Associations between early life exposure to persistent organic pollutants and mitochondrial DNA copy number in...

Early-life exposure to persistent organic pollutants (POPs) has adverse effects on fetuses and infants. However, little is known about the impact of POPs on mitochondrial DNA copy number (mtDNAcn) in neonates, which may lie on the pathway linking POPs exposure to adverse health impacts. To investigate the individual and joint associations between the multiple POPs and neonatal mtDNAcn, and to identify the most critical pollutants, we recruited 352 newborns at Hunan Children's Hospital, China and collected their basic information along with that of their parents, as well as blood samples from the newborns upon their initial hospital admission. 41 POPs were quantified by gas chromatography system coupled with a 7010B triple quadrupole tandem mass spectrometer. MtDNAcn in neonatal blood was measured by real-time quantitative polymerase chain reaction. We utilized generalized linear regression, least absolute shrinkage and selection operator regression, and two multi-pollutant models (bayesian kernel machine regression and weighted quantile sum regression [WQS]) to evaluate the potential effects of both individual POP exposure and POPs mixtures on neonatal mtDNAcn. After adjusting for covariates, γ-BHC, β-Endosulfan, Anthracene, Dibenz(a,h)anthracene, BDE-100, and BDE-99 were inversely associated with mtDNAcn. Results from the WQS model indicated a significant inverse correlation between mixed exposure to POPs and mtDNAcn (%Change = -20.63, 95 %CI: -34.43, -3.92). Meanwhile, BDE-99 predominated in the mixture index with the highest weight (19.7 %). These findings suggested that early-life exposure to specific POPs was associated with reduced neonatal mtDNAcn, with BDE-99 serving as the primary contributor. However, the association between exposure to POPs mixtures and decreased mtDNAcn was only observed in the WQS model. Future studies are needed to confirm these findings and to clarify the potential long-term hazards of early-life exposure to POPs.