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Background: Ambient air pollution during pregnancy has been linked with postpartum depression up to 12 months, but few studies have investigated its impact on persistent depression beyond 12 months postpartum. This study aimed to evaluate prenatal ambient air pollution exposure and the risk of persistent depression over 3 years after childbirth and to identify windows of susceptibility., Methods: This study included 361 predominantly low-income Hispanic/Latina participants with full-term pregnancies in the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort. We estimated daily residential PM 2.5 , PM 10 , NO 2 , and O 3 concentrations throughout 37 gestational weeks using inverse-distance squared spatial interpolation from monitoring data and calculated weekly averaged levels. Depression was assessed by the 20-item Center for Epidemiologic Studies-Depression (CES-D) scale at 12, 24, and 36 months postpartum, with persistent postpartum depression defined as a CES-D score ≥16 at any of these timepoints. We performed robust Poisson log-linear distributed lag models (DLM) via generalized estimating equations (GEE) to estimate the adjusted risk ratio (RR)., Results: Depression was observed in 17.8 %, 17.5 %, and 13.4 % of participants at 12, 24, and 36 months, respectively. We found one IQR increase (3.9 ppb) in prenatal exposure to NO 2 during the identified sensitive window of gestational weeks 13-29 was associated with a cumulative risk ratio of 3.86 (95 % CI: 3.24, 4.59) for persistent depression 1-3 years postpartum. We also found one IQR increase (7.4 μg/m 3 ) in prenatal exposure to PM 10 during gestation weeks 12-28 was associated a cumulative risk ratio of 3.88 (95 % CI: 3.04, 4.96) for persistent depression. No clear sensitive windows were identified for PM 2.5 or O 3 ., Conclusions: Mid-pregnancy PM 10 and NO 2 exposures were associated with nearly 4-fold increased risks of persistent depression after pregnancy, which has critical implications for prevention of perinatal mental health outcomes., Competing Interests: Declaration of competing interest We declare no actual or potential competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

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.)

Objective: It is known that exposure to air pollution is associated with an increased risk for cardiovascular and respiratory diseases. This review aimed to summarise observational studies on the impact of short and long-term exposure to ambient air pollution on prevalence of hospitalisations and/or emergency department visits caused by respiratory diseases in children and adolescents., Sources: Pubmed, Scopus, Embase and Cochrane Library databases were searched for the years 2018 to December 2022, including studies in any language., Summary of the Findings: A total of 15 studies published between 2018 and 15 January 2022 were included in this review. PM 2.5 was the most type of particulate matter studied. Short-term exposure to PM 2,5 , PM 10 , NO 2 , SO 2 and O 3 , even at concentrations less than the current health-based guidelines, was significantly correlated with increased risk of outpatient/hospital visits and hospitalisations for respiratory diseases by children., Conclusions: Our findings emphasise the importance and urgency of long-term control of air pollution and pollution-related diseases, especially among children and adolescents. There is a need for further research employing more homogeneous methodologies for assessing exposure and outcome measurements, in order to enable systematic reviews with meta-analysis., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

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).)

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.)

Exposure to ambient ozone (O 3 ) is linked to increased mortality risks from various diseases, but epidemiological investigations delving into its potential implications for cancer mortality are limited. We aimed to examine the association between short-term O 3 exposure and site-specific cancer mortality and investigate vulnerable subgroups in Brazil. In total 3,459,826 cancer death records from 5570 Brazilian municipalities between 2000 and 2019, were included. Municipal average daily O 3 concentration was calculated from a global estimation at 0.25°×0.25° spatial resolution. The time-stratified case-crossover design was applied to assess the O 3 -cancer mortality association. Subgroup analyses by age, sex, season, time-period, region, urban hierarchy, climate classification, quantiles of GDP per capita and illiteracy rates were performed. A linear and non-threshold exposure-response relationship was observed for short-term exposure to O 3 with cancer mortality, with a 1.00% (95% CI: 0.79%-1.20%) increase in all-cancer mortality risks for each 10-μg/m 3 increment of three-day average O 3 . Kidney cancer was most strongly with O 3 exposure, followed by cancers of the prostate, stomach, breast, lymphoma, brain and lung. The associated cancer risks were relatively higher in the warm season and in southern Brazil, with a decreasing trend over time. When restricting O 3 concentration to the national minimum value during 2000-2019, a total of 147,074 (116,690-177,451) cancer deaths could be avoided in Brazil, which included 17,836 (7014-28,653) lung cancer deaths. Notably, these associations persisted despite observed adaptation within the Brazilian population, highlighting the need for a focus on incorporating specific measures to mitigate O 3 exposure into cancer care recommendations., (© 2024 The Author(s). International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

