Environmental Endocrine-Disrupting Chemical Exposure: Role in Non-Communicable Diseases

Abstract

The exponential growth of pollutant discharges into the environment due to increasing industrial and agricultural activities is a rising threat for human health and a biggest concern for environmental health globally. Several synthetic chemicals, categorized as potential environmental endocrine-disrupting chemicals (EDCs), are evident to affect the health of not only livestock and wildlife but also humankind. In recent years, human exposure to environmental EDCs has received increased awareness due to their association with altered human health as documented by several epidemiological and experimental studies. EDCs are associated with deleterious effects on male and female reproductive health; causes diabetes, obesity, metabolic disorders, thyroid homeostasis and increase the risk of hormone-sensitive cancers. Sewage effluents are a major source of several EDCs, which eventually reach large water bodies and potentially contaminate the drinking water supply. Similarly, water storage material such as different types of plastics also leaches out EDCs in drinking Water. Domestic wastewater containing pharmaceutical ingredients, metals, pesticides and personal care product additives also influences endocrine activity. These EDCs act via various receptors through a variety of known and unknown mechanisms including epigenetic modification. They differ from classic toxins in several ways such as low-dose effect, non-monotonic dose and trans-generational effects. This review aims to highlight the hidden burden of EDCs on human health and discusses the non-classical toxic properties of EDCs in an attempt to understand the magnitude of the exposome on human health. Present data on the environmental EDCs advocate that there may be associations between human exposure to EDCs and several undesirable health outcomes that warrants further human bio-monitoring of EDCs.

Keywords: endocrine-disrupting chemicals; exposome; hormone receptor; pollutant; trans-generational effects.

Figure 1

Sources of environmental EDCs and their effects on metabolism. DEP, Diethyl phthalate; DEHP, Diethylhexyl phthalate; DBP, Dibutyl phthalate; PFOS, Perfluorooctanote; DDT, Dichlorodiphenyltrichloro ethane; PBDE, Polybrominated diphenyl ether; TPTO, bis (triphenyltin) oxide; TBT, Tributyltin.

Figure 2

Health Effect of Endocrine disrupting chemicals. Tributyltin (TBT), PerfluorooctaneSulfonate (PFOS), Perfluorinated compounds (PFCs), Perfluorooctanoic acid (PFOA), Bisphenol A (BPA), Diethylstilbestrol (DES), hexachlorobenzene (HCB), dichlorodiphenyltri-chloroethane (DDT), Polybrominated diphenyls ethers (PBDEs), constitutive androstane receptor (CAR), Thyroid Hormone Receptor (ThR), glucocorticoid receptor (GR), Aryl hydrocarbon receptor (Ahr), Androgen receptor (AR), Peroxisome proliferator-activated receptor (PPAR), Estrogen receptor (ER), Liver X Receptor (LXR).

Figure 3

Total plastic waste generation by country, measured in million tons per year for the year 2010 and disease burden from non-communicable diseases (from 1990 to 2016). Total disease burden from non-communicable diseases (NCDs), measured in DALYs (Disability-Adjusted Life Years) per year. DALYs are used to measure total burden of disease—both from years of life lost and years lived with a disability. One DALY equals 1 lost year of healthy life. Base map courtesy of mapchart.net (http://www.mapchart.net) [Source: (10, 11)].

Figure 4

Trends of global diabetes, obesity, and plastic production during the period of 1980–2008 [Data source: https://ourworldindata.org/plastic-pollution and (9, 12)].