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Program - Society of Toxicology

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44 th Annual Meeting<br />

and ToxExpo<br />

<strong>Program</strong> Description<br />

TUESDAY<br />

Tuesday Afternoon, March 8<br />

1:30 PM to 4:30 PM<br />

Room RO8<br />

SYMPOSIUM SESSION: UPDATE ON MECHANISMS FOR<br />

ENVIRONMENTAL TOBACCO SMOKE-INDUCED HEALTH<br />

EFFECTS<br />

Chairperson(s): Chris A. Pritsos, University <strong>of</strong> Nevada, Reno, NV and Kevin<br />

E. Pinkerton, University <strong>of</strong> California, Davis, Davis, CA.<br />

Endorsed by:<br />

Occupational and Public Health SS<br />

Risk Assessment SS<br />

Epidemiological evidence has demonstrated an association between exposure to<br />

environmental tobacco smoke (ETS) and disease. Diseases associated with ETS<br />

exposure include a variety <strong>of</strong> cancers, cardiovascular disease, COPD, asthma<br />

and a number <strong>of</strong> perinatal manifestations, to name a few. While many <strong>of</strong> these<br />

exposure/disease associations are strong, the mechanism(s) by which ETS exposure<br />

influences the etiology <strong>of</strong> these diseases remains unclear. There are a great<br />

number <strong>of</strong> confounding factors which make ascribing any ETS-induced mechanism<br />

for disease difficult. Included amongst these factors is the immense<br />

complexity <strong>of</strong> the substituents which make up ETS. ETS is comprised <strong>of</strong> both a<br />

vapor phase and particulate phase with over 4000 chemicals identified to date.<br />

One must not only consider the effect <strong>of</strong> individual compounds but must also<br />

consider potential synergism between compounds. Another factor which needs<br />

to be considered is the fact that exposure to tobacco smoke compounds is<br />

substantially less than for smokers, due to dilution <strong>of</strong> the smoke. Chemical reactivity<br />

or “aging” <strong>of</strong> the ETS components can also modify their chemical nature.<br />

Also, an individual’s susceptibility to the harmful effects <strong>of</strong> ETS exposure can<br />

be greatly influenced by their genetic makeup. While quite complex, certain<br />

mechanistic themes are beginning to emerge as characteristic <strong>of</strong> ETS’s association<br />

with these diseases. The speakers will provide recent advances in our<br />

understanding <strong>of</strong> the mechanisms by which ETS can influence the etiology <strong>of</strong><br />

these diseases and provide a linkage between the epidemiological and biochemical/pathophysiological<br />

