In the last decade, increasing incidence of type 1 diabetes (T1D) stabilized in Finland, a phenomenon that coincides with tighter regulation of perfluoroalkyl substances (PFAS). Here, we quantified PFAS to examine their effects, during pregnancy, on lipid and immune-related markers of T1D risk in children. In a mother-infant cohort (264 dyads), high PFAS exposure during pregnancy associated with decreased cord serum phospholipids and progression to T1D-associated islet autoantibodies in the offspring. This PFAS-lipid association appears exacerbated by increased human leukocyte antigen-conferred risk of T1D in infants. Exposure to a single PFAS compound or a mixture of organic pollutants in non-obese diabetic mice resulted in a lipid profile characterized by a similar decrease in phospholipids, a marked increase of lithocholic acid, and accelerated insulitis. Our findings suggest that PFAS exposure during pregnancy contributes to risk and pathogenesis of T1D in offspring.

在过去的十年中，芬兰的1型糖尿病（T1D）发病率不断上升，这一现象与对全氟烷基物质（PFAS）的严格监管相吻合。在这里，我们对PFAS进行了定量，以检查它们在怀孕期间对儿童T1D风险的脂质和免疫相关标记的影响。在一个母婴队列（264个双胞胎）中，怀孕期间的高PFAS暴露与脐带血磷脂减少以及后代发展为T1D相关的胰岛自身抗体有关。婴儿中人类白细胞抗原赋予的T1D风险增加似乎加剧了PFAS-脂质的关联。在非肥胖型糖尿病小鼠中暴露于单一PFAS化合物或有机污染物的混合物会导致脂质分布，其特征是磷脂的减少类似，石胆酸显着增加，和加速性岛炎。我们的发现表明，怀孕期间暴露于PFAS会增加后代T1D的风险和发病机理。