Outdoor air pollution is a major public health issue. Many studies correlate ambient air pollution with acute and chronic pulmonary disease. However, its interactions with airborne bacteria remain insufficiently characterized. In particular, the mechanisms linking pollutants to microbial adaptation and pathogenicity are not clearly established. An increasing body of evidence shows that airborne bacteria respond actively to atmospheric pollutants. These responses affect their survival, behavior, and functional traits. However, a comprehensive synthesis of pollutant-driven microbial adaptation and its implications for virulence and public health, is still lacking. This review synthesizes current knowledge on the interactions between atmospheric pollutants and airborne bacteria within an integrative mechanistic and One Health framework. The nature and sources of major atmospheric pollutants are first outlined. The mechanisms by which these pollutants induce oxidative and nitrosative stress in bacteria are then analyzed, with a focus on the generation of reactive oxygen and nitrogen species and their cellular impacts. Bacterial adaptive responses to these stresses are subsequently discussed. These include antioxidant defenses, membrane remodeling, biofilm formation, and horizontal gene transfer. The potential contribution of these processes to bacterial persistence, virulence-associated traits, and antibiotic resistance is discussed. The implications for human and environmental health are then addressed. Particular attention is given to respiratory infections, the enrichment of airborne resistomes, and the emergence of opportunistic taxa in polluted environments. Finally, future research directions including key knowledge gaps are summarized.
Current epidemiological evidence on the association between air pollutants and non-accidental mortality remains limited, particularly in developing countries. This study aimed to investigate the short-term association between ambient air pollution and non-accidental mortality, and to quantify the attributable disease burden in Shantou, a subtropical coastal city in China. Daily data on non-accidental mortality, meteorological factors, and ambient air pollutants including PM2.5, PM10, SO2, NO2, CO, and O3 were collected in Shantou from 2016 to 2020. A Poisson generalized additive model (GAM) was applied to estimate the acute effects of air pollutants on non-accidental mortality, with stratification analyses by gender, age, and season. Attributable fractions (AFs) and attributable numbers (ANs) were further estimated based on the World Health Organization (WHO) air quality guidelines and Chinese air quality standards. Non-accidental mortality in Shantou was significantly associated with exposure to PM2.5, PM10, SO2, NO2 and O3, but not with CO. Per 10 μg/m3 increase in air pollutant concentration, the strongest relative risks (RRs) and 95% confidence intervals (CIs) for non-accidental mortality were 1.0199 (1.0106-1.0294) for PM2.5 at lag03 days, 1.0146 (1.0085-1.0209) for PM10 at lag 03 days, 1.1268 (1.0773-1.1786) for SO2 at lag 07 days, 1.0256 (1.0093-1.0422) for NO2 at lag 03 days, and 1.0048 (1.0013-1.0083) for O₃ at lag 04 days, respectively. Stratified analyses showed that individuals aged 65 years and older were more susceptible only to O₃. The significant adverse effect of O₃ was significantly stronger in the warm season than in the cold season, while no significant difference was found between males and females. Overall, 4.23% (5,576 cases) of non-accidental deaths were attributable to excess exposure to air pollution exceeding the WHO air quality guidelines. Short-term exposure to PM2.5, PM10, SO2, NO2 and O3 was significantly associated with elevated non-accidental mortality in Shantou, a coastal subtropical city, imposing a considerable disease burden. Our findings highlight the urgent need for effective air pollution control strategies to reduce the related disease burden.
