Rethinking Environmental Carcinogenesis

Abstract

The 2010 report of the President's Cancer Panel concluded that the burden of cancer from chemical exposures is substantial, while the programs for testing and regulation of carcinogens remain inadequate. New research on the role of early life exposures and the ability of chemicals to act via multiple biological pathways, including immunosuppression, inflammation, and endocrine disruption as well as mutagenesis, further supports the potential for chemicals and chemical mixtures to influence disease. Epidemiologic observations, such as higher leukemia incidence in children living near roadways and industrial sources of air pollution, and new in vitro technologies that decode carcinogenesis at the molecular level, illustrate the diverse evidence that primary prevention of some cancers may be achieved by reducing harmful chemical exposures. The path forward requires cross-disciplinary approaches, increased environmental research investment, system-wide collaboration to develop safer economic alternatives, and community engagement to support evidence-informed action. Engagement by cancer researchers to integrate environmental risk factors into prevention initiatives holds tremendous promise for reducing the rates of disease.See all articles in this CEBP Focus section, "Environmental Carcinogenesis: Pathways to Prevention."

Cancer Incidence Projections in the United States Between 2015 and 2050

“…If the prevalence of causal factors associated with higher cancer risk declined in the population, so too could cancer incidence. Multiple opportunities exist to disrupt the initiation or promotion of different cancers in adults by reducing exposures to carcinogens, promoting social and physical environments that support healthy behaviors, and preventing chronic conditions such as obesity and diabetes (23,24). The Community Guide (www.thecommunityguide.org/) provides recommended community-based strategies to reduce the prevalence of several common behavioral risk factors.…”

β-Hexachlorocyclohexane Drives Carcinogenesis in the Human Normal Bronchial Epithelium Cell Line BEAS-2B

“…The experimental concentration of 10 µM for β-HCH is the same as that already employed in our previous works and corresponds to the average plasma levels detected in a population-based epidemiologic study in the Valle del Sacco [ 21 ]. It is well established in the literature that chemical substances may cause carcinogenesis via both genotoxic and non-genotoxic mechanisms by altering cellular signaling networks or inducing DNA damage [ 39 ].…”

In Vitro Approaches to Determine the Potential Carcinogenic Risk of Environmental Pollutants

“…However, NAMs still exhibit several uncertainties and, thus, it is not currently possible to fully replace in vivo studies with alternative approaches [8]. Nonetheless, it is believed that applying an evaluation strategy that integrates data from several NAMs would efficiently allow us to prioritize data needed for the preliminary determination of the risks posed by exposures [9,10].…”