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Background: Air pollution is one of the most serious environmental risks to mortality of stroke. However, there exists a noteworthy knowledge gap concerning the different stroke subtypes, causes of death, the susceptibility of stroke patient, and the role of greenness in this context., Methods: We analyzed data from an ecological health cohort, which included 334,261 patients aged ≥40 years with stroke (comprising 288,490 ischemic stroke and 45,771 hemorrhagic stroke) during the period 2013-2019. We used Cox proportional hazards models with time-varying exposure to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) to assess the associations of annual average fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) with both all-cause and cause-specific mortality. Additionally, we conducted analyses to examine the effect modification by greenness and identify potential susceptibility factors through subgroup analyses., Result: In multivariable-adjusted models, long-term exposure to PM 2.5 and NO 2 was associated with increased risk of all-cause mortality (HR: 1.038, 95% CI: 1.029-1.047 for PM 2.5 ; HR: 1.055, 95% CI: 1.026-1.085 for NO 2 , per 10 μg/m 3 , for ischemic stroke patients; similar for hemorrhagic stroke patients). Gradually increasing effect sizes were shown for CVD mortality and stroke mortality. The HRs of mortality were slightly weaker with high versus low vegetation exposure. Cumulative exposures increased the HRs of pollutant-related mortality, and greater greenness decreased this risk. Two subtypes of stroke patients exhibited diverse patterns of benefit., Conclusion: Increasing residential greenness attenuates the increased risk of mortality with different patterns due to chronic air pollutants for ischemic and hemorrhagic stroke, offering valuable insights for precise tertiary stroke prevention strategies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Co-exposure to air pollution and neighborhood disadvantage may influence cognition decline. We tested these associations in the context of dementia risk., Methods: We leveraged a cohort of adults ≥65 years (n = 5397) enrolled from 2011 to 2018 in the National Health and Aging Trends Study (NHATS). Particulate matter (PM) ≤ 10 μm in diameter, PM ≤ 2.5 μm in diameter, carbon monoxide, nitric oxide, and nitrogen dioxide - and neighborhood disadvantage were tested for joint associations with dementia risk. Pollutant concentrations at the 2010 census tract level were assigned using the US Environmental Protection Agency's Community Multiscale Air Quality Modeling System. Neighborhood disadvantage was defined using the tract Social Deprivation Index (SDI). Dementia was determined through self- or proxy-report or scores indicative of "probable dementia" according to NHATS screening tools. Joint effects of air pollutants and SDI were tested using quantile g-computation Cox proportional hazards models. We also stratified joint air pollution effects across SDI tertiles. Analyses adjusted for age at enrollment, sex, education, partner status, urbanicity, income, race and ethnicity, years at residence, census segregation, and census region., Results: SDI score (aHR = 1.08; 95% CI 0.96, 1.22), joint air pollution (aHR = 1.03, 95% CI 0.92, 1.16) and joint SDI with air pollution (aHR = 1.04, 95% CI 0.89, 1.22) were not associated with dementia risk. After accounting for competing risk of death, joint SDI with air pollution was not associated with dementia risk (aHR = 1.06; 95% CI 0.87, 1.29). In stratified models, joint air pollution was associated with greater risk of dementia at high (aHR = 1.19; 95% CI 0.87, 1.63), but not at medium or low SDI., Conclusion: Air pollution was associated with greater dementia risk in disadvantaged areas after accounting for competing risks. Air pollution associations with dementia incidence may be attenuated when other risk factors are more prominent in disadvantaged neighborhoods., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Aisha S. Dickerson reports financial support was provided by National Institute of Environmental Health Sciences. Aisha S. Dickerson reports financial support was provided by Bloomberg American Health Initiative. Roland J. Thorpe, Jr. reports financial support was provided by National Institute on Aging. Roland J. Thorpe, Jr. reports financial support was provided by National Institute on Minority Health and Health Disparities. Cavin Ward-Caviness reports a relationship with Clock Foundation that includes: board membership. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Evidence of the potential causal links between long-term exposure to particulate matters (PM, i.e., PM 1 , PM 2.5 , and PM 1-2.5 ) and T2DM mortality based on large cohorts is limited. In contrast, the existing evidence usually suffers from inherent bias with the traditional association assessment. A prospective cohort of 580,757 participants in the southern region of China were recruited during 2009 and 2015 and followed up through December 2020. PM exposure at each residential address was estimated by linking to the well-established high-resolution simulation dataset. Hazard ratios (HRs) were calculated using time-varying marginal structural Cox models, an established causal inference approach, after adjusting for potential confounders. During follow-up, a total of 717 subjects died from T2DM. For every 1 μg/m 3 increase in PM 2.5 , the adjusted HRs and 95% confidence interval (CI) for T2DM mortality was 1.036 (1.019-1.053). Similarly, for every 1 μg/m 3 increase in PM 1 and PM 1-2.5 , the adjusted HRs and 95% CIs were 1.032 (1.003-1.062) and 1.085 (1.054-1.116), respectively. Additionally, we observed a generally more pronounced impact among individuals with lower levels of education or lower residential greenness which as measured by the Normalized Difference Vegetation Index (NDVI). We identified substantial interactions between NDVI and PM 1 (P-interaction = 0.003), NDVI and PM 2.5 (P-interaction = 0.019), as well as education levels and PM 1 (P-interaction = 0.049). The study emphasizes the need to consider environmental and socio-economic factors in strategies to reduce T2DM mortality. We found that PM 1 , PM 2.5 , and PM 1-2.5 heighten the peril of T2DM mortality, with education and green space exposure roles in modifying it., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Air pollutants, such as fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ), have been associated with adverse birth outcomes, including low birth weight, often exhibiting sex-specific effects. However, the modifying effect of placental telomere length (TL), reflecting cumulative lifetime oxidative stress in mothers, remains unexplored., Method: Using data from a Northeastern U.S. birth cohort (n = 306), we employed linear regression and weighted quantile sum models to assess trimester-average air pollution exposures and birth weight for gestational age (BWGA) z-scores. Placental TL, categorized by median split, was considered as an effect modifier. Interactions among air pollutants, placental TL, infant sex, and BWGA z-score were evaluated., Results: Without placental TL as a modifier, only 1 st trimester O 3 was significantly associated with BWGA z-scores (coefficient: 0.33, 95% CI: 0.03, 0.63). In models considering TL interactions, a significant modifying effect was observed between 3 rd trimester NO 2 and BWGA z-scores (interaction p-value = 0.02). Specifically, a one interquartile range (1-IQR) increase in 3 rd trimester NO 2 was linked to a 0.28 (95% CI: 0.06, 0.52) change in BWGA z-score among shorter placental TL group, with no significant association among longer TL group. Among male infants, there were significant associations between 3 rd trimester PM 2.5 exposure and BWGA z-scores in the longer TL group (coefficient: -0.34, 95% CI: -0.61, -0.02), and between 1 st trimester O 3 exposure and BWGA z-scores among males in the shorter TL group (coefficient: 0.59, 95% CI: 0.06, 1.08). For females, only a negative association in 2 nd trimester mixture model was observed within the longer TL group (coefficient: -0.10, 95% CI: -0.21, -0.01)., Conclusion: These findings highlight the need to consider the complex interactions among prenatal air pollutant exposures, placental TL, and fetal sex to better elucidate those at greatest risk for adverse birth outcomes., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Haze weather, characterized by low visibility due to severe air pollution, has aroused great public concern. However, haze definitions are inconclusive, and multicentre studies on the health impacts of haze are scarce. We collected data on the daily number of deaths and environmental factors in 190 Chinese cities from 2014 to 2020. The city-specific association was estimated using quasi-Poisson regression and then pooled using meta-analysis. We found a negative association between daily visibility and non-accidental deaths, and mortality risk sharply increased when visibility was < 10 km. Haze weather, defined as a daily average visibility of < 10 km without a limit for humidity, produced the best model fitness and greatest effect on mortality. A haze day was associated with an increase of 2.53% (95% confidence interval [CI]:1.96, 3.10), 2.84 (95% CI: 2.13, 3.56), and 2.99% (95% CI: 1.94, 4.04) in all non-accident, cardiovascular and respiratory mortality, respectively. Haze had the greatest effect on lung cancer mortality. The haze-associated risk of mortality increased with age. Severe haze (visibility <2 km) and damp haze (haze with relative humidity >90%) had greater health impacts. Our findings can help in the development of early warning systems and effective public health interventions for haze., 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.)

Objective: Factors that shape individuals' vulnerability to the effects of air pollution on COVID-19 severity remain poorly understood. We evaluated whether the association between long-term exposure to ambient NO 2 , PM 2.5 , and PM 10 and COVID-19 hospitalisation differs by age, sex, individual income, area-level socioeconomic status, arterial hypertension, diabetes mellitus, and chronic obstructive pulmonary disease., Methods: We analysed a population-based cohort of 4,639,184 adults in Catalonia, Spain, during 2020. We fitted Cox proportional hazard models adjusted for several potential confounding factors and evaluated the interaction effect between vulnerability indicators and the 2019 annual average of NO 2 , PM 2.5 , and PM 10 . We evaluated interaction on both additive and multiplicative scales., Results: Overall, the association was additive between air pollution and the vulnerable groups. Air pollution and vulnerability indicators had a synergistic (greater than additive) effect for males and individuals with low income or living in the most deprived neighbourhoods. The Relative Excess Risk due to Interaction (RERI) was 0.21, 95 % CI, 0.15 to 0.27 for NO 2 and 0.16, 95 % CI, 0.11 to 0.22 for PM 2.5 for males; 0.13, 95 % CI, 0.09 to 0.18 for NO 2 and 0.10, 95 % CI, 0.05 to 0.14 for PM 2.5 for lower individual income and 0.17, 95 % CI, 0.12 to 0.22 for NO 2 and 0.09, 95 % CI, 0.05 to 0.14 for PM 2.5 for lower area-level socioeconomic status. Results for PM 10 were similar to PM 2.5 . Results on multiplicative scale were inconsistent., Conclusions: Long-term exposure to air pollution had a larger synergistic effect on COVID-19 hospitalisation for males and those with lower individual- and area-level socioeconomic status., 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.)

