Phthalate exposure increases interferon- during pregnancy: The Atlanta African American Maternal-Child Cohort

Background: The immune system undergoes unique adaptations during pregnancy and is particularly sensitive to environmental chemicals, such as phthalates, which are associated with acute and chronic inflammatory medical conditions. However, current knowledge of how phthalate exposures are associated with systemic inflammation in pregnant people is limited by cross-sectional study designs and single chemical models. Our objective was to estimate the association between repeated measures of prenatal phthalate exposures, examined individually and collectively, and a panel of clinical inflammatory biomarkers. Methods: In the Atlanta African American Maternal -Child Cohort, biospecimens were collected at mean 11 and 26 weeks gestation (N = 126). Concentrations of eight urinary phthalate metabolites and five serum inflammatory biomarkers, including CRP, IFN-gamma, IL -6, IL -10, and TNF-alpha, were measured. Linear mixed effect regression and quantile g -computation models were used to estimate the associations for single phthalates and their exposure mixture, respectively. Results: Participants who self -reported any use of alcohol, tobacco, or marijuana in the month prior to pregnancy had increased MEP, MBP, MiBP, and CRP, relative to those with no substance use. IFN-gamma was elevated in response to MECPP (% change = 17.35, 95 % confidence interval [CI] = 0.32, 32.27), MEHHP (% change = 12.75, 95 % CI = 2.22, 24.36), MEOHP (% change = 11.63, 95 % CI = 1.21, 23.12), and their parent phthalate, EDEHP (% change = 15.03, 95 % CI = 0.28, 31.94). The phthalate mixture was also associated with an increase in IFN-gamma (% change = 15.03, 95 % CI = 6.18, 24.61). Conclusions: Our findings suggest DEHP metabolites induce systemic inflammation during pregnancy. The proinflammatory cytokine IFN-gamma may play an important role in the relationship between prenatal phthalate exposures and adverse pregnancy outcomes.