Debunking Human Health Risk, APPENDIX D - LBAMspray.com

A P P E N D I X D 

Human Health Risk Assessment

LIGHT BROWN APPLE MOTH ERADICATION PROGRAM 

Draft 

Programmatic Environmental Impact Report 

HUMAN HEALTH RISK ASSESSMENT 

JULY 2009 

Prepared by 

Prepared for 

ENVIRON International Corporation 

6001 ShellmoundStreet, Suite 700 

Emeryville, CA 94608 

T 510.420.2583 • F 510.655.9517 

ENTRIX, Inc. 

2300 Clayton Road, Suite 200 

Concord, CA 94520 

T 925.935.9920 • F 925.935.5368 

California Department of Food and Agriculture 

Plant Health and Pest Prevention Services 

1220 N Street 

Sacramento, CA 95814 

T 916.445.2180 • F 916.445.2427

Table of Contents 

Executive Summary ...............................................................................................................1-1 

S E C T I O N D 1 Introduction..........................................................................................1-1 

S E C T I O N D 2 Problem Formulation ..........................................................................2-1 

D2.1 Program Area............................................................................2-1 

D2.1.1 Program Area Location................................................2-1 

D2.2 Overview of Proposed Program Alternatives ...........................2-2 

D2.2.1 No Program Alternative...............................................2-3 

D2.2.2 Alternative Mating Disruption (MD): MD-1, 

Twist Ties; MD-2, Ground; MD-3, Aerial ..................2-3 

D2.2.3 Male Moth Attractant (MMA) Alternative..................2-4 

D2.2.4 Organic Treatment Alternative ....................................2-4 

D2.3 Management Goals and Assessment Endpoints for 

Estimating Risk.........................................................................2-4 

D2.3.1 Risk Hypothesis...........................................................2-5 

D2.3.2 Human Health Assessment Methods ...........................2-5 

S E C T I O N D 3 Toxicity Assessment.............................................................................3-1 

D3.1 No Program: Continued Use of Currently Approved 

Pesticides by Individual Growers and Households...................3-3 

D3.1.1 Chlorpyrifos.................................................................3-3 

D3.1.2 Carriers and Dispersants of Chlorpyrifos ..................3-14 

D3.1.3 Lambda-Cyhalothrin..................................................3-24 

D3.1.4 Carriers and Dispersants of Lambda-Cyhalothrin .....3-35 

D3.1.5 Permethrin .................................................................3-40 

D3.1.6 Inert Ingredients of Permethrin E-Pro .......................3-58 

D3.2 Alternative Mating Disruption (MD): MD-1, Twist Ties; 

MD-2, Ground; MD-3, Aerial.................................................3-61 

D3.2.1 HERCON Disrupt Bio-Flake ® LBAM ......................3-62 

D3.2.2 Toxicity of HERCON Disrupt Bio-Flake ® 

LBAM........................................................................3-66 

D3.2.3 CheckMate ® LBAM-F...............................................3-69 

D3.2.4 Isomate ® -LBAM PLUS .............................................3-75 

D3.2.5 Environmental Transport and Degradation of 

Isomate.......................................................................3-76 

JULY 2009 

App D_HHRA_508.doc D-i

LIGHT BROWN APPLE MOTH ERADICATION PROJECT 

APPENDIX D 

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D3.2.6 SPLAT LBAM.......................................................3-78 

D3.2.7 Toxicity of SPLAT LBAM....................................3-79 

D3.2.8 No Mate ® LBAM MEC .............................................3-81 

D3.2.9 Toxocity of NoMate ® LBAM MEC ..........................3-83 

D3.2.10 Interpretation of Human Toxicity Based on 

Animal Studies ..........................................................3-84 

D3.3 Male Moth Attractant (MMA) Alternative.............................3-84 

D3.4 Organic-Approved Insecticides (Alternatives Bt and S) ........3-85 

D3.4.1 Spinosad.....................................................................3-85 

D3.4.2 Bacillus thuringiensis (Bt) .........................................3-92 

D3.4.3 Interpretation of Human Toxicity............................3-100 

S E C T I O N D 4 Exposure Assessment...........................................................................4-1 

D4.1 Exposure Pathways and Exposure Point Concentrations..........4-1 

D4.2 Development of Exposure Point Concentrations......................4-1 

D4.2.1 Exposure Point Concentrations Developed from 

Air Modeling ...............................................................4-2 

D4.2.2 Additional Estimation Techniques Used to 

Calculate Exposure Point Concentrations....................4-3 

D4.3 Intakes.......................................................................................4-4 

D4.3.1 Ingestion and Inhalation Exposure ..............................4-4 

D4.3.2 Intake Parameters.........................................................4-7 

D4.4 Human Receptor Populations .................................................4-14 

D4.4.1 Nursery/Program Workers.........................................4-14 

D4.4.2 Agricultural Workers.................................................4-14 

D4.4.3 Adult and Child Residents.........................................4-14 

D4.4.4 Adult Gardeners.........................................................4-15 

D4.4.5 Adult and Child Recreational Park Users..................4-15 

D4.5 No Program Alternative..........................................................4-15 

D4.6 Mating Disruption (MD) Alternative......................................4-24 

D4.6.1 Alternative MD-1.......................................................4-24 




D4.8 Organic treatment ALTERNATIVE.......................................4-43 

S E C T I O N D 5 Risk Characterization..........................................................................5-1 

D5.1 Methods Used to Characterize Human Health Risk .................5-1 

D-ii App D_HHRA_508.doc JULY 2009

TABLE OF CONTENTS 

D5.1.1 Toxicity Values............................................................5-2 

D5.2 Interpretation of Results ...........................................................5-7 

D5.3 No Program...............................................................................5-7 

D5.3.1 Nursery/Program Workers and Agricultural 

Workers .......................................................................5-7 

D5.3.2 Adult and Child Residents...........................................5-9 

D5.3.3 Adult Gardener ..........................................................5-12 

D5.3.4 Adult and Child Recreational Park Users..................5-13 

D5.4 Mating Disruption Alternative................................................5-15 

D5.4.1 MD-1 .........................................................................5-15 

D5.4.2 MD-2 .........................................................................5-18 

D5.4.3 MD-3 .........................................................................5-21 


D5.5.1 Nursery/Program Workers.........................................5-25 

D5.5.2 Agricultural Workers.................................................5-25 


D5.5.4 Adult Resident Gardener ...........................................5-28 

D5.5.5 Adult and Child Recreational Park User....................5-29 

D5.6 Organic Treatment Alternative ...............................................5-32 

D5.6.1 Nursery/Program Workers and Agricultural 

Workers .....................................................................5-32 


D5.6.3 Adult Resident Gardener ...........................................5-35 

D5.6.4 Adult and Child Recreational Park User....................5-35 

S E C T I O N D 6 Human Health Risk Conclusions and Uncertainties ........................6-1 

D6.1 Uncertainties in the Assessment of Human Health Risks.........6-1 

D6.2 Conclusions on Human Health Risks .......................................6-4 

D6.2.1 No Program..................................................................6-4 

D6.2.2 Mating Disruption (MD) Alternative...........................6-4 

D6.2.3 Male Moth Attractant (MMA) Alternative..................6-6 

D6.2.4 Organic Treatment Alternative ....................................6-7 

S E C T I O N D 7 References.............................................................................................7-1 

JULY 2009 

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T A B L E S 

Table D1-1 Condensed Summary of LBAM Eradication Alternatives Evaluated in the EIR ............1-2 

Table D3-1 Chemical Hazard Classifications .....................................................................................3-1 

Table D3-2 

Table D3-3 

Table D3-4 

Table D3-5 

Physical and Chemical Properties of Chlorpyrifos..........................................................3-5 

Acute Toxicity of Chlorpyrifos........................................................................................3-8 

Genotoxicity of Chlorpyrifos in vivo.............................................................................3-11 

Toxicity Criteria for Chlorpyrifos..................................................................................3-13 

Table D3-6 Chemical and Physical Properties of 1,2,4-trimethylbenzene .......................................3-14 

Table D3-7 

Table D3-8 

Chemical and Physical Properties of Ethylbenzene.......................................................3-15 

Chemical and Physical Properties of Ethyltoluene........................................................3-15 

Table D3-9 Chemical and Physical Properties of Xylenes ...............................................................3-16 

Table D3-10 Noncancer Toxicity Criteria for Ethylbenzene ..............................................................3-21 

Table D3-11 

Cancer Criteria for Ethylbenzene...................................................................................3-22 

Table D3-12 Physical-Chemical Properties of Lambda-Cyhalothrin .................................................3-27 

Table D3-13 Toxicity Profile of Lambda-Cyhalothrin .......................................................................3-30 

Table D3-14 

Table D3-15 

Genotoxicity of Type II Pyrethroids In Vivo.................................................................3-32 

Toxicity Criteria for Lambda-Cyhalothrin.....................................................................3-35 

Table D3-16 Physical and Chemical Properties of Naphthalene ........................................................3-36 

Table D3-17 Physical and Chemical Properties of Propylene Glycol ................................................3-37 

Table D3-18 

Chemical Property Data of Permethrin..........................................................................3-41 

Table D3-19 Summary of Subchronic Toxicity and Studies of Permethrin .......................................3-45 

Table D3-20 

Table D3-21 

Summary of Chronic Toxicity and Carcinogenicity of Permethrin...............................3-51 

Results of Studies of the Genotoxicity of Permethrin....................................................3-54 

Table D3-22 Noncancer Oral Toxicity Criteria for Permethrin ..........................................................3-56 

Table D3-23 

Table D3-24 

Noncancer Inhalation Toxicity Criteria for Permethrin.................................................3-58 

Chemical and Physical Properties of Stoddard Solvent.................................................3-59 

Table D3-25 General Characteristics of Five LBAM-Specific Pheromones Considered for Use ......3-61 

Table D3-26 

Table D3-27 

Table D3-28 

Physical and Chemical Properties of HERCON Disrupt Bio-Flake® LBAM...............3-63 

Sub-chronic toxicity data for four SCLPs (1-nonanol, 1-decanol, 2-trans,4-transdecadienal, 

and 1-dodecanol).........................................................................................3-66 

Summary of Mammalian Toxicity Studies for HERCON Disrupt Bio-Flake® 

LBAM............................................................................................................................3-67 

Table D3-29 Physico-Chemical Properties of CheckMate® LBAM-F ..............................................3-70 

Table D3-30 

Table D3-31 

Table D3-32 

Summary of Mammalian Toxicity Studies for CheckMate® LBAM-F........................3-72 

Physical and Chemical Properties of CheckMate® LBAM-F Ingredients....................3-72 

Toxicity Studies of CheckMate® LBAM-F Inert Ingredients.......................................3-74 

D-iv App D_HHRA_508.doc JULY 2009


Table D3-33 

Table D3-34 

Table D3-35 

Physical and Chemical Properties of Isomate Twist Ties..............................................3-76 

Physical and Chemical Properties of Isomate Twist Ties..............................................3-77 

Physical-Chemical Properties of Isomate® – LBAM Plus Twist-Ties (properties 

of dispenser)...................................................................................................................3-77 

Table D3-36 Physico-Chemical Properties of SPLAT LBAM .......................................................3-79 

Table D3-37 Summary of Mammalian Toxicity Reference Values for SPLAT LBAM ................3-80 

Table D3-38 Physico-Chemical Properties of NoMate® LBAM MEC .............................................3-82 

Table D3-39 

Table D3-40 

Summary of Toxicity Data for NoMate® LBAM MEC................................................3-83 

Toxicity Values for BIO-TAC®....................................................................................3-84 

Table D3-41 Physical and Chemical Properties of Spinosyns A and D .............................................3-86 

Table D3-42 

Acute Toxicity of Technical Grade Spinosad and Spinosyn A and D...........................3-88 

Table D3-43 Acute Mammalian Toxicity of Bacillus thuringiensis kurstaki .....................................3-98 

Table D3-44 Subchronic and Chronic Toxicity of Bacillus thuringiensis kurstaki ............................3-99 

Table D3-45 

Post-spray Symptoms Reported by Ground-spray Workers and Controls1.................3-101 

Table D3-46 Ground Spray Worker Exposures to Btk .....................................................................3-103 

Table D4-1 Exposure Assumptions ....................................................................................................4-7 

Table D4-2 

Table D4-3 

Dermal Absorption Factors............................................................................................4-11 

Intake Factors.................................................................................................................4-12 

Table D4-4 Exposure Point Concentrations – No Program Alternative ...........................................4-19 

Table D4-5 

Table D4-6 

Chemical-Specific Intakes Factors for Nursery/Program Workers – No Program 

Alternative .....................................................................................................................4-19 

Chemical-Specific Intakes Factors for Agricultural Workers – No Program 

Alternative .....................................................................................................................4-20 

Table D4-7 Chemical-Specific Intakes for Adult Residents – No Program Alternative ..................4-20 

Table D4-8 

Table D4-9 

Chemical-Specific Intakes for Child Residents – No Program Alternative...................4-21 

Chemical-Specific Intakes for Residential Adult Gardener – No Program 

Alternative .....................................................................................................................4-22 

Table D4-10 Chemical-Specific Intakes for Adult Park User – No Program Alternative ..................4-22 

Table D4-11 Chemical-Specific Intakes for Child Park User – No Program Alternative ..................4-23 

Table D4-12 Exposure Point Concentrations – Mating Disruption Alternative, Twist Ties ..............4-24 

Table D4-13 

Table D4-14 

Table D4-15 

Table D4-16 

Chemical-Specific Intakes for Nursery/Program Workers and Agricultural 

Workers – Mating Disruption Alternative, Twist Ties ..................................................4-24 

Chemical-Specific Intakes for Adult and Child Resident – Mating Disruption 

Alternative, Twist Ties ..................................................................................................4-25 

Chemical-Specific Intakes for Residential Adult Gardener – Mating Disruption 

Alternative, Twist Ties ..................................................................................................4-29 

Chemical-Specific Intakes for Adult and Child Recreational Park User – Mating 

Disruption Alternative, Twist Ties ................................................................................4-29 

JULY 2009 

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Table D4-17 

Exposure Point Concentrations – Mating Disruption Alternative, Ground 

Application.....................................................................................................................4-30 

Table D4-18 Chemical-Specific Intakes for Nursery/Program and Agricultural Workers – 

Mating Disruption Alternative, Ground Application.....................................................4-30 

Table D4-19 

Table D4-20 

Table D4-21 

Table D4-22 

Table D4-23 

Table D4-24 

Table D4-25 

Table D4-26 

Table D4-27 

Table D4-28 

Table D4-29 

Table D4-30 

Table D4-31 

Table D4-32 

Table D4-33 

Table D4-34 

Table D4-35 

Table D4-36 

Table D4-37 

Table D4-38 

Table D4-39 

Chemical-Specific Intakes for Adult Resident – Mating Disruption Alternative, 

Ground Application .......................................................................................................4-31 

Chemical-Specific Intakes for Child Resident – Mating Disruption Alternative, 



Alternative, Ground Application ...................................................................................4-32 

Chemical-Specific Intakes for Adult Park User – Mating Disruption Alternative, 


Chemical-Specific Intakes for Child Park User – Mating Disruption Alternative, 


Exposure Point Concentrations – Mating Disruption Alternative, Aerial 

Application.....................................................................................................................4-33 


Workers – Mating Disruption Alternative, Aerial Application .....................................4-34 

Chemical-Specific Intakes for Adult and Child Residents – Mating Disruption 

Alternative, Aerial Application......................................................................................4-35 


Alternative, Aerial Application......................................................................................4-35 

Chemical-Specific Intakes for Adult and Child Recreational Park User – Mating 

Disruption Alternative, Aerial Application....................................................................4-36 

Exposure Point Concentrations – Male Moth Attractant...............................................4-37 

Chemical-Specific Intakes Factors for Nursery/Program Workers – Male Moth 

Attractant .......................................................................................................................4-37 

Chemical-Specific Intakes Factors for Agricultural Workers – Male Moth 

Attractant .......................................................................................................................4-38 

Chemical-Specific Intake Factors for Adult Resident – Male Moth Attractant.............4-39 

Chemical-Specific Intake Factors for Child Resident – Male Moth Attractant.............4-40 

Chemical-Specific Intakes for Residential Adult Gardener – Male Moth 

Attractant .......................................................................................................................4-41 

Chemical-Specific Intakes for Adult Recreational Park User – Male Moth 

Attractant .......................................................................................................................4-42 

Chemical-Specific Intakes for Child Recreational Park User – Male Moth 

Attractant .......................................................................................................................4-43 

Exposure Point Concentrations – Organic Treatment Alternative.................................4-44 


Workers – Organic Treatment Alternative.....................................................................4-44 

Chemical-Specific Intakes for Adult and Child Resident – Organic Treatment 

Alternative .....................................................................................................................4-45 

D-vi App D_HHRA_508.doc JULY 2009


Table D4-40 

Table D4-41 

Table D5-1 

Table D5-2 

Chemical-Specific Intakes for Residential Adult Gardener – Organic Treatment 

Alternative .....................................................................................................................4-45 

Chemical-Specific Intakes for Adult and Child Recreational Park User – Organic 

Treatment Alternative ....................................................................................................4-46 

Toxicity Values................................................................................................................5-5 

Nursery/Program Worker Hazard Quotients – No Program Alternative.........................5-8 

Table D5-3 Agricultural Worker – No Program Alternative ..............................................................5-9 

Table D5-4 

Table D5-5 

Table D5-6 

Adult Resident Cancer Risks and Hazard Quotients – No Program Alternative...........5-10 

Child Resident Hazard Quotient – No Program Alternative..........................................5-11 

Residential Adult Gardener Cancer Risks and Hazard Quotient – No Program 

Alternative .....................................................................................................................5-12 

Table D5-7 Adult Park User Cancer Risks and Hazard Quotients – No Program Alternative .........5-13 

Table D5-7 Adult Park User Cancer Risks and Hazard Quotients – No Program Alternative .........5-14 

Table D5-8 Child Park User Cancer Risks and Hazard Quotients – No Program Alternative .........5-15 

Table D5-9 

Table D5-10 

Table D5-11 

Nursery/Program Worker Hazard Quotients – Mating Disruption Alternative, 

Twist Ties ......................................................................................................................5-16 

Agricultural Worker Hazard Quotients – Mating Disruption Alternative, Twist 

Ties ................................................................................................................................5-16 

Adult Resident Hazard Quotients – Mating Disruption Alternative, Twist Ties...........5-17 

Table D5-12 Child Resident Hazard Quotients – Mating Disruption Alternative, Twist Ties ...........5-17 

Table D5-13 

Residential Adult Gardener Hazard Quotients – Mating Disruption Alternative, 

Twist Ties ......................................................................................................................5-17 

Table D5-14 Adult Park User Hazard Quotients – Mating Disruption Alternative, Twist Ties .........5-18 

Table D5-15 Child Park User Hazard Quotients – Mating Disruption Alternative, Twist Ties .........5-18 

Table D5-16 

Table D5-17 

Table D5-18 

Table D5-19 

Table D5-20 

Table D5-21 

Table D5-22 

Table D5-23 



Agricultural Worker Hazard Quotients – Mating Disruption Alternative, Ground 

Application.....................................................................................................................5-19 

Adult Resident Hazard Quotients – Mating Disruption Alternative, Ground 

Application.....................................................................................................................5-20 

Child Resident Hazard Quotients – Mating Disruption Alternative, Ground 

Application.....................................................................................................................5-20 



Adult Park User Hazard Quotients – Mating Disruption Alternative, Ground 

Application.....................................................................................................................5-21 

Child Park User Hazard Quotients – Mating Disruption Alternative, Ground 

Application.....................................................................................................................5-21 


Aerial Application..........................................................................................................5-22 

JULY 2009 

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DRAFT PEIR 


Table D5-24 

Table D5-25 

Table D5-26 

Table D5-27 

Table D5-28 

Table D5-29 

Table D5-30 

Agricultural Worker Hazard Quotients – Mating Disruption Alternative, Aerial 

Application.....................................................................................................................5-22 

Adult Resident Hazard Quotients – Mating Disruption Alternative, Aerial 

Application.....................................................................................................................5-23 

Child Resident Hazard Quotients – Mating Disruption Alternative, Aerial 

Application.....................................................................................................................5-23 


Aerial Application..........................................................................................................5-23 

Adult Park User Hazard Quotients – Mating Disruption Alternative, Aerial 

Application.....................................................................................................................5-24 

Child Park User Hazard Quotients – Mating Disruption Alternative, Aerial 

Application.....................................................................................................................5-24 

Nursery/Program Worker Cancer Risks and Hazard Quotients – Male Moth 

Attractant .......................................................................................................................5-25 

Table D5-31 Agricultural Worker Cancer Risks and Hazard Quotients – Male Moth Attractant ......5-26 

Table D5-32 

Table D5-33 

Table D5-34 

Table D5-35 

Adult Resident Cancer Risks and Hazard Quotients – Male Moth Attractant...............5-27 

Child Resident Cancer Risks and Hazard Quotients – Male Moth Attractant...............5-28 

Residential Adult Gardener Cancer Risks and Hazard Quotients – Male Moth 

Attractant .......................................................................................................................5-28 

Adult Park User Cancer Risks and Hazard Quotients – Male Moth Attractant.............5-30 

Table D5-36 Child Park User Cancer Risks and Hazard Quotients – Male Moth Attractant .............5-31 

Table D5-37 Nursery/Program Worker Hazard Quotients–Organic Treatment Alternative ..............5-33 

Table D5-38 

Agricultural Worker Hazard Quotients – Organic Treatment Alternative.....................5-33 

Table D5-39 Adult Resident Hazard Quotients – Organic Treatment Alternative .............................5-34 

Table D5-40 Child Resident Hazard Quotients – Organic Treatment Alternative .............................5-34 

Table D5-41 Residential Adult Gardener Hazard Quotients – Organic Treatment Alternative .........5-35 

Table D5-42 Adult Park User Hazard Quotients – Organic Treatment Alternative ...........................5-36 

Table D5-43 

Child Park User Hazard Quotients – Organic Treatment Alternative............................5-36 

D-viii App D_HHRA_508.doc JULY 2009


F I G U R E S 

Figure D3-1 Chemical Structure of Chlorpyrifos (ATSDR 1997) .......................................................3-4 

Figure D3-2 

Structure of 1,2,4-Trimethylbenzene (from National Library of Medicine)..................3-14 

Figure D3-3 Structure of Ethylbenzene (from National Library of Medicine) ..................................3-15 

Figure D3-4 Structure of Meta-Ethyltoluene (from National Library of Medicine) ..........................3-16 

Figure D3-5 

Figure D3-6 

Figure D3-7 

Figure D3-8 

Figure D3-9 

Structure of Xylenes (from National Library of Medicine)...........................................3-16 

Chemical Structure of Lambda-Cyhalothrin..................................................................3-25 

Structure of naphthalene (from National Library of Medicine).....................................3-36 

Structure of Propylene Glycol (from National Library of Medicine)............................3-37 

Permethrin is Produced Through the Chemical Reaction of a Carboxylic Acid 

with an Alcohol (ATSDR 2003)....................................................................................3-40 

Figure D3-10 Structure of Triacetin .....................................................................................................3-59 

Figure D3-11 

Molecular Structure of (Z)-11-Tetradecenyl Acetate, a Typical Straight Chain 

Lepidopteran Pheromone (SCLP)..................................................................................3-63 

Figure D3-12 Chemical Structure of Spinosad and Metabolites (from Gao et al. 2007) .....................3-85 

Figure D3-13 

Figure D4-1 

Figure D4-2 

Figure D4-3 

Sympton Frequency vs Btk Exposure Group...............................................................3-102 

Conceptual Site Model for Potential Exposure Pathways for Chemicals Released 

by the Male Moth Attractant, Organic Treatment, sand No Program Alternatives .......4-17 

Conceptual Site Model for Potential Exposure Pathways for Pheromones 

Released by Ground Application Methods through the Mating Disruption 

Alternative .....................................................................................................................4-27 

Potential Exposure Pathways for Pheromones Released by Aerial Application 

under the Mating Disruption Alternative.......................................................................4-28 

JULY 2009 

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A B B R E V I A T I O N S & A C R O N Y M S 

°C degrees Centigrade 

APHIS 

ATSDR 

BCF 

BIU 

Bt 

Btk 

CAS 

CDFA 

CEQA 

CFR 

CFU 

ChE 

CheckMate 

CI 

Cry 

CSF 

CSM 

CWA 

DOD 

DPR 

EIR 

EPC 

FAO 

FDA 

FIFRA 

FOB 

GABA 

GD 

GRAS 

HERCON 

HI 

HQ 

HSDB 

Animal and Plant Health Inspection Service 

Agency for Toxic Substances and Disease Registry 

bioconcentration factor 

billion international units 

Bacillus thuringiensis 

Bacillus thuringiensis kurstaki 

Chemical Abstracts Service 

California Department of Food and Agriculture 

California Environmental Quality Act 

Code of Federal Regulations 

colony forming unit 

cholinesterase 

CheckMate ® LBAM-F - pheromone treatment formulation 

confidence interval 

crystal 

cancer slope factor 

conceptual site model 

Clean Water Act 

Department of Defense 

California Department of Pesticide Regulation 

Environmental Impact Report 

exposure point concentration 

Food and Agricultural Organization of the United Nations 

United States Food and Drugs Administration 

Federal Insecticide, Fungicide and Rodenticide Act 

functional observational battery 

γ-aminobutyric acid 

gestation day 

Generally Recognized as Safe 

HERCON Disrupt Bio-Flake ® LBAM - pheromone treatment formulation 

hazard index 

hazard quotient 

Hazardous Substances Database 

D-x App D_HHRA_508.doc JULY 2009


IARC International Agency for Research on Cancer 

IPCS International Program on Chemical Safety 

IRIS Integrated Risk Information System 

Isomate Isomate ® LBAM Plus - LBAM pherome formulation 

ISCA ISCA Technologies 

IUPAC International Union of Pure and Applied Chemistry 

ip 

intraperitoneal 

iv 

intravenous 

JEFCA Joint Environmental Committee on Food Additives 

JMPR Joint Meeting on Pesticide Registration 

K OC 

K OW 

LBAM 

LC 50 

LD 50 

LEL 

LLNA 

organic carbon partition coefficient 

octanol-water partition coefficient 

Light Brown Apple Moth 

median lethal concentration for 50% of the test animals 

median lethal dose for 50% of the test animals 

lowest effect level 

localized lymph node assay 

LOAEL/LOEL lowest observed adverse effect level/lowest observed effect level 

MD Mating Disruption 

MLC minimum lethal concentration 

MMA male moth attractant 

MOE margin-of-exposure 

MRID Master Record Identification Number 

MRL minimal risk level 

MSDS material safety datasheet 

nAChR nicotinic acetylcholine receptors 

NOAEL/NOEL no observed adverse effect level/no observed effect level 

NOEC no observed adverse effect concentration 

NoMate NoMate ® LBAM MEC - pheromone treatment formulation 

NPTN National Pesticide Telecommunications Network 

NRC National Research Council 

NTP National Toxicology Program 

OECD Organization for Economic Cooperation and Development 

OEHHA California’s Office of Environmental Health Hazard Assessment 

OPP US Environmental Protection Agency Office of Pesticide Programs 

ORNL Oak Ridge National Laboratory 

JULY 2009 

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PEIR 

PND 

ppm 

RBC 

REL 

RfC 

RfD 

RR 

S 

SCLP 

SIT 

SPLAT 

TCP 

TOXNET 

TSCA 

TSH 

UF 

USDA 

USEPA 

UV 

WHO 

Programmatic Environmental Impact Report 

post-natal day 

parts per million 

red blood cell 

reference exposure level 

reference concentration 

reference dose 

relative risk 

spinosad 

Straight Chain Lepidopteran Pheromone 

Sterile Insect Technique 

SPLAT LBAM - pheromone treatment formulation 

3,5,6-trichloro-2-pyridinol 

database maintained by the National Library of Medicine 

Toxic Substances Control Act 

thyroid stimulating hormone 

uncertainty factor 

United States Department of Agriculture 

United States Environmental Protection Agency 

ultraviolet 

World Health Organization 

D-xii App D_HHRA_508.doc JULY 2009

Executive Summary 

This human health risk assessment (HHRA) evaluates the potential health effects from those 

treatment methodologies that comprise the Light Brown Apple Moth (LBAM) Program 

Alternatives. The HHRA focuses specifically on those alternatives that involve the use of 

chemical or biologically based pesticides; these are the No Program, Mating Disruption, Male 

Moth Attractant, and Organic-Approved alternatives. Potential health effects were not evaluated 

for the Inundative Parasitic Wasp Release or the Sterile Insect Technique alternatives. 

A goal of this HHRA was to use a consistent set of exposure assumptions in conjunction with 

predicted environmental concentrations of Program chemicals to evaluate the potential health 

effects associated with each Program alternative. This approach allows direct comparisons 

between the health effects attributable to each alternative, which in turn, can be used to inform 

the selection of one or more alternatives by California’s Department of Food and Agriculture 

(CDFA). 

The assessment was necessarily broadly focused, as the state-wide extent of the Program 

precludes characterization of potential effects to specific individuals or populations. Instead, this 

screening-level evaluation assessed the potential for adverse health effects using conservative 

exposure assumptions designed to be protective of all populations, including the most sensitive. 

The protection of sensitive populations was also a key consideration when toxicity criteria were 

selected or derived. 

This evaluation began by reviewing the toxicological literature on each of the pesticides 

regarding its potential for human toxicity. This review focused on identifying regulatory 

literature or other information sources that defined dose response relationships for noncancer 

and/or cancer endpoints. For those pesticides with noncancer effects, the review focused on 

identifying a no observed adverse effect level (NOAEL) or a lowest adverse effect level 

(LOAEL) for each exposure route and exposure duration (depending on availability). These 

NOAELS or LOAELS typically provide the basis for the development of noncancer reference 

toxicity criteria, which in turn are used to interpret the significance of calculated human doses. 

For the two carcinogens evaluated, permethrin and ethylbenzene, the toxicity evaluation resulted 

in the selection of toxicity criteria to characterize both noncancer effects and the risk of cancer. 

Cancer risk is estimated by multiplying the estimated dose by a toxicity criterion known as a 

cancer slope factor (CSF). That CSF represents the theoretical upper bound probability of excess 

cancer cases occurring in an exposed population assuming a lifetime exposure to the chemical. 

Details of the methodology used to quantify adverse effects from pesticides considered for use 

are provided in Section D5. 

Depending on the availability of data for each pesticide, toxicity criteria (e.g., reference doses 

[RfDs], CSFs) were identified for one or more routes of exposure. These toxicity criteria were 

obtained from documents and on-line sources from the United States Environmental Protection 

Agency (USEPA) Office of Pesticide Programs (OPP), Office of Environmental Health Hazard 

Assessment (OEHHA), UESPA Integrated Risk Information System (IRIS), and the Agency for 

Toxic Substances and Disease Registry (ATSDR). If a criterion was not available from these 

sources, information in other regulatory documents or the primary literature was relied on. When 

JULY 2009 App D_HHRA_508.doc D1-1



DRAFT PEIR 


toxicity criteria were developed for this assessment (e.g., from data in the regulatory or primary 

literature), uncertainty factors (UFs) were incorporated to address data gaps, effects on sensitive 

receptors, and variability in study and/or human populations, an approach that is consistent with 

methods of the USEPA, OEHHA, and the ATSDR. 

To characterize potential human exposure to pesticides considered for use, a number of 

hypothetical human receptor populations were identified: Nursery/Program Workers, 

Agricultural Workers, Adult Residents, Child Residents, Adult Gardeners, and Adult and Child 

Recreational Park Users. The Child Residents and Child Recreational Park Users represent the 

sensitive receptor populations considered in this assessment. Each of these receptor populations 

was evaluated under each alternative, with exposure (dose) quantified for inhalation, incidental 

ingestion of soil, dermal contact with soil or vegetation, and ingestion of produce. Using 

conservative air dispersion modeling results (Appendix C) that generated predicted 

concentrations of pesticides in air, and on soil and vegetation, chemical-specific intakes were 

calculated for each chemical for each alternative (as appropriate). 

For chemicals with noncarcinogenic effects, these intakes were compared to toxicity criteria(the 

RfD) to estimate whether the calculated doses might exceed the toxicity criterion (if a calculated 

dose exceeds the criterion. This comparison yields a ration (of the dose to the RfD) known as a 

hazard quotient (HQ – for a single exposure pathway), or a hazard index (HI –calculated for 

multiple pathways or for exposure to multiple chemicals). If the value of the HQ or the HI 

exceeds 1, it indicates a potential for adverse health effects to occur. For the carcinogens 

permethrin and ethylbenzene, predicted intakes were multiplied by a CSF to yield an estimate of 

the probability (risk) of cancer, e.g., 1 x 10 -6 (one in a million). For certain substances and/or 

certain exposure pathways, no regulatory agency had derived toxicity criteria, and the toxicity 

data were not sufficient to support the derivation of such values. In these instances, it was not 

possible to quantify the relationship between exposure and the potential for adverse health 

effects. Instead, a semi-quantitative comparison was made of the likelihood of adverse effects by 

comparing the predicted intake to a range of values obtained from toxicity testing. 

SUMMARY OF RESULTS 

The No Program Alternative addresses the use of spinosad, Btk, lambda-cyhalothrin, 

permethrin, or chlorpyrifos by private landowners to control the LBAM, while maintaining state 

and federal quarantines. Because there is no basis to assume that more than one of these 

chemicals would be used at a given time, additive effects were not evaluated. Cancer risks above 

1 x 10 -6 were identified for Nursery/Program Workers, Adult and Child Residents, Adult 

Gardeners, and Adult and Child Park Users. All of these risks are attributable to dermal doses 

potentially acquired from contact with permethrin-contaminated vegetation. Chronic noncancer 

HIs exceeded the threshold value of 1 for Nursery/Program Workers (lambda-cyhalothrin and 

chlorpyrifos); Agricultural Workers (chlorpyrifos), Adult Resident (chlorpyrifos), Child Resident 

(lambda-cyhalothrin and chlorpyrifos, Adult Gardener (chlorpyrifos), Adult Park User 

(chlorpyrifos), and the Child Park User (chlorpyrifos). 

For the MD Alternative, potential exposures to LBAM pheromone formulations were evaluated 

for twist ties (MD-1, Isomate), ground-based application (MD-2, SPLAT and HERCON), or 

aerial application (MD-3, SPLAT and HERCON). 

D1-2 App D_HHRA_508.doc JULY 2009

EXECUTIVE SUMMARY 

The HQs for both acute and subchronic inhalation exposures calculated for Alternative MD-1 

were all very low, approximately one million to one hundred thousand-fold below the threshold 

value of 1. In addition, both child receptor populations were evaluated for potential health effects 

attributed to the accidental ingestion of a twist tie. The HI from this ingestion exposure is 0.05, 

indicating that no adverse effects are expected in the unlikely event that a child ingested (or 

chewed on) a twist tie. 

Estimated chronic inhalation intakes of the LBAM pheromones were also low, ranging from 

approximately one millionth to several millionths of a mg/kg-day. There is no information to 

indicate that long-term exposures to the pheromones at these very low levels will be associated 

with adverse effects. The low subchronic HQs for Isomate exposures provide further support for 

the conclusion that long-term exposures are not likely to be a concern (also see OEHHA, 2009b). 

As reviewed in Section D3, there is no evidence to indicate that SCLPs are genotoxic or 

carcinogenic, and their structural similarity to certain fatty acids indicates they are likely to be 

metabolized into substances of “no known toxicological concern” (OEHHA, 2009b). 

Accordingly, it is considered unlikely that long-term (or short-term) use of the twist ties will 

result in any impacts on human health. OEHHA (2009b), who had access to information on the 

additives in Isomate, has also determined that the additives, as well as exposure to the product 

itself, “are not likely to pose a health hazard to adults and children.” 

The acute and subchronic inhalation HQs for all receptor populations evaluated under 

Alternative MD-2 are approximately a hundred to a thousand fold lower than the threshold 

value of 1. Because of these low HQs, adverse effects from acute and subchronic inhalation 

exposures are not considered likely. Chronic exposures to the pheromones in SPLAT and 

HERCON -whether by inhalation, incidental ingestion of soil, or dermal contact - could not be 

quantitatively evaluated due to the absence of suitable toxicity criteria. However, the predicted 

chronic intakes of the pheromones are low, ranging from approximately several hundredths of a 

mg per kg-day to less than a millionth of a mg/kg-body weight (depending on exposure 

pathway). As noted for the twist ties, there are no data to indicate that exposures to SCLPs at 

these very low levels are associated with adverse effects, and, for the reasons discussed under 

Alternative MD-1, it is considered unlikely that long-term exposure to the pheromones released 

from SPLAT or HERCON would result in any impacts on human health. 

Although the quantitative analyses of potential health effects (see preceding discussion) indicates 

that adverse effects are not likely from exposures to the pheromones in SPLAT or HERCON, 

there is some information which indicates that the LBAM pheromones may cause dermal 

sensitization following direct contact (OEHHA 2008b; OEHHA et al 2008). Results from dermal 

sensitization assays indicate that SPLAT may have some sensitizing potential (see Section D3). 

HERCON (manufactured as a flake, with the pheromones sandwiched between two starch 

layers) could only be tested in one of the two sensitization assays – the results from that assay 

were negative regarding the products sensitization potential. The likelihood of sensitization from 

exposure to the pheromones cannot be quantified because there is not sufficient information 

available to determine what levels of pheromones, what types of exposure, or what other 

variables may be involved in this response in humans. Despite the uncertainties regarding the 

potential for sensitization, the possibility that dermal sensitization could occur from contact with 

LBAM pheromone-containing products cannot be excluded (OEHHA 2008b) 




DRAFT PEIR 


Aerial treatment (Alternative MD-3) is expected to release pheromones directly to air, with 

subsequent deposition to soil and vegetation. The calculated acute and subchronic inhalation 

HQs range from approximately a thousand to ten thousand fold or more below the reference HQ 

of 1. On the basis of these low HQs, adverse effects from acute and subchronic inhalation 

exposures are not considered likely. 

As was the case for the other application methods (twist ties, ground application), chronic 

exposures could not be quantitatively evaluated due to the absence of chronic toxicity criteria for 

SCLPs. However, the estimated chronic intakes of the pheromones are low for this mode of 

application as well, ranging from approximately one hundredth of a mg per kg-day to less than a 

millionth of a mg/kg body weight-day (depending on pathway). It is considered unlikely that 

long-term exposure to the pheromones released from SPLAT or HERCON will result in adverse 

impacts on human health. 

Because the same products are being considered for both the ground and aerial applications, the 

comments regarding the potential for dermal and respiratory sensitization provided above are 

also relevant to SPLAT and HERCON applied aerially. 

In the MMA Alternative, the pheromone formulation SPLAT will be applied with Permethrin 

E-Pro to attract and kill LBAM. The permethrin product is a formulation that contains 

ethylbenzene and 1,2,4-trimethylbenzene as well as permethrin as the active ingredient. Because 

permethrin and ethylbenzene are classified as carcinogens, carcinogenic risks attributable to 

potential permethrin and ethylbenzene exposure were calculated, as well as non-cancer HIs from 

permethrin, ethylbenzene, and 1,2,4-trimethylbenzene. Additive HIs were calculated to address 

potential noncancer effects from concurrent exposures to permethrin, ethylbenzene, and 1,2,4- 

trimethylbenzene, and additive cancer risks were calculated to address risks from concurrent 

exposures to the carcinogens permethrin and ethylbenzene. 

Cancer risks above 1 x 10 -6 , all attributable to permethrin, were calculated for Nursery/Program 

Workers, Adult and Child Residents, Adult Gardeners, and both Adult and Child Park Users. 

Ethylbenzene did not contribute significantly to cancer risk for any population, and thus the total 

risks from permethrin and ethylbenzene are equivalent to those calculated for permethrin alone. 

Those noncancer HQs calculated for individual chemicals and individual pathways, as well as 

HIs calculated for all pathways and all chemicals are below 1 for all receptor populations. 

As noted in the discussion of MD-2 and MD-3, chronic exposures to the pheromones in SPLAT 

cannot be quantitatively evaluated due to the absence of chronic toxicity data. In this Alternative 

as well, the predicted chronic intakes of the pheromones in SPLAT are low, ranging from 

approximately several hundredths of a mg/kg-day to less than a millionth of a mg/kg-day 

(depending on pathway). As noted previously, there are no data to indicate that exposures to 

SCLPs at these levels are likely to be associated with effects on human health. However, the 

cautions regarding the potential sensitizing action of the LBAM pheromones (see MD 

Alternative and discussions in Section D3) pertain to the use of SPLAT in this alternative as 

well. 

The Organic Treatment Alternative considers the use of spinosad and the biopesticide Btk for 

control and eradication of LBAM. The evaluation of health effects from potential exposure to 

these materials is subject to the availability of toxicity data; those data are not sufficient to 

quantify effects from all exposure pathways or for all exposure durations. When quantitative 


EXECUTIVE SUMMARY 

estimates of health effects were not possible, comparisons were made between intakes of Btk or 

spinosad and available toxicity data to support an understanding of the likelihood of adverse 

effects that may occur from exposure. 

For both Btk and spinosad, acute inhalation HIs are below 1 for all receptor populations, 

indicating that health effects from acute exposures are not expected. Subchronic inhalation RfDs 

are not available for either spinosad or Btk. However, the intakes for this exposure pathway for 

all receptor populations are very low, and are approximately ten-fold lower (or more) than the 

intakes used to develop the acute inhalation HIs, indicating that effects of subchronic inhalation 

exposure are not likely. An additional comparison can be made for spinosad using the chronic 

RfD. If that RfD is used to develop an HI using the subchronic inhalation intake, the result – for 

all receptor populations – are HIs that are a hundred-fold to approximately 10,000 times lower 

than the HI threshold value of 1. Based on this evaluation, adverse effects of subchronic 

exposure to spinosad are not expected for any receptor population. 

All chronic HQs for spinosad, and the HI obtained from summing all HQs, are less than 1 for all 

receptor populations. Consequently, health effects from long-term exposure to spinosad are not 

likely. 

No chronic RfD is available for Btk; however estimated chronic intakes range from about a 

hundredth of a mg/kg day to roughly a millionth of a mg/ kg day. These intakes are far below 

quantities of Btk (e.g., 10 9 spores/kg-d, roughly equivalent to a g/kg-day [or five-fold higher than 

the highest estimated intake in this HRA], and 8.4 g/kg-d) that have been tolerated with only 

minimal effects in animal studies. These data suggest that long-term exposures to Btk at the 

levels estimated here are not likely to result in adverse health effects. These conclusions 

regarding the relative safety of Btk are also supported by its long usage history, and by an 

extensive body of evidence from large-scale ground and aerial applications which have yielded 

no evidence of significant or persistent health effects from exposure. 




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S E C T I O N D 1 

Introduction 

The light brown apple moth (LBAM), Epiphyas postvittana (Walker) (Lepidoptera: Tortricidae) 

is originally from Australia. An invasive pest species, LBAM is reported to attack more than 120 

plant genera in over 50 families, including many economically important species. LBAM feeding 

“destroys, stunts, or deforms young seedlings, spoils the appearance of ornamental plants, and 

injures deciduous fruit-tree crops, citrus, and grapes” (United States Environmental Protection 

Agency [USEPA] 2008). Because the LBAM is a new pest to the North American Continent, 

and affects a broad range of plants (as many as 2,042 plants, including native plants, forest 

species, agronomically important crops and ornamentals), both the United States Department of 

Agriculture’s (USDA) Animal and Plant Health Inspection Service (APHIS) and the California 

Department of Food and Agriculture (CDFA) have taken action to eradicate LBAM from 

California to prevent its spread to susceptible host plants throughout the United States and 

neighboring Mexico and Canada. The pest is prolific, and the number of generations produced in 

a growing season varies from one to more than four (depending on environmental conditions). 

LBAM infestations can be either local or regional at present, and the overall strategy is to 

eradicate the pest rather than control it because eradication was determined by the CDFA to be 

feasible. 

A total of 71,867 detections of the moth in California as of March 13, 2009, have been confirmed 

by the CDFA, including 10,285 in 2007 and 62,346 in 2008. LBAM has the potential to cause 

significant economic losses due to increased production costs and the possible loss of 

international and domestic markets. USDA estimates the impact on plant production costs may 

exceed $100 million in the State of California (USEPA 2007). A recent find has confirmed apple 

moth invasion in Healdsburg, Sonoma County (Press Democrat, March 11, 2009). 

The LBAM Program Area has changed as the infestation area has grown. For this human health 

risk assessment (HHRA) it is defined as all areas of the State of California that could become 

infested with LBAM, (see Figure 2-1 in Section D2 of the Programmatic Environmental Impact 

Report [PEIR]), meaning approximately 57 of the 58 counties in California, excluding alpine and 

desert areas and Imperial County, could contain the moth if allowed to spread. At present, the 

moth infestations are located in 13 counties, and LBAM is expected to continue to spread until 

full-scale eradication and treatment activities are implemented following completion of the 

PEIR. 

The proposed alternatives for control of the LBAM and the chemicals proposed for use are 

summarized in Table D1-1. This table represents a highly truncated description of the application 

scenarios detailed in Section D2 of the PEIR. The California Environmental Quality Act (CEQA) 

Guidelines require assessment of the potential effects of any proposed project or activity (such as 

insecticide applications by the CDFA) deemed to have a potential adverse effect on human 

health. Thus, this screening level HHRA examines the potential health effects associated with the 

use of (1) five different LBAM-specific pheromone treatment formulations for aerial or ground 

treatment: HERCON Disrupt Bio-Flake ® LBAM (HERCON), SPLAT LBAM (SPLAT), and 




DRAFT PEIR 


Isomate ® -LBAM Plus (Isomate) as the three proposed pheromone formulations of primary 

interest for the eradication Program, as well as two microcapsule formulations CheckMate ® 

LBAM-F (CheckMate) and Scentry Biologicals, Inc.’s (SBI’s) NoMate ® LBAM MEC (NoMate) 

that are not currently proposed for use in the Program), (2) proposed use of Bacillus 

thuringiensis kurstaki (Btk) for ground treatment, (3) proposed use of another bacterial 

insecticide, spinosad, for ground treatment and (4) proposed use of permethrin with a pheromone 

in male attractant treatments for ground application. In addition, evaluation of the No Program 

Alternative examines the increased use of several of the chemicals currently registered for use by 

the USEPA and the California Department of Pesticide Regulation (DPR) for control or 

prevention of LBAM including, but not limited to, chlorpyrifos, permethrin, lambda-cyhalothrin, 

spinosad, and Btk. 

Table D1-1 

Condensed Summary of LBAM Eradication Alternatives Evaluated in the EIR 

Alternative Application Method Chemical (s) 

No Program 

As per label directions 

Chlorpyrifos, Permethrin, Lambda-cyhalothrin, Spinosad, 

Btk 

Mating Disruption - 1 Twist Ties Isomate (LBAM pheromones) 

Mating Disruption - 2 Ground Applications HERCON, SPLAT (LBAM pheromones) 

Mating Disruption - 3 Aerial Release HERCON, SPLAT (LBAM pheromones) 

Male Moth Attractant (Alternative MMA) 

Ground Application 

SPLAT (LBAM pheromones), Permethrin (inert 

ingredients: ethylbenzene; 1,2,4-trimethylbenzene) 

Organic Treatment (Alternative Bt) Ground Treatments Bacillus thuringiensis kurstaki 

Organic Treatment (Alternative S, spinosad) Ground Treatments Spinosad 

Inundative Parasite Wasp Release (Alternative Bio-P) 

Sterile Insect Technique (Alternative SIT) 

None–not considered further in this Risk Assessment 

None–not considered further in this Risk Assessment 

This Appendix D to the PEIR follows standard HHRA protocols (National Research Council 

[NRC] 1983, 1994; California’s Office of Environmental Health Hazard Assessment [OEHHA] 

2003) and addresses the four key elements of risk assessment — hazard identification, 

identification of chemicals of potential concern; exposure assessment; dose-response assessment; 

and risk characterization. This screening level assessment examines only potential toxicological 

impacts to hypothetical human receptor populations from the use of the chemical formulations 

proposed for use to eradicate LBAM. Other impact analyses are provided in the other appendices 

of this report, consistent with CEQA Guidelines. Findings in this Appendix D are integrated into 

the PEIR, in Section 8 Human Health and in other appropriate sections. 

This screening level risk assessment uses default parameters and assumptions to assess potential 

health effects of exposure to chemicals proposed for use and other chemicals previously used or 

available for use under No Program. No site-specific or other data attributable to actual human 

populations are used. The likelihood of adverse health effects resulting from programmatic 

activities was estimated by calculating chemical-specific intakes to each of four hypothetical 

receptor populations. These intakes were calculated from the estimated exposure point 

concentrations (EPCs) of each of the different chemicals for each complete exposure pathway. 

Estimated intakes were then compared against toxicity criteria obtained from the literature or 

derived in this assessment if sufficient toxicity data were available. These comparisons were 

used to evaluate whether any of the chemicals may pose potential hazards or risks to the receptor 

populations. 


SECTION D1 

INTRODUCTION 

In screening level risk assessments, conservative exposure assumptions are typically applied to 

yield estimates of risk and hazard that are protective of the general population and sensitive 

subpopulations. This type of screening approach is consistent with regulatory guidance for risk 

assessment, and addresses the objective of providing information useful for risk management 

decisions. Risk and hazard estimates generated by a screening level health risk assessment 

should not be interpreted as expected rates of illness or disease in the exposed population but 

rather as estimates of potential risk, based on current knowledge and a number of assumptions 

(OEHHA 2003). Actual risks may be much lower than estimated in this analysis, and are most 

appropriately viewed as a tool for comparison rather than a literal prediction of disease incidence 

(OEHHA 2003). 




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Problem Formulation 

D2.1 PROGRAM AREA 

The overall Program Area is defined as all areas of the State of California that could become 

infested with LBAM, meaning approximately 57 of the 58 counties in California, excluding 

alpine and desert areas and Imperial County. Given this large area, the discussion is necessarily 

broad. 

D2.1.1 

Program Area Location 

The Program Area is intended to include all portions of the state in which climatic conditions are 

suitable to the LBAM. The moths prefer cool areas with moderate rainfall and moderate to high 

relative humidity (mean temperatures of ~56ºF, ~ 29 inches rain/year and ~70 % humidity) and 

are unlikely to thrive in the hot, dry conditions that exist in the southern parts of California… 

although it may be able to establish itself in the irrigated areas (USDA 2008). In addition, LBAM 

have no diapause (resting) stage and can only survive in areas where it can continuously breed 

and where sufficient hosts are available. Thus, desert areas with sparse vegetation, including 

most of Imperial County and the eastern portions of San Bernardino, Riverside, Los Angeles, 

Kern and Inyo counties, and areas of extensive cold, including elevations above 5,000 feet in the 

Sierra Nevada Mountains and the eastern portions of Modoc and Lassen counties are not 

expected to harbor LBAM. The threat is greatest along the coast from the Oregon border to the 

Mexican border. LBAM is expected to survive in the central valley and foothills below 5,000 

feet. 

As discussed in Section D2.1 of the PEIR, the immediate Program Area is located in the 13 

quarantined counties of the state where infestations occur as of January 2009: Alameda, Contra 

Costa, San Francisco, Napa, Marin, Sonoma, Solano, San Mateo, Santa Clara, San Benito, 

Monterey, Santa Cruz, and Santa Barbara. The areas proposed for eradication activities cover 

approximately 2,000 square miles. Within the 13 counties, eradication activities would be 

focused in the areas with the greatest infestation problems. 

Specific treatment area boundaries are determined based on trapping within any infested counties 

within California. The detection of 2 or more moths within a 3-mile radius within a time period 

equal to 1 LBAM life cycle places the area within the Program Area. 

Small, isolated infestations will continue to be treated with twist ties containing LBAM 

pheromone. Small infestations near larger infested areas will be treated with the moth pheromone 

applied to utility poles and trees and shrubs to confuse the male moths. Medium and large 

infestations will be treated with the moth pheromone and permethrin applied to utility poles and 

street trees. See Section D2 of the PEIR for a full description of the chemical treatment 

alternatives. 




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D2.2 OVERVIEW OF PROPOSED PROGRAM ALTERNATIVES 

The CDFA has published an Eradication Strategy for 2008–2015 (September 2008) that outlines 

treatment methodologies and application techniques (CDFA 2008). All of these methodologies 

and techniques are considered alternatives for analysis under CEQA. The Strategy is described in 

greater detail in the sections below to facilitate comprehensive and thorough analysis of potential 

environmental effects. Each method proposed under the Program is discussed as a separate 

alternative, with different application options under some of the alternatives. The alternatives are 

categorized as either chemical treatment or nonchemical treatment methods. The chemical 

alternatives (mating disruption and pesticidal control, including No Program) are presented first 

for consistency with the ecological and HHRA; then the sterile insect and biological 

control/parasitic wasp alternatives are presented. The subsequent impact analysis addresses the 

alternatives in this order as well. The order of presentation and discussion does not imply greater 

(or lesser) use of the alternative over the course of the eradication program. Methods considered 

but eliminated from the Program alternatives are discussed in Chapter 15 of this PEIR. The 

Program anticipates using all of the chemical and nonchemical alternatives (and options) in 

combination as part of an integrated pest management Program. However, should any one 

alternative become infeasible for effectiveness or economic or environmental reasons, the other 

alternatives would be used. Furthermore, the quarantine, inspection, detection, and private 

pesticide use components of No Program would continue until LBAM eradication is achieved. 

In summary, the alternatives are as follows: 

NO PROGRAM ALTERNATIVES 

• Quarantine, inspection, and detection 

• Chemical treatment with registered chemicals or biopesticides 

Chlorpyrifos 

Lambda-cyhalothrin 

Permethrin 

Spinosad 

Btk 

PROGRAM ALTERNATIVES 

Chemical Treatment Alternatives 

• Mating Disruption (MD) 

Twist ties (pheromones), 

Ground application of pheromones, 

Aerial application of pheromones 

• Male Moth Attractant (Alternative MMA) 

• Organic-Approved Insecticides (Alternatives Bacillus thuringiensis [Bt] and Spinosad [S]) 

Bacillus thuringiensis kurstaki 


SECTION D2 

PROBLEM FORMULATION 

Spinosad 

Nonchemical Treatment 

• Inundative Parasite Wasp Releases (Alternative Bio-P) 

• Sterile Insect Technique (Alternative SIT) 

D2.2.1 

No Program Alternative 

The No Program Alternative consists of maintaining the current state and federal Quarantine 

Orders without further action by the state or USDA. Private landowners would manage LBAM 

infestations on their land using currently approved chemicals and treatments without state or 

federal oversight. 

This risk assessment considers the potential health effects from the expanded use of the 

pesticides chlorpyrifos, permethrin, lambda-cyhalothrin, spinosad, and Btk for the No Program 

Alternative - these pesticides are currently registered for use for LBAM and other pests by the 

DPR. Analysis of risks from the No Program Alternative has assumed that use of these chemicals 

would be implemented at local scales through ground application, and that no aerial application 

of these chemicals would be permitted. 

D2.2.2 Alternative Mating Disruption (MD): MD-1, Twist Ties; MD-2, Ground; MD-3, Aerial 

Up to five different pheromone treatment formulations are being investigated for aerial or ground 

treatment: HERCON, SPLAT Isomate, and the microcapsule formulations CheckMate and 

NoMate. However, CDFA is proposing to use only three of these for the Proposed Program: 

HERCON, Isomate, and SPLAT. Mating pheromones act by attracting the male LBAMs to the 

pheromone lure, and thus reduce the probability of finding a female mate. The artificial 

pheromones do not kill the moths. They would be applied in three different ways, for urban 

infestations and for small and isolated areas, a ground treatment tool using pheromone twist ties 

will be used as well as ground-based application of pheromone via truck-based spray. Aerial 

application may be used for heavily infested, inaccessible areas such as forests and agricultural 

lands. 

For ground applications to trees and utility poles on public and private property and aerial 

application of pheromone in remote areas, the treatment area considered for this risk assessment 

is a 1.5 mile radius around each LBAM detection, with a projected 30 to 90 day spray interval. 

For ground treatment using twist ties, 250 twist ties per acre in a 200 meter radius around each 

LBAM detection are applied and subsequently replaced every 3 to 6 months. Treatment areas 

may be adjusted to provide the public with identifiable treatment boundaries. After two life 

cycles of treatment without any LBAM detections, treatment would cease. Post-treatment 

monitoring traps will remain in place for one additional life cycle. 

The area for aerial applications is a 1.5 mile radius around each location where LBAM have been 

detected. After two life cycles of mating disruption applications without any LBAM detections, 

these applications will cease. Once the pheromone has dropped to levels that will not interfere 

with trap efficacy, post-treatment monitoring traps will remain in place for one additional life 

cycle. If no additional LBAM are detected, this area will be declared free from LBAM and 

trapping levels will return to detection levels. 




DRAFT PEIR 


D2.2.3 

Male Moth Attractant (MMA) Alternative 

This alternative considers the application of the LBAM pheromone-containing formulation 

SPLAT and the permethrin-containing formulation Permethrin E-Pro. Application of this 

combination of chemicals by ground-based methods is designed to attract the moths by the use of 

SPLAT, and to kill them with the permethrin. This alternative is being considered for both urban 

and nonurban areas, and involves the use of small amounts of pheromone and Permethrin E-Pro 

in a thick matrix of SPLAT, which is applied to poles and trees. Each male attraction station will 

have 5 milliliters (mL) of the mixture applied to utility poles and trees, on both private and 

public property. The specific application method involves use of a metered hand-held wand that 

will release a squirt of mixture. All application sites are at least 8 feet aboveground level to 

minimize the potential for tampering or other disturbance. Applications will be made at the rate 

of 1200 treatments per square mile (approximately 2 per acre). Because of the slow release of the 

pheromone, male moth attractant (MMA) treatments only need to be repeated at 60-day 

intervals. 

D2.2.4 

D2.2.4.1 

Organic Treatment Alternative 

Bacillus thuringiensis kurstaki (Btk) 

Use of the bacterial insecticide Btk is being considered for ground treatment in heavily infested 

areas. Foliar ground treatments targeting the LBAM larvae would use Btk in the formulations 

DiPel ® DF and/or DiPel ® PRO DF. Application would be by backpack or truck-mounted sprayer. 

Up to 6 applications of Btk would occur at approximately 10- to 14-day intervals, although in 

most cases only one to three applications would be made. The Btk formulations would be applied 

with water as the carrier. 

D2.2.4.2 

Spinosad 

Use of the bacterially derived insecticide spinosad is being considered for ground treatment in 

heavily infested areas. It is also an approved treatment that could be employed by landowners in 

the event the No Program Alternative is selected through the Environmental Impact Report (EIR) 

process; however, for the purposes of this risk assessment, spinosad is considered as a distinct 

component of the Organic Treatment Alternative. Foliar application would be by backpack or 

truck-mounted sprayer. To reduce the potential for developing insecticide resistance, no more 

than 3 applications of spinosad can occur over a 30-day period with a maximum of 6 applications 

per year. Spinosad formulations would be applied with water as the carrier. 

D2.3 MANAGEMENT GOALS AND ASSESSMENT ENDPOINTS FOR ESTIMATING 

RISK 

The management goal for this HHRA is to protect human populations from avoidable risks of 

injury from the proposed use of chemicals or biopesticides to eradicate LBAM in California. 

This goal is consistent with the regulatory goals of the federal Toxic Substances Control Act 

(TSCA §2[b][1], Clean Water Act (304(a)CWA), the Federal Insecticide, Fungicide and 

Rodenticide Act (FIFRA), and OEHHA (various regulations). 

Estimated noncancer hazards and cancer risk from potential exposure to Program chemicals and 

formulation constituents represent the assessment endpoints used to characterize risks to 

potentially exposed human populations throughout the 57-county Program Area. 


SECTION D2 

PROBLEM FORMULATION 

D2.3.1 

Risk Hypothesis 

Based on the description of the Program alternatives, the primary exposures to Program 

chemicals or biopesticides will result from the intentional use of these materials to control 

LBAM populations. Because these materials will be released via ground-based spraying, 

volatilization from twist ties, or aerial application, ambient air will be the primary environmental 

medium affected. Once released to air, Program chemicals or biopesticides may deposit onto 

surface soil and vegetation. Thus, the exposure points through which human receptor populations 

could contact or otherwise receive ‘doses’ include inhalation of ambient air; incidental ingestion 

of soil; dermal contact with soil; dermal contact with ornamental vegetation, commercially 

grown produce, or homegrown produce; and ingestion of commercially grown or homegrown 

produce. Based on the release and transport mechanisms, and the associated human activities that 

may influence exposure, health effects to human receptor populations are potentially significant. 

The null and alternative hypotheses assumed for this screening level assessment are as follows: 

• Ho. Program chemicals or biopesticides applied in accordance with label instructions will 

yield significant toxicologically based impacts to human receptor populations. 

• Ha. Program chemicals or biopesticides applied in accordance with label instructions will not 

yield significant toxicologically based impacts to human receptor populations. 

D2.3.2 

Human Health Assessment Methods 

Methods used for assessing potential human health effects follow standard regulatory guidance 

(NRC 1983; 1994; USEPA 1989; OEHHA 2003). The health effects assessment addresses two 

fundamentally different types of toxic response to exposure (i.e., cancer and noncancer effects). 

Chemicals with sufficient evidence of carcinogenicity, as determined by a regulatory agency 

such as the USEPA or OEHHA, were evaluated for their ability to induce cancer at the predicted 

levels and durations that result from the No Program Alternative or from Program activity 

(MMA Alternative). Carcinogens (chemicals that can cause cancer) typically also can induce 

noncancer toxicity, and were evaluated for these effects as well. Noncarcinogens were evaluated 

only for noncancer health effects. As described more fully in Sections D3 and D5, carcinogens 

were evaluated by the use of a cancer slope factor (CSF) - a parameter that describes the 

quantitative relationship between the estimated dose and the probability of developing cancer. 

Noncancer health effects are evaluated using toxicity values known as reference doses (RfDs). 

Depending on the availability of data for each pesticide, toxicity criteria (e.g., RfDs, CSFs) were 

identified for one or more routes of exposure. These toxicity criteria were obtained from 

documents and on-line sources from the USEPA Office of Pesticide Programs (OPP), OEHHA, 

UESPA Integrated Risk Information System (IRIS), and the Agency for Toxic Substances and 

Disease Registry (ATSDR). If a criterion was not available from these sources, information in 

other regulatory documents or the primary literature was relied on. When toxicity criteria were 

developed for this assessment (e.g., from data in the regulatory or primary literature), uncertainty 

factors (UFs) were incorporated to address data gaps, effects on sensitive receptors, and 

variability in study and/or human populations. Additional details of the quantitative risk 

assessment methods used to assess potential health effects are provided in Section D5. 




DRAFT PEIR 





Toxicity Assessment 

The toxicity assessment portion of this risk assessment summarizes environmental fate, transport 

and toxicity hazard data developed on the compound(s) identified for use under the No Program 

and Program alternatives. Toxicological literature on the inert ingredients in the various 

pheromone and pesticide formulations used or proposed to be used to control LBAM are 

reviewed in this section to determine the most appropriate toxicity criteria. By comparing 

estimated exposure (dose) to these criteria, it is possible to estimate the potential health effects to 

human receptor populations from the treatment chemicals identified for each alternative. Fate, 

transport, and persistence of the various inert ingredients in the pesticide and pheromone 

formulations considered are also discussed to assess the potential for longer term exposure to 

formulation constituents or their breakdown products. 

A central tenet of toxicology is that for noncarcinogens, some dose level exists at which no effect 

is measurable in the response tested; this paradigm is considered a valid model for this 

assessment. This dose or concentration is known as the no observable adverse effect level or 

concentration (NOAEL/NOEL). The lowest observable (adverse) effect level or LOAEL (LOEL) 

corresponds to the lowest dose at which a biological and/or statistically significant effect is 

measurable relative to an unexposed control group. Beyond these typical measures, standard 

toxicological terms include the LD 50 and the LC 50 , the exposure dose or concentration, 

respectively that kills 50% of the animals tested. Table D3-1 summarizes chemical hazard 

classifications based on toxicity testing results, as applied by the USEPA. 

Table D3-1 

Chemical Hazard Classifications 

Hazard 

Indicators I II III IV Hazard Category 

Oral LD50 

Dermal 

LD50 

Inhalation 

LD50 

Eye 

Irritation 

Up to and 

including 

50 mg/kg 

Up to and 

including 

200 mg/kg 

Up to and 

including 

0.2 mg/liter 

Corrosive; 

corneal 

opacity not 

reversible 

within 

7 days 

>50 through 

500 mg/kg 

>200 through 

2,000 mg/kg 

>0.2 through 2 

mg/liter 

Corneal 

opacity 

reversible 

within 7 days, 

irritation 

persisting for 

7 days 

>500 through 

5,000 mg/kg 

>2,000 

through 

20,000 mg/kg 

>2 through 

20 mg/liter 

No corneal 

opacity; 

irritation 

reversible 

within 7 days 

Acute Oral or 

Dermal LD50 

mg/kg 

Mammals 

Acute 

Inhalation 

LC50 ppm 

>5,000 mg/kg Very highly toxic 20 mg/liter Moderately toxic 51-500 501-1,000 

No irritation Slightly toxic 501-2,000 1,001-5,000 




DRAFT PEIR 


Table D3-1 

Chemical Hazard Classifications 

Mammals 

Hazard 

Indicators I II III IV Hazard Category 

Acute Oral or 

Dermal LD50 

mg/kg 

Acute 

Inhalation 

LC50 ppm 

Skin 

Irritation 

Corrosive 

Severe 

irritation at 72 

hours 

Moderate 


hours 

Mild or slight 


hours 

Practically nontoxic >2,000 >5,000 

Source: 

40 CFR 156.62 

The fate and transport information summarized in this chapter allows for an evaluation of the 

expected mobility, degradation and persistence of the chemicals associated with the proposed 

treatment and alternatives, in both abiotic media (e.g., soil, water, air) and biotic media 

(biological tissues). The potential for persistence of chemicals in biological tissues is commonly 

characterized through measures of bioconcentration or bioaccumulation. Bioconcentration of a 

chemical can occur in an organism when it accumulates chemicals in its tissues following direct 

exposure, at a concentration greater than that found in the exposure media (e.g., water, air, soil, 

sediment). If the organism is then consumed (i.e., predated upon) by another organism resulting 

in a higher concentration of the chemical in the predator, then the chemical is considered to 

bioaccumulate. The bioaccumulation of organic chemicals in animals is a function of their 

lipophilicity (i.e., the tendency of the chemical to partition to and solubilize in lipids [fats]). Fat 

soluble (hydrophobic, nonpolar) chemicals that are also chemically stable are prone to 

bioaccumulate because they are cleared from the fat slowly. Chemicals that are insoluble or 

relatively insoluble in lipid tend to be polar and water soluble. In general, these substances are 

metabolized and eliminated more rapidly than lipophilic substances and generally, do not 

bioaccumulate or bioconcentrate. The bioconcentration factor (BCF) is a measure of the 

tendency for a substance in water to accumulate in organisms, especially fish. 

