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Background: Previous studies reported that short-term exposure to ground-level ozone is associated with mortality risk. However, due to the limited monitored areas, existing studies were limited in assessing the nationwide risk and suggesting specific vulnerable populations to the ozone-mortality risk., Methods: We performed a nationwide time-stratified case-crossover study to evaluate the association between short-term ozone and cause-specific mortality in South Korea (2015-2019). A machine learning-ensemble prediction model (a test R 2  > 0.96) was used to assess the short-term ozone exposure. Stratification analysis was conducted to examine the high-risk populations, and the excess mortality due to non-compliance with the WHO guideline was also assessed., Results: For all-cause mortality (1,343,077 cases), the risk associated with ozone (lag0- 1) was weakly identified (odd ratio: 1.005 with 95% CI: 0.997-1.014), and the risk was prominent in mortality with circulatory system diseases. In addition, based on the point estimates, the ozone-mortality risk was higher in people aged less than 65y, and this pattern was also observed in circulatory system disease deaths and urban areas., Conclusions: This study provides national estimates of mortality risks associated with short-term ozone. Results showed that the benefits of stricter air quality standards could be greater in vulnerable populations., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Previous studies based on animal models have raised concerns about salbutamol use in ozone air pollution with regard to ozone related lung injury. We conducted a double-blind, randomized, placebo-controlled crossover study including 18 subjects diagnosed with EIB by a eucapnic voluntary hyperpnea (EVH) test. Participants completed 30 min of standardized moderate to vigorous exercise in four conditions: ozone plus salbutamol; room air plus salbutamol; ozone plus placebo medication; and room air plus placebo medication. Spirometry, fraction of exhaled nitric oxide, and symptoms were measured before, immediately after, 30 min after and 1 h after exercise. Measurements between the four conditions were compared using percent change from pre to post exercise. There was a statistically significant difference between the salbutamol and placebo medication groups for spirometric variables including FEV1 (Estimate = 6.3, 95% CI: 4.23-8.37, p < 0.001). No differences were observed between ozone and room air exposures. There were no significant differences in FeNO response between experimental conditions. We found that salbutamol improved pulmonary function in individuals with EIB when exercising in ozone and did not increase eosinophilic airway inflammation as indicated by FeNO. This evidence suggests that it is safe for people with EIB to continue to use salbutamol as proscribed when ozone levels are elevated., (© 2024 The Author(s). Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Background: Exposure to ambient air pollutants has emerged as a risk for metabolic-dysfunction associated steatotic liver disease (MASLD)., Objectives: We sought to examine associations between short-term (prior month) and long-term (prior year) ambient air pollution exposure with hepatic fat fraction (HFF) and liver stiffness in Latino youth with obesity. A secondary aim was to investigate effect modification by patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype and liver disease severity., Methods: Data was analyzed from 113 Latino youth (age 11-19) with obesity in Southern California. Individual exposure to particulate matter with aerodynamic diameter ≤ 2.5μm (PM 2.5 ), ≤ 10μm (PM 10 ), nitrogen dioxide (NO 2 ), 8-hour maximum ozone (8hrMax-O 3 ), 24-hr O 3 , and redox-weighted oxidative capacity (O x wt ) were estimated using residential address histories and United States Environmental Protection Agency air quality observations. HFF and liver stiffness were measured using magnetic resonance imaging. Linear models were used to determine associations between short-term and long-term exposure to air pollutants with HFF and liver stiffness. Modification by PNPLA3 and liver disease severity was then examined., Results: Short-term exposure to 8hrMax-O 3 was positively associated with HFF. Relationships between air pollution exposure and HFF were not impacted by PNPLA3 genotype or liver disease severity. Long-term exposure to 8hrMax-O 3 and O x wt were positively associated with liver stiffness. Associations between air pollution exposure and liver stiffness depended on PNPLA3 genotype, such that individuals with GG genotypes exhibited stronger, more positive relationships between short-term exposure to PM 10 , 8hrMax-O 3 , 24-hr O 3, and O x wt and liver stiffness than individuals with CC/CG genotypes. In addition, relationships between short-term exposure to NO 2 and liver stiffness were stronger in those with severe liver disease., Discussion: Air pollution exposure may be a risk factor for liver disease among Latino youth with obesity, particularly in those with other preexisting risks for liver damage., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Rohit Kohli reports a relationship with Mirum Biopharma that includes: consulting or advisory. Rohit Kohli reports a relationship with Ipsen that includes: consulting or advisory. Michael Goran reports a relationship with YUMI foods that includes: consulting or advisory. Michael Goran reports a relationship with Bobbie Labs that includes: consulting or advisory. Michael Goran receives royalties from Penguin Random House for Sugarproof If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Emerging evidence suggests that air pollution is a significant contributor to the global burden of kidney disease. Although acute kidney injury (AKI) is a common secondary event in ill patients, evidence regarding the association between air pollution and AKI accompanied by specific comorbidities is limited. This study aimed to estimate the association between short-term exposure to air pollution (fine particulate matter ≤2.5 μm [PM 2.5 ] and ozone [O 3 ]) and incident AKI by comorbid diseases using the Korea National Health Information Database (NHID). Total of 160,390 incident AKI cases, defined as an emergency department (ED) visit due to AKI, were observed within the period 2015-2021 in inland South Korea. A time-stratified case-crossover design was applied for PM 2.5 and O 3 individually, using a conditional logistic regression model within each case and its own control (three or four days of the same day of the week in the same month) to estimate the association between short-term air pollution exposure and ED visits due to AKI. Short-term exposure to PM 2.5 and O 3 was associated with ED visits due to AKI with ORs of 1.008 (95% confidence interval [CI]: 0.999, 1.017) and 1.019 (95% CI: 1.005, 1.033) for an interquartile range (IQR) increase in lag 0-1 day PM 2.5 and O 3 respectively, although OR for PM 2.5 was marginally significant. The odds of incident AKI associated with PM 2.5 was evident in conjunction with ischemic heart disease, cerebrovascular disease, gastrointestinal bleeding, and pneumonia. For O 3 , the estimated odds was prominent for AKI with ischemic heart disease. In addition, the comorbid disease-specific odds of AKI attributed to air pollution varied by sex and age. Our findings provide epidemiological evidence of a plausible mechanism between air pollution and incident AKI and suggest the need for personalized AKI prevention strategies attributed to air pollution., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Youngrin Kwag, Eunhee Ha reports financial support was provided by Korea Ministry of Science and ICT. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Evidence regarding the link between long-term ambient ozone (O 3 ) exposure and childhood sleep disorders is little. This study aims to examine the associations between long-term exposure to O 3 and sleep disorders in children. We conducted a population-based cross-sectional survey, including 185,428 children aged 6-18 years in 173 schools across 14 Chinese cities during 2012 and 2018. Parents or guardians completed a checklist using Sleep Disturbance Scale for Children, and O 3 exposure at residential and school addresses was estimated using a satellite-based spatiotemporal model. We used generalized linear mixed models to test the associations with adjustment for factors including socio-demographic variables, lifestyle, meteorology and multiple pollutants. Mean concentrations of O 3 , particulate matter with diameters ≤2.5 mm (PM 2.5 ) and nitrogen dioxide (NO 2 ) were 89.0 μg/m 3 , 42.5 μg/m 3 and 34.4 μg/m 3 , respectively. O 3 and NO 2 concentrations were similar among provinces, while PM 2.5 concentration varied significantly among provinces. Overall, 19.4% of children had at least one sleep disorder. Long-term exposure to O 3 was positively associated with odds of sleep disorders for all subtypes. For example, each interquartile increment in home-school O 3 concentrations was associated with a higher odds ratio for global sleep disorder, at 1.22 (95% confidence interval: 1.18, 1.26). Similar associations were observed for sleep disorder subtypes. The associations remained similar after adjustment for PM 2.5 and NO 2 . Moreover, these associations were heterogeneous regionally, with more prominent associations among children residing in southeast region than in northeast and northwest regions in China. We concluded that long-term exposure to O 3 is positively associated with risks of childhood sleep disorders. These associations varied by geographical region of China., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Objectives: Long-term exposure to air pollution has been associated with higher risk of cardiovascular mortality. Less is known about the association of air pollution with initial development of cardiovascular disease. Herein, the association between low-level exposure to air pollutants and subclinical carotid atherosclerosis in adults without known clinical cardiovascular disease was investigated., Design: Cross-sectional analysis within a prospective cohort study., Setting: The Canadian Alliance for Healthy Hearts and Minds Cohort Study; a pan-Canadian cohort of cohorts., Participants: Canadian adults (n = 6645) recruited between 2014-2018 from the provinces of British Columbia, Alberta, Ontario, Quebec, and Nova Scotia, were studied, for whom averages of exposures to nitrogen dioxide (NO2), ozone (O3), and fine particulate matter (PM2.5) were estimated for the years 2008-2012., Main Outcome Measure: Carotid vessel wall volume (CWV) measured by magnetic resonance imaging (MRI)., Results: In adjusted linear mixed models, PM2.5 was not consistently associated with CWV (per 5 μg/m3 PM2.5; adjusted estimate = -8.4 mm3; 95% Confidence Intervals (CI) -23.3 to 6.48; p = 0.27). A 5 ppb higher NO2 concentration was associated with 11.8 mm3 lower CWV (95% CI -16.2 to -7.31; p<0.0001). A 3 ppb increase in O3 was associated with 9.34 mm3 higher CWV (95% CI 4.75 to 13.92; p<0.0001). However, the coarse/insufficient O3 resolution (10 km) is a limitation., Conclusions: In a cohort of healthy Canadian adults there was no consistent association between PM2.5 or NO2 and increased CWV as a measure of subclinical atherosclerosis by MRI. The reasons for these inconsistent associations warrant further study., Competing Interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: RJ de Souza has served as an external resource person to the World Health Organization’s Nutrition Guidelines Advisory Group on trans fats, saturated fats, and polyunsaturated fats. The WHO paid for his travel and accommodation to attend meetings from 2012-2017 to present and discuss this work. He has presented updates of this work to the WHO in 2022. He has also done contract research for the Canadian Institutes of Health Research’s Institute of Nutrition, Metabolism, and Diabetes, Health Canada, and the World Health Organization for which he received remuneration. He has received speaker’s fees from the University of Toronto, and McMaster Children’s Hospital. He has held grants from the Canadian Institutes of Health Research, Canadian Foundation for Dietetic Research, Population Health Research Institute, and Hamilton Health Sciences Corporation as a principal investigator, and is a co-investigator on several funded team grants from the Canadian Institutes of Health Research. He has served as an independent director of the Helderleigh Foundation (Canada). He serves as a member of the Nutrition Science Advisory Committee to Health Canada (Government of Canada), and a co-opted member of the Scientific Advisory Committee on Nutrition (SACN) Subgroup on the Framework for the Evaluation of Evidence (Public Health England). Dr Anand reported receiving grants from Canadian Partnership Against Cancer, Heart and Stroke Foundation of Canada, and Canadian Institutes of Health Research, and a Canadian Institutes of Health Research Foundation grant during the conduct of the study and serving as the Tier 1 Canada Research Chair Ethnicity and Cardiovascular Disease and as the Michael G Degroote Heart and Stroke Foundation Chair in Population Health Research, and receiving grants from Heart and Stroke Foundation of Canada and Canadian Institutes of Health Research, and receiving personal fees from Bayer outside the submitted work. Dr Friedrich reported receiving personal fees from Circle CVI Inc for serving as a board member and adviser and being a shareholder outside the submitted work. Dr Dummer reported receiving grants from Canadian Partnership Against Cancer during the conduct of the study. Dr Lear reported receiving grants from the Canadian Institutes of Health Research and grants from Michael Smith Foundation for Health Research during the conduct of the study and personal fees from Curatio Inc outside the submitted work. Dr Tardif reported receiving grants from Amarin, Ceapro, Esperion, Ionis, Novartis, Pfizer, RegenXBio, Sanofi, AstraZeneca, and DalCor Pharmaceuticals, receiving personal fees from AstraZeneca, HLS Pharmaceuticals, Pendopharm, and DalCor Pharmaceuticals, and having a minor equity interest in DalCor Pharmaceuticals Minor outside the submitted work. In addition, Dr Tardif had a patent for Pharmacogenomics-Guided CETP Inhibition issued by DalCor Pharmaceuticals, a patent for Use of Colchicine After Myocardial Infarction pending, and a patent for Genetic Determinants of Response to Colchicine pending. No other disclosures were reported. Dr Brauer served on the WHO Guideline Development Group (no remuneration was provided but travel costs to meetings were covered). This does not alter our adherence to PLOS ONE policies on sharing data and materials., (Copyright: © 2024 Azab et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

