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PERCHLOROETHYLENE CAS No: 127-18-4 I. PHYSICAL AND CHEMICAL PROPERTIES (From HSDB, 1998) Molecular weight 165.83 Boiling point 121 o C Melting point -19 o C Vapor pressure 18.47 mm Hg @ 25 o C Air concentration conversion 1 ppm = 6.78 mg/m 3 @ 25 o C II. HEALTH ASSESSMENT VALUES Unit Risk Factor: 5.9 E-6 (µg/m 3 ) -1 Slope Factor: 2.1 E-2 (mg/kg-day) -1 [Male mouse hepatocellular adenoma and carcinoma incidence data (NTP, 1986), cancer risk estimate calculated using a linearized multistage procedure and PBPK model dose adjustment (CDHS, 1991). III. CARCINOGENIC EFFECTS Human Studies Epidemiological studies of perchloroethylene (PCE) exposure have been reviewed by Reichert (1983) and by the U.S. EPA (1985). Blair et al. (1979) analyzed the death certificates of 330 union laundry and dry-cleaning workers (out of a cohort of 10,000). Of 330 decedents, 279 had worked solely in dry-cleaning establishments. Increased mortality from cancers of the respiratory tract, cervix, and skin was documented, and when all malignancies were evaluated together, the number of observed deaths was significantly greater than expected (p < 0.05). Although an excess of liver cancer and leukemia was also observed, these increases were not statistically significant. In an expanded study, Blair et al. (1990) reported on mortality among 5,365 dry cleaning union members. Statistically significant excesses of cancer of the esophagus and cervix and non-significant excesses for cancer of the larynx, lung, bladder, and thyroid were reported. Lack of PCE exposure data and lack of accounting for potential confounding factors, such as economic status, tobacco, or alcohol use, prevents any firm conclusion as to the association of PCE exposure and excess cancer. Katz and Jowett (1981) analyzed the mortality patterns of 671 white female laundry and dry-cleaning workers. Occupational codes listed on the certificates did not distinguish between the two types of work. Data on the duration of employment were not available, nor were the investigators able to determine to which solvent(s) the individuals were exposed. Smoking history was not known. A significant increase in risk of death from cancer of the kidneys (p < 0.05) and genitals (p < 0.01) was 479
documented. An excess risk from skin and bladder cancer was also found; however, neither increase was statistically significant. Other studies of laundry and dry-cleaning workers have also reported an increased risk of death from cervical cancer (Blair et al., 1979; Kaplan, 1980); however, these investigators have not compared mortality data by low-wage occupation. Although not definitive, the findings of Katz and Jowett (1981) suggest that factor(s) other than (or in addition to) solvent exposure are important contributors to cervical cancer. Kaplan (1980) completed a retrospective mortality study of 1,597 dry-cleaning workers exposed to PCE for at least one year (prior to 1960). The solvent history of approximately half of the dry-cleaning establishments was known. The inability of Kaplan to quantify solvent exposure adds an important confounding variable to the study (Kaplan, 1980). The mean exposure concentration of individuals to PCE was calculated to be 22 ppm for dry-cleaning machine operators and 3.3 ppm for all other jobs. Kaplan found an elevated SMR (182) for malignant neoplasms of the colon (11 observed deaths, 6.77 to 6.98 expected deaths). In addition to colon cancer, malignant neoplasms of the rectum, pancreas, respiratory system, urinary organs, and “other and unspecified sites (major)” were observed (Kaplan, 1980). Although the relatively small cohort in this study limits conclusions about the carcinogenic potential of PCE, the study (Kaplan, 1980) results suggest a relationship between colon cancer and solvent exposure. A group of Danish laundry and dry-cleaning workers was identified from the Danish Occupational Cancer Register (Lynge et al., 1990). From cancer incidence data for a 10-year period, a significant excess risk was found for primary liver cancer among 8,567 women (standardized incidence ratio 3.4, 95% confidence interval 1.4-7.0). No case of primary liver cancer was observed among 2,033 men, for whom the expected value was 1.1. Excess alcohol consumption did not appear to account for the excess primary liver cancer risk for women. However, no data was available on actual exposures of the study group to PCE or other chemicals. Duh and Asal (1984) studied the cause(s) of mortality among 440 laundry and dry-cleaning workers from Oklahoma who died during 1975 to 1981. Smoking histories were not available and separation of the two groups by occupation was not possible. NIOSH reported that, although 75% of dry-cleaning establishments in the U.S. use PCE, Oklahoma may be unique in that petroleum solvents account for more that 50% of total solvents used during this period (NIOSH, 1980). Analysis of deaths due to cancer showed an increase for cancers of the respiratory system, lung, and kidney. Brown and Kaplan (1987) conducted a retrospective, cohort-mortality study of workers employed in the dry-cleaning industry to evaluate the carcinogenic potential from occupational exposure to PCE. The study cohort consisted of 1,690 members of four labor unions (located in Oakland, Detroit, Chicago, and New York City). Individuals selected for the study had been employed for at least one year prior to 1960 in dry-cleaning shops using PCE as the primary solvent. Complete solvent-use histories were not known for about half of the shops included in the study. Because petroleum solvents were widely used by dry cleaners prior to 1960, most of the cohort had known or potential exposure to 480
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Air Toxics Hot Spots Program Risk A
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Prepared by: John D. Budroe, Ph.D.
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This document is one of five docume
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TABLE OF CONTENTS PREFACE i INTRODU
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N-Nitrosodimethylamine 401 N-Nitros