Air pollution remains a significant global health challenge and is increasingly recognized as a critical exposomic risk factor for adverse birth outcomes. Although numerous epidemiological studies have linked prenatal air pollution exposure to low birth weight, preterm birth, and stillbirth, important uncertainties remain regarding the underlying biological mechanisms, critical exposure windows, and the interplay between different pollutants and susceptibility factors. This narrative review synthesizes epidemiological findings and mechanistic evidence identified through literature searches in PubMed, Scopus, and Web of Science to provide a comprehensive overview of how maternal exposure to air pollutants affects fetal development and pregnancy outcomes. The reviewed epidemiological evidence largely supports an association between maternal air pollution exposure and adverse birth outcomes. For example, a 10 µg/m3 increase in fine particulate matter (PM2.5) exposure during the second trimester has been associated with an 11.8 g reduction in birth weight and a 23.1% increase in the risk of preterm birth. Oxidative stress, inflammation, endocrine disruption, vascular dysfunction, and epigenetic modifications are considered key biological pathways through which air pollution may impair placental function, alter fetal growth trajectories, and increase the likelihood of pregnancy complications. The placenta serves as a critical interface between maternal and fetal health and is particularly vulnerable to environmental insults, with air pollution exposure linked to changes in placental morphology, perfusion, and metabolic function. However, challenges persist in disentangling the effects of individual pollutants, establishing causality, identifying critical windows of susceptibility, and determining the extent to which sociodemographic, lifestyle, and genetic factors modify these associations. Current research gaps underscore the need for studies integrating high-resolution exposure assessment, multi-pollutant modeling, and mechanistic investigations to better clarify the impact of air pollution on pregnancy outcomes. Air pollution and adverse birth outcomes.
This study aimed to examine the association between ambient air pollution and hospital admissions for ischemic stroke, as well as the attributable disease burden, in Zhangzhou, a subtropical city in China. Daily data on hospital admissions for ischemic stroke, meteorological factors, and ambient air pollutants (PM2.5, PM10, SO2, NO2, CO, and O3) were collected in Zhangzhou from 2020 to 2023. A Poisson generalized additive model (GAM) was used to evaluate the acute effects of air pollutants on ischemic stroke admissions, with stratification by sex, age, and season. Attributable fractions (AFs) and attributable numbers (ANs) were further estimated based on the World Health Organization (WHO) Air Quality Guidelines and Chinese air quality standards. Ischemic stroke admissions were significantly associated with exposure to PM2.5, PM10, NO2 and O3, but not with SO2 or CO. For per 10 μg/m3 increment in PM2.5, PM10, NO2, and O3 at lag01, the corresponding relative risks (RRs) and 95% confidence intervals (CIs) were 1.0356 (1.0107-1.0611), 1.0196 (1.0052-1.0341), 1.0387 (1.0045-1.0740), and 1.0106 (1.0030-1.0183), respectively. These associations were stronger in males, individuals under 65 years of age, and during the cold season. Overall, 7.0% (854 cases) of ischemic stroke admissions in Zhangzhou were attributable to air pollutant concentrations exceeding the WHO Air Quality Guidelines. Short-term exposure to PM2.5, PM10, NO2, and O3 was significantly associated with increased hospital admissions for ischemic stroke and contributed to a certain disease burden in Zhangzhou. Our findings highlight the need for effective air pollution control strategies to reduce the related health burden.
Fine particulate matter (PM2.5) is pervasive in the atmosphere, particularly in densely populated industrial areas with multiple fugitive emission sources, such as opencast coal mining regions. Open-cast coal mining operations generate substantial particulate matter pollution, raising environmental and health concerns in the areas surrounding the mines. While PM2.5 levels are routinely regulated in mining regions, the chemical composition and toxicity of PM2.5, which may substantially influence health risks remain inadequately characterized. In this study, the composition, toxicity, and health risk of PM2.5 at six locations (two roadsides, three residential sites, and one residential background site) around an active opencast coal mining area in eastern Maharashtra, India were investigated. PM2.5-bound elemental carbon (EC), organic carbon (OC), metals, trace metals, polycyclic aromatic hydrocarbons (PAHs), and oxidative potential (OP) were examined. Highest PM2.5 levels were found at the roadsides (~ 400 µg m-3) and at 2 and 5 km from the mine (122 ± 43.4 µg m-3and 116 ± 35.5 µg m-3, respectively). Carbonaceous species and metals comprised ~ 40-50% of PM2.5 mass with Cr, Ni, Fe, Mg, and Zn nearly five-ten folds higher at the roadsides and residential sites closest to the mine compared to the background and the 10 km residential site. EC exhibited a high cancer risk (10-3), suggesting a serious health burden. Toxicity of PM, measured as OPvAA and OPvDTT, was higher at the roadside (18.05 ± 15.54 nmol min-1 m-3 and ~ 8.15 ± 9.94 nmol min-1 m-3), respectively, driven by metals and organics (r = 0.3-0.5, p < 0.05). Benzo(a)pyrene and naphthalene dominated the PAHs fraction having 5-tenfold higher concentrations than other PAHs. Multivariate regression model explained 25-40% of the variability in OPvAA and OPvDTT, primarily affected by Fe, Cr, Zn and EC. Overall, communities residing near active opencast coal mines experienced elevated exposure to PM2.5-bound chemical components, resulting in substantial toxicity and health risks. These findings demonstrate the value of integrating chemical composition, oxidative potential, and health risk assessment to better characterize PM2.5-linked health risks and burdens in communities impacted by mining and industrial sources. This bridges a significant gap in current air quality and health risk studies and provides evidence to inform future policy and regulatory decisions.
