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This study aimed to investigate the association between long-term exposure to fine particulate matter (PM 2.5 ) and its constituents (black carbon (BC), ammonium (NH 4 + ), nitrate (NO 3 - ), organic matter (OM), inorganic sulfate (SO 4 2- )) and incident female breast cancer in Beijing, China. Data from a prospective cohort comprising 85,504 women enrolled in the National Urban Cancer Screening Program in Beijing (2013-2019) and the Tracking Air Pollution in China dataset are used. Monthly exposures were aggregated to calculate 5-year average concentrations to indicate long-term exposure. Cox models and mixture exposure models (weighted quantile sum, quantile-based g-computation, and explanatory machine learning model) were employed to analyze the associations. Findings indicated increased levels of PM 2.5 and its constituents were associated with higher breast cancer risk, with hazard ratios per 1-μg/m 3 increase of 1.02 (95% confidence interval (CI): 1.01, 1.03), 1.39 (95% CI: 1.16, 1.65), 1.28 (95% CI: 1.12, 1.46), 1.15 (95% CI: 1.05, 1.24), 1.05 (95% CI: 1.02, 1.08), and 1.15 (95% CI: 1.07, 1.23) for PM 2.5 , BC, NH 4 + , NO 3 - , OM, and SO 4 2- , respectively. Exposure-response curves demonstrated a monotonic risk increase without an evident threshold. Mixture exposure models highlighted BC and SO 4 2- as key factors, underscoring the importance of reducing emissions of these pollutants., 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 B.V. All rights reserved.)

Leukemia and lymphoma are the two most common forms of hematologic malignancy, and their etiology is largely unknown. Pathophysiological mechanisms suggest a possible association with air pollution, but little empirical evidence is available. We aimed to investigate the association between long-term residential exposure to outdoor air pollution and risk of leukemia and lymphoma. We pooled data from four cohorts from three European countries as part of the "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration. We used Europe-wide land use regression models to assess annual mean concentrations of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC) and ozone (O 3 ) at residences. We also estimated concentrations of PM 2.5 elemental components: copper (Cu), iron (Fe), zinc (Zn); sulfur (S); nickel (Ni), vanadium (V), silicon (Si) and potassium (K). We applied Cox proportional hazards models to investigate the associations. Among the study population of 247,436 individuals, 760 leukemia and 1122 lymphoma cases were diagnosed during 4,656,140 person-years of follow-up. The results showed a leukemia hazard ratio (HR) of 1.13 (95% confidence intervals [CI]: 1.01-1.26) per 10 μg/m 3 NO 2 , which was robust in two-pollutant models and consistent across the four cohorts and according to smoking status. Sex-specific analyses suggested that this association was confined to the male population. Further, the results showed increased lymphoma HRs for PM 2.5 (HR = 1.16; 95% CI: 1.02-1.34) and potassium content of PM 2.5 , which were consistent in two-pollutant models and according to sex. Our results suggest that air pollution at the residence may be associated with adult leukemia and lymphoma., 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 Ltd. All rights reserved.)

Background: Ambient air pollution exposure has been associated with childhood asthma, but previous studies have primarily focused on prevalence of asthma and asthma-related outcomes and urban traffic-related exposures., Objective: We examined nationwide associations between pre- and postnatal exposure to ambient air pollution components and asthma incidence in children age 0-19 y., Methods: Asthma incidence was identified from hospital admission, emergency room, and outpatient contacts among all live-born singletons born in Denmark between 1998 and 2016. We linked registry data with monthly mean concentrations of particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ) and PM with aerodynamic diameter ≤ 10 μ m ( PM 10 ), nitrogen dioxide ( NO 2 ), nitrogen oxides, elemental carbon, and organic carbon (OC), sulfur dioxide, ozone, sulfate, nitrate, ammonium, secondary organic aerosols, and sea salt. Associations were estimated with Cox proportional hazard models using fixed prenatal exposure means and time-varying postnatal exposures., Results: Of the 1,060,154 children included, 6.1% had asthma during the mean follow-up period of 8.8 y. The risk of asthma increased with increasing prenatal exposure to all pollutants except for O 3 and sea salt. We also observed increased risk after restriction to asthma after age 4 y, after additional adjustment for area-specific socioeconomic status, and for postnatal exposure to most pollutants. The hazard ratio (HR) associated with an interquartile range increase of 2.4 and 8.7   μ g / m 3 in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for PM 2.5 and 1.04 (95% CI: 1.02, 1.05) for NO 2 , respectively. This association with PM 2.5 was stable after adjustment for NO 2 , whereas it attenuated for NO 2 to 1.01 (95% CI: 0.99, 1.03) after adjustment for PM 2.5 . For a 0.5 - μ g / m 3 increase in prenatal OC exposure, for which biomass is an important source, the HR was 1.08 (95% CI: 1.06, 1.10), irrespective of adjustment for PM 2.5 ., Discussion: These findings suggest that early-life exposure to ambient air pollution from multiple sources contributes to asthma development. https://doi.org/10.1289/EHP11539.

A hygroscopic tandem differential mobility analyser (H-TDMA) was used to observe the size-resolved hygroscopic characteristics of submicron particles in January and April 2018 in urban Beijing. The probability distribution of the hygroscopic growth factor (HGF-PDF) in winter and spring usually showed a bimodal pattern, with more hygroscopic mode (MH) being more dominant. The seasonal variation in particle hygroscopicity was related to the origin of air mass, which received polluted southerly air masses in spring and clean northwesterly air masses in winter. Particles showed stronger hygroscopic behaviour during heavy pollution episodes (HPEs) with elevated concentrations of secondary aerosols, especially higher mass fraction of nitrate, which were indicated using the PM 2.5 (particulate matter with diameter below 2.5 µm) mass concentration normalised by CO mass concentration. The hygroscopic parameter (κ) values were calculated using H-TDMA (κ htdma ) and chemical composition (κ chem ). The closure study showed that κ chem was overestimated in winter afternoon when compared with κ htdma , because the organic particle hygroscopic parameter (κ org ) was overestimated in the calculations. It was influenced by the presence of a high concentration of hydrocarbon-like organic aerosol (HOA) with a weak water uptake ability. A positive relationship was observed between κ org and the ratio of oxygenated organic aerosol (OOA) and HOA, thereby indicating that the strong oxidation state enhanced the hygroscopicity of the particles. This study revealed the effect of local emission sources and secondary aerosol formation processes on particle hygroscopicity, which is of great significance for understanding the pollution formation mechanism in the North China Plain., 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 © 2021. Published by Elsevier B.V.)

Introduction: Long-term exposure to ambient fine particulate matter (PM 2.5 ) has been linked to increases in the incidence of lung cancer. However, more evidence is needed to conclude its effects on lung cancer survival., Objectives: The study aimed to explore the relationship between long-term PM 2.5 exposure and lung cancer survival and evaluated the benefits of clean air actions in Beijing., Methods: A whole-population cohort study was conducted on lung cancer patients diagnosed between 2001 and 2017. An atmospheric chemical transport model was used to estimate exposure under a counterfactual scenario without the policy and then quantified the effect of the policy. Cox regression models were used with the seasonality-adjusted PM 2.5 as the main effect., Results: A 10 μg/m 3 increase in PM 2.5 was estimated to be with a 6.5 % (95 % CI: 4.8 %, 8.2 %) increase in the mortality rates. The association was heterogeneous and modified by individual-level characteristics. The clean air actions were estimated to have prevented 3548 (95 % CI: 3280, 3825) premature deaths and to have prolonged survival time by 4.29 months (95 % CI: 0.01, 25.11)., Conclusion: Our findings suggest that PM 2.5 exposure lowers the survival rate for lung cancer. The clean air actions implemented in Beijing can protect lung cancer patients by increasing their survival time., Synopsis: Long-term exposure to PM 2.5 can lower lung patients' survival rates whereas the clean air actions in Beijing have prolonged these patients' survival time by reducing PM 2.5 level., 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.)

Background: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited., Objective: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts., Methods: Within the project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC), and ozone (O 3 ), as well as 8 PM 2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders., Results: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM 2.5 (hazard ratio per 5 µg/m 3 : 1.25; 95% confidence interval: 1.01-1.55), NO 2 (1.13; 0.95-1.34 per 10 µg/m 3 ), and BC (1.12; 0.94-1.34 per 0.5 × 10 -5 m -1 ), and a negative association with O 3 (0.74; 0.58-0.94 per 10 µg/m 3 ). Associations of PM 2.5 , NO 2 , and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM 2.5 remained robust when adjusted for NO 2 (1.24; 0.95-1.62) or BC (1.28; 0.96-1.71), whereas associations with NO 2 or BC attenuated to null. O 3 associations remained negative, but no longer statistically significant in models with PM 2.5 . We detected suggestive positive associations with the potassium component of PM 2.5 ., Conclusion: Long-term exposure to PM 2.5 , at levels well below current EU air pollution limit values, may contribute to PD mortality., 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 Ltd.. All rights reserved.)

