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Highway vehicle emissions can result in adverse health problems to nearby residents and workers, especially during traffic congestion. In response, the policy to implement electronic toll collection (ETC) has helped alleviate traffic congestion, as compared to manual toll collection (MTC) and has led to reduced air pollution and improved public health. However, the effect of ETC in reducing particulate matter polluting the air is not well understood, especially in the ultrafine particle (UFP) range (particle diameter <100 nm). To the best of our knowledge, this is the first study to investigate how ETC affects the traffic pattern and air quality, especially UFP and PM 2.5 . We selected a site in Tainan, Taiwan, and measured UFP and PM 2.5 concentrations before and after the construction of the ETC system. The computed traffic volumes during peak travel periods (7:00 AM to 9:00 AM and 4:00 PM to 6:00 PM) respectively, accounted for approximately 23-25% and 14-18% before and after the implementation of ETC, indicating that peak traffic volumes were more homogeneous after ETC. Moreover, the results indicate that the full implementation of ETC can help reduce UFP number concentrations and PM 2.5 mass concentrations in the highway downwind area by 4 × 10 3 #/cm 3 and 20.5 μg/m 3 , respectively. After the full implementation of the ETC, significant reductions in both the UFP number concentration and PM 2.5 mass concentration were seen. Furthermore, excessive lifetime cancer risks (ELCR) from exposure to PM 2.5 and UFP together were reduced 49.3% after the implementation of the ETC. Accordingly, ETC not only helps alleviate traffic congestion but also reduces traffic emissions and lifetime cancer risk for people living or working near highways.

Fine particulate matter (PM 2.5 ) emitted from electric arc furnaces (EAFs) poses health concerns. However, little research has been done on the impact of EAF on the health of community residents. This cross-sectional study conducted a PM 2.5 exposure assessment and health examination of community residents living near an EAF. A total of 965 residents aged 40-90 years were recruited. The residents' exposure to PM 2.5 was categorized according to the distance of their residence from the EAFs (<500, 500-1000, 1000-1500, 1500-2000, and > 2000 m). Average ambient PM 2.5 concentrations were estimated using a hybrid kriging/land-use regression (LUR) model. In addition, we selected two air-sampling sites to monitor the 2-year levels of PM 2.5 and particle-bound metals. A spot urine sample and blood samples were collected and ten heavy metal concentrations in the blood were analyzed. Inflammation- and oxidative stress-related biomarkers were measured. The associations between environmental factors and a biochemical examination were estimated using a generalized linear model. Active air sampling and hybrid kriging/LUR model simulation indicated increased levels of PM 2.5 near the EAF. The metal concentrations in PM 2.5 included Fe, Pb, Mn, Ni, As, Cu, Ni, Zn, and Al, which also significantly increased near the EAF. PM 2.5 levels were significantly associated with an increased total cholesterol-high-density lipoprotein (TC/HDL) ratio. High levels of PM 2.5 and malondialdehyde were associated with a 1.72-fold increased risk of TC/HDL ratio ≥ 4 (95% CI: 1.12-2.65) after adjusting for potential confounding factors. Blood Pb levels were significantly associated with increased systolic and diastolic blood pressure and decreased estimated glomerular filtration rate but negatively associated with distance from the EAF. The results show that people living near EAFs should pay more attention to adverse health problems, including atherogenic dyslipidemia, hypertension, and chronic kidney disease associated with exposure to PM 2.5 and particle-bound metals., 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 Elsevier B.V. All rights reserved.)

Background: Exposure to occupational noise might increase the risk of hypertension. However, limited cohort studies have investigated the relationship between time-varying exposure to occupational noise and the development of hypertension., Methods: We conducted a 17-year cohort study involving 2459 workers to assess the relationship between time-varying exposure to occupational noise and incident hypertension in the aerospace industry. We performed an extended Cox proportional hazard model considering occupational noise exposure as time-varying covariates. Furthermore, we employed the distributed lag nonlinear models (DLNMS) to examine the exposure-response relationship., Results: In the extended Cox proportional model, as workers were exposed to noise over 80 dBA, the hazard ratios (HRs) of hypertension significantly increased with a noise increase of 5 dBA (HR = 1.16, 95% CI: 1.04-1.29). In exposure-response associations, the HRs of hypertension steadily increased between noise levels of 82 and 106 dBA (HRs ranged from 1.04 to 1.46). After additionally adjusting for personal protection equipment (PPE), the HRs decreased dramatically between 107 and 124 dBA (HRs ranged from 1.45 to 1.00)., Conclusions: Our study refined the exposure assessment by integrating time-varying exposures to occupational noise and taking work history into consideration. Our findings suggested that workers exposed to noise levels between 82 and 106 dBA for 3-17 years may increase the risk of hypertension with a non-linear exposure-response pattern. We further provided evidence that workers wearing PPE could effectively reduce noise exposure and avoid the development of hypertension., Competing Interests: Declaration of competing interest The work was supported by China Medical University (CMU 107-Z-04), Taichung, TAIWAN and National of Science Council (NSC102-2314-B-039-025), Taipei, TAIWAN. The authors declare they have no actual or potential competing financial interests., (Copyright © 2020 Elsevier GmbH. All rights reserved.)