This study investigates the projected impact of air pollution on mortality and Disability-Adjusted Life Years (DALYs) across SAARC countries. Utilizing Time Series and Machine Learning methodologies such as Autoregressive Integrated Moving Average, Exponential Smoothing, and Neural Network, the research aims to accurately forecast the mortality and DALYs attributed to air pollution from 2020 to 2030. Statistical analyses reveal a consistent upward trend in deaths and DALYs during the forecasting period, primarily driven by Ambient Particulate Matter Pollution (APM) and Ambient Ozone Pollution (AOP). Comparing the predictive accuracy of the models, Neural Network outperformed other methods, as indicated by Root Mean Square Error (RMSE) values. Specifically, the study finds that deaths and DALYs due to Ambient Particulate Matter pollution are least prevalent in the Maldives, while India and Pakistan exhibit the highest rates, and deaths and DALYs due to Ambient Ozone pollution are lowest in the Maldives and highest in Bangladesh and Pakistan. Moreover, deaths and DALYs attributed to Household Air Pollution (HAP) are lowest in Pakistan and highest in Nepal. These findings underscore the urgent need for air pollution control measures and informed policymaking in SAARC countries to mitigate the escalating health burden associated with air pollution., (© 2024. The Author(s).)

Objectives: We performed a systematic review and meta-analysis on long-term exposure to nitrogen dioxide (NO 2 ) and ozone (O 3 ) with mortality, to expand evidence that informed 2021 the WHO Air Quality Guidelines and guide the Health Risks of Air Pollution in Europe project., Methods: We included cohorts investigating NO 2 and O 3 mortality from all-causes, respiratory diseases, chronic obstructive pulmonary disease (COPD), acute lower respiratory infections (ALRI); and NO 2 mortality from circulatory, ischemic heart, cerebrovascular diseases and lung cancer. We pooled estimates by random-effects models and investigated heterogeneity. We assessed the certainty of the evidence using the Grading of Recommendations Assessment Development approach and Evaluation (GRADE)., Results: We selected 83 studies for NO 2 and 26 for O 3 for the meta-analysis. NO 2 was associated with all outcomes, except for cerebrovascular mortality. O 3 was associated with respiratory mortality following annual exposure. There was high heterogeneity, partly explained by region and pollutant levels. Certainty was high for NO 2 with COPD and ALRI, and annual O 3 with respiratory mortality., Conclusion: An increasing body of evidence, with new results from countrywide areas and the Western Pacific, supports certainty, including new outcomes., Competing Interests: The authors declare that they do not have any conflicts of interest., (Copyright © World Health Organization 2024. Licensee Frontiers Media SA and Stiftung Swiss School of Public Health plus.)

Background: While stationary links between childhood hand, foot and mouth disease (HFMD) and air pollution are known, a comprehensive study on their heterogeneous relationships (nonstationarity), jointly considering numerical, temporal and spatial dimensions, has not been reported., Methods: Monthly HFMD incidence and air pollution data were collected at the county level from Sichuan-Chongqing, China (2009-2011), alongside meteorological and social environmental covariates. Key influential factors were identified using random forest (RF) under the stationary assumption. Factors' numerically, temporally, and spatially heterogeneous relationships with HFMD were assessed using generalized additive model (GAM) and geographically and temporally weighted regression (GTWR)., Results: Our findings highlighted the relatively higher stationary contributions of fine particulate matter (PM 2.5 ) and ozone (O 3 ) to HFMD incidence across Sichuan-Chongqing counties. We further uncovered heterogeneous impacts of PM 2.5 and O 3 from three nonstationary perspectives. Numerically, PM 2.5 showed an inverse 'V'-shaped relationship with HFMD incidence, while O 3 exhibited a complex pattern, with increased HFMD incidence at low PM 2.5 and moderate O 3 concentrations. Temporally, PM 2.5 's impact peaked in autumn and was weakest in spring, whereas O 3 's effect was strongest in summer. Spatially, hotspot mapping revealed high-risk clusters for PM 2.5 impact across all seasons, with notable geographical variations, and for O 3 in spring, summer, and autumn, concentrated in specific regions of Sichuan-Chongqing., Conclusions: This study underscores the nuanced and three-perspective heterogeneous influences of air pollution on HFMD in small areas, emphasizing the need for differentiated, localized, and time-sensitive prevention and control strategies to enhance the precision of dynamic early warnings and predictive models for HFMD and other infectious diseases, particularly in the fields of environmental and spatial epidemiology., (© 2024. The Author(s).)

Rationale: Few studies have examined the effects of long-term childhood air pollution exposure on adult respiratory health, including whether childhood respiratory effects underlie this relation. Objectives: To evaluate associations between childhood air pollution exposure and self-reported adult bronchitic symptoms while considering child respiratory health in the Southern California Children's Health Study. Methods: Exposures to nitrogen dioxide (NO 2 ), ozone, and particulate matter <2.5 μm and <10 μm in diameter (PM 10 ) assessed using inverse-distance-squared spatial interpolation based on childhood (birth to age 17 yr) residential histories. Bronchitic symptoms (bronchitis, cough, or phlegm in the past 12 mo) were ascertained via a questionnaire in adulthood. Associations between mean air pollution exposure across childhood and self-reported adult bronchitic symptoms were estimated using logistic regression. We further adjusted for childhood bronchitic symptoms and asthma to understand whether associations operated beyond childhood respiratory health impacts. Effect modification was assessed for family history of asthma, childhood asthma, and adult allergies. Measurements and Main Results: A total of 1,308 participants were included (mostly non-Hispanic White [56%] or Hispanic [32%]). At adult assessment (mean age, 32.0 yr; standard deviation [SD], 4.7), 25% reported bronchitic symptoms. Adult bronchitic symptoms were associated with NO 2 and PM 10 childhood exposures. Odds ratios per 1-SD increase were 1.69 (95% confidence interval, 1.14-2.49) for NO 2 (SD, 11.1 ppb) and 1.51 (95% confidence interval, 1.00-2.27) for PM 10 (SD, 14.2 μg/m 3 ). Adjusting for childhood bronchitic symptoms or asthma produced similar results. NO 2 and PM 10 associations were modified by childhood asthma, with greater associations among asthmatic individuals. Conclusions: Childhood NO 2 and PM 10 exposures were associated with adult bronchitic symptoms. Associations were not explained by childhood respiratory health impacts; however, participants with childhood asthma had stronger associations.

