Heating of asphalts to facilitate use in paving and roofing applications produces fumes containing polycyclic aromatic compounds (PAC). Regulatory organizations have suggested
asphalt fumes of concern to humans due to possible carcinogenic effects but data are inadequate to classify. Two-year rodent inhalation studies and recent European epidemiology research have shown that
asphalt fume alone does not pose a carcinogenic risk to humans. Dermal exposure to
asphalt fume condensate have produced skin
tumors in mouse skin painting studies but no
skin cancer studies in humans have been reported occupationally. Mechanistic research explores underlying processes to assess relevance of findings in animals to humans.
DNA adducts are useful as
biological dosimeters of exposure, but DNA repair processes, lack of correlation with more definitive genotoxic and
cancer results in animals and humans limits reliability as a predictor of carcinogenic hazard. Inhibition of gap junction intercellular communication and stimulation of intracellular signaling by
asphalt fume condensate can relate to
tumor development. Up and down-regulation of expression in genes involved in the metabolism and action of
asphalt fume demonstrates intrinsic activity at the cellular level but changes were inconsistent. The relationship of reported effects on the immune system to
carcinogenesis is unclear. Overall, results of mechanistic studies provide insights into
biological activity from
asphalt fume exposure but compositional differences, level of human exposure and detoxification processes must be considered in translating these findings to
cancer risk.