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Background: Air pollution is a major environmental risk factor. Hypertension is one of the most important modifiable risk factors for cardiovascular diseases. However, few studies have evaluated the impact of exposure to ambient air pollution on hypertension hospitalizations., Objective: This study aims to explore the correlation between exposure to air pollution and hospital admissions for hypertension, to evaluate the short-term effects of air pollution on hypertension hospitalizations and its lag effects., Methods: We collected air pollution concentration and hypertension hospitalization data from 2013 to 2020. Distributed lag non-linear models were employed to assess the impact of air pollution on hypertension hospitalizations in Lanzhou City. We also performed subgroup analyses and sensitivity analyses., Results: A total of 47,884 cases of hypertension hospitalizations were included. Short-term exposure to NO 2 and CO increased the risk of hypertension hospitalization. For each 10 µg/m 3 increase in NO 2 and each 1 mg/m 3 increase in CO, the relative risk (RR) for hypertension hospitalization were highest at lag0-3 (RR: 1.0427; 95% CI: 1.0196, 1.0663) and lag3 (RR: 1.0986; 95% CI: 1.0350, 1.1661), respectively. SO 2 at different lag structures showed opposite effects on hypertension hospitalization. O 3 was significantly negatively associated with hypertension hospitalization. No correlation was observed between PM 2.5 and PM 10 and hypertension hospitalization. Females and individuals aged ≥ 65 were more susceptible to air pollution. The harmful effects of air pollution are greater in the cold season., Conclusion: Short-term exposure to ambient air pollution increases risk of hypertension hospitalization., Competing Interests: Declarations. Ethics approval and consent to participate: The Institutional Review Board (IRB) at School of Public Health, Lanzhou University has waived the ethics approval and the informed consent for the study. The study adhered to the guidelines and regulations outlined in the Declaration of Helsinki. This exemption is due to the fact that the data used in the study was provided by government agencies and consented for use in this research. The data did not involve any direct or indirect identification of hospital patients’ personal information. And the waiver of informed consent has been reviewed and approved by the research ethics committee. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Background: People living with HIV (PLWH) are more vulnerable to infectious and non-infectious comorbidities due to chronic inflammation and immune dysfunction. Air pollution is a major global health risk, contributing to millions of deaths annually, primarily from cardiovascular and respiratory diseases. However, the link between air pollution and mortality risk in PLWH is underexplored. This systematic review assesses the association between exposure to pollutants such as particulate matter (PM), nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), ozone (O 3 ), and carbon monoxide (CO) and mortality risk in PLWH., Methods: A systematic search of PubMed, Web of Science, and Embase was conducted for studies published up to August 2024. Eligibility criteria included cohort, case-control, and cross-sectional studies assessing air pollution exposure and mortality in PLWH. Nested-Knowledge software was used for screening and data extraction. The Newcastle-Ottawa Scale was applied for quality assessment. A narrative approach and tabular summarization were used for data synthesis and presentation., Results: Nine studies, mostly from China, demonstrated a significant association between long-term exposure to PM 1 , PM 2.5 , and PM 10 and increased risks of AIDS-related and all-cause mortality in PLWH. Hazard ratios for mortality increased by 2.38-5.13% per unit increase in PM concentrations, with older adults (> 60), females, and those with lower CD4 counts (< 500 cells/µL) being more vulnerable. Short-term exposure to ozone and sulfur dioxide also increased mortality risks, particularly during the warm season and in older populations. Specific pollutants like ammonium (NH4⁺) and sulfate (SO4²⁻) had the strongest links to elevated mortality., Conclusion: Air pollution, especially fine particulate matter and ozone, is associated with a higher risk of mortality in PLWH. Targeted interventions to reduce pollution exposure in vulnerable subgroups are crucial. Further research is needed to confirm these findings in diverse regions and develop effective mitigation strategies., Competing Interests: Declarations. Human ethics and Consent to participate declarations: Not applicable Consent to Participate: Not applicable since this is a review and not involved any human. Competing interests: The authors declare no competing interests. Financial support and sponsorship: None Ethical considerations: Not applicable, (© 2024. The Author(s).)

Background: Air pollution is considered one of the risk factors for stroke prevalence in the long term and incidence in the short term. Tabriz is one of the most important industrial cities in Iran. Hence, air pollution has always been one of the main concerns in environmental health in the region., Method: The patient data were retrieved from electronic health records of the primary tertiary hospital of the city (Imam Reza Hospital). Air pollution data was obtained from the Environmental Protection Agency and is generated by 8 sensor stations spread across the city. Average daily values were calculated for CO, NO, NO, NOx, O3, SO2, PM2.5, and PM10 from hourly measurement data. Autoregressive integrated moving average (ARIMA-X) model with 3 lag days was developed to assess the correlation., Results: Air pollutants and hospital admission data were collected for 1821 day and includes 4865 stroke cases. our analysis showed no statistically significant association between the daily concentrations of CO (p = 0.41), NOx (p = 0.96), O3 (p = 0.65), SO2 (p = 0.91), PM2.5 (p = 0.44), and PM10 (p = 0.36). Only the binary COVID variable which was used to distinguish between COVID-19 era and other days, was significant (p value = 0.042). The goodness of fit measures, Root Mean Squared Error (RMSE), and Median Absolute Error (MAE) were 1.81 and 1.19, respectively., Conclusion: In contrast to previous reports on the subject, we did not find any pollutant significantly associated with an increased number of stroke patients., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Razzaghi 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.)

Background: A growing body of epidemiologic and toxicologic literature indicates that fine airborne particulate matter (PM 2.5 ) pollution is neurotoxic and threatens children's neurobehavioral development, resulting in reduced cognitive function. Understanding the magnitude of this effect is critical for establishing public health policies that will protect children's health, preserve human capital, and support societal progress., Objective: To quantify the association between ambient PM 2.5 air pollution and loss of cognitive function in children, as measured by Intelligence Quotient (IQ) scores, through a systematic literature review and meta-analysis., Methods: Following PRISMA guidelines, we conducted a systematic literature search across seven databases: Agricultural and Environmental Science, BIOSIS Citation Index, Embase, GreenFILE, PubMed, Scopus, and Web of Science to identify original scientific studies that investigated the impact of PM 2.5 exposure during pre-and postnatal periods on IQ loss during childhood. Using data from studies included for final review, we conducted a meta-analysis, using a random effects model to compute a beta coefficient that quantifies the overall effect of PM 2.5 exposure on Full-Scale IQ (FSIQ), Performance IQ (PIQ), and Verbal IQ (VIQ)., Findings: Of the 1,107 unique publications identified, six studies met the inclusion criteria for final review, representing 4,860 children across three continents (North America, Europe, and Asia). The mean PM 2.5 concentration across all studies was 30.4 ± 24.4 µg/m 3 . Exposure timing ranged from the prenatal period to mid-childhood. Children were an average of 8.9 years old at the time of cognitive testing. We found that each 1 µg/m 3 increase in PM 2.5 concentration is associated with a -0.27 point change in FSIQ (p < 0.001), 0.39 point change in PIQ (p = 0.003), and -0.24 point change in VIQ (p = 0.021)., Conclusion: Through a systematic review and meta-analysis, we identified a statistically significant relationship between increased exposure to PM 2.5 air pollution and reduced cognitive function in children, with the most pronounced impact on PIQ. This analysis will enable estimation of the burden of adverse neurobehavioral development attributable to PM 2.5 in pediatric populations and will inform local and global strategies for exposure prevention., Competing Interests: Declarations Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Background: Growing epidemiological evidence suggests an association between exposure to air pollutants and breast cancer. Yet, the underlying mechanisms remain poorly understood. This study explored the mediating role of thirteen metabolic health biomarkers in the relationship between exposure to three air pollutants, i.e. nitrogen dioxide (NO 2 ), polychlorinated biphenyls 153 (PCB153), and benzo[a]pyrene (BaP), and breast cancer risk., Methods: We used data from a nested case-control study within the French national prospective E3N-Generations cohort, involving 523 breast cancer cases and 523 matched controls. The four-way decomposition mediation of total effects for thirteen biomarkers was applied to estimate interaction and mediation effects (controlled direct, reference interaction, mediated interaction, and pure indirect effects)., Results: The analyses indicated a significant increase in breast cancer risk associated with BaP exposure (odds ratio (OR) Q4 vs Q1  = 2.32, 95% confidence intervals (CI): 1.00-5.37). PCB153 exposure showed a positive association only in the third quartile (OR Q3 vs Q1  = 2.25, CI 1.13-4.57), but it appeared to be non-significant in the highest quartile (OR Q4 vs Q1  = 2.07, CI 0.93-4.61). No association was observed between NO 2 exposure and breast cancer risk. Estradiol was associated with an increased risk of breast cancer (OR per one standard deviation (SD) increment = 1.22, CI 1.05-1.42), while thyroid-stimulating hormone was inversely related to breast cancer risk (OR per 1SD increase = 0.87, CI 0.75-1.00). We observed a suggestive mediated effect of the association between the three pollutants and breast cancer risk, through albumin, high-density lipoproteins cholesterol, low-density lipoprotein cholesterol, parathormone, and estradiol., Conclusion: Although limited by a lack of statistical power, this study provides relevant insights into the potential mediating role of certain biomarkers in the association between air pollutant exposure and breast cancer risk, highlighting the need for further in-depth studies in large populations., Competing Interests: Declarations Ethics approval and consent to participate Our research utilized data from the existing French prospective cohort E3N. All participants provided informed consent and the study received approval from the French National Commission for Data Protection and Privacy (CNIL). Due to ethical considerations and the specific consent signed by the participants, the datasets generated and/or analysed during the current study are not publicly available, however, data can be obtained from the E3N-Generations team through the corresponding author upon reasonable request. Consent for publication Not applicable. Competing interests The authors declare that they have no competing interests., (© 2024. The Author(s).)