The ability of air pollution to induce acute exacerbation of asthma is well documented. However, the ability of ozone (O 3 ), the most reactive gaseous component of air pollution, to function as a modulator during sensitization is not well established. C57BL/6 J male mice were intranasally sensitized to house dust mite (HDM) (40 μg/kg) for 3 weeks on alternate days in parallel with once-a-week O 3 exposure (1 ppm). Mice were euthanized 24 h following the last HDM challenge. Lung lavage, histology, lung function (both forced oscillation and forced expiration-based), immune cell profiling, inflammation (pulmonary and systemic), and immunoglobulin production were assessed. Compared to HDM alone, HDM + O 3 leads to a significant increase in peribronchial inflammation (p < 0.01), perivascular inflammation (p < 0.001) and methacholine-provoked large airway hyperreactivity (p < 0.05). Serum total IgG and IgE and HDM-specific IgG1 were 3-5 times greater in HDM + O 3 co-exposure compared to PBS and O 3 -exposed groups. An increase in activated/mature lung total and monocyte-derived dendritic cells (p < 0.05) as well as T-activated, and T memory lymphocyte subset numbers (p < 0.05) were noted in the HDM + O 3 group compared to HDM alone group. Concurrent O 3 inhalation and HDM sensitization also caused significantly greater (p < 0.05) lung tissue interleukin-17 pathway gene expression and mediator levels in the serum. Redox imbalance was manifested by impaired lung antioxidant defense and increased oxidants. O 3 inhalation during allergic sensitization coalesces in generating a significantly worse T H 17 asthmatic phenotype., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Tropospheric ozone is an air pollutant that poses a public health problem in Europe. Climate change could increase the formation of ozone. Applying past and predicted annual total (all-cause) mortality data and modeled daily ozone concentrations, we performed a nationwide health impact assessment estimating annual ozone-related (attributable) deaths in Austria. Different approaches were compared. Estimates were based on maximal 1-h averages of ozone. Until the decade from 2045 till 2055, more people will die in Austria because of the demographic trends. Therefore, more deaths will also be attributable to ozone. Higher greenhouse gas emission scenarios (e.g. Representative Concentration Pathway RCP8.5 compared to RCP2.6) will lead to more ozone-related deaths, mostly due to the national emission of ozone precursors (a difference of 250-340 cases per year, depending on the model), but to a lesser extent because of global climate change. Increases in attributable deaths will be affected mostly by national, not global mitigation measures. National emission reduction will certainly have a strong and beneficial effect on local atmospheric chemistry, air quality, and public health., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Public Health Association.)

Scarlet fever (SF) is an acute respiratory transmitted disease that primarily affects children. The influence of meteorological factors and air pollutants on SF in children has been proved, but the relevant evidence in Northwest China is still lacking. Based on the weekly reported cases of SF in children in Lanzhou, northwest China, from 2014 to 2018, we used geographical detectors, distributed lag nonlinear models (DLNM), and bivariate response models to explore the influence of meteorological factors and air pollutants with SF. It was found that ozone (O 3 ), carbon monoxide (CO), sulfur dioxide (SO 2 ), temperature, pressure, water vapor pressure and wind speed were significantly correlated with SF based on geographical detectors. With the median as reference, the influence of high temperature, low pressure and high pressure on SF has a risk effect (relative risk (RR) > 1), and under extreme conditions, the dangerous effect was still significant. High O 3 had the strongest effect at a 6-week delay, with an RR of 5.43 (95%CI: 1.74,16.96). The risk effect of high SO 2 was strongest in the week of exposure, and the maximum risk effect was 1.37 (95%CI: 1.08,1.73). The interactions showed synergistic effects between high temperatures and O 3 , high pressure and high SO 2 , high nitrogen dioxide (NO 2 ) and high particulate matter with diameter of less than 10 μm (PM 10 ), respectively. In conclusion, high temperature, pressure, high O 3 and SO 2 were the most important factors affecting the occurrence of SF in children, which will provide theoretical support for follow-up research and disease prevention policy formulation., (© 2024. The Author(s) under exclusive licence to International Society of Biometeorology.)

Objectives: We aimed to assess the effect of air pollution on incident cardiovascular disease (CVD) in people with type 2 diabetes mellitus (T2DM)., Methods: We tracked 486 T2DM patients from 2012 to 2021. Cox regression models were applied to assess the hazard of exposure to particulate matter, carbon monoxide (CO), ozone, nitrogen dioxide, and sulfur dioxide (SO 2 ) on incident CVD, revealing hazard ratios (HRs)., Results: CVD incidents occurred in 73 individuals. Among men, each 1-ppm increase in CO levels raised the risk of CVD (HR: 2.66, 95% CI: 1.30-5.44). For women, a 5-ppb rise in SO 2 increased CVD risk (HR: 1.60, 95% CI: 1.11-2.30). No notable impact of particulate pollutants was found., Conclusions: Persistent exposure to gaseous air pollutants, specifically CO and SO 2 , is linked to the development of CVD in men and women with T2DM., Competing Interests: Conflict of interest: None declared., (Copyright © 2024 American College of Occupational and Environmental Medicine.)

Background: Fewer studies have examined the relationship between air pollution and depressive or anxiety symptoms in rural residents. Social economic status (SES), as an important indicator of the current state of socioeconomic development, we know little about how it modifies the relationship between air pollution and symptoms of depression or anxiety., Methods: The patient health questionnaire (PHQ-2) and generalized anxiety scale (GAD-2) were used to learn about the prevalence of depressive and anxiety symptoms, the social economic status of the participants was categorized into two levels: lower and higher, and a binary logistic regression model was used to analyze the relationship between air pollution and residents' symptoms of depression or anxiety., Results: A total of 10,670 adults were enrolled in this study, of which a total of 1292 participants suffered from depressive symptoms and 860 suffered from anxiety symptoms. Short-term exposure to PM 2.5 and O 3 , singly or in combination, may be associated with the onset of depression symptoms, and there was a significant interaction between SES and exposure to PM 2.5 or O 3 . Residents of areas with higher SES may have a lower risk of suffering from anxiety symptoms after O 3 exposure compared to participants living in lower SES., Limitations: The study was a cross-sectional study, which may have lowered the quality level of the evidence., Conclusions: Short-term PM 2.5 and O 3 exposure may be associated with an increased prevalence risk of depressive symptoms. Higher levels of SES may reduce the adverse effects of air pollution on depressive or anxiety symptoms., Competing Interests: Declaration of competing interest The authors declare that there are no conflict of interests., (Copyright © 2024. Published by Elsevier B.V.)

Background: Renal sympathetic denervation (RDN) reduces blood pressure (BP)., Methods: This single-arm open-label study enrolled patients with resistant hypertension (RH) and treat them by CT-guided ozone mediated lumbar-renal sympathetic denervation (L-RDN). The primary endpoint was to assess the changes of BP over 24-h ambulatory BP monitoring (ABPM) and to evaluate the anti-hypertensive medication burden (AHMB) at 3-month follow-up. This study was registered in Chictr.org.cn (ChiCTR2300071375)., Results: 17 patients (mean age 65.12 ± 10.77 years) with AHMB of 4.12 ± 1.11 were enrolled. After the procedure, 7 patients (46.7 %) matched the criteria for antihypertensive medication reduction. The AHMB decreased to 3.87 ± 0.96 for the whole objectives and from 3.87 ± 0.96 to 3.55 ± 0.78 for patients with normal baseline renal function. On top of the lessened AHMB, L-RDN further reduced morning systolic BP (SBP) by -8.6 ± 4.0 mmHg (p = 0.034) and diastolic BP (DBP) by -4.6 ± 2.1 mmHg (p = 0.032) for all participants and morning SBP by -13.2 ± 3.6 mmHg (p < 0.001), morning DBP by -6.2 ± 2.4 mmHg (p = 0.011) and daytime SBP by -4.1 ± 1.6 mmHg (p = 0.009) for those with normal baseline renal function at 3-month of follow-up. No adverse events were reported intra- and post operation., Conclusions: CT-guided ozone-mediated L-RDN might be an innovative approach of RDN for treating RH. Confirmatory studies are warranted., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Growing evidence suggests that long-term air pollution exposure is a risk factor for cardiovascular mortality and morbidity. However, few studies have investigated air pollution below current regulatory limits, and causal evidence is limited. We use a double negative control approach to examine the association between long-term exposure to air pollution at low concentration and cardiovascular hospitalizations among US Medicare beneficiaries aged ≥65 years between 2000 and 2016. The expected values of the negative outcome control (preceding-year hospitalizations) regressed on exposure and negative exposure control (subsequent-year exposure) are treated as a surrogate for omitted confounders. With analyses separately restricted to low-pollution areas (PM 2.5  < 9 μg/m³, NO 2  < 75.2 µg/m 3 [40 ppb], warm-season O 3  < 88.2 μg/m 3 [45 ppb]), we observed positive associations of the three pollutants with hospitalization rates of stroke, heart failure, and atrial fibrillation and flutter. The associations generally persisted in demographic subgroups. Stricter national air quality standards should be considered., (© 2024. The Author(s).)