Background: Epidemiological evidence on the association of PM 2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) and its specific components with hypertension and blood pressure is limited., Methods: We applied information of participants from the World Health Organization's (WHO) Study on Global Ageing and Adult Health (SAGE) to estimate the associations of long-term PM 2.5 mass and its chemical components exposure with blood pressure (BP) and hypertension incidence in Chinese adults ≥ 50 years during 2007-2018. Generalized linear mixed model and Cox proportional hazard model were applied to investigate the effects of PM 2.5 mass and its chemical components on the incidence of hypertension and BP, respectively., Results: Each interquartile range (IQR = 16.80 μg/m 3 ) increase in the one-year average of PM 2.5 mass concentration was associated with a 17 % increase in the risk of hypertension (HR = 1.17, 95 % CI: 1.10, 1.24), and the population attributable fraction (PAF) was 23.44 % (95 % CI: 14.69 %, 31.55 %). Each IQR μg/m 3 increase in PM 2.5 exposure was also related to increases of systolic blood pressure (SBP) by 2.54 mmHg (95 % CI:1.99, 3.10), and of diastolic blood pressure (DBP) by 1.36 mmHg (95 % CI: 1.04, 1.68). Additionally, the chemical components of SO 4 2- , NO 3 - , NH 4 + , OM, and BC were also positively associated with an increased risk of hypertension incidence and elevated blood pressure., Conclusions: These results indicate that long-term exposure to PM 2.5 mass and its specific components may be major drivers of escalation in hypertension diseases., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: The adverse effect of air pollution on mortality is well documented worldwide but the identification of more vulnerable populations at higher risk of death is still limited. The aim of this study was to evaluate the association between natural mortality (overall and cause-specific) and short-term exposure to five air pollutants (PM 2.5 , PM 10 , NO 2 , O 3 and black carbon) and identify potential vulnerable populations in Belgium., Methods: We used a time-stratified case-crossover design with conditional logistic regressions to assess the relationship between mortality and air pollution in the nine largest Belgian agglomerations. Then, we performed a random-effect meta-analysis of the pooled results and described the global air pollution-mortality association. We carried out stratified analyses by individual characteristics (sex, age, employment, hospitalization days and chronic preexisting health conditions), living environment (levels of population density, built-up areas) and season of death to identify effect modifiers of the association., Results: The study included 304,754 natural deaths registered between 2010 and 2015. We found percentage increases for overall natural mortality associated with 10 μg/m 3 increases of air pollution levels of 0.6% (95% CI: 0.2%, 1.0%) for PM 2.5 , 0.4% (0.1%, 0.8%) for PM 10 , 0.5% (-0.2%, 1.1%) for O 3 , 1.0% (0.3%, 1.7%) for NO 2 and 7.1% (-0.1%, 14.8%) for black carbon. There was also evidence for increases of cardiovascular and respiratory mortality. We did not find effect modification by individual characteristics (sex, age, employment, hospitalization days). However, this study suggested differences in risk of death for people with preexisting conditions (thrombosis, cardiovascular diseases, asthma, diabetes and thyroid affections), season of death (May-September vs October-April) and levels of built-up area in the neighborhood (for NO 2 )., Conclusions: This work provided evidence for the adverse health effects of air pollution and contributed to the identification of specific population groups. These findings can help to better define public-health interventions and prevention strategies., (© 2024. The Author(s).)

Background: The independent effects of short-term exposure to increased air temperature and air pollution on mortality are well-documented. There is some evidence indicating that elevated concentrations of air pollutants may lead to increased heat-related mortality, but this evidence is not consistent. Most of these effects have been documented through time-series studies using city-wide data, rather than at a finer spatial level. In our study, we examined the possible modification of the heat effects on total and cause-specific mortality by air pollution at municipality level in the Attica region, Greece, during the warm period of the years 2000 to 2016., Methods: A municipality-specific over-dispersed Poisson regression model during the warm season (May-September) was used to investigate the heat effects on mortality and their modification by air pollution. We used the two-day average of the daily mean temperature and daily mean PM 10 , NO 2 and 8 hour-max ozone (O 3 ), derived from models, in each municipality as exposures. A bivariate tensor smoother was applied for temperature and each pollutant alternatively, by municipality. Α random-effects meta-analysis was used to obtain pooled estimates of the heat effects at different pollution levels. Heterogeneity of the between-levels differences of the heat effects was evaluated with a Q-test., Results: A rise in mean temperature from the 75th to the 99th percentile of the municipality-specific temperature distribution resulted in an increase in total mortality of 12.4% (95% Confidence Interval (CI):7.76-17.24) on low PM 10 days, and 21.25% (95% CI: 17.83-24.76) on high PM 10 days. The increase on mortality was 10.09% (95% CI: - 5.62- 28.41) on low ozone days, and 14.95% (95% CI: 10.79-19.27) on high ozone days. For cause-specific mortality an increasing trend of the heat effects with increasing PM 10 and ozone levels was also observed. An inconsistent pattern was observed for the modification of the heat effects by NO 2 , with higher heat effects estimated in the lower level of the pollutant., Conclusions: Our results support the evidence of elevated heat effects on mortality at higher levels of PM 10 and 8 h max O 3. Under climate change, any policy targeted at lowering air pollution levels will yield significant public health benefits., (© 2024. The Author(s).)

Evidence on the potential causal links of long-term air pollution exposure with lung cancer incidence (reflected by mortality and hospital admission) was limited, especially based on large cohorts. We examined the relationship between lung cancer and long-term exposure to particulate matter (PM, including PM 2.5 , PM 10 and PM 10-2.5 ) and nitrogen dioxide (NO 2 ) among a large cohort of general Chinese adults using causal inference approaches. The study included 575 592 participants who were followed up for an average of 8.2 years. The yearly exposure of PM and NO 2 was estimated through satellite-based random forest approaches and the ordinary kriging method, respectively. Marginal structural Cox models were used to examine hazard ratios (HRs) of mortality and hospital admission due to lung cancer following air pollution exposure, adjusting for potential confounders. The HRs of mortality due to lung cancer were 1.042 (95% confidence interval [CI]: 1.033-1.052), 1.032 (95% CI:1.024-1.041) and 1.052 (95% CI:1.041-1.063) for each 1 μg/m 3 increase in PM 2.5 , PM 10 and NO 2 , respectively. In addition, we observed statistically significant effects of PMs on hospital admission due to lung cancer. The HRs (95%CI) were 1.110 (1.027-1.201), 1.067 (1.020-1.115) and 1.079 (1.010-1.153) for every 1 μg/m 3 increase in PM 2.5 , PM 10 , PM 10-2.5 , respectively. Furthermore, we found larger effect estimates among the elderly and those who exercised more frequently. We provided the most comprehensive evidence of the potential causal links between two outcomes of lung cancer and long-term air pollution exposure. Relevant policies should be developed, with special attention to protecting the vulnerable groups of the population., (© 2023 UICC.)

Background: Although converging lines of research have pointed to the adverse neural effects of air pollution, evidence linking ozone (O 3 ) and neural damage remains limited., Objectives: To investigate the subclinical neural effects of short-term ozone (O 3 ) exposure in elderly adults., Methods: A panel of healthy elderly individuals was recruited, and five repeated measurements were conducted from December 2018 to April 2019 in Xinxiang, China. Serum neural damage biomarkers, including brain-derived neurotrophic factor (BDNF), neurofilament light chain (NfL), neuron-specific enolase (NSE), protein gene product 9.5 (PGP9.5), and S100 calcium-binding protein B (S100B) were measured at each follow-up session. Personal O 3 exposure levels were calculated based on outdoor monitoring and sampling times. A linear mixed-effects model was adopted to quantify the acute effect of O 3 on serum neural damage biomarkers. Stratification analysis based on sex, education level, physical activity, and glutathione S-transferases (GST) gene polymorphism analysis was performed to explore their potential modifying effects., Results: A total of 34 healthy volunteers aged 63.7 ± 5.7 y were enlisted and completed the study. The concentration of the daily maximum 8-h average O 3 (O 3 -8h) ranged from 19.5 to 160.5 μg/m 3 during the study period. Regression analysis showed that short-term O 3 exposure was associated positively with serum concentrations of neural damage biomarkers. A 10 μg/m 3 increase in O 3 -8h exposure was associated with an increment of 74 % (95 % CI:1 %-146 %) and 197 % (95 % CI:39 %-356 %) in BDNF (lag 2 d) and NfL (lag 1 d), respectively. The stratification results suggest that males, people with lower education levels, lower physical activity, and GST theta 1 (GSTT1)-sufficient genotype might be marginally more vulnerable., Conclusions: This study provides new evidence for the neural damage risk posed by O 3 exposure, even at relatively low concentrations, which, therefore, requires that stringent air quality standards be developed and implemented., 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. Mention of trade names or commercial products does not constitute endorsement or recommendation for use., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Pregnancy loss, a major health issue that affects human sustainability, has been linked to short-term exposure to ground-surface ozone (O 3 ). However, the association is inconsistent, possibly because of the co-occurrence of O 3 and heat episodes, as increased temperature is a risk factor for pregnancy loss. To explain this inconsistency, the effect of O 3 on pregnancy loss needs to be examined jointly with that of high temperature., Methods: A total of 247,305 pregnancy losses during the warm season were extracted from fetal death certificates from the 386 counties in contiguous United States from 1989 to 2005. We assessed environmental exposure based on the daily maximum 8 h average of O 3 from Air Quality System monitors and the 24 h average temperature from the North American Regional Reanalysis product. We conducted a bidirectional, time-stratified case-crossover study of the association between pregnancy loss and exposures to O 3 and temperature and their multiplicative interaction. The main time window for the exposure assessment was the day of case occurrence and the preceding 3 days. To estimate the association, we used conditional logistic regression with adjustment for relative humidity, height of the planetary boundary layer, and holidays. Sensitivity analyses were performed on the lagged structure, nonlinearity, and between-subpopulation heterogeneity of the estimated joint effect., Results: The joint effect was first estimated by the regression against categorical exposure by tertile. Compared to the low-low exposure group (O 3  ≤ 78 μg/m 3 and temperature ≤ 18 °C), the odds of pregnancy loss was significantly higher by 6.0 % (95 % confidence interval [CI] 2.4-9.7 %), 9.8 % (6.1-13.8 %), and 7.5 % (4.7-10.3 %) in the high-low (>104 μg/m 3 and ≤18 °C), low-high (≤78 μg/m 3 and >23 °C), and high-high (>104 μg/m 3 and >23 °C) groups. The model of linear exposure and the multiplicative interaction yielded similar results. Each increment of 10 μg/m 3 in O 3 and 1 °C in temperature was associated with a 3.0 % (2.0 %-4.0 %) and 3.9 % (3.5 %-4.3 %), respectively, increase in the odds of pregnancy loss. A decrease in odds of 0.2 % (0.1 %-0.2 %) was associated with the temperature × O 3 interaction. The finding of an antagonistic interaction between temperature and O 3 was confirmed by models parametrizing the joint exposure as alternative nonlinear terms (i.e., a two-dimensional spline term or a varying-coefficient term) and was robust to a variety of exposure lags and stratifications. Therefore, the marginal effect of O 3 was estimated to vary by climate zone. A significant association between O 3 and pregnancy loss was observed in the northern, but not southern, United States., Conclusion: Joint exposure to O 3 and high temperature can increase the risk for pregnancy loss. The adverse effect of O 3 is potentially modified by ambient temperature. In high-latitude cities, controlling for O 3 pollution could protect maternal health., 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 © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Published literature considering the association between ambient air pollution and blood pressure is highly inconsistent, which may be explained by the different proportions of susceptible subpopulations. We hypothesized that hypertensive patients are more sensitive to air pollution due to the disruption of neurohumoral system. The study aimed to reveal the association between PM 2.5 and its carbon components and blood pressure, and whether this association is modified by hypertension status. We conducted a panel study in Beijing, China. Four repeated measurements were performed from 2016 to 2018. Linear mixed-effects models and generalized additive mixed models were performed to investigate the associations between PM 2.5 and its carbon components and blood pressure. Subgroup analyses were performed by hypertension status to reveal potential effect modification. Among hypertensive patients, for every 1 μg/m 3 increment of PM 2.5 , TC, OC, and EC in 1-day to 2-day MA, SBP increased from 0.16 mmHg (95% CI, 0.03 to 0.29) to 6.75 mmHg (95% CI, 2.82 to 10.68), and PP increased from 0.14 mmHg (95% CI, 0.02 to 0.26) to 6.03% (95% CI, 2.46 to 9.59%), but no significant association was observed among non-hypertensive subjects. The p values for the interaction between pollutants and hypertension status in 1-day to 2-day MA were less than 0.05. These findings suggest that hypertensive patients may be more susceptible to the adverse effects of air pollution than non-hypertensive subjects, which might provide guidance to hypertensive patients living in areas with high levels of particle pollution., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: Both Nitrogen dioxide (NO 2 ) exposure and antenatal anxiety have individually been associated with small for gestational age (SGA). Little is known, however, about whether there is effect modification of antenatal anxiety on NO 2 -related SGA., Methods: The prospective birth cohort study included 1823 mother-newborn pairs in Guangzhou, China, from January 2017 to April 2020. Exposure to NO 2 during the pre-conceptional and prenatal periods was estimated using an inverse distance weighted method. Antenatal anxiety was assessed by Trait Anxiety Inventory. SGA was determined by the Chinese gestational age- and sex-specific birthweight standards. Cox proportional hazards regression models was used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs) for SGA as per 10 μg/m 3 increase in NO 2 . Modifying effects of trait anxiety on NO 2 -related SGA were identified by stratified analyses, and three-dimensional response surface plots and two-dimensional heat maps., Results: Each 10 μg/m 3 increase in NO 2 exposure during the third trimester was significantly associated with SGA risk among overall participants (HR = 1.221, 95 % CI: 1.014-1.471) and primipara (HR = 1.271, 95 % CI: 1.023-1.579). We found significant effect modification of anxiety level for NO 2 -related SGA in the third trimester (P interaction  < 0.05). Pregnant women with higher levels of trait anxiety were more likely to deliver SGA newborns, particularly for those with high trait anxiety (HR = 1.781, 95 % CI: 1.007-2.945). Primiparous women were more susceptible., Conclusions: This study provides evidence that antenatal trait anxiety may modify the effects of maternal NO 2 exposure on SGA risk. The third trimester could be a critical window of susceptibility., 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 © 2023 Elsevier B.V. All rights reserved.)

