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Background: Ambient air pollution, including particulate matter (such as PM 10 and PM 2·5 ) and nitrogen dioxide (NO 2 ), has been linked to increases in mortality. Whether populations' vulnerability to these pollutants has changed over time is unclear, and studies on this topic do not include multicountry analysis. We evaluated whether changes in exposure to air pollutants were associated with changes in mortality effect estimates over time., Methods: We extracted cause-specific mortality and air pollution data collected between 1995 and 2016 from the Multi-Country Multi-City (MCC) Collaborative Research Network database. We applied a two-stage approach to analyse the short-term effects of NO 2 , PM 10 , and PM 2·5 on cause-specific mortality using city-specific time series regression analyses and multilevel random-effects meta-analysis. We assessed changes over time using a longitudinal meta-regression with time as a linear fixed term and explored potential sources of heterogeneity and two-pollutant models., Findings: Over 21·6 million cardiovascular and 7·7 million respiratory deaths in 380 cities across 24 countries over the study period were included in the analysis. All three air pollutants showed decreasing concentrations over time. The pooled results suggested no significant temporal change in the effect estimates per unit exposure of PM 10 , PM 2·5 , or NO 2 and mortality. However, the risk of cardiovascular mortality increased from 0·37% (95% CI -0·05 to 0·80) in 1998 to 0·85% (0·55 to 1·16) in 2012 with a 10 μg/m 3 increase in PM 2·5 . Two-pollutant models generally showed similar results to single-pollutant models for PM fractions and indicated temporal differences for NO 2 ., Interpretation: Although air pollution levels decreased during the study period, the effect sizes per unit increase in air pollution concentration have not changed. This observation might be due to the composition, toxicity, and sources of air pollution, as well as other factors, such as socioeconomic determinants or changes in population distribution and susceptibility., Funding: None., 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.)

Objective: To determine whether long term exposure to outdoor nitrogen dioxide (NO2) is associated with all-cause or cause-specific mortality., Methods: MEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was conducted using random effects models, heterogeneity among included studies was assessed using Cochran's Q and I2 measures, and sources of heterogeneity were evaluated using meta-regression. Sensitivity of pooled estimates to individual studies was examined and publication bias was evaluated using Funnel plots, Begg's and Egger's tests, and trim and fill., Results: Seventy-nine studies based on 47 cohorts, plus one set of pooled analyses of multiple European cohorts, met inclusion criteria. There was a consistently high degree of heterogeneity. After excluding studies with probably high or high risk of bias in the confounding domain (n = 12), pooled hazard ratios (HR) indicated that long term exposure to NO2 was significantly associated with mortality from all/ natural causes (pooled HR 1.047, 95% confidence interval (CI), 1.023-1.072 per 10 ppb), cardiovascular disease (pooled HR 1.058, 95%CI 1.026-1.091), lung cancer (pooled HR 1.083, 95%CI 1.041-1.126), respiratory disease (pooled HR 1.062, 95%CI1.035-1.089), and ischemic heart disease (pooled HR 1.111, 95%CI 1.079-1.144). Pooled estimates based on multi-pollutant models were consistently smaller than those from single pollutant models and mostly non-significant., Conclusions: For all causes of death other than cerebrovascular disease, the overall quality of the evidence is moderate, and the strength of evidence is limited, while for cerebrovascular disease, overall quality is low and strength of evidence is inadequate. Important uncertainties remain, including potential confounding by co-pollutants or other concomitant exposures, and limited supporting mechanistic evidence. (PROSPERO registration number CRD42018084497)., Competing Interests: The authors have declared that no competing interests exist.

