Effect of perfluoroalkyl exposure in pregnancy and infancy on intrauterine and childhood growth and anthropometry. Sub study from COPSAC2010 birth cohort

Sevelsted, Astrid; Gürdeniz, Gözde; Rago, Daniela; Pedersen, Casper-Emil Tingskov; Lasky‐Su, Jessica; Checa, Antonio; Zhang, Pei; Wheelock, Craig E.; Normann, Stine S; Kristensen, David M.; Rasmussen, Morten; Schullehner, Jörg; Sdougkou, Kalliroi; Martin, Jonathan W.; Stokholm, Jakob; Bønnelykke, Klaus; Bisgaard, Hans; Chawes, Bo

doi:10.1016/j.ebiom.2022.104236

Cited by 15 publications

(16 citation statements)

References 51 publications

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“…This is because maternal PFAS concentrations are influenced by her previous pregnancy and breastfeeding history, likely due to transfer of PFAS during pregnancy, delivery, and breastfeeding. 12,[35][36][37][38] Given that past breastfeeding predicts future breastfeeding, 39 bias could be produced if multiparous women who had previously breastfed had lower concentrations of PFAS and were also more likely to breastfeed for a longer duration for the current pregnancy. Because the Healthy Start study did not collect data about prior breastfeeding, the observed relationships in multiparous women may be due to residual confounding that biased the estimates away from the null.…”

Section: Discussionmentioning

confidence: 99%

Maternal serum per- and polyfluoroalkyl substances during pregnancy and breastfeeding duration

Friedman

Dabelea

Keil

et al. 2023

Environmental Epidemiology

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Background/objectives: Per-and polyfluoroalkyl substances (PFAS) are endocrine-disrupting chemicals that may affect breastfeeding duration. We examined associations between maternal PFAS concentrations during pregnancy and breastfeeding cessation. We investigated potential effect modification by parity status. Methods: Among 555 women enrolled in the Healthy Start study (2009)(2010)(2011)(2012)(2013)(2014), we quantified maternal serum concentrations of 5 PFAS during mid-to late-pregnancy (mean 27 weeks of gestation). Participants self-reported their breastfeeding practices through 18-24 months postnatally. Among all participants and stratified by parity, we estimated associations between maternal PFAS concentrations and breastfeeding discontinuation by 3 and 6 months, using Poisson regression, and breastfeeding duration, using Cox regression. Results: Median PFAS concentrations were similar to those in the general US population. Associations between PFAS and breastfeeding duration differed by parity status. After adjusting for covariates, among primiparous women, associations between PFAS and breastfeeding cessation by 3 and 6 months were generally null, with some inverse associations. Among multiparous women, there were positive associations between perfluorohexane sulfonate, perfluorooctane sulfonate, perfluorooctanoate (PFOA), and perfluorononanoate and breastfeeding cessation by 3 and 6 months. For example, per ln-ng/mL increase in PFOA, the risk ratio for breastfeeding discontinuation by 6 months was 1.45 (95% confidence interval, 1.18, 1.78). Hazard ratios reflected similar patterns between PFAS and breastfeeding duration. Conclusions: Among primiparous women, we did not find evidence for associations between PFAS concentrations and breastfeeding duration. In contrast, among multiparous women, PFAS serum concentrations were generally inversely associated with breastfeeding duration, though estimates may be biased due to confounding by unmeasured previous breastfeeding.

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Section: Discussionmentioning

confidence: 99%

Maternal serum per- and polyfluoroalkyl substances during pregnancy and breastfeeding duration

Friedman

Dabelea

Keil

et al. 2023

Environmental Epidemiology

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“…PFOA, absorbed primarily through contaminated food and water and, to a lesser extent, through polluted air, exhibit a lipophilic nature, distributing throughout the body with a notable affinity for accumulating in fatty tissues [ 47 ]. The slow elimination of PFOA poses challenges, contributing to their persistence and potential long-term health implications, as evidenced by associations with intrauterine growth and asthma [ 2 ]. These findings underscore the need for continued research and regulatory scrutiny to address the complexities of xenobiotic exposure during critical developmental stages and suggest a possible path through breastfeeding [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Pregnancy, birth, and the first months of life are crucial in early childhood disease development [ 1 , 2 ]. It is assumed that during pregnancy and early childhood, the mother and child experience a shared exposure to nutrients and environmental intake of chemical compounds (metabolites) [ 2 ]. Further, many metabolites are the consequence of enzymatic biochemical conversions stemming from host genomics, or the gut microbiome, which can also shared between mother and child [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, metabolomics represents a mechanistic information layer for understanding the mode of action for exposures like diet, exercise, and pollutants on disease progression [ 7 ]. Understanding which metabolites get passed down from mother to child is crucial in discerning prenatal maternal impacts on the child’s health [ 2 , 8 , 9 , 10 ]. For example, per- and poly-fluoroalkyl substances (PFAS), metabolites associated with high rates of vertical transfer [ 11 ], have been associated with premature birth [ 12 ] and adverse child growth [ 2 ] but also show the potential to affect the lipidome [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Vertical Metabolome Transfer from Mother to Child: An Explainable Machine Learning Method for Detecting Metabolomic Heritability

