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The relationship of fine particulate matter (PM2.5) exposure and insulin resistance remains inclusive. Our study aimed to investigate this association in the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR). Specifically, we examined the associations between long-term PM2.5 exposure and three surrogate indicators of insulin resistance: the triglyceride-glucose index (TyG), TyG with waist circumference (TyG-WC) and metabolic score for insulin resistance (METS-IR). Additionally, we explored potential effect modification of dietary intake and components. Generalized estimating equations were used to evaluate the associations between PM2.5 and the indicators with an unbalanced repeated measurement design. Our analysis incorporated a total of 162,060 observations from 99,329 participants. Each 10 μg/m3 increment of PM2.5 was associated with an increase of 0.22 % [95 % confidence interval (CI): 0.20 %, 0.25 %], 1.60 % (95 % CI: 1.53 %, 1.67 %), and 2.05 % (95 % CI: 1.96 %, 2.14 %) in TyG, TyG-WC, and METS-IR, respectively. These associations were attenuated among participants with a healthy diet, particularly those with sufficient intake of fruit and vegetable, fish or tea (pinteraction

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 NO2, PM2.5, and PM10 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 NO2, PM2.5, and PM10. 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 NO2 and 0.16, 95 % CI, 0.11 to 0.22 for PM2.5 for males; 0.13, 95 % CI, 0.09 to 0.18 for NO2 and 0.10, 95 % CI, 0.05 to 0.14 for PM2.5 for lower individual income and 0.17, 95 % CI, 0.12 to 0.22 for NO2 and 0.09, 95 % CI, 0.05 to 0.14 for PM2.5 for lower area-level socioeconomic status. Results for PM10 were similar to PM2.5. 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.

Background: Epidemiological evidence on the association of PM2.5 (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 PM2.5 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 PM2.5 mass and its chemical components on the incidence of hypertension and BP, respectively. Results: Each interquartile range (IQR = 16.80 μg/m3) increase in the one-year average of PM2.5 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/m3 increase in PM2.5 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 SO42−, NO3−, NH4+, 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 PM2.5 mass and its specific components may be major drivers of escalation in hypertension diseases.

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 (PM10), PM ≤ 2.5 μm (PM2.5), nitrogen dioxide (NO2), and ozone (O3) 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 75th to the 99th 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 PM10 was equal to 10 or 90 μg/m3, respectively. Corresponding estimates when daily O3 concentrations were 40 or 160 μg/m3 were 2.9 % (1.1 %, 4.7 %) and 12.5 % (6.9 %, 18.5 %), respectively. Similarly, a 10 μg/m3 increment in PM10 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 1st and 99th city-specific percentiles, respectively. Corresponding mortality estimate for O3 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 PM2.5 and NO2. 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.

Background: Short-term associations between heat and cardiovascular disease (CVD) mortality have been examined mostly in large cities. However, different vulnerability and exposure levels may contribute to spatial heterogeneity. This study assessed heat effects on CVD mortality and potential vulnerability factors using data from three European countries, including urban and rural settings. Methods: We collected daily counts of CVD deaths aggregated at the small-area level in Norway (small-area level: municipality), England and Wales (lower super output areas), and Germany (district) during the warm season (May-September) from 1996 to 2018. Daily mean air temperatures estimated by spatial–temporal models were assigned to each small area. Within each country, we applied area-specific Quasi-Poisson regression using distributed lag nonlinear models to examine the heat effects at lag 0–1 days. The area-specific estimates were pooled by random-effects meta-analysis to derive country-specific and overall heat effects. We examined individual- and area-level heat vulnerability factors by subgroup analyses and meta-regression, respectively. Results: We included 2.84 million CVD deaths in analyses. For an increase in temperature from the 75th to the 99th percentile, the pooled relative risk (RR) for CVD mortality was 1.14 (95% CI: 1.03, 1.26), with the country-specific RRs ranging from 1.04 (1.00, 1.09) in Norway to 1.24 (1.23, 1.26) in Germany. Heat effects were stronger among women [RRs (95% CIs) for women and men: 1.18 (1.08, 1.28) vs. 1.12 (1.00, 1.24)]. Greater heat vulnerability was observed in areas with high population density, high degree of urbanization, low green coverage, and high levels of fine particulate matter. Conclusion: This study provides evidence for the heat effects on CVD mortality in European countries using high-resolution data from both urban and rural areas. Besides, we identified individual- and area-level heat vulnerability factors. Our findings may facilitate the development of heat-health action plans to increase resilience to climate change.

