Prenatal serum concentrations of 13 PFAS, including PFBS, are measured among 500 participants in the New York University Children’s Health and Environment Study between 2016 and 2019 to investigate associations of PFAS exposures with demographic characteristics, including location of residence, and an exploratory factor analysis to investigate common sources of exposure.
Abstract
Relatively few epidemiologic studies in the US have measured the short-chain replacement per- or polyfluoroalkyl substance (PFAS) perfluorobutanesulfonic acid (PFBS), and little is known about its health impacts. We measured prenatal serum concentrations of 13 PFAS, including PFBS, among 500 participants in the New York University Children’s Health and Environment Study (NYU CHES) between 2016 and 2019. We investigated associations of PFAS exposures with demographic characteristics, including location of residence, and conducted an exploratory factor analysis to investigate common sources of exposure. PFBS concentrations were quantified in 95.6% of samples (median 0.40 ng/mL), which was unexpectedly higher than serum PFBS concentrations reported in other US-based cohorts. PFBS concentrations were not correlated with other PFAS, though they were positively correlated with each other. Unlike other PFAS, PFBS concentrations were not associated with participant characteristics, and there was no evidence for spatial autocorrelation. The changing PFAS exposure landscape warrants further investigation into the health effects of short-chain replacements, particularly in vulnerable populations.
The findings suggest that exposure to low levels of some alternative and precursor PFAS may be widespread in Canada and reinforce the role of pregnancy and breastfeeding as excretion pathways for legacy PFAS and support previous investigations demonstrating that exposure to some PFAS may be lower amongst financially disadvantaged populations.
Michael M. Borghese, Rebecca Lelievre, Sara Packull-McCormick et al.· Environmental Health· 0 citations
Limiting to directly measured exposures, incorporating the full NHANES design in the primary regression, and triangulating across complementary mixture frameworks provide a more rigorous platform than prior single-pollutant or design-naive approaches.
Rifa Tasnia, E. Obeng-Gyasi· Journal of Xenobiotics· 0 citations
PER: and polyfluoroalkyl substances (PFAS) have been implicated in metabolic dysregulation; however, longitudinal evidence linking PFAS to metabolic syndrome (MS) across the transition from adolescence or young adulthood into early adulthood is still lacking. We analyzed 516 participants aged 12-30 years in the Young Taiwanese Cohort (YOTA) with baseline examinations in 2006-2008 and follow-up in 2017-2019. Eleven plasma PFAS and MS components were quantified at both time points. We used joint models that simultaneously included baseline PFAS and long-term PFAS changes to evaluate associations with follow-up MS and its components. A PFAS exposure index was derived as the mean of standardized ln-PFAS. The baseline PFAS exposure index was not associated with MS or its components. Among individual baseline PFAS, linear PFOA was inversely associated with impaired fasting glucose, and both linear PFOA and PFHxS were inversely associated with elevated blood pressure. In contrast, the PFAS exposure index change was inversely associated with follow-up MS (OR 0.36, q = 0.050) and follow-up MS waist (OR 0.22, q < 0.001). Among individual PFAS changes, follow-up MS was inversely associated with changes in linear PFOA, PFHxS, and PFDoA, and MS waist was inversely associated with changes in linear PFOA, linear PFOS, PFNA, PFDA, PFUdA, and PFDoA. The associations between PFAS exposure index change with MS and MS waist were robust across sensitivity analyses, including qgcomp. Analyses of continuous metabolic traits showed concordant patterns for waist circumference and HDL-C. Exploratory backward models further suggested that adiposity change may influence measured PFAS change. In this Taiwanese cohort, higher ΔPFAS exposure index was associated with lower odds of MS and abdominal obesity, but the findings are consistent with reciprocal coupling rather than a protective effect of PFAS exposure. Studies with three or more repeated measurements are needed to clarify causal direction and underlying mechanisms.
Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) represents a critical developmental concern because several PFAS cross the placenta and may perturb biological programming during sensitive windows. Although epidemiological and experimental studies have linked prenatal exposure to several measured PFAS, primarily legacy perfluoroalkyl acids such as perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), Perfluorohexane Sulfonic Acid (PFHxS), and Perfluorononanoic Acid (PFNA), to diverse offspring outcomes, the strength of evidence differs substantially across compounds and health domains. Current human evidence is strongest for impaired vaccine antibody responses and altered growth or metabolic trajectories in studies dominated by legacy PFAS, whereas evidence for other congeners, short-chain PFAS, ether-based alternatives, and fluorotelomer compounds remains sparse. Mechanistically, placental transfer, nuclear receptor perturbation, thyroid hormone transport disruption, mitochondrial stress, immune modulation, and epigenetic reprogramming may jointly contribute to developmental susceptibility. We further discuss how emerging PFAS alternatives and real-world mixture exposures challenge single-chemical and adult-centered assessment paradigms. Finally, we outline a conceptual framework for developmental hazard assessment, in which exposure-window characterization, congener-specific toxicokinetics, human-relevant models, multi-omics biomarkers, and PBPK/PBTK modeling are positioned as complementary components rather than as a fully operational assessment system.
Bin Deng, Xuan Xia, Xiaoxiang Sun· Frontiers in Public Health· 0 citations
Per- and polyfluoroalkyl substances (PFAS) are pervasive organic compounds that have garnered significant attention due to their potential impacts on human health, particularly in relation to asthma, though current evidence remains limited. This study aimed to examine the association between PFAS exposure and adult asthma using a sample of 7106 participants aged 20 years and older from the NHANES survey, spanning 2003 to 2018. Survey-weighted multivariable logistic regression models, subgroup analysis, weighted quantile sum and Bayesian kernel machine regression models were employed to probe the relationship between PFAS and asthma. In the multivariable logistic regression analysis, higher log10-transformed perfluorooctane sulfonic acid (PFOS) and PFNA concentrations were significantly associated with lower odds of asthma (PFOS: OR = 0.76, 95% CI: 0.61–0.96; PFNA: OR = 0.77, 95% CI: 0.60–0.99). The inverse link between PFAS co-exposure and asthma incidence persisted across multi-pollutant models, weighted quantile sum regression, and Bayesian kernel machine regression models, with PFOS emerging as the primary negative influencer. In conclusion, this study highlights PFAS exposure is inversely associated with asthma risk in adults.
Tiankai Shan, Kai Wu, Jing-Xian Jiang· Medicine· 0 citations
Per and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants with endocrine-disrupting and carcinogenic potential. However, their bioaccumulation profiles and clinical relevance in human breast cancer remain largely unexplored.
In this preliminary study we quantified the absolute concentrations of 33 PFAS congeners (ng/g) in paired tumour and adjacent non-tumorous tissues from 11 breast cancer patients (
n
= 11) using LC–MS/MS to evaluate their tissue distribution and clinical correlations.
The detection rates for six compounds (HFPOTA, PFOA, PFNA, PFUnDA, PFOS, and 6:2Cl-PFESA) were greater than 40%. In paired samples, several congeners showed higher concentrations in tumour than in adjacent non-tumorous tissue; using a two-sided exact Wilcoxon signed-rank test with Hodges–Lehmann effect sizes, tumour enrichment remained significant after Benjamini–Hochberg correction for HFPOTA (
q
= 0.041), PFNA (
q
= 0.047) and PFUnDA (
q
= 0.047). HFPOTA showed by far the highest tissue burden (median 654 ng/g). Clinically, PFOS concentrations were descriptively higher in Luminal B than in Luminal A tumours and were positively correlated with the proliferation marker Ki-67; a high 6:2Cl-PFESA–PR rank correlation was observed in four samples but was not statistically significant on the raw p-value (p ≈ 0.051) and is exploratory. Bioinformatic analyses indicated that computationally predicted shared target genes of PFAS and breast cancer are enriched in the PPAR signaling pathway, lipid metabolism, and steroid hormone biosynthesis.
Collectively, PFAS bioaccumulation was associated with breast cancer clinicopathological characteristics. Because the target genes are predicted rather than experimentally validated and the cohort is small (
n
= 11), these are exploratory, hypothesis-generating findings that require validation in larger cohorts. This study underscores the need to reassess the biosafety of novel PFAS alternatives and provides new insights into the environmental etiology of breast cancer.
Bei Sun, Zhanhua Gao, Xiyue Liu et al.· Frontiers in Public Health· 0 citations