The COVID-19 containment response policies (CRPs) had a major impact on air quality (AQ). These CRPs have been time-varying and location-specific. So far, despite having numerous studies on the effect of COVID-19 lockdown on AQ, a knowledge gap remains on the association between stringency of CRPs and AQ changes across the world, regions, nations, and cities. Here, we show that globally across 1851 cities (each more than 300 000 people) in 149 countries, after controlling for the impacts of relevant covariates (e.g., meteorology), Sentinel-5P satellite-observed nitrogen dioxide (NO 2 ) levels decreased by 4.9% (95% CI: 2.2, 7.6%) during lockdowns following stringent CRPs compared to pre-CRPs. The NO 2 levels did not change significantly during moderate CRPs and even increased during mild CRPs by 2.3% (95% CI: 0.7, 4.0%), which was 6.8% (95% CI: 2.0, 12.0%) across Europe and Central Asia, possibly due to population avoidance of public transportation in favor of private transportation. Among 1768 cities implementing stringent CRPs, we observed the most NO 2 reduction in more populated and polluted cities. Our results demonstrate that AQ improved when and where stringent COVID-19 CRPs were implemented, changed less under moderate CRPs, and even deteriorated under mild CRPs. These changes were location-, region-, and CRP-specific.

Evidence of the respiratory effects of ambient organic aerosols (e.g., polycyclic aromatic hydrocarbons, PAHs) among patients with chronic diseases is limited. We aimed to assess whether exposure to ambient particle-bound PAHs could worsen small airway functions in patients with chronic obstructive pulmonary disease (COPD) and elucidate the underlying mechanisms involved. Forty-five COPD patients were recruited with four repeated visits in 2014-2015 in Beijing, China. Parameters of pulmonary function and pulmonary/systemic inflammation and oxidative stress were measured at each visit. Linear mixed-effect models were performed to evaluate the associations between PAHs and measurements. In this study, participants experienced an average PAH level of 61.7 ng/m 3 . Interquartile range increases in exposure to particulate PAHs at prior up to 7 days were associated with reduced small airway functions, namely, decreases of 17.7-35.5% in forced maximal mid-expiratory flow. Higher levels of particulate PAHs were also associated with heightened lung injury and inflammation and oxidative stress. Stronger overall effects were found for PAHs from traffic emissions and coal burning. Exposure to ambient particulate PAHs was capable of impairing small airway functions in elderly patients with COPD, potentially via inflammation and oxidative stress. These findings highlight the importance of control efforts on organic particulate matter from fossil fuel combustion emissions.

Background: The majority of studies have shown higher greenness exposure associated with reduced mortality risks, but few controlled for spatially correlated air pollution and traffic noise exposures. We aim to address this research gap in the ELAPSE pooled cohort., Methods: Mean Normalized Difference Vegetation Index (NDVI) in a 300-m grid cell and 1-km radius were assigned to participants' baseline home addresses as a measure of surrounding greenness exposure. We used Cox proportional hazards models to estimate the association of NDVI exposure with natural-cause and cause-specific mortality, adjusting for a number of potential confounders including socioeconomic status and lifestyle factors at individual and area-levels. We further assessed the associations between greenness exposure and mortality after adjusting for fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ) and road traffic noise., Results: The pooled study population comprised 327,388 individuals who experienced 47,179 natural-cause deaths during 6,374,370 person-years of follow-up. The mean NDVI in the pooled cohort was 0.33 (SD 0.1) and 0.34 (SD 0.1) in the 300-m grid and 1-km buffer. In the main fully adjusted model, 0.1 unit increment of NDVI inside 300-m grid was associated with 5% lower risk of natural-cause mortality (Hazard Ratio (HR) 0.95 (95% CI: 0.94, 0.96)). The associations attenuated after adjustment for air pollution [HR (95% CI): 0.97 (0.96, 0.98) adjusted for PM 2.5 ; 0.98 (0.96, 0.99) adjusted for NO 2 ]. Additional adjustment for traffic noise hardly affected the associations. Consistent results were observed for NDVI within 1-km buffer. After adjustment for air pollution, NDVI was inversely associated with diabetes, respiratory and lung cancer mortality, yet with wider 95% confidence intervals. No association with cardiovascular mortality was found., Conclusions: We found a significant inverse association between surrounding greenness and natural-cause mortality, which remained after adjusting for spatially correlated air pollution and traffic noise., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

We assessed mortality risks associated with source-specific fine particles (PM 2.5 ) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM 2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM 2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 μg/m 3 increase) across five identified sources. On a 1 μg/m 3 basis, the residual oil-related PM 2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM 2.5 mass, suggesting that past estimates using the generic PM 2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.

Rationale: Ambient air pollution exposure has been linked to mortality from chronic cardiorespiratory diseases, while evidence on respiratory infections remains more limited. Objectives: We examined the association between long-term exposure to air pollution and pneumonia-related mortality in adults in a pool of eight European cohorts. Methods: Within the multicenter project ELAPSE (Effects of Low-Level Air Pollution: A Study in Europe), we pooled data from eight cohorts among six European countries. Annual mean residential concentrations in 2010 for fine particulate matter, nitrogen dioxide (NO 2 ), black carbon (BC), and ozone were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and pneumonia, influenza, and acute lower respiratory infections (ALRI) mortality. Measurements and Main Results: Of 325,367 participants, 712 died from pneumonia and influenza combined, 682 from pneumonia, and 695 from ALRI during a mean follow-up of 19.5 years. NO 2 and BC were associated with 10-12% increases in pneumonia and influenza combined mortality, but 95% confidence intervals included unity (hazard ratios, 1.12 [0.99-1.26] per 10 μg/m 3 for NO 2 ; 1.10 [0.97-1.24] per 0.5 10 -5 m -1 for BC). Associations with pneumonia and ALRI mortality were almost identical. We detected effect modification suggesting stronger associations with NO 2 or BC in overweight, employed, or currently smoking participants compared with normal weight, unemployed, or nonsmoking participants. Conclusions: Long-term exposure to combustion-related air pollutants NO 2 and BC may be associated with mortality from lower respiratory infections, but larger studies are needed to estimate these associations more precisely.

Background: The association between long-term exposure to air pollution and mortality from cardiorespiratory diseases is well established, yet the evidence for other diseases remains limited., Objectives: To examine the associations of long-term exposure to air pollution with mortality from diabetes, dementia, psychiatric disorders, chronic kidney disease (CKD), asthma, acute lower respiratory infection (ALRI), as well as mortality from all-natural and cardiorespiratory causes in the Danish nationwide administrative cohort., Methods: We followed all residents aged ≥ 30 years (3,083,227) in Denmark from 1 January 2000 until 31 December 2017. Annual mean concentrations of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC), and ozone (warm season) were estimated using European-wide hybrid land-use regression models (100 m × 100 m) and assigned to baseline residential addresses. We used Cox proportional hazard models to evaluate the association between air pollution and mortality, accounting for demographic and socioeconomic factors. We additionally applied indirect adjustment for smoking and body mass index (BMI)., Results: During 47,023,454 person-years of follow-up, 803,881 people died from natural causes. Long-term exposure to PM 2.5 (mean: 12.4 µg/m 3 ), NO 2 (20.3 µg/m 3 ), and/or BC (1.0 × 10 -5 /m) was statistically significantly associated with all studied mortality outcomes except CKD. A 5 µg/m 3 increase in PM 2.5 was associated with higher mortality from all-natural causes (hazard ratio 1.11; 95% confidence interval 1.09-1.13), cardiovascular disease (1.09; 1.07-1.12), respiratory disease (1.11; 1.07-1.15), lung cancer (1.19; 1.15-1.24), diabetes (1.10; 1.04-1.16), dementia (1.05; 1.00-1.10), psychiatric disorders (1.38; 1.27-1.50), asthma (1.13; 0.94-1.36), and ALRI (1.14; 1.09-1.20). Associations with long-term exposure to ozone (mean: 80.2 µg/m 3 ) were generally negative but became significantly positive for several endpoints in two-pollutant models. Generally, associations were attenuated but remained significant after indirect adjustment for smoking and BMI., Conclusion: Long-term exposure to PM 2.5 , NO 2 , and/or BC in Denmark were associated with mortality beyond cardiorespiratory diseases, including diabetes, dementia, psychiatric disorders, asthma, and ALRI., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed., Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC), warm season ozone (O 3 ) and eight PM 2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders., Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM 2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93-1.27) per 5 µg/m 3 for 2010 exposure and 1.06 (95% CI: 0.99-1.14) for baseline exposure. Effect estimates for NO 2 , BC and O 3 were close to unity. A positive association was observed with PM 2.5 zinc (HR 1.08; 95% CI: 1.00-1.16 per 10 ng/m 3 )., Conclusions: We found suggestive evidence of an association between long-term PM 2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM 2.5 suggests the importance of industrial emissions., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)