Background: Nitrogen dioxide (NO 2 ) is a pervasive urban pollutant originating primarily from vehicle emissions. Ischemic heart disease (IHD) is associated with a considerable public health burden worldwide, but whether NO 2 exposure is causally related to IHD morbidity remains in question. Our objective was to determine whether short term exposure to outdoor NO 2 is causally associated with IHD-related morbidity based on a synthesis of findings from case-crossover and time-series studies., Methods: MEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts between reviewers were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was conducted using random effects models, heterogeneity among included studies was assessed using Cochran's Q and I 2 measures, and sources of heterogeneity were evaluated using meta-regression. Sensitivity of pooled estimates to individual studies was examined using Leave One Out analysis and publication bias was evaluated using Funnel plots, Begg's and Egger's tests, and trim and fill., Results: Thirty-eight case-crossover studies and 48 time-series studies were included in our analysis. NO 2 was significantly associated with IHD morbidity (pooled odds ratio from case-crossover studies: 1.074 95% CI 1.052-1.097; pooled relative risk from time-series studies: 1.022 95% CI 1.016-1.029 per 10 ppb). Pooled estimates for case-crossover studies from Europe and North America were significantly lower than for studies conducted elsewhere. The high degree of heterogeneity among studies was only partially accounted for in meta-regression. There was evidence of publication bias, particularly for case-crossover studies. For both case-crossover and time-series studies, pooled estimates based on multi-pollutant models were smaller than those from single pollutant models, and those based on older populations were larger than those based on younger populations, but these differences were not statistically significant., Conclusions: We concluded that there is a likely causal relationship between short term NO 2 exposure and IHD-related morbidity, but important uncertainties remain, particularly related to the contribution of co-pollutants or other concomitant exposures, and the lack of supporting evidence from toxicological and controlled human studies.

Background: There is scant information as to whether traffic-related air pollution is associated with the incidence of breast cancer. Nitrogen dioxide (NO 2 ) and ultrafine particles (UFPs, <0.1µm), are two pollutants that capture intra-urban variations in traffic-related air pollution and may also be associated with incidence., Methods: We conducted a population-based, case-control study of street-level concentrations of NO 2 and UFPs and incident postmenopausal breast cancer in Montreal, Canada. Incident cases were identified between 2008 and 2011 from all but one hospital that treated breast cancer in the Montreal area. Population controls were identified from provincial electoral lists of Montreal residents and frequency-matched to cases using 5-year age groups. Concentrations of NO 2 and UFPs were estimated using two separate land-use regression models. Exposures were assigned to residential locations at the time of recruitment, and we identified residential histories of women who had lived in these residences for 10 years or more. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression models adjusting for individual-level and ecological covariates. We assessed the functional form of NO 2 and UFP exposures using natural cubic splines., Results: We found that the functional form of the response functions between incident postmenopausal breast cancer and concentrations of NO 2 and UFPs were consistent with linearity. For NO 2 , we found increasing risks of breast cancer for all subjects combined and stronger associations when analyses were restricted to those women who had lived at their current address for 10 years or more. Specifically, the OR, adjusted for personal covariates, per increase in the interquartile range (IQR=3.75 ppb) of NO 2 was 1.08 (95%CI: 0.92-1.27). For women living in their homes for 10 years or more, the adjusted OR was 1.17 (95%CI: 0.93-1.46; IQR=3.84 ppb); for those not living at that home 10 years before the study, it was 0.93 (95%CI: 0.64, 1.36; IQR=3.65 ppb). For UFPs, the ORs were lower than for NO 2 , with little evidence of association in any of the models or sub-analyses and little variability in the ORs (about 1.02 for an IQR of ~3500cm -3 ). On the other hand, we found higher ORs amongst cases with positive oestrogen and progesterone receptor status; namely for NO 2 , the OR was 1.13 (95%CI: 0.94-1.35) and for UFPs it was 1.05 (95%CI: 0.96-1.14)., Conclusions: Our findings suggest that exposure to ambient NO 2 and UFPs may increase the risk of incident postmenopausal breast cancer especially amongst cases with positive oestrogen and progesterone receptor status., (Copyright © 2017. Published by Elsevier Inc.)

