Ambient Air Pollution Research Articles (Page 1)

Association between long-term exposure to a mixture of ambient air pollutants and the incidences of bladder and kidney cancers.

The impact of exposure to different ambient air pollutants on sperm quality: A retrospective cohort study.

Outdoor thermal comfort is a critical determinant of urban livability and public health, particularly in the face of the increasing frequency and intensity of extreme weather events. While meteorological variables are well-established drivers of thermal stress, the influence of ambient air pollution on human thermal perception remains poorly understood and largely overlooked in urban climate research. To address this gap, this study investigates the multidimensional effects of six major air pollutants PM2.5, PM10, SO2, NO2, O3, and CO on the Universal Thermal Climate Index (UTCI) across 370 Chinese cities from 2020 to 2024. Using integrated spatiotemporal analysis, we found significant seasonal, diurnal, and climatic heterogeneity in pollutant–UTCI interactions. Our findings reveal that O3 and PM10 amplify thermal stress during summer daytime through photochemical heating and radiative forcing, whereas PM2.5 and CO reduce nocturnal heat loss in winter by trapping long-wave radiation, effectively acting as thermal insulators. These effects are further modulated by local climate: arid regions (e.g., Lanzhou) experience exacerbated O3-driven heat stress, while cold zones (e.g., Harbin) benefit from particulate-induced warming in winter. Meteorological factors serve as dual regulators; temperature and solar radiation directly elevate the UTCI, while wind and humidity govern pollutant dispersion and thus indirectly shape thermal comfort. This study not only advances the scientific understanding of air pollution’s role in urban thermal environments but also provides actionable, data-driven insights for climate-resilient urban planning, public health interventions, and integrated environmental policies that jointly address air quality and thermal comfort in rapidly urbanizing regions.

Background: Ambient air pollution has been linked to atrial fibrillation (AF), yet the underlying metabolic mechanisms remain poorly understood. Methods: We analyzed 227,324 UK Biobank participants without baseline AF. We constructed an air pollution score by aggregating all four pollutants (PM 2.5 , PM 10 , NO 2 , NO x ). Nuclear magnetic resonance metabolomics identified pollution-related metabolic signatures through elastic net regression. Associations between air pollutants, metabolic signatures and AF were analyzed using Cox models. Mediation analysis was employed to examine the role of metabolic signatures in the association between air pollutants and AF. Results: During follow-up, 16,235 participants (7.14%) developed AF. We identified 65-metabolite signatures significantly associated with air pollution, predominantly comprising lipoprotein lipid concentrations (32.31%), lipoprotein subclasses (15.38%), fatty acids (13.85%), and amino acids (12.31%). Each standard deviation increase in this metabolic signature was associated with 18% higher AF risk (HR=1.18, 95%CI:1.03-1.35). The metabolic profile mediated 15.45% of the relationship between air pollution and AF, with lipoprotein parameters showing the strongest mediation effects. Conclusion: Air pollution-related metabolic signatures independently predict AF risk and mediate a significant portion of pollution’s arrhythmogenic effects. These findings provide novel insights into biological mechanisms linking environmental exposures to AF.

Background: Ambient air pollution is associated with ischemic heart disease (IHD), but the metabolic mechanisms mediating this relationship remain unclear. Methods: In 218,047 UK Biobank participants without baseline IHD, we identified plasma metabolic signatures associated with air pollution (PM 2.5 , PM 10 , NO 2 , NO x ) using elastic net regression. Cox proportional hazards models assessed relationships between air pollution, metabolic signatures, and incident IHD. Mediation analyses quantified the contribution of metabolic signatures to pollution-IHD associations. Results: We identified 41 metabolites significantly associated with air pollution, primarily comprising lipoprotein lipid concentrations, fatty acids, and amino acids. During follow-up, 18,911 participants developed IHD. High metabolic signature scores were associated with 26% increased IHD risk compared to low scores (HR=1.26, 95% CI: 1.20-1.32). The metabolic signature mediated 19.49% of the total effect of air pollution on IHD risk, with stronger mediation for PM 2.5 (21.24%). Associations were more pronounced in older individuals (≥65 years) and those with lower genetic susceptibility to IHD. Conclusions: Air pollution exposure induces specific plasma metabolic alterations that independently predict IHD risk and substantially mediate pollution-IHD associations. These findings provide novel insights into biological pathways linking environmental exposures to cardiovascular pathology and identify vulnerable subpopulations.