Traffic-related air pollution (TRAP) has shown enormous environmental toxicity, but its cardiorespiratory health impact on chronic obstructive pulmonary disease (COPD) has been less studied. We followed a panel of 45 COPD patients with 4 repeated clinical visits across 14 months in a traffic-predominated urban area of Beijing, China, with concurrent measurements of TRAP metrics (fine particulate matter, black carbon, oxides of nitrogen and carbon monoxide). Linear mixed-effect models were performed to evaluate the associations and potential pathways linking traffic pollution to indicators of spirometry, cardiac injury, inflammation and oxidative stress. We observed that interquartile range increases in moving averages of TRAP exposures at prior up to 7 days were associated with significant reductions in large and small airway functions, namely decreases in forced vital capacity of 3.1-9.3% and forced expiratory flow 25-75% of 5.9-16.4%. Higher TRAP levels were also associated with worsening of biomarkers relevant to lung injury (hepatocyte growth factor and surfactant protein D) and cardiac injury (high-sensitivity cardiac troponin I, B-type natriuretic peptide and soluble ST2), as well as enhanced airway/systemic inflammation and oxidative stress. Mediation analyses showed that TRAP exposures may prompt cardiac injury, possibly via worsening pulmonary pathophysiology. These findings highlight the importance of traffic pollution control priority in urban areas., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: While air pollution has been linked to the development of chronic obstructive pulmonary disease (COPD), evidence on the role of environmental noise is just emerging. We examined the associations of long-term exposure to air pollution and road traffic noise with COPD incidence., Methods: We defined COPD incidence for 24 538 female nurses from the Danish Nurse Cohort (age >44 years) as the first hospital contact between baseline (1993 or 1999) and 2015. We estimated residential annual mean concentrations of particulate matter with an aerodynamic diameter <2.5 µm (PM 2.5 ) since 1990 and nitrogen dioxide (NO 2 ) since 1970 using the Danish Eulerian Hemispheric Model/Urban Background Model/Air Geographic Information System modelling system, and road traffic noise (L den ) since 1970 using the Nord2000 model. Time-varying Cox regression models were applied to assess the associations of air pollution and road traffic noise with COPD incidence., Results: 977 nurses developed COPD during a mean of 18.6 years' follow-up. We observed associations with COPD for all three exposures with HRs and 95% CIs of 1.19 (1.01-1.41) per 6.26 µg·m -3 for PM 2.5 , 1.13 (1.05-1.20) per 8.19 µg·m -3 for NO 2 and 1.15 (1.06-1.25) per 10 dB for L den . Associations with NO 2 and L den attenuated slightly after mutual adjustment, but were robust to adjustment for PM 2.5 . Associations with PM 2.5 were attenuated to null after adjustment for either NO 2 or L den . No potential interaction effect was observed between air pollutants and noise., Conclusion: Long-term exposure to air pollution, especially traffic-related NO 2 , and to road traffic noise were independently associated with COPD., Competing Interests: Conflict of interest: S. Liu has nothing to disclose. Conflict of interest: Y-H. Lim has nothing to disclose. Conflict of interest: M. Pedersen has nothing to disclose. Conflict of interest: J.T. Jørgensen has nothing to disclose. Conflict of interest: H. Amini has nothing to disclose. Conflict of interest: T. Cole-Hunter has nothing to disclose. Conflict of interest: A.J. Mehta has nothing to disclose. Conflict of interest: R. So has nothing to disclose. Conflict of interest: L.H. Mortensen has nothing to disclose. Conflict of interest: R.G.J. Westendorp has nothing to disclose. Conflict of interest: S. Loft has nothing to disclose. Conflict of interest: E.V. Bräuner has nothing to disclose. Conflict of interest: M. Ketzel has nothing to disclose. Conflict of interest: O. Hertel has nothing to disclose. Conflict of interest: J. Brandt has nothing to disclose. Conflict of interest: S.S. Jensen has nothing to disclose. Conflict of interest: J.H. Christensen has nothing to disclose. Conflict of interest: T. Sigsgaard has nothing to disclose. Conflict of interest: C. Geels has nothing to disclose. Conflict of interest: L.M. Frohn has nothing to disclose. Conflict of interest: M. Brborić has nothing to disclose. Conflict of interest: J. Radonić has nothing to disclose. Conflict of interest: M. Turk Sekulic has nothing to disclose. Conflict of interest: K. Bønnelykke has nothing to disclose. Conflict of interest: C. Backalarz has nothing to disclose. Conflict of interest: M.K. Simonsen has nothing to disclose. Conflict of interest: Z.J. Andersen has nothing to disclose., (Copyright ©The authors 2021. For reproduction rights and permissions contact permissions@ersnet.org.)