The U.S. Environmental Protection Agency (USEPA) regulates pesticides under two major 

statutes: the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) and the Federal Food, 

Drug, and Cosmetic Act (FFDCA). Pesticides are defined under FIFRA as, “any substance 

intended for preventing, destroying, repelling, or mitigating any pest.” FIFRA requires that 

pesticides be registered (licensed) by the USEPA before they may be sold or distributed for use 

in the United States, and that they perform their intended functions without causing unreasonable 

adverse effects on people and the environment when used according to USEPA-approved label 

directions. 

Current FIFRA regulations do not require manufacturers to reveal the inert ingredients in 

pesticide formulations, as FIFRA regulates the active ingredients only. Thus, the identity of some 

of the inert ingredients in the commercial formulations of the various pesticide products on the 

market have not been provided to the USEPA. Toxicity studies conducted under FIFRA are 

required to evaluate the product formulations only, and not the toxicity of the individual inert 

ingredients that may be used to facilitate absorption and uptake of the pesticide. However, 

because the formulations are tested, the potential additive or synergistic effect of inert 

ingredients on toxicity is addressed through the testing protocols adopted. Special uses of 

pesticides, outside their original label specifications, can be considered on a case-by-case basis 


SECTION D3 

TOXICITY ASSESSMENT 

through FIFRA Section 24C (US Code of Regulations 2008). However, the use of the LBAM 

pheromone formulations considered for use in this PEIR are already authorized in the State of 

California by the CDPR, and uses will conform to the approved label restrictions. 

The FFDCA authorizes the USEPA to set tolerances, or maximum legal limits, for pesticide 

residues in food. Thus, the FFDCA does not expressly regulate pesticide use, but residue limits 

established by this agency may result in a change in the use pattern regulated under FIFRA. The 

USEPA also requires extensive scientific research and supporting test data as part of its pesticide 

review and approval process before granting a registration for most pesticides. These studies 

allow the USEPA to assess risks to human health, domestic animals, wildlife, plants, 

groundwater, and beneficial insects, and to assess the potential for other environmental effects. 

When new evidence raises questions about the safety of a registered pesticide, the USEPA may 

take action to suspend or cancel its registration and revoke the associated residue tolerance. The 

USEPA may also undertake extensive special review of a pesticide’s risks and benefits or work 

with manufacturers and users to implement changes in a pesticide’s use (e.g., reducing 

application rates, or cancellation of a pesticide’s use). 

D3.1 NO PROGRAM: CONTINUED USE OF CURRENTLY APPROVED 

PESTICIDES BY INDIVIDUAL GROWERS AND HOUSEHOLDS 

This section provides information on the physical and chemical properties, environmental fate, 

and toxicity of three of the five active ingredients already approved for use by DPR by 

homeowners and/or nurseries that could be applied to control LBAM at local levels: 

chlorpyrifos, lambda-cyhalothrin, and permethrin. The formulations that are evaluated include 

Dursban 4E ® (chlorpyrifos as the active ingredient, with xylenes, ethyltoluenes, 

trimethylbenzenes, and ethylbenzene present as inert ingredients); Warrior ® (lambda-cyhalothrin 

as the active ingredient, with naphthalene and propylene glycol present as inert ingredients); and 

Permethrin E-Pro (permethrin as the active ingredient, with naphthalene and propylene glycol 

present as inert ingredients). The other two active ingredients also approved for use under the No 

Program Alternative, spinosad and Btk, are the focus of a directed alternative that addresses the 

use of approved organic insecticides (see Section D3.4.1). 

D3.1.1 

Chlorpyrifos 

Chlorpyrifos (O,O-diethyl O-3,5,6-trichloro-2-pyridyl) (Chemical Abstracts Service [CAS] 

number 2912-88-2) is a broad spectrum organophosphate pesticide introduced by Dow 

Chemical Company in 1965 (ATSDR 1997). It is one of the most widely used organophosphate 

pesticides in the United States, and is effective against members of the insect orders Coleoptera, 

Diptera, Lepidoptera, and Isoptera (Agency for Toxic Substances and Disease Registry 

[ATSDR] 1997; OEHHA 2008a). Chlorpyrifos was used extensively in residential applications 

until 2000, when the USEPA restricted or eliminated the sale of most chlorpyrifos-containing 

home products (USEPA 2000a). In 2006, the most recent year for which data are available, 

1,919,625 pounds of chlorpyrifos were used in California agriculture (OEHHA 2008a). 

Chlorpyrifos is synthesized by reacting 3,5,6-trichloro-2-pyridinol (TCP) and O,Odiethylphosphorochloridothioate 

under basic conditions (Sittig 1985). The chemical structure of 

chlorpyrifos is shown on Figure D3-1. Chlorpyrifos is registered as the active ingredient in 

several trade name pesticides, including Dursban ® , Lorsban ® , Brodan ® , and Stipend ® (ATSDR 




DRAFT PEIR 


1997). Chlorpyrifos is available in numerous different formulations, including emulsifiable 

concentrate, dust, flowable, granular wettable powder, microcapsule, pellet, and spray. 

Figure D3-1 Chemical Structure of Chlorpyrifos (ATSDR 1997) 

Major impurities in chlorpyrifos formulations can include sulfotep, which has a higher toxicity 

than chlorpyrifos by oral, inhalation, and dermal routes of exposure (World Health Organization 

[WHO] 2006), the S-alkyl isomer of chlorpyrifos (iso-chlorpyrifos), and the oxon of chlorpyrifos 

(WHO 2006). The Food and Agricultural Organization of the United Nations (FAO) and the 

WHO Joint Meeting on Pesticide Registration (JMPR) determined that sulfotep was the only 

toxicologically relevant impurity in chlorpyrifos, since the alkyl isomer is not readily formed 

under normal storage conditions for chlorpyrifos and the oxon is metabolized rapidly in humans 

(WHO 2006). 

D3.1.1.1 

Environmental Fate and Chemistry 

D3.1.1.1.1 Chemical and Physical Properties of the Active Ingredient 

Chlorpyrifos has a molecular formula of C 9 H 11 C l3 NO 3 PS and a molecular weight of 350.6. 

Technical grade chlorpyrifos is a crystalline solid that is white to tan or amber-colored (ATSDR 

1997). Chlorpyrifos has a vapor pressure of 2.5 x 10 -8 atm at 25°C, relatively low aqueous 

solubility (0.7 to 2 mg/L at 20-25°C), and a Henry’s Law Constant of 6.6 x 10 -6 atm-m 3 mol 

(ATSDR 1997). These properties indicate that chlorpyrifos will tend to volatilize from water to 

air, persisting primarily in the vapor phase. Volatilization rates for chlorpyrifos from soil can 

vary greatly and depend on the interaction among chlorpyrifos sorbed to soil, dissolved in soil 

water, and present in the soil air. For example, the volatilization rate of chlorpyrifos applied at 

11 µg/cm 2 ranged from 80 to 290 g/hectare/day in the first 3 days after application, with a 

simulated wind speed of 1 km/hour. 

Once in the atmosphere, chlorpyrifos can partition to particulate matter; in terrestrial systems, 

chlorpyrifos will partition to soils and sediments (ATSDR 1997). The extent of this partitioning 

is dependent on the octanol-water partition coefficient (log K OW of 4.82) and the organic carbon 

content of particulates and soils; measured organic carbon content-adjusted organic carbon 

partition coefficients (K OC ) range from 973 to 31,000 (ATSDR 1997). Chlorpyrifos has a strong 

affinity for organic matter, indicating that it will have a tendency to partition to soil and 

sediments, and that it is not likely to have substantial mobility in soil. In laboratory leaching 

studies, chlorpyrifos has been shown to stay within the top 5 centimeters (cm) of several 

different soils after sample elution with water (Harris et al. 1988; McCall et al. 1985). This 

finding has been confirmed in field studies where chlorpyrifos remained in the top 12 inches of 

soil after application (Oliver et al. 1987). 

The ATSDR (1997) gives the aquatic BCF for chlorpyrifos or its metabolites as a single set of 

values that range from 1 to 5100. These values have been determined experimentally with 


SECTION D3 


different organisms under varying experimental conditions; they indicate that chlorpyrifos has 

the potential to bioaccumulate, with the extent of that accumulation dependent on the species, the 

dose of chlorpyrifos, and the duration of exposure (ATSDR 1997). 

Table D3-2 summarizes some of the important physical and chemical properties of chlorpyrifos. 

Table D3-2 

Physical and Chemical Properties of Chlorpyrifos 

Parameter 

Value(s) and conditions 

Vapor pressure 2.5 x 10 -8 atm at 20 or 25°C 

Density 

1.398 g/cm 3 at 43.5°C 

Melting point, 

41.0 to 42.0°C 

Temperature of decomposition 

~160°C 

Solubility in water 

0.7 mg/L at 20°C 

2 mg/L at 25°C 

Octanol/water partition coefficient (KOW) Log KOW=4.7001 at 20°C 

Organic carbon partition coefficient (KOC) 973-31,000 

Henry’s Law Constant 

1.23x 10 -5 atm-m 3 /mol 

Direct photo-transformation was observed in buffer solutions and river waters, 

Photolysis 

under both natural and artificial lighting conditions. Approximately 50% 

degradation had occurred after 30-40 days. 

Source: 

ATSDR 1997 

D3.1.1.1.2 Environmental Transformation and Degradation 

AIR 

Chlorpyrifos and its major environmental degradation product, TCP, undergo photodegradation 

in the presence of sunlight; the estimated half-life of chlorpyrifos in the atmosphere is 6.34 hours 

(Atkinson 1987). 

WATER 

In water, chlorpyrifos degrades via abiotic hydrolysis and photosensitized oxidation (Macalady 

and Wolfe 1983). Hydrolysis of chlorpyrifos is pH-dependent. The half-life of chlorpyrifos in 

distilled water with a pH of 6.1 at 20°C is 120 days, and 53 days at a pH of 7.4 (Freed et al. 

1979). Temperature also plays a major role in the half-life of chlorpyrifos in water. At 21°C, the 

half-life of chlorpyrifos was reported to be 4.8 days, while at 4°C, the half-life increased to 27 

days (Frank et al. 1991). The disappearance of chlorpyrifos from water is also dictated by its rate 

of volatilization. Chlorpyrifos’ moderate vapor pressure and relative insolubility in water 

indicate that it will likely volatilize from surface waters. Additionally, because chlorpyrifos has a 

high affinity for organic particles, it partitions from water to soils and sediments (ATSDR 1997). 

In sediment or slurry systems, the half-life of chlorpyrifos has ranged from 12 to 30 days, as 

calculated from first-order degradation rate constants (Walker et al. 1988). 

SOIL 

On soil surfaces, chlorpyrifos undergoes photodegradation via abiotic hydrolysis, dechlorination, 

oxidation, and microbial degradation. The products of oxidation and dechlorination will break 

down further to form the chloropyridinols (including the oxon) and O,O-diethyl phosphorothioic 




DRAFT PEIR 


acid (Walia et al. 1988). The oxon of chlorpyrifos is very unstable and hydrolyzes more rapidly 

than the parent compound (ATSDR 1997). The half-life of chlorpyrifos in loamy soils is between 

2.5 and 16 weeks depending on temperature (28°C and 3°C, respectively); the half-life in 

“muck” was between 6 and >24 weeks for the same temperature range (Miles et al. 1979, 1983). 

PLANTS 

Reports vary on whether chlorpyrifos can be taken up by plant roots or leaves. For example, 

hydroponically grown cranberry bean plants were treated with 50 parts per million (ppm) of 

chlorpyrifos in an emulsifiable concentrate. About 0.7 - 0.1% of chlorpyrifos was taken up into 

the plant (Kenaga et al. 1965; Smith et al. 1967). Smith et al. (1967) reported similar results after 

treating a leaf of a cranberry bean plant with 1 mg of chlorpyrifos (Smith et al. 1967). However, 

Rouchard et al. (1991) observed translocation of chlorpyrifos into the leaves of cauliflower and 

brussels sprout plants after soil around the plant was treated. A concentration of ≥ 1 miligram per 

kilogram (mg/kg) (fresh tissue) of chlorpyrifos was measured in plants up to 44 days after 

treatment of brussels sprouts and up to 3.5 days-post treatment in cauliflower plants (Rouchard et 

al. 1991). 

D3.1.1.2 

Mammalian Toxicity 

D3.1.1.2.1 Mechanism of Action in Mammals and Humans 

The toxicity of chlorpyrifos is due primarily to its action as a cholinesterase (ChE) inhibitor. Like 

other organophosphates, chlorpyrifos acts by inhibiting the action of ChEs, enzymes that break 

down acetylcholine and related neurotransmitters of the central and peripheral nervous systems. 

The result is prolonged excitation of the nerves that enervate muscle or other tissue. Inhibition of 

ChE is dose-dependent, with neurological effects ranging from tremor and nausea to paralysis 

and, given large enough doses, death. Chlorpyrifos targets ChE in plasma, erythrocytes, and the 

brain. Recent data indicate that chlorpyrifos has actions on the developing brain that are likely 

distinct from ChE inhibition. These include interference with cell signaling and replication; 

lowered levels of nerve cell receptor proteins; and inhibition of adenyl cyclase-mediated cell 

replication, development, cell acquisition, and neuritic outgrowth (see following). 

D3.1.1.2.2 Metabolism and Elimination 

Chlorpyrifos is rapidly absorbed by ingestion, inhalation, and dermal contact, with dermal 

absorption occurring more slowly than absorption following either oral or inhalation exposure 

(ATSDR 1997). Once absorbed, chlorpyrifos is rapidly metabolized in the liver by oxidative 

desulfuration via a cytochrome P-450-dependent pathway to form its highly reactive oxon 

(Nolan et al. 1984; ATSDR 1997). The oxon of chlorpyrifos is reportedly 400 times more potent 

than the parent compound (WHO 1973), and Huff et al. (1994) reported that the chlorpyrifos 

oxon can inhibit brain ChE at a rate that is 3 orders of magnitude faster than chlorpyrifos (Huff et 

al. 1994). The inhibitory effects of both chlorpyrifos and its oxon occur in a dose-dependent 

manner (Huff et al. 1994; ATSDR 1997). However, the chlorpyrifos oxon is rapidly detoxified 

by hydrolysis to form TCP, the major metabolite of chlorpyrifos (Ma and Chambers 1994; 

Sultatos 1984, 1988). TCP does not inhibit ChE and is not mutagenic (Sultatos and Murphy 

1983). 

Chlorpyrifos is primarily eliminated in the urine as water-soluble metabolites, (ATSDR 1997; 

OEHHA 2008). Nolan et al. (1984) estimated that the average half-life for appearance of TCP in 


SECTION D3 


the blood of exposed individuals is about 22.5 hours, with the half-life of elimination estimated 

to be about 27 hours after either oral or dermal exposures (Nolan et al. 1984). The absorption and 

elimination of chlorpyrifos follows first order kinetics following dermal, oral, and inhalation 

exposures, indicating that chlorpyrifos is not likely to bioaccumulate in humans (Nolan et al. 

1984). 

D3.1.1.2.3 Acute Toxicity 

Chlorpyrifos is acutely toxic when exposures occur via oral, inhalation, or dermal routes. In 

humans, symptoms of acute toxicity include headache, nausea, dizziness, vomiting, catatonia, 

meiosis, tachycardia, muscle weakness, respiratory problems, lethargy, cyanosis, and other 

symptoms associated with parasympathetic stimulation (ATSDR 1997). One of the phenomena 

associated with acute exposure to chlorpyrifos is delayed (deferred) neurotoxicity. A number of 

documented instances of acute exposure to unspecified quantities of chlorpyrifos have resulted in 

impaired memory, paresthesia, and/or lowered scholastic performance in children; these effects 

persisted for up to 6 months after exposure. Anecdotal reports following dermal exposure to 

chlorpyrifos cite reactions such as skin flushing (Ames et al. 1989), skin irritation, and dermal 

sensitization as well as neurological and behavioral effects similar to those observed in humans 

and animals after oral exposures (ATSDR 1997). 

In experimental animals, the median lethal dose required to kill 50% of the test animals (LD 50 ) 

appears to depend on the formulation. A recent review of rat oral LD 50 gives a range of 205-1414 

mg/kg for liquid formulations; 224-1630 mg/kg for granular formulations, 180-235 mg/kg for 

wettable powders; and for orally administered sprays, 710 to > 5,000 mg/kg (Cochran et al. 

1992). Data are contradictory as to whether females rats may be more susceptible to chlorpyrifos 

than males. For example, Gaines (1969) reported a chlorpyrifos oral LD 50 of 82 mg/kg in female 

Sherman rats and 155 mg/kg for male Sherman rats whereas McCollister et al. (1974) 

documented an LD 50 of 155 mg/kg or 118 mg/kg in female and male rats, respectively. Acute 

toxicity data for chlorpyrifos are summarized in Table D3-3. 

Only limited acute inhalation toxicity data are available for chlorpyrifos. The median lethal 

concentration required to kill 50% of the test animals (LC 50 ) has been reported to be greater than 

5.22 mg/L for rats (WHO 2006). The WHO (2006) also cites a minimum lethal concentration 

(MLC) for chlorpyrifos in rats as > 36 mg/m 3 (Table D3-3) 

Chlorpyrifos is not markedly toxic via dermal exposures (Table D3-3). The rat LD 50 for dermal 

exposures to chlorpyrifos ranges from 202 to > 2,000 mg/kg (ATSDR 1997; Gaines 1969; WHO 

2006). 




DRAFT PEIR 


Table D3-3 

Acute Toxicity of Chlorpyrifos 

Species 

Test 

Duration and conditions or 

guideline adopted, purity 

Result 

Rat, Sprague Dawley (m,f) Acute oral purity 99.3% LD50 (m,f) = 320 mg/kg bw (260-393) LD50 

(m) = 276 mg/kg bw (167-455) LD50 (f) = 

350 mg/kg bw (285-429) 

Rat, Sprague Dawley (m,f) Acute dermal purity 99.3% LD50 >2,000 mg/kg 

Rat, Sprague Dawley (m,f) Acute dermal purity 98.5% LD50 >2,000 mg/kg 

Rat, Sprague Dawley (m,f) Acute inhalation purity 99.3% MLC (m,f) >36 mg/m 3 (32-40), no deaths. 

Rat, Sprague-Dawley (m,f) Acute inhalation purity 97.8% LC50 >5.22 mg/l 

Rabbit, New Zealand white (sex not 

stated) 

Rabbit, New Zealand white (sex not 

stated) 

Skin irritation purity 99.3% Mild irritant. No corrosive effects. 

Eye irritation purity 99.3% Mild irritant (class 4, modified Kay & 

Calandra classification), all rabbits 

showed positive effects. 

Guinea pig, albino Dunkin-Hartley (f) Skin sensitization purity 99.3% Nonsensitizer. 

Source: 

WHO 2006 

Notes: 

LD50 = Median lethal dose for 50% of test animals 

MCL = Minimum lethal concentration 

D3.1.1.2.4 Subchronic and Chronic Toxicity 

Effects seen in humans and animals after chronic exposures to low levels of chlorpyrifos are 

manifested as decreased concentration, memory loss, impairment of spatial associations, 

irritability, and depression (Shaw 1961; Metcalf and Holmes 1969). These effects can be very 

subtle, especially where ChE is not severely inhibited by exposure to chlorpyrifos (Huff et al. 

1994). As with acute exposures, deferred neurotoxicity is characteristic of longer-term exposure 

to chlorpyrifos; both sensory loss and peripheral neuropathy have been documented in humans 

(ATSDR 1997). 

Steenland et al. (2000) investigated neurological function in 191 pesticide applicators who had 

applied chlorpyrifos as a termiticide. The average exposure duration for members of the group 

was 2.5 years. In neurobehavioral evaluations, the exposed group did not perform as well as a 

control group in pegboard turning tests and postural sway tests. Exposed individuals also had a 

higher incidence of memory problems, reports of fatigue, loss of muscle strength, and altered 

emotional states. The two groups did not differ significantly in more quantitative clinical 

evaluations, however. 

Terry et al. (2007) studied the neurologic effects in rats given subcutaneous injections of 

chlorpyrifos (2.5-18.0 mg/kg) every other day for 30 days. The exposure period was followed by 

a 2-week “wash out” period, where chlorpyrifos was not administered. Tests conducted during 

the wash out period documented a dose-dependent decrease in behavioral function in 

chlorpyrifos-treated rats. Additionally, ChE inhibition was still evident after the 2-week wash out 

period, even though chlorpyrifos and the metabolite TCP were barely detectable in the brain and 

plasma. The highest dose of chlorpyrifos (18 mg/kg) was associated with decreases in nerve 

growth factor receptors, vesicular acetylcholine transporters, high affinity choline transporters, 

and the α7-nicotinic acetylcholine receptor proteins. The study also found decreases in axonal 


SECTION D3 


transport in the sciatic nerves ex vivo. Terry et al. (2007) hypothesized that these neurochemical 

changes may be causally related to deficits in information processing and cognitive function 

linked to chlorpyrifos. 

D3.1.1.2.5 Developmental Toxicity 

Three separate ongoing epidemiology studies in the United States, and one study of agricultural 

workers in India were reviewed by OEHHA (2008a). All studies examined the potential 

association between maternal exposure to chlorpyrifos or other pesticides and adverse effects on 

their offspring. These studies differed significantly with respect to the ethnic composition of the 

study population; the potential exposure frequency, magnitude, and duration; and the endpoints 

examined. Adverse effects associated with chlorpyrifos exposure include lower birth weight, 

decreased length at birth, smaller head circumference, delays in mental and motor development, 

behavioral problems, and DNA damage. 

A series of recent studies provide considerable evidence that chlorpyrifos has specific targeted 

adverse effects on the developing brain that are distinct from its action as a ChE inhibitor. 

Chlorpyrifos-induced effects that appear to be unrelated to ChE inhibition include effects on the 

developing brain during cell division; interference with RNA synthesis during differentiation; 

interruption of cell signaling; interference with nuclear transcription factors involved in cell 

differentiation; effect on the catecholamine system in the developing brain; oxidative stress in 

the developing brain; and interference with gliogenesis and axonogenesis (see review by 

OEHHA 2008a). 

For example, Campbell et al. (1997) investigated the effects of chlorpyrifos exposures on cell 

development in the brains of neonatal rats. Chlorpyrifos administered intramuscularly on postnatal 

day (PND) 1 to 4 (1 or 5 mg/kg) or 11 to 14 (5 or 25 mg/kg) caused cell death in the 

developing brain. A significant loss in cells of the brainstem was seen in animals given 5 mg/kg 

on PND 1-4, although this group also sustained significant mortality. In neonates treated on PND 

11 to 14, the primary target of chlorpyrifos shifted from the brainstem to the forebrain, with cell 

loss occurring on PND 15 to 21 after treatment had ceased. Neither survival nor growth was 

affected in this group of animals. Cells in the cerebellum of both groups of neonates had early, 

short-term increases in DNA levels subsequent to chlorpyrifos exposure; DNA levels decreased 

to below normal levels in the cerebellum coincident with the loss of cells in the brainstem and 

forebrain, an effect that was interpreted as evidence of cell death in this region of the brain. 

Although the doses of chlorpyrifos administered in this study are above those likely to be 

incurred by environmental exposures, they indicate that chlorpyrifos can induce significant 

adverse effects on the developing brain at doses that do not cause overt toxicity. 

Slotkin (1999) reviewed a body of experimental data that examined the underlying mechanisms 

of toxicity of chlorpyrifos on the developing brain. Consistent with its action on ChE, 

chlorpyrifos administered to developing rats at doses that were not overtly toxic decreased DNA 

synthesis and caused cell loss in regions of the brain innervated with cholinergic receptors. In rat 

embryo cultures, chlorpyrifos induced cell death during neurulation. However, in vitro data from 

neuronal cell cultures with few cholinergic receptors indicate that chlorpyrifos also interferes 

with adenyl cyclase-mediated cell replication, development, cell acquisition, and neuritic 

outgrowth - a mechanism of toxicity distinct from ChE inhibition. These dual actions indicate 

that chlorpyrifos may impair neural cell development for a period that extends from 

embryogenesis through post-natal development. 




DRAFT PEIR 


Notwithstanding the effects of chlorpyrifos that are distinct from its action on ChE, inhibition of 

ChE continues to be used as a sensitive indicator of chlorpyrifos exposure. OEHHA (2008a) has 

recently reviewed a series of toxicity studies that measured inhibition of red blood cell (RBC), 

plasma, or brain ChE, and/or physical and cognitive impairment to assess chlorpyrifos-induced 

developmental toxicity. Those studies reveal a pattern of treatment-related decreases in neonatal 

weight, growth, or survival; inhibition of brain ChE; behavioral changes; and impaired learning 

or memory loss. The lowest NOAEL was identified in rats by Maurissen et al. (2000) as 0.3 

mg/kg, with the LOAEL in that study, 1 mg/kg, associated with impairment of brain ChE. 

Chlorpyrifos exposure during gestation may result in behavioral changes that manifest long after 

exposure has ended and ChE levels have recovered. Delayed-onset deficits in memory have been 

observed in adolescent and adult rats exposed in utero, an effect that has been postulated to be 

due to disruption of development of normal cholinergic activity (OEHHA 2008a). 

D3.1.1.2.6 Teratogenicity 

Chlorpyrifos, but not TCP, appears to be teratogenic when administered in sufficiently large 

doses. Chlorpyrifos given as a single intraperitoneal injection (80 mg/kg) caused a significant 

increased incidence of fetal mortality, fetal resorption, cleft palate, missing thoracic vertebrae, 

and a decrease in caudal vertebrae when administered to mice on gestation day (GD) 10. 

Significant maternal toxicity was not observed (Tian et al. 2005). Chlorpyrifos adversely affected 

fetal weight and caused an increase in resorption and fetal death when provided to rats by gavage 

at 25 mg/kg on GD 6-15. Doses of 5 or 15 mg/kg did not yield any evidence of teratogenicity. 

Maternal toxicity occurred in the highest dose group as well, and may have caused or contributed 

to the adverse effects seen in fetuses (Farag et al. 2003). An evaluation of TCP for its teratogenic 

potential utilized doses of 0-150 mg/kg chlorpyrifos for rats (GD 6-15) and 0-250 mg/kg for 

rabbits (GD 7-19). No effects occurred in either species on fetal weight, viability, or any type of 

abnormality despite the induction of maternal toxicity in the higher dose groups (Hanley et al. 

2000). 

D3.1.1.2.7 Reproductive Toxicity 

Epidemiological evidence suggests that exposures to chlorpyrifos may be related to increased 

DNA damage in sperm as well as other reproductive effects. In a case-control study involving 

men from Minnesota and Missouri, Swan et al. (2003) linked increased levels of TCP to 

decreased sperm quality (Swan et al. 2003). A series of cross-sectional studies based on the same 

study population also linked increased TCP metabolites in urine to increased DNA damage in the 

sperm of the study population (Meeker 2004a, 2004b), lower reproductive hormone levels, 

including testosterone and estradiol (Meeker 2006a, 2008), and higher thyroid stimulating 

hormone (TSH) levels (Meeker 2006b). 

In separate two-generation studies, chlorpyrifos administered as Dursban ® (to 1.2 mg/kg) or as 

97.8% pure compound (to 5 mg/kg) did not affect indices of reproduction or fertility in male or 

female rats despite the induction of significant RBC-, plasma-, and brain-ChE inhibition by the 5 

mg/kg dose (OEHHA 2008a). Reduced pup weights and increased pup mortality observed at the 

5 mg/kg dose in the study occurred only at a dose that caused parental toxicity and, thus, are not 

considered reproductive effects. Substantially higher doses of chlorpyrifos (7.5, 12.5, and 17.5 

mg/kg) administered to male rats by gavage for 30 days, resulted in a significant decrease in 

testes weight, sperm counts, and in serum testosterone concentrations. These effects were 

associated with degenerative changes in the seminiferous tubules. Histological examination of 


SECTION D3 


testicular tissue from the low-dose group revealed a decrease in the number of sperm and the 

presence of irregular epithelia; these alterations increased in severity with increasing dose (Joshi 

et al. 2007 as cited in OEHHA 2008a). 

D3.1.1.2.8 Genotoxicity 

Chlorpyrifos has been evaluated for genotoxicity in an array of in vitro assays that examined 

mutagenicity in bacteria; mutation, gene conversion, or mitotic crossover in yeast; and 

unscheduled DNA synthesis, chromosomal aberrations, sister chromatid exchange, or induction 

of micronuclei in mammalian cells (Table D3-4). Chlorpyrifos appears to be clastogenic in vitro, 

in that it has induced a dose-dependent increase in the induction of micronuclei in mammalian 

bone marrow cells (Amer and Fahmy 1982); an increase in sister chromatid exchange (Sobti et 

al. 1982); and in chromosome aberrations (Amer and Aly 1992). Some evidence exists that 

chlorpyrifos may be genotoxic in vivo. Chlorpyrifos has induced mutations and chromosome 

loss in Drosophila (Patnaik and Tripathy 1992; Woodruff et al. 1983), respectively. Mehta et al. 

(2008) found dose dependent increases in DNA damage in the liver and brain of rats following 

acute or chronic intramuscular exposures of 50 and 100 mg/kg, or 1.12 and 2.24 mg/kg 

chlorpyrifos, respectively. 

Table D3-4 

Genotoxicity of Chlorpyrifos in vivo 

Species (test system) End point Results Reference 

Fly (Drosophila melanogaster) germ cells Complete chromosome loss + Woodruff et al. 1983 

Fly (Drosophila melanogaster) germ cells Partial chromosome loss — Woodruff et al. 1983 

Fly (Drosophila) somatic and germ cells Induction of mosaic wing spots + Patnaik and Tripathy 1992 

Fly (Drosophila) somatic and germ cells Induction of sex-linked recessive lethals + Patnaik and Tripathy 1992 

Mouse (Swiss) bone marrow 

Source: 

ATSDR 1997; OEHHA 2008 

Polychromatic erythrocytes (PE) and PE 

with micronuclei 

+ Amer and Fahmy 1982 

Escherichia coli Mutation - OEHHA 2008 

Salmonella typhimurium Mutation - OEHHA 2008 

Bacillus subtilis Mutation + OEHHA 2008 

D3.1.1.2.9 Carcinogenicity 

A prospective epidemiological study on the health of pesticide applicators in Iowa and North 

Carolina found a positive association between chlorpyrifos exposure and an increased risk of 

lung cancer (Relative Risk [RR]= 2.18; 95% CI = 1.31-3.64) (Lee et al. 2004). The correlation 

between exposure to chlorpyrifos and lung cancer remained after controlling for smoking 

history, other pesticide exposures, and certain demographic variables. 

No evidence from animals studies exists to indicate that chlorpyrifos is carcinogenic, although 

the ATSDR (1997) cites only a single chronic-duration study to support this conclusion. In that 

study, male and female rats and beagle dogs exposed to chlorpyrifos up to 3 mg/kg per day for 1 

to 2 years did not have an increased incidence of tumors compared to controls (McCollister et al. 

1974). Chlorpyrifos is not listed as a carcinogen by the International Agency for Research on 

Cancer (IARC), the USEPA, the National Toxicology Program (NTP), or under California’s 

Proposition 65. 




DRAFT PEIR 


D3.1.1.3 

Interpretation of Human Toxicity Based on Animal Studies 

LBAM eradication goals include consideration of a No Program Alternative, in which certain 

pesticides that are known to be effective against the apple moth would continue to be used in 

nurseries, in agriculture, and for home use to treat or help to prevent infestations (under current 

EPA registration, only extremely limited residential of use of chlorpyrifos is permitted). These 

uses may result in human exposure. Although the significance of these exposures is likely to be 

minimal when the products are used in accordance with label directions, chlorpyrifos’ ability to 

persist in the environment indicates that human exposure to low concentrations may occur. 

When quantitative human toxicity data are not available for a chemical, as is the case for 

chlorpyrifos, regulatory agencies necessarily rely on data from animal studies to characterize 

exposure levels deemed to be safe for humans. Noncancer toxicity criteria for chlorpyrifos have 

been developed by the ATSDR (2003) and the USEPA (2009a). Notwithstanding the use of 

different terminology for their respective toxicity criteria (minimal risk levels [MRLs] for 

ATSDR, and RfDs for the USEPA), both of the agencies use comparable methodology to derive 

the noncancer toxicity criteria. 

The USEPA focuses its noncancer toxicity criteria on long-term i.e., chronic oral exposure. For 

these exposures, the USEPA develops an oral RfD, with the analogous value for inhalation 

exposures referred to as the reference concentration (RfC) or inhalation RfDinh (USEPA 2009b). 

The RfD and RfC/RfDinh are each defined as the daily exposure level for the “…human 

population (including sensitive subgroups) that is likely to be without an appreciable risk of 

deleterious effects during a lifetime” (USEPA 2009b). RfDs or RfCs are typically derived by 

selecting the most scientifically appropriate NOAEL, or if it is not available the LOAEL, from 

relevant animal toxicology studies, and then applying one or more UFs of 3 or 10 to address data 

limitations. These UFs are used to account for intraspecies variability, interspecies variability, 

the extrapolation of data from animals to humans, differences in duration between the 

experimental period and lifetime exposure, use of the LOAEL rather than the NOAEL, and/or for 

the overall quality and completeness of available toxicity data (USEPA 2009b). 

The ATSDR defines a MRL as an “ estimate of daily human exposure to a substance that is 

likely to be without appreciable risk of adverse effects (noncarcinogenic) over a specified 

duration of exposure.” 

The ATSDR also identifies NOAELs as the basis for the derivation of its noncancer toxicity 

criteria, although it may develop MRLs for different exposure periods than those considered by 

the USEPA. MRLs are derived by the ATSDR (2008) “…when reliable and sufficient data exist 

to identify the target organ(s) of effect or the most sensitive health effect(s) for a specific 

duration within a given route of exposure.” 

The ATSDR (1997) and the USEPA (2009a) relied on the same data for the development of oral 

toxicity criteria for chlorpyrifos, although each agency interpreted the data somewhat differently. 

The study in question is not publicly available, but involved a group of human adult male 

volunteers who were given chlorpyrifos once a day for up to 28 days (cited variously as Coulston 

et al. 1972 [reference not provided by ATSDR] or as Dow Chemical Co. 1972). The 

administered doses of chlorpyrifos ranged from 0, 0.014, 0.03, or 0.1 milligrams per kilogram 

per day (mg/kg-d). According to the review in ATSDR (1997), the 0.014 and 0.03 mg/kg-d dose 

groups were treated for 28 and 21 days, respectively, but treatment of the high dose group (0.1 


SECTION D3 


mg/kg-d) was terminated after 9 days due to one of the four subjects experiencing mild adverse 

effects (faintness, runny nose, blurred vision). ChE measurements, urinalyses, and serum 

chemistry tests were conducted periodically throughout the experiment. Mean plasma ChE levels 

were reduced by 66% in the high dose individuals at the time treatment ceased at 9 days. At the 

study’s end, the 0.03 mg/kg-d dose group had plasma ChE levels that were an average of 30% 

lower than controls, although this difference was not significant. The ATSDR identified this dose 

level, 0.03 mg/kg-d, as the NOAEL. As supporting evidence of the representativeness of this 

NOAEL, the ATSDR (1997) cited a separate study by Deacon et al. (1980) that identified a 

NOAEL of 0.1 mg/kg-d in rats, where the LOAEL in that experiment addressed both fetotoxicity 

and ChE inhibition. The USEPA (2009a) identified the same NOAEL as did the ATSDR (1997) 

from the Coulston et.al/Dow Chemical (1972) data, i.e., 0.03 mg/kg-d. The ATSDR considered 

the NOAEL to be applicable to the derivation of both an acute and intermediate duration MRL 

(with application of an UF of 10); the USEPA considered the same data to be appropriate for 

derivation of a chronic RfD, also with an UF of 10. These values are listed in Table D3-5. As 

part of the 2006 re-registration of chlorpyrifos (USEPA 2006a), the USEPA identified a shortterm 

(1-30 days) and an intermediate term (1-6 months) inhalation NOAEL of 0.1 mg/ kg-d. 

Pesticide re-registration documents do not contain citations that provide the source of the 

original data, but the USEPA indicated that this NOAEL was selected based on an absence of 

effects in two rat inhalation studies. In those studies, 43% plasma ChE inhibition and 41% RBC 

ChE inhibition were observed at the LOAEL of 0.3 mg/kg-d when chlorpyrifos was administered 

over a 2-week period. The USEPA (2006a) identified a margin-of-exposure (MOE) value for 

infants, children, and females ages 13-50 (a sensitive population) of 1,000, and an MOE of 100 

for all other populations. Although the USEPA (2006a) does not calculate a RfD from these 

parameters, if the MOEs are considered equivalent to UFs, RfDs are readily calculated by 

dividing the NOAEL by the MOE. That calculation yields an acute inhalation RfD of 3 x 10 -4 for 

sensitive populations, and an acute inhalation RfD of 3 x 10 -3 for all other populations. For 

exposures that occur for periods of time greater than 6 months, the USEPA (2006a) identified a 

NOAEL of 0.03 mg/kg-d. That value was derived from five studies in which dogs or rats were 

exposed to chlorpyrifos for 90 days or 2 years. Significant plasma and RBC ChE inhibition were 

seen at 0.22 to 0.3 mg/kg-d. The USEPA (2006a) selected the same MOEs as for the acute 

exposures, and again, did not develop toxicity criteria from the NOAELs. By completing 

analogous calculations to those noted for the acute inhalation RfD yields long-term, or chronic 

RfDs of 3 x 10 -5 for sensitive populations, and a chronic inhalation RfD of 3 x 10 -4 for all other 

populations. 

Table D3-5 

Toxicity Criteria for Chlorpyrifos 

Oral (mg/kg-d) 

Inhalation (mg/kg-d) 

Acute Subchronic Chronic Acute Subchronic Chronic 

3 x 10 -3 a 3 x 10 -3 a 3 x 10 -3 b 

1 x 10 -3 c 

1 x 10 -4d 

1 x 10 -3 c 

1 x 10 -4d 

Notes: 

a 

ATSDR 1997 

b 

USEPA 2009a 

c 

derived from data in USEPA 2006a 

d 

applicable to sensitive receptors (USEPA 2006a). 

The values denoted in bold font were used as toxicity values in the human health quantitative risk assessment. 

3 x 10 -4 c 

3 x 10 -5d 




DRAFT PEIR 


D3.1.2 

Carriers and Dispersants of Chlorpyrifos 

DuraGuard ® ME and Dursban ® 4E are chlorpyrifos-containing products approved for the control 

or prevention of LBAM at nurseries and/or in crop production areas. The DuraGuard ® ME 

material safety datasheet (MSDS) (Whitmire MicroGen 2001) does not list any specific inert 

ingredients, noting only that these comprise 80% of the product, with chlorpyrifos making up the 

remaining 20%. The Dursban ® 4E MSDS lists xylene range aromatic solvents and emulsifiers as 

comprising 55.1% of the product, and provides CAS numbers for xylenes, ethyl toluenes, 

trimethyl benzenes, and ethylbenzene. Specific quantities are not given for these inert ingredients 

(DowElanco 1998). In the following discussion, information on 1,2,4-trimethylbenzene is 

provided in lieu of general information on the category of compounds known as 

trimethylbenzenes. Both 1,2,4-trimethylbenzene and ethylbenzene are also components of the 

permethrin formulation (Permethrin E-Pro) proposed for use in both the No Program Alternative 

and the MMA Program Alternative. 

D3.1.2.1 

Environmental Fate and Chemistry of Inert Ingredients 

D3.1.2.1.1 Chemical and Physical Properties of Inert Ingredients 

1,2,4-TRIMETHYLBENZENE 

1,2,4-trimethylbenzene (molecular formula C 9 H 12 , CAS number is 95-63-6) is used as an 

intermediate in the manufacture of dyes, pharmaceuticals, and the synthesis of the chemical 

pseudocumidine, although it’s primary industrial use is as a solvent and paint thinner (Hazardous 

Substances Database [HSDB] 2009). Key chemical and physical properties of 1,2,4- 

trimethylbenzene are given in Table D3-6. The structure of 1,2,4-trimethylbenzene is given on 

Figure D3-2. 

Table D3-6 

Chemical and Physical Properties of 1,2,4-trimethylbenzene 

Property 

Parameter 

Molecular weight, grams 120.191 

Color and state 

Clear colorless liquid 

Boiling point 

168.89ºC 

Solubility in water 57 mg/L at 25ºC 

Log octanol-water partition coefficient (KOW) 3.78 

Vapor pressure at 25ºC 

2.10 mmHg 

Henry’s Law Constant at 20ºC 

6.16 x 10 -3 atm m 3 /mol 

Source: 

HSDB 2009 

Figure D3-2 

Structure of 1,2,4-Trimethylbenzene (from National Library of Medicine) 


SECTION D3 


ETHYLBENZENE 

Ethylbenzene (molecular formula C 8 H 10 , CAS number 100-41-4) is typically synthesized by the 

reaction of benzene and ethylene with an aluminum trichloride catalyst, although other 

manufacturing methods are also used (ATSDR 2007a; HSDB 2009). In the United States, 

ethylbenzene is ranked as one of the top 50 chemicals produced on a mass basis, with 11.6 

billion pounds produced in 2005 (ATSDR 2007a). Chemical and physical properties of 

ethylbenzene are given in Table D3-7, and the structure is shown on Figure D3-3. 

Table D3-7 

Chemical and Physical Properties of Ethylbenzene 

Source: 

HSDB 2009 

Property 

Parameter 



Boiling point 


Colorless liquid 

136.1ºC 

0.014 g/mL at 15ºC 

169 mg/L at 25ºC 

Log octanol-water partition coefficient (KOW) 3.15 

Vapor pressure at 25ºC 9.6 mmHg at 25ºC 


7.88 x 10 -3 atm m 3 /mol 

Figure D3-3 

Structure of Ethylbenzene (from National Library of Medicine) 

ETHYLTOLUENES 

Ethyltoluene refers to an aromatic hydrocarbon mixture comprised of ortho-, meta-, and paraisomers 

represented by CAS no. 2550-14-5. Individual isomers have a molecular weight of 

120.19 grams, and molecular formula of C 9 H 12 . The chemical and physical properties of these 

aromatic hydrocarbons are listed in Table D3-8, and the structure of the meta-isomer is depicted 

on Figure D3-4. 

Table D3-8 

Source: 

Cameo 2009 

Chemical and Physical Properties of Ethyltoluene 

Property 

Parameter 




Boiling point 

324.9ºF 


Not available 


10.34 mmHg (temperature not specified) 




DRAFT PEIR 


Figure D3-4 

Structure of Meta-Ethyltoluene (from National Library of Medicine) 

XYLENES 

Xylenes (dimethylbenzene) is a colorless, flammable liquid that is used as a solvent in the 

printing, rubber, and leather industries and as a cleaner and paint thinner, in paints or coatings, or 

as a blend in gasoline. It occurs naturally in petroleum and coal tar (Oak Ridge National 

Laboratory [ORNL] 2005; USEPA 2003). Xylenes (CAS no. 1330-20-7) have the molecular 

formula C 8 H 10 , and a molecular weight of 106.17. Xylenes are liquid at room temperature, but 

readily volatilize to air given their low vapor pressure (USEPA 2003). Commercial formulations 

of xylenes are typically composed of a mixture of three isomers, meta-xylene (m-xylene), orthoxylene 

(o-xylene), and para-xylene (p-xylene), of which the m-isomer usually predominates 

(USEPA 2003). The chemical and physical properties of xylenes are listed in Table D3-9, and 

the structure is given on Figure D3-5. 

Table D3-9 

Chemical and Physical Properties of Xylenes 

Property 

Parameter 

Source: 

HSDB 2009 




Boiling point 

137-140ºC 

Water solubility 

Practically insoluble 

Log octanol-water partition coefficient 3.12-3.2 

Vapor pressure at 25 ºC 7.99 mmHg at 25 ºC 

Figure D3-5 

Structure of Xylenes (from National Library of Medicine)*** 

D3.1.2.1.2 Environmental Transformation and Degradation of Carriers and Dispersants 

1,2,4-TRIMETHYLBENZENE 

If released to the atmosphere, 1,2,4-trimethylbenzene will exist in the vapor phase, where it is 

subject to degradation by hydroxyl and nitrate radicals but not by direct photolysis (HSDB 

2009). 1,2,4-trimethylbenzene is expected to partition to organic matter if released to soil; and as 

a result, should have only limited mobility in this environmental compartment. Aerobic 

biodegradation may occur in soils. In surface waters, 1,2,4-trimethylbenzene will partition to 

sediment, although some is also expected to volatilize based on the Henry’s Law Constant. 

Hydrolysis is not a significant loss process (HSDB 2009). 


SECTION D3 


ETHYLBENZENE 

Like 1,2,4-trimethylbenzene, if ethylbenzene is released to the atmosphere, it will exist in the 

vapor phase where it is subject to degradation by hydroxyl radicals (HSDB 2009). The Henry’s 

Law Constant reflects a tendency to volatilize readily from moist soils; volatilization from dry 

soils will also occur (HSDB 2009). In surface waters, ethylbenzene will tend to sorb to 

suspended solids and to sediments, although if released to the surface, volatilization will also 

occur. Hydrolysis is not expected to occur. Measured BCFs of 0.67 to 15 indicate a minimal 

potential for bioaccumulation (HSDB 2009). 

ETHYLTOLUENES 

No information on the environmental fate of the ethyltoluenes was found. 

XYLENES 

Xylenes released to ambient air are expected to exist solely in the vapor phase. Once in the 

atmosphere, xylenes react with hydroxyl radicals, resulting in a relatively short half-life for 

xylenes of 1 to 2 days (HSDB 2009). If released to moist soil or to water, xylenes will tend to 

volatilize to air, although some of the material may remain sorbed to soil or sediment organic 

carbon. In surface waters, the estimated half-life ranges from 3 to 99 hours (HSDB 2009). 

Biodegradation of xylenes occurs in soil and groundwater under both aerobic and anaroebic 

conditions (HSDB 2009). A BCF of 20 was determined experimentally in eels. Although not 

definitive because data are available for only a single species, this low BCF suggests little 

potential exists for bioconcentration of xylenes in aquatic organisms (HSDB 2009). 

D3.1.2.2 

Mammalian Toxicity of Carriers and Dispersants 

D3.1.2.2.1 1,2,4-Trimethylbenzene 

The potential adverse health effects of exposure to 1,2,4-trimethylbenzene will not be 

quantitatively evaluated when present as an inert ingredient of a product formulation used in the 

No Program Alternative. However, 1,2,4-trimethylbenzene will be quantitatively evaluated when 

introduced as a component of Permethrin E-Pro used in the MMA Alternative. 

Toxicity data for 1,2,4-trimethylbenzene are extremely limited. The HSDB (2009) reports that 

1,2,4-trimethylbenzene is a central nervous system depressant and respiratory irritant. It is also 

irritating to the skin and eyes (HSDB 2009). No exposure data were provided to characterize the 

concentrations of 1,2,4-trimethylbenzene or duration of exposure associated with induction of 

these effects. TOXNET (2009) summarizes acute toxicity data for 1,2,4-trimethylbenzene. These 

data include a 48-hour LC > 2000 parts per million, and oral LD 50 s that range from 2720 mg/kg 

to 6000 mg/kg. Chronic inhalation exposure can result in bronchitis, although this outcome is 

likely associated with exposure to high concentrations that occur over long periods of time 

(HSDB 2009). The USEPA has identified a provisional RfC for 1,2,4-trimethylbenzene of 

7 x 10 -3 mg/m 3 which is equivalent to 2 x 10 -3 mg/kg-d (USEPA 2008). A subchronic RfC of 

7 x 10 -2 mg/m 3 , equivalent to 2 x 10 -2 mg/kg-d is also cited in the Provisional Peer Reviewed 

Toxicity Values (USEPA 2008b). An inhalation RfD of 2 x 10 -3 mg/kg-d and subchronic 

inhalation RfD of 2 x 10 -2 mg/kg-d were used as toxicity values in the HHRA. 




DRAFT PEIR 


D3.1.2.2.2 Ethylbenzene 

METABOLISM AND ELIMINATION 

Ethylbenzene can be absorbed following exposure by inhalation, ingestion, or dermal contact; it 

can also cross the placenta (HSDB 2009; ORNL 1997). In humans and animals exposed by 

inhalation, a substantial portion of the administered dose was retained (49 to 64% for humans, 

and 44% for animals).of an inhaled dose was retained in the body (NTP 1999). 

Following inhalation, ethylbenzene distributes to the liver, fat, and gastrointestinal tissues. An 

oral exposure resulted in the detection of ethylbenzene in the intestine, liver, and kidney (ORNL 

1997). 

Differences exist in the metabolism of ethylbenzene between humans and animals, with the 

dominant human metabolites mandelic acid (64 to 70%) and phenylglyoxylic acid (25%) (ORNL 

1997). These metabolites are also produced by animals, although they are of relatively minor 

importance. Hippuric acid, glycine conjugates of benzoic acid, phenylacetic acid, mandelic acid, 

and glucuronide conjugates of methylphenylcarbinol and phenylethanol have all been identified 

as metabolites of ethylbenzene in animals (ORNL 1997). These metabolites are water-soluble, 

and urinary elimination is the primary route of ethylbenzene elimination (ORNL 1997). 

ACUTE TOXICITY 

In animals, oral LD 50 values reportedly range from 3.5 to 5.5 g/kg in rats (ORNL 1997). 

Ingestion of sublethal amounts may cause central nervous system depression, gastric upset, and 

vomiting (ORNL 1997). 

SUBCHRONIC TOXICITY 

Inhalation exposure of rats and mice to 0 to 1,000 ppm ethylbenzene, 6 hours/day, 5 days/week 

for 90 days resulted in dose-dependent increases in liver weights at doses of 250 ppm and above, 

and altered liver enzyme levels at doses above 500 ppm. An increase in relative kidney weights 

was documented in animals exposed to 500, 750, and 1,000 ppm (OEHHA 1999) 

Female rats administered 408 or 680 mg/kg-d ethylbenzene, 5 days/week for 6 months by oral 

intubation developed slight, statistically significant increases in liver and kidney weights and 

cloudy swelling of the parenchymal cells of the liver and renal tubular epithelial cells (ORNL 

1997). No adverse effects were seen at dose levels of 13.6 and 136 mg/kg-d 

Developmental malformations were induced in the offspring of rats administered ethylbenzene at 

2400 mg/m 3 , 24 hours/day, 7 days/week on days 7 to 15 of gestation (OEHHA 1999). The 

offspring of animals exposed to 0, 600, 1200 mg/m 3 , as well as those in the high dose group 

exhibited skeletal malformations. Rabbits exposed to the same concentrations and by the same 

exposure protocol did not produce any live fetuses that could be evaluated for abnormalities. 

Some maternal toxicity was reported in the 1,000-ppm group, but it is not clear if maternal 

toxicity was a factor for other dose groups as well. 

Other developmental study results cited by OEHHA (1999) reported no effects in the offspring 

of rabbits exposed to ethylbenzene (0, 100, or 1,000 ppm) 6 or 7 hours/day, 7 days/week during 

days 1 through 24 of gestation. Rats exposed to ethylbenzene via the same protocol displayed 

maternal toxicity in the high dose group, and fetuses from this group had an increase in skeletal 

variations (OEHHA 1999). 


SECTION D3 


CHRONIC TOXICITY 

Rats and mice exposed to ethylbenzene by inhalation (0 to 750 ppm) for 2 years (6 hours/day, 5 

days/week for 104 weeks) had lower body weights than controls. Additionally, high-dose male 

rats exhibited renal tubule hyperplasia, nephropathy, and an increased incidence of renal tumors. 

Nephropathy was also noted in female rats (all dose groups), although the incidence became 

statistically significant only in the 750-ppm group (OEHHA 1999). Mice in the high dose group 

had lung and liver tumors, and a significant increase in eosinophilic liver foci (females). 

Numerous pathological changes occurred in the livers of male mice (dose levels not specified by 

OEHHA 1999). The incidence of hypertrophy of the pituitary gland (250- and 750-ppm females) 

and thyroid gland follicular cell hyplerplasia (750-ppm males and females) were significantly 

different than controls (OEHHA 1999). 

GENOTOXICITY 

ATSDR (1999) has reviewed the ability of ethylbenzene to induce mutations or DNA damage in 

vitro and in vivo. Ethylbenzene is not mutagenic in Salmonella reverse mutation assays, in 

Escherichia coli assays, or in gene conversion assays in Saccharomyces cerevisiae (ATSDR 

1999). At levels that were cytotoxic, ethylbenzene induced mutations in L5178Y mouse 

lymphoma cells. Ethylbenzene has not induced chromosomal damage in mammalian cells, nor 

has it caused an increase in sister chromatid exchange or chromosomal aberrations in Chinese 

hamster ovary cells (ATSDR 1999). Ethylbenzene did not affect the incidence of micronuclei in 

bone marrow cells of rodents following single or repeated exposures (ATSDR 1999). OEHHA 

(2007) cites data indicating that two metabolites of ethylbenzene may induce DNA damage in 

vitro. 

CARCINOGENICITY 

No epidemiological information is available on the potential carcinogenicity of ethylbenzene in 

humans. 

OEHHA (2007) reviewed the results of a carcinogenicity bioassay of ethylbenzene conducted by 

the NTP. That study exposed rats or mice to ethylbenzene by inhalation (0, 75, 250, or 750 ppm), 

6.25 hours/day, 5 days/week for 104 weeks. Rats had significant increases in the incidence of 

renal tumors (adenoma and carcinoma in males; adenoma only in females) in the high dose 

group. High dose male rats also had a significant increase in testicular adenomas. In mice, 

incidence of alveolar/bronchiolar adenoma and adenoma or carcinoma (combined) increased in 

high dose male mice. Among female mice, the incidences of combined hepatocellular adenoma 

or carcinoma and hepatocellular adenoma alone were significantly increased over control 

animals. The NTP concluded that evidence of carcinogenicity was clear in male rats and some 

evidence in female rats, based on the renal tumorigenicity findings. Additionally, some evidence 

of carcinogenicity existed in male and female mice. Based on the NTP data, California has 

developed CSFs for ethylbenzene, and has listed ethylbenzene as a carcinogen under Proposition 

65 (OEHHA 2007). 

The IARC (2000) has classified ethylbenzene as Group 2B, possibly carcinogenic to humans. 

D3.1.2.2.3 Interpretation of Human Toxicity Based on Animal Studies 


ethylbenzene, regulatory agencies necessarily rely on data from animal studies to characterize 




DRAFT PEIR 


exposure levels deemed to be safe for humans. Noncancer toxicity criteria for ethylbenzene have 

been developed by the ATSDR (2007a) and the USEPA (2009a). Notwithstanding the use of 

different terminology for their respective toxicity criteria (MRLs for ATSDR, and RfDs for the 

USEPA), both of the agencies use comparable methodology to derive the noncancer toxicity 

criteria. 



exposures referred to as the RfC or inhalation RfDinh. The RfD and RfC/RfDinh are each 

defined as the daily exposure level for the “…human population (including sensitive subgroups) 

that is likely to be without an appreciable risk of deleterious effects during a lifetime” (USEPA 

2009b). RfDs or RfCs are typically derived by selecting the most scientifically appropriate 

NOAEL from relevant animal toxicology studies, and then applying one or more UFs of 3 or 10 

to address data limitations. These UFs are used to account for intraspecies variability, 

interspecies variability, the extrapolation of data from animals to humans, differences in duration 

between the experimental period and lifetime exposure, and/or for the overall quality and 

completeness of available toxicity data (USEPA 2009b). 

The ATSDR defines a MRL as an “estimate of daily human exposure to a substance that is likely 

to be without appreciable risk of adverse effects (noncarcinogenic) over a specified duration of 

exposure.” 






In deriving the oral RfD for ethylbenzene, the USEPA (2009a) relied on a study (Wolf et al. 

1956) that identified a no observed effect level (NOEL) of 136 mg/kg (converted to 97.1 mg/kgd 

by USEPA 2009a). In that study, the LOAEL of 408 mg/kg-d was associated with 

histopathological evidence of liver and kidney toxicity when ethylbenzene was given 

5 days/week at doses of 13.6 to 680 mg/kg. The USEPA applied a net UF of 1,000 to the NOEL 

and obtained the RfD of 1.0 x 10 -1 mg/kg. 

The USEPA RfC for ethylbenzene is 1.0 x 10 1 mg/m 3 (USEPA 2009a). That value was 

developed from an inhalation study (Andrew et al. 1981) in which rats and rabbits were exposed 

to ethylbenzene at concentrations of 0 to 1,000 ppm 6 to7 hours/day, 7 days/week during days 1- 

19 and 1-24 of gestation, respectively. For rabbits, a NOAEL of 100 ppm was identified, where 

the LOAEL was associated with a decrease in the number of live kits per litter. No evidence 

existed of major or minor malformations or ‘common variants’ in fetal rabbits from exposed 

groups. Rats exposed during gestation showed a statistically significant increase in the incidence 

of supernumerary and rudimentary ribs in the high exposure group, and an increase in the 

incidence of extra ribs in the 1,000 ppm group. Some maternal toxicity was observed in the high 

dose group. The USEPA considered 1,000 ppm to be a LOAEL. When the NOAEL is converted 

from ppm to mg/m 3 , it yields a value of 434 mg/m 3 . Applying an UF of 300 gives the RfC of 

1 mg/m 3 , equivalent to an RfD of 2.9 x 10 -1 mg/kg-d. 


SECTION D3 


OEHHA derived a chronic reference exposure level (REL) for ethylbenzene of 2 mg/m 3 

(equivalent to 5.7 x 10 -1 mg/kg-d). This REL was based on data from a lifetime toxicity and 

carcinogenicity study in rats and mice conducted by the National Toxicology Program and cited 

by OEHHA (1999). Animals were exposed for 6 hours/day, 5 days/week for 103 weeks. The 

study results identified nephrotoxicity, body weight reductions, cellular alterations and necrosis 

of the liver, and hyperplasia of the pituitary gland as effects of exposure to ethylbenzene. A 

NOAEL of 75 ppm was identified, and OEHHA applied a cumulative uncertainty factor of 30 to 

account for interspecies variability (3) and intraspecies variability (10) to develop the REL of 0.4 

ppm, equivalent to the value of 2 mg/m 3 cited above. 

The ATSDR’s acute inhalation MRL for ethylbenzene is based on a study that evaluated auditory 

damage subsequent to exposure (Cappaert et al. 2000). Rats were exposed to 0 to 500 ppm 

ethylbenzene, 8 hours/day for 5 days. The study authors identified a NOAEL of 300 ppm, and a 

LOAEL of 400 ppm based on a significant deterioration in compound action potential auditory 

threshold, and significant outer hair cell loss. Applying a compound UF of 30 gives an acute 

inhalation MRL of 10 ppm. ATSDR’s intermediate inhalation MRL for ethylbenzene was 

derived from a study in which rats were exposed to 0 to 800 ppm ethylbenzene 6 hours/day, 6 

days/week for 13 weeks (Gagnaire et al. 2007). As in the Cappaert et al. (2000) study, the 

Gagnaire et al. study used sensitive and specific measurements to evaluate ototoxicity. Gagnaire 

et al. (2007) reported that ethylbenzene exposure resulted in higher audiometric thresholds in 

animals exposed to 400, 600, and 800 ppm ethylbenzene relative to controls. Significant losses 

occurred in the hair cells in the organ of Corti in rats exposed to 200 ppm, with a dose-related 

loss of these cells in the 600 and 800 ppm groups. The LOAEL for hair cell loss was 200 ppm, 

with no NOAEL established. ATSDR (2007a) applied a compound UF of 300 to yield a 

subchronic inhalation MRL of 0.7 ppm. 

ATSDR based the chronic inhalation MRL on data from the NTP’s 2-year study of toxicology 

and carcinogenesis of ethylbenzene. Groups of rats or mice were exposed to ethylbenzene by 

inhalation (0, 75, 250, or 750 ppm), 6.25 hours/day, 5 days/week for 104 weeks. An increase in 

the severity of nepropathy was observed in female rats at doses of 75 ppm and above, and in 

males exposed to 750 ppm. High dose male rats also had a higher incidence of renal tubule 

proliferative lesions, of renal tubule hyperplasia, and degeneration of the liver relative to control 

animals. Female mice exhibited a significant increase in the incidence of hyperplasia of the 

pituitary gland pars distalis, whereas high dose male mice had a significant increase in the 

incidence of alveolar epithelial metaplasia. Female mice displayed eosinophilic foci of the liver 

(750 ppm); male mice at all dose levels had alterations in hepatocytes, with the increase 

becoming significant at doses above 250 ppm. The findings from this study relative to the 

induction of tumors was previously reviewed (see section on carcinogenicity of ethylbenzene). 

This study identified a LOAEL of 75 ppm based on increases in the severity of nephropathy in 

female rats. The ATSDR applied a compound UF of 300, to yield a chronic inhalation MRL for 

ethlybenzene of 0.3 ppm. 

The toxicity criteria that have been developed for ethylbenzene are summarized in Tables D3-10 

and D3-11. 

Table D3-10 

Noncancer Toxicity Criteria for Ethylbenzene 

Acute MRL a Intermediate Chronic MRL RfD RfC REL 




DRAFT PEIR 


10ppm 

(12.4 mg/kg-d) a 

MRL b 

0.7 ppm 

(8.7 x 10 -1 mg/kgd) 

a 

0.3 ppm 

(3.7 x 10 -1 mg/kgd) 

a 1.0 x 10 -1 mg/kg b 

1.0 x 10 1 mg/m 3 

(2.9 x 10 -1 ) mg/kg b 

Notes: 

a The Acute MRL was converted to units of mg/kg-d and provides the basis for the Acute Inhalation RfD used in the risk calculations. 

b The Intermediate MRL was converted to units of mg/kg-d and provides the basis for the Subchronic Inhalation RfD used in the risk calculations 

c ATSDR 2007a 

d USEPA 2008 

e OEHHA 2000b 


2 mg/m 3 

(5.7 x 10- 1 mg/kg-d) c 

Table D3-11 

Cancer Criteria for Ethylbenzene 

Proposed NSRL a 

(oral) µg/d 

Proposed NSRL a 

(inhalation) µg/d 

Cancer Slope Factor (inhalation) b 

(mg/kg-d) -1 

Cancer Slope Factor (oral) b 

(mg/kg-d) -1 

41 54 8.7 x 10 -3 1.1 x 10 -2 

Notes: 

aOEHHA 2009a 

bOEHHA 2009a 


D3.1.2.2.4 Ethyltoluenes 

Only extremely limited toxicity data are available on the ethyltoluenes. No toxicity criteria were 

identified, and no evidence was found to indicate that this substance has been evaluated for 

genotoxicity or for carcinogenicity. Of the numerous databases available through the National 

Library of Medicine, only the National Oceanic and Atmospheric Administration’s Cameo 

(Cameo) database contained information, and that was only summary in nature (Cameo 2009). 

The Cameo summary indicates that ethyltoluene vapors are irritating to the eyes and respiratory 

tract. Consistent with other aromatic hydrocarbons (e.g., xylenes, ethylbenzene), exposure to the 

ethyltoluenes can cause dizziness and headache, and at high enough concentrations (not 

specified), anesthesia and respiratory arrest (Cameo 2009). Ingestion causes vomiting, diarrhea, 

and respiratory depression (Cameo 2009). No exposure data were provided to characterize the 

concentrations of ethylbenzenes or duration of exposure associated with induction of these 

effects. 

D3.1.2.2.5 Xylenes 


Xylenes are small nonpolar compounds that are readily absorbed across the skin or the epithelia 

of the gut and lungs. In animals, the extent of oral absorption varies depending on the isomer, 

with some data indicting that the para (p-) isomer is most extensively absorbed, following the 

meta (m-) and othor (o-) isomers (ORNL 2005). In humans exposed by inhalation, 

approximately 60% of the available xylenes were absorbed, regardless of isomer (ORNL 2005). 

Dermal absorption of liquid xylenes can be significant, but dermal absorption of xylenes present 

in air represents only a minor exposure pathway (ORNL 2005). 

Subsequent to exposure, xylenes distribute to blood and tissues, where they tend to accumulate in 

muscle and fat (ORNL 2005). The half-life for elimination of xylene from subcutaneous fat has 

been estimated to be greater than 40 hours in humans, indicating accumulation may occur with 

repeated exposure (ORNL 2005). The xylene that is not retained in tissues is subject to oxidation 


SECTION D3 


of the methyl group to the corresponding methylbenzoic acid and methylhippuric acids. These 

metabolites are water-soluble, and are eliminated in urine (ORNL 2005). 

TOXICITY 

High-dose exposure to xylenes by either oral or inhalation routes can result in death due to 

respiratory failure accompanied by pulmonary congestion (ORNL 2005). Nonlethal levels of 

xylene vapor may cause eye and respiratory tract irritation, and contact with liquid xylenes may 

result in dermatitis (ATSDR 2007b; ORNL 2005). Chronic occupational exposure to xylene has 

been associated with headaches, chest pain, electrocardiographic abnormalities, fever, 

leukopenia, malaise, impaired lung function, and confusion (ORNL 2005). 

Experimental data from animal studies have demonstrated that neurological effects are the most 

sensitive effect of xylene inhalation exposure; effects on certain neurobehavioral endpoints have 

been observed at xylene concentrations as low as 100 ppm following subchronic exposure 

(USEPA 2003). At higher inhalation exposure levels, changes in bodyweight have been reported, 

but this effect has not been consistently observed (USEPA 2003). Repeated inhalation exposure 

to xylenes has been linked to neurological impairment and developmental effects in addition to 

transient respiratory tract irritation and neurological impairment from acute exposure. Data 

reviewed by the USEPA (2003) identified a threshold of 100-200 ppm for short-term reversible 

irritant and neurological effects from xylene exposure. Exposure to the m-isomer (> 100 ppm, 6 

hours/day, 5 days/week) can result in ‘persistent’ adverse effects on certain neurological function 

in adult rats, including hearing loss (USEPA 2003). 

