Long-term air pollution was associated with higher risks of clinically significant liver-related outcomes and a possible role of proteomic aging in the association between air pollution and liver-related outcomes is suggested, warranting further investigation.
Abstract
Although air pollution is recognized as a contributor to accelerated biological aging, its associations with clinically significant liver-related outcomes and the potential role of proteomic aging remain unclear. We aimed to evaluate the associations of key air pollutants with liver-related outcomes and the potential mediating role of proteomic aging clocks. Among 504,006 China Kadoorie Biobank participants without liver disease or cancer, we used time-varying Cox regression to assess associations of PM2.5, PM10, NO2, and warm-season O3, and their mixtures with liver-related events (LRE) and liver-related mortality (LRM), and mediation analyses to examine the role of proteomic aging clocks (i.e., ProtAge). Long-term exposure to PM2.5, PM10, NO2, and warm-season O3 showed significant positive associations with LRE, while PM2.5, PM10, and NO2 were also positively associated with LRM. A 1-unit increment in the weighted pollutant score was associated with an 81% higher risk of LRE (hazard ratio [HR]=1.81 [1.65-1.98]) and a 17% higher risk of LRM (HR=1.17 [1.05-1.31]). Acceleration in ProtAge was associated with higher risks of LRE (HR=1.86 [1.16-2.97]) and LRM (HR=4.43 [3.02-6.50]). ProtAge accounted for an estimated 7.1% and 12.5% of the associations of pollutant mixtures with LRE and LRM, respectively. Among proteins in ProtAge, CD248, GDF15, TNFRSF6B, and XG showed concordant associations in pollutant mixture-protein and protein-LRE analyses. Long-term air pollution was associated with higher risks of clinically significant liver-related outcomes. These findings suggest a possible role of proteomic aging in the association between air pollution and liver-related outcomes, warranting further investigation.
Air pollution is the leading environmental cause of disease burden worldwide and is increasingly recognized as a potent driver of accelerated biological aging. Rather than acting through organ-specific toxicity alone, air pollutants appear to affect the fundamental hallmarks of aging itself, including oxidative stress, chronic inflammation, epigenetic dysregulation, telomere attrition, mitochondrial dysfunction, and cellular senescence. The pollutants of greatest concern are fine and ultrafine particulate matter (PM2.5, PM0.1), traffic-related air pollution, and household combustion emissions. This review synthesizes epidemiological and mechanistic evidence linking ambient and household air pollution to biological aging across the full spectrum of biomarker classes, including molecular measures (epigenetic clocks, telomere length, transcriptomic signatures), system-level indices (composite clinical biomarkers, proteomic aging clocks, inflammatory markers), and whole-organism measures (frailty). The strength of evidence varies meaningfully across biomarker classes. System-level composite measures, particularly the Klemera-Doubal method biological age, PhenoAge, and frailty scores, show the most robust and consistent associations with air pollution. Causal mediation analyses across independent cohorts support the role of biological aging as a mechanistic pathway linking air pollution exposure to clinical disease outcomes, including cardiovascular disease, neuropsychiatric disorders, and chronic kidney disease. Epigenetic clock findings remain inconclusive at the meta-analytic level despite strong biological plausibility, likely reflecting differences in exposure assessment methods, study design, and cell composition of the target tissue. Life-course vulnerability windows are also examined, with prenatal and early-life exposures shown to shape biological aging trajectories that persist into later life. Key research gaps include underrepresentation of household air pollution and low-income settings, and the shortage of longitudinal multimarker or multi-omics study designs. Air quality improvements and clean cooking fuel transitions have been shown to partially reverse air pollution-associated aging acceleration, reinforcing the public health relevance of these findings. Reducing air pollution thus remains the most equitable strategy for slowing biological aging at the population level, and incorporating aging-focused endpoints into environmental health research and regulatory policy is both a scientific and public health priority.
P. Poursafa, J. Jylhävä· Ageing Research Reviews· 0 citations
It is suggested that air pollution might contribute to T2D risk through inflammation-related proteins, highlighting the potential of proteomics as a tool for precision public health.
Shenghao Yuan, Yongxuan Li, Yujia Bao et al.· Ecotoxicology and Environmen...· 0 citations
This systematic review investigates the mediating factors in the relationship between ambient air pollution exposure and cognitive aging. We identified 16 studies examining 72 unique exposure-mediator-outcome associations for six pollutants (PM2.5, PM10, NO2, NOX, black carbon, and PM1 components). The most studied pollutant was PM2.5 (65% of analyses). Cognitive outcomes included memory, cognitive processing speed, and clinically diagnosed conditions such as dementia incidence. Potential mediators spanned mental health outcomes (depression, anxiety, stress), lung function (FEV1, FVC, PEF), vascular diseases (stroke, hypertension), inflammation (CRP), metabolic factors (type 2 diabetes), sleep, and neuroanatomical changes. The quality of mediation analysis reporting was generally good, but most studies had some risk of bias, particularly in outcome assessment and confounding adjustment. Cardio and Cerebro-vascular diseases emerged as a potential key mediator. Mental health outcomes, sleep, and lung function also showed mediating potential, but further research is needed to confirm these findings. This review highlights the need for rigorous causal mediation analyses and standardized reporting to better understand the complex pathways linking air pollution to cognitive aging, in order to identify targeted preventive measures to reduce the negative impact of ambient air pollution on cognitive health.
M. Z. Sakhvidi, E. Burte, A. Mehrparvar et al.· Ageing Research Reviews· 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
Evidence on the link between air pollution and inflammatory responses is scarce, especially during early life. This study investigates the associations between air pollution exposure, respiratory outcomes, and cytokine responses during the first year of life, and whether these are modified by sex and temperature. The association of residential exposure to ambient PM2.5, PM10, and NO2 with the prevalence of bronchitis and wheezing in 1-year-old infants (n = 606) was examined using logistic regression. In the subcohort (n = 508) with cytokine data (TNF-α, MCP-1, IL-8, IL-6, and IL-10, pg/mL) after lipopolysaccharide stimulation, single pollutants were correlated with inflammatory biomarkers by linear regression, and mixture effects were estimated using Bayesian kernel machine regression (BKMR). All models were stratified by sex and adjusted for covariates and residential greenness. Estimates were calculated per IQR increase in PM2.5, PM10, and NO2 exposures: 2.0, 2.8, and 9.1 μg/m3, respectively. In boys, an IQR increase in PM2.5 was associated with higher odds of bronchitis (aOR = 1.50, 95% CI: 1.02 - 2.23) and IL-8 concentrations (23.8%, 95% CI: 11.2 - 37.9%). In girls, an IQR increase in PM2.5 was associated with elevated concentrations of IL-8 (31.9%, 95% CI: 18.6 - 46.7%) and TNF-α (12.8%, 95% CI: 3.9 - 22.6%). All air pollutants were consistently associated with increased IL-10 concentrations in girls, with PM2.5 having the strongest effect (35.7%, 95% CI: 14.4 - 61.1%) per IQR increment. BKMR mixture analyses revealed a positive non-linear association between the air pollutant mixture, IL-8, and TNF-α when all air pollutants exceeded their 60th percentile. Infants in the upper temperature tertile showed stronger associations with IL-8 in response to PM2.5 and NO2 exposures. Altogether, our findings suggest that PM2.5 is the primary predictor of respiratory outcomes and inflammatory responses during the first year of life.
S. Gómez-Olarte, S. Röder, K. de Hoogh et al.· Environmental Pollution· 0 citations
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