Association between Long-Term Ambient PM2.5 Exposure and Hypertension and Metabolic Syndrome among Ghanaian Adults.

Associations of long-term PM2.5 exposure and genetic susceptibility with prevalent metabolic syndrome and subsequent cardiovascular disease risk: A UK Biobank cohort study.

Long-term PM2.5 exposure is implicated in cardiometabolic disorders, but its interactions with genetic susceptibility and the underlying epigenetic mechanisms remain unclear. We sought to examine the joint associations of long-term PM2.5 exposure and genetic susceptibility with prevalent metabolic syndrome (MetS) and subsequent cardiovascular disease (CVD) risk among individuals with MetS. Among 324,887 UK Biobank participants, logistic regression analyses indicated greater odds of MetS at higher PM2.5 exposure (adjusted OR = 1.04, 95% CI: 1.03-1.05). Among 64,832 individuals with MetS, Cox regression with inverse probability weighting showed elevated incident CVD risk at higher PM2.5 exposure (adjusted HR = 1.04, 95% CI: 1.01-1.06). Additive interaction analyses revealed significant synergy of PM2.5 exposure with both the polygenic risk score (PRS) for MetS (relative excess risk due to interaction [RERI] = 0.11, 95% CI: 0.02-0.20) and the PRS for CVD (RERI = 0.13, 95% CI: 0.05-0.21). 1 PM2.5-associated CpG site related to MetS and five related to CVD were identified by summary-data-based Mendelian randomization (SMR) analyses. Among these, cg13235717 near SFN emerged as a key locus across phenotypes, and gene-environment interaction analyses further supported its potential role as an epigenetic modifier. Overall, these findings indicate that long-term PM2.5 exposure is associated with prevalent MetS and subsequent CVD risk among individuals with MetS, particularly among genetically susceptible individuals, with DNA methylation potentially serving as an epigenetic link in these associations.

Association between ambient fine particulate matter and hemorrhagic stroke in Yancheng, China

Objectives Ambient air pollution, particularly fine particulate matter (PM2.5), has been linked to cerebrovascular disease. However, findings on the short-term effects of PM2.5 exposure on hemorrhagic stroke (HS) have been inconsistent across studies. Therefore, this study investigated the association between short-term PM2.5 exposure and HS hospitalization in Yancheng, China. Methods An individual-level time-stratified case-crossover study was conducted using hospitalization records of patients with HS from four major hospitals in Yancheng between 2022 and 2024. Conditional logistic regression models were applied to estimate the associations between short-term PM2.5 exposure and HS hospitalization across different lag structures. Stratified analyses were further performed according to sex, age, hypertension, diabetes, smoking, alcohol consumption, and season. Results A total of 2,312 patients hospitalized for HS were included in the analysis. The strongest association was observed at lag01, where each 10 μg/m3 increase in PM2.5 concentration was associated with a 3.24% increase in HS hospitalization (95% CI: 0.55%−6.00%). Significant increases were also observed at lag0 and lag1, with corresponding effect estimates of 2.50% (95% CI: 0.11%−4.95%) and 2.76% (95% CI: 0.32%−5.27%), respectively. The associations remained significant after adjustment for ozone (O3) but were no longer statistically significant after adjustment for sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO). Relatively stronger effect estimates were observed among females, older adults, individuals with hypertension or diabetes, smokers, alcohol consumers, and during the cold season. Conclusion Short-term PM2.5 exposure was associated with an increased risk of HS hospitalization in Yancheng, China, with the strongest effects observed within the first two days after exposure. The associations were more pronounced among susceptible populations and during the cold season.

Ambient PM2.5 exposure and cancer incidence in Nigerian adults: A prospective cohort study.

BACKGROUND Ambient PM2.5 is an IARC Group 1 carcinogen, yet prospective evidence from sub-Saharan Africa remains scarce. We investigated long-term exposure to PM2.5, PM10, and NO₂ and incident cancer risk in a Nigerian adult cohort. METHODS We studied 5621 adults across Lagos, Kano, and Rivers States with median follow-up of 4.7 years (25,418 person-years). Annual pollutant concentrations were estimated using hybrid satellite-land use regression at 1 km resolution. Incident cancers were confirmed histopathologically. Biomarkers of oxidative stress and inflammation were measured in a subsample. Hazard ratios (HRs) were estimated using Cox regression with mediation analysis. RESULTS Mean PM2.5 was 50.4 μg/m³ , tenfold above WHO guidelines. A total of 147 incident cancers occurred. Each 10 μg/m³ PM2.5 increment was associated with a 12% increase in all-cancer incidence (HR 1.12; 95% CI: 1.06-1.19). Highest versus lowest PM2.5 quartile had 82% elevated hazard (HR 1.82; 95% CI: 1.29-2.57). Site-specific associations were strongest for lung, breast, and hematopoietic malignancies. Dose-dependent elevations in oxidative stress and inflammatory markers were observed. Mediation analysis indicated this pathway accounted for 41.3% of the total PM2.5-cancer association. CONCLUSIONS In this first prospective sub-Saharan African cohort, chronic PM2.5 exposure was positively associated with incident cancer risk. Oxidative stress and inflammation mediate a substantial proportion of this association. These findings support integrating air quality monitoring into national cancer control strategies.