Results from subchronic oral exposures in rodents indicate that decreases in body weight may 

results from repeated oral exposure to xylenes when doses are > 500-800 mg/kg-d. Other 

experimental observations from xylene-exposed animals include increases in liver weight 

(without histological changes), and increases in kidney weights (with evidence of nephropathy) 

(USEPA 2003). Neurological effects from oral exposure occur only at levels greater than those 

associated with changes in body weight. For example, the USEPA (2003) cites a NTP study of 

13 weeks duration that identified various signs of neurological impairment in mice exposed to 

2,000 mg/kg xylenes (mixed isomers), but not in animals exposed to 1,000 mg/kg. 

Developmental effects, such as cleft palates, have been observed in fetuses of mice exposed to 

2060 mg/kg-d on GDs 6-15; a separate study noted the same effect in the fetuses of mice 

exposed to 1960 mg/kg, but no in animals exposed to 780 mg/kg (USEPA 2003). In other 

developmental studies, decreased fetal body weight and decreased fetal survival occurred in 

animals exposed to xylene isomers by inhalation at 350 or 700 ppm (duration not specified), or 

to xylene mixtures (780 ppm, 24 hours/day, duration not specified) (USEPA 2003). However, 

these effects occurred at concentrations above those that elicited neurological effects in adults. 

GENOTOXICITY 

The ATSDR (2007b) has reviewed the extensive database on the genotoxicity on xylenes, and 

concluded that the majority of evidence suggests that xylenes are not mutagenic or capable of 

inducing chromosomal aberrations. That conclusion is based on the fact that xylenes have 

consistently given negative results in reverse mutation assays in vitro; in in vivo assays of sister 

chromatid exchange, chromosomal aberrations, or micronuclei formation, or in in vitro assays of 

DNA damage. 




DRAFT PEIR 



No epidemiological information is available on the potential carcinogenicity of xylenes in 

humans. 

The USEPA has determined that data are inadequate for an assessment of the carcinogenic 

potential of xylenes (USEPA 2009a). This conclusion is based on the fact that adequate human 

data on the carcinogenicity of xylenes are not available, and the available animal data are not 

conclusive with respect to the potential of xylenes to cause a carcinogenic response. As noted by 

the USEPA (2009a), a number of human occupational studies have suggested that chronic 

inhalation exposure to xylenes may be linked to possible carcinogenicity; however, in each case 

co-exposure to other chemicals was a confounding factor, and made it impossible to assess the 

effects of chronic exposure to xylenes alone. 

The USEPA (2009a) cites data developed by the NTP, in which a 2-year bioassay of xylenes was 

conducted. Rats were exposed to 0, 250, or 500 mg/kg-d of mixed xylenes by gavage for 

5 days/week for 103 weeks. No evidence of carcinogenesis was seen in male or female rats. Mice 

exposed to 0, 500, or 1,000 mg/kg-d for 2 years also showed no evidence of a carcinogenic 

response. 


As an inert ingredient present in a product formulation used only in the No Program Alternative, 

potential adverse health effects of exposure to xylenes will not be quantitatively evaluated. 

However, OEHHA (1999) has derived acute and chronic RELs for xylenes, and the basis of 

these values is provided here as background information. 

OEHHA’s acute REL for xylenes was developed based on data from three studies of human 

volunteers. Individuals were exposed to xylenes at concentrations up to 3,000 mg/m 3 for periods 

less than 1 hour. In all three studies, adverse effects of exposure were eye, nose, and throat 

irritation. Considered collectively, OEHHA identified a NOAEL for eye irritation (the most 

sensitive endpoint measured) of 100 ppm (430 mg/m 3 ). OEHHA applied an UF of 10 to account 

for intraspecies variability, and calculated the acute REL of 5 ppm (22 mg/m 3 , or 22,000 μg/m 3 ). 

The chronic REL for xylene is based on a human occupational study, in which 175 xyleneexposed 

factory workers were evaluated relative to a control population of 241 factory workers. 

Exposures occurred by inhalation during an 8-hour work day, and took place over a 7-year 

period. The geometric mean exposure concentration was 14.2 ppm, which was also identified as 

the LOAEL. A NOAEL could not be identified. Documented adverse effects included a 

concentration-related increase in the prevalence of eye irritation, sore throat, poor appetite, and a 

floating sensation. OEHHA applied a cumulative UF of 30 to the LOAEL (3 for use of a LOAEL 

instead of a LOAEL, and 10 for intraspecies variability), to derive the chronic REL of 0.2 ppm 

(0.7 mg/m 3 , or 700 μg/m 3 ). The value is applicable to mixed xylenes or to a total concentration 

of individual isomers. 

D3.1.3 

Lambda-Cyhalothrin 

Lambda-cyhalothrin ([1-alpha(S*),3-alpha(Z)]-cyano(3-phenoxyphenyl)methyl-3-(2-chloro- 

3,3,3-trifluoro-1-propenyl)-2,2-dimethylcyclopropanecarboxylate (9CI)) (CAS number 91465- 

08-6) is a fourth generation broad spectrum type II pyrethroid introduced by Zeneca 


SECTION D3 


Agrochemicals in 1986 (ATSDR 2003a). Pyrethroids are synthetic chemical analogues of 

pyrethrins, which are naturally occurring insecticidal compounds produced in the flowers of 

Chrysanthemums. Fourth generation pyrethroids are the most recent generation of pyrethroids, 

having relatively low application rates, high photostability and low volatility compared to earlier 

pyrethroids. In contrast to Type I pyrethroids, Type II pyrethroids, including lambda-cyhalothrin, 

have a positive temperature coefficient; that is, increased effectiveness with increased ambient 

temperature (Scott 1995). Lambda-cyhalothrin is the active ingredient in a number of registered 

pesticides including: Warrior ® , Karate ® , Scimitar ® , Demand ® , Icon ® , and Matado ® that are 

labeled for agricultural and public health use; it is also an active ingredient in a number of home 

use pesticides available to the public. 

Cyhalothrin is created through the esterification of 3-(2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2- 

dimethylcyclopropanecarboxylic acid chloride with alpha-cyano-3-phenoxybenzyl alcohol. This 

process produces a racemic (equal proportions) mixture of four stereo isomers in two 

enantiomeric pairs of differing insecticidal activity. The more biologically active of the pairs of 

enantiomers are crystallized from cyhalothrin to form lambda-cyhalothrin. Lambda-cyhalothrin 

was registered for use by the USEPA in 1988 (Syngenta 2007). The structure of lambdacyhalothrin 

is shown on Figure D3-6. 

Figure D3-6 

Chemical Structure of Lambda-Cyhalothrin 

Lambda-cyhalothrin is used as an agricultural pesticide on a wide range of crops and it may also 

be used for structural pest management or in public health applications to control insects such as 

cockroaches, mosquitoes, ticks and flies, which may act as disease vectors (ATSDR 2003a). In 

the Sacramento, San Joaquin, and Central Valleys of California, the use of lambda-cyhalothrin 

increased during the period 1998 to 2003, from 692 pounds per year to 8432 pounds per year, 

respectively (Oros and Werner 2005). In 2005, 37,000 pounds were used statewide (DPR, 2007). 

D3.1.3.1 

Environmental Fate and Chemistry of Lambda-cyhalothrin 

Once introduced into the environment, the fate of lambda-cyhalothrin is controlled by adsorption 

to particles. It dissipates from water by adsorption, biodegradation and photolysis with an 

apparent half-life of less than 1 day. It degrades by photolysis in soil if exposed to sunlight, but 

in soil it degrades primarily by microbial action (I). Half lives in soil are reported from 9 to 84 

days with a representative half-life of 30 days. Lambda-cyhalothrin partitions readily to the 

organic material in sediment, which can protect it from degradation processes (National Pesticide 

Telecommunications Network [NPTN] 2001). 

D3.1.3.1.1 Physical Chemistry 

Lambda-cyhalothrin is one of several fourth generation pyrethroids designed to have low LD 50 , 

low vapor pressure, and low solubility in water (Ware and Whitacre 2004). Technical grade 

lambda-cyhalothrin is a beige solid and can appear yellowish in solution. 




DRAFT PEIR 


Lambda-cyhalothrin has a high K OW (7.00 log K OW at 20°C) and a high soil adsorption 

coefficient (K OC 2.4–3.3 x 10 5 cm 3 /g) so tends to adsorb onto mineral soil components and 

partition into organic soil components. Pesticides with K OC greater than 1,000 are considered 

immobile in soil, and unlikely to contaminate groundwater by leaching as dissolved residues in 

percolating waters (McCarty et al. 2003). Transport of bound residues on particles in water is the 

most likely mechanism for movement of lambda-cyhalothrin in the environment (He et. al. 

2008). 

Lambda-cyhalothrin is stable in water at pH 5, and as pH levels rise, racemization occurs to 

create a 1:1 mixture of enantiomers and at pH 9, the ester bond is readily hydrolyzed with a halflife 

of 7 days (see Table D3-12). 


SECTION D3 


Table D3-12 

Physical-Chemical Properties of Lambda-Cyhalothrin 

CAS number 91465-08-6 

Molecular formula 

Molecular weight 

C23H19ClF3NO3 

449.9 g/mol 

Density 1.33 g/mL at 25°C 

Melting point 

Boiling point 

49.2°C 

187–190°C at 0.2 mmHg 

Vapor pressure 0.0002 mPa at 20°C 


0.018 Pa-m 3 /mole 

Water solubility 0.005 mg/L at 20°C 

Solubility in other solvents (e.g., acetone) 

> 500,000 mg/L 

Octanol-water partition Coefficient (log KOW at 20°C) 7.00 

Source: 

Ware and Whitacre 2004 

Hydrolysis half-life (d) -- 

pH 5 

pH 7 

Stable 

Stable 

pH 9 8.66 

Photolysis half-life (d) -- 

Soil 53.7 

BCF (fish) 2,240 

Soil Partition Coefficient KOC 247,000–330,000 cm 3 /g 


AIR 

Due to both a low vapor pressure (1.5 x 10 -9 mmHg) and Henry’s Law Constant (0.018 Pam 

3 /mole) lambda-cyhalothrin does not volatilize into the atmosphere. 

WATER 

Lambda-cyhalothrin has extremely low water solubility and once is adsorbed it is tightly bound 

to soil; it is therefore not expected to be prevalent in surface waters (Ware and Whitacre 2004). 

Photolysis appears to be an important route for the degradation of lambda-cyhalothrin 

(International Program on Chemistry Safety [IPCS] 1990). Studies found lambda-cyhalothrin 

dissipated from the water phase of ditch water more quickly than is predicted by photolysis, with 

less than 30 % of the applied amount remaining after 1 day, and was undetectable only 4 days 

after application in simulated rice paddy water (He et.al. 2008). Also in a study of runoff from an 

alfalfa field, vegetation in return ditches was shown to significantly reduce dissolved residues of 

lambda-cyhalothrin (Gill 2008). These data suggest that adsorption to plants and particles 

contributes significantly to the removal of dissolved lambda-cyhalothrin from surface water. 

SOIL 

Due to the high K OC , lambda-cyhalothrin is not expected to be mobile in soil. The strength of the 

adsorption to soil varies with the amount and polarity of soil organic components. Leaching 




DRAFT PEIR 


studies show that lambda-cyhalothrin applied to the soil surface is unlikely to move more than 

about 15 cm into the soil column (He et al. 2008). Studies comparing sterile to nonsterile soil 

found relatively quick dissipation of lambda-cyhalothrin from the nonsterile systems indicating 

biodegradation is a potential environmental removal mechanism (He et al. 2008). Field soil 

dissipation studies found that dissipation rates change; with an initial rapid dissipation due to 

photolysis and hydrolysis, followed by a slower steady decline due to biodegradation (He et al. 

2008). 

Field studies show the half-life of lambda-cyhalothrin is close to 30 days in most soils; 

degradation in soil occurs primarily through hydroxylation followed by cleavage of the ester 

linage to give two main degradation products, the same as for water degradation, which are 

further degraded to carbon dioxide (IPCS 1990). 

D3.1.3.2 


Lambda-cyhalothrin is comprised of two stereo isomers of the four-isomer racemic parent 

compound, cyhalothrin (IPCS 1990). Given this common chemistry, many of the toxicity studies 

submitted to the USEPA (e.g., 2002a) in support of lambda-cyhalothrin pesticide tolerance 

evaluations were conducted with cyhalothrin. In the following discussion, toxicity data are 

considered for both compounds, with preference given to data specific to lambda-cyhalothrin, 

when available. 

D3.1.3.2.1 Mechanism of Action in Mammals and Humans 

Pyrethroids are separated into two broad categories–Type I and Type II– based on distinct 

chemical and toxicological properties (Bloomquist 1996; ATSDR 2003a). In general, the Type II 

group, which includes lambda-cyhalothrin, contain a cyano-3-phenoxybenzyl alcohol substituent 

(Bloomquist, 1996; ATSDR 2003a). Pyrethroid’s primary toxicity is manifested in the nervous 

system of insects as well as mammals, where they act as neurotoxins. Lambda-cyhalothrin’s 

neurotoxicity is a function of its ability to prolong sodium ion permeability in neuronal 

membranes during the excitatory phase of the action potential, and by so doing, interfere with 

nerve impulse generation. In insects, the Type II pyrethroids cause predominantly ataxia and 

incoordination, while in mammals they produce “sinuous writhing” and salivation (Bloomquist 

1996). Pyrethroids affect nerve impulse generation in both sensory and motor neurons of the 

peripheral nervous system, as well as in interneurons of the central nervous system (Bloomquist 

1996; ATSDR 2003a). Type II pyrethroids, like lambda-cyhalothrin, can also affect chloride and 

calcium channels, further affecting nerve function. Because they are lipophilic, pyrethroids are 

readily absorbed by biological membranes and tissues (IPCS 1990; USEPA 2002a). 

D3.1.3.2.2 Metabolism and Elimination 

Studies in multiple species indicate that cyhalothrin is fairly well absorbed following oral 

administration, with approximately 50% (rats), 50-80% (dogs), and 80% (cows) absorbed, 

respectively (Harrison et al. 1981, 1984a, 1984b, 1984c, 1984d; Prout and Howard 1985). In 

humans, oral and dermal uptake studies documented oral absorption quantities that ranged from 

50.35 to 56.71%. Dermal absorption was reportedly quite limited, ranging from 0.115 to 0.122% 

(USEPA 2007b, 2007c). 

The distribution, metabolism, and elimination of lambda-cyhalothrin and cyhalothrin were not 

appreciably different when rats were given radiolabeled doses of either compound, and followed 


SECTION D3 


for 119 days (Prout and Howard 1985). The pattern of distribution of cyhalothrin is similar 

regardless of whether the exposure is a single or multiple events (USEPA 2002a). 

Following absorption, cyhalothrin is eliminated in the urine as water-soluble metabolites, as well 

as unchanged in the feces. In those animal species studied to date, the dominant metabolic 

pathway is by hydrolysis of the ester linkage followed by glucuronide conjugation, oxidation, 

and/or sulfation. Significant mammalian metabolites include cyclopropyl carboxylic acid, 3- 

phenoxybenzoic acid, glucuronide-conjugated 3-4”-hydroxyphenoxybenzoic acid, and a sulfate 

conjugate (IPCS 1990; USEPA 2002a). 

Lambda-cyhalothrin did not accumulate in the tissues of cows fed at doses of 1, 5, or 25 mg/kg 

for up to 30 days, and levels declined when treatment was discontinued. As would be expected 

from its lipophilic character, the highest levels of lambda-cyhalothrin were documented in fat 

(Sapiets 1985). 


Consistent with its action on sodium channel permeability, acute exposure to lambda-cyhalothrin 

has been linked with changes in neurological function when administered at a single dose of 0, 

2.5, 10, or 35 mg/kg-d (USEPA 2002a). Rats exposed for 4 hours to an aerosol of cyhalothrin at 

concentrations of 3.68 to 68 mg/m 3 exhibited a concentration-dependent increase in signs of 

eurotoxicity. Effects ranged from lethargy and salivation at the lowest concentration, to death 

(shortly after termination of exposure) at the highest concentration (Curry and Bennett 1985). 

The median lethal oral dose (LD 50 ) of lambda-cyhalothrin has been reported at 56 to 79 mg/kg 

for female and male rats, respectively or as high as 144 mg/kg (Ray 1991). Technical-grade 

lambda-cyhalothrin is less toxic when exposure occurs dermally, given its relatively poor 

absorption by this route; dermal LD 50 s of 632 mg/kg and 696 mg/kg for male and female rats 

have been cited. One of the formulated products, Karate ® , can cause significant skin and eye 

irritation (Ray 1991). 

D3.1.3.2.4 Subchronic and Chronic Toxicity 

Table D3-13 summarizes the results of subchronic and chronic toxicity studies of lambdacyhalothrin 

and cyhalothrin, based on data provided in USEPA (2002a, 2004a, 2007b, 2007c) 

and ATSDR (2003a). The data in this table primarily encompass studies conducted in mice, rats, 

and dogs exposed orally, with one study that has evaluated the effects of inhalation exposure. 

Lambda-cyhalothrin and cyhalothrin have been repeatedly and consistently documented to cause 

decreased body weight gain and reduced food consumption from exposure levels as low as 0.9 

mg/kg-d, with numerous study results yielding NOAELs of 1 to 2.5 mg/kg-d. Signs of 

neurotoxicity and changes in organ weights are also common effects of exposure to lambdacyhalothrin 

and cyhalothrin (USEPA 2002a, 2004a, 2007b, 2007c). 




DRAFT PEIR 


Table D3-13 

Toxicity Profile of Lambda-Cyhalothrin 

Study Type Year/Doses Results 

Acute neurotoxicity–rat 

(lambda-cyhalothrin) 

13-Week feeding–rat 

(cyhalothrin) 

13-Week feeding–rat (lambdacyhalothrin) 

28-Day feeding–rat 

(cyhalothrin) 

28-Day feeding–rat 

(cyhalothrin) 

4-Week feeding–mouse 

(cyhalothrin) 

26-Week feeding–dog 

(cyhalothrin) 

21-Day dermal toxicity - rabbit 

(cyhalothrin) 

21-Day dermal toxicity - rat 


21-Day inhalation toxicity - rat 


Developmental toxicity–rat 

(cyhalothrin) 

Developmental toxicity–rabbit 

(cyhalothrin) 

1999/ 0, 2.5, 10, 35 mg/kg-d NOAEL a : 10 mg/kg 

LOAEL b : 35 mg/kg 

Clinical observations indicative of neurotoxicity and changes in 

functional 

observational battery (FOB) parameters. 

1981/0, 0.5, 2.5, 12.5 mg/kg-d NOAEL: 2.5 mg/kg-d 

LOAEL: 12.5 mg/kg-d 

Decreased body weight gain in males. 



Reduced body weight gain and food consumption in both sexes and 

food efficiency in females. 

1984/0, 2, 10, 25, 50, 75 mg/kg-d. NOAEL: 2 mg/kg-d 

LOAEL: 10 mg/kg-d 

Clinical signs of neurotoxicity. At higher doses, decreases in body 

weight gain and food consumption and changes in organ weights. 

1984/0, 0.1, 0.5, 1.0, 2.0, 25.0 

mg/kg-d 

1981/ 0, 0.65, 3.30, 13.5, 64.2, 309 

mg/kg-d (males). 

0, 0.80, 4.17, 15.2, 77.9, 294 

mg/kg-d (females). 

NOAEL: 1.0 mg/kg-d 


Decreases in mean body weight gain in females. 

NOAEL: 64.2/77.9 mg/kg-d 

LOAEL: 309/294 mg/kg-d 

Mortality, clinical signs of toxicity, decreases in bodyweight gain and 

food consumption. Changes in hematology and organ weights 

minimal centrilobularhepatocyte enlargement. 



Increase in liquid feces. At 10.0 mg/kg-d, clinical signs of 

neurotoxicity. 

1982/0, 10, 100, 1,000 mg/kg-d for 

6 hours/day, 5 days/week for total 

of 15 applications. 

1989/0, 1, 10 mg/kg-d for 6 

hours/day for 21 consecutive days; 

2-3 applications at 100 mg/kg-d, 

reduced to 50 mg/kg-d for 21 

consecutive days. 

1990/0, 0.3, 3.3, 16.7 [mu]g/L; 

approx. 0, 0.08, 0.90, 4.5 mg/kg-d 

NOAEL: 100 mg/kg-d 

LOAEL: 1,000 mg/kg-d 

Significant weight loss. 

NOAEL: 10 mg/kg-d 

LOAEL: 50 mg/kg-d (clinical signs of toxicity, decreased body weight 

and body weight gain) 

NOAEL: 0.08 mg/kg-d 


Clinical signs of neurotoxicity, decreased body weight gains, 

increased incidence of punctuate foci in cornea, slight reductions in 

females, slight changes in selected urinalysis parameters. 

1981/0, 5, 10, 15 mg/kg-d Maternal NOAEL: 10 mg/kg-d 

Maternal LOAEL: 15 mg/kg-d Uncoordinated limbs, reduced body 

weight gain and food consumption. 

Developmental NOAEL: 15 mg/kg-d, the highest dose tested 

(HDT) Developmental LOAEL: >15 mg/kg-d 

1981/0, 3, 10, 30 mg/kg-d Maternal NOAEL: 10 mg/kg-d 

Maternal LOAEL: 30 mg/kg-d 

Reduced body weight gain and food consumption. 

Developmental NOAEL: 30 mg/kg-d 

(HDT) Developmental LOAEL: >30 mg/kg-d 


SECTION D3 


Table D3-13 

Toxicity Profile of Lambda-Cyhalothrin 

Study Type Year/Doses Results 

3-Generation Reproduction–rat 

(cyhalothrin) 

Year oral–dog (capsule: 

lambda-cyhalothrin) 

Carcinogenicity –mouse 

(cyhalothrin) 

Chronic/Carcinogenicity - rat 

(cyhalothrin) 

1984/0, 0.5, 1.5, 5.0 mg/kg-d Parental/Offspring NOAEL: 1.5 mg/kg-d 

Parental/Offspring LOAEL: 5.0 mg/kg-d 

Decreased parental body weight and body 

weight gain during premating and gestation periods and reduced pup 

weight and weight gain during lactation. 

Reproductive NOAEL: 5.0 mg/kg-d (HDT) 



Clinical signs of neurotoxicity. 

1984/0, 3, 15, 75 mg/kg-d. NOAEL: 15 mg/kg-d 

LOAEL: 75 mg/kg-d 

Increased incidence of piloerection, hunched posture; decreased 

body weight gain in males. Not oncogenic under conditions of study. 

HDT inadequate. New study not required at this time. 



Decreases in mean body weight. Not oncogenic under conditions of 

study. 

Notes: 

a NOAEL = no observed adverse effect level 

b LOAEL = lowest observed adverse effect level from USEPA 2002a, 2004a, 2007b, 2007c; ATSDR 2003a 

D3.1.3.2.5 Developmental Toxicity 

Two of the studies listed in Table D3-13 summarize the results of studies in which cyhalothrin 

was evaluated for developmental toxicity in rats or rabbits. Few details of those studies are 

publically available, but the information provided by the USEPA (2002a, 2004a) indicates that 

the maternal NOAEL was 10 mg/kg-d for both species. The developmental NOAEL was the 

highest dose tested in each study; in rats, it was 15 mg/kg-d, and in rabbits, 30 mg/kg-d. 

D3.1.3.2.6 Reproductive Toxicity 

In a reproductive study of cyhalothrin (see Table D3-13) rats were dosed with 0, 0.5, 1.5, or 5.0 

mg/kg-d over three generations. The LOAEL of 5.0 mg/kg-d elicited adverse effects in both the 

parents and pups, with toxicity manifested as reduced body weight and body weight gain in the 

parents, and reduced pup weight and reduced pup weight gain during lactation. Although the 

USEPA (2002a, 2004a) lists the reproductive NOAEL as 5 mg/kg-d, the summary provided 

indicates that the NOAEL should have been identified as the next lowest dose level of 1.5 

mg/kg-d. 

D3.1.3.2.7 Genotoxicity 

No genotoxicity data for cyhalothrin or lambda-cyhalothrin were identified in the ATSDR 

(2003a) review, or in recent USEPA pesticide tolerance documents (USEPA 2002a, 2004a, 

2007b, 2007c). Genotoxicity data for other Type II pyrethroids (summarized in ATSDR 2003) 

and excerpted as Table D3-14, show that the Type II pyrethroids appear to be clastogenic in 

mammalian test systems. Although not all test results are consistent, as a class, this type of 

pyrethroid can induce chromosomal aberrations, sister chromatid exchange, micronuclei, and 

DNA fragmentation. However, the available carcinogenicity data (see following) do not indicate 

that this clastogenicity is associated with tumorigenic potential. 




DRAFT PEIR 


Table D3-14 

Genotoxicity of Type II Pyrethroids In Vivo 

Species (test system) Chemical End point Results Reference 

Eukaryotic organisms: 

Drosophila Cypermethrin Sex-linked recessive lethal ± Batiste-Alentorn et al. 1986 

Drosophila Cypermethrin Sex-chromosome loss – Batiste-Alentorn et al. 1986 

Drosophila Cypermethrin Nondisjunction – Batiste-Alentorn et al. 1986 

Drosophila Supercyper-methrin Sex-linked recessive lethal – Miadoková et al. 1992 

Drosophila 

Mammalian systems: 

Supercyper-methrin 

Sex-chromosome loss, 

nondisjunction, frequency of deletion 

– Miadoková et al. 1992 

Rat bone marrow Cypermethrin Chromosomal aberrations + Institóris et al. 1999b 

Rat bone marrow Cypermethrin Chromosomal aberrations – Nehéz et al. 2000 

Mouse bone marrow Cypermethrin Chromosomal aberrations +, – Bhunya and Pati 1988 

Mouse bone marrow Cypermethrin Chromosomal aberrations + Amer et al. 1993 

Mouse spleen cells Cypermethrin Chromosomal aberrations + Amer et al. 1993 

Mouse bone marrow Cypermethrin Sister chromatid exchange + Chauhan et al. 1997 

Mouse bone marrow Cypermethrin Sister chromatid exchange + Amer et al. 1993 

Rat bone marrow Cypermethrin Micronuclei – Hoellinger et al. 1987 

Mouse bone marrow Cypermethrin Micronuclei + Bhunya and Pati 1988 

Mouse sperm Cypermethrin Cellular abnormalities + Bhunya and Pati 1988 

Rat bone marrow Deltamethrin Chromosomal aberrations + Agarwal et al. 1994 

Mouse bone marrow Deltamethrin Chromosomal aberrations + Bhunya and Pati 1990 

Mouse bone marrow Deltamethrin Chromosomal aberrations – Poláková and Vargová 1983 

Mouse bone marrow Deltamethrin Sister chromatid exchange + Chauhan et al. 1997 

Rat bone marrow Deltamethrin Micronuclei + Agarwal et al. 1994 

Rat bone marrow Deltamethrin Micronuclei – Hoellinger et al. 1987 

Mouse bone marrow Deltamethrin Micronuclei + Bhunya and Pati 1990 

Mouse bone marrow Deltamethrin Micronuclei + Gandhi et al. 1995 

Rat testes Deltamethrin DNA fragmentation + El-Gohary et al. 1999 

Mouse sperm Deltamethrin Cellular abnormalities + Bhunya and Pati 1990 

Mouse Deltamethrin Dominant lethal mutations – Shukla and Taneja 2000 

Rat bone marrow Mouse 

bone marrow 

Fenpropathrin 

(Meothrin) 

Fenpropathrin 

Micronuclei Micronuclei + – Oraby 1997 Ryu et al. 1996 

Rat bone marrow Fenvalerate Chromosomal aberrations + Chatterjee et al. 1982 

Mouse bone marrow Fenvalerate Chromosomal aberrations + Ghosh et al. 1992 

Mouse bone marrow Fenvalerate Chromosomal aberrations + Pati and Bhunya 1989 

Mouse sperm Fenvalerate Cellular abnormalities + Pati and Bhunya 1989 

Mouse bone marrow Flumethrin Chromosomal aberrations +, – Nakano et al. 1996 

Mouse bone marrow Flumethrin Micronuclei +, – Nakano et al. 1996 

Source: ATSDR 2003a 

Notes: 

– negative result 

+ positive result 

± weak positive result 

+, – both positive and negative results 

DNA deoxyribonucleic acid 


SECTION D3 


D3.1.3.2.8 Carcinogenicity 

The USEPA Hazard Identification Assessment Review Committee (USEPA 2002b) reviewed 

two studies that provide information on lambda-cyhalothrin’s carcinogenic potential. The first of 

these studies, study MRID 00154803, was a chronic feeding study in which rats were given 

cyhalothrin in the diet (0-12.5 mg/kg-d for 2 years). No treatment-related effects were observed 

in the two lowest dose groups (0.5 or 2.5 mg/kg-d). A decrease in both body weight and food 

consumption was observed in males and females given 12.5 mg/kg-d; this dose level defined the 

study LOAEL. The NOAEL was 2.5 mg/kg-d. As noted by the USEPA (2002a), under the 

conditions of the study, “…there was no indication of oncogenic activity”. Study MRID 

00150842 was a two-year feeding study of cyhalothrin, in which male and female mice were 

given doses of approximately 0-75 mg/kg-d. The study defined a NOAEL of 3 mg/kg-d. An 

increased incidence of piloerection was documented in male mice between weeks 13 and 52. 

Male and female animals in the high dose groups (75 mg/kg-d) exhibited an increased incidence 

of piloerection, along with hunched posture up to 78 weeks into the study. After this time, the 

incidence of hunched posture was not distinguishable from controls. Decreased body weight gain 

was observed in males during the first 13 weeks and for the two-year period, was 77% of 

controls. Females exhibited an increase in mammary tumors that appeared to be dose-related 

(1/52, 0/52, 7/52, 6/52). The USEPA (2002b) noted concern over the adequacy of the dosing in 

the study, without providing details of the specific nature of those concerns. However, the 

agency’s conclusion was that cyhalothrin should be classified as a Group D chemical i.e., Not 

Classifiable as to Human Carcinogenicity. The DPR (2007) cited the increased incidence of 

mammary tumors in mice, and the USEPA's conclusion that lambda-cyhalothrin was not 

classifiable as to its carcinogenicity in prioritizing lambda-cyhalothrin for risk assessment 

initiation. More recent USEPA pesticide program documents refer to lambda-cyhalothrin as `not 

likely to be carcinogenic to humans.' (USEPA 2007b) or as studies on lambda-cyhalothrin or 

cyhalothrin as yielding ‘no evidence of carcinogenicity’ (USEPA 2004a). Neither lambdacyhalothrin 

nor cyhalothrin are listed as carcinogens by the IARC, the USEPA, the NTP, or 

under California’s Proposition 65. 

D3.1.3.3 


LBAM eradication goals include consideration of a No Program Alternative, in which certain 

pesticides, such as lambda-cyhalothrin, that are known to be effective against the apple moth 

would continue to be used in nurseries, in agriculture, and for home use to treat or help to 

prevent infestations. These uses will yield a potential for human exposure. Although the 

significance of these exposures is likely to be minimal when the products are used in accordance 

with label directions, lambda-cyhalothrin’s ability to persist in the environment indicates that 

human exposure to low concentrations may occur. 


lambda-cyhalothrin or cyhalothrin, regulatory agencies necessarily rely on data from animal 

studies to characterize exposure levels deemed to be safe for humans. Noncancer oral toxicity 

criteria for cyhalothrin have been developed by the ATSDR (2003a) and the USEPA (2009a). 

Notwithstanding the use of different terminology for their respective toxicity criteria (MRLs for 

ATSDR, and RfDs for the USEPA), both of the agencies use comparable methodology to derive 

the noncancer toxicity criteria. 




DRAFT PEIR 


The USEPA focused its noncancer toxicity criteria on long-term i.e., chronic oral exposure. For 


exposures referred to as the RfC or inhalation RfDinh. The RfD and RfC/RfDinh are each 

defined as the daily exposure level for the “…human population (including sensitive subgroups) 

that is likely to be without an appreciable risk of deleterious effects during a lifetime” (USEPA 

2009c). RfDs or RfCs are typically derived by selecting the most scientifically appropriate 





completeness of available toxicity data (USEPA 2009b). 



exposure.” 



the USEPA. MRLs are derived by the ATSDR (2003a) “…when reliable and sufficient data exist 



The ATSDR (2003a) relied on a 26-week study of cyhalothrin for derivation of the acute and 

intermediate-duration oral MRLs. That study was apparently documented in early (1961) 

USEPA documents that are not readily available for public review. Dogs were given a range of 

doses of cyhalothrin in capsule form over the duration of the study, with the LOAEL identified 

based on the induction of gastrointestinal effects (diarrhea) at 2.5 mg/kg-d. The NOAEL was 1 

mg/kg-d. The ATSDR applied a cumulative UF of 100 to the NOAEL to develop the MRL of 1 x 

10 -2 mg/kg-d (see Table D3-15). 

In determining the chronic oral RfD for cyhalothrin, the USEPA (2009a) relied on a study 

(Coopers Animal Health and Imperial Chemical Industries 1984) in which cyhalothrin was 

administered in the diet of rats at dose levels of 0, 10, 30, and 100 ppm for three generations 

(exact exposure duration and dosing regimen were not provided). According to the summary 

provided by the USEPA (2009a), the primary adverse effect of cyhalothrin exposure was a 

smaller gain in body weight for both males and females during the premating periods and for 

pups during the weaning period. Also, the number of viable pups in the F2A and F3B 

generations appeared to decrease at the highest dose level (100 ppm). A NOEL of 10 ppm (0.5 

mg/kg-d) was identified, with the lowest effect level (LEL) of 30 ppm (1.5 mg/kg-d). The 

USEPA applied an UF of 10 to account for interspecies variability, with an additional UF of 10 

used to account for intraspecies variability. The resulting chronic RfD is 5 × 10 -3 mg/kg-d (Table 

D3-15). 

The USEPA (2007b) identified an inhalation exposure study of lambda-cyhalothrin conducted in 

rats that the agency considered appropriate for characterizing potential risk from “all exposure 

durations” i.e., acute, subchronic, and chronic periods. In that study (MRID number 41387702), 

rats were exposed to lambda-cyhalothrin (81.5% purity) by nose for 6 hours/day, 5 days/week for 

21 days. Exposure concentrations were estimated to be approximately 0, 0.08, 0.9, or 4.5 mg/kg- 


SECTION D3 


d. No treatment related effects were observed at the lowest dose, but exposure to 0.9 mg/kg 

induced salivation, tearing, splayed gait, decreased body weight and body weight gain, as well as 

numerous other signs of neurotoxicity. The study results led the USEPA to identify a LOAEL of 

0.9 mg/kg-d and a NOAEL of 0.08 mg/kg-d. Although the study was of relatively limited 

duration, the USEPA (2007b) reasoned that because the route of administration (inhalation) is 

directly relevant to deriving inhalation toxicity criteria, and because the concentrations used 

elicited the effects of concern (neurotoxicity), the NOAEL should be protective of longer-term 

exposure. That conclusion was supplemented by the observation that longer-duration studies 

have not shown that lambda-cyhalothrin toxicity is induced at lower dose levels when exposure 

occurs over longer periods of time. Although the USEPA did not derive an inhalation RfD, they 

identified a cumulative UF of 100 for application to the NOAEL, which reflects an UF (or 

“variability factor”) of 10 to account for intraspecies variability, and a variability factor of 10 to 

account for interspecies variability. Application of the cumulative variability factor of 100 to the 

NOAEL of 0.08 mg/kg-d gives an RfD of 8 x 10 -4 mg/kg-d. This RfD is applicable to acute, 

subchronic, and chronic exposure scenarios. 

Table D3-15 

Toxicity Criteria for Lambda-Cyhalothrin 

Oral (mg/kg-d) 

Inhalation (mg/kg-d) 

Acute MRL Subchronic MRL Chronic Acute Subchronic Chronic 

1 x 10 -2 a 1 x 10 -2 a 5 x 10 -3 b 8 x 10 -4 c 8 x 10 -4 c 8 x 10 -4 c 

Notes: 

a ATSDR 2003 

b USEPA 2009a 

c derived from data in USEPA 2007b 


D3.1.4 

Carriers and Dispersants of Lambda-Cyhalothrin 

Warrior ® is the lambda-cyhalothrin-containing product approved for the control or prevention of 

LBAM at nurseries and/or in crop production areas. The MSDS for Warrior ® (Syngenta 2009) 

lists naphthalene (< 1.5%), propylene glycol (percentage not provided), and petroleum solvent 

(percentage not provided) as the inert ingredients of Warrior ® . The following sections provide 

information on the chemistry, environmental fate, and toxicity of naphthalene and propylene 

glycol. Because no CAS number or other specific identifying information was provided by 

Syngenta (2009) on the petroleum solvents, they are not discussed here. 

D3.1.4.1 Environmental Fate and Chemistry of Inert Ingredients of Warrior ® 

D3.1.4.1.1 Physical and Chemical Properties of Inert Ingredients of Warrior ® 

NAPHTHALENE 

Naphthalene occurs naturally as a component of crude oil, and is purified by distillation and 

fractionation of coal tar (ATSDR 2003b). Naphthalene produced from petroleum, the principal 

source in the United States, is approximately 99% pure (ATSDR 2003b). Naphthalene also 

occurs naturally in the roots of Radix and Herba ononidis (HSDB 2009). In the United States, the 

production of naphthalene in 2004 was an estimated 215 million pounds (ATSDR 2003b). 

Naphthalene is used in the manufacture of phthalic anhydride, which is an intermediary in the 




DRAFT PEIR 


production of phthalate plasticizers, resins, dyes, pharmaceutical materials, and insect repellants 

(HSDB 2009). 

Napthalene has a molecular formula of C 10 H 8 , a molecular weight of 128.17, and a CAS number 

of 91-20-3. Naphthalene is a white crystalline flake or solid at room temperature, with an odor of 

tar or mothballs (HSDB 2009; ATSDR 2003b). Key chemical and physical properties of 

naphthalene are summarized in Table D3-16, and the structure of naphthalene is shown on 

Figure D3-7. 

Table D3-16 

Physical and Chemical Properties of Naphthalene 

Parameter 


Source: 

HSDB 2009 

Molecular weight 128.17 

Vapor pressure 0.85 mmHg at 25°C 

Vapor Density 4.42 

Melting point, 

80.2°C 

Solubility in water 31 mg/L at 25°C 

Log Octanol/water partition coefficient (KOW) 

Log KOW=3.30 

Organic carbon partition coefficient (KOC) 440-830 


4.4x 10 -4 atm-m 3 /mol 

Figure D3-7 

Structure of naphthalene (from National Library of Medicine) 

PROPYLENE GLYCOL 

Propylene glycol is produced and used as an emollient (skin softener) in cosmetics and other 

pharmaceuticals; as a corrosion inhibitor, in the manufacture of resins; as a temperature stabilizer 

in paints; as a de-icing fluid, and as a solvent in food coloring and flavorings (HSDB 2009). 

Propylene glycol is a colorless viscous liquid that is nearly without odor. It has a molecular 

formula of C 3 H 8 O 2 , a molecular weight of 76.09, and a CAS no. of 57-55-6. It’s chemical and 

physical properties are summarized in Table D3-17 and it structure is given on Figure D3-8. 


SECTION D3 


Table D3-17 

Physical and Chemical Properties of Propylene Glycol 

Source: 

HSDB 2009 

Parameter 


Molecular weight 76.09 

Vapor pressure 0.13mmHg at 25°C 

Density 1.036, 25°C 

Boiling point 

188.2°C 

Solubility in water Miscible (1.1 x 10 6 mg/L 20°C 

Log Octanol/water partition coefficient (KOW) 

Log KOW=-0.92 


1.3 x 10 -8 atm-m 3 /mol 

Figure D3-8 

Structure of Propylene Glycol (from National Library of Medicine) 

D3.1.4.1.2 Environmental Transport and Degradation of Inert Ingredients of Warrior ® 

NAPHTHALENE 

If released to ambient air, naphthalene will exist primarily as vapor; once in the atmosphere, 

naphthalene reacts with hydroxyl and nitrate radicals, and is also subject to photolytic 

degradation (HSDB 2009). The atmospheric half-life of naphthalene is 18-60 hours (HSDB 

2009). Naphthalene has a moderate K O C (range of 440-1300), indicating that if released to soils 

or sediments, it will tend to sorb to organic matter. This sorption to organic materials indicates 

that naphthalene is likely to be only moderately mobile in soils. The soil half-life of naphthalene 

of 2-18 days reflects the fact that naphthalene undergoes biodegradation by soil microorganisms 

(HSDB 2009). If released to moist soils or surface water, naphthalene tends to volatilize (see 

Henry’s Law Constant). Hydrolysis is not a significant degradation pathway (HSDB 2009). BCF 

values from fish (23-168) indicate that naphthalene may bioconcentrate in some organisms 

(HSDB 2009). 

PROPYLENE GLYCOL 

Propylene glycol’s relatively high vapor pressure indicates that if it released to air, it will exist as 

a vapor (HSDB 2009). In the atmosphere, propylene glycol is degraded by reaction with 

hydroxyl radicals, resulting in a half-life of approximately 32 hours (HSDB 2009). Its low K OC 

(8) indicates it sorbs only minimally to organic materials present in soils and sediments, and if 

released to soil, propylene glycol will readily move through the soil column (HSDB 2009). 

Propylene glycol’s low Henry’s Law Constant reflects its tendency not to volatilize from moist 

soils or surface water (HSDB 2009). Hydrolysis is not a significant loss process for propylene 

glycol (HSDB 2009). Experimental data have shown that it can undergo considerable 

biodegradation, with 73-78% of the parent material being degraded to CO 2 (HSDB 2009). 




DRAFT PEIR 


D3.1.4.2 

Mammalian Toxicity of Carriers and Dispersants 

D3.1.4.2.1 Naphthalene 


Naphthalene is absorbed when exposure occurs by inhalation, orally, or by dermal contact 

(USEPA 1998a). Once absorbed into the circulatory system, naphthalene is distributed 

throughout the body. Data from animal studies indicate that the majority of naphthalene 

distributes to the lung, liver, kidney, heart, and spleen–all richly perfused organs. This pattern of 

distribution is broadly consistent across species USEPA (1998a). 

Naphthalene initially undergoes metabolic oxidation, followed by conjugation of the oxidative 

metabolite by glucuronides and sulfonic acid. The oxidative metabolite can also react with 

glutathione-S-transferase to form a cysteine conjugate. The complex metabolic scheme of 

naphthalene is reviewed and presented in USEPA (1998a). Metabolites of naphthalene are 

primarily eliminated in urine, with small amounts eliminated in the feces (USEPA 1998a). 

TOXICITY 

Exposure to naphthalene can cause hemolytic anemia, cataracts, and both cancer and noncancer 

toxicity of the respiratory tract. Hemolytic anemia has occurred following oral, inhalation, and 

dermal exposures to naphthalene (USEPA 1998a). Although the mechanism by which 

naphthalene induces hemolytic anemia is not fully characterized, anemia is thought to result from 

the action of one or more metabolites. Individuals who are deficient in glucose-6-phosphate 

dehydrogenase, a metabolic enzyme, are more susceptible to this effect of naphathalene than 

individuals with normal levels of this enzyme (USEPA 1998a). For reasons potentially due to 

differences in metabolism, animals appear to be less susceptible to naphthalene toxicity than 

humans (USEPA 1998a). 

GENOTOXICITY 

Naphthalene was not mutagenic in reverse mutation assays with Salmonella typhimurium in the 

presence or absence of metabolic activation (ATSDR 2003b). Naphthalene did not induce 

mutations at the hprt and tk loci in human lymphoblastoid cells, but did induce chromosomal 

aberrations in Chinese hamster ovary cells (ATSDR 2003b). In mammalian cells naphthalene did 

not induce transformations, DNA single-strand breaks, or unscheduled DNA synthesis (ATSDR 

2003b). Naphthalene was mutagenic in Drosophila melanogaster, and induced micronuclei in 

erythrocytes of salamander larvae exposed to concentrations of 0.5 mm. Naphthalene did not 

induce micronuclei in bone marrow of mice given single oral doses (ATSDR 2003b). These 

results give an equivocal picture of naphthalenes genotoxicity, indicating that naphthalene can 

potentially-but not necessarily-induce mutations and chromosomal damage. 


Two studies have evaluated naphthalene’s carcinogenicity (reviewed in ATSDR 2003b). Those 

studies identified respiratory tissues as the most sensitive target of chronic naphthalene exposure, 

in that naphthalene exposure induced benign and neoplastic lesions in the nose of rats, benign 

lesions in the nose of mice, and benign and neoplastic lesions in the lungs of mice exposed to 

naphthalene by inhalation for 10 or 30 ppm (mice), or 10, 30, or 60 ppm (rats). Exposures 

occurred 6 hours/day 5 days/week for 104 weeks. From an analysis of the data in these studies, 

the NTP and the IARC (2002) concluded that evidence of naphthalene’s carcinogenicity in 


SECTION D3 


animals is sufficient (USEPA 1998a). The USEPA (2009a) classifies naphthalene as a Group C 

possible human carcinogen based on the inadequate data of carcinogenicity in humans exposed 

to naphthalene by oral and inhalation routes, and the limited evidence of carcinogenicity in 

animals exposed by inhalation. Napthalene has been listed under California’s Proposition 65 as 

“known to the state to cause cancer”. OEHHA has established a CSF for naphthalene of 1.2 x 10 - 

1 (mg/kg-d) -1 . 

The mechanism by which naphthalene induces benign respiratory tract tumors is not fully 

understood, but is believed to be due to the action of reactive oxidative metabolites. The USEPA 

considers a genotoxic mechanism of action unlikely (USEPA 2009a). 



potential adverse health effects of exposure to naphthalene will not be quantitatively evaluated. 

However, OEHHA (2008c) has derived a chronic RELs for naphthalene, and the basis of that 

value is provided here as background information. The chronic REL is considered to be the most 

relevant toxicity criterion for naphthalene given that inhalation exposure will likely be the 

dominant route of exposure subsequent to application of Warrior ® . 

California’s OEHHA relied on data from the NTP study cited above, in which mice were 

exposed to naphthalene by inhalation at 0, 10, or 30 ppm 6 hours/day, 5 days/week for 104 

weeks. The critical effects observed were nasal inflammation, olfactory epithelial metaplasia, 

and respiratory epithelial hyperplasia. The study identified a LOAEL of 10ppm, a concentration 

associated with a 96% incidence of lesions in males, and a 100% incidence in females. A 

NOAEL was not defined. OEHHA applied a cumulative UF of 1,000 to account for intraspecies 

variability, interspecies variability, and uncertainty in extrapolating from a LOAEL to a NOAEL. 

The resulting chronic REL is 0.002 ppm (0.009 mg/m 3 , 9 μg/m 3 ). 

D3.1.4.2.3 Propylene Glycol 

Propylene glycol is designated by the United States Food and Drug Administration (FDA) as a 

Generally Recognized as Safe (GRAS) additive (ATSDR 1997). It has very low acute oral 

toxicity, with LD 50 values ranging from 21800 to 33500 mg/kg (TOXNET 2009). Propylene 

glycol is more poorly absorbed by inhalation or dermal routes than when exposures occur orally. 

It is mildly irritating to the eyes and skin, and has been shown to be capable of eliciting dermal 

sensitization in humans (TOXNET 2009). 

Repeated exposures to extremely large doses of propylene glycol (> 8,000 mg/kg) by oral, 

dermal, or intravenous exposure resulted in central nervous system depression in animals 

(TOXNET 2009), and liver toxicity was induced by repeated administration of > 12,000 mg/kg 

of propylene glycol in water for 140 days (TOXNET 2009). Much lower doses, albeit still large 

(1200 or 2400 mg/kg) have induced minor liver damage in rats (TOXNET 2009). 

The FDA exempts residues of propylene glycol from tolerance requirements when it is used as a 

solvent or cosolvent. These uses must be in accordance with good agricultural practices as an 

inert (or occasionally active) ingredient in pesticide formulations applied to crops or to raw 

agricultural commodities (TOXNET 2009). 




DRAFT PEIR 


GENOTOXICITY 

Propylene glycol was not mutagenic when tested in bacterial reverse mutation assays with or 

without metabolic activation, but has induced chromosomal damage in Chinese hamster 

fibroblasts (TOXNET 2009b) 


ATSDR (1997) cites a study in which no treatment-related increases in tumors were observed 

when rats were exposed to propylene glycol at 2,500 mg/kg-d. Additional details of the study 

were not provided 



potential adverse health effects of exposure to propylene glycol will not be quantitatively 

evaluated. Propylene glycol is relatively nonvolatile, and any incidental exposures that may 

occur would likely be from incidental ingestion or dermal contact. Although no toxicity criteria 

have been developed for propylene glycol, its low toxicity, coupled with its designation as 

GRAS, indicate that the low environmental levels that may result from its use in the LBAM 

Eradication Program are not expected to cause adverse health effects. 

D3.1.5 

Permethrin 

Pyrethrum is a naturally occurring substance with insecticidal properties obtained from certain 

species of Chrysanthemum (C. cinerariaefolium and C. cineum), and is one of many synthetic 

analogs of pyrethrum known as pyrethroids that have been commercially developed as 

insecticides (ATSDR 2003a). Commercial pyrethroid research has focused on the synthesis of 

chemicals with enhanced insecticidal action and environmental stability relative to the parent 

compound, pyrethrum (ATSDR 2003a). 

Pyrethroids are effective against insects in the orders Coleoptera, Diptera, Hemiptera, 

Hymenoptera, Lepidoptera, Orthoptera, and Thysanoptera, and are used to control insect pests on 

grain and other edible products (ATSDR 2003a). In 2001, over 1 million pounds of permethrin 

were applied to control various insects on alfalfa, corn, cotton, grains, lettuce, onion, peaches, 

potatoes, and tomatoes on commercial crops as well as on home gardens (ATSDR 2003a). 

Permethrin is also used in pet sprays and shampoos (ATSDR 2003a). 

Permethrin is synthesized by the chemical reaction of a dichlorochrysanthemic acid and a 

phenoxybenzyl alcohol, as indicated on Figure D3-9. 

Acid Alcohol Permethrin 

Figure D3-9 Permethrin is Produced Through the Chemical Reaction of a Carboxylic Acid with an Alcohol (ATSDR 2003) 


SECTION D3 


D3.1.5.1 


D3.1.5.1.1 Chemical and Physical Properties of Permethrin 

Permethrin is chemically identified as (3-phenoxyphenyl)methyl (1RS)-cis,trans-3-(2,2- 

dichloroethenyl)-2,2-dimethylcyclopropanecarboxylate. The CAS number is 52645-53-1. 

Technical-grade permethrin is a mixture of four isomers, with the 1 R, cis isomer possessing the 

greatest insecticidal activity (IPCS 1999). Considered as a group, the pyrethyroids tend to be 

nonpolar, with correspondingly low water solubility and limited volatility; these characteristics, 

combined with their high K OW drive a tendency to partition to soils and sediments where they 

bind strongly (Laskowski 2002). The chemical property data of permethrin are summarized in 

Table D3-18. 

Table D3-18 

Chemical Property Data of Permethrin 

Chemical Property 

Molecular Weight 391.29 

Aqueous solubility (20ºC) 

< 0.1 mg/L 

Melting Point 

cis isomer 

63-65ºC 

trans isomer 

44-47ºC 

Boiling Point 

200ºC 1 mmHg 

Vapor Pressure 

2.2x10 -8 mmHg 

Mean organic carbon coefficient (KOC) 81,600 

Henry's Law Constant 1.9 x 10 -6 atm-m 3 /mol, 25ºC 

Log Octanol Water Partition Coefficient (KOW) 6.5 

Source: 

IPCS 1999; ATSDR 2003a; Laskowski 2002 

Value 

D3.1.5.1.2 Environmental Transport, Persistence and Degradation of Permethrin 

AIR 

Based on the low vapor pressure and low Henry’s Law Constant, permethrin is not likely to 

volatilize to air, though drift is possible during aerial applications (ATSDR 2003a). 

WATER 

In general, permethrin is less stable in fresh water than in sediment. Over a 12-week study 

period, permethrin degraded more rapidly in lake water than in flooded sediments, with the transpermethrins 

degrading to below detectable levels, and the cis-permethrins degrading to less than 

50% of the original amount (Sharom and Solomon 1981). The same authors also showed that 

more than 95% of the permethrin sorbed onto lake sediments following the initial application, 

with only 7-9% removed by multiple washings. 

The relative stability of permethrin in sediment compared to water is also supported by the data 

of Rawn et. al. (1982). In experiments that used outdoor artificial ponds, permethrin levels in the 

water were significantly decreased after 12 hours, with the photolytic half-lives estimated to be 

19.6±2.3 hours for the trans isomers and 27.1±4.4 hours for the cis isomers. Permethrin remained 

detectable in pond sediments up to a year later. 




DRAFT PEIR 


In water as well as soil, permethrin is degraded to 3-phenoxybenzyl alcohol and dichlorovinyl 

acid through cleavage of the ester bond (Holmstead 1978). 

SOIL 

Estimates of the persistence and degradation of permethrin in soils have been developed under a 

variety of experimental conditions, with the resulting estimates spanning a considerable range of 

time. For example, Laskowski (2002) cites a mean half-life for permethrin in aerobic soil of 39.5 

days, and a corresponding value of 197 days for anaerobic soils. 

Soils incubated with 1ppm permethrin for up to 64 days at 10, 25, and 40°C yielded estimated 

half lives for the cis isomer of 12-55 days, and for the trans isomers of 4 to 14 days. Jordan and 

Kaufman (1986) examined permethrin degradation in flooded soil by applying 0.1% or 1% 

permethrin and incubating the samples in the dark at 25°C. The half-life of trans-permethrin was 

32 and 34 days for the 0.1% and 1% applications respectively. However, cis-permethrin 

exhibited a half-life greater than 64 days, regardless of the concentration applied. 

Experiments with sterile and nonsterile soils indicate that microbial degradation is a significant 

environmental removal mechanism for permethrin. Eight weeks after application of 1ppm 

permethrin, only 16% remained in natural organic soil (pH 7.1-7.2), while no removal (loss) was 

observed in sterile soils (Chapman et al. 1982). 

Permethrin’s tendency to sorb to organic matter results in its persistence in soils and sediments. 

Given its low aqueous solubility, permethrin does not solubilize significantly in soil pore water, 

resulting in a limited potential for leaching to groundwater. 

POTENTIAL FOR BIOACCUMULATION 

Permethrin’s hydrophobicity, low vapor pressure, and limited aqueous solubility (Table D3-18) 

indicate a potential for permethrin to concentrate and accumulate in biota. Experimentally 

determined BCF in fish confirm the tendency for bioconcentration: Laskowski (2002) calculated 

an average fish BCF of 558 from available data. However, the potential for bioaccumulation of 

permethrin in mammals is limited by its rapid metabolism to water-soluble metabolites that are 

eliminated in urine (ATSDR 2003a). Experimental data confirm that while permethrin partitions 

to both muscle and fat of mammals, it does not accumulate in these tissues with repeated 

exposure (IPCS 1979, 1999). 

D3.1.5.2 


D3.1.5.2.1 Mode of Action 

Pyrethroids are separated into two broad categories–Type I and Type II- based on distinct 

chemical and toxicological properties (Bloomquist 1996; ATSDR 2003a). In general, the Type I 

group, which includes permethrin, does not contain a cyano group, whereas members of the 

Type II pyrethroids contain a cyano-3-phenoxybenzyl alcohol substituent (Bloomquist 1996; 

ATSDR 2003a). Pyrethroid’s primary toxicity is manifested in the nervous system of insects as 

well as mammals, where they act as neurotoxins. This manifestation is consistent with the signs 

of toxicity elicited by Type I pyrethroids in general; i.e., hyperexcitability and convulsions in 

insects, and whole body tremors in mammals (Bloomquist 1996). Permethrin’s neurotoxicity is a 

function of its ability to prolong sodium ion permeability in neuronal membranes during the 

excitatory phase of the action potential, and by so doing, interfere with nerve impulse generation. 


SECTION D3 


In mammals, Type I pyrethroids affect nerve impulse generation in both sensory and motor 

neurons of the peripheral nervous system, as well as in interneurons of the central nervous 

system (Bloomquist 1996; ATSDR 2003a). 

D3.1.5.2.2 Absorption, Distribution, and Elimination 

Experimental data obtained from studies in multiple species (rats, cattle, goats, and chickens) 

have demonstrated that orally administered permethrin is rapidly absorbed and widely distributed 

(IPCS 1999). Estimates of the extent of the oral absorption of Type I and Type II pyrethroids 

range from 40 to 60%, with the recognition that removal by first-pass metabolism may make this 

a significant underestimate (ATSDR 2003a). For example, whole-body radiography studies in 

rats have demonstrated that a single orally administered dose of permethrin is rapidly absorbed, 

with peak blood concentrations reached within 1.5 hours of dosing. Permethrin distributed to 

many tissues and organs, with the highest levels detected in the stomach, intestines, liver, 

kidneys, and fat. The same authors also provided data indicating that virtually all of a single 

orally administered dose of radiolabeled permethrin was eliminated in urine and feces within 12 

days. Some differences appear in the physiological fate of the cis and trans isomer, however, as 

rats given the trans isomer excreted greater proportions of the radiolabel in urine and lower 

proportions of radiolabel in feces than animals given the cis isomer. In goats and cows, and in 

hens, approximately 65% or 90% of an orally administered dose of radiolabeled permethrin was 

recovered in excreta, respectively (IPCS 1999). Residues of radiolabel were detected in liver and 

milk samples (goat and cow), and in egg and liver samples from hens (IPCS, 1999). 

Very limited information, inferred from occupational studies, indicates that permethrin is 

absorbed subsequent to inhalation exposure (IPCS 1999; ATSDR 2003a). Leng et al. (1997) 

documented the appearance of urinary metabolites within 30 minutes of exposure to an 

unspecified pyrethroid, suggesting that absorption may be rapid. No data are available, either 

from experimental animals or from human studies that characterize the distribution of permethrin 

or of other pyrethroids following inhalation (ATSDR 2003a). 

Data from clinical application of permethrin-containing products to control dermal parasites, 

coupled with occupational data, indicate that permethrin is absorbed following dermal exposure 

(IPCS 1999; ATSDR 2003a). More recent clinical data provide some insight into the rate of 

absorption when permethrin-containing products are dermally applied. Permethrin was absorbed 

when administered either via a hair rinse solution or as a cream to volunteers. Depending on the 

product, the rate of urinary metabolite production peaked at 12.3 to 14.6 hours, with metabolite 

elimination exhibiting a half-life of 28.8 to 37.8 hours (Tomalik-Scharte et al. 2005). The extent 

of dermal absorption in the study was “small,” which is consistent with Meinking and Taplin 

(1996) (0.6% absorption in an in vitro model), van der Rhee et al. (1989) (1-2.1% absorption 

from permethrin cream), and ATSDR (2003a). ATSDR (2003a) cites an estimate for the dermal 

absorption of pyrethroids as < 2% of an applied dose. 

D3.1.5.2.3 Metabolism 

Permethrin is extensively metabolized in mammals, yielding water-soluble metabolites that are 

eliminated in the urine and feces. The principal metabolic reactions include cleavage of the ester 

bond to produce an acid and alcohol (see Figure D3-9), followed by hydroxylation and oxidation 

reactions, and glucuronide conjugation (IPCS 1999; ATSDR 2003a). Rats, cows, goats, and 

chickens all produced 4’hydroxypermethrin, dichlorovinyl acid, and phenoxybenzyl alcohol as 




DRAFT PEIR 


metabolites of permethrin. Dichlorovinyl acid, and phenoxybenzyl alcohol have also been 

identified as permethrin metabolites in humans (IPCS 1999). 


The acute toxicity of permethrin varies considerably, and is dependent on the relative proportion 

of cis and trans isomers, the vehicle, the route of administration, and the species. 

In humans, acute effects observed subsequent to ingestion of permethrin included nausea, 

vomiting, abdominal pain, headache, dizziness, anorexia, and hypersalivation. Reports of severe 

poisoning are rare and usually follow ingestion of substantial, but poorly described, amounts of 

permethrin. Symptoms of severe poisoning include impaired consciousness, muscle 

fasciculation, convulsions, and noncardiogenic pulmonary edema (ATSDR 2003a). 

Acute oral studies conducted with rats by the Department of Defense (DOD 1977) showed that 

exposure to permethrin caused tremors, weight loss, and increased liver and kidney weights 

starting at 185 mg/kg. The NOAELs in the DOD studies ranged from 92 to 210 mg/kg. 

Oral LD 50 1 values in rats range from 220 mg/kg to 8900 mg/kg and in mice, from 230 mg/kg to 

1,700 mg/kg (IPCS 1999). The lethal dose of permethrin depended both on the vehicle in which 

permethrin was administered, as well as the cis/trans composition of the mixture. The effect of 

vehicle on permethrin’s toxicity becomes evident by comparing two sets of data in which male 

and female Wistar rats were administered a 40:60 cis/trans permethrin mixture with or without a 

maize oil vehicle. The corresponding LD 50 values were 1200 mg/kg and 8900 mg/kg (IPCS 

1999). The greater toxicity of the cis isomer is seen by comparing two studies in which an 80:20 

or a 20:80 cis/trans mixture of permethrin was administered in maize oil to rats. The respective 

LD 50 s were 200 mg/kg and 6,000 mg/kg. The underlying basis for the greater toxicity of the cis 

isomer, or of permethrin administered in maize oil has not been characterized (IPCS 1999). 

The LC 50 

2 

was estimated to be >24 mg/L in male and female rats exposed for 4 hours to a 40:60 

cis/trans mixture of permethrin (Braun and Killeen 1976). 

Permethrin is only slightly toxic via the dermal route, with an LD 50 > 2,000 mg/kg in rabbits 

(Braun and Killeen 1975b; Sauer 1980b). Permethrin of various cis/trans formulations has 

caused only very mild irritation when applied to either intact or abraded skin of rabbits (Braun 

and Killeen 1975b, 1975c; Sauer 1980c, 1980d). Dermal exposure in humans can cause tingling 

and pruritus with blotchy erythema on exposed skin, and has caused transient paresthesia 

(ATSDR 2003a). 

The USEPA (2006b) has classified permethrin as category III for acute oral and acute dermal 

toxicity; category III for eye irritation potential, and category IV for dermal irritation potential. 

Technical grade permethrin is not considered a skin sensitizer (USEPA 2006b). 

D3.1.5.2.5 Subchronic Toxicity 

Table D3-19 summarizes the results of subchronic toxicity studies of permethrin, based on data 

provided in IPCS (1999). The data in this table encompass studies conducted in mice, rats, dogs, 

1 The LD 50 represents the median lethal dose (LD 50 ) required to kill 50% of the test animals. 

2 The LC 50 represents the median lethal concentration (LC 50 ) required to kill 50% of the test animals. 


SECTION D3 


rabbits, and guinea pigs, and oral, inhalation, and dermal routes of exposure. Because of the 

range of species, dosing protocols, dose or concentration levels and the differing cis/trans ratios 

of permethrin, no clear dose-response relationship is readily apparent. Considerable consistency 

exists, however, in the nature of the adverse effects documented at the LOAEL or lowest 

observed adverse effect concentration (LOAEC); tremor or other symptoms of neurotoxicity, 

decreased body weight, and increased liver weight being the most frequently observed effects of 

permethrin exposure. 

Table D3-19 

Summary of Subchronic Toxicity and Studies of Permethrin 

Species 

Mice 

Rats 

Rats 

Rats 

Rats 

Study Duration 

(route) 

28 d 

(oral) 

28 d 

(oral) 

28 d 

(oral) 

30 d 

(oral) 

5 weeks 

(oral) 

Dose or 

Concentration 

Cis/trans 

Ratio 

NOAEL or 

NOAEC a 

0-560 mg/kg 39:56 140 mg/kg 

Primary Effect at 

LOAEL or 

LOAEC b 

Increased 

incidence, 

eosinophilia of 

hepatocytes 

0-1,000 mg/kg 38:52 50 mg/kg Tremors 

0-800 mg/kg 

(males); 

0-820 mg/kg 

(females) 

0-630 mg/kg 

(males); 

0-660 mg/kg 

(females) 

0-300 mg/kg 

N/A c 

250 mg/kg 

40:60 120 mg/kg 

N/A 

30 mg/kg 

Rats 90 days (oral) 0-200 mg/kg N/A 60 mg/kg 

Rats 90 days (oral) 0-50 mg/kg 55:45 30 mg/kg 

Rats 

Rats 

Rabbits 

Guinea 

Pigs 

26 weeks 

(oral) 

5 days/week 

13 weeks 

(inhalation) 

21 days 

(dermal) 

6h/d 

5 days/week 

13 weeks 

(inhalation) 

0-100 mg/kg 

36.1:61.1 5 mg/kg 

0-500 mg/m 3 60:40 250 mg/ m 3 

0-1,000 mg/kg 

Decreased 

bodyweight 

Tremors, 

Decreased 

bodyweight 

Increased 

liver weight 

Increased spleen 

and lung weight 

(males); 

decreased 

adrenal gland 

weight (females) 

Increased 

liver weight 

Increased 

liver weight 

Tremors, 

convulsions 

Reference 

Chapp et al. 

1977a 

Chapp et al. 

1977b 

Killeen and Rapp 

1974 


1975a 

Butterworth and 

Hend 1976 

Williams et al. 

1976a 

Becci and Parent 

1980 

Hart et al. 1977a 

US Army 1978 

41.56:46.5 1,000 mg/kg None Metker et al. 1977 

0-500 mg/m 3 60:40 500 mg/ m 3 None US Army 1978 

Dogs 14 days (oral) 0-500 mg/kg 40:60 250 mg/kg Tremors, ataxia 

Dogs 96 days (oral) 0-500 mg/kg 40:60 50 mg/kg 

Dogs 90 days (oral) 0-500 mg/kg 54:46 5 mg/kg 

Increased liver 

weight, tremors 

Tremors, ataxia, 

other neurological 

symptoms of 

toxicity 


1975b 


1976 

Becci et al. 1980 




DRAFT PEIR 


Table D3-19 

Summary of Subchronic Toxicity and Studies of Permethrin 

Species 

Study Duration 

(route) 

Dose or 

Concentration 

Cis/trans 

Ratio 

NOAEL or 

NOAEC a 

Primary Effect at 

LOAEL or 

LOAEC b 

Reference 

Dogs 180 days (oral) 0-250 mg/kg 25:75 250 mg/kg None 

Dogs 52 weeks (oral) 0-1,000 mg/kg 323.3:60.2 5 mg/kg 

Dogs 

Rats 

6h/d 

5 days/week 

13 weeks 

(inhalation) 

GDs 6-15 

(garage) 

Decreased body 

weight 

Reynolds et al. 

