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Smoking Increases Carcinogenic Polycyclic Aromatic Hydrocarbons in Human Lung Tissue¹

Georgetown University Medical Center, Lombardi Cancer Center, Washington, DC 20007 [R. G., L. E., S. S. K., P. G. S.]; Research Triangle Institute, Research Triangle Park, North Carolina 27709 [E. P., J. B. B.]; and Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892 [E. D. B.]

Tobacco smoke is a major source of human exposure to polycyclic aromatichydrocarbons (PAHs). The concentration of PAHs in lung tissue would reflect an individual’s dose, and its variation could perhaps reflect cancer risk. Eleven PAHs were measured in 70 lung tissue samples from cancer-free autopsy donors by gas chromatography-mass spectrometry. There were 37 smokers and 33 nonsmokers as estimated by serum cotinine concentration. The sum of PAH concentrations was higher in smokers (P = 0.01), and there was a dose-response relationship for greater smoking (P < 0.01). Smoking increased the concentration of five PAHs including benzo(a)pyrene, which increased 2-fold. The risk for increasing carcinogenic PAHs (odds ratio, 8.20; 95% confidence interval, 2.39–28.09) was 3-fold compared with noncarcinogenic PAHs (odds ratio, 2.61; 95% confidence interval, 0.75–9.12). A higher concentration of PAHs was detected in the lung tissue of males, although the estimated smoking was similar in males and females. Race was not associated with PAH concentrations overall, but PAH concentrations appeared to be higher in African-American males than in any other group. Age was weakly correlated with an increase in fluoranthene and pyrene. The measurement of PAHs in human lung tissue can be used to estimate the actual dose to the target organ.

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