Search

The long-term joint impacts of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) on mortality are inconclusive. To bridge this research gap, we included 283,568 adults from the Taiwan MJ cohort between 2005 and 2016 and linked with the mortality data until 31 May 2019. Participants' annual average exposures to PM 2.5 , NO 2 , and O 3 were estimated using satellite-based spatial-temporal models. We applied elastic net-regularised Cox models to construct a weighted environmental risk score (WERS) for the joint effects of three pollutants on non-accidental, cardiovascular, and cancer mortality and evaluated the contribution of each pollutant. The three pollutants jointly raised non-accidental mortality risk with a WERS hazard ratio (HR) of 1.186 (95% CI: 1.118-1.259) per standard deviation increase in each pollutant and weights of 72.8%, 15.2%, and 12.0% for PM 2.5 , NO 2 , and O 3 , respectively. The WERS increased cardiovascular death risk [HR: 1.248 (1.042-1.496)], with PM 2.5 as the first contributor and O 3 as the second. The WERS also elevated the cancer death risk [HR: 1.173 (1.083-1.270)], where PM 2.5 played the dominant role and NO 2 ranked second. Coordinated control of these three pollutants can optimise the health benefits of air quality improvements., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Evidence regarding the link between long-term ambient ozone (O 3 ) exposure and childhood sleep disorders is little. This study aims to examine the associations between long-term exposure to O 3 and sleep disorders in children. We conducted a population-based cross-sectional survey, including 185,428 children aged 6-18 years in 173 schools across 14 Chinese cities during 2012 and 2018. Parents or guardians completed a checklist using Sleep Disturbance Scale for Children, and O 3 exposure at residential and school addresses was estimated using a satellite-based spatiotemporal model. We used generalized linear mixed models to test the associations with adjustment for factors including socio-demographic variables, lifestyle, meteorology and multiple pollutants. Mean concentrations of O 3 , particulate matter with diameters ≤2.5 mm (PM 2.5 ) and nitrogen dioxide (NO 2 ) were 89.0 μg/m 3 , 42.5 μg/m 3 and 34.4 μg/m 3 , respectively. O 3 and NO 2 concentrations were similar among provinces, while PM 2.5 concentration varied significantly among provinces. Overall, 19.4% of children had at least one sleep disorder. Long-term exposure to O 3 was positively associated with odds of sleep disorders for all subtypes. For example, each interquartile increment in home-school O 3 concentrations was associated with a higher odds ratio for global sleep disorder, at 1.22 (95% confidence interval: 1.18, 1.26). Similar associations were observed for sleep disorder subtypes. The associations remained similar after adjustment for PM 2.5 and NO 2 . Moreover, these associations were heterogeneous regionally, with more prominent associations among children residing in southeast region than in northeast and northwest regions in China. We concluded that long-term exposure to O 3 is positively associated with risks of childhood sleep disorders. These associations varied by geographical region of China., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Information on the relation of air pollution with non-alcoholic fatty liver disease (NAFLD) is scarce. We thus conducted a large cross-sectional study in Asia to investigate the role of air pollution in NAFLD., Methods: We recruited 329,048 adults (mean age: 41.0 years) without other liver disease (hepatitis and cirrhosis) or excessive alcohol consumption in Taiwan and Hong Kong from 2001 to 2018. The concentrations of nitrogen dioxide (NO 2 ) and ozone (O 3 ) were estimated using a space-time regression model, and the concentrations of fine particulate matter (PM 2.5 ) was evaluated using a satellite-based spatio-temporal model. NAFLD was determined using either the fatty liver index (FLI) or the hepatic steatosis index (HSI). The NAFLD-related advanced fibrosis was defined according to BARD score or the fibrosis-4 (FIB-4). A logistic regression model was adopted to explore the relationships of ambient air pollution with the odds of NAFLD and NAFLD-related advanced fibrosis., Results: We found positive relationships between PM 2.5 and the odds of NAFLD and advanced fibrosis, with every standard deviation (SD, 7.5 µg/m 3 ) increases in PM 2.5 exposure being associated with a 10% (95% confidence interval [CI]: 9%-11%) increment in the prevalence of NAFLD and an 8% (95% CI: 7%-9%) increment in the prevalence of advanced fibrosis. Similarly, the prevalence of NAFLD and advanced fibrosis increased by 8% (95% CI: 7%-9%) and 7% (95% CI: 6%-8%) with per SD (18.9 µg/m 3 ) increasement in NO 2 concentration, respectively. Additionally, for every SD (9.9 µg/m 3 ) increasement in O 3 concentration, the prevalence of NAFLD and advanced fibrosis decreased by 12% (95% CI: 11%-13%) and 11% (95% CI: 9%-12%), respectively., Conclusion: Higher ambient PM 2.5 and NO 2 are linked with higher odds of NAFLD and advanced fibrosis. Our findings indicate that reducing PM 2.5 and NO 2 concentrations may be an effective way for preventing NAFLD. Further studies on O 3 are warranted., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Due to the non-linearity in ozone (O 3 ) formation, reducing the emission of nitrogen oxides (NO x ) may increase O 3 concentration. Given the counteractive O 3 response to NO x reduction, overall impact of air pollution controls can be ambiguous when the assessments focus on the changes in pollutant concentrations. In this study, a risk-based method was used to gauge the net effect of air pollution controls on mortality risk in the Beijing-Tianjin-Hebei (BTH) region during the 2022 Winter Olympics and Paralympics (WOP). This mega-event presents a unique opportunity to investigate the efficacy of deep cuts in pollutant emissions. Results show that O 3 concentrations greatly increased as nitrogen dioxide (NO 2 ) concentrations decreased in the BTH. Due to the active photochemical formations, O 3 became the dominant pollutant that affected human health during the WOP. Despite the substantial O 3 increases, the health benefits of NO 2 reductions overwhelmed the adverse health effects of O 3 increases in most regions of the BTH (at 81 out of 112 stations). After considering the impacts of particulate matter, the integrated health risk of air pollution mixtures declined almost everywhere in the BTH. Our results underscore the great necessity of changing the assessment paradigm of pollution control from using concentration-based methods to using risk-based methods. Together with the carbon neutrality policy, stringent control of NO x emission from combustion sources is a promising way to achieve synergistic control solutions for air pollution and climate change., Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022. Published by Elsevier B.V.)