Interstitial lung diseases (ILDs) lead to increased morbidity and premature deaths, imposing a significant burden on public health worldwide. Recently, several studies have linked ambient air pollution with the acute exacerbation of certain ILDs, but the evidence remains limited and inconclusive. With a multicenter hospital-based case-crossover design, we investigated 9128 patients who resided in Jiangsu province, China, and were admitted for ILDs between 2019 and 2022. Residential exposure to particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM 2.5 ), PM 10 , sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), carbon monoxide (CO), and ozone (O 3 ) was assessed using our validated grid datasets. We fitted conditional logistic regression models to examine associations of exposure to air pollutants with ILD admission. A 10 µg/m 3 increment of exposure to SO 2 and NO 2 was positively associated with a 16.18 % (95 % confidence interval [CI]: 3.79 %, 30.03 %) and 4.06 % (0.75 %, 7.49 %) increase in odds of ILD admission, respectively. All these associations appeared to be linear and the association of SO 2 exposure was significantly stronger among older adults. We estimated that over 10 % of ILD admissions could be attributable to exposure to SO 2 and NO 2 . This study provides compelling evidence on the association of exposure to ambient air pollutants (including SO 2 and NO 2 ) with an increased odds of ILD hospitalizations. Our findings indicate that SO 2 and NO 2 exposures can lead to the exacerbation of ILDs, especially in elderly, and that the disease burden is considerable., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Hong Sun and Yuewei Liu were supported by Jiangsu Provincial Health Commission. 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.)

Air pollutants have been investigated to be associated with many health issues. Recently, increasing epidemiological studies have suggested the association between air pollution exposure and risk of frailty with inconsistent findings. This systematic review and meta-analysis was to summarize and evaluate effects of exposure to various air pollutants on risk of frailty. PubMed, Embase, Scopus and Web of Science were systematically searched for relevant studies published before May 11, 2024. Studies that explored the potential relationship between exposure to air pollutants (PM 2.5 , PM 10 , O 3 , NO x , solid fuel, secondhand tobacco, and air quality) and risk of frailty were included. The quality of cross-sectional and cohort studies was evaluated using an eight-item assessment instrument for epidemiological studies and Newcastle-Ottawa Scale, respectively. A total of 9,929 papers were retrieved, of which 20 met the inclusion criteria. Meta-analysis indicated that PM 2.5 exposure was significantly associated with frailty assessed by the frailty index [OR (95% CI): 1.24 (1,11-1.38) per 10 μg/m 3 increment]. Moreover, solid fuel exposures were significantly associated with an increased risk of frailty assessed by the frailty phenotype [OR (95% CI): 1.91 (1.09-3.34)] or the frailty index [OR (95% CI): 1.25 (1.11-1.41)]. Exposure to PM 2.5 and solid fuel increases the risk of frailty. Environmental protection policies and public health measures should be developed to reduce PM 2.5 concentrations. Effective measures, such as improving stoves and using clean fuels, should be taken to reduce indoor air pollution levels., 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 Ltd. All rights reserved.)

Epidemiologic research and quantitative risk assessment play a crucial role in transferring fundamental scientific knowledge to policymakers so they can take action to reduce the burden of ambient air pollution. This commentary addresses several challenges in quantitative risk assessment of air pollution that require close attention. The background to this discussion provides a summary of and conclusions from the epidemiological evidence on ambient air pollution and health outcomes accumulated since the 1990s. We focus on identifying relevant exposure-health outcome pairs, the associated concentration-response functions to be applied in a risk assessment, and several caveats in their application. We propose a structured and comprehensive framework for assessing the evidence levels associated with each exposure-health outcome pair within a health impact assessment context. Specific issues regarding the use of global or regional concentration-response functions, their shape, and the range of applicability are discussed., Competing Interests: Declarations Ethics approval and consent to participate There was no need to consent as there are no individual data. Consent for publication There was no need of consent. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Background: The prevalence of eczema has increased with industrialization. Industrial practices generate ambient air pollution, including fine particulate matter of diameter ≤ 2.5μm (PM2.5). Studies investigating the relationship between PM2.5 and eczema in the US are scarce. The objective of this study was to determine the risk of eczema with PM2.5 exposure in a diverse national cohort of American adults., Methods: In this cross-sectional study, eczema cases in the All of Us Research Program were linked via three-digit zip code to average annual PM2.5 concentrations from the Center for Air, Climate, and Energy Solutions. Eczema cases and controls were compared using Pearson's χ2 test for categorical variables and one-way analysis of variance for continuous variables. The relationship between PM2.5 and eczema was assessed via logistic regression adjusting for demographic factors, smoking, and atopic comorbidities., Results: Individuals with eczema (n = 12,695) lived in areas with significantly higher PM2.5 concentrations than did individuals without eczema (n = 274,127) (0.83 x 10 μg/m3 v. 0.81 x 10 μg/m3, P < .001). PM2.5 concentration was significantly associated with eczema in univariable analysis (odds ratio 1.97, 95% confidence interval 1.77-2.19, P < .001), and in multivariable analyses, both controlling for demographics and smoking status (odds ratio 2.21, 95% confidence interval 1.98-2.47, P < .001) and with the addition of atopic comorbidities (odds ratio 2.38, 95% confidence interval 2.12-2.67, P < .001)., Conclusions: The odds of eczema increased with greater PM2.5 concentration in this large, diverse, adult American cohort. Ambient air pollution is an environmental hazard that influences inflammatory skin disease, suggesting possible targeted interventions., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Chen 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.)

Air pollution is one of the leading causes of early deaths worldwide, with particulate matter (PM) as an emerging factor contributing to this trend. PM is classified based on its physical size, which ranges from PM 10 (diameter ≤10 μm) to PM 2.5 (≤2.5 μm) and PM 0.5 (≤0.5 μm). Smaller-sized PM can move freely through the air and readily infiltrate deep into the lungs, intensifying existing health issues and exacerbating complications. Lung complications are the most common issues arising from PM exposure due to the primary site of deposition in the respiratory system. Conditions such as asthma, COPD, idiopathic pulmonary fibrosis, lung cancer and various lung infections are all susceptible to worsening due to PM exposure. PM can epigenetically modify specific target sites, further complicating its impact on these conditions. Understanding these epigenetic mechanisms holds promise for addressing these complications in cases of PM exposure. This involves studying the effect of PM on different gene expressions and regulation through epigenetic modifications, including DNA methylation, histone modifications and microRNAs. Targeting and manipulating these epigenetic modifications and their mechanisms could be promising strategies for future treatments of lung complications. This review mainly focuses on different epigenetic modifications due to PM 2.5 exposure in the various lung complications mentioned above., Competing Interests: Conflict of interest: All the authors have nothing to disclose., (Copyright ©The authors 2024.)

To investigate air pollution's effect in the form of PM 2.5 (particulate matter measuring less than 2.5 microns) on head and neck aerodigestive cancer incidence, an epidemiological cohort analysis was performed using data from the Surveillance Epidemiology and End Results national cancer database from the years 2002-2012. The relationship between US county mean PM 2.5 levels and head and neck cancer (HNC) incidence rates were examined using a linear mixed model. Lagged effect of the pollutant's effect on HNC incidence was analyzed. Our results showed a significant association between the incidence of HNC and certain subtypes with PM 2.5 exposure after controlling for demographic characteristics, smoking and alcohol use. We observed the highest association at a 5-year lag period (β = 0.24, p value < 0.001). We observed significant associations at no lag (β = 0.16, p value = 0.02) and up to a 20-year lag period (β = 0.15, p value < 0.001). PM 2.5 exposure is associated with an increased incidence of HNC, with the strongest association at a 5-year lag period. To better understand the relationships between exposure and cancer pathogenesis, further subgroup analysis is needed., Competing Interests: Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Purpose The relationship between exposure doses of 2.5-micrometer Particulate Matter (PM 2.5 ), Inhalable particles (PM 10 ), Sulfur Dioxide (SO 2 ), Nitrogen Dioxide (NO 2 ) and Ozone (O 3 ) in the first trimester and spontaneous abortion of pregnant women was evaluated by global average method and nearest monitoring station method, respectively. Method Retrospective analysis of the clinical data of pregnant women with spontaneous abortion and full-term pregnant women in the Department of Obstetrics and Gynecology of two third-class hospitals in a valley city in Northwest China. According to the age factor, the eligible pregnant women were matched at a ratio of 1 : 4. The global average method and the nearest monitoring station method were used to evaluate the exposure of pollutants. The rank-sum test and conditional logistic regression were used to analyze the correlation between air pollutants and spontaneous abortion. Results Although the global average method and the nearest monitoring station method are slightly different in the assessment of exposure dose, they do not affect the correlation evaluation with spontaneous abortion. The exposure of pregnant women to PM 2.5 (OR 1  = 1.156, OR 2  = 1.036), SO 2 (OR 1  = 1.432, OR 2  = 1.429) and NO 2 (OR 1  = 1.121, OR 2  = 1.159) in the first trimester is related to the occurrence of spontaneous abortion.(OR 1 : the global average method, OR 2 : the nearest monitoring station method) Conclusion The exposure of PM 2.5 , SO 2 and NO 2 in the first trimester in valley cities is associated with the occurrence of spontaneous abortion in pregnant women., Competing Interests: Declarations Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

The study aimed to analyse the association between the digit ratio in adult women and the degree of air pollution (suspended particulate matter, sulphur dioxide, nitric dioxide, benzene levels) in the place of residence of their mothers during pregnancy. The data was collected from female students in several Polish cities. Measurements were taken, and questionnaire data were collected. 2D:4D ratios were calculated for the left and the right hand. The ratio was analysed as a continuous variables. Air quality information was retrieved from reports by the Chief Inspectorate for Environmental Protection. Statistically significant differences both in right- and left-hand 2D:4D ratio were found for PM 10 and benzene. In addition, the right-hand 2D:4D differed significantly depending on PM 2.5 . The association between digit ratio and the complex air pollution index was also found. Poor air quality was associated with higher values of the ratio. Our results indicate that a high airborne pollutant level, especially suspended particulate matter, is associated with a higher digit ratio., (© 2024. The Author(s).)