Background and Objective: Genetic and environmental factors have been recognized to play an important role in autism. The possibility that exposure to outdoor air pollution increases the risk of autism spectrum disorder (ASD) has been an emerging area of research. Herein, we present a systematic review, and meta-analysis of published epidemiological studies that have investigated these associations., Methods: We undertook a comprehensive search strategy to identify studies that investigated outdoor air pollution and autism in children. Overall, seven cohorts and five case-control studies met our inclusion criteria for the meta-analysis. We summarized the associations between exposure to air pollution and ASD based on the following critical exposure windows: (i) first, second and third trimester of pregnancy, (ii) entire pregnancy, and (iii) postnatal period. Random effects meta-analysis modeling was undertaken to derive pooled risk estimates for these exposures across the studies., Results: The meta-estimates for the change in ASD associated with a 10μg/m 3 increase in exposure in PM 2.5 and 10 ppb increase in NO 2 during pregnancy were 1.34 (95% CI:0.83, 2.17) and 1.05 (95% CI:0.99, 1.11), respectively. Stronger associations were observed for exposures received after birth, but these estimates were unstable as they were based on only two studies. O 3 exposure was weakly associated with ASD during the third trimester of pregnancy and during the entire pregnancy, however, these estimates were also based on only two studies., Conclusion: Our meta-analysis support the hypothesis that exposure to ambient air pollution is associated with an increased risk of autism. Our findings should be interpreted cautiously due to relatively small number of studies, and several studies were unable to control for other key risk factors., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: We examined the impact of data source and exposure measurement error for ambient NO2 on risk estimates derived from a case-crossover study of emergency room visits for asthma in Windsor, Canada between 2002 and 2009., Methods: Paired personal and fixed-site NO2 data were available from an independent population (47 children and 48 adults) in Windsor between 2005 and 2006. We used linear regression to estimate the relationship and measurement error variance induced between fixed site and personal measurements of NO2, and through a series of simulations, evaluated the potential for a Bayesian model to adjust for this change in scale and measurement error. Finally, we re-analyzed data from the previous case-crossover study adjusting for the estimated change in slope and measurement error., Results: Correlations between paired NO2 measurements were weak (R(2)≤0.08) and slopes were far from unity (0.0029≤β≤0.30). Adjusting the previous case-crossover analysis suggested a much stronger association between personal NO2 (per 1ppb) (Odds Ratio (OR)=1.276, 95% Credible Interval (CrI): 1.034, 1.569) and emergency room visits for asthma among children relative to the fixed-site estimate (OR=1.024, 95% CrI 1.004-1.045)., Conclusions: Our findings suggest that risk estimates based on fixed-site NO2 concentrations may differ substantially from estimates based on personal exposures if the change in scale and/or measurement error is large. In practice, one must always keep the scale being used in mind when interpreting risk estimates and not assume that coefficients for ambient concentrations reflect risks at the personal level., (Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.)

BackgroundThe tremendous global health burden related to COVID-19 means that identifying determinants of COVID-19 severity is important for prevention and intervention. We aimed to explore long-term exposure to ambient air pollution as a potential contributor to COVID-19 severity, given its known impact on the respiratory system.MethodsWe used a cohort of all people with confirmed SARS-CoV-2 infection, aged 20 years and older and not residing in a long-term care facility in Ontario, Canada, during 2020. We evaluated the association between long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ground-level ozone (O3), and risk of COVID-19-related hospital admission, intensive care unit (ICU) admission and death. We ascertained individuals' long-term exposures to each air pollutant based on their residence from 2015 to 2019. We used logistic regression and adjusted for confounders and selection bias using various individual and contextual covariates obtained through data linkage.ResultsAmong the 151 105 people with confirmed SARS-CoV-2 infection in Ontario in 2020, we observed 8630 hospital admissions, 1912 ICU admissions and 2137 deaths related to COVID-19. For each interquartile range increase in exposure to PM2.5 (1.70 μg/m3), we estimated odds ratios of 1.06 (95% confidence interval [CI] 1.01-1.12), 1.09 (95% CI 0.98-1.21) and 1.00 (95% CI 0.90-1.11) for hospital admission, ICU admission and death, respectively. Estimates were smaller for NO2. We also estimated odds ratios of 1.15 (95% CI 1.06-1.23), 1.30 (95% CI 1.12-1.50) and 1.18 (95% CI 1.02-1.36) per interquartile range increase of 5.14 ppb in O3 for hospital admission, ICU admission and death, respectively.InterpretationChronic exposure to air pollution may contribute to severe outcomes after SARS-CoV-2 infection, particularly exposure to O3.