We present a dataset integrating physico-chemical air quality measurements with long-read PacBio HiFi shotgun metagenomic sequences from culture-enriched airborne samples collected in Sudwala Caves, one of the oldest known cave systems in South Africa. This resource provides baseline characterization of airborne microbial communities and associated environmental parameters within a subterranean karst ecosystem. A total of 106 air samples were collected across six different cave compartments and three external reference sites spanning two seasonal periods, the winter-spring transition (September-October 2024) and the summer-autumn window (February-March 2025). Environmental metadata include temperature, relative humidity, particulate matter (PM₁.₀, PM₂.₅, PM₁₀), and formaldehyde (HCHO) concentrations, enabling direct linkage between microbial composition and air quality dynamics. Post-quality control of eighteen (18) culture-enriched metagenome datasets yielded 7.7 × 10⁴ to 7.8 × 10⁵ HiFi reads per sample corresponding to 0.63-6.71 Gb of high-accuracy sequence data per sample. Kaiju classification assigned 65.1-83.4% of assembled sequences to reference taxa. Domain-level profiles were dominated by Bacteria (98.7-99.9% of classified sequences), with minor representation of Eukaryota (0.06-0.15%) and extremely low abundances of Archaea (0.002-0.009%) and Viruses (0.000-0.001%). At the phylum level, airborne bacterial communities were consistently dominated by Bacillota (mean relative abundance: 46.92%), Pseudomonadota (34.28%), and Actinomycetota (15.71%) across all sampling sites and seasons, with Pseudomonadota and Actinomycetota exhibiting proportionally higher representation within cave interior environments relative to outdoor reference sites. At the genus level, Staphylococcus, Bacillus, Microbacterium, Arthrobacter, and Pseudomonas were among the most consistently detected and abundant airborne genera within cave compartments, whilst outdoor aerobiome communities were characterised by greater relative abundances of Planococcus, Sphingomonas, Stenotrophomonas, and Arthrobacter. Functional annotation using the DRAM pipeline identified 1205,651 predicted genes, with 579,682 KEGG orthologs (KO), 62,261 MEROPs peptidases, 904,193 Pfam domains, and 21,859 CAZy genes annotated. This dataset supports investigations of culturable airborne microbial composition, functional capacity, bioaerosol dynamics, and environmental health indicators in dolomitic subterranean karst systems, providing a reference framework for comparative studies of low-biomass atmospheric environments.
Despite growing concern, the developmental effects of prenatal exposure to indoor and ambient particulate pollution remain poorly characterized. This study examined their individual and joint associations with infant growth. Embedded in the PKUBC-T birth cohort (initiated in June 2018, China), this study included 1068 mother-infant pairs. The PM1 and PM2.5 concentrations from the last menstrual period to delivery were predicted via a validated machine learning model, whereas PM2.5 constituents' concentrations were derived via a modified Community Multiscale Air Quality Model. Indoor air pollution was assessed via questionnaires covering four dimensions. Infant growth was evaluated using body mass index (BMI) Z-scores and weight-for-length (WFL) Z-scores at one year, with overweight/obesity (OWOB) defined by World Health Organization standards. Generalized linear regression indicated that increased exposure to indoor air pollution was associated with elevated BMI Z-scores (β = 0.089, 95 % CI: 0.007, 0.171) and WFL Z-scores (β = 0.094, 95 % CI: 0.013, 0.176) in offspring. PM1 and PM2.5 also exhibited positive associations with these growth indicators. Infants whose mothers were exposed to higher levels of organic carbon (OC), elementary carbon (EC), NH4+ and SO42- had an elevated risk of overweight/obesity (OWOB). Stratified analyses revealed that joint exposure to PM₁ above the median and indoor air pollution was related to increased infant growth, despite nonsignificant multiplicative interaction effects. Similar joint effects were observed for indoor air pollution and PM2.5, along with its constituents. This study highlights synergistic harms of combined indoor-outdoor air pollution on infant growth, reinforcing the need for integrated policies targeting indoor combustion and ambient PM reduction to safeguard early-life development.