Despite increasing concerns about the detrimental effects of air pollution on respiratory health, limited evidence is available on these effects in the Hong Kong population, especially in children. In this prospective cohort study between 2012 and 2017, we aimed to investigate the associations between exposure to air pollution (concentrations of fine particulate matter [PM 2.5 ] and nitrogen dioxide [NO 2 ]) and respiratory health (lung function parameters and respiratory diseases and symptoms) in schoolchildren. We recruited 5612 schoolchildren aged 6-16 years in Hong Kong. We estimated the annual average concentrations of ambient PM 2.5 and NO 2 at each participant's address using spatiotemporal models. We conducted spirometry tests on all participants to measure their lung function parameters and used a self-administered questionnaire to collect information on their respiratory diseases and symptoms and a wide range of covariates. Linear mixed models were used to investigate the associations between exposure to air pollution and lung function. Mixed-effects logistic regression models with random effects were used to investigate the associations of exposure to air pollution with respiratory diseases and symptoms. In all of the participants, every 5-μg/m 3 increase in the ambient PM 2.5 concentration was associated with changes of - 13.90 ml (95 % confidence interval [CI]: -23.65 ml, -4.10 ml), - 4.20 ml (-15.60 ml, 7.15 ml), 27.20 ml/s (-3.95 ml/s, 58.35 ml/s), and - 19.80 ml/s (-38.35 ml/s, -1.25 ml/s) in forced expiratory volume in 1 s, forced vital capacity, peak expiratory flow, and maximal mid-expiratory flow, respectively. The corresponding lung function estimates for every 5-μg/m 3 increase in the ambient NO 2 concentration were - 2.70 ml (-6.05 ml, 0.60 ml), - 1.40 ml (-5.40 ml, 2.60 ml), - 6.60 ml/s (-19.75 ml/s, 6.55 ml/s), and - 3.05 ml/s (-11.10 ml/s, 5.00 ml/s), respectively. We did not observe significant associations between PM 2.5 /NO 2 exposure and most respiratory diseases and symptoms. Stratified analyses by sex and age showed that the associations between exposure to air pollution and lung function parameters were stronger in male participants and older participants (11-14 year old group) than in female participants and younger participants (6-10 year old group), respectively. Our results suggest that chronic exposure to air pollution is detrimental to the respiratory health of schoolchildren, especially that of older boys. Our findings reinforce the importance of air pollution mitigation to protect schoolchildren's respiratory health., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Lao Xiangqiang reports financial support was provided by Institute of Health and Medical Research. JC and YZ are supported by the Ph.D. Studentship of the Chinese University of Hong Kong. CG is in part supported by the Research Grants Council Postdoctoral Fellowship Scheme of Hong Kong. XW is supported by the Research Grants Council Hong Kong PhD Fellowship Scheme., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Introduction: Habitual exercise may amplify the respiratory uptake of air pollutants in the lung, exacerbating the adverse effects of air pollution. However, it is unclear whether this can reduce the health benefits of habitual exercise (referred to as leisure-time exercise). Thus, the combined effects of habitual exercise and chronic exposure to ambient fine particulate matter 2.5 on cardiovascular mortality were examined among adults in Taiwan., Methods: A total of 384,128 adults were recruited between 2001 and 2016 and followed up to May 31, 2019. Participants' vital status was obtained by matching their unique identification numbers with records of cardiovascular death in the National Death Registry of Taiwan. A time-varying Cox regression model was used to analyze the data. Analyses were conducted in 2021., Results: Cardiovascular death risks were inversely associated with habitual exercise and positively associated with chronic exposure to particulate matter 2.5. The beneficial effects of habitual exercise on cardiovascular mortality were not modified by chronic exposure to particulate matter 2.5. Inactive participants with high particulate matter 2.5 exposure exhibited a 123% higher risk of cardiovascular death than high-exercise-group participants exposed to low levels of particulate matter 2.5 (95% CI=89, 163)., Conclusions: High level of habitual exercise combined with low exposure level of ambient particulate matter 2.5 is associated with the lowest risk of cardiovascular death. A higher level of habitual exercise is associated with a lower risk of cardiovascular death at all levels of particulate matter 2.5 exposure studied. The results indicate that habitual exercise is a safe health promotion strategy even for people residing in relatively polluted regions., (Copyright © 2022 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.)

PM 2.5 -hypertension association were well documented in adults, while the effects of life-course exposure to PM 2.5 on adulthood hypertension remained unclear. This study aimed to investigate the associations between life-course exposure to ambient PM 2.5 and incident hypertension in adulthood in Asia. We included 4272 participants with 17,814 medical visits from two open cohorts in Taiwan and Hong Kong between 2000 and 2018. We used a satellite-based model to assess 2-year average PM 2.5 exposure at a resolution of 1 km 2 . A linear mixed model was used to examine the association with blood pressure. A Cox regression model with time-dependent covariates was used to examine the overall association with the development of hypertension in adulthood. Life-course mixed models were used to examine the effects of PM 2.5 exposure at different life stages on blood pressure and hypertension. For every 10 μg/m 3 increase in PM 2.5 , the overall risk of adulthood hypertension increased by 40% (95% confidence interval [CI] 8-80%). The health effects of PM 2.5 exposure at different life-stages on incident hypertension were generally independent of each other. In critical model, the risk of developing hypertension increased 23%, 27%, and 55% for each 10 μg/m 3 increase in PM 2.5 exposure during school age, adolescence, and adulthood, respectively. Similar associations were found between life-course PM 2.5 exposure and blood pressure. Association between PM 2.5 and adulthood hypertension can be traced back to childhood. Our study suggests that life-course control of air pollution exposure should be implemented to alleviate the huge burden of adulthood hypertension., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: To investigate the associations between long-term exposure to ambient air pollution and age at menopause and the risk of early menopause in two Asian cohorts., Methods: A total of 53,167 female adults were enrolled from two ongoing cohorts, one each in Taiwan and Hong Kong, between 2003 and 2018, yielding 200,000 person-years of follow-up. We performed a Cox regression model with time-dependent covariates to investigate associations between air pollution and menopause., Results: The mean age at baseline and at natural menopause was 34.4 and 51.0 years, respectively. In the single-pollutant models, we found that increase in PM 2.5 and NO 2 was associated a younger age at menopause [hazard ratios (HRs) (95% confidence interval, CI): 1.16 (1.09-1.23) and 1.04 (1.01-1.06), respectively, for each 10 µg/m 3 increase in air pollution]. In the multiple-pollutant models, the NO 2 -menopause associations were attenuated after adjusting for PM 2.5 and O 3 , whereas the associations of menopause with PM 2.5 and O 3 remained stable. Similar associations were observed for the risk of early menopause (age at menopause ≤ 45 years)., Conclusions: Long-term exposure to ambient air pollution was associated with the age at menopause and the risk of early menopause. More effective strategies to mitigate air pollution are required., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Few studies have examined the effects of multi-pollutant air pollution on renal health, especially in children and adolescents. This study investigated the association between long-term ambient air pollution exposure and renal health in Asian children and adolescents., Methods: This study included 10,942 children and adolescents from Taiwan and Hong Kong between 2000 and 2017. PM 2.5 , NO 2 and O 3 concentrations were estimated using satellite-based spatiotemporal regression models. Two-year average concentrations, those of the year of visit and the preceding year, were used. Linear mixed models were used to examine the association between air pollution and yearly changes in estimated glomerular filtration rate (eGFR). Cox regression models with time-dependent covariates were used to examine the association between air pollution and the development of chronic kidney disease (CKD)., Results: Median age of the participants was 19 years (range: 2-25). The overall average concentration of PM 2.5 , NO 2 and O 3 was 26.7 μg/m 3 , 44.1 μg/m 3 and 51.1 μg/m 3 , respectively. The mean yearly change in eGFR was 0.37 μL/min/1.73 m 2 and the incidence rate of CKD was 6.8 per 1,000 person-years. In single-pollutant models, each 10 μg/m 3 increase in PM 2.5 was associated with a 0.45 μL/min/1.73 m 2 [95% confidence interval (CI): 0.28-0.63] reduction in the yearly increase in eGFR and 53% [hazard ratio (HR): 1.53 (95%CI: 1.07-2.2)] greater risk of incident CKD. Each 10 μg/m 3 increase in NO 2 was associated with a 7% [HR (95%CI): 1.07 (1.00-1.15)] higher risk of incident CKD, while an equivalent increase in O 3 was associated with a 19% [HR (95%CI): 0.81 (0.67-0.98)] lower risk., Conclusions: Long-term exposure to ambient PM 2.5 and NO 2 was associated with a slower growth of eGFR and a higher risk of incident CKD in children and adolescents. Our findings suggest that air pollution control in early life is imperative to improve lifelong renal health and alleviate the CKD burden., 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 Elsevier Inc. All rights reserved.)

