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Previous studies have found associations between the incidence of metabolic syndrome (MetS) and exposure to air pollution or road traffic noise. However, investigations on environmental co-exposures are limited. This study aimed to investigate the association between co-exposure to air pollution and road traffic noise and MetS and its subcomponents. Participants living in Taipei City who underwent at least two health checkups between 2010 and 2016 were included in the study. Data were sourced from the MJ Health database, a longitudinal, large-scale cohort in Taiwan. The monthly traffic noise exposure (L den and L night ) was computed using a dynamic noise map. Monthly fine particulate data at one kilometer resolution were computed from satellite imagery data. Cox proportional hazards regression models with month as the underlying time scale were used to estimate hazard ratios (HRs) for the impact of PM 2.5 and road traffic noise exposure on the risk of developing MetS or its subcomponents. Data from 10,773 participants were included. We found significant positive associations between incident MetS and PM 2.5 (HR: 1.88; 95% CI 1.67, 2.12), L den (HR: 1.10; 95% CI 1.06, 1.15), and L night (HR: 1.07; 95% CI 1.02, 1.13) in single exposure models. Results further showed significant associations with an elevated risk of incident MetS in co-exposure models, with HRs of 1.91 (95% CI 1.69, 2.16) and 1.11 (95% CI 1.06, 1.16) for co-exposure to PM 2.5 and L den , and 1.90 (95% CI 1.68, 2.14) and 1.08 (95% CI 1.02, 1.13) for co-exposure to PM 2.5 and L night . The HRs for the co-exposure models were higher than those for models with only a single exposure. This study provides evidence that PM 2.5 and noise exposure may elevate the risk of incident MetS and its components in both single and co-exposure models. Therefore, preventive approaches to mitigate the risk of MetS and its subcomponents should consider reducing exposure to PM 2.5 and noise pollution., (© 2024. The Author(s).)

Urban greenery can help to improve air quality, reduce health risks and create healthy livable urban communities. This study aimed to explore the role of urban greenery in reducing air pollution at the community level in Tainan City, Taiwan, using air quality sensors and street-view imagery. We also collected the number of road trees around each air quality sensor site and identified the species that were best at absorbing PM 2.5 . Three greenness metrics were used to assess community greenery in this study: two Normalized Difference Vegetation Indices (NDVI) from different satellites and the Green View Index (GVI) from Google Street View (GSV) images. Land-use Regression (LUR) was used for statistical analysis. The results showed that a higher GVI within a 500 m buffer was significantly associated with decreased PM 2.5 . Neither NDVI metrics within a 500 m circular buffer were significantly associated with decreased PM 2.5 . Evergreen trees were significantly associated with lower ambient PM 2.5 , compared with deciduous and semi-deciduous trees. Because localized changes in air quality profoundly affect public health and environmental equity, our findings provide evidence for future urban community greenspace planning and its beneficial impacts on reducing air pollution., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Introduction: 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., Objective: 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., Materials and Methods: 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., Results: 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., Conclusion: 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., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Exposure to air pollutants may elevate the injury severity scores (ISSs) for road traffic injuries (RTIs). This multicenter cross-sectional study aimed to investigate the associations between air pollution, weather conditions, and RTI severity. This retrospective study was performed in Taiwan in 2018. The location of each road traffic accident (RTA) was used to determine the nearest air quality monitoring and weather station, and the time of each RTA was matched to the corresponding hourly air pollutant concentration and weather factors. Five multiple logistic regression models were used to compute the risk of sustaining severe injury (ISS ≥ 9). Of the 14,973 patients with RTIs, 2853 sustained severe injury. Moderate or unhealthy air quality index, higher exposure to particulate matter ≤2.5 μm in diameter, bicyclists or pedestrians, greater road width, nighttime, and higher temperature and relative humidity were significant risk factors for severe injury. Exposure to nitrogen oxide and ozone did not increase the risk. Auto occupants and scene-to-hospital time were the protective factors. Sensitivity analyses showed consistent results between air pollutants and the risk of severe injury. Poor air quality and hot and humid weather conditions were associated with severe RTIs. Active commuters were at higher risk of sustaining severe RTI.