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 [PM2.5]) 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 PM2.5, 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 O3, 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.

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 PM2.5, NO2 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: PM2.5 and NO2 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 PM2.5 was 1.041 (1.038, 1.045) per IQR increase (4.0 µg/m3) 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/m3 PM2.5. Ozone was only positively associated with CVD, CHD and CBV hospitalization for the low-exposure subgroup (

• PM 2.5 is associated with the increased surrogate indices of insulin resistance (IR). • Healthy diet could reduce the harm of long-term PM 2.5 exposure on surrogate indices. • IR is also attenuated by rational diet components despite challenge of PM 2.5 control. The relationship of fine particulate matter (PM 2.5) exposure and insulin resistance remains inclusive. Our study aimed to investigate this association in the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR). Specifically, we examined the associations between long-term PM 2.5 exposure and three surrogate indicators of insulin resistance: the triglyceride-glucose index (TyG), TyG with waist circumference (TyG-WC) and metabolic score for insulin resistance (METS-IR). Additionally, we explored potential effect modification of dietary intake and components. Generalized estimating equations were used to evaluate the associations between PM 2.5 and the indicators with an unbalanced repeated measurement design. Our analysis incorporated a total of 162,060 observations from 99,329 participants. Each 10 μg/m3 increment of PM 2.5 was associated with an increase of 0.22 % [95 % confidence interval (CI): 0.20 %, 0.25 %], 1.60 % (95 % CI: 1.53 %, 1.67 %), and 2.05 % (95 % CI: 1.96 %, 2.14 %) in TyG, TyG-WC, and METS-IR, respectively. These associations were attenuated among participants with a healthy diet, particularly those with sufficient intake of fruit and vegetable, fish or tea (p interaction < 0.0028). For instance, among participants with a healthy diet, TyG increased by 0.11 % (95 % CI: 0.08 %, 0.15 %) per 10 μg/m3 PM 2.5 increment, significantly lower than the association observed in those with an unhealthy diet. The findings of this study emphasize the potential of a healthy diet to mitigate these associations, highlighting the urgency for improving air quality and implementing dietary interventions among susceptible populations in China. [ABSTRACT FROM AUTHOR]

• Evidence for those vulnerable to effects of long-term air pollution on severe COVID-19 is scarce. • We evaluate the interaction effect on both multiplicative and additive scales. • Males and those with lower socioeconomic status are the most vulnerable groups. 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. 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. 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. 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. [ABSTRACT FROM AUTHOR]

[Display omitted] • This is a national cohort study focusing on PM 2.5 and hyphenation across China. • Long-term exposure to PM 2.5 may increase blood pressure and risk of hypertension. • We found different effects of PM 2.5 components on blood pressure and hypertension. • BC and OM have greater effects on SBP in patients with hypertensive than others. • These effects were modified by sex, urbanicity, smoking status, and cooking fuel type. 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. 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. Each interquartile range (IQR = 16.80 μg/m3) 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/m3 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. 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. [ABSTRACT FROM AUTHOR]