Environmental exposures are recognized as determinants of health, particularly in vulnerable populations such as hemodialysis patients, whose impaired kidney function may heighten susceptibility. This study assesses the association between meteorological and air-pollution factors and the risk of hospital admission and mortality in end-stage kidney disease patients, considering both acute peaks and sustained exposure through weekly and monthly averages. A retrospective cohort of 336 hemodialysis patients treated between 2016 and 2024 at Hospital Universitario Príncipe de Asturias (Madrid, Spain) was analyzed, including 563 admissions and 90 deaths. Time-to-event analyses were conducted separately for mortality and admissions. Cox proportional hazards and parametric survival models (Weibull, log-normal, log-logistic) were applied for mortality, while recurrent-event models (Andersen-Gill, Prentice-Williams-Peterson, frailty) used for admissions. Sulfur dioxide (SO2) was consistently associated with increased risk in both acute and cumulative exposure models for mortality and admissions. Nitrogen dioxide (NO2) predicted mortality only in long-term analyses, suggesting a cumulative effect. Solar radiation was linked to accelerated mortality in non-linear models, whereas atmospheric pressure appeared protective for admissions. These findings highlight the influence of environmental exposures, particularly SO2, on adverse outcomes in hemodialysis patients and support incorporating environmental indicators into clinical risk prediction and public health strategies. Bad Weather, Dirty Air: How Pollution and Climate Increase the Risk of Hospitalization and Death for Kidney Failure Patients Environmental exposures are increasingly recognized as serious health factors, especially for high-risk groups like hemodialysis patients. These individuals have severely compromised kidney function, meaning their bodies struggle to detoxify, potentially making them highly susceptible to environmental toxins and climate stressors. This study aimed to determine if changes in local air quality and weather patterns increase the risk of hospital admission and mortality for patients with end-stage kidney disease. We analyzed data from 336 hemodialysis patients treated in Madrid, Spain, between 2016 and 2024, examining 563 hospital admissions and 90 deaths. We looked at two types of exposure: acute (short-term pollution peaks) and sustained (weekly and monthly averages of environmental data). Our statistical analysis showed strong links between environmental factors and adverse health outcomes. Sulfur dioxide (SO2) pollution was the most consistent threat, significantly increasing the risk of both hospitalization and death under both acute and sustained exposure scenarios. Nitrogen dioxide (NO2) was linked to a higher risk of mortality only when patients were exposed to sustained long-term averages, suggesting a cumulative impact. Regarding weather, solar radiation was associated with accelerated mortality in certain models, while atmospheric pressure appeared to offer a protective effect against hospital admissions. These findings emphasize that environmental factors, particularly SO2, are critical and preventable drivers of adverse clinical outcomes in the hemodialysis population. The study supports integrating environmental data and warning systems into clinical risk assessment and public health strategies to better protect this highly vulnerable group.
Environmental pollution is a major global issue. Ports, heavy traffic, and the presence of industries increase this pollution in some megacities like Abidjan. This study assessed potentially toxic elements in aerosols and rainwater and estimated associated health risks in Abidjan, Côte d'Ivoire. Aerosol and rainwater samples were collected in the communes of Cocody and Treichville during 2019 and 2020, taking into account the two main climatic seasons. Analysis of trace metal element (TME) and polycyclic aromatic hydrocarbon (PAH) levels revealed a dual origin both natural and anthropogenic for these pollutants in the environments studied with concentration between not determined (nd) and 0.056 ng·m-3 in aerosol and between nd and 0.0805 meq·L-1 in rainwater for TME. PAH concentrations vary from nd to 0.0798 ng·m-3 in aerosols. The ILCR values for inhaling BaP calculated are between nd and 4.02 × 10-16 and from nd to 1.44 × 10-15, respectively, for adult and children. The cancer risk levels calculated in rainwater for TMEs through oral and dermal pathways were all below 1 × 10-6 in rainwater. The results show that children are more vulnerable than adults and highlight the importance of continuous monitoring to anticipate and mitigate health risks, especially for the most vulnerable groups.