Improving air quality in indoor environments where people live is of importance to protect human health. In this systematic review, we assessed the effectiveness of personal-level use of air filtration units in reducing indoor particulate matters (PM) concentrations under real-world situations following systematic review guidelines. A total of 54 articles were included in the review, in which 20 randomized controlled/crossover trials that reported the changes in indoor fine PM (PM 2.5 ) concentrations were quantitatively assessed in meta-analysis. Standardized mean differences (SMDs) were calculated for changes in indoor PM concentrations following air filtration interventions. Moderate-to-large reductions of 11%-82% in indoor PM 2.5  concentrations were observed with SMD of -1.19 (95% CI: -1.50, -0.88). The reductions in indoor PM concentrations varied by geographical locations, filtration technology employed, indoor environmental characteristics, and air pollution sources. Most studies were graded with low-to-moderate risk of bias; however, the overall certainty of evidence for indoor PM concentration reductions was graded at very low level. Considering the effectiveness of indoor air filtration under practical uses, socio-economic disparities across study populations, and costs of air filter replacement over time, our results highlight the importance of reducing air pollution exposure at the sources., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Epidemiological evidence on cardiometabolic health of particulate organic matter (POM) and its sources is sparse. In a panel of 73 healthy adults in Beijing, China, daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) and n-alkanes were measured throughout the study period, and Positive Matrix Factorization approach was used to identity PAHs sources. Linear mixed-effect models and mediation analyses were applied to examine the associations and potential interlink pathways between POM and biomarkers indicative of hemodynamics, insulin resistance, vascular calcification and immune inflammation. We found that significant alterations in cardiometabolic measures were associated with POM exposures. In specific, interquartile range increases in PAHs concentrations at prior up to 9 days were observed in association with significant elevations of 2.6-2.9% in diastolic blood pressure, 6.6-8.1% in soluble ST2, 10.5-14.5% in insulin, 40.9-45.7% in osteoprotegerin, and 36.3-48.7% in interleukin-17A. Greater associations were generally observed for PAHs originating from traffic emissions and coal burning. Mediation analyses revealed that POM exposures may prompt the genesis of hemodynamic abnormalities, possibly via worsening insulin resistance and calcification potential. These findings suggested that cardiometabolic health benefits would be achieved by reducing PM from combustion emissions., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Introduction: Epidemiological cohort studies have consistently found associations between long-term exposure to outdoor air pollution and a range of morbidity and mortality endpoints. Recent evaluations by the World Health Organization and the Global Burden of Disease study have suggested that these associations may be nonlinear and may persist at very low concentrations. Studies conducted in North America in particular have suggested that associations with mortality persisted at concentrations of particulate matter with an aerodynamic diameter of less than 2.5 μm (PM 2.5 ) well below current air quality standards and guidelines. The uncertainty about the shape of the concentration-response function at the low end of the concentration distribution, related to the scarcity of observations in the lowest range, was the basis of the current project. Previous studies have focused on PM 2.5 , but increasingly associations with nitrogen dioxide (NO 2 ) are being reported, particularly in studies that accounted for the fine spatial scale variation of NO 2 . Very few studies have evaluated the effects of long-term exposure to low concentrations of ozone (O 3 ). Health effects of black carbon (BC), representing primary combustion particles, have not been studied in most large cohort studies of PM 2.5 . Cohort studies assessing health effects of particle composition, including elements from nontailpipe traffic emissions (iron, copper, and zinc) and secondary aerosol (sulfur) have been few in number and reported inconsistent results. The overall objective of our study was to investigate the shape of the relationship between long-term exposure to four pollutants (PM 2.5 , NO 2 , BC, and O 3 ) and four broad health effect categories using a number of different methods to characterize the concentration-response function (i.e., linear, nonlinear, or threshold). The four health effect categories were (1) natural- and cause-specific mortality including cardiovascular and nonmalignant as well as malignant respiratory and diabetes mortality; and morbidity measured as (2) coronary and cerebrovascular events; (3) lung cancer incidence; and (4) asthma and chronic obstructive pulmonary disease (COPD) incidence. We additionally assessed health effects of PM 2.5 composition, specifically the copper, iron, zinc, and sulfur content of PM 2,5 ., Methods: We focused on analyses of health effects of air pollutants at low concentrations, defined as less than current European Union (EU) Limit Values, U.S. Environmental Protection Agency (U.S. EPA), National Ambient Air Quality Standards (NAAQS), and/or World Health Organization (WHO) Air Quality Guideline values for PM 2.5 , NO 2 , and O 3 . We address the health effects at low air pollution levels by performing new analyses within selected cohorts of the ESCAPE study (European Study of Cohorts for Air Pollution Effects; Beelen et al. 2014a) and within seven very large European administrative cohorts. By combining well-characterized ESCAPE cohorts and large administrative cohorts in one study the strengths and weaknesses of each approach can be addressed. The large administrative cohorts are more representative of national or citywide populations, have higher statistical power, and can efficiently control for area-level confounders, but have fewer possibilities to control for individual-level confounders. The ESCAPE cohorts have detailed information on individual confounders, as well as country-specific information on area-level confounding. The data from the seven included ESCAPE cohorts and one additional non-ESCAPE cohort have been pooled and analyzed centrally. More than 300,000 adults were included in the pooled cohort from existing cohorts in Sweden, Denmark, Germany, the Netherlands, Austria, France, and Italy. Data from the administrative cohorts have been analyzed locally, without transfer to a central database. Privacy regulations prevented transfer of data from administrative cohorts to a central database. More than 28 million adults were included from national administrative cohorts in Belgium, Denmark, England, the Netherlands, Norway, and Switzerland as well as an administrative cohort in Rome, Italy. We developed central exposure assessment using Europewide hybrid land use regression (LUR) models, which incorporated European routine monitoring data for PM 2.5 , NO 2 , and O 3 , and ESCAPE monitoring data for BC and PM 2.5 composition, land use, and traffic data supplemented with satellite observations and chemical transport model estimates. For all pollutants, we assessed exposure at a fine spatial scale, 100 × 100 m grids. These models have been applied to individual addresses of all cohorts including the administrative cohorts. In sensitivity analyses, we applied the PM 2.5 models developed within the companion HEI-funded Canadian MAPLE study (Brauer et al. 2019) and O 3 exposures on a larger spatial scale for comparison with previous studies. Identification of outcomes included linkage with mortality, cancer incidence, hospital discharge registries, and physician-based adjudication of cases. We analyzed natural-cause, cardiovascular, ischemic heart disease, stroke, diabetes, cardiometabolic, respiratory, and COPD mortality. We also analyzed lung cancer incidence, incidence of coronary and cerebrovascular events, and incidence of asthma and COPD (pooled cohort only). We applied the Cox proportional hazard model with increasing control for individual- and area-level covariates to analyze the associations between air pollution and mortality and/or morbidity for both the pooled cohort and the individual administrative cohorts. Age was used as the timescale because of evidence that this results in better adjustment for potential confounding by age. Censoring occurred at the time of the event of interest, death from other causes, emigration, loss to follow-up for other reasons, or at the end of follow-up, whichever came first. A priori we specified three confounder models, following the modeling methods of the ESCAPE study. Model 1 included only age (time axis), sex (as strata), and calendar year of enrollment. Model 2 added individual-level variables that were consistently available in the cohorts contributing to the pooled cohort or all variables available in the administrative cohorts, respectively. Model 3 further added area-level socioeconomic status (SES) variables. A priori model 3 was selected as the main model. All analyses in the pooled cohort were stratified by subcohort. All analyses in the administrative cohorts accounted for clustering of the data in neighborhoods by adjusting the variance of the effect estimates. The main exposure variable we analyzed was derived from the Europewide hybrid models based on 2010 monitoring data. Sensitivity analyses were conducted using earlier time periods, time-varying exposure analyses, local exposure models, and the PM 2.5 models from the Canadian MAPLE project. We first specified linear single-pollutant models. Two-pollutant models were specified for all combinations of the four main pollutants. Two-pollutant models for particle composition were analyzed with PM 2.5 and NO 2 as the second pollutant. We then investigated the shape of the concentration-response function using natural splines with two, three, and four degrees of freedom; penalized splines with the degrees of freedom determined by the algorithm and shape-constrained health impact functions (SCHIF) using confounder model 3. Additionally, we specified linear models in subsets of the concentration range, defined by removing concentrations above a certain value from the analysis, such as for PM 2.5 25 μg/m 3 (EU limit value), 20, 15, 12 μg/m 3 (U.S. EPA National Ambient Air Quality Standard), and 10 μg/m 3 (WHO Air Quality Guideline value). Finally, threshold models were evaluated to investigate whether the associations persisted below specific concentration values. For PM 2.5 , we evaluated 10, 7.5, and 5 μg/m 3 as potential thresholds. Performance of threshold models versus the corresponding no-threshold linear model were evaluated using the Akaike information criterion (AIC)., Results: In the pooled cohort, virtually all subjects in 2010 had PM 2.5 and NO 2 annual average exposures below the EU limit values (25 μg/m 3 and 40 μg/m 3 , respectively). More than 50,000 had a residential PM 2.5 exposure below the U.S. EPA NAAQS (12 μg/m 3 ). More than 25,000 subjects had a residential PM 2.5 exposure below the WHO guideline (10 μg/m 3 ). We found significant positive associations between PM 2.5 , NO 2 , and BC and natural-cause, respiratory, cardiovascular, and diabetes mortality. In our main model, the hazard ratios (HRs) (95% [confidence interval] CI) were 1.13 (CI = 1.11, 1.16) for an increase of 5 μg/m 3 PM 2.5 , 1.09 (CI = 1.07, 1.10) for an increase of 10 μg/m 3 NO 2 , and 1.08 (CI = 1.06, 1.10) for an increase of 0.5 × 10 -5 /m BC for natural-cause mortality. The highest HRs were found for diabetes mortality. Associations with O 3 were negative, both in the fine spatial scale of the main ELAPSE model and in large spatial scale exposure models. For PM 2.5 , NO 2 , and BC, we generally observed a supralinear association with steeper slopes at low exposures and no evidence of a concentration below which no association was found. Subset analyses further confirmed that these associations remained at low levels: below 10 μg/m 3 for PM 2.5 and 20 μg/m 3 for NO 2 . HRs were similar to the full cohort HRs for subjects with exposures below the EU limit values for PM 2.5 and NO 2 , the U.S. NAAQS values for PM 2.5 , and the WHO guidelines for PM 2.5 and NO 2 . The mortality associations were robust to alternative specifications of exposure, including different time periods, PM 2.5 from the MAPLE project, and estimates from the local ESCAPE model. Time-varying exposure natural spline analyses confirmed associations at low pollution levels. HRs in two-pollutant models were attenuated but remained elevated and statistically significant for PM 2.5 and NO 2 . In two-pollutant models of PM 2.5 and NO 2 HRs for natural-cause mortality were 1.08 (CI = 1.05, 1.11) for PM 2.5 and 1.05 (CI = 1.03, 1.07) for NO 2 . Associations with O 3 were attenuated but remained negative in two-pollutant models with NO 2 , BC, and PM 2.5 . We found significant positive associations between PM 2.5 , NO 2 , and BC and incidence of stroke and asthma and COPD hospital admissions. Furthermore, NO 2 was significantly related to acute coronary heart disease and PM 2.5 was significantly related to lung cancer incidence. We generally observed linear to supralinear associations with no evidence of a threshold, with the exception of the association between NO 2 and acute coronary heart disease, which was sublinear. Subset analyses documented that associations remained even with PM 2.5 below 20 μg/m 3 and possibly 12 μg/m 3 . Associations remained even when NO 2 was below 30 μg/m 3 and in some cases 20 μg/m 3 . In two-pollutant models, NO 2 was most consistently associated with acute coronary heart disease, stroke, asthma, and COPD hospital admissions. PM 2.5 was not associated with these outcomes in two-pollutant models with NO 2 . PM 2.5 was the only pollutant that was associated with lung cancer incidence in two-pollutant models. Associations with O 3 were negative though generally not statistically significant. In the administrative cohorts, virtually all subjects in 2010 had PM 2.5 and NO 2 annual average exposures below the EU limit values. More than 3.9 million subjects had a residential PM 2.5 exposure below the U.S. EPA NAAQS (12 μg/m 3 ) and more than 1.9 million had residential PM 2.5 exposures below the WHO guideline (10 μg/m 3 ). We found significant positive associations between PM 2.5 , NO 2 , and BC and natural-cause, respiratory, cardiovascular, and lung cancer mortality, with moderate to high heterogeneity between cohorts. We found positive but statistically nonsignificant associations with diabetes mortality. In our main model meta-analysis, the HRs (95% CI) for natural-cause mortality were 1.05 (CI = 1.02, 1.09) for an increase of 5 μg/m 3 PM 2.5 , 1.04 (CI = 1.02, 1.07) for an increase of 10 μg/m 3 NO 2 , and 1.04 (CI = 1.02, 1.06) for an increase of 0.5 × 10 -5 /m BC, and 0.95 (CI = 0.93, 0.98) for an increase of 10 μg/m 3 O 3 . The shape of the concentration-response functions differed between cohorts, though the associations were generally linear to supralinear, with no indication of a level below which no associations were found. Subset analyses documented that these associations remained at low levels: below 10 μg/m 3 for PM 2.5 and 20 μg/m 3 for NO 2 . BC and NO 2 remained significantly associated with mortality in two-pollutant models with PM 2.5 and O 3 . The PM 2.5 HR attenuated to unity in a two-pollutant model with NO 2 . The negative O 3 association was attenuated to unity and became nonsignificant. The mortality associations were robust to alternative specifications of exposure, including time-varying exposure analyses. Time-varying exposure natural spline analyses confirmed associations at low pollution levels. Effect estimates in the youngest participants (<65 years at baseline) were much larger than in the elderly (>65 years at baseline). Effect estimates obtained with the ELAPSE PM 2.5 model did not differ from the MAPLE PM 2.5 model on average, but in individual cohorts, substantial differences were found., Conclusions: Long-term exposure to PM 2.5 , NO 2 , and BC was positively associated with natural-cause and cause-specific mortality in the pooled cohort and the administrative cohorts. Associations were found well below current limit values and guidelines for PM 2.5 and NO 2 . Associations tended to be supralinear, with steeper slopes at low exposures with no indication of a threshold. Two-pollutant models documented the importance of characterizing the ambient mixture with both NO 2 and PM 2.5 . We mostly found negative associations with O 3 . In two-pollutant models with NO 2 , the negative associations with O 3 were attenuated to essentially unity in the mortality analysis of the administrative cohorts and the incidence analyses in the pooled cohort. In the mortality analysis of the pooled cohort, significant negative associations with O 3 remained in two-pollutant models. Long-term exposure to PM 2.5 , NO 2 , and BC was also positively associated with morbidity outcomes in the pooled cohort. For stroke, asthma, and COPD, positive associations were found for PM 2.5 , NO 2 , and BC. For acute coronary heart disease, an increased HR was observed for NO 2 . For lung cancer, an increased HR was found only for PM 2.5 . Associations mostly showed steeper slopes at low exposures with no indication of a threshold., (© 2021 Health Effects Institute. All rights reserved.)