With the prevalence of stroke rising due to both aging societies and more people getting strokes at a younger age, a comprehensive investigation into the relationship between urban characteristics and age-specific stroke mortality for the development of a healthy built environment is necessary. Specifically, assessment of various dimensions of urban characteristics (e.g. short-term environmental change, long-term environmental conditions) is needed for healthy built environment designs and protocols. A multifactorial assessment was conducted to evaluate associations between environmental and sociodemographic characteristics with age-stroke mortality in Hong Kong. We found that short-term (and temporally varying) daily PM 10 , older age and being female were more strongly associated with all types of stroke deaths compared to all-cause deaths in general. Colder days, being employed and being married were more strongly associated with hemorrhagic stroke deaths in general. Long-term (and spatially varying) regional-level air pollution were more strongly associated with non-hemorrhagic stroke deaths in general. These associations varied by age. Employment (manual workers) and low education were risk factors for stroke mortality at younger ages (age <65). Greenness and open space did not have a significant association with stroke mortality. Since a significant connection was expected, this leads to questions about the health-inducing efficacy of Hong Kong's compact open spaces (natural greenery being limited to steep slopes, and extensive impervious surfaces on public open spaces). In conclusion, urban plans and designs for stroke mortality prevention should implement age-specific health care to neighborhoods with particular population segments., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Background: Global climate change could have potential impact on enterovirus (EV)-induced infectious diseases. However, the environmental factors promoting acute hemorrhagic conjunctivitis (AHC) circulation remain inconclusive. This study aimed to quantify the relationship between the environment and AHC., Methods: We retrieved the monthly counts and incidence of AHC, meteorological variables and air quality in mainland China between 2013 and 2018. Exposure risks were evaluated by multivariate distributed lag nonlinear models., Results: A total of 219,599 AHC cases were reported in 31 provinces of China, predominantly in southern and central China, seasonally increased in summer. AHC incidence increased by 7% between 2013 and 2018, from 2.6873 to 2.7570 per 100,000 people. A moderate positive correlation was seen between AHC and monthly mean temperature, relative humidity (RH) and precipitation. Each unit increment was associated with a relative risk for AHC of 1.058 at 17°-32 °C at lag 0 months, 1.017 at 65-71% RH at lag 1.4 months, and 1.039 at 400-569 mm at lag 2.4 months. By contrast, a negative correlation was seen between monthly ambient NO 2 and AHC., Conclusion: Long-term exposure to higher mean temperature, RH and precipitation were associated with an increased risk of AHC. The general public, especially susceptible populations, should pay close attention to weather changes and take protective measures in advance to any AHC outbreak as the above situations occur., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Although socio-environmental factors which may affect dementia have widely been studied, the mortality of dementia and socio-environmental relationships among older adults have seldom been discussed., Method: A retrospective, observational study based on territory-wide register-based data was conducted to evaluate the relationships of four individual-level social measures, two community-level social measures, six short-term (temporally varying) environmental measures, and four long-term (spatially varying) environmental measures with dementia mortality among older adults in a high-density Asian city (Hong Kong), for the following decedents: (1) all deaths: age >= 65, (2) "old-old": age > = 85, (3) "mid-old": aged 75-84, and (4) "young-old": aged 65-74., Results: This study identified 5438 deaths (3771 old-old; 1439 mid-old; 228 young-old) from dementia out of 228,600 all-cause deaths among older adults in Hong Kong between 2007 and 2014. Generally, regional air pollution, being unmarried or female, older age, and daily O 3 were associated with higher dementia mortality, while more urban compactness and greenness were linked to lower dementia mortality among older adults. Specifically, being unmarried and the age effect were associated with higher dementia mortality among the "old-old", "mid-old" and "young-old". Regional air pollution was linked to increased dementia mortality, while urban compactness and greenness were associated with lower dementia mortality among the "old-old" and "mid-old". Higher daily O 3 had higher dementia mortality, while districts with a greater percentage of residents whose native language is not Cantonese were linked to lower dementia mortality among the "old-old". Economic inactivity was associated with increased dementia mortality among the "young-old". Gender effect varied by age., Conclusion: The difference in strengths of association of various factors with dementia mortality among different age groups implies the need for a comprehensive framework for community health planning. In particular, strategies for air quality control, usage of greenspace and social space, and activity engagement to reduce vulnerability at all ages are warranted.

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.)

Scarlet fever has resurged in China starting in 2011, and the environment is one of the potential reasons. Nationwide data on 655,039 scarlet fever cases and six air pollutants were retrieved. Exposure risks were evaluated by multivariate distributed lag nonlinear models and a meta-regression model. We show that the average incidence in 2011-2018 was twice that in 2004-2010 [RR = 2.30 (4.40 vs. 1.91), 95% CI: 2.29-2.31; p < 0.001] and generally lower in the summer and winter holiday (p = 0.005). A low to moderate correlation was seen between scarlet fever and monthly NO 2 (r = 0.21) and O 3 (r = 0.11). A 10 μg/m 3 increase of NO 2 and O 3 was significantly associated with scarlet fever, with a cumulative RR of 1.06 (95% CI: 1.02-1.10) and 1.04 (95% CI: 1.01-1.07), respectively, at a lag of 0 to 15 months. In conclusion, long-term exposure to ambient NO 2 and O 3 may be associated with an increased risk of scarlet fever incidence, but direct causality is not established.