Epidemiological studies have consistently demonstrated that exposure to fine particulate matter (PM 2.5) is associated with increased risks of mortality. To a lesser extent, a series of studies suggest that living in greener areas is associated with reduced risks of mortality. Only a handful of studies have examined the interplay between PM 2.5 , greenness, and mortality. We investigated the role of residential greenness in modifying associations between long-term exposures to PM 2.5 and non-accidental and cardiovascular mortality in a national cohort of non-immigrant Canadian adults (i.e., the 2001 Canadian Census Health and Environment Cohort). Specifically, we examined associations between satellite-derived estimates of PM 2.5 exposure and mortality across quintiles of greenness measured within 500 m of individual's place of residence during 11 years of follow-up. We adjusted our survival models for many personal and contextual measures of socioeconomic position, and residential mobility data allowed us to characterize annual changes in exposures. Our cohort included approximately 2.4 million individuals at baseline, 194,270 of whom died from non-accidental causes during follow-up. Adjustment for greenness attenuated the association between PM 2.5 and mortality (e.g., hazard ratios (HRs) and 95% confidence intervals (CIs) per interquartile range increase in PM 2.5 in models for non-accidental mortality decreased from 1.065 (95% CI: 1.056–1.075) to 1.041 (95% CI: 1.031–1.050)). The strength of observed associations between PM 2.5 and mortality decreased as greenness increased. This pattern persisted in models restricted to urban residents, in models that considered the combined oxidant capacity of ozone and nitrogen dioxide, and within neighbourhoods characterised by high or low deprivation. We found no increased risk of mortality associated with PM 2.5 among those living in the greenest areas. For example, the HR for cardiovascular mortality among individuals in the least green areas was 1.17 (95% CI: 1.12–1.23) compared to 1.01 (95% CI: 0.97–1.06) among those in the greenest areas. Studies that do not account for greenness may overstate the air pollution impacts on mortality. Residents in deprived neighbourhoods with high greenness benefitted by having more attenuated associations between PM 2.5 and mortality than those living in deprived areas with less greenness. The findings from this study extend our understanding of how living in greener areas may lead to improved health outcomes. • Exposure to air pollution had a lower impact on risk of dying in greener areas. • This pattern held in neighbourhoods characterised by high or low deprivation. • Not accounting for greenness may overstate air pollution impacts on health. • This study extends our understanding of how living in greener areas improves health. • We found no link between PM 2.5 and risk of dying among those in the greenest areas. [ABSTRACT FROM AUTHOR]

Abstract Background Migraine is a chronic and agonizing neurological disorder prevalent worldwide. Although its pathogenesis remains unclear, limited evidence exists on the role of air pollution. Objective We aimed to assess the association of short-term air pollution exposure with migraine in conjunction with the synergistic effect of temperature. Methods We identified 18,921 patients who visited emergency departments (EDs) for migraine as a primary disease in Seoul from the national emergency database between 2008 and 2014. We conducted a time-stratified, case-crossover analysis to compare levels of particles <2.5 μm (PM 2.5), particles <10 μm (PM 10), nitrogen dioxide (NO 2), sulfur dioxide (SO 2), ozone (O 3), and carbon monoxide (CO) on ED visit days and those on the control days matched to day of the week, month, and year. We evaluated the synergistic effects of air pollution and temperature using an interaction term. Results Higher air pollution levels were significantly associated with risk of migraine over various lag structures. In the best fitting lags, the odds ratio (OR) associated with an interquartile range increase of PM 2.5 , PM 10 , NO 2 , O 3 , and CO was 1.031 (95% CI: 1.010–1.053), 1.032 (95% CI: 1.007–1.057), 1.053 (95% CI: 1.022–1.085), 1.034 (95% CI: 1.001–1.067), and 1.029 (95% CI: 1.005–1.053), respectively. The SO 2 effect was positive but not significant (OR 1.019 [95% CI: 0.991–1.047]). The PM effect was significantly stronger on high-temperature days (above the 75th percentile) than on low-temperature days (PM 2.5 , high: OR 1.068, low: OR 1.021, P interact = 0.03; PM 10 , high: OR 1.066, low: OR 1.014, P interact = 0.02). Conclusion Our study provides new evidence that air pollution exposure may trigger migraine especially on high-temperature days, and this finding may contribute in establishing preventive measures against migraine. Highlights • We assessed a short-term association between ambient air pollution and migraine. • We examined a synergistic effect of air pollution and temperature on migraine. • PM 2.5 , PM 10 , NO 2 , O 3 , and CO significantly increased the risk of migraine. • The PM 2.5 and PM 10 effects were significantly stronger on high-temperature days. [ABSTRACT FROM AUTHOR]