1978 

Kalinowski et al. 

1982 

0-500 mg/m 3 60:40 500 mg/ m 3 None US Army 1978 

N/A 40:60 150 mg/kg Developmental USEPA 1991 

Rats 90 days (diet) N/A 45:55 73.6 mg/kg 

Rats 13 weeks (diet) N/A 50:50 150.35 mg/kg 

Rats 13 weeks (diet) N/A 50:50 15.5 mg/kg 

Dog 1 year (oral) N/A 40:60 100 mg/kg 

Source: 

ATSDR 2003a and IPCS 1999 

Notes: 

a NOAEL = no observed adverse effect level; NOAEC = no observed adverse effect concentration 

b LOAEL = lowest observed adverse effect level; LOAEC = lowest observed adverse effect concentration 

c N/A indicates the data are not available 

Unspecified 

effects on liver 

Unspecified 

effects on body 

weight 

Tremors, 

staggered gait, 

hind limb splay 

Tremors, 

uncoordinated 

gait, convulsions, 

excessive 

salivation 

DOD 1977 

USEPA 1994 

USEPA 1994 

USEPA 1983 

D3.1.5.2.6 Chronic Toxicity and Carcinogenicity 

The results of cancer bioassays of permethrin provide only an equivocal understanding of its 

carcinogenic potential (see Table D3-20). Data from three rat studies have been reviewed by 

USEPA (1988, 1989a, 1989b, 1989c, 1989d, 2002c, 2005) and the DPR (1994) has conducted an 

independent evaluation of data previously reviewed by the USEPA and additional studies. The 

USEPA concluded that a study by Braun and Rinehart (1977) provided evidence of 

carcinogenicity to rats (USEPA 2002); however, DPR (1994) did not concur with this finding. 

Data from the other two rat studies (Ishmael and Litchfield 1988; McSheehy et al. 1980) were 

considered negative for oncogenicity by both the USEPA and DPR. Data from mouse studies 

(FMC Mouse II 1979; Tierney and Rinehart 1979) evaluated by the USEPA supported a 

conclusion that there were statistically significant increases in combined liver 

adenoma/carcinoma in male and female mice and statistically significant increases in lung 

carcinoma in female mice only. The DPR (1994) concurred with USEPA that the study was 

positive for oncogenic effects but identified a major deficiency in the study regarding inadequate 

husbandry. 


SECTION D3 


All other long-term studies of the chronic toxicity of permethrin (Table D3-20) provide no 

evidence of any carcinogenic potential, and the IPCS concluded that the “weight of evidence 

supports the conclusion that permethrin has very weak oncogenic potential, and the probability 

that it has oncogenic potential in humans is remote.” The USEPA’s IRIS contains an evaluation 

of permethrin completed in 1992, which has not been revised since that time (USEPA 1992). 

That evaluation notes that a carcinogen assessment of permethrin was under review in 1990, but 

no indication exists that it was ever completed (USEPA 1992). At this time, neither the WHO (a 

supporting agency of the IPCS evaluation) nor the IARC have classified permethrin as 

carcinogenic. IARC has concluded that permethrin is unclassifiable as to its carcinogenicity to 

humans (IARC 1991). In California, under Proposition 65, permethrin is currently being 

considered by OEHHA for listing as a carcinogen (OEHHA 2009a). 

Permethrin was classified by the USEPA in 2002 as a Category C carcinogen (likely to be 

carcinogenic to humans) under the agency’s 1999 Interim Final Guidelines for Carcinogen Risk 

Assessment (USEPA 2002c). This classification was based on two reproducible benign tumor 

types (lung and liver) in the mouse (Tierney and Rinehart 1979), equivocal evidence of 

carcinogenicity in Long-Evans rats (Braun and Rinehart 1977), and supporting structural activity 

relationships (SAR) information (USEPA 2002c). This decision has been supported in 

subsequent data reviews by the USEPA (2004b, 2009c, 2009d). Most recently, the USEPA has 

evaluated permethrin as a carcinogen (likely to be carcinogenic to humans) in the human health 

risk assessments for the Reregistration Eligibility Decision (RED) for Permethrin (USEPA 

2009d). A cancer slope factor of 9.6 x 10 -3 (mg/kg-d)-1 was used in the risk assessments, as 

derived and documented by the USEPA (2002c). 

A summary of toxicity evaluations of permethrin conducted by the USEPA, DPR, ATSDR, and 

other health organizations are presented in the following sections. As discussed below, the 

significance of these findings has not been consistently interpreted by reviewing agencies. 

D3.1.5.2.7 Permethrin Study Data Reviews 

Data from rat and mouse studies submitted by investigators for permethrin are summarized in 

Table D3-20. These data have been reviewed by the USEPA (1988, 1989a, 1989b, 1989c, 1989d, 

2002c, 2005), DPR (1994), and ATSDR (2003a) for evaluating the carcinogenic potential of 

permethrin. The oncogenic database reviewed by the USEPA and DPR includes three rat studies 

(Braun and Rinehart 1977; Ishmael and Litchfield 1988; Wellcome 1980). Three mouse studies 

(Tierney and Rinehart 1979; Barton et al. 1980) reviewed by USEPA have been used as the basis 

for concluding that permethrin should be classified as a Category C (possible human carcinogen) 

by the oral route along with evidence in the Long-Evans rat that was considered equivocal but 

suggestive Braun and Rinehart 1977). The DPR reviewed four mouse oncogenicity studies 

(Hogan and Rinehart 1977, Ishmael and Litchfield (1988), Tierney and Rinehart 1979, James 

1980). Based on significant deviations from FIFRA requirements all four mouse studies were 

considered unacceptable to DPR (1994). 

RAT STUDIES 

MRID 92142123, ICI 1977 (Ishmael and Litchfield 1988; Richards et al. 1990): In a chronic 

oral toxicity/oncogenicity study, permethrin was administered to Wistar rats (60/sex/group) in 

the feed at concentrations of 0, 500, 1,000 or 2,500 ppm. The mean estimated compound intake 

for male rats was 0, 19.4, 36.9, or 91.5 mg/kg-d, respectively, and for females was 0, 19.1, 40.2, 

or 10 4 mg/kg-d. The USEPA concluded that the incidence of tumor-bearing rats or incidence of 




DRAFT PEIR 


any specific tumor type in either sex was observed at the doses tested; permethrin was not 

carcinogenic to the rat. Based on tremors and hypersensitivity, as well as liver effects, dosing 

was considered adequate. This chronic toxicity/oncogenicity study in the rat met the USEPA 

acceptable/guideline and satisfied the guideline requirements for a chronic toxicity/oncogenicity 

oral study (OPPTS 870.4300 [§83-5A]) in the rat. 

DPR concurred that this study was acceptable but identified several deficiencies. 

As per a review of these data by ATSDR (2003a), no evidence of carcinogenicity was observed 

in rats. 

Braun and Rinehart 1977: Permethrin was administered in a 2-year feeding study of 60 Long- 

Evans rats/sex/group at 0, 20, 100, or 500 mg/kg corresponding to a dose of 0, 1, 5 or 25 mg/kgd. 

Initial examination of lung tissue from male rats suggested that the presence of lung tumors 

was dose-related but was not statistically significant at any dose level. The lung tissue was 

reexamined after step-sectioning at 250 micron intervals and the incidence from the second 

reading was not statistically significant. The USEPA adjusted the incidence by the amount of 

lung tissue examined, resulting in an adjusted incidence at the mid- and high-dose level that was 

marginally significant (p=0.10) by pair-wise comparison with concurrent controls. 

Although the USEPA concluded that the evidence for lung tumors in the male rats was 

equivocal, the DPR (1994) did not consider the changes toxicologically significant since a 

Maximum Tolerated Dose (MTD) was not established during the study. 

MRID 97441; Wellcome 1980 (McSheehy et al. 1980): In a second combined 

toxicity/carcinogenicity study, permethrin was administered to groups (60/sex/group) of Wistar 

strain rats ( at dietary concentrations delivering doses of 0, 10, 50, or 250 mg/kg-d for up to 104 

weeks. There were no treatment related increases in tumor incidences at any dose of the test 

material when compared to the control tumor incidences. Dosing was considered adequate based 

on clinical signs of neurotoxicity at the high dose. At the mid- and high-dose levels, there was an 

increased incidence of hepatocyte fatty vacuolation and periacinar hepatocyte hypertrophy, also 

evidence that dosing was adequate. The USEPA (2005) concluded that this 

chronic/carcinogenicity study in the rat is unacceptable/guideline (upgradeable) but could be 

upgraded upon submission of data listing on the study deficiencies section. It should be noted 

that this study was conducted before Subdivision F or OPPTS 870.4300 guidelines were 

established. 

DPR (1994) concluded that the findings from this study supported an oncogenic effect but 

considered the study inadequate since it did not conform to FIFRA guidelines due to the lack of 

dose level justification and information regarding the purity of the test material was not reported. 

D3.1.5.2.8 Mouse Studies 

MRID 00062806, 92142033; FMC 33297 (Tierney and Rinehart 1979): In a carcinogenicity 

study permethrin was administered to Charles River CD-1 mice (75/sex/dose) in the diet. 

Concentrations in feed were 0, 20, 500, or 2,000 ppm for males (equivalent to 0, 3, 71, or 286 

mg/kg-d, respectively) and 0, 20, 2500, or 5000 ppm for females (equivalent to 0, 3, 357, or 714 

mg/kg-d, respectively) for 24 months. 


SECTION D3 


This study had been previously evaluated in December 1988 by the USEPA Health Effects 

Division (HED) Peer Review Committee (USEPA 1989) and concluded that there were 

statistically significant increases in liver adenomas at all doses for males and at mid- and highdoses 

for females with a significant dose-related trend in both sexes. Statistically significant 

increases of combined liver adenoma/carcinoma also were observed at mid- and high-doses for 

male and female mice. In females only, statistically significant lung adenomas and combined 

adenoma/carcinoma at all doses were observed. The incidence of carcinoma increased at all 

doses but was statistically significant only at the highest dose tested. The incidences of adenoma 

and carcinoma at mid- and high-doses were outside historical control ranges. Statistically 

significant dose-related trends were also observed for lung adenomas, carcinomas, and combined 

adenoma/carcinomas in female mice. The incidences of lung tumors in male mice (adenoma or 

carcinoma, or combined) were not statistically significant at any dose and there were no doserelated 

trends. The adequacy of the dose levels tested was deemed adequate. The USEPA 

classified this carcinogenicity study in mice as acceptable/guideline (OPPT 870.4200b; §832b) 

for the evaluation of carcinogenicity. 

The DPR (1994) concurred with the USEPA that the Mouse II study was positive for an 

oncogenic effect but identified inadequate husbandry as a major deficiency in this study. 

This study is not publically available, but was reviewed by IPCS (1999). Tierney and Rinehart’s 

data (1979) were developed after an earlier study (Hogan and Rinehart 1977; Rapp 1978) was 

compromised by methodological problems. However, the IPCS review (IPCS 1999) relied on the 

absence of tumors in the Hogan and Rinehart (1977) and Rapp (1978) study to support a finding 

of a lack of biological significance for an increased incidence of alveolar-cell adenomas and 

carcinomas found in female mice by Tierney and Rinehart (1979). Tierney and Rinehart (1979) 

also reported a dose-related increased incidence of hepatocellular carcinomas in mid- and highdose 

male mice. For reasons that were not adequately explained by IPCS (1999), these 

carcinomas were deemed to represent spontaneous lesions unrelated to treatment. 

MRID 00102110, 94142032; ICI 1977 (Ishmael and Litchfield 1988): In another mouse 

carcinogenicity study, permethrin was administered to pathogen free Alderley Park mice 

(70/sex/dose). Dietary dose levels were 0, 250, 1,000, or 2,500 ppm (equivalent to 0, 26.9, 110.5, 

or 287.2 mg/kg bw/day for males and 0, 29, 124.2, or 316.1 mg/kg bw/day for females) up to 98 

weeks. Necropsies were performed on ten males and females per group for 26- and 52-week 

interim studies. Hematology and clinical chemistry parameters were also measured. 

There was no evidence of significant increase in tumor types or in tumor-bearing animals 

compared to controls, at the doses tested. A non-significant increase in lung adenomas in male 

mice and in lung adenomas plus carcinomas in female mice at the highest dose administered 

(2,500 ppm in the diet) but was not considered evidence of carcinogenicity. Doses were 

considered adequate. This carcinogenicity study in mice was classified as acceptable/guideline 

and satisfied the guideline requirement for a carcinogenicity study (OPPTS 870.4200b; 

Organization for Economic Cooperation and Development [OECD] 451). The USEPA considered this 

study negative for oncogenic effects. 

DPR (1994) identified a number of deficiencies with this study due to the lack of overt toxicity, 

inadequate analysis of diet, a misdosing incident, and the lack of pathology for non-neoplastic 

lesions. 




DRAFT PEIR 


IPCS (1999) reviewed the Ishmael and Litchfield (1988) mouse data collectively with data from 

an unpublished study of Hart et al. (1977b), noting “no significant increase in the incidence of 

tumors of unusual types or in the number of tumor bearing animals.” This conclusion was based 

on IPCS’ analysis, in which the high dose male mice (the same treatment group referred to by 

ATSDR 2003a) had a significant increase in benign lung tumors only if one “unconfirmed” 

tumor was included in the statistical analysis. The IPCS (1999) did not find these data to be 

sufficient evidence of a carcinogenic effect of permethrin. The ATSDR did not provide a 

conclusion regarding the significance of the Ishmael and Litchfield (1988) data. 

MRID 45507105, Carcinogenicity/Reversibility Study 2000: Permethrin was administered to 

groups of 50 to 109 Crl:CD-1 ® (ICR)BR female mice through the diet in a non-guideline mouse 

carcinogenicity study. This study was designed to test the progression and possible reversal of 

toxic effects, including benign liver and lung tumors. Doses were administered at 0 or 5,000 

mg/kg (equivalent to 780-807 mg/kg bw/day) for 39, 52, 65, or 78 weeks. Statistically significant 

increases of liver adenomas were present in female mice exposed to permethrin at 5000 mg/kg in 

the diet up to 79 weeks, with recovery to week 101 although the tumors were not dose-related. 

Incidences of lung tumors increased immediately after treatment and continued to increase 

during the recovery periods compared to controls. There was no progression to carcinoma 

observed in either the lung or liver. 

DPR (1994) did not review data from this study. 

D3.1.5.2.9 Non-cancer Chronic Toxicity 

Long-term exposure to permethrin (Table D3-20) is associated with many of the same adverse 

effects observed in subchronic studies (Table D3-19). These effects include decreased body 

weight, liver hypertrophy, increased liver weight, and an increased incidence of eosinophilia of 

hepatocytes. Overt neurological symptoms such as tremors, hypersensitivity, or ataxia were 

noted in the initial phases of many of the studies cited in Table D3-20, but in general, these 

symptoms did not persist for the duration of the study. 

The range of NOAELs identified for chronic permethrin exposure encompasses a smaller set of 

values than seen in the subchronic data, likely due to the smaller number of studies as well as to 

the fewer number of species studied for chronic effects. Nonetheless, both chronic and 

subchronic studies have identified a NOAEL as low as 5 mg/kg in rats, with two subchronic 

studies identifying this as a NOAEL for dogs. These NOAELs were derived in animals exposed 

to permethrin with different proportions of cis/trans isomers, and the primary effect observed at 

the LOAEL differed in each case. Despite these differences, the identification of 5 mg/kg as a 

NOAEL in multiple studies and in two different species provides support for identification of 

this dose of permethrin as a level not likely to elicit substantial toxicity if prolonged exposure 

occurs. 


SECTION D3 


Table D3-20 

Summary of Chronic Toxicity and Carcinogenicity of Permethrin 

Species 

Study 

Duration 

Formulation 

Concentration in 

Feed 

mg/kg 

Intake 

mg/kg-d 

Long-Evans Rat 104 weeks Unspecified 0-500 0-25 

Wistar Rat 104 weeks Not specified 0-2500 

Wistar Rat 

CD-1 Mice 

104 weeks 

2 years 

Charles River 

CD-1 Mice 24 months Not specified 

Alderley Park 

Mice 

98 weeks 

0-91.5 

(males) 

0-104 

(females) 

Technical grade, 

purity not 

specified Not specified 0-250 

Purity unknown; 

cis-trans 40:60 0-4000 0-600 

0-2000 (males) 

0-5000 (females) 

PP557 94.0- 

98.9% a.i.; 

cis-trans 40:60 0-2500 

0-286 (males) 

0-714 

(females) 

0-287.2 

(males); 

0-316.1 

(females) 

Tumor Data 

NOAEL a 

mg/kg-d 

Primary Effect 

at LOAEL b 

Equivocal for lung tumors 

in males (USEPA 1981); 

considered negative for 

tumors (DPR 1994). N/A c NA 

No statistically significant 

incidence of tumors in 

either males or females 

(USEPA 2002 and DPR 

1994) 40 


incidence of tumors 

(USEPA 2005 and DPR 

1994) 50 

Non-neoplastic 

liver effects 


weights (USEPA 

as cited in DPR 

2004) 


incidence of tumors (study 

considered invalid by 

USEPA 1989; study 

deficiencies cited by DPR 

1994) 75 d N/A 

Statistically significant 

increases in liver 

adenoma/carcinoma at 

mid- and high-doses for 

male and females; 

statistically significant lung 

adenomas and combined 

adenoma/carcinoma in 

females only (USEPA 

2002); DPR (1994) 

considered the study 

positive for an oncogenic 

effect. 


incidence of tumors 

(USEPA 2005; study 

deficiencies cited by DPR 

1994) 

N/A due to study 

deficiencies; 

study may not 

be used for 

assessment of 

chronic toxicity 

(USEPA 2004b) 

110.5 (males) 

124.2 (females) 

N/A due to study 

deficiencies; 

study may not be 

used for 

assessment of 

chronic toxicity 

(USEPA 2004b) 

Liver effects 

(proliferation of 

smooth 

endoplasmic 

reticulum; 

Reference 

Braun and Rinehart 1977 as 

cited in DPR 1994; also 

referenced as Braun and 

Rinehart 1977 

MRID 92142123 as cited in 

USEPA 2002; 2005; also 

referenced as ICI 1977; 

Richards et al. 1977; Ishmael 

and Litchfield 1988. 


USEPA 2005; also referenced 

as Wellcome 1980 and 

McSheehy et al. 1980. 

Bio/dynamics Mouse I 1977 

as cited in DPR 1994; also 

referenced as Hogan and 

Rinehart 1977. 

MRID 00062806, 92142033; 

FMC 33297 as cited in 

USEPA 2002 and 2004b; also 

referenced as FMC Mouse II, 

Pathology Work Group Study 

1979 and Tierney and 

Rinehart 1979. 

MRID 00102110, 92142032 

as cited in USEPA 2005; also 

referenced as ICI 1977; Hartz 

et al. 1977; Ishmael and 

Litchfield 1988. 



DRAFT PEIR 



Table D3-20 


Species 

Crl:CD- 

1 ® (ICR)BR 

female mice 

CFLP mice 

Study 

Duration 

100 weeks 

91 weeks 

Formulation 


Feed 

mg/kg 

Intake 

mg/kg-d 

Technical grade, 

94.7 a.i. 0 or 5000 780-807 

Purity unknown; 

cis-trans 25:75 Not specified 0-250 

Tumor Data 

NOAEL a 

mg/kg-d 


at LOAEL b 

increased 

peroxisomes in 

centrilobular 

hepatocytes, 

eosinophilia of 

hepatocytes) 


increases of lung 

brachioloalveolar 

adenomas; increased 

incidences of basophillic 

hepatocellular adenoma 

unrelated to treatment 

duration; no progression to 

carcinoma in lung or liver 

(USEPA 2002; not 

reviewed by DPR) N/A N/A 


increases in benign lung 

tumors (study did not 

conform to FIFRA 

guidelines according to 

DPR 1994; USEPA as 

cited in DPR 1994) 

Dog 

1 year 

Purity 92.5%; cistrans 

ratio 32:60 Not specified 0-1000 N/A 10 d 

Notes: 

a NOAEL = No observed adverse effect level 

b LOAEL = Lowest observed adverse effect level 

c N/A indicates that data is not available 

d No observed effect level 

250 d 


weights 

Liver 

hypertrophy, 

adrenal 

alterations, and 

decreased 

weight gain 

Reference 


USEPA 2002; also referenced 

as 

Carcinogenicity/Reversibility 

Study 2000 and Barton et al. 

2000. 

Wellcome 1980 as cited in 

DPR 1994; also referenced 

as James 1980 

Kalinowski et al. 1982 as 

cited in DPR 1994 

Source: 

Braun, W. G. and W. E. Rinehart (Biodynamics). 1977. A twenty-four month oral toxicity/carcinogenicity study of FMC 33297 in rats. FMC Corp. DPR Vol. 378-010, -011, -022, and -024, #13347, #13348, #989535, and 


SECTION D3 


Table D3-20 


Species 

Study 

Duration 

Formulation 


Feed 

mg/kg 

Intake 

mg/kg-d 

Tumor Data 

NOAEL a 

mg/kg-d 


at LOAEL b 

Reference 

#989579. 

California Environmental Protection Agency, Department of Pesticide Regulation (DPR). 1994. Permethrin (Permanone Tick Repellant). Risk Characterization Document (Revised). May 9. 

Hogan, G. K., and W. E. Rinehart (Bio/dynamics, Inc.). 1977. A twenty-four month oral carcinogenicity study of some pyrethroids. Mutat. Res. 130:244. 

Ishmael, J. and M. H. Litchfield. 1988. Chronic toxicity and carcinogenic evaluation of permethrin in rats and mice. Fund. Appl. Toxicol. 11:308-322. Unpublished reports: (1) Hart, D., P. B. Banham, J. R. Glaister, I. Pratt and T. 

M. Weight, 1977 PP557: whole life feeding study in mice. ICI Americas, Inc. Report No. CTL/P/359. DPR Vol. 378-053 and -054, #989517 and #989509. (2) Richards, D. P. B. Banham, I.S. Chart, J. R. Glaister, G. W. Gore, I. 

Pratt, K. Taylor, and T. M. Weight, 1977. PP557: Two year feeding study in rats. ICI Americas, Inc. Report No. CTL/P/357. DPR Vol. 378-051 and -052, #989518 and #989510. Also known as MRIDs 00102110 and 94142123. 

Kalinowski, A. E., P. B. Banham, I. S. Chart, S. K. Cook, G. W. Gore, S. F Moreland, and B. H. Woollen. 1982. Permethrin: One year oral dosing in dogs. ICI Americas, Inc. Report No. CTL/P/647. DPR Vol. 378-297, #04866. 

McSheehy, T, W., R Ashby, P. A. Marin, P. L. Hepworth, and J. P. Finn (Wellcome Foundation Ltd.). 1980. 21Z: Potential toxicity and oncogenicity in dietary administration to rats for a period of 104 weeks. Coopers Animal 

Health Inc. DRP Vol. 378-299 to -305, #48981 - #48987. Also referenced as MRID 974411. 

MRID 92142123. Richards, D. et al (1977) Phase 3 reformat of MRIDs 69701 and 120268: Permethrin (PP557): 2 year Feeding Study in Rats (Volume I and II). ICI Central Toxicology Laboratory, Alderley Park, Macclesfield, 

Cheshire SK10 4TJ, UK. CTL Report Number: CTL/P/357, December 19, 1977; reformatted April 30, 1990. 

MRID 00062806. Ellison, T. (1979) Analysis of Physical Observations, Twenty-four Month Oral Carcinogenicity Study of FMC 33297 in Mice. Bio/dynamics, Inc., Mettlers Road, East Milestone, New Jersey 08873. Bio/dynamics 

Study Number: 76-1695, FMC Study Number: ACT 115.35, October 9, 1979. Unpublished. 

MRID 45597105. Barton, S.J., S. Robinson, and T. Martin (2000) Permethrin Technical: 100 Week Carcinogenicity/Reversibility Study in Mice with Administration by the Diet. Inveresk Research, Tranent, EH33 2NE, Scotland. 

Inveresk Report No. 16839, Project No. 45695, FMC Study No. A95-4264, May 24, 2000. Unpublished. 

Tierney W. J. and W. E. Rhinehart (Biodynamics Inc.). 1979. A twenty-four month oral carcinogenicity study of FMC 33297 in mice (Mouse II). FMC Corp. DPR Vol. 378-342, #57754. 

USEPA. 2002c. Memorandum. Kidwell, J. Permethrin: Report of the Cancer Assessment Review Committee (Third Evaluation). Health Effects Division, Office of Pesticides Program, USEPA. TXR No. 0051220. Dated October 

23, 2002. 

USEPA. 2004b. Memorandum. Kidwell, J. Permethrin - Third Report of the Hazard Identification Assessment Review Committee. Health Identification Assessment Review Committee, Health Effects Division (7509C). USEPA 

TXR No.: 0052543. Dated May 12, 2004. 

USEPA. 2005. Memorandum. Kinard, S., Y. Yang, S. Ary. Permethrin: HED Chapter of the Reregistration Eligibility Decision Document (RED). PC Code 109701, Case No. 52645-53-1, DP Barcode D319234. Health Effects 

Division, Office of Pesticides Program. USEPA. Dated July 19, 2005. 




DRAFT PEIR 


D3.1.5.2.10 

Genotoxicity 

The genotoxicity of permethrin has been evaluated in a comprehensive suite of assays that have 

utilized mammalian cells, Drosophila, and the bacteria Escherichia, Salmonella, and Bacillus, to 

examine permethrin’s ability to induce forward and reverse mutations, gene conversions, mitotic 

recombination, chromosomal loss, sex-linked recessive mutation, unscheduled DNA synthesis, 

sister chromatid exchange, or micronuclei formation (Table D3-21). Results of these assays have 

given consistently negative results when permethrin has been tested for the ability to induce 

specific mutations (e.g., in the Ames assay with Salmonella typhimurium). However, permethrin 

has induced chromosomal aberrations in human lymphocytes and in Chinese hamster ovary cells 

when tested with an absence of metabolic activation (S9 fraction), with equivocal results 

obtained for human lymphocytes when tested in the presence of S9. Permethrin has also yielded 

evidence, ranging from clearly positive to equivocal results, of its ability to induce micronucleus 

formation, sister chromatid exchange, and chromosomal aberrations in either human or 

nonhuman, mammalian systems in vitro. These data were sufficient for the IPCS (1999) to 

conclude that permethrin is clastogenic in vitro. No data are available to assess whether 

permethrin is clastogenic in vivo as well. 

Table D3-21 

Results of Studies of the Genotoxicity of Permethrin 

End-point Test object Concentration 

In vitro 

cis: trans 

ratio 

Purity 

(%) Result Reference 

Differential toxicity E. coli W3110/ p3478 5,000 µg/disc 38:52 90.4 Negative ± S9 

Differential toxicity B. Subtilis H17/M45 5,000 µg/disc 38:52 90.4 Negative ± S9 

Reverse mutation 








S.typhimurium TA100, 

TA98, TA1538, 

TA1537, TA1535 


TA98, TA1538, 

TA1537, TA1535 


TA98, TA1538, 

TA1537, TA1535 


TA98 


TA98, TA1538, 

TA1537, TA1535 


TA98 


TA98 


TA98, TA1538, 

TA1537, TA1535 

5 µl/plate 44:56 93.6 Negative ± S9 

Simmon et al. 

1979 

Simmon et al. 

1979 

Brusick and Weir 

1976 

1,000 µg/plate NR 95.7 Negative ± S9 Simmon 1976 

7,500 µg/plate 38:52 90.4 Negative ± S9 

980 µg/plate NR NR Negative ± S9 

Simmon et al. 

1979 

Bartsch et al. 

1980 

5,000 µg/plate NR NR Negative ± S9 Moriya et al. 1983 

3,000 µg/plate NR 95 Negative ± S9 

5,460 µg/plate NR NR Negative ± S9 

6,000 µg/plate NR 

cis, 99 

trans, 100 

Negative ± S9 

Pluijmen et al. 

1984 

Pednekar et al. 

1987 

Herrera and 

Laborda 1988 

Reverse mutation E. coli WP2 1,000 µg/plate NR 95.7 Negative ± S9 Simmon 1976 

Reverse mutation E. coli WP2 7,500 µg/plate 38:52 90.4 Negative ± S9 

Simmon et al. 

1979 

Reverse mutation E. coli WP2 hcr 5,000 µg/plate NR NR Negative ± S9 Moriya et al. 1983 


SECTION 3 


Table D3-21 

Results of Studies of the Genotoxicity of Permethrin 

End-point Test object Concentration 

cis: trans 

ratio 

Purity 

(%) Result Reference 

Gene conversion 

S. cerevisiae D4, try 

locus 

5 µl/plate 44:56 93.6 Negative ± S9 

Mitotic recombination S. cerevisiae D3 50,000 µg/ml 38:52 90.4 Negative ± S9 

Chromosomal loss D. melanogaster 5 µg/ml feed NR NR Negative a 

Sex-linked recessive 

mutation 

Unscheduled DNA 

synthesis 

Gene mutation 

Gene mutation 

Gene mutation 

Chromosomal 

aberration 

Sister chromatid 

exchange 

D. melanogaster 1.2 µg/ml feed 45:55 91.1 Negative a 

Fischer 344 rat primary 

hepatocytes 

Chinese hamster lung 

V79 cells 

Hprt locus 


V79 cells 

OuaR 

Mouse lymphoma 

L5178Y cells, Tk locus 

Chinese hamster ovary 

cells 

5,000 µg/ml 38:52 90.4 Negative a 

40 µg/ml NR 95 Negative ± S9 

40 µg/ml NR 95 Negative ± S9 

Brusick and Weir 

1976 

Simmon et al. 

1979 

Woodruff et al. 

1983 

Mehr et al. 

1988;Gupta et al. 

1990 

Simmon et al. 

1979 


1984 


1984 

94 µg/ml NR NR Negative ± S9 Clive 1977 

100 µg/ml NR 99.5 Positive - S9 

Human lymphocytes 50 µg/ml NR 99.5 Equivocal + S9 

Micronucleus formation Human lymphocytes 50 µg/ml NR 99.5 Positive - S9 

Micronucleus formation Human lymphocytes 100 µg/ml NR 95 Equivocal a 

Micronuclei (with 

inhibition of excision 

repair) 

Micronuclei (with 

inhibition of excision 

repair) 

Chromosomal 

aberration 

Inhibition of gapjunctional 

intercellular 

communication 

In vivo 

Human lymphocytes 100 µg/ml NR 97 Equivocal a 

Human lymphocytes 10 µg/ml NR 97 Positive a 

Human lymphocytes 75 µg/ml NR 99.5 


V79 cells 

Positive - S9 

Equivocal + S9 

8 µg/ml NR NR Negative a 

Barrueco et al. 

1994 


1992; Herrera et 

al. 1992 


1992; Herrera et 

al. 1992 

Surrallès et al. 

1995a 


1995a 


1995a 


1992, 1994 

Flodström et al. 

1988 

Dominant lethal 

mutation 

Male CD -1 mice 

452 mg/kg bw × 5 

orally 

NR NR Negative 

Chesher et al. 

1975 

Source: 

IPCS 1999 

Notes: 

a Not tested in the presence of S9 

NR, not reported; S9, 9000 × g supernatant of rat liver 




DRAFT PEIR 


D3.1.5.3 


LBAM eradication goals may require repeated application of permethrin to fenceposts, telephone 

poles, or similar structures in conjunction with a pheromone attractant. This mode of application 

will yield a very low potential for human exposure to permethrin. Nonetheless, permethrin’s 

ability to persist in the environment for days or weeks (see Section D3.1.5.1) indicates that 

human exposure to low concentrations may occur. 

When human toxicity data are not available for a chemical, as is the case for permethrin, 

regulatory agencies necessarily rely on data from animal studies to characterize exposure levels 

deemed to be safe for humans. Noncancer toxicity criteria for permethrin have been developed 

by the ATSDR (2003a) and the USEPA IRIS (2009a). Notwithstanding the use of different 

terminology for their respective toxicity criteria (MRLs for ATSDR, and RfDs for the USEPA), 

both of the agencies use comparable methodology to derive the noncancer toxicity criteria. 



exposures referred to as the RfC (USEPA 2009b). The RfD and RfC are each defined as the daily 

exposure level for the “…human population (including sensitive subgroups) that is likely to be 

without an appreciable risk of deleterious effects during a lifetime” (USEPA 2009b). RfDs or 

RfCs are typically derived by selecting the most scientifically appropriate NOAEL from relevant 

animal toxicology studies, and then applying one or more UFs of 3 or 10 to address data 

limitations. These UFs are used to account for intraspecies variability, interspecies variability, 

the extrapolation of data from animals to humans, differences in duration between the 

experimental period and lifetime exposure, and/or for the overall quality and completeness of 

available toxicity data (USEPA 2009b). 



exposure.” 





duration within a given route of exposure.” Table D3-22 summarizes the toxicity criteria for 

permethrin that have been derived by regulatory agencies. 

Table D3-22 

Noncancer Oral Toxicity Criteria for Permethrin 

Toxicity Criterion Value (mg/kg-d) Reference 

Acute-duration MRL 0.3 ATSDR 2003a 

Intermediate-duration MRL 0.2 ATSDR 2003a 

Chronic RfD 0.05 USEPA 2009a 

Chronic RfD 0.25 USEPA 2007 

Note: 



SECTION 3 


ATSDR’s acute-duration MRL is based on the data of McDaniel and Moser (1993), who 

administered a single gavage dose of technical-grade permethrin to rats at 0, 25, 75, or 150 

mg/kg. Neurological toxicity, manifested as an increase in excitability and aggressiveness, 

decreased motor activity, and abnormal motor movement, was observed in animals given 75 

mg/kg, but not at 25 mg/kg. Consequently, the dose level of 75 mg/kg represents the LOAEL, 

and 25 mg/kg represents the NOAEL. To that NOAEL, ATSDR applied a UF of 10 to account 

for extrapolation from animals to humans, and an additional UF of 10 to account for 

‘intrahuman’ variation, yielding the acute-duration MRL of 0.3 mg/kg-d. 

ATSDR cites a 1994 USEPA review (USEPA 1994) from the Office of Pesticides and Toxic 

Substances as the basis of their intermediate-duration MRL (ATSDR 2003a). In the study 

described in ATSDR (2003a), male and female rats were administered technical-grade 

permethrin in the diet for 13 weeks. Time-weighted average doses were 0, 15.5, 91.5, or 150.4 

mg/kg for males, and 0, 18.7, 111.4, or 189.7 mg/kg for females. Hindlimb splay and other 

unspecified signs of neurotoxicity were documented at 91.5 and 111.4 mg/kg in males and 

females, respectively. These doses represent the gender-specific LOAELs, with the NOAEL of 

15.5 mg/kg selected as the lowest dose from either gender showing an absence of neurotoxicity. 

As with the acute-duration MRL, the ATSDR applied an UF of 10 to account for extrapolation 

from animals to humans, and an additional UF of 10 to account for “intrahuman” variation. The 

resulting intermediate-duration MRL is 0.2 mg/kg-d. 

The USEPA’s chronic RfD for permethrin was derived from a 2-year feeding study in which rats 

were given 0, 1, 5, or 25 mg/kg of permethrin for 104 weeks. The study was conducted by FMC 

and submitted to the USEPA to support registration of permethrin-containing pestcides. The 

study is not available for review. However, based on information provided in the USEPA’s IRIS 

summary for permethrin (USEPA 2009a), no adverse effects of permethrin were observed at 1 

mg/kg, but a slight increase in liver weights was observed at 5 mg/kg. A marked increase in liver 

weight was documented for the 25 mg/kg dose groups. The increase in liver weights in the 5 

mg/kg was slight enough to be considered toxicologically insignificant, and 5 mg/kg was 

identified as the NOAEL. The USEPA applied an UF of 10 to account for the extrapolation from 

animals to humans, and an additional UF of 10 to account for within-species variability. The 

resulting chronic RfD is 0.05 mg/kg-d. This information was developed in 1992, and has not 

been revised to reflect more current toxicologic information on permethrin. Recent toxicity data 

on permethrin have been incorporated into the USEPA’s reregistration of permethrin (see 

following), and the chronic RfD from that assessment is used to assess potential effects of 

chronic oral exposure to permethrin. 

The USEPA (2007) identified a chronic oral NOAEL of 25 mg/kg-d that was developed in 

support of the reregistration of permethrin. That RfD was based on an acute study in rats that 

identified a LOAEL of 75 mg/kg-d based on signs of aggression, abnormal and/or decreased 

movement, and increased body temperature. No other details of the study were provided. An 

uncertainty factor of 100 was applied to the NOAEL to develop the chronic RfD of 0.25 mg/kgd. 

Inhalation toxicity data for permethrin are extremely limited, and neither ATSDR nor the 

USEPA have developed inhalation toxicity criteria for permethrin (ATSDR 2003a; USEPA 

2009a). In analyses developed to support the reregistration of permethrin (USEPA 2005), agency 

toxicologists identified a 15-day inhalation study in rats (MRID No. 00096713) as the basis of 




DRAFT PEIR 


the inhalation component of their risk assessment. That study exposed animals by whole body 

inhalation (as opposed to nose-only) to concentrations of 0, 0.0061, 0.042, or 0.583 mg/L for 6 

hours/day for 2 days during week 1; 5 days during weeks 2 and 3; and 3 days during week 4. The 

LOAEL was the highest concentration administered, 0.583 mg/L. Animals in that group 

exhibited body tremors and hypersensitivity to noise. The NOAEL was identified as 0.042 mg/L, 

or 11 mg/kg-d. The USEPA (2005) considered the NOAEL, with a cumulative UF of 100, to be 

applicable to all exposure durations. Dividing the NOAEL of 11 mg/kg-d by 100 gives a RfDinh 

of 1.1 x 10 -1 mg/kg-d (see Table D3-23). 

Table D3-23 

Noncancer Inhalation Toxicity Criteria for Permethrin 

Toxicity criterion Value (mg/kg-d) Reference 

Acute-duration inhalation reference dose 1.1 x 10 -1 USEPA 2005 

Intermediate-duration inhalation reference dose 1.1 x 10 -1 USEPA 2005 

Chronic-duration inhalation reference dose 1.1 x 10 -1 USEPA 2005 

Note: 


Permethrin was classified by the USEPA in 2002 as a Category C carcinogen (likely to be 

carcinogenic to humans) under the agency’s 1999 Interim Final Guidelines for Carcinogen Risk 

assessment (USEPA 2002c). This classification was based on two reproducible benign tumor 

types (lung and liver) in the mouse (Tierney and Rinehart 1979), equivocal evidence of 

carcinogenicity in Long-Evans rats (Braun and Rinehart 1977), and supporting structural activity 

relationship information (USEPA 2002c). This decision has been supported in subsequent data 

reviews by the USEPA (2004b, 2005, 2007). Most recently, the USEPA has evaluated 

permethrin as a carcinogen in the human health risk assessments for the RED for Permethrin 

(USEPA 2007). A cancer slope factor of 9.6 x 10 -3 mg/kg-d -1 was used in the risk assessments, as 

derived and documented by the USEPA (2002c). 

D3.1.6 

Inert Ingredients of Permethrin E-Pro 

The formulation Permethrin E Pro consists of 36.8% permethrin and 63.2% other ingredients 

(Etigra, undated). The other ingredients include 26.0% of hydrocarbon solvents (CAS no. 8052- 

41-3, which refers to Stoddard solvent); 25.9% triacetin (CAS no. 102-76-1); < 10.0% of a 

surfactant blend (no CAS number provided); < 4.0% 1,2,4-trimethylbenzene (CAS no. 95-63-6); 

and > 0.03% ethylbenzene (CAS no. 100-41-4) (Etigra, undated). 1,2,4-trimethylbenzene and 

ethylbenzene are also components of Dursban ® 4E, one of the chlorpyrifos-containing products 

considered under the No Program Alternative and addressed previously; 1,2,4-trimethylbenzene 

and ethylbenzene were also previously evaluated as inert ingredients of Dursban ® 4E. In the 

following sections, information on the chemistry, environmental fate, and toxicity of Stoddard 

solvent and triacetin are provided. Because no specific identifying information was provided by 

Etigra (undated MSDS) on the identity of the surfactant blend, that material could not be 

evaluated. 


SECTION 3 


D3.1.6.1 

Environmental Fate and Chemistry of Ingredients of Permethrin E-Pro 

D3.1.6.1.1 Physical and Chemical Properties of Inert Ingredients of Permethrin E-Pro 

STODDARD SOLVENT 

Stoddard solvent is a mixture of C 7 -C 12 hydrocarbons (alkanes, cycloalkanes, and aromatic 

compounds), with the majority in the C 9 to C 12 range (ATSDR 1995). It is produced by refining 

crude oil, and its composition varies depending on the refinery and time of production (ATSDR 

1995). Table D3-24 lists chemical and physical properties of Stoddard solvent. 

Table D3-24 

Chemical and Physical Properties of Stoddard Solvent 

Source: 

ATSDR 1995 

Property 

Parameter 

Molecular weight (range, grams) 135-145 


Clear liquid 

Boiling point 

154-202ºC 


Insoluble 

Log octanol-water partition coefficient (KOW) 3.16-7.06 

Log organic carbon partition coefficient (KOC) 2.85-6.74 


4-4.5 mmHg 


4.4x 10-4-7.4 atm m 3 /mol 

TRIACETIN 

Triacetin is typically used as a topically applied anti-fungal agent, as a fixative in perfumes, as a 

cellulose plasticizer in cigarette filters, as a component in binders for solid rocket fuels, and in 

the manufacture of cosmetics. (TOXNET 2009b). It is manufactured by the reaction of glycerol 

with acetic acid in the presence of twitchell reagent; or in a benzene solution of glycerol and 

boiling acetic acid in the presence of cationic resin that has been pretreated with dilute sulfuric 

acid (TOXNET 2009b). 

Triacetin, or the triacetate ester of glycerol, is a clear, combustible and oily liquid. It has a 

molecular formula of C 9 H 14 O 6 , a molecular weight of 219.20, and a boiling point between 258- 

259ºC (TOXNET 2009b). The log K OW is 0.25, indicating that triacetin is not likely to 

bioaccumulate or bioconcentrate. Triacetin is slightly soluble in water but is unlikely to volatize 

from water or air due to its low Henry’s Law Constant (1.2 × 10 -8 atm-m 3 /mol at 25ºC [USEPA 

2003]) and low vapor pressure (0.00248 mmHg at 25°C) (TOXNET 2009b). The structure of 

triacetin is given on Figure D3-10. 

Figure D3-10 Structure of Triacetin 




DRAFT PEIR 


D3.1.6.1.2 Environmental Transport, Persistence, and Degradation of Inert Ingredients 


The relatively high K OC and K OW indicate that Stoddard solvent will tend to sorb to organic 

matter (ATSDR 1995). Although some of the higher molecular weight compounds of the mixture 

are not water-soluble, the alkylbenzene components may dissolve in water. If that water is in 

contact with soil, the solution may move downward through the soil column. Alkane components 

of Stoddard solvent are expected to sorb to soil organic matter but tend not to dissolve in soil 

water. Volatilization from surface soil or surface water will be an important loss process for 

Stoddard solvent in the environment; especially true for the alkane components, whereas higher 

molecular weight components may undergo biodegradation (ATSDR 1995). In aqueous systems, 

substituted benzenes and naphthalene components may be photo-oxidized, while other 

components are not photolabile (ATSDR 1995). No data are available on the potential for 

Stoddard solvent to bioaccumulate (ATSDR 1995). 

TRIACETIN 

Once in the atmosphere, triacetin tends to be degraded by interaction with highly reactive 

hydroxyl radicals; the estimated half-life for this process is estimated to be 1.9 days. Triacetin is 

not known to be subject to photolytic degradation. The K OC has been estimated to be 33, 

indicating that triacetin may be mobile in soil. This K OC also indicates that if triacetin is released 

to surface waters, it will tend to partition to sediments. TOXNET cites an estimated aquatic halflife 

of 130 and 12 days at pH values of 7 and 8, respectively (TOXNET 2009b). 

D3.1.6.1.3 Mammalian Toxicity of Permethin E Pro Inert Ingredients 


Stoddard solvent is volatile, and is readily absorbed by inhalation. Following rapid distribution to 

blood and other tissues, it is quickly cleared from the blood, but exhibits much more prolonged 

and slower elimination from other physiological compartments (HSDB 2009). Central nervous 

toxicity is a well-recognized target of acute and longer-term inhalation exposure to Stoddard 

solvent. Gastorintestinal and hepatic effects have also been documented following ingestion, and 

can be severe if sufficient quantities were administered or consumed (HSDB 2009). Little to no 

evidence exists of genotoxocity for Stoddard solvent. One short-term assay of mutagenicity 

reported positive results, but only at concentrations that were cytotoxic (ATSDR 1995). Stoddard 

solvent has not been classified as a carcinogen by the USEPA or by OEHHA. No toxicity criteria 

for Stoddard solvent have been developed by the ATSDR, USEPA, OEHHA. 

TRIACETIN 

Triacetin is considered to have low toxicity; it has been classified by the FDA as ‘generally 

recognized as safe’ when added directly to human food (Code of Cederal Regulations [CFR] 

2005a). It has also been exempted from tolerance requirements when used as a solvent or 

cosolvent ‘in accordance with good agricultural practice’ as an inert ingredient in pesticide 

formulations applied to animals (CFR 2005b). 

Human dermal toxicity and sensitization studies of triacetin reviewed in TOXNET (2009) 

indicate that a solution of triacetin (50% dilution, but concentrations not otherwise specified) was 

neither a dermal irritant nor a sensitizer. Triacetin has caused ocular irritation, pain, and redness. 

The irritation potential of triacetin may depend on the presence and concentration of monoacetin 


SECTION 3 


and diacetin, with diacetin reportedly capable of inducing greater irritation than triacetin 

(TOXNET 2009). No other toxicity data on triacetin were identified. 

D3.2 ALTERNATIVE MATING DISRUPTION (MD): MD-1, TWIST TIES; MD-2, 

GROUND; MD-3, AERIAL 

Up to five different pheromone treatment formulations are being evaluated for use under this 

alternative: (1) HERCON, (2) SPLAT, (3) Isomate, and the microcapsule formulations (4) 

CheckMate and (5) NoMate (Table D3-25). (The Microcapsule formulations are not part of the 

proposed Program, but are evaluated in response to public scoping comments for the PEIR.) 

They are to be applied in several ways, for urban infestations and for small and isolated areas, a 

ground treatment tool using pheromone twist ties will be used. Ground-based application of 

pheromones via the use of a pod gun, caulk gun, metered spray gun, or a truck-based spray gun 

will be used to apply pheromones to trees and shrubs in residential yards, or to trees and 

telephone poles on public property (see Section D2.3.2.2 for additional details of the different 

application methods). Aerial application may be used for heavily infested, inaccessible areas 

such as forested and agricultural land. 

Broadly defined, pheromones are chemical compounds produced by animals that modify the 

behavior of other individuals of the same species. Lepidopteran pheromones are those 

pheromones produced by members of the insect order Lepidoptera, which includes moths and 

butterflies. Mating pheromones are released by females to attract males of the same species; 

when used as biopesticides, these substances act by attracting males to the site of the trap or bait, 

and by so doing confuse and diminish the likelihood of successful mating with females. The 

pheromones do not kill the moths. 

While only small amounts of pheromone are necessary in the environment to disrupt mating, the 

pheromone is highly volatile and degrades rapidly when exposed to the environment. Therefore, 

if mating disruption is to continue beyond a few days before another application of pheromone is 

necessary, the pheromone must be formulated in such a way as to provide for a slow release to 

the atmosphere. Several formulations will do this and allow one application of pheromone to 

provide sufficient levels of pheromone in the environment to disrupt mating for between 30 to 90 

days. These formulations are manufactured as microcapsules, biodegradable flakes, or in a 

paraffin wax-based matrix that can provide a delayed release of pheromone (USDA 2008). The 

four formulations considered in this EIR reflect this array of delivery styles. 

Table D3-25 

General Characteristics of Five LBAM-Specific Pheromones Considered for Use 

Product Characteristics Formulation on Product Label Product Description 

HERCON 

SPLAT 

Isomate 

LBAM pheromones in starch-based 

flakes, approximately 1/8 inch 

square by 1/16 inch thick, applied 

with a sticking agent 

LBAM pheromones in an amorphous 

sticky polymer, size of drops 

depends on application 

characteristics 

LBAM pheromones in a brown 

plastic tube dispenser with an 

aluminum wire for attachment of the 

14.29% (E)-11-Tetradecen-1-yl 

acetate 

0.71% (E,E)-9,11-Tetradecadien-1-yl 

acetate 

85% Inert Ingredients 

9.5% (E)-11-Tetradecen-1-yl acetate 


acetate 



Acetate, 


Pheromones embedded in starchbased 

flakes 

Pheromones in a mixture of wax, 

emulsifiers and carriers. 

. 

Pheromones in a plastic tube with 

ingredients to minimize UV 

degradation and oxidation 




DRAFT PEIR 


Table D3-25 

General Characteristics of Five LBAM-Specific Pheromones Considered for Use 

Product Characteristics Formulation on Product Label Product Description 

twist-tie 

Acetate 

33.48% Inert Ingredients 

NoMate 

LBAM pheromones in microcapsule 

shell, aqueous suspension 


Acetate, 


Acetate 


Bio-Tac adhesive to hold capsules 

on foliage - Polybutene 

CheckMate 

LBAM pheromone in microcapsule 

shell, aqueous suspension 


Acetate, 


Acetate 

82.39% Inert Ingredients 

--- 

For ground applications to trees and utility poles on public and private property and aerial 

application of pheromone in remote areas, the treatment area is a 1.5 mile radius around each 

LBAM detection, with a projected 30 to 90 day spray interval. For ground treatment using twist 

ties, 250 twist ties per acre in a 200 meter radius around each LBAM detection are applied and 

subsequently replaced every 3 to 6 months. Treatment areas may be adjusted to provide the 

public with identifiable treatment boundaries. After two life cycles of treatment without any 

LBAM detections, treatment would cease. Post-treatment monitoring traps will remain in place 

for one additional life cycle. 

The area for aerial applications is a 1.5 mile radius around each location where a LBAM is 

detected. After two life cycles of mating disruption applications without any LBAM detections, 

these applications will cease. Once the pheromone has dropped to levels that will not interfere 

with trap efficacy, post-treatment monitoring traps will remain in place for one additional life 

cycle. If no additional LBAM are detected, this area will be declared free from LBAM and 

trapping levels will return to detection levels. 

Twist ties utilize LBAM-specific pheromone that is contained within a sealed polyethylene tube 

that contains 63.88% (E)-11-tetradecen-1-yl acetate and 2.64% of (E,E)-9,11-tetradecadien-1-yl 

acetate (the two compounds that comprise the LBAM-specific pheromone) (Pacific Biocontrol 

Isomate Label, no date). 

The following discussion considers the available environmental fate and toxicity hazard 

information on the pheromone formulations under evaluation. 

D3.2.1 

HERCON Disrupt Bio-Flake ® LBAM 

HERCON is a sprayable starch-based flake pheromone treatment. The active ingredients are the 

synthetically manufactured LBAM pheromones (E)-11-tetradecenyl acetate and (E,E)-9,11- 

tetradecadienyl acetate. HERCON is manufactured by Hercon Environmental (HE) for use as a 

mating disruptor of the LBAM (HE 2008). It has no other known uses. HERCON targets light 

brown apple moths and has no attractant, physiological or hormonal effect on fish, reptiles, birds, 

or mammals. However, the LBAM pheromones may have some ability to affect Tortricid moths 

(CDFA 2009). 


SECTION 3 


HERCON is manufactured as a biodegradable polymeric controlled release flake; each flake is 

approximately 1/8 inch x 1/8 inch square, with the pheromone contained between two outer 

protective layers of starch-based polymer (HE 2009). This layered structure protects the 

contained pheromone from environmental degradation and rapid evaporation, resulting in 

controlled release over extended periods. 

D3.2.1.1 Physical and Chemical Properties of Active Ingredient of HERCON Disrupt Bio- 

Flake ® LBAM 

The majority of Lepidopteran pheromones are naturally occurring unbranched aliphatic 

compounds of 9 to 18 carbons with up to three double bonds that terminate in an alcohol, an 

aldehyde, or an acetate functional group (OECD 2002; USEPA 1995). The lengthy aliphatic 

chain gives rise to the designation of this class of compounds as Straight Chain Lepidopteran 

Pheromones, or SCLPs - a category that includes most of the known pheromones produced by 

insects in the order Lepidoptera (OECD 2002; USEPA 1995). In developing pesticide tolerance 

exemptions for SCLPs, the USEPA has included both naturally occurring as well as synthetically 

produced compounds that are identical to a known Lepidopteran pheromone, as well those 

pheromones that are stereoisomers or mixtures of isomers (USEPA 1995). Because of their 

selective and relatively low toxicity, the USEPA exempts SCLPs from pesticide tolerance 

requirements in or on all raw agricultural commodities when the pheromone is applied to 

growing crops at a rate that does not exceed 150 grams per year of active ingredient (see for 

example USEPA 1995). Figure D3-11 gives the structure of a typical SCLP. 

Figure D3-11 Molecular Structure of (Z)-11-Tetradecenyl Acetate, a Typical Straight Chain Lepidopteran Pheromone 

(SCLP) 

The simple straight chain hydrocarbon structure of the SCLPs that are present in HERCON, 

combined with an absence of environmentally persistent chemical substituents indicate that the 

SCLPs would not be expected to persist, accumulate, or concentrate in biota or in the 

environment. 

Table D3-26 summarizes the physical and chemical properties of HERCON (HE 2009). 

Table D3-26 

Physical and Chemical Properties of HERCON Disrupt Bio-Flake ® LBAM 

Source: 

HE 2009 

Parameter 


Vapor pressure 

Not determined 

Odor 

Mild 

Melting point 300°F 


Insoluble 

Octanol/water partition coefficient 

Not Reported 

Hydrolysis characteristics 

Not Reported 

Photolysis characteristics 

Not Reported 

Dissociation characteristics 

Not Reported 




DRAFT PEIR 


D3.2.1.2 

Environmental Transport, Persistence and Degradation 

Information on the environmental fate and persistence for HERCON could not be identified. 

However, the product is designed so that the LBAM pheromones slowly migrate to the outside 

edges of the flake, where they are released from the surface of the flake over 80-90 days. 

Following the release of its pheromone component, the remaining product consists mainly of 

starch. During the time the product is exposed to the environment, several microsopic organisms 

such as bacteria and molds are expected to degrade the product, causing it to decompose. 

D3.2.1.3 

Mammalian Toxicity of SCLPs 

D3.2.1.3.1 Metabolism 

By analogy to the structurally similar long-chain fatty acids, the USEPA (1995) predicted that 

SCLPs would be metabolized either by -oxidation to yield a series of two-carbon compounds, 

or by glucuronide conjugation and subsequent urinary elimination. 

STRAIGHT CHAIN LEPIDOPTERAN PHEROMONES 

Data submitted to the USEPA (USEPA 1995, 2006c, 2007d) in support of the pesticide tolerance 

exemptions for SCLPs provide evidence of and support for “nontoxic” or “practically nontoxic” 

classifications when SCLPs were tested by inhalation, dermal, and skin and eye irritation. No 

data indicate that SCLPs are genotoxic (USEPA 2007d). The USEPA’s interpretation of the low 

toxicity of SCLPs is shared by the OECD (2002). The OECD notes that these substances are 

inherently different from conventional pesticides in their “nontoxic, target-specific mode of 

action.” Further, SCLPs are effective at low concentrations (low application rates), and, 

consistent with their action as attractants, are volatile (OECD 2002). 

ACUTE TOXICITY OF SCLPS 

As a class, toxicity data indicate extremely limited toxicity of SCLPs to mammals. Data cited in 

the OECD (2002) list the LD 50 as >5,000 mg/kg for acute oral exposure; an LD 50 > 2,000 mg/kg 

for acute dermal toxicity, the LC 50 as “generally” > 5 mg/L, and no evidence of mutagenicity as 

tested in the Ames assay with Salmonella typhimurium. The USEPA (1995) cites an absence of 

significant acute toxicity from the administration of straight chain (unbranched) alcohols, 

acetates, and aldehydes of 6 to 16 carbon atoms in length (species and doses not specified). 

Additionally, Beroza et al. (1975) reported no mortality in rats exposed to aerosols of different 

pure SCLPs (3.8 to 6.7 µg/L) for one hour. The SCLPs evaluated were (Z)-7-hexadecen-1- 

olacetate, (Z)-7-dodeden-1-ol acetate, and (z)-7-dodecen-1-ol. Inscoe and Ridgeway (1992) 

reported inhalation LC 50 of > 5 mg/L to > 75 mg/L for (Z+E) 8-dodecenol acetate, (Z)-9- 

tetradecenal, (Z+E)-11-tetradecenal, and (Z)-11-hexadecenal. The SCLP (Z,Z+ZE)-7,11- 

hexadecadienol acetate was reported to have an acute inhalation LC 50 of > 3.3 mg/L (Inscoe and 

Ridgeway 1992). 

Recently conducted acute toxicity tests of the LBAM pheromone active ingredient (reviewed by 

OEHHA 2008c) provide evidence that the pheromones are in Toxicity Category IV (the lowest 

toxicity category) for oral administration (LD 50 > 5,000 mg/kg). The dermal irritation testing 


SECTION 3 


cited by OEHHA (2008c) indicated that these substances can induce moderate irritation 

(Toxicity Category III). Of the two dermal sensitization tests that are currently available, one – 

the Buehler dermal assay – did not indicate that the LBAM pheromones induce dermal 

sensitization. The second test – the LLNA or Localized Lymph Node Assay, was not conducted 

on the active ingredients. However, when conducted on other LBAM pheromone-containing 

formulations, the results of these two different assays of dermal sensitization have provided 

apparently contradictory results. OEHHA (2008c) discussed the reasons for the different results 

between the Buehler and LLNA tests, and noted that each measures the response to exposure at a 

different phase in the development of a sensitization reaction, i.e., “…it is possible that the 

products are active in the initial phase of the sensitization process, which is what the LLNA 

measures, but inactive in the later phases, what the guinea pig assay [Buehler assay] measures.” 

The OEHHA concluded that “In the absence of additional data, the health-protective approach is 

to treat the products [LBAM pheromone-containing products] as potential dermal sensitizers, 

meaning that they have the potential to cause allergic type reactions from skin contact.” 

SUBCHRONIC TOXICITY OF SCLPS 

Evidence of the relatively low toxicity of SCLPs also comes from the subchronic toxicity study 

of tridecyl acetate in rats (Daughtrey et al. 1990). Tridecyl acetate is a 15-carbon straightchain 

hydrocarbon ending in an acetate group, and as such, is structurally similar to the SCLPs. In the 

Daughtrey et al. (1990) study, rats were given relatively large doses of tridecyl acetate-0.1, 0.5, 

or 1.0 g/kg-d, 5 days/week for 90 days. The NOAEL was identified as the lowest dose 

administered (0.1 g/kg-d). Male and female animals in the 0.5 and 1.0 g/kg-d groups exhibited 

increased liver weights and/or in the ratios of liver to body weight, increased kidney weight 

and/or in the kidney to body weight ratios; males also developed kidney nephropathy. While 

these results indicate that subchronic exposure to tridecyl acetate can elicit adverse effects, these 

effects were seen at large doses (> 0.5 g/kg per day). These quantities are substantially greater 

than any environmental levels of LBAM pheromone expected to be present as a result of the 

LBAM program. 

OEHHA (2009b) reviewed and summarized additional subchronic toxicity data on SCLPs (see 

Table D3-27). According to OEHHA’s review, Nelson et al. (1990) exposed animals to the 

maximum-achievable concentrations of 1-nonanol (150 mg/m 3 ) and 1-decanol (150 mg/m 3 ), 6-7 

hours/day during gestation. Neither the pregnant females nor the fetuses exhibited evidence of 

toxicity from exposure, supporting the identification of NOAELs of > 30 mg/kg and > 17 mg/kg 

for 1-nonanol and 1-decanol, respectively. OEHHA (2009b) also cites two studies of the 

subchronic oral toxicity of SCLPs (WHO 2004; Hansen 1992). The WHO report describes the 

results of an unpublished study of a the SCLP 2-trans,4-trans-decadienal, but with very few 

details provided (see Table D3-27). As reported by OEHHA (2009b), the Hansen (1992) study 

examined both the subchronic toxicity and the reproductive/developmental toxicity of 1- 

dodecanol. Doses of 100, 500, or 2000 mg/kg were administered in the diet for 37 days to male 

and female rats. There were no adverse effects on the fetuses. Pregnancy rates were reduced in 

the high dose group, but not to a level that was statistically significant. There were no observed 

effects on body weight, weight gain, food consumption, or food efficiency at any dose, although 

a statistically significant decrease in white blood cell counts were documented for the two 

highest dose groups. The study defined a NOAEL of 100 mg/kg-d. Both the United States and 

Europe permit the use of 1-dodecanol as a food additive (OEHHA 2009b). 




DRAFT PEIR 


Table D3-27 

Sub-chronic toxicity data for four SCLPs (1-nonanol, 1-decanol, 2-trans,4-trans-decadienal, 

and 1-dodecanol) 

Chemical 

Test 

animals 

Route of exposure 

and doses used 

Exposure 

duration 

NOAEL and the reported health 

effects 

Reference 

1-nonanol 

1-decanol 

2-trans,4-transdecadienal 

Pregnant 

rats 

Pregnant 

rats 

rats 

Inhalation, one dose 

group 

Inhalation, one dose 

group 

Oral, gavage, one 

dose group 

1-dodecanol rats Oral, feed, 

0, 100, 500, or 2000 

mg/kg-d 

19 days >30 mg/kg-d based on absence of effects 

at this dose level; no fetal effects 

19 days >17 mg/kg-d based on absence of effects 

at this dose level; no fetal effects 

Nelson et al. 1990 

Nelson et al. 1990 

14 weeks 34 mg/kg-d (LOAEL not described) WHO Technical 

Report Series 922 

2004 

37 days 100 mg/kg-d based on small decrease in 

mean white blood cell counts at 500 

mg/kg-d; no reproductive or 

developmental effects 

Hansen 1992 

Source: 

OEHHA 2009b 

CHRONIC TOXICITY OF SCLPS 

Literature searches conducted for this HRA, as well as those conducted by OEHHA (2009b) 

have not identified any studies that characterize the chronic toxicity of SCLPs. As OEHHA 

(2009b) notes, “However the concern of any health effects associated with long-term exposure to 

the SCLPs is mitigated by the very low application rates and low acute and sub-chronic toxicities 

of these chemicals. There is no evidence to indicate the SCLPs are mutagenic. In addition, the 

SCLPs are structurally similar to some common fatty acids and are likely to be metabolized by 

the body into by-products that have no known toxicological concern.” 

D3.2.2 

Toxicity of HERCON Disrupt Bio-Flake ® LBAM 

A series of acute toxicity studies of HERCON were completed in 2008, with results submitted to 

the USDA. Those studies are summarized in Table D3-28. A review of these data by the DPR 

(2008a) determined that the studies of acute dermal toxicity, primary eye and dermal irritation, 

and dermal sensitization studies are acceptable to support use of the product. The acute dermal 

toxicity and primary eye and dermal irritation study results further indicate that HERCON is a 

Toxicity Category IV for these exposure routes and endpoints. With respect to the dermal 

sensitization potential of HERCON, the Buehler guinea pig dermal sensitization study indicates 

that the product is not a dermal sensitizer. An attempt to evaluate HERCON in the LLNA dermal 

sensitization study was not successful due to the physical and chemical properties of the product 

(DPR 2008a). However, as noted in the discussion of SCLPs, LBAM pheromone-containing 

products have given differing results in the LLNA and Buehler tests; thus the absence of data on 

HERCON’s sensitization potential in the LLNL assay leaves uncertainties as to whether 

HERCON may have sensitizing abilities or not. HERCON could not be evaluated for oral or 

inhalation toxicity in that multiple attempts to grind the flake to an acceptable size for 

administration by these routes of exposure were not successful (see Table D3-28). 


SECTION 3 


Table D3-28 

Summary of Mammalian Toxicity Studies for HERCON Disrupt Bio-Flake ® LBAM 

Author/ Study Study Design Toxicity EPA Hazard Rating 

Kuhn 2008 Stillmeadow 11754-08 


Cructchfield 2008. 

11756-08 


Kuhn 2008. Stillmeadow 11758-08 



Disrupt Bio-Flake ® LBAM Acute 

Oral (UDP) Toxicity in Rats 


Dermal Toxicity in Rats 


Inhalation Toxicity in Rats 

Disrupt Bio-Flake ® LBAM Eye 

Irritation Study in Rabbits 


Dermal Irritation Study in 

Rabbits. 

Disrupt Bio-Flake ® LBAM Skin 

Sensitization: Local Lymph 

Node Assay in Mice 

Disrupt Bio-Flake ® LBAM Skin 

Sensitization Study in Guinea 

Pigs 

5050 mg/kg Practically nontoxic 

2.10 mg/L. A study of primary eye irritation found no instances of 

corneal opacity or iritis, and although mild conjunctiva was induced (grade 1), it was clearing 

within 24 hours. When evaluated for primary dermal irritation, no treatment-related edema was 

observed, and only mild transient erythema (DPR 2008e). A dermal sensitization study reported 

only “faint erythema” in a small percentage of test animals at 24 or 48 hours after exposure. The 

DPR (2008e) placed Micro-TacII ® in acute toxicity category IV (the lowest toxicity rating) for 

these exposure routes, while concluding that it is not a dermal contact sensitizer. 