Background: Air pollution exposure poses significant health risks for the general population, but particularly for women with acute and chronic respiratory conditions. Given the increasing global burden of air pollution-related illnesses, understanding these biomarkers is crucial for developing targeted interventions and improving respiratory health outcomes in vulnerable populations. In this systematic review, we aimed to determine potential dysregulated respiratory inflammatory blood biomarker candidates in adult female patients who experience varying levels and sources of inhaled pollutant exposure., Methods: We searched the Cochrane Library, PubMed, and Web of Science with nuanced search terms to retrieve articles published in English between 1 January 2000 and 12 June 2023, to ensure relevancy. We filtered our findings to generate a focussed narrative analysis and used the Risk of Bias In Non-randomized Studies-of Exposures (ROBINS-E) and Risk-of-bias VISualization (robVIS) tools to ensure the validity of the data and the quality of the conclusions being made., Results: We identified 916 articles from the databases used in our search, 16 of which met the criteria of our focussed narrative analysis. Among blood biomarkers, platelet-activating factor and eosinophilia could be used to assess the severity of asthma conditions, as a lack or reduction thereof indicates specific conditions. Pro-inflammatory cytokines require further validation, as some studies with a high risk of bias have reported conflicting results compared to more recent research on whether these markers are up-regulated or down-regulated. We found one study to be at a very high risk of bias, two had a high risk of bias, one had some concerns of confounding factors which may not have affected their results, and 12 studies had a low risk of bias., Conclusions: There were narrowed-down blood biomarker candidates that could be used in future research and avenues of research like generating specific microRNA sequences to test for prognostic/diagnostic tests., Registration: PROSPERO: 42023435721., Competing Interests: Disclosure of interest: The authors completed the ICMJE Disclosure of Interest Form (available upon request from the corresponding author) and disclose no relevant interests., (Copyright © 2024 by the Journal of Global Health. All rights reserved.)

Background: Although numerous studies have discussed about the impact of air pollution on cognitive function, a consensus has yet to be reached, necessitating further exploration of their relationship. The aim of this study is to reveal the effects of major air pollutants on cognitive function in Chinese middle-aged and older adults, while considering the lagged effects of pollution., Methods: Panel data were constructed by integrating the air pollutants concentration (particulate matter diameter ≤1 µm (μm) (PM 1 ), PM 2.5 , PM 10 , nitrogen dioxide (NO 2 ), and ozone (O 3 )) among 28 provinces in China and the personal characteristics from China Health and Retirement Longitudinal Study participants during the period of 2011-2015. To explore the effects of single pollutants and their interactions on cognitive function, panel linear regression using ordinary least squares method was employed, and first-order lag effects (two-year interval) of air pollution were introduced into the models., Results: Our study revealed that, after adjusting for confounding factors, higher levels of particulate matter (PM 1 , coefficient (Coef.) = -0.093, P = 0.001; PM 2.5 , Coef. = -0.051, P = 0.001; PM 10 , Coef. = -0.030, P = 0.001) and NO 2 (Coef. = -0.094, P = 0.006) were associated with lower cognitive function scores among the participants. Moreover, the interaction between the five major pollutants exhibited a negative effect on cognitive function(Coef. = -2.89, P = 0.004)., Conclusions: PM 1 , PM 2.5 , PM 10 have detrimental effects on the cognitive function of middle-aged and elderly adults in China, where increasing particle diameter correlates with a less negative impacts, providing theoretical underpinnings for the formulation of environmental protection policies., Competing Interests: Disclosure of interest: The authors completed the ICMJE Disclosure of Interest Form (available upon request from the corresponding author) and disclose no relevant interests, (Copyright © 2024 by the Journal of Global Health. All rights reserved.)

Background: There is limited evidence regarding the modifying effects of parents' age at childbirth on the relationship between air pollution and obesity in plateau areas. This study aimed to explore the association between particulate matter (PM) and child obesity, specifically investigating whether parents' age at childbirth could modify this relationship in the Tibetan plateau, China., Methods: Satellite-based random forest models were used to estimate the concentrations of PM 2.5 (particulate matter with aerodynamic diameters ≤ 2.5 μm), PM c (particulate matter with aerodynamic diameters between 2.5 μm and 10 μm), and PM 10 (particulate matter with aerodynamic diameters ≤ 10 μm). Linear and logistic regression models were employed to assess associations between PM exposure and obesity indicators, and effect estimates of PM across different particle sizes were compared., Results: The study comprised 2,015 children under five years old. Postnatal exposure to PM was positively associated with overweight and obesity (OWO), waist-to-hip ratio (WHR) and body mass index (BMI). Among these pollutants, PM 10 exhibited the strongest association with BMI and OWO, whereas PM c showed the strongest association with WHR. An interquartile range (IQR) increase in PM 2.5 (5.67 µg/m 3 ), PM c (5.25 µg/m 3 ), and PM 10 (11.06 µg/m 3 ) was positively associated with OWO (odd ratio [OR] for PM 2.5 = 1.52, 95% confidence interval [CI] for PM 2.5 = 1.24 to 1.85; OR for PM c = 1.50, 95% CI for PM c = 1.19 to 1.88; OR for PM 10  = 1.56, 95% CI for PM 10  = 1.25 to 1.96), respectively. Stratified analysis by parents' age at childbirth indicated that the effects of PM on obesity indicators were more pronounced in the advanced age group., Conclusions: Long-term exposure to PM was positively associated with OWO, WHR, and BMI. Our findings also underscore the importance of examining the effects of ambient PM exposure on OWO, particularly in parents of advanced age at childbirth., (© 2024. The Author(s).)

There is a growing interest in the health impacts of PM 2.5 originating from landscape fires. We conducted a time-series study to investigate the association between daily exposure to landscape fire PM 2.5 and hospital admissions for cardiovascular events in 184 major Chinese cities. We developed a machine learning model combining outputs from chemical transport models, meteorological information and observed air pollution data to determine daily concentrations of landscape fire PM 2.5 . Furthermore, we fitted quasi-Poisson regression to evaluate the link between landscape fire PM 2.5 concentrations and cardiovascular hospitalizations in each city, and conducted random-effects meta-analysis to pool the city-specific estimates. Here we show that, on a national scale, a rise of 1-μg/m 3 in landscape fire PM 2.5 concentrations is positively related to a same-day 0.16% (95% confidence interval: 0.01%-0.32%) increase in hospital admissions for cardiovascular disease, 0.28% (0.12%-0.44%) for ischemic heart disease, and 0.25% (0.02%-0.47%) for ischemic stroke. The associations remain significant even after adjusting for other sources of PM 2.5 . Our findings indicate that transient elevation in landscape fire PM 2.5 levels may increase risk of cardiovascular diseases., (© 2024. The Author(s).)

We estimated the association between combined exposure to air pollutants and the development of cardiometabolic multimorbidity (CM) and all-cause mortality. An air pollution score was calculated to determine the combined exposure to five air pollutants. CM was defined as the instance of at least two types of diseases. A genetic risk score (GRS) was calculated for each individual. A multistate regression model was used to investigate the effect of the combined associations of air pollutants on each stage of CM progression. After multivariable adjustment, the air pollution score was related with greater susceptibility of CM and all-cause mortality, and those with a high GRS for cardiovascular disease (CVD) or coronary heart disease (CHD) and a high air pollution score had a greater susceptibility of incident CM and all-cause mortality. The multistate model revealed that the greater air pollution score was connected with the susceptibility of progressing from disease-free baseline to having one cardiometabolic disease, and next to CM, and eventually to death. Combined exposure to five air pollutants were related with greater susceptibility of CM and all-cause mortality in a dose-dependent style and is related with the progression of CM and with all-cause mortality., (© 2024. The Author(s).)

Background: During the COVID-19 pandemic, non-therapeutic interventions (NPIs), such as traffic restrictions, work stoppages, and school suspensions, have led to a sharp decline in the concentration of air pollutants in the epidemic sites. However, few studies focused on the impact of air pollutant changes on the risk of nonaccidental death., Method: We selected Yancheng City, China, as the study site and applied a Generalized Additive Model (GAM) based on the quasi-Poisson distribution to evaluate the impact of atmospheric pollutants exposure on the nonaccidental death of local residents. The time span of this study was set from January 1, 2013, to December 21, 2022, that is, before and after the outbreak of COVID-19., Results: The concentration of some air pollutants has greatly varied after the outbreak of COVID-19, with a significant decline for PM 2.5 (- 43.4%), PM 10 (- 38.5%), SO 2 (- 62.9%), and NO 2 (- 22.6%), but an increase for O 3 (+ 4.3%). Comparative analysis showed that PM 2.5 contributed to an increased risk of nonaccidental death after the outbreak of COVID-19. With an increase in PM 2.5 by 10 µg/m³, the excess relative risks (ER) of nonaccidental death of residents increased by 1.01% (95%CI: 0.19%,1.84%). The stratified analysis revealed that air pollutants impacted nonaccidental deaths in both men and women before the outbreak of COVID-19. After the outbreak of COVID-19, PM 10 had a significant effect on male nonaccidental deaths. The concentrations of PM 2.5 , PM 10 , and SO 2 increased by 10 µg/m³, the ER of PM 2.5 , PM 10 , and SO 2 on female nonaccidental death increased by 1.52% (0.38%,2.67%), 0.58% (0.02%,1.13%), and 15.09% (5.73%,25.28%), respectively. Before the outbreak of COVID-19, five air pollutants had an impact on the death of residents from cardiovascular disease (CVD). After the outbreak of COVID-19, only PM 10 significantly affected the death risk of CVD. In addition, we discovered that PM 2.5 , PM 10 , and SO 2 significantly impacted the risk of death due to respiratory diseases before and after the outbreak of COVID-19., Conclusions: Air pollutants have different effects on nonaccidental deaths before and after the COVID-19 outbreak. A decrease in air pollutant concentration due to the NPIs for COVID-19 had a significant effect on the reduction of the risk of nonaccidental death., (© 2024. The Author(s).)