The epidemiological evidence on the interaction between heat and ambient air pollution on mortality is still inconsistent. To investigate the interaction between heat and ambient air pollution on daily mortality in a large dataset of 620 cities from 36 countries. 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. We analyzed 22,630,598 deaths. An increase in mean temperature from the 75th to the 99th 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/m3, respectively. Corresponding estimates when daily O 3 concentrations were 40 or 160 μg/m3 were 2.9 % (1.1 %, 4.7 %) and 12.5 % (6.9 %, 18.5 %), respectively. Similarly, a 10 μg/m3 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 1st and 99th 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. 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. [ABSTRACT FROM AUTHOR]

• Heat effect on CVD mortality was examined using data from both urban and rural areas. • Heat was associated with an increased risk for CVD mortality in European countries. • Women were more at risk from heat compared with men. • Heat effect was modified by population density, urbanization, greenness, and PM 2.5. Short-term associations between heat and cardiovascular disease (CVD) mortality have been examined mostly in large cities. However, different vulnerability and exposure levels may contribute to spatial heterogeneity. This study assessed heat effects on CVD mortality and potential vulnerability factors using data from three European countries, including urban and rural settings. We collected daily counts of CVD deaths aggregated at the small-area level in Norway (small-area level: municipality), England and Wales (lower super output areas), and Germany (district) during the warm season (May-September) from 1996 to 2018. Daily mean air temperatures estimated by spatial–temporal models were assigned to each small area. Within each country, we applied area-specific Quasi-Poisson regression using distributed lag nonlinear models to examine the heat effects at lag 0–1 days. The area-specific estimates were pooled by random-effects meta-analysis to derive country-specific and overall heat effects. We examined individual- and area-level heat vulnerability factors by subgroup analyses and meta-regression, respectively. We included 2.84 million CVD deaths in analyses. For an increase in temperature from the 75th to the 99th percentile, the pooled relative risk (RR) for CVD mortality was 1.14 (95% CI: 1.03, 1.26), with the country-specific RRs ranging from 1.04 (1.00, 1.09) in Norway to 1.24 (1.23, 1.26) in Germany. Heat effects were stronger among women [RRs (95% CIs) for women and men: 1.18 (1.08, 1.28) vs. 1.12 (1.00, 1.24)]. Greater heat vulnerability was observed in areas with high population density, high degree of urbanization, low green coverage, and high levels of fine particulate matter. This study provides evidence for the heat effects on CVD mortality in European countries using high-resolution data from both urban and rural areas. Besides, we identified individual- and area-level heat vulnerability factors. Our findings may facilitate the development of heat-health action plans to increase resilience to climate change. [ABSTRACT FROM AUTHOR]

Abstract Many previous literatures suggested that high temperature and diurnal temperature range (DTR) are prominent risk factors to increase risk of mortality. However, the role of effect modification of temperature on the DTR-related mortality is unclear. We examined whether temperature was an effect modifier on the DTR-mortality association and how the modification patterns differed by cause of deaths and different regional climates using a nationwide 47 prefecture data in Japan (1972–2015). We used a two-stage analysis. For the first stage, we used a time-series regression with a distributed lag model to estimate the DTR-mortality association according to five levels of temperature (extreme cold, cold, moderate, hot, and extreme hot days) for each prefecture stratified by twelve cause-specific deaths. Then, we applied a meta-analysis to pool the estimates across the 47 prefectures in Japan and separately by cooler vs. warmer regions. Our findings showed that the risk of mortality associated with DTR was strongly modified by temperature for all causes and cardiovascular deaths (p < 0.001) in the total population, suggesting that the influence of DTR on mortality increases at higher levels of temperature. These findings were consistent across warmer and cooler regions. Similar patterns were observed for respiratory and renal disease deaths which demonstrated the associations with DTR were the highest during extreme hot days, although it was statistically not significant and varied depending on the climate regions. Our findings suggest that the DTR-related mortality may be modified by daily mean temperature and the most elevated during extremely hot temperatures. Highlights • We aimed to identify the DTR-related mortality with cause-specific deaths. • Weather and 12-specific deaths data of Japan (47 prefectures; 1972–2015) were used. • We found the DTR-related risks were highest in respiratory and renal deaths. • The modification of temperature was significant in total and cardiovascular deaths. • The DTR-related mortality changed during the study period. [ABSTRACT FROM AUTHOR]

