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Does Low Maternal Exposure to Per- and Polyfluoroalkyl Substances Elevate the Risk of Spontaneous Preterm Birth? A
Xiaotu Liu1, Da Chen1, Bin Wang2,3
1School of Environment, Guangdong Key Laboratory of Environmental Pollution and Health, Jinan University, Guangzhou 510632, China.
Insights
Maternal exposure to per- and polyfluoroalkyl substances (PFASs) was not linked to spontaneous preterm birth (SPB) risk in a Chinese study. However, PFASs may affect inflammation pathways, potentially impacting fetal development.
Area of Science:
- Environmental Health
- Reproductive Toxicology
- Per- and Polyfluoroalkyl Substances (PFASs) Research
Background:
- Maternal exposure to per- and polyfluoroalkyl substances (PFASs) is a growing concern for adverse birth outcomes.
- Spontaneous preterm birth (SPB) is a leading cause of infant mortality and morbidity, necessitating research into its contributing factors.
- Previous studies suggest potential links between PFAS exposure and negative pregnancy outcomes.
Purpose of the Study:
- To investigate the association between prenatal PFAS exposure and spontaneous preterm birth (SPB) risk.
- To examine the relationship between PFAS exposure and biomarkers of oxidative stress and systemic inflammation.
- To assess the impact of common PFASs like PFOA and PFOS on pregnancy outcomes in a Chinese population.
Main Methods:
- A prospective nested case-control study was conducted with 4229 women in Shanxi Province, China (2009-2013).
- Maternal plasma/serum samples from 144 SPB cases and 375 controls were analyzed for 17 PFASs.
- Biomarkers including monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), and heme oxygenase-1 (HO-1) were measured.
Main Results:
- No significant association was found between maternal plasma PFAS levels and spontaneous preterm birth (SPB) risk after adjusting for confounders.
- Perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), and 6:2 chlorinated polyfluoroether sulfonic acid (6:2 Cl-PFESA) were detected in over 90% of samples.
- PFOS and 6:2 Cl-PFESA showed a positive association with MCP-1, while PFOA was inversely associated with IL-8, suggesting inflammation pathway disturbance.
Conclusions:
- Low-level maternal PFAS exposure in this cohort did not elevate the risk of spontaneous preterm birth (SPB).
- Prenatal PFAS exposure may influence biochemical pathways related to inflammation, potentially affecting fetal and newborn development.
- Further research is warranted to understand the implications of PFAS-induced inflammation on birth and developmental outcomes.
Abstract:
Previous animal and human studies suggest potential links between maternal exposure to per- and polyfluoroalkyl substances (PFASs) and adverse birth outcomes. As spontaneous preterm birth (SPB) represents a major cause of infant mortality and precursor to future morbidity, we conducted a prospective nested case-control study in Shanxi Province, China to investigate the association between prenatal PFAS exposure and SPB risk, as well as the associations with biomarkers of oxidative stress and systemic inflammation. Among 4229 women enrolled during 2009-2013, 144 SPB cases and 375 controls were included in this study. Seventeen PFASs, as well as monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), and heme oxygenase-1 (HO-1), were measured in maternal plasma or serum collected during 4th-22nd gestational weeks. Perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), and its alternative chlorinated polyfluoroether sulfonic acid (6:2 Cl-PFESA) were detected in more than 90% samples with a median concentration of 0.79, 1.79, and 0.34 ng/mL, respectively. The analyses revealed no significant associations between plasma PFASs and the SPB risk after adjusting for potential confounders. However, concentrations of PFOS and 6:2 Cl-PFESA were both significantly and positively associated with MCP-1 levels, while PFOA was inversely associated with IL-8. Our findings suggested that maternal exposure to the determined low levels of PFAS did not induce an elevated risk of SPB, but the exposure may disturb potential biochemical pathways of inflammation. The latter has important implications for possible birth outcome effects and developmental effects in fetuses and newborns, which warrants close attention.
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