In this study, we aimed to examine the combined associations of particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5) and habitual exercise with pneumonia mortality. We included 384,130 persons aged ≥18 years from Taiwan, Republic of China, during 2001-2016. We followed participants until May 31, 2019, to obtain information on vital status. A time-dependent Cox regression model was used for statistical analysis. We found that risks of pneumonia mortality were reduced by 55% (hazard ratio (HR) = 0.45, 95% confidence interval (CI): 0.36, 0.55) and 36% (HR = 0.64, 95% CI: 0.52, 0.80) in participants who engaged in high and moderate levels of exercise, respectively, as compared with inactive persons. By contrast, each 10-μg/m3 increase in chronic PM2.5 exposure was associated with a 30% (HR = 1.30, 95% CI: 1.17, 1.45) higher risk of pneumonia mortality. Risk of pneumonia death was 72% lower (HR = 0.28, 95% CI: 0.20, 0.41) for persons with a high exercise level and a low PM2.5 level. Lower risk of pneumonia mortality was associated with both higher exercise and lower PM2.5 air pollution levels. For adults exposed to different levels of PM2.5, exercise benefits remained. Our findings suggest that engaging in exercise is a safe and effective strategy for alleviating the burden of pneumonia mortality, even for people who reside in a moderately polluted area., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Little evidence is available regarding the impact of different sizes of inhaled particulate matter (PM) on inflammatory responses in healthy young adults in connection with toxicological responses. We conducted a five-time repeated measurement panel study on 88 healthy young college students in Guangzhou, China from December 2017 to January 2018. Blood samples were collected from each participant and tested for tumor necrosis factor alpha (TNF-α) levels every week for 5 consecutive weeks. Mass concentrations of ambient PM 2.5 , PM 1 , PM 0.5 and number concentrations of ambient PM 0.1 were measured. RAW 264.7 macrophages were exposed to PM (PM 10 - 2.5 , PM 2.5 - 1 , PM 1 and TNF-α level were consistent in lag 0 and 3 days, and the relative risk decreased as the particle size decreased. All the ambient air pollutants had the similar change trends in lag 1, 4 and 5 days. Similar results in RAW 264.7 macrophages were found; PM - 0.2 , PM 0.2 ) collected at the same time as the panel study. Cytotoxicity, oxidation and inflammatory parameters, cell cycle and genotoxicity were tested. Particles were characterized for their chemical composition. The trends of associations between PM 2.5 , PM 1 , PM 0.5 and TNF-α level were consistent in lag 0 and 3 days, and the relative risk decreased as the particle size decreased. All the ambient air pollutants had the similar change trends in lag 1, 4 and 5 days. Similar results in RAW 264.7 macrophages were found; PM 10 - 2.5 induced the greatest TNF-α and macrophage inflammatory protein 2 (MIP-2) productions and oxidative damage. PM 1 - 0.2 and PM 0.2 induced more significant dose-dependent increases of cell cycle and genotoxic response. In the component concentrations of PM samples, metal elements were PM 10 - 2.5 > PM 2.5 - 1 > PM 0.2 ≥ PM 1 - 0.2 ; ions and polycyclic aromatic hydrocarbons (PAHs) were PM 0.2 > PM 1 - 0.2 > PM 2.5 - 1 > PM 10 - 2.5 . Our results suggested that exposure to all particle sizes was significantly associated with inflammation among healthy young adults and toxicological responses in RAW 264.7 macrophages. Different human and toxicological reactions caused by PM samples indicated the importance of investigating various particle sizes., Competing Interests: Declaration of competing interest The authors declare they have no actual or potential competing interests., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Objectives: Exercise may increase the inhaled amount of air pollutants and exacerbate the adverse health effects. We investigated the combined effects of chronic exposure to fine particulate matter with an aerodynamic diameter less than 2.5 µm (PM 2.5 ) and habitual exercise on C reactive protein (CRP), a sensitive marker of inflammation., Methods: We selected 40 209 Taiwanese adults who joined a standard medical screening programme between 2001 and 2016. The PM 2.5 exposure was estimated at each participant's address using a satellite-based spatiotemporal model. Information on habitual exercise was collected using a standard self-administered questionnaire. Mixed-effects linear regression models were used to investigate the associations of CRP with PM 2.5 and exercise. An interaction term of PM 2.5 and exercise was introduced in the models to test the modifying effects., Results: A greater amount of habitual exercise was associated with a decreased level of CRP, while a higher concentration of PM 2.5 exposure was associated with an increased level of CRP. The inverse associations of habitual exercise with CRP were not modified by chronic exposure to PM 2.5 . The participants in the group with a low level of exercise and a high level of PM 2.5 exposure exhibited a 19.1% higher level of CRP than those in the group with a high level of exercise and a low level of PM 2.5 exposure (95% CI: 13.7% to 24.8%; p<0.001). The longitudinal and sensitivity analyses yielded similar results., Conclusions: Increased levels of exercise and reduced exposure levels of PM 2.5 are associated with a lower CRP level. Habitual exercise reduces CRP level regardless of the levels of chronic PM 2.5 exposure. Our results support that habitual exercise is a safe approach for reducing systemic inflammation to improve cardiovascular health even for people residing in relatively polluted areas., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Cohort studies on the association between long-term exposure to fine particulate matter (PM2.5) and mortality have been well established for America and Europe, but limited and inconsistent in Asia with much higher air pollution. This study aims to investigate the associations between ambient PM2.5 and all-cause and cause-specific mortality over a period of rising and then declining PM2.5., Methods: We enrolled a total of 400,459 adults from an open cohort between 2001 and 2016, and followed them up until 31 May 2019. We obtained mortality data from the National Death Registry maintained by the Ministry of Health and Welfare in Taiwan. We estimated ambient PM2.5 exposures using a satellite-based spatiotemporal model. We performed a Cox regression model with time-dependent covariates to investigate the associations of PM2.5 with deaths from all causes and specific causes., Results: This study identified 14,627 deaths and had a total of 5 million person-years of follow-up. Each 10 µg/m3 increase in PM2.5 was associated with an increased hazard risk of 29% (95% confidence interval: 24%-35%) in all-cause mortality. Risk of death increased by 30% for natural causes, 20% for cancer, 42% for cardiovascular disease (CVD) causes, and 53% for influenza and pneumonia causes, for each 10 µg/m3 increase in PM2.5. Sensitivity analyses generally yielded similar results., Conclusion: Long-term exposure to ambient PM2.5 was associated with increased risks of all-cause mortality and deaths from cancers, natural causes, CVD, and influenza and pneumonia. Longitudinal study design should be encouraged for air pollution epidemiologic investigation., Competing Interests: The authors report no conflicts of interest., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Exercise may increase the inhalation and deposition of air pollutants, which may counteract its beneficial effects. We thus examined the combined effects of chronic exposure to fine particulate matter (PM2.5) and habitual exercise on the risk of death from cancer in Taiwan., Patients and Methods: A total of 384 128 adults (≥18 years of age) were recruited for a medical screening programme between 2001 and 2016, yielding 842 384 medical-examination records. All participants were followed up until 31 May 2019. Vital data were obtained from the National Death Registry of Taiwan and the ambient PM2.5 exposure was estimated using a satellite-based spatiotemporal model. Information on habitual exercise was collected using a standard self-administered questionnaire. The time-dependent Cox-regression model was used to evaluate the combined effects., Results: A greater amount of habitual exercise was associated with lower risk of death from cancer, whilst a higher level of PM2.5 exposure was associated with a higher risk of death from cancer. The inverse associations of habitual exercise with death from cancer were not modified by chronic exposure to PM2.5. The participants in the group with a high level of exercise and a low level of PM2.5 exposure exhibited a 35% lower risk of death from cancer than those in the group with a low level of exercise and a high level of PM2.5 exposure (95% confidence interval: 28%, 42%)., Conclusions: Increased levels of exercise and reduced exposure levels of PM2.5 are associated with a lower risk of death from cancer. Habitual exercise reduces the risk of death from cancer regardless of the levels of chronic PM2.5 exposure. Our results indicate that habitual exercise is a suitable health-promotion strategy even for people who reside in moderately polluted regions., (© The Author(s) 2021; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Previous studies on long-term ozone (O 3 ) variations in China have reported inconsistent conclusions on the role of meteorological factors in controlling said variations. In this study, we used an observation-based decomposition model to conduct an up-to-date investigation of the effects of meteorological factors on the variations in nitrogen dioxide (NO 2 ) and O 3 concentrations in China in the summer from 2013 to 2020. The variations in NO 2 and O 3 concentrations after removing the major meteorological effects were then analyzed to improve our understanding of O 3 formation regimes. Ground measurements show that both NO 2 and O 3 concentrations decreased in eastern, central, and southeastern China (e.g., NO 2 and O 3 concentrations in Wuhan reduced by 4.3 and 6.2 ppb, respectively), which was not anticipated. Analyses of meteorological effects showed that reduced wind strength, decreased temperature, and increased relative humidity significantly reduced O 3 concentrations in eastern and central China (e.g., by 10.5 ppb in Wuhan). After removing the major meteorological effects, the O 3 trends were reversed in eastern and central China (e.g., increased by 4.9 ppb in Wuhan). The contrasting trends in NO 2 and O 3 concentrations suggest that their O 3 formations were sensitive to volatile organic compounds (VOC-limited regime). In southeastern China, both NO 2 and O 3 concentrations decreased, implying that the O 3 formation regimes changed to mixed sensitive or nitrogen oxide-limited (NO x -limited) regimes. The meteorological effects varied by region and may play a dominant role in controlling the long-term O 3 variation. Our results indicate that the attribution of O 3 variation to emission control without accounting for meteorological effects can be misleading., 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.)

