Children’s white blood cell counts in relation to developmental exposures to methylmercury and persistent organic pollutants
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CitationOulhote, Y., Z. Shamim, K. Kielsen, P. Weihe, P. Grandjean, L.P. Ryder, and C. Heilmann. 2017. “Children’s White Blood Cell Counts in Relation to Developmental Exposures to Methylmercury and Persistent Organic Pollutants.” Reproductive Toxicology 68 (March): 207–214. doi:10.1016/j.reprotox.2016.08.001.
AbstractBackground: To explore possible markers of developmental immunotoxicity, we prospectively examined 56 children to determine associations between exposures to mercury and persistent organic pollutants since birth and the comprehensive differential counts of white blood cells (WBC) at age 5 years.
Materials and methods: Extended differential count included: neutrophils, eosinophils, basophils, lymphocytes (including T cells, NK cells, and B cells), and monocytes. Organochlorine compounds (OCs) including polychlorinated biphenyls (PCBs) and pesticides, five perfluoroalkyl substances (PFASs), and mercury (Hg) were measured in maternal (n=56) and children’s blood at 18 months (n=42) and 5 years (n=56). We constructed latent functions for exposures at three different ages using factor analyses and applied structural equations models adjusted for covariates.
Results: Prenatal mercury exposure was associated with depleted total WBC, especially for lymphocytes, where a one standard deviation (SD) increase in the exposure was associated with a decrease by 23% SD (95% CI: -43, -4) in the cell count. Prenatal exposure to OCs was marginally associated with decreases in neutrophil counts. In contrast, the 5-year PFASs concentrations were associated with higher basophil counts (B= 46% SD, 95% CI: 13, 79). Significantly reduced subpopulations of lymphocytes such as B cells, CD4-positive T helper cells and CD4 positive recent thymic emigrants may suggest cellular immunity effects and dysregulation of T-cell mediated immunity.
Conclusion: Thus prenatal exposure to mercury and PFASs appears to have differential impacts on WBC counts.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:37221735
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