Per- and polyfluoroalkyl substance (PFAS) exposure, maternal metabolomic perturbation, and fetal growth in African American women: A meet-in-the-middle approach

Chang, Che-Jung; Barr, Dana Boyd; Ryan, P. Barry; Panuwet, Parinya; Smarr, Melissa M.; Liu, Ken; Kannan, Kurunthachalam; Yakimavets, Volha; Tan, Youran; Ly, ViLinh; Marsit, Carmen J.; Jones, Dean P.; Corwin, Elizabeth J.; Dunlop, Anne L.; Liang, Donghai

doi:10.1016/j.envint.2021.106964

Cited by 95 publications

(60 citation statements)

References 149 publications

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“…In addition, as a PPAR-α agonist, PFOA may affect the status of the liver, β-oxidation of fatty acids, or hormone levels, which promises to trigger the reduction in birthweight. ,− On another aspect, PFOS causes controversy regarding fetal growth restriction, including reduction of HMG-CoA reductase activity, changes in the hypothyroid status, binding to specific proteins, altering the hormone or lipid metabolism, and so forth. Meanwhile, some researchers have proposed that PFAS lead to human fetal growth restriction by interfering with the metabolism of amino acids, lipids, and vitamins, as well as altering the status of the liver and gallbladder …”

Section: Discussionmentioning

confidence: 99%

Global Exposure to Per- and Polyfluoroalkyl Substances and Associated Burden of Low Birthweight

Fan

Tang

Wang

et al. 2022

Environ. Sci. Technol.

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Low birthweight (LBW) is a worldwide public health concern, while the global burden of LBW attributable to endocrine-disrupting chemicals, such as per- and polyfluoroalkyl substances (PFAS), has not yet been evaluated. Here, we established a large dataset for the biomonitoring of seven representative congeners of PFAS by examining data from 2325 publications. Global exposure to perfluorooctanesulfonic acid (PFOS) was the highest, followed by perfluorohexanesulfonic acid (PFHxS) and perfluorooctanoic acid (PFOA). Spatiotemporal exposure to PFAS varied considerably, with daily intake estimated in the range of 0.01–1.7 ng/kg/day. Moreover, decreasing trends in PFOS, PFHxS, and PFOA exposure were noted in most regions of the world over the past two decades, but such trends were not observed for other PFAS with long carbon chains, especially in East Asia. Furthermore, we estimated that human exposure to PFOA contributed to approximately 461,635 (95% confidence interval: 57,418 to 854,645) cases per year of LBW during the past two decades, predominantly from Asian regions. Although our estimation may be constrained by uncertainties from the dose–response curve and data availability, this study has unveiled that PFAS might be a contributor to global LBW prevalence during 2000–2019, supporting continuous actions to mitigate PFAS contamination.

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Section: Discussionmentioning

confidence: 99%

Global Exposure to Per- and Polyfluoroalkyl Substances and Associated Burden of Low Birthweight

Fan

Tang

Wang

et al. 2022

Environ. Sci. Technol.

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“…We applied to columns to maximize metabolomic coverage. [27][28][29] The sheath gas and auxiliary gas were set at 30 (arbitrary units) and 5 (arbitrary units) for the negative ESI, respectively. For the positive ESI, the sheath gas and the auxiliary gas were set at 45 (arbitrary units) and 25 (arbitrary units), respectively.…”

Section: High-resolution Metabolomicsmentioning

confidence: 99%

Length of PM2.5 exposure and alterations in the serum metabolome among women undergoing infertility treatment

Hood

Liang

Tang

et al. 2022

Environmental Epidemiology

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Both short-and long-term exposure to PM 2.5 has been related to adverse health outcomes. However, the biological pathways underlying these health effects are largely unknown. We identified several unique serum metabolomic pathways associated with acute and chronic PM 2.5 exposure. Major pathways associated with acute PM 2.5 exposure included amino acid, energy, and lipid metabolism. Major pathways associated with chronic PM 2.5 exposure included pro-inflammatory and anti-inflammatory pathways. Seven unique metabolites were identified with level-1 evidence.

