UNASSIGNED: We evaluated the long-term effects of air pollution controls on health and health inequity among Chinese >45 years of age.
UNASSIGNED: Data were derived from the China Health Aging and Retirement Longitudinal Survey and the China National Environmental Monitoring Centre. Decreases in PM2.5 and PM10 were scaled to measure air quality controls. We used a quasi-experimental design to estimate the impact of air quality controls on self-reported health and health inequity. Health disparities were estimated using the concentration index and the horizontal index.
UNASSIGNED: Air pollution controls significantly improved self-reported health by 20% (OR 1.20, 95% CI, 1.02-1.42). The poorest group had a 40% (OR 1.41, 95% CI, 0.96-2.08) higher probability of having excellent self-reported health after air pollution controls. A pro-rich health inequity was observed, and the horizontal index decreased after air pollution controls.
UNASSIGNED: Air pollution controls have a long-term positive effect on health and health equity. The poorest population are the main beneficiaries of air pollution controls, which suggests policymakers should make efforts to reduce health inequity in air pollution controls.

UNASSIGNED: In recent years, the prevalence of obesity has continued to increase as a global health concern. Numerous epidemiological studies have confirmed the long-term effects of exposure to ambient air pollutant particulate matter 2.5 (PM2.5) on obesity, but their relationship remains ambiguous.
UNASSIGNED: Utilizing large-scale publicly available genome-wide association studies (GWAS), we conducted univariate and multivariate Mendelian randomization (MR) analyses to assess the causal effect of PM2.5 exposure on obesity and its related indicators. The primary outcome given for both univariate MR (UVMR) and multivariate MR (MVMR) is the estimation utilizing the inverse variance weighted (IVW) method. The weighted median, MR-Egger, and maximum likelihood techniques were employed for UVMR, while the MVMR-Lasso method was applied for MVMR in the supplementary analyses. In addition, we conducted a series of thorough sensitivity studies to determine the accuracy of our MR findings.
UNASSIGNED: The UVMR analysis demonstrated a significant association between PM2.5 exposure and an increased risk of obesity, as indicated by the IVW model (odds ratio [OR]: 6.427; 95% confidence interval [CI]: 1.881-21.968; P FDR = 0.005). Additionally, PM2.5 concentrations were positively associated with fat distribution metrics, including visceral adipose tissue (VAT) (OR: 1.861; 95% CI: 1.244-2.776; P FDR = 0.004), particularly pancreatic fat (OR: 3.499; 95% CI: 2.092-5.855; PFDR =1.28E-05), and abdominal subcutaneous adipose tissue (ASAT) volume (OR: 1.773; 95% CI: 1.106-2.841; P FDR = 0.019). Furthermore, PM2.5 exposure correlated positively with markers of glucose and lipid metabolism, specifically triglycerides (TG) (OR: 19.959; 95% CI: 1.269-3.022; P FDR = 0.004) and glycated hemoglobin (HbA1c) (OR: 2.462; 95% CI: 1.34-4.649; P FDR = 0.007). Finally, a significant negative association was observed between PM2.5 concentrations and levels of the novel obesity-related biomarker fibroblast growth factor 21 (FGF-21) (OR: 0.148; 95% CI: 0.025-0.89; P FDR = 0.037). After adjusting for confounding factors, including external smoke exposure, physical activity, educational attainment (EA), participation in sports clubs or gym leisure activities, and Townsend deprivation index at recruitment (TDI), the MVMR analysis revealed that PM2.5 levels maintained significant associations with pancreatic fat, HbA1c, and FGF-21.
UNASSIGNED: Our MR study demonstrates conclusively that higher PM2.5 concentrations are associated with an increased risk of obesity-related indicators such as pancreatic fat content, HbA1c, and FGF-21. The potential mechanisms require additional investigation.