Background Although epidemiological studies have reported associations between mortality and both ambient air pollution and air temperature, it remains uncertain whether the mortality effects of air pollution are modified by temperature and vice versa. Moreover, little is known on the interactions between ultrafine particles (diameter ≤ 100 nm, UFP) and temperature. Objective We investigated whether the short-term associations of particle number concentration (PNC in the ultrafine range (≤100 nm) or total PNC ≤ 3000 nm, as a proxy for UFP), particulate matter ≤ 2.5 μm (PM 2.5 ) and ≤ 10 μm (PM 10 ), and ozone with daily total natural and cardiovascular mortality were modified by air temperature and whether air pollution levels affected the temperature-mortality associations in eight European urban areas during 1999–2013. Methods We first analyzed air temperature-stratified associations between air pollution and total natural (nonaccidental) and cardiovascular mortality as well as air pollution-stratified temperature-mortality associations using city-specific over-dispersed Poisson additive models with a distributed lag nonlinear temperature term in each city. All models were adjusted for long-term and seasonal trend, day of the week, influenza epidemics, and population dynamics due to summer vacation and holidays. City-specific effect estimates were then pooled using random-effects meta-analysis. Results Pooled associations between air pollutants and total and cardiovascular mortality were overall positive and generally stronger at high relatively compared to low air temperatures. For example, on days with high air temperatures (>75th percentile), an increase of 10,000 particles/cm 3 in PNC corresponded to a 2.51% (95% CI: 0.39%, 4.67%) increase in cardiovascular mortality, which was significantly higher than that on days with low air temperatures (<25th percentile) [−0.18% (95% CI: −0.97%, 0.62%)]. On days with high air pollution (>50th percentile), both heat- and cold-related mortality risks increased. Conclusion Our findings showed that high temperature could modify the effects of air pollution on daily mortality and high air pollution might enhance the air temperature effects. [ABSTRACT FROM AUTHOR]

Background The linkage between ambient fine particle pollution (PM 2.5 ) and chronic obstructive pulmonary disease (COPD) and the attributable risk remained largely unknown. This study determined the cross-sectional association between ambient PM 2.5 and prevalence of COPD among adults ≥50 years of age. Methods We surveyed 29,290 participants aged 50 years and above in this study. The annual average concentrations of PM 2.5 derived from satellite data were used as the exposure indicator. A mixed effect model was applied to determine the associations and the burden of COPD attributable to PM 2.5. Results Among the participants, 1872 (6.39%) were classified as COPD cases. Our analysis observed a threshold concentration of 30 μg/m 3 in the PM 2.5 -COPD association, above which we found a linear positive exposure-response association between ambient PM 2.5 and COPD. The odds ratio (OR) for each 10 μg/m 3 increase in ambient PM 2.5 was 1.21(95% CI: 1.13, 1.30). Stratified analyses suggested that males, older subjects (65 years and older) and those with lower education attainment might be the vulnerable subpopulations. We further estimated that about 13.79% (95% CI: 7.82%, 21.62%) of the COPD cases could be attributable to PM 2.5 levels higher than 30 μg/m 3 in the study population. Conclusion Our analysis indicates that ambient PM 2.5 exposure could increase the risk of COPD and accounts for a substantial fraction of COPD among the study population. [ABSTRACT FROM AUTHOR]