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Hot Spots Unit Risk and Cancer Pote
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Additional ATES and PETS documents
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data. If several data sets (dose an
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US EPA Calculation of Carcinogenic
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exposure to a concentration of 1 µ
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incidences for each of the dose lev
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computes the surface area of a sphe
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Comparison of Hot Spots Cancer Unit
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Gold, L., de Veciana, M., Backman,
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Animal Studies Rats Woutersen et al
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ased on sufficient evidence of carc
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ACETAMIDE CAS No: 60-35-5 I. PHYSIC
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Methodology Expedited Proposition 6
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cancer mortality. However, US EPA (
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Table 2. Lung adenoma incidence in
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Table 3 (continued). Acrylamide-ind
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Robinson M, Bull RJ, Knutsen GL, Sh
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Also, a trend was observed correlat
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eported. Cause-specific expected de
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Bio/Dynamics Inc. conducted a study
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examination. Interim sacrifices wer
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Table 8. Tumor incidence in male an
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Gaffey WR and Strauss ME. 1981. A m
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(technical grade; 98% pure) by gava
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International Agency for Research o
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still alive in the low-dose control
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ANILINE CAS No: 62-53-3 I. PHYSICAL
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fibrosarcomas, stromal sarcomas, ca
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ARSENIC (INORGANIC) CAS No: 7440-38
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elationship between arsenic exposur
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al. (1988) did not induce lung tumo
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A risk assessment was also conducte
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Chen C, Chuang Y, You S, Lin T and
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Schrauzer G, White D, McGinness J,
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Table 1: Summary of epidemiologic s
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had at least one animal demonstrati
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mesothelioma, recommended lifetime
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National Institute for Occupational
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BENZENE CAS No: 71-43-2 I. PHYSICAL
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Animal Studies Available experiment
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Table 3: Summary of NTP bioassay re
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Table 4: Summary of benzene low-dos
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Maltoni C, Conti B and Cotti G. 198
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a benign tumor of the kidney. No ba
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al. (1968) found no tumors in lifet
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following relationship, where C(t 1
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Miakawa M. and Yoshida O. 1975. Pro
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human population and that BPDE-DNA
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demonstrated the tumor initiating a
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Table 4: Bronchoalveolar tumors fro
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Table 5: IARC groupings of PAHs, mi
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Table 6 (continued): IARC Group 3 P
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Potency Equivalency Factors (PEF) f
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This was rounded to a PEF of 0.1. 1
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experiment (Takayama et al., 1985)
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Deutsch-Wenzel RP, Brune H, Grimmer
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Krewski D, Thorslund T and Withey J
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U.S. Environmental Protection Agenc
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Sorahan et al. (1983) studied cance
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Lijinsky W. 1986. Chronic bioassay
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the drinking water (Schroeder and M
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Table II. Effective dose, upper-bou
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BIS(2-CHLOROETHYL)ETHER CAS No: 111
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IV. DERIVATION OF CANCER POTENCY Ba
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BIS(CHLOROMETHYL)ETHER CAS No: 542-
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Table 1. Bis(chloromethyl)ether-ind
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Drew RT, Laskin S, Kuschner M and N
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ates for the 1968 U.S. male populat
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Table 1: Incidence of primary tumor
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National Institute of Occupational
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was less than 0.05 when controlling