Background: Several studies reported that long-term exposure to fine particulate matter (PM 2.5 ) was associated with an increased risk of chronic obstructive pulmonary disease (COPD). It remains unclear whether reduced PM 2.5 can decrease the risk of COPD development., Objective: To investigate the associations of dynamic changes (including deterioration and improvement) in long-term exposure to ambient PM 2.5 with changes in lung function and the incidence of COPD., Methods: A total of 133,119 adults (aged 18 years or older) were recruited in Taiwan between 2001 and 2014. All participants underwent at least two standard medical examinations including spirometry test. We estimated PM 2.5 concentrations using a high-resolution (1 km 2 ) satellite-based spatio-temporal model. The change in PM 2.5 (ΔPM 2.5 ) was defined as the difference in concentration of PM 2.5 between the respective visit and the previous visit. We used a multivariable mixed linear model and time-varying Cox model to investigate the associations of change in PM 2.5 with annual change of lung function and the incidence of COPD, respectively., Result: The PM 2.5 concentration in Taiwan increased during 2002-2004 and began to decrease around 2005. Every 5-µg/m 3 /year decrease in the annual change of PM 2.5 (i.e., ΔPM 2.5 /year of 5 µg/m 3 /year) was associated with an average increase of 19.93 mL/year (95 %CI: 17.42,22.43) in forced expiratory volume in 1 s (FEV 1 ), 12.76 mL/year (95 %CI: 9.84,15.66) in forced vital capacity (FVC), 70.22 mL/s/year (95 %CI: 64.69,76.16) in midexpiratory flow between 25 and 75% of the forced vital capacity (MEF25-75), 0.27%/year (95 %CI: 0.21%, 0.32%) in FEV 1 /FVC/year. Every 5 µg/m 3 decrease in PM 2.5 (i.e., ΔPM 2.5 of 5 µg/m 3 ) was associated with a 12% (95 %CI: 7%, 17%) reduced risk of COPD development. The stratified and sensitivity analyses generally yielded similar results., Conclusion: An improvement in PM 2.5 pollution exposure was associated with an attenuated decline in lung function parameters of FEV 1 , FVC, MEF25-75, and FEV 1 /FVC, and a decreased risk of COPD development. Our findings suggest that strategies aimed at reducing air pollution may effectively combat the risk of COPD development., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