Background: Information on the association between long-term exposure to PM 2.5 and gastrointestinal cancer mortality is scarce., Objectives: 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., Methods: 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 km 2 . 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., Results: We found that each 10 µg/m 3 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., Conclusions: 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., 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 © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

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.)

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.)

Haze is an extreme weather event that can severely increase air pollution exposure, resulting in higher burdens on human health. Few studies have explored the health effects of haze, and none have investigated the spatiotemporal interaction between temperature, air quality and urban environment that may exacerbate the adverse health effects of haze. We investigated the spatiotemporal pattern of haze effects and explored the additional effects of temperature, air pollution and urban environment on the short-term mortality risk during hazy days. We applied a Poisson regression model to daily mortality data from 2007 through 2014, to analyze the short-term mortality risk during haze events in Hong Kong. We evaluated the adverse effect on five types of cause-specific mortality after four types of haze event. We also analyzed the additional effect contributed by the spatial variability of urban environment on each type of cause-specific mortality during a specific haze event. A regular hazy day (lag 0) has higher all-cause mortality risk than a day without haze (odds ratio: 1.029 [1.009, 1.049]). We have also observed high mortality risks associated with mental disorders and diseases of the nervous system during hazy days. In addition, extreme weather and air quality contributed to haze-related mortality, while cold weather and higher ground-level ozone had stronger influences on mortality risk. Areas with a high-density environment, lower vegetation, higher anthropogenic heat, and higher PM 2.5 featured stronger effects of haze on mortality than the others. A combined influence of haze, extreme weather/air quality, and urban environment can result in extremely high mortality due to mental/behavioral disorders or diseases of the nervous system. In conclusion, we developed a data-driven technique to analyze the effects of haze on mortality. Our results target the specific dates and areas with higher mortality during haze events, which can be used for development of health warning protocols/systems., (Copyright © 2017 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)

Background: Dust events have long been recognized to be associated with a higher mortality risk. However, no study has investigated how prolonged dust events affect the spatial variability of mortality across districts in a downwind city., Methods: In this study, we applied a spatial regression approach to estimate the district-level mortality during two extreme dust events in Hong Kong. We compared spatial and non-spatial models to evaluate the ability of each regression to estimate mortality. We also compared prolonged dust events with non-dust events to determine the influences of community factors on mortality across the city., Results: The density of a built environment (estimated by the sky view factor) had positive association with excess mortality in each district, while socioeconomic deprivation contributed by lower income and lower education induced higher mortality impact in each territory planning unit during a prolonged dust event. Based on the model comparison, spatial error modelling with the 1st order of queen contiguity consistently outperformed other models. The high-risk areas with higher increase in mortality were located in an urban high-density environment with higher socioeconomic deprivation., Conclusion: Our model design shows the ability to predict spatial variability of mortality risk during an extreme weather event that is not able to be estimated based on traditional time-series analysis or ecological studies. Our spatial protocol can be used for public health surveillance, sustainable planning and disaster preparation when relevant data are available.

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.

Air pollution has been shown to be significantly associated with morbidity and mortality in urban areas, but there is lack of studies focused on extreme pollution events such as extreme dust episodes in high-density Asian cities. However, such cities have had extreme climate episodes that could have adverse health implications for downwind areas. More importantly, few studies have comprehensively investigated the mortality risks of extreme dust events for socioeconomically vulnerable populations. This paper examined the association between air pollutants and mortality risk in Hong Kong from 2006 to 2010, with a case-crossover analysis, to determine the elevated risk after an extreme dust event in a high-density city. The results indicate that PM 10-2.5 dominated the all-cause mortality effect at the lag 0 day (OR: 1.074 [1.051, 1.098]). This study also found that people who were aged ≥ 65, economically inactive, or non-married had higher risks of all-cause mortality and cardiorespiratory mortality during days with extreme dust events. In addition, people who were in areas with higher air pollution had significantly higher risks of all-cause mortality and cardiorespiratory mortality. In conclusion, the results of this study can be used to target the vulnerable among a population or an area and the day(s) at risk to assist in health protocol development and emergency planning, as well as to develop early warnings for the general public in order to mitigate potential mortality risk for vulnerable population groups caused by extreme dust events. [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]