Based on the monitoring data of atmospheric pollutants and the meteorological data in Harbin in 2017, the temporal spatial distribution characteristics of PM 2.5 pollution and the relationships between PM 2.5 concentration and meteorological factors in this region were analyzed. The PM 2.5 concentration data and the meteorological data in 2017 were comprehensively analyzed by using ArcGIS and R. The results show that spatially, the PM 2.5 concentration in the central districts of Harbin are high in the southeast and low in the northwest; temporally, PM 2.5 pollution is most serious in autumn and winter, with multiple spells of heavy pollution and an obvious "weekend effect", while the air quality is better in spring and summer; overall, relative humidity is positively correlated to PM 2.5 concentration, while temperature, wind direction, and wind speed are negatively correlated to PM 2.5 mass concentration, and low wind speed and high relative humidity are major contributors to increase of PM 2.5 concentration. Implications : Highlight: The use of big data to deal with the data of air pollution and meteorology.Key points: The air pollution data of Harbin in autumn and winter is more serious than that in spring and summer, and is closely related to meteorological factors. Attraction: Big data is used to process air pollution data and meteorological data, and R language is used to describe the relationship between them.

Background: Ambient air pollution is likely a risk factor for asthma, and recent evidence suggests the possible relevance of road traffic noise., Objectives: We examined the associations of long-term exposure to air pollution and road traffic noise with adult-asthma incidence., Methods: We followed 28,731 female nurses (age > 44 years) from the Danish Nurse Cohort, recruited in 1993 and 1999, for first hospital contact for asthma from 1977 until 2015. We estimated residential annual mean concentrations of particulate matter with diameter < 2.5 µm (PM 2.5 ) since 1990 and nitrogen dioxide (NO 2 ) since 1970 with the Danish DEHM/UBM/AirGIS modeling system, and road traffic noise (L den ) since 1970 with the Nord2000 model. Time-varying Cox regression models were used to associate air pollution and road traffic noise exposure with asthma incidence., Results: During 18.6 years' mean follow-up, 528 out of 23,093 participants had hospital contact for asthma. The hazard ratios (HR) and 95% confidence intervals for asthma incidence associated with 3-year moving average exposures were 1.29 (1.03, 1.61) per 6.3 µg/m 3 for PM 2.5 , 1.16 (1.07, 1.27) per 8.2 µg/m 3 for NO 2 , and 1.12 (1.00, 1.25) per 10 dB for L den . The HR for NO 2 remained unchanged after adjustment for either PM 2.5 or L den , while the HRs for PM 2.5 and L den attenuated to unity after adjustment for NO 2 ., Conclusions: Long-term exposure to air pollution was associated with adult-asthma incidence independently of road traffic noise, with NO 2 most relevant. Road traffic noise was not independently associated with adult-asthma incidence., (Copyright © 2021. Published by Elsevier Ltd.)

Background: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ) and black carbon (BC) with asthma incidence in adults., Methods: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders., Results: Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 μg·m -3 for PM 2.5 , 1.17 (95% CI 1.10-1.25) per 10 µg·m -3 for NO 2 and 1.15 (95% CI 1.08-1.23) per 0.5×10 -5  m -1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM 2.5 and NO 2 . NO 2 and BC estimates remained unchanged in two-pollutant models with PM 2.5 , whereas PM 2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold., Conclusions: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values., Competing Interests: Conflict of interest: S. Liu has nothing to disclose. Conflict of interest: J.T. Jørgensen has nothing to disclose. Conflict of interest: P. Ljungman has nothing to disclose. Conflict of interest: G. Pershagen has nothing to disclose. Conflict of interest: T. Bellander has nothing to disclose. Conflict of interest: K. Leander has nothing to disclose. Conflict of interest: P.K.E. Magnusson has nothing to disclose. Conflict of interest: D. Rizzuto has nothing to disclose. Conflict of interest: U.A. Hvidtfeldt has nothing to disclose. Conflict of interest: O. Raaschou-Nielsen has nothing to disclose. Conflict of interest: K. Wolf has nothing to disclose. Conflict of interest: B. Hoffmann has nothing to disclose. Conflict of interest: B. Brunekreef has nothing to disclose. Conflict of interest: M. Strak has nothing to disclose. Conflict of interest: J. Chen has nothing to disclose. Conflict of interest: A. Mehta has nothing to disclose. Conflict of interest: R.W. Atkinson has nothing to disclose. Conflict of interest: M. Bauwelinck has nothing to disclose. Conflict of interest: R. Varraso has nothing to disclose. Conflict of interest: M-C. Boutron-Ruault has nothing to disclose. Conflict of interest: J. Brandt has nothing to disclose. Conflict of interest: G. Cesaroni has nothing to disclose. Conflict of interest: F. Forastiere has nothing to disclose. Conflict of interest: D. Fecht has nothing to disclose. Conflict of interest: J. Gulliver has nothing to disclose. Conflict of interest: O. Hertel has nothing to disclose. Conflict of interest: K. de Hoogh has nothing to disclose. Conflict of interest: N.A.H. Janssen has nothing to disclose. Conflict of interest: K. Katsouyanni has nothing to disclose. Conflict of interest: M. Ketzel has nothing to disclose. Conflict of interest: J.O. Klompmaker has nothing to disclose. Conflict of interest: G. Nagel has nothing to disclose. Conflict of interest: B. Oftedal has nothing to disclose. Conflict of interest: A. Peters has nothing to disclose. Conflict of interest: A. Tjønneland has nothing to disclose. Conflict of interest: S.P. Rodopoulou has nothing to disclose. Conflict of interest: E Samoli has nothing to disclose. Conflict of interest: D.T. Kristoffersen has nothing to disclose. Conflict of interest: T. Sigsgaard has nothing to disclose. Conflict of interest: M. Stafoggia has nothing to disclose. Conflict of interest: D. Vienneau has nothing to disclose. Conflict of interest: G. Weinmayr has nothing to disclose. Conflict of interest: G. Hoek has nothing to disclose. Conflict of interest: Z.J. Andersen has nothing to disclose., (Copyright ©ERS 2021.)

Background: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤ 2.5   μ m [fine particulate matter ( PM 2.5 )] components and mortality have been reported, partly related to challenges in exposure assessment., Objectives: We investigated the associations between long-term exposure to PM 2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM 2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms., Methods: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM 2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100 × 100   m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM 2.5 mass and nitrogen dioxide ( NO 2 ) separately., Results: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM 2.5 and NO 2 . HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2   ng / m 3 , adjusting for PM 2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models., Conclusion: Long-term exposure to V in PM 2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.

