Title: Lactation history, serum concentrations of persistent organic pollutants, and maternal risk of diabetes.
Authors: Zong, Geng; Grandjean, Philippe; Wang, Xiaobin; Sun, Qi
Published In Environ Res, (2016 Oct)
Abstract: Lactation may help curb diabetes risk and is also known as an excretion route for some environmental pollutants. We evaluated associations of lifetime lactation history with serum concentrations of persistent organic pollutants (POPs) in the National Health and Nutrition Examination Survey 1999-2006, and examined whether potentially diabetogenic POPs account for associations between lactation and diabetes.Among 4479 parous women, breastfeeding history was defined as the number of children breastfed ≥1 month. Diabetes was identified by self-report or hemoglobin A1c >6.5%. Twenty-four POPs were measured in serum among subsamples of 668 to 1073 participants.Compared with women without lactation history, odds ratios (95% confidence intervals) of having diabetes among those with 1-2 and ≥3 lactation periods were 0.83(0.61, 1.13) and 0.63(0.44, 0.91; P trend=0.03). Lifetime lactation history was inversely associated with serum concentrations of 17 out of the 24 organochlorine pesticides, polychlorinated biphenyl congeners (PCBs), and perfluoroalkyl substances (Ptrend<0.05). Comparing the ≥3 lactations group with women without a lactation history, the relative reduction of POPs ranged from 12% (PCB-196) to 30% (oxychlordane). The inverse association between lactation and diabetes was slightly attenuated after adjustment for POPs. Age-stratified analyses showed that the inverse association between lactation periods and serum POP concentrations was observed primarily among participants <60 years, whereas age did not significantly modify the association between lactation history and diabetes prevalence.Crudely-classified lifetime lactation history was inversely associated with concurrent serum POP concentrations and diabetes prevalence. Prospective studies are needed to clarify how lactation could complement diabetes prevention through decreasing the POP body burdens.
PubMed ID: 27336232
MeSH Terms: No MeSH terms associated with this publication