Objectives: To explore the associations of air pollutants and Air Quality Index (AQI) with risk of sudden sensorineural hearing loss (SSNHL) DESIGN: Cross-sectional study SETTING: Medical record data and local population data collected between 2014 and 2022 in Changshu, China were retrospectively reviewed., Participants: Adults aged 18 years and above who were diagnosed with SSNHL in Changshu No. 1 People's Hospital or Changshu No. 2 People's Hospital from the spring of 2014 to the fall of 2022 were included in the study., Outcome Measure: SSNHL was diagnosed by clinicians using the Chinese diagnostic criteria for SSNHL., Results: Compared with those exposed to the lowest tertile of carbon monoxide (CO), the prevalence ratio for those exposed to middle and high tertiles of CO were 1.113 (95% CI 1.022 to 1.213) and 1.230 (95% CI 1.105 to 1.369), respectively. The risk of SSNHL was increased by 30.6% (95% CI 9.9% to 55.4%) per doubling increment of CO. No categorical association was found between ozone (O 3 ) exposure and risk of SSNHL, however, an increased risk of 22.2% (0.8%-48.2%) was identified for each doubling of O 3 . No association was identified between other pollutants and AQI and risk of SSNHL., Conclusions: In this study, CO and O 3 were associated with an increased risk of SSNHL in Changshu, China. Further studies are warranted to confirm our findings., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Future climate change may bring local benefits or penalties to surface air pollution, resulting from changing temperature, precipitation, and transport patterns, as well as changes in climate-sensitive natural precursor emissions. Here, we estimate the climate penalties and benefits at the end of this century with regard to surface ozone and fine particulate matter (PM[Formula: see text]; excluding dust and smoke) using a one-way offline coupling between a general circulation model and a global 3-D chemical-transport model. We archive meteorology for the present day (2005 to 2014) and end of this century (2090 to 2099) for seven future scenarios developed for Phase 6 of the Coupled Model Intercomparison Project. The model isolates the impact of forecasted anthropogenic precursor emission changes versus that of climate-only driven changes on surface ozone and PM[Formula: see text] for scenarios ranging from extreme mitigation to extreme warming. We then relate these changes to impacts on human mortality and crop production. We find ozone penalties over nearly all land areas with increasing warming. We find net benefits due to climate-driven changes in PM[Formula: see text] in the Northern Extratropics, but net penalties in the Tropics and Southern Hemisphere, where most population growth is forecast for the coming century., Competing Interests: Competing interests statement:The authors declare no competing interest.

Background: The short-term adverse effects of ambient fine particulate matter (PM 2.5 ) and ozone (O 3 ) on anxiety disorders (ADs) remained inconclusive., Methods: We applied an individual-level time-stratified case-crossover study, which including 126,112 outpatient visits for ADs during 2019-2021 in Guangdong province, China, to investigate the association of short-term exposure to PM 2.5 and O 3 with outpatient visits for ADs, and estimate excess outpatient visits in South China. Daily residential air pollutant exposure assessments were performed by extracting grid data (spatial resolution: 1 km × 1 km) from validated datasets. We employed the conditional logistic regression model to quantify the associations and excess outpatient visits., Results: The results of the single-pollutant models showed that each 10 μg/m 3 increase of PM 2.5 and O 3 exposures was significantly associated with a 3.14 % (95 % confidence interval: 2.47 %, 3.81 %) and 0.88 % (0.49 %, 1.26 %) increase in odds of outpatient visits for ADs, respectively. These associations remained robust in 2-pollutant models. The proportion of outpatient visits attributable to PM 2.5 and O 3 exposures was up to 7.20 % and 8.93 %, respectively. Older adults appeared to be more susceptible to PM 2.5 exposure, especially in cool season, and subjects with recurrent outpatient visits were more susceptible to O 3 exposure., Limitation: As our study subjects were from one single hospital in China, it should be cautious when generalizing our findings to other regions., Conclusion: Short-term exposure to ambient PM 2.5 and O 3 was significantly associated with a higher odds of outpatient visits for ADs, which can contribute to considerable excess outpatient visits., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests of personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Nationwide evidence linking maternal ozone exposure with fetal growth restriction (FGR) was extensively scarce, especially in the Middle East with dry climate and distinct religious culture., Methods: We carried out a national retrospective birth cohort study using registry-based records from 749 hospitals across 31 provinces in Iran from 2013 to 2018. Monthly concentrations of maximum daily average 8-hour (MDA8) ozone at 0.125° × 0.125° resolution were extracted from well-validated spatiotemporal grid dataset. Linear and logistic regression models were employed to evaluate associations of maternal MDA8 ozone exposure with birthweight outcomes. Assuming causality, the comparative risk assessment framework was utilized to estimate the burden of low birthweight (LBW), small for gestational age (SGA), and birthweight loss per livebirth (BLL) attributable to ambient ozone pollution., Results: Of 4030383 livebirths included in the study, 264304 (6.6%) were LBW and 484405 (12.0%) were SGA. Each 10-ppb increase in MDA8 ozone exposure was associated with an odds ratio of 1.123 (95% confidence interval [CI]: 1.104 to 1.142) for LBW and 1.210 (95% CI: 1.197 to 1.223) for SGA, and a 30.5-g (95% CI: 29.0 to 32.0) reduction in birthweight. We observed approximately linear exposure-response relationships of maternal MDA8 ozone exposure with LBW (P nonlinear = 0.786), SGA (P nonlinear = 0.156), and birthweight reduction (P nonlinear = 0.104). Under the premise of causal association, we estimated 6.6% (95% CI: 5.7 to 7.5) of LBW, 10.1% (95% CI: 9.6 to 10.6) of SGA, and 18.8 g (95% CI: 17.9 to 19.7) of BLL could be attributable to maternal ozone exposure in Iran. Considerably greater risk and burden of ozone-related FGR were observed among younger, less-educated, and rural-dwelling mothers., Conclusions: Our study provided compelling evidence that maternal ozone exposure was associated with heightened FGR risk and burden, particularly among socioeconomically disadvantaged mothers. These findings underscored the urgent need for government to incorporate socioeconomic factors into future ozone-related health policies, not only to mitigate pollution, but also minimize inequality., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Prolonged exposure to air pollution has been linked to adverse respiratory health, yet the evidence concerning its association with chronic obstructive pulmonary disease (COPD) is inconsistent. The evidence of a greenness effect on chronic respiratory diseases is limited., Objective: This study aimed to investigate the association between long-term exposure to particulate matter (PM 2.5 and PM 10 ), black carbon (BC), nitrogen dioxide (NO 2 ), ozone (O 3 ) and greenness (as measured by the normalized difference vegetation index - NDVI) and incidence of self-reported chronic bronchitis or COPD (CB/COPD)., Methods: We analyzed data from 5355 adults from 7 centers participating in the Respiratory Health in Northern Europe (RHINE) study. Mean exposures to air pollution and greenness were assessed at available residential addresses in 1990, 2000 and 2010 using air dispersion models and satellite data, respectively. Poisson regression with log person-time as an offset was employed to analyze the association between air pollution, greenness, and CB/COPD incidence, adjusting for confounders., Results: Overall, there were 328 incident cases of CB/COPD during 2010-2023. Despite wide statistical uncertainty, we found a trend for a positive association between NO 2 exposure and CB/COPD incidence, with incidence rate ratios (IRRs) per 10 μg/m³ difference ranging between 1.13 (95% CI: 0.90-1.41) in 1990 and 1.18 (95% CI: 0.96-1.45) in 2000. O 3 showed a tendency for inverse association with CB/COPD incidence (IRR from 0.84 (95% CI: 0.66-1.07) in 2000 to 0.88 (95% CI: 0.69-1.14) in 2010. No consistent association was found between PM, BC and greenness with CB/COPD incidence across different exposure time windows., Conclusion: Consistent with prior research, our study suggests that individuals exposed to higher concentrations of NO 2 may face an elevated risk of developing COPD, although evidence remains inconclusive. Greenness was not associated with CB/COPD incidence, while O 3 showed a tendency for an inverse association with the outcome., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Uncertainty remains about the long-term effects of air pollutants (AP) on multiple diseases, especially subtypes of cardiovascular disease (CVD). We aimed to assess the individual and joint associations of fine particulate matter (PM 2.5 ), along with its chemical components, nitrogen dioxide (NO 2 ) and ozone (O 3 ), with risks of 32 health conditions., Methods: A total of 17,566 participants in Sichuan Province, China, were included in 2018 and followed until 2022, with an average follow-up period of 4.2 years. The concentrations of AP were measured using a machine-learning approach. The Cox proportional hazards model and quantile g-computation were applied to assess the associations between AP and CVD., Results: Per interquartile range (IQR) increase in PM 2.5 mass, NO 2 , O 3 , nitrate, ammonium, organic matter (OM), black carbon (BC), chloride, and sulfate were significantly associated with increased risks of various conditions, with hazard ratios (HRs) ranging from 1.06 to 2.48. Exposure to multiple air pollutants was associated with total cardiovascular disease (HR 1.75, 95% confidence intervals (CIs) 1.62-1.89), hypertensive diseases (1.49, 1.38-1.62), cardiac arrests (1.52, 1.30-1.77), arrhythmia (1.76, 1.44-2.15), cerebrovascular diseases (1.86, 1.65-2.10), stroke (1.77, 1.54-2.03), ischemic stroke (1.85, 1.61-2.12), atherosclerosis (1.77, 1.57-1.99), diseases of veins, lymphatic vessels, and lymph nodes (1.32, 1.15-1.51), pneumonia (1.37, 1.16-1.61), inflammatory bowel diseases (1.34, 1.16-1.55), liver diseases (1.59, 1.43-1.77), type 2 diabetes (1.48, 1.26-1.73), lipoprotein metabolism disorders (2.20, 1.96-2.47), purine metabolism disorders (1.61, 1.38-1.88), anemia (1.29, 1.15-1.45), sleep disorders (1.54, 1.33-1.78), renal failure (1.44, 1.21-1.72), kidney stone (1.27, 1.13-1.43), osteoarthritis (2.18, 2.00-2.39), osteoporosis (1.36, 1.14-1.61). OM had max weights for joint effects of AP on many conditions., Conclusions: Long-term exposure to increased levels of multiple air pollutants was associated with risks of multiple health conditions. OM accounted for substantial weight for these increased risks, suggesting it may play an important role in these associations., (© 2024. The Author(s).)