Air pollution is the leading environmental cause of death globally, and most mortality occurs in resource-limited settings such as sub-Saharan Africa. The African continent experiences some of the worst ambient air pollution in the world, yet there are relatively little African data characterizing ambient pollutant levels and source admixtures. In Uganda, ambient PM2.5 levels exceed international health standards. However, most studies focus only on urban environments and do not characterize pollutant sources. We measured daily ambient PM2.5 concentrations and sources in Mbarara, Uganda from May 2018 through February 2019 using Harvard impactors fitted with size-selective inlets. We compared our estimates to publicly available levels in Kampala, and to World Health Organization (WHO) air quality guidelines. We characterized the leading PM2.5 sources in Mbarara using x-ray fluorescence and positive matrix factorization. Daily PM2.5 concentrations were 26.7 μg m-3 and 59.4 μg m-3 in Mbarara and Kampala, respectively (p<0.001). PM2.5 concentrations exceeded WHO guidelines on 58% of days in Mbarara and 99% of days in Kampala. In Mbarara, PM2.5 was higher in the dry as compared to the rainy season (30.8 vs 21.3, p<0.001), while seasonal variation was not observed in Kampala. PM2.5 concentrations did not vary on weekdays versus weekends in either city. In Mbarara, the six main ambient PM2.5 sources identified included (in order of abundance): traffic-related, biomass and secondary aerosols, industry and metallurgy, heavy oil and fuel combustion, fine soil, and salt aerosol. Our findings confirm that air quality in southwestern Uganda is unsafe and that mitigation efforts are urgently needed. Ongoing work focused on improving air quality in the region may have the greatest impact if focused on traffic and biomass-related sources.

Climate change is increasing the frequency and intensity of heatwaves, raising concerns about their detrimental effects on air quality. However, a role for heatwave-human-environment interactions in air pollution exacerbation has not been established. In the summer of 2022, record-breaking heatwaves struck China and Europe. In this study, we use integrated observational data and machine learning to elucidate the formation mechanism underlying one of the most severe ozone pollution seasons on record in central eastern China, an area that encompasses approximately half of China\'s total population and sown land. Our findings reveal that the worsened ozone and nitrogen dioxide pollution resulted from a mismatch between energy demand and supply, which was driven by both heatwaves and energy policy-related factors. The observed adverse heatwave-energy-environment feedback loop highlights the need for the diversification of clean energy sources, more resilient energy structures and power policies, and further emission control to confront the escalating climate challenge in the future.

Although epidemiological studies have demonstrated significant associations of long-term exposure to particulate matter (PM) air pollution with stroke, evidence on the long-term effects of PM exposure on cause-specific stroke incidence is scarce and inconsistent. We incorporated 33,282 and 33,868 individuals aged 35 to 75 years without a history of ischemic or hemorrhagic stroke at the baseline in 2014, who were followed up till 2021. Residential exposures to particulate matter with an aerodynamic diameter less than 2.5 μm (PM2.5) and particulate matter with an aerodynamic diameter less than 10 μm (PM10) for each participant were predicted using a satellite-based model with a spatial resolution of 1×1 km. We employed time-varying Cox proportional hazards models to assess the long-term effect of PM pollution on incident stroke. We identified 926 cases of ischemic stroke and 211 of hemorrhagic stroke. Long-term PM exposure was significantly associated with increased incidence of both ischemic and hemorrhagic stroke, with almost 2 times higher risk on hemorrhagic stroke. Specifically, a 10 μg/m³ increase in 3-year average concentrations of PM2.5 was linked to a hazard ratio (HR) of 1.35 (95% confidence interval (CI): 1.18-1.54) for incident ischemic stroke and 1.79 (95% CI: 1.36-2.34) for incident hemorrhagic stroke. The HR related to PM10, though smaller, remained statistically significant, with a HR of 1.25 for ischemic stroke and a HR of 1.51 for hemorrhagic stroke. The excess risks are larger among rural residents and individuals with lower educational attainment. The present cohort study contributed to the mounting evidence on the increased risk of incident stroke associated with long-term PM exposures. Our results further provide valuable evidence on the heightened sensitivity of hemorrhagic stroke to air pollution exposures compared with ischemic stroke.

Smoke from wildfires poses a substantial threat to health in communities near and far. To mitigate the extent and potential damage of wildfires, prescribed burning techniques are commonly employed as land management tools; however, they introduce their own smoke-related risks. This study investigates the impact of prescribed fires on daily average PM2.5 and maximum daily 8-h averaged O3 (MDA8-O3) concentrations and estimates premature deaths associated with short-term exposure to prescribed fire PM2.5 and MDA8-O3 in Georgia and surrounding areas of the Southeastern US from 2015 to 2020. Our findings indicate that over the study domain, prescribed fire contributes to average daily PM2.5 by 0.94 ± 1.45 μg/m3 (mean ± standard deviation), accounting for 14.0% of year-round ambient PM2.5. Higher average daily contributions were predicted during the extensive burning season (January-April): 1.43 ± 1.97 μg/m3 (20.0% of ambient PM2.5). Additionally, prescribed burning is also responsible for an annual average increase of 0.36 ± 0.61 ppb in MDA8-O3 (approximately 0.8% of ambient MDA8-O3) and 1.3% (0.62 ± 0.88 ppb) during the extensive burning season. We estimate that short-term exposure to prescribed fire PM2.5 and MDA8-O3 could have caused 2665 (95% confidence interval (CI): 2249-3080) and 233 (95% CI: 148-317) excess deaths, respectively. These results suggest that smoke from prescribed burns increases the mortality. However, refraining from such burns may escalate the risk of wildfires; therefore, the trade-offs between the health impacts of wildfires and prescribed fires, including morbidity, need to be taken into consideration in future studies.