Background: We evaluated methods for the analysis of multi-level survival data using a pooled dataset of 14 cohorts participating in the ELAPSE project investigating associations between residential exposure to low levels of air pollution (PM 2.5 and NO 2 ) and health (natural-cause mortality and cerebrovascular, coronary and lung cancer incidence)., Methods: We applied five approaches in a multivariable Cox model to account for the first level of clustering corresponding to cohort specification: (1) not accounting for the cohort or using (2) indicator variables, (3) strata, (4) a frailty term in frailty Cox models, (5) a random intercept under a mixed Cox, for cohort identification. We accounted for the second level of clustering due to common characteristics in the residential area by (1) a random intercept per small area or (2) applying variance correction. We assessed the stratified, frailty and mixed Cox approach through simulations under different scenarios for heterogeneity in the underlying hazards and the air pollution effects., Results: Effect estimates were stable under approaches used to adjust for cohort but substantially differed when no adjustment was applied. Further adjustment for the small area grouping increased the effect estimates' standard errors. Simulations confirmed identical results between the stratified and frailty models. In ELAPSE we selected a stratified multivariable Cox model to account for between-cohort heterogeneity without adjustment for small area level, due to the small number of subjects and events in the latter., Conclusions: Our study supports the need to account for between-cohort heterogeneity in multi-center collaborations using pooled individual level data., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: An association between long-term exposure to fine particulate matter (PM 2.5 ) and lung cancer has been established in previous studies. PM 2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the "Effects of Low-level Air Pollution: A Study in Europe" (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM 2.5 and lung cancer incidence., Methods: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM 2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants' baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status)., Results: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m 3 PM 2.5  K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m 3 PM 2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m 3 PM 2.5  S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m 3 PM 2.5  V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO 2 ). After adjustment for PM 2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative., Conclusions: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM 2.5 components may prove helpful in future lung cancer prevention strategies., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background/aim: Ambient air pollution has been associated with lung cancer, but the shape of the exposure-response function - especially at low exposure levels - is not well described. The aim of this study was to address the relationship between long-term low-level air pollution exposure and lung cancer incidence., Methods: The "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration pools seven cohorts from across Europe. We developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO 2 ), fine particulate matter (PM 2.5 ), black carbon (BC), and ozone (O 3 ) to assign exposure to cohort participants' residential addresses in 100 m by 100 m grids. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). We fitted linear models, linear models in subsets, Shape-Constrained Health Impact Functions (SCHIF), and natural cubic spline models to assess the shape of the association between air pollution and lung cancer at concentrations below existing standards and guidelines., Results: The analyses included 307,550 cohort participants. During a mean follow-up of 18.1 years, 3956 incident lung cancer cases occurred. Median (Q1, Q3) annual (2010) exposure levels of NO 2 , PM 2.5 , BC and O 3 (warm season) were 24.2 µg/m 3 (19.5, 29.7), 15.4 µg/m 3 (12.8, 17.3), 1.6 10 -5 m -1 (1.3, 1.8), and 86.6 µg/m 3 (78.5, 92.9), respectively. We observed a higher risk for lung cancer with higher exposure to PM 2.5 (HR: 1.13, 95% CI: 1.05, 1.23 per 5 µg/m 3 ). This association was robust to adjustment for other pollutants. The SCHIF, spline and subset analyses suggested a linear or supra-linear association with no evidence of a threshold. In subset analyses, risk estimates were clearly elevated for the subset of subjects with exposure below the EU limit value of 25 µg/m 3 . We did not observe associations between NO 2 , BC or O 3 and lung cancer incidence., Conclusions: Long-term ambient PM 2.5 exposure is associated with lung cancer incidence even at concentrations below current EU limit values and possibly WHO Air Quality Guidelines., (Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD), but evidence is sparse and inconsistent., Objectives: We examined the association between long-term exposure to low-level air pollution and COPD incidence., Methods: Within the 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE) study, we pooled data from three cohorts, from Denmark and Sweden, with information on COPD hospital discharge diagnoses. Hybrid land use regression models were used to estimate annual mean concentrations of particulate matter with a diameter < 2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ), and black carbon (BC) in 2010 at participants' baseline residential addresses, which were analysed in relation to COPD incidence using Cox proportional hazards models., Results: Of 98,058 participants, 4,928 developed COPD during 16.6 years mean follow-up. The adjusted hazard ratios (HRs) and 95% confidence intervals for associations with COPD incidence were 1.17 (1.06, 1.29) per 5 µg/m 3 for PM 2.5 , 1.11 (1.06, 1.16) per 10 µg/m 3 for NO 2 , and 1.11 (1.06, 1.15) per 0.5 10 -5 m -1 for BC. Associations persisted in subset participants with PM 2.5 or NO 2 levels below current EU and US limit values and WHO guidelines, with no evidence for a threshold. HRs for NO 2 and BC remained unchanged in two-pollutant models with PM 2.5 , whereas the HR for PM 2.5 was attenuated to unity with NO 2 or BC., Conclusions: Long-term exposure to low-level air pollution is associated with the development of COPD, even below current EU and US limit values and possibly WHO guidelines. Traffic-related pollutants NO 2 and BC may be the most relevant., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Objective: We aimed to establish a representative exposure response function between PM 2.5 and lung cancer to evaluate the impact on lung cancer burden and the benefits gained in association with the environmental policy change in Beijing, China., Methods: Based on population-based cancer registration data during 2001-2016, using a spatiotemporal Poisson regression model, long-term concentrations of PM 2.5 were linked to sex-age adjusted incidence rates of total lung cancer and its pathological subtypes. We calculated the health and monetary benefits associated with air quality improvement using the cost of illness method., Results: In the constructed regression model, a 10 μg/m 3 increment of PM 2.5 was associated with increases of 6.0% (95% confidence interval [95% CI]: 4.3%, 7.7%), 14.8% (10.3%, 19.4%), and 6.5% (3.3%, 9.8%) in the incidence of total lung cancer, squamous cell carcinoma, and adenocarcinoma, respectively. The estimated associations indicate that long-term exposure to PM 2.5 contributed 1947 to 3059 incident cases of lung cancer per year among the residents in Beijing during the study period. Clean air actions saved 4978 (95% CI: 2711, 7417) lung cancer cases, which brought a savings of 218 (118, 324) million RMB (~31 [17, 46] million US dollars) in direct inpatient medical expenditures. If air quality had met national standards of long-term PM 2.5 (35 μg/m 3 ) in 2014-2016, 10,003 (95% CI: 9325, 10,650) lung cancer cases could have been prevented and direct inpatient medical expenditures of 438 (409, 466) million RMB (~63 [58, 67] million US dollars) could have been saved., Conclusions: This study enriches epidemiological study, confirming the association between exposure to PM 2.5 and lung cancer or its subtypes, and provides novel evidence for the notable reduction in lung cancer burden and medical expenditure savings that were achieved through air quality improvements in Beijing from 2014 to 2016., 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 The Authors. Published by Elsevier B.V. All rights reserved.)

Rationale: Chronic air pollutant exposure has been associated with development of Acute Respiratory Distress Syndrome (ARDS) in patients at risk, particularly from severe trauma. We recently reported that shorter peripheral blood leukocyte (PBL) telomere length (TL) was associated with worse outcomes and higher severity of ARDS in critically ill patients. Since most major air pollutants are potent oxidants that can induce cellular oxidative stress, and oxidative stress can accelerate telomere shortening, we hypothesized that higher levels of chronic air pollutant exposure would be associated with shorter telomere length in critically ill patients including patients with ARDS., Methods: PBL-TL was measured in genomic DNA collected on the morning of ICU day 2 in 772 critically ill patients enrolled in a prospective observational study. Exposures to air pollutants including ozone (warm-season only), particulate matter < 2.5 µm (PM 2.5 ), particulate matter < 10 µm (PM 10 ), CO, NO 2 and SO 2 , were estimated by weighted average of daily levels from all monitors within 50 km of each patient's residential address for the 3 years prior to admission. Associations of each air pollutant exposure and PBL-TL were investigated by multivariable linear regression models adjusting for age, ethnicity, sex, smoking history, alcohol abuse, insurance status, median household income, history of malignancy and APACHE II., Results: Contrary to our hypothesis, TL increased across exposure quartiles in both ozone and PM 2.5 analyses (p < 0.05). In a regression model controlling for potential confounders, long term ozone exposure was significantly associated with an increase in TL in the entire cohort (0.31 kb per 10 ppb), as well as in subgroups with sepsis, trauma and ARDS (all p < 0.05). In multivariable models, entire-year exposure to PM 2.5 , PM 10 , CO, NO 2 and SO 2 was not associated with TL after adjustment for potential confounders. In an analysis restricted to warm-season levels to assess the effect of seasonality, higher warm-season PM 2.5 and CO exposures were independently associated with longer TL., Conclusions: Long-term exposure to ozone is associated with longer peripheral blood TL in critically ill patients. Further studies are needed to investigate the potential underlying mechanisms for this unexpected positive association between telomere length and air pollution exposure in critical illness., Competing Interests: Declaration of Competing Interest None of the authors report conflicts of interest relevant to this study., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Tropospheric ozone (O 3 ) is a pollutant of widespread concern in the world and especially in China for its negative effects on agricultural crops. For the first time, yield and economic losses of wheat between 2014 and 2017 were estimated for the North China Plain (NCP) using observational hourly O 3 data from 312 monitoring stations and exposure-response functions based on AOT40 index (accumulated hourly O 3 concentration above 40 ppb) from a Chinese study. AOT40 values from 2014 to 2017 during the wheat growing seasons (75-days, 44 before and 30 after mid-anthesis) ranged from 3.1 to 14.9 ppm h, 4.9-17.5 ppm h, 7.3-17.6 ppm h, and 0.5-18.6 ppm h, respectively. The highest AOT40 values were observed in the Beijing-Tianjin-Hebei region. The values of relative yield losses from 2014 to 2017 were in the ranges of 6.4-30.5%, 10.0-35.8%, 14.9-34.1%, and 21.6-38.2%, respectively. The total wheat production losses in NCP for 2014-2017 accounted for 18.5%, 22.7%, 26.2% and 30.8% in the whole production, while the economic losses amounted to 6,292 million USD, 8,524 million USD, 10,068 million USD, and 12,404 million USD, respectively. The important impact of O 3 in this area, which is of global importance, should be considered when assessing wheat yield production. Our results also show an increasing trend in AOT40, relative yield loss, total crop production loss and economic loss in the four consecutive years., 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 © 2019 Elsevier Ltd. All rights reserved.)

