Author(s): Schreiner CA
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Abstract 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. Copyright © 2010 Elsevier Inc. All rights reserved.
This article was published in Regul Toxicol Pharmacol
and referenced in Journal of Clinical Toxicology