Rationale: Outdoor particulate and gaseous air pollutants impair respiratory health in children, and these associations may be influenced by particle composition. Objectives: To examine whether associations between shortterm variations in fine particulate air pollution, oxidant gases, and respiratory hospitalizations in children are modified by particle constituents (metals and sulfur) or oxidative potential. Methods: We conducted a case-crossover study of 10,500 children (0-17 years of age) across Canada. Daily fine particle mass concentrations and oxidant gases (nitrogen dioxide and ozone) were collected from ground monitors. Monthly estimates of fine particle constituents (metals and sulfur) and oxidative potential were also measured. Conditional logistic regression models were used to estimate associations between air pollutants and respiratory hospitalizations, above and below median values for particle constituents and oxidative potential. Measurements and Main Results: Lag-1 fine particulate matter mass concentrations were not associated with respiratory hospitalizations (odds ratio and 95% confidence interval per 10 -g/m3 increase in fine particulate matter: 1.004 [0.955-1.056]) in analyses ignoring particle constituents and oxidative potential. However, when models were examined above or below median metals, sulfur, and oxidative potential, positive associations were observed above the median. For example, the odds ratio and 95% confidence interval per 10 -g/m3 increase in fine particulate matter were 1.084 (1.007-1.167) when copper was above the median and 0.970 (0.929-1.014) when copper was below the median. Similar trends were observed for oxidant gases. Conclusions: Stronger associations were observed between outdoor fine particles, oxidant gases, and respiratory hospitalizations in children when metals, sulfur, and particle oxidative potential were elevated. [ABSTRACT FROM AUTHOR]

Air pollution is a major threat to public health. Understanding the spatial distribution of air pollution concentration is of great interest to government or local authorities, as it informs about target areas for implementing policies for air quality management. Cluster analysis has been popularly used to identify groups of locations with similar profiles of average levels of multiple air pollutants, efficiently summarising the spatial pattern. This study aimed to cluster locations based on the seasonal patterns of multiple air pollutants incorporating the location‐specific characteristics such as socio‐economic indicators. For this purpose, we proposed a novel non‐parametric Bayesian sparse latent factor model for covariate‐dependent multivariate functional clustering. Furthermore, we extend this model to conduct clustering with temporal dependency. The proposed methods are illustrated through a simulation study and applied to time‐series data for daily mean concentrations of ozone (O3$$ {\mathrm{O}}_3 $$), nitrogen dioxide (NO2$$ \mathrm{N}{\mathrm{O}}_2 $$), and fine particulate matter (PM2.5$$ \mathrm{P}{\mathrm{M}}_{2.5} $$) collected for 25 cities in Canada in 1986–2015. [ABSTRACT FROM AUTHOR]

