Abstract
Polycyclic aromatic hydrocarbon (PAH) exposure is widespread, and many PAHs are considered carcinogenic. The PAH-contaminated AWI Superfund site in Virginia provides a model for studying a complex PAH mixture and its extrapolation to cancer risk and PAH exposure in the general population. We examined cancer risk at the Superfund site due to sediment-derived PAHs and then evaluated PAH sources in the general population and potentially vulnerable subpopulations upon PAH mixture exposure. The PAH mixture was assessed for potential carcinogenicity using the US EPA's OncoLogic™ ranking tool and the US EPA list of priority PAHs. Cancer risk due to PAH exposure was calculated for Superfund site users and compared to the US EPA assessment. Human intake and health endpoints of PAHs within the mixture were extracted from USEtox® chemical fate database, while mean intake exposure was calculated for U.S. adults for select PAHs using NHANES database urinary biomarkers. Eleven PAH compounds within the mixture were of carcinogenic concern, and seven PAHs conveyed significant excess cancer risk at the Superfund site and in the general population, wherein PAH-contaminated seafood ingestion was a main contributor. Other dietary sources of PAHs derived from PAH-contaminated soil or water could also play a role in total exposure. Vulnerable populations to PAH exposure and coinciding increased cancer risk may include, in addition to smokers, children and non-Hispanic blacks, which is a public health concern.
Highlights
From prenatal days until death, humans are each subjected to their own variable exposome [1], a sum of individual environmental exposures from their source to their biological and health effects [2,3,4]
We model our investigations after previously obtained Polycyclic aromatic hydrocarbons (PAHs)-contaminated sediment samples derived from a Superfund site Atlantic Wood Industries (AWI) located in Portsmouth, Virginia, along the Southern Branch of the Elizabeth River
Based on the high level of PAHs and the complexity of the AWI Superfund site mixture, as well as the knowledge that many PAHs are carcinogenic, we postulated that the sediment-derived PAH mixture components would prove to be cancer relevant and confer cancer risk on the users of the Superfund site through various activities relevant to sediment exposure. As this Superfund site mixture is a model complex PAH mixture that may occur in other regions, we further proposed that increased cancer risk and health effects would be applicable for the wider U.S population
Summary
From prenatal days until death, humans are each subjected to their own variable exposome [1], a sum of individual environmental exposures from their source to their biological and health effects [2,3,4]. PAHs are released from anthropogenic and natural activities. PAH emissions and human exposure originate from sources of incomplete organic fuel combustion, including tobacco smoke, charred or smoked meat, industrial byproduct emissions, forest fires, volcanic eruptions, and even contaminated food [5]. Single PAH chemical studies have been helpful in the research realm for studying toxicity, but realistic exposure to chemicals occurs in mixtures rather than by single While air emission sources such as tobacco smoke, and subsequent inhalation of volatile PAHs, has dominated analyses of exposure, dietary sources have been suggested as significant contributors to PAH exposure and potential health risks [6,7,8,9].
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