Fine particulate matter with a diameter ≤2.5 μm (PM2.5) pollution poses a global public health crisis, demonstrating significant threats to human health. This study focused on the strategically important Chengdu-Chongqing Economic Circle in western China, systematically comparing the toxic effects of urban and rural PM2.5 across five levels. PMF and regression analysis were used to identify source contributions, dual-omics to pinpoint key molecules, and epidemiological data with a GAM model to assess health risks. Findings demonstrate that rural PM2.5 possesses greater biotoxicity than its urban counterpart. Cytotoxicity in urban and rural PM2.5 originated from road dust/vehicle emissions and biomass burning, respectively. Subsequently, integrated omics and molecular biology analyses identify kinesin family member 20A (KIF20A) as a shared key target, which mediates toxicity induced by both urban and rural PM2.5. Finally, epidemiological analysis reveals that females and ≥65 years old exhibit relatively high sensitivity to urban PM2.5 exposure trends, with rhinitis showing a comparatively higher impact among various related diseases. The novelty of this work lies in its pioneering application of a multi-tiered investigative approach. This approach spans "environmental samples-cellular mechanisms-population health" within the Chengdu-Chongqing economic circle context, systematically elucidating common and distinct respiratory health risk of urban and rural PM2.5. This work offers a vital scientific foundation for advancing region-specific, precise air pollution prevention and control measures.
Inhaling smoke PM2.5 can cause adverse health effects ranging from acute (e.g., asthma, lung irritation) to chronic (e.g., COPD, lung cancer). Acute health effects have immediate implications for public health, requiring rapid response to minimize harm during an exposure window. Estimating acute health effects requires short-term (e.g., daily) estimates of fire-specific smoke PM2.5 concentrations at ground level. Any temporal discrepancy (e.g., missing fire emissions information) may result in underestimated smoke exposure in an epidemiology study. This paper introduces a method to estimate daily fire-specific PM2.5 smoke concentration at ground level in the western US from 2007-2019 to provide smoke characterizations (i.e., exposure estimates) for time-series studies investigating acute health effects. The smoke exposure model incorporates data on fire characteristics, such as fuel type, fire size, and fire distance, enabling a more detailed analysis of health impacts. This method utilizes updated fire emissions information as inputs to an atmospheric dispersion model, which determines the concentration and location of fire smoke after transport. These results are combined with a Bayesian time-series model to determine the smoke-specific portion of PM2.5 measured from nine ground-based EPA monitors in the western US. The Bayesian model includes meteorology and season to estimate the background PM2.5 concentrations. Using this data set with retained fire characteristics provides valuable insight into the differences between PM2.5 concentrations at different locations. We found that fires with the largest burned area during the study period (~1×108 m2) affected six of our nine stations, showing how widespread smoke impacts from large fires can be. The Lindon, UT station was impacted by the greatest number of fires over the period (398), but the average smoke PM2.5 concentration per fire was ~2 μg m-3 and the highest smoke PM2.5 concentration was 35 μg m-3. In comparison, the Carson City, NV station was impacted by less than half the number of fires over the study period (177), but the average smoke PM2.5 concentration per fire was three times higher (~6 μg m-3), and the highest smoke PM2.5 concentration was 159 μg m-3. These examples highlight two significantly different smoke exposure conditions that could plausibly lead to different health outcomes. Being able to investigate the health effects of the fire-specific smoke characteristics improves our understanding of the impacts of smoke exposure and ensures that management strategies are mitigating all possible outcomes of fires, including transported smoke.