It remains unknown whether reduced air pollution levels can prevent type 2 diabetes mellitus. In this study, we investigated the associations between dynamic changes in long-term exposure to ambient fine particulate matter, defined as particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5), and changes in fasting plasma glucose (FPG) levels and incidence of type 2 diabetes. A total of 151,398 adults (ages ≥18 years) were recruited in Taiwan between 2001 and 2014. All participants were followed up for a mean duration of 5.0 years. Change in PM2.5 (ΔPM2.5) was defined as the value at a follow-up visit minus the corresponding value at the immediately preceding visit. The PM2.5 concentration in Taiwan increased during 2002-2004 and began to decrease in 2005. Compared with participants with little or no change in PM2.5 exposure, those with the largest decrease in PM2.5 had a decreased FPG level (β = -0.39, 95% confidence interval: -0.47, -0.32) and lower risk of type 2 diabetes (hazard ratio = 0.86, 95% confidence interval: 0.80, 0.93). The sensitivity analysis and analyses stratified by sex, age, body mass index, smoking, alcohol drinking, and hypertension generally yielded similar results. Improved PM2.5 air quality is associated with a better FPG level and a decreased risk of type 2 diabetes development., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Many countries have dedicated to the mitigation of air pollution in the past several decades. However, evidence of beneficial effects of air quality improvement on chronic kidney disease (CKD) remains limited. We thus investigated the effects of dynamic changes (including deterioration and improvement) in air quality on the incidence of CKD in a longitudinal study in Taiwan. During 2001-2016, this study recruited a total of 163,197 Taiwanese residents who received at least two standard physical examinations. The level of fine particle matter (PM 2.5 ) was estimated using a high-resolution (1 km 2 ) satellite-based spatio-temporal model. We defined changes of PM 2.5 concentrations (ΔPM 2.5 ) as the difference between the two-year average measurements during follow-up and during the immediately preceding visit. The time-dependent Cox regression model was adopted to evaluate the relationships between ΔPM 2.5 and the incidence of CKD after adjusting for a series of covariates. The concentrations of PM 2.5 in Taiwan peaked around 2004 and began to decrease since 2005. We observed an approximate linear concentration-response relationship of ΔPM 2.5 with CKD incidence. Every 5 μg/m 3 decrease in the ambient concentration of PM 2.5 was associated with a 25% reduced risk of CKD development [hazard ratio (HR): 0.75; 95% CI: 0.73, 0.78]. In conclusion, this study demonstrated that the improvement of PM 2.5 air quality might be associated with a lower risk of CKD development. Our findings indicate that reducing air pollution may effectively prevent the development of CKD.

Background: We investigated the joint associations of habitual physical activity (PA) and long-term exposure to fine particulate matter (PM 2.5 ) with the development of hypertension in a longitudinal cohort in Taiwan., Methods: We selected 140 072 adults (≥18 years of age) without hypertension who joined a standard medical screening program with 360 905 medical examinations between 2001 and 2016. PM 2.5 exposure was estimated at each participant's address using a satellite data-based spatiotemporal model with 1 km 2 resolution. Information on habitual PA and a wide range of covariates was collected using a standard self-administered questionnaire. We used the Cox regression model with time-dependent covariates to examine the joint associations., Results: The mean age of all observations was 41.7 years, and 48.8% were male. The mean value for systolic and diastolic blood pressure was 112.5 and 68.7mm Hg, respectively. Approximately 34.2% of all observations were inactive (0 metabolic equivalence values-hours), 29.8% had moderate-PA (median [interquartile range]; 3.75 [3.38 to 4.38] metabolic equivalence values-hours), and 36.0% had high-PA (15.7 [10.3 to 24.8] metabolic equivalence values-hours). The mean±SD of PM 2.5 was 26.1±7.3 μg/m 3 . The prevalence of cardiovascular disease, diabetes mellitus, and cancer was 2.1%, 2.9%, and 1.5%, respectively. After adjusting for a wide range of covariates (including a mutual adjustment for PA or PM 2.5 ), a higher PA level was associated with a lower risk of hypertension (hazard ratio [HR] for the moderate- and high-PA was 0.93 [95% CI, 0.89-0.97] and 0.92 [95% CI, 0.88-0.96], respectively, as compared with the inactive-PA), whereas a higher level of PM 2.5 was associated with a higher risk of hypertension (HR for the moderate- and high-PM 2.5 was 1.37 [95% CI, 1.32-1.43] and 1.92 [95% CI, 1.81-2.04], respectively, as compared with the low-PM 2.5 group]. No significant interaction was observed between PA and PM 2.5 (HR 1.01 [95% CI, 1.00-1.02])., Conclusions: A high-PA and low PM 2.5 exposure were associated with a lower risk of hypertension. The negative association between PA and hypertension remained stable in people exposed to various levels of PM 2.5 , and the positive association between PM 2.5 and hypertension was not modified by PA. Our results indicated that PA is a suitable hypertension prevention strategy for people residing in relatively polluted regions.

Human exposure to PM 2.5 , represented by population-weighted mean PM 2.5 concentration (c ρ ), declines under three conditions: (1) mean PM 2.5 concentration declines, (2) PM 2.5 concentration within urban areas goes through more of a decrease than within rural areas, or (3) city planning relocates people into cleaner areas. Decomposing these effects on human exposure is essential to guide future environmental policies. The lack of ground PM 2.5 observations limits the assessment of human exposure to PM 2.5 over China. This study proposed a novel diagnostic framework using satellite observations to decompose the variation in c ρ resulting from change in the mean PM 2.5 concentration, spatial difference in PM 2.5 change, and demographic change. In this framework, we decomposed c ρ into mean PM 2.5 concentration (c 0 ) and pollution-population-coincidence induced PM 2.5 exposure (PPCE). We then used this framework to decompose the variation in c ρ over China within three recent Five-Year Plans (FYPs) (2001-2015). The results showed that the decline in c 0 reduced c ρ in most provinces within the eleventh and twelfth FYPs. The spatial difference in PM 2.5 change reduced the PPCE and c ρ in most provinces within the tenth and twelfth FYPs, with the most substantial reduction rate of -3.64 μg m -3 ·yr -1 in Tianjin within the twelfth FYP. Rural-to-urban migration resulting from rapid urbanization, however, increased the PPCE and c ρ (by as much as 0.22 μg m -3 ·yr -1 ) in all provinces except Taiwan within all three FYPs. The demographic change reduced c ρ in Taiwan because of the migration of population into less polluted areas. To better reduce human exposure, it is recommended that control efforts further target populous residential areas and urbanization planning relocates people into less polluted areas. Our decomposition framework paves a new way to decompose the human exposure to other air pollutants in China and other regions., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: The association between long-term exposure to ambient fine particulate matter with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ) and lung function in young people remains uncertain, particularly in Asia, where air pollution is generally a serious problem., Objectives: This study investigated the association between long-term exposure to ambient PM 2.5 and lung function in Taiwanese children, adolescents, and young adults., Methods: This study comprised 24,544 participants 6-24 years of age, with 33,506 medical observations made between 2000 and 2014. We used a spatiotemporal model to estimate PM 2.5 concentrations at participants' addresses. Spirometry parameters, i.e., forced vital capacity (FVC), forced expiratory volume in 1 s ( FEV 1 ), and maximum midexpiratory flow (MMEF), were determined. A generalized linear mixed model was used to examine the associations between long-term exposure to ambient PM 2.5 and lung function. The odds ratios (ORs) of poor lung function were also calculated after adjusting for a range of covariates., Results: Every 10 - μ g / m 3 increase in the 2-y average PM 2.5 concentration was associated with decreases of 2.22% [95% confidence interval (CI): - 2.60 , - 1.85 ], 2.94 (95% CI: - 3.36 , - 2.51 ), and 2.79% (95% CI: - 3.15 , - 2.41 ) in the FVC, FEV 1 , and MMEF, respectively. Furthermore, it was associated with a 20% increase in the prevalence of poor lung function (OR: 1.20; 95% CI: 1.12, 1.29)., Conclusions: Two-year ambient PM 2.5 concentrations were inversely associated with lung function and positively associated with the prevalence of poor lung function in children, adolescents, and young adults in Taiwan. https://doi.org/10.1289/EHP5220.

