In this study, we investigated by using comet assay the effects of polycyclic aromatic hydrocarbon (PAH) as a major factor on DNA damage of workers exposed to exhaust fumes. Twenty-four workers from three automobile emission inspection companies, 28 workers from a waste incinerating company, and 43 matched, unexposed healthy subjects were enrolled in the study. The mean values of 1-hydroxypyrene (1-OHP) in automobile emission inspection and waste incineration workers were 0.27+/-0.19 and 0.57+/-0.46 micromol/mol creatinine, respectively, and the mean values of 2-naphthol in automobile emission inspectors and waste incineration workers were 4.80+/-4.01 and 8.30+/-4.79 mol/mol creatinine, respectively. Significant difference in urinary metabolites, 1-hydroxypyrene and 2-naphthol was found between smokers and non-smokers in exposed groups and it may be due to the amounts of smoking cigarettes. In T-lymphocytes, DNA damage in control subjects, emission inspection workers and incineration workers were 1.42+/-0.22, 1.41+/-0.22 and 1.76+/-0.27, respectively. DNA damage of B-lymphocytes in the three groups showed the most significant differences of three cell types. The tail moments of the B-lymphocytes of control subjects, emission inspection and incineration workers were 1.40+/-0.27, 2.44+/-0.32 and 2.36+/-0.37, respectively. In granulocytes, DNA damage was also different, the tail moments being 2.72+/-0.59, 3.32+/-0.38 and 2.85+/-0.49, respectively. Although 1-OHP and 2-naphthol levels were statistically increased in smokers in workers exposed to PAHs, exposed smoking and non-smoking workers did not show any significantly difference in terms of Olive tail moments. Our results suggest that PAH causes single strand DNA breakage in human T- and B-lymphocytes, and granulocytes. A comparison of DNA damage in three groups showed that B-lymphocytes are useful target in the biomonitoring of human exposure.