To BaP or not to BaP? That is the question.

[a]pyrene (BaP), a polycyclic aromatic hydrocarbon (PAH) and animal carcinogen, is used by regulators as the basis for quantitative risk estimation of PAH-containing combustion by-products (1). Is BaP an appropriate predictor of cancer risk for products of incomplete combustion? A multidose, 2-year (chronic) feeding protocol developed by the National Institute of Environmental Health Sciences is a study design for identifying and characterizing chemicals that pose a cancer risk. The National Center for Toxicological Research (NCTR) of the U.S. Food and Drug Administration and EPRI used this protocol to study tumor outcomes in mice fed BaP and coal tar (2). Coal tar is a BaP-containing material found in Superfund sites and in sites once used in the production of manufactured gas. Tumor incidence was very different for coal tar and BaP. Coal tar caused tumors in lung, skin, forestomach, small intestine, and liver and also caused hemangiosarcomas and histiosarcomas in various organs. BaP caused tumors in forestomach, tongue, esophagus, and larynx. In mice fed coal tar, the lung was the most sensitive organ site for tumor formation. In mice fed BaP, the forestomach was the most sensitive site for tumor formation. Significantly, BaP did not induce lung tumors, even though there was evidence that BaP or an active metabolite of BaP had reached lung tissue (3). Ingested coal tar is a systemic tumorigen; ingested BaP is a contact tumorigen. When an agent causes tumors in more than one site, as is the case for ingested coal tar and BaP, tumor incidence in the most sensitive tissue site is used for risk assessment. In the NCTR/EPRI study, health risks of coal tar would be based on lung tumor incidence and health risks of BaP would be based on forestomach tumor incidence. Gaylor et al. (4) concluded that " ... carcinogenicity of coal tars cannot be fully accounted for by BaP content [of coal tar] since BaP alone did not induce tumors of the lung. " The findings of the 2-year feeding study are consistent with other data on the contribution of BaP to lung tumor induction by environmental PAHs. In 1972 the Committee on Biological Effects of Atmospheric Pollutants of the National Academy of Sciences evaluated the relationship of BaP dose and lung cancer mortality. Based on epidemiologic evidence from urban dwellers, British gas workers, and topside coke-oven workers, the committee concluded that a BaP lung cancer mortality ratio relationship " lacks …