Numerous epidemiologic studies on adverse health effects of air pollution have been well documented; however, assessment on health benefits of air quality improvement from air pollution control measures has been limited in developing countries. We assessed the mortality benefits associated with air pollution improvement over 11 years in Guangzhou, China (2006-2016). A time series analysis with Generalized additive Poisson models was used to estimate mortality effects of ozone (O 3 ) and nitrogen dioxide (NO 2 ), adjusting for time trend, day of week, public holiday, temperature and relative humidity. We further estimated the changes in mortality burden of O 3 and NO 2 , including attributable fraction (AF, in %) and attributable mortality (AM, in number of death) during study period. We lastly estimated mortality effects during the 2010 Asian Games (November 12 to December 18, 2010) compared to a baseline period consisting of 4-week before and 4-week after the game. During the study period, average annual concentrations of NO 2 decreased from 42.3 μg/m 3 in 2006 to 33.8 μg/m 3 in 2016; while O 3 levels remained stable over time. We observed significant increases in mortality of O 3 and NO 2 , with approximately linear exposure-response relationships. In specific, each increase of 10 μg/m 3 in O 3 and NO 2 at 2 prior days was associated with increases of 0.60% (95% confidence interval (CI): 0.47, 0.74) and 1.89% (95%CI: 1.49, 2.29) in total mortality, respectively. We further estimated that AF on total mortality attributed to NO 2 decreased from 1.38% (95%CI: 1.09, 1.68) in 2006-2010 to 0.43% (95%CI: 0.34, 0.52) in 2011-2016, corresponding to AM on total mortality of 2496 deaths (95%CI: 1964, 3033) to 1073 deaths (95%CI: 846, 1301). During the 2010 Asian Games, we observed decrease in total mortality of 9.3% (95%CI: -15.0, -3.2) in comparison with that observed in the baseline period. Similar mortality benefits in cardiovascular diseases were also observed. Our results showed reduced mortality burden from air pollution improvement in Guangzhou in recent years, which provide strong rationale for continuing to reduce air pollution through comprehensive and rigorous air quality management in the area., (Copyright © 2019. Published by Elsevier Ltd.)

Background: Ambient air pollution has been associated with acute cardiovascular events; however, the underlying mechanisms remain incompletely understood. We aimed to examine the impacts of ambient air pollutants on cardiac ventricular repolarization in a highly polluted urban region., Methods: Seventy-three healthy non-smoking young adults (66% female, mean age of 23.3 ± 5.4 years) were followed with four repeated 24-h electrocardiogram recordings in 2014-2016 in Beijing, China. Continuous concentrations of ambient particulates in size fractions of 5-560 nm diameter, black carbon (BC), nitrogen dioxide (NO 2 ), carbon monoxide (CO), sulfur dioxide (SO 2 ), and ozone (O 3 ) were measured at a fixed-location air pollution monitoring station. Generalized linear mixed models, with adjustment for individual risk factors, time-varying factors and meteorological parameters, were used to evaluate the effects of air pollution on 5-min segments of heart rate-corrected QT interval (QTc), an index of cardiac ventricular repolarization., Results: During the study period, the mean levels of number concentrations of particulates in size range of 5-560 nm (PNC 5-560 ) were 20,711 particles/cm 3 . Significant increases in QTc of 0.56% (95% CI: 0.27, 0.84) to 1.76% (95% CI: 0.73, 2.79) were associated with interquartile range increases in PNC 50-560 at prior 1-5 moving average days. Significant increases in QTc were also associated with increases in exposures to traffic-related air pollutants (BC, NO 2 and CO), a combustion pollutant SO 2 , and the secondary pollutant O 3 . The associations were stronger in participants who were male, overweight, with abdominal obesity, and with higher levels of high-sensitivity C-reactive protein., Conclusions: Our findings suggest that exposures to higher levels of ambient particulates in small size fractions and traffic pollutants were associated with cardiac repolarization abnormalities in healthy adults, and the cardio-metabolic risks may modify the adverse cardiac effects attributable to air pollution., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Polycyclic aromatic hydrocarbons (PAHs) have been of health concern due to its carcinogenesis and mutagenesis. In this study, we aimed to assess the variations, sources, and lifetime excessive cancer risk (ECR) attributable to PAHs bound to ambient particulate matters with aerodynamic diameter less than 2.5μm (PM 2.5 ) in metropolitan Beijing, China. We collected 24-hour integrated PM 2.5 samples on daily basis between November 2014 and June 2015 across both central heating (cold months) and non-heating (warm months) seasons, and further analyzed the PAH components in these daily PM 2.5 samples. Our results showed that total concentrations of PM 2.5 -bound PAHs varied between (88.6±75.4)ng/m 3 in the cold months and (11.0±5.9)ng/m 3 in the warm months. Benzo[a]pyrene (BaP), the carcinogenic marker of PAHs, averaged at 5.7 and 0.4ng/m 3 in the cold and warm months, respectively. Source apportionment analyses illustrated that gasoline, biomass burning, diesel, coal combustion and cooking were the major contributors, accounting for 12.9%, 17.8%, 24.7%, 24.3% and 6.4% of PM 2.5 -bound PAHs, respectively. The BaP equivalent lifetime ECR from inhalation of PM 2.5 -bound PAHs was 16.2 cases per million habitants. Our results suggested that ambient particulate reduction from energy reconstruction and adaption of clean fuels would result in reductions PM 2.5 -bound PAHs and its associated cancer risks. However, as only particulate phased PAHs was analyzed in the present study, the concentration of ambient PAHs could be underestimated., (Copyright © 2018. Published by Elsevier B.V.)

Numerous studies have reported associations between ambient particulate matter (PM) and daily mortality; however, little is known about temporal variations in ambient air pollution associated mortality risks, particularly in developing countries with limited long time-series air monitoring data. In present study, we assessed the associations and temporal relationships between ambient PM and daily mortality in Guangzhou, China, during 2006-2016. With this unique 11-year dataset, we related daily concentrations of PM with aerodynamic diameter < 2.5 μm (PM 2.5 ), between 2.5 and 10 μm (PM 10-2.5 ) and <10 μm (PM 10 ) to daily mortality in Guangzhou. We applied overdispersed Poisson regression with adjustment for time trend and potential confounding factors. Multiple level sensitivity analyses were conducted to examine the robustness of main results. Between 2006 and 2016, annual concentrations of PM 2.5 decreased by 50.8% to 27.0 μg/m 3 , of PM 10-2.5 by 27.6% to 16.2 μg/m 3 , and of PM 10 by 44.1% to 43.3 μg/m 3 in Guangzhou. In this study, per 10 μg/m 3 increases in mean concentrations at current day and 6 prior days of death (lag06), we observed increases in total mortality risks of 0.55% (95% Confidence Interval (CI): 0.24%, 0.86%) for PM 2.5 , 0.99% (95%CI: 0.48%, 1.50%) for PM 10-2.5 , and 0.44% (95%CI: 0.22%, 0.65%) for PM 10 . Stronger associations were observed for ambient PM on cardio-respiratory mortality and people at age ≥ 65 years. Despite drastic reductions in annual PM levels, PM 2.5 associated cardiovascular and respiratory mortality risks remained significant at 1.26% (95%CI: 0.19%, 2.35%) and 1.91% (95%CI: 0.25%, 3.60%) during 2014-2016. Further, PM 2.5 and PM 10 associated respiratory mortality risks showed increasing trend over time (p-value = 0.03 for PM 2.5 ). In summary, though ambient PM levels decreased substantially in Guangzhou in recent years, PM 2.5 and PM 10 associated cardio-respiratory mortality risks remained significant and respiratory mortality risks even increased. Our findings provide strong rationale for continuation of ambient air pollution control effort for public health protection in the future., (Copyright © 2018. Published by Elsevier B.V.)