Long-Term Air Pollution Exposure, Cardiovascular Disease, and Cardiometabolic Risk Factors in Middle-Aged and Older Chinese Adults: A Prospective Cohort Study

The substantial burden of cardiovascular disease (CVD) attributable to air pollution remains a critical public health challenge, yet its combined effect with cardiometabolic factors is not fully understood. This study leveraged data from the Global Burden of Disease Study (GBD) and the China High Air Pollutants (CHAP) database to evaluate the CVD burden attributable to air pollution, which was found to increase progressively with age. We conducted a cross-sectional analysis using baseline (2011) data from 7420 participants aged ≥ 45 years in the China Health and Retirement Longitudinal Study (CHARLS), and a prospective cohort analysis in 8792 participants followed through 2020. In the longitudinal analysis, long-term exposure to PM2.5 (HR = 1.09, 95% CI: 1.03–1.16) and PM10 (HR = 1.07, 95% CI: 1.04–1.10) was significantly associated with an elevated risk of incident CVD, whereas the association for NO2 was nominally significant (HR = 1.12, 95% CI: 1.00–1.24) and that for O3 was not statistically significant (HR = 1.08, 95% CI: 0.93–1.27). Furthermore, prolonged exposure to these pollutants was associated with a higher prevalence of hypertension, diabetes, dyslipidemia, and obesity, and with adverse levels of metabolic indicators, including the TyG, TyG-BMI, and TyG-WC indices. A random forest model showed modest discrimination for incident CVD (AUC = 0.656), identifying PM10 and PM2.5 as the most important predictors. In conclusion, long-term exposure to ambient air pollution, particularly particulate matter, is associated with an increased risk of CVD and cardiometabolic disorders in middle-aged and older Chinese adults.

The association between carbon monoxide and cardiovascular-kidney-metabolic syndrome in the Chinese populations: China Health and Retirement Longitudinal Study.

Long-term exposure to ambient air pollution and an increased risk of hyperuricemia.

OBJECTIVES Evidence suggests that ambient air pollution contributes to metabolic dysregulation, including hyperuricemia. However, previous studies were limited to specific groups or regions with relatively high air pollutant concentrations. This study examined the association between long-term exposure to ambient air pollutants and hyperuricemia in a general population exposed to relatively low pollution concentrations. METHOD This cross-sectional study analyzed 20,117 adults who underwent health screenings in the Republic of Korea (2015-2019). Annual mean concentrations of PM2.5, PM10, NO2, SO2, and CO were estimated at residential addresses using the Community Multiscale Air Quality model. Hyperuricemia was defined as serum uric acid level > 7.0 mg/dL (males) or > 6.0 mg/dL (females). Multivariable logistic regression estimated odds ratios (ORs) per interquartile range (IQR) increase in pollutant exposure, adjusting for confounders including estimated glomerular filtration rate. RESULTS Among 20,117 participants, 3,078 (15.3%) had hyperuricemia. All five pollutants were significantly associated with hyperuricemia. The ORs (95% CIs) per IQR increase were 1.06 (1.01-1.10) for PM2.5, 1.15 (1.08-1.21) for PM10, 1.07 (1.00-1.14) for NO2, 1.13 (1.07-1.19) for SO2, and 1.06 (1.01-1.11) for CO. Associations were stronger among current smokers, older adults, and individuals with dyslipidemia or central obesity (all P for interaction < 0.05). CONCLUSIONS Long-term exposure to air pollutants was significantly associated with hyperuricemia, independent of renal function and even at low concentrations. These findings suggest that air pollution is an important environmental risk factor for metabolic disease, emphasizing the need for stricter regulations to protect vulnerable populations. Key Points • Long-term exposure to major ambient air pollutants is significantly associated with an increased risk of hyperuricemia, even at relatively low concentrations. • The association between air pollution and hyperuricemia persists independent of renal function, suggesting a potential role in systemic metabolic dysregulation. • Vulnerable populations, including older adults, current smokers, and individuals with metabolic conditions, exhibit stronger associations between air pollution exposure and hyperuricemia.