Background: Fine particulate matter (PM2.5) is increasingly recognized as a cardiovascular risk factor, with both short- and long-term exposure associated with higher rates of atrial fibrillation (Afib). However, few studies have assessed its relationship with Afib using comprehensive burden metrics such as disability-adjusted life years (DALYs) at the population level. Aim: To evaluate the association between long-term PM2.5 exposure and the burden of Afib, measured in DALYs, across U.S. states from 2000 to 2021. Methods: We conducted a longitudinal ecological analysis using state-level data from the Global Burden of Disease (GBD) study and the U.S. Environmental Protection Agency (EPA). Afib-related DALYs, deaths, and prevalence were age-standardized and sex-combined. Annual PM2.5 concentrations were averaged across the study period. Covariates included summary exposure values for obesity, smoking, hypertension, high fasting plasma glucose, high LDL cholesterol, and kidney dysfunction. Multivariable linear regression assessed the independent association between PM2.5 and Afib DALYs, adjusted for all covariates. Interaction terms between PM2.5 and both obesity and smoking were tested in secondary models. Choropleth maps and trend plots were used to visualize spatial and temporal patterns. Results: Afib DALY rates varied across states, with the largest increase in California (+46%) and the largest decrease in Pennsylvania (–5%). Higher long-term PM2.5 exposure was independently associated with increased Afib DALY rates (β = 1.21, p < 0.0001; 95% CI: 0.89–1.53). PM2.5 was also associated with Afib prevalence (β = 13.47, p < 0.0001), but not with deaths (β = 0.011, p = 0.16). No significant interactions were observed with obesity or smoking. While PM2.5 declined nationally, Afib burden increased or plateaued in most states. Conclusions: Ambient air pollution is independently associated with Afib burden and prevalence across U.S. states, even after adjustment for cardiometabolic and renal risk factors. These findings align with recent international research linking PM2.5 to increased Afib incidence and provide new evidence of its contribution to population-level disease burden in the U.S. This highlights air quality as a potential modifiable contributor to the growing Afib epidemic and underscores the importance of environmental health policy in arrhythmia prevention.

Background: Subclinical arrhythmias such as atrial high-rate episodes (AHREs) and ventricular high-rate episodes (VHREs), detected by cardiac implantable electronic devices (CIEDs), are established predictors of future cardiovascular events. While ambient air pollution has been linked to various adverse cardiovascular outcomes, limited evidence exists regarding its association with subclinical arrhythmias, especially in CIED patients. This study is the first to assess this relationship using real-time cardiac monitoring and high-resolution exposure data. Objective: To evaluate the association between exposure to ambient air pollutants and subclinical arrhythmias, with a specific focus on VHREs, in patients with CIEDs. Methods: We conducted a nationwide retrospective analysis of 225 CIED patients enrolled across eight tertiary hospitals in South Korea between 2017 and 2019. Daily exposures to PM2.5, PM10, NO2, SO2, CO, and O3 were estimated using Air Korea monitoring stations located near patient residences. Generalized Estimating Equations (GEE) were used to assess associations between pollutant exposure and the occurrence of AHREs and VHREs. Results: Out of 93,881 monitored episodes, 1,210 arrhythmia events were identified, comprising 1,065 AHREs and 173 VHREs. No air pollutant showed a significant association with AHREs. However, VHREs were significantly associated with NO2 exposure (OR 1.174, 95% CI 1.027–1.341). A sensitivity analysis excluding 14 patients assigned exposure based on proxy addresses due to long distances from monitoring stations showed a strengthened association (OR 1.180, 95% CI 1.030–1.351). No significant associations were observed for PM2.5, PM10, NO2, SO2, CO, and O3. . Conclusion: NO2 exposure was associated with an increased risk of VHREs in CIED patients. As this study was conducted prior to the COVID-19 pandemic, it provides a valuable reference for cardiovascular risk assessment under typical, unmasked air pollution conditions. These findings emphasize the importance of managing environmental risk factors and highlight the value of continuous cardiac monitoring in vulnerable populations. Keywords: particulate matter, air pollution, arrhythmia, cardiovascular disease, AHRE, VHRE, CIED

