scholarly journals Association between Atmospheric Particulate Pollutants and Mortality for Cardio-Cerebrovascular Diseases in Chinese Korean Population: A Case-Crossover Study

2018 ◽  
Vol 15 (12) ◽  
pp. 2835 ◽  
Author(s):  
Chao Zhang ◽  
Zhenyu Quan ◽  
Qincheng Wu ◽  
Zhezhen Jin ◽  
Joseph Lee ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cerebrovascular Disease ◽  
Cerebrovascular Diseases ◽  
Air Pollutant ◽  
Aerodynamic Diameter ◽  
Case Crossover ◽  
Disease Mortality ◽  
Particulate Pollutants ◽  
Pm2.5 And Pm10 ◽  
The Relationship

Background: Air pollution in large Chinese cities has led to recent studies that highlighted the relationship between particulate matters (PM) and elevated risk of cardio-cerebrovascular mortality. However, it is unclear as to whether: (1) The same adverse relations exist in cities with relatively low levels of air pollution; and (2) the relationship between the two are similar across ethnic groups. Methods: We collected data of PM2.5 (PM with an aerodynamic diameter ≤ 2.5 µm) and PM10 (aerodynamic diameter ≤ 10 µm) in the Yanbian Korean Autonomous Prefecture between 1 January 2015 and 31 December 2016. Using a time-stratified case-crossover design, we investigated whether levels of particulate pollutants influence the risk of cardio-cerebrovascular disease mortality among ethnic Korean vs. ethnic Han residents residing in the Yanbian Korean Autonomous Prefecture. Results: Under the single air pollutant model, the odds ratios (ORs) of cardio-cerebrovascular disease were 1.025 (1.024–1.026) for each 10 μg/m3 increase in PM2.5 at lag0 day, 1.012 (1.011–1.013) for each 10 μg/m3 increase in PM10 at lag1 day. In the multi-pollutant model adjusted by PM10, SO2, and NO2, the ORs of cardio-cerebrovascular disease were 1.150 (1.145–1.155) for ethnic Koreans and 1.154 (1.149–1.158) for ethnic Hans for each 10 μg/m3 increase in PM2.5. In the multi-pollutant model adjusted by PM2.5, SO2, and NO2, the ORs of cardio-cerebrovascular disease were 1.050 (1.047–1.053) for ethnic Koreans and 1.041 (1.039–1.043) for ethnic Hans for each 10 μg/m3 increase in PM10. Conclusion: This study showed that PM2.5 and PM10 were associated with increased risks of acute death events in residential cardio-cerebrovascular disease in Yanbian, China.

scholarly journals Short-term effects of outdoor air pollution on acute ischaemic stroke occurrence: a case-crossover study in Tianjin, China

2020 ◽  
Vol 77 (12) ◽  
pp. 862-867
Author(s):  
Xuemei Qi ◽  
Zhongyan Wang ◽  
Xiaokun Guo ◽  
Xiaoshuang Xia ◽  
Juanjuan Xue ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Ischaemic Stroke ◽  
Acute Ischaemic Stroke ◽  
Ambient Air ◽  
Air Pollutant ◽  
Aerodynamic Diameter ◽  
Stroke Incidence ◽  
Case Crossover ◽  
Increased Risk

ObjectiveAmbient air pollution is associated with ischaemic stroke incidence. However, most of the previous studies used stroke-related hospital admission rather than stroke onset itself. This study aimed to evaluate the relationship between ambient air pollutant exposures and acute ischaemic stroke based on the timing of symptom onset.MethodsA time-stratified, case-crossover analysis was performed among 520 patients who had ischaemic stroke admitted to the Second Hospital of Tianjin Medical University (Tianjin, China) between 1 April 2018 and 31 March 2019 (365 days). Daily air pollutant concentrations of particulate matter with aerodynamic diameter 2.5 µm, particulate matter with aerodynamic diameter 10 µm (PM10), sulfur dioxide, nitrogen dioxide, carbon monoxide and ozone were obtained from fixed-site monitoring stations. We used conditional logistic regression to estimate OR and 95% CI corresponding to an increase in IQR of each air pollutant after adjusting for the effects of temperature and relative humidity.ResultsOverall, a higher risk of ischaemic stroke was found between April and September. During this period PM10 was associated with an increased risk of ischaemic stroke (1-day lag: OR=1.49, 95% CI 1.09 to 2.02; 3-day mean: OR=1.58, 95% CI 1.09 to 2.29) among patients between 34 and 70 years old. Positive associations were also observed between PM10 (1-day lag: OR=1.51, 95% CI 1.10 to 2.07; 3-day mean: OR=1.57, 95% CI 1.08 to 2.29), ozone (1-day lag: OR=1.83, 95% CI 1.16 to 2.87; 3-day mean: OR=1.90, 95% CI 1.06 to 3.42) and ischaemic stroke occurrence among those with hyperlipidaemia.ConclusionOur results suggest that air pollution is associated with a higher risk of ischaemic stroke in younger people or people with hyperlipidemia. These findings still need to be further investigated.

