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Smoking, sex, air pollution, lifestyle, and diet may act independently or in concert with each other to contribute to the different outcomes of lung cancer (LC). This study aims to explore their associations with the carcinogenesis of LC, which will be useful for formulating further preventive strategies. This retrospective, longitudinal follow-up cohort study was carried out by connecting to the MJ Health Database, Taiwan Cancer Registry database, and Taiwan cause of death database from 2000 to 2015. The studied subjects were persons attending the health check-ups, distributed throughout the main island of Taiwan. Cox proportional hazards regression models were used to investigate the risk factors associated with LC development and mortality after stratifying by smoking status, with a special emphasis on ambient two-year average PM 2.5 exposure, using a satellite-based spatiotemporal model at a resolution of 1 km 2 , and on dietary habit including consumption of fruits and vegetables. After a median follow-up of 12.3 years, 736 people developed LC, and 401 people died of LC-related causes. For never smokers, the risk of developing LC (aHR: 1.32, 95%CI: 1.12-1.56) and dying from LC-related causes (aHR: 1.28, 95%CI: 1.01-1.63) rises significantly with every 10 μg/m 3 increment of PM 2.5 exposure, but not for ever smokers. Daily consumption of more than two servings of vegetables and fruits is associated with lowering LC risk in ever smokers (aHR: 0.68, 95%CI: 0.47-0.97), and preventing PM 2.5 exposure is associated with lowering LC risk for never smokers.

Rationale & Objective: Limited evidence concerns fine particulate matter (with aerodynamic diameter ≤ 2.5μm [PM 2.5 ]) exposure and the risk for kidney failure with replacement therapy (KFRT). This study assessed whether PM 2.5 exposure was associated with progression of chronic kidney disease (CKD) to KFRT., Study Design: Prospective cohort study., Setting & Participants: 6,628 adult patients with CKD were recruited from the Advanced CKD Program in Taiwan between 2003 and 2015., Exposure: Satellite-based spatiotemporal models were used to calculate each individual's 1-year PM 2.5 exposure before the date of enrollment into the Advanced CKD Program., Outcomes: Time to KFRT (defined as initiation of maintenance hemodialysis, peritoneal dialysis, or kidney transplantation) and time to all-cause mortality., Analytical Approach: Multivariable proportional hazard regression analyses were used to estimate the association of PM 2.5 with KFRT and all-cause mortality. Restricted cubic splines were used to explore dose-response relationships., Results: The study population included 6,628 adult patients with CKD who were aged 20 to 90 years. 941 KFRT events and 1,653 deaths occurred during follow-up. The adjusted HR for progression to KFRT was 1.19 (95% CI, 1.08-1.31) per 7.8μg/m 3 greater PM 2.5 , an amount spanning the interquartile range. There was evidence of a dose-response relationship (adjusted HRs of 1.16 [95% CI, 0.90-1.51], 1.19 [95% CI, 0.94-1.52], and 1.42 [95% CI, 1.12-1.80] for low, medium, and high PM 2.5 levels). There was no significant association between PM 2.5 and all-cause mortality (adjusted HR, 1.01 [95% CI, 0.95-1.08])., Limitations: Misclassification of PM 2.5 exposure assessment and the potential for residual confounding., Conclusions: Our findings suggest that long-term exposure to PM 2.5 is associated with increased risk for progression to KFRT in patients with CKD., (Copyright © 2020 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

The Yangtze River Delta region (YRD) is one of the most densely populated regions in the world, and is frequently influenced by fine particulate matter (PM 2.5 ). Specifically, lung cancer mortality has been recognized as a major health burden associated with PM 2.5 . Therefore, this study developed a multistage approach 1) to first create dasymetric population data with moderate resolution (1 km) by using a random forest algorithm, brightness reflectance of nighttime light (NTL) images, a digital elevation model (DEM), and a MODIS-derived normalized difference vegetation index (NDVI), and 2) to apply the improved population dataset with a MODIS-derived PM 2.5 dataset to estimate the association between spatiotemporal variability of long-term population exposure to PM 2.5 and lung cancer mortality attributable to PM 2.5 across YRD during 2010-2016 for microscale planning. The created dasymetric population data derived from a coarse census unit (administrative unit) were fairly matched with census data at a fine spatial scale (street block), with R 2 and RMSE of 0.64 and 27,874.5 persons, respectively. Furthermore, a significant urban-rural difference of population exposure was found. Additionally, population exposure in Shanghai was 2.9-8 times higher than the other major cities (7-year average: 192,000 μg·people/m 3 ·km 2 ). More importantly, the relative risks of lung cancer mortality in high-risk areas were 28%-33% higher than in low-risk areas. There were 12,574-14,504 total lung cancer deaths attributable to PM 2.5 , and lung cancer deaths in each square kilometer of urban areas were 7-13 times higher than for rural areas. These results indicate that moderate-resolution information can help us understand the spatiotemporal variability of population exposure and related health risk in a high-density environment., Competing Interests: Declaration of competing interest None., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