Air pollution, mostly from fossil fuel sources, is the leading environmental cause of global morbidity and mortality and is intricately linked to climate change. There is emerging evidence indicating that air pollution imposes most of its risk through proximate cardiovascular kidney and metabolic (CKM) etiologies. Indeed, there is compelling evidence linking air pollution to the genesis of insulin resistance, type 2 diabetes, hypertension, and other risk factors. Air pollution frequently coexists with factors such as noise, with levels and risks influenced substantially by additional factors such as social determinants and natural and built environment features. Persistent disparities regarding the impact and new sources of air pollution, such as wildfires attributable to climate change, have renewed the urgency to better understand root sources, characterize their health effects, and disseminate this information for personal protection and policy impacts. In this review, we summarize evidence associating air pollution with cardiovascular health, the impact of air pollution on CKM health, and how interactions with other exposures and personal characteristics may modify these associations. Finally, we discuss new integrated approaches to capture risk from air pollution in the context of an exposomic framework., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

Importance: The associations of exposure to fine particulate matter (PM2.5) and its constituents with spontaneous preterm birth (sPTB) remain understudied. Identifying subpopulations at increased risk characterized by socioeconomic status and other environmental factors is critical for targeted interventions., Objective: To examine associations of PM2.5 and its constituents with sPTB., Design, Setting, and Participants: This population-based retrospective cohort study was conducted from 2008 to 2018 within a large integrated health care system, Kaiser Permanente Southern California. Singleton live births with recorded residential information of pregnant individuals during pregnancy were included. Data were analyzed from December 2023 to March 2024., Exposures: Daily total PM2.5 concentrations and monthly data on 5 PM2.5 constituents (sulfate, nitrate, ammonium, organic matter, and black carbon) in California were assessed, and mean exposures to these pollutants during pregnancy and by trimester were calculated. Exposures to total green space, trees, low-lying vegetation, and grass were estimated using street view images. Wildfire-related exposure was measured by the mean concentration of wildfire-specific PM2.5 during pregnancy. Additionally, the mean exposure to daily maximum temperature during pregnancy was calculated., Main Outcomes and Measures: The primary outcome was sPTB identified through a natural language processing algorithm. Discrete-time survival models were used to estimate associations of total PM2.5 concentration and its 5 constituents with sPTB. Interaction terms were used to examine the effect modification by race and ethnicity, educational attainment, household income, and exposures to green space, wildfire smoke, and temperature., Results: Among 409 037 births (mean [SD] age of mothers at delivery, 30.3 [5.8] years), there were positive associations of PM2.5, black carbon, nitrate, and sulfate with sPTB. Adjusted odds ratios (aORs) per IQR increase were 1.15 (95% CI, 1.12-1.18; P < .001) for PM2.5 (IQR, 2.76 μg/m3), 1.15 (95% CI, 1.11-1.20; P < .001) for black carbon (IQR, 1.05 μg/m3), 1.09 (95% CI, 1.06-1.13; P < .001) for nitrate (IQR, 0.93 μg/m3), and 1.06 (95% CI, 1.03-1.09; P < .001) for sulfate (IQR, 0.40 μg/m3) over the entire pregnancy. The second trimester was the most susceptible window; for example, aORs for total PM2.5 concentration were 1.07 (95% CI, 1.05-1.09; P < .001) in the first, 1.10 (95% CI, 1.08-1.12; P < .001) in the second, and 1.09 (95% CI, 1.07-1.11; P < .001) in the third trimester. Significantly higher aORs were observed among individuals with lower educational attainment (eg, less than college: aOR, 1.16; 95% CI, 1.12-1.21 vs college [≥4 years]: aOR, 1.10; 95% CI, 1.06-1.14; P = .03) or income (<50th percentile: aOR, 1.17; 95% CI, 1.14-1.21 vs ≥50th percentile: aOR, 1.12; 95% CI, 1.09-1.16; P = .02) or who were exposed to limited green space (<50th percentile: aOR, 1.19; 95% CI, 1.15-1.23 vs ≥50th percentile: aOR, 1.12; 95% CI, 1.09-1.15; P = .003), more wildfire smoke (≥50th percentile: aOR, 1.19; 95% CI, 1.16-1.23 vs <50th percentile: aOR, 1.13; 95% CI, 1.09-1.16; P = .009), or extreme heat (aOR, 1.51; 95% CI, 1.42-1.59 vs mild temperature: aOR, 1.11; 95% CI, 1.09-1.14; P < .001)., Conclusions and Relevance: In this study, exposures to PM2.5 and specific PM2.5 constituents during pregnancy were associated with increased odds of sPTB. Socioeconomic status and other environmental exposures modified this association.

Considering the limited information on the impact of PM 2.5 content on ocular health, a follow-up study was conducted on 50 healthy adults. Samples were collected twice, once before the PM 2.5 exposure season and again after exposure. Daily PM 2.5 concentration data was gathered from Thung Satok monitoring station. All subjects completed the self-structured ocular symptom questionnaire. The concentrations of 1-OHP were determined using HPLC-FLD. Logistic regression analysis investigated the relationship between PM 2.5 toxicity and ocular symptoms. The findings revealed that daily PM 2.5 concentrations surpassed the WHO-recommended range by around threefold. Exposure to PM 2.5 significantly raised the likelihood of ocular redness (adjusted OR: 12.39, 95% CI), watering (adjusted OR: 2.56, 95% CI), and dryness (adjusted OR: 5.06, 95% CI). Additionally, these symptoms had an exposure-response relationship with increasing 1-OHP levels. Ocular symptoms worsened in frequency and severity during the high PM 2.5 season, showing a strong link to elevated PM 2.5 levels. Lymphocyte counts were also positively correlated with redness, watering, and dryness during high PM 2.5 exposure. In conclusion, our study shows that subjects exposed to higher PM 2.5 levels presented more significant ocular surface alterations., (© 2024. The Author(s).)

Background: Eosinophil activation is associated with asthma. Whether air pollution affects the activation of blood eosinophils in patients with asthma remains unknown. In this study, we investigated the correlation between transcriptional activity in eosinophils and air pollutant exposure in patients receiving different levels of Global Initiative for Asthma (GINA) treatment., Methods: We evaluated the expression levels of activation- and function-related genes in eosinophils from patients with GINA 4 or 5 (n = 20), those with GINA 3 (n = 12), and normal individuals (n = 7); the eosinophils were activated with interleukin (IL)-5 or IL-17. A land use regression model was used to estimate air pollutant exposure. The correlations between mRNA expression, lung function, and air pollutant exposure were investigated., Results: The expression levels of TGFB1, IL7R, and TLR3 were significantly higher for patients with GINA 4 or 5 than for those with GINA 3 or normal individuals. The expression of certain genes, particularly in IL-17-activated eosinophils, was correlated with lung function decline in patients with GINA 4 or 5. For patients with GINA 4 or 5, NO 2 exposure was correlated with upregulated TGFB1 expression in IL-5-activated eosinophils. For patients with GINA 3, O 3 exposure was correlated with upregulated CCR5, IL5RA, IL7R, and TGFB1 expression in IL-17-activated eosinophils and upregulated IL7R expression in IL-5-activated eosinophils., Conclusion: Patients with GINA 4 or 5 may exhibit elevated transcriptional activity in eosinophils; this elevation is correlated with lung function decline. Air pollution may affect eosinophil mRNA expression in patients with asthma., (© 2024 The Author(s). Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.)

It is important to understand the effects of environmental factors such as air pollution on mitochondrial structure and function, especially when these changes increase cardiovascular disease risk. Although lifestyle choices directly determine many mitochondrial diseases, increasingly, it is becoming clear that the structure and function of mitochondria may be affected by pollutants found in the atmosphere (e.g., gases, pesticides herbicide aerosols, or microparticles). To date, the role of such agents on mitochondria and the potential impact on cardiovascular fitness is neglected. Here we offer a review of airborne stressors and pollutants, that may contribute to impairments in mitochondrial function and structure to cause heart disease., (© 2024 The Author(s). Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Background: Obesity, characterized by excessive or abnormal fat accumulation, is a major public health concern. Air pollution is a significant potential obesogenic factor, but the clear direct and indirect correlations between air pollution and obesity remain unclear. This study aims to provide a comprehensive understanding of the relationship between air pollution and obesity by identifying both direct and indirect causal correlations., Methods: We used nationally representative data from the China Family Panel Survey. Air pollution concentrations were quantified as the mass (μg) of air pollutants per cubic meter (m 3 ) based on nationally representative statistical data. To minimize statistical bias inherent in traditional methods, the direct relationship between air pollution and obesity was estimated using a regression discontinuity model, while the potential underlying mechanisms were explored through structural equation modeling., Results: Air pollution was generally positively associated with overweight/obesity ( O R O W A Q I = 1.109, [95%CI = 1.027:1.305], O R O B A Q I = 1.032, [95%CI = 1.006:1.217], O R SO A Q I = 1.069, [95%CI = 1.014:1.208], PM 2.5 and PM 10 positively affected overweight/obesity ( O R O W PM 2.5 = 1.173, [95%CI = 1.094:1.252], O R O B PM 2.5 = 1.022, [95%CI = 1.016:1.028], O R SO PM 2.5 = 1.035 [95%CI = 1.015:1.055], O R O W PM 10 = 1.053, [95%CI = 1.030:1.076], O R O B PM 10 = 1.008 [95%CI = 1.006:1.010], O R SO PM 10 = 1.013 [95%CI = 1.007:1.019]), and SO 2 and CO posed negative impacts on overweight/obesity ( O R O W SO 2 = 0.972, [95%CI = 0.965:0.979], O R O B SO 2 = 0.997, [95%CI = 0.996:0.998], O R SO SO 2 = 0.994, [95%CI = 0.991:0.997], O R O W C O = 0.986, [95%CI = 0.980:0.992], O R O B C O = 0.998, [95%CI = 0.997:0.999], O R SO C O = 0.999, [95%CI = 0.998:0.999]). The impact of air pollution on overweight/obesity was more significant among men, older individuals, and rural populations compared to women, younger individuals, and urban populations. Furthermore, the relationship between air pollution and overweight/obesity was mediated by social behavior determinants, including physical activity ( β = 0.18, [95%CI = 0.04:0.29]), sedentary behavior ( β = 0.12, [95%CI = 0.04:0.16]), sleep (β = 0.06, [95%CI = 0.02:0.13], smoking (β = 0.07, [95%CI = 0.02:0.15]), alcohol consumption (β = 0.08, [95%CI = 0.04:0.11]), and mental health (β = 0.06, [95%CI = 0.01:0.09])., Conclusion: Air pollution was generally associated with an increased risk of overweight and obesity, with PM 2.5 and PM 10 having a positive influence, while SO 2 and CO had a negative impact. The effect of air pollution was more pronounced among men, older individuals, and rural populations compared to women, younger individuals, and urban populations. Additionally, social behavior factors, such as physical activity, sedentary behavior, sleep, smoking, alcohol consumption, and mental health, predominantly mediated the relationship between air pollution and obesity., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yu, Xie and Liu.)