Long-Term Exposure to PM2.5 and Cognitive Decline: A Longitudinal Population-Based Study

2021 ◽  
pp. 1-9
Author(s):  
Giulia Grande ◽  
Jing Wu ◽  
Petter L.S. Ljungman ◽  
Massimo Stafoggia ◽  
Tom Bellander ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cognitive Decline ◽  
Population Based ◽  
Cerebrovascular Diseases ◽  
Air Pollutant ◽  
National Study ◽  
Piecewise Regression ◽  
Risk Increase ◽  
Restricted Cubic Splines

Background: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear. Objectives: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association. Methods: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5μm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25%fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model. Results: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2–3.2) per interquartile range difference up to mean PM2.5 level (8.6μg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74–1.06). The presence of cerebrovascular diseases further increased such risk by 6%. Conclusion: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.

scholarly journals Ambient Air Pollution and Hospital Admissions for Peptic Ulcers in Taipei: A Time-Stratified Case-Crossover Study

2019 ◽  
Vol 16 (11) ◽  
pp. 1916 ◽  
Author(s):  
Shang-Shyue Tsai ◽  
Hui-Fen Chiu ◽  
Chun-Yuh Yang
Keyword(s):  
Air Pollution ◽  
Peptic Ulcer ◽  
Crossover Study ◽  
Air Pollutants ◽  
Hospital Admissions ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Research Database ◽  
Case Crossover

Very few studies have been performed to determine whether there is a relationship between air pollution and increases in hospitalizations for peptic ulcer, and for those that have occurred, their results may not be completely relevant to Taiwan, where the mixture of ambient air pollutants differ. We performed a time-stratified case-crossover study to investigate the possible association between air pollutant levels and hospital admissions for peptic ulcer in Taipei, Taiwan. To do this, we collected air pollution data from Taiwan's Environmental Protection Agency and hospital admissions for peptic ulcer data for the years 2009–2013 from Taiwan's National Health Insurance's research database. We used conditional logistic regression to analyze the possible association between the two, taking temperature and relative humidity into account. Risk was expressed as odds ratios and significance was expressed with 95% confidence intervals. In our single pollutant model, peptic ulcer admissions were significantly associated with all pollutants (PM10, PM2.5, SO2, NO2, CO, and O3) on warm days (>23 °C). On cool days (<23 °C), peptic ulcer admissions were significantly associated with PM10, NO2, and O3. In our two-pollutant models, peptic ulcer admissions were significantly associated NO2 and O3 when combined with each of the other pollutants on warm days, and with PM10, NO2, and O3 on cool days. It was concluded that the likelihood of peptic ulcer hospitalizations in Taipei rose significantly with increases in air pollutants during the study period.

Long-Term Exposure to PM2.5 and Cognitive Decline: A Longitudinal Population-Based Study

2021 ◽  
Author(s):  
Giulia Grande ◽  
Jing Wu ◽  
Petter L.S. Ljungman ◽  
Massimo Stafoggia ◽  
Tom Bellander ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cognitive Decline ◽  
Population Based ◽  
Cerebrovascular Diseases ◽  
Air Pollutant ◽  
National Study ◽  
Piecewise Regression ◽  
Risk Increase ◽  
Particulate Matter 2.5

Background: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear. Objectives: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association. Methods: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5 μm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25% fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model. Results: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2–3.2) per interquartile range difference up to mean PM2.5 level (8.6 μg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74–1.06). The presence of cerebrovascular diseases further increased such risk by 6%. Conclusion: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.

scholarly journals Association between exposure to ambient air pollution and hospital admission, incidence, and mortality of stroke: an updated systematic review and meta-analysis of more than 23 million participants

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Zhiping Niu ◽  
Feifei Liu ◽  
Hongmei Yu ◽  
Shaotang Wu ◽  
Hao Xiang
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Hospital Admission ◽  
Air Pollutants ◽  
Meta Analysis ◽  
Air Pollutant ◽  
Pollutant Concentration ◽  
Aerodynamic Diameter ◽  
Stroke Incidence ◽  
Incidence And Mortality

