Can Exposure to Environmental Chemicals Increase the Risk of Diabetes Type 1 Development?

Abstract

Type 1 diabetes mellitus (T1DM) is an autoimmune disease, where destruction of beta-cells causes insulin deficiency. The incidence of T1DM has increased in the last decades and cannot entirely be explained by genetic predisposition. Several environmental factors are suggested to promote T1DM, like early childhood enteroviral infections and nutritional factors, but the evidence is inconclusive. Prenatal and early life exposure to environmental pollutants like phthalates, bisphenol A, perfluorinated compounds, PCBs, dioxins, toxicants, and air pollutants can have negative effects on the developing immune system, resulting in asthma-like symptoms and increased susceptibility to childhood infections. In this review the associations between environmental chemical exposure and T1DM development is summarized. Although information on environmental chemicals as possible triggers for T1DM is sparse, we conclude that it is plausible that environmental chemicals can contribute to T1DM development via impaired pancreatic beta-cell and immune-cell functions and immunomodulation. Several environmental factors and chemicals could act together to trigger T1DM development in genetically susceptible individuals, possibly via hormonal or epigenetic alterations. Further observational T1DM cohort studies and animal exposure experiments are encouraged.

Exposure to polychlorinated biphenyl-153 decreases incidence of autoimmune Type 1 diabetes in non-obese diabetic mice

“…In agreement with the latest review about the risk assessment of POPs in T1D development (Bodin et al 2015), further observational T1D cohort studies together with animal and cellular exposure experiments will be needed to support this hypothesis. Although only mouse models were used in this study, as it is the convention in many federal agencies (including the National Toxicology Program), it is important to comment that the burgeoning field of molecular epidemiology and ''omics'' approaches (Milan et al 2015;Hong et al 2016) will allow further understanding of the biological consequences and milieu invoked by environmental exposures to PCBs.…”

“…Taylor et al (2013) and Bodin et al (2015) recently emphasized several areas that need to be extensively researched regarding the association of POP with diabetes, one being relationships between POP and specifically T1D; to date, only one prospective study (Rignell-Hydbom et al 2010) has been done. In the context of this data gap, we believe our study adds to the knowledge about the relation between PCB-153 and T1D.…”

“…This study chose to study PCB-153 as it is the most prevalent PCB congener with its concentration often used as a representative of total PCB concentration (RPCB) in human sera. Considering recent reviews by Taylor et al (2013), Tang et al (2014), and Bodin et al (2015) pointing at the substantial knowledge gained about the role of PCBs in Type 2 diabetes, and speculating (in the absence of experimental evidence) about a positive association between PCBs and T1D, this study sheds a light on PCB-153 action in the context of experimental T1D. Whereas PCB-153 levels in sera of treated mice were not identified here, the doses and route of exposure were comparable to those used in previous animal studies (Smialowicz et al 1997;Ropstad et al 2006;Strathmann et al 2006;Duffy-Whritenour et al 2010).…”

“…Although many environmentallyrelated hypotheses, including hygiene, diet, viral infections and chemicals have been proposed, the reason for such an increase in T1D is still unknown (Knip & Simell 2012). Over the past several years, research investigating the role of environmental pollutants in diabetes development has been substantially expanding (Taylor et al 2013;Bodin et al 2015).…”

Exposure to environmental chemicals and type 1 diabetes: an update

“…A separate 2015 narrative review also determined that it was plausible that environmental chemical and air pollution exposures could contribute to T1DM development, by impairing immune or beta cell function 4. Chemical exposures could affect the developing immune system and increasing the risk of autoimmunity as well as affect the beta cells, increasing their susceptibility to an autoimmune attack 5.…”