Many countries dedicated in mitigation of air pollution in the past several decades. However, little is known about how air quality improvement affects health. Therefore, we conducted current study to investigate dynamic changes in long-term exposure to ambient particulate matter (PM 2.5 ) and incidence of hypertension in a large longitudinal cohort. We recruited 134 978 adults aged 18 years or above between 2001 and 2014. All the participants received a series of standard medical examinations, including measurements of blood pressure. The PM 2.5 concentration was estimated using a satellite-based spatiotemporal model at a high resolution (1×1 km 2 ). The change in long-term exposure to PM 2.5 (ΔPM 2.5 ) was defined as the difference between the values measured during follow-up and during the immediately preceding visit, and a negative value indicated an improvement in PM 2.5 air quality. Time-varying Cox model was used to examine the associations between ΔPM 2.5 and the development of hypertension. The results show that PM 2.5 concentrations increased in 2002, 2003, and 2004, but began to decrease in 2005. Every 5 µg/m 3 change in exposure to PM 2.5 (ie, a ΔPM 2.5 of 5 µg/m 3 ) was associated with a 16% change in the incidence of hypertension (hazard ratio, 0.84; 95% CI, 0.82-0.86). Both stratified and sensitivity analyses generally yielded similar results. We found that an improvement in PM 2.5 exposure is associated with a decreased incidence of hypertension. Our findings demonstrate that air pollution mitigation is an effective strategy to reduce the risk of cardiovascular disease.

Background: Evidence of the effects of long-term exposure to fine particulate matter (PM 2.5 ) air pollution on the development of dyslipidaemia is limited. This study aimed to investigate the association between long-term exposure to ambient PM 2.5 and incident dyslipidaemia in a large cohort., Methods: We studied 66,702 participants aged ≥18 years belonging to a cohort from a standard medical examination programme conducted in Taiwan between 2001 and 2014. The PM 2.5 concentration at each participant's address was estimated using a satellite-based spatiotemporal model at a high resolution (1 km 2 ). A time-varying Cox regression model was used to examine the association between long-term exposure to ambient PM 2.5 and the development of dyslipidaemia. Additionally, sensitivity analyses were conducted to examine the stability of these associations., Results: Compared with participants exposed to the 1st tertile of PM 2.5 , participants exposed to the 2nd and 3rd tertiles of PM 2.5 had respective hazard ratios of 1.02 [95% confidence interval (CI): 0.98-1.06] and 1.08 (95%CI: 1.04-1.13) for incident dyslipidaemia. Sensitivity analyses generally yielded similar results., Conclusion: Long-term exposure to ambient PM 2.5 is associated with a higher risk of dyslipidaemia. Global strategies for reducing air pollution are needed to prevent the development of dyslipidaemia., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Variations in aerosol characteristics play an essential role in satellite remote sensing of PM 2.5 concentrations. The lack of measurement of aerosol characteristics, however, limits the assessment of their effects. This study presented an observation-based model that directly considered the effects of aerosol characteristics. In this model, we used an integrated humidity coefficient (γ') and an integrated reference value ( K) to delineate the effects of aerosol characteristics. We then investigated the effects of the long-term variations in aerosol characteristics on satellite remote sensing of PM 2.5 concentration in Hong Kong from 2004 to 2012. The results show that the γ' value peaked in 2009 because the percentages of highly hygroscopic components (e.g., sulfate and nitrate) in aerosols reached their peaks. The K value increased from 2004 to 2011 because of the increasing percentages of strong light-extinction components (e.g., organic matter) and the decreasing fine mode fraction in aerosols. The accuracy of PM 2.5 retrieval improved greatly after accounting for the long-term variations in aerosol characteristics (e.g., correlation coefficient increased from 0.56 to 0.80). The results underscore the need to incorporate the variations in aerosol characteristics in the PM 2.5 estimation models.