Increased systemic oxidative stress, implicated in adverse pregnancy outcomes for both mothers and fetuses, has been associated with gestational exposure to air pollutants such as polycyclic aromatic hydrocarbons (PAHs), fine particulate matter (PM2.5), and nitrogen dioxide (NO2). However, it is unclear whether exposure to pollutants at levels below the current air quality standards can increase oxidative stress in pregnant women. In a cohort of 305 pregnant persons residing in western New York, we examined the association between exposure to PM2.5, NO2, and PAHs (measured as urinary 1-hydroxypyrene) and urinary biomarkers of oxidative stress (malondialdehyde [MDA] and 8-hydroxy-2\'-deoxyguanosine [8-OHdG]) measured in each trimester. After controlling for gestational stage, maternal age, lifestyles, and socioeconomic factors, each interquartile range (IQR) increase in 1-hydroxypyrene concentration (65.8 pg/ml) was associated with a 7.73% (95%CI: 3.18%,12.3%) higher in MDA levels throughout the pregnancy and in the first and second trimester. An IQR increase in PM2.5 concentration (3.20 μg/m3) was associated with increased MDA levels in the first trimester (8.19%, 95%CI: 0.28%,16.1%), but not the 2nd (-7.99%, 95% CI: -13.8%, -2.23%) or 3rd trimester (-2.81%, 95% CI: -10.0%, 4.38%). The average cumulative PM2.5 exposures in the 3-7 days before urine collection were associated with increased 8-OHdG levels during the second trimester, with the largest difference (22.6%; 95% CI: 3.46%, 41.7%) observed in relation to a one IQR increase in PM2.5 concentration in the previous 7 days. In contrast, neither oxidative stress biomarker was associated with NO2 exposure. Observed in pregnant women exposed to low-level air pollution, these findings expanded previously reported associations between systemic oxidative stress and high-level PM2.5 and PAH concentrations. Further, the first and second trimesters may be a susceptible window during pregnancy for oxidative stress responses to air pollution exposure.

UNASSIGNED: Air pollution is a recognized risk factor associated with chronic diseases, including respiratory and cardiovascular conditions, which can lead to physical and cognitive impairments in later life. Although these losses of function, individually or in combination, reduce individuals\' likelihood of living independently, little is known about the association of air pollution with this critical outcome.
UNASSIGNED: To investigate associations between air pollution and loss of independence in later life.
UNASSIGNED: This cohort study was conducted as part of the Environmental Predictors Of Cognitive Health and Aging study and used 1998 to 2016 data from the Health and Retirement Study. Participants included respondents from this nationally representative, population-based cohort who were older than 50 years and had not previously reported a loss of independence. Analyses were performed from August 31 to October 15, 2023.
UNASSIGNED: Mean 10-year pollutant concentrations (particulate matter less than 2.5 μm in diameter [PM2.5] or ranging from 2.5 μm to 10 μm in diameter [PM10-2.5], nitrogen dioxide [NO2], and ozone [O3]) were estimated at respondent addresses using spatiotemporal models along with PM2.5 levels from 9 emission sources.
UNASSIGNED: Loss of independence was defined as newly receiving care for at least 1 activity of daily living or instrumental activity of daily living due to health and memory problems or moving to a nursing home. Associations were estimated with generalized estimating equation regression adjusting for potential confounders.
UNASSIGNED: Among 25 314 respondents older than 50 years (mean [SD] baseline age, 61.1 [9.4] years; 11 208 male [44.3%]), 9985 individuals (39.4%) experienced lost independence during a mean (SD) follow-up of 10.2 (5.5) years. Higher exposure levels of mean concentration were associated with increased risks of lost independence for total PM2.5 levels (risk ratio [RR] per 1-IQR of 10-year mean, 1.05; 95% CI, 1.01-1.10), PM2.5 levels from road traffic (RR per 1-IQR of 10-year mean, 1.09; 95% CI, 1.03-1.16) and nonroad traffic (RR per 1-IQR of 10-year mean, 1.13; 95% CI, 1.03-1.24), and NO2 levels (RR per 1-IQR of 10-year mean, 1.05; 95% CI, 1.01-1.08). Compared with other sources, traffic-generated pollutants were most consistently and robustly associated with loss of independence; only road traffic-related PM2.5 levels remained associated with increased risk after adjustment for PM2.5 from other sources (RR per 1-IQR increase in 10-year mean concentration, 1.10; 95% CI, 1.00-1.21). Other pollutant-outcome associations were null, except for O3 levels, which were associated with lower risks of lost independence (RR per 1-IQR increase in 10-year mean concentration, 0.94; 95% CI, 0.92-0.97).
UNASSIGNED: This study found that long-term exposure to air pollution was associated with the need for help for lost independence in later life, with especially large and consistent increases in risk for pollution generated by traffic-related sources. These findings suggest that controlling air pollution could be associated with diversion or delay of the need for care and prolonged ability to live independently.

