scholarly journals Long-Term Ambient Air Pollutant Exposure and Risk of Recurrent Headache in Children: A 12-Year Cohort Study

Author(s):  
Syuan-Yu Hong ◽  
Lei Wan ◽  
Hui-Ju Lin ◽  
Cheng-Li Lin ◽  
Chang-Ching Wei

Although studies have suggested environmental factors to be triggers of headache, the contribution of long-term air pollution exposure to recurrent headaches is poorly understood. Hence, we executed this nationwide cohort study to investigate associations between levels of ambient air pollutants and risks of recurrent headaches in children in Taiwan from 2000 to 2012. We used data from the Taiwan National Health Insurance Research Database and linked them to the Taiwan Air Quality Monitoring Database. Overall, 218,008 children aged < 18 were identified from 1 January 2000, and then followed until they were diagnosed by a physician for ≥3 times with recurrent headaches or until 31 December 2012. We categorized the annual average concentration of each air pollutant (fine particulate matter, total hydrocarbon, methane, sulfur dioxide, and nitrogen dioxide) into quartiles (Q1–Q4). We measured the incidence rate, hazard ratios (HRs), and the corresponding 95% confidence intervals for recurrent headaches. stratified by the quartiles. A total of 28,037 children (12.9%) were identified with recurrent headaches. The incidence rate and adjusted HR for recurrent headaches increased with higher-level exposure of air pollutants, except sulfur dioxide. We herein demonstrate that long-term ambient air pollutant exposure might be a risk factor for childhood recurrent headaches.

2020 ◽  
Author(s):  
Syuan-Yu Hong ◽  
Lei Wan ◽  
Hui-Ju Lin ◽  
Cheng-Li Lin ◽  
Chang-Ching Wei

Abstract Background Although research has suggested environmental factors to be triggers of headache, the contribution of long-term air pollution exposure to migraine and recurrent headaches (migraine/headaches) is poorly understood. Hence, we executed this nationwide cohort study to investigate the association of levels of ambient air pollution with the incidence and the risk of migraine/headaches in Taiwan children from 2000 to 2012. Methods We collected data from the Taiwan National Health Insurance Research Database and linked them to the Taiwan Air Quality Monitoring Database. Overall 218,008 children aged <18 (0-17) years old were identified from January 1, 2000 and then followed until they were diagnosed by a physician >=3 times with migraine/headaches or until December 31, 2012. We categorized the annual average concentration of each air pollutant (fine particulate matter, total hydrocarbon, methane, sulfur dioxide, and nitrogen dioxide) into quartiles (Q1-Q4). We measured the incidence rate, hazard ratios (HRs), and the corresponding 95% confidence intervals for migraine/headaches stratified by the quartiles. Results A total of 28037 children (12.9%) were identified with migraine/headaches. The incidence rate and adjusted HR for migraine/headaches increased with higher-level exposure of air pollutants, except sulfur dioxide. Conclusions We herein demonstrate that long-term ambient air pollutant exposure might be a risk factor for childhood migraine/headaches.


Author(s):  
Shang-Shyue Tsai ◽  
Hui-Fen Chiu ◽  
Chun-Yuh Yang

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.


2020 ◽  
Vol 191 ◽  
pp. 110116
Author(s):  
Yan Wang ◽  
Xiaotian Liu ◽  
Gongbo Chen ◽  
Runqi Tu ◽  
Tanko Abdulai ◽  
...  

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 145.3-145
Author(s):  
K. S. K. MA ◽  
L. T. Wang

Background:Recent studies suggest that air pollution may play a role in autoimmune diseases. However, few of them report the correlation between air pollution and primary Sjögren’s syndrome (pSS).Objectives:We sought to determine whether people exposed to environmental fine particulate of air pollution have a higher risk of developing pSS.Methods:We performed a retrospective population-based cohort study from the National Health Insurance Research Database (NHIRD) of Taiwan’s population, using the international Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) to categorize each disease diagnosis. Air pollution data on Nitric oxide (NO), methane (CH4), and carbon monoxide (CO) were obtained from the Taiwan Air Quality-Monitoring Database (TAQMD), where daily air pollution data from community-based monitoring sites (78 sites since 1993) was available on a real-time basis. We followed up from January 1st, 1998 to the endpoint of SS diagnosis or to December 31, 2011.The daily average air pollutant concentrations were divided into 4 quartile-based groups (Q1-Q4). The incidence rate, hazard ratios (HRs), as well as 95% confidence intervals for pSS, were stratified by the quartiles of air pollutant concentration, and calculated with a Cox proportional regression model. Finally, Ingenuity Systems Pathway Analysis (IPA) was conducted to identify activated pathways among air way epithelial cells exposed to airborne coarse, fine, and ultrafine particles, and parotid gland tissues from pSS patients using Z-score visualization.Results:A total of 200 patients were diagnosed with SS. The mean age of patients with pSS was 53.1 years. The incidence of pSS was 0.11%. With the increase in exposure concentrations of nitrogen dioxide, methane, and carbon monoxide (from Q1 to Q4), the incidence rate for pSS of per 1000 person-years increased from 0.7 to 1.19, from 0.93 to 2.14, and from 0.57 to 1.06, respectively. Moreover, compared with Q1, the adjusted HR in Q4 after adjusting for age, gender, monthly income and urbanization levels increased to 1.86, 2.21 and 2.04, respectively. IPA analyses suggested that the underlying cellular mechanisms involved up-regulation of chronic inflammatory pathways including fibrosis signaling pathway.Conclusion:Exposure to air pollutants, specifically NO, CH4, and CO, was associated with SS development, mostly driven by fibrotic signaling cascades occurred during chronic inflammation.Disclosure of Interests:None declared


Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Ming-Shun Hsieh ◽  
Chorng-Kuang How ◽  
Pau-Chung Chen

Objective: Many studies had reported the association between air pollution and cardiovascular diseases. In this current study, we aimed to evaluate the risk of long-term exposure to air pollution (PM2.5, CO and NO2) to the development of PAOD. Methods: We linked two nation-scale databases, the national health insurance database and the air quality-monitoring database of Taiwan to conduct this cohort study between 2003 and 2013. Cox proportional regression with time-dependent model was used to evaluate the hazard ratio (HR) of air pollutants to PAOD. The residential areas were divided into four categories according to the daily average concentration of air pollutants, Q1 to Q4 (Q4 = the worst). The cumulative incidence of PAOD was examined by the Kaplain-Meier analysis with log-rank test. Results: A total of 1,598 PAOD cases were identified during the follow-up period with 98,540 non-PAOD ones (demographic characteristics were showed in Table 1). In the multivariate analysis, after adjusting for age, gender, urbanization level, residential area, baseline comorbidities, and drug use, the adjusted HRs were that PM2.5 = 1.14 (95% CI 1.13-1.16), NO2 = 1.03 (95% CI 1.02-1.04), and CO = 2.35 (95% CI 1.95-2.84), respectively (Table 2). The Kaplain-Meier analysis showed that CO concentration was strongly associated with cumulative incidence rate of PAOD during the follow-up period (Figure 1). Conclusion: Besides of well-known risk factors, air pollutants may also play a potential role in PAOD pathogenesis.


2020 ◽  
Vol 188 ◽  
pp. 109755
Author(s):  
Zhicheng Luo ◽  
Yitan Hou ◽  
Gongbo Chen ◽  
Fang Wang ◽  
Runqi Tu ◽  
...  

2021 ◽  
Author(s):  
Bingxiao Li ◽  
Han Cao ◽  
Kuo Liu ◽  
Li Pan ◽  
Ze Cui ◽  
...  

Abstract Background:The association between long-term air pollutants exposure with blood pressure and hypertension defined by 2017 American College of Cardiology (ACC)/American Heart Association (AHA) Hypertension Guideline is still conflicting. This study was designed to investigate the associations between long-term exposure to air pollutants, blood pressure and hypertension defined by Chinese and ACC/AHA guideline in Chinese adults. Methods: Our study was based on the baseline survey of the Cohort Study on Chronic Disease of Communities Natural Population in Beijing, Tianjin and Hebei (CHCN-BTH) from 2017 to 2019. A spatial statistical model was used to assessed three-year (2014-2016) average pollutant concentrations for PM2.5, and other pollutants concentration (PM10, SO2, NO2) was assessed by data of air monitoring stations. Results: A total of 32,135 adults aged 18-80 years were included, each interquartile range (IQR) increment of PM2.5, PM10, SO2 and NO2 was associated with increases of 0.66mmHg (95%CI: 0.29, 1.03), 040mmHg (0.00, 0.81), 1.38mmHg (0.92, 1.84) and 0.54mmHg (0.16, 0.91) in SBP, respectively. SO2 was associated with increases 0.42mmHg (0.11, 0.72) in DBP. PM2.5, PM10, SO2 and NO2 was associated with an 14% (Odds ratio [OR]:1.14, 95%CI:1.06-1.23), 6% (1.06, 1.00-1.13), 9% (1.09, 1.02-1.17) and 8% (1.08, 1.01-1.16) increase of hypertension defined by Chinese guideline. PM2.5 and SO2 was associated with 16% (1.166, 1.093-1.245) and 10% (1.10, 1.03-1.18) increase of hypertension defined by ACC/AHA guideline. Two-pollutants model, traffic-related pollution model and stratified analysis yielded similar results. Conclusions: We found that long-term exposure to PM2.5, NO2 and SO2 is associated with increase of blood pressure and hypertension defined by both Chinses and ACC/AHA guideline. PM10 is associated with higher SBP and risk of hypertension defined by Chinese guideline.


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