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up period. The final cohort include
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If the cadmium-exposed workers incl
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on personnel records (20%); (3) eva
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were exposed to a continuous (23.5
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procedure (NLIN), the parameters we
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International Agency for Research o
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Two reports were published on cance
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Mendel rats, respectively), and sub
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Eschenbrenner A and Miller E. 1946.
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III. CARCINOGENIC EFFECTS Human Stu
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cancers, were less than expected. T
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and no cases of cancer (although cl
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There was a statistically significa
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NTP (1982a) also conducted an carci
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Several pathologists have independe
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hepatocellular adenoma/carcinoma tu
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carcinogenic potency may decline in
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Cochrane W, Singh J and Miles W. 19
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North Atlantic Treaty Organization,
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CHLORINATED PARAFFINS (average chai
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ased on dose-response data for beni
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chloroform in drinking water with k
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Overall, the present epidemiologica
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female dogs received toothpaste bas
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Calculated q 1 * values from the ab
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Hogan MD, Chi Py, Hoel DG and Mitch
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Table 1. Study design summary for N
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V. REFERENCES California Environmen
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toluidine. Followup of this subcoho
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feeding studies on by NCI (1979) us
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CHROMIUM (HEXAVALENT) CAS No: 18540
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expected rate may be inflated becau
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Oral Borneff et al. (1968) exposed
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CREOSOTE (COAL TAR-DERIVED) CAS No:
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from an inhalation exposure study (
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Table 1. Study design summary for N
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Table 1. Experimental design for ca
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Hazardous Substance Data Bank (HSDB
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Table 1: Tumor induction in Fischer
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Table 1. Experimental design of 2,4
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Additional analysis of these data b
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Jackson RJ, Greene CJ, Thomas JT, M
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Table 1. Tumor incidence in rats ex
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Girard R, Tolot F, Martin P and Bou
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exposed more than 16 years before t
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interpretation of dose extrapolatio
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1, 1-DICHLOROETHANE CAS No: 75-34-3
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Table 1b. Study design for carcinog
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National Cancer Institute (NCI) 197
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mice, hepatocellular carcinoma inci
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V. REFERENCES California Department
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DAB/day by gavage for the life of t
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2,4-DINITROTOLUENE CAS No: 121-14-2
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Ellis et al.(1979) (also reported b
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Final Statement of Reasons for OAL,
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to the small sample size and short
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In an inhalation study, Torkelson e
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V. REFERENCES American Conference o
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EPICHLOROHYDRIN CAS No: 106-89-8 I.
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espiratory tumors were noted in the
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Table 4. Epichlorohydrin-induced fo
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Konishi Y, Kawabata A, Denda A, Ike
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exposed to arsenicals for 20 months
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espectively (all statistically sign
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ETHYLENE DICHLORIDE CAS No: 107-06-
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Several factors have been suggested
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myelogenous leukemias (4 and 8 year
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statistically significant. CDHS not
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combined with the incidence in the
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incidence of primary brain tumors.