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).)

Introduction: While associations between ambient air pollution and respiratory health in chronic obstructive pulmonary disease (COPD) patients are well studied, little is known about individuals' personal exposure to pollution and associated health effects by source., Aim: To separate measured total personal exposure into indoor-generated and outdoor-generated pollution and use these improved metrics in health models for establishing more reliable associations with exacerbations and respiratory symptoms., Methods: We enrolled a panel of 76 patients with COPD and continuously measured their personal exposure to particles and gaseous pollutants and location with portable monitors for 134 days on average. We collected daily health information related to respiratory symptoms through diary cards and peak expiratory flow (PEF). Mixed-effects models were applied to quantify the relationship between total, indoor-generated and outdoor-generated personal exposures to pollutants with exacerbation and symptoms occurrence and PEF., Results: Exposure to nitrogen dioxide from both indoor and outdoor sources was associated with exacerbations and respiratory symptoms. We observed an increase of 33% (22%-45%), 19% (12%-18%) and 12% (5%-20%) in the odds of exacerbation for an IQR increase in total, indoor-generated and outdoor-generated exposures. For carbon monoxide, health effects were mainly attributed to indoor-generated pollution. While no associations were observed for particulate matter 2.5 with COPD exacerbations, indoor-generated particles were associated with a significant decrease in PEF., Conclusions: Indoor-generated and outdoor-generated pollution can deteriorate COPD patients' health. Policy-makers, physicians and patients with COPD should note the importance of decreasing exposure equally to both source types to decrease risk of exacerbation., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published by BMJ.)

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).)

PM 2.5 is a fine particulate matter with an aerodynamic equivalent diameter of less than or equal to 2.5 μm, and it is the primary pollutant that causes haze. In recent years, numerous research results have shown that PM 2.5 is associated with various ophthalmic diseases and its pathogenic mechanism is complex. It can disrupt the homeostasis of the tear film and the function of the meibomian glands, leading to dry eye; increase the risk of allergic and other types of conjunctivitis; may cause blepharitis; affect the homeostasis of the corneal epithelium and promote the development of keratopathy; the correlation with cataract is controversial; it is related to the risk of glaucoma; it is associated with age-related macular degeneration; it may also indirectly promote diabetic retinopathy. Prevention and control measures include controlling the level of PM 2.5 , strengthening publicity and screening, reducing going out and wearing goggles, etc. PM 2.5 is closely related to ophthalmic diseases, but its specific pathogenic mechanism still requires more research to explore.

Background: Epidemiological evidence regarding the association between air pollutants and cardiopulmonary disease, mortality in individuals with preserved ratio impaired spirometry (PRISm), and their combined effects remains unclear., Methods: We followed 36,149 participants with PRISm in the UK Biobank study. Annual concentrations of PM 2.5 , PM 10 , NO 2 , NO x , and SO 2 at residential addresses were determined using a bilinear interpolation method, accounting for address changes. A multistate model assessed the dynamic associations between air pollutants and cardiopulmonary diseases and mortality in PRISm. Quantile g-computation was used to investigate the joint effects of air pollutants., Results: Long-term exposure to PM 2.5 , PM 10 , NO 2 , NO x , and SO 2 was significantly associated with the risk of cardiopulmonary disease in PRISm. The corresponding hazard ratios (HRs) [95 % confidence intervals (95 % CIs)] per interquartile range (IQR) were 1.49 (1.43, 1.54), 1.52 (1.46, 1.57), 1.34 (1.30, 1.39), 1.30 (1.26, 1.34), and 1.44 (1.41, 1.48), respectively. For mortality, the corresponding HRs (95 % CIs) per IQR were 1.36 (1.25, 1.47), 1.35 (1.24, 1.46), 1.27 (1.18, 1.36), 1.23 (1.15, 1.31), and 1.29 (1.20, 1.39), respectively. In PRISm, quantile g-computation analysis demonstrated that a quartile increase in exposure to a mixture of all air pollutants was positively associated with the risk of cardiopulmonary disease and mortality, with HRs (95 % CIs) of 1.84 (1.76, 3.84) and 1.45 (1.32, 1.57), respectively., Conclusion: Long-term individual and joint exposure to air pollutants (PM 2.5 , PM 10 , NO 2 , NO x , and SO 2 ) might be an important risk factor for cardiopulmonary disease and mortality in high-risk populations with PRISm., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

