Biological monitoring of fire fighters: sister chromatid exchange and polycyclic aromatic hydrocarbon-DNA adducts in peripheral blood cells.
Fire fighters are exposed to potentially carcinogenic combustion and pyrolysis products during the course of their work. The present study was designed to test 43 fire fighters and matched controls for DNA damage which might be related to occupational carcinogen exposures. Using peripheral blood lymphocytes, we examined (a) baseline sister chromatid exchange (SCE) frequency and (b) SCE induction by in vitro mutagenic challenge with mitomycin C. Using nucleated peripheral blood cells, we examined (c) polycyclic aromatic hydrocarbon-DNA adduct levels by assessing benzo(a)pyrene diol epoxide (BPDE)-DNA antigenicity. Exposures were determined from histories of fire-fighting activity. The presence of confounding factors (e.g., tobacco smoking, charcoal-broiled food consumption, etc.) was determined by questionnaire. Plasma cotinine levels were measured to assess recent exposures to tobacco smoke. White fire fighters exhibited a significantly higher risk for the presence of detectable BPDE-DNA antigenicity than white controls (odds ratio, 3.4; 95% confidence interval, 1.08-10.5 after adjustment). Consumption of charcoal-broiled food less than 3 times a month was associated with a smaller proportion of individuals exhibiting measurable (positive) BPDE-DNA antigenicity, while consumption of broiled food greater than 3 times a month did not affect the proportion of positive individuals. Daily alcohol consumption was associated with a larger proportion of individuals exhibiting positive BPDE-DNA antigenicity, (P = 0.07). Tobacco smoking and charcoal-broiled food consumption, but not fire fighting, were associated with increased levels of baseline SCE. Sensitivity to SCE induced by mitomycin C in cultured peripheral lymphocytes was similar in fire fighter and control groups. However, sensitivity of individual fire fighters to mitomycin C-induced SCE was correlated with number of fires fought in the previous 24 h.
Liou
S H
SH
Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland.
Jacobson-Kram
D
D
Poirier
M C
MC
Nguyen
D
D
Strickland
P T
PT
Tockman
M S
MS
D015123:7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide / Q000097:blood*; D000328:Adult; D000428:Alcohol Drinking; D002274:Carcinogens, Environmental; D003296:Cooking; D003367:Cotinine / Q000097:blood; D004247:DNA / Q000097:blood*; D018736:DNA Adducts; D004249:DNA Damage; D004101:Dihydroxydihydrobenzopyrenes / Q000097:blood*; D004784:Environmental Monitoring / Q000379:methods; D006801:Humans; D007962:Leukocytes / Q000032:analysis; D008297:Male; D016685:Mitomycin; D008937:Mitomycins; D012307:Risk Factors; D012854:Sister Chromatid Exchange / Q000187:drug effects; D012907:Smoking / Q000009:adverse effects / Q000097:blood
D002274:Carcinogens, Environmental; D018736:DNA Adducts; D004101:Dihydroxydihydrobenzopyrenes; D008937:Mitomycins; C043931:benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide-DNA; D016685:Mitomycin; D015123:7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide; D004247:DNA; D003367:Cotinine