Halogenated Aromatic Hydrocarbons and Cardiovascular Disease

Abstract

Halogenated aromatic hydrocarbons (HAHs) are ubiquitous environmental pollutants and include polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs). Most humans accumulate these chemicals over a lifetime via a diet of fish, meat, poultry, and dairy products. A large number of human epidemiology studies have been conducted in an effort to elucidate the degree to which exposure to PCDDs, PCDFs, and PCBs may increase the morbidity and/or mortality from cardiovascular disease. Additionally, numerous laboratory-based cell culture and experimental animal studies have investigated the cardiovascular toxicity of HAH exposure and provide evidence for the biological plausibility and potential mechanism of action of HAH-induced cardiovascular disease. This chapter will review HAH-related human epidemiology data and laboratory-based experimental studies that have been conducted. Cardiovascular disease etiology is multifactorial and heterogeneous, and gene–environment interactions are important risk factors for disease pathogenesis. The data from both human epidemiology and laboratory animal studies strongly suggest that sustained activation of the aryl hydrocarbon receptor (AHR) by exposure to HAHs represents an important gene–environment interaction that has the potential to contribute to the burden of human cardiovascular disease morbidity and mortality.