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“…In humans, elevated serum PFAS correlated with changes in systemic metabolic pathways that provide precursors for monoamine synthesis . The changes in the metabolic pathway for tryptophan, an amino acid precursor for serotonin synthesis, were found to correlate with PFHxS and PFNA exposure.…”

Section: Pfas Effects On Neurotransmittersmentioning

confidence: 91%

“…The changes in the metabolic pathway for tryptophan, an amino acid precursor for serotonin synthesis, were found to correlate with PFHxS and PFNA exposure. Moreover, changes in the metabolic pathway for glutamate, the most prevalent amino acid and neurotransmitter in the brain, were correlated with PFOS, PFHxS, and PFNA exposure . Rat kidney cells exposed to PFOS or PFOA demonstrated decreases in phenylalanine (a tyrosine precursor), tyrosine (a dopamine and norepinephrine precursor), and tryptophan (a serotonin precursor) levels compared to the controls .…”

Section: Pfas Effects On Neurotransmittersmentioning

confidence: 99%

Neurotransmission Targets of Per- and Polyfluoroalkyl Substance Neurotoxicity: Mechanisms and Potential Implications for Adverse Neurological Outcomes

Brown-Leung

Cannon

2022

Chem. Res. Toxicol.

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Per- and polyfluoroalkyl substances (PFAS) are a group of persistent environmental pollutants that are ubiquitously found in the environment and virtually in all living organisms, including humans. PFAS cross the blood–brain barrier and accumulate in the brain. Thus, PFAS are a likely risk for neurotoxicity. Studies that measured PFAS levels in the brains of humans, polar bears, and rats have demonstrated that some areas of the brain accumulate greater amounts of PFAS. Moreover, in humans, there is evidence that PFAS exposure is associated with attention-deficit/hyperactivity disorder (ADHD) in children and an increased cause of death from Parkinson’s disease and Alzheimer’s disease in elderly populations. Given possible links to neurological disease, critical analyses of possible mechanisms of neurotoxic action are necessary to advance the field. This paper critically reviews studies that investigated potential mechanistic causes for neurotoxicity including (1) a change in neurotransmitter levels, (2) dysfunction of synaptic calcium homeostasis, and (3) alteration of synaptic and neuronal protein expression and function. We found growing evidence that PFAS exposure causes neurotoxicity through the disruption of neurotransmission, particularly the dopamine and glutamate systems, which are implicated in age-related psychiatric illnesses and neurodegenerative diseases. Evaluated research has shown there are highly reproduced increased glutamate levels in the hippocampus and catecholamine levels in the hypothalamus and decreased dopamine in the whole brain after PFAS exposure. There are significant gaps in the literature relative to the assessment of the nigrostriatal system (striatum and ventral midbrain) among other regions associated with PFAS-associated neurologic dysfunction observed in humans. In conclusion, evidence suggests that PFAS may be neurotoxic and associated with chronic and age-related psychiatric illnesses and neurodegenerative diseases. Thus, it is imperative that future mechanistic studies assess the impact of PFAS and PFAS mixtures on the mechanism of neurotransmission and the consequential functional effects.

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Per- and polyfluoroalkyl substance (PFAS) exposure, maternal metabolomic perturbation, and fetal growth in African American women: A meet-in-the-middle approach

Cited by 95 publications

References 149 publications

Global Exposure to Per- and Polyfluoroalkyl Substances and Associated Burden of Low Birthweight

Global Exposure to Per- and Polyfluoroalkyl Substances and Associated Burden of Low Birthweight

Length of PM2.5 exposure and alterations in the serum metabolome among women undergoing infertility treatment

Neurotransmission Targets of Per- and Polyfluoroalkyl Substance Neurotoxicity: Mechanisms and Potential Implications for Adverse Neurological Outcomes

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