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Table 6 (continued): Organ/Sex Mali
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An Upper 95% Confidence Limit (UCL)
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ETHYLENE THIOUREA (ETU) CAS No: 96-
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male and female rats. Tumor inciden
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FORMALDEHYDE CAS No: 50-00-0 I. PHY
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presented an extension of a previou
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Methodology In developing a spectru
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Casanova M, Morgan KT, Steinhagen W
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Tobe M, Kaneko T, Uchida Y, Kamata
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Table 1. Hexachlorobenzene-induced
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50 pups (F 1 ) of each sex were ran
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Ertürk E, Lambrecht RW, Peters HA,
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Table 1. Liver hepatoma incidence i
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1988). An airborne unit risk factor
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HYDRAZINE CAS No: 302-01-2 I. PHYSI
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Methodology Inhalation A linearized
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LEAD AND LEAD COMPOUNDS (INORGANIC)
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and other occupational carcinogens
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y inhalation is similar for rats an
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Goyer RA. 1992. Nephrotoxicity and
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LINDANE (g-Hexachlorocyclohexane) C
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Using these relationships, a human
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METHYL TERT-BUTYL ETHER (MTBE) CAS
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Tumor incidences according to the r
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kidney changes indicative of chroni
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Interspecies scaling for oral doses
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Table 4 (continued): Dose Response
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Experimental Pathology Laboratories
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Animal Studies Male and female HaM/
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Gold L, Sawyer C, Magaw R, Backman
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Using the statistical tests (one-ta
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Table 1: Methylene chloride-induced
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Significant treatment-related incre
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National Toxicology Program (NTP) 1
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noted; however, the study duration
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Crump KS, Howe RB, Van Landingham C
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Table 1. Michler’s ketone-induced
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NICKEL AND NICKEL COMPOUNDS CAS No:
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the high exposure group was 14.0. A
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male and 121 female rats, was expos
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2.1 - 2.6 × 10 -4 (µg/m 3 ) -1 .
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The increased incidence of bladder
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A linearized multistage procedure w
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N-NITROSO-N-METHYLETHYLAMINE CAS No
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propylamine in drinking water at 0.
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N-NITROSODIETHYLAMINE CAS No: 55-18
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Table 2. Treatment groups, concentr
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California Department of Health Ser
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animals and the second generation t
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ationale for selection of the OEHHA
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A unit risk value based upon air co
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N-NITROSODIPHENYLAMINE CAS No: 86-3
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Methodology Dosage estimates of NDP
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Crump KS, Howe RB. 1984. The multis
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Table 1. P-Nitrosodiphenylamine-ind
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N-NITROSOMORPHOLINE CAS No: 59-89-2
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N-NITROSOPIPERIDINE CAS No: 100-75-
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Table 3. N-Nitrosopiperidine-induce