D3.2.2.3 


When quantitative human toxicity data are not available for a chemical, as is the case for SCLPs 

in general and HERCON specifically, regulatory agencies necessarily rely on data from animal 




DRAFT PEIR 


studies to characterize exposure levels deemed to be safe for humans. To quantify the potential 

for adverse effects to occur as a consequence of exposure to HERCON, this assessment relies on 

a series of toxicity criteria derived by OEHHA (2009b) for SCLPs. OEHHA’s derivation of the 

SCLP toxicity criteria (i.e., RfDs) follows methods previously described for the USEPA and 

ATSDR (e.g., see the Interpretation of Human Toxicity discussion for lambda-cyhalothrin). 

When HERCON was subjected to acute inhalation toxicity testing (DPR 2008a), the testing 

laboratory was not able to grind the flakes to an acceptable size for inhalation dosing despite 

applying two different techniques (e.g., grinding in a grinder for 24 hours). The physical 

properties of HERCON that made it unsuitable for testing also indicate that the material will 

have extremely limited bioavailability. However, the inherent chemical properties of the 

pheromones that comprise the active ingredients of HERCON indicate that human populations 

may be exposed as the pheromones volatilize (see following). In their evaluation of the LBAM 

pheromone formulation Isomate, OEHHA (2009b) relied on data in the Isomate MSDS (Pacific 

Biocontrol 2007), the USEPA (1994 referenced in OEHHA 2009b), and Health Canada (2002 - 

referenced in OEHHA 2009b) in concurring that SCLPs have low acute inhalation toxicity and 

LC 50 s > 5 mg/L. That concentration (5 mg/L) was identified as a NOAEL, and was converted to 

yield an acute inhalation NOAEL for SCLPs of 229 mg/kg-hour (OEHHA 2009b). By applying 

UFs of 10 to account for intraspecies variability and 10 for interspecies variability, OEHHA 

derived an acute inhalation RfD of 2.29 mg/kg-hour (OEHHA 2009b). That acute inhalation RfD 

is used in Section D5 to quantify potential effects from exposure to the LBAM pheromones 

present in HERCON. 

OEHHA (2009b) determined that both of the Nelson et al. (1990) studies (Table D3-27) are 

appropriate for assessing potential effects of subchronic inhalation exposure to SCLPs. OEHHA 

(2009b) selected the lower NOAEL from these two studies ( > 17 mg/kg-d) as the basis for 

estimating a subchronic inhalation RfD; the agency applied UFs of 10 to account for intraspecies 

variability, 10 for interspecies variability, and an additional factor of 3 (basis not specified) to 

yield a subchronic inhalation RfD of 5.7 x 10 -2 . That subchronic inhalation RfD is used in 

Section D5 to quantify potential effects from exposure to the LBAM pheromones present in 

HERCON. No chronic toxicity data are available for SCLPs, thus a chronic inhalation RfD could 

not be developed. 

SCLPs are capable of causing slight to mild eye irritation, although the degree of irritation 

depends on the specific pheromone. However, no acute toxicity criterion has been identified by 

OEHHA (2009b) or the USEPA to characterize the potential for SCLPs to induce eye irritation. 

The likelihood of dermal sensitization from HERCON exposures cannot be assessed given that 

currently available data does not support a complete understanding of the dermal sensitization 

potential of the LBAM pheromones. Because HERCON may be applied aerially, the following 

conclusion from OEHHA (2008b), reached in reference to the aerial application of Checkmate, 

should also be noted “…the acute toxicity testing of several LBAM pheromone formulations 

indicates low acute toxicity to individuals who could have been exposed by ingesting, breathing, 

or getting the product on their skin. However, due to the positive results of the LLNA, we cannot 

dismiss the possibility that in sensitive individuals, contact with particles could cause allergictype 

responses, though the negative results of the Buehler assays do not provide a compelling 

argument for such a link.” OEHHA (2008b) went on to note that “We find the results of the 

studies support our previous conclusionthat we cannot definitively determine whether or not 


SECTION 3 


there is a link between the reported symptoms and the Checkmate applications and support our 

recommendation for enhancing the systems for symptoms reporting.” 

The extremely low mammalian toxicity of SCLPs has led the USEPA to waive food tolerance 

requirements when application rates do not exceed 150 g of active ingredient per acre per year 

(USEPA 1995). The acute mammalian toxicity tests summarized in the preceding section 

confirm the low toxicity of the HERCON product and of the active ingredients, indicating that 

HERCON is not a dermal toxin, or an eye irritant. HERCON’s dermal sensitization potential 

remains unclear. Because of the physical characteristics of HERCON, sufficient quantites could 

not be administered experimentally to evaluate acute oral or inhalation toxicity. Those same 

physical characteristics suggest that if a human inadvertently ingested or inhaled small quantities 

of HERCON product present in the environment, that the material is not compatible with 

acquisition of a significant dose of the pheromone active ingredient. Inhalation of the LBAM 

pheromones that volatilize from HERCON are evaluated using the acute and subchronic RfDs 

developed above. 

D3.2.3 CheckMate ® LBAM-F 

CheckMate contains the active ingredients (E)-11-tetradecenyl acetate and (E,E)-9,11- 

tetradecadienyl acetate. According to the CDFA (2007), additional ingredients in CheckMate 

include water, crosslinked polyurea polymer, butylated hydroxytoluene, polyvinyl alcohol, 

tricaprylyl methyl ammonium chloride, sodium phosphate, ammonium phosphate, 1,2- 

benzisothiozoli-3-one, and 2-hydroxy-4-n-octyloxybenzophenone. 

CheckMate is manufactured by Suterra for use as a mating disruptor of the LBAM. It has no 

other known uses. 

D3.2.3.1 


D3.2.3.1.1 Physical and Chemical Properties of Active Ingredients of CheckMate 

CheckMate is an aqueous suspension of LBAM pheromones containing micro-bead/dispensers 

with a mild, waxy odor (Suterra 2007). This microcapsule structure protects the contained 

pheromone from environmental degradation and rapid evaporation. 

The active ingredient (E)-11-tetradecen-1-yl acetate (16.9%) has the CAS no. 33189-72-9 and 

chemical formula C 16 H 30 O 2 ; the other active ingredient (E,E)-9,11-tetradecadien-1-yl acetate 

(0.71%) has CAS no. 54664-98-1 and chemical formula C 16 H 28 O 2 . The product has a low 

solubility in water. Those chemical and physical properties that have been determined for 

CheckMate are listed in Table D3-28. 

The CheckMate pheromones are SCLPs, a category that includes most of the known pheromones 

produced by insects in the order Lepidoptera (OECD 2002; USEPA 1995). The simple straight 

chain hydrocarbon structure, combined with an absence of environmentally persistent chemical 

substituents, indicate that the SCLPs would not be expected to persist, accumulate, or 

concentrate in biota or in the environment. 

Known physical and chemical properties of the active ingredients in CheckMate are summarized 

in Table D3-28. 




DRAFT PEIR 


Table D3-29 

Physico-Chemical Properties of CheckMate ® LBAM-F 

Parameter 


Melting point, boiling point and/or temperature of decomposition 

Source: 

Suterra 2007 







Not applicable 

Boiling Point ~100°C for water component 

Low solubility for pheromone 

Not Reported 

Not Reported 

Not Reported 

Not Reported 

D3.2.3.1.2 Environmental Fate and Chemistry of CheckMate ® LBAM-F 

No information was publicly available from the manufacturer of CheckMate on the persistence 

or degradation of this product in the environment (Suterra 2007). However, the inert ingredients 

include a poly-urea polymer that is expected to be stable and remain in the environment for an 

extended period of time. Due to the volatile nature of the pheromone active ingredients, they are 

not expected to persist in the environment for more than ~60 days (Suterra 2007). 

D3.2.3.1.3 Mammalian Toxicity 

METABOLISM 

By analogy to the structurally similar long-chain fatty acids, the USEPA (1995) predicted that 

SCLPs would be metabolized either by -oxidation to yield a series of two-carbon compounds, 

or by glucuronide conjugation and subsequent urinary elimination. 


The toxicity of SCLPs was reviewed in the discussion of HERCON. Additional information is 

provided here that relates specifically to CheckMate or similar LBAM pheromone-containing 

products. 

D3.2.3.2 

CheckMate ® LBAM-F 

In September 2007, the CDFA (in cooperation with the USDA), aerially applied two pheromone 

products in Monterey and Santa Cruz counties. The products were CheckMate ® OLR-F and 

CheckMate ® LBAM-F. Prior to the aerial application, the DPR and OEHHA submitted a report 

to the secretaries of the California Environmental Protection Agency, the California Health and 

Human Services agency, and CDFA (i.e., the 2007 “consensus report”, cited but not formally 

referenced in OEHHA et al. 2008). As noted in OEHHA et al. (2008), the consensus report 

concluded “The toxicity data on the pheromones and on microencapsulated products suggest the 

possibility that exposure to a sufficient amount of airborne CheckMate microcapsule particles 

could result in some level of eye, skin, or respiratory irritation. However, as the product is 

diluted and applied over a large area, the degree of exposure as well as the potential for irritation 

should decrease significantly.” 


SECTION 3 


Subsequent to the pheromone aerial applications, a number of individuals in these counties 

reported symptoms of exposure to the spray (OEHHA et al. 2008). Staff of OEHHA, DPR, and 

the California Department of Public Health evaluated symptom reports from Monterey and Santa 

Cruz counties. These symptom reports were obtained from physicians, a CDFA call center, and “ 

various websites” (OEHHA et al. 2008). The dominant symptoms in these reports were those 

affecting the respiratory system, and included cough, shortness of breath, runny nose, upper 

respiratory irritation and/or pain, and wheezing. The respiratory symptoms represented 70% of 

the 463 symptom reports evaluated. Seventy four individuals sought medical attention for their 

symptoms, and of these, 62 were for respiratory effects. 

OEHHA et al. (2008) were not able to determine if there was a link between the reported 

symptoms and aerial spraying of the LBAM pheromone products. Among the factors that 

interfered with establishing potential causality were the lack of confirmatory medical tests 

available to establish exposure, the fact that < 25% of the symptom reports identified a date or 

location of exposure, and that < 10% of the symptom reports were supported by documentation 

from medical providers that could have provided information such as date, time, and duration of 

exposure etc. Additionally, OEHHA et al. (2008) cited the likely very low level of human 

exposure that may have occurred (based on DPR estimates). Further, the nature of the reported 

dominant adverse effects – respiratory symptoms – also complicated interpretation of the cause 

of the symptoms given that they are non-specific in nature and present at background rates of 15- 

25% in adult Californians. However, as noted previously, positive results of certain LBAM 

pheromone formulations in the LLNA of dermal sensitization led OEHHA to note separately that 

“…we cannot dismiss the possibility that in sensitive individuals, contact with the particles could 

cause allergic-type responses, though the negative results of the Buehler assays do not provide a 

compelling argument for such a link” (OEHHA 2008b). 

D3.2.3.2.1 Acute Toxicity CheckMate ® LBAM-F 

In addition to the above information, a series of results from acute toxicity studies of CheckMate 

are available. These studies were completed in 2008, with results submitted to the USDA. Study 

results are summarized in Table D3-30. A review of these data by the California Department of 

Pesticide Registration (DPR 2008b) determined that the studies of oral, dermal, and inhalation 

toxicity, as well as those that evaluated primary eye and dermal irritation are acceptable to 

support use of the product, and indicate Toxicity Category IV hazards (the lowest toxicity 

rating). The LLNA dermal sensitization study was also deemed acceptable; data from that study 

indicate that CheckMate is a potential skin sensitizer. Results from the Buehler guinea pig 

dermal sensitization study–also deemed acceptable by DPR–gave negative results. Both the 

LLNL and Buehler tests represent accepted methodologies for testing skin sensitization potential, 

and the different outcome of the two studies leave the question of CheckMate’s skin sensitizing 

potential unresolved. As noted above in the discussion of SCLPs, several LBAM pheromone 

products have given different results between the Buehler and LLNA tests. The reason for this 

phenomenon is not known, and has led OEHHA to caution that “In the absence of additional 

data, the health-protective approach is to treat the products as potential dermal sensitizers, 

meaning that they have the potential to cause allergic type reactions from skin contact….While 

we cannot view the LLNA tests as evidence that exposure to the pheromone products can cause 

respiratory sensitization, this possibility cannot be ruled out.” 




DRAFT PEIR 


Table D3-30 

Summary of Mammalian Toxicity Studies for CheckMate ® LBAM-F 

Author/ Study Study Design Toxicity EPA Hazard Rating 


CheckMate ® LBAM-F Acute 

Oral (DUDP) Toxicity in Rats 

Acute oral LD50 >5,000mg/kg 

Toxicity Category IV 



Dermal Toxicity in Rats 

>5050mg/kg body weight 


Cructchfield 2008.11750-08 


Inhalation Toxicity in Rats 

LC50 >2.07 mg/L No clinical 

signs of toxicity some discolored 

lungs & liver in test animals from 

4 hr exposure. 



CheckMate ® LBAM-F Eye 

Irritation Study in Rabbits 

No positive effects in any eyes. 





Rabbits. 

72 hour Observation minimally 

irritating 



CheckMate ® LBAM-F Skin 



Sensitizer Produced a 

stimulation index of > 3 in two 

test groups 



CheckMate ® LBAM-F Skin 


Pigs 

Did not elicit a sensitizing 

reaction in Guinea Pigs 


PHYSICAL AND CHEMICAL PROPERTIES OF INERT INGREDIENTS 

CDFA (2007) lists the inert ingredients in CheckMate as: water, crosslinked polyurea polymer, 

butylated hydroxytoluene, polyvinyl alcohol, tricaprylyl methyl ammonium chloride, sodium 

phosphate, ammonium phosphate, 1,2-benzisothiozoli-3-one, and 2-hydroxy-4-noctyloxybenzophenone. 

No specific data from the manufacturer of CheckMate were available for these ingredients 

(Suterra 2007). The following information was obtained from a review of various MSDS from 

other sources. The physical and chemical properties of the carrier, inert, and dispersant 

ingredients are listed in Table D3-31. 

Table D3-31 

Physical and Chemical Properties of CheckMate ® LBAM-F Ingredients 

Chemical a 

Butylated Hydroxytoluene b 

Properties 

Appearance: Crystalline solid 

Color: White to yellowish 

Odor: Phenolic 

Molecular Weight: 220.36 g/mol 

pH: N/A 

Specific Gravity: 1.048 

Solubility in water: Insoluble in cold water 


SECTION 3 


Table D3-31 


Chemical a 

Properties 

Polyvinyl Alcohol c 

Tricaprylyl Methyl Ammonium Chloride d 

Sodium Phosphate e 

Ammonium Phosphate f 

1,2- Benzisothiozoli-3-one g 

2-Hydroxy-4-n-octyloxybenzophenone h 

Appearance: Solid powder 

Color: Off-white to white 

Odor: Odorless 

Molecular Weight: (44.05)n g/mol 

pH: N/A 

Specific Gravity: 1.19 – 1.31 

Solubility in water: Soluble 

Appearance: Clear liquid 

Color: Reddish-brown 

Odor: N/A 

Molecular Weight: 404.17 

pH: N/A 

Specific Gravity: N/A 

Solubility in water: >10% 

Appearance: Granular or crystalline powder 

Color: White 

Odor: Odorless 


pH: 4.4 to 4.5 


Solubility in water: Soluble 

Appearance: Crystals of granules 

Color: Brilliant white 

Odor: Faint acid odor 


pH: 4.2 


Solubility in water: N/A 

Appearance: Crystalline 

Color: Light yellow 

JULY 2009 App D_HHRA_508.doc D3-73 

Odor: 


pH: N/A 

Specific Gravity: N/A 

Solubility in water: N/A 

Appearance: Granules, flakes, beads 

Color: Pale yellow 

Odor: Faint 

Molecular Weight: 326 

pH: N/A 


Solubility in water:



DRAFT PEIR 


Table D3-31 


Chemical a 

e MSDS for Sodium phosphate. Ted Pella, Inc. January 26, 2004. 

f MSDS for Ammonium phosphate. J.T.Baker and Mallinchrodt Chemicals. August 2, 2007. 

g MSDS for 1,2-Bezisothiazol-3-one. Sigma-Aldrich. December 30, 2008. 

h MSDS for 2-Hydroxy-4-n-octyloxybenzophenone. Chemtura. January 1, 2006. 

Properties 

MAMMALIAN TOXICITY OF INERT INGREDIENTS 

The toxicity of carrier and dispersant ingredients of CheckMate are summarized in Table D3-32 

below. 

Table D3-32 

Toxicity Studies of CheckMate ® LBAM-F Inert Ingredients 

Chemical 

Butylated Hydroxytoluene 

Polyvinyl Alcohol 

Tricaprylyl Methyl Ammonium Chloride 

Source: 

Suterra 2007 

Sodium Phosphate 

Ammonium Phosphate 

1,2-benzisothiozoli-3-one 

Toxicity as listed on MSDS 

ORAL (LD50): 

Acute: 890 mg/kg [Rat]. 

650 mg/kg [Mouse]. 

10700 mg/kg [Guinea pig]. 

Oral rat LD50: > 20 gm/kg. 

ORAL (LD50): Acute: 223 mg/kg [Rat]. 

280 mg/kg 

[Mouse]. 

Oral-rat LD50: 8290 mg/kg. 

Intra-rat LD50: 250 mg/Kg. 

Eye-rabbit LD50: 150 mg/kg. 

Skin- rabbit LD50: 7940 mg/kg 

Humans: Mild irritation effect on eyes. 

No LD50/LC50 information found 

Inhalation: Causes irritation to the respiratory tract. 

Symptoms may include coughing, shortness of breath. 

Ingestion: Causes irritation to the gastrointestinal tract. 

Symptoms may include nausea, vomiting and diarrhea. 

Skin Contact: Causes irritation to skin. Symptoms include 

redness, itching, and pain. 

Eye Contact: Causes irritation, redness, and pain. 

Chronic Exposure: No information found. 

Hazardous Decomposition Products: Carbon monoxide, 

Carbon dioxide, Nitrogen oxides, Sulfur dioxide. 

Oral Rat 1020 mg/kg LD50 

Oral Mouse 1150 mg/kg LD50 


The acute mammalian toxicity tests of CheckMate summarized in the preceding section support 

an interpretation of the low toxicity of the product and the active ingredients, indicating that 

CheckMate is not a significant oral, inhalation, or dermal toxin or an eye irritant; its potential 

action as a dermal sensitizer is unclear given the differing results from two separate testing 

methods used to evaluate this endpoint. However, the low acute toxicity of CheckMate and 

SCLPs in general indicate that environmental exposures to this material are not likely to result in 

a significant dose of the pheromone active ingredient. As previously described in the discussion 


SECTION 3 


of SCLP toxicity, OEHHAs evaluated SCLP toxicity data as part of a human health risk 

assessment of Isomate OEHHA (2009b). OEHHA (2009b) relied on data in the Isomate MSDS 

(Pacific Biocontrol 2007), the USEPA (1994 referenced by OEHHA 2009b), and Health Canada 

(2002 - referenced in OEHHA 2009b) in concurring that SCLPs have low acute inhalation 

toxicity and LC 50 s > 5 mg/L. Data provided in Table D3-32 indicate that while CheckMate has a 

low inhalation toxicity that is consistent with that of other SCLPs, it is somewhat lower (> 2.07 

mg/L) than the value used by OEHHA (2009b) to evaluate the acute inhalation toxicity of 

Isomate (> 5 mg/L). Applying the methodology of OEHHA (2009b) to the CheckMate LC 50 of 

2.07 mg/L yields an acute inhalation RfD of 9.49 x 10 -1 mg/kg-hour. Note that this value is 

provided for information purposes only as CheckMate is not included as a chemical in any of the 

LBAM Program alternatives. 

As described for HERCON, OEHHA (2009b) determined that the Nelson et al. (1990) studies 

(Table D3-27) are appropriate for assessing potential effects of subchronic inhalation exposure to 

SCLPs and calculated a subchronic inhalation RfD for SCLPs of 5.7 x 10 -2 . As with the acute 

inhalation RfD, this value is provided for information purposes only as CheckMate is not 

included as a chemical in any of the LBAM Program alternatives. 

The likelihood of dermal sensitization from CheckMate exposures cannot be assessed based on 

currently available data. However, as previously noted, OEHHA (2008b) has determined that 

“these products should be treated as potential dermal sensitizers, meaning that they have the 

potential to cause allergic type reactions from skin contact….While we cannot view the LLNA 

tests as evidence that exposure to the pheromone products can cause respiratory sensitization, 

this possibility cannot be ruled out.”. 

Although butylated hydroxytoluene, and tricaprylyl methyl ammonium chloride have somewhat 

greater toxicity that the LBAM pheromone active ingredients, neither of these ingredients–or any 

of the other inert ingredients - are expected to be introduced into the environment in sufficient 

quantities to cause toxicologically significant effects. 

D3.2.4 Isomate ® -LBAM PLUS 

Isomate is a mixture of the two LBAM pheromones, (E)-11-Tetradecen-1-yl Acetate (63.88 %) 

and (E,E)-9,11-Tetradecadien-1-yl Acetate (2.64 %) contained within a twist-tie dispenser. The 

dispenser is composed of a polyethylene plastic tube parallel to an aluminum wire, and is similar 

in size to a pipe cleaner (Pacific Biocontrol Fact Sheet, no date). The pheromone active 

ingredients are contained within the dispenser tube and do not come in contact with crops or 

other vegetation except as may occur incidentally by placement of the twist tie (Pacific 

Biocontrol Fact Sheet, no date). Non-active ingredients comprise 33.48% of Isomate; 28.68% of 

these ingredients are not added to the product, but are present as a result of the manufacturing 

process (Pacific Biocontrol Fact Sheet, no date). Inert ingredients comprise the remaining 4.8% 

of Isomate. The primary purpose for the addition of these inert ingredients is to protect the 

pheromones from ultraviolet-mediated degradation as well as from exposure to oxidants (Pacific 

Biocontrol Fact Sheet, no date). The inert ingredients have been approved by the National 

Organic Program for organic use when used in this type of twist-tie dispenser (Pacific Biocontrol 

Fact Sheet, no date). 




DRAFT PEIR 


Isomate is manufactured by Shin-Etsu Chemical Co. and is registered and sold by Pacific 

Biocontrol Corporation (2007) for use as a mating disruptor of the LBAM. It has no other known 

uses. 

D3.2.4.1 


D3.2.4.1.1 Physical and Chemical Properties of Active Ingredients of Isomate 

The Isomate formulation is contained within the twist-tie dispenser, and has the appearance of 

“… a colorless or light yellow transparent liquid with an oily-fatty, slightly waxy odor” (Pacific 

Biocontrol, 2007). 

The molecular formulas and molecular weights of the pheromones (E)-11-Tetradecen-1-yl 

Acetate and (E,E)-9,11-Tetradecadien-1-yl Acetate are C 16 H 30 O 2 (254.41g) and C 16 H 28 O 2 

(252.4g), respectively. The corresponding CAS numbers are 33189-72-9 and 30562-09-5. No 

other chemical and physical property data are available for the Isomate formulation. 

Known physical and chemical properties of the active ingredients in Isomate are summarized in 

Table D3-33. 

Table D3-33 

Physical and Chemical Properties of Isomate Twist Ties 

Parameter 

Melting Point 

Boiling Point 

Evaporation Rate 

Vapor Pressure 

Specific Gravity 

Solubility(oil) 

Octanol/Water Partition Coefficient 

pH 

Source: 

MSDS Pacific Biocontrol Corporation 2007 

Value(s) and Conditions 

102-106°C 

Solid 

0.035 mg/dispenser/hour (maximum) 

Solid 

0.92 g/mL 

Soluble in hydrocarbon and clorohydrocarbon at high temperatures 

Insoluble in water or octanol 

7 (the same as water) 

D3.2.5 

Environmental Transport and Degradation of Isomate 

Product information developed by Pacific Biocontrol Corporation (Pacific Biocontrol Fact Sheet, 

no date) indicates that the LBAM pheromones are emitted from the twist-ties “ over at least a 

180 day period”. The volatile nature of the LBAM pheromones, and SCLPs in general, indicates 

that the pheromones would not be expected to persist for significant periods beyond the 180 

estimated release period. 

D3.2.5.1 


D3.2.5.1.1 Straight chain lepidopteran pheromones 

The toxicity of SCLPs was reviewed in the discussion of HERCON. 


SECTION 3 


D3.2.5.1.2 Isomate ® -LBAM PLUS 

The material safety data sheet for Isomate (Pacific Biocontrol 2007) provides information on the 

acute toxicity of the pheromone active ingredient within the twist-tie dispenser tubes. That 

information is provided in Table D3-34. Isomate-LBAM Plus is in EPA Toxicity Category III 

(Pacific Biocontrol 2007). 

Table D3-34 

Physical and Chemical Properties of Isomate Twist Ties 

Source: 

Pacific Biocontrol, 2007 

Endpoint 

Oral LD50 (rats) 

Dermal LD50 (rats) 

Primary eye irritation (rabbits) 

Inhalation LC50 

Primary dermal irritation (rabbits) 

Dermal maximization (guinea pigs) 

Value 

> 5000 mg/kg 

> 2000 mg/kg 

All eye irritation cleared by 72 hours 

> 5.26 mg/L 

Slight to moderate skin irritation 

Not considered a skin sensitizer 

To characterize the acute oral toxicity of Isomate and other SCLPs, OEHHA (2009b) examined 

the Inscoe and Ridgeway (1992) review, the USEPA (1994), and an acute oral toxicity study 

with rats of the SCLPs that target LBAM (MB Research Laboratories 2008a as cited in OEHHA, 

2009b). The MB Research Laboratories data reportedly identified an oral LD 50 > 5000 mg/kg, 

which OEHAA (2009b) selected as the most appropriate NOAEL for acute oral exposures. (Note 

that this value is consistent with the Isomate-specific LD 50 cited in Table D3-34). 

D3.2.5.2 Physical and Chemical Properties of Isomate Inert Ingredients 

The twist-tie dispenser is a polyethylene plastic, with one side of the dispenser tube containing a 

thin piece of aluminum used to affix the twist-tie to vegetation (Pacific Biocontrol Fact Sheet, no 

date). The physical properties of the dispenser are provided in Table D3-35. 

Table D3-35 

Physical-Chemical Properties of Isomate ® – LBAM Plus Twist-Ties (properties of dispenser) 

Parameter 



Not applicable (dispenser is a solid) 

Boiling point 

Not available (dispenser is a solid) 

Solubility in oil 

Liquid suspension disperses in water 


Insoluble in water or octanol 

Appearance 

Brown plastic tube 

pH 7 

Evaporation rate 

0.035 mg/dispenser/hour maximum 

D3.2.5.3 Interpretation of Human Toxicity Based on Animal Studies 

As discussed in the corresponding sections for HERCON and CheckMate, OEHHA (2009b) has 

prepared a human health risk assessment of Isomate OEHHA (2009b). OEHHA (2009b) 

provided a review of SCLP toxicity as an integral part of that assessment, relying on data in the 




DRAFT PEIR 


Isomate MSDS (Pacific Biocontrol 2007), the USEPA (1994), and Health Canada (2002, both 

referenced in OEHHA 2009b) in concurring that SCLPs have low acute inhalation toxicity and 

LC 50 s > 5 mg/L. This LC 50 is consistent with the Isomate-specific LC 50 provided in Table D3-34. 

The LC 50 concentration (5 mg/L) was identified as a NOAEL, and was converted to yield an 

acute inhalation NOAEL for SCLPs of 229 mg/kg-hour (OEHHA 2009b). By applying UFs of 

10 to account for intraspecies variability and 10 for interspecies variability, OEHHA derived an 

acute inhalation RfD of 2.29 mg/kg-hour (OEHHA 2009b). That acute inhalation RfD is used in 

Section D5 to quantify potential effects from exposure to the LBAM pheromones present in 

Isomate. 

The previous discussions of HERCON and CheckMate have provided the basis for the derivation 

of the subchronic RfD for SCLPs of 5.7 x 10 -2 . This value is used to quantitatively evaluate the 

potential adverse effects from subchronic inhalation of Isomate. 

Although the MSDS data on Isomate do not indicate it is a skin sensitizer, as with the other 

LBAM pheromone-containing formulations, the likelihood of dermal sensitization from Isomate 

exposures cannot be assessed based on currently available data. As noted in previous discussions 

of this issue, OEHHA (2008) has determined that “In the absence of additional data, the healthprotective 

approach is to treat the products as potential dermal sensitizers, meaning that they 

have the potential to cause allergic type reactions from skin contact.” 

Because there is some potential – albeit considered to be quite small – that a child could ingest 

one of the Isomate-containing twist ties, OEHHA characterized the acute oral toxicity of 

Isomate. OEHHA (2009b) began that evaluation by examining the Inscoe and Ridgeway (1992) 

review, the USEPA (1994), and an acute oral toxicity study with rats of the SCLPs that target 

LBAM (MB Research Laboratories 2008a as cited in OEHHA 2009b). The MB Research 

Laboratories data reportedly identified an oral LD 50 > 5000 mg/kg, which OEHAA (2009b) 

selected as the most appropriate NOAEL for acute oral exposures. (Note that this value is 

consistent with the Isomate-specific LD 50 cited in Table D3-34). By applying UFs of 10 to 

account for intraspecies variability and 10 for interspecies variability, OEHHA derived an acute 

oral RfD of 50 mg/kg (OEHHA 2009b). This value is used in Section D5 to address the potential 

adverse effects from the accidental ingestion of a twist tie by a child. 

D3.2.6 

SPLAT LBAM 

SPLAT (Specialized Pheromone & Lure Application Technology) is a proprietary matrix 

formulation of LBAM pheromones and biologically inert materials that is designed to provide a 

sustained and controlled release of the LBAM pheromones. SPLAT is manufactured by ISCA 

Technologies for use as a mating disruptor of the LBAM (ISCA 2008). It has no other known 

uses. 

D3.2.6.1 

Environmental Fate and Chemistry of Pheromones 

D3.2.6.1.1 Physical and Chemical Properties of Active Ingredient of SPLAT LBAM 

The active ingredients of SPLAT are (E)-11-Tetradecen-1-yl acetate and (E,E)-9,11- 

Tetradecadien-1-yl acetate; their respective molecular formulas and weights are C 16 H 30 O 2 

(254.41) and C 16 H 28 O 2 (252.4). The corresponding CAS numbers are 33189-72-9 and 30562-09- 


SECTION 3 


5 (ISCA 2008) (see Table D3-36). The product is manufactured as a waxy emulsion that protects 

the entrained pheromone from environmental degradation and rapid evaporation (ISCA 2008). 

SPLAT is creamy dark grey in color, with a slightly waxy floral odor (ISCA 2008). It has limited 

solubility, a pH of 6.88, and is stable under ordinary conditions of use and storage. The active 

ingredients comprise 10% of the product with 90% of the ingredients listed as ‘other’ (ISCA 

2008). 

The simple straight chain hydrocarbon structure of the SPLAT pheromones (see Figure D3-11), 

combined with an absence of environmentally persistent chemical substituents, indicate that the 

SCLPs would not be expected to persist, accumulate, or concentrate in biota or in the 

environment (OECD 2002; USEPA 1995). 

Table D3-36 

Source: 

ISCA 2008 

Physico-Chemical Properties of SPLAT LBAM 

Parameter 


Boiling point 







Not available 

100°C at 760 mmHg 

Limited 

Not available 

Not available 

Not available 

Not available 

D3.2.6.2 Environmental Transport and Degradation of SPLAT LBAM 

SPLAT has a wide range of viscosities with an amorphous flowable quality allowing for a 

variety of application methods including hand spraying, aerial spraying, and via a caulking gun 

(ISCA 2008). It is designed to be placed in dollops at varying densities of varying sizes, allowing 

the number of SPLAT point sources to be tailored to the pest density without changing the 

amount of material applied per acre. Once cured (2-3 hours after application), SPLAT becomes 

resistant to ultraviolet (UV) degradation and rainfall, and can remain effective for up to 6 months 

(ISCA undated). 



The toxicity of SCLPs was reviewed in the discussion of HERCON. Additional information from 

symptom reports following the aerial application of two CheckMate formulations was provided 

in the discussion of CheckMate toxicity. 

D3.2.7 

Toxicity of SPLAT LBAM 

In 2008, a series of acute toxicity studies of SPLAT were completed by independent toxicology 

laboratories, with results submitted to the USDA. Those studies are summarized in Table D3-37. 

A review of these data by the DPR (2008c) determined that the studies of acute oral, dermal, and 

inhalation toxicity, as well as those that evaluated primary eye and dermal irritation are 




DRAFT PEIR 


acceptable to support use of the product. For the acute oral, dermal, and inhalation routes of 

exposure, SPLAT is considered to be in Toxicity Category IV hazard (the lowest toxicity 

rating). Results of the LLNA dermal sensitization study were also deemed acceptable; data from 

that study indicate that SPLAT is a potential skin sensitizer. 

However, as is the case for CheckMate, the Buehler guinea pig dermal sensitization study 

yielded no evidence to indicate that SPLAT is a dermal sensitizer. As previously noted, both the 

LLNL and Buehler tests represent accepted methodologies for testing skin sensitization potential, 

and the different outcome of the two study types for certain LBAM pheromone-containing 

formulations leave the question of SPLAT skin sensitizing potential unresolved. OEHHA 

(2008b) has recommended that the health-protective interpretation of the skin-sensitization 

potential of the LBAM pheromones is to consider the products to be potential dermal sensitizers. 

This means that these products may have the potential to induce allergic type reactions from skin 

contact. Table D3-37 summarizes the findings of mammalian toxicity studies completed on 

SPLAT. 

Table D3-37 

Summary of Mammalian Toxicity Reference Values for SPLAT LBAM 

Author/ Study Material Toxicity Hazard Rating 


SPLAT LBAM Acute Oral 

Toxicity Study (UDP) in Rats. 

SPLAT LBAM Acute Dermal 

Toxicity Study in Rats. 

SPLAT LBAM Skin 


Pigs 

Acute oral LD50 >5,000mg/kg. 

Very low toxicity; USEPA 

Category IV 


Category IV 


LD50 >5050mg/kg 




No evidence of irritation or 

sensitization 

LC50 >2.07 mg/L 

No clinical signs of toxicity, 

although some discoloration of 

lungs and liver in test animals 

from 4 hr exposure 

Sensitizer 

Produced a stimulation index of 

> 3 in all test groups 

No positive effects in any eyes. 

Rated minimally irritating, 

assigned Toxicity Category IV 

72 hour Observation slightly 

irritating 

Crutchfield 2008. Stillmeadow 

11762-08 

SPLAT LBAM Acute 

Inhalation Toxicity Study in Rats. 


Category IV 


SPLAT LBAM Skin 



Potential skin sensitizer 


SPLAT LBAM Eye Irritation 

Study in Rabbits 

Mildly irritating; USEPA 

Category IV 


SPLAT LBAM Acute Dermal 

Irritation Study in Rabbits. 

Slightly irritating; USEPA 

Category IV 

Source: 

DPR 2008c 

D3.2.7.1 

Physical and Chemical Properties of Inert Ingredients 

The carrier and dispersant ingredients of SPLAT are characterized in the MSDS as a mixture of 

wax, emulsifiers, and carriers that are all listed by the USEPA as exempt from the requirement of 

tolerance (ISCA 2008). No additional information on the carrier and dispersant ingredients of 

SPLAT is available. 


SECTION 3 


D3.2.7.2 

Environmental Transport and Degradation of Inert Ingredients 

The label for SPLAT states it should be applied when the ambient temperature is above 55°F and 

below 95°F. SPLAT dollops typically cure within 2-3 hours following application, after which 

point they become rain fast and UV resistant (ISCA 2008). The label also states not to apply if 

rain is expected within 1-2 hours of application or the temperature is outside the recommended 

range (ISCA undated). If applied in a manner consistent with label recommendations, SPLAT 

can remain effective for up to 6 months (ISCA 2008). 

D3.2.7.3 

Mammalian Toxicity of Inert Ingredients 

The mixture of wax, emulsifiers, and carriers that comprise the inert ingredients of SPLAT are 

all listed by the USEPA as exempt from the requirement of tolerance, indicating that these 

substances to have little to no inherent toxicity (ISCA 2008). No additional information on the 

potential toxicity of the inert ingredients of SPLAT is available. 

D3.2.7.4 


As noted in discussions in the corresponding sections for HERCON, CheckMate, and Isomate, 

OEHHA (2009b) reviewed SCLP toxicity as an integral part of an HRA of Isomate, determining 

that SCLPs have low acute inhalation toxicity and LC 50 s > 5 mg/L. Data provided in Table D3- 

37 indicate that while SPLAT has a low inhalation toxicity that is generally consistent with that 

of other SCLPs, SPLATs LC 50 is somewhat lower (> 2.07 mg/L) than the value used by OEHHA 

(2009b) to evaluate the acute inhalation toxicity of Isomate (> 5 mg/L). Applying the 

methodology of OEHHA (2009b) to the SPLAT LC 50 of 2.07 mg/L yields an acute inhalation 

RfD of 9.49 x 10 -1 mg/kg-hour (OEHHA 2009b). This value is used in the quantitative 

evaluation of potential health effects associated with inhalation of the pheromones contained in 

SPLAT. 

The previously-derived SCLP subchronic inhalation RfD of 5.7 x 10 -2 is used to quantitatively 

evaluate the potential adverse effects from subchronic inhalation of SPLAT. 

The acute toxicity data for SPLAT (Table D3-37) provide another example of apparently 

contradictory skin sensitization data for a LBAM pheromone-containing product, That is, 

SPLAT was negative for skin sensitization when tested in the Buehler assay, but gave a positive 

result in the LLNA. In the absence of additional data, OEHHA (2008b) recommends that these 

products be treated “.. as potential dermal sensitizers…”. However, because of the limited data 

that are available on skin sensitization, it is not possible to quantify the likelihood of a 

sensitization reaction being induced from the low environmental concentrations associated with 

the LBAM Program alternatives. 

D3.2.8 No Mate ® LBAM MEC 

NoMate is a mixture of the two LBAM pheromones, (E)-11-Tetradecen-1-yl Acetate (19.2%) 

and (E,E)-9,11-Tetradecadien-1-yl Acetate (0.8%) in a micro-capsule product provided as an 

aqueous suspension (Scentry Biologicals Inc. 2008). Eighty % of the product is comprised of 

inert ingredients (SBI 2008) 

NoMate is manufactured by SBI for use as a mating disruptor of the LBAM. It has no other 

known uses. 




DRAFT PEIR 


D3.2.8.1 


D3.2.8.1.1 Physical and Chemical Properties of Active Ingredients 

The NoMate formulation is an off-white to light brown, viscous liquid with a mild, sweet odor. 

The liquid suspension disperses in water and has a pH between 7.5 and 8.5 (SBI 2008) (See 

Table D3-38). The molecular formulas and weights of the pheromones (E)-11-Tetradecen-1-yl 

Acetate and (E,E)-9,11-Tetradecadien-1-yl Acetate are C 16 H 30 O 2 (254.41g) and C 16 H 28 O 2 

(252.4g), respectively. The corresponding CAS numbers are 33189-72-9 and 30562-09-5 (ISCA 

2008). 

Table D3-38 

Physico-Chemical Properties of NoMate ® LBAM MEC 

Parameter 


Source: 

SBI 2008 


Not available 

Boiling point 212ºF 



Appearance 

Liquid suspension disperses in water 

Not available (aqueous mixture) 

Off-white to light brown viscous liquid 

pH 7.5-8.5 


Not available 


Product information developed by SBI indicates that NoMate will last no more that 40 days in 

the environment. Weather conditions can reportedly affect the persistence of this material (e.g., 

UV radiation, rainfall), but details are not available (SBI, undated). 

The NoMate pheromones are SCLPs, a category that, as previously noted, includes most of the 

known pheromones produced by insects in the order Lepidoptera (OECD 2002; USEPA 1995). 

The straight chain hydrocarbon structure (Figure D3-11), combined with an absence of 

environmentally persistent chemical substituents indicate that the SCLPs would not be expected 

to persist, accumulate, or concentrate in biota or in the environment. 


METABOLISM 

As noted in previous sections on pheromone-containing products, the USEPA (1995) predicted 

that SCLPs would be metabolized either by -oxidation to yield a series of two-carbon 

compounds, or by glucuronide conjugation and subsequent urinary elimination. 


The toxicity of SCLPs was initially reviewed in the discussion of HERCON. Additional 

information from symptom reports following the aerial application of two CheckMate 

formulations was provided in the discussion of CheckMate toxicity. 


SECTION 3 


D3.2.9 

Toxocity of NoMate ® LBAM MEC 

Analogous to the other LBAM pheromone-containing products discussed earlier, a series of 

acute toxicity studies were completed by independent toxicology laboratories in 2008, with 

results submitted to the USDA. The study results for NoMate are summarized in Table D3-39. A 

review of these data by the DPR (2008d) determined that the studies of acute oral, dermal, and 

inhalation toxicity, as well as those that evaluated primary eye and dermal irritation are 

acceptable to support use of the product, and indicate Toxicity Category IV hazards (the lowest 

toxicity rating). Results of the LLNA dermal sensitization study was also deemed acceptable; 

data from that study indicate that NoMate is a potential skin sensitizer. Results from the Buehler 

guinea pig dermal sensitization study–also considered to be acceptable by DPR - yielded no 

evidence to indicate that NoMate is a dermal sensitizer. Table D3-39 summarizes the findings of 

mammalian toxicity studies completed on NoMate. 

Table D3-39 

Summary of Toxicity Data for NoMate ® LBAM MEC 

Author/ Study Material Toxicity EPA Hazard Rating 




Crutchfield 2008. Stillmeadow 11768- 

08 




NoMate ® LBAM MEC Acute 

Oral Toxicity Study (UDP) in 

Rats. 


Dermal Toxicity Study in Rats. 

NoMate ® LBAM MEC Skin 


Pigs 


Inhalation Toxicity Study in 

Rats. 

NoMate ® LBAM MEC Skin 




Eye Irritation Study in Rabbits 



Rabbits. 

Acute oral LD50 >5,000mg/kg. 

LD50 >5050mg/kg 



LC50 >2.12 mg/L Decreased 

activity & piloerection caused 

by exposure, but effects 

reversible and no longer 

evident by Day 6. No 

observable abnormalities from 

4 hr exposure. 

Sensitizer 

Produced a stimulation index of 

> 3 in 2 test groups. 

No positive effects in eyes. 

Rated minimally irritating 

72 hour observation period. 

Nonirritating; 


Category IV 


Category IV 

Negative. Not a skin sensitizer 

in this assay 


Category IV 

Positive. Evidence of potential 

for skin sensitization 


Category IV 


Category IV 

D3.2.9.1 Physical and Chemical Properties of Inert Ingredients 

As noted above, 80% of NoMate consists of inert ingredients (SBI 2008). Although the specific 

identity of these ingredients have not been made publicly available by the manufacturer, the inert 

ingredients in the formulation meet National Organic Program standards, and are on USEPA list 

4A and 4B, indicating they are biodegradable (SBI 2008). 

BIO-TAC ® is an adhesive used to hold NoMate products on plant foliage. The principal 

functional agent of BIO-TAC ® is polybutene, which has been registered in the United States 

since 1960 for use as an insect control agent, since 1963 as a bird repellent, and since 1967 as a 

tree squirrel repellent. The mode of action of BIO-TAC ® is more to trap than repel (USEPA 




DRAFT PEIR 


1994). Polybutene is a highly stable polymeric substance, which is resistant to physical or 

chemical change from aging or temperature (USEPA 1994). 

D3.2.9.2 

Environmental Transformation and Degradation of Inert Ingredients 

See previous section on the Environmental transformation and degradation of NoMate. 

D3.2.9.3 

Mammalian Toxicity of Inert Ingredients 

Available toxicity data for BIO-TAC ® are summarized in Table D3-40. These data indicate that 

although BIO-TAC ® does not induce skin sensitization or dermal irritation, it is an irritant when 

applied directly to the eyes. BIO-TAC ® has low to very low acute oral or dermal toxicity. 

Table D3-40 Toxicity Values for BIO-TAC ® 

Source: 

USEPA 1994 

Oral LD50-Rat LD50 >5.0 g/kg Very low toxicity. Category IV 

Dermal LD50-Rabbit LD50 >2.0 g/kg Low toxicity. Category III 

Eye Irritation-Rabbit Irritating Category II 

Dermal Irritation-Rabbit Not irritating; Very low toxicity. Category IV 

Dermal Sensitization- Guinea pig Not sensitizing Negative. Not a skin sensitizer 

D3.2.10 


The acute mammalian toxicity tests summarized in the preceding section confirm the low 

toxicity of NoMate, and indicate that is not a significant acute oral, inhalation, or dermal toxin or 

an eye irritant. As with SPLAT and CheckMate its potential action as a dermal sensitizer is 

unclear due to the different outcomes of the dermal sensitization assays. The low acute toxicity 

of NoMate and the minimal toxicity of SCLPs in general indicate that environmental exposures 

to this material are not likely to result in significant human exposure to the pheromone active 

ingredient. 

Although NoMate is not proposed for use in any of the Program alternatives, the acute inhalation 

RfD of 2.29 mg/kg-hour and the subchronic inhalation RfD of 5.7 x 10 -2 mg/kg-d previously 

derived for LBAM pheromone-containing products are also considered applicable to the NoMate 

formulation. 

D3.3 MALE MOTH ATTRACTANT (MMA) ALTERNATIVE 

This alternative involves ground treatment with an LBAM-specific pheromone in combination 

with the insecticide permethrin. MMA Alternative is conducted in advance of the aerial mating 

disruption (if needed) to enhance the efficacy of the aerial mating disruption pheromone 

applications. The treatment consists of a 1.5-mile radius around any detection site. Treatments 

may occur on street trees and utility poles, 8 feet above the ground. MMA sites will be out of 

reach of the general public. 

This alternative will be used in certain areas where insecticides and pheromones cannot be 

applied by broadcast methods. These treatments consist of the use of SPLAT to deliver a 1% 

concentration of the LBAM pheromones and a 6.0 % concentration of permethrin. The 


SECTION 3 


application method consists of using ground-based equipment to apply a gel material to 

telephone poles and trees using a metered hand-held wand. 

The pheromones and the pheromone products that are considered for use in this alternative were 

addressed in Section D3.2. 

The permethrin product proposed for use in the MMA is Permethrin E-Pro. The product MSDS 

(Etigra, undated) indicates that the formulation consists of 36.8% permethrin and 63.2% other 

ingredients. The other ingredients include 26.0% of hydrocarbon solvents (CAS no. 8052-41-3 

which corresponds to Stoddard solvent); triacetin 25.9%; a surfactant blend (< 10.0%); 1,2,4- 

trimethylbenzene( < 4.0%); and ethylbenzene (>0.03%). Permethrin and the inert ingredients for 

which data are available were reviewed under the No Program Alternative. 

D3.4 ORGANIC-APPROVED INSECTICIDES (ALTERNATIVES BT AND S) 

This section provides information on the physical and chemical properties, environmental fate, 

and toxicity of two insecticides that are approved for use with organic crops; the bacterially 

derived spinosad and the biopesticide Btk. Both of these treatments would be applied by 

hydraulic spraying using either truck-based or backpack-based equipment. No information is 

publicly available on the formulation ingredients of either material; accordingly, the following 

sections provide information on the chemistry, environmental fate, and toxicity of the active 

ingredients of spinosad and Btk. 

D3.4.1 

Spinosad 

Spinosad is an insecticidal mixture derived from the soil bacterium Saccharopolyspora spinosa. 

Two of the mixtures components, spinosyn A and spinosyn D typically comprise ~ 88% of 

spinosad; the majority of the insecticidal activity of spinosad has been attributed to these two 

compounds (IPCS 2001). Spinosad contains other structurally related spinosyns (Figure D3-12 

[from Gao et al. 2007]) and may also contain proteinaceous, carbohydrate, and inorganic salt 

compounds (IPCS 2001). 

Figure D3-12 Chemical Structure of Spinosad and Metabolites (from Gao et al. 2007) 

Spinosyns A and D are metabolites of S. spinosa grown on nutrient media under aerobic 

conditions. These and other metabolic products are extracted and processed to form spinosad. 

Purified spinosad is a crystalline solid, light gray to white in color; it reportedly has an “earthy” 

odor (Thompson et al. 1999). 




DRAFT PEIR 


Spinosad was developed by DowElanco, with the first spinosad-containing products reaching the 

market in 1997. Initially registered for use on nonfood crops such as turf, cotton and 

ornamentals, spinosad has now been approved for use by the USEPA for over 150 food and 

nonfood crop uses, and is registered for use in 30 countries (DOW AgroSciences 2001). 

Spinosad is also registered in the United States for dermal application to cattle (USEPA 2006d). 

Spinosad is active on contact with insect eggs, larvae, and adults (DOW AgroSciences 2008). 

Spinosad is particularly effective against pests in the orders Lepidoptera (moths and butterflies), 

Diptera (flies), Thysanoptera (thrips), as well as against certain Coleoptera (beetles) (Millar and 

Denholm 2007; DOW AgroSciences 2001). Spinosad is the active ingredient in the 

commercially available products Tracer ® , Naturalyte ® , Success Naturalyte ® , and Conserve SC 

Specialty Insecticide ® . 

D3.4.1.1 

Environmental Fate and Chemistry of Spinosad 

Once introduced to the environment, spinosad degrades primarily by photolysis and microbial 

action (Dow AgroSciences 2004). In outdoor (aerobic) microcosms, spinosad exhibited a halflife 

greater than 25 days (USEPA 2006d); a half-life on plant surfaces of 1 to 16 days has been 

reported (Tomlin 2007). Hydrolysis can contribute to the removal of spinosad from aquatic 

systems, but only under highly alkaline conditions where half-lives of approximately 8 months 

have been documented (Cleveland et al. 2002). In sunlit surface water where degradation is 

driven by photolysis, the half-life of spinosad ranges from < 1 to 2 days (Cleveland et al. 2002). 

Spinosad partitions readily to sediment where it can persist with a half-life of 161-250 days 

under anaerobic conditions (USEPA 2006d). 

In soil exposed to sunlight, photolytic degradation of the spinosyns is moderately rapid, with 

spinosyn A exhibiting a half-life of approximately 9 to 17 days, and spinosyn D a half-life of 

somewhat over 9 days (DOW AgroSciences 2004). Laboratory analyses of spinosad degradation 

in soil in the absence of sunlight (20ºC) yielded half-lives from 5 to 68 days (DOW 

AgroSciences 2001). Spinosad is “moderately to strongly” sorbed to soil (Kd 4-337 mL/g) and, 

thus, is not expected to mobilize (DOW AgroSciences 2001). 

D3.4.1.2 

Chemical and Physical Properties 

The physical properties of spinosyns A and D have been characterized by the manufacturer, 

DOW AgroSciences, LLC (2001 2004). Those properties are summarized in Table D3-41 

Table D3-41 

Physical and Chemical Properties of Spinosyns A and D 

Spinosyn A 

Spinosyn A 

CAS Number 131929-60-7 131929-63-0 

Molecular Weight 731.976 745.988 

Empirical Formula C42H67NO16 C41H65NO16 

Melting Point 84-99ºC 161-170ºC 

Vapor Pressure at 25ºC (mmHg) 2.4 ×10 -10 1.6 ×10 -10 

Solubility in water at pH 5.0, 20ºC (mg/L) 290 28.7 



Log Octanol-water partition coefficient at pH 5.0 2.78 3.23 



SECTION 3 


Table D3-41 

Physical and Chemical Properties of Spinosyns A and D 

Spinosyn A 

Spinosyn A 


Source: 

Dow AgroSciences 2001, 2004 

BCF < 100 Not available 

The spinosyns’ molecular weight, low vapor pressure, and moderate lipophilicity (characterized 

by the log octanol/water partition coefficient) indicate that spinosad has some potential to persist 

in the environment and in biota (Table D3-41). For example, spinosad applied directly to the skin 

of sheep (5.8 mg/kg) yielded detectable residues in fat, muscle, liver, and kidney, with the 

highest concentrations measured in fat 3-7 days after treatment (Rothwell et al. 2005). Dairy 

cows given doses of spinosad of up to 10 µg/g for 28 days had the highest concentrations of 

spinosad in cream and fat (1.9 and 5.7 µg/g, respectively), and hens dosed with spinosad for 42 

days accumulated residues in eggs (0.19 µg/g) and fat (1.2 µg/g ) in a dose-dependent manner 

(Rutherford et al. 2000). 

The BCFs of spinosad characterized from the muscle, viscera, and whole bodies of fish are 7.5, 

28.8, and 21.1, respectively (USEPA 2006d). However, because spinosad is cleared from fish 

tissues fairly rapidly once exposure ends (half-life of approximately 1 day), the potential for 

food-chain bioaccumulation is not considered “substantial” (USEPA 2006d). 

D3.4.1.3 Mammalian Toxicity from Spinosad Exposure 

The USEPA has classified spinosad as Toxicity Category III for acute oral and dermal toxicity, 

and Toxicity Category IV for acute inhalation toxicity, primary eye irritation, and primary skin 

irritation (USEPA 2006d). Determinations of allowable spinosad residues in crop, meat, eggs, 

and dairy products concluded that spinosad is not likely to be carcinogenic in humans (USEPA 

2000b, 2007e). These determinations were made on the basis of experimental animal data as no 

data characterize the effects of spinosad exposure in humans (see following discussion). 

The insecticidal mechanism of action of spinosad appears to be unique, with the primary site of 

attack being nicotinic acetylcholine receptors (nAChRs) and the secondary site of attack being γ- 

aminobutyric acid (GABA) receptors (Salgado 1998; Salgado et al. 1998; Watson 2001; Salgado 

and Sparks 2005; Millar and Denholm 2007). Spinosad is thought to exert its toxicity primarily 

by activating a nAChR subtype (Salgado and Sparks 2005). However, the toxicological basis for 

the selectivity of spinosad between insects and mammals is not well understood. 

Spinosyn A and spinosyn D are well absorbed by rats following oral administration 

(approximately 70%), with the remainder eliminated without undergoing absorption. Spinosyns 

A and D are eliminated rapidly in rats, with ~70-90% of a dose eliminated in the first 24 hours, 

and only ~1 to 3% remaining 7 days after dosing (IPCS 2001). The rate of absorption appears to 

be saturable and dose-dependent, with low doses (10 mg/kg) yielding peak blood concentrations 

within 1 hour and a dose of 100 mg/kg producing a peak blood concentration only after 6 to 12 

hours (IPCS 2001). The spinosyns distribute to muscle, organs, and fat following oral 

administration (Mendrala et al. 1995a, 1995b reviewed in IPCS 2001), with clearance from the 

thyroid markedly slower than from other organs (IPCS 2001). Spinosyn A is absorbed across the 




DRAFT PEIR 


skin to a limited extent (< 1% after 24h); comparable data are not available for spinosyn D. No 

data are available on the absorption, distribution, or elimination of spinosad following inhalation 

exposure (IPCS 2001). Spinosyn A and D are metabolized either by direct binding to glutathione 

or by binding to glutathione following demethylation. 


Technical grade spinosad and spinosyns A and D have low acute mammalian toxicity following 

oral, dermal, or inhalation exposure (reviewed in IPCS 2001). A summary of the results of acute 

toxicity testing, provided as either the LD 50 or LC 50 required to kill 50% of the test animals, is 

provided in Table D3-38. The differences in acute toxicity are likely attributable to differences in 

the response of different species, different genders, and the routes of exposure. The data 

summarized in Table D3-42 were developed by DOW Chemical Co., and submitted to the WHO 

as unpublished reports. The original studies are not available, and the summary provided by 

IPCS (2001) provides no details on the signs and symptoms of acute toxicity following exposure 

to spinosad or the spinosyns. 

Table D3-42 

Acute Toxicity of Technical Grade Spinosad and Spinosyn A and D 

Chemical Exposure Route LD50 or LC50 Species 

Technical grade spinosad 

(~88%) 

spinosyn A and D (46.1:50.2) 

Source: 

IPCS 2001 

Oral > 2,000 to > 7,500 (mg/kg) Rats, Mice 

Dermal 

> 2,000 to > 5,000 

(no deaths) (mg/kg) 

Rabbits 

Inhalation > 5.2 (mg/L) Rats 

Oral 

Males 4,400 

Females > 5,000 (mg/kg) 

Rats 

Dermal > 5,000 (mg/kg) Rabbits 

Dermal application of spinosad or a mixture of ~ 50:50 spinosyns A and D to the intact skin of 

rabbits (500 to 5,000 mg/kg) for up to 24h did not cause mortality, dermal irritation, or any other 

evidence of toxicity (IPCS 2001). A single dose of spinosad or a ~50:50 mixture of spinosyns A 

and D applied to the eyes of rabbits was mildly irritating; signs of irritation resolved within 24 to 

48h (IPCS 2001). Neither spinosad or a ~50:50 mixture of spinosyns A and D induced contact 

hypersensitivity (IPCS 2001). 

D3.4.1.3.2 Subchronic Toxicity 

The IPCS (2001) evaluated the subchronic toxicity of spinosad based on a series of reports 

submitted by DOW Chemical Co. to the WHO. With the exception of data subsequently 

published as Stebbins et al. (2002) and Yano et al. (2002) these data are not publically available. 

However, the IPCS analysis provides details of study protocols (species, doses used, route of 

administration) and results. Tissue vacuolation was a common feature of subchronic spinosad 

exposure in mice, rats, and dogs. In rodents administered spinosad in the diet, the severity of 

vacuolation was generally dose-related, with the number of tissues involved increasing with 

increasing dose (Stebbins et al. 2002; Yano et al. 2002). Spinosad increased absolute and relative 

weights of the liver, kidney and spleen in rats (> 133 mg/kg) and mice (> 57 mg/kg), and heart 


SECTION 3 


and thyroid weights in rats (Stebbins et al. 2002; Yano et al. 2002). Studies that characterized 

spinosads’ toxicity in dogs identified a LOAEL for tissue vacuolation of 6.5 mg/kg from a 28- 

day study and a NOAEL of 2.7 mg/kg from a study that lasted 12 months (IPCS 2001). 

D3.4.1.3.3 Chronic Toxicity 

In 2000, the USEPA (2000b) proposed that spinosad be placed in Group E as Not Likely to be 

Carcinogenic to Humans. Current USEPA Guidelines for Carcinogen Risk Assessment (USEPA 

2005) recommend this designation “when the available data are considered robust for deciding 

that there is no basis for human hazard concern.” As of 2008, a final classification of spinosads’ 

carcinogenicity has not been made. The data that supported the USEPA’s 2000 proposal were 

not explicitly cited, but information provided in USEPA (2000b) indicates that the USEPA was 

referring to study results subsequently published as Yano et al. (2002) and Stebbins et al. (2002) 

(see following). 

Stebbins et al. (2002) conducted two separate 18-month studies to evaluate spinosads’ 

carcinogenicity in mice. The first of these studies administered dietary doses of up to 50.9 mg/kg 

(males) and 67.0 mg/kg (females). Excessive mortality occurred in high-dose females, but 

surviving animals showed no statistically significant difference in any tumor type, or in the 

incidence of all cancers combined. A companion study that utilized lower doses of spinosad (up 

to 32.7 mg/kg in males, and up to 41.5 mg/kg in females) also found no increase in tumor 

incidence relative to controls (Stebbins et al. 2002). Dietary administration of spinosad to rats for 

up to 24 months (at doses that ranged to 49.4 mg/kg in males and to 62.8 mg/kg in females) also 

yielded no evidence of carcinogenicity (Yano et al. 2002). Vacuolation of the thyroid was seen at 

doses of spinosad > 9.5 mg/kg, with lung, thyroid, and lymph tissue affected by inflammation at 

higher doses. Thyroid necrosis and increased kidney weights were observed at doses > 9.5 mg/kg 

as well (Yano et al. 2002). 

The inactivity of spinosad in long-term cancer bioassays (Yano et al. 2002, Stebbins et al. 2002) 

is consistent with short-term studies of spinosads’ genotoxicity. Spinosad (88%) has been 

evaluated for genotoxicity in both in vitro and in vivo assays (reviewed by IPCS 2001). In the 

Ames Assay with Salmonella typhimurium, spinosad tested negative for the induction of reverse 

mutations both with and without exogenous metabolic activation. Additional in vitro assays that 

examined the ability of spinosad to induce forward mutation (mouse lymphoma cells), or 

chromosomal aberrations or unscheduled DNA synthesis (Chinese hamster ovary cells) were 

also negative. Spinosad did not induce micronuclei in mice dosed orally at 0, 500, 1,000, or 

5,000 mg/kg for 2 days. Collectively, these results provide no indication that spinosad possesses 

genotoxic activity. 

The neurotoxicity of spinosad has been evaluated in studies in which spinosad was administered 

as a single gavage dose (to 2,000 mg/kg) to rats (Albee et al. 1994), by dietary administration to 

rats (to 43 mg/kg) for 13 weeks (Wilmer et al. 1993) or 12 months (to 49 mg/kg) (Bond et al. 

1995), or by dietary administration to dogs (to 8.2 mg/kg) for 12 months (Harada 1995) (all 

studies reviewed in IPCS 2001). These studies utilized batteries of tests to assess neurological 

function, and in the studies of Wilmer et al. (1993) and Bond et al. (1995), functional tests were 

supplemented with histological examination of tissues of the central and peripheral nervous 

systems. No treatment-related effects of spinosad were observed on neurological function or on 

neurological tissues. 




DRAFT PEIR 


Spinosad administered at 100 mg/kg in the diets of rats over two generations resulted in parental 

toxicity that included decreased body weights in adult males. Increases in absolute and relative 

weights of the liver, kidney, heart, spleen, and thyroid were also observed. Histological 

examination of tissues showed evidence of vacuolation in kidneys, lungs, lymph nodes, spleen, 

and thyroid of second generation adult males and females. Gestation survival was lower in F2 

litters, with smaller litter sizes seen in post-natal days 1 to 4 in all generations treated with 100 

mg/kg (Hanley et al. 2000). Treatment-related toxicity observed in dams during birth and 

lactation was linked to reduced survival of pups. Pup body weight gains in the 100 mg/kg group 

were lower throughout lactation, with significantly lower weights on post-natal day 21 in all 

generations. Because the effects on offspring occurred only in the highest dose group, and were 

associated with overt parental toxicity, spinosad does not appear to be a direct developmental 

toxin. That finding is generally consistent with the data of Breslin et al. (2000) who examined the 

potential of spinosad to induce adverse developmental effects by administering spinosad to rats 

and rabbits during gestation. In high dose rats (200 mg/kg), maternal body weight was 

significantly decreased at times during treatment, although final body weights were not affected. 

Spinosad did not affect the rate of pregnancy, implantation number, litter size, resorption rate, 

fetal viability, fetal body weight, or fetal sex ratio (Breslin et al. 2000). Micropthalmia was 

observed in 1 fetus from the 50 mg/kg dose group, and in two fetuses from two separate highdose 

(200 mg/kg) litters. ICPS (2001) provides a discussion of the documented incidence of 

unilateral micropthalmia; while acknowledging that it is quite rare, ICPS (2001) cites data to 

support the fact that small clusters of micropthalmia have occurred randomly and at similar 

incidence in several research labs. Given an absence of evidence for spinosads’ reproductive 

toxicity (Hanley et al. 2000) or developmental toxicity in rabbits (Breslin et al. 2000 -see 

following), it appears likely that the micropthalmia was not treatment-related. No other effects of 

spinosad treatment were observed in the Hanley et al. (2000) study. Breslin et al. (2000) also 

studied the developmental toxicity of spinosad by administering doses of 10 to 50 mg/kg 

spinosad to rabbits during gestation. Animals given 10 mg/kg displayed no adverse effects of 

treatment. High dose females had significantly lower body weight gain than controls, and two 

animals aborted their litters. The digestive tract, gall bladder, and kidney from one of these 

animals showed clear signs of toxicity; the other animal appeared normal based on macroscopic 

examination. Fetuses from these animals showed no evidence of treatment-related effects, 

indicating the failure to carry the litters to term was likely due to maternal toxicity. No 

parameters of fetal health were altered at any of the doses studied. 

D3.4.1.4 


The ability of spinosad to persist in the environment for days or weeks (see Section D3.4.1.1) 

coupled with LBAM eradication goals that may require repeated application of spinosad indicate 

that humans may potentially be exposed repeatedly to low-level concentrations of spinosad. 

When human toxicity data are not available for a chemical, as is the case for spinosad, regulatory 

agencies necessarily rely on data from animal studies to characterize exposure levels deemed to 

be safe for humans. For long-term i.e., chronic oral exposure, a RfD is developed. The analogous 

value for inhalation exposures is referred to as the RfC (USEPA 2009c). The RfD and RfC are 

each defined as the daily exposure level for the “…human population (including sensitive 

subgroups) that is likely to be without an appreciable risk of deleterious effects during a 

lifetime.” RfDs or RfCs are typically derived by selecting the most scientifically appropriate 




SECTION 3 




completeness of available toxicity data (USEPA 2009c). 

Spinosad’s chronic NOAEL comes from a series of chronic toxicity studies with mice, rats, 

rabbits, and dogs that have characterized its general toxicity, neurotoxicity, reproductive toxicity, 

developmental toxicity, and carcinogenicity (IPCS 2001; USEPA 2000b; Yano et al. 2002; 

Hanley et al. 2002; Stebbins et al. 2002). In these studies spinosad has been administered orally, 

either in the diet or by gavage. In general, long-term dosing with spinosad causes treatmentrelated 

effects in a number of tissues, with the most notable and consistent effect being tissue 

vacuolation. Additional effects observed in multiple species that received high doses of spinosad 

include increased liver, kidney, and thyroid weights, skeletal muscle myopathy, as well as 

inflammation and degeneration in multiple tissues and organs (IPCS 2001; USEPA 2000b; Yano 

et al. 2002; Hanley et al. 2002; Stebbins et al. 2002). The phenomenon of spinosad-induced 

tissue vacuolation has been attributed to phospholipidosis i.e., an accumulation of phospholipids 

accompanied by the development of lamellar bodies following inhibition and/or inactivation of 

the enzymes (phospholipases) that degrade phospholipids (Reasor and Kacew 2001; Yano et al. 

2002). Despite the almost ubiquitous nature of this response to spinosad, and its induction in 

humans by drugs such as amiodarone and fluoxetine, it is not known whether it represents a 

biologically significant effect (Reasor and Kacew 2001). 

