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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.)

Environmental pollution significantly impacts global disease burden. However, the contribution of environmental pollution to kidney disease is often overlooked in nephrology. This review examines the growing body of research demonstrating the significant impacts of environmental pollutants, with a focus on air pollution as a primary factor, and acknowledges the roles of other pollutants, such as heavy metals, in the development and progression of kidney diseases. Short-term exposure to air pollution is linked with an increased risk of kidney disease-related events, including hospital admissions, and death, predominantly occurring in vulnerable populations. In contrast, long-term exposure, even at low to moderate levels, may lead to progressive pathophysiological changes, such as chronic systemic inflammation and oxidative stress, that contribute to the development of kidney disease. In addition, air pollution may exacerbate traditional kidney disease risk factors such as hypertension and diabetes, thereby accelerating disease progression. The review also explores how climate change may interact with various pollutants, including air pollution, influencing kidney disease indirectly. The examined evidence underscores the urgent need for an interdisciplinary approach to research further into environmental kidney disease. Environmental health policies could play a crucial role in the prevention, intervention, and improvement of kidney health worldwide., (Copyright © 2024 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

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.)

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.

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.)

Aims/hypothesis: Information on the associations of long-term exposure to fine particulate matter (with an aerodynamic diameter less than 2.5 μm; PM 2.5 ) with the development of type 2 diabetes is scarce, especially for south-east Asia, where most countries are experiencing serious air pollution. This study aimed to investigate the long-term effects of exposure to ambient PM 2.5 on the incidence of type 2 diabetes in a population of Taiwanese adults., Methods: A total of 147,908 participants without diabetes, at least 18 years of age, were recruited in a standard medical examination programme between 2001 and 2014. They were encouraged to take medical examinations periodically and underwent at least two measurements of fasting plasma glucose (FPG). Incident type 2 diabetes was identified as FPG ≥7 mmol/l or self-reported physician-diagnosed diabetes in the subsequent medical visits. The PM 2.5 concentration at each participant's address was estimated using a satellite-based spatiotemporal model with a resolution of 1 × 1 km 2 . The 2 year average of PM 2.5 concentrations (i.e. the year of and the year before the medical examination) was treated as an indicator of long-term exposure to ambient PM 2.5 air pollution. We performed Cox regression models with time-dependent covariates to analyse the long-term effects of exposure to PM 2.5 on the incidence of type 2 diabetes. A wide range of covariates were introduced in the models to control for potential effects, including age, sex, education, season, year, smoking status, alcohol drinking, physical activity, vegetable intake, fruit intake, occupational exposure, BMI, hypertension and dyslipidaemia (all were treated as time-dependent covariates except for sex)., Results: Compared with the participants exposed to the first quartile of ambient PM 2.5 , participants exposed to the second, third and fourth quartiles of ambient PM 2.5 had HRs of 1.28 (95% CI 1.18, 1.39), 1.27 (95% CI 1.17, 1.38) and 1.16 (95% CI 1.07, 1.26), respectively, for the incidence of type 2 diabetes. Participants who drank occasionally or regularly (more than once per week) or who had a lower BMI (<23 kg/m 2 ) were more sensitive to the long-term effects of exposure to ambient PM 2.5 ., Conclusions/interpretation: Long-term exposure to ambient PM 2.5 appears to be associated with a higher risk of developing type 2 diabetes in this Asian population experiencing high levels of air pollution.

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: Chronic kidney disease (CKD) is a serious global public health challenge, but there is limited information on the connection between air pollution and risk of CKD., Objective: The aim of this study was to investigate the association between long-term exposure to particulate matter (PM) with an aerodynamic diameter of less than [Formula: see text] ([Formula: see text]) and the development of CKD in a large cohort., Methods: A total of 100,629 nonCKD Taiwanese residents age 20 y or above were included in this study between 2001 and 2014. Ambient [Formula: see text] concentration was estimated at each participant's address using a satellite-based spatiotemporal model. Incident CKD cases were identified by an estimated glomerular filtration rate (eGFR) of less than [Formula: see text]. We collected information on a wide range of potential confounders/modifiers during the medical examinations. Cox proportional hazard regression was applied to calculate hazard ratios (HRs)., Results: During the follow-up, 4,046 incident CKD cases were identified, and the incidence rate was 6.24 per 1,000 person-years. In contrast with participants with the first quintile exposure of [Formula: see text], participants with the fourth and fifth quintiles exposure of [Formula: see text] had increased risk of CKD development, adjusting for age, sex, educational level, smoking, drinking, body mass index, systolic blood pressure, fasting glucose, total cholesterol, and self-reported heart disease or stroke, with an HR [95% confidence interval (CI)] of 1.11 (1.02, 1.22) and 1.15 (1.05, 1.26), respectively. A significant concentration-response trend was observed ([Formula: see text]). Every [Formula: see text] increment in the [Formula: see text] concentration was associated with a 6% higher risk of developing CKD (HR: 1.06, 95% CI: 1.02, 1.10). Sensitivity and stratified analyses yielded similar results., Conclusions: Long-term exposure to ambient [Formula: see text] was associated with an increased risk of CKD development. Our findings reinforce the urgency to develop global strategies of air pollution reduction to prevent CKD. https://doi.org/10.1289/EHP3304.

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: 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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: 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 PM2.5 and NO2 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/m3 increase in air pollution]. In the multiple-pollutant models, the NO2-menopause associations were attenuated after adjusting for PM2.5 and O3, whereas the associations of menopause with PM2.5 and O3 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. [ABSTRACT FROM AUTHOR]

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. • We proposed a novel framework to decompose the variation in human exposure. • We used satellite observations to delineate human exposure to PM 2.5 in China. • Spatial difference in PM 2.5 change extensively reduced population exposure. • Population migration increased human exposure in all provinces except Taiwan. • The framework paves a new way to apply for other air pollutants in other regions. [ABSTRACT FROM AUTHOR]

Background: We investigated the joint associations of habitual physical activity (PA) and long-term exposure to fine particulate matter (PM2.5) 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. PM2.5 exposure was estimated at each participant's address using a satellite data-based spatiotemporal model with 1 km2 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 PM2.5 was 26.1±7.3 μg/m3. 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 PM2.5), 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 PM2.5 was associated with a higher risk of hypertension (HR for the moderate- and high-PM2.5 was 1.37 [95% CI, 1.32-1.43] and 1.92 [95% CI, 1.81-2.04], respectively, as compared with the low-PM2.5 group]. No significant interaction was observed between PA and PM2.5 (HR 1.01 [95% CI, 1.00-1.02]).Conclusions: A high-PA and low PM2.5 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 PM2.5, and the positive association between PM2.5 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. [ABSTRACT FROM AUTHOR]