Background Adverse effects of traffic-related air pollution (AP) and noise on cognitive functions have been proposed, but little is known about their interactions and the combined effect of co-exposure. Methods Cognitive assessment was completed by 4086 participants of the population-based Heinz Nixdorf Recall cohort study using five neuropsychological subtests and an additively calculated global cognitive score (GCS). We assessed long-term residential concentrations for size-fractioned particulate matter (PM) and nitrogen oxides with land use regression. Road traffic noise (weighted 24-h (L DEN ) and night-time (L NIGHT ) means) was assessed according to the EU directive 2002/49/EC. Linear regression models adjusted for individual-level characteristics were calculated to estimate effect modification of associations between AP and noise with cognitive function. We used multiplicative interaction terms and categories of single or double high exposure, dichotomizing the potential effect modifier at the median (AP) or at an a priori defined threshold (road traffic noise). Results In fully adjusted models, high noise exposure increased the association of AP with cognitive function. For example, for an interquartile range increase of PM 2.5 (IQR 1.43), association s with GCS were: estimate ( β ) = − 0.16 [95% confidence interval: − 0.33; 0.01] and β = − 0.48 [− 0.72; − 0.23] for low and high L DEN , respectively. The association of noise with GCS was restricted to highly AP-exposed participants. We observed stronger negative associations in those participants with double exposure compared to the addition of effect estimates of each single exposure. Conclusions Our study suggests that AP and road traffic noise might act synergistically on cognitive function in adults. [ABSTRACT FROM AUTHOR]

Background Lead and psychosocial stress disrupt similar but not completely overlapping mechanisms. Exposure during the prenatal period to each of these insults singularly has been found to alter normal neurodevelopment; however, longitudinal associations with stress modifying the effect of lead have not been sufficiently analyzed in epidemiologic studies. Objective To evaluate prenatal stress as an effect modifier of gestational lead neurotoxicity. Methods We used a structural equations modeling approach with a trivariate response to evaluate cognitive, language and motor scores of the Bayley Scales of Infant Development-III in 24 month-old children ( n = 360). Maternal blood lead levels were measured at the 2nd and 3rd trimester and psychosocial stress during pregnancy was assessed using a negative life events (NLE) scale derived from the CRYSIS questionnaire. Results 3rd trimester lead (mean 3.9 ± 3.0 SD μg/dL) and stress (median = 3 NLE) were negatively associated with Bayley III scores. Using the model's results we generated profiles for 0, 2, 4 and 6 NLE across lead levels (up to 10 μg/dL) and observed a dose–response for the developmental scores when lead levels were below 2 μg/dL. Each NLE curve had a different shape across increasing lead levels. Higher stress (NLE = 6) resulted in lower cognitive scores for both sexes, in lower language scores in girls but not boys. In the absence of stress we saw a negative association with lead for all scores, however for language and motor scores, higher stress seemed to mask this association. Conclusions Our work examined and confirmed prenatal stress exposure as a modifier of the well-known neurotoxic effects of prenatal lead. It adds to the existing evidence pointing at the importance of studying the co-exposure of chemical and non-chemical exposures, specifically of considering the emotional environment of children at early developmental stages of life. [ABSTRACT FROM AUTHOR]

• Heat effect modification by air pollution on cardiovascular and respiratory mortality was investigated across 482 cities. • Heat effect was seen to be significantly modified by air pollutants PM 10, PM 2.5, O 3, and NO 2. • This study is the most extensive research to date investigating the heat effect modification on cardiovascular and respiratory mortality. • This is the first-ever study to deeply investigate effect modifications by air pollutants such as PM 2.5 and NO 2. Evidence on the potential interactive effects of heat and ambient air pollution on cause-specific mortality is inconclusive and limited to selected locations. 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. 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. 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. 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. [ABSTRACT FROM AUTHOR]

Many time-series studies have characterized the relationship between short-term ozone exposure and adverse health outcomes, controlling for temperature as a confounder. Temperature may also modify ozone effects, though this has been largely under-investigated. In this study, we explored whether temperature modifies the effect of short-term ozone exposure on mortality. We used the database developed for the National Morbidity and Mortality Air Pollution Study to estimate ozone mortality risks in 97 US cities in May through September, 1987–2000. We treated temperature as a confounder as well as an effect modifier by estimating risks at low, moderate, and high temperature categories. When temperature was treated as a confounder, a 10-ppb increase in daily 24-h ozone was associated with a 0.47% (95% CI: 0.19%–0.76%) increase in mortality. When we assessed effect modification by temperature, the interaction between ozone and temperature was not statistically significant. However, there was a U-shaped pattern in mortality risk, which was greater at the low (< 25th percentile) and high (> 75th percentile) temperature levels than moderate temperature levels. At the high temperature category, a 10% increase in AC prevalence mitigated mortality risk associated with 10-ppb of ozone exposure by − 0.18% (95% CI: − 0.35%, − 0.02%). Furthermore, ozone mortality risk in the high temperature category increased as we restricted our analyses to hotter days. On days where temperatures exceeded the 75th, 90th, and 95th percentile temperatures, a 10-ppb increase in ozone was associated with a 0.65% (95% CI: 0.20%–1.09%), 0.83% (95% CI: 0.17%–1.48%), and 1.35% (95% CI: 0.44%–2.27%) increase in mortality, respectively. These results suggested that high temperatures may exacerbate physiological responses to short-term ozone exposure. [ABSTRACT FROM AUTHOR]