Background: The epidemiological evidence on the interaction between heat and ambient air pollution on mortality is still inconsistent., Objectives: To investigate the interaction between heat and ambient air pollution on daily mortality in a large dataset of 620 cities from 36 countries., Methods: We used daily data on all-cause mortality, air temperature, particulate matter ≤ 10 μm (PM 10 ), PM ≤ 2.5 μm (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) from 620 cities in 36 countries in the period 1995-2020. We restricted the analysis to the six consecutive warmest months in each city. City-specific data were analysed with over-dispersed Poisson regression models, followed by a multilevel random-effects meta-analysis. The joint association between air temperature and air pollutants was modelled with product terms between non-linear functions for air temperature and linear functions for air pollutants., Results: We analyzed 22,630,598 deaths. An increase in mean temperature from the 75 th to the 99 th percentile of city-specific distributions was associated with an average 8.9 % (95 % confidence interval: 7.1 %, 10.7 %) mortality increment, ranging between 5.3 % (3.8 %, 6.9 %) and 12.8 % (8.7 %, 17.0 %), when daily PM 10 was equal to 10 or 90 μg/m 3 , respectively. Corresponding estimates when daily O 3 concentrations were 40 or 160 μg/m 3 were 2.9 % (1.1 %, 4.7 %) and 12.5 % (6.9 %, 18.5 %), respectively. Similarly, a 10 μg/m 3 increment in PM 10 was associated with a 0.54 % (0.10 %, 0.98 %) and 1.21 % (0.69 %, 1.72 %) increase in mortality when daily air temperature was set to the 1 st and 99 th city-specific percentiles, respectively. Corresponding mortality estimate for O 3 across these temperature percentiles were 0.00 % (-0.44 %, 0.44 %) and 0.53 % (0.38 %, 0.68 %). Similar effect modification results, although slightly weaker, were found for PM 2.5 and NO 2 ., Conclusions: Suggestive evidence of effect modification between air temperature and air pollutants on mortality during the warm period was found in a global dataset of 620 cities., 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 © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Studies suggested that greenness could reduce death risks related to ambient exposure to particulate matter (PM), while the available evidence was mixed across the globe and substantially exiguous in low- and middle-income countries. By conceiving an individual-level case-crossover study in central China, this analysis primarily aimed to quantify PM-mortality associations and examined the modification effect of greenness on the relationship., Methods: We investigated a total of 177,058 nonaccidental death cases from 12 counties in central China, 2008-2012. Daily residential exposures to PM 2.5 (aerodynamic diameter <2.5 µm), PM c (aerodynamic diameter between 2.5 and 10 µm), and PM 10 (aerodynamic diameter <10 µm) were assessed at a 1 × 1-km resolution through satellite-derived machine-learning models. Residential surrounding greenness was assessed using satellite-derived enhanced vegetation index (EVI) and normalized difference vegetation index (NDVI) at multiple buffer sizes (250, 500, and 1000 m). To quantify the acute mortality risks associated with short-term exposure to PM 2.5 , PM c , and PM 10 , a time-stratified case-crossover design was utilized in conjunction with a conditional logistic regression model in our main analyses. To investigate the effect modification of greenness on PM-mortality associations, we grouped death cases into low, medium, and high greenness levels using cutoffs of 25th and 75th percentiles of NDVI or EVI exposure, and examined potential effect heterogeneity in PM-related mortality risks among these groups., Results: Mean concentrations (standard deviation) on the day of death were 73.8 (33.4) μg/m 3 for PM 2.5 , 43.9 (17.3) μg/m 3 for PM c , and 117.5 (44.9) μg/m 3 for PM 10 . Size-fractional PM exposures were consistently exhibited significant associations with elevated risks of nonaccidental and circulatory mortality. For every increase of 10-μg/m 3 in PM exposure, percent excess risks of nonaccidental and circulatory mortality were 0.271 (95% confidence interval [CI]: 0.010, 0.533) and 0.487 (95% CI: 0.125, 0.851) for PM 2.5 at lag-01 day, 0.731 (95% CI: 0.108, 1.359) and 1.140 (95% CI: 0.267, 2.019) for PM c at lag-02 day, and 0.271 (95% CI: 0.010, 0.533) and 0.386 (95% CI: 0.111, 0.662) for PM 10 at lag-01 day, respectively. Compared to participants in the low-level greenness areas, those being exposed to higher greenness were found to be at lower PM-associated risks of nonaccidental and circulatory mortality. Consistent evidence for alleviated risks in medium or high greenness group was observed in subpopulations of female and younger groups (age <75)., Conclusions: Short-term exposure to particulate air pollution was associated with elevated risks of nonaccidental and circulatory death, and individuals residing in higher neighborhood greenness possessed lower risk of PM-related mortality. These findings emphasized the potential public health advantages through incorporating green spaces into urban design and planning., 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 © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Cardiovascular disease (CVD) mortality is associated with long-term particulate matter (PM) exposure. However, evidence from large, highly-exposed population cohort and observational-data-based causal inference approaches remains limited., Aims: We examined the potential causal links between PM exposure and the CVD mortality in South China., Methods: 580,757 participants were recruited during 2009-2015 and followed up through 2020. Satellite-based annual concentrations of PM 2.5 , PM 10 , and PM coarse (i.e., PM 10 - PM 2.5 ) at 1 km 2 spatial resolution were estimated and assigned to each participant. Marginal structural Cox models with time-varying covariates, adjusted using inverse probability weighting, were developed to evaluate the association between prolonged PM exposure and CVD mortality., Results: For overall CVD mortality, the hazard ratios and 95% confidence interval for each 1 μg/m 3 increase in the annual average concentration of PM 2.5 , PM 10 , and PM coarse were 1.033 (1.028-1.037), 1.028 (1.024-1.032), and 1.022 (1.012-1.033), respectively. All three PMs were linked to a higher mortality risk for myocardial infarction and ischemic heart disease (IHD). The mortality risk of chronic IHD and hypertension was linked to PM 2.5 and PM 10 . Significant association between PM coarse and other heart disease mortality was also observed. The older, women, less-educated participants, or inactive participants exhibited particularly higher susceptibility. Participants who were generally exposed to PM 10 concentrations below 70 μg/m 3 were more vulnerable to PM 2.5 -, PM 10 - and PM coarse -CVD mortality risks., Conclusion: This large cohort study provides evidence for the potential causal links between increased CVD mortality and ambient PM exposure, as well as socio-demographics linked to the highest vulnerability., 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 © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Evidence on the potential interactive effects of heat and ambient air pollution on cause-specific mortality is inconclusive and limited to selected locations., Objectives: We investigated the effects of heat on cardiovascular and respiratory mortality and its modification by air pollution during summer months (six consecutive hottest months) in 482 locations across 24 countries., Methods: Location-specific daily death counts and exposure data (e.g., particulate matter with diameters ≤ 2.5 µm [PM 2.5 ]) were obtained from 2000 to 2018. We used location-specific confounder-adjusted Quasi-Poisson regression with a tensor product between air temperature and the air pollutant. We extracted heat effects at low, medium, and high levels of pollutants, defined as the 5th, 50th, and 95th percentile of the location-specific pollutant concentrations. Country-specific and overall estimates were derived using a random-effects multilevel meta-analytical model., Results: Heat was associated with increased cardiorespiratory mortality. Moreover, the heat effects were modified by elevated levels of all air pollutants in most locations, with stronger effects for respiratory than cardiovascular mortality. For example, the percent increase in respiratory mortality per increase in the 2-day average summer temperature from the 75th to the 99th percentile was 7.7% (95% Confidence Interval [CI] 7.6-7.7), 11.3% (95%CI 11.2-11.3), and 14.3% (95% CI 14.1-14.5) at low, medium, and high levels of PM 2.5 , respectively. Similarly, cardiovascular mortality increased by 1.6 (95%CI 1.5-1.6), 5.1 (95%CI 5.1-5.2), and 8.7 (95%CI 8.7-8.8) at low, medium, and high levels of O 3 , respectively., Discussion: We observed considerable modification of the heat effects on cardiovascular and respiratory mortality by elevated levels of air pollutants. Therefore, mitigation measures following the new WHO Air Quality Guidelines are crucial to enhance better health and promote sustainable development., 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 © 2023. Published by Elsevier Ltd.)