Introduction: Prenatal and early-life exposure to air pollution and extreme temperatures are associated with childhood asthma and wheeze. However, potential windows of susceptibility and their sex-specific and interactive effects have not been fully elucidated. We aimed to identify critical windows of susceptibility and evaluate sex-specific effects in these associations, and evaluate exposure interactions., Methods: We analyzed data from 468 mother-child pairs enrolled in the PROGRESS birth cohort in Mexico City. Daily residential levels of PM 2.5 , NO 2 , and temperature were generated from our validated spatiotemporally resolved models from conception to age 4 years. Childhood asthma and wheeze outcomes were collected at 4-6 and 7-8 years. Distributed lag nonlinear models (DLNMs) were used to identify susceptible windows for prenatal weekly-specific and postnatal monthly-specific associations of air pollution and temperature with respiratory outcomes adjusting for covariates. To evaluate sex-specific effects, DLNMs were stratified. Joint effects were assessed using relative excess risk due to interaction and attributable proportion., Results: Mid-gestation was a critical window for both PM 2.5 (weeks 20-28, cumulative OR: 1.18 [95% CI: 1.01, 1.37]; weeks 19-26, cumulative OR: 1.18 [95% CI: 1.02, 1.36]) and NO 2 (weeks 18-25, cumulative OR: 1.16 [95% CI: 1.02, 1.31]) exposure, associated with higher odds of wheeze. Postnatal exposure to PM 2.5 and NO 2 during the first year of life was also linked to higher odds of wheeze. The warmer and colder temperatures showed mixed effects on respiratory outcomes. We observed a synergistic interaction between high PM 2.5 and high temperature exposure during the first year of life, associated with higher odds of current wheeze. The associations of prenatal air pollution and temperature exposure with respiratory outcomes were more pronounced in males., Conclusions: Early-life air pollution exposure contributes to the development of childhood asthma and wheeze, while exposure to temperature showed mixed associations with respiratory outcomes., 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 Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Being unhoused can increase vulnerability to adverse health effects due to air pollution. We aimed to quantify changes in emergency-department visits during and after exposure to wildfire-specific and non-wildfire particulate matter 2·5 μm or less in diameter (PM 2·5 ) in San Diego County (CA, USA) in people who were both unhoused and housed., Methods: For this time-stratified case-crossover study, we used data on exposure to wildfire-specific PM 2·5 in California and individual-level data for people admitted to the emergency departments of two hospitals (UC San Diego Health emergency departments at La Jolla and Hillcrest, San Diego) in San Diego County between July 1, 2012, and Dec 31, 2020. People with a postcode outside of San Diego County were excluded. Demographic information was age group, race or ethnicity, and transport to the emergency department. Wildfire-specific PM 2·5 concentration at the postcode level was previously estimated using an ensemble model that combined multiple machine-learning algorithms and explanatory variables obtained via data on 24-h mean PM 2·5 concentrations from the US Environmental Protection Agency Air Quality System. Conditional logistic regression models were applied, adjusting for specific humidity, wind velocity, and maximum temperature extracted from the US Gridded Surface Meteorological Dataset. Housing status was established by registration staff or triage nurses on arrival at the emergency department. For people who were unhoused, exposure was defined based on the weighted mean PM 2·5 concentration at the city level proportional to the number of people who were unhoused in each specific city across urban centres in San Diego County. For people who were housed, we used residence postcode to measure exposure. We assessed the association between PM 2·5 from wildfire and non-wildfire sources and emergency-department visits in people who were housed and unhoused., Findings: There were 587 562 emergency-department visits at the two hospitals, 76 407 (13·0%) of which were by people who were unhoused. People who were housed had a higher exposure to overall PM 2·5 (24-h mean over the study period of 9·904 mg/m 3 , SD 3·445) and non-wildfire PM 2·5 (9·663, 2·977) than people who were unhoused (9·863, 3·221; 9·557, 2·599). However, people who were unhoused had a higher exposure to wildfire-specific PM 2·5 (0·305, 1·797) than people who were housed (0·240, 1·690). Overall PM 2·5 exposure was associated with increased odds of emergency-department visits for both people who were housed (odds ratio 1·003, 95% CI 1·001-1·004 per 1 μg/m 3 PM 2·5 for 0-3 days after exposure) and people who were unhoused (1·004, 1·000-1·008 for 0-3 days after exposure). We found that non-wildfire PM 2·5 was associated with emergency-department visits among people who were housed (1·003, 1·002-1·005 for 0-3 days after exposure) and wildfire-specific PM 2·5 was associated with emergency-department visits in people who were unhoused (1·006, 1·001-1·011 for 0-3 days after exposure)., Interpretation: People who were unhoused in San Diego County were more likely to visit emergency departments after exposure to increased wildfire-specific PM 2·5 . As the intensity and frequency of wildfires increase, understanding risk factors for vulnerable populations, such as people who are unhoused, is crucial to develop effective adaptation strategies., Funding: US National Institutes of Health, National Institute on Aging., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Limited evidence was available on ambient air pollution and pediatric atopic dermatitis (AD). The study aimed to evaluate the associations between short-term exposure to air pollutants and outpatient visits for pediatric AD. From 2016-2018, we collected data on six criteria air pollutants (PM 2.5 , PM 10 , NO 2 , SO 2 , CO and O 3 ) and daily outpatient visits for pediatric AD in 66 hospitals, covering all districts in Shanghai, China. The over-dispersed Poisson generalized additive model (GAM) was applied to fit the associations of criteria air pollutants with hospital visits. Two-pollutant models were fitted and stratified analyses by sex, age and season were conducted. We identified 477,833 outpatient visits for pediatric AD. Each interquartile range (IQR) increase in PM 2.5 (IQR: 30.9 μg/m 3 ), PM 10 (8.9 μg/m 3 ), NO 2 (25.5 μg/m 3 ), SO 2 (5.8 μg/m 3 ) and CO (0.283 mg/m 3 ) on the concurrent day was significantly associated with increments of 2.08 % (95 % CI: 0.53 %, 3.65 %), 2.53 % (95 % CI: 0.87 %, 4.22 %), 8.14 % (95 % CI: 6.24 %, 10.08 %), 5.67 % (95 % CI: 3.58 %, 7.80 %), and 2.27 % (95 % CI: 0.70 %, 3.87 %) in pediatric AD outpatient visits, respectively. The effects of NO 2 remained robust after adjustment for other air pollutants. The exposure-response curves for PM 2.5 and PM 10 were steeper for moderate-lower concentrations, with a flatten curves at high concentration; nearly linear relationships were found for NO 2 . Higher associations of NO 2 exposure on AD were detected in children under 6 years old (p=0.01); and we observed larger effect of air pollutants in cool seasons (p<0.001 for PM 2.5 , PM 10 , NO 2 and CO; p=0.043 for SO 2 ). This study indicated that short-term exposure to air pollution could increase risk of outpatient visits for pediatric AD., 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.)

Introduction: Air pollution presents a major public health threat to India, affecting more than three quarters of the country's population. In the current project, GEOHealth Health Effects of Selected Environmental Exposomes Across the Life CourSe-India, we aim to study the effect of environmental exposomes-fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), ozone (O 3 ) and extremes of temperature-on multiple health outcomes using a modified life course approach. The associated training grant aims to build capacity in India to address the unique environmental health problems., Methods and Analysis: The project aims to (A) Develop exposure assessments in seven cities, namely Delhi, Chennai, Sonipat, Vizag, Pune, Hyderabad and Bikaner, for: (1) A fine-scale spatiotemporal model for multiple pollutants (PM 2.5 , NO 2 , O 3, temperature); (2) Combined ground monitoring and modelling for major chemical species of ambient PM 2.5 at seven cities; and (3) Personal exposure assessment in a subsample from the six cities, except Pune, and (B) Conduct health association studies covering a range of chronic non-communicable diseases and their risk factors leveraging a unique approach using interdigitating cohorts. We have assembled existing pregnancy, child, adolescent, adult and older adult cohorts across India to explore health effects of exposomes using causal analyses. We propose to use Bayesian kernel machine regression to assess the effects of mixtures of all pollutants including species of PM 2.5 on health while accounting for potential non-linearities and interactions between exposures. This builds on earlier work that constructed a fine spatiotemporal model for PM 2.5 exposure to study health outcomes in two Indian cities., Ethics and Dissemination: Ethical clearance for conduct of the study was obtained from the Institutional Ethics Committee (IEC) of the Centre for Chronic Disease Control, and all the participating institutes and organisations. National-level permission was provided by the Indian Council of Medical Research. The research findings will be disseminated through peer-reviewed publications, policy briefs, print and social media, and communicating with the participating communities and stakeholders. Training of Indian scientists will build the capacity to undertake research on selected adverse environmental exposures on population health in India., 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.)