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 (PM 2.5 ) 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 PM 2.5 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 PM 2.5 and PA on pulmonary function. We also performed stratified analyses by different levels of PM 2.5 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 (FEV 1 ), and maximum mid-expiratory flow (MMEF), respectively, after adjusting for PM 2.5 exposure and a wide range of covariates including age, sex education, body mass index, lifestyles, and health conditions. Each 10 μg/m 3 increase in PM 2.5 was associated with a lower FVC, FEV 1 , and MMEF (2.43%, 2.78% and 3.10%, respectively). Negative interactions were observed, and PM 2.5 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 PM 2.5 and habitual PA, suggesting that the increased intake of PM 2.5 due to PA may attenuate the benefits of habitual PA on lung function. However, the PA benefits generally remained stable at different stratum of PM 2.5 in the stratified analyses, and habitual PA may still be recommended to 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.

Objectives: Animal experiments indicate that exposure to particulate matter (PM) can induce hepatotoxic effects but epidemiological evidence is scarce. We aimed to investigate the associations between long-term exposure to PM air pollution and liver enzymes, which are biomarkers widely used for liver function assessment., Methods: A cross-sectional analysis was performed among 351 852 adult participants (mean age: 40.1 years) who participated in a standard medical screening programme in Taiwan. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and γ-glutamyl transferase (GGT) levels were measured. A satellite-based spatio-temporal model was used to estimate the concentrations of ambient fine particles (PM with an aerodynamic diameter ≤2.5 µm, PM 2.5 ) at each participant's address. Linear and logistic regression models were used to investigate the associations between PM 2.5 and the liver enzymes with adjustment for a wide range of potential confounders., Results: After adjustment for confounders, every 10 µg/m 3 increment in 2-year average PM 2.5 concentration was associated with 0.02%(95% CI: -0.04% to 0.08%), 0.61% (95% CI: 0.51% to 0.70%) and 1.60% (95% CI: 1.50% to 1.70%) increases in AST, ALT and GGT levels, respectively. Consistently, the odds ratios of having elevated liver enzymes (>40 IU/L) per 10 µg/m 3 PM 2.5 increment were 1.06 (95% CI: 1.04 to 1.09), 1.09 (95% CI: 1.07 to 1.10) and 1.09 (95% CI: 1.07 to 1.11) for AST, ALT and GGT, respectively., Conclusions: Long-term exposure to PM 2.5 was associated with increased levels of liver enzymes, especially ALT and GGT. More studies are needed to confirm our findings and to elucidate the underlying mechanisms., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

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.

Fine particulate matter (PM 2.5 ) has been recognized as a key air pollutant that can influence population health risk, especially during extreme cases such as wildfires. Previous studies have applied geospatial techniques such as land use regression to map the ground-level PM 2.5 , while some recent studies have found that Aerosol Optical Depth (AOD) derived from satellite images and machine learning techniques may be two elements that can improve spatiotemporal prediction. However, there has been a lack of studies evaluating use of different machine learning techniques with AOD datasets for mapping PM 2.5 , especially in areas with high spatiotemporal variability of PM 2.5 . In this study, we compared the performance of eight predictive algorithms with the use of multiple remote sensing datasets, including satellite-derived AOD data, for the prediction of ground-level PM2.5 concentration. Based on the results, Cubist, random forest and eXtreme Gradient Boosting were the algorithms with better performance, while Cubist was the best (CV-RMSE = 2.64 μg/m3, CV-R 2  = 0.48). Variable importance analysis indicated that the predictors with the highest contributions in modelling were monthly AOD and elevation. In conclusion, appropriate selection of machine learning algorithms can improve ground-level PM2.5 estimation, especially for areas with nonlinear relationships between PM2.5 and predictors caused by complex terrain. Satellite-derived data such as AOD and land surface temperature (LST) can also be substitutes for traditional datasets retrieved from weather stations, especially for areas with sparse and uneven distribution of stations., (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: 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: 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 (PM 2.5 ) may induce systemic inflammation., Objective: To investigate the joint effects of habitual PA and long-term exposure to PM 2.5 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 PM 2.5 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 PM 2.5 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 PM 2.5 exposure and a wide range of confounders. Long-term PM 2.5 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 PM 2.5 exposure (P for interaction=0.59)., Conclusions: Habitual PA was associated with statistically significant lower markers of systemic inflammation across different levels of PM 2.5 . Effects of PA and PM 2.5 exposure on systemic inflammation are independent., (Copyright © 2017 Elsevier GmbH. All rights reserved.)