Air pollution remains a critical environmental health challenge in Thailand, yet evidence linking high-resolution exposure to short-term respiratory health and inequality at the national scale remains limited. This study presents the first nationwide, high-resolution, daily assessment of PM2.5 and NO2 in Thailand, jointly quantifies short-term respiratory impacts and spatial inequality from 2019 to 2023. Daily pollutant concentrations at 0.01° resolution were reconstructed using Light Gradient Boosting Machine model integrating ground observations, satellite products, meteorological reanalysis, atmospheric chemical fields, and socio-environmental indicators, achieving strong predictive performance (R2 = 0.88 for PM2.5 and 0.92 for NO2; RMSE = 5.73 and 5.27 μg/m3, respectively). Distributed lag non-linear models were used to quantify short-term exposure-response relationships between air pollution and hospital admissions for asthma, chronic obstructive pulmonary disease (COPD), and all respiratory diseases. Pollutant-attributable fractions and inequality metrics were subsequently estimated. Long-term population exposure to PM2.5 was dominant, with nearly all residents persistently exposed to concentrations exceeding WHO guideline levels, whereas NO2 exposure was geographically constrained but concentrated in densely populated urban centers. Despite its limited spatial footprint, NO2 exhibited stronger short-term associations with respiratory admissions and generated disproportionately high, population-amplified attributable burdens. During high-pollution episodes, NO2 exposure accounted for an additional ∼11% of daily asthma and COPD admissions in urban areas, with attributable fractions for all respiratory diseases reaching ∼33%. These findings demonstrate that pollutants with contrasting exposure regimes impose distinct acute health and equity impacts, highlighting the need for pollutant-specific and regionally differentiated air quality management strategies in Thailand.
Poor outdoor air quality episodes-driven by wildfire smoke, traffic-related emissions, and unfavorable atmospheric conditions-increasingly are common, and patients routinely ask whether and how to continue exercising outdoors. The health benefits of regular physical activity are well established, yet exposure to fine particulate matter and ozone is associated with adverse cardiopulmonary outcomes; during exercise, increased minute ventilation increases inhaled dose, sharpening the clinical counseling dilemma. Existing recommendations from public health and professional organizations largely provide population-level messaging and are not optimized for rapid, individualized decisions in routine outpatient care. In this How I Do It article, we translate epidemiologic, experimental, and guideline-based evidence into a pragmatic counseling approach anchored to the US Air Quality Index (AQI). We present a 4-step framework: (1) stratify patients by cardiopulmonary vulnerability; (2) interpret local, real-time, pollutant-specific air quality data; (3) apply AQI-based action thresholds tailored to risk tier; and (4) prescribe specific, operational modifications to exercise timing, location and route, intensity, and duration, with mitigation strategies when exposure cannot be avoided. This framework emphasizes dose reduction and modification, rather than blanket cessation, explicitly acknowledges heterogeneity in individual susceptibility and access to mitigation resources, and supports shared decision-making at the point of care. By integrating air quality awareness into routine exercise counseling, clinicians can deliver clear, equitable, and clinically actionable guidance that helps patients to remain active while minimizing avoidable exposure during pollution events.
Climate and air pollution are associated with pediatric allergic diseases; however, their relative impacts remain poorly understood, particularly in subtropical climates. This study quantified and compared the contributions of meteorological variables and air pollutants to childhood allergic rhinitis (AR), asthma and atopic dermatitis (AD). We analyzed 1,516,996 pediatric hospital visits in Chongqing, China (2014-2019, 2023-2024), including AR (n = 456,807), asthma (n = 775,181), and AD (n = 285,008). Using distributed lag non-linear models, we examined associations with temperature, humidity, atmospheric pressure, wind speed, PM₂.₅, PM₁₀, NO₂, SO₂, CO, and O₃, comparing effect magnitudes through standardized coefficients and attributable disease burdens. Temperature demonstrated the strongest associations across all diseases, with opposing effects: positive associations with respiratory allergies (AR: RR = 1.25, 95% CI: 1.16-1.35 at 30 °C, attributing 84,640 cases [18.5% of total burden]; asthma: RR = 1.10, 95% CI: 1.05-1.16 at 32 °C, attributing 58,058 cases [7.5%]) versus inverse association with AD (RR = 0.75, 95% CI: 0.68-0.83 at 30 °C, associated with 58,270 fewer cases [20.4% reduction]). Seasonal analyses demonstrated marked heterogeneity: summer concentrated AR burden (temperature attributing 18,896 cases, 22.3% of annual burden), while winter concentrated asthma NO₂ effects (21,558 cases, 11.1% of winter burden). Individual air pollutants showed substantially smaller effects than temperature. Temperature demonstrated stronger short-term associations with childhood allergic disease burden than individual air pollutants in subtropical settings. Disease-specific environmental susceptibility patterns (opposing temperature effects for respiratory versus dermatological allergies) necessitate tailored prevention strategies. These results support integrating climate adaptation measures alongside air quality management in pediatric environmental health policies, with season-specific interventions during high-burden periods.