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Crump KS, Howe RB, Van Landingham C
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testicular tumors were noted in the
Page 437 and 438: PARTICULATE MATTER FROM DIESEL-FUEL
Page 439 and 440: etired railroad workers who had had
Page 441 and 442: employment (χ 2 test for trend: p
Page 443 and 444: elevated smoking-adjusted risk esti
Page 445 and 446: Table 1 (continued): Reference Miln
Page 447 and 448: Table 1 (continued): Reference Damb
Page 449 and 450: Table 1 (continued): Reference Burn
Page 451 and 452: Table 1 (continued): Reference Raff
Page 453 and 454: Table 1 (continued): Epidemiologica
Page 455 and 456: Table 1 (continued): Epidemiologica
Page 457 and 458: Table 1 (continued): Reference Wegm
Page 459 and 460: Animal Studies Section 6.1 (Animal
Page 461 and 462: The variability, or heterogeneity,
Page 463 and 464: estimate for those studies for whic
Page 465 and 466: Figure 1: Estimates of Relative Ris
Page 467 and 468: q 1 * = Excess relative risk × CA
Page 469 and 470: Table 3: Number of Workers in the E
Page 471 and 472: u nexposed workers at zero concentr
Page 473 and 474: for each µg/m 3 of diesel exhaust
Page 475 and 476: Table 4: Values from Unit Risk for
Page 477 and 478: their findings that a reasonable es
Page 479 and 480: Garshick E, Schenker M, Woskie S an
Page 481 and 482: Lewis T, Green, FH MW, Burg J and L
Page 483 and 484: Rothman K. 1986. Modern epidemiolog
Page 485 and 486: PENTACHLOROPHENOL CAS No: 87-86-5 I
Page 487: The default lifespan for mice is 10
Page 491 and 492: B6C3F 1 mice and F344/N rats were e
Page 493 and 494: This model, rather than a time depe
Page 495 and 496: POLYCHLORINATED BIPHENYLS (PCBs) CA
Page 497 and 498: several benign adenomatous lesions
Page 499 and 500: Ito et al. (1973) exposed groups of
Page 501 and 502: could not be characterized by chlor
Page 503 and 504: exposure (all pathways and mixtures
Page 505 and 506: National Toxicology Program 1993. T
Page 507 and 508: Table 1. Potassium bromate-induced
Page 509 and 510: 1,3-PROPANE SULTONE CAS No: 1120-71
Page 511 and 512: IV. DERIVATION OF CANCER POTENCY Ba
Page 513 and 514: PROPYLENE OXIDE CAS No: 75-56-9 I.
Page 515 and 516: oxide. In the NTP carcinogenicity s
Page 517 and 518: 1,1,2,2-TETRACHLOROETHANE CAS No: 7
Page 519 and 520: assumed a body weight of 70 kg and
Page 521 and 522: total); an untreated control group
Page 523 and 524: TOLUENE DIISOCYANATE CAS No: 26471-
Page 525 and 526: Animal Studies The National Toxicol
Page 527 and 528: Mortillaro PT and Schiavon M. 1982.
Page 529 and 530: male or female rats. Increases in h
Page 531 and 532: TRICHLOROETHYLENE CAS No: 79-01-6 I
Page 533 and 534: A mortality analysis of a cohort of
Page 535 and 536: elative to that of the controls whi
Page 537 and 538: applied or metabolized. The range o
Page 539 and 540:
Katz RM and Jowett D. 1981. Female
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10,000 ppm 2,4,6-trichlorophenol in
Page 543 and 544:
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Bionetics Research Laboratories. 19
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control; females: 6/10 exposed, 0/1
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over controls (p < 0.04). Other tum
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was increased (100/314 exposed vs.
Page 553 and 554:
Table 3. Cancer potency estimates f
Page 555 and 556:
Crouch E. 1983. Uncertainties in in
Page 557 and 558:
VINYL CHLORIDE CAS No: 75-01-4 I. P
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Table 1 (continued): A Summary of E
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al., 1983). Histopathology of all o
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Table 3: Tumor incidences in 100 pp
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experiment, animals were exposed to
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Experiment BT1 Most previous risk a
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No statistical analyses of mortalit
Page 571 and 572:
Table 11 gives unit risk estimates
Page 573 and 574:
Bertazzi PA, Villa A, Foa V, Saia B
Page 575 and 576:
Nicholson WJ, Hammond EC, Seidman H
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immunotoxicity, reproductive toxici
Page 579 and 580:
scheme. TEFs for two major noncance
Page 581 and 582:
NATO/CCMS (1988a) Pilot Study on In
Page 583 and 584:
Table 2 Toxicity Equivalency Factor
Page 585 and 586:
Table 4 A Comparison of CTEF- and I
Page 587 and 588:
Office of Environmental Health Haza
Page 589 and 590:
Group 4: The agent is probably not
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TECHNICAL SUPPORT DOCUMENT FOR DESC
Page 593 and 594:
US EPA IRIS Inhalation Unit Risk an
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TECHNICAL SUPPORT DOCUMENT FOR DESC
Page 597 and 598:
as appropriate, and revise IRIS fil
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Chemical Exposure Route Study Type
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Page 603 and 604:
Page 605 and 606:
Methyl tert-butyl ether p. 5: Added
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