Jul 2026· Journal of Hazardous Materials· Vol 514, pp.
142906
· 0 citations· 57 references
Medicine
TL;DR
These findings underscore the potential contribution of individual PM2.5 constituents and their mixtures in COPD mortality, while suggesting actionable source-control priorities and coordinated precursor-reduction strategies, as well as population-specific prevention approaches.
Abstract
Chronic obstructive pulmonary disease (COPD) imposes a major burden on global health, yet evidence on the prolonged health effects of individual PM2.5 constituents remains limited. Previous research has primarily employed traditional models, which may struggle to capture the complex correlations among the PM2.5 components and be less effective in confounding adjustment. We conducted a prospective cohort study involving 182,009 participants from the Pearl River Cohort (2013-2015) followed through 2020, applying inverse probability-weighted marginal structural Cox models and quantile g-computation (QGC) to assess the associations of individual PM2.5 components and their mixtures with COPD mortality, followed by stratified analyses for effect modification. Over 1.18 million person-years of follow-up, 422 COPD deaths were documented. Long-term exposure to ammonium (NH4+), black carbon (BC), nitrate (NO3-), organic matter (OM) and chloride (Cl-) was associated with higher COPD mortality, with HRs (95% CI) of 2.75 (1.86-4.05), 2.41 (1.64-3.55), 1.86 (1.45-2.39), 1.85 (1.33-2.57) and 1.45 (1.15-1.82), respectively. Mixture analysis showed that each one-quartile increase in the PM2.5 component mixture was associated with a 39% (29%-50%) higher risk of COPD mortality, primarily driven by OM, Cl-, and NO3- (weights = 0.34, 0.34, 0.32). Stratified analyses indicated greater associations among older adults, suggesting increased susceptibility in this group. Our findings underscore the potential contribution of individual PM2.5 constituents and their mixtures in COPD mortality, while suggesting actionable source-control priorities and coordinated precursor-reduction strategies, as well as population-specific prevention approaches.
OBJECTIVE
The component‑specific toxicity of fine particulate matter (PM2.5) and the underlying metabolic pathways driving airflow impairment in chronic obstructive pulmonary disease (COPD) remain unclear. We evaluated how specific PM2.5 constituents alter circulating metabolites and mediate short‑term changes in peak expiratory flow (PEF) among COPD patients.
METHODS
A panel study was conducted in 32 patients with stable COPD in Beijing (2018-2019). Participants were followed-up across four seasons, yielding 3363 daily PEF measurements and 208 serum samples for untargeted metabolomics. PM2.5 components concentrations were obtained from a high-resolution (1 km) dataset integrating ground observations, satellite retrievals, and model simulations. Linear mixed-effects models were used to estimate the associations between PM2.5 components and PEF, and a meet-in-the-middle strategy was adopted to identify mediating metabolites and pathways.
RESULTS
PEF declines were associated with interquartile range increase in several PM2.5 components (lag0-7 days moving average), most notably for black carbon [-5.88 (-8.76 ~ -3.01) L/min] and sulfate [-4.78 (-8.82 ~ -0.73) L/min]. Metabolomic analysis identified 12 metabolites significantly linked to PEF (q < 0.05). Pathway enrichment highlighted urea cycle/amino group metabolism (P = 0.041) and bile acid biosynthesis (P = 0.012) as key biological response routes. Five metabolites were identified as mediators of the associations between PM2.5 components and PEF, notably Nb-arachidoyltryptamine and 6-nitrochrysene.
CONCLUSION
These findings highlight black carbon and sulfate as primary drivers of PM2.5-related lung function impairment in COPD patients, likely acting through systemic metabolic perturbations. Our study supports targeted emission controls and suggests metabolic profiling as a potential approach for targeted prevention in vulnerable populations.
Jiachen Li, Lirong Liang, Y. Cai et al.· Respiratory Research· 0 citations
Positive associations between long-term exposure to NO2 and CKD incidence were greater in never smokers than in ever-smokers, and stronger associations among never-smokers suggest that environmental exposures may independently influence kidney health.
Gonzalo Hevia-Ramos, Jiawei Zhang, Stephane Tuffier et al.· Journal of Exposure Science...· 0 citations
Ambient fine particulate matter (PM2.5) is a proven human lung carcinogen associated with lung cancer incidence. However, the relative toxicity of the various chemical components of PM2.5 and their joint association with all-cause mortality following lung cancer diagnosis remain unclear. We conducted a cohort study of 528,127 adults aged ≥65 years with lung cancer diagnosed between 2000-2019, derived from the SEER-Medicare database. Patients were followed annually from diagnosis until death, loss to follow-up, or end of the study in 2019. Two-year moving average exposures to 15 PM2.5 chemical components were estimated using high-resolution spatiotemporal models and linked to each patient based on residential ZIP code in each year. We used generalized weighted quantile sum regression with random holdouts to estimate both the joint association of PM2.5 component mixtures with all-cause mortality and the relative contribution of each component, adjusted for demographics, histological type, stage, first-course treatments, comorbidities, and neighborhood-level covariates. We found that joint exposure to PM2.5 component mixtures was associated with increased mortality, with relative risk of 1.011 (95% confidence interval [CI]: 1.010, 1.013) per decile increase in all components. Although differences in contributions were modest, silicon, nitrate, vanadium, zinc, and iron appeared to be more influential contributors, suggesting that controlling related sources, such as road dust, traffic emissions, fossil fuel combustion, and heavy fuel oil combustion, may obtain greater potential benefits. Exploratory subgroup analyses suggested that the joint association may be stronger among patients with non-small cell lung cancer, those with later-stage disease, and female patients.
Yaguang Wei, Jiaowei Gong, Edgar Castro et al.· Environmental Research· 0 citations
INTRODUCTION
Air pollution is a leading environmental risk factor for cardiovascular disease (CVD), yet its relationship with metabolic syndrome (MetS) and its components in sub-Saharan Africa are unclear. This study aimed to examine the association between long-term PM2.5 exposure and MetS (and its component conditions) in a Ghanaian adult cohort.
METHODS
We performed a cross-sectional analysis of 1,833 adults (40-60 years) from the Awi-Gen study. Long-term PM2.5 exposure (2007-2015) was estimated via a satellite-based model. MetS was defined using harmonized criteria. We used multivariable logistic regression with sequential adjustment for covariates.
RESULTS
A positive association was observed between PM2.5 and hypertension, while no association was found for MetS overall or its component conditions. Each 1 μg/m3 increase in PM2.5 was associated with 6% higher odds of hypertension (OR: 1.06, 95% CI: 1.02-1.11). PM2.5 quartiles also showed a dose-response relationship with hypertension (p-trend=0.003), with the highest exposure linked to a 50% greater likelihood of hypertension. The calculated population attributable fraction for PM2.5 and hypertension was 18.6%.
INTERPRETATION
In this rural Ghanaian population, long-term PM2.5 exposure was associated with hypertension but not with metabolic syndrome or its other components. These findings provide important evidence from an understudied sub-Saharan African population and support the integration of air quality management into cardiovascular disease prevention strategies.
Ali Moro, E. Nonterah, Godfred Agongo et al.· Environmental Research· 0 citations
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.
Xue-Hua Wang, Zhaohui Wang, Yan Wang· Bioengineering· 0 citations