This is a proposal to study the free radical chemistry of cigarette smoke, woodsmoke, smoke from plastics and elastomers, and automobile exhaust. We will elucidate the mechanisms for production of radicals in these smokes and determine the structures and reactivities of the radicals. There is considerable inferential evidence that radicals often mediate the reactions of components of these smoke streams with pulmonary target molecules. Our long-term aim is to develop insight into the chemistry of the radicals in these smoke streams so the biological reactions they initiate can be predicted and understood. Cigarette smoke places an oxidative burden on the lungs of the smoker, and the very high concentration of carbon - and oxy- radicals in smoke suggests they may be implicated in this effect. Recent evidence also demonstrates loss of pulmonary function for persons exposed to woodsmoke, which our preliminary evidence show contains even more radicals than does tobacco smoke.
Our specific aims are: (1) Use FTIR and other methods to study the oxidation of N0 to N02 in tobacco smoke and in the model systems we have developed. This is a critical test of our hypothesis that the radicals in cigarette smoke are being continuously produced by NOx-olefin reactions. (2) Utilize electron-spin resonance spin- trap methods to probe which materials (wood, plastics, elastomers) burn to produce radicals and determine their yields and structures. (3) Use spin traps methods to determine the yields and structure of the radicals in both spark ignition and diesel exhaust and the effects of engine operating variables on radical yields.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL025820-11
Application #
3338270
Study Section
Toxicology Subcommittee 2 (TOX)
Project Start
1981-06-01
Project End
1993-08-31
Budget Start
1992-05-01
Budget End
1993-08-31
Support Year
11
Fiscal Year
1992
Total Cost
Indirect Cost
Name
Louisiana State University A&M Col Baton Rouge
Department
Type
Schools of Arts and Sciences
DUNS #
075050765
City
Baton Rouge
State
LA
Country
United States
Zip Code
70803
Stone, K; Bermudez, E; Zang, L Y et al. (1995) The ESR properties, DNA nicking, and DNA association of aged solutions of catechol versus aqueous extracts of tar from cigarette smoke. Arch Biochem Biophys 319:196-203
Stone, K K; Bermudez, E; Pryor, W A (1994) Aqueous extracts of cigarette tar containing the tar free radical cause DNA nicks in mammalian cells. Environ Health Perspect 102 Suppl 10:173-8
Evans, M D; Pryor, W A (1994) Cigarette smoking, emphysema, and damage to alpha 1-proteinase inhibitor. Am J Physiol 266:L593-611
Bermudez, E; Stone, K; Carter, K M et al. (1994) Environmental tobacco smoke is just as damaging to DNA as mainstream smoke. Environ Health Perspect 102:870-4
Winston, G W; Church, D F; Cueto, R et al. (1993) Oxygen consumption and oxyradical production from microsomal reduction of aqueous extracts of cigarette tar. Arch Biochem Biophys 304:371-8
Evans, M D; Pryor, W A (1992) Damage to human alpha-1-proteinase inhibitor by aqueous cigarette tar extracts and the formation of methionine sulfoxide. Chem Res Toxicol 5:654-60
Nakayama, T; Church, D F; Pryor, W A (1989) Quantitative analysis of the hydrogen peroxide formed in aqueous cigarette tar extracts. Free Radic Biol Med 7:9-15
Lachocki, T M; Church, D F; Pryor, W A (1988) Persistent free radicals in the smoke of common household materials: biological and clinical implications. Environ Res 45:127-39
Borish, E T; Pryor, W A; Venugopal, S et al. (1987) DNA synthesis is blocked by cigarette tar-induced DNA single-strand breaks. Carcinogenesis 8:1517-20
Pryor, W A; Dooley, M M; Church, D F (1986) The inactivation of alpha-1-proteinase inhibitor by gas-phase cigarette smoke: protection by antioxidants and reducing species. Chem Biol Interact 57:271-83

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