Search

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 Methods: We studied 361,560 adults [greater than or equal to]18 y 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 P[M.sub.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 P[M.sub.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 P[M.sub.2.5] and incident hypertension. Results: Each 10-[micro]g/[m.sup.3] increment in the 2-y average P[M.sub.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-[micro]g/[m.sup.3] increment in the 2-y average P[M.sub.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 P[M.sub.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, Introduction Cardiovascular disease (CVD) is a leading cause of death worldwide, contributing to 17.7 million deaths in 2015 (WHO 2017). Many epidemiological studies have shown that long-term exposure to particulate [...]

Aims/hypothesis: Information on the associations of long-term exposure to fine particulate matter (with an aerodynamic diameter less than 2.5 μm; PM2.5) 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 PM2.5 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 PM2.5 concentration at each participant's address was estimated using a satellite-based spatiotemporal model with a resolution of 1 × 1 km2. The 2 year average of PM2.5 concentrations (i.e. the year of and the year before the medical examination) was treated as an indicator of long-term exposure to ambient PM2.5 air pollution. We performed Cox regression models with time-dependent covariates to analyse the long-term effects of exposure to PM2.5 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 PM2.5, participants exposed to the second, third and fourth quartiles of ambient PM2.5 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/m2) were more sensitive to the long-term effects of exposure to ambient PM2.5. Conclusions/interpretation: Long-term exposure to ambient PM2.5 appears to be associated with a higher risk of developing type 2 diabetes in this Asian population experiencing high levels of air pollution. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. 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 km2). 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. 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. 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. • This is the largest longitudinal cohort study consisting of 66,702 adults. • The mean PM 2.5 was 27.0 μg/m3 and the interquartile range was 9.6 μg/m3 with a range of 5.8–50.3 μg/m3 • Ambient PM 2.5 is associated with a higher risk of dyslipidaemia. [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]

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.)

Previous studies have reported inconsistent results of the associations of alanine transaminase (ALT), aspartate transaminase (AST), gamma-glutamyltransferase (GGT) and alkaline phosphatase (ALP) with incident type 2 diabetes (diabetes hereafter). We aimed to resolve the controversy by taking nonalcoholic fatty liver disease (NAFLD) into account. The study population comprised 132,377 non-diabetic individuals (64,875 men and 67,502 women) aged 35-79 who had two or more health examinations during 1996-2014. A total of 6,555 incident diabetes (3,734 men and 2,821 women) were identified, on average, over 5.8 years of follow-up. Cox regression was used to calculate the hazard ratio (HR) for incident diabetes, adjusting for classical confounders. The risk of incident diabetes was significantly associated with NAFLD [HR = 2.08 (men) and 2.65 (women)]. Elevated ALT, AST, GGT and ALP were also significantly associated with the increased risk of diabetes, with HRs of 1.27, 1.23, 1.58 and 1.37, respectively, in men, and 1.56, 1.18, 1.48 and 1.44, respectively in women. Our results suggest that NAFLD, ALT, AST, GGT and ALP are independent predictors for incident diabetes in both men and women.