Abstract
The potential for persistent organic pollutants (POPs), including dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs), to increase the risk of incident diabetes in adults has been extensively studied. However, there is substantial variability in the reported associations both between and within studies. Emerging data from rodent studies suggest that dioxin disrupts glucose homeostasis in a sex-specific manner. Thus, we performed a review and meta-analysis of relevant epidemiological studies to investigate sex differences in associations between dioxin or DL-PCB exposure and type 2 diabetes incidence. Articles that met our selection criteria (n = 81) were organized into the following subcategories: data stratified by sex (n = 13), unstratified data (n = 45), and data from only 1 sex (n = 13 male, n = 10 female). We also considered whether exposure occurred either abruptly at high concentrations through a contamination event (“disaster exposure”) or chronically at low concentrations (“non-disaster exposure”). There were 8 studies that compared associations between dioxin/DL-PCB exposure and diabetes risk in males versus females within the same population. When all sex-stratified or single-sex studies were considered in the meta-analysis (n = 18), the summary relative risk (RR) for incident diabetes among those exposed relative to reference populations was 1.78 (95% CI = 1.37–2.31) and 1.95 (95% CI = 1.56–2.43) for female and males, respectively. However, when we restricted the meta-analysis to disaster-exposed populations, the RR was higher in females than males (2.86 versus 1.59, respectively). In contrast, in non-disaster exposed populations the RR for females was lower than males (1.40 and 2.02, respectively). Our meta-analysis suggests that there are sex differences in the associations between dioxin/DL-PCBs exposure and incident diabetes, and that the mode of exposure modifies these differences.
Highlights
The incidence of diabetes is increasing worldwide at a rate that cannot be explained solely by genetic predisposition or lifestyle (Knip et al, 2005; Butalia et al, 2016; Franks and McCarthy 2016), prompting investigations into alternative etiological risk factors
When examining pooled data from all 18 studies, we found that both sexes showed a statistically significant positive association between pollutant exposure and type 2 diabetes (T2D) (Figure 3; Table 2)
We looked for sex differences when studies were further subcategorized by population location or type of pollutant (Table 2)
Summary
The incidence of diabetes is increasing worldwide at a rate that cannot be explained solely by genetic predisposition or lifestyle (Knip et al, 2005; Butalia et al, 2016; Franks and McCarthy 2016), prompting investigations into alternative etiological risk factors. There is emerging evidence of a causal association between environmental pollutant exposure and the incidence of type 2 diabetes (T2D) (Carpenter 2008; Hectors et al, 2011; Ngwa et al, 2015). Persistent organic pollutants (POPs) are manmade toxins, released into the environment through industrial, electrical, and agricultural sources (Wikoff, Fitzgerald, and Birnbaum 2012; Hens and Hens 2017). POPs are typically lipophilic, resistant to degradation, and highly mobile, leading to ubiquitous global dispersion and bioaccumulation (Fisher 1999). Pollutant exposure can occur abruptly at high levels, as in a disaster event such as an industrial accident or sudden food contamination, but more frequently occurs at chronic low levels (Marinković et al, 2010). Human exposure to POPs occurs typically through the consumption of fish, meat, eggs, and dairy (Schecter et al, 2006; Srogi 2008). Despite global efforts to restrict POP production, use still continues in some countries (Azandjeme et al, 2014; Jaacks et al, 2019) and biomonitoring studies continue to detect POPs in serum and urine of the general population in North America (Haines and Murray 2012; Haines et al, 2017)
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