Objectives: The city of Windsor is recognized to have poor air quality in comparison with other Canadian cities. However, relatively few studies have evaluated associations between day-to-day fluctuations in air pollution levels and respiratory health in Windsor. In this study, we examined associations between short-term changes in ambient air pollution and emergency department (ED) visits for asthma in Windsor. Methods: A time-stratified case-crossover design was applied to 3,728 ED visits for asthma that occurred in Windsor area hospitals between 2002 and 2009. Daily air pollution levels for the region were estimated using Environment Canada's network of fixed-site monitors. ED visits were identified through the National Ambulatory Care Reporting System (NACRS). Odds ratios and their corresponding 95% confidence intervals were estimated using conditional logistic regression, and were adjusted for the confounding influence of daily number of influenza ED visits and weather variables using natural spline functions. Results: Statistically significant associations were observed between ambient air pollution levels and ED visits for asthma in Windsor. Effects were particularly pronounced among children 2 to 14 years of age between April and September. Namely, increases in the interquartile range with 1-day lagged exposure to SO2, NO2 and CO levels were associated with increased risks of an asthma visit of 19%, 25% and 36%, respectively. Conclusion: Exposure in Windsor to ambient air pollution increases the risk of ED visits for asthma, particularly among children. Key words: Air pollution; asthma; child; risk; cross-over studies Objectifs : La ville de Windsor est reconnue pour avoir une qualite d'air inferieure comparativement a d'autres villes canadiennes. Toutefois, peu d'etudes ont evalue l'association entre des fluctuations quotidiennes dans les niveaux de polluants atmospheriques et des problemes respiratoires a Windsor. Le but de cette etude est d'evaluer l'association entre le changement a court terme de polluants atmospheriques et les admissions a l'urgence dans la ville de Windsor. Methodes : Un devis d'etude cas-temoins de croisement stratifie sur le temps a ete applique a 3 728 visites dans les departements d'urgence des hopitaux de la ville de Windsor entre 2002 et 2009. Les niveaux de polluants atmospheriques pour cette region ont ete estimes en utilisant les sites de surveillance de la pollution atmospherique d'Environnement Canada. Les visites a l'urgence ont ete identifiees avec le Systeme national d'information sur les soins ambulatoires (SNISA). Des rapports de cote (RC) accompagnes d'intervalle de confiance a 95 % ont ete generes en utilisant la regression logistique conditionnelle et ont ete ajustes pour les facteurs confondants d'admissions quotidiennes a l'urgence pour un diagnostique d'influenza et des variables climatiques en utilisant des fonctions splines naturelles. Resultats : Des associations statistiquement significatives ont ete observes entre les polluants atmospheriques et les admissions a l'urgence pour de l'asthme a Windsor. Les effets etaient particulierement prononces chez les enfants de 2 a 14 ans entre les mois d'avril et septembre. Specifiquement, une augmentation dans l'ecart interquartile avec un decalage d'une journee dans l'exposition au S[O.sub.2], N[O.sub.2] et CO augmentait le risque d'une visite a l'urgence pour de l'asthme de 19 %, 25 % et 36 %, respectivement. Conclusion : L'exposition a la pollution de l'air ambiante a Windsor augmente le risque d'admission a l'urgence pour de l'asthme, particulierement chez les enfants. Mots cles : pollution de l'air; asthme; enfant; risque; cas-temoins de croisement, Ambient air pollution is recognized to adversely affect respiratory health. Several studies conducted in Canada (1-3) and elsewhere (4-7) have found that day-to-day increases in pollution levels are associated with [...]

Background: Maternal prenatal exposure to air pollution has been associated with adverse birth outcomes. However, previous studies focused on a priori time intervals such as trimesters reported inconsistent associations.Objectives: We investigated time-varying vulnerability of birth weight to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) using flexible time intervals.Methods: We analyzed 1,300 live, full-term births from Maternal-Infant Research on Environmental Chemicals, a Canadian prospective pregnancy cohort spanning 10 cities (2008-2011). Daily PM2.5 and NO2 concentrations were estimated from ground-level monitoring, satellite models, and land-use regression, and assigned to participants from pre-pregnancy through delivery. We developed a flexible two-stage modeling method-using a Bayesian Metropolis-Hastings algorithm and empirical density threshold-to identify time-dependent vulnerability to air pollution without specifying exposure periods a priori. This approach identified critical windows with varying lengths (2-363 days) and critical windows that fell within, or straddled, predetermined time periods (i.e., trimesters). We adjusted the models for detailed infant and maternal covariates.Results: Critical windows associated with reduced birth weight were identified during mid- to late-pregnancy for both PM2.5 and NO2: -6 g (95% credible interval: -11, -1 g) and -5 g (-10, -0.1 g) per µg/m3 PM2.5 during gestational days 91-139 and 249-272, respectively; and -3 g (-5, -1 g) per ppb NO2 during days 55-145.Discussion: We used a novel, flexible selection method to identify critical windows when maternal exposures to air pollution were associated with decrements in birth weight. Our results suggest that air pollution impacts on fetal development may not be adequately captured by trimester-based analyses. [ABSTRACT FROM AUTHOR]

