22 Witten et al16 suggested that exposure to petrol or diesel engine exhausts may increase the risk of lung cancer and neurological conditions in rats. A recent study in the US showed that breathing air polluted by exhaust fumes was responsible for more than 70% of the cancer risk in the South Coast Air Basin in California.41 selleck inhibitor Lopez-Abente et al42 correlated gastric cancer risk to consumption of a local wine sealed with a tar like substance obtained through boiling and distilling fir and pinewood which contains PAHs. Sinha et al43 associated increased risk of colorectal adenomas with benzo(a)pyrene intake in food. Tobacco smoke, which contains PAHs, has been implicated in the lung cancer.44 An association between PAH-DNA adducts and breast cancer incidences have also been reported.

18,19,36,45 Furthermore, there was a positive correlation regarding the distance to source of pollution and the level of 1-hydroxypyrene in blood samples of exposed animals. 1-hydroxypyrene level was significantly (P < 0.05) increased in groups of rats that had experienced dermal and inhaled exposure to the generator fumes compared to the group of unexposed rats (control). This points to the fact that the closer the rat to the generator exhaust source, the higher the absorption of these carcinogens after inhalation and dermal contact. Reports have suggested that most PAHs are well absorbed in mammals.30,46 Rapid absorption has been recorded in rats exposed to benzo(a)pyrene through inhalation.46 There is a high tendency of malignant tumor development in these PAH poisoned rats due to mutation arising from PAH-DNA adducts disrupting normal DNA transcription, translation, and replication.

However, gene polymorphisms in most enzymes have been identified in human beings and this could modulate individual cancer susceptibility. Ueng et al47 reported that exposure of rats to motorcycle exhaust and organic extracts of the exhaust particulate causes a dose- and time-dependent increase in cytochrome P-450-dependent monooxygenases as well as glutathione-S-transferase in the liver, kidney, and lung microsomes. This occurs as these enzymes metabolize the PAHs to polar nucleophilic metabolites that bind with the adenine and guanine bases of the DNA.47 Lin et al28 reported that the cytotoxicity of traffic related nano/ultrafine particle extracts was significantly higher than for coarser particles. This would be most likely due to the higher PAH concentration Carfilzomib in the fine generator exhaust particles. Conclusion The data available from this study shows that generator fumes contribute significantly to the atmospheric level of PAHs and that the level is dependent on the distance from the point of generation.