Abstract
BackgroundThe incidence of type 1 diabetes in Europe is increasing at a rate of about 3% per year and there is also an increasing incidence throughout the world. Type 1 diabetes is a complex disease caused by multiple genetic and environmental factors. Persistent organochlorine pollutants (POPs) have been suggested as a triggering factor for developing childhood type 1 diabetes. The aim of this case-control study was to assess possible impacts of in utero exposure to POPs on type 1 diabetes.Methodology/ Principal FindingsThe study was performed as a case-control study within a biobank in Malmö, a city located in the Southern part of Sweden. The study included 150 cases (children who had their diagnosis mostly before 18 years of age) and 150 controls, matched for gender and day of birth. 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB-153) and the major DDT metabolite 1,1-dichloro-2,2-bis (p-chlorophenyl)-ethylene (p,p′-DDE) were used as a biomarkers for POP exposure. When comparing the quartile with the highest maternal serum concentrations of PCB-153 with the other quartiles, an odds ratio (OR) of 0.73 (95% confidence interval [CI] 0.42, 1.27) was obtained. Similar results was obtained for p,p′-DDE (OR 0.56, 95% CI 0.29, 1.08).ConclusionsThe hypothesis that in utero exposure to POPs will trigger the risk for developing type 1 diabetes was not supported by the results. The risk estimates did, although not statistically significant, go in the opposite direction. However, it is not reasonable to believe that exposure to POPs should protect against type 1 diabetes.
Highlights
The incidence of type 1 diabetes in Europe and many other parts of the world is increasing at a rate of about 3% per year [1,2,3,4,5]
The hypothesis that in utero exposure to Persistent organochlorine pollutants (POPs) will trigger the risk for developing type 1 diabetes was not supported by the results
It is not reasonable to believe that exposure to POPs should protect against type 1 diabetes
Summary
The incidence of type 1 diabetes in Europe and many other parts of the world is increasing at a rate of about 3% per year [1,2,3,4,5]. Type 1 diabetes is an autoimmune disease that is characterized by destruction of insulin-producing pancreatic b-cells, resulting in a lack of or even absence of insulin production and disturbed glucose homeostasis [8] It is a complex disease caused by multiple genetic and environmental factors. Several studies support the hypothesis that prenatal exposure to environmental factors are of importance In this context, advanced maternal age, blood group incompatibility between mother and child [12], maternal enterovirus infections during pregnancy [13,14] and being born with congenital rubella [15] are associated with an increased risk of developing the disease later in life. The aim of this case-control study was to assess possible impacts of in utero exposure to POPs on type 1 diabetes
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