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).)

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.)

The River Sacco Basin (Rsb) is a site of National interest, characterized by several environmental pressures such as industrial facilities. This study investigates the association between long-term exposure to industrial-PM10 and -NOx and cause-specific mortality (non-accidental, cardiovascular, respiratory, and cancer) in the Rsb in the 2006-2018 period. We enrolled 301,681 residents near 14 major industrial plants (grouped into 5 30-km2 spatial domains). Residential exposure to annual PM10 and NOx was considered as categorical exposure (high (>80th percentile), medium (50th-80th), and low (<50th)). We applied adjusted domain specific Cox regression models (covariates: age, sex, and deprivation index) and performed a relative meta-analysis. We obtain a pooled 34% increase in respiratory mortality for high PM10 levels. Elevated risks were also observed for non-accidental and cancer mortality, highlighting the need for continuous monitoring and preventive interventions.

Background: reducing air emissions is the fundamental action necessary to mitigate the negative health effects caused by air pollution. However, increased public awareness has highlighted the need to identify protective measures that can mitigate the personal health risks associated with air pollution., Objectives: examine the evidence regarding personal protection strategies capable of mitigating the health effects caused by air pollution, with a focus on healthy individuals and at-risk categories.  Design: narrative review., Setting and Participants: this study examines the most effective personal protection strategies for healthy and at-risk individuals, considering children, the elderly, and individuals with cardiovascular and respiratory diseases; the examined strategies include the use of air purifiers, respiratory masks, exposure limitation, physical activity, alternative means of transportation, and environmental monitoring systems., Main Outcomes Measures: reduction of individual exposure to air pollution, respiratory and cardiovascular outcomes, total and all-cause mortality., Results: the evidence indicates that these measures can reduce exposure and promote well-being. For at-risk individuals, it is crucial to limit exposure during periods and in locations with high pollution levels, with an emphasis on physical activity. The use of high-efficiency air purifiers can reduce the negative effect of air pollution on individuals with respiratory and cardiovascular conditions, especially those with asthma. In healthy individuals, multiple mitigation actions have been identified, with evidence suggesting that the benefits of physical activity persist even in environments with high levels of air pollution., Conclusions: this narrative review provides an overview of personal strategies capable of reducing air pollution exposure and consequently mitigating its negative impact on health. These findings can support the development of recommendations and communication and prevention interventions, promoting risk reduction policies and increased awareness and engagement from both healthcare and non-healthcare networks at the local level. Although more robust systematic approaches are needed, this review serves as a useful tool for stakeholders and citizens, while also providing a simple instrument with significant communicative potential, applicable on a large scale.

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.)

