Reproductive disorders are considered a global health problem influenced by physiological, genetic, environmental, and lifestyle factors. The increased exposure to bisphenols, a chemical used in large quantities for the production of polycarbonate plastics, has raised concerns regarding health risks in humans, particularly their endocrine-disrupting effects on female reproductive health. To provide a basis for future research on environmental interference and reproductive health, we reviewed relevant studies on the exposure patterns and levels of bisphenols in environmental matrices and humans (including susceptible populations such as pregnant women and children). In addition, we focused on in vivo, in vitro, and epidemiological studies evaluating the effects of bisphenols on the female reproductive system (the uterus, ovaries, fallopian tubes, and vagina). The results indicate that bisphenols cause structural and functional damage to the female reproductive system by interfering with hormones; activating receptors; inducing oxidative stress, DNA damage, and carcinogenesis; and triggering epigenetic changes, with the damaging effects being intergenerational. Epidemiological studies support the association between bisphenols and diseases such as cancer of the female reproductive system, reproductive dysfunction, and miscarriage, which may negatively affect the establishment and maintenance of pregnancy. Altogether, this review provides a reference for assessing the adverse effects of bisphenols on female reproductive health.

Particulate matter of size ≤ 2.5 μm (PM_2.5) is a critical environmental threat that considerably contributes to the global disease burden. However, accompanied by the rapid research progress in this field, the existing research on developmental toxicity is still constrained by limited data sources, varying quality, and insufficient in-depth mechanistic analysis. This review includes the currently available epidemiological and laboratory evidence and comprehensively characterizes the adverse effects of PM_2.5 on developing individuals in different regions and various pollution sources. In addition, this review explores the effect of PM_2.5 exposure to individuals of different ethnicities, genders, and socioeconomic levels on adverse birth outcomes and cardiopulmonary and neurological development. Furthermore, the molecular mechanisms involved in the adverse health effects of PM_2.5 primarily encompass transcriptional and translational regulation, oxidative stress, inflammatory response, and epigenetic modulation. The primary findings and novel perspectives regarding the association between public health and PM_2.5 were examined, highlighting the need for future studies to explore its sources, composition, and sex-specific effects. Additionally, further research is required to delve deeper into the more intricate underlying mechanisms to effectively prevent or mitigate the harmful effects of air pollution on human health.

Ambient particulate matter (PM_2.5) is a potential risk factor for metabolic damage to the liver. Epidemiological studies suggest that elevated PM_2.5 concentrations cause changes in hepatic metabolism, but there is a lack of laboratory evidence. Here, we aimed to evaluate the effects of PM_2.5 exposure on liver metabolism in C57BL/6j female mice (10 months old) and to explore the mechanisms underlying metabolic alterations and differential gene expressions by combining metabolomics and transcriptomics analyses. The metabolomics results showed that PM_2.5 exposure notably affected the metabolism of amino acids and organic acids and caused hepatic lipid and bile acid accumulation. The transcriptomic analyses revealed that PM_2.5 exposure led to a series of metabolic pathway abnormalities, including steroid biosynthesis, steroid hormone biosynthesis, primary bile acid biosynthesis, etc. Among them, the changes in the bile acid pathway might be one of the causes of liver damage in mice. In conclusion, this study clarified the changes in liver metabolism in mice caused by PM_2.5 exposure through combined transcriptomic and metabolomic analyses, revealed that abnormal bile acid metabolism is the key regulatory mechanism leading to metabolic-associated fatty liver disease (MAFLD) in mice, and provided laboratory evidence for further clarifying the effects of PM_2.5 on body metabolism.

Bisphenol A (BPA) continuously leaches from consumer products and accumulates in the human body, with detectable levels in urine. Emerging evidence suggests potential associations between prolonged BPA exposure and subclinical nephrotoxicity accompanied by metabolic dysregulation, though the gene regulatory mechanisms underlying these associations remain insufficiently characterized. In this study, bioinformatics analyses were employed to systematically reveal the potential transcriptional regulation of chronic renal injury due to BPA exposure. Complementary positron emission tomography/computed tomography (PET/CT) imaging revealed pronounced renal inflammatory responses and localized tissue damage in murine models following 6-week oral BPA administration. Histopathological examination of the kidney revealed exfoliation of renal tubular epithelial cells, with collagen fibers and mucus deposits. Further multi-omics integration (transcriptomic-metabolomic) analysis identified significant perturbations in cortisol biosynthesis, aldosterone regulation, and MAPK signaling cascades induced by BPA exposure. These findings were further validated through molecular docking studies and MAPK inhibitor intervention studies in cellular models. In summary, a critical pathway in BPA-induced renal injury involves the modulation of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) expression, which is mediated by p38 MAPK. This process impacts cortisol metabolism and aldosterone synthesis, suggesting that the biosynthesis of renal steroid hormones is intricately linked to MAPK regulation in renal injury following BPA exposure. Our findings furnish a theoretical foundation for elucidating the mechanisms underlying BPA-induced nephrotoxicity and contribute a holistic viewpoint to environmental health risk assessments.

In recent years, coal-combustion-related air pollution has declined markedly, whereas tropospheric ozone (O₃) pollution has emerged as a growing environmental concern. Long-term exposure to O₃ can severely impact human health and ecosystems, constraining socioeconomic development. The Fenwei Plain has complex topographical conditions and a relatively simple industrial structure, and at present, O₃ is one of the main pollutants affecting air quality in this region. Therefore, studying the distribution of O₃ pollution in the Fenwei Plain can provide a reference for developing plans to control O₃ pollution in the area, which is important for safeguarding local public health and economic development. Currently, the number of pollutant monitoring stations in China is limited, spatially discontinuous, and significantly affected by environmental factors, making it difficult to obtain high-precision, large-scale observational data. Satellite-based remote sensing provides broad spatial coverage and is free from topographic constraints, thereby serving as an effective complement to ground-based monitoring networks. This provides important technical support for studying the distribution characteristics of O₃ pollution and its associated health risks. This study focuses on the Fenwei Plain, utilizing machine learning models to estimate continuous O₃ concentrations from 2015 to 2022 and analyze the spatiotemporal distribution of O₃. Based on this, an assessment and analysis of the health risks associated with near-surface O₃ exposure in the study area will be conducted, incorporating the population exposed in the Fenwei Plain and individuals with chronic obstructive pulmonary disease (COPD).