Long-term exposed to ambient particulate matter (PM) has been recognized as a risk factor for cardiovascular diseases (CVDs) mortality but few studies examine the utility of WHO's interim targets (2006) concerning PM control on CVD mortality. This review aimed to synthesize the long-term exposed to ambient PM exposures on overall CVD mortality according to WHO's interim targets; meanwhile, subgroup analysis by ethnicity, smoking status and PM assessment method were also conducted. We systematically searched studies published between January 1974 and Jul 2017 in PubMed and Embase. Quality of each study was assessed using Critical Appraisal Skill Programme (CASP) checklist. Fixed-effects or random-effects model of meta-analysis was determined by the test of heterogeneity. Subgroup analyses were conducted according to ethnicity, smoking status, PM assessment method and interim PM targets of WHO guidelines. Overall, 16 eligible studies were included, covering 15,511,997 participants and 542,991 CVD deaths. Five studies concerning PM2.5 were rated as good quality. The pooled hazard ratio (HR) of every 10μg/m3 increment of PM2.5 exposure for CVD mortality was 1.12 (95%CI = 1.08-1.16), but it was not significant for PM10 (HR = 1.02, 95%CI = 0.89-1.16). Compared with the annual PM2.5 exposure level within WHO's interim targets (1.11-1.16), significantly smaller HR was observed for subjects with an exposure level below WHO's air quality guideline (HR = 1.03, 95%CI = 1.02-1.04). The pooled HR was relatively higher for studies in Asian and with at least 11 years' follow-up and those adopting relatively poor methods (category 1) in assessing PM2.5, whilst the risk was similar regardless of smoking status. Egger and Begg's tests showed no evidence for publication bias. Long-term ambient PM2.5 exposure level was positively associated with the overall CVD mortality. Different interim targets above the WHO's Air Quality Guideline level exerted a similar scale of CVD risk, but there is no evidence for a threshold., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: The prothrombotic effects of particulate matter (PM) may underlie the association of air pollution with increased risks of cardiovascular disease. This study aimed to investigate the association between long-term exposure to PM with an aerodynamic diameter ≤2.5 μm (PM 2.5 ) and platelet counts, a marker of coagulation profiles., Methods: The study participants were from a cohort consisting of 362,396 Taiwanese adults who participated in a standard medical examination program between 2001 and 2014. Platelet counts were measured through Complete Blood Count tests. A satellite-based spatio-temporal model was used to estimate 2-year average ambient PM 2.5 concentration at each participant's address. Mixed-effects linear regression models were used to investigate the association between PM 2.5 exposure and platelet counts., Results: This analysis included 175,959 men with 396,248 observations and 186,437 women with 397,877 observations. Every 10-μg/m 3 increment in the 2-year average PM 2.5 was associated with increases of 0.42% (95% CI: 0.38%, 0.47%) and 0.49% (95% CI: 0.44%, 0.54%) in platelet counts in men and women, respectively. A series of sensitivity analyses, including an analysis in participants free of cardiometabolic disorders, confirmed the robustness of the observed associations. Baseline data analyses showed that every 10-μg/m 3 increment in PM 2.5 was associated with higher risk of 17% and 14% of having elevated platelet counts (≥90th percentile) in men and women, respectively., Conclusions: Long-term exposure to PM 2.5 appears to be associated with increased platelet counts, indicating potential adverse effects on blood coagulability., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: Information on the effects of long-term exposure to fine particulate matter with an aerodynamic diameter of 2·5 μm or less (PM 2·5 ) on lung health is scarce. We aimed to investigate the associations between long-term exposure to PM 2·5 , lung function, and chronic obstructive pulmonary disease (COPD) in a large-scale longitudinal cohort., Methods: We included 285 046 participants aged 20 years or older from the Taiwan MJ Health Management Institution cohort, who were recruited between 2001 and 2014 and had spirometric tests during the medical examination visit. We used a satellite-based spatiotemporal model to estimate the 2-year average ground concentration of PM 2·5 (for the calendar year of each participant's medical examination and for the previous year) at each participant's address. We used the generalised linear mixed model to examine the associations between PM 2·5 concentrations and lung function and the Cox proportional hazard regression model with time-dependent covariates to investigate the PM 2·5 effects on COPD development., Findings: Every 5 μg/m 3 increment in PM 2·5 was associated with a decrease of 1·18% for forced vital capacity (FVC), 1·46% for forced expiratory volume in 1 s (FEV 1 ), 1·65% for maximum mid-expiratory flow (MMEF), and 0·21% for FEV 1 :FVC ratio. The decrease accelerated over time. Additional annual declines were observed for FVC (0·14%), FEV 1 (0·24%), MMEF (0·44%), and FEV 1 :FVC ratio (0·09%). Compared with the participants exposed to the first quartile of PM 2·5 , participants exposed to the fourth, third, and second quartiles of PM 2·5 had a hazard ratio of 1·23 (95% CI 1·09-1·39), 1·30 (1·16-1·46), and 1·39 (1·24-1·56) for COPD development, respectively., Interpretation: Long-term exposure to ambient PM 2·5 is associated with reduced, and faster declines in, lung function. Long-term exposure to ambient PM 2·5 is also associated with an increased risk of the incidence of COPD. This study reinforces the urgency of global strategies to mitigate air pollution for improvement of pulmonary health and prevention of COPD., Funding: Environmental Health Research Fund of the Chinese University of Hong Kong and PhD Studentship of the Chinese University of Hong Kong., (Copyright © 2018 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Objectives: Environmental exposure to chemicals has been considered a potential factor contributing to deteriorated semen quality. However, previous literature on exposure to air pollution and semen quality is inconsistent. We therefore investigated the health effects of short-term and long-term exposure to fine particulate matter (PM 2.5 ) on semen quality in Taiwanese men from the general population., Methods: A cross-sectional study was conducted among 6475 male participants aged 15-49 years who participated in a standard medical examination programme in Taiwan between 2001 and 2014. Semen quality was assessed according to the WHO 1999 guidelines, including sperm concentration, total motility, progressive motility and morphology. Three-month and 2-year average PM 2.5 concentrations were estimated at each participant's address using a spatiotemporal model based on satellite-derived aerosol optical depth data. Multivariable linear and logistic regressions were used to examine the associations between PM 2.5 and semen quality., Results: A robust association was observed between exposure to PM 2.5 and decreased normal morphology. Every increment of 5 µg/m 3 in 2-year average PM 2.5 was significantly associated with a decrease of 1.29% in sperm normal morphology and a 26% increased risk of having the bottom 10% of sperm normal morphology, after adjusting for a wide range of potential confounders (p<0.001). On the other hand, an increment of 5 µg/m 3 in 2-year average PM 2.5 was associated with an increase of 1.03×10 6 /mL in sperm concentration and a 10% decreased risk of being the bottom 10% of sperm concentration (both p<0.001). Similar results were found for 3-month PM 2.5 ., Conclusions: Exposure to ambient PM 2.5 air pollution is associated with a lower level of sperm normal morphology and a higher level of sperm concentration., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Background: Long-term exposure to particulate matter (PM) air pollution may increase blood pressure and the risk of hypertension. However, epidemiological evidence is scarce and inconsistent., Objectives: We investigated the associations between long-term exposure to PM with an aerodynamic diameter <2.5μm (PM 2.5 ), blood pressure, and incident hypertension in a large Taiwanese cohort., Methods: We studied 361,560 adults ≥18y old from a large cohort who participated in a standard medical examination program during 2001 to 2014. Among this group, 125,913 nonhypertensive participants were followed up. A satellite-based spatiotemporal model was used to estimate the 2-y average PM 2.5 concentrations at each participant's address. Multivariable linear regression was used in the cross-sectional data analysis with the 361,560 participants to investigate the associations between PM 2.5 and systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP), and Cox proportional hazard regression was used in the cohort data analysis with the 125,913 participants to investigate the associations between PM 2.5 and incident hypertension., Results: Each 10-μg/m 3 increment in the 2-y average PM 2.5 concentration was associated with increases of 0.45 mmHg [95% confidence interval (CI): 0.40, 0.50], 0.07 mmHg (95% CI: 0.04, 0.11), and 0.38 mmHg (95% CI: 0.33, 0.42) in SBP, DBP, and PP, respectively, after adjusting for a wide range of covariates and possible confounders. Each 10-μg/m 3 increment in the 2-y average PM 2.5 concentration was associated with an increase of 3% in the risk of developing hypertension [hazard ratio=1.03 (95% CI: 1.01, 1.05)]. Stratified and sensitivity analyses yielded similar results., Conclusions: Long-term exposure to PM 2.5 air pollution is associated with higher blood pressure and an increased risk of hypertension. These findings reinforce the importance of air pollution mitigation strategies to reduce the risk of cardiovascular disease. https://doi.org/10.1289/EHP2466.