Rationale: Current evidence on the relationship between long-term exposure to air pollution and new onset of chronic lung disease is inconclusive.Objectives: To examine associations of incident chronic obstructive pulmonary disease (COPD) and adult-onset asthma with past exposure to fine particulate matter ≤ 2.5 μm in diameter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and the redox-weighted average of NO2 and O3 (Ox) and characterize the concentration-response relationship.Methods: We conducted a population-based cohort study of all Ontarians, aged 35-85 years, from 2001 to 2015. A 3-year moving average of residential exposures to selected pollutants with a 1-year lag were estimated during follow-up. We used Cox proportional hazard models and Aalen additive-hazard models to quantify the pollution-disease associations and characterized the shape of these relationships using newly developed nonlinear risk models.Measurements and Main Results: Among 5.1 million adults, we identified 340,733 and 218,005 incident cases of COPD and asthma, respectively. We found positive associations of COPD with PM2.5 per interquartile-range (IQR) increase of 3.4 μg/m3 (hazard ratio, 1.07; 95% confidence interval, 1.06-1.08), NO2 per IQR increase of 13.9 ppb (1.04; 1.02-1.05), O3 per IQR increase of 6.3 ppb (1.04; 1.03-1.04), and Ox per IQR increase of 4.4 ppb (1.03; 1.03-1.03). By contrast, we did not find strong evidence linking these pollutants to adult-onset asthma. In addition, we quantified that each IQR increase in pollution exposure yielded 3.0 (2.4-3.6), 3.2 (2.0-4.3), 1.9 (1.3-2.5), and 2.3 (1.7-2.9) excess cases of COPD per 100,000 adults for PM2.5, NO2, O3, and Ox, respectively. Furthermore, most pollutant-COPD relationships exhibited supralinear shapes.Conclusions: Air pollution was associated with a higher incidence of COPD but was not associated with a higher incidence of adult-onset asthma. [ABSTRACT FROM AUTHOR]

Background: Nitrogen dioxide (NO2) is a pervasive urban pollutant originating primarily from vehicle emissions. Ischemic heart disease (IHD) is associated with a considerable public health burden worldwide, but whether NO2 exposure is causally related to IHD morbidity remains in question. Our objective was to determine whether short term exposure to outdoor NO2 is causally associated with IHD-related morbidity based on a synthesis of findings from case-crossover and time-series studies. Methods: MEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts between reviewers were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was conducted using random effects models, heterogeneity among included studies was assessed using Cochran's Q and I2 measures, and sources of heterogeneity were evaluated using meta-regression. Sensitivity of pooled estimates to individual studies was examined using Leave One Out analysis and publication bias was evaluated using Funnel plots, Begg's and Egger's tests, and trim and fill. Results: Thirty-eight case-crossover studies and 48 time-series studies were included in our analysis. NO2 was significantly associated with IHD morbidity (pooled odds ratio from case-crossover studies: 1.074 95% CI 1.052–1.097; pooled relative risk from time-series studies: 1.022 95% CI 1.016–1.029 per 10 ppb). Pooled estimates for case-crossover studies from Europe and North America were significantly lower than for studies conducted elsewhere. The high degree of heterogeneity among studies was only partially accounted for in meta-regression. There was evidence of publication bias, particularly for case-crossover studies. For both case-crossover and time-series studies, pooled estimates based on multi-pollutant models were smaller than those from single pollutant models, and those based on older populations were larger than those based on younger populations, but these differences were not statistically significant. Conclusions: We concluded that there is a likely causal relationship between short term NO2 exposure and IHD-related morbidity, but important uncertainties remain, particularly related to the contribution of co-pollutants or other concomitant exposures, and the lack of supporting evidence from toxicological and controlled human studies. [ABSTRACT FROM AUTHOR]