Background: Exposure to air pollution can affect the health of individuals with respiratory disease, but may also impede the health and performance of athletes. This is potentially relevant for people travelling to and competing in the Olympic and Paralympic Games (OPG) in Paris. We describe anticipated air quality in Paris based on historical monitoring data and describe the impact of the process on the development of monitoring strategies for future international sporting events., Methods: Air pollutant data for July to September 2020-2023 and pollen data for 2015-2022 were provided by Airparif (particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ) and ozone (O 3 )) and RNSA stations in the Paris region. Airparif's street-level numerical modelling provided spatial data for the OPG venues., Results: The maximum daily mean PM 2.5 was 11±6 µg/m 3 at traffic stations, below the WHO recommended daily air quality threshold (AQT). Daily NO 2 concentrations ranged from 5±3 µg/m 3 in rural areas to 17±14 µgm 3 in urban areas. Near traffic stations, this rose to 40±24 µg/m 3 exceeding the WHO AQT. Both peaked around 06:00 and 20:00 UTC (coordinated universal time). The ambient O 3 level exceeded the AQT on 20 days per month and peaked at 14:00 UTC. The main allergenic taxa from June to September was Poaceae (ie, grass pollen variety)., Conclusion: Air pollutant levels are expected to be within accepted air quality thresholds at the Paris OPG. However, O 3 concentrations may be significantly raised in very hot and clear conditions and grass pollen levels will be high, prompting a need to consider and manage this risk in susceptible individuals., Competing Interests: Competing interests: VB, RV, RSE, DB, GO and GF declare having no conflict of interest. A few authors declared they work for a non-profit organisation: NV is resident of the RNSA (French aerobiological monitoring network), is on the Board of the French Societies ATMO (no retribution – non-profit organisation), responsible for air quality monitoring in France, and APPA (association for the prevention of atmospheric pollution, non-profit organisation). He declared receiving funds from French ANSES and ARS (National Research Agency) for projects on pollen pollution and pollinators. VG, FA and JB from Airparif are involved in a project with SOLIDEO (Société de livraison d’ouvrages olympiques) to evaluate cleaning solutions implemented in the Olympic Village., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Air pollution exposure has been linked with increased risk of preterm birth, which is one of the leading causes of infant mortality. Limited studies have attempted to explore these associations in low-polluted areas. In this study, we aimed to assess the association between short-term exposure to ambient air pollution and preterm birth in Sweden., Method: In this population-based study we included preterm births between 2014 and 2019 from the Swedish Pregnancy Register. We applied a spatiotemporal model to estimate daily levels of particulate matter <2.5 μm (PM 2.5 ), PM < 10 μm (PM 10 ), nitrogen dioxide (NO 2), and ozone (O 3 ) at the residential address of each participant. We applied a time-stratified case-crossover design with conditional logistic regression analysis to estimate odds ratios (OR) of preterm birth per 10 μg/m 3 (PM 10 , NO 2 , O 3 ) and 5 μg/m 3 (PM 2.5 ) increase in air pollution exposure at 0-6-day lag. Two-pollutant models were applied to evaluate the independent association of each exposure on preterm birth. We also stratified by maternal characteristics to identify potential effect modifiers., Results: 28,216 (4.5%) preterm births were included. An increase in O 3 exposure was associated with increased odds of preterm birth [OR = 1.06 per 10 μg/m 3 (95% CI, 1.02; 1.10]. PM 2.5 and PM 10 were not significantly associated with preterm birth, and NO 2 displayed a negative nonlinear association with preterm birth. We did not observe any notable effect modification, but we found suggestive larger associations between O 3 and preterm birth when stratifying by male sex, spontaneous delivery, and spring season., Conclusions: Increased O 3 exposure one week before delivery was associated with an increased risk of preterm birth in Sweden, a country with levels of air pollution below the current World Health Organization air quality guidelines. Increases in O 3 levels with climate change make these findings especially concerning., (Copyright © 2024 The Authors. Published by Elsevier GmbH.. All rights reserved.)

The relationship between maternal peripheral blood mitochondrial DNA and adverse pregnancy outcomes, specifically preterm birth (PTB), remains uncertain. To investigate the effects of preconception mitochondrial DNA copy number (mtDNAcn) on the association between prenatal air pollutants exposure and PTB risk, a total of 1871 expectant mothers from six regions in Henan Province were recruited. Information regarding air pollutants was obtained from 151 environmental monitoring sites, and relative mtDNAcn was evaluated using real-time PCR analysis. After adjusting for potential confounding variables, it was determined that the risk of PTB increased with elevated levels of inhalable particulate matter (PM 10 ), fine particulate matter (PM 2.5 ), sulfur dioxide (SO 2 ), carbon monoxide (CO) and ozone (O 3 ) exposure (P < 0.05) but decreased with higher nitrogen dioxide (NO 2 ) exposure (0.05 < P < 0.10) during the entire pregnancy. Additionally, the preconception relative mtDNAcn was lower in the PTB group (0.82 ± 0.23) compared to the term group (0.92 ± 0.29). Furthermore, for each 0.1-unit increase in preconception mtDNAcn, the risk of PTB decreased by 14.8%. Stratified analyses revealed that the risk of PTB rose with increasing O 3 concentrations, regardless of the relative mtDNAcn. Moreover, the study found a significant association between PTB risk and prenatal exposure to elevated PM 10 , PM 2.5 , SO 2 , and CO, particularly in mothers with low mtDNAcn (≤0.88) (P < 0.05). Conversely, a decrease in the PTB risk was observed with elevated NO 2 exposure in mothers with high mtDNAcn (>0.88). Interaction analysis revealed that exposure to PM 10 , PM 2.5 , SO 2 , NO 2 , and CO interacted with mtDNAcn, respectively, affecting PTB risk (P -interaction <0.05). These findings indicate a noteworthy association between PTB risk and prenatal air pollutants exposure, which is influenced by the preconception mtDNAcn., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Background: Executive function, which develops rapidly in childhood, enables problem-solving, focused attention, and planning. Animal models describe executive function decrements associated with ambient air pollution exposure, but epidemiologic studies are limited., Methods: We examined associations between early childhood air pollution exposure and school-aged executive function in 1235 children from three US pregnancy cohorts in the ECHO-PATHWAYS Consortium. We derived point-based residential exposures to ambient particulate matter ≤2.5 µm in aerodynamic diameter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) at ages 0-4 years from spatiotemporal models with a 2-week resolution. We assessed executive function across three domains, cognitive flexibility, working memory, and inhibitory control, using performance-based measures and calculated a composite score quantifying overall performance. We fitted linear regressions to assess air pollution and child executive function associations, adjusting for sociodemographic characteristics, maternal mental health, and health behaviors, and examined modification by child sex, maternal education, and neighborhood educational opportunity., Results: In the overall sample, we found hypothesized inverse associations in crude but not adjusted models. Modified associations between NO 2 exposure and working memory by neighborhood education opportunity were present ( Pinteraction = 0.05), with inverse associations more pronounced in the "high" and "very high" categories. Associations of interest did not differ by child sex or maternal education., Conclusion: This work contributes to the evolving science regarding early-life environmental exposures and child development. There remains a need for continued exploration in future research endeavors, to elucidate the complex interplay between natural environment and social determinants influencing child neurodevelopment., Competing Interests: Disclosure: The authors report no conflicts of interest., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Rationale: It is unknown whether air pollution is associated with radiographic features of interstitial lung disease in individuals with chronic obstructive pulmonary disease (COPD). Objectives: To determine whether air pollution increases the prevalence of interstitial lung abnormalities (ILA) or percent high-attenuation areas (HAA) on computed tomography (CT) in individuals with a heavy smoking history and COPD. Methods: We performed a cross-sectional study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study), focused on current or former smokers with COPD. Ten-year exposure to particulate matter ⩽2.5 μm in aerodynamic diameter (PM 2.5 ), nitrogen oxides (NO x ), nitrogen dioxide (NO 2 ), and ozone before enrollment CT (completed between 2010 and 2015) were estimated with validated spatiotemporal models at residential addresses. We applied adjusted multivariable modified Poisson regression and linear regression to investigate associations between pollution exposure and relative risk (RR) of ILA or increased percent HAA (between -600 and -250 Hounsfield units), respectively. We assessed for effect modification by MUC5B -promoter polymorphism (variant allele carriers GT or TT vs. GG at rs3705950), smoking status, sex, and percent emphysema. Results: Among 1,272 participants with COPD assessed for HAA, 424 were current smokers, and 249 were carriers of the variant MUC5B allele. A total of 519 participants were assessed for ILA. We found no association between pollution exposure and ILA or HAA. Associations between pollutant exposures and risk of ILA were modified by the presence of MUC5B polymorphism ( P value interaction term for NO x  = 0.04 and PM 2.5  = 0.05) and smoking status ( P value interaction term for NO x  = 0.05; NO 2  = 0.01; and ozone = 0.05). With higher exposure to NO x and PM 2.5 , MUC5B variant carriers had an increased risk of ILA (RR per 26 ppb NO x , 2.41; 95% confidence interval [CI], 0.97-6.0; and RR per 4 μg ⋅ m -3 PM 2.5 , 1.43; 95% CI, 0.93-2.2, respectively). With higher exposure to NO 2 , former smokers had an increased risk of ILA (RR per 10 ppb, 1.64; 95% CI, 1.0-2.7). Conclusions: Exposure to ambient air pollution was not associated with interstitial features on CT in this population of heavy smokers with COPD. MUC5B modified the association between pollution and ILA, suggesting that gene-environment interactions may influence prevalence of interstitial lung features in COPD.