Objective: Coastal cities, due to their proximity to coastlines and unique climatic conditions, face growing challenges from extreme temperature events associated with climate change. Research on the impact of extreme temperatures on tuberculosis (TB) in these cities is limited, and findings from different regions lack consensus. This study focuses on Shantou, a coastal city in China, to investigate the influence of extreme temperatures on TB within this distinctive geographical context., Methods: Distributed Lag Non-Linear Models (DLNM) were employed to evaluate the effect of extreme temperatures on TB incidence risk in Shantou, a coastal city in China, spanning from 2014 to 2021. Daily TB case data were provided by the Shantou Tuberculosis Prevention and Control Institute. Daily meteorological information was sourced from the Reliable Prognosis website, while daily air pollutant data were obtained from the China Air Quality Online Monitoring and Analysis Platform., Results: The study revealed a significant association between extreme temperatures and TB incidence, with the impact peaking at a lag of 27 days after exposure. Notably, extreme cold temperatures led to a temporary decrease in TB incidence with a lag of 1-2 days. Subgroup analysis indicated that males had a notably higher risk of TB under extreme temperature conditions compared to females. Additionally, individuals aged 65 years and above showed a significant cumulative effect in such conditions., Conclusions: This research enhances our comprehension of the effects of extreme temperatures on TB in coastal cities and carries substantial public health implications for TB prevention in China., Competing Interests: Declarations 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. Ethical responsibility of authors This study did not involve human or animal subjects, and thus, no ethical approval was required., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: Air pollution, a significant global health concern, notably impacts human well-being. Children, owing to their distinctive physiology and behavior, are particularly susceptible to its adverse effects. This prospective study examines air quality variations and respiratory risks in children residing in critically polluted areas (CPA) compared to relatively non-polluted areas (NPA), utilizing a prospective design to understand the impacts of air pollution on children's respiratory health, including measures like relative risk (RR) and attributable risk (AR)., Methods: This prospective study tracked 739 students of 5th- 7th grade residing in CPA and NPA for one year, and measured the ambient and indoor air quality levels in both these areas. Throughout the study, based on the observed respiratory symptoms new episodes of upper and lower respiratory tract illnesses were recorded for each child on a weekly basis. Incidence rate, RR and AR for both the illnesses were compared. Statistical analysis was performed with SPSS 26.0., Results: The study observes higher concentration for particulate matter and gaseous pollutants at CPA in comparison to NPA. Children living in CPA exhibited a notably greater weekly occurrence of both upper and lower respiratory tract illnesses compared to those in NPA, with RR of 1.26 (95% CI: 1.16-1.37) and 1.74 (95% CI: 1.34-2.27), respectively. The AR associated with air pollution for upper and lower respiratory tract illnesses among CPA students was found to be 20.7% and 42.7%, respectively., Conclusion: This research underscores the pressing need to address air pollution in critically polluted areas and its profound effects on children's respiratory health. Public health interventions, such as reducing emissions from industries and creating green spaces, should be prioritized. Furthermore, early respiratory health screening in schools within polluted areas could aid in the timely diagnosis and management of respiratory issues in children., Competing Interests: Declarations Ethical approval Study was approved from Institutional Ethical Committee of ICMR-National Institute of Occupational Health, Ahmedabad with document reference No. ICMR-NIOH/ ethics/ 2018/Agenda 3.10 on 28.09.2018. Conflict of interest None., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

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.)