Background: Green space is a newly modifiable environmental factor which would bring health benefits, and identifying potential pathways is important to better promote public health. Nowadays, limited evidence is available on residential green space and risk of incident type 2 diabetes (T2D). To evaluate the longitudinal association between residential green space and incident T2D, and further illustrate the role of air pollution, we conducted a prospective analysis in UK Biobank., Methods: Incident cases of T2D were ascertained through medical linkage of hospital admissions. Residential green space indicated by percentage of green space at 300 m buffer was estimated using land use data. Annual average air pollution was modelled using Land Use Regression model. Cox proportional hazard regression models were used to determine the association between the exposure and incident T2D. Effect modification of air pollution was assessed using log-likelihood tests. Casual mediation analysis including interaction of green space and air pollution was used to quantity pure natural indirect effect of air pollution., Results: Of 379,238 participants at baseline, 15564 incident T2D cases were identified with 12.4 years of follow-up. In main models, individuals who exposed to residential green space at 300 m buffer in high level (≥75 %) had 14.4 % (95 % CI: 8.0 %, 20.3 %) lower risk of incident T2D compared with those in low level (<25 %). This association was modified by NO 2 , with green space indicating higher protective effect in low NO 2 level (P interaction = 0.098). PM 2.5 had a high mediation effect of 37.0 % in the association., Conclusion: Elevated residential green space level was associated with lower risk of incident T2D, and air pollution played an important role in this association. These findings would contribute to policy making and healthy city construction to take air pollution into consideration while planning green space, which would maximize public health benefits., 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 © 2023 Elsevier B.V. All rights reserved.)

Background: Although the association between short-term air pollution exposure and certain hospitalizations has been well documented, evidence on the effect of longer-term (e. g., monthly) air pollution on a comprehensive set of outcomes is still limited., Method: A total of 68,416 people in South China were enrolled and followed up during 2019-2020. Monthly air pollution level was estimated using a validated ordinary Kriging method and assigned to individuals. Time-dependent Cox models were developed to estimate the relationship between monthly PM 10 and O 3 exposures and the all-cause and cause-specific hospitalizations after adjusting for confounders. The interaction between air pollution and individual factors was also investigated., Results: Overall, each 10 μg/m 3 increase in PM 10 concentration was associated with a 3.1% (95% CI : 1.3%-4.9%) increment in the risk of all-cause hospitalization. The estimate was even greater following O 3 exposure (6.8%, 5.5%-8.2%). Furthermore, each 10 μg/m 3 increase in PM 10 was associated with a 2.3%-9.1% elevation in all the cause-specific hospitalizations except for those related to respiratory and digestive diseases. The same increment in O 3 was relevant to a 4.7%-22.8% elevation in the risk except for respiratory diseases. Additionally, the older individuals tended to be more vulnerable to PM 10 exposure ( P interaction : 0.002), while the alcohol abused and those with an abnormal BMI were more vulnerable to the impact of O 3 ( P interaction : 0.052 and 0.011). However, the heavy smokers were less vulnerable to O 3 exposure ( P interaction : 0.032)., Conclusion: We provide comprehensive evidence on the hospitalization hazard of monthly PM 10 and O 3 exposure and their interaction with individual factors., 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 © 2023 Ju, Yimaer, Du, Wang, Cai, Chen, Zhang, Wu, Wu, Lin, Wang, Jiang, Hu, Zhang and Hao.)

Numerous epidemiological studies have reported that ozone (O 3 ) and temperature are independently associated with health outcomes, but modification of the effects of O 3 on health outcomes by temperature, and vice versa, has not been fully described. This study aimed to investigate effect modification by temperature on the association between O 3 and emergency ambulance dispatches (EADs) in Japan. Data on daily air pollutants, ambient temperature, and EADs were obtained from eight Japanese cities from 2007 to 2015. A distributed lag non-linear model combined with Poisson regression was performed with temperature as a confounding factor and effect modifier to estimate the effects of O 3 on EADs at low (<25th percentile), moderate (25th-75th percentile), and high (>75th percentile) temperature for each city. The estimates obtained from each city were pooled by random-effects meta-analysis. When temperature was entered as a confounder, the estimated effects of O 3 on EADs for all acute, cardiovascular, and respiratory illnesses were largest at lag 0 (current-day lag). Therefore, this lag was used to further estimate the effects of O 3 on EADs in each temperature category. The estimated effects of O 3 on EADs for all acute, cardiovascular, and respiratory illnesses in all eight Japanese cities increased with increasing temperature. Specifically, a 10 ppb increase in O 3 was associated with 0.80 % (95 % CI: 0.25 to 1.35), 0.19 % (95 % CI: -0.85 to 1.25), and 1.14 % (95 % CI: -0.01 to 2.31) increases in the risk of EADs for all acute, cardiovascular, and respiratory illnesses, respectively, when city-specific daily temperature exceeded the 75th percentile. Our findings suggest that the association between O 3 and EADs for all acute, cardiovascular, and respiratory illnesses is the highest during high temperature. Finding of this study can be used to develop potential mitigation measures against O 3 exposure in high temperature environment to reduce its associated adverse health effects., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have influenced the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Objective: Ambient extreme temperatures have been associated with mental and behavior disorders (MBDs). However, few studies have assesed whether vulnerability factors such as ambient air pollution, pre-existing mental health conditions and residential environmental factors increase susceptibility. This study aims to evaluate the associations between short-term variations in outdoor ambient extreme temperatures and MBD-related emergency department (ED) visits and how these associations are modified by vulnerability factors., Methods: We conducted a case-crossover study of 9,958,759 MBD ED visits in Alberta and Ontario, Canada made between March 1st, 2004 and December 31st, 2020. Daily average temperature was assigned to individual cases with ED visits for MBD using gridded data at a 1 km × 1 km spatial resolution. Conditional logistic regression was used to estimate associations between extreme temperatures (i.e., risk of ED visit at the 2.5th percentile temperature for cold and 97.5th percentile temperature for heat for each health region compared to the minimal temperature risk) and MBD ED visits. Age, sex, pre-existing mental health conditions, ambient air pollution (i.e. PM 2.5 , NO 2 and O 3 ) and residential environmental factors (neighborhood deprivation, residential green space exposure and urbanization) were evaluated as potential effect modifiers., Results: Cumulative exposure to extreme heat over 0-5 days (odds ratio [OR] = 1.145; 95% CI: 1.121-1.171) was associated with ED visits for any MBD. However, cumulative exposure to extreme cold was associated with lower risk of ED visits for any MBD (OR = 0.981; 95% CI: 0.976-0.987). We also found heat to be associated with ED visits for specific MBDs such as substance use disorders, dementia, neurotic disorders, schizophrenia and personality behavior disorder. Individuals with pre-existing mental health conditions, those exposed to higher daily concentrations of NO 2 and O 3 and those residing in neighborhoods with greater material and social deprivation were at higher risk of heat-related MBD ED visits. Increasing tree canopy coverage appeared to mitigate risks of the effect of heat on MBD ED visits., Conclusions: Findings provide evidence that the impacts of heat on MBD ED visits may vary across different vulnerability factors., 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., (Crown Copyright © 2022. Published by Elsevier Inc. All rights reserved.)

Emerging evidence suggests residential surrounding green space is beneficial for human health. The association between green space and GDM showed inconsistent results, and potential effect modification of green space with air pollution is still unclear. This study aims to evaluate the association between green space and GDM, and further explore potential interaction and medication effects. Participants were recruited from a retrospective cohort study between 2015 and 2020 in Henan, China. Residential green space based on normalized difference vegetation index (NDVI) and air pollution exposure were estimated using spatial-statistical models. Multivariate logistic regression was applied to evaluate the association between per 0.1 unit increase in NDVI with 4 buffer sizes (250 m, 500 m, 1000 m, 2000 m) and GDM. We examined potential interaction of green space and air pollutants on GDM. Mediating effects of air pollution associated with green space exposure on GDM were also investigated by causal mediation analyses. A total of 46,665 eligible pregnant women were identified. There were 4092 (8.8 %) women diagnosed with GDM according to the IADPSG criteria. We found that per 0.1-unit increment in NDVI 250 m , NDVI 500 m , NDVI 1000 m and NDVI 2000 m in second trimester were associated with the decreased risk of GDM, with adjusted OR of 0.921(95 %CI: 0.890-0.953), 0.922 (95 %CI: 0.891-0.953), 0.921 (95 %CI: 0.892-0.952) and 0.921 (95 %CI: 0.892-0.951), respectively. We identified significant interactions between second trimester PM 2.5 and O 3 exposure and NDVI for GDM (P interaction < 0.001). The causal mediation analysis showed that PM 2.5 mediated approximately 2.5-5.5 % of the association between green space and GDM, while the estimated mediating effect of O 3 was approximately 30.1-38.5 %. In conclusion, our study indicates that residential green space was associated with a reduced risk of GDM, particularly second trimester. Green space may benefit to GDM partly mediated by a reduction in PM 2.5 and O 3 ., 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 © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Socioeconomic status (SES) was a crucial influencing factor of household air pollution (HAP). However, few studies have explored the potential effect modification of SES on the associations of HAP with type 2 diabetes mellitus (T2DM) and glucose homeostasis., Methods: A total of 20900 participants were obtained from the Henan Rural Cohort. HAP reflected by cooking fuel type and cooking duration was assessed via questionnaire. SES was evaluated by two dimensions: educational level and average monthly income. Associations of cooking fuel type, cooking duration with T2DM and glucose homeostasis indices (insulin, fasting plasma glucose (FPG), and HOMA-β) were assessed by the generalized linear model. Analyses were also conducted in different SES groups to explore the potential effect modification., Results: Significant negative association of cooking fuel type and cooking duration with T2DM, FPG, and HOMA-β was not observed. However, cooking with solid fuel and long-duration cooking were associated with decreased insulin level in women, and the adjusted coefficients were - 0.35 (95% confidence interval (95% CI): - 0.53, - 0.17) and - 0.36 (95% CI: -0.50, -0.21), respectively. Results from stratified analyses showed that these associations were more prominent in women with low average monthly income, with corresponding coefficient of - 0.57 (95% CI: -0.77, -0.37) for cooking with solid fuel and - 0.34 (95% CI: -0.52, -0.16) for long-duration cooking. Among women with low average monthly income, the largest decreased insulin level was observed in those who cooked with solid fuel, long-duration and poor kitchen ventilation, while the negative association of cooking fuel type and cooking duration with insulin level was slightly alleviated in the good kitchen ventilation group., Conclusions: Low average monthly income aggravated the negative association of HAP and insulin level among rural women, while improving kitchen ventilation may be a practical intervention., Trail Registration: The Henan Rural Cohort Study has been registered at Chinese Clinical Trial Register (Registration number: ChiCTR-OOC-15006699). Date of registration: 06 July, 2015. http://www.chictr.org.cn/showproj.aspx?proj=11375., 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 © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Children are vulnerable to the respiratory effects of air pollution, and their lung function has been associated with long-term exposure to low air pollution level in developed countries. However, the impact of contemporary air pollution level in developing countries as a result of recent efforts to improve air quality on children's lung function is less understood., Methods: We obtained a cross-sectional sample of 617 schoolchildren living in three differently polluted areas in Anhui province, China. 2-year average concentrations of air pollutants at the year of spirometry and the previous year (2017-2018) obtained from district-level air monitoring stations were used to characterize long-term exposure. Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV 1 ), and forced expiratory flow between 25 and 75% of FVC (FEF 25-75 ) were determined under strict quality control. Multivariable regression was employed to evaluate the associations between air pollution level and lung function parameters, overall and by demographic characteristics, lifestyle, and vitamin D that was determined by liquid chromatography tandem mass spectrometry., Results: Mean concentration of fine particulate matter was 44.7 μg/m 3 , which is slightly above the interim target 1 standard of the World Health Organization. After adjusting for confounders, FVC, FEV 1 , and FEF 25-75 showed inverse trends with increasing air pollution levels, with children in high exposure group exhibiting 87.9 [95% confidence interval (CI): 9.5, 166.4] mL decrement in FEV 1 and 195.3 (95% CI: 30.5, 360.1) mL/s decrement in FEF 25-75 compared with those in low exposure group. Additionally, the above negative associations were more pronounced among those who were younger, girls, not exposed to secondhand smoke, non-overweight, physically inactive, or vitamin D deficient., Conclusions: Our study suggests that long-term exposure to relatively high air pollution was associated with impaired lung function in children. More stringent pollution control measures and intervention strategies accounting for effect modification are needed for vulnerable populations in China and other developing countries., 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 © 2022 Teng, Li, Yang, Cui, Xia, Chen, Zheng, Bao, Wang, Shen, Zhang, Meng, Wang, Wu, Xu, Wang, Ding, Duan and Li.)