UNASSIGNED: Although there is increasing awareness of the health risks of air pollution as a global issue, few studies have focused on the methods for assessing individuals\' perceptions of these risks. This scoping review aimed to identify previous research evaluating individuals\' perceptions of air pollution and its health effects, and to explore the measurement of perceptions, as a key resource for health behaviour.
UNASSIGNED: The review followed the methodological framework proposed by Arksey and O\'Malley. PubMed and Web of Science were searched. After initial and full-text screening, we further selected studies with standardised scales that had previously been tested for reliability and validity in assessing awareness and perceptions.
UNASSIGNED: After full-text screening, 95 studies were identified. \'Perception/awareness of air quality\' was often measured, as well as \'Perception of health risk.\' Only nine studies (9.5%) used validated scaled questionnaires. There was considerable variation in the scales used to measure the multiple dimensions of risk perception for air pollution.
UNASSIGNED: Few studies used structured scales to quantify individuals\' perceptions, limiting comparisons among studies. Standardised methods for measuring health risk perception are needed.
Main findings: Among 95 studies assessing health risk perception of air pollution, only nine studies used standardised scales.Added knowledge: There was considerable variation in the scales measuring the multiple dimensions of risk perception for air pollution, which makes comparison among the studies difficult.Global health impact for policy and action: This review highlights the need for the development of globally standardised scale to measure the health risk perception of air pollution.

UNASSIGNED: Fine particulate matter (PM2.5) promotes atherosclerosis progression and plaque vulnerability. Consequently, patients with a high atherosclerotic burden may be at especially increased risk when exposed to air pollution.
UNASSIGNED: The purpose of this study was to examine the relationship between chronic ambient PM2.5 exposure and adverse outcomes after percutaneous coronary interventions (PCI).
UNASSIGNED: Baseline clinical and procedural data from U.S. veterans undergoing elective PCI (2005-2018) were linked to annual ambient PM2.5 exposure. The association between PM2.5 exposure and major adverse cardiovascular events (MACEs) (myocardial infarction, stroke, or all-cause mortality) was determined using time-varying Cox regression models. Using flexible parametric models, we also evaluated the average life months lost for specific PM2.5 levels over the 15-year period.
UNASSIGNED: In the 73,425 veterans that underwent an elective PCI, the mean annual PM2.5 exposure was 8.4 ± 1.8 μg/m3 (median follow-up 6.75 years). The incidence of MACE was 28%, 48%, and 65% at 5, 10, and 15 years, respectively. In adjusted models, each 1-μg/m3 increase in PM2.5 exposure was associated with an 8.7% (95% CI: 8.4%-8.9%; P < 0.001) increase in MACE. Compared to patients exposed to 5 μg/m3, those exposed to 10 μg/m3 lost 1.1, 3.8, and 7.6 months of life at 5, 10, and 15 years of exposure, respectively.
UNASSIGNED: Veterans undergoing elective PCI are at increased risk of MACE and significant life years lost with long-term exposure to fine particulate matter pollution, even at the current low levels in the United States. These findings emphasize the need for improved air quality standards and patient interventions to better protect vulnerable populations.