Objectives: The study aims to explore whether short-term exposure to meteorological factors has a potential association with the risk of diabetes mellitus (DM) mortality., Methods: During the period 2015-2018, we collected daily data on meteorological factors and deaths of diabetic patients in Hefei. A total of 1101 diabetic deaths were recorded. We used structural equation modeling to initially explore the relationships among air pollutants, meteorological variables, and mortality, and generalized additive modeling (GAM) and distributional lag nonlinear modeling (DLNM) to explore the relationship between meteorological factors and the mortality risk of DM patients. We also stratified by age and gender. The mortality risk in diabetic patients was expressed by relative risks (RR) and 95% confidence intervals (CI) for both single and cumulative days., Results: Single-day lagged results showed a high relative humidity (RH) (75th percentile, 83.71%), a fairly high average temperature (T mean) (95th percentile, 30.32 °C), and an extremely low diurnal temperature range (DTR) (5th percentile, 3.13 °C) were positively related to the mortality risk of DM. Stratified results showed that high and very high levels of T mean were significantly positively linked to the mortality risk of DM among females and the elderly, while very high levels of DTR were linked to the mortality risk in men and younger populations., Conclusion: In conclusion, this study found that short-duration exposure to quite high T mean, high RH, and very low DTR were significantly positively related to the mortality risk of DM patients. For women and older individuals, exposure to high and very high T mean environments should be minimized. Men and young adults should be aware of daily temperature changes., Competing Interests: Declarations Conflict of interest This study does not conflict with other authors. Ethics approval Ethical approval for in this study was not sought, and it is a secondary analysis research., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Scientific literature on the health effects of air pollution is diverse, and broadly acknowledges the importance of human experience and social and economic precarity as modifying factors. Still, the inclusion of the embodied experience of air pollution has been limited. Also, the health effects of pollution are often studied at the group or population level, without adequately considering individual difference. This paper uses a Bio 3 Science framework, which integrates biology, biography, and biosphere, to explore how air pollution affects residents in Medellín, Colombia. By using qualitative research on individual experiences of air pollution (biography) to probe the intersection of individual health (biology) and environment (biosphere), we illustrate how pollution shapes lived rhythms at multiple scales. Our findings emphasize that air pollution's health impacts extend beyond measurable pollutants to include the complex synergies of smoke, noise, stress, and disruptions to daily life. This comprehensive approach provides a nuanced understanding of how air pollution materially shapes the lives of individuals and communities, advocating for research models that capture the subtle, everyday experiences often overlooked by traditional group or population-level analyses., 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 Ltd.. 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.)

Purpose of Review: Respiratory allergies are non-communicable diseases caused by the hypersensitivity of the immune system to environmental aeroallergens. The culprits are aero-transported proteins eliciting respiratory symptoms in sensitized/allergic individuals. This review intends to provide a holistic overview on the categorization of aeroallergens into protein families (Part 1) and to exploit the impact of physicochemical properties on inhalant protein allergenicity (Part 2). This first part will focus particularly on aeroallergen organization into families and how this classification fits their physicochemical properties., Recent Findings: Aeroallergen classification into protein families facilitates the identification of common physicochemical properties, thus aiding a better comprehension of known allergens, while predicting the behavior of novel ones. The available online databases gathering important features of aeroallergens are currently scarce. Information on distinct aeroallergen classification is still lacking, as data is dispersed and often outdated, hampering an efficient evaluation of new aeroallergens., (© 2024. The Author(s).)

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.)

Objectives: To investigate the associations between PM 2.5 and its chemical constituents with blood pressure (BP), assess effects across BP quantiles, and identify the key constituent elevating BP., Methods: A total of 36 792 adults were included in the cross-sectional study, representing 25 districts/counties of southeast China. Quantile regression models were applied to estimate the associations of PM 2.5 and its chemical constituents (ammonium [NH 4+ ], nitrate [NO 3- ], sulfate [SO 42- ], black carbon [BC], organic matter [OM]) with systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean artery pressure (MAP). A weighted quantile sum (WQS) index was used to estimate the relative importance of each PM 2.5 chemical constituent to the joint effect on BP., Results: The adverse effects of each interquartile range (IQR) increase in PM 2.5 , NH 4+ , NO 3- , SO 42- , and BC on BP were found to be greater with elevated BP, especially when SBP exceeded 133 mmHg and DBP exceeded 82 mmHg. Each IQR increase in all five PM 2.5 chemical constituents was associated with elevated SBP ( β [95% CI]: 0.90 [0.75, 1.05]), DBP ( β : 0.44 [0.34, 0.53]), and MAP ( β : 0.57 [0.45, 0.69]), NH 4+ (for SBP: weight = 99.43%; for DBP: 12.78%; for MAP: 60.73%) and BC (for DBP: 87.06%; for MAP: 39.07%) predominantly influencing these effects. The joint effect of PM 2.5 chemical constituents on risks for elevated SBP and DBP exhibited an upward trend from the 70 th quantile (SBP exceeded 133 mmHg, DBP exceeded 82 mmHg)., Conclusion: Long-term exposure to PM 2.5 and its chemical constituents was associated with increased risk for elevated BP, with NH 4+ and BC being the main contributors, and such associations were significantly stronger at 70th to 90th quantiles (SBP exceeded 133 mmHg, DBP exceeded 82 mmHg)., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Increasing research has focused on the impact of air pollution on brain health. As the prevalence of air pollution is increasing alongside other environmental harms, the importance of studying the effects of these changes on human health has become more significant. Additionally, gaining insight into how air pollution exposure, measured at different points in the lifespan, can affect brain structure is critical, as this could be a precursor to cognitive decline later in life. The purpose of this review was to synthesize the literature on the association between air pollutant exposure and cortical thickness, a structural change with known associations with later cognition and neurodegenerative disease. After screening, twelve studies were included in this systematic review. Across a majority of studies, results suggest significant associations between increasing air pollution exposure and decreases in cortical thickness, primarily in areas such as prefrontal cortex, precuneus, and temporal regions of the brain. These results did differ somewhat between age groups and different air pollutants, with the most prominent results being found with exposure to PM 2.5 , the smallest particulate matter size included in the review. In the future, it is important to continue studying cortical thickness as it is essential to brain functioning and can be influential in disease progression. Furthermore, conducting more longitudinal studies in which air pollution is measured as a cumulation throughout the lifespan would help elucidate when exposure is most impactful and when brain structural changes become observable., 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 International Brain Research Organization (IBRO). Published by Elsevier Inc. All rights reserved.)

