Neonatal exposure to environmental pollutants and placental mitochondrial DNA content: A multi-pollutant approach. (September 2017)

• Record Type: Journal Article
• Authors: Vriens, Annette; Nawrot, Tim S.; Baeyens, Willy; Den Hond, Elly; Bruckers, Liesbeth; Covaci, Adrian; Croes, Kim; De Craemer, Sam; Govarts, Eva; Lambrechts, Nathalie; Loots, Ilse; Nelen, Vera; Peusens, Martien; De Henauw, Stefaan; Schoeters, Greet; Plusquin, Michelle
• Is Part Of: Environment international. Volume 106(2017)
• Page Start: 60
• Page End: 68
• Publication Date: 2017-09
• Subjects: Placenta -- Mitochondrial DNA content -- Environmental pollution -- Newborns; Environmental protection -- Periodicals; Environmental health -- Periodicals; Environmental monitoring -- Periodicals; Environmental Monitoring -- Periodicals; Environnement -- Protection -- Périodiques; Hygiène du milieu -- Périodiques; Environnement -- Surveillance -- Périodiques; Environmental health; Environmental monitoring; Environmental protection; Periodicals; 333.705
• DOI: 10.1016/j.envint.2017.05.022
• Languages: English
• ISSNs: 0160-4120

Abstract

Abstract: Background: Placental mitochondrial DNA (mtDNA) content can be indicative of oxidative damage to the placenta during fetal development and is responsive to external stressors. In utero exposure to environmental pollutants that may influence placental mtDNA needs further exploration. Objectives: We evaluated if placental mtDNA content is altered by environmental pollution in newborns and identified pollutants independently associated to alterations in placental mtDNA content. Methods: mtDNA content was measured in placental tissue of 233 newborns. Four perfluoroalkyl compounds and nine organochlorine compounds were quantified in cord blood plasma samples and six toxic metals in whole cord blood. We first applied a LASSO (least absolute shrinkage and selection operator) penalized regression model to identify independent associations between environmental pollutants and placental mtDNA content, without penalization of several covariates. Then adjusted estimates were obtained using an ordinary least squares (OLS) regression model evaluating the pollutants' association with placental mtDNA content, adjusted for several covariates. Results: Based on LASSO penalized regression, oxychlordane, p, p′-dichlorodiphenyldichloroethylene, β-hexachlorocyclohexane, perfluorononanoic acid, arsenic, cadmium and thallium were identified to be independently associated with placental mtDNA content. The OLS model showed a higher placental mtDNA content of 2.71% (95% CI: 0.3 to 5.2%; p = 0.03) and 1.41% (0.1 to 2.8%, p = 0.04) for a 25% concentration increase of respectively cord blood β-hexachlorocyclohexane and arsenic. For a 25% concentration increase of cord blood thallium, a 4.88% lower placental mtDNA content (95% CI: -9.1 to − 0.5%, p = 0.03) was observed. Conclusion: In a multi-pollutant approach, low fetal exposure levels of environmental organic and inorganic pollutants might compromise placental mitochondrial function as exemplified in this study by alterations in mtDNA content. Highlights: Mitochondrial DNA (mtDNA) copy number can sense environmental perturbations. We studied neonatal exposure to environmental pollutants in relation to placental mtDNA. Using a multi-pollution approach we identified independent exposures influencing mtDNA. Arsenic, Thallium and β-HCH are associated with placental mtDNA content. Placental mtDNA content is sensitive to low levels of exposure.