In establishing pesticide tolerances for spinosad in food, the USEPA (2000b) considered a 

chronic toxicity study conducted in dogs that yielded NOAELs of 2.68 mg/kg (males) and 2.78 

mg/kg (females) and a chronic study in rats that identified NOAELs of 9.5 mg/kg and 12.0 

mg/kg for male and female rats, respectively. From these data, the USEPA (2000b) derived a 

RfD for spinosad of 0.027 mg/kg based on the NOAEL of 2.7 mg/kg in dogs (the value 

approximately intermediate between 2.68 and 2.78 mg/kg), to which they applied an UF of 10 to 

account for interspecies variability, and an additional UF of 10 to address intraspecies variability. 

Although the USEPA did not provide citations for the chronic toxicity data used in RfD 

development, the dog toxicity data are apparently those of Harada (1995 as cited in IPCS 2001). 

The Harada data are not publically available, but are well described in IPCS (2001). This 12- 

month study identified a NOAEL of 2.7 mg/kg, with animals at the LOAEL i.e., the next highest 

dose above the NOAEL, exhibiting tissue vacuolation and increases in two clinical chemistry 

parameters. The rat data discussed by the USEPA (2000b) have since been published as Yano et 

al. (2002). In the published data, Yano et al. (2002) reported a lower NOAEL (2.4 mg/kg) than 

referred to in the USEPA (2000). Effects observed at the LOAEL of 9.5 mg/kg, were limited to 

vacuolation of the thyroid, with higher spinosad doses inducing inflammation of the lung and 

thyroid, thyroid necrosis, and increased kidney weights as previously noted (Yano et al. 2002). 

The Yano et al. (2002) data are appropriate for derivation of a chronic RfD. These study results 

not only provide a lower NOAEL than Harada’s data, but were based on the administration of 

spinosad for up to 2 years. Although the study periods used in both studies are appropriate for 

determination of a chronic RfD, the Yano et al. (2002) were selected due to the longer study 

duration–a time period that approximates the life span of rodents. IPCS (2001) also identified the 

NOAEL of 2.4 mg/kg as the lowest relevant NOAEL for a long-term study (data source cited as 

Bond et al. 1995, a report submitted by DOW to the WHO). 

Data from exposures of rats, mice, and dogs (IPCS 2001) indicate considerable consistency in 

the nature of the adverse effects induced by spinosad, providing confidence that available data 




DRAFT PEIR 


reasonably characterize the nature of spinosad’s chronic toxicity. Histologic changes in multiple 

organs have been observed across species at many of the higher doses, with vacuolation and 

inflammatory changes the most commonly observed effects. Because no human data for 

spinosad exist, an UF of 10 was selected to account for extrapolation of data from animals to 

humans. An additional UF of 10 was selected to account for human intraspecies variability to 

insure that sensitive individuals are protected. Applying the combined UF of 100 to the NOAEL 

of 2.4 mg/kg yields a chronic RfD of 0.024 mg/kg. 

Spinosad’s inhalation toxicity has not been well characterized in any species. The IPCS (2001) 

determined that technical-grade spinosad had “little acute toxicity” regardless of exposure route, 

and cited dermal and oral LD 50 s in excess of 2,000 mg/kg. Spinosad also appears to have low 

acute inhalation toxicity, with a reported LC 50 greater than 5.2 mg/L (IPCS 2001). The Office of 

Pesticide Programs of the USEPA (2007) identified an oral NOAEL of 4.9 mg/kg-d that was 

considered appropriate for characterizing short-term (1-30 days) inhalation toxicity of spinosad. 

As with other pesticide evaluations, the USEPA (2007) gave only summary information on the 

(apparently) unpublished study; that information indicates the NOAEL was obtained in a 

subchronic feeding study in dogs that identified a LOAEL of 9.73 mg/kg-d based on histological 

changes in various organs, decreases in mean body weights and food consumption, anemia, and 

potential liver damage. If the USEPA-selected cumulative UF of 100-to address intraspecies and 

interspecies variability-is applied to the NOAEL of 4.9 mg/kg-d, it yields a short-term (acute) 

inhalation RfD of 4.9 x 10 -2 mg/kg. To characterize the potential effects of long-term (chronic) 

inhalation exposure, the USEPA (2007e) identified an oral NOAEL of 2.7 mg/kg-d from a 

chronic toxicity study in dogs. While it is likely that the study in question is from Harada et al. 

1995 (as reviewed in IPCS 2001), the USEPA document does not list the study authors. 

Nonetheless, applying the USEPA’s assumptions of 100% absorption via inhalation exposure, 

and a cumulative UF of 100, gives a chronic inhalation RfD of 2.7 x 10 -2 mg/kg-d. 

D3.4.2 

Bacillus thuringiensis (Bt) 

Bacillus thuringiensis (Bt) and its subspecies (ssp) are bacteria that have been used as pest 

control agents for nearly 50 years (McClintlock et al. 1995; WHO 1999). The bacterium’s 

selective insecticidal activity derives from crystalline proteins, encoded by extra chromosomal 

plasmids, which are formed in the endospore. These crystal (Cry) proteins are toxic to insects in 

the orders Lepidoptera (moths, butterflies), Coleoptera (beetles), and Diptera (flies). The Cry 

proteins are protoxins in that the biologically active compounds are derived by the action of 

proteolytic enzymes on the protoxin in the insect gut. Btk produce 2 or 3 protoxins that are toxic 

to Lepidopteran and Dipteran larvae (Widner and Whiteley 1997). As of 1999 when the WHO 

reviewed Bt, 67 different ssp of Bt had been identified; Btk is one of these (WHO 1999). 

Commercial Bt formulations were first marketed in Europe for forestry and agricultural uses 

(Siegel 2001). Currently, Bt is applied to food crops such as soybeans, tomatoes, potatoes, and 

grain; nonfood crops such as cotton, and forest trees for the control of pest species such as the 

gypsy moth and spruce budworm (WHO 1999). Bt was first registered for use by the USEPA in 

1961, and was re-registered in 1998 (USEPA 1998b). Between the years 1961 and 1995, the 

USEPA registered 177 Bt products (Siegel 2001). Depending on the manufacturer, the target 

pest, and the mode of application, Bt formulations are either wettable powders, suspension 

concentrates, water-dispersable granules, oil-miscible granules, or capsule suspensions (WHO 

1999). Two essentially identical formulations are proposed for use in the state’s LBAM 

eradication program, DiPel ® DF and DiPel ® PRO DF. Both products have been approved for use 


SECTION 3 


against the LBAM (CDFA Phytosanitary Advisory NO. 15-2008 Approved Treatments for Light 

Brown Apple Moth (LBAM) in Nurseries). 

Along with Btk, Bt israelensis and Bt aizawai are commonly used strains, with more than 1 

million pounds of these Bt formulations applied annually in the Unites States (Bernstein et al. 

1999). The WHO has estimated that approximately 13,000 metric tons of Bt products are 

produced yearly using aerobic fermentation technology (WHO 1999). Commercially produced 

Bt-based pesticides are a complex mixture of Bt spores, both intact and partial Cry proteins, 

residual growth medium, bacterial cell wall debris, and vegetative cells (Seligy et al. 1997). 

Analyses of Bt formulations indicate that these mixtures are comprised primarily of spores (up to 

1013 spores/Liter [L]) and the Cry proteins. The latter may be present in concentrations that 

range from 25 to 50% of the spore content (Dubois 1968; Seligy and Rancourt 1999). The 

International Union of Pure and Applied Chemistry (IUPAC) has established quality standards 

for Bt fermentation products, which include concentration limits for contaminants such as molds 

and various non-Bt bacteria that may be present in trace amounts (WHO 1999). 

D3.4.2.1 


D3.4.2.1.1 Physical Chemistry 

Bt is a gram-positive, spore-forming facultative anaerobic bacterium (WHO 1999; Siegel 2001). 

Unfavorable environmental conditions trigger vegetative cells to begin the process of sporulation 

(spore formation). On completion of sporulation, the parent bacterium lyses to release the spore 

and the cytoplasmic inclusions, the Cry proteins. Solution-grown spores of Bt have an average 

length of 2.0 µm and an average width of 872 nm; plate-grown spores have an average length of 

2.17 µm and an average width of 937 nm (Plomp et al. 2005). Vegetative cells of Bt are 3-5 × 

1.0-1.2 µm (as cited in Green et al. 1990). Due to their size, Bt spores and vegetative cells are 

respirable. 

D3.4.2.2 Environmental Transport and Degradation 

Bacillus thuringiensis and its subspecies are naturally occurring bacteria that have been detected 

in soil, from leaf and needle surfaces of trees, from vegetables, fruits, herbs, grain, and in water 

bodies (WHO 1999; Valaderes de Amorim et al. 2001; Frederiksen et al. 2006). Some recent 

analyses of food products have been unable to distinguish whether the bacterium’s presence on 

these materials was attributable to natural sources or to pesticide residue (Frederiksen et al. 

2006) 

On plant surfaces, the insecticidal activity of Bt spores is degraded primarily by UV light, 

although high leaf-surface temperatures and leaf type may also be a factor (WHO 1999). 

Reported half-lives of Bt spores on different leaf surfaces range from 0.63 days to 2 weeks, 

whereas Bt formulations may persist up to 1 year (WHO 1999). 

Bt spores can persist in soil for 12-24 months, but vegetative cells and the Cry proteins do not 

(WHO 1999). Forest applications of commercially available Bt formulations resulted in elevated 

numbers of Bt spores in forest soils for 12 months (Visser and Addison 1994 as cited in Smith 

and Barry 1997) to 24 months (Smith and Barry 1997). Spore recovery frequency and the 

number of Bt spores quantified per gram of soil corresponded to the number of applications and 

the interval since the last application; spore numbers provided no indication that proliferation 




DRAFT PEIR 


had occurred in the environment (Smith and Barry 1997). Bt spores do not germinate or grow in 

many naturally occurring soils. Spores do not accumulate in soil to an appreciable extent, and are 

relatively immobile, remaining in the top several centimeters of the soil column (WHO 1999). 

The WHO (1999) cited environmental half-lives for the Cry proteins of Bt of 3 to 6 days. At 

least one of the environmental removal mechanisms of the Cry proteins is metabolism by non-Bt 

microorganisms (WHO 1999). 

Molecular analysis techniques have led to the detection of Btk in surface waters of Victoria, 

British Colombia, prior to aerial application of Btk to control the European gypsy moth 

(Valaderes de Amorim et al. 2001). Btk can persist in fresh water and in saltwater for 70 days 

and 40 days, respectively (reviewed in WHO 1999). 

D3.4.2.3 


Bt’s insecticidal activity derives from the Cry proteins formed in the bacterium’s endospore. 

When the Bt spore is ingested by insects, these proteins undergo proteolysis in the insect gut, 

forming a biologically active compound known as a delta-endotoxin. This toxin subsequently 

binds to insect-specific receptors on the gut cell walls, disrupting the cellular osmotic balance 

and causing the death of the cell and ultimately, of the insect. Mammals do not have equivalent 

receptors, and no data indicate Bt acts similarly in mammals (reviewed in Betz et al. 2000). The 

isolated reports of adverse effects from Bt in humans as well as in experimental animals have not 

been linked to any specific mechanism of action. The USEPA has classified DiPel ® DF, the Btk 

formulation to be used in the LBAM eradication program, as USEPA toxicity category IV and III 

for oral and dermal toxicity, respectively (Valent Biosciences 2003). The inhalation toxicity of 

DiPel ® DF has not been classified due to the fact sufficiently high concentrations of respirable 

particles could not be generated (Valent Biosciences 2003). 

Some subspecies of Bt produce an additional insecticidal compound known as a -exotoxin. 

This heat-stable chemical acts by inhibiting RNA polymerases, enzymes critical to gene 

transcription in vertebrates and invertebrates alike. While the -exotoxin causes adverse effects 

in both mammals and insects, these toxins are not produced by Btk (WHO 1999). 

As a species of Bacillus, Bt is related to B cereus (Bc), B mycoides, and other members of the 

genus. Bt cannot be distinguished from the enteropathic species Bc morphologically, by substrate 

utilization, or by many common methods of genotypic differentiation. The two species can be 

separated by Bt’s formation of Cry proteins during sporulation (WHO 1999). However, the 

plasmids that encode the Cry proteins can be transferred from Bt to Bc, conveying Cry protein 

biosynthetic capabilities to Bc, and making the two species indistinguishable (WHO 1999). 

Although Bc can transfer genetic material to Bt as well, the likelihood of toxicologically 

significant genetic transfer occurring is considered unlikely (USEPA 1986b cited in USDA FS 

1995). 

Bt administration has frequently been accompanied by the detection of Bt in organs or excreta 

for considerable periods of time after exposure (McClintlock et al. 1995; WHO 1999; Jensen et 

al. 2002). However, because detection has not been accompanied by evidence of bacterial 

multiplication and/or toxin production (McClintlock et al. 1995; Siegel 2001), these data provide 

evidence of Bt’s persistence, not of its pathogenicity. Unpublished studies submitted to the 

USEPA in support of product registration, and cited by McClintlock et al. (1995), provide 


SECTION 3 


evidence that Bt passes through the gastrointestinal tract of rodents after oral exposure and does 

not distribute to other organs or tissues (McClintlock et al. 1995). In rodents exposed to Btk by 

intratracheal or intranasal dosing, colony forming units (CFUs i.e., viable spores that produce a 

single colony when grown on appropriate medium) declined during the first 24 hours after 

treatment, although the lungs still retained some Btk at day 21 when the study was terminated 

(McClintlock et al. 1995). Rats injected intravenously with Btk initially yielded viable CFUs 

from blood, liver, kidney, spleen, and other organs; Btk was still detectable in the liver and 

spleen up to 128 days post-exposure (McClintlock et al.1995). 

D3.4.2.3.1 Toxicity to Humans 

Human exposure to Bt occurs during commercial production, during application of Bt products 

to crops or other vegetation, and by exposure to Bt residues on food and other agricultural 

products. The WHO notes that over the many years of commercial production of Bt, no reports 

of adverse effects occurring to workers in manufacturing facilities have been made (WHO 1999). 

Widespread aerial and/or ground application of Bt formulations to control the gypsy moth, 

spruce budworm, or other forest pests have taken place over large areas and have involved 

exposure of the applicators as well as the general public (WHO 1999). Noble et al. (1992) 

reported that workers that sprayed Btk (Foray 48B ® ) to control gypsy moths were exposed to 

mean concentrations of 3 × 10 5 to 5.9 × 10 6 Btk spores/m 3 , with maximum estimated cumulative 

concentrations reaching 7.2 × 10 8 Btk spores/m 3 . Transient, nonspecific symptoms documented 

among these workers ranged from dry skin, eye irritation and nasal drip. Potential impacts in the 

general population during the same Btk spraying program were tracked by evaluating records 

from the emergency room, those of private physicians, and of bacterial cultures of infections 

collected by area hospitals. Noble and his co-workers also specifically considered whether 

asthmatics, HIV-positive individuals, or others with immunosuppressive disease might be at a 

greater risk of infection. Btk was isolated from many individuals during the 10-week spray 

program (thus documenting exposure), but no evidence existed that these exposures were 

associated with disease, even in individuals with compromised immune systems. No adverse 

effects of spraying were observed in the general population or in sensitive individuals (Noble et 

al. 1992). 

Cook (1994) published a detailed analysis of 120 ground spray workers exposed in the same 

spray program evaluated by Noble et al. (1992). Filter cassettes attached to the chest of workers 

provided exposure data for each worker. Samples were collected for 1- hour periods, with most 

workers sampled a single time. However, to evaluate the variability of individual exposure 

levels, certain workers, selected at random, were sampled 3 to 6 times during differing phases of 

the operation. Quantitative assay methods were used to assay the number of Btk spores on the 

filters, with exposure concentrations reported as CFU/m 3 . Cumulative exposure of each worker 

was calculated by multiplying the mean exposure concentration by the number of hours of actual 

exposure. The number of hours of exposure was not reported. Cumulative Btk exposures ranged 

from 7 x 10 5 CFU to 7.2 x 10 8 CFU. Based on questionnaire-developed data, approximately 

twice the number of workers reported adverse effects compared to controls (63% and 38%, 

respectively). Effects were generally minor and short-lived, and included dry skin, chapped lips, 

respiratory system irritation, and eye irritation. However, Cook (1994) reported a positive doseresponse 

relationship between total reported symptom frequency and cumulative Btk exposure. 

Total reported symptom frequency ranged from 0.8 per person (controls) to 1.5 in the low 




DRAFT PEIR 


exposure group (5.4 to 100 x 10 6 CFU), to 1.9 per person in the medium exposure group (101- 

300 x 10 6 CFU) and 2.9 per person in the high exposure group (>300 to 720 x 10 6 CFU). 

Btk is respirable, and Pearce et al. (2002) examined its potential to exacerbate asthma in children 

exposed during spray episodes on Vancouver Island. Foray 48B ® was applied at 4L/hectare at 

three separate times, separated by 10 day intervals. The average concentration of Btk in the spray 

zone during application periods was 739 CFU/m 3 . Sampling indicated that small numbers of the 

“control” population were exposed as well. Although limited in scope (29 asthmatic children and 

an equal number of controls) the results indicate that spraying did not affect either population. A 

companion study (Valadares de Amorin et al. 2001) found that the frequency of detection of Btk 

in nasal swabs increased among members of the general public inside the Btk spray zone, and in 

some cases, the increase was statistically significant. The presence of Btk did not appear to be 

biologically significant however, as the detection of Btk in nasal mucosa was not linked to 

adverse health effects as measured by a change in the frequency of emergency room visits. 

Two epidemiological studies in New Zealand have evaluated the health of individuals in 

populations exposed to Foray 48B ® (Aer’aqua Medicine 2001; Petrie et al. 2003). The largest of 

these, Aer’aqua Medicine (2001) relied on tracking of morbidity by participating physicians, 

coupled with self-reporting of symptoms by members of the general public. This study is 

noteworthy for the large exposed population (~86,000) and the extensive set of endpoints 

evaluated. At the end of the spray program, no effects were noted on the incidence of birth 

defects, birth weights, gestational age, anaphalaxis, meningococcal infection, or infection with 

Btk. No newly identified onset of asthma or of an increase in medical visits for existing asthma 

during spraying were noted. Similarly, no increase was documented in autoimmune illness or in 

medical visits for existing autoimmune illness during spraying. The greatest numbers of selfreported 

specific symptoms were respiratory, skin, and eye irritation. The incidence of these 

symptoms was neither reported nor evaluated for statistical significance. Foray 48B ® was applied 

at the rate of 5L/hectare, but estimates or measurements of airborne concentrations were not 

made by the study authors. 

Petrie et al. (2003) surveyed individuals before and after aerial application of Foray 48B ® , with 

181 of the original 239 participants completing the study. The application rate of Foray 48B ® 

was not specified, although Durkin (2004) has estimated concentrations of 100 to 4,000 CFU/m 3 

based on typical label-recommended application rates. Petrie et al. (2003) documented a 

statistically significant increase in self-reported sleep problems, dizziness, difficulty 

concentrating, irritated throat, itchy nose, diarrhea, and stomach discomfort. No increase in 

overall symptoms was reported among individuals with previously diagnosed asthma, but a 

significant increase in symptoms occurred among previously diagnosed hay fever sufferers. 

Because spraying occurred during hay fever season, symptoms of irritated throat and itchy nose 

cannot be definitively attributed to Btk exposure. These symptoms are similar however, to those 

described by Cook (1994) and in the Aer’Aqua Medicine 2001 studies. The study authors noted 

that participation was relatively poor (62%) among the cohort, and that individuals who believed 

themselves to be adversely affected were more likely to respond than individuals who felt 

unaffected. Among study participants, no change occurred in the number of visits to physicians 

after spraying, indicating that the effects were transient and were not deemed severe enough to 

warrant medical consultation. 


SECTION 3 


During the 1980s in Oregon, aerial spraying of the Btk formulation DiPel ® DF impacted an area 

with a population of 80,000 or 40,000 in each of the 2 years of the program, respectively. DiPel ® 

DF was applied at an application rate of 16 billion international units (BIU) per acre (cited in 

Durkin 2004). A public health surveillance program was established to track any species of 

Bacillus identified in clinical cultures during the period of spraying. A total of 55 Btk-positive 

isolates were identified, with 52 of these 55 cultures ultimately attributed to probable laboratory 

contamination as opposed to environmental sources (i.e., from spraying). Of the three remaining 

isolates, Btk could not be ruled in or ruled out as a cause of illness. However, all three 

individuals that yielded positive Btk cultures had existing medical conditions, and if Bt infection 

did occur, it may have developed because the immune systems of these individuals were 

compromised (Green et al. 1990). 

During approximately 50 years of commercial use of Bt-based insecticides, only a few isolated 

instances of human infection with Bt have been documented. These reports indicate Bt appears 

to be pathogenic only in individuals who may be unable to mount a fully functional immune 

response. The WHO (1999) references four reports in which Bt has been linked to disease. None 

of the Bt strains involved were Btk, and one of the reports (Jackson et al. 1995) appears to have 

inappropriately attributed gastroenteritis to Bt instead of to Bc. Two other reports involve 

isolation of Bt from burns or war wounds (Damgaard et al. 1997; Hernandez et al. 1998). 

Damgaard et al. (1997) cultured Bt from burns of immuno-supressed patients, contaminated by 

water used in treatment. Similarly, Hernandez et al. (1998) identified Bt ssp konkukian from a 

severe war wound, and confirmed the pathogenicity of the subspecies by successfully inducing 

infection in mice. Notably, the bacterium only caused infection in immuno-suppressed animals. 

A Btk commercial product, DiPel ® DF, was linked to development of a corneal ulcer after an 

individual splashed the product in his face. Analyses of this incident (see discussion in WHO 

1999 and Siegel 2001) make it clear that while Btk was cultured from the affected eye, Btk’s 

presence may have been coincidental as opposed to causative, as a comprehensive screen for 

other organisms was not conducted. 

Btk is capable of inducing immune responses in individuals, but it is important to recognize that 

these responses–measured by the induction of antibodies or skin sensitization reactions–are 

distinct from pathogenicity. For example, aqueous extracts of a commercial Bt product, or 

antigens obtained from sporulation cultures of Btk induced immune responses in individuals, 

characterized by positive skin and antibody tests (Bernstein et al. 1999). Despite evidence of 

induced skin sensitivity to both spore and vegetative components of Btk, no clinical evidence of 

disease existed (Bernstein et al. 1999). The WHO (1999) cites similar data from Lafarriere et al. 

(1987) who documented antibody development to Btk spore-crystal complexes, vegetative cells, 

and to spores in approximately 10% of workers involved in a 2-year spraying program. No 

adverse effects were observed in these individuals. 

Human volunteers have ingested 1 gram (g) of Btk formulation (3 x 10 9 spores per g of powder) 

daily for 5 days, and some of these same individuals also inhaled 100 mg of the Btk powder 

daily for a 5-day period. No evidence existed of adverse effects from these exposures (Fisher and 

Rosner 1959 as cited in WHO 1999). McClintlock et al. (1995) cites an additional study in which 

5 human males and 5 females ingested 1 x 10 10 viable spores per day for 3 days. Individuals 

were followed for 30-days after the end of exposure without evidence of adverse effects. 




DRAFT PEIR 


No data indicate that Btk or any of the Btk formulations are genotoxic or carcinogenic (WHO 

1999). 

D3.4.2.3.2 Toxicity to Animals 

McClintlock et al. (1995) summarized mammalian toxicity data submitted to the USEPA in 

support of registration of Bt-based pesticides prior to 1989. Data excerpted from the McClintlock 

et al. (1995) review are summarized in Tables D3-43 and D3-44. For acute exposure by oral, 

inhalation, or dermal routes of exposure, no evidence exists of infectivity or toxicity from studies 

with experimental animals. 

Table D3-43 

Acute Mammalian Toxicity of Bacillus thuringiensis kurstaki 

Route of exposure Species LD50 or LC50 1 NOAEL 2 

Oral Rat > 4.7 x 10 11 spores/kg No infectvity/toxicity 

Dermal Rat > 3.4 x 10 11 spores/kg No infectvity/toxicity 

Inhalation Rabbit > 2.6 x 10 7 spores/L No infectvity/toxicity 

Source: 

McClintlock et al.1995 

Notes: 

1 Median lethal dose (LD50) or median lethal concentration (LC50) required to kill 50% of test animals. 

2 NOAEL: No Observed Adverse Effect Level 

Conclusions from the acute studies regarding Btk’s toxicity were reached after observing animals 

for mortality, changes in body weight, clinical signs of toxicity, gross necropsies, and by 

evaluating the patterns of clearance of Btk from the test animals. The USEPA requires an 

intraperitoneal injection test for Bt-based products in which spores, crystals, and fermentation 

material (10 6 to 10 8 CFU) are injected into mice. Although intraperitoneal injections of technicalgrade 

Btk administered at 10 6 to 10 7 CFU did not cause mortality, injection of Btk product 

produced significant mortality in half of the treated groups (McClintlock et al. 1995). These 

results show that very high doses of commercial Btk formulations can be toxic when 

administered intraperitoneally, although, this route of exposure is not directly relevant to 

humans. The WHO provides data on two additional acute oral toxicity studies of Btk, and note 

that no mortality was observed in rats given 10 7 to 10 11 CFU (WHO 1999). 

Some subspecies of Bt, although not Btk, have caused moderate to slight skin irritation following 

a single dermal exposure. Specifically, dermal exposure of rabbits to Btk spores or to the Btkcontaining 

product Thuricide 32B ® (2,000 mg/kg or 3.4 x 10 8 spores/kg) did not cause dermal 

irritation in rabbits (McClintlock et al. 1995). 

In addition to the acute toxicity data summarized by McClintlock et al. (1995), both the WHO 

(1999) and Durkin (2004) present comprehensive summaries of the numerous studies submitted 

in support of Btk-containing insecticides. Despite the completion of additional toxicity studies 

since McClintlock’s 1995 review, the conclusions are unchanged i.e., that acute oral, inhalation, 

or dermal exposure to Btk or to Btk formulations are neither toxic nor infective. 

Acute ocular exposures (0.1 mL) of different Btk formulations have produced redness and 

discharge that have persisted up to 10 days, and the administration of massive doses of Btk either 

intratracheally (summarized in Durkin 2004) or by intranasal instillation (see discussion of 


SECTION 3 


Hernandez et al. 1999, 2000) have produced mortality, pulmonary irritation, and pulmonary 

lesions. Data are also limited on mortality in experimental animals following intravenous (iv) or 

intraperitoneal (ip) injection of Btk (Durkin 2004). With the exception of the ocular exposures, 

none of these routes of exposure are applicable or relevant to circumstances of potential human 

exposure, and are minimally informative with respect to the inherent toxicity of likely 

environmental levels of Btk. The doses administered were substantial (3 x 10 9 CFU/g [iv] or up 

to 10 8 CFU/mouse [ip]), and are well above quantities that the general public might encounter in 

the environment from application of Btk-containing insecticides. 

Hernandez et al. (1999, 2000) has investigated the pathogenicity of different Bt strains in 

immuno-competent and immuno-compromised mice. In the first of two reports, Hernandez et al. 

exposed animals by nasal instillation to spore suspensions of Btk. Nasal instillation of 10 8 spores 

of Btk in water–a massive dose–resulted in 80% mortality within 24 hours of exposure 

(Hernandez et al. 1999). The lungs of these animals exhibited hemorrhagic lesions, ulceration, 

edema, and alveolar damage, which Hernandez et al. (1999) attributed to the action of Bt-derived 

hemolysins. In a follow-up study, Hernandez et al. (2000) dosed mice via intranasal instillation 

with 10 2 , 10 4 , or 10 7 spores of Btk with or without influenza virus (2% or 4% of the viral LD 50 ). 

Co-infection of mice with Btk and 4% of the viral LD 50 caused Btk dose-related mortality (20% 

mortality with 10 2 Btk spores vs 70% mortality with 107 spores). Parallel experiments with 2% 

of the LD 50 of influenza virus did not produce mortality in any treatment group. In mice exposed 

only to Btk (10 2 , 10 4 , or 10 7 spores), lung inflammation was the only adverse effect reported, 

albeit without any discussion of severity or potential presence of a dose-response relationship. 

The subchronic and chronic studies of Btk reviewed by McClintlock et al. (1995) and 

summarized in Table D3-40 show that even very substantial doses of Btk (e.g., 8.4 g/kg-day) can 

be tolerated with minimal effect. In the 2-year feeding study, the only reported adverse effect 

was decreased weight gain in females, seen initially at week 10 and persisting to the termination 

of the study (McClintlock et al. 1995). McClintlock et al. (1995) did not address whether animals 

in the 90-day study also exhibited decreased weight gain at the (same) NOAEL, nor did they 

specify whether the quantities of Btk used in the 90-day and 2-year studies pertained to Btk 

spores or to a Btk formulation. The WHO has stated that a commercial formulation was used, 

however (WHO 1999). 

Table D3-44 

Subchronic and Chronic Toxicity of Bacillus thuringiensis kurstaki 

Route of Exposure Species Study Duration NOAEL 1 

Oral (gavage) Rat 13 weeks 1.3 x 10 9 spores/kg-day 

Oral (diet) Rat 90 days 8.4 g/kg-day 

Oral (diet) Rat 2 years 8.4 g/kg-day 

Source: 

McClintlock et al.1995 

Notes: 

1 NOAEL: No Observed Adverse Effect Level 

In addition to the data presented in Table D3-40, summary data are available on sheep exposed 

to Btk for 60 days (Hadley et al. 1987). In that study, sheep were fed either DiPel ® DF or 

Thuricide HP ® for 5 months at a concentration of ~10 12 spores per day. Diarrhea was observed in 




DRAFT PEIR 


some of the treated animals, but not in untreated or vehicle controls. No other effects of exposure 

were documented. 

D3.4.3 

Interpretation of Human Toxicity 

Animal toxicity data submitted in support of registration of Bt-based pesticides provide a 

compelling body of evidence that demonstrates that Btk is not toxic or infective when exposure 

occurs dermally, and causes only minimal toxicity when massive doses are provided by 

ingestion or inhalation (McClintlock et al. 1995). This response pattern has been consistently 

observed and documented across multiple species for acute, subchronic, and chronic exposure 

durations–not only in the early studies (McClintlock et al. 1995), but in later summaries reported 

by the WHO (1999) and Durkin (2004). A single noteworthy exception to this otherwise clear 

pattern of Btk’s minimaltoxicity comes from the data of Hernandez et al. (1999, 2000). In these 

studies, large doses of Btk spores (10 8 ) induced 80% mortality when administered to mice via 

intranasal instillation. Lower spore numbers of Btk (10 2 to 10 7 ) caused pulmonary inflammation 

but no lethality. Parallel experiments with 10 8 spores of Bt israelensis and Bt konkukian resulted 

in the deaths of 100 % (ssp. konkukian) or 40% (ssp. israelensis) of treated mice. As with Btk 

however, intranasal installation of 10 5 or 10 7 spores of Bt israelensis or Bt konkukian caused 

only localized inflammation. The pulmonary lesions induced by all Bt subspecies were similar, 

and included ulceration, edema, and alveolar damage. Because spores were administered in an 

aqueous suspension, these effects are clearly attributable to the bacteria and not to the vehicle. 

What is less clear however, is whether the pulmonary toxicity and mortality are a function of the 

innate toxicity of certain subspecies of Bt, or whether the response is due–wholly or in part–to a 

physically mediated effect attributable to the sheer number of spores that came into contact with 

lung tissue. Certain gram positive bacteria, including some species of Bacillus, have the ability to 

cause the lysis of RBCs (hemolysis), and Hernandez et al. (1999, 2000) have proposed that 

hemolysis is a factor for the lesions and/or mortality observed in their mice. That possibility 

notwithstanding, significant questions exist regarding the relevance of the dose, the route of 

exposure, and the effects cited in the Hernandez papers to humans who may be exposed to 

environmental concentrations of Btk. Thus, while the data of Hernandez et al. (1999, 2000) 

appear to indicate that large doses of intransally instilled spores of Btk can cause significant 

toxicity, the fact that humans would never be exposed in this manner or to such enormous 

concentrations makes these data largely irrelevant to an understanding of potential effects in 

humans exposed to much lower environmental concentrations. 

To better understand the potential for adverse effects in humans who may be exposed to Btk 

subsequent to environmental applications, the epidemiologic studies of Cook (1994), Aer’Aqua 

Medicine (2001), and Petrie et al. (2003) are informative. Considered together, these studies 

present a pattern of evidence that links environmental release (application) of Btk to irritation of 

the respiratory tract, eyes, and skin. All three studies examined the linkage between exposure to 

the commercial Btk formulation Foray 48B ® and adverse effects. These effects were documented 

by self-reporting (Cook 1994; Petrie et al. 2003) or by self-reporting plus physician reporting 

(Aer’Aqua Medicine 2001). Although the use of self-reporting as a method to evaluate effects 

incidence is inherently subjective, the consistency in reports of eye, skin, and respiratory tract 

irritation increase the weight of evidence that these effects are exposure related. 

In the Aer’Aqua Medicine report (2001), respiratory concerns were the most frequently reported 

effect by individuals in the spray zone, with approximately 220 of 375 people reporting 

symptoms. “General” health concerns were the next most common complaint (~120 persons), 


SECTION 3 


with eye (~90 persons), neurological complaints (~75 persons), skin (~75 persons), and “social” 

concerns (~75 persons) also eliciting relatively large numbers of complaints. These data were not 

evaluated for statistical significance, nor were they presented in a way that would support such 

an analysis. Concentrations of Btk were not measured or reported. As a consequence, these data 

provide support for Btk’s ability to cause respiratory tract, eye, and skin irritation (as well as 

other minor effects), but are not adequate to support a quantitative understanding of Btk’s doseresponse 

relationship for these endpoints. 

The Petrie et al. (2003) data found a number of statistically significant reported symptoms 

among residents of an area sprayed with Btk. Rates of throat irritation doubled, and were notable 

for the degree of difference between exposed and unexposed individuals (p = 0.0001). Other 

symptoms that also increased significantly among exposed individuals–although to a lesser 

extent than throat irritation–were itchy nose, gastrointestinal distress, sleep problems, dizziness, 

and concentration problems. With the exception of itchy nose (which is consistent with an 

irritant response), it seems likely that these effects are attributable to anxiety about the spray 

program and do not represent Btk-induced effects. Although Petrie et al. (2003) did not monitor 

exposure concentrations, Durkin (2004) estimated that Btk concentrations ranged from 

10 2 to 4 x 10 3 CFU/m 3 based on label-recommended application rates. Nonetheless, because 

these concentration estimates cannot be linked to different effects incidence or severity, the data 

of Petrie et al. (2003) are also not sufficient to support an understanding of the relationship 

between different exposure concentrations of Btk and adverse effects. They do however provide 

qualitative support for the existence of a relationship between Btk exposure and throat irritation. 

Of the three studies that have documented respiratory tract, and/or eye, and/or skin irritation, 

only Cook (1994) measured actual exposure concentrations. Those exposure data were obtained 

for workers, and represent concentrations that are likely much higher than any the general public 

might encounter. Mean exposure concentrations ranged from 3.0 × 10 5 to 5.9 × 10 6 Btk 

spores/m 3 (see companion study of Noble et al. 1992) with maximum estimated cumulative 

concentrations (CFU/m 3 x hours of exposure) reaching 7.2 x 10 8 Btk CFU/m 3 . Cumulative 

concentrations represent exposures incurred by the workers intermittently over the ~ 3-month 

period of the ground-spray program, and represent exposure during at least two work shifts. 

Further details of how cumulative exposures were incurred were not provided by Noble et al. 

(1992) or by Cook (1994). Table D3-45 provides the symptom frequency in workers based on 

data in Cook (1994). 

Table D3-45 Post-spray Symptoms Reported by Ground-spray Workers and Controls 1 

Symptoms 

Controls 

(n=29) 

Number (%) 

Workers 

(n=120) 

Dermal (dry or itchy skin, chapped lips) 3 (10%) 41 (34%) 

Eyes (redness, itch, burning, puffiness) 4 (13%) 24 (20%) 

Headache 3 (10%) 8 (7%) 

Throat (dry, sore) 2 (7%) 35 (29%) 

Runny nose or stuffiness 4 (13%) 32 (27%) 

Respiratory (cough, tightness) 1 (3%) 24 (20%) 

Digestive (nausea, diarrhea) 3 (10%) 8 (7%) 

Total (all symptoms combined) 11 (38%) 76 (63%) 




DRAFT PEIR 


Table D3-45 Post-spray Symptoms Reported by Ground-spray Workers and Controls 1 

Symptoms 

Controls 

(n=29) 

Number (%) 

Workers 

(n=120) 

Notes: 

1. Data from Cook 1994. Table D3, p. 22. 

Cook (1994) did not evaluate his symptom incidence data for statistical significance, but this 

analysis was conducted separately by Durkin (2004). Applying the Fisher Exact Test, dermal 

irritation (dry itchy skin and chapped lips), throat irritation, and respiratory irritation were 

statistically significant (p < 0.05). However, a more stringent statistical method that accounts for 

multiple comparisons (Bonferroni correction) found skin and throat irritation to be marginally 

significant and respiratory irritation no longer significant. 

Cook (1994) grouped cumulative exposures into three categories (Low, Medium, High), and 

evaluated overall symptom frequency relative to each exposure level (Figure D3-13). That 

evaluation demonstrated a dose response relationship between cumulative exposure to the Btk 

formulation Foray 48B ® and total reported symptoms (Cook 1994). Dose-response data for 

specific symptom categories such as skin and throat irritation, or respiratory irritation, are not 

available from Cook’s data. The biological significance of these effects appears to be modest, as 

all effects were reversible, none were associated with infection or pathogenicity of Btk, and none 

were severe enough to result in lost work days. 

Figure D3-13 Symptom Frequency vs Btk Exposure Group 

Equation D3-1 

 

 

CFU 10 

6 

3 

M 

hours 

 

exposed 

 


SECTION 3 


In summary, the data of Cook (1994) document Btk exposure-related skin and throat irritation, in 

keeping with similar reports by Aer’Aqua Medicine (2001) and Petrie et al. (2003). The timing 

of the exposures documented by Cook (1994) is not available and, thus, it is not possible to 

determine with certainty whether exposure to the maximum measured concentration occurred at 

a single time or repeatedly. However, based on discussions in Cook (1994), it appears that the 

Btk exposures were both acute (single) and subchronic (repeated). Consequently, the effects 

described from Btk exposure likely occurred subsequent to either exposure duration. 

The data of Cook (1994) represent the only quantitative human dose-response data available on 

Btk; despite a number of ambiguities in the data, they do support the existence of a 

concentration-response relationship. That relationship, summarized in Figure D3-13, indicates 

that the LOAEL for irritant effects, measured as cumulative exposure, is represented by the 

lower end of the range of values reported for the “Low” exposure group (range of < 1 x 10 6 to 

100 x 10 6 CFU/m 3 ). Based on data provided in Cook (1994) and presented in Table D3-42, the 

LOAEL of 0.7 x 10 6 mean CFU/m 3 was documented for Contractor B “PR” workers. 

Table D3-46 

Ground Spray Worker Exposures to Btk 

Worker Job Category Number of samples Mean CFU/m 3 

Contractor A 

Sprayer 30 3.1 x 10 6 

Hose handler 16 2.2 x 10 6 

Auditor 30 2.0 x 10 6 

PR 10 2.0 x 10 6 

Contractor B 

Sprayer 8 5.9 x 10 6 

Hose handler 6 1.7 x 10 6 

Auditor 6 1.4 x 10 6 

PR 4 0.7 x 10 6 

Source: 

Cook 1994. Table 2, p. 21. 

Taking the LOAEL of 0.7 x 10 6 mean CFU/m 3 and applying an UF of 10 to account for 

variability in the human population, and an additional UF of 10 to account for the use of a 

LOAEL instead of a NOAEL yields a RfC of 7 x 10 3 CFU/m 3 . Because it is unclear whether the 

data of Cook (1994) reflect effects from anything other than acute exposure, this RfC is 

considered appropriate only for the quantification of potential adverse effects of Btk from an 

acute exposure period. To support quantitative risk assessment for Btk exposure, the RfC was 

converted from CFU/m 3 to mg/m 3 as follows. 

Capalbo et al. (2001) determined that there are approximately 10 9 CFUs (viable spores) per gram 

of Bt tolworthi. If it assumed that Btk spores have approximately the same mass as Bt tolworthi, 

and that all of the spores released to combat the apple moth are viable, the RfC can be translated 

into mg of spores per cubic meter (mg/m 3 ) by dividing 7 x 10 3 CFU/m 3 by 10 9 CFUs, and 

multiplying by 10 3 to convert grams to milligrams. This calculation yields an RfC of 7 x 10 -3 

mg/m 3 . This RfC can be converted to an inhalation RfDinh of 2 x 10 -3 mg/kg-d as shown in Eq. 

3-2. 




DRAFT PEIR 


Equation D3-2 

Where: 

RfC = Reference concentration (mg/m 3 ) 

RfD = Reference dose (mg/kg-d) 

BW = Body weight (70kg) 

IR = Inhalation rate (20 m 3 /d) 



Exposure Assessment 

In this chapter, potential exposures to human receptor populations are characterized from each of 

the proposed alternatives based on exposure parameters and exposure point concentrations of 

insecticides developed from projected application practices. Calculation of chemical-specific 

intakes was conducted from estimated EPCs in lieu of empirical measurements of exposure 

media, to gauge exposure levels based on application rates and delivery mechanisms of relevance 

to human populations. 

D4.1 EXPOSURE PATHWAYS AND EXPOSURE POINT CONCENTRATIONS 

As described in more detail under the sections that address each of the alternatives, humans may 

potentially be exposed to chemical or biological insecticides used to control LBAM. These 

exposures may occur by inhalation (chlorpyrifos, lambda cyhalothrin, permethrin, ethylbenzene, 

1,2,4-trimethylbenzene, spinosad, Btk, and the LBAM pheromones present in SPLAT, 

HERCON, and Isomate (hereafter referred to as SPLAT, HERCON, or Isomate as distinct from 

the LBAM pheromones present in these products); by incidental ingestion of soil (chlorpyrifos, 

lambda cyhalothrin, permethrin, ethylbenzene, 1,2,4-trimethylbenzene, spinosad, Btk, SPLAT, 

and HERCON); dermal contact with soil or vegetation (chlorpyrifos, lambda cyhalothrin, 

permethrin, spinosad, SPLAT, and HERCON); ingestion of commercial produce (chlorpyrifos, 

lambda cyhalothrin, SPLAT, HERCON, spinosad, Btk), and ingestion of home-grown produce 

(chlorpyrifos, lambda-cyhalothrin, SPLAT, HERCON, spinosad, and Btk. Dermal exposure of 

human receptor populations to Btk was not evaluated, as no evidence indicates that Btk can be 

absorbed across or otherwise enter intact skin. Exposures to triacetin, an inert ingredient of the 

permethrin formulation Permethrin E-Pro was not evaluated given that the material is essentially 

nontoxic. Because no direct treatment of surface water will occur, any contact human 

populations may have with water would be extremely limited and would not result in appreciable 

exposure. Accordingly, no potential exposures associated with surface water were evaluated for 

humans. 

D4.2 DEVELOPMENT OF EXPOSURE POINT CONCENTRATIONS 

The EPCs, provided for each alternative in the following sections, are key determinants of the 

theoretical dose incurred by human receptor populations as the dose will differ depending on the 

environmental medium and the quantity or concentration of chemical or biological insecticide in 

that medium. Human uptake is also dependent on the different physiological characteristics and 

activity patterns of each receptor population - characterized in this HRA by population-specific 

exposure parameters. 

The EPCs for each alternative were developed through application of the air modeling 

methodologies described in Appendix C and summarized below. The EPCs for incidental 

ingestion and dermal uptake of soil, and incidental ingestion of contaminated produce 

(commercial crops or homegrown produce) require the use of additional estimation techniques to 

translate the model-derived deposition quantities of insecticide into the EPC. Those estimation 




DRAFT PEIR 


techniques are briefly described below following the summary of assumptions used in the air 

modeling to develop EPCs. 

D4.2.1 

Exposure Point Concentrations Developed from Air Modeling 

Numerous assumptions were necessary in conducting the air dispersion modeling for this statewide 

program. A detailed presentation of those assumptions and the air modeling methodologies 

are provided in Appendix C. Those assumptions that directly affect the development of EPCs for 

the HHRA are summarized below. 

• Maximum modeled air dispersion and deposition rates. These were used as the input 

parameters to define estimated exposure point concentrations in soil and vegetation. For the 

air dispersion modeling that provided the key EPCs data for all human health risk 

calculations, additional assumptions include: 

Model selection – Either very conservative screening-level models were used (e.g., box 

models) or more refined models were used in a screening-mode (e.g., the industrial 

source complex [ISC] model using screening level meteorology). The models were run in 

this manner so the results would be applicable statewide. As a result, the estimated 

concentrations and deposition quantities are likely higher than what a more refined model 

would predict for a specific location using site-specific information. 

That the maximum concentrations and deposition quantities could occur at the same time 

– The maximum concentration and maximum deposition amounts were estimated in 

separate model runs because the environmental conditions and application characteristics 

that result in maximum airborne concentrations tend to minimize the amount of material 

that deposits and visa versa. It is therefore unlikely that the maximum concentration and 

maximum deposition would occur at the same time; assuming simultaneous exposure to 

both would over predict the associated human health impacts. 

Utilized maximum application rates – The emission rates for each treatment formulation 

were calculated based on the maximum application rate and the fraction of the active 

ingredients obtained from the product labels. Pesticide label application rates are often 

provided as a range for each treatment formulation for different pests and application 

settings. When this proved to be the case for a given pesticide, the most conservative of 

the potentially applicable application rates was used. Because of this approach, it is 

possible that the emission estimates used to predict air concentrations and deposition 

quantities likely overestimate the true emissions. 

Overestimated the quantity of material that would likely volatilize. For volatile 

compounds and for certain methods of application (e.g., pod guns and metered jet guns) 

estimates of the amount of material that would volatilize or be present as drift were 

required. With different environmental conditions likely to be encountered across the 

state and different application methods, conservative assumptions regarding volatilization 

were made. These assumptions include, but are not limited to, assuming 100 percent of 

the volatile materials volatilize between applications and that 10 percent of the 

permethrin applied would either volatilize or be present in drift for Alternative MMA, 

even though it is likely nonvolatile. Thus, the resulting concentration estimates likely 

over predict the actual concentrations that might be encountered by human populations. 


SECTION D4 

EXPOSURE ASSESSMENT 

Assumed three applications per treatment option – To determine the number of applications for 

each treatment alternative, the Program calls for up to two life cycles without LBAM being 

detected before treatment is halted. However, it was necessary to quantify this value in more 

precise terms to perform the modeling and post-processing calculations and it was assumed that 

each treatment alternative would be applied 3 times. If the number of applications increases or 

decreases, then the resulting concentrations and depositions would also increase or decrease. 

• Hydraulic spraying only during daylight hours. It was assumed that the hydraulic spraying 

for both the No Program and Organic Approved Pesticides (Btk and S) alternatives would 

only occur during daylight hours. As such, a limited set of meteorological data was used, 

representing conditions that occur during daylight hours. In particular, the most stable 

atmospheric conditions that only occur at night were excluded from the analyses. This 

assumption would under-estimate concentrations if spraying were to occur at night. 

Inhalation exposure. The maximum 1-hour ambient air concentration modeled for each 

chemical and treatment alternative was used to estimate acute inhalation exposure. The 1- 

hour maximum concentrations were the highest air borne concentrations projected from 

air dispersion modeling. For chronic inhalation exposures, the period average air 

concentration for each treatment chemical was used; this metric accounts for both air 

concentrations during (active OR concurrent) application treatments and volatilized 

concentrations from past treatments. 

D4.2.2 Additional Estimation Techniques Used to Calculate Exposure Point 

Concentrations 

The average concentration of a contaminant in soil is related to the quantity of material deposited 

during application (mass per unit area), soil mixing depth, and soil bulk density. The calculation 

of the amount of pesticide deposited (see Appendix C) accounts for the label-specified 

application rate, the number of applications during the treatment period, and specific 

environmental loss processes that are applicable to a given pesticide. Because the pesticide 

deposition terms accounts for these parameters, the average concentration of a pesticide in soil 

can be estimated by applying Equation D4-1. This equation is used, along with an intake factor 

(see following), to determine the amount of pesticide exposure incurred by incidental ingestion 

of soil. 

Equation D4-2 

Concentration on vegetation 

Cv = (Ds × IF × CF ) / Y 

Where: 

Cv = Average vegetation concentration over the evaluation period 

(mg/kg) 

Ds = Deposition onto soil (g/ m 2 ) 

IF = Intercept fraction (0.2 unitless, OEHHA 2003) 

CF = Conversion Factor (g/mg) 

Y = Yield (2 kg/m 2 , OEHHA 2003) 




DRAFT PEIR 


D4.3 INTAKES 

The intake of chemicals for each human receptor population was calculated using methods 

consistent with those of OEHHA (2003), supplemented by methods in USEPA et al. (1997) and 

USEPA (2001). Recommended population and exposure-route-specific intake factors were 

selected from OEHHA (2003) when available, and were supplemented by values from the more 

comprehensive USEPA Exposure Factors Handbook (USEPA 1997) as needed (see following). 

The USEPA (1997) does not necessarily provide recommended parameters for all activities or 

receptor populations. In those cases, such as the Recreational Park User (see following), 

professional judgment was used to either select appropriate values from USEPA (1997) (if 

available) or to define select parameters as needed. The specific exposure parameters that were 

used to quantify exposure for each receptor population are provided in Table D4-1. Footnotes to 

that table give the source of each assumption or parameter e.g., USEPA (1997) or OEHHA 

(2003). 

D4.3.1 

Ingestion and Inhalation Exposure 

The general intake equations for soil or vegetation ingestion exposure , acute inhalation 

exposure, and both subchronic and chronic inhalation exposure, are given in equations 4-3, 4-4, 

and 4-5, respectively. 

Equation D4-3 

Soil or vegetation ingestion intake factor 

IF = (IR × CF × EF × ED)/(BW × AT) 

Where: 

IF = Ingestion Intake Factor, kilograms (kg) soil or vegetation/kg body 

weight-day 

IR = Ingestion Rate, milligrams (mg)/day 

CF = Conversion Factor, kg/mg 

EF = Exposure Frequency, days/year 

ED = Exposure Duration, years 

BW = Body Weight, kg 

AT = Averaging Time, days 

Equation D4-4 

Acute vapor inhalation intake factor 

IF = (IR × EF × ED)/(BW × AT) 

Where: 

IF = Inhalation intake factor in cubic meters of air/kilogram body 

weight-day 

IR = Inhalation Rate, cubic meters (m 3 )/hour 

EF = Exposure Frequency, hours/day 

ED = Exposure Duration, days 


SECTION D4 




Equation D4-5 

Subchronic and chronic vapor inhalation intake factor 

IF = (IR × EF × ED)/(BW × AT) 

Where: 

IF = Inhalation intake factor in cubic meters of air/kilogram body 

weight-day 

IR = Inhalation Rate, cubic meters (m 3 )/day 





D4.3.1.1 Dermal Dose from Soil or Vegetation 

Equation D4-6 is the equation used to estimate dermal exposure from contact with contaminated 

soil. 

Equation D4-6 

dermal intake factor from soil 

IF = (SA × AF × ABS × CF × EF × ED)/(BW × AT) 

Where: 

IF = Dermal Intake Factor, kilograms (kg) soil /kg body weight-day 

SA = Surface Area of Exposed Skin, square centimeters (cm 2 )/day 

AF = Soil-to-Skin Adherence Factor, milligrams (mg)/ cm 2 

ABS = Absorption Factor (unitless) 

CF = Conversion Factor, kg/mg 





Equation D4-7 provides the general approach used to estimate dermal intake from contact with 

pesticide-contaminated vegetation, and is consistent with methods described in Sections D2.2, 

D3.2, and D4.2 of USEPA et al. (1997), and USEPA (2001) (see following). 

Equation D4-7 

dermal intake factor from vegetation 

IF = (Tc × ABS × ET × EF × ED × CF)/(BW × AT) 




DRAFT PEIR 


Where: 

IF = Intake factor for exposure via dermal contact with vegetation, 

square meters (m 2 )/kilogram (kg)-day 

TC = Transfer Coefficient, square centimeters (cm 2 )/hour 

ABS = Chemical-specific Dermal Absorption Factor, unitless 

ET = Exposure Time, hours/day 



CF = Conversion Factor, m 2 /cm 2 



It is important to note that the USEPA et al. (1997) methodology contains terms that are not 

included in Equation D4-6, specifically, AR (application rate of active ingredient in mass/area), 

F (fraction of active ingredient retained on foliage (unitless) and (1-D)t for the fraction of residue 

that dissipates daily (unitless). In the HRA calculations, these terms were replaced by an air 

modeling-derived value that represents the mass of active ingredient per unit area (see Appendix 

C). The air modeling accounted for the pesticide application rate as well as environmental loss 

processes such as volatilization (where appropriate), dispersion, and degradation. The USEPA et 

al. (1997) method was also modified to include the chemical-specific dermal absorption factor 

(ABS in Eq. 4-7), a term which accounts for the uptake (absorption) of a chemical across the 

skin and into the circulation (Table D4-2). 

Transfer coefficients used to estimate dermal dose from ornamental vegetation for Adult and 

Child Residents, Adult and Child Recreational Park Users, and Adult Gardeners (Table D4-1) 

are those applicable to intermediate-term contact with turf (USEPA 2001). The transfer 

coefficient used to calculate dermal dose to a home gardener (Table D4-1) is from USEPA et al. 

(1997). 

Dermal dose incurred by Agricultural Workers from post-application harvesting of commercial 

crops was calculated by applying USEPA et al. (1997) methods for a resident harvesting fruit 

(Eq. 4-6), but with a worker-appropriate exposure time (8 hours/day) and transfer coefficient (see 

following). Because the HRA needs to address virtually all crops grown in the State of 

California, but cannot characterize exposure from each crop type due to the sheer number and 

variety, a single transfer coefficient was developed from data provided in DPR (2009). 

Specifically, the set of all non-zero transfer coefficients in DPR (2009) (range of 100 cm 2 /h to 

16500 cm 2 /h) were evaluated to determine the distribution of best fit. The transfer coefficients 

were found to be consistent with a log-normal distribution with a mean of 2144 cm 2 /hour and a 

standard deviation of 3712 cm 2 /hour. The seventy-fifth percentile of the distribution, 2371 

cm 2 /hour, was selected as a transfer coefficient to represent typical foliage contact activities of 

an Agricultural Worker. Dermal doses incurred by Nursery/Program Workers from postapplication 

contact with ornamental vegetation were calculated in a manner consistent with the 

approach described for Agricultural Workers. The 75th percentile value of the distribution of 

transfer coefficients from DPR (2009) data was used for these workers as well (2371 cm 2 /hour), 


SECTION D4 


because the very limited number of available transfer coefficients for ornamental vegetation 

precluded the development of a separate distribution for these workers. 

D4.3.1.1.1 Accidental Ingestion 

The LBAM pheromone-containing twist ties are designed to be hung in trees or similar 

vegetation at a height of 6 to 10 feet (OEHHA 2009b). While unlikely, it is possible that a child 

might obtain one of the twist ties and chew on it, thus receiving a dose of the LBAM 

pheromones. To evaluate the dose of pheromone that a child might incur from this process, 

OEHHA (2009b) assumed that 25% of the total mass of pheromone active ingredients could be 

ingested. The quantity of active ingredient available for ingestion was calculated by OEHHA 

from manufacturers information that each twist tie contains 188 mg of chemicals, of which 95% 

is active ingredient. The dose can be estimated by equation 4-8: 

Equation D4-8 

intake from direct ingestion (twist ties) 

IF = (T × pAI × pI )/(BW) 

Where: 

IF = Intake from direct ingestion of twist ties milligram (mg)/kilogram 

(kg) 

T = Total chemical ingredients, 188 milligrams (mg) 

pAI = percent active ingredient, 0.95 (unitless) 

pI = percent active ingredient available for ingestion, 0.25 (unitless) 

BW = Body Weight child, 18 kg 

D4.3.2 Intake Parameters 

The exposure parameters given in Table D4-1 represent a combination of average and “highend” 

assumptions. For all receptor populations, exposure was calculated first as a pathwayspecific 

intake, which accounts for an environmental medium-specific intake (such as a 

breathing rate of air), as well as for exposure frequency, exposure duration, body weight, and 

averaging time (see preceding section). 

Table D4-1 

Exposure Assumptions 

Potentially Exposed Populations 

Commercial Resident Recreational Park User 

Nursery/ 

Agricultural 

Program 

Adult 

Worker 

Parameter Symbol Worker 

Gardener Adult Child Adult Child 

Target Risk TR 1.0E-06 a 1.0E-06 a 1.0E-06 a 1.0E-06 a 1.0E-06 a 1.0E-06 a 1.0E-06 a 

Target Hazard 

Quotient HI 1 a 1 a 1 a 1 a 1 a 1 a 1 a 

Inhalation of Vapors and Particulates - Chronic Exposures 

Inhalation Rate 

(m 3 /hour) IRhour 1.3 b 1.3 b 1.6 c 0.79 d 0.34 e 1.6 c 1.2 f 




DRAFT PEIR 


Table D4-1 




Parameter 

Symbol 

Nursery/ 

Program 

Worker 

Agricultural 

Worker 

Adult 


Exposure Time 

(hours/day) ET 8 a 8 a 2 g 24 a 24 a 2 h 2 h 


(m 3 /day) IRday 10 i 10 i 3.2 i 19 i 8.1 i 3.2 i 2.4 i 

Exposure Frequency 

(days/year) EF 245 a 245 a 100 j 350 a 350 a 100 k 100 k 

Inhalation of Vapors and Particulates - Subchronic Exposures 



Exposure Time 

(hours/day) ET 8 a 8 a 2 g 24 a 24 a 2 h 2 h 


(m 3 /day) IRday 10.4 i 10.4 i 3.2 i 19 i 8.1 i 3.2 i 2.4 i 

Exposure Duration 

(weeks) ED 6 l 6 l 6 l 6 l 6 l 6 l 6 l 


(days/week) EF 5 a 5 a 7 a 7 a 7 a 2 k 2 k 

Averaging Time 

(days) AT 270 m 270 m 270 m 270 m 270 m 270 m 270 m 

Inhalation of Vapors and Particulates - Acute Exposures 



Exposure Time 

(hours/day) ET 1 1 1 1 1 1 1 


(days) EF 1 1 1 1 1 1 1 


(days) AT 1 1 1 1 1 1 1 

Ingestion of Soil 

Ingestion Rate 

(mg/day) IR 100 a 100 a 107 n 107 n 157 n 54 o 79 o 



Conversion Factor 

(kg/mg) CF 1.0E-06 1.0E-06 1.0E-06 1.0E-06 1.0E-06 1.0E-06 1.0E-06 

Dermal Contact with Soil 

Surface Area 

(cm 2 /day) SA 5,800 p 5,800 p 5,500 p 4,700 p 2,778 p 4,700 p 2,778 p 

Adherence Factor 

(mg/cm 2 ) AF 0.5 q 0.5 q 0.3 q 0.2 a 0.2 a 0.2 a 0.2 a 

Absorption Factor 

(unitless) 

ABS 

r 

r 



r 

r 

r 

r 

chemspec 

chemspec 

chemspec 

chemspec 

chemspec 

chemspec 

chemspec 

r 


SECTION D4 


Table D4-1 


Parameter 

Symbol 

Nursery/ 

Program 

Worker 



Agricultural 

Worker 

Adult 



(kg/mg) CF 1.0E-06 1.0E-06 1.0E-06 1.0E-06 1.0E-06 1.0E-06 1.0E-06 

Ingestion of Commercial Crops 

Ingestion Rate 

Commercially Grown 

Produce (g/day) IR NA NA 346 s 346 s 108 s 346 s 108 s 

Ingestion Rate of 

Produce 

(g/kg bw-day) IR NA NA 6.46 t 6.46 t 7.08 t 6.46 t 7.08 t 

Fraction of Exposed 

Commercially Grown 

Produce FEcc NA NA 0.85 u 0.85 u 0.85 u 0.85 u 0.85 u 


(days/year) EF NA NA 350 a 350 a 350 a 350 a 350 a 


(kg/g) CF NA NA 1.0E-03 1.0E-03 1.0E-03 1.0E-03 1.0E-03 

Dermal Contact with Commercial Crops 

Transfer Coefficient 

(cm 2 /hour) Tc NA 2,371 v NA NA NA NA NA 

Exposure Time 

(hours/day) ET NA 8 a NA NA NA NA NA 


(unitless) ABS NA 

chemspec 

r NA NA NA NA NA 


(days/year) EF NA 245 a NA NA NA NA NA 


(m 2 /cm 2 ) CF NA 1.0E-04 NA NA NA NA NA 

Ingestion of Homegrown Produce 


Homegrown Produce 

(g/day) IR NA NA 61 w 61 w 19 w NA NA 


Produce (g/kg bwday) 

IR NA NA 6.46 t 6.46 t 7.08 t NA NA 

Fraction of Exposed 

Homegrown Produce FEhp NA NA 0.15 x 0.15 x 0.15 x NA NA 


(days/year) EF NA NA 350 a 350 a 350 a NA NA 


(kg/g) CF NA NA 1.0E-03 1.0E-03 1.0E-03 NA NA 

Dermal Contact with Homegrown Produce 


(cm 2 /hour) Tc NA NA 10,000 y NA NA NA NA 

Exposure Time 

(hours/day) ET NA NA 0.67 y NA NA NA NA 




DRAFT PEIR 


Table D4-1 




Parameter 

Symbol 

Nursery/ 

Program 

Worker 

Agricultural 

Worker 

Adult 



(unitless) ABS NA NA 

chemspec 

r NA NA NA NA 


(days/year) EF NA NA 100 j NA NA NA NA 


(m 2 /cm 2 ) CF NA NA 1.0E-04 NA NA NA NA 

Dermal Contact with Ornamental Vegetation 


(cm 2 /hour) Tc 2,371 v NA 7,300 y 7,300 y 2,600 y 7,300 y 2,600 y 

Exposure Time 

(hours/day) ET 8 a NA 2 y 2 y 2 y 2 y 2 y 


(unitless) 

ABS 

chemspec 

r NA 


(days/year) EF 245 a NA 100 j 350 a 350 a 100 k 100 k 


(m 2 /cm 2 ) CF 1.0E-04 NA 1.0E-04 1.0E-04 1.0E-04 1.0E-04 1.0E-04 

Population-Specific Assumptions _Chronic Exposures 

Exposure Duration 

(years) ED 7 z 7 z 7 z 7 z 7 z 7 z 7 z 

Body Weight (kg) BW 70 aa 70 aa 63 aa 63 aa 18 aa 63 aa 18 aa 

Averaging Time for 

Carcinogens (days) ATc 25,550 ab 25,550 ab 25,550 ab 25,550 ab 25,550 ab 25,550 ab 25,550 ab 


(chronic) for 

Noncarcinogens 

(days) ATnc 2,555 ac 2,555 ac 2,555 ac 2,555 ac 2,555 ac 2,555 ac 2,555 ac 

Notes: 

NA = Not applicable 

m 2 = squared meters; m 3 = cubic meters; mg = milligram; kg = kilogram; cm 2 = square centimeters; g = grams; bw = body weight 

a Cal/EPA 2003a 

b Cal/EPA 2003a, Chapter 5, Table D5.4; inhalation rate for an off-site worker. 

c USEPA 1997, Table D5-23. It was assumed that an adult gardener or an adult park user has an inhalation rate corresponding to a moderate activity level in short-term 

exposures. 

d Calculated based on the 80th percentile value for inhalation rate of 302 L/kg-day (Cal/EPA, 2003) and the body weights listed under Population-Specific Assumptions in 

this table. 

e Cal/EPA 2003a, Chapter 5, Table D5.4; average inhalation rate for a child, under the 9-year exposure scenario. 

f USEPA 1997, Table D5-23. It was assumed that a child park visitor has an inhalation rate corresponding to a moderate activity level. 

g It is assumed that a home gardener spends two hours gardening. 

h Adult and child park visitors are assumed to visit a developed park for two hours/day. 

i Value represents the hourly inhalation rate multiplied by the exposure time. 

j Assumes home gardener gardens two days/week for 50 weeks/year based on a year-around growing season in California 

k Assumes adult and child park users visit a park two days/week for 50 weeks/year. 

l CDFA 2009. Personal communication. 

m Averaging time is equal to the number of days in the exposure duration, and depends on the Alternative (No Program and Organic Alternatives[42 days]; MD-1 [90 

days]; MD-2 and MMA [60 days]; and MD-3 [30 days].. 

n Cal/EPA 2003a. Values were calculated from the soil ingestion rate and the body weights listed under Population-Specific Assumptions in this table. 

o Soil ingestion rate was assumed to be one-half the soil ingestion rate used for the adult resident and the child resident based on the lower exposure time of park use. 

p Cal/EPA 2003a, Table D5-6. The high-end value for a 30-year exposure duration was used for the gardener (refer to Excel table). 

q USEPA 2004. Exhibit 3-3. 95th percentile value for gardening activities for residential adults and for nursery/agricultural workers and adult gardeners, respectively. 

r The chemical-specific dermal absorption factors are as presented in Table D4.2. 

r 

r 

r 

r 

chemspec 

chemspec 

chemspec 

chemspec 

chemspec 

r 


SECTION D4 


Table D4-1 


Parameter 

Symbol 

Nursery/ 

Program 

Worker 



Agricultural 

Worker 

Adult 


s Amount of commercial produce ingested assumes ingestion of leafy and exposed produce only, as listed in HotSpots Table D5.10. Value is derived by multiplying the 

sum of the average values for daily produce ingestion in grams of produce/kg BW-day for leafy and exposed produce, by the fraction of consumed produced assumed to 

be commercially grown. 

t Cal/EPA 2003a. Conservative estimate based on Table D5.10. 

u Cal/EPA 2003a, page 5-21. The fraction of ingested produce which is commercially grown is assumed to be the fraction remaining after subtracting the amount for 

homegrown produce in non-urban (0.15) sites, or 0.85 . 

v Derived from data in DPR 2009. See equation 4-7 of this report. 

w Amount of total produce ingested assumes ingestion of leafy and exposed produce only, as listed in Cal/EPA 2003 Table D5.10. Value is derived by multiplying the 

sum of the average consumption rate of leafy and exposed produce in g/kg BW-day by the fraction of produce assumed to be homegrown in an urban setting, 0.15. 

x Cal/EPA 2003a, page 5-21. The fraction of ingested produce which is homegrown for urban and non-urban sites: 0.052 and 0.15, respectively. 

y USEPA 2001. 

z CDFA 2008. The exposure duration is based on the currently-proposed length of the LBAM eradication program, which is scheduled to begin in 2009 and extend 

through 2015. 

aa Cal/EPA (2003a), Table D5-6. 

ab Averaging time for carcinogens is equal to 365 days times 70 years. 

ac Averaging time for non-carcinogens is equal to the number of days in the exposure duration of 7 years. 

