Journal of environmental science and public health最新文献

Cardiovascular diseases are a significant cause of mortality worldwide, and their prevalence can be amplified by a range of environmental factors. This review article critically evaluated the published information on the epidemiology and pathophysiological mechanisms of various environmental factors such as air indoor and outdoor air pollution, water pollution, climate change, and soil pollution. Preventative measures to mitigate these effects including public health responses are discussed with gaps in our knowledge for future studies.

The health outcomes of an individual are shaped by a combination of genetic predisposition and environmental influences. While some diseases stem solely from environmental factors, others like atopic eczema, also known as neurodermatitis or atopic dermatitis, are multifaceted, with environmental variables playing a significant role in its initiation and severity. Atopic eczema is a prevalent chronic condition observed globally, particularly in Western industrialized nations where its prevalence is estimated to range from 2.5% to 3.5% in adults and 10% to 15% among children. The increasing incidence of atopic eczema in industrialized countries over recent decades suggests that this trend may be due to environmental changes rather than genetic predispositions. Therefore, by thoroughly examining environmental factors and their role in atopic dermatitis, one may be able to gain a better understanding of its disease pattern and develop possible preventative measures. This article provides a comprehensive analysis of how the surrounding environment contributes to the pathogenesis of atopic eczema.

Empirical evidence from human studies has demonstrated a correlative relationship between perfluorooctane sulfonate (PFOS) exposure and increased risks of preeclampsia and fetal developmental complications. Although experimental and circumstantial data suggest that PFOS induces endothelial dysfunction, leading to decreased uterine arterial blood flow and gestational hypertension, the precise regulatory mechanisms responsible for this effect remain unknown. To address this issue, we treated human uterine artery endothelial cells (hUAECs) isolated from pregnant women with 10 μmol/L PFOS or vehicle and conducted comparative transcriptomic analyses. We identified a total of 19 differentially expressed genes, 9 of which were upregulated and 10 were down-regulated in PFOS-treated pregnant hUAECs. Pre-ranked gene set enrichment analysis unveiled a distinct set of activated genes involved in osmotic stress, cellular stress response, translation regulation, metabolic regulation, and oxidation-reduction processes in PFOS-treated pregnant hUAECs. Furthermore, PFOS treatment resulted in the downregulation of genes implicated in cardiac muscle cell proliferation, embryonic morphogenesis, and muscle cell proliferation. In addition, we observed differential splicing events in 2678 genes in hUAECs exposed to PFOS, with cross-comparison analysis revealing 4 genes that were both differentially expressed and alternatively spliced and were implicated in oxidative stress and cardiac development. In conclusion, this study provides a comprehensive understanding of the molecular mechanisms underlying PFOS-induced gestational uterine artery endothelial dysfunction during pregnancy, offering a valuable resource for future research in this field.

Perfluorooctane sulfonate (PFOS), a synthetic chemical used in various commercial applications and industrial settings, has led to contamination of drinking water and has been detected in the bloodstream of pregnant women with gestational complications. Recent investigations have indicated that PFOS disrupts placental function; however, the mechanism remains elusive. Given the significant abundance of mitochondria in the placenta, which play a pivotal role in fulfilling the heightened energy requirements of pregnancy, our research aimed to examine the repercussions of PFOS exposure on mitochondrial dynamics within placental trophoblasts. Specifically, human trophoblasts (HTR-8/SVneo) were exposed to environmentally relevant concentrations of PFOS ranging from 0.1 to 50 μM for 48 hours. Findings revealed that PFOS exposure elicited a concentration-dependent decrease in basal, maximal, and ATP-linked respiration. PFOS inhibited the activity of electron transport complexes I, II, and III, resulting in diminished ATP production. Furthermore, PFOS reduced mitochondrial DNA copy number, indicating less mitochondrial content. Concurrently, there was a downregulation in the expression of mitochondrial biogenesis-related genes, including PGC-1α, NRF1, and NRF2. Notably, PFOS perturbed mitochondrial dynamics by suppressing the expression of fission-related genes (FIS1 and DRP1) and fusion-related genes (MFN1 and MFN2). In summary, our findings suggest that PFOS exposure leads to a decline in mitochondrial content and compromises the bioenergetic capacity of trophoblasts by impairing cellular respiration. This reduction in mitochondrial biogenesis and alterations in fission/fusion dynamics induced by PFOS may contribute to mitochondrial dysfunction in trophoblasts. Consequently, strategies that preserve mitochondrial function in trophoblasts may mitigate PFOS-induced impairment of placental energy metabolism.