Background: Ambient air pollution exposure increases the incidence and severity of pediatric asthma. Despite this, we lack effective therapies to protect patients from the impact of ambient air pollution exposure. A roadblock is the inability to identify patients that are affected by air pollution., Objective: To examine the association between AAP sensitivity determined by individual exposure prior to asthma exacerbations and the severity of asthma in pediatric patients., Methods: We assess the association between spikes in ambient air pollution and asthma exacerbations. Patients were considered sensitive to a specific pollutant if they experienced an asthma exacerbation immediately following a spike in the concentration of that pollutant. Cut off values for these spikes were determined as two standard deviations above the mean concentration two weeks prior and two weeks post the days leading up to an asthma exacerbation., Results: We included 8129 pediatric patients with over 34,346 associated asthma exacerbations. In a multinomial log-linear logistic regression model comparing patients with mild asthma to patients with moderate or severe asthma, sensitivity to Ozone, SO 2 , PM 2.5 and PM 10 was significantly associated to severe as opposed to mild asthma (OR 1.39 with CI 1.08-1.78, 1.58 with CI 1.12-2.23, 1.37 with CI 1.07-1.76, and 1.63 with CI 1.12-2.37 respectively). Furthermore, moderate as opposed to mild asthma was significantly associated with sensitivity to SO 2 and PM 2.5 (OR 1.24 with CI 1.06-1.44 and 1.26 with CI 1.12-1.43, respectively)., Impact Statement: There is a subpopulation of pediatric asthma patients that experience asthma exacerbations just following spikes in ambient air pollution. This subgroup of patients has more severe asthma despite correction for significant confounders. The presented work is the first to reveal the clinically significant impact of variation in ambient air pollution sensitivity in pediatric asthma, highlighting the importance of accounting for variable sensitivity in the study of the effects of ambient air pollution exposure on pediatric asthma., (© 2023. The Author(s), under exclusive licence to Springer Nature America, Inc.)

Air pollution exposure during pregnancy may affect fetal growth. Fetal growth restriction (FGR) is associated with reduced lung function in children that can persist into adulthood. Using an established model of asymmetrical FGR in Long-Evans rats, this study investigated sex differences in effects of early life ozone exposure on lung development and maturation. Adverse health effects for i) gestational exposure (with impacts on primary alveolarization), ii) peri-adolescent exposure (with impacts on secondary alveolarization), and iii) cumulative exposure across both periods were evaluated. Notably, female offspring were most affected by gestational ozone exposure, likely because of impaired angiogenesis and corresponding decreases in primary alveolarization. Females had diminished lung capacity, fewer mature alveoli, and medial hypertrophy of small and large pulmonary arteries. Males, especially FGR-prone offspring, were more affected by peri-adolescent ozone exposure. Males had increased ductal areas, likely due to disrupted secondary alveolarization. Altered lung development may increase risk of developing diseases, such as pulmonary arterial hypertension or chronic obstructive pulmonary disease. Pulmonary arterial hypertension disproportionately affects women. In the United States, chronic obstructive pulmonary disease prevalence is increasing, especially in women; and prevalence for both men and women is highest in urbanized areas. This investigation underlines the importance of evaluating results separately by sex, and provides biologic plausibility for later consequences of early-life exposure to ozone, a ubiquitous urban air pollutant., (Published by Elsevier Inc.)

Outdoor air pollution is ubiquitous, and no safe level of exposure has been identified for the most common air pollutants such as ozone and particle pollution. Children are uniquely more susceptible to the harms of outdoor air pollution, which can cause and exacerbate respiratory disease. Although challenging to identify the effects of outdoor air pollution on individual patients, understanding the basics of outdoor air pollution is essential for pediatric respiratory health care providers. This review covers basic information regarding outdoor air pollution, unique considerations for children, mechanisms for increased susceptibility, and association with incident and exacerbation of respiratory disease in children., Competing Interests: Disclosure Dr Rosser's time contribution was supported by NIHK08 HL159333., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Gestational diabetes mellitus (GDM) can have negative effects on both the pregnancy and perinatal outcomes, as well as the long-term health of the mother and the child. It has been suggested that exposure to air pollution may increase the risk of developing GDM. This study investigated the relationship between exposure to air pollutants with gestational diabetes., Methods: The present study is a retrospective cohort study. We used data from a randomised community trial conducted between September 2016 and January 2019 in Iran. During this period, data on air pollutant levels of five cities investigated in the original study, including 6090 pregnant women, were available. Concentrations of ozone (O 3 ), nitric oxide (NO), nitrogen dioxide (NO 2 ), nitrogen oxides (NOx), sulphur dioxide (SO 2 ), carbon monoxide (CO), particulate matter < 2.5 (PM 2.5 ) or <10 μm (PM 10 ) were obtained from air pollution monitoring stations. Exposure to air pollutants during the three months preceding pregnancy and the first, second and third trimesters of pregnancy for each participant was estimated. The odds ratio was calculated based on logistic regression in three adjusted models considering different confounders. Only results that had a p  < .05 were considered statistically significant., Results: None of the logistic regression models showed any statistically significant relationship between the exposure to any of the pollutants and GDM at different time points (before pregnancy, in the first, second and third trimesters of pregnancy and 12 months in total) ( p  > .05). Also, none of the adjusted logistic regression models showed any significant association between PM 10 exposure and GDM risk at all different time points after adjusting for various confounders ( p  > .05)., Conclusions: This study found no association between GDM risk and exposure to various air pollutants before and during the different trimesters of pregnancy. This result should be interpreted cautiously due to the lack of considering all of the potential confounders.

Objective: To evaluate the influence of environmental factors and prematurity relating to juvenile dermatomyositis (JDM), its course and refractoriness to treatment., Methods: A case-control study with 35 patients followed up at a tertiary hospital and 124 healthy controls, all residents of São Paulo. Patients were classified according to monocyclic, polycyclic or chronic disease courses and refractoriness to treatment. The daily concentrations of pollutants (inhalable particulate matter-PM 10 , sulfur dioxide-SO 2 , nitrogen dioxide-NO 2 , ozone-O 3 and carbon monoxide-CO) were provided by the Environmental Company of São Paulo. Data from the population were obtained through a questionnaire., Results: Fifteen patients had monocyclic courses, and 19 polycyclic/chronic courses. Eighteen patients were refractory to treatment. Maternal occupational exposure to inhalable agents (OR = 17.88; IC 95% 2.15-148.16, p = 0.01) and exposure to O 3 in the fifth year of life (third tertile > 86.28µg/m 3 ; OR = 6.53, IC95% 1.60-26.77, p = 0.01) were risk factors for JDM in the multivariate logistic regression model. The presence of a factory/quarry at a distance farther than 200 meters from daycare/school (OR = 0.22; IC 95% 0.06-0.77; p = 0.02) was a protective factor in the same analysis. Prematurity, exposure to air pollutants/cigarette smoke/sources of inhalable pollutants in the mother's places of residence and work during the gestational period were not associated with JDM. Prematurity, maternal exposure to occupational pollutants during pregnancy as well as patient's exposure to ground-level pollutants up to the fifth year of life were not associated with disease course and treatment refractoriness., Conclusion: Risk factors for JDM were maternal occupational exposure and exposure to O 3 in the fifth year of life., (© 2024. The Author(s).)

Impaired cognitive health is the leading cause of various disabilities and disorders. Air pollution has been dramatically increasing over the last few decades and has been identified as a potential risk factor for impaired cognitive health. This study investigates the effect of air pollutants, particulate matter (PM 2.5 , PM 10 ), sulfur dioxide (SO 2 ), and ground-level ozone, on global cognitive health. The data on environmental pollutants and cognitive health were recorded from PubMed, Web of Science, Scopus, and Google Scholar. Initially, 790 articles were identified after screening for duplicates and applying the inclusion and exclusion criteria, 21 studies were included, and data was synthesized to get a pooled result. The overall results revealed that increased exposure to PM 2.5 was positively and significantly associated with cognitive decline (OR 1.49; 95% CI 1.11, 1.99; p = 0.01). The risk of cognitive impairment due to PM 10 (OR 1.30; 95% CI 1.00-1.70, p = 0.05), and SO 2  (OR 1.39; 95% CI 1.27-1.51; p < 0.01) exposure were also significantly heightened. The study findings show that overall exposure to particulate matter PM 2.5, PM 10, and SO 2 was associated with an increased risk of a decrease in global cognitive functions. The findings suggest that reducing levels of air pollutants could be a strategic approach to mitigate cognitive health risks in populations worldwide., (© 2024. The Author(s).)