Abstract: Background: Heterogeneity in the response to PM2.5 is hypothesized to be related to differences in particle composition across monitoring sites which reflect differences in source types as well as climatic and topographic conditions impacting different geographic locations. Identifying spatial patterns in particle composition is a multivariate problem that requires novel methodologies. Objectives: Use cluster analysis methods to identify spatial patterns in PM2.5 composition. Verify that the resulting clusters are distinct and informative. Methods: 109 monitoring sites with 75% reported speciation data during the period 2003–2008 were selected. These sites were categorized based on their average PM2.5 composition over the study period using k-means cluster analysis. The obtained clusters were validated and characterized based on their physico-chemical characteristics, geographic locations, emissions profiles, population density and proximity to major emission sources. Results: Overall 31 clusters were identified. These include 21 clusters with 2 or more sites which were further grouped into 4 main types using hierarchical clustering. The resulting groupings are chemically meaningful and represent broad differences in emissions. The remaining clusters, encompassing single sites, were characterized based on their particle composition and geographic location. Conclusions: The framework presented here provides a novel tool which can be used to identify and further classify sites based on their PM2.5 composition. The solution presented is fairly robust and yielded groupings that were meaningful in the context of air-pollution research. [Copyright &y& Elsevier]

Abstract: Background: The importance of describing, understanding and regulating multi-pollutant mixtures has been highlighted by the US National Academy of Science and the Environmental Protection Agency. Furthering our understanding of the health effects associated with exposure to mixtures of pollutants will lead to the development of new multi-pollutant National Air Quality Standards. Objectives: Introduce a framework within which diagnostic methods that are based on our understanding of air pollution mixtures are used to validate the distinct air pollutant mixtures identified using cluster analysis. Methods: Six years of daily gaseous and particulate air pollution data collected in Boston, MA were classified solely on their concentration profiles. Classification was performed using k-means partitioning and hierarchical clustering. Diagnostic strategies were developed to identify the most optimal clustering. Results: The optimal solution used k-means analysis and contained five distinct groups of days. Pollutant concentrations and elemental ratios were computed in order to characterize the differences between clusters. Time-series regression confirmed that the groups differed in their chemical compositions. The mean values of meteorological parameters were estimated for each group and air mass origin between clusters was examined using back-trajectory analysis. This allowed us to link the distinct physico-chemical characteristics of each cluster to characteristic weather patterns and show that different clusters were associated with distinct air mass origins. Conclusions: This analysis yielded a solution that was robust to outlier points and interpretable based on chemical, physical and meteorological characteristics. This novel method provides an exciting tool with which to identify and further investigate multi-pollutant mixtures and link them directly to health effects studies. [Copyright &y& Elsevier]

Abstract: Acute respiratory infections are common in children below 5years and recent studies suggest a possible link with air pollution. In this study, we investigated the association between ambient nitrogen oxides (NOx) and bronchitis or upper airway inflammation. This longitudinal study was conducted in Teplice and Prachatice districts, Czech Republic. Children were followed from birth to 4.5years of age. Data were compiled from medical records at delivery and at follow up, and from self-administered questionnaires from the same two time points. Air pollution monitoring data were used to estimate exposure over five different averaging periods ranging from three to 45days prior to an episode. To quantify the association between exposure and outcome, while accounting for repeated measure correlation we conducted logistic regression analysis using generalized estimating equations. During the first 2years of life, the adjusted rate ratio for bronchitis associated with interquartile increase in the 30-day average NOx was 1.31 [95% confidence interval (CI): 1.07, 1.61] and for two to 4.5year olds, it was 1.23 (95% CI: 1.01, 1.49). The 14-day exposure also had stable association across both age groups: below 2years it was 1.25 (95% CI: 1.06, 1.47) and for two to 4.5years it was 1.21 (95% CI: 1.06, 1.39). The association between bronchitis and NOx increased with child''s age in the under 2years group, which is a relatively novel finding. The results demonstrate an association between NOx and respiratory infections that are sufficiently severe to come to medical attention. The evidence, if causal, can be of public health concern because acute respiratory illnesses are common in preschool children. [Copyright &y& Elsevier]