Lovrić,

Horner,

Chen

et al. 2024

Metabolites

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Vertical transmission of metabolic constituents from mother to child contributes to the manifestation of disease phenotypes in early life. This study probes the vertical transmission of metabolites from mothers to offspring by utilizing machine learning techniques to differentiate between true mother–child dyads and randomly paired non-dyads. Employing random forests (RF), light gradient boosting machine (LGBM), and logistic regression (Elasticnet) models, we analyzed metabolite concentration discrepancies in mother–child pairs, with maternal plasma sampled at 24 weeks of gestation and children’s plasma at 6 months. The propensity of vertical transfer was quantified, reflecting the likelihood of accurate mother–child matching. Our findings were substantiated against an external test set and further verified through statistical tests, while the models were explained using permutation importance and SHapley Additive exPlanations (SHAP). The best model was achieved using RF, while xenobiotics were shown to be highly relevant in transfer. The study reaffirms the transmission of certain metabolites, such as perfluorooctanoic acid (PFOA), but also reveals additional insights into the maternal influence on the child’s metabolome. We also discuss the multifaceted nature of vertical transfer. These machine learning-driven insights complement conventional epidemiological findings and offer a novel perspective on using machine learning as a methodology for understanding metabolic interactions.

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Caspase-3/GSDME dependent pyroptosis contributes to offspring lung injury induced by gestational PFOS exposure via PERK/ATF4 signaling

Li,

Zhang,

et al. 2023

Arch Toxicol

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Perfluorooctane sulfonate (PFOS) is widely used in industry and consumer products. Previous studies have showed that PFOS gestational exposure is associated with offspring lung damage in rat. However, the underlying mechanisms remain poorly understood. In this study, we investigated the role of gasdermin E (GSDME) in lung injury of offspring and its underlying mechanisms using in vivo and in vitro approaches. Pregnant SD rats were exposed to PFOS (1 mg/kg BW/d) between gestational day 12–18, and the lung tissue of the offspring was evaluated on postnatal day 7. PFOS treated animals exhibited alveolar septal thickening and inflammation-related damages, with an increased expression of GSDME in alveolar type II epithelial cells (AECII). Furthermore, in vitro experiments demonstrated that PFOS exposure (with 225 μM and up) upregulated the caspase-3/GSDME signaling pathway in AECII. Also, ultrastructure analysis revealed significant changes in the endoplasmic reticulum (ER) structure in PFOS-induced pyroptotic cells, which is consistent with the ER stress detected in these cells. Additionally, PFOS exposure led to increased expression of ER stress-related proteins, including p-PERK, p-eIF2α, ATF4, and CHOP. Subsequently, using specific inhibitors, we found that the PERK/ATF4 pathway acted as an upstream signal regulating GSDME-dependent pyroptosis. Overall, our findings show that GSDME-dependent pyroptosis plays a crucial role in the lung injury induced by gestational PFOS exposure, and the PERK/ATF4 pathway may function as a possible mediator of this process.

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Effect of perfluoroalkyl exposure in pregnancy and infancy on intrauterine and childhood growth and anthropometry. Sub study from COPSAC2010 birth cohort

Cited by 15 publications

References 51 publications

Maternal serum per- and polyfluoroalkyl substances during pregnancy and breastfeeding duration

Maternal serum per- and polyfluoroalkyl substances during pregnancy and breastfeeding duration

Vertical Metabolome Transfer from Mother to Child: An Explainable Machine Learning Method for Detecting Metabolomic Heritability

Caspase-3/GSDME dependent pyroptosis contributes to offspring lung injury induced by gestational PFOS exposure via PERK/ATF4 signaling

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