There is a lack of evidence from cohort studies on the causal association of long-term exposure to ambient fine particulate matter (PM 2.5 ) and its chemical components with the risk of nasopharyngeal carcinoma (NPC) recurrence. Based on a 10-year prospective cohort of 1184 newly diagnosed NPC patients, we comprehensively evaluated the potential causal links of ambient PM 2.5 and its chemical components including black carbon (BC), organic matter (OM), sulfate (SO 4 2- ), nitrate (NO 3 - ), and ammonium (NH 4 + ) with the recurrence risk of NPC using a marginal structural Cox model adjusted with inverse probability weighting. We observed 291 NPC patients experiencing recurrence during the 10-year follow-up and estimated a 33% increased risk of NPC recurrence (hazard ratio [HR]: 1.33, 95% confidence interval [CI]: 1.02-1.74) following each interquartile range (IQR) increase in PM 2.5 exposure. Each IQR increment in BC, NH 4 + , OM, NO 3 - , and SO 4 2- was associated with HRs of 1.36 (95%CI: 1.13-1.65), 1.35 (95%CI: 1.07-1.70), 1.33 (95%CI: 1.11-1.59), 1.32 (95%CI: 1.06-1.64), 1.31 (95%CI: 1.08-1.57). The elderly, patients with no family history of cancer, no smoking history, no drinking history, and those with severe conditions may exhibit a greater likelihood of NPC recurrence following exposure to PM 2.5 and its chemical components. Additionally, the effect estimates of the five components are greater among patients who were exposed to high concentration than in the full cohort of patients. Our study provides solid evidence for a potential relationship between long-term exposure to PM 2.5 and its components and the risk of NPC recurrence., (© 2024 UICC.)

Background: Traffic-related air pollutants have been associated with a variety of adverse human health impacts, including cancers. In the United States, numerous studies have documented racial inequities in neighborhood exposures to traffic-related air pollution. Emerging evidence suggests that structural racism may influence neighborhood exposures to air pollutants. However, existing research has largely focused on residential racial segregation, one indicator of structural racism. This study developed a multidimensional measure of structural racism to examine the relationship between structural racism and estimated cancer risk from air pollutants in Georgia., Methods: Carcinogenic air toxics data were obtained from the US Environmental Protection Agency's 2019 Air Toxics Screening Assessment and sociodemographic data from the American Community Survey. Guided by stakeholder input, county-level data on residential segregation, education, employment, incarceration, economic status, political participation, and homeownership were used to create a multidimensional county-level structural racism index. Relative risks (RRs) were estimated for associations between structural racism and elevated (top 10% in Georgia) estimated cancer risk from air toxics., Results: Multilevel analyses revealed a significant association between multidimensional structural racism and exposure to carcinogenic traffic-related air pollutants. Neighborhoods in the highest quartile of structural racism exhibited an elevated cancer risk from traffic-related air pollutants (RR, 7.84; 95% CI, 5.11-12.05) compared to neighborhoods with lower levels of structural racism., Conclusions: Multidimensional structural racism was associated with estimated cancer risk from traffic-related air pollution in Georgia. Findings can inform future studies and policy interventions that address racial inequalities in exposure to traffic-related air pollution., (© 2024 American Cancer Society.)

