Organophosphate pesticides exposure in pregnant women and maternal and cord blood thyroid hormone concentrations. (November 2019)

• Record Type: Journal Article
• Authors: Mulder, Tessa A.; van den Dries, Michiel A.; Korevaar, Tim I.M.; Ferguson, Kelly K.; Peeters, Robin P.; Tiemeier, Henning
• Is Part Of: Environment international. Volume 132(2019)
• Publication Date: 2019-11
• Subjects: Organophosphate pesticides -- Repeated measurements -- Thyroid function -- Pregnancy -- Cord blood -- 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.2019.105124
• Languages: English
• ISSNs: 0160-4120

Abstract

Abstract: Background: Animal studies suggest that organophosphate (OP) pesticides exposure affects thyroid function, but evidence in humans remains sparse and inconclusive. Gestational exposure is of particular interest, since thyroid hormone is essential for fetal brain development. OP pesticides are able to cross the placental and blood-brain barrier and may interfere with fetal development processes regulated by thyroid hormone. Objective: To investigate the association of gestational OP pesticides exposure during pregnancy with maternal and cord blood thyroid hormone concentrations. Methods: This study was embedded within Generation R (Rotterdam, the Netherlands), a prospective population-based birth cohort. Mother-child pairs with OP pesticides assessment and maternal ( N = 715) or cord blood ( N = 482) thyroid hormone measurements were included. OP pesticides exposure was assessed at <18, 18–25, and >25 weeks gestation by measuring six urinary dialkylphosphate (DAP) metabolites. Thyroid stimulating hormone (TSH) and free thyroxine (FT4) were measured in maternal and cord blood. Maternal measures also included total thyroxine (TT4) and TPO antibodies (TPOAbs). To study the association of creatinine-adjusted DAP metabolite concentrations with thyroid function and TPO antibodies, multivariable linear regression models including relevant confounders were used. Results: There was no association of DAP metabolites with maternal TSH, FT4, TT4 or TPOAb concentrations during pregnancy. Similarly, there was no association of DAP metabolites with cord blood TSH or FT4. Results did not change when DAP concentrations were analyzed at individual time points or as mean gestational exposure. Conclusion: Gestational OP pesticides exposure, as assessed by repeatedly measured urinary DAP metabolite concentrations in an urban population, was not associated with maternal or cord blood thyroid hormone concentrations. These findings do not support a mediating role for serum thyroid hormone availability in the relation of early life exposure to low levels of OP pesticides with child neurodevelopment. However, disruption of the thyroid system at tissue level cannot be excluded. In addition, this is one of the first studies on this subject and measurement error in DAP metabolites might have resulted in imprecise estimates. Future studies should use more urine samples to increase precision and should investigate specific OP pesticide metabolites. Highlights: We explored whether gestational OP pesticide exposure is associated with maternal or cord thyroid parameters. Maternal urinary concentrations of six DAP metabolites were measured during early, mid, and late pregnancy. DAP metabolite concentrations were 2–3 times higher than those in most other birth cohorts. Thyroid hormones were measured during early pregnancy and in cord blood. Maternal DAP concentrations were not associated with maternal or cord blood thyroid hormone concentrations.