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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.

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.)