Background: Particulate matter (PM) air pollution is associated with the risk of cardiovascular morbidity and mortality. However, the biological mechanism underlying the associations remains unclear. Atherosclerosis, the underlying pathology of cardiovascular disease, is a chronic inflammatory process. We therefore investigated the association of long-term exposure to fine PM (PM2.5) with C-reactive protein (CRP), a sensitive marker of systemic inflammation, in a large Taiwanese population., Methods: Participants were from a large cohort who participated in a standard medical examination programme with measurements of high-sensitivity CRP between 2007 and 2014. We used a spatiotemporal model to estimate 2-year average PM2.5 exposure at each participant's address, based on satellite-derived aerosol optical depth data. General regression models were used for baseline data analysis and mixed-effects linear regression models were used for repeated data analysis to investigate the associations between PM2.5 exposure and CRP, adjusting for a wide range of potential confounders., Results: In this population of 30 034 participants with 39 096 measurements, every 5 μg/m3 PM2.5 increment was associated with a 1.31% increase in CRP [95% confidence interval (CI): 1.00%, 1.63%) after adjusting for confounders. For those participants with repeated CRP measurements, no significant changes were observed between the first and last measurements (0.88 mg/l vs 0.89 mg/l, P = 0.337). The PM2.5 concentrations remained stable over time between 2007 and 2014., Conclusions: Long-term exposure to PM2.5 is associated with increased level of systemic inflammation, supporting the biological link between PM2.5 air pollution and deteriorating cardiovascular health. Air pollution reduction should be an important strategy to prevent cardiovascular disease., (© The Author 2017. Published by Oxford University Press on behalf of the International Epidemiological Association)

Fine particulate matter (PM 2.5 ) is an air pollutant that is receiving intense regulatory attention in Taiwan. In previous studies, the effect of air pollution on bladder cancer has been explored. This study was conducted to elucidate the effect of atmospheric PM 2.5 and other local risk factors on bladder cancer mortality based on available 13-year mortality data. Geographically weighted regression (GWR) was applied to estimate and interpret the spatial variability of the relationships between bladder cancer mortality and ambient PM 2.5 concentrations, and other variables were covariates used to adjust for the effect of PM 2.5 . After applying a GWR model, the concentration of ambient PM 2.5 showed a positive correlation with bladder cancer mortality in males in northern Taiwan and females in most of the townships in Taiwan. This is the first time PM 2.5 has been identified as a risk factor for bladder cancer based on the statistical evidence provided by GWR analysis.

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 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]

Background: Particulate matter (PM) air pollution is associated with the risk of cardiovascular morbidity and mortality. However, the biological mechanism underlying the associations remains unclear. Atherosclerosis, the underlying pathology of cardiovascular disease, is a chronic inflammatory process. We therefore investigated the association of long-term exposure to fine PM (PM2.5) with C-reactive protein (CRP), a sensitive marker of systemic inflammation, in a large Taiwanese population.Methods: Participants were from a large cohort who participated in a standard medical examination programme with measurements of high-sensitivity CRP between 2007 and 2014. We used a spatiotemporal model to estimate 2-year average PM2.5 exposure at each participant's address, based on satellite-derived aerosol optical depth data. General regression models were used for baseline data analysis and mixed-effects linear regression models were used for repeated data analysis to investigate the associations between PM2.5 exposure and CRP, adjusting for a wide range of potential confounders.Results: In this population of 30 034 participants with 39 096 measurements, every 5 μg/m3 PM2.5 increment was associated with a 1.31% increase in CRP [95% confidence interval (CI): 1.00%, 1.63%) after adjusting for confounders. For those participants with repeated CRP measurements, no significant changes were observed between the first and last measurements (0.88 mg/l vs 0.89 mg/l, P = 0.337). The PM2.5 concentrations remained stable over time between 2007 and 2014.Conclusions: Long-term exposure to PM2.5 is associated with increased level of systemic inflammation, supporting the biological link between PM2.5 air pollution and deteriorating cardiovascular health. Air pollution reduction should be an important strategy to prevent cardiovascular disease. [ABSTRACT FROM AUTHOR]