Air pollution is a leading threat to human health (WHO, 2021) but has been largely overlooked in the study of psychopathology. As the burden of poor mental health grows, a consideration of new contributors to psychopathology is needed to identify novel prevention and intervention approaches. Consequently, collaboration between clinical psychological scientists and experts in atmospheric research, pollution, and built environments holds great potential for advancing knowledge and addressing these threats. The current project brings together a cross-disciplinary team to summarize the state of existing research linking air quality to the development and maintenance of psychopathology. We then identify some traditional challenges to collaboration across our disciplines before identifying promising areas for future research and providing concrete advice to psychological scientists interested in similar collaborations, including recommendations for the measurement and application of outdoor and indoor air quality, ways to strengthen causal inference, and considerations for environmental justice.
Exposure to ambient air pollution, including ozone and fine particulate matter (PM2.5), is the world's leading environmental health risk factor. Estimating how this burden may change in the future depends on projecting population growth and age structure as well as understanding how future meteorological changes may impact the production and removal of pollutants from the atmosphere. The net impact of these factors on a global scale has not been well-characterized. Here, we leverage recent meteorology, exposure, and mortality output from general circulation, atmospheric chemistry, and health impact models to isolate how changes in meteorology and populations will impact future global air-pollution-related mortality and the associated monetized impacts by the degree of global temperature change. In contrast to previous studies, we estimate that changes in meteorologically driven air pollution, in the absence of pollutant precursor emission changes, will result in 180 000 fewer deaths annually by 2100 relative to current levels, an annual monetized benefit of $7.3 trillion. Reductions are driven by decreases in PM2.5-attributable mortality in populated regions but are substantially offset by global increases in ozone-related mortality. We also highlight striking regional differences in the sign of net pollutant impacts by 2100, with net pollution decreases in the Northern Hemisphere driven by reductions in nitrate aerosol, while increases in both ozone and organic aerosol at higher temperatures lead to net increases in pollutant impacts in the Southern Hemisphere. Lastly, we assess sensitivities of these results to meteorological projections, health impact functions, and 10 000 future warming scenarios.
This interdisciplinary longitudinal study examines the association between PM2.5 levels at sites downwind of a coal-fired thermal power plant (TPP) near the India-Bangladesh border and respiratory health in the exposed population, assessed using spirometry and fractional exhaled nitric oxide levels. Pulmonary function tests indicate significantly worse lung health at downwind sites in both India and Bangladesh compared with an upwind location. With averaged forced expiratory volume in one second (FEV1) values < 80% of predicted, evidence of preserved ratio impaired spirometry (PRISm), and significantly lower forced expiratory flow between 25% and 75% of vital capacity (FEF25-75), the population at the Indian downwind site is clearly at risk of developing obstructive pulmonary and related diseases. Although PM2.5 concentrations decline sharply during the monsoon across all sites, this does not translate into a recovery in lung health at the downwind location, consistent with chronic, irreversible effects potentially related to long-term exposure to TPP-associated PM2.5. Moreover, poorer socioeconomic conditions and exposure to emissions from biomass-based indoor cooking are associated with exacerbated respiratory effects. Overall, the study advocates transitioning to cleaner fuels for power generation and household use and recommends locating power plants away from densely populated areas to minimize health impacts.