Background: Ambient air pollution has become a challenging global health issue since industrialization, especially affecting respiratory diseases. However, the causal link between air pollution and allergic respiratory diseases (ARDs) remains unclear due to confounding factors in conventional epidemiological studies across different populations. Thus, we aimed to clarify the causal associations between air pollution and ARDs in European and East Asian populations using Mendelian randomization (MR)., Methods: MR utilizes genetic variants and provides a satisfactory level of causal evidence. Genetic data for exposures (PM 2.5 , PM 2.5 absorbance, PM 10 , PM coarse , NO 2 and NO x ) and outcomes (allergic rhinitis, chronic rhinosinusitis, asthma, and obesity related asthma) were obtained from genome-wide association studies. Instrumental variables were strictly filtered based on core assumptions. Two-sample MR and sensitivity analyses were conducted separately for European and East Asian populations., Results: PM coarse was causally associated with an increased risk of chronic rhinosinusitis (OR = 1.588 [1.002-2.518]; p = 0.049) and obesity related asthma (OR = 1.956 [1.012-3.780]; p = 0.046) in European population, and PM 10 was associated with a decreased risk of allergic rhinitis in East Asian population (OR = 0.882 [0.798-0.974]; p = 0.013). No heterogeneity or pleiotropy was detected in any significant causal association., Conclusion: Our findings indicate that ambient air pollution has opposite impacts on the etiology of ARDs in European and East Asian populations, which provides evidence for decisions on public policies and suggests that different responses to environmental factors such as air pollution may contribute to racial heterogeneity of ARDs., 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.)

Air pollution is one of the main causes of global disease burden, especially in low-income and middle-income countries. Estimation of the current situation and prediction of the future health effects of death and incidence of stroke and coronary heart disease (CHD) attributed to PM 2.5 were done using BenMAP-CE software. Estimating and forecasting the economic burden of these diseases were done in 4 scenarios: Stability of the current PM 2.5 concentration, annual 10 % reduction of PM 2.5 concentration, reduction to 5 µg/m3, and reduction to 12 µg/m3, with three approaches for calculating the economic burden in mortality costs, including the human capital(HC), years of life lost(YLL) and value of statistical life(VSL) was performed. With the stability of the PM 2.5 concentration, the economic burden of stroke attributed to PM 2.5 with the approach of calculating the cost of death with the HC, the YLL, and VSL will reach from 64, 82 and 172 million USD in 2020-849, 1120 and 2703 million USD in 2030 and these costs for CHD in the mentioned approaches of calculating the cost of death will reach respectively from 499, 568 and 898 million USD in 2020-7096, 8088, and 13,621 million USD in 2030. We find that the morbidity economic burden (including direct, indirect, and intangible costs) of stroke compared to the cost of death with the HC, and YLL approaches are 67.58 times, 3.15 times respectively, and in the VSL approach is 47.32 % of stroke death cost. Also, the costs of CHD morbidity economic burden compared to the cost of death in the method of calculating the cost of death with the HC, YLL, and VSL approaches are 42.09, 7.25, and 1.16 times, respectively. This study provides comprehensive baseline information for health policymakers to understand the benefits of air pollution control policies globally, especially in LMICs., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Zohreh Kazemi reports financial support was provided by Iran National Science Foundation. 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.)

Fine particulate matter (PM 2.5 ) is suggested to pose a severe risk to the kidneys by inducing functional degradation and chronic kidney diseases (CKD). This study aims to explore the nephrotoxicity of PM 2.5 exposure and the underlying mechanism. Herein, based on the UK Biobank, it is found that per interquartile range (IQR) increase in PM 2.5 is associated with a 6% (95% CI: 1%-11%), 7% (95% CI: 3%-11%), 9% (95% CI: 4%-13%), 11% (95% CI: 9%-13%), and 10% (95% CI: 8%-12%) increase in the risk of nephritis, hydronephrosis, kidney stone, acute renal failure, and CKD, respectively. In experimental study, noticeable kidney injury, which is the initiation of kidney diseases, is observed with PM 2.5 exposure in C57BL/6N mice (n = 8), accompanied with oxidative stress, autophagy and pyroptosis. In vitro, HK-2 cells with PM 2.5 -stimulation exhibit tubulopathy, increased reactive oxygen species (ROS) generation and activated pyroptosis and autophagy. All changes are abolished by ROS scavenger of N-acetyl-L-cysteine (NAC) both in vivo and in vitro. In conclusion, the study provides evidence showing that PM 2.5 exposure is associated with 5 kinds of kidney diseases by directly inducing nephrotoxicity, in which ROS may be the potential target by triggering autophagy and pyroptosis., (© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.)

Objective: Air pollution is increasing and threatening human health. The objective of this study is to investigate the population distribution characteristics of elderly osteoporosis fractures in Hebei Province and Xinjiang Uygur Autonomous Region and to analyze the effects of air pollutants on the number of elderly osteoporosis fracture inpatients in the two regions., Method: A retrospective collection of elderly osteoporosis fracture cases was conducted in selected hospitals in Hebei Province and Xinjiang Uygur Autonomous Region from January 1, 2018 to December 31, 2022. The chi-square test was used to compare the distributional characteristics of the population in the two regions. Additionally, we used a distributed lag nonlinear model (DLNM) in order to assess the effect of air pollutants on the number of daily hospital admissions of elderly osteoporosis fracture patients in different regions., Result: A total of 19,203 elderly osteoporosis fracture patients were included in the study. The average age of these patients was 76.66 ± 7.55 years, and the majority of them were female (13,514 instances, 70.37%). The disparities in age distribution (χ 2  = 133.9 p < 0.001), fracture site (χ 2  = 62.0 p < 0.001), and hospitalization cost (Z = -15.635 p < 0.001) between the two regions were statistically significant. The lag effect curves of PM2.5, PM10, and NO 2 on the number of elderly osteoporosis fracture hospitalizations in Xinjiang Uygur Autonomous Region exhibited a similar pattern resembling a "W"-shaped curve. All three pollutants reached their highest values after a lag time of 14 days (PM2.5: RR = 1.053, 95% CI: 1.031, 1.074; PM10: RR = 1.031, 95% CI: 1.018, 1.043; NO 2 : RR = 1.125, 95% CI: 1.070, 1.182). In Hebei Province, the largest impacts of PM2.5 and PM10 were observed after a lag of 14 days (PM2.5: RR = 1.022, 95% CI: 1.013, 1.028; PM10: RR = 1.013, 95% CI: 1.008, 1.018). Similarly, the maximum effect of NO 2 was observed after a lag of 11 days (RR = 1.020, 95% CI: 1.010, 1.028)., Conclusion: There were differences in the epidemiological characteristics of hospitalized patients with osteoporosis fractures between the two regions, PM2.5, PM10, and NO 2 increased the number of hospitalizations for osteoporosis fractures. Exposure to air pollutants such as PM2.5 increases the risk of osteoporosis fractures in the elderly population., (© 2024 The Author(s). Orthopaedic Surgery published by Tianjin Hospital and John Wiley & Sons Australia, Ltd.)

Now more than ever, complex socio-ecological challenges require timely and integrated responses from scientists and policymakers. Air quality is one such challenge. Under the Clean Air Act, the U.S. Environmental Protection Agency establishes ambient air quality standards to protect public welfare from known or anticipated adverse effects of air pollutants. As our understanding of the environment and awareness of social values grow, there is a need to improve characterization of "adversity to the public welfare." Scientific assessment can link ecological effects to public welfare using modern scientific approaches that incorporate ecological complexity and multiple value systems held by the public. We propose ideas for the future of scientific assessments meant to inform air quality and other environmental decision-making, including concrete ways we can focus on vulnerable species and ecosystems, incorporate a multiplicity of values, climate and multiple stressors, and partner to diversify the knowledge upon which protective policies are based., (© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

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.)

The present study explores the modifications of cardiovascular autonomic control (CAC) during wake and sleep time and the systemic inflammatory profile associated with exposure to indoor air pollution (IAP) in a cohort of healthy subjects. Twenty healthy volunteers were enrolled. Indoor levels of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ) and volatile organic compounds (VOCs) were monitored using a portable detector for 7 days. Together, a 7-day monitoring was performed through a wireless patch that continuously recorded electrocardiogram, respiratory activity and actigraphy. Indexes of CAC during wake and sleep time were derived from the biosignals: heart rate and low-frequency to high-frequency ratio (LF/HF), index of sympathovagal balance with higher values corresponding to a predominance of the sympathetic branch. Cyclic variation of heart rate index (CVHRI events/hour) during sleep, a proxy for the evaluation of sleep apnea, was assessed for each night. After the monitoring, blood samples were collected to assess the inflammatory profile. Regression and correlation analyses were performed. A positive association between VOC exposure and the CVHRI (Δ% = +0.2% for 1 μg/m 3 VOCs, p = 0.008) was found. The CVHRI was also positively associated with LF/HF during sleep, thus higher CVHRI values corresponded to a shift of the sympathovagal balance towards a sympathetic predominance (r = 0.52; p = 0.018). NO 2 exposure was positively associated with both the pro-inflammatory biomarker TREM-1 and the anti-inflammatory biomarker IL-10 (Δ% = +1.2% and Δ% = +2.4%, for 1 μg/m 3 NO 2 ; p = 0.005 and p = 0.022, respectively). The study highlights a possible causal relationship between IAP exposure and higher risk of sleep apnea events, associated with impaired CAC during sleep, and a pro-inflammatory state counterbalanced by an increased anti-inflammatory response in healthy subjects. This process may be disrupted in vulnerable populations, leading to a harmful chronic pro-inflammatory profile. Thus, IAP may emerge as a critical and often neglected risk factor for the public health that can be addressed through targeted preventive interventions., 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.)