Air pollution stands as an environmental risk to child mental health, with proven relationships hitherto observed only in urban areas. Understanding the impact of pollution in rural settings is equally crucial. The novelty of this article lies in the study of the relationship between air pollution and behavioural and developmental disorders, attention deficit hyperactivity disorder (ADHD), anxiety, and eating disorders in children below 15 living in a rural area. The methodology combines spatio-temporal models, Bayesian inference and Compositional Data (CoDa), that make it possible to study areas with few pollution monitoring stations. Exposure to nitrogen dioxide (NO 2 ), ozone (O 3 ), and sulphur dioxide (SO 2 ) is related to behavioural and development disorders, anxiety is related to particulate matter (PM 10 ), O 3 and SO 2 , and overall pollution is associated to ADHD and eating disorders. To sum up, like their urban counterparts, rural children are also subject to mental health risks related to air pollution, and the combination of spatio-temporal models, Bayesian inference and CoDa make it possible to relate mental health problems to pollutant concentrations in rural settings with few monitoring stations. Certain limitations persist related to misclassification of exposure to air pollutants and to the covariables available in the data sources used., (© 2024. The Author(s).)

Background: Exposure to air pollution is a major health problem worldwide. This study aimed to investigate the effect of the level of air pollutants and meteorological parameters with their related lag time on the transmission and severity of coronavirus disease 19 (COVID-19) using machine learning (ML) techniques in Shiraz, Iran. Study Design: An ecological study., Methods: In this ecological research, three main ML techniques, including decision trees, random forest, and extreme gradient boosting (XGBoost), have been applied to correlate meteorological parameters and air pollutants with infection transmission, hospitalization, and death due to COVID-19 from 1 October 2020 to 1 March 2022. These parameters and pollutants included particulate matter (PM2), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), nitric oxide (NO), ozone (O 3 ), carbon monoxide (CO), temperature (T), relative humidity (RH), dew point (DP), air pressure (AP), and wind speed (WS)., Results: Based on the three ML techniques, NO 2 (lag 5 day), CO (lag 4), and T (lag 25) were the most important environmental features affecting the spread of COVID-19 infection. In addition, the most important features contributing to hospitalization due to COVID-19 included RH (lag 28), T (lag 11), and O 3 (lag 10). After adjusting for the number of infections, the most important features affecting the number of deaths caused by COVID-19 were NO 2 (lag 20), O 3 (lag 22), and NO (lag 23)., Conclusion: Our findings suggested that epidemics caused by COVID-19 and (possibly) similarly viral transmitted infections, including flu, air pollutants, and meteorological parameters, can be used to predict their burden on the community and health system. In addition, meteorological and air quality data should be included in preventive measures., (© 2024 The Author(s); Published by Hamadan University of Medical Sciences. This is an open-access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.)

Allergic rhinitis （AR） is a nasal hypersensitivity disease that is influenced by environmental factors, genetic factors, and various inflammatory factors. The role and mechanisms of ozone, as a component of air pollution, in the pathogenesis of AR are not yet fully understood. This article provides a review of the impact of ozone on the epidemiology and pathology of AR, as well as its possible mechanisms, to provide new insights into the prevention and treatment of AR., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Although previous studies have suggested that meteorological factors and air pollutants can cause dry eye disease (DED), few clinical cohort studies have determined the individual and combined effects of these factors on DED. We investigated the effects of meteorological factors (humidity and temperature) and air pollutants [particles with a diameter ≤ 2.5 μ m (PM 2.5 ), ozone (O 3 ), nitrogen dioxide (NO 2 ), and carbon monoxide (CO)] on DED. A retrospective cohort study was conducted on 53 DED patients. DED was evaluated by Symptom Assessment in Dry Eye (SANDE), tear secretion, tear film break-up time (TBUT), ocular staining score (OSS), and tear osmolarity. To explore the individual, non-linear, and joint associations between meteorological factors, air pollutants, and DED parameters, we used generalized linear mixed model (GLMM) and Bayesian kernel machine regression (BKMR). After adjusting for all covariates, lower relative humidity or temperature was associated with a higher SANDE (p < 0.05). Higher PM 2.5 , O 3 , and NO 2 levels were associated with higher SANDE and tear osmolarity (p < 0.05). Higher O 3 levels were associated with lower tear secretion and TBUT, whereas higher NO 2 levels were associated with higher OSS (p < 0.05). BKMR analyses indicated that a mixture of meteorological factors and air pollutants was significantly associated with increased SANDE, OSS, tear osmolarity, and decreased tear secretion., (© 2024. The Author(s).)

Introduction: The health effects of ambient ozone have been investigated in many previous studies. However, the effects of long-term exposure to ambient ozone on the incidence of cardiovascular disease (CVD) remain inconclusive., Objectives: To estimate the associations of long-term exposure to maximum daily 8-hours average ozone (MDA8 O 3 ) with the incidence of total CVD, heart disease, hypertension, and stroke., Methods: This was a prospective cohort study, and the data was obtained from the China Health and Retirement Longitudinal Survey (CHARLS) implemented during 2011-2018 and the China Family Panel Studies (CFPS) implemented during 2010-2018. We applied a Cox proportional hazards regression model to evaluate the associations of MDA8 O 3 with total CVD, heart disease, hypertension, and stroke risks, and the corresponding population-attributable fractions (PAF) attributable to MDA8 O 3 were also calculated. All analyses were conducted by R software., Results: The mean MDA8 O 3 concertation of all included participants in the CHARLS and CFPS were 51.03 part per billion (ppb) and 51.15 ppb, respectively. In the CHARLS including 18,177 participants, each 10 ppb increment in MDA8 O 3 concentration was associated with a 31% increase [hazard ratio (HR) = 1.31, 95% confidence interval (CI): 1.22-1.42] in the risk of incident heart disease, and the corresponding population-attributable fractions (PAF) was 13.79% [10.12%-17.32%]. In the CFPS including 30,226 participants, each 10 ppb increment in MDA8 O 3 concentration was associated with an increase in the risk of incident total CVD (1.07 [1.02-1.13]), and hypertension (1.10 [1.03-1.18]). The PAFs of total CVD, and hypertension attributable to MDA8 O 3 were 3.53% [0.82%-6.16%], and 5.11% [1.73%-8.38%], respectively. Stratified analyses showed greater associations in males, urban areas, and Southern China., Conclusions: Long-term exposure to MDA8 O 3 may increase the incidence of CVD. Therefore, the policies that control O 3 and related precursors are persistently needed., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Production and hosting by Elsevier B.V.)

Background and Aims: Uncertainty of the causality determinations for ambient ozone (O 3 ) on cardiovascular events is heightened by the limited understanding of the mechanisms involved in humans. We aimed to examine the pro-atherothrombotic impacts of O 3 exposure and to explore the potential mediating roles of dysfunctional neutrophils, focusing on neutrophil extracellular traps (NETs)., Methods: A longitudinal panel study of 152 healthy adults was conducted in the cool to cold months with relatively low levels of O 3 between September 2019 and January 2020 in Beijing, China. Four repeated measurements of indicators reflecting atherothrombotic balance and NETs were performed for each participant., Results: Daily average exposure levels of ambient O 3 were 16.6 μg/m 3 throughout the study period. Per interquartile range increase in average concentrations of O 3 exposure at prior up to 7 days, we observed elevations of 200.1-276.3% in D-dimer, 27.2-36.8% in thrombin-antithrombin complex, 10.8-60.3% in plasminogen activator inhibitor 1, 13.9-21.8% in soluble P-selectin, 16.5-45.1% in matrix metalloproteinase-8, and 2.4-12.4% in lipoprotein-associated phospholipase A2. These pro-atherothrombotic changes were accompanied by endothelial activation, lung injury, and immune inflammation. O 3 exposure was also positively associated with circulating NETs indicators, including citrullinated histone H3, neutrophil elastase, myeloperoxidase, and double-stranded DNA. Mediation analyses indicated that NETs could mediate O 3 -associated pro-atherothrombotic responses. The observational associations remained significant and robust after controlling for other pollutants, and were generally greater in participants with low levels of physical activity., Conclusions: Ambient O 3 exposure was associated with significant increases in NETs and pro-atherothrombotic potential, even at exposure levels well below current air quality guidelines of the World Health Organization., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Objectives: To assess the association between air pollution exposure and housing context during pregnancy and adverse birth outcomes., Methods: We linked air pollution data from the Environmental Protection Agency and housing data from the American Community Survey with birth records from Wisconsin counties over a 9-year period. We calculated average daily pregnancy exposure to fine particulate matter and ozone and modeled its relationship to preterm birth, low birthweight and NICU admission, adjusting for individual characteristics and housing context., Results: Ozone exposure and housing cost-burden had substantive and statistically significant negative associations with birthweight and gestational age, and positive associations with NICU admission, while a poor-quality housing environment had a significant negative effect on weeks of gestation. Fine particulate matter exposure had a negligible correlation with these outcomes., Conclusions for Practice: An additional tenth of one part-per-million daily average exposure to ozone is associated with a 33 g decrease in birthweight. This decrease in birthweight is about the same size as the association of gestational diabetes (32 g), larger than the association of chronic hypertension (22 g), and about 40% the size of the effect of smoking during pregnancy on birthweight (84 g). Given the magnitudes of the associations with atmospheric ozone and adverse birth outcomes, reducing atmospheric ozone should be a public health priority. Inclusion of controls for housing cost-burden and poor-quality housing reduces the magnitude of the association with mothers who identify as Black, suggesting the importance of these structural factors in understanding adverse birth outcomes by race., (© 2024. The Author(s).)