Background: There is strong evidence of mortality being associated to extreme temperatures but the extent to which individual or residential factors modulate this temperature vulnerability is less clear., Methods: We conducted a multi-city study with a time-stratified case-crossover design and used conditional logistic regression to examine the association between extreme temperatures and overall natural and cause-specific mortality. City-specific estimates were pooled using a random-effect meta-analysis to describe the global association. Cold and heat effects were assessed by comparing the mortality risks corresponding to the 2.5 th and 97.5 th percentiles of the daily temperature, respectively, with the minimum mortality temperature. For cold, we cumulated the risk over lags of 0 to 28 days before death and 0 to 7 days for heat. We carried out stratified analyses and assessed effect modification by individual characteristics, preexisting chronic health conditions and residential environment (population density, built-up area and air pollutants: PM 2.5 , NO 2 , O 3 and black carbon) to identify more vulnerable population subgroups., Results: Based on 307,859 deaths from natural causes, we found significant cold effect (OR = 1.42, 95%CI: 1.30-1.57) and heat effect (OR = 1.17, 95%CI: 1.12-1.21) for overall natural mortality and for respiratory causes in particular. There were significant effects modifications for some health conditions: people with asthma were at higher risk for cold, and people with psychoses for heat. In addition, people with long or frequent hospital admissions in the year preceding death were at lower risk. Despite large uncertainties, there was suggestion of effect modification by air pollutants: the effect of heat was higher on more polluted days of O 3 and black carbon, and a higher cold effect was observed on more polluted days of PM 2.5 and NO 2 while for O 3 , the effect was lower., Conclusions: These findings allow for targeted planning of public-health measures aiming to prevent the effects of extreme temperatures., 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 © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Active mobility (AM), defined as walking and cycling for transportation, can improve health through increasing regular physical activity. However, these health improvements could be outweighed by harm from inhaling traffic-related air pollutants during AM participation. The interaction of AM and air pollutants on health is complex physiologically, manifesting as acute changes in health indicators that may lead to poor long-term health consequences. The aim of this study was to systematically review the current evidence of effect modification by air pollution (AP) on associations between AM and health indicators. Studies were included if they examined associations between AM and health indicators being modified by AP or, conversely, associations between AP and health indicators being modified by AM. Thirty-three studies met eligibility criteria. The main AP indicators studied were particulate matter, ultrafine particles, and nitrogen oxides. Most health indicators studied were grouped into cardiovascular and respiratory indicators. There is evidence of a reduction by AP, mainly ultrafine particles and PM 2.5 , in the short-term health benefits of AM. Multiple studies suggest that long-term health benefits of AM are not negatively associated with levels of the single traffic-related pollutant NO 2 . However, other studies reveal reduced long-term health benefits of AM in areas affected by high levels of pollutant mixtures. We recommend that future studies adopt consistent and rigorous study designs and include reporting of interaction testing, to advance understanding of the complex relationships between AM, AP, and health indicators., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Objective: To investigate the potential effect of modification of antihypertensive medications on the association of nitrogen dioxide (NO 2 ) long-term exposure and chronic kidney disease (CKD)., Methods: Data of the national representative sample of adult population from the China National Survey of Chronic Kidney Disease (2007-2010) were included in the analyses, and exposure data of NO 2 were collected and matched. Generalized mixed-effects models were used to analyze the associations between NO 2 and CKD, stratified by the presence of hypertension and taking antihypertensive medications. The stratified exposure-response curves of NO 2 and CKD were fitted using the natural spine smoothing function. The modifying effects of antihypertensive medications on the association and the exposure-response curve of NO 2 and CKD were analyzed., Results: Data of 45 136 participants were included, with an average age of (49.5±15.3) years. The annual average exposure concentration of NO 2 was (7.2±6.4) μg/m 3 . Altogether 6 517 (14.4%) participants were taking antihypertensive medications, and 4 833 (10.7%) participants were identified as having CKD. After adjustment for potential confounders, in the hypertension population not using antihypertensive medications, long-term exposure to NO 2 was associated with a significant increase risk of CKD ( OR : 1.38, 95% CI : 1.24-1.54, P < 0.001); while in the hypertension population using antihypertensive medications, no significant association between long-term exposure to NO 2 and CKD ( OR : 0.96, 95% CI : 0.86-1.07, P =0.431) was observed. The exposure-response curve of NO 2 and CKD suggested that there was a non-linear trend in the association between NO 2 and CKD. The antihypertension medications showed significant modifying effects both on the association and the exposure-response curve of NO 2 and CKD (interaction P < 0.001)., Conclusion: The association between long-term exposure to NO 2 and CKD was modified by antihypertensive medications. Taking antihypertensive medications may mitigate the effect of long-term exposure to NO 2 on CKD.

Background: Maternal exposure to air pollution has been associated with birth outcomes; however, few studies examined biologically critical exposure windows shorter than trimesters or potential effect modifiers., Objectives: To examine associations of prenatal fine particulate matter (PM 2.5 ), by trimester and in biologically critical windows, with birth outcomes and assess potential effect modifiers., Methods: This study used two pregnancy cohorts (CANDLE and TIDES; N = 2099) in the ECHO PATHWAYS Consortium. PM 2.5 was estimated at the maternal residence using a fine-scale spatiotemporal model, averaged over pregnancy, trimesters, and critical windows (0-2 weeks, 10-12 weeks, and last month of pregnancy). Outcomes were preterm birth (PTB, <37 completed weeks of gestation), small-for-gestational-age (SGA), and continuous birthweight. We fit multivariable adjusted linear regression models for birthweight and Poisson regression models (relative risk, RR) for PTB and SGA. Effect modification by socioeconomic factors (maternal education, household income, neighborhood deprivation) and infant sex were examined using interaction terms., Results: Overall, 9% of births were PTB, 10.4% were SGA, and mean term birthweight was 3268 g (SD = 558.6). There was no association of PM 2.5 concentration with PTB or SGA. Lower birthweight was associated with higher PM 2.5 averaged over pregnancy (β -114.2, 95%CI -183.2, -45.3), during second (β -52.9, 95%CI -94.7, -11.2) and third (β -45.5, 95%CI -85.9, -5.0) trimesters, and the month prior to delivery (β -30.5, 95%CI -57.6, -3.3). Associations of PM 2.5 with likelihood of SGA and lower birthweight were stronger among male infants (p-interaction ≤0.05) and in those with lower household income (p-interaction = 0.09)., Conclusions: Findings from this multi city U.S. birth cohort study support previous reports of inverse associations of birthweight with higher PM 2.5 exposure during pregnancy. Findings also suggest possible modification of this association by infant sex and household income., (Copyright © 2022. Published by Elsevier Inc.)

Background: Air pollution and previous abortion have been reported to be related to preterm birth (PTB). But rare study examined the effect of air pollution on PTB risk among mothers with previous abortion., Objective: To estimate the effect of air pollution on PTB and the potential effect modification of previous abortion on such an association in rural part of Henan province (China)., Method: Based on National Free Preconception Health Examination Project (NFPHEP), information from the medical records of 57,337 mothers with previous abortion were obtained. An inverse distance-weighted model was used to estimate exposure levels of air pollutants. The effect of air pollution on the risk of PTB was estimated with a multiple logistic regression model. Stratified and interaction analyses were undertaken to explore the potential effect modification of previous abortion on this association., Results: The risk of PTB was positively associated with exposure to levels of nitrogen dioxide (NO 2 ; OR: 1.03; 95%CI: 1.02-1.04)], and sulfur dioxide (SO 2 ; 1.04; 1.02-1.07), and negatively associated with ozone (O 3 ) exposure (0.97; 0.97-0.98) during the entire pregnancy. Besides, we observed a positive effect of carbon monoxide (CO) exposure during the third trimester of pregnancy on PTB (1.14; 1.01-1.29). The type of previous abortion could modify the effect of air pollution on the PTB risk (P- interaction < 0.05). Compared with mothers with previous induced abortion, mothers with previous spontaneous abortion carried a higher risk of PTB induced by NO 2 , CO, and O 3 ., Conclusions: The risk of PTB was positively associated with levels of NO 2 , SO 2 and CO, and negatively associated with the O 3 level. The types of previous abortion could modify the effect of air pollution on PTB. Mothers who had an abortion previously, especially spontaneous abortion, should avoid exposure to air pollution to improve their pregnancy outcome., (Copyright © 2022 Elsevier Inc. All rights reserved.)

