BackgroundExisting evidence indicates that exposure to per- and polyfluoroalkyl substances (PFASs) may increase the risk of hypertension, but the findings are inconsistent. Therefore, we aimed to explore the relationship between PFASs and hypertension through this systematic review and meta-analysis.MethodsWe searched PubMed, Embase, and the Web of Science databases for articles published in English that examined the relationship between PFASs and hypertension before 13 August 2022. The random effects model was used to aggregate the evaluation using Stata 15.0 for Windows. We also conducted subgroup analyses by region and hypertension definition. In addition, a sensitivity analysis was carried out to determine the robustness of the findings.ResultsThe meta-analysis comprised 15 studies in total with 69,949 individuals. The risk of hypertension was substantially and positively correlated with exposure to perfluorooctane sulfonate (PFOS) (OR = 1.31, 95% CI: 1.14, 1.51), perfluorooctanoic acid (PFOA) (OR = 1.16, 95% CI: 1.07, 1.26), and perfluorohexane sulfonate (PFHxS) (OR = 1.04, 95% CI: 1.00, 1.09). However, perfluorononanoic acid (PFNA) exposure and hypertension were not significantly associated (OR = 1.08, 95% CI: 0.99, 1.17).ConclusionWe evaluated the link between PFASs exposure and hypertension and discovered that higher levels of PFOS, PFOA, and PFHxS were correlated with an increased risk of hypertension. However, further high-quality population-based and pathophysiological investigations are required to shed light on the possible mechanism and demonstrate causation because of the considerable variability.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/ PROSPERO, registration number: CRD 42022358142.
Perfluorooctane sulfonate (PFOS), a new type of persistent
organic
pollutant in the environment of water, has drawn significant attention
in recent years due to its widespread prevalence and high toxicity.
Neurotoxicity is regarded as one of the major toxic effects of PFOS,
while research studies on PFOS-induced depression and the underlying
mechanisms remain scarce. In this study, behavioral tests revealed
the depressive-like behaviors in PFOS-exposed male mice. Neuron damages
including pyknosis and staining deepening were identified through
hematoxylin and eosin staining. Then, we noticed the elevation of
glutamate and proline levels as well as the decline of glutamine and
tryptophan levels. Proteomics analysis identified 105 differentially
expressed proteins that change in a dose-dependent manner and revealed
that PFOS exposure activated the glutamatergic synapse signaling pathway,
which were further confirmed by Western blot, and the data were consistent
with the findings of the proteomics analysis. Additionally, the downstream
signaling cyclic AMP-responsive element-binding protein (CREB)/brain-derived
neurotrophic factor (BDNF) and synaptic plasticity-related postsynaptic
density protein 95, synaptophysin, were downregulated. Our results
highlight that PFOS exposure may inhibit the synaptic plasticity of
the hippocampus via glutamatergic synapse and the CREB/BDNF signaling
pathway to cause depressive-like behaviors in male mice.
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