Yinyin Cai

Climate change can reduce cold exposure while increasing heat exposure, making thermal-welfare change difficult to measure. The Thermal Deviation Index (TDI) applies a nonlinear, two-sided response function to temperature relative to a human-centered optimum and accumulates the resulting values over time. Higher TDI denotes greater accumulated deviation and lower thermal welfare. Across 243,616 land cells over 1940-2024, baseline thermal position predicts the direction of change, while migration and leisure choices are associated with lower-TDI environments. Increasing TDI is associated with lower national output and employment and greater heat-related work-hour losses. Among the population living in cells with increasing TDI, 52.1% experience displacement exceeding twice the local detrended variability. The share remains 40.1% after AR(1) adjustment. Under CMIP6 projections with fixed 2020 population weights, warming concentrates losses among warmer, lower-income populations. TDI provides an accounting measure for climate economics.

Could the global transition to renewable energy create a green dilemma that pits carbon reduction against biodiversity conservation? This study examined the effect of policies promoting solar photovoltaics on local avian biodiversity using a panel dataset covering 2344 counties in China from 2014 to 2023. Policies that favored photovoltaic expansion led to reductions in bird diversity, disproportionately affecting wealthier and nondesert regions, as well as widespread species. The mechanism operated primarily through land conversion: Cropland and grassland were transformed into developed areas, reducing the diversity of vegetation. Paradoxically, the leaf area index increased, a pattern we term “inferior greening,” whereby diverse natural landscapes were replaced by dense but ecologically homogeneous vegetation. We argue that future photovoltaic development should be accompanied by strict biodiversity safeguards, especially in economically developed regions with high habitat complexity.

The burden of disease and death attributable to environmental pollution is a growing public health challenge worldwide, particularly in developing countries. While the adverse effects of environmental pollution on oral health have garnered increasing attention, a comprehensive and systematic assessment remains lacking. This article delves into the intricate relationship between environmental pollution and oral health, highlighting significant impacts on various aspects such as dental caries, periodontal diseases, oral facial clefts, cancer, as well as other oral diseases. Our results suggested that secondhand smoke, particulate matters (PM) and heavy metals are the most important risk factors affecting oral health. Additional contributors, such as radiation pollutants, electronic cigarette, phthalates, gaseous air pollutants, pesticides, solvents, wood dust, formaldehyde and excessive fluoride were investigated, though evidence for their impacts remains limited and often inconclusive. The review also explores potential mechanisms underlying these impacts, including microorganism, inflammation, oxidative stress, genetic influences, and toxicant exposures from heavy metals and other pollutants. For instance, PM2.5 may contribute to dental caries by disrupting oral pH balance and absorbing heavy metals such as lead and cadmium which have been considered as caries promoting elements. It is also associated with adverse inflammatory responses and tissue damage in periodontal tissues by causing oxidative stress, potentially leading to periodontitis. Drawing on current evidence, it provides a comprehensive analysis of these associations, offering critical insights to guide the development of preventive strategies and public health interventions. The findings highlight the pressing need for future research to validate the causal links between environmental pollution and oral diseases and to unravel the underlying biological mechanisms. Ultimately, greater attention must be directed toward addressing the relationship between environmental pollution and oral diseases, with a focus on pollution control and the reduction of preventable environmental risks to safeguard oral health on a broader scale.

Although previous studies have presented that fine particulate matter (PM2.5) regulates liver enzyme levels in the development of liver diseases, the evidence regarding the relationship between PM2.5 exposure and liver enzyme is not robust. We further aimed to conduct a systematic review and meta-analysis of observational studies to summarize the recent evidence on the effects of PM2.5 on liver enzyme in humans. In the meta-analysis, we retrieved online databases including PubMed and Web of Science database from 1982 up to 2022. A random-effects model was applied to evaluate the correlation between PM2.5 and liver enzyme level. A total of 10 studies fulfilled the inclusion criteria, including five prospective cohort studies, two cross-sectional studies, two longitudinal studies, and one time-series analysis. Each 10 μg/m³ increase in PM2.5 concentration was significantly correlated with a 4.45% increase in alanine aminotransferase (ALT) level (95% CI: 0.51–8.38%, p = 0.03), a 3.99% increase in aspartate transferase (AST) level (95% CI: 0.88–7.10%, p = 0.01), and a 2.91% increase in gamma-glutamyl transferase (GGT) level (95% CI: 1.18–4.64%, p < 0.001), but this significant association was not observed in alkaline phosphatase (ALP). Subgroup analysis revealed that PM2.5 has a significant correlation with ALT (5.07%, 95% CI: 0.81–9.33%), AST (4.11%, 95% CI: 0.74–7.48%), and GGT (2.74%, 95% CI: 1.09–4.38%) in Asia. Our meta-analysis showed that increments in PM2.5 exposure were significantly associated with a higher level of ALT, AST, and GGT. In addition, investigations into liver enzyme subtypes and specific chemical components of PM2.5 are important directions for future research.

Although fine particulate matter (PM2.5) is a known carcinogen, evidence of the association between PM2.5 and chronic liver disease is controversial. In the present meta-analysis study, we reviewed epidemiological studies to strengthen evidence for the association between PM2.5 and chronic liver disease. We searched three online databases from 1990 up to 2022. The random-effect model was applied for detection of overall risk estimates. Sixteen eligible studies, including one cross-sectional study, one retrospective cohort study, and 14 prospective cohort studies, fulfilled inclusion criteria with more than 330 thousand participants from 13 countries. Overall risk estimates of chronic liver disease for 10 μg/m³ increase in PM2.5 was 1.27 (95% confidence interval (CI): 1.19–1.35, p < 0.001). We further analyzed the relationship between PM2.5 exposure and different chronic liver diseases. The results showed that increments in PM2.5 exposure significantly increased the risk of liver cancer, liver cirrhosis, and fatty liver disease (hazard ratio (HR) = 1.23, 95% CI: 1.14–1.33; HR = 1.17, 95% CI: 1.06–1.29; HR = 1.51, 95% CI: 1.09–2.08, respectively). Our meta-analysis indicated long-term exposure to PM2.5 was associated with increased risk of chronic liver disease. Moreover, future researches should be focused on investigating subtypes of chronic liver diseases and specific components of PM2.5.