Background: Exercise may exacerbate the adverse health effects of air pollution by increasing the inhalation of air pollutants. We investigated the combined effects of long-term exposure to fine particle matter (PM2.5) and habitual exercise on deaths from natural causes in Taiwan.Methods: We recruited 384 130 adults (aged ≥ 18 yr) with 842 394 medical examination records between 2001 and 2016, and followed all participants until May 31, 2019. We obtained vital data from the National Death Registry of Taiwan. We estimated PM2.5 exposure using a satellite-based spatiotemporal model, and collected information on exercise habits using a standard self-administered questionnaire. We analyzed the data using a Cox regression model with time-dependent covariates.Results: A higher level of habitual exercise was associated with a lower risk of death from natural causes, compared with inactivity (hazard ratio [HR] 0.84, 95% confidence interval [CI] 0.80-0.88 for the moderate exercise group; HR 0.65, 95% CI 0.62-0.68 for the high exercise groups), whereas a higher PM2.5 exposure was associated with a higher risk of death from natural causes compared with lower exposure (HR 1.02, 95% CI 0.98-1.07, and HR 1.15, 95% CI 1.10-1.20, for the moderate and high PM2.5 exposure groups, respectively). Compared with inactive adults with high PM2.5 exposure, adults with high levels of habitual exercise and low PM2.5 exposure had a substantially lower risk of death from natural causes. We found a minor, but statistically significant, interaction effect between exercise and PM2.5 exposure on risk of death (HR 1.03 95% CI 1.01-1.06). Subgroup analyses, stratified by PM2.5 categories, suggested that moderate and high levels of exercise were associated with a lower risk of death in each PM2.5 stratum, compared with inactivity.Interpretation: Increased levels of exercise and reduced PM2.5 exposure are associated with a lower risk of death from natural causes. Habitual exercise can reduce risk regardless of the levels of PM2.5 exposure. Our results suggest that exercise is a safe health improvement strategy, even for people residing in relatively polluted regions. [ABSTRACT FROM AUTHOR]

Background: Physical activity (PA) increases a person's inhalation of air pollutants due to greater ventilation, possibly leading to larger adverse health effects. This study aims to investigate the combined effects of long-term exposure to fine particulate matter (PM2.5) and habitual PA on lung function in adults.Methods: This was a longitudinal cohort study that included 278,065 Taiwan residents with an age of 20 years old or above who joined a standard medical screening programme between 2001 and 2014. Each participant received at least one medical examination (including spirometric, blood, and urinary tests and a standard self-administered questionnaire survey) during the study period. We estimated the 2-year average PM2.5 concentrations at each participant's address using a new physical model based on observational data. Information on the participants' PA was collected using the standard self-administrated questionnaire. Generalised linear mixed models were used to investigate the combined effects of PM2.5 and PA on pulmonary function. We also performed stratified analyses by different levels of PM2.5 exposure and habitual PA.Results: Each 10 MET-h increase in PA was associated with a higher level of 0.20%, 0.16%, and 0.19% in forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and maximum mid-expiratory flow (MMEF), respectively, after adjusting for PM2.5 exposure and a wide range of covariates including age, sex education, body mass index, lifestyles, and health conditions. Each 10 μg/m3 increase in PM2.5 was associated with a lower FVC, FEV1, and MMEF (2.43%, 2.78% and 3.10%, respectively). Negative interactions were observed, and PM2.5 exposure was associated with a greater reduction in lung function among the participants with higher PA levels.Conclusions: We found significant negative interaction effects between long-term exposure to PM2.5 and habitual PA, suggesting that the increased intake of PM2.5 due to PA may attenuate the benefits of habitual PA on lung function. However, the PA benefits generally remained stable at different stratum of PM2.5 in the stratified analyses, and habitual PA may still be recommended to people residing in relatively polluted regions. [ABSTRACT FROM AUTHOR]

Background: Relatively few studies have explored the relationship between air pollution and cause-specific mortality among hypertensive patients. This study evaluated whether short term exposures to nitrogen dioxide (NO2), ozone (O3), particulate matter <10 mm in diameter (PM10) were associated with higher risk of mortality among a large hypertensive patients.Methods: A total of 223,287 hypertensive patients who attended any public health-care services in Hong Kong and prescribed at least 1 antihypertensive agent for the first time between 2001 and 2005 were followed up until 2010. A time-stratified, bi-directional case-crossover design was adopted to study the association between environmental exposures and mortality outcomes.Results: For all-cause mortality, significant positive associations were observed for NO2 and PM10 at lag 0 to 3 days per 10 MIUg/m3 increase in concentration and the excess risks ranged from 1.187%- 2.501%. Significant positive associations were found for O3 at lag 1 and 2 days and the excess risks were 1.654% (95% C.I. 0.469%, 2.852%) and 1.207% (95% C.I. 0.025%, 2.404%), respectively. We found similarly positive associations between NO2 (excess risks: 1.786%-2.798%), PM10 (1.126%-1.847%), O3 (3.035%-3.355%) and mortality due to respiratory disease. In stratified analysis, these significant results were observed amongst those aged >65 years and in cold seasons only.Conclusions: Older hypertensive patients are susceptible to all-cause and respiratory disease-specific deaths from these air pollutants in cold weather. This implies urgent need for protective air pollution standards for this susceptible population. [ABSTRACT FROM AUTHOR]

Background: The protective effects of physical activity (PA) against chronic disease can be partially ascribed to its anti-inflammatory effects. On the other hand, long-term exposure to particulate matter with an aerodynamic diameter less than 2.5μm (PM2.5) may induce systemic inflammation.Objective: To investigate the joint effects of habitual PA and long-term exposure to PM2.5 on systemic inflammation in a large cohort of Taiwanese adults.Methods: We studied 359,067 adult participants from a cohort consisting of Taiwanese residents who participated in a standard medical examination program from 2001 to 2014. Peripheral white blood cell (WBC) and differential counts were measured as indicators of systemic inflammation. Two-year average concentration of PM2.5 was estimated at each participant's address using a satellite-based spatio-temporal model. Habitual PA level was assessed by questionnaire (inactive, low, moderate and high). Mixed-effects linear regression model was used to examine the associations of WBC counts with PM2.5 and PA.Results: Compared with inactive participants, those with low, moderate or high PA levels had 0.36% [95% confidence interval (CI): 0.31%, 0.41%], 0.70% (95%CI: 0.65%, 0.76%) and 1.16% (95%CI: 1.11%, 1.22%) lower WBC counts, respectively, after adjusting for PM2.5 exposure and a wide range of confounders. Long-term PM2.5 exposure was associated with increased WBC counts at all PA levels. Analyses for differential counts generated similar results. No significant interaction was observed between PA and PM2.5 exposure (P for interaction=0.59).Conclusions: Habitual PA was associated with statistically significant lower markers of systemic inflammation across different levels of PM2.5. Effects of PA and PM2.5 exposure on systemic inflammation are independent. [ABSTRACT FROM AUTHOR]