• PM 2.5 and NO 2 were positively associated with CVD hospitalization. • Ozone was only positively associated with CVD hospitalization at low exposure levels. • Associations of PM 2.5 were stronger with higher greenness. • Associations of PM 2.5 were stronger with lower temperature, specific humidity and O x. 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. 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. 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/m3) 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/m3 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. 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. [ABSTRACT FROM AUTHOR]

Little information exists on the lipidemic effects of ozone exposure. Few studies have focused on the different patterns of the association among older adults population, and little attention has been given to comprehensive lipid indices when evaluating the effect of O3 exposure on the metabolism. We conducted a longitudinal study involving 201 older adults in Beijing, China between 2016 and 2018. A mixed regression model was applied with random effects to investigate the relationship between O3 and lipid profiles. O3 exposure positively correlated with TC, LDL-C, CRI-I, CRI-II and AC at short-term and medium-term exposure periods. The largest increases in TC, LDL-C, CRI-I and CRI-II were found in the 28-days moving average indicating accumulative effects over prolonged exposure period. A 10 μg/m3 increase of O3 at the 28-days moving average was associated with a significant increase of 3.9% (95% CI: 1.0, 6.9) in TC, 8.2% (95% CI: 4.2, 12.4) in LDL-C, 4.8% (95% CI: 1.1, 8.5) in CRI-I and 7.0% (95% CI: 2.7, 11.5) in CRI-II. Stratification by health status and characteristics revealed different patterns of lipid changes among older adults, lipid status, age, sex and BMI may modify the relationship between O3 exposure and lipid profiles. Our findings suggest that short-term and medium-term O3 exposure is associated with lipid profiles abnormalities among the older adults. Evidence also suggests there are patterns within population which differ according to both health status and demographic characteristics. • Association between ambient O3 exposure and lipid profiles in older adults were assessed. • O3 exposure positively correlated with TC, LDL-C, CRI-I, CRI-II and AC at different exposure periods among the older adults. • O3 influenced different lipid profiles depending on both health status and demographic characteristics. • These results should inform policies to prevent adverse health effects in older adults. [ABSTRACT FROM AUTHOR]

Background: Heterogeneity in the response to PM2.5 is hypothesized to be related to differences in particle composition across monitoring sites which reflect differences in source types as well as climatic and topographic conditions impacting different geographic locations. Identifying spatial patterns in particle composition is a multivariate problem that requires novel methodologies., Objectives: Use cluster analysis methods to identify spatial patterns in PM2.5 composition. Verify that the resulting clusters are distinct and informative., Methods: 109 monitoring sites with 75% reported speciation data during the period 2003-2008 were selected. These sites were categorized based on their average PM2.5 composition over the study period using k-means cluster analysis. The obtained clusters were validated and characterized based on their physico-chemical characteristics, geographic locations, emissions profiles, population density and proximity to major emission sources., Results: Overall 31 clusters were identified. These include 21 clusters with 2 or more sites which were further grouped into 4 main types using hierarchical clustering. The resulting groupings are chemically meaningful and represent broad differences in emissions. The remaining clusters, encompassing single sites, were characterized based on their particle composition and geographic location., Conclusions: The framework presented here provides a novel tool which can be used to identify and further classify sites based on their PM2.5 composition. The solution presented is fairly robust and yielded groupings that were meaningful in the context of air-pollution research., (Copyright © 2013 Elsevier Ltd. All rights reserved.)