Background: Adverse cardiovascular effects associated with air pollution exposure have been widely demonstrated. However, inconsistent cardiovascular responses were observed from reducing indoor air pollution exposure. We aimed to assess whether short-term air filtration intervention could benefit cardiovascular health in elderly living in high pollution area., Methods: A randomized crossover intervention study of short-term indoor air filtration intervention on cardiovascular health was conducted among 35 non-smoking elderly participants living in Beijing in the winter of 2013, as part of Beijing Indoor Air Purifier StudY (BIAPSY). Portable air filtration units were randomly allocated to active filtration for 2 weeks and sham filtration for 2 weeks in the households. Twelve-hour daytime ambulatory heart rate variability (HRV) and blood pressure (ABP) were measured during active and sham filtration. Concurrently, real-time indoor and outdoor particulate matter with diameter less than 2.5 µm (PM 2.5 ) and indoor black carbon (BC) concentrations were measured. We applied generalized additive mixed models to evaluate the associations of 1- to 10-h moving average (MA) exposures of indoor PM 2.5 and BC with HRV and ABP indices, and to explore whether these associations could be modified by air filtration., Results: We observed decreases of 34.8% in indoor PM 2.5 and 35.3% in indoor BC concentrations during active filtration. Indoor PM 2.5 and BC exposures were significantly associated with reduced HRV and increased ABP indices, and greater changes were observed during sham filtration. In specific, each 10 μg/m 3 increase in indoor PM 2.5 at MA8-h was associated with a significant reduction of 1.34% (95% CI: -2.42, -0.26) in SDNN during sham filtration, compared with a non-significant reduction of 0.81% (95% CI: -6.00, 4.68) during active filtration (P inter < 0.001). Each 1 μg/m 3 increase in indoor BC at MA8-h was associated with a significant increase of 2.41% (95% CI: 0.38, 4.47) in SBP during sham filtration, compared with a non-significant increase of -1.09% (95% CI: -4.06, 1.96) during active filtration (P inter = 0.135). Nonlinear inverse exposure-response relationships of indoor air pollution exposures with predicted HRV and ABP indices also confirmed some cardiovascular benefits of short-term air filtration intervention., Conclusions: Our results suggested that short-term indoor air filtration intervention can be of some cardiovascular benefits in elderly living with high pollution episodes., (Copyright © 2018 Elsevier Inc. All rights reserved.)

With rapid economic development and urbanization in recent decades, China has experienced the worsening of ambient air quality. For better air quality management to protect human health, Chinese government revised national ambient air quality standards (NAAQS) for particulate matter (PM) in 2012 (GB3095-2012). To assess the effectiveness of current NAAQS for PM on public health in Chinese population, we conducted a meta-analysis on published studies examining the mortality risk of short-term exposure to PM with aerodynamic diameters less than 10 and 2.5μm (PM 10 and PM 2.5 ) in China. The reported 24-hour concentrations of PM 10 and PM 2.5 in studies ranged from 43.5 to 150.1μg/m 3 and 37.5 to 176.7μg/m 3 . In the pooled excess, mortality risk estimates of short-term exposure to PM. In specific, per 10μg/m 3 increase in PM 10 , we observed increases of 0.40% (95%CI: 0.33%, 0.47%), 0.57% (95%CI: 0.44%, 0.70%) and 0.49% (95%CI: 0.40%, 0.58%) in total, respiratory and cardiovascular mortality, per 10μg/m 3 increase in PM 2.5 , we observed increases of 0.51% (95%CI: 0.38%, 0.63%), 0.62% (95%CI: 0.52%, 0.73%) and 0.75% (95%CI: 0.54%, 0.95%) in total, respiratory and cardiovascular mortality. Finally, we derived 125μg/m 3 for PM 10 and 62.5μg/m 3 for PM 2.5 as 24-hour recommendation values based on the pooled estimates. Our results indicated that current Chinese NAAQS for PM could be sufficient in mitigating the excess mortality risk from short-term exposure to ambient PM. However, future research on long-term exposure cohort studies in Chinese population is also essential in revising annual averages for PM in Chinese NAAQS., (Copyright © 2018. Published by Elsevier B.V.)

To evaluate the ozone (O 3 ) sensitivity among peach tree (Prunus persica) cultivars widely planted in Beijing region and explore the possible eco-physiological response mechanisms, thirteen cultivars of peach seedlings were exposed to either charcoal-filtered air or elevated O 3 (E-O 3 , non-filtered ambient air plus 60 ppb) for one growing season in open-top chambers. Leaf structure, stomatal structure, gas exchange and chlorophyll a fluorescence, photosynthetic pigments, antioxidant defense system and lipid peroxidation were measured in three replicated chambers. Results showed that E-O 3 significantly reduced abaxial epidemis thickness, but no effects on the thicknesses of adaxial epidemis, palisade parenchyma and spongy parenchyma. Stomatal area, density and conductance were not significantly affected by E-O 3 . E-O 3 significantly accelerated leaf senescence, as indicated by increased lipid peroxidation and more declines in light-saturated photosynthetic rate and pigments contents. The reduced ascorbate content (ASC) was decreased but antioxidant enzyme activity (CAT, APX and SOD) and total antioxidant capacity (TAC) were significantly increased by E-O 3 among cultivars. The cultivars with visible symptoms also had more reductions in net photosynthetic rate than those without visible symptoms. Ozone sensitivity among cultivars was strongly linked to leaf mass per area (LMA), antioxidant enzymes activity e.g. SOD, APX rather than stomatal parameters (stomatal area, density and conductance) and ASC. Results could provide a theoretical basis for selecting and breeding the ozone-resistant cultivars of peach trees grown in high O 3 -polluted regions., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Tropospheric ozone (O3) is a phytotoxic air pollutant adversely affecting plant growth. High O3 exposures are often concurrent with summer drought. The effects of both stresses on plants are complex, and their interactions are not yet well understood. Here, we investigate whether drought can mitigate the negative effects of O3 on plant physiology and growth based on a meta‐analysis. We found that drought mitigated the negative effects of O3 on plant photosynthesis, but the modification of the O3 effect on the whole‐plant biomass by drought was not significant. This is explained by a compensatory response of water‐deficient plants that leads to increased metabolic costs. Relative to water control condition, reduced water treatment decreased the effects of O3 on photosynthetic traits, and leaf and root biomass in deciduous broadleaf species, while all traits in evergreen coniferous species showed no significant response. This suggested that the mitigating effects of drought on the negative impacts of O3 on the deciduous broadleaf species were more extensive than on the evergreen coniferous ones. Therefore, to avoid over‐ or underestimations when assessing the impact of O3 on vegetation growth, soil moisture should be considered. These results contribute to a better understanding of terrestrial ecosystem responses under global change. Summary statement: Drought mitigated the negative effects of elevated O3 on some photosynthesis‐related parameters but not on the growth of the whole plant. The mitigation effects of drought on O3‐induced reductions in photosynthesis and biomass were greater in the deciduous species than in the evergreen species. [ABSTRACT FROM AUTHOR]

Based on the monitoring data of atmospheric pollutants and the meteorological data in Harbin in 2017, the temporal spatial distribution characteristics of PM2.5 pollution and the relationships between PM2.5 concentration and meteorological factors in this region were analyzed. The PM2.5 concentration data and the meteorological data in 2017 were comprehensively analyzed by using ArcGIS and R. The results show that spatially, the PM2.5 concentration in the central districts of Harbin are high in the southeast and low in the northwest; temporally, PM2.5 pollution is most serious in autumn and winter, with multiple spells of heavy pollution and an obvious "weekend effect", while the air quality is better in spring and summer; overall, relative humidity is positively correlated to PM2.5 concentration, while temperature, wind direction, and wind speed are negatively correlated to PM2.5 mass concentration, and low wind speed and high relative humidity are major contributors to increase of PM2.5 concentration. Implications: Highlight: The use of big data to deal with the data of air pollution and meteorology. Key points: The air pollution data of Harbin in autumn and winter is more serious than that in spring and summer, and is closely related to meteorological factors. Attraction: Big data is used to process air pollution data and meteorological data, and R language is used to describe the relationship between them. [ABSTRACT FROM AUTHOR]