Air pollution is a critical global issue with extensive implications beyond respiratory health, significantly affecting neurological and psychiatric disorders. Emerging evidence establishes a link between exposure to fine particulate matter (PM < 2.5 µm), sulfur dioxide (SO 2 ), and nitrogen dioxide (NO 2 ) and heightened risks of dementia, Alzheimer's disease, schizophrenia, ADHD, stroke, Parkinson's disease, and multiple sclerosis. Mechanistic pathways include neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and blood-brain barrier disruption. Epidemiological studies indicate increased susceptibility among urban residents, particularly men, middle-aged individuals, and married persons, to the mental health impacts of air pollution. Additionally, socioeconomic factors, such as GDP per capita, access to health resources, green spaces, and sports facilities, modulate these health outcomes. Addressing this public health challenge necessitates stricter industrial emission controls, sustainable agricultural practices, promotion of cleaner energy sources, and incorporation of pollution exposure history into clinical assessments. Enhanced public awareness and interdisciplinary research are vital for mitigating the detrimental effects of air pollution on neurological and psychiatric health, ultimately striving for a cleaner and healthier environment for future generations., (Copyright © 2024 Instituto Mexicano del Seguro Social (IMSS). Published by Elsevier Inc. All rights reserved.)

Epidemiologic studies have suggested a possible association between air pollution and chronic obstructive pulmonary disease (COPD), but it is controversial and difficult to draw causal inferences. Five methods were adopted to evaluate the causal relationship between air pollution and COPD in European and East Asian populations by using MR Analysis. A statistically significant causal relationship between PM2.5 and COPD was observed in the European population (OR: 2.34; 95% CI: 1.06-5.05; p  = 0.033). Statistical significance remained after adjustment for confounding factors (adjusted OR: 2.28; 95% CI: 1.01-5.20; p  = 0.048). In East Asian populations, PM2.5 absorbance, a proxy for black carbon, was statistically associated with COPD (OR: 1.41; 95% CI: 1.09-1.81; p  = 0.007). We did not adjust for confounders in East Asian populations, as the association was independent of known confounders (e.g. smoking, respiratory tract infections, etc.). In conclusion, increased concentrations of PM2.5 and PM2.5 absorbance were associated with an increased risk of COPD.

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.)

Background: Childhood-onset lupus nephritis (cLN) is a severe form of systemic lupus erythematosus (SLE) with high morbidity and mortality. The impact of long-term exposure to fine particulate matter (PM 2.5 ) on adverse outcomes in cLN remains unclear., Methods: We combined a 19-years cLN cohort from seven provinces in China with high-resolution PM 2.5 dataset from 2001 to 2020, investigating the association between long-term exposure to PM 2.5 and its constituents (sulfate, nitrate, organic matter, black carbon, ammonium) with the risk of death and kidney failure, analyzed with multiple variables Cox models. We also evaluated the association between 3-year average PM 2.5 exposure before study entry and baseline SLE disease activity index (SLEDAI) scores using linear regression models., Results: Each 10 μg/m 3 increase in annual average PM 2.5 exposure was associated with an increased risk of death and kidney failure (HR = 1.58, 95 % CI: 1.24-2.02). Black carbon showed the strongest association (HR = 2.14, 95 % CI: 1.47-3.12). Higher 3-year average exposures to PM 2.5 and its constituents were significantly associated with higher baseline SLEDAI scores., Conclusions: These findings highlight the significant role of environmental pollutants in cLN progression and emphasize the need for strategies to mitigate exposure to harmful PM2.5 constituents, particularly in vulnerable pediatric populations., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)