The associations between particulate matter (PM) exposure, psychosocial stress and blood cell parameters are bringing novel insights to characterize the early damage of multiple diseases. Based on two studies conducted in three Chinses cities using cross-sectional (Beijing, 425 participants) and panel study (Tianjin and Shanghai, 92 participants with 361 repeated measurements) designs, this study explored the associations between short-term exposure to ambient PM and blood cell parameters, and the effect modification by psychosocial stress. Increasing PM 2.5 exposure was significantly associated with decreases in red blood cell (RBC) count and mean corpuscular hemoglobin concentration (MCHC), and increases in mean corpuscular volume (MCV), platelets count (PLT) and platelet hematocrit (PCT) in both studies. For instance, a 10 μg/m 3 increment in PM 2.5 concentration was associated with a 1.04% (95%CI: 0.16%, 1.92%) increase in PLT (4-d) and a 1.09% (95%CI: 0.31%, 1.87%) increase in PCT (4-d) in the cross-sectional study, and a 0.64% (95%CI: 0.06%, 1.22%) increase in PLT (1-d) and a 0.72% (95%CI: 0.33%, 1.11%) increase in PCT (1-d) in the panel study, respectively. In addition, stronger increases in MCV, PLT, and PCT associated with PM 2.5 exposure were found in higher psychosocial stress group compared to lower psychosocial stress group (p for interaction <0.10), indicating that blood cell parameters of individuals with higher psychosocial stress might be more susceptible to the early damages of PM 2.5 exposure., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: The health effects of fine particulate matter (PM 2.5 ) may be worse at higher temperatures., Objective: To investigate temperature's effect on PM 2.5 -mortality/morbidity associations in Lima, Peru., Methods: Time-series regressions relating PM 2.5 and temperature to mortality and emergency room (ER) visits during 2010-2016. Daily PM 2.5 levels (assigned to 40 Lima districts) and daily maximum temperature (Lima-wide) were estimated based on ground monitors, remote sensing, and modeling. We analyzed all-cause, cardiovascular (ICD codes I00-I99), and respiratory (ICD codes J00-J99) mortality, and cardiovascular and respiratory causes for ER visits., Results: The average PM 2.5 concentration was 20.9 µg/m 3 (IQR 17.5-23.5). The mean daily maximum temperature was 23.8 °C (IQR 20.8-26.9). PM 2.5 's effect on all-cause, respiratory, and circulatory disease mortality was significantly (p < 0.05) stronger at temperatures above the maximum temperature median. The rate ratios per increase of 10 µg/m 3 of PM 2.5 for all cause, respiratory, and circulatory mortality respectively were 1.03 (1.00-1.06), 1.04 (0.98-1.10), and 1.04 (0.98-1.10) at temperatures below the median, vs. 1.08 (1.04-1.12), 1.11 (1.03-1.19), and 1.14 (1.05-1.25) when temperatures were above the median. Results were analogous for ER visits for respiratory but not circulatory disease., Significance: Results strengthen the evidence that air pollution may be more dangerous when temperatures are higher., Impact: Our data contribute to a growing body of literature which indicates that the damaging effects of PM 2.5 may be worse at higher temperature, adding new evidence from Lima, Peru., (© 2021. The Author(s), under exclusive licence to Springer Nature America, Inc.)

Epidemiologic cohort studies have consistently demonstrated that long-term exposure to ambient fine particles (PM 2.5 ) is associated with mortality. Nevertheless, extrapolating results to understudied locations may involve considerable uncertainty. To explore this issue, this review discusses the evidence for (i) the associated risk of mortality, (ii) the shape of the concentration-response function, (iii) a causal interpretation, and (iv) how the source mix/composition of PM 2.5 and population characteristics may alter the effect. The accumulated evidence suggests the following: (i) In the United States, the change in all-cause mortality risk per μg/m 3 is about 0.8%. (ii) The concentration-response function appears nonlinear. (iii) Causation is overwhelmingly supported. (iv) Fossil fuel combustion-related sources are likely more toxic than others, and age, race, and income may modify the effect. To illustrate the use of our findings in support of a risk assessment in an understudied setting, we consider Kuwait. However, given the complexity of this relationship and the heterogeneity in reported effects, it is unreasonable to think that, in such circumstances, point estimates can be meaningful. Consequently, quantitative probabilistic estimates, which cannot be derived objectively, become essential. Formally elicited expert judgment can provide such estimates, and this review provides the evidence to support an elicitation.

Hand, foot, and mouth disease (HFMD) poses a great disease burden in China. However, there are few studies on the relationship between temperature variability (TV) and HFMD. Moreover, whether air pollutions have modified effects on this relationship is still unknown. Therefore, this study aims to explore the modified effects of air pollutants on TV-HFMD association in Zibo City, China. Daily data of HFMD cases, meteorological factors, and air pollutants from 2015 to 2019 were collected for Zibo City. TV was estimated by calculating standard deviation of minimum and maximum temperatures over the exposure days. We used generalized additive model to estimate the association between TV and HFMD. The modified effects of air pollutants were assessed by comparing the estimated TV-HFMD associations between different air stratums. We found that TV increased the risk of HFMD. The effect was strongest at TV03 (4 days of exposure), when the incidence of HFMD increased by 3.6% [95% CI: 1.3-5.9%] for every 1℃ increases in TV. Males, children aged 0-4 years, were more sensitive to TV. We found that sulfur dioxide (SO 2 ) enhanced TV's effects on all considered exposure days, while ozone (O 3 ) reduced TV's effects on some exposure days in whole concerned population. However, we did not detect significant effect modification by particulate matter less than 10 microns in aerodynamic diameter (PM 10 ). These findings are of significance in developing policies and public health practices to reduce the risks of HFMD by integrating changes in temperatures and air pollutants., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: A large body of evidence has linked air pollution and temperature with chronic kidney disease (CKD) prevalence and hospitalizations. However, most studies have focused on the influence of heat stress on CKD prevalence, and the potential effect modification of temperature on the association between air pollution and CKD has not been well-investigated. In this study, we examined the associations of the whole temperature spectrum and air pollution with CKD-related hospital visits and explored whether temperature modifies the short-term association of air pollution with CKD-related hospital visits., Methods and Findings: We collected 40 276 CKD-related hospital visits from the first Affiliated Hospital of Anhui Medical University and Anhui Provincial Hospital in Hefei, China, during 2015-2019. A two-stage time-series design was conducted to investigate the associations of air pollution and daily mean temperature with CKD-related hospital visits. First, we estimated the associations between air pollution and CKD-related hospital visits as well as temperature and CKD-related hospital visits. Second, we analyzed the associations of air pollution with CKD hospital visits at different temperatures. We found that NO 2 exposure and low temperature were associated with an increased risk of CKD-related hospital visits. Low temperature enhanced the association between NO 2 exposure and CKD-related hospital visits, with an increase of 4.30% (95% CI: 2.47-5.92%) per 10 μg/m 3 increment in NO 2 at low temperature. Effect modification of the association between NO 2 and the risk of CKD-related hospital visits was stronger at low temperature across the whole population., Conclusions: Our findings indicate that low temperature-related chronic kidney damage should be of immediate public health concern. Impact of NO 2 exposure on the risk of CKD-related hospital visits may increase under the low temperature, which suggests the need for NO 2 exposure mitigation strategies in the context of climate change and an enhanced understanding of the mechanisms underlying the temperature variance of air pollution effect to help reduce the magnitude of the CKD burden on the healthcare systems., (Copyright © 2022. Published by Elsevier Inc.)

Background: Many studies have found associations between early life air pollution exposure and subsequent onset of autism spectrum disorder (ASD). However, characteristics that affect susceptibility remain unclear., Objective: This systematic review examined epidemiologic studies on the modifying roles of social, child, genetic and maternal characteristics in associations between prenatal and early postnatal air pollution exposure and ASD., Methods: A systematic literature search in PubMed and Embase was conducted. Studies that examined modifiers of the association between air pollution and ASD were included., Results: A total of 19 publications examined modifiers of the associations between early life air pollution exposures and ASD. In general, estimates of effects on risk of ASD in boys were larger than in girls (based on 11 studies). Results from studies of effects of family education (2 studies) and neighborhood deprivation (2 studies) on air pollution-ASD associations were inconsistent. Limited data (1 study) suggest pregnant women with insufficient folic acid intake might be more susceptible to ambient particulate matter less than 2.5 μm (PM 2.5 ) and 10 μm (PM 10 ) in aerodynamic diameter, and to nitrogen dioxide (NO 2 ). Children of mothers with gestational diabetes had increased risk of ozone-associated ASD (1 study). Two genetic studies reported that copy number variations may amplify the effect of ozone, and MET rs1858830 CC genotype may augment effects of PM and near-roadway pollutants on ASD., Conclusions: Child's sex, maternal nutrition or diabetes, socioeconomic factors, and child risk genotypes were reported to modify the effect of early-life air pollutants on ASD risk in the epidemiologic literature. However, the sparsity of studies on comparable modifying hypotheses precludes conclusive findings. Further research is needed to identify susceptible populations and potential targets for preventive intervention., (Copyright © 2021. Published by Elsevier Inc.)

Mounting evidence indicated the associations between air pollution and outpatient visits for allergic rhinitis (AR), while few studies assessed the effect modification of these associations by ambient temperature and relative humidity (RH). In this study, dataset of AR outpatients was obtained from Chinese People's Liberation Army Strategic Support Force Characteristic Medical Center in Beijing during 2014 to 2019, and the average concentrations of air pollutants including particulate matter ≤2.5 μm in diameter (PM 2.5 ) and ≤10 μm (PM 10 ), nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), and meteorological factors (temperature and RH) at the same period were collected from one nearby air monitoring station. We performed a time-series study with Poisson regression model to examine the effects of air pollutants on AR outpatients after adjustment for potential confounders. And the effects modification analysis was further conducted by stratifying temperature and RH by tertiles into three groups of low, middle and high. In total of 33,599 outpatient visits for AR were recorded during the study period. Results found that a 10 μg/m 3 increase in PM 2.5 , PM 10 , NO 2 and SO 2 was associated with significant increases in AR outpatients of 1.24% (95% confidence interval (CI): 0.69%, 1.78%), 0.79% (95% CI: 0.43%, 1.15%), 3.05% (95% CI: 1.72%, 4.40%) and 5.01% (95% CI: 1.18%, 8.96%), respectively. Stronger associations were observed in males than those in females, as well as in young adults (18-44 years) than those in other age groups. Air pollution effects on AR outpatients increased markedly at low temperature (<33.3th percentile) and high RH (>66.7th percentile). Findings in this study indicate that air pollution is associated with increased risk of AR outpatients, and the effects of air pollution on AR could be enhanced at low temperature and high RH., 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 © 2022. Published by Elsevier B.V.)