Gasoline evaporation is a significant source of urban volatile organic compounds (VOCs). In this study, we selected Nanjing, a major city in the Yangtze River Delta of China, and developed a high-resolution (1 km × 1 km) gridded VOC species emission inventory for gas stations based on measured VOC emission characteristics and statistical data on gasoline and diesel sales. The results show that VOC emissions from gas stations were correlated with population density and road networks, and were mainly concentrated in the downtown area. The emitted VOCs were dominated by alkanes (58%) and oxygenated VOCs (19%), with i-pentane, n-butane, and methyl tert-butyl ether (MTBE) as the major components. C4-C5 alkenes were identified as the key contributors to ozone (O3) formation, while aromatics contributed most to secondary organic aerosol (SOA) formation. Health risk assessment indicates that, for gas station workers, both carcinogenic and non-carcinogenic risks associated with gasoline and diesel VOC evaporation exceed acceptable thresholds. Benzene, 1,2-dichloroethane, and 1,2-dibromoethane posed the highest carcinogenic risks, whereas acrolein, benzene, and 1,3-butadiene contributed most to non-carcinogenic risks. For urban residents, the health risks from gas station VOC emissions were generally within acceptable levels; however, under unfavorable meteorological conditions, residents living near gas stations may still face elevated health risks. This study highlights the significant impacts of gas station-related VOC emissions on air quality and human health, and informs targeted control and mitigation strategies for gasoline evaporation.
The concentration of atmospheric fine particles (PM2.5) has been considerably lowered in Beijing as a result of the implementation of a number of air pollution control initiatives. Nevertheless, the understanding of the impact of clean air measures on the health risks of PM2.5-bound trace elements is still limited. In this study, the concentrations and chemical fractionation of 14 trace elements in PM2.5 in Beijing after the "coal-to-gas" conversion measure were measured and compared with our previous study in Beijing before the measure. The major elements changed from Fe, Zn, and Pb before the measure to Fe, Ti, and Cu after the measure. The bioavailability of Pb, Zn, Cu, Sr, Ba, and Cr increased by approximately 5 %-44 % after the measure, while the bioavailability of Cd, Mn, As, Co, V, Fe, Ni, and Ti decreased by approximately 0.5 %-31 %, which may be mainly attributed to changes in their emission sources. After the measure, the relative contribution of traffic-related emissions to the total concentration of 14 elements increased by 12.1 %, and coal combustion decreased by 17.5 %. Traffic-related emissions (92.8 %) were the primary causes of carcinogenic risk after the measure, while traffic-related emissions (52.2 %) and coal combustion (41.4 %) dominated before the measure. This study elucidates changes in concentrations, chemical fractionation, bioavailability, sources, and health risks of PM2.5-bound trace elements in Beijing before and after the "coal-to-gas" conversion measure and suggests that traffic-related emissions should still be the main focus in the future.
Due to their ubiquitous emissions and associated health risks, atmospheric volatile organic compounds (VOCs) have been extensively studied in urban and industrial areas. However, small residential areas located near industrial facilities have received relatively little attention. Community-scale monitoring of VOCs was conducted using passive air samplers deployed at 7 sites in small residential areas near industrial complexes in Ulsan, South Korea. Among the 59 VOCs analyzed, aromatic compounds such as m,p,o-xylenes (13.6 ± 8.6 µg/m3), toluene (11.7 ± 11.9 µg/m3), and ethylbenzene (5.3 ± 4.0 µg/m3) were predominant. Elevated total VOC concentrations were observed at sites strongly influenced by solvent-related industrial activities. Correlation analysis between measured concentrations and industrial emissions within radii of 0.5, 1, 2, and 3 km indicated that facilities within 3 km were likely major sources of VOCs. Results of diagnostic ratios and principal component analysis indicated that VOCs were primarily influenced by local industrial activities, such as solvent use, fuel combustion, cleaning/degreasing, and petrochemical refining, rather than by regional or long-range atmospheric transport. Among the 23 VOCs evaluated for health risks, naphthalene was the only compound exceeding the US EPA threshold for acute non-cancer risk, primarily affecting the respiratory system. In contrast, cancer and non-cancer risk estimates for chronic exposure remained within acceptable levels. These findings highlight that residents within 3 km of the industrial complexes may be exposed to significant health risks. Therefore, continuous monitoring of VOC levels over various exposure durations (e.g., acute, subchronic, and chronic) is needed, even in small residential areas.