Smoking increases carcinogenic polycyclic aromatic hydrocarbons in human lung tissue

Tobacco smoke is a major source of human exposure to polycyclic aromatic hy drocarbons (PAHs). The concentration of PAHs in lung tissue would reflect a n individual's dose, and its variation could perhaps reflect cancer risk. E leven 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-respo nse relationship for greater smoking (P < 0.01). Smoking increased the conc entration of five PAHs including benzo(a)pyrene, which increased <similar t o>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 P AHs (odds ratio, 2.61; 95% confidence interval, 0.75-9.12). A higher concen tration of PAHs was detected in the lung tissue of males, although the esti mated smoking was similar in males and females. Race was not associated wit h PAH concentrations overall, but PAH concentrations appeared to be higher in African-American males than in any other group. Age was weakly correlate d with an increase in fluoranthene and pyrene. The measurement of PAHs in h uman lung tissue can be used to estimate the actual dose to the target orga n.