• This is a large cohort study consisting of 385,650 adults aged ≥18 years in Taiwan. • PM 2.5 was associated with higher risk of gastrointestinal cancer mortality. • PM 2.5 was associated with higher risk of liver and colorectal cancers mortality. Information on the association between long-term exposure to PM 2.5 and gastrointestinal cancer mortality is scarce. This study investigated the association between long-term exposure to PM 2.5 and deaths from gastrointestinal cancer and its subtypes in adults in Taiwan. A total of 385,650 Taiwanese adults (≥18 years old) jointed a standard medical examination program between 2001 and 2014 and were followed up until 2016. Their vital data were obtained from the National Death Registry maintained by the Ministry of Health and Welfare in Taiwan. We estimated the ambient PM 2.5 concentration at individual's address utilising a satellite-based spatiotemporal model at a resolution of 1 km2. Cox proportional hazard regression model was used to investigate the associations between ambient PM 2.5 and deaths from gastrointestinal, stomach, colorectal and liver cancers. We found that each 10 µg/m3 increase in PM 2.5 was associated with an increased hazard risk (HR) of 1.09 (95% confidence interval (CI): 1.03–1.16) and 1.13 (95%CI: 1.02–1.24) in deaths from gastrointestinal and liver cancers, respectively. The association between PM 2.5 and death from colorectal cancer was marginally statistically significant [HR: 1.13 (95%CI: 1.00–1.26)]. We did not find significant associations between PM 2.5 and mortality from stomach cancer. Long-term exposure to ambient PM 2.5 was associated with an increased risk of deaths from gastrointestinal cancers, liver cancer and also potentially colorectal cancer. Air pollution control strategies are necessary to reduce the burden of gastrointestinal cancer. [ABSTRACT FROM AUTHOR]

Green space and air pollution have been recognized as vital health determinants. There is a paucity of studies examining the interplay between green space, fine particulate matter (PM 2.5), and the incidence of specific cancers. We aimed to explore the contributions of green space and ambient PM 2.5 to the risk of specific cancers in terms of the most common cancers based on incidence or mortality rate in Taiwan and to ascertain the interaction between green space and PM 2.5 and their role in cancer risk. This retrospective longitudinal cohort study included 407,415 participants. Data were obtained from the 2000–2015 Mei Jau Health Examination Database linked to the Taiwan Cancer Registry and Causes of Death datasets. All participants were aged ≥20 years and had no history of cancer. The environmental exposure were the normalized difference vegetation index (NDVI) and the 2-year average PM 2.5 at baseline. Multivariate adjusted hazard ratios (HRs) were calculated using Cox proportional hazards models. We adjusted for covariates including demographics, anthropometrics, comorbidities, health behaviors, biochemical data, and environmental factors. During a median follow-up of 10.37 years, 11,576 cancer cases were reported. PM 2.5 exposure increased the risk of all cancers (HR: 1.11, [95% CI: 1.06–1.15]), stomach cancer (HR: 1.27, [1.02–1.58]), endocrine gland cancer (HR: 2.13, [1.39–3.26]), breast cancer (HR: 1.12, [1.03–1.22]), and lung cancer (HR: 1.12, [1.01–1.24]). An increase in NDVI reduced the risk of prostate cancer (HR: 0.93, [0.88–0.99]) and lung cancer (HR: 0.95, [0.91–0.99]). NDVI influenced the incidence of prostate and all cancers by reducing PM 2.5 concentrations. Long-term PM 2.5 exposure is associated with an increased risk of some types of cancers. In contrast, an increase in environmental green space exposure is associated with lowering of the risk of prostate and lung cancer. • There is a paucity of research regarding the interplay between green space and air pollution on cancer incidence. • Long-term PM2.5 exposure is a possible risk factor for all cancers, and specific cancers. • Green space plays a possible protective role against the incidence of prostate and lung cancer. • There was no significant interaction between PM2.5 and green space on cancer incidence. [ABSTRACT FROM AUTHOR]