Background: Ambient air pollutants such as fine particulate matter (PM 2.5 ), nitrogen oxides (NO x ), and carbon monoxide (CO) contribute to cardiovascular (CV) morbidity. However, the role of social vulnerability in modifying pollution-related CV risk remains underexplored, especially in high-risk populations with coronary artery disease (CAD). We evaluated the associations between air pollutant exposures, the Social Vulnerability Index (SVI), and CV outcomes, hypothesizing that higher exposures would be associated with worse outcomes, particularly among socially vulnerable individuals. Methods: The study consisted of 1,602 participants (mean age of 62, 63% men, 62% White race, 31% Black race) undergoing coronary angiography enrolled in the Emory Cardiovascular Biobank. Participants were stratified into high vs. low pollutant exposure groups based on pollutant medians (PM 2.5 : 10.6 μg/m 3 ; NO x : 39.4 ppb; CO: 635 ppb) estimated at residential address using a 250m-resolution model. Clinical characteristics and SVI domains (socioeconomic status, household characteristics, racial/ethnic minority status, housing and transportation, and overall SVI ranking) were compared between high vs. low pollutant groups. SVI domain scores were obtained from the CDC/ATSDR Social Vulnerability Index linked by residential census tract. Cox models assessed associations between pollutants and CV outcomes (CV death, myocardial infarction [MI], stroke, heart failure [HF], and their composite [MACE]), and tested for effect modification by SVI domains. Results: Participants with hypertension, female sex, and higher SVI were more likely to fall in the high PM 2.5 group (all p<0.05). Similar gradients were observed across NO x and CO strata. In adjusted models, PM 2.5 and CO were significantly associated with increased MACE (PM 2.5 : HR 1.73, p=0.002; CO: HR 1.001, p=0.005), and PM 2.5 was associated with HF (HR 1.16, p=0.003). SVI significantly modified the relationship between air pollution and CV events with stronger pollutant-outcome associations among those with higher SVI—particularly for NO x and risk of HF (p=0.033) and stroke (p=0.025), and for CO and HF (p=0.046). Conclusion: In patients with CAD, PM 2.5 and CO exposure were associated with increased risk of MACE. Social vulnerability amplified the adverse effects of NO x and CO exposures on CV events highlighting the need to consider neighborhood-level social determinants of health in pollution-related CV disease prevention efforts.

Objective To assess the burden of chronic obstructive pulmonary disease (COPD) in Ghana within a global context, analyze temporal trends and risk factor attribution from 1990 to 2021, and project the future burden through 2050. Study design Secondary analysis of Global Burden of Disease (GBD) 2021 data, using statistical modeling to evaluate trends in COPD prevalence, incidence, mortality, disability-adjusted life years (DALYs), and attributable risk factors. Future projections were generated using Bayesian Age-Period-Cohort (BAPC) modeling. Data source GBD 2021 study, providing standardized estimates for 369 diseases across 204 countries and territories. Main outcome measures COPD-related deaths, prevalence, incidence, DALYs, age-standardized rates (ASRs), risk factor attribution, percentage change, age-specific death rates, and projections to 2050. Results From 1990 to 2021, Ghana experienced a 157% increase in COPD deaths (from 693 to 1,782), compared to a 49% global increase. Ghana's age-standardized death rate (ASDR) declined by only 7%, far below the global reduction of 37%. COPD prevalence in Ghana tripled, rising from 0.1 to 0.3 million, while incidence increased by 215% and DALYs by 171%. Globally, DALYs rose by 40% over the same period. In Ghana, household air pollution from solid fuel use accounted for 40% of COPD deaths, followed by ambient air pollution (25%). Globally, particulate matter pollution (41%) and smoking (36%) were dominant. Projections show continued increases in prevalence and incidence, particularly among adults aged 40–64, with plateauing DALYs and declining ASDR by the 2040s. Mortality increases sharply after age 60, with higher burden among males. Cohort analysis reveals rising mortality risk among those born after 1960. Conclusion Despite modest ASDR reductions, Ghana's absolute COPD burden is increasing, driven by preventable risk factors such as household air pollution. These findings highlight the need for targeted interventions, including clean cook-stove programs, improved air quality monitoring, and expanded access to spirometry and early screening. Such efforts are essential to reduce COPD-related morbidity and mortality and advance Sustainable Development Goal (SDG) 3.4.

This study aims to examine the impact of ambient air pollution exposure on the prevalence of acute respiratory infections (ARI) among outdoor workers. Given the increasing urban air pollution levels in Indonesia, outdoor laborers such as street vendors, construction workers, and traffic police represent a vulnerable population with prolonged exposure to hazardous air pollutants. A cross-sectional observational study was conducted among 300 outdoor workers in three urban areas with varying pollution levels. Air quality data, including concentrations of particulate matter (PM2.5 and PM10), were obtained from local monitoring stations. Health outcomes were assessed through standardized questionnaires on respiratory symptoms and medical history, alongside clinical examinations conducted by health professionals. Logistic regression analysis was applied to evaluate the association between exposure levels and ARI prevalence, controlling for confounders such as age, smoking habits, and socioeconomic status. The study revealed a significantly higher prevalence of ARI among outdoor workers in high-pollution areas compared to those in lower-pollution regions (37.2% vs. 18.9%; p < 0.01). Logistic regression analysis indicated that exposure to elevated PM2.5 levels was strongly associated with increased risk of ARI (OR = 2.41, 95% CI: 1.52–3.82). Smoking and low socioeconomic status were also identified as contributing risk factors, though air pollution remained the strongest predictor. Air pollution substantially elevates the risk of ARI among outdoor workers. These findings highlight the urgent need for targeted occupational health interventions, improved air quality policies, and the provision of personal protective measures to safeguard vulnerable populations.