Sources: 

California Environmental Protection Agency (Cal/EPA). 2003a. Air Toxics "Hot Spots" Program Risk Assessment Guidelines Part, The Air Toxics Hot Spots Program 

Guidance Manual for Preparation of Health Risk Assessments. August. Appendix 1. Sacramento, California. January. 

California Environmental Protection Agency (Cal/EPA). 2003b. Air Resources Board Recommended Interim Risk Management Policy for Inhalation -Based Residential 

Cancer Risk. Sacramento, CA. October 9. 

Department of Pesticide Regulation (DPR). 2009. Exposure Assessment Policy and Procedure - Default Transfer Coefficients. Memorandum from J.P. Frank to All Staff, 

Worker Health and Safety Branch. 

United States Environmental Protection Agency (USEPA). 1997. Exposure Factors Handbook. Volume I - General Factors. EPA/600/P-95/002Fa. August. 

United States Environmental Protection Agency (USEPA). 2001. Science Advisory Council for Exposure. Policy Number 12. Recommended Revisions to the Standard 

Operating Procedures (SOPs) for Residential Exposure Assessments. February 22, 2001. 

United States Environmental Protection Agency (USEPA). 2004. RAGS Part E - See footnote for Table D4-2. 

United States Environmental Protection Agency (USEPA). 2009. Permethrin HED reference footnote for Table D4-2. 

Table D4-2 lists the chemical-specific dermal absorption factors used to estimate dermal dose 

from soil or vegetation. 

Table D4-2 

Dermal Absorption Factors 

Chemical Dermal Absorption Factor (unitless) Source 

HERCON (LBAM pheromone) 0.1 USEPA 2004 

SPLAT (LBAM pheromone) 0.1 USEPA 2004 

Isomate (LBAM pheromone) 0.1 USEPA 2004 

Btk NA* McClintock 1995 

Spinosad 0.01 IPCS 2001 

Permethrin 0.15 USEPA 2005 

Lambda-Cyhalothrin 0.1 USEPA 2004 

Chlorpyrifos 0.03 USEPA 2006 

Ethylbenzene 0 USEPA 2004 

1,2,4-Trimethylbenzene 0 USEPA 2004 

Notes: 

NA = Not Applicable 




DRAFT PEIR 


Table D4-2 

Dermal Absorption Factors 

Chemical Dermal Absorption Factor (unitless) Source 

*Btk is not dermally absorbed. Exposure via dermal absorption is not evaluated 

Sources: 

International Programme on Chemical Safety (IPCS). 2001. Pesticide Residues in Food. Toxicological Evaluations. 

Spinosad.http://www.inchem.org/documents/jmpr/jmpmono/2001pr12.htm 

McClintock, J. T., Schaffer, C. R., and Sjoblad, R. D. 1995. A comparative review of the mammalian toxicity of Bacillus thuringiensis-based pesticides. Pesticide 

Science 45:95-105. World Health Organization (WHO). 1999. Microbial pest control agent: Bacillus thuringiensis. Environmental Health Criteria 217. 

United States Environmental Protection Agency (USEPA), 2004. Risk Assessment Guidance for Superfund. Volume I. Human Health Evaluation Part E. Supplemental 

Guidance for Dermal Risk Assessment. Final. EPA/540/99/005 

United States Environmental Protection Agency (USEPA), 2005. Permethrin: HED chapter of the reregistration eligibility decision document. PC Code 2, case no. 

2510, DP Barcode D357566. 

United States Environmental Protection Agency (USEPA), 2006. Reregistration Eligibility Decision for Chlorpyrifos. Office of Pesticide Programs. July 31 

2006.http://www.epa.gov/oppsrrd1/REDs/chlorpyrifos_ired.pdf 

Pathway-specific intake factors for each receptor population are provided in Table D4-3. 

Chemical-specific intake quantities are provided in the discussion of each alternative. Those 

intakes were calculated by multiplying each of the pathway-specific intakes listed in Table D4-3 

by the appropriate EPC (provided for each alternative -see following). The total exposure of a 

given receptor population to a chemical or group of chemicals (as appropriate) was calculated by 

summing chemical-specific intakes from all pathways. 

Table D4-3 

Intake Factors 


Exposure 

Pathway 

Nursery/Program 

Worker 

Agricultural 

Worker 

Residential 

Gardener 

Adult 

Resident 

Child 

Resident 

Adult 

Recreational 

Park User 

Child 

Recreational 

Park User 

CARCINOGENIC 

AIR 

SOIL 

Inhalation of 

Vapors 

(m³/kg-day) 9.97E-03 9.97E-03 1.39E-03 2.89E-02 4.32E-02 1.39E-03 3.65E-03 


(kg/kg-day) 9.59E-08 9.59E-08 4.65E-08 1.63E-07 8.34E-07 2.33E-08 1.20E-07 

Dermal Contact 

with Soil 

(kg/kg-day) a 2.78E-06 2.78E-06 7.18E-07 1.43E-06 2.96E-06 4.09E-07 8.46E-07 

VEGETATION 

Ingestion of 

Commercial 

Produce 

(kg/kg-day) NC NC 5.27E-04 5.27E-04 5.77E-04 5.27E-04 5.77E-04 


with Commercial 

Produce 

(m 2 /kg-day) a NC 1.82E-03 NC NC NC NC NC 

Ingestion of 

Homegrown 

Produce NC NC 9.29E-05 9.29E-05 1.02E-04 NC NC 


SECTION D4 


Table D4-3 



Exposure 

Pathway 


Worker 

Agricultural 

Worker 

Residential 

Gardener 

Adult 

Resident 

Child 

Resident 

Adult 

Recreational 

Park User 

Child 

Recreational 

Park User 

(kg/kg-day) 


with Homegrown 

Produce 

(m 2 /kg-day) a NC NC 2.91E-04 NC NC NC NC 


with Ornamental 

Vegetation 

(m 2 /kg-day) a 4.44E-03 NC 6.35E-04 2.22E-03 2.77E-03 6.35E-04 7.91E-04 

NONCARCINOGENIC 

AIR 

Inhalation of 

Vapors 


Subchronic 

Inhalation of 

Vapors 


Acute Inhalation of 

Vapors 


SOIL 


(kg/kg-day) 9.59E-07 9.59E-07 4.65E-07 1.63E-06 8.34E-06 2.33E-07 1.20E-06 


with Soil 

(kg/kg-day) a 2.78E-05 2.78E-05 7.18E-06 1.43E-05 2.96E-05 4.09E-06 8.46E-06 

VEGETATION 

Ingestion of 

Commercial 

Produce 

(m 2 /kg-day) a NC NC 5.27E-03 5.27E-03 5.77E-03 5.27E-03 5.77E-03 


with Commercial 

Produce 

(kg/kg-day) a NC 1.82E-02 NC NC NC NC NC 

Ingestion of 

Homegrown 

Produce 

(kg/kg-day) NC NC 9.29E-04 9.29E-04 1.02E-03 NC NC 


with Homegrown 

Produce 

(m 2 /kg-day) a NC NC 2.91E-03 NC NC NC NC 


with Ornamental 

Vegetation 

(m 2 /kg-day) a 4.44E-02 NC 6.35E-03 2.22E-02 2.77E-02 6.35E-03 7.91E-03 

Notes: 




DRAFT PEIR 


Table D4-3 


Exposure 

Pathway 


Worker 

Agricultural 

Worker 


Residential 

Gardener 

Adult 

Resident 

Child 

Resident 

Adult 

Recreational 

Park User 

Child 

Recreational 

Park User 

m 3 = cubic meter kg = kilogram 

NC = pathway not calculated for the receptor. 

a To calculate chemical specific intake factors via dermal contact with soil, produce, and vegetation multiply listed value by chemical specific dermal absorption 

fraction listed in Table D4-2. 

D4.4 HUMAN RECEPTOR POPULATIONS 

To quantify the potential health effects of Program chemicals and biological insecticides, five 

hypothetical receptor populations were identified: Nursery/Program Workers, Agricultural 

Workers, Residents (adult and child), Adult Gardeners, and Recreational Park Users (adult and 

child). The rationale for selecting each of these populations for evaluation, and the exposure 

pathways evaluated for each receptor population are discussed below. 

D4.4.1 

Nursery/Program Workers 

Nursery/Program Workers are individuals who may be exposed to chemical or biological 

pesticides to control LBAM while working in nurseries or other locations where infestations of 

LBAM are a concern. Although Nursery/Program Workers will wear protective clothing to 

minimize or prevent any significant exposures from occurring during application, potential 

exposure of this receptor population was assessed to address exposures that may occur after 

application has ended. Immediately following spray application, these workers may inhale a 

chemical that is present in ambient air (acute inhalation). Nursery/Program Workers may also 

incur exposures to residual material present in air from repeated applications (subchronic 

inhalation). Chronic inhalation exposure may occur due to potential persistence and/or 

resuspension of a chemical from soil or vegetation. Nursery/Program Workers may also be 

exposed by the incidental ingestion of soil where chemicals have deposited, and by dermal 

contact with soil, and dermal contact with ornamental vegetation. These latter pathways are 

evaluated under the assumption that these exposures occur for extended periods of time. 

D4.4.2 Agricultural Workers 

Agricultural Workers represent a population that may be exposed to chemical or biological 

pesticides to control LBAM while working in agriculture and engaged in activities such as 

harvesting commercial food crops The exposure pathways evaluated for Agricultural Workers 

are the same as those considered for Nursery/Program Workers, except that dermal uptake of 

chemicals by contact with contaminated commercial crops is evaluated instead of dermal uptake 

from contact with ornamental vegetation. 

D4.4.3 

Adult and Child Residents 

Because the LBAM infestation area may encompass residential neighborhoods, potential 

exposures to chemical and biological insecticides were also calculated for residential receptor 

populations. Separate exposure estimates were developed for adults and for children that may 

reside in the Program Area. Children were evaluated as a separate population using child-specific 


SECTION D4 


exposure factors, which addresses the fact that relative to adults, children have a greater skin 

surface area that may come in contact with soil or vegetation, and greater soil and food ingestion 

rates (see Table D4-1). These higher intakes, attributable to anatomical differences as well as 

activity and behavior patterns that are distinct from adults (OEHHA 2003), make children 

potentially more vulnerable (sensitive) to any health effects of insecticides. The child resident 

represents one of two sensitive populations evaluated. Exposures of Adult and Child Residents to 

insecticides may potentially occur by acute, subchronic, or chronic inhalation; by incidental 

ingestion of soil; by ingestion of home-grown or commercial produce; or by dermal contact with 

home-grown produce or ornamental vegetation. 

D4.4.4 

Adult Gardeners 

The characteristics of this receptor population were developed to evaluate a hypothetical adult 

who may receive higher exposures than an adult Resident by virtue of their activities in a home 

garden. While the relevant exposure pathways for this receptor population are the same as for an 

adult Resident, exposure of this population was assessed by incorporating higher breathing rates 

than were used for residential receptors (Table D4-1) to address the possibility that gardening is 

associated with a higher activity level than is typical for an average Resident. The estimation of 

dermal dose for this receptor population also utilized a higher transfer coefficient than for the 

Adult Resident, reflecting the likelihood that gardeners will engage in a greater frequency of 

activities that bring them into contact with contaminated foliage. 

D4.4.5 

Adult and Child Recreational Park Users 

Potential exposure of individuals who may recreate in areas treated for LBAM infestation was 

evaluated for a hypothetical Recreational Park User. As with the residential receptor population, 

separate exposure parameters were developed for adults and for children. As discussed in Section 

D4.3.3, anatomical and behavioral characteristics of children can lead to relatively greater 

exposures than adults, which may leave children more vulnerable to any health effects of 

insecticide exposure. Thus, the child Recreational Park User represents the second sensitive 

receptor population evaluated. Exposure of recreational populations to chemical or biological 

insecticides may occur by acute, subchronic, or chronic inhalation, by ingestion of soil, ingestion 

of commercial food crops is shown on Figure D4-1, or by dermal contact with soil and 

contaminated ornamental vegetation. 

D4.5 NO PROGRAM ALTERNATIVE 

For this alternative, exposures were evaluated for all of the receptor populations noted above. 

Potential acute, subchronic, and chronic inhalation exposures of human receptor populations to 

spinosad, Btk, lambda-cyhalothrin, chlorpyrifos, and permethrin were estimated from the 

corresponding air concentrations (EPCs) listed in Table D4-4. Inhalation exposures are 

consistent with the ground-based method of application of the chemicals, which would generate 

airborne quantities that could be inhaled during and immediately after application (acute 

inhalation exposure). Figure D4-1 is a conceptual site model (CSM) that provides a diagram of 

potential exposure routes for this alternative. This CSM is consistent with product labels that 

limit application technologies to the use of backpack and/or truck-mounted sprayers (or their 

equivalent). The potential persistence of residual amounts of chemicals in the environment, 

followed by volatilization or resuspension from soils or vegetation, could contribute to inhalation 

exposures over longer periods of time. These potential exposures were addressed by quantifying 

subchronic and chronic inhalation exposure. Because application could also lead to residues on 




DRAFT PEIR 


soil and vegetation that may persist for extended periods of time, potential exposure was 

evaluated by estimating the dose that could result from incidental ingestion of soil, dermal 

contact with soil, ingestion of commercially grown and home-grown produce, dermal contact 

with commercially grown and home-grown produce, and dermal contact with ornamental 

vegetation (lawns, shrubs). The EPCs used to estimate dose for the noninhalation exposure 

pathways are also listed in Table D4-4. Chemical-specific intakes for Nursery/Program Workers 

and for Agricultural Workers are given in Table D4-5 and 4-6, respectively. The corresponding 

values for Adult and Child Residents are given in Table D4-7 and 4-8; for the Adult Gardener, in 

Table D4-9; and for the Adult and Child Recreational Park Users in Tables D4-10 and D4-11. 


SECTION D4 


Figure D4-1 

Conceptual Site Model for Potential Exposure Pathways for Chemicals Released by the Male Moth Attractant, Organic Treatment, sand No Program Alternatives 



DRAFT PEIR 





SECTION D4 


Table D4-4 

Exposure Point Concentrations – No Program Alternative 

Air 

(mg/m 3 ) 

Environmental Media 

Ground Conventional Applications 

Deposition Rate 

(mg/m 2 ) 

Soil 

(mg/kg-soil) 

Vegetation 

(mg/kg-veg) 

Chemical Acute Subchronic Chronic Chronic Chronic Chronic 

Btk 8.17E-03 1.36E-04 1.36E-04 1.36E+02 6.79E-01 1.36E+01 

Spinosad 3.24E-04 9.64E-07 9.64E-07 2.05E+00 1.32E-01 2.05E-01 

Permethrin 1.51E-03 4.49E-06 4.49E-06 1.84E+01 1.19E+00 1.84E+00 

Lambda- 

Cyhalothrin 3.08E-04 9.16E-07 9.16E-07 2.58E+00 1.66E-01 2.58E-01 

Chlorpyrifos 6.68E-03 3.37E-04 3.37E-04 8.78E+00 1.21E+00 8.78E-01 

Table D4-5 

Chemical-Specific Intakes Factors for Nursery/Program Workers – No Program Alternative 

Lifetime Carcinogenic Average Daily Intakes 

Noncarcinogenic Intakes 

Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Air 

Soil 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Units: mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d 

Btk 

Spinosad 

Permethrin 

Lambda- 

Cyhalothrin 

Chlorpyrifos 

--- --- --- --- 

--- --- --- --- 

4.48E- 

08 

8.82E- 

09 

3.84E- 

08 

5.02E-03 

--- --- --- --- 

--- --- --- --- 

mg/kgd 

1.36E- 

05 

9.61E- 

08 

4.48E- 

07 

9.13E- 

08 

3.36E- 

05 

1.44E-05 

1.02E-07 

4.76E-07 

9.72E-08 

3.58E-05 

1.52E- 

04 

6.02E- 

06 

2.80E- 

05 

5.72E- 

06 

6.51E- 

07 

9.83E- 

09 

8.82E- 

08 

1.24E- 

08 

mg/kg-d 

--- --- 

Notes: 

--- = Not Applicable 

NE = Not evaluated because permethrin is registered by the USEPA primarily for as a termiticide and on non-food crops (Etigra. 2007. Product Label for 

Permethrin E-Pro. Revised July 9, 2007). 

mg/kg-d = milligram per kilogram - day 

1.24E- 

04 

4.21E- 

08 

2.85E- 

09 

3.84E- 

07 

3.59E- 

08 

3.66E- 

08 

3.73E-04 

5.02E-02 

4.69E-03 

4.79E-03 




DRAFT PEIR 


Table D4-6 

Chemical-Specific Intakes Factors for Agricultural Workers – No Program Alternative 


Exposure 

Medium: 

Air Soil Ornamental Vegetation 

Pathways: Inhalation Incidental Ingestion Dermal Contact Dermal Contact 

Units: mg/kg-d mg/kg-d mg/kg-d mg/kg-d 

Btk --- --- --- --- 

Spinosad --- --- --- --- 

Permethrin 4.48E-08 8.82E-09 3.84E-08 NE 

Lambda- 

Cyhalothrin 

--- --- --- --- 

Chlorpyrifos --- --- --- --- 


Air 

Soil 

Ornamental 

Vegetation 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Units: mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d 

Btk 1.36E-05 1.44E-05 1.52E-04 6.51E-07 --- --- 

Spinosad 9.61E-08 1.02E-07 6.02E-06 9.83E-09 2.85E-09 3.73E-04 

Permethrin 4.48E-07 4.76E-07 2.80E-05 8.82E-08 3.84E-07 NE 

Lambda- 

Cyhalothrin 

9.13E-08 9.72E-08 5.72E-06 1.24E-08 3.59E-08 4.69E-03 

Chlorpyrifos 3.36E-05 3.58E-05 1.24E-04 4.21E-08 3.66E-08 4.79E-03 

Notes: 





Table D4-7 

Chemical-Specific Intakes for Adult Residents – No Program Alternative 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce - 

Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 


Btk --- --- --- --- --- --- 

Spinosad --- --- --- --- --- --- 

Permethrin 1.30E-07 1.50E-08 1.97E-08 6.13E-03 NE NE 

Lambda- 

Cyhalothrin 

--- --- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- --- 


Exposure Medium: Air Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 


SECTION D4 


Table D4-7 

Chemical-Specific Intakes for Adult Residents – No Program Alternative 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 


Btk 3.94E-05 4.11E-05 1.03E-04 1.11E-06 --- --- 7.15E-02 1.26E-02 

Spinosad 2.79E-07 2.91E-07 4.07E-06 1.67E-08 1.47E-09 4.56E-04 1.08E-03 1.90E-04 

Permethrin 1.30E-06 1.35E-06 1.90E-05 1.50E-07 1.97E-07 6.13E-02 NE NE 

Lambda- 

Cyhalothrin 

2.65E-07 2.76E-07 3.87E-06 2.10E-08 1.85E-08 5.73E-03 1.36E-03 2.40E-04 

Chlorpyrifos 9.75E-05 1.02E-04 8.40E-05 7.16E-08 1.88E-08 5.85E-03 4.62E-03 8.16E-04 

Notes: 





Table D4-8 

Chemical-Specific Intakes for Child Residents – No Program Alternative 

Exposure 

Medium: 

Pathways: 

Air 

Inhalation 

Incidental 

Ingestion 


Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 


Btk --- --- --- --- --- --- 

Spinosad --- --- --- --- --- --- 


Lambda- 

--- --- --- --- --- --- 

Cyhalothrin 

Chlorpyrifos --- --- --- --- --- --- 


Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 


Btk 5.87E-05 6.13E-05 1.53E-04 5.67E-06 --- --- 7.84E-02 1.38E-02 



Lambda- 

Cyhalothrin 

3.95E-07 4.12E-07 5.78E-06 1.08E-07 3.82E-08 7.15E-03 1.49E-03 2.63E-04 

Chlorpyrifos 1.45E-04 1.52E-04 1.25E-04 3.66E-07 3.90E-08 7.30E-03 5.07E-03 8.94E-04 

Notes: 








DRAFT PEIR 


Table D4-9 

Chemical-Specific Intakes for Residential Adult Gardener – No Program Alternative 


Exposure 

Medium: Air Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

Units: mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d 

Btk --- --- --- --- --- --- --- 

Spinosad --- --- --- --- --- --- --- 

Permethrin 6.25E-09 4.28E-09 9.90E-09 1.75E-03 NE NE NE 

Lambda- 

Cyhalothrin 

--- --- --- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- --- --- 


Exposure Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

Units: mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d 

Btk 1.89E-06 6.92E-06 2.07E-04 3.16E-07 --- --- 7.15E-02 1.26E-02 --- 

Spinosad 1.34E-08 4.90E-08 8.23E-06 4.77E-09 7.36E-10 1.30E-04 1.08E-03 1.90E-04 5.97E-05 

Permethrin 6.25E-08 2.28E-07 3.83E-05 4.28E-08 9.90E-08 1.75E-02 NE NE NE 

Lambda- 

Cyhalothrin 

1.27E-08 4.65E-08 7.82E-06 6.00E-09 9.26E-09 1.64E-03 1.36E-03 2.40E-04 7.52E-04 

Chlorpyrifos 4.69E-06 1.71E-05 1.70E-04 2.04E-08 9.45E-09 1.67E-03 4.62E-03 8.16E-04 7.67E-04 

Notes: 





Table D4-10 

Chemical-Specific Intakes for Adult Park User – No Program Alternative 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal Contact Ingestion Dermal Contact 

Units: mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d 

Btk --- --- --- --- --- 

Spinosad --- --- --- --- --- 

Permethrin 6.25E-09 2.14E-09 5.64E-09 NE 1.75E-03 

Lambda- 

--- --- --- --- --- 

Cyhalothrin 

Chlorpyrifos --- --- --- --- --- 


SECTION D4 


Table D4-10 

Chemical-Specific Intakes for Adult Park User – No Program Alternative 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 


Btk 1.89E-06 1.98E-06 2.07E-04 1.58E-07 --- 7.15E-02 8.63E-01 

Spinosad 1.34E-08 1.40E-08 8.23E-06 2.39E-09 4.19E-10 1.08E-03 1.30E-04 

Permethrin 6.25E-08 6.52E-08 3.83E-05 2.14E-08 5.64E-08 NE 1.75E-02 

Lambda- 

Cyhalothrin 

1.27E-08 1.33E-08 7.82E-06 3.00E-09 5.27E-09 1.36E-03 1.64E-03 

Chlorpyrifos 4.69E-06 4.89E-06 1.70E-04 1.02E-08 5.39E-09 4.62E-03 1.67E-03 

Notes: 


NE = Not evaluated because permethrin is registered by the USEPA primarily for as a termiticide and on non-food crops (Etigra. 2007. Product Label 

for Permethrin E-Pro. Revised July 9, 2007). 


Table D4-11 

Chemical-Specific Intakes for Child Park User – No Program Alternative 

Exposure 

Medium: 

Pathways: 

Air 

Inhalation 

Incidental 

Ingestion 


Soil 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 


Btk --- --- --- --- --- 

Spinosad --- --- --- --- --- 

Permethrin 1.64E-08 1.11E-08 1.17E-08 NE 2.18E-03 

Lambda- 

--- --- --- --- --- 

Cyhalothrin 

Chlorpyrifos --- --- --- --- --- 


Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 


Btk 4.97E-06 5.19E-06 5.45E-04 8.17E-07 --- 7.84E-02 --- 


Permethrin 1.64E-07 1.71E-07 1.01E-04 1.11E-07 1.17E-07 NE 2.18E-02 

Lambda- 

Cyhalothrin 

3.35E-08 3.49E-08 2.05E-05 1.55E-08 1.09E-08 1.49E-03 2.04E-03 

Chlorpyrifos 1.23E-05 1.28E-05 4.45E-04 5.28E-08 1.11E-08 5.07E-03 2.08E-03 




DRAFT PEIR 


Table D4-11 

Chemical-Specific Intakes for Child Park User – No Program Alternative 

Notes: 


NE = Not evaluated because permethrin is registered by the USEPA primarily for as a termiticide and on non-food crops (Etigra. 2007. Product Label 

for Permethrin E-Pro. Revised July 9, 2007). 


D4.6 MATING DISRUPTION (MD) ALTERNATIVE 

The MD Alternative considers the application of the LBAM pheromone by three different 

methods. For urban infestations and for small and isolated areas, a ground treatment will be used 

that relies on pheromone-containing twist ties (MD-1). Ground-based applications of 

pheromones to trees and utility poles via specialized application equipment will also be 

conducted (MD-2). Figure D4-2 depicts the potential exposure routes for each receptor 

population for the ground-based applications considered for this alternative. Aerial application 

(MD-3) may be used for heavily infested, inaccessible areas such as forested and agricultural 

lands; Figure D4-3 presents the potential exposure routes for each receptor population for the 

proposed aerial application of the pheromone-containing products SPLAT and HERCON. 

D4.6.1 

Alternative MD-1 

For this alternative, exposures were evaluated for of all of the receptor populations described in 

Section D4.3. Potential exposure to human populations from acute, subchronic, and chronic 

inhalation exposures that may result from the use of pheromone-containing twist ties were 

estimated from the EPCs listed in Table D4-12. Inhalation exposures are consistent with the 

volatile nature of the LBAM pheromones, which are formulated as Isomate to release low 

quantities of pheromones over time. Inhalation intakes of pheromones released from Isomate for 

Nursery/Program Workers and for Agricultural Workers are given in Table D4-13; for Adult and 

Child residents in Table D4-14; for the Adult Gardener in Table D4-15; and for the Adult and 

Child Recreational Park Users in Table D4-16. The intake of pheromones from the accidental 

ingestion of a twist tie by a child (calculated as per Eq. 4-8) is equal to 2.5 mg/kg. 

Table D4-12 

Exposure Point Concentrations – Mating Disruption Alternative, Twist Ties 


Twist Ties 

Air 

(mg/m 3 ) 

Soil 

(mg/kg-soil) 


(mg/m 2 ) 

Vegetation 

(mg/kg-veg) 

Chemical Acute Subchronic Chronic Chronic Acute Chronic 

Isomate 

(LBAM pheromones) 3.22E-04 1.65E-05 1.65E-05 --- --- --- 

Table D4-13 

Chemical-Specific Intakes for Nursery/Program Workers and Agricultural Workers – Mating 

Disruption Alternative, Twist Ties 



Ornamental 

Vegetation 


SECTION D4 


Table D4-13 


Disruption Alternative, Twist Ties 


Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 



Isomate 

(LBAM pheromones) 

1.65E-06 1.75E-06 5.98E-06 --- --- --- 


Commercial 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 


Agricultural Workers 

Isomate 


Notes: 



1.65E-06 1.75E-06 5.98E-06 --- --- --- 

Table D4-14 

Chemical-Specific Intakes for Adult and Child Resident – Mating Disruption Alternative, 

Twist Ties 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 


Adult Resident 

Isomate 

(LBAM 

pheromones) 

Child Resident 

4.78E-06 4.98E-06 4.05E-06 --- --- --- --- --- 

Isomate 

(LBAM 7.12E-06 7.43E-06 3.09E-07 --- --- --- --- --- 

pheromones) 

Notes: 






DRAFT PEIR 




SECTION D4 


Figure D4-2 

Conceptual Site Model for Potential Exposure Pathways for Pheromones Released by Ground Application Methods through the Mating Disruption Alternative 



DRAFT PEIR 



Figure D4-3 

Potential Exposure Pathways for Pheromones Released by Aerial Application under the Mating Disruption Alternative 


SECTION 4 


Table D4-15 

Chemical-Specific Intakes for Residential Adult Gardener – Mating Disruption Alternative, 

Twist Ties 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 


Isomate 

(LBAM 

pheromones) 

Notes: 



2.30E-07 8.38E-07 8.17E-06 --- --- --- --- --- --- 

Table D4-16 

Chemical-Specific Intakes for Adult and Child Recreational Park User – Mating Disruption 

Alternative, Twist Ties 

Exposure 


Commercial 

Produce 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 


Adult Recreational Park User 

Isomate 

(LBAM 

pheromones) 

2.30E-07 2.40E-07 8.17E-06 --- --- --- --- 

Child Recreational Park User 

Isomate 

(LBAM 6.03E-07 6.29E-07 2.15E-05 --- --- --- --- 

pheromones) 

Notes: 



D4.6.2 Alternative MD-2 

Two pheromone formulations, SPLAT and HERCON, could be used in the ground-based 

component of this alternative. Potential exposure to human populations from acute, subchronic, 

and chronic inhalation exposures to LBAM pheromones that may result from the use of SPLAT 

and HERCON were estimated from the EPCs listed in Table D4-17. Inhalation exposures are 

consistent with the volatile nature of the pheromones, which are formulated to release low 

quantities of pheromones over time. Because the method of application may result in quantities 

of SPLAT or HERCON on soil or vegetation, incidental ingestion of soil, dermal contact with 

soil, dermal contact with commercial- or home-grown produce, and dermal contact with 

ornamental vegetation were also evaluated. Chemical-specific intakes of the pheromones present 

in SPLAT and HERCON for Nursery/Program Workers and for Agricultural Workers are given 

in Table D4-18; for Adult and Child Residents in Tables D4-19 and D4-20; for the Adult 




DRAFT PEIR 


Gardener in Table D4-21; and for the Adult and Child Recreational Park Users in Table D4-22 

and 4-23. 

Table D4-17 

Exposure Point Concentrations – Mating Disruption Alternative, Ground Application 


Air 

(mg/m 3 ) 

Soil 

(mg/kg-soil) 

Deposition 

Rate 

(mg/m 2 ) 

Vegetation 

mg/kg-veg) 


HERCON (LBAM 

pheromones) 3.54E-01 2.81E-03 2.81E-03 6.91E-02 1.38E+01 1.38E+00 

SPLAT (LBAM pheromones) 1.50E+00 5.85E-03 5.85E-03 1.04E-01 2.08E+01 2.08E+00 

Table D4-18 

Chemical-Specific Intakes for Nursery/Program and Agricultural Workers – Mating Disruption 

Alternative, Ground Application 



Ornamental 

Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 



HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

2.80E-04 2.98E-04 6.58E-03 6.63E-08 1.92E-07 2.51E-02 

5.83E-04 6.20E-04 2.78E-02 9.95E-08 2.89E-07 3.78E-02 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


2.80E-04 2.98E-04 6.58E-03 6.63E-08 1.92E-07 2.51E-02 

5.83E-04 6.20E-04 2.78E-02 9.95E-08 2.89E-07 3.78E-02 


SECTION D4 


Table D4-19 

Chemical-Specific Intakes for Adult Resident – Mating Disruption Alternative, Ground 

Application 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


8.12E-04 8.47E-04 4.46E-03 1.13E-07 9.89E-08 3.07E-02 7.28E-03 1.28E-03 

1.69E-03 1.76E-03 1.88E-02 1.69E-07 1.49E-07 4.61E-02 1.09E-02 1.93E-03 

Table D4-20 

Chemical-Specific Intakes for Child Resident – Mating Disruption Alternative, Ground 

Application 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Ingestion 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


1.21E-03 1.26E-03 6.65E-03 5.77E-07 2.05E-07 2.80E-02 

2.52E-03 2.63E-03 2.80E-02 8.66E-07 3.07E-07 4.20E-02 

3.83E- 

02 

5.75E- 

02 

7.98E-03 

1.20E-02 

1.41E-03 

2.11E-03 




DRAFT PEIR 


Table D4-21 


Ground Application 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


3.91E-05 1.43E-04 9.00E-03 3.22E-08 4.96E-08 8.78E-03 7.28E-03 1.28E-03 4.03E-03 

8.14E-05 2.97E-04 3.80E-02 4.83E-08 7.45E-08 1.32E-02 1.09E-02 1.93E-03 6.05E-03 

Table D4-22 

Chemical-Specific Intakes for Adult Park User – Mating Disruption Alternative, Ground 

Application 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


3.91E-05 4.07E-05 9.00E-03 1.61E-08 2.83E-08 7.28E-03 8.78E-03 

8.14E-05 8.48E-05 3.80E-02 2.42E-08 4.24E-08 1.09E-02 1.32E-02 


SECTION D4 


Table D4-23 

Chemical-Specific Intakes for Child Park User – Mating Disruption Alternative, Ground 

Application 



Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 


HERCON 


SPLAT 


Note: 


1.03E-04 1.07E-04 2.36E-02 8.31E-08 5.85E-08 7.98E-03 1.09E-02 

2.14E-04 2.23E-04 9.97E-02 1.25E-07 8.78E-08 1.20E-02 1.64E-02 

D4.6.3 

Alternative MD-3 

SPLAT and HERCON may also be applied by aerial application if infestations of LBAM 

develop in nonurban areas. Potential exposure to human populations from acute, subchronic, and 

chronic inhalation exposures to LBAM pheromones that may result from the application of 

SPLAT and HERCON were estimated from the EPCs listed in Table D4-24. Because aerial 

application may result in the deposition of SPLAT and HERCON onto soil and vegetation, 

incidental ingestion of soil, dermal contact with soil, dermal contact with commercial- or homegrown 

produce, and dermal contact with ornamental vegetation were also evaluated. Chemicalspecific 

intakes of the LBAM pheromones in SPLAT and HERCON for Nursery/Program 

Workers and for Agricultural Workers are given in Table D4-25; for Adult and Child Residents 

in Table D4-26; for the Adult Gardener in Table D4-27; and for the Adult and Child Recreational 

Park Users in Table D4-28. 

Table D4-24 

Exposure Point Concentrations – Mating Disruption Alternative, Aerial Application 

Chemical 

Air 

(mg/m 3 ) 


Pheromone Aerial Applications 

Soil 

(mg/kg-soil) 


(mg/m 2 ) 

Vegetation 

(mg/kg-veg 

Acute Subchronic Chronic Chronic Chronic Chronic 

HERCON 

(LBAM pheromones) 7.14E+03 6.23E-05 6.23E-05 2.92E-02 5.84E+00 5.84E-01 

SPLAT 

(LBAM pheromones) 2.63E-02 9.95E-05 9.95E-05 2.47E-02 4.94E+00 4.94E-01 




DRAFT PEIR 


Table D4-25 


Disruption Alternative, Aerial Application 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Units: mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-d mg/kg-day 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

6.22E-06 6.61E-06 1.33E-04 2.80E-08 8.13E-08 1.06E-02 

9.92E-06 1.06E-05 4.89E-04 2.37E-08 6.88E-08 8.99E-03 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


6.22E-06 6.61E-06 1.33E-04 2.80E-08 8.13E-08 1.06E-02 

9.92E-06 1.06E-05 4.89E-04 2.37E-08 6.88E-08 8.99E-03 


SECTION D4 


Table D4-26 

Chemical-Specific Intakes for Adult and Child Residents – Mating Disruption Alternative, 

Aerial Application 

Exposure 


Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 


Incidental 

Ingestion 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 



HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

1.80E-05 1.88E-05 8.98E-05 4.76E-08 4.18E-08 1.30E-02 3.08E-03 5.43E-04 

2.88E-05 3.00E-05 3.31E-04 4.03E-08 3.54E-08 1.10E-02 2.60E-03 4.59E-04 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


2.69E-05 2.80E-05 1.34E-04 2.44E-07 8.65E-08 1.62E-02 3.37E-03 5.95E-04 

4.29E-05 4.48E-05 4.93E-04 2.06E-07 7.32E-08 1.37E-02 2.85E-03 5.04E-04 

Table D4-27 


Aerial Application 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 


HERCON 

(LBAM 

pheromones) 

8.67E-07 3.17E-06 1.81E-04 1.36E-08 2.10E-08 3.71E-03 3.08E-03 5.43E-04 

SPLAT 

(LBAM 1.38E-06 5.05E-06 6.68E-04 1.15E-08 1.77E-08 3.14E-03 2.60E-03 4.59E-04 

pheromones) 

Note: 


Dermal 

Contact 

mg/kgd 

1.70E- 

03 

1.44E- 

03 




DRAFT PEIR 


Table D4-28 

Chemical-Specific Intakes for Adult and Child Recreational Park User – Mating Disruption 

Alternative, Aerial Application 



Commercial 

Produce 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 



HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

8.67E-07 9.04E-07 1.81E-04 6.81E-09 1.19E-08 3.08E-03 3.71E-03 

1.38E-06 1.44E-06 6.68E-04 5.76E-09 1.01E-08 2.60E-03 3.14E-03 


HERCON 

(LBAM 

pheromones) 

SPLAT 

(LBAM 

pheromones) 

Note: 


2.28E-06 2.37E-06 4.76E-04 3.51E-08 2.47E-08 3.37E-03 4.63E-03 

3.63E-06 3.79E-06 1.75E-03 2.97E-08 2.09E-08 2.85E-03 3.91E-03 


This alternative considers the application of the LBAM pheromone-containing formulation 

SPLAT and the permethrin-containing formulation Permethrin E-Pro. The formulation 

Permethrin E-Pro also contains the inert ingredients ethylbenzene, 1,2,4-trimethylbenzene, and 

triacetin. Application of this combination of chemicals by ground-based methods is designed to 

attract the moths by the use of SPLAT, and to kill them with the permethrin. 

For this alternative, exposures to SPLAT, permethrin, ethylbenzene, and 1,2,4-trimethylbenzene 

were evaluated for all of the receptor populations described in Section D4.3. Triacetin was not 

evaluated because it is essentially nontoxic at the very low quantities that may be released to the 

environment (see Section D3 – triacetin is used as a food additive) (CFR 2005a, 2005b). 

Potential exposure to human populations from acute, subchronic, and chronic inhalation 

exposures that may result from the use of SPLAT and Permethrin E-Pro were estimated from the 

EPCs listed in Table D4-29. Inhalation exposures are consistent with the volatile nature of the 

pheromones, permethrin, ethylbenzene, and 1,2,4-trimethylbenzene. Because the ground-based 

method of application may result in small quantities of SPLAT or Permethrin E-Pro on soil or 

vegetation, incidental ingestion of soil, dermal contact with soil, dermal contact with 

commercial- or home-grown produce, and dermal contact with ornamental vegetation were also 

evaluated. Chemical-specific intakes of SPLAT (LBAM pheromones), permethrin, ethylbenzene, 

and 1,2,4-trimethylbenzene for Nursery/Program Workers are given in Table D4-30; for 

Agricultural Workers in Table D4-31; for Adult and Child Residents in Tables D4-32 and D4-33, 


SECTION D4 


respectively; for the Adult Gardener in Table D4-34; and for the Adult and Child Recreational 

Park Users in Tables D4-35 and D4-36. 

Table D4-29 

Exposure Point Concentrations – Male Moth Attractant 

Air 

(mg/m 3 ) 


Ground Applications 

Soil 

(mg/kg-soil) 


(mg/m 2 ) 

Vegetation 

(mg/kg-veg) 


SPLAT (LBAM 

pheromones) 1.04E-03 4.14E-06 4.14E-06 2.60E-04 5.19E-02 5.19E-03 

Permethrin 1.25E-03 4.85E-06 4.85E-06 3.61E-03 7.21E-01 7.21E-02 

Ethylbenzene 1.02E-05 4.00E-08 4.00E-08 1.27E-06 2.54E-04 2.54E-05 

1,2,4- 

Trimethylbenzene 1.35E-03 5.33E-06 5.33E-06 1.69E-04 3.38E-02 3.38E-03 

Table D4-30 

Chemical-Specific Intakes Factors for Nursery/Program Workers – Male Moth Attractant 


Air 


Soil 

Ornamental 

Vegetation 



SPLAT 


--- --- --- --- 

Permethrin 4.83E-08 3.46E-10 1.50E-09 1.97E-04 

Ethylbenzene 3.99E-10 1.22E-13 --- --- 

1,2,4-Trimethylbenzene --- --- --- --- 



Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 


SPLAT 


4.13E-07 4.39E-07 1.93E-05 2.49E-10 7.22E-10 9.44E-05 

Permethrin 4.83E-07 5.14E-07 2.31E-05 3.46E-09 1.50E-08 1.97E-03 

Ethylbenzene 3.99E-09 4.24E-09 1.89E-07 1.22E-12 --- --- 

1,2,4-Trimethylbenzene 5.32E-07 5.66E-07 2.52E-05 1.62E-10 --- --- 

Notes: 






DRAFT PEIR 


Table D4-31 

Chemical-Specific Intakes Factors for Agricultural Workers – Male Moth Attractant 


Exposure Medium: Air Soil Commercial Produce 



SPLAT 


--- --- --- --- 

Permethrin 4.83E-08 3.46E-10 1.50E-09 NE 

Ethylbenzene 3.99E-10 1.22E-13 --- --- 

1,2,4-Trimethylbenzene --- --- --- --- 


Exposure Medium: Air Soil Commercial Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 


SPLAT 


4.13E-07 4.39E-07 1.93E-05 2.49E-10 7.22E-10 9.44E-05 

Permethrin 4.83E-07 5.14E-07 2.31E-05 3.46E-09 1.50E-08 NE 

Ethylbenzene 3.99E-09 4.24E-09 1.89E-07 1.22E-12 --- --- 

1,2,4-Trimethylbenzene 5.32E-07 5.66E-07 2.52E-05 1.62E-10 --- --- 

Notes: 


NE = Not evaluated because permethrin is registered by the USEPA primarily for use as a termiticide and on nonfood crops (Etigra. 2007. Product Label for 

Permethrin E-Pro. Revised July 9 2007)mg/kg-d = milligram per kilogram - day 


SECTION D4 


Table D4-32 

Chemical-Specific Intake Factors for Adult Resident – Male Moth Attractant 

Exposure 

Medium: 

Pathways: 

Air 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 


SPLAT 

(LBAM 

pheromones) 

--- --- --- --- --- --- 


Ethylbenzene 1.16E-09 2.07E-13 --- --- 1.34E-08 2.36E-09 

1,2,4- 

Trimethylbenzene 

Exposure 

Medium: 

Pathways: 

Inhalation 

--- --- --- --- --- --- 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 


SPLAT 

(LBAM 

pheromones) 

1.20E-06 1.25E-06 1.31E-05 4.23E-10 3.71E-10 1.15E-04 2.73E-05 4.82E-06 


Ethylbenzene 1.16E-08 1.21E-08 1.28E-05 2.07E-12 --- --- 1.34E-07 2.36E-08 

1,2,4- 


1.54E-06 1.61E-06 1.70E-05 2.76E-10 --- --- 1.78E-05 3.14E-06 

Notes: 







DRAFT PEIR 


Table D4-33 

Chemical-Specific Intake Factors for Child Resident – Male Moth Attractant 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 


SPLAT 

(LBAM 

pheromones) 

--- --- --- --- --- --- 


Ethylbenzene 1.73E-09 1.06E-12 --- --- 1.46E-08 2.58E-09 

1,2,4- 


--- --- --- --- --- --- 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 


SPLAT 

(LBAM 1.79E-06 1.86E-06 1.95E-05 2.17E-09 7.68E-10 1.44E-04 2.99E-05 5.28E-06 

pheromones) 


Ethylbenzene 1.73E-08 1.80E-08 1.91E-07 1.06E-11 --- --- 1.46E-07 2.58E-08 

1,2,4- 


2.30E-06 2.40E-06 2.54E-05 1.41E-09 --- --- 1.95E-05 3.45E-06 

Notes: 



Permethrin E-Pro. Revised July 9 2007) 



SECTION D4 


Table D4-34 

Chemical-Specific Intakes for Residential Adult Gardener – Male Moth Attractant 

Exposure 


Pathways: 

Inhalation 

Incidental 

Ingestion 


Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ingestion 

Homegrown 

Produce 

Dermal 

Contact 


SPLAT 

(LBAM 

pheromones) 

--- --- --- --- --- --- --- 

Permethrin 6.74E-09 1.68E-10 3.88E-10 6.87E-05 NE NE NE 

Ethylbenzene 5.56E-11 5.91E-14 --- --- 1.34E-08 2.36E-09 --- 

1,2,4- 


Exposure 

Medium: 

Pathways: 

Inhalation 

--- --- --- --- --- --- --- 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ingestion 

Homegrown 

Produce 

Dermal 

Contact 


SPLAT 

(LBAM 

pheromones) 

5.76E-08 2.10E-07 2.64E-05 1.21E-10 1.86E-10 3.29E-05 2.73E-05 4.82E-06 1.51E-05 

Permethrin 6.74E-08 2.46E-07 3.16E-05 1.68E-09 3.88E-09 6.87E-04 NE NE NE 

Ethylbenzene 5.56E-10 2.03E-09 2.58E-07 5.91E-13 --- --- 1.34E-07 2.36E-08 --- 

1,2,4- 


7.42E-08 2.71E-07 3.44E-05 7.88E-11 --- --- 1.78E-05 3.14E-06 --- 

Notes: 







DRAFT PEIR 


Table D4-35 

Chemical-Specific Intakes for Adult Recreational Park User – Male Moth Attractant 

Exposure 


Pathways: 

Inhalation 

Incidental 

Ingestion 


Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 


SPLAT 

(LBAM 

pheromones) 

--- --- --- --- --- 

Permethrin 6.74E-09 8.40E-11 2.21E-10 6.87E-05 NE 

Ethylbenzene 5.56E-11 2.96E-14 --- --- 1.34E-08 

1,2,4- 


--- --- --- --- --- 


Exposure 


Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 


SPLAT 

(LBAM 

pheromones) 

5.76E-08 6.00E-08 2.64E-05 6.04E-11 1.06E-10 3.29E-05 2.73E-05 

Permethrin 6.74E-08 7.03E-08 3.16E-05 8.40E-10 2.21E-09 6.87E-04 NE 

Ethylbenzene 5.56E-10 5.80E-10 2.58E-07 2.96E-13 --- --- 1.34E-07 

1,2,4- 


7.42E-08 7.74E-08 3.44E-05 3.94E-11 --- --- 1.78E-05 

Notes: 






SECTION D4 


Table D4-36 

Chemical-Specific Intakes for Child Recreational Park User – Male Moth Attractant 

Exposure 


Pathways: 

Inhalation 

Incidental 

Ingestion 


Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 


SPLAT 

(LBAM 

pheromones) 

--- --- --- --- --- 

Permethrin 1.77E-08 4.34E-10 4.58E-10 8.56E-05 NE 

Ethylbenzene 1.46E-10 1.53E-13 --- --- 1.46E-08 

1,2,4- 


--- --- --- --- --- 


Exposure 


Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 


SPLAT 

(LBAM 

pheromones) 

1.51E-07 1.58E-07 6.93E-05 3.12E-10 2.19E-10 4.11E-05 2.99E-05 

Permethrin 1.77E-07 1.85E-07 8.31E-05 4.34E-09 4.58E-09 8.56E-04 NE 

Ethylbenzene 1.46E-09 1.52E-09 6.77E-07 1.53E-12 --- --- 1.46E-07 

1,2,4- 


1.95E-07 2.03E-07 9.03E-05 2.04E-10 --- --- 1.95E-05 

Notes: 





D4.8 ORGANIC TREATMENT ALTERNATIVE 

Under the Organic Treatment Alternative, the organic-approved insecticide spinosad, and the 

biopesticide Btk could be used. Both of these materials would be applied by hydraulic spraying 

using either truck-based or backpack-based equipment. For this alternative, exposures to 

spinosad and Btk were evaluated for of all of the receptor populations described in Section D4.3. 

Potential exposure to human populations from acute, subchronic, and chronic inhalation 

exposures that may result from the use of spinosad and Btk were estimated from the EPCs listed 

in Table D4-37. Although neither spinosad nor Btk are volatile, the method of application is 

expected to introduce these substances into the air during application, which would potentially 

result in acute and subchronic exposures. The presence of residual material after application may 

result in longer-term i.e., chronic inhalation exposure, albeit at quite low levels. The groundbased 

method of application may also result in quantities of spinosad or Btk that deposit on soil 




DRAFT PEIR 


or vegetation. To address this possibility, incidental ingestion of soil, dermal contact with soil, 

dermal contact with commercial- or home-grown produce, dermal contact with ornamental 

vegetation, and ingestion of produce were also evaluated for spinosad. With the exception of the 

dermal pathways, these same exposure routes were also evaluated for Btk. As noted in Section 

D4.1, dermal exposures to Btk were not evaluated as no evidence indicates that Btk can be 

absorbed across or otherwise enter intact skin. 

Chemical-specific intakes of spinosad and Btk for Nursery/Program Workers and Agricultural 

Workers are given in Table D4-38; for Adult and Child Residents in Table D4-39; for the Adult 

Gardener in Table D4-40; and for the Adult and Child Recreational Park Users in Table D4-41. 

Table D4-37 

Exposure Point Concentrations – Organic Treatment Alternative 


Organic Treatment Applications 

Air 

(mg/m 3 ) 

Soil 

(mg/kg-soil) 


(mg/m 2 ) 

Vegetation 

(mg/kg-veg) 


Btk 8.17E-03 1.36E-04 1.36E-04 6.79E-01 1.36E+02 1.36E+01 

Spinosad 3.24E-04 5.40E-06 5.40E-06 5.73E-02 1.15E+01 1.15E+00 

Table D4-38 

Chemical-Specific Intakes for Nursery/Program Workers and Agricultural Workers – Organic 

Treatment Alternative 


Exposure Medium: Air Soil Ornamental Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 



Btk 1.36E-05 1.44E-05 1.52E-04 6.51E-07 --- --- 



Btk 1.36E-05 1.44E-05 1.52E-04 6.51E-07 --- --- 


Notes: 


mg/kg-d = milligram per kilogram–day 


SECTION D4 


Table D4-39 

Chemical-Specific Intakes for Adult and Child Resident – Organic Treatment Alternative 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 



Btk 3.94E-05 4.11E-05 1.03E-04 1.11E-06 --- --- 7.15E-02 1.26E-02 



Btk 5.87E-05 6.13E-05 1.53E-04 5.67E-06 --- --- 7.84E-02 1.38E-02 


Notes: 



Table D4-40 

Chemical-Specific Intakes for Residential Adult Gardener – Organic Treatment Alternative 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 


Btk 1.89E-06 6.92E-06 2.07E-04 3.16E-07 --- --- 7.15E-02 1.26E-02 --- 

Spinosad 

7.51E-08 2.74E-07 8.23E-06 2.67E-08 

Notes: 



4.11E- 

09 

7.28E-04 6.04E-03 1.07E-03 

3.34E- 

04 




DRAFT PEIR 


Table D4-41 

Chemical-Specific Intakes for Adult and Child Recreational Park User – Organic Treatment 

Alternative 



Commercial 

Produce 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 



Btk 1.89E-06 1.98E-06 2.07E-04 1.58E-07 --- 7.15E-02 --- 



Btk 4.97E-06 5.19E-06 5.45E-04 8.17E-07 --- 7.84E-02 --- 


Notes: 





Risk Characterization 

D5.1 METHODS USED TO CHARACTERIZE HUMAN HEALTH RISK 

The following discussion describes the methods used to assess the potential adverse health effects 

associated with each alternative. For noncarcinogens, the likelihood that adverse effects would 

develop as a result of exposure is evaluated by use of a hazard index (HI) approach. That approach 

involves the calculation of an HI, which represents the ratio of the estimated level of total exposure 

to the relevant noncancer toxicity criterion, in this case, the RfD. When the ratio is calculated for a 

specific exposure pathway (or for a single substance), the ratio is called a hazard quotient (HQ). The 

HQs are summed over all exposure pathways and all chemicals to develop the total HI. The 

noncancer toxicity criterion is developed by identifying a NOAEL or LOAEL if an appropriate 

NOAEL is not available, and applying one or more UFs (see Section D3). If the value of the HI is 

less than one, it is considered unlikely that exposure will cause adverse health effects; conversely, if 

the HI is greater than 1 then health effects may result from exposure. Unlike cancer risk estimates 

that are expressed as probabilities (e.g., 1 in a million), HIs do not represent the probability of health 

effects developing, but are presented to provide context to the relationship between the known 

toxicity of a substance and the estimated magnitude of exposure. The equations used to calculate 

HQs and HIs are shown below: 

Equation D5-1 

Hazard Quotient (HQ) = Exposure (dose) 

RfD 

Where: 

HQ = Hazard Quotient (unitless) 

Exposure = dose, milligrams (mg) per kilogram (kg)-day 

RfD = Reference Dose, milligrams (mg) per kilogram (kg)-day 

Equation D5-2 

Hazard Index (HI) = HQ 

Where: 

HI = Hazard Index (unitless) 

HQ = Hazard Quotient (unitless) 

Carcinogenic risks are estimated by calculating the upper-bound incremental probability that an 

individual will develop cancer over a lifetime as a direct result of exposure to a potential carcinogen. 

The CSF is the toxicity value used to estimate cancer risk, and is defined by OEHHA (2003) as “the 

theoretical upper bound probability of extra cancer cases occurring in an exposed population 

assuming a lifetime exposure to the chemical when the chemical dose is expressed in exposure units 

of milligrams/kilogram-day (mg/kg-d).” For this assessment, cancer risks were calculated for 



DRAFT PEIR 



chronic exposure periods only (i.e., not for sub-chronic or acute exposure periods). As noted in 

OEHHA (2003), the agency does not support the use of cancer potency factors to evaluate cancer 

risk for exposures of less than 9 years. OEHHA notes that if such risks must be evaluated (i.e., for 

periods less than 9 years), “ …we recommend assuming that average daily dose for short-term 

exposure is assumed to last for a minimum of 9 years.” The LBAM Eradication Program is currently 

set to last 7 years, and this 7-year period was the value used for exposure duration and averaging 

time when assessing chronic exposure and risk. Although this approach is not in strict accordance 

with OEHHAs guidance, use of the 7-year period yields slightly higher estimates of risk than if a 9- 

year period were used, and thus does not underestimate risk to potentially affected receptor 

populations. 

The equation used to calculate potential excess cancer risk (Eq. 5-3) is: 

Equation D5-3 

Excess Cancer Risk = Exposure (dose) × CSF 

Where: 

Exposure = dose, milligrams (mg) per kilogram (kg)-day 

CSF = Cancer Slope Factor, [milligrams (mg)/kilogram (kg)-day(d)] -1 

D5.1.1 

Toxicity Values 

The toxicity values used to estimate the likelihood of adverse effects from Program alternatives were 

identified and discussed in Section D3; the specific toxicity criteria used to estimate cancer risk and 

noncancer hazard for all Program chemicals and biopesticides are provided in Table D5-1. Note that 

the Section D3 discussions included toxicity criteria, where available, from multiple regulatory 

sources. In selecting values to use for the quantification of adverse health effects, toxicity criteria 

(e.g., RfDs, CSFs) were identified for one or more routes of exposure. These toxicity criteria were 

obtained from documents and on-line sources from the USEPA, OPP, OEHHA, USEPA’s IRIS, and 

the ATSDR. If a criterion was not available from these sources, information in other regulatory 

documents or the primary literature was relied on. When toxicity criteria were developed for this 

assessment (e.g., from data in the regulatory or primary literature), UFs were incorporated to address 

data gaps, effects on sensitive receptors, and variability in study and/or human populations. 

The toxicity values in Table D5-1 reflect this use of multiple information sources. Not all toxicity 

criteria that were identified for a chemical in Section D3 were used (although values selected for use 

were identified in Section D3); however, all values were retained in Section D3 for information 

purposes. 

Of the chemicals and biopesticides evaluated for use under each of the Program alternatives, 

spinosad, chlorpyrifos, lambda-cyhalothrin, 1,2,4-trimethylbenzene, Btk, and the pheromonecontaining 

products SPLAT, HERCON, and Isomate, are not classified as carcinogens. Accordingly, 

these substances were evaluated only for potential noncarcinogenic effects. Both permethrin and 

ethylbenzene, an inert ingredient of Permethrin E-Pro, are classified as carcinogens (see Section D3), 

and were evaluated for both carcinogenic as well as noncarcinogenic effects under MMA 

Alternative. Only active ingredients were evaluated under the No Program Alternative. Not all 

chemicals or biopesticides had toxicity criteria available for all potential exposure pathways and 

exposure durations. Accordingly, only those pathways and exposure durations that had applicable 


SECTION D5 

RISK CHARACTERIZATION 

toxicity criteria could be quantitatively evaluated. Where toxicity criteria were not available, 

chemical-specific intakes are discussed by reference to toxicity data and EPCs to provide a basis for 

the interpretation of these intakes. 



DRAFT PEIR 





SECTION D5 


Table D5-1 


Carcinogenic Toxicity Values 

Noncarcinogenic Toxicity Values 

Pesticide or 

Chemical 

Inhalation CSF 

(mg/kg-d) -1 

Oral CSF 

(mg/kg-d) -1 

Chronic Inhalation RfD 

(mg/kg-d) 

Subchronic Inhalation RfD 

(mg/kg-d) 

Acute Inhalation RfD 

(mg/kg-d) 

Oral RfD 

(mg/kg-d) 

Hercon --- --- --- --- --- --- 5.70E-02 

Splat --- --- --- --- --- --- 5.70E-02 

Isomate --- --- --- --- --- --- 5.70E-02 

Bacillus 

thuringiensis 

kurstaki 

OEHHA 

2009a 

OEHHA 

2009a 

OEHHA 

2009a 

2.29E+00 

9.49E-01 

2.29E+00 

OEHHA 

2009a 

Crutchfield 

2008 

OEHHA 

2009a 

--- --- 

--- --- 

--- --- 

--- --- --- --- --- --- --- --- 2.00E-03 Cook 1994 --- --- 

Spinosad --- --- --- --- 2.70E-02 

Permethrin --- --- 9.60E-03 

USEPA 

2005 

1.10E-01 

Lambda-Cyhalothrin --- --- --- --- 8.00E-04 

Chlorpyrifos --- --- --- --- 

Ethylbenzene 

1,2,4- 


8.70E-03 

OEHHA 

2009b 

1.10E-02 

OEHHA 

2009b 

3.00E-04 

(adult) 

3.00E-05 

(child) 

5.71E-01 

--- --- --- --- 2.00E-03 

Notes: 

CSF = cancer slope factor 

RfD = reference dose 

mg/kg-d = milligram per kilogram per day 

--- = no cancer slope factor or noncancer reference dose available 

USEPA 

2007a 

USEPA 

2005 

USEPA 

2007b 

USEPA 

2006 

OEHHA 

2009b 

PPRTV 

2009 

--- --- 4.90E-02 

1.10E-01 

8.00E-04 

1.00E-03 

8.70E-01 

2.00E-02 

USEPA 

2005 

USEPA 

2007a 

USEPA 

2006 

ATSDR 

2008 

PPRTV 

2009 

1.10E-01 

8.00E-04 

1.00E-03 

1.24E+01 

USEPA 

2007a 

USEPA 

2005 

USEPA 

2007b 

USEPA 

2006 

ATSDR 

2008 

2.40E-02 

2.50E-01 

5.00E-03 

3.00E-03 

1.00E-01 

IPCS 

2001 

USEPA 

2005 

USEPA 

2009 

USEPA 

2009 

USEPA 

2009 

--- --- --- --- 

Sources: 

ATSDR. 2008. Minimal Risk Levels. December. http://www.atsdr.cdc.gov/mrls/index.html 

Crutchfield. 2008. SPLAT LBAM Acute Inhalation Toxicity Study in Rats. Stillmeadow 11762-08. 

IPSC. 2001. Toxicology evaluations on spinosad. http://inchem.org/documents/jmpr/jmpmono/2001pr12.htm. 

Cook. 1994. Major Paper Submitted in Partial Fulfillment of MHSc Degree, (Community Medicine) in the Department of Health Care and Epidemiology. Faculty of Medicine. The University of British Colombia. 

OEHHA. 2009a. Human Health Risk Assessment of Isomate LBAM Plus. February 2009. 

OEHHA. 2009b. Toxicity criteria database. http://oehha.ca.gov/risk/chemicaldb/index.asp. 

PPRTV Database. 2009. http://hhpprtv.ornl.gov/pprtv.shtml. 



DRAFT PEIR 



Table D5-1 


USEPA. 2009. Permethrin: HED chapter of the reregistration eligibility decision document. PC Code 109701, case no. 2501, DP Barcode D357566. 

USEPA. 2006. Office of Pesticide Programs, Reregistration eligibility decision for chlorpyrifos. July 31 

USEPA. 2007a. Spinosad and spinetoram. Human health assessment for application of spinosad to pineapple and the spice subgroup (19B, except black pepper). 

USEPA. 2007b. Lambda-Cyhalothrin; Pesticide Tolerance. Federal Register: August 15, 2007.Volume 72, Number 157. Rules and Regulations. pages 45656-45663. http://www.epa.gov/EPA-PEST/2007/August/Day- 

15/p16050.htm 

USEPA. 2009. Integrated Risk Information System. http://cfpub.epa.gov/ncea/iris/index.cfm 


SECTION D5 


D5.2 INTERPRETATION OF RESULTS 

Health effects assessment outcomes for the Alternatives discussed in the following sections are 

provided as noncancer HQs or HIs, or as cancer risks (see following). For noncancer effects, an 

HQ or HI less than one indicates that adverse effects are not expected to occur if exposure occurs 

as assumed in a given scenario. If an HQ or an HI exceeds 1, then adverse effects may occur. In 

general, the lower the HQ or HI, the lower the likelihood of an adverse effect, and the greater the 

HI, the greater the likelihood of an adverse effect. However, since the RfDs used to develop the 

HIs incorporate large margins of safety from the use of UFs, it is possible that no adverse effects 

may occur even if the threshold value of 1 is exceeded. For the PEIR that this HHRA supports, 

HQs or HIs above 1 are considered potentially significant under CEQA. 

As noted in Section D5.1, cancer risks represent the incremental probability of cancer, assuming 

exposure occurs over a lifetime. Cancer risks are expressed as probabilities e.g., one in a million 

(1 x 10 -6 ), one in one hundred thousand (1 x 10 -5 ). Risks that fall within the range of 1 x 10 -6 to 

1 x 10 -4 are generally considered acceptable (USEPA 1990). For the PEIR that this HHRA 

supports, risks greater than 1 x 10 -6 are considered potentially significant under CEQA. 

D5.3 NO PROGRAM 

The estimated EPCs and intakes of Btk and spinosad are the same under the No Program 

Alternative as for the Organic Treatment alternative due to assumed similarities in the method 

and rate of application (see Appendix C). Interpretation of the potential health effects from use of 

these materials is presented in Section D5.5. 

D5.3.1 Nursery/Program Workers and Agricultural Workers 

Nursery/Program Workers and Agricultural Workers that inhale permethrin, lambda-cyhalothrin, 

or chlorpyrifos are not likely to experience any adverse effects from acute, subchronic, or 

chronic inhalation exposures, based on calculated HIs that are less than 1 (Tables D5-2 and D5- 

3). Dermal contact with ornamental vegetation contaminated with lambda-cyhalothrin or 

chlorpyrifos (Nursery/Program Workers) and dermal contact with commercial produce 

contaminated with chlorpyrifos (Agricultural Workers) are associated with HIs above 1. Cancer 

risks are in excess of 1 x 10 -6 for Nursery/Program Workers who are assumed to come in regular 

dermal contact with permethrin-contaminated vegetation. These HIs above 1 and cancer risks 

above 1 x 10 -6 indicate that adverse health effects may occur if workers regularly contact 

contaminated vegetation without the use of protective clothing. For permethrin, lambdacyhalothrin, 

and chlorpyrifos, no other exposure routes are associated with outcomes that 

indicate there may be a potential for adverse effects. 




DRAFT PEIR 


Table D5-2 

Nursery/Program Worker Hazard Quotients – No Program Alternative 

Chemical-Specific Cancer Risks 


Air 

Soil 

Ornamental 

Vegetation 

Total 

Cancer 

Risk 

Pathway: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

All 

Pathways 

Bacillus 

thuringiensis 

kurstaki 

--- --- NA NA --- 

Spinosad --- --- --- --- --- 

Permethrin --- 8.5E-11 3.7E-10 4.8E-05 5.E-05 

Lambda-Cyhalothrin --- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- 

Chemical-Specific Noncarcinogenic Hazard Quotients 


Air 

Soil 

Ornamental 

Vegetation 

Total 

Chronic HI 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

All 

Pathways 

Bacillus 

thuringiensis 

kurstaki 

--- --- 7.6E-02 --- NA NA --- 

Spinosad 3.6E-06 --- 1.2E-04 4.1E-07 1.2E-07 1.6E-02 2.E-02 

Permethrin 4.1E-06 4.3E-06 2.5E-04 3.5E-07 1.5E-06 2.0E-01 2.E-01 

Lambda-Cyhalothrin 1.1E-04 1.2E-04 7.2E-03 2.5E-06 7.2E-06 9.4E-01 9.E-01 

Chlorpyrifos 1.1E-01 3.6E-02 1.2E-01 1.4E-05 1.2E-05 1.6E+00 2.E+00 

Notes: 

--- = Appropriate toxicity value is not available 


These cancer risks ands HIs were calculated based on conservative exposure scenarios and exposure parameters selected to avoid underestimation of risk to 

the public. They are not meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the expected rate of disease in a population (see 

Section D6). 


SECTION D5 


Table D5-3 

Agricultural Worker – No Program Alternative 

Exposure 

Medium: 

Pathway: 

Bacillus 

thuringiensis 

kurstaki 

Air 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Dermal 

Contact 

Total 

Cancer 


All 

Pathways 

--- --- NA NA --- 

Spinosad --- --- --- --- --- 

Permethrin --- 8.5E-11 3.7E-10 NE 5.E-10 

Lambda- 

Cyhalothrin 

--- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- 

Exposure 

Medium: 

Pathway: 

Bacillus 

thuringiensis 

kurstaki 

Inhalation 


Air 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Dermal 

Contact 

Total 

Chronic HI 

All 

Pathways 

--- --- 7.6E-02 --- NA NA --- 


Permethrin 4.1E-06 4.3E-06 2.5E-04 3.5E-07 1.5E-06 NE 6.E-01 

Lambda- 

Cyhalothrin 

1.1E-04 1.2E-04 7.2E-03 2.5E-06 7.2E-06 9.4E-01 9.E-01 

Chlorpyrifos 1.1E-01 3.6E-02 1.2E-01 1.4E-05 1.2E-05 1.6E+00 2.E+00 

Notes: 



NE = Not evaluated because permethrin is registered by the USEPAprimarily for use as a termiticide and on non-food crops (Etigra, 2007. Product Label for 

Permethrin E-Pro. Revised July 9, 2007) 



Section D6). 