bases <strong>of</strong> disease. The symposium will have two<br />

presentations each dealing with: ETS and cardiovascular disease, ETS and<br />

cancer and ETS and respiratory diseases.<br />

#1008 1:30 UPDATE ON MECHANISMS FOR<br />

ENVIRONMENTAL TOBACCO SMOKE-<br />

INDUCED HEALTH EFFECTS. C. A. Pritsos 1 and<br />

K. E. Pinkerton 2 . 1 Nutrition, University <strong>of</strong> Nevada,<br />

Reno, NV and 2 Center for Health and the Environment,<br />

University <strong>of</strong> California, Davis, CA.<br />

#1009 1:35 IMPACT OF WORKPLACE ETS EXPOSURE ON<br />

RISK FACTORS FOR CORONARY HEART<br />

DISEASE. C. A. Pritsos 1 , G. R. Cutter 2 , S. St. Jeor 3 , J.<br />

A. Ashley 1 , S. Perumean-Chaney 2 , S. Clodfelter 1 , J. E.<br />

Woodrow 1 , A. C. Collier 1 , L. D. Bowen 1 , N. J. Martin 1<br />

and K. L. Pritsos 1 . 1 Nutrition, University <strong>of</strong> Nevada,<br />

Reno, NV, 2 Biostatistics, University <strong>of</strong> Alabama,<br />

Birmingham, Birmingham, AL and 3 Internal Medicine,<br />

University <strong>of</strong> Nevada, Reno, NV.<br />

#1010 2:00 IMPACT OF PRENATAL CARDIOVASCULAR<br />

DISEASE RISK FACTOR EXPOSURE ON<br />

MITOCHONDRIAL DAMAGE AND ADULT<br />

HEART DISEASE DEVELOPMENT. S. W.<br />

Ballinger 1 , Z. Yang 1 and A. Penn 2 . 1 Pathology,<br />

University Alabama at Birmingham, Birmingham, AL<br />

and 2 Veterinary Medicine, Louisiana State University,<br />

Baton Rouge, LA.<br />

#1011 2:30 IMMUNOLOGIC DETECTION OF<br />

CARCINOGEN-DNA AND PROTEIN ADDUCTS.<br />

R. M. Santella. Environmental Health Sciences,<br />

Columbia University, New York.<br />

#1012 3:00 ETS IMPACT ON ALLERGIC AIRWAYS<br />

RESPONSES TO ANTIGEN. A. penn 1 , D. Paulsen 2<br />

and D. Horohov 3 . 1 CBS, LSU Vet.Med., Baton Rouge,<br />

LA, 2 PBS, LSU Vet.Med., Baton Rouge, LA and 3 Vet.<br />

Sciences., University <strong>of</strong> KY, Lexington, KY.<br />

#1013 3:30 GESTATIONAL STAGE-SPECIFIC ETS-<br />

INDUCED OXIDATIVE DNA DAMAGE. L. M.<br />

Anderson 1 , A. Maciag 1 , I. Espiritu 2 , A. Bialkowska 1 , K.<br />

Kasprzak 1 and H. Witschi 2 . 1 Lab. Comparative<br />

Carcinogenesis, National Cancer Inst., Frederick, MD<br />

and 2 Center for Health and the Environment, University<br />

<strong>of</strong> California, Davis, CA.<br />

#1014 4:00 EFFECTS OF ENVIRONMENTAL TOBACCO<br />

SMOKE ON CYTOKINES AND<br />

NEUROTROPHINS IN THE NEONATAL LUNG.<br />

K. E. Pinkerton, J. P. Joad and M. Yu. Center for Health<br />

and the Environment, University <strong>of</strong> California, Davis,<br />

CA.<br />

Abstract 1015 is located on page 150.<br />

Tuesday Afternoon, March 8<br />

1:30 PM to 4:30 PM<br />

Room 220<br />

WORKSHOP SESSION: CURRENT AND FUTURE SCIENCE-BASED<br />

APPROACHES TO DRUG SAFETY EVALUATION: AN ASSESSMENT<br />

OF POTENTIAL CANCER RISK<br />

Chairperson(s): Martha M. Moore, U.S. FDA, Jefferson, AR and David<br />

Jacobson-Kram, U.S. FDA, Rockville, MD.<br />

Endorsed by:<br />

Carcinogenesis SS*<br />

Regulatory and Safety Evaluation SS<br />

Risk Assessment SS<br />

Student Advisory Committee<br />

Currently the preclinical safety evaluation <strong>of</strong> pharmaceuticals for potential<br />

cancer risk includes the application <strong>of</strong> genetic toxicology assays and the rodent<br />

cancer bioassay. While data from rodent carcinogenicity studies are generally<br />

available prior to marketing approval, data from short-term studies is used to<br />

assess cancer risk during the drug development phases. Although this has generally<br />

been a successful approach there is wide discussion as to the appropriate<br />

role <strong>of</strong> the genetic toxicology assays and the possibility that other assays such as<br />

the Syrian hamster embryo (SHE) test and the shorter term transgenic cancer<br />

bioassays (Trp53 and rasH2) might be useful. The emerging “omics” technologies<br />

provide for possible new and improved approaches to understanding<br />

whether new drugs might cause an increased cancer risk. In addition, both<br />

present and future technologies have the potential to be applied within the<br />

context <strong>of</strong> the clinical trials. This session will provide a forum to discuss these<br />

issues. The first speaker will provide an overview <strong>of</strong> the current approaches and<br />

issues relevant to preclinical drug safety assessment. Additional speakers will<br />

discuss the current thinking on the use <strong>of</strong> genetic toxicology assays, the SHE<br />

assay and the transgenic cancer bioassays. The last two speakers will consider<br />

both the present and potential future applications <strong>of</strong> “omic” technologies and<br />

our ability to utilize individuals in clinical trials to provide a better assessment<br />

<strong>of</strong> the potential human cancer risk from pharmaceutical drugs.<br />

128<br />

SOT’s 44 th Annual Meeting

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