Background: Regional differences in the oxidative potential of fine particulate air pollution (PM2.5) may modify its impact on the risk of myocardial infarction.Methods: A case-crossover study was conducted in 16 cities in Ontario, Canada to evaluate the impact of regional PM2.5 oxidative potential on the relationship between PM2.5 and emergency room visits for myocardial infarction. Daily air pollution and meteorological data were collected between 2004 and 2011 from provincial monitoring sites and regional estimates of glutathione (OP(GSH)) and ascorbate-related (OP(AA)) oxidative potential were determined using an acellular assay based on a synthetic respiratory tract lining fluid. Exposure variables for the combined oxidant capacity of NO2 and O3 were also examined using their sum (Ox) and a weighted average (Ox (wt)) based on their redox potentials.Results: In total, 30,101 cases of myocardial infarction were included in the analysis. For regions above the 90(th) percentile of OP(GSH) each 5 μg/m(3) increase in same-day PM2.5 was associated with a 7.9 % (95 % CI: 4.1, 12) increased risk of myocardial infarction whereas a 4.1 % (95 % CI: 0.26, 8.0) increase was observed in regions above the 75(th) percentile and no association was observed below the 50(th) percentile (p-interaction = 0.026). A significant 3-way interaction was detected with the strongest associations between PM2.5 and myocardial infarction occurring in areas with high regional OP(GSH) and high Ox (wt) (p-interaction < 0.001).Conclusions: Regional PM2.5 oxidative potential may modify the impact of PM2.5 on the risk of myocardial infarction. The combined oxidant capacity of NO2 and O3 may magnify this effect. [ABSTRACT FROM AUTHOR]

An amendment to this paper has been published and can be accessed via the original article. [ABSTRACT FROM AUTHOR]

• We examined the association between air pollution and AKI death in 6 countries. • Increased PM 2.5 , O 3 , and NO 2 was associated with an increased risk of AKI death. • The risk of AKI death fluctuated for four weeks after exposure to air pollution. • 1.9%–6.3% of AKI deaths were attributed to pollution level above the WHO guideline. Recent studies have reported that air pollution is related to kidney diseases. However, the global evidence on the risk of death from acute kidney injury (AKI) owing to air pollution is limited. Therefore, we investigated the association between short-term exposure to air pollution—particulate matter ≤ 2.5 μm (PM 2.5), ozone (O 3), and nitrogen dioxide (NO 2)—and AKI-related mortality using a multi-country dataset. This study included 41,379 AKI-related deaths in 136 locations in six countries during 1987–2018. A novel case time-series design was applied to each air pollutant during 0–28 lag days to estimate the association between air pollution and AKI-related deaths. Moreover, we calculated AKI deaths attributable to non-compliance with the World Health Organization (WHO) air quality guidelines. The relative risks (95% confidence interval) of AKI-related deaths are 1.052 (1.003, 1.103), 1.022 (0.994, 1.050), and 1.022 (0.982, 1.063) for 5, 10, and 10 µg/m3 increase in lag 0–28 days of PM 2.5 , warm-season O 3 , and NO 2 , respectively. The lag-distributed association showed that the risk appeared immediately on the day of exposure to air pollution, gradually decreased, and then increased again reaching the peak approximately 20 days after exposure to PM 2.5 and O 3. We also found that 1.9%, 6.3%, and 5.2% of AKI deaths were attributed to PM 2.5 , warm-season O 3 , and NO 2 concentrations above the WHO guidelines. This study provides evidence that public health policies to reduce air pollution may alleviate the burden of death from AKI and suggests the need to investigate the several pathways between air pollution and AKI death. [ABSTRACT FROM AUTHOR]