The most up-to-date estimate of the global burden of disease indicates that ambient air pollution, including fine particulate matter and ozone, contributes to an estimated 5.2 million deaths each year. In this review, we highlight the challenges in estimating population exposure to air pollution and attributable health risks, particularly in low- and middle-income countries and among vulnerable populations. To protect public health, the evidence so far confirms urgent needs to prioritize interdisciplinary research on air pollution exposure and risk assessment and to develop evidence-based intervention policies and risk communication strategies. Here, we synthesize the emerging evidence supporting the monitoring and evaluation of the progress in implementation of the Global Air Quality Guidelines prepared by the World Health Organization.

Objectives: To identify the long-term spatiotemporal trend of ozone-related chronic obstructive pulmonary disease (COPD) burden by sex and country and to explore potential drivers., Methods: We retrieved data of ozone-related COPD death and disability adjusted life year (DALY) from the Global Burden of Disease 2019. We used a linear regression of natural logarithms of age-standardized rates (ASRs) with calendar year to examine the trends in ASRs and a panel regression to identify country-level factors associated with the trends., Results: Global ozone-attributable COPD deaths increased from 117,114 to 208,342 among men and from 90,265 to 156,880 among women between 1990 and 2019. Although ASRs of ozone-related COPD death and DALY declined globally, they increased in low and low-middle Socio-demographic Index (SDI) regions, with faster rise in women. Elevated average maximum temperature was associated with higher ozone-attributable COPD burden, while more green space was associated with lower burden., Conclusion: More efforts are needed in low and low-middle SDI regions, particularly for women, to diminish inter-country inequality in ozone-attributable COPD. Global warming may exacerbate the burden. Expanding green space may mitigate the burden., Competing Interests: The authors declare that they do not have any conflicts of interest., (Copyright © 2024 Wang, Cheng, Xu, Wang, Wang, Feng, Hu and Wang.)

Long-term mortality effects of particulate air pollution have been investigated in a causal analytic frame, while causal evidence for associations with gaseous air pollutants remains extensively lacking, especially for carbon monoxide (CO) and sulfur dioxide (SO 2 ). In this study, we estimated the causal relationship of long-term exposure to nitrogen dioxide (NO 2 ), CO, SO 2 , and ozone (O 3 ) with mortality. Utilizing the data from National Morbidity, Mortality, and Air Pollution Study, we applied a variant of difference-in-differences (DID) method with conditional Poisson regression and generalized weighted quantile sum regression (gWQS) to investigate the independent and joint effects. Independent exposures to NO 2 , CO, and SO 2 were causally associated with increased risks of total, nonaccidental, and cardiovascular mortality, while no evident associations with O 3 were identified in the entire population. In gWQS analyses, an interquartile range-equivalent increase in mixture exposure was associated with a relative risk of 1.067 (95% confidence interval: 1.010-1.126) for total mortality, 1.067 (1.009-1.128) for nonaccidental mortality, and 1.125 (1.060-1.193) for cardiovascular mortality, where NO 2 was identified as the most significant contributor to the overall effect. This nationwide DID analysis provided causal evidence for independent and combined effects of NO 2 , CO, SO 2 , and O 3 on increased mortality risks among the US general population., (© 2024. The Author(s).)

Air pollution has the potential to disrupt ecologically- and economically-beneficial services provided by invertebrates, including pollination and natural pest regulation. To effectively predict and mitigate this disruption requires an understanding of how the impacts of air pollution vary between invertebrate groups. Here we conduct a global meta-analysis of 120 publications comparing the performance of different invertebrate functional groups in unpolluted and polluted atmospheres. We focus on the pollutants ozone, nitrogen oxides, sulfur dioxide and particulate matter. We show that beneficial invertebrate performance is reduced by air pollution, whereas the performance of plant pest invertebrates is not significantly affected. Ozone pollution has the most detrimental impacts, and these occur at concentrations below national and international air quality standards. Changes in invertebrate performance are not dependent on air pollutant concentrations, indicating that even low levels of pollution are damaging. Predicted increases in tropospheric ozone could result in unintended consequences to global invertebrate populations and their valuable ecological services., (© 2024. The Author(s).)

Background: The effects of air pollution on endothelial function remain unclear across populations. We aimed to use brachial artery flow-mediated dilatation (FMD) to identify demographic differences in the effects of air pollution exposure on endothelial dysfunction., Methods: We measured FMD in 850 participants from October 2016 to January 2020. Location-specific concentrations of fine particulate matter < 2.5 μm aerodynamic diameter (PM 2.5 ), inhalable particulate matter < 10 μm aerodynamic diameter (PM 10 ), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), carbon monoxide (CO), and ozone (O 3 ) measured by fixed ambient air monitoring stations were collected for short- and long-term exposure assessment. Multiple linear regression models and restricted cubic splines were used to assess the associations before and after stratification by age and sex., Results: This study eventually included 828 participants [551 (66.5%) younger than 65 years and 553 (66.8%) men]. Each 10 µg/m 3 increase in 7-day exposure to PM 2.5 and PM 10 was significantly linearly associated with a 0.07% (β = -0.07, 95% CI: -0.13 to -0.004) and 0.05% (β = -0.05, 95% CI: -0.10 to -0.004) decrease in FMD in the fully adjusted model. After full adjustment, long-term exposure to all air pollutants was significantly associated with impaired FMD. Each 10 µg/m 3 increase in long-term exposure to PM 2.5 and PM 10 was significantly associated with a -0.18% (95% CI: -0.34 to -0.03) and - 0.23% (95% CI: -0.40 to -0.06) change in FMD, respectively. After stratification, the associations of lower FMD with long-term exposure to PM 2.5 , PM 10 , SO 2 , NO 2 , and CO significantly persisted in men and participants younger than 65 years instead of women or older participants. For short-term exposure, we observed differences consistent with long-term exposure and a stronger effect of 7-day exposure to SO 2 in men due to a significant interaction effect., Conclusion: Short- and long-term exposure to different air pollutants are strongly associated with decreased endothelial function, and susceptibility to air pollution varies significantly with age and sex., (© 2024. The Author(s).)

Background and Aim: The increasing prevalence of precocious puberty (PP) has emerged as a significant medical and social problem worldwide. However, research on the relationship between long-term air pollution exposure and PP has been relatively limited. We thus investigated the association between long-term air pollution exposure and the onset of PP in South Korea., Methods: We investigated a retrospective cohort using the Korea National Health Insurance Database. Six-year-old children born from 2007 to 2009 were examined (2013-2015). We included boys ≤10 years and girls aged ≤9 years who visited hospitals for early pubertal development, were diagnosed with PP per the ICD-10 (E228, E301, and E309), and received gonadotropin-releasing hormone agonist treatment. We analyzed data for boys up until 10 years old (60-month follow-up) and for girls up to 9 years old (48-month follow-up). We assessed the association between long-term air pollution exposure and the onset of PP using a Cox proportional hazard model. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) per 1 μg/m 3 increase in fine particulate matter (PM 2.5 ) and particulate matter (PM 10 ) and per 1 ppb increase in sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), and ozone (O 3 )., Results: This study included 1,205,784 children aged six years old between 2013 and 2015. A positive association was found between the 48-month moving average PM 2.5 (HR: 1.019; 95% CI: 1.012, 1.027), PM 10 (HR: 1.009; 95% CI: 1.006, 1.013), SO 2 (HR: 1.037; 95% CI: 1.018, 1.055), and O 3 (HR: 1.006; 95% CI: 1.001, 1.010) exposure and PP in girls but not boys., Conclusions: This study provides valuable insights into the harmful effects of air pollution during childhood and adolescence, emphasizing that air pollution is a risk factor that should be managed and reduced., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Previous studies of air pollution and respiratory disease often relied on aggregated or lagged acute respiratory disease outcome measures, such as emergency department (ED) visits or hospitalizations, which may lack temporal and spatial resolution. This study investigated the association between daily air pollution exposure and respiratory symptoms among participants with asthma and chronic obstructive pulmonary disease (COPD), using a unique dataset passively collected by digital sensors monitoring inhaled medication use. The aggregated dataset comprised 456,779 short-acting beta-agonist (SABA) puffs across 3,386 people with asthma or COPD, between 2012 and 2019, across the state of California. Each rescue use was assigned space-time air pollution values of nitrogen dioxide (NO 2 ), fine particulate matter with diameter ≤ 2.5 µm (PM 2.5 ) and ozone (O 3 ), derived from highly spatially resolved air pollution surfaces generated for the state of California. Statistical analyses were conducted using linear mixed models and random forest machine learning. Results indicate that daily air pollution exposure is positively associated with an increase in daily SABA use, for individual pollutants and simultaneous exposure to multiple pollutants. The advanced linear mixed model found that a 10-ppb increase in NO 2 , a 10 μg m -3 increase in PM 2.5 , and a 30-ppb increase in O 3 were respectively associated with incidence rate ratios of SABA use of 1.025 (95 % CI: 1.013-1.038), 1.054 (95 % CI: 1.041-1.068), and 1.161 (95 % CI: 1.127-1.233), equivalent to a respective 2.5 %, 5.4 % and 16 % increase in SABA puffs over the mean. The random forest machine learning approach showed similar results. This study highlights the potential of digital health sensors to provide valuable insights into the daily health impacts of environmental exposures, offering a novel approach to epidemiological research that goes beyond residential address. Further investigation is warranted to explore potential causal relationships and to inform public health strategies for respiratory disease management., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: All co-authors affirm the absence of any conflict of interest related to this research, with the exception of Meredith Barrett and Vy Vuong, who are employees of ResMed (to which Propeller Health is affiliated) and receive salary and stock., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)