Abstract Background Previous studies have suggested that exposure to air pollution may increase stroke risk, but the results remain inconsistent. Evidence of more recent studies is highly warranted, especially gas air pollutants. Methods We searched PubMed, Embase, and Web of Science to identify studies till February 2020 and conducted a meta-analysis on the association between air pollution (PM2.5, particulate matter with aerodynamic diameter less than 2.5 μm; PM10, particulate matter with aerodynamic diameter less than 10 μm; NO2, nitrogen dioxide; SO2, sulfur dioxide; CO, carbon monoxide; O3, ozone) and stroke (hospital admission, incidence, and mortality). Fixed- or random-effects model was used to calculate pooled odds ratios (OR)/hazard ratio (HR) and their 95% confidence intervals (CI) for a 10 μg/m3 increase in air pollutant concentration. Results A total of 68 studies conducted from more than 23 million participants were included in our meta-analysis. Meta-analyses showed significant associations of all six air pollutants and stroke hospital admission (e.g., PM2.5: OR = 1.008 (95% CI 1.005, 1.011); NO2: OR = 1.023 (95% CI 1.015, 1.030), per 10 μg/m3 increases in air pollutant concentration). Exposure to PM2.5, SO2, and NO2 was associated with increased risks of stroke incidence (PM2.5: HR = 1.048 (95% CI 1.020, 1.076); SO2: HR = 1.002 (95% CI 1.000, 1.003); NO2: HR = 1.002 (95% CI 1.000, 1.003), respectively). However, no significant differences were found in associations of PM10, CO, O3, and stroke incidence. Except for CO and O3, we found that higher level of air pollution (PM2.5, PM10, SO2, and NO2) exposure was associated with higher stroke mortality (e.g., PM10: OR = 1.006 (95% CI 1.003, 1.010), SO2: OR = 1.006 (95% CI 1.005, 1.008). Conclusions Exposure to air pollution was positively associated with an increased risk of stroke hospital admission (PM2.5, PM10, SO2, NO2, CO, and O3), incidence (PM2.5, SO2, and NO2), and mortality (PM2.5, PM10, SO2, and NO2). Our study would provide a more comprehensive evidence of air pollution and stroke, especially SO2 and NO2.

scholarly journals The first 1000 days of life: traffic-related air pollution and development of wheezing and asthma in childhood. A systematic review of birth cohort studies

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Alessandra Bettiol ◽  
Elena Gelain ◽  
Erika Milanesio ◽  
Federica Asta ◽  
Franca Rusconi
Keyword(s):  
Systematic Review ◽  
Air Pollution ◽  
Cohort Studies ◽  
Exposure Assessment ◽  
Birth Cohort ◽  
Early Life ◽  
Air Pollutants ◽  
Air Pollutant ◽  
Increased Risk ◽  
The Relationship

Abstract Background The first 1000 days of life -including pregnancy and the first 2 years after birth- represent a critical window for health interventions. This systematic review aimed to summarize the evidence on the relationship between traffic-related air pollutants exposure in the first 1000 days of life and the development of wheezing and asthma, with a particular focus on windows of exposure. Methods Medline and Embase were searched from January 2000 to May 2020 to retrieve population-based birth-cohort studies, including registries, providing quantitative information on the association between exposure to traffic-related air pollutants during pregnancy or early life, and the risk of developing wheezing and asthma in childhood. Screening and selection of the articles were completed independently by three reviewers. The quality of studies was assessed using the Newcastle-Ottawa scale. Results Out of 9681 records retrieved, 26 studies from 21 cohorts were included. The most common traffic-related air pollutant markers were particulate matter (PM) and nitric oxides (NOx). The variability in terms of pollutants, exposure assessment methods, and exposure levels chosen to present the results did not allow a meta-analysis. Exposure to PM and NOx in pregnancy (10 cohorts) was consistently associated with an increased risk of asthma development, while the association with wheezing development was unclear. The second trimester of pregnancy seemed to be particularly critical for asthma risk. As for exposure during early life (15 cohorts), most studies found a positive association between PM (7/10 studies) and NOx (11/13 studies) and the risk of asthma development, while the risk of wheezing development was controversial. The period of postnatal exposure, however, was less precisely defined and a partial overlap between the period of exposure measurement and that of outcome development was present in a consistent number of studies (14 out of 15) raising doubts on the associations found. Conclusions Traffic-related air pollution during pregnancy is associated with an increased risk of asthma development among children and adolescents. The relationship between exposure in the first two years of life and the development of wheezing and asthma needs to be confirmed in studies with more precise exposure assessment.

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