Objectives: Evidence of childhood asthma hospitalizations associated with temperature variability (TV) and the attributable risk are limited in China. We aim to use a comprehensive index that reflected both intra- and inter-day TV to assess the TV-childhood asthma relationship and disease burden, further to identify seasonality vulnerable populations, and to explore the effect modification of PM 2.5 ., Methods: A quasi-distributed lagged nonlinear model (DLNM) combined with a linear threshold function was applied to estimate the association between TV and childhood asthma hospitalizations during 2013-2016 in Hefei, China. Subgroup analysis was conducted by age and sex. Disease burden is reflected by the attributable fraction and attributable number. Besides, modifications of PM 2.5 were tested by introducing the cross-basis of TV and binary PM 2.5 as an interaction term., Results: The risk estimates peaked at TV 0-3 and TV 0-4 in the cool and the warm season separately, with RR of 1.051 (95%CI: 1.021-1.081) and 1.072 (95%CI: 1.008-1.125), and the effects lasted longer in the cool season. The school-age children in the warm season and all subgroups except pre-school children in the cool season were vulnerable to TV. It is estimated that the disease burden related to TV account for 6.2% (95% CI: 2.7%-9.4%) and 4% (95% CI: 0.6%-7.1%) during the cool and warm seasons in TV 0-3 . In addition, the risks of TV were higher under the high PM 2.5 level compared with the low PM 2.5 level in the cool season, although no significant differences between them., Conclusions: TV exposure significantly increases the risk and disease burden of childhood asthma hospitalizations, especially in the cool season. More medical resources should be allocated to school-age children. Giving priority to pay attention to TV in the cool season in practice could obtain the greatest public health benefits and those days with high TV and high PM 2.5 need more attention., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Increasing number of studies have linked air pollution exposure with renal function decline and disease. However, there is a lack of data on its impact among end-stage kidney disease (ESKD) patients and its potential modifying effect from extreme heat events (EHE)., Methods: Fresenius Kidney Care records from 28 selected northeastern US counties were used to pool daily all-cause mortality (ACM) and all-cause hospital admissions (ACHA) counts. County-level daily ambient PM 2.5 and ozone (O 3 ) were estimated using a high-resolution spatiotemporal coupled climate-air quality model and matched to ESKD patients based on ZIP codes of treatment sites. We used time-stratified case-crossover analyses to characterize acute exposures using individual and cumulative lag exposures for up to 3 days (Lag 0-3) by using a distributed lag nonlinear model framework. We used a nested model comparison hypothesis test to evaluate for interaction effects between air pollutants and EHE and stratification analyses to estimate effect measures modified by EHE days., Results: From 2001 to 2016, the sample population consisted of 43,338 ESKD patients. We recorded 5217 deaths and 78,433 hospital admissions. A 10-unit increase in PM 2.5 concentration was associated with a 5% increase in ACM (rate ratio [RR Lag0 - 3 ]: 1.05, 95% CI: 1.00-1.10) and same-day O 3 (RR Lag0 : 1.02, 95% CI: 1.01-1.03) after adjusting for extreme heat exposures. Mortality models suggest evidence of interaction and effect measure modification, though not always simultaneously. ACM risk increased up to 8% when daily ozone concentrations exceeded National Ambient Air Quality Standards established by the United States, but the increases in risk were considerably higher during EHE days across lag periods., Conclusion: Our findings suggest interdependent effects of EHE and air pollution among ESKD patients for all-cause mortality risks. National level assessments are needed to consider the ESKD population as a sensitive population and inform treatment protocols during extreme heat and degraded pollution episodes., Competing Interests: Declaration of competing interest Dr. Raimann reported being an employee of the Renal Research Institute (a wholly owned subsidiary of Fresenius Medical Care [FMC]) and owning stock in FMC. Dr. Kotanko reported receiving honoraria from UpToDate, being an employee of the Renal Research Institute, and owning stock in FMC. Dr. Maddux reported owning stock in and being employed by FMC. No other disclosures were reported., (Copyright © 2021. Published by Elsevier B.V.)

Air pollution risk assessments typically estimate ozone-attributable mortality counts using concentration-response (C-R) parameters from epidemiologic studies that treat temperature as a potential confounder. However, some recent epidemiologic studies have indicated that temperature can modify the relationship between short-term ozone exposure and mortality, which has potentially important implications when considering the impacts of climate change on public health. This proof-of-concept analysis quantifies counts of temperature-modified ozone-attributable mortality using temperature-stratified C-R parameters from a multicity study in which the pooled ozone-mortality effect coefficients change in concert with daily temperature. Meteorology downscaled from two global climate models is used with a photochemical transport model to simulate ozone concentrations over the 21st century using two emission inventories: one holding air pollutant emissions constant at 2011 levels and another accounting for reduced emissions through the year 2040. The late century climate models project increased summer season temperatures, which in turn yields larger total counts of ozone-attributable deaths in analyses using temperature-stratified C-R parameters compared to the traditional temperature confounder approach. This analysis reveals substantial heterogeneity in the magnitude and distribution of the temperature-stratified ozone-attributable mortality results, which is a function of regional variability in both the C-R relationship and the model-predicted temperature and ozone.

Background: Studies have observed associations between long-term air pollution and cardiovascular disease hospitalization. Little is known, however, about effect modification of these associations by greenness, temperature and humidity., Methods: We constructed an open cohort consisting of all fee-for-service Medicare beneficiaries, aged ≥ 65, living in the contiguous US from 2000 through 2016 (~63 million individuals). We assigned annual average PM 2.5 , NO 2 and ozone zip code concentrations. Cox-equivalent Poisson models were used to estimate associations with first cardiovascular disease (CVD), coronary heart disease (CHD) and cerebrovascular disease (CBV) hospitalization., Results: PM 2.5 and NO 2 were both positively associated with CVD, CHD and CBV hospitalization, after adjustment for potential confounders. Associations were substantially stronger at the lower end of the exposure distributions. For CVD hospitalization, the hazard ratio (HR) of PM 2.5 was 1.041 (1.038, 1.045) per IQR increase (4.0 µg/m 3 ) in the full study population and 1.327 (1.305, 1.350) per IQR increase for a subgroup with annual exposures always below 10 µg/m 3 PM 2.5 . Ozone was only positively associated with CVD, CHD and CBV hospitalization for the low-exposure subgroup (<40 ppb). Associations of PM 2.5 were stronger in areas with higher greenness, lower ozone and O x , lower summer and winter temperature and lower summer and winter specific humidity., Conclusion: PM 2.5 and NO 2 were positively associated with CVD, CHD and CBV hospitalization. Associations were more pronounced at low exposure levels. Associations of PM 2.5 were stronger with higher greenness, lower ozone and O x , lower temperature and lower specific humidity., (Copyright © 2021. Published by Elsevier Ltd.)

Background: The effects of exposure to particulate matter with aerodynamic diameter less than 2.5 μm (PM 2.5 ) on children's respiratory system were investigated in numerous epidemiological literatures. However, studies on the association between PM 2.5 and pediatric outpatient visits for respiratory diseases, especially considering the multicenter studies were limited in China., Objectives: To study the association between the short-term exposure to PM 2.5 and the number of children's outpatient visits for respiratory diseases in four Chinese cities as well as the pooled health effects., Methods: Data of pediatric outpatient visits for respiratory diseases (RD, ICD: J00-J99) from representative hospitals in Shijiazhuang (SJZ), Xi'an (XA), Nanjing (NJ) and Guangzhou (GZ) in China from 2015 to 2018 were collected and the air quality data for the same period were collected from environmental protection departments. Generalized additive model (GAM) with quasi-Poisson regression was conducted to analyze the effects of PM 2.5 on the number of pediatric outpatient visits in each city. Single-day lag model (lag0 to lag7) and moving average lag model (lag01 and lag07) were used to examine the lag effects and cumulative effects. Random-effects meta-analysis was used to pool the estimated risks of four cities. The interactions between PM 2.5 and temperature were also explored., Results: The average daily/total outpatient visits for RD, in SJZ, XA, NJ and GZ from 2015 to 2018 were 854.2/1,245,384, 2353.9/3,439,025, 1267.2/1,851,438 and 1399.5/2,044,740 respectively. The percentages of acute upper respiratory infections (URD, ICD: J00-J06) and other acute lower respiratory infections (LRD, ICD: J20-J22) in RD were 33%, 13% (SJZ), 43%, 32% (XA), 26%, 21% (NJ) and 54%, 26% (GZ). The largest pooled estimates of single-day lag effects for RD, URD, and LRD were at lag0, lag0 and lag1. Every 10 μg/m 3 increase in PM 2.5 concentration was associated with a 0.46% (95%CI: 0.21%-0.70%), 0.50% (95%CI: 0.19%-0.81%) and 0.42% (95%CI: 0.06%-0.79%) increased number of outpatient visits significantly. While max cumulative effects which were all at lag 07 were 1.10% (95%CI: 0.46%-1.74%), 0.96% (95%CI: 0.20%-1.73%) and 1.06% (95%CI: 0.12%-2.00%). Less polluted cities (GZ and NJ) showed greater city-specific excess risks, but the excess risks significantly decreased after adjusting for NO 2 in two-pollutant models. Generally, PM 2.5 showed larger health hazards on lower temperature days., Conclusions: Our study showed that exposure to the ambient PM 2.5 was associated with the increase of the number of outpatient visits with pediatric respiratory diseases in four Chinese cities. The health effects of PM 2.5 may not be independent of other air pollutants and could be modified by temperature., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Background and Objectives: Sulfur dioxide (SO 2 ) is a ubiquitous air pollutant and its concentration in China remains at a higher level in the world. However, evidence regarding short-term effect of SO 2 on years of life lost (YLL) from stroke is scarce. We aim to estimate the short-term association between SO 2 pollution and YLL for stroke and the related excess life years and economic loss., Methods: A national time-series study was conducted in 48 Chinese cities from 2013 to 2017. Generalized additive model coupled with random-effects model were used to explore the effects of SO 2 on YLL from stroke. Stratified analyses were performed by demographical and geographical factors, and the effect modification of city-level factors was estimated. In addition, the related economic loss was calculated using the method of the value per statistical life year (VSLY)., Results: Averaged daily mean SO 2 concentration was 27.1 μg/m 3 in 48 Chinese cities from 2013 to 2017. Per 10 μg/m 3 increase in the concentration of SO 2 (lag03) was associated with an increment of 0.70% (95% confidence interval: 0.27%,1.13%), 0.51% (-0.01%,1.04%), 0.71% (0.14%,1.28%) increase in YLL from total stroke, hemorrhagic and ischemic stroke, respectively. The effect of short-term ambient SO 2 exposure on YLL from stroke was more pronounced in the less-educated population and those living in the south. The corresponding excess economic loss during the study period due to SO 2 -related YLL from stroke accounted for 0.08% (0.03%, 0.13%) of the GDP in China., Conclusions: Our results provide evidence from China that short-term exposure to SO 2 is positively associated with YLL from stroke and its major subtypes in certain subgroups of population. This study calls for greater awareness of the adverse health effect due to SO 2 in China and other developing countries, as well as local-specific implementation of air pollution mitigation measures., 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 © 2020 Elsevier Ltd. All rights reserved.)