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.)

Air pollution is a critical global health issue that significantly impacts cardiovascular health. The air pollutant PM 2.5 (particulate matter with a diameter of 2.5 micrometres or less) has been positioned as a leading environmental risk factor for morbidity and mortality, especially from cardiovascular diseases (CVDs). Using data from the World Health Organization (WHO), Global Health Observatory, and the United Nations Environment Programme, we explored global trends in air pollution, with a focus on PM 2.5 levels, the implications for cardiovascular health, and the policy measures aimed at reducing their impact. Despite progress in reducing pollution levels in high-income countries, global trends show a limited annual reduction in PM 2.5 concentration. The analysis highlights disparities between regions, with low- and middle-income countries bearing the brunt of air pollution-related CVDs. In 2019 alone, ambient air pollution was responsible for approximately 4.2 million deaths worldwide. Of these, 70% were caused by CVDs, with approximately 1.9 million deaths from ischemic heart disease and 900,000 deaths from stroke. Policy gaps remain a challenge, with many countries lacking adequate legally binding air quality standards. We recommend the adoption of WHO air quality guidelines, enhanced monitoring of air pollution levels, and increased investment in interdisciplinary research to understand the full scope of air pollution's effects on cardiovascular health. Addressing the global cardiovascular crisis linked to air pollution will require coordinated efforts from policymakers, healthcare systems, and global health organisations., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

Background: A large body of data shows that fetal brain development is vulnerable to disruption by air pollution experienced by the mother during pregnancy, adversely affecting cognitive and psychomotor capabilities during childhood (De Asis-Cruz et al., Biol Psychiatry 7:480-90, 2022; Morgan ZEM et al., Environ Health 22:11, 2023). This study has sought to identify gestational windows of susceptibility to prenatal exposure to air pollution., Methods: 470 African American and Latina mother/child pairs participated in a prospective cohort study based in the low-income communities of Northern Manhattan and the South Bronx, New York City. Gestational exposure to respirable particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) was assessed through validated models in relation to cognitive and motor development assessed at ages 1, 2, and 3 years using the Bayley-II Scales. Multiple linear regression models and distributed lag models (DLM) were used to identify critical windows of exposure by trimester and week of pregnancy., Results: By linear regression, average exposures to NO 2 during the first and second trimesters and the entire pregnancy were significantly and negatively associated with the mental developmental index (MDI) at age 1. Average exposures to PM 2.5 during the second trimester and the entire pregnancy were also significantly, inversely associated with age 1 MDI. No significant associations were found between these exposures and MDI at age 2. NO 2 exposure during the first trimester was significantly negatively associated with MDI at age 3. Using DLM, exposures to NO 2 at lags 29-30 weeks (within the first trimester) and PM 2.5 at lags 17-18 weeks (second trimester) were significantly and inversely associated with MDI at age 1. Significant, inverse associations were found between exposures to NO 2 at lag 29 weeks and PM 2.5 at lags 27-29 weeks and children's MDI at age 3. No significant associations were found between psychomotor index (PDI) and prenatal exposures to NO 2 or PM 2.5 at ages 1, 2 or 3., Conclusions: Our finding that prenatal exposure to air pollution in the first and second trimesters was associated with lower scores for cognitive development at ages 1 and 3 is of concern because of the potential consequences of these outcomes for long-term functioning. They underscore the need for stronger policies to protect pregnant individuals and offspring, particularly during vulnerable, early life-stage of development., (© 2024. The Author(s).)

Anthropogenic emissions alter atmospheric composition and therefore the climate, with implications for air pollution- and climate-related human health. Mortality attributable to air pollution and non-optimal temperature is a major concern, expected to shift under future climate change and socioeconomic scenarios. In this work, results from numerical simulations are used to assess future changes in mortality attributable to long-term exposure to both non-optimal temperature and air pollution simultaneously. Here we show that under a realistic scenario, end-of-century mortality could quadruple from present-day values to around 30 (95% confidence level:12-53) million people/year. While pollution-related mortality is projected to increase five-fold, temperature-related mortality will experience a seven-fold rise, making it a more important health risk factor than air pollution for at least 20% of the world's population. These findings highlight the urgent need to implement stronger climate policies to prevent future loss of life, outweighing the benefits of air quality improvements alone., (© 2024. The Author(s).)

Background: Despite progress, under-five mortality remains high, especially in Sub-Saharan Africa and South Asia, where around 13,400 children die daily. Environmental pollutants, including PM2.5 from outdoor air and household air pollution, significantly contribute to these preventable deaths., Methods: This cross-country study combined satellite data with 113 surveys from the IPUMS-DHS dataset (1998-2019) to examine under-five child mortality in 41 developing countries. The integration of Global Annual Particulate Matter with a diameter of 2.5 micrometres or less (PM2.5) Grids from Socioeconomic Data and Applications Center (SEDAC) and geospatial data from the DHS Program enabled a focused analysis of the association between indoor and outdoor air pollution, particularly PM2.5, and child mortality rates using both logistic and multilevel logistic regression models, as well as estimating Population Attributable Fractions (PAF) to quantify the mortality burden attributable to these pollutants., Results: Outdoor air pollution, measured by a one standard deviation increase in PM2.5, significantly increased the risk of child mortality (Odds Ratio [OR]: 1.14; 95% Confidence Interval [CI]: 1.10-1.18; p < 0.001). Moderate and high household air pollution exposure also heightened this risk, with increases of 37% (OR: 1.37; 95% CI: 1.24-1.53; p < 0.001) and 40% (OR: 1.40; 95% CI: 1.26-1.56; p < 0.001), respectively, compared to no exposure. Multilevel models (Models 5a and 10a) produced similar estimates to standard logistic regression, indicating robust associations. Additionally, Population Attributable Fraction analysis revealed that approximately 11.9% of under-five mortality could be prevented by reducing ambient PM2.5 exposure and 12.0% by mitigating household air pollution. The interaction between indoor and outdoor pollution revealed complex dynamics, with moderate and high household exposure associated with a reduction in mortality risk when combined with PM2.5. Geographical disparities were observed, with stronger correlations between outdoor air pollution and child mortality in Africa compared to Asia, and more pronounced impacts in low-income countries. However, household air pollution had stronger association with child mortality in Africa and lower- and middle-income countries., Conclusions: Our findings could serve as a guide for policy development aimed at reducing under-five mortality, ultimately contributing to the attainment of the Sustainable Development Goal (SDGs)., (© 2024. The Author(s).)

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).)

Introduction: This study aimed to elucidate the effects of outdoor air pollution and allergic conjunctivitis and population-based lagged effects of air pollution., Methods: We included data on six major air pollutants, PM 10 , PM 2.5 , carbon monoxide (CO), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), and ozone (O3), and 3325 allergic conjunctivitis outpatient visits in Urumqi, northwest China, from 1 January 2013 to 31 December 2020. We developed quasi-Poisson generalized linear regression models with distributed lagged nonlinear models (DLNM), and single and multi-pollutant models were constructed to investigate single-day and cumulative lagged effects in detail., Results: Our results confirmed that elevated PM 10 and NO 2 levels are significantly associated with increased allergic conjunctivitis outpatient visits with lags of 2 and 3 days respectively, and subgroup analyses further suggest that the effects of PM 10 and NO 2 on allergic conjunctivitis are more pronounced during the warm season. Women are more sensitive to PM 10 exposure and the effect of air pollution on allergic conjunctivitis is influenced by age (e.g., infancy and older people)., Discussion: Our work provides the first time-series study in Urumqi, the world's furthest inland city from the ocean. Further implementation of specific outdoor air pollution controls such as the burning of fossil fuels like coal, as well as special population protection policies remain necessary. Multicenter studies with larger sample sizes are needed., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Liu, Gui, Wang, Wang, Qiao, Tao, Tao, Jiang and Yi.)

Background: Previous studies have typically explored daily lagged relationships among pertussis and meteorology, with little assessment of effect and interaction among pollutants mixtures., Methods: Our researchers collected pertussis cases data from 2017-2022 as well as meteorological and contaminative factors for the Jining region. First, we reported the application of the Moving Epidemic Method (MEM) to estimate epidemic threshold and intensity level. Then we developed a Weighted Quantile Sum (WQS) regression and Bayesian Kernel Machine Regression (BKMR) model to assess single, multiple effects and interaction of meteorological and pollution factors on pertussis cases for different sex, delayed and epidemic threshold groups., Results: There has been a yearly upward trend in the incidence of pertussis in Jining regions. High prevalence threshold years were in 2018-2019, the epidemic peak was mainly concentrated in 32 weeks. Totally, pertussis infections disease was separately 2.1% (95% confidence Interval (CI) = 1.3, 2.8) and 1.1% (95% CI = 0.3, 1.9) higher per decile increase in temperature and sulphur dioxide (SO 2 ). And pertussis infections disease was 1.1% lower per decile increase in humidity. In the different stratified analyses, air pressure was a strong negative effect in males and in the lagged 11-20 days group, with 7.3 and 14.7%, respectively. Sulphur dioxide had a relatively weak positive effect in males, females and the group after 20 days lag, ranging from 0.5 to 0.6%. The main positive effectors affecting the onset of disease at low and high threshold levels were ozone (O 3 ) and SO 2 , respectively, while the negative effectors were SO 2 and carbon monoxide (CO), respectively., Conclusions: This is the first mathematically based study of seasonal threshold of pertussis in China, which allows accurate estimation of epidemic level. Our findings support that short-term exposure to pollutants is the risk factor for pertussis. We should concentrate on pollutants monitoring and effect modeling., Competing Interests: Disclosure of interest: The authors completed the ICMJE Disclosure of Interest Form (available upon request from the corresponding author) and disclose no relevant interests., (Copyright © 2024 by the Journal of Global Health. All rights reserved.)