Ambient Air Pollution and Environmental Injustice in Perinatal Health.

Association between ambient air pollution and increased risk of respiratory diseases in Vellore and Ranipet, Tamil Nadu, India: A retrospective study.

Although health effects of ambient air pollution are well established in the general population, the impact of exposure in working populations remains poorly understood. Outdoor workers are disproportionately exposed to ambient air pollution, particularly with increasing wildfire smoke events and global climate change. An international interdisciplinary group of experts including worker representation assembled to review the current state of knowledge regarding the impact of occupational air pollution exposure on worker health and develop recommendations for research and actions to evaluate, mitigate, and regulate occupational air pollution exposure. The group identified health risks likely resulting from air pollution based on studies of the general population, noting that additional risks may be encountered from coexposures, as well as exertion increasing the work of breathing. High-risk groups were identified, including agricultural workers, construction workers, and wildland firefighters; others working in warehouses and indoor spaces are likely at risk via ambient air pollutant infiltration. It was estimated that at least 20 million outdoor U.S. workers are exposed to air pollution at work, which limits productivity and increases absenteeism. Participants recommended using air quality to guide work modifications and adoption of the hierarchy of exposure controls as a model to reduce exposures, as used by some states and proposed by the National Institute for Occupational Safety and Health for agricultural and other outdoor workers. Existing research supports the urgent need for policies to protect workers from exposure. Research gaps remain, including medical surveillance strategies, improved technology to protect workers, and studies specifically evaluating the impacts of occupational air pollution exposure.

Air pollution, noise, greenspace and pneumonia, a nation-wide cohort study from Denmark.

Genetic sensitivity moderates the effects of joint exposure to air pollution on depression risk: a genome-wide by environment interaction analysis.

Hypertension (HTN), a major contributor to cardiovascular diseases, is linked to ambient air pollution and residential greenness. However, their joint associations remain unclear. This research focuses on assessing the individual and joint associations of ambient air pollution and residential greenness on HTN among Northwestern Chinese adults. In this cross-sectional analysis, 4,214,199 participants in Northwestern China were included. HTN was assessed via standardized assessment protocols. Air pollutant concentrations were estimated via the Space-Time Extra-Trees model, and greenness was assessed through the Normalized Difference Vegetation Index (NDVI). Generalized regression models were employed to assess the individual and joint effects of air pollutants and residential greenness on HTN. The prevalence of HTN was 20.43%. The adjusted odd ratio of HTN for each 10 µg/m3 increase in PM1, PM2.5, PM10 and SO2 were 1.571 (95% CI: 1.556-1.585), 1.070 (95% CI: 1.068-1.072), 1.021 (95% CI: 1.020-1.021) and 1.798 (95% CI: 1.770-1.827), each 0.1-unit increase in NDVI were 0.943 (95% CI: 0.940-0.946) respectively. The negative association of residential greenness with HTN appeared to weaken at higher concentrations of air pollutants. Mediation analysis indicated that body mass index (BMI) partially mediated the effects of both air pollutants and NDVI on HTN risk. Our findings reveal that air pollutants are positively correlated with HTN, while residential greenness shows a negative association. However, this negative association is attenuated at higher concentrations of air pollutants. Additionally, the associations of air pollutants and residential greenness with HTN appear partially mediated by BMI.

Association between ambient air pollution and ischemic stroke hospitalization: A multicenter case-crossover study in Tianjin, China

Measurement error correction methods for the effects of ambient air pollution on mortality and morbidity using the UK Biobank cohort: the MELONS study.

Air pollution is the risk factor for psychiatric disorders: a two-step Mendelian randomization study.

Abstract Formaldehyde is a known air pollutant recognised for its risks associated with cancer due to prolonged exposure. This study examines the spatial and temporal variability of HCHO and related cancer risk in India using the high-resolution GEOS-Chem Chemical Transport Model for the year 2022. The findings indicate notable regional disparities in HCHO pollution in India, with higher levels in industrial centres, coastal zones and intense agricultural regions. The highest cancer risk associated with HCHO exposure is found in northern IGP, Northeast India and Kerala, where up to 81280 individuals per million may potentially develop cancer. Sensitivity assessment indicates that a 25% and 50% reduction in nitrogen oxide emissions lead to 2.60% and 6.74% reduction in cancer risks, respectively. The findings emphasize the need to regulate ambient HCHO pollution in India, where limited healthcare and expensive treatments make reducing emissions and air pollution essential to limiting cancer risks.