Toxicogenomics of persistent organic pollutants: potential impacts on biodiversity and infectious diseases

Abstract

Pollution is recognized as one of the main causes of biodiversity loss. Growing evidence also points to pollution as an important risk factor for the emergence or reemergence of infectious diseases that affect humans and other animals. However, the mechanisms and pathways that explain how pollution erodes biodiversity and favors infectious diseases are poorly explored. Using the Dirty Dozen (aldrin, chlordane, dichlorodiphenyl trichloroethane - DDT, dieldrin, dioxins, endrin, furans, heptachlor, hexachlorobenzene, mirex, polychlorinated biphenyls - PCBs, and toxaphene) persistent organic pollutants (POPs) as a study model, in this article we demonstrate through toxicogenomic approaches that these POPs affect thousands of genes involved in the immune system and metabolic processes, among other biological pathways (n=19,086 genes from multiple organisms). One of the major findings indicate that POPs interact with hormone receptor genes prominently (i.e., Esr1, Nr1i2 and Ar genes). This finding highlights the activity of these pollutants as hormonal disruptors, with potentially deleterious consequences for the metabolism and reproduction of a wide range of species. These pollutants also have an important genotoxic activity, contributing to genomic instability and other related consequences. In summary, disturbances in the immune system can favor infection and the spread of pathogens, and changes in metabolism and genotoxic effects triggered by pollutants in multiple body systems can reduce fitness, harming the species’ survival in natural environments. The results of this exploratory toxicogenomic analysis represent a new piece in the puzzle that increasingly points to pollution as a major risk factor for both biodiversity loss and emerging infectious diseases.