Evidence from cohort studies on the effects of long-term exposure to air pollution on mortality is limited in South Korea, which has high concentration of particles compared to North America, Western Europe, and Japan, and low exposure compared to China. To reduce knowledge gaps between other countries and South Korea, we investigated the association between all-cause, cardiovascular, and respiratory mortality and long-term exposure to PM 10 and, as a surrogate for fine particles from local emission sources, SO 2 and NO 2 . Participants comprised 18,220 subjects (97,114.4 person-years) residing in 73 districts of seven major cities of South Korea who were assigned to measurements of fixed-site monitoring stations and followed up. We applied Cox proportional hazard models with time-varying exposure up to three years average of air pollutants. We adjusted for individual and district-level covariates measured at baseline such as age, sex, socioeconomic positions, and health behaviors. We found that hazard ratios of PM 10 and SO 2 for all-cause mortality leveled off over approximately 5 ppb of SO 2 and 35-50 μg/m 3 of PM 10 . Interquartile range increases of PM 10 (5.05 μg/m 3 ), SO 2 (2.09 ppb), and NO 2 (11.41 ppb) were associated with 14.4% (95% CI: -0.4, 31.4), 18.1% (-4.5, 46.0), and 18.9% (-8.7, 54.7) increases in cardiovascular mortality, respectively. We did not find positive associations for respiratory mortality. The increase in cardiovascular mortality varied by sex (for PM 10 , in females, 27.4% (5.8, 53.5) increase), smoking (in non-smokers, 35.9% (12.7, 64.0) increase), drinking (in drinkers, 24.5% (2.1, 51.8) increase), marital status (in those not married, 23.1% (1.1, 49.9)), employment status (for SO 2 , in those employed, 79.4% (16.1, 177.3) increase), body mass index (in those ≥23, 47.6% (10.4, 97.3) increase), and community deprivation (for PM 10 , in less deprived communities, 21.0% (1.3, 44.4) increase). In summary, long-term exposure to air pollution is associated with mortality risk in South Korea. Our results suggest that the health effect of long-term exposure to air pollution may not be equal by sex, health behaviors and socioeconomic positions., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: Evidence on the acute effect of short-term exposure to nitrogen dioxide (NO 2 ) on years of life lost (YLL) is rare, especially in multicity setting., Methods: We conducted a time series study among 48 major Chinese cities covering more than 403 million people from 2013 to 2017. The relative percentage changes of NO 2 -YLL were estimated by generalized additive models in each city, then were pooled to generate average effects using random-effect models. In addition, stratified analyses by individual demographic factors and temperature as well as meta-regression analyses incorporating city-specific air pollutant concentrations, meteorological conditions, and socioeconomic indicators were performed to explore potential effect modification., Results: A 10 μg/m 3 increase in two-day moving average (lag01) NO 2 concentration was associated with 0.64% (95% CI: 0.47%, 0.81%), 0.47% (95% CI: 0.27%, 0.68%), and 0.68% (95% CI: 0.34%, 1.02%) relative increments in YLL due to nonaccidental causes, cardiovascular diseases (CVD), and respiratory diseases (RD), respectively. These associations were generally robust to the adjustment of co-pollutants, except for NO 2 -CVD that might be confounded by fine particulate matter. The increased YLL induced by NO 2 were more pronounced in elderly people, hotter days, and cities characterized by less severe air pollution or higher temperature., Conclusions: Our results demonstrated robust evidence on the associations between NO 2 exposure and YLL due to nonaccidental causes, CVD, and RD, which provided novel evidence to better understand the disease burden related to NO 2 pollution and to facilitate allocation of health resources targeting high-risk subpopulation., 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 © 2020 Elsevier Ltd. All rights reserved.)

It is unknown whether giving birth via caesarean section (c-section) is a modifier for the association between air pollution and asthma. From 2012 to 2013, 59,754 children between the ages of 2 and 17 were randomly selected from 94 middle schools, elementary schools and kindergartens in seven Chinese cities for a cross-sectional study. The children's parents or guardians completed questionnaires, from which data on asthma as well as asthma-related symptoms were obtained. Participants' exposure to particles with an aerodynamic diameter ≤1.0 μm (PM 1 ), ≤2.5 μm (PM 2.5 ), and ≤10 μm (PM 10 ) and exposure to nitrogen dioxide (NO 2 ) were estimated using random forest models. We used mixed effects logistic regression models and added an interaction term between mode of delivery and ambient air pollution into the model to estimate effect modification from c-sections after appropriate adjustments for potential confounding variables. Among children delivered by c-section, the adjusted ORs for asthma and its symptoms per interquartile range (IQR) increase of PM 1 , PM 2.5 , PM 10 and NO 2 (1.20 95% CI: 1.07-1.34 to 2.04 95% CI: 1.87-2.24) were significantly higher than those of children delivered vaginally (1.05 95% CI: 0.92-1.19 to 1.33 95%CI: 1.21-1.47). The interactions between c-sections and ambient air pollution were statistically significant for all studied respiratory disorders, except current wheeze. Delivery via c-section may increase the risks of air pollution on asthma and its symptoms in Chinese children., 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 © 2020 Elsevier Ltd. All rights reserved.)

Environmental factors affect the health and wellbeing of urban residents. However, they do not act individually on humans, but instead show potential synergistic or antagonistic effects. Questions that arise from this are: How does a combination of air pollutants with other environmental factors impact health? How well are these associations evidenced? What methods can we use to look at them? In this article, methodical approaches regarding the effects of a combination of various environmental factors are first described. Environmental factors are then examined, which together with different air pollutants, have an impact on human health such as ambient temperature, noise, and pollen as well as the effect of green spaces. Physical activity and nutrition are addressed regarding the attenuation of health effects from air pollution.While there is often clear evidence of health effects of single environmental stressors, there are still open questions in terms of their interaction. The research methods required for this still need to be further developed. The interrelationship between the different environmental factors make it clear that (intervention) measures for reducing single indicators are also interlinked. Regarding traffic, switching from passive to active transport (e.g., due to safe cycle paths and other measures) leads to less air pollutants, smaller increases in temperature in the long term, and at the same time improved health of the individual. As a result, sensible planning of the built environment has great potential to reduce environmental stressors and improve people's health and wellbeing.

Studies of the health effects of air pollution have traditionally controlled for ambient temperature as a confounder, and vice versa. However, season might be an important factor contributing to adverse health effects of air pollution. Given the current inconsistencies in results of previous studies on the effect modification of air pollution on morbidity by season, a systematic review and meta-analysis was conducted to synthesize the current evidence on effects of season on air pollution and morbidity. The electronic databases including PubMed, Web of Science, Embase, CNKI, and Wanfang were used to identify papers published up to the 30st of November in 2019. We identified 4284 articles, after screening, eighty papers met the inclusion criteria. Significant effect modification of CO, O 3 , SO 2 and NO 2 on morbidity by season was observed, with corresponding ratio of relative risk of 1.0009 (95% CI: 1.0001-1.0018), 1.0080 (95% CI: 1.0021-1.0138), 0.9828 (95% CI: 0.9697-0.9962) and 0.9896 (95% CI: 0.9824-0.9968), respectively. Season significantly modified the effect of CO on pneumonia, the effect of SO 2 on cardiovascular disease, the effect of PM 10 on stroke, and the effect of O 3 on stroke, asthma and pneumonia. The effect modifications of air pollution by season were similar among males and females, while the effect estimates seem to be higher among children under 18 years old and the elderly aged 75 or over. Further research is needed to better understand the mechanisms underlying the seasonal variance of the effect of air pollutants on morbidity., 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 © 2020 Elsevier B.V. All rights reserved.)

Background: Ambient PM 2.5 has been identified as the top leading cause of risk-attributable deaths worldwide, particularly in China. Evidence suggested that PM 1 contributed the most majority of PM 2.5 concentrations in Chinese cities. However, epidemiologic knowledge to date is of wide lack regarding PM 1 -associated health effects., Methods: We collected daily records of all-cause emergency department visits (EDVs) and ground measurements of ambient air pollutants and meteorological factors in Guangzhou and Shenzhen, China, 2015-2016. Case-crossover design and conditional logistic regression models were used to comparatively assess the short-term effects of ambient PM 1 , PM 2.5 , and PM 10 on EDVs. Stratified analyses by gender, age and season were performed to identify vulnerable groups and periods., Results: PM 1 , PM 2.5 and PM 10 were all significantly associated with increased EDVs in both cities. Population risks for EDVs increased by 2.2% [95% confidence interval, 1.8 to 2.6] in Guangzhou and 1.7% [1.0 to 2.4] in Shenzhen, for a 10 μg/m 3 rise in PM 1 at lag 0-1 days and lag 0-4 days, respectively. Relatively lower risks were found to be associated with PM 2.5 and PM 10 . PM-EDVs associations exhibited no gender differences, but varied across age groups. Compared with adults and the elderly, children under 14 years-of-age suffered higher PM-induced risks. Results from both cities suggested greatly significant effect modification by season, with consistently stronger PM-EDVs associations during cold months., Conclusions: Our study added comparative evidence for increased EDVs risks associated with short-term exposures to ambient PM 1 , PM 2.5 and PM 10 . Besides, PM-associated effects were significantly stronger among children and during cold months., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Introduction: Epidemiologic studies have reported associations between short-term exposure to particulate matter <2.5 μm in aerodynamic diameter (PM 2.5 ) and mortality, but the role of modifiers remains unclear with studies reporting inconsistent results. We evaluated the impact of individual (age, gender and education) and township (geographic area, socioeconomic status, background air pollution and road density) level factors on the relationship between short-term variation in PM 2.5 with cause-specific mortality in Beijing (population: 21.7 million in 2016), China., Methods: Daily PM 2.5 concentrations in each township (n = 327; township population: 2000-359,400; township area: 1-392 km 2 ) within Beijing were estimated by kriging with external drift using measurements from 35 air quality monitoring stations and geographic variables. Time-stratified case-crossover analysis with township-level mortality data from Oct. 1st, 2012 to Dec. 31st, 2013 was then used to examine associations between PM 2.5 exposure estimates and cause-specific mortality, stratified by the potential effect modifiers., Results: A 10-μg/m 3 increase in PM 2.5 concentration was associated with a 0.17% [95% confidence interval (CI): 0.05%-0.29%] and 0.27% (95%CI:0.01%-0.52%) increase in non-accidental and stroke mortality with no lag, a 0.81% (95%CI:0.39%-1.23%) and 0.96% (95%CI:0.35%-1.57%) increase in respiratory disease (RD) and chronic obstructive pulmonary disease (COPD) mortality at a lag of two-day moving average. For individual-level effect modifiers, the elderly showed higher effects for all the specific causes of mortality; those with lower education level showed higher effects for non-accidental, cardiovascular disease and stroke mortality; females showed higher effects for non-accidental and cause-specific cardiovascular diseases. For township-level effect modifiers, effect estimates tended to be larger for suburban areas, areas of lower road density, lower PM 2.5 and lower socioeconomic status., Conclusions: Short-term exposure to township-level ambient PM 2.5 was associated with increased mortality in Beijing, with indications of effect modification by both individual and township-level factors., Competing Interests: Declaration of competing interest The authors declare that they have no competing interest., (Copyright © 2019. Published by Elsevier Inc.)