Potential additive effects from exposure to multiple chemicals were not evaluated, due to the fact 

that there is no basis for assuming that more than one chemical at a time would be applied to 

control LBAM. 

D5.3.2 


D5.3.2.1 

Adult Residents 

Adult Residents that inhale permethrin, or lambda-cyhalothrin, or chlorpyrifos are not expected 

to experience any adverse effects from acute exposure, based on calculated HQs for acute 

inhalation that are less than 1 (Table D5-4). Subchronic or chronic inhalation exposure of 




DRAFT PEIR 


Residents to permethrin, lambda-cyhalothrin, or chlorpyrifos also yield HQs less than 1. Dermal 

contact with ornamental vegetation (lambda-cyhalothrin and chlorpyrifos) and dermal contact 

with commercial produce (chlorpyrifos) is associated with HQs (and total chronic HIs) greater 

than 1. Dermal contact with permethrin-contaminated ornamental vegetation resulted in a cancer 

risk above 1 x 10 -6 . The HQs above 1 and cancer risks above 1 x 10 -6 indicates that adverse 

health effects may occur to Residents if exposure occurs as assumed. 

Table D5-4 

Adult Resident Cancer Risks and Hazard Quotients – No Program Alternative 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Cancer 


Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

All 

Pathways 

Btk --- --- NA NA --- --- --- 

Spinosad --- --- --- --- --- --- --- 

Permethrin --- 1.4E-10 1.9E-10 5.9E-05 NE NE 6.E-05 

Lambda- 

Cyhalothrin 

Chlorpyrifo 

s 

--- --- --- --- --- --- --- 

--- --- --- --- --- --- --- 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

All 

Pathways 

Btk --- --- 5.1E-02 --- NA NA --- --- --- 

Spinosad 1.0E-05 --- 8.3E-05 7.0E-07 6.1E-08 1.9E-02 4.5E-02 7.9E-03 7.E-02 

Permethrin 1.2E-05 1.2E-05 1.7E-04 6.0E-07 7.9E-07 2.5E-01 NE NE 2.E-01 

Lambda- 

Cyhalothrin 

Chlorpyrifo 

s 

3.3E-04 3.5E-04 4.8E-03 4.2E-06 3.7E-06 1.1E+00 2.7E-01 4.8E-02 1.E+00 

3.2E-01 1.0E-01 8.4E-02 2.4E-05 6.3E-06 2.0E+00 1.5E+00 2.7E-01 4.E+00 

Notes: 







Section D6). 

Potential additive effects from exposure were not evaluated (see 5.2.1). 

D5.3.2.2 

Child Residents 

The analyses of the potential adverse health effects of No Program Alternative chemicals to 

Child Residents used methods consistent with those used for other receptor populations. 

However, the calculations of Child Resident HQ for the chronic inhalation of chlorpyrifos is 


SECTION D5 


based on an RfD (see Table D5-1 and Section D3) that incorporated an additional UF of 10 to 

account for the greater sensitivity of children relative to adults (USEPA 2006). That UF (for 

chronic inhalation) in combination with child-specific exposure parameters, tends to give Child 

Resident HQs for chlorpyrifos that are greater than those developed for an Adult Resident. 

The estimated HQs for acute inhalation exposure of a Child Resident to permethrin, or lambdacyhalothrin 

and chlorpyrifos are less than or equal to 1, indicating that adverse effects are not 

expected (Table D5-5). Subchronic inhalation exposure of Child Resident to permethrin and 

lambda-cyhalothrin give HQs less than 1. For chlorpyrifos, subchronic inhalation exposure of 

Child Residents is associated with an HQ of 2. This HQ indicates that a Child Resident may be 

adversely affected if exposure to chlorpyrifos occurs under the conservative exposure 

assumptions assumed in this evaluation. 

Chronic exposure of a Child Resident was calculated by summing chronic HQs across all 

pathways to yield chemical-specific HIs. Those HIs (Table D5-5) indicate that lambdacyhalothrin 

and chlorpyrifos use is associated with the potential for adverse health effects (HI of 

2 and 9, respectively). Additive effects from exposure were not evaluated (see 5.2.1). 

Dermal contact with permethrin-contaminated ornamental vegetation resulted in a cancer risk for 

the Child Resident above 1 x 10 -6 . 

Table D5-5 

Child Resident Hazard Quotient – No Program Alternative 

Chemical-Specific Cancer Risk 

Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Cancer Risk 

Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

All 

Pathways 

Btk --- --- NA NA --- --- --- 

Spinosad --- --- --- --- --- --- --- 


Lambda- 

Cyhalothrin 

--- --- --- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- --- --- 



Ornamental 

Vegetation 

Commerci 

al Produce 

Homegrown 

Produce 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion Ingestion All Pathways 

Btk --- --- 7.7E-02 --- NA NA --- --- --- 



Lambda- 

Cyhalothrin 

4.9E-04 5.2E-04 7.2E-03 2.2E-05 7.6E-06 1.4E+00 3.0E-01 5.3E-02 2.E+00 

Chlorpyrifos 4.8E+00 1.5E+00 1.3E+00 1.2E-04 1.3E-05 2.4E+00 1.7E+00 3.0E-01 9.E+00 

Notes: 







DRAFT PEIR 


Table D5-5 

Child Resident Hazard Quotient – No Program Alternative 


These cancer risks ands HIs were calculated based on conservative exposure scenarios and exposure parameters selected to avoid underestimation of risk to the 

public. They are not meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the expected rate of disease in a population (see Section 

D6). 

D5.3.3 

Adult Gardener 

Short-term inhalation exposures of Adult Gardeners to permethrin, or lambda-cyhalothrin, or 

chlorpyrifos yield acute inhalation HQs less than 1 (Table D5-6). Subchronic inhalation 

exposures of Adult Gardeners to permethrin lambda-cyhalothrin, and chlorpyrifos are associated 

with HQs less than 1. In this assessment, the effects of chronic exposure of the Adult Gardener 

population was estimated based on inhalation, incidental ingestion of soil, dermal contact with 

soil, dermal contact with ornamental vegetation, ingestion of both commercially grown and 

home-grown produce, and by dermal contact with homegrown produce. The chronic HIs (Table 

D5-6) indicate that permethrin and lambda-cyhalothrin use is associated with HIs less than 1. 

The total chronic HI for (3) chlorpyrifos, indicates that chronic exposure may be associated with 

adverse health effects. 


the Adult Gardener above 1 x 10 -6 . 

Additive effects from exposure to multiple Program chemicals were not evaluated (see 5.2.1). 

Table D5-6 

Residential Adult Gardener Cancer Risks and Hazard Quotient – No Program Alternative 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 


Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Btk --- --- NA NA --- --- NA --- 

Spinosad --- --- --- --- --- --- --- --- 

Permethrin --- 4.1E-11 9.5E-11 1.7E-05 NE NE NE 2.E-05 

Lambda- 

Cyhalothrin 

--- --- --- --- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- --- --- --- 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Btk --- --- 1.0E-01 --- NA NA --- --- NA --- 

Spinosad 5.0E-07 --- 1.7E-04 2.0E-07 3.1E-08 5.4E-03 4.5E-02 7.9E-03 2.5E-03 6.E-02 

Permethrin 5.7E-07 2.1E-06 3.5E-04 1.7E-07 4.0E-07 7.0E-02 NE NE NE 7.E-02 

Lambda- 

Cyhalothrin 

1.6E-05 5.8E-05 9.8E-03 1.2E-06 1.9E-06 3.3E-01 2.7E-01 4.8E-02 1.5E-01 8.E-01 

Chlorpyrifos 1.6E-02 1.7E-02 1.7E-01 6.8E-06 3.2E-06 5.6E-01 1.5E+00 2.7E-01 2.6E-01 3.E+00 


SECTION D5 


Table D5-6 

Residential Adult Gardener Cancer Risks and Hazard Quotient – No Program Alternative 

Notes: 



NE = Not evaluated because permethrin is registered by the USEPA primarily for use as a termiticide and on non-food crops (Etigra, 2007. Product Label for 

Permethrin E-Pro. Revised July 9 2007). 



D6). 

D5.3.4 

Adult and Child Recreational Park Users 

D5.3.4.1 


Adult Recreational Park Users that inhale permethrin, lambda-cyhalothrin, or chlorpyrifos are 

not expected to develop any adverse effects from acute exposure, based on calculated HQs for 

acute inhalation that are less than 1 (Table D5-7). The subchronic inhalation HQs for permethrin, 

lambda-cyhalothrin, and chlorpyrifos are all less than 1. 

Chronic HIs for the Adult Recreational Park User were calculated based on HQs from the 

incidental ingestion of soil, dermal contact with soil, ingestion of commercial produce, and 

dermal contact with ornamental vegetation. With the exception of chlorpyrifos, chemical-specific 

chronic HIs are less than 1, indicating that Adult Recreational Park Users are not expected to be 

affected by the use of permethrin, or lambda-. The chronic HI for chlorpyrifos is 2, indicating the 

possibility for adverse effects. 


the Adult Park User above 1 x 10 -6 .Additive effects from exposure to multiple Program 

chemicals were not evaluated (see 5.2.1). 

Table D5-7 

Adult Park User Cancer Risks and Hazard Quotients – No Program Alternative 


Exposure 

Medium: 

Pathways: 

Air 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 

Total 


All 

Pathways 

Btk --- --- NA --- NA --- 

Spinosad --- --- --- --- --- --- 

Permethrin --- 2.1E-11 5.4E-11 NE 1.7E-05 2.E-05 

Lambda- 

Cyhalothrin 

--- --- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- --- 




DRAFT PEIR 


Table D5-7 

Adult Park User Cancer Risks and Hazard Quotients – No Program Alternative 


Exposure 

Medium: 

Air 

Soil 

Commerc 

ial 

Produce 

Ornamental 

Vegetation 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Btk --- --- 1.0E-01 --- NA --- NA --- 

Spinosad 5.0E-07 --- 1.7E-04 9.9E-08 1.7E-08 4.5E-02 5.4E-03 5.E-02 

Permethrin 5.7E-07 5.9E-07 3.5E-04 8.6E-08 2.3E-07 NE 7.0E-02 7.E-02 

Lambda- 

Cyhalothrin 

1.6E-05 1.7E-05 9.8E-03 6.0E-07 1.1E-06 2.7E-01 3.3E-01 6.E-01 

Chlorpyrifos 1.6E-02 4.9E-03 1.7E-01 3.4E-06 1.8E-06 1.5E+00 5.6E-01 2.E+00 

Notes: 




Permethrin E-Pro. Revised July 9 2007).These cancer risks ands HIs were calculated based on conservative exposure scenarios and exposure parameters 

selected to avoid underestimation of risk to the public. They are not meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the 

expected rate of disease in a population (see Section D6). 

D5.3.4.2 


Acute and subchronic inhalation HQs calculated for the Child Recreational Park User indicate 

that chlorpyrifos is the only chemical associated with an HQ greater than 1 (HQ of 4 for the 

acute inhalation route of exposure) (Table D5-8). 

The potential health impact of chronic exposures to the Child Recreational Park User were 

evaluated for the same pathways identified in Section D5.2.5. That evaluation indicates that 

permethrin and lambda-cyhalothrin are not expected to elicit adverse noncancer health effects to 

this receptor population when exposure occurs for an extended period. The chlorpyrifos HI of 3 

indicates that use of chlorpyrifos under the No Program Alternative is associated with potential 

adverse health effects for the Child Recreational Park User population. 

Dermal dose from contact with permethrin-contaminated ornamental vegetation resulted in a 

cancer risk for the Child Park User above 1 x 10 -6 . 

Additive effects from exposure to multiple Program chemicals were not evaluated (see 5.2.1). 


SECTION D5 


Table D5-8 

Child Park User Cancer Risks and Hazard Quotients – No Program Alternative 


Exposure 

Medium: 

Pathways: 

Air 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 

Total 


All 

Pathways 

Btk --- --- NA --- NA --- 

Spinosad --- --- --- --- --- --- 

Permethrin --- 1.1E-10 1.1E-10 NE 2.1E-05 2.E-05 

Lambda- 

Cyhalothrin 

--- --- --- --- --- --- 

Chlorpyrifos --- --- --- --- --- --- 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 


Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 

Total 

Chronic HI 

All 

Pathways 

Btk --- --- 2.7E-01 --- NA --- NA --- 


Permethrin 1.5E-06 1.6E-06 9.2E-04 4.4E-07 4.7E-07 NE 8.7E-02 9.E-02 

Lambda- 

Cyhalothrin 

4.2E-05 4.4E-05 2.6E-02 3.1E-06 2.2E-06 3.0E-01 4.1E-01 7.E-01 

Chlorpyrifos 4.1E-01 1.3E-01 4.5E+00 1.8E-05 3.7E-06 1.7E+00 6.9E-01 3.E+00 

Notes: 


NA = Appropriate toxicity value is not available 





Section D6). 

D5.4 MATING DISRUPTION ALTERNATIVE 

D5.4.1 

MD-1 

Under Alternative MD-1, Nursery/Program Workers, Agricultural Workers, Adult and Child 

Residents, Gardeners, and Adult and Child Recreational Park Users were evaluated for potential 

adverse effects from acute and subchronic inhalation of the LBAM pheromones that volatilize 

from the Isomate twist ties. Given the mode of application and the volatile nature of the 

pheromones, inhalation is expected to be the only exposure route for all adult receptor 

populations. Chronic inhalation exposures could not be quantitatively evaluated due to the 

absence of a suitable toxicity criterion. The HQs for both acute and subchronic inhalation 

exposure for adult receptor populations were all very low – approximately one million to one 

hundred thousand fold below the threshold value of 1 (Tables D5-9, D5-10, D5-11, D5-13). 

Chronic inhalation intakes (see Tables D4-13 through D4-16) are also very low – on the order of 




DRAFT PEIR 


one millionth to several millionths of a mg per kg body weight. There is no other specific 

information to indicate that exposures to SCLPs at these very low levels have been associated 

with adverse effects; furthermore, the low subchronic HQs also provide support for the 

conclusion that long-term exposures to the pheromones in Isomate are not likely to be a concern 

(see OEHHA, 2009). Additionally, there is no evidence to indicate that SCLPs are genotoxic or 

carcinogenic; their structural similarity to certain fatty acids indicates they are likely to be 

metabolized into substances of “no known toxicological concern” (OEHHA, 2009). Accordingly, 

it is considered unlikely that long-term (or short-term) use of the twist ties will result in any 

impacts on human health. OEHHA (2009), who had access to information on the additives in 

Isomate, has determined that exposure to the additives as well as to the active ingredients “are 

not likely to pose a health hazard to adults and children.” 

The Child Resident and the Child Recreational Park Users also had acute and subchronic 

inhalation HQs well below 1 (factors of approximately 10 million to ten thousand below 1, 

respectively – see Tables D5-12 and D5-16). In addition, both child receptor populations were 

evaluated for potential health effects attributed to the accidental ingestion of a twist tie. The HQ 

from this ingestion exposure is 0.05, indicating that no adverse effects are expected in the 

unlikely event that a child ingested (or chewed on) a twist tie. The preceding discussion 

regarding the very low potential for adverse effects to adult populations from long-term exposure 

to the pheromones in Isomate are directly relevant to the child receptor populations as well. 

Table D5-9 

Nursery/Program Worker Hazard Quotients – Mating Disruption Alternative, Twist Ties 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Isomate --- 3.1E-05 2.6E-06 --- --- --- 

Notes: 

--- = Appropriate toxicity value is not available. 

These HIs were calculated based on conservative exposure scenarios and exposure parameters selected to avoid underestimation of risk to the public. They are 

not meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the expected rate of disease in a population (see Section D6). 

Table D5-10 

Agricultural Worker Hazard Quotients – Mating Disruption Alternative, Twist Ties 


Exposure 

Medium: 

Air Soil Food 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Isomate --- 3.1E-05 2.6E-06 --- --- --- 

Notes: 





SECTION D5 


Table D5-11 

Adult Resident Hazard Quotients – Mating Disruption Alternative, Twist Ties 



Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Isomate --- 8.7E-05 1.8E-06 --- --- --- --- --- 

Ingestion 

Notes: 




Table D5-12 

Child Resident Hazard Quotients – Mating Disruption Alternative, Twist Ties 



Pathways: 

Inhalation 

Subchroni 

c 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Isomate --- 1.3E-04 1.4E-07 --- --- --- --- --- 

Ingestion 

Notes: 




Table D5-13 

Residential Adult Gardener Hazard Quotients – Mating Disruption Alternative, Twist Ties 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Isomate --- 1.5E-05 3.6E-06 --- --- --- --- --- --- 

Dermal 

Contact 

Notes: 







DRAFT PEIR 


Table D5-14 

Adult Park User Hazard Quotients – Mating Disruption Alternative, Twist Ties 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Isomate --- 4.2E-06 3.6E-06 --- --- --- --- 

Notes: 




Table D5-15 

Child Park User Hazard Quotients – Mating Disruption Alternative, Twist Ties 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Isomate --- 1.1E-05 9.4E-06 --- --- --- --- 

Notes: 




D5.4.2 

MD-2 

Under Alternative MD-2, the pheromone-containing products SPLAT and HERCON will be 

applied by ground-based methods. These methods of application may result in LBAM 

pheromone releases to ambient air, soil, and vegetation. As with the twist ties, potential hazard 

was evaluated to all of the receptor populations of interest (Nursery/Program Workers, 

Agricultural Workers, Adult and Child Residents, Adult Residential Gardener, Adult and Child 

Recreational Park Users). Because the mode of application is expected to release pheromones to 

multiple environmental media, EPCs were calculated for inhalation, soil, and vegetation-based 

exposure pathways (see Table D4-17). 

The acute and subchronic inhalation HQs for all receptor populations are approximately a 

hundred to a thousand fold lower than the threshold value of 1 (Tables D5-17 to D5-23). Because 

of these low HQs, adverse effects from acute and subchronic inhalation exposures are not 

considered likely. 

Chronic exposures - whether by inhalation, incidental ingestion of soil, or dermal contact - could 

not be quantitatively evaluated due to the absence of suitable toxicity criteria. However, the 

predicted chronic intakes of the pheromones are low (see Tables D4-18 through D4-23), ranging 

from approximately several hundredths of a mg to less than a millionth of a mg per kilogram 

body weight (depending on pathway). As noted for the twist ties, there are no data to indicate 


SECTION D5 


that exposures to SCLPs at these very low levels are associated with adverse effects, and, for the 

reasons discussed under Alternative MD-1, it is considered unlikely that long-term exposure to 

the pheromones released from SPLAT or HERCON will result in any impacts on human health. 

Ground-based application of SPLAT and HERCON may result in greater opportunities for 

individuals to come in contact with these products than with the Isomate twist ties. Results from 

dermal sensitization assays indicate that SPLAT may have some sensitizing potential, although 

the conclusions regarding this potential differed between the two assays used (see Section D3). 



were negative regarding the products sensitization potential. While acknowledging the 

uncertainties regarding the potential for sensitization, OEHHA (2008b) noted that it is prudent to 

treat the LBAM pheromone-containing products as dermal sensitizers in the absence of 

additional data. 

Table D5-16 

Nursery/Program Worker Hazard Quotients – Mating Disruption Alternative, Ground 

Application 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 


Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Hercon --- 5.2E-03 2.9E-03 --- --- --- 

Splat --- 1.1E-02 2.9E-02 --- --- --- 

Notes: 




Table D5-17 

Agricultural Worker Hazard Quotients – Mating Disruption Alternative, Ground Application 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 


Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Dermal 

Contact 

Hercon --- 5.2E-03 2.9E-03 --- --- --- 

Splat --- 1.1E-02 2.9E-02 --- --- --- 

Notes: 

iate toxicity value is not available. 






DRAFT PEIR 


Table D5-18 

Adult Resident Hazard Quotients – Mating Disruption Alternative, Ground Application 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Hercon --- 1.5E-02 1.9E-03 --- --- --- --- --- 

Splat --- 3.1E-02 2.0E-02 --- --- --- --- --- 

Notes: 




Table D5-19 

Child Resident Hazard Quotients – Mating Disruption Alternative, Ground Application 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Hercon --- 2.2E-02 2.9E-03 --- --- --- --- --- 

Splat --- 4.6E-02 3.0E-02 --- --- --- --- --- 

Notes: 




Table D5-20 

Residential Adult Gardener Hazard Quotients – Mating Disruption Alternative, Ground 

Application 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

Hercon --- 2.5E-03 3.9E-03 --- --- --- --- --- --- 

Splat --- 5.2E-03 4.0E-02 --- --- --- --- --- --- 

Notes: 





SECTION D5 


Table D5-21 

Adult Park User Hazard Quotients – Mating Disruption Alternative, Ground Application 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 


Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Hercon --- 7.1E-04 3.9E-03 --- --- --- --- 

Splat --- 1.5E-03 4.0E-02 --- --- --- --- 

Ingestion 

Notes: 




Table D5-22 

Child Park User Hazard Quotients – Mating Disruption Alternative, Ground Application 

Exposure 

Medium: 

Pathways: 

Inhalation 

Air 

Subchronic 

Inhalation 


Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Hercon --- 1.9E-03 1.0E-02 --- --- --- --- 

Splat --- 3.9E-03 1.1E-01 --- --- --- --- 

Ingestion 

Notes: 




D5.4.3 

MD-3 

The potential health effects from the aerial application of SPLAT and HERCON were evaluated 

to the receptor populations of interest; Nursery/Program Workers, Agricultural Workers, Adult 

and Child Residents, Adult Residential Gardener, and Adult and Child Recreational Park Users. 

Aerial treatment is expected to release pheromones to air, with subsequent deposition to soil and 

vegetation. Accordingly, both EPCs and intakes were calculated for inhalation, soil, and 

vegetation-based exposure pathways (see Tables D4-24 through D4-28). 

The acute and subchronic inhalation HQs for all receptor populations are approximately a 

thousand to ten thousand fold or more below the reference HQ of 1 (see Tables D5-24 to D5-30) 

On the basis of these low HQs, adverse effects from acute and subchronic inhalation exposures 

are not considered likely. 


exposures -could not be quantitatively evaluated due to the absence of appropriate toxicity 

criteria. However, the chronic intakes of the pheromones are low (see Tables D4-25 through D4- 

28), and range from approximately one hundredth of a mg to less than a millionth of a mg per 

kilogram body weight (depending on pathway). There are no data to indicate that exposures to 




DRAFT PEIR 


SCLPs at these concentrations are associated with any adverse effects, and it is not likely that 

long-term exposure to the pheromones released from SPLAT or HERCON will result in any 



comments discussing the potential for dermal sensitization provided in Section D5.4.2 are also 

relevant to SPLAT and HERCON applied aerially. 

Table D5-23 

Nursery/Program Worker Hazard Quotients – Mating Disruption Alternative, Aerial 

Application 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Hercon --- 1.2E-04 5.8E-05 --- --- --- 

Splat --- 1.9E-04 5.1E-04 --- --- --- 

Note: 




Table D5-24 

Agricultural Worker Hazard Quotients – Mating Disruption Alternative, Aerial Application 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Hercon --- 1.2E-04 5.8E-05 --- --- --- 

Splat --- 1.9E-04 5.1E-04 --- --- --- 

Note: 





SECTION D5 


Table D5-25 

Adult Resident Hazard Quotients – Mating Disruption Alternative, Aerial Application 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Hercon --- 3.3E-04 3.9E-05 --- --- --- --- --- 

Splat --- 5.3E-04 3.5E-04 --- --- --- --- --- 

Ingestion 

Note: 


These HIs were calculated based on conservative exposure scenarios and exposure parameters selected to avoid underestimation of risk to the public. They 

are not meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the expected rate of disease in a population (see Section D6). 

Table D5-26 

Child Resident Hazard Quotients – Mating Disruption Alternative, Aerial Application 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Hercon --- 4.9E-04 5.8E-05 --- --- --- --- 

Splat --- 7.9E-04 5.2E-04 --- --- --- --- --- 

Ingestion 

Note: 




Table D5-27 

Residential Adult Gardener Hazard Quotients – Mating Disruption Alternative, Aerial 

Application 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

Hercon --- 5.6E-05 7.9E-05 --- --- --- --- --- --- 

Splat --- 8.9E-05 7.0E-04 --- --- --- --- --- --- 

Notes: 







DRAFT PEIR 


Table D5-28 

Adult Park User Hazard Quotients – Mating Disruption Alternative, Aerial Application 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Pathways: 

Inhalation 

Subchroni 

c 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Hercon --- 1.6E-05 7.9E-05 --- --- --- --- 

Splat --- 2.5E-05 7.0E-04 --- --- --- --- 

Notes: 




Table D5-29 

Child Park User Hazard Quotients – Mating Disruption Alternative, Aerial Application 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Hercon --- 4.2E-05 2.1E-04 --- --- --- --- 

Splat --- 6.6E-05 1.8E-03 --- --- --- --- 

Notes: 





In this alternative, SPLAT will be applied along with Permethrin E-Pro, a formulation that 

contains the active ingredient permethrin, as well as ethylbenzene and 1,2,4-trimethylbenzene. 

Although triacetate is also present in Permethrin E-Pro, it was not evaluated as it is only 

minimally toxic (Section D3.1.6.1.3). SPLAT and Permethrin E-Pro will be applied to trees, 

utility poles, and similar structures with a specialized squirt gun, resulting in releases to air, soil, 

and vegetation. Carcinogenic risk attributable to permethrin and ethylbenzene, and noncancer 

hazard attributable to permethrin, ethylbenzene, and 1,2,4-trimethylbenzene were evaluated for 

all receptor populations - subject to availability of toxicity criteria (e.g., 1,2,4-trimethylbenzene 

lacks acute and subchronic inhalation toxicity criteria). Additive HIs were calculated to address 




The discussion in section 5.4.2 regarding the uncertainties of the dermal and respiratory 

sensitization potential of LBAM pheromones is applicable to this Alternative as well (use of 

SPLAT). 


SECTION D5 


D5.5.1 


The total incremental excess cancer risk for Nursery/Program Workers exposed to permethrin by 

chronic inhalation, incidental ingestion of soil, dermal contact with soil, and dermal contact with 

vegetation is 2 x 10 -6 (2 in 1,000,000); risk attributable to ethylbenzene is 3 x 10 -12 . Total risk 

from exposure to permethrin and ethylbenzene is also 2 x 10 -6 , and is dominated by the risks 

from permethrin. (Table D5-31). HQs calculated for individual pathways and individual 

chemicals, as well as HIs calculated for all pathways and all chemicals are below 1. Although the 

potential effects of chronic exposure to SPLAT could not be quantitatively evaluated due to a 

lack of appropriate toxicity data, adverse effects are not expected (see discussion provided for 

Alternative MD-2). 

Table D5-30 

Nursery/Program Worker Cancer Risks and Hazard Quotients – Male Moth Attractant 

Exposure 

Medium: 

Pathway: 

Air 

Inhalation 


Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Total Cancer 


All Pathways 

Splat --- --- --- --- --- 

Permethrin --- 3.3E-12 1.4E-11 1.9E-06 2E-06 

Ethylbenzene 3.5E-12 1.3E-15 NA NA 3E-12 

1,2,4- 


--- NA NA NA --- 


Exposure 

Medium: 

Pathway: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Total Chronic 

HI 

All Pathways 

Splat --- 7.7E-06 2.0E-05 --- --- --- --- 

Permethrin 4.4E-06 4.7E-06 2.1E-04 1.4E-08 6.0E-08 7.9E-03 8E-03 

Ethylbenzene 7.0E-09 4.9E-09 1.5E-08 1.2E-11 NA NA 7E-09 

1,2,4- 


2.7E-04 2.8E-05 --- --- NA NA 3E-04 

Notes: 





Section D6). 

D5.5.2 


The total incremental excess cancer risk for Agricultural Workers exposed to permethrin by 

chronic inhalation, incidental ingestion of soil, dermal contact with soil, and dermal contact with 

vegetation is 2 x 10 -11 ; risk attributable to ethylbenzene is 3 x 10 -12 . Total risk from exposure to 

permethrin and ethylbenzene is also 2 x 10 -11 . (Table D5-32). Where toxicity data supported 

quantitative assessments, HQs calculated for individual pathways and individual chemicals, as 

well as HIs calculated for all pathways and all chemicals are below 1. Potential adverse effects 




DRAFT PEIR 


from long-term exposure to SPLAT by Agricultural Workers could not be evaluated due to a 

lack of chronic toxicity data. However, adverse effects are not considered likely, for the reasons 

discussed in Section D5.4.2 (SPLAT evaluated for ground-based application under MD-2). 

Table D5-31 

Agricultural Worker Cancer Risks and Hazard Quotients – Male Moth Attractant 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Total 

Cancer 


Pathway: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

All 

Pathways 

Splat --- --- --- --- --- 

Permethrin --- 3E-12 1E-11 NE 2E-11 

Ethylbenzene 3E-12 1E-15 NA NA 3E-12 

1,2,4- 


--- --- NA NA --- 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Total 

Chronic HI 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

All 

Pathways 

Splat --- 8E-06 2E-05 --- --- --- --- 

Permethrin 4E-06 5E-06 2E-04 1E-08 6E-08 NE 4E-06 

Ethylbenzene 7E-09 5E-09 2E-08 1E-11 NA NA 7E-09 

1,2,4- 


3E-04 3E-05 --- --- NA NA 3E-04 

Notes: 







Section D6). 

D5.5.3 


Tables D5-33 and D5-34 summarize the results of the calculated cancer risk and noncancer 

hazard for Adult and Child Residents, respectively. For the Adult Resident, cancer risk 

attributable to permethrin is 2 x 10 -6 ; risks from ethylbenzene are 2 x 10 -10 . The risk from 

permethrin drives the risk from simultaneous exposure to these substances, yielding a total risk 

of 2 x 10 -6 . HQs calculated for individual pathways and individual chemicals, as well as HIs 

calculated for all pathways and all chemicals are below 1. 

For the Child Resident, cancer risk attributable to permethrin is 3 x 10 -6 ; risks from ethylbenzene 

are 2 x 10 -10 . As with the Adult Resident, the risk from permethrin drives the risk from 

simultaneous exposure to these substances, yielding a total risk of 2 x 10 -6 . Based on available 

toxicity data, HQs calculated for individual pathways and individual chemicals, as well as HIs 


SECTION D5 


calculated for all pathways and all chemicals are below 1. Because the HQs and HIs are below 1 

for both receptor populations, noncancer adverse effects are not expected to occur. 

For both the Adult and Child Residents, potential effects of chronic exposure to SPLAT could 

not be quantified due to a lack of chronic toxicity criteria. For the reasons discussed in Section 

D5.4.2 (SPLAT evaluated for ground-based application under MD-2), potential adverse effects 

from long-term exposure to SPLAT are not likely. 

Table D5-32 

Adult Resident Cancer Risks and Hazard Quotients – Male Moth Attractant 


Exposure 

Medium: 

Pathways: 

Air 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Homegrown 

Produce 

Ingestion 

Total 


All 

Pathways 

Splat --- --- --- --- --- --- --- 


Ethylbenzene 1.0E-11 2.3E-15 NA NA 1.5E-10 2.6E-11 2.E-10 

1,2,4- 


--- --- NA NA --- --- --- 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

All 

Pathways 

Splat --- 2.2E-05 1.4E-05 --- --- --- --- --- --- 


Ethylbenzene 2.0E-08 1.4E-08 1.0E-08 2.1E-11 NA NA 1.3E-06 2.4E-07 2.E-06 

1,2,4- 


7.7E-04 8.0E-05 --- --- NA NA --- --- 8.E-04 

Notes: 







D6). 




DRAFT PEIR 


Table D5-33 

Child Resident Cancer Risks and Hazard Quotients – Male Moth Attractant 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 


Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

All 

Pathways 

Splat --- --- --- --- --- --- --- 

Permethrin --- 2.9E-11 1.5E-11 2.9E-06 NE NE 3E-06 

Ethylbenzene 1.5E-11 1.2E-14 NA NA 1.6E-10 2.8E-11 2E-10 

1,2,4- 


--- --- NA NA --- --- --- 



Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion Ingestion All Pathways 

Splat --- 3.3E-05 2.1E-05 --- --- --- --- --- --- 

Permethrin 1.9E-05 2.0E-05 2.1E-04 1.2E-07 6.4E-08 1.2E-02 NE NE 1E-02 

Ethylbenzene 3.0E-08 2.1E-08 1.5E-08 1.1E-10 NA NA 1.5E-06 2.6E-07 2E-06 

1,2,4- 


1.2E-03 1.2E-04 --- --- NA NA --- --- 1E-03 

Notes: 




Permethrin E-Pro. Revised July 9 2007).These cancer risks ands HIs were calculated based on conservative exposure scenarios and exposure parameters selected 

to avoid underestimation of risk to the public. They are not meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the expected rate of 

disease in a population (see Section D6). 

D5.5.4 

Adult Resident Gardener 

Residential Adult Gardeners are predicted to have an incremental excess cancer risk from 

permethrin is 7 x 10 -7 and risks from ethylbenzene of 2 x 10 -10 (Table D5-35). As with all 

receptor populations considered for this alternative, the risk from permethrin drives the risk from 

concurrent exposure to these substances, yielding a total risk of 7 x 10 -7 . For those chemicals that 

had the requisite supporting toxicity data, HQs calculated for individual pathways and individual 

chemicals, as well as HIs calculated for all pathways and all chemicals are below 1, indicating 

that noncancer adverse effects of exposure are not expected to occur. 

For the reasons discussed in Section D5.4.2 (SPLAT evaluated for ground-based application 

under MD-2), potential adverse effects from long-term exposure to SPLAT are not likely. 

Table D5-34 

Residential Adult Gardener Cancer Risks and Hazard Quotients – Male Moth Attractant 



SECTION D5 


Exposure 

Medium: 

Pathways: 

Air 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ingestion 

Homegrown 

Produce 

Dermal 

Contact 

Splat --- --- --- --- --- --- --- --- 

Total 

Cancer 


All 

Pathways 

Permethrin --- 1.6E-12 3.7E-12 6.6E-07 NE NE NE 7E-07 

Ethylbenzene 4.8E-13 6.5E-16 NA NA 1.5E-10 2.6E-11 NA 2E-10 

1,2,4- 

Trimethylbenze 

ne 

--- --- NA NA --- --- NA 


--- 

Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

All Pathways 

Splat --- 3.7E-06 2.8E-05 --- --- --- --- --- --- --- 

Permethrin 6.1E-07 2.2E-06 2.9E-04 6.7E-09 1.6E-08 2.7E-03 NE NE NE 3E-03 

Ethylbenzene 9.7E-10 2.3E-09 2.1E-08 5.9E-12 NA NA 1.3E-06 2.4E-07 NA 2E-06 

1,2,4- 

Trimethylbenze 

ne 

3.7E-05 1.4E-05 --- --- NA NA --- --- NA 

Notes: 


NA = No applicable 

NE = Not evaluated because permethrin is registered by the USEPA primarily for use as a termiticide and on non-food crops (Etigra, 2007. Product Label for Permethrin 

E-Pro. Revised July 9 2007).These cancer risks ands HIs were calculated based on conservative exposure scenarios and exposure parameters selected to avoid 

underestimation of risk to the public. They are not meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the expected rate of disease in a 

population (see Section D6). 

4E-05 

D5.5.5 

Adult and Child Recreational Park User 

Tables D5-36 and D5-37 summarize the results of the calculations of cancer risk and noncancer 

hazard for Adult and Child Recreational Park Users, respectively. 




DRAFT PEIR 


Table D5-35 

Adult Park User Cancer Risks and Hazard Quotients – Male Moth Attractant 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Ornamental 

Vegetation 

Total 


Pathways: 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Splat --- --- --- --- --- --- 

Permethrin --- 8.1E-13 2.1E-12 NE 6.6E-07 7E-07 

Ethylbenzene 4.8E-13 3.3E-16 NA 1.5E-10 NA 5E-13 

1,2,4- 


--- --- NA --- NA --- 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Ornamental 

Vegetation 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Splat --- 1.1E-06 2.8E-05 --- --- --- --- --- 

Permethrin 6.1E-07 6.4E-07 2.9E-04 3.4E-09 8.8E-09 NE 2.7E-03 3E-03 

Ethylbenzene 9.7E-10 6.7E-10 2.1E-08 3.0E-12 NA 1.3E-06 NA 1E-09 

1,2,4- 


3.7E-05 3.9E-06 --- --- NA --- NA 4E-05 

Notes: 







Section D6). 


SECTION D5 


Table D5-36 

Child Park User Cancer Risks and Hazard Quotients – Male Moth Attractant 


Exposure 

Medium: 

Pathways: 

Air 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Commercial 

Produce 

Ingestion 

Ornamental 

Vegetation 

Dermal 

Contact 

Total 


All 

Pathways 

Splat --- --- --- --- --- --- 

Permethrin --- 4.2E-12 4.4E-12 NE 8.2E-07 8E-07 

Ethylbenzene 1.3E-12 1.7E-15 NA 1.6E-10 NA 1E-12 

1,2,4- 


--- --- NA --- NA --- 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Ornamental 

Vegetation 

Total 

Chronic HI 

Pathways: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Splat --- 2.8E-06 7.3E-05 --- --- --- --- --- 

Permethrin 1.6E-06 1.7E-06 7.6E-04 1.7E-08 1.8E-08 NE 3.4E-03 3E-03 

Ethylbenzene 2.6E-09 1.8E-09 5.5E-08 1.5E-11 NA 1.5E-06 NA 3E-09 

1,2,4- 


9.7E-05 1.0E-05 --- --- NA --- NA 1E-04 

Notes: 







Section D6). 

The Adult Park User has an estimated risk from permethrin and ethylbenzene of 7 x 10 -7 and 

5 x 10 -13 , respectively. Total cancer risk to this receptor from permethrin and ethylbenzene is 

7 x 10 -7 . The Child Park User has predicted risks from permethrin and ethylbenzene of 8 x 10 -7 

and 1 x 10 -12 , respectively. Total cancer risk to this receptor from permethrin and ethylbenzene is 

8 x 10 -7 . 

For both the Adult Park User and the Child Park User, HQs calculated for individual pathways 

and individual chemicals, as well as HIs calculated for all pathways and all chemicals are 

below 1. These results indicate that noncancer adverse effects of exposure are not expected to 

occur. 




DRAFT PEIR 


D5.6 ORGANIC TREATMENT ALTERNATIVE 

Application of Btk and spinosad by backpack and/or truck-mounted spray equipment is expected 

to result in the release of these materials to air, soil, and vegetation. The evaluation of health 

effects from potential exposure to Btk or spinosad is subject to the availability of toxicity data; 

those data are not sufficient to quantify effects from all exposure pathways or for all exposure 

durations. When quantitative estimates of health effects are not possible, comparisons were made 

between intakes of Btk or spinosad and available toxicity data. Like the quantitative evaluations 

that result in HQs or HIs, these comparisons support an understanding – albeit semi-quantitative 

- of the likelihood of adverse effects that may occur from exposure. 

D5.6.1 

Nursery/Program Workers and Agricultural Workers 

Nursery/Program Workers and Agricultural Workers are predicted to incur exposure to Btk or 

spinosad via similar pathways, with Agricultural Workers evaluated for the additional pathway 

of dermal contact with commercial produce (spinosad only) (Table D4-38). Based on acute 

inhalation HQs that are less than 1, neither Btk nor spinosad should cause adverse health effects 

to these Worker populations (Tables D5-38 and D5-39). Subchronic inhalation RfDs are not 

available for either spinosad or Btk. However, the intakes for this exposure pathway (Table D4- 

38) are very low, and are approximately ten-fold lower than the intakes used to develop the acute 

inhalation HQs. Additionally, spinosad has a chronic RfD (Table D5-1) that can be used to 

estimate an approximate HQ using the subchronic inhalation intake. Because that comparison 

gives an approximate HQ that is about 10000 times lower than the HQ threshold value of 1, 

adverse effects of subchronic exposure to spinosad are not expected for either worker population. 

All chronic HQs for spinosad, and the HI obtained from summing all HQs, are less than 1. These 

results indicate that health effects from long-term exposure to spinosad are not likely for these 

populations. 

No chronic RfD is available for Btk. Estimated chronic intakes (Table D4-38) are about a 

hundred thousandth to roughly a millionth of a mg per kg day. These intakes are very low; for 

comparison, long-term toxicity studies of Btk (see McClintlock et al 1995 and discussion in 

Section D3) cite data in which very large quantities of Btk (e.g., 10 9 spores/kg-d, roughly 

equivalent to a g/kg-day, and 8.4 g/kg-d) were tolerated with minimal effects. These data suggest 

that long-term exposures to Btk at the levels estimated here are not likely to result in adverse 

health effects. 


SECTION D5 


Table D5-37 

Nursery/Program Worker Hazard Quotients–Organic Treatment Alternative 



Pathway: 

Bacillus thuringiensis 

kurstaki 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Total Chronic 

HI 

All Pathways 

--- --- 7.6E-02 --- NA NA --- 


Notes: 





Table D5-38 

Agricultural Worker Hazard Quotients – Organic Treatment Alternative 


Exposure 

Medium: 

Pathway: 

Inhalation 

Air 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Soil 

Dermal 

Contact 

Ornamental 

Vegetation 

Dermal 

Contact 

Total Chronic 

HI 

All Pathways 

Bacillus 

thuringiensis --- --- 7.6E-02 --- NA NA --- 

kurstaki 


Notes: 





D5.6.2 


Adult and Child Residents are not expected to incur adverse health effects from acute inhalation 

exposure to spinosad or Btk (HQs are less than 1 for both materials) (Tables D5-40 and D5-41). 

As explained in the preceding discussion for Nursery/Program Workers and Agricultural 

workers, subchronic inhalation RfDs are not available for either spinosad or Btk. Similar to the 

worker populations, the intakes for this exposure pathway (Table D4-39) are very low, and are 

either approximately equal to (spinosad) or about ten-fold lower (Btk) than the intakes used to 

develop the acute inhalation HQs. If a subchronic inhalation HQ is approximated by using 

spinosad’s chronic RfD (Table D5-1) with the subchronic inhalation intakes, the resulting HQs 

are 6 x 10 -5 (Adult Resident) or 9 x 10 -5 (Child resident). These values are far below the 

threshold of 1, and suggest that adverse effects of subchronic exposure to spinosad are not 

anticipated. 




DRAFT PEIR 


All chronic HQs for spinosad, and the HI obtained from summing all HQs, are less than 1 for the 

Adult and Child Residents. These results indicate that health effects from long-term exposure to 

spinosad are not likely for these populations. 

Because a chronic RfD is not available for Btk, estimated chronic intakes (Table D4-39) can be 

examined to obtain an understanding of the magnitude of exposure. Those pathway-specific 

intakes range from several hundred thousandths to approximately one-one hundredth of a mg per 

kg-day, well below levels associated with toxicity (see preceding discussion for workers, as well 

as Section D3). Additionally, it is important to recognize that the highest intakes are attributable 

to ingestion of homegrown and commercial produce. These are very conservative intake 

estimates, and do not account for removal of Btk from produce by washing prior to ingestion. By 

not accounting for removal by washing, intakes are probably overestimated to a considerable 

degree. 

Table D5-39 

Adult Resident Hazard Quotients – Organic Treatment Alternative 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commerci 

al Produce 

Homegrow 

n Produce 

Total 

Chronic HI 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

All 

Pathways 

Bacillus 

thuringiensis --- --- 5.1E-02 --- NA NA --- --- --- 

kurstaki 


Notes: 





Table D5-40 

Child Resident Hazard Quotients – Organic Treatment Alternative 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Chronic 

HI 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

All 

Pathways 

Bacillus 

thuringiensis --- --- 7.7E-02 --- NA NA --- --- --- 

kurstaki 


Notes: 






SECTION D5 


D5.6.3 

Adult Resident Gardener 

Calculated HQs for the Adult Resident Gardener are provided in Table D5-42. The HQs from 

acute inhalation exposure to spinosad or Btk are less than 1 for both materials. 

The analyses and comparisons made for the worker and resident populations regarding 

subchronic inhalation to Btk and spinosad are applicable to the Adult Gardener as well. They 

support a conclusion that the subchronic exposure duration is not expected to be associated with 



Adult Gardener. These results indicate that health effects from long-term exposure to spinosad 

are not likely for this population. 

A comparison of chronic intakes for Btk (Table D4-40) to the toxicity data previously cited (see 

Section D3 and preceding discussions for this Alternative) indicate that intakes of Btk for the 

Adult Gardener are also expected to be below levels of concern. 

Table D5-41 

Residential Adult Gardener Hazard Quotients – Organic Treatment Alternative 


Exposure 

Medium: 

Air 

Soil 

Ornamental 

Vegetation 

Commercial 

Produce 

Homegrown 

Produce 

Total 

Chronic 

HI 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Dermal 

Contact 

Ingestion 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Bacillus 

thuringiensis 

kurstaki 

--- --- 1.0E-01 --- NA NA --- --- NA --- 

Spinosad 2.8E-06 --- 1.7E-04 1.1E-06 1.7E-07 3.0E-02 2.5E-01 4.4E-02 1.4E-02 3.E-01 

Notes: 



These HIs were calculated based on conservative exposure scenarios and exposure parameters selected to avoid underestimation of risk to the public. They are not 

meant to reflect actual estimates of exposure, nor interpreted as actual estimates of the expected rate of disease in a population (see Section D6). 

D5.6.4 Adult and Child Recreational Park User 

The HQs for the Adult and Child Recreational Park Users are provided in Tables D5-43 and D5- 

44. The HQs from acute inhalation exposure to spinosad or Btk are less than 1 for both 

substances and both receptor populations. 

Previous analyses (see Sections D5.6, D5.6.2, and D5.6.3) regarding subchronic inhalation to 

Btk and spinosad are also applicable to the Adult and Child Recreational Park users, These 

analyses support a conclusion that subchronic exposures are not expected to be associated with 





DRAFT PEIR 



Adult and Child Park Users. Consequently, health effects from long-term exposure to spinosad 

are not likely for this population. 

Chronic intakes for Btk (Table D4-41) to the toxicity data previously cited (see Section D3 and 

preceding discussions for this Alternative) indicate that intakes of Btk for the Adult and Child 

Park Users are also below levels of concern. 

Table D5-42 

Adult Park User Hazard Quotients – Organic Treatment Alternative 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Ornamental 

Vegetation 

Total Chronic 

HI 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Bacillus 

thuringiens --- --- 1.0E-01 --- NA --- NA --- 

is kurstaki 


Notes: 





Table D5-43 

Child Park User Hazard Quotients – Organic Treatment Alternative 


Exposure 

Medium: 

Air 

Soil 

Commercial 

Produce 

Ornamental 

Vegetation 

Total 

Chronic 

HI 

Pathway: 

Inhalation 

Subchronic 

Inhalation 

Acute 

Inhalation 

Incidental 

Ingestion 

Dermal 

Contact 

Ingestion 

Dermal 

Contact 

All 

Pathways 

Bacillus 

thuringiensis --- --- 2.7E-01 --- NA --- NA --- 

kurstaki 


Notes: 






SECTION D5 





Human Health Risk 

Conclusions and Uncertainties 

D6.1 UNCERTAINTIES IN THE ASSESSMENT OF HUMAN HEALTH RISKS 

Understanding the degree of uncertainty associated with each component of a risk assessment is 

critical to interpreting the assessment results. In their discussion of risk assessments conducted 

by the USEPA, the NRC (1994) noted that [a risk assessment should include] “ a full and open 

discussion in the body of each EPA risk assessment, including prominent display of critical 

uncertainties in the risk characterization.” The NRC (1994) further states that “…when EPA 

reports estimates of risk to decision-makers and the public, it should present not only point 

estimates of risk, but also the sources and magnitude of uncertainty associated with these 

estimates.” These principles are considered applicable to this risk assessment, and accordingly, 

some of the key uncertainties are discussed below. 

Important uncertainties in this risk assessment are attributable to the availability of toxicity data 

used to understand and characterize the relationship between exposure and the likelihood of 

adverse effects. For the pheromone formulations Isomate, SPLAT, and HERCON, formulationspecific 

toxicity data are limited to those developed for acute (short-term) exposure periods. 

These data provide important information on the short-term toxicity of the formulations by oral, 

dermal and inhalation exposures, as well as on the potential for eye and dermal irritation, and 

dermal sensitization. However, formulation-specific data that characterize potential effects – if 

any – of subchronic and chronic exposures are not currently available. Instead, subchronic 

toxicity data for SCLPs were used to support development of a subchronic RfD for the LBAM 

pheromones. No chronic data are available on SCLPs in general, or the LBAM pheromones in 

particular, that can support a full understanding of potential health hazards of long-term 

exposures to these substances. While there is nothing in the structure of SCLPs or in the history 

of their usage to indicate that such health hazards are associated with long-term use, having this 

specific information available would have reduced this important uncertainty. 

Another important uncertainty for the LBAM pheromones relates to their potential action as 

dermal sensitizers. Symptom reports from Santa Cruz and Monterey counties following the 2007 

aerial application of two different Checkmate products triggered a detailed examination of 

possible linkages between exposure to the LBAM pheromones, dermal allergic reactions, and 

respiratory complaints (as well as other, less-frequently reported symptoms) (OEHHA et al. 

2008). While that examination determined that there was a low potential for acute adverse 

effects, the agencies also concluded that not enough information was available to determine if 

there was a relationship between the symptoms and the pheromone applications. A subsequent 

evaluation of dermal sensitization data from four LBAM pheromone formulations, supplemented 

by studies on the LBAM pheromone active ingredients, led OEHHA (2008b) to conclude that 

they could not rule out the possibility that for sensitive individuals, contact could cause “allergic 

–type responses, although….[certain study results] do not provide a compelling argument for 




DRAFT PEIR 


such a link.” The uncertainties associated with the potential of the LBAM pheromones to act as 

sensitizing agents in susceptible individuals can only be addressed through further study. 

These uncertainties notwithstanding, long experience with other structurally similar compounds 

indicate that straight chain Lepidopteran pheromones have minimal toxicity. That fact, coupled 

with the extremely low predicted environmental concentrations of the pheromones present in 

Isomate, SPLAT, or HERCON, and the correspondingly small calculated potential exposure 

levels indicate that the possibility of adverse effects from the proposed use of these materials is 

quite limited, and is likely extremely small. 

Additionally, it is important to note that when HERCON was tested for acute inhalation and oral 

toxicity (see Section D3), the testing laboratory was able to grind less than 0.1% of the test 

substance into a form sufficiently small for testing. Although the physical form of HERCON 

made it unfeasible to develop key toxicity data, that physical form also indicates that the product 

will not be biologically available in significant quantities when exposure occurs either orally or 

by inhalation. (These comments do not apply to inhalation of the pheromones released from 

HERCON to ambient air.) Furthermore, the calculated intakes of HERCON are based on 

estimated theoretical releases of the product to air and subsequent deposition to soil and 

vegetation. Those intakes do not explicitly take into account the size of the HERCON flake or its 

bioavailability and, thus, likely represent overestimates of the magnitude of actual exposure. 

For both SPLAT and HERCON, intake estimates do not account for removal of these materials 

from vegetation by washing prior to ingestion. Because the products are visible, it is likely that 

produce would be washed before being eaten to remove visible residues. Not accounting for the 

process of removal by washing likely overestimates the potential exposures that might be 

incurred by ingestion. 

The cancer risks attributable to permethrin are predominantly due to doses potentially incurred 

via dermal absorption from contact with contaminated ornamental vegetation (No Program and 

MMA). For the MMA in particular, these risk estimates are highly conservative given the 

targeted mode of application (specialized squirt gun) and height of application (8 feet above 

ground). The risk estimates address the possibility that some of the permethrin (added to 

SPLAT) will miss the target and inadvertently end up on vegetation. However, CDFA has 

controls and processes in place to minimize this from occurring. Furthermore, in the event that 

some SPLAT/permethrin misses the target, it is not likely that an individual would have 

opportunities for regular sustained exposure to these materials as is assumed in this HRA. For 

these reasons, cancer risks attributable to permethrin are uncertain and likely overestimate the 

actual risks. 

Uncertainties also exist regarding the derivation of toxicity criteria for some of the 

nonpheromone pesticides evaluated in this assessment. For Btk, no data from either 

epidemiological or animal toxicity studies have linked exposure to Btk at environmentally 

relevant doses to biologically and/or statistically significant effects. However, because of the 

need to provide a means to quantify the effects of exposure to Btk despite the absence of clearly 

appropriate studies, an inhalation RfD was developed for acute inhalation exposure. That 

inhalation RfD was based on human effects data that indicated only transient effects of exposure. 

These effects are not believed to be biologically significant. The development of that RfD 

implies a greater certainty of the exposure-response relationship of Btk than are supported by 


SECTION D6 

CONCLUSIONS AND UNCERTAINTIES 

available data. An additional uncertainty relevant to Btk, and previously noted for HERCON, 

and SPLAT is that the calculated intakes from ingestion of contaminated homegrown or 

commercial produce do not account for removal by washing. Since washing of produce is a 

common practice, it is likely that actual intakes of Btk from produce would be substantially less 

as a result of removal of these materials by washing. 

With the exception of an oral toxicity criterion identified for chlorpyrifos and the inhalation 

criterion developed for Btk (as noted), all other toxicity data used in this risk assessment are 

based on dose-response data obtained from studies in experimental animals. Use of animal data 

to interpret potential human outcomes is associated with many uncertainties, including the 

sensitivity and appropriateness of the endpoints evaluated, the quality of the studies, and the 

greater genetic variability of humans relative to experimental animals. Although UFs were 

applied to account for these and other variables, the true nature and magnitude of the 

uncertainties associated with these extrapolations is difficult to quantify. 

The selection of pathways used to quantify potential exposure and health effects were made 

based on conceptual “site” models (see Figures D4-1 through D4-3) that identified those 

pathways associated with each mode of application for a set of hypothetical receptor populations. 

For a number of receptor populations, potential exposures that could occur shortly after 

application were evaluated, despite the fact that label requirements, workplace safety 

precautions, and general safety practices dictate the use of protective equipment to minimize or 

eliminate such exposures. Label requirements, workplace practices, and safe handling procedures 

would also limit the likelihood of individuals being exposed to concentrations of pesticides 

during application, and this pathway was not evaluated. Although such exposures are possible, 

quantification of exposures via this pathway are not expected to have changed the conclusions 

regarding the relative health effects attributed to each alternative. 

In regulatory risk assessment, conservative exposure assumptions (exposure parameters) are 

typically utilized to yield estimates of risk that are protective of human health. Use of these 

parameters is “…designed to err on the side of health protection to avoid underestimation of risk 

to the public (OEHHA 2003). Because of this inherent conservatism, the risk estimates provided 

in this assessment are not meant to be interpreted as the expected rate of morbidity in a 

population (OEHHA 2003), but instead, are best used as a basis for comparing different sources 

of exposure to one another and thus, to allow the prioritization or selection of alternatives. In 

keeping with this health-protective approach, a majority of the exposure parameters used to 

characterize potential exposure from the different pesticides were obtained from OEHHA (2003). 

Although certain exposure parameters represent mean values (e.g., the ingestion rate of 

homegrown produce), others are “high end” i.e., they are values selected from the upper range of 

a distribution of values for a particular parameter. For example, this assessment utilized the 

assumption that workers will be exposed 8 hours/day, 5 days/week for the period of active 

treatment (subchronic exposures) or 245 days/year over the 7 year period of the Program 

(chronic exposures). Potential health effects to hypothetical Residential Receptors were 

characterized with similarly conservative assumptions (e.g., chronic exposures may occur 24 

hours/day, 350 days/year for 7 years. To put the latter assumption in perspective, adult residents 

typically spend 68-73% of their total daily time at home (USEPA 1997), whereas this risk 

assessment assumed that value to be 100%. 




DRAFT PEIR 


D6.2 CONCLUSIONS ON HUMAN HEALTH RISKS 

The goal of this HHRA was to use a consistent set of exposure assumptions in conjunction with 

predicted environmental concentrations of Program chemicals to evaluate the potential health 

effects associated with each Program Alternative. This approach allows direct comparisons 

between the health effects attributable to each alternative, which in turn, can be used to inform 

the selection of one or more alternatives by CDFA. 

The assessment was necessarily broadly focused, as the statewide extent of the Program 

precludes characterization of potential effects to specific individuals or populations. Instead, this 

screening-level evaluation assessed the potential for adverse health effects using conservative 

exposure assumptions designed to be protective of all populations, including the most sensitive. 

No Program Alternative. 

The risks and hazards provided in Section D5 and summarized in the following discussion, were 

developed based on conservative exposure parameters and air modeling methods selected to 

avoid underestimation of risk to the public. They are not meant to reflect actual estimates of 

exposure, not are they meant to be interpreted as actual estimates of the expected rate of disease 

in a population (see OEHHA 2003). 

D6.2.1 

No Program 

The No Program Alternative addresses the use of spinosad, Btk, lambda-cyhalothrin, permethrin, 

or chlorpyrifos by private landowners to control the LBAM, while maintaining state and federal 

quarantines. Because no basis exists to assume that more than one of these chemicals would be 

used at a given time, additive effects were not evaluated. 

Cancer risks above 1 x 10 -6 were identified for Nursery/Program Workers, Adult and Child 

Residents, Adult Gardeners, and Adult and Child Park Users. All of these risks are attributable to 

dermal doses potentially acquired from contact with permethrin-contaminated vegetation. 

Chronic noncancer HIs exceeded the threshold value of 1 for Nursery/Program Workers 

(lambda-cyhalothrin and chlorpyrifos); Agricultural Workers (chlorpyrifos), Adult Resident 

(chlorpyrifos), Child Resident (lambda-cyhalothrin and chlorpyrifos, Adult Gardener 

(chlorpyrifos), Adult Park User (chlorpyrifos), and the Child Park User (chlorpyrifos). 

D6.2.2 

Mating Disruption (MD) Alternative 

For the MD Alternative, potential exposures to LBAM pheromone formulations were evaluated 

for twist ties (MD-1, Isomate), ground-based application (MD-2, SPLAT and HERCON), or 

aerial application (MD-3, SPLAT and HERCON). 

D6.2.2.1 

MD-1 

The HQs for both acute and subchronic inhalation exposures calculated for Alternative MD-1 

were all very low, approximately one million to one hundred thousand-fold below the threshold 

value of 1. In addition, both child receptor populations were evaluated for potential health effects 

attributed to the accidental ingestion of a twist tie. The HI from this ingestion exposure is 0.05, 

indicating that no adverse effects are expected in the unlikely event that a child ingested (or 

chewed on) a twist tie. 


SECTION D6 


Estimated chronic inhalation intakes of the LBAM pheromones were also low, ranging from 

approximately one millionth to several millionths of a mg/kg-day. There is no information to 

indicate that long-term exposures to the pheromones at these very low levels will be associated 

with adverse effects. The low subchronic HQs for Isomate exposures provide further support for 

the conclusion that long-term exposures are not likely to be a concern (also see OEHHA, 2009b). 

As reviewed in Section D3, there is no evidence to indicate that SCLPs are genotoxic or 

carcinogenic, and their structural similarity to certain fatty acids indicates they are likely to be 

metabolized into substances of “no known toxicological concern” (OEHHA, 2009). Accordingly, 

it is considered unlikely that long-term (or short-term) use of the twist ties will result in any 


OEHHA (2009b), who had access to information on the additives in Isomate, has also 

determined that the additives , as well as exposure to the product itself, “are not likely to pose a 

health hazard to adults and children.” 

D6.2.2.2 MD-2 

The acute and subchronic inhalation HQs for all receptor populations evaluated under 

Alternative MD-2 are approximately a hundred to a thousand fold lower than the threshold value 

of 1. Because of these low HQs, adverse effects from acute and subchronic inhalation exposures 

are not considered likely. 

Chronic exposures - whether by inhalation, incidental ingestion of soil, or dermal contact -could 

not be quantitatively evaluated due to the absence of suitable toxicity criteria. However, the 

predicted chronic intakes of the pheromones are low (see Tables D4-18 through D4-23), ranging 

from approximately several hundredths of a mg per kg-day to less than a millionth of a mg/kgbody 

weight (depending on pathway). As noted for the twist ties, there are no data to indicate 

that exposures to SCLPs at these very low levels are associated with adverse effects, and, for the 

reasons discussed under Alternative MD-1, it is considered unlikely that long-term exposure to 

the pheromones released from SPLAT or HERCON would result in any impacts on human 

health. 

Although the quantitative analyses of potential health effects (see preceding discussion) indicates 

that adverse effects are not likely from exposures to the pheromones in SPLAT or HERCON, 

there is some information which indicates that the LBAM pheromones may cause dermal 

sensitization following direct contact (OEHHA 2008b; OEHHA et al 2008). Results from dermal 

sensitization assays indicate that SPLAT may have some sensitizing potential (see Section D3). 



were negative regarding the products sensitization potential. The likelihood of sensitization from 

exposure to the pheromones cannot be quantified because there is not sufficient information 

available to determine what levels of pheromones, what types of exposure, or what other 

variables may be involved in this response in humans. Despite the uncertainties regarding the 

potential for sensitization, the possibility that dermal sensitization could occur from contact with 

LBAM pheromone-containing products cannot be excluded (OEHHA 2008b) 




DRAFT PEIR 


D6.2.2.3 

MD-3 

Aerial treatment is expected to release pheromones directly to air, with subsequent deposition to 

soil and vegetation. The calculated acute and subchronic inhalation HQs range from 

approximately a thousand to ten thousand fold or more below the reference HQ of 1. On the 

basis of these low HQs, adverse effects from acute and subchronic inhalation exposures are not 

considered likely. 


exposures could not be quantitatively evaluated due to the absence of chronic toxicity criteria for 

SCLPs. However, the estimated chronic intakes of the pheromones are low (see Tables D4-25 

through D4-28), and range from approximately one hundredth of a mg per kg-day to less than a 

millionth of a mg/kg body weight-day (depending on pathway). There are no data to indicate that 

exposures to SCLPs at these concentrations are associated with any adverse effects, and it is not 

likely that long-term exposure to the pheromones released from SPLAT or HERCON will result 

in any impacts on human health. 


comments regarding the potential for dermal and respiratory sensitization provided above are 

also relevant to SPLAT and HERCON applied aerially. 

D6.2.3 

Male Moth Attractant (MMA) Alternative 

In the MMA Alternative, the pheromone formulation SPLAT will be applied with Permethrin E- 

Pro to attract and kill LBAM. The permethrin product is a formulation that contains 

ethylbenzene and 1,2,4-trimethylbenzene as well as permethrin as the active ingredient. Because 

permethrin and ethylbenzene are classified as carcinogens, carcinogenic risks attributable to 

potential permethrin and ethylbenzene exposure were calculated, as well as non-cancer HIs from 

permethrin, ethylbenzene, and 1,2,4-trimethylbenzene. Additive HIs were calculated to address 




Cancer risks above 1 x 10 -6 , all attributable to permethrin, were calculated for Nursery/Program 

Workers, Adult and Child Residents, Adult Gardeners, and both Adult and Child Park Users. 

Ethylbenzene did not contribute significantly to cancer risk for any population, and thus the total 

risks from permethrin and ethylbenzene are equivalent to those calculated for permethrin alone. 

Those noncancer HQs calculated for individual chemicals and individual pathways, as well as 

HIs calculated for all pathways and all chemicals are below 1 for all receptor populations. 

Chronic exposures to the pheromones in SPLAT could not be quantitatively evaluated due to the 

absence of chronic toxicity data. However, the predicted chronic intakes of the pheromones in 

SPLAT are low (see Tables D4-18 through D4-23), ranging from approximately several 

hundredths of a mg to less than a millionth of a mg/kg-body weight (depending on pathway). As 

discussed for the MD Alternative, there are no data to indicate that exposures to SCLPs at these 

very low levels are likely to be associated with effects on human health. However, the cautions 

regarding the potential sensitizing action of the LBAM pheromones (see MD Alternative and 

discussions in Section D3) pertain to the use of SPLAT in this alternative as well. 


SECTION D6 


D6.2.4 

Organic Treatment Alternative 

The Organic Treatment Alternative considers the use of spinosad and the biopesticide Btk for 

control and eradication of LBAM. The evaluation of health effects from potential exposure to 

these materials is subject to the availability of toxicity data; those data are not sufficient to 

quantify effects from all exposure pathways or for all exposure durations. When quantitative 

estimates of health effects were not possible, comparisons were made between intakes of Btk or 

spinosad and available toxicity data to support an understanding of the likelihood of adverse 

effects that may occur from exposure. 

For both Btk and spinosad, acute inhalation HIs are below 1 for all receptor populations, thus 

health effects from acute exposures are not expected. Subchronic inhalation RfDs are not 

available for either spinosad or Btk. However, the intakes for this exposure pathway for all 

receptor populations are very low, and are approximately ten-fold lower (or more) than the 

intakes used to develop the acute inhalation HIs, indicating that effects of subchronic inhalation 

exposure are not likely. An additional comparison can be made for spinosad, which has a chronic 

RfD (Table D5-1). If that value is used to develop an HI using the subchronic inhalation intake, 

the result – for all receptor populations – are HIs that are a hundred-fold to approximately 10,000 

times lower than the HI threshold value of 1. Based on this evaluation, adverse effects of 

subchronic exposure to spinosad are not expected for any receptor population. 

All chronic HQs for spinosad, and the HI obtained from summing all HQs, are less than 1 for all 

receptor populations. Consequently, health effects from long-term exposure to spinosad are not 

likely. 

No chronic RfD is available for Btk; however estimated chronic intakes range from about a 

hundredth of a mg per kg day to roughly a millionth of a mg per kg day. These intakes are far 

below quantites of Btk (e.g., 10 9 spores/kg-d, roughly equivalent to a g/kg-day [or five-fold 

higher than the highest estimated intake in this HRA], and 8.4 g/kg-d) that have been tolerated 

with only minimal effects in animal studies. These data suggest that long-term exposures to Btk 

at the levels estimated here are not likely to result in adverse health effects. These conclusions 

regarding the relative safety of Btk are also supported by its long usage history, and by an 

extensive body of evidence from large-scale ground and aerial applications which have yielded 

no evidence of significant or persistent health effects from exposure. 




DRAFT PEIR 





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