Background: Short-term exposure to ozone (O 3 ) has been associated with higher stroke mortality, but it is unclear whether this association differs between urban and rural areas. The study aimed to compare the association between short-term exposure to O 3 and ischaemic and haemorrhagic stroke mortality across rural and urban areas and further investigate the potential impacts of modifiers, such as greenness, on this association., Methods: A multi-county time-series analysis was carried out in 19 counties of Shandong Province from 2013 to 2019. First, we employed generalized additive models (GAMs) to assess the effects of O 3 on stroke mortality in each county. We performed random-effects meta-analyses to pool estimates to counties and compare differences in rural and urban areas. Furthermore, a meta-regression model was utilized to assess the moderating effects of county-level features., Results: Short-term O 3 exposure was found to be associated with increased mortality for both stroke subtypes. For each 10-µg/m 3 (lag0-3) rise in O 3 , ischaemic stroke mortality rose by 1.472% in rural areas and 1.279% in urban areas. For each 0.1-unit increase in the Enhanced Vegetation Index (EVI) per county, the ischaemic stroke mortality caused by a 10-µg/m 3 rise in O 3 decreased by 0.60% overall and 1.50% in urban areas., Conclusions: Our findings add to the evidence that short-term O 3 exposure increases ischaemic and haemorrhagic stroke mortality and has adverse effects in urban and rural areas. However, improving greenness levels may contribute to mitigating the detrimental effects of O 3 on ischaemic stroke mortality., (© 2024. The Author(s).)

Following up the previously published systematic review on the same topic and realizing that new studies and evidence had emerged on the matter, we conducted an update on the same research terms. With the objective of updating the information relating environmental risk factors on neurodegenerative diseases and the geographic approaches used to address them, we searched PubMed, Web of Science and Scopus for all scientific studies considering the following three domains: neurodegenerative disease, environmental atmospheric factor and geographical analysis, using the same keywords as in the previously published systematic review. From February 2020 to February 2023, 35 papers were included versus 34 in the previous period, with dementia (including Alzheimer's disease) being the most focused disease (60.0%) in this update, opposed to multiple sclerosis on the last review (55.9%). Also, environmental pollutants such as PM 2.5 and NO 2 have gained prominence, being represented in 65.7% and 42.9% of the new studies, opposed to 9.8% and 12.2% in the previous review, compared to environmental factors such as sun exposure (5.7% in the update vs 15.9% in the original). The mostly used geographic approach remained the patient's residence (82.9% in the update vs 21.2% in the original and 62.3% in total), and remote sensing was used in 45.7% of the new studies versus 19.7% in the original review, with 42.0% of studies using it globally, being the second most common approach, usually to compute the environmental variable. This review has been registered in PROSPERO with the number CRD42020196188., (© 2024. The Author(s).)

Background: Particulate matter (PM), including the major risk factor for lung cancer (LC), greatly impacts human health. Although numerous studies have highlighted spatiotemporal patterns and PM-LC associations, these studies have not been well-reviewed. Thus, we examined epidemiological studies linked with PM-LC and provided concise, up-to-date data., Methods: We used certain keywords to review articles published in PubMed, Web of Science, Scopus, and Google Scholar until 30th June 2024 and identified 1474 research articles. We then filtered the research articles based on our criteria and ultimately dropped down to 30 for this review., Results: Out of the thirty reviewed studies on the PM-LC relation, twenty-four focused on PM 2.5 , four on PM 10 , and two on both, indicating that approximately 80% of the respondents were inclined toward fine particles and their health impacts. The study revealed that 22 studies used visualization, 12 used exploration, and 15 used modeling methods. A strong positive relationship was reported between LC and PM 2.5 , ranging from 1.04 to 1.60 (95% CI) for a 10 µg/m 3 increase in PM 2.5 exposure. However, compared to PM 2.5 , PM 10 was found to have a significantly less positive association., Conclusions: Very few studies have used advanced spatiotemporal methods to examine the association between LC and PM. Advanced spatiotemporal analysis techniques should be employed to explore this association in specific geographical locations. Further research should utilize spatiotemporal epidemiological approaches to study the link between PM and lung cancer., (© 2024. The Author(s).)

Background and Aim: Woodsmoke from household fireplaces contributes significantly to outdoor air pollution in the Netherlands. The current understanding of the respiratory health effects of exposure to smoke from residential wood burning is limited. This study investigated the association between short-term changes in outdoor woodsmoke exposure and lung function, respiratory symptoms, and medication use in adults in the Netherlands., Methods: This study was co-created with citizen scientists and other relevant stakeholders. A panel study was conducted with repeated observations in 46 adults between February and May 2021 in four Dutch towns. Participants recorded their symptoms and medication use in daily diaries, and conducted morning and evening home spirometry measurements. Woodsmoke exposure was characterized by measuring levoglucosan (most specific marker for woodsmoke exposure), black/brown carbon, fine and ultrafine particulate matter at central monitoring sites. Individual woodsmoke perception (smell) was recorded in daily diaries. Linear and logistic regression models were used to investigate the association between respiratory health and woodsmoke exposure. Models were adjusted for time-varying confounders and accounted for repeated observations within participants., Results: Consistent positive associations were found between levoglucosan and shortness of breath (SOB) during rest and extra respiratory medication use. Odds ratios for current day exposure to levoglucosan were 1.12 (95% CI: 0.97, 1.30) for SOB during rest and 1.19 (95% CI: 1.07, 1.33) for extra medication use, expressed per interquartile range of levoglucosan concentrations (69.16 ng/m 3 ). Positive non-significant associations were found between levoglucosan and nasal symptoms, cough and waking up with SOB. No consistent association was found between levoglucosan and lung function. Associations found between woodsmoke markers, SOB during rest and extra medication use remained after the inclusion of PM 2.5 and UFP in two-pollutant models., Conclusions: Adults experienced more SOB during rest, nasal symptoms and used more medication to treat respiratory symptoms on days with higher levels of outdoor woodsmoke concentrations., (© 2024. The Author(s).)

Background: Evidence for the relationship between individual and combined volatile organic compounds (VOCs) and cardiovascular disease (CVD) is limited. Besides, the mediating role of biological aging (BA) has not been studied. Therefore, this study aimed to examine the association between VOCs and CVD risk and to explore the mediating effects of BA., Methods: Logistic regression models were used to investigate the relationships of metabolites of volatile organic compounds (mVOCs) and BA with CVD. In addition, weighted quantile sum (WQS) regression, adaptive elastic networks, and Environmental Risk Score (AENET-ERS) were utilized to assess overall associations of mixed VOCs co-exposure with CVD. Mediation analyses were used to identify potential mediating effects of BA., Results: In the single-pollutant model, CYMA was shown to be associated with an increased risk of CVD. Additionally, we identified significantly positive associations between the WQS index and CVD (odds ratio (OR) = 1.292, 95% confidence interval (CI): 1.006, 1.660), and DHBMA had the greatest contribution for CVD (0.246). Furthermore, the AENET-ERS results showed that 8 mVOCs were significantly associated with CVD, and ERS was related to an elevated risk of CVD (OR = 1.538, 95%CI: 1.255, 1.884). Three BA indicators mediated the association of the mVOCs mixture with CVD, with mediating effect proportions of 11.32%, 34.34%, and 7.92%, respectively., Conclusion: The risk of CVD was found to increase with both individual and combined exposure to VOCs. BA mediates the positive effects of VOCs on CVD, suggesting that this pathway may be one of the mechanisms of CVD., (© 2024. The Author(s).)

Background: Current evidence linking long-term exposure to fine particulate matter (PM 2.5 ) exposure and mortality is primarily based on persons that live in the same residence, city and/or country throughout the study, with few residential moves or relocations. We propose a novel method to quantify the health impacts of PM 2.5 for United States (US) diplomats who regularly relocate to international cities with different PM 2.5 levels., Methods: Life table methods were applied at an individual-level to US mortality statistics using the World Health Organization's database of city-specific PM 2.5 annual mean concentrations. Global Burden of Disease concentration-response (C-R) functions were used to estimate cause-specific mortality and days of life lost (DLL) for a range of illustrative 20-year diplomatic assignments for three age groups. Time lags between exposure and exposure-related mortality risks were applied. Sensitivity analysis of baseline mortality, exposure level, C-R functions and lags was conducted. The effect of mitigation measures, including the addition of air purifiers, was examined., Results: DLL due to PM 2.5 exposure for a standard 20-year assignment ranged from 0.3 days for diplomats' children to 84.1 days for older diplomats. DLL decreased when assignments in high PM 2.5 cities were followed by assignments in low PM 2.5 cities: 162.5 DLL when spending 20 years in high PM 2.5 cities compared to 62.6 DLL when spending one of every four years (5 years total) in a high PM 2.5 city for older male diplomats. Use of air purifiers and improved home tightness in polluted cities may halve DLL due to PM 2.5 exposure. The results were highly sensitive to lag assumptions: DLL increased by 68% without inception lags and decreased by 59% without cessation lags for older male diplomats., Conclusion: We developed a model to quantify health impacts of changing PM 2.5 exposure for a population with frequent relocations. Our model suggests that alternating assignments in high and low PM 2.5 cities may help reduce PM 2.5 -related mortality burdens. Adding exposure mitigation at home may help reduce PM 2.5 related mortality. Further research on outcome-specific lag structures is needed to improve the model., (© 2024. The Author(s).)