Few studies have assessed the association between fine particulate matter (PM 2.5 ) exposure during pregnancy and infancy and pediatric rheumatic diseases (PRDs). The goal of this study was to investigate the association of PM 2.5 with PRDs, and to explore sensitive windows of exposure. Therefore, we conducted a cohort-based case-control study to investigate the association between weekly exposure to PM 2.5 and PRDs in Taiwan. Our birth cohort consisted of infants born in 2004-2014 (n = 1,991,592) who were followed from conception to the end of 2015. There were 2363 cases of incident PRDs in children, and 23,630 children served as controls using density matching (1:10) based on date of birth, gender, and gestational week. We used a linear mixed effect (LME) model to incorporate the aerosol optical depth (AOD), meteorological variables, and land-use data to predict daily PM 2.5 concentrations. We also performed conditional logistic regression with distributed lag non-linear models (DLNMs) to assess the effects of weekly average PM 2.5 on PRDs, as well as dose-response relationships. In DLNMs, exposure to PM 2.5 during pregnancy (11-40 weeks) or infancy (1-14 weeks after birth) was associated with incident PRDs adjusting for potential confounding factors, and for carbon monoxide and sulfur dioxide. In the dose-response association, the odds ratios of PRDs were significantly increased for PM 2.5 exposures between 26 and 54 μg/m 3 . In addition, exposure to PM 2.5 above 81 μg/m 3 dramatically increased the risk of PRDs. In conclusions, our study provides new data to suggest that PM 2.5 exposure from 11-40 gestational weeks to 1-14 weeks after birth can increase the risk for PRDs in a non-linear dose-response fashion., 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.)

Work stress and burnout have become important issues. Changes in work patterns frequently, long working hours, and too much pressure among workers in high-tech companies may result in the chronic fatigue symptoms and increase the risk of cardiovascular diseases, even leading to sudden death. Changes of heart rate variability (HRV) can be treated as a warning from the autonomic nervous systems and as a long-term monitoring method for chronic disease, for example, cardiovascular diseases and sudden death. The purpose of this study was to explore the association between occupational burnout and HRV.Proportional stratified convenient sampling was performed and in total, 120 individuals participated in this study. Questionnaires and the "occupational burnout inventory" were used to collect biographical and burnout information. A novel wrist physiological monitor was used to measure autonomic nervous system-related data, including HRV, low-frequency (LF) %, high-frequency (HF) %, and LF/HF ratio. Descriptive statistics and logistic regressions were computed using SPSS 17.0 (Chinese version, IBM Corp., New York, NY).The results show that participants who were 20 to 25 years old, work overtime because of onerous personal tasks, had a medical history, and recently felt unwell have higher "personal burnout." "Participants with a graduate degree, with onerous tasks, who were indirect staff, and with a regular-hour job tended to overcommit to their work." Significant associations were found among medical history, recently feeling unwell, and "work-related burnout." There was a positive association between HRV and job seniority. LF%, HF%, and LF/HF ratio were significantly correlated with job category. "Work overcommitment" was related to LF/HF ratio among men. Some items in "personal burnout" and "work overcommitment" were also associated with HRV among women.The findings suggest that the measurement of HRV can be applied in occupational settings to assess burnout. It not only allows administrators to quickly select the colleagues who need health care, but also provides timely and appropriate care, thereby promoting the health of the worker.

Air pollution is a modifiable and preventable factor, and it is a possible risk factor for dementia. However, evidence from epidemiological studies is still limited. We conducted a systematic review and meta-analysis to summarize the epidemiological evidence for long-term effects of particulate matter with an aerodynamic diameter ≤2.5 μm (PM 2.5 ) on dementia/Alzheimer's disease (AD). Our inclusion criteria for eligible studies were: longitudinal cohort study design, no overlap in study population, age of study subject ≥50 years, detailed description of exposure assessment for PM 2.5 , outdoor assessment of exposure to PM 2.5 , usage of a clear definition of dementia/AD, and accessibility of sufficient information for meta-analysis. Six databases were searched for eligible studies. The random-effect model was used to synthesize the associations between PM 2.5 and dementia. After exclusion of all irrelevant studies, we analyzed the results of four cohort studies conducted in Canada, Taiwan, the UK, and the US during 2015-2018 among more than 12 million elderly subjects aged ≥50 years (N = 12,119,853). Our meta-analysis reveals that exposure to a 10 μg/m 3 increase in PM 2.5 was significantly and positively associated with dementia (pooled HR = 3.26, 95% CI: 1.20, 5.31). In subgroup analyses, exposure to a 10 μg/m 3 increase in PM 2.5 was found to be positively associated with AD (pooled HR = 4.82, 95% CI: 2.28, 7.36). Analysis of current epidemiological research on PM 2.5 and dementia confirmed that exposure to PM 2.5 was positively associated with a higher risk for dementia. However, it is to be noted that the included studies mainly relied on claim-based diagnosis and showed large differences in methods of exposure assessment, hence further epidemiological studies with well validated outcomes and with standardized exposure assessment models are required to ascertain the relationship between PM 2.5 and dementia/AD., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Systemic lupus erythematosus (SLE) is a multi-systemic chronic autoimmune disease, the etiology of SLE is still unclear. Only a few studies evaluated the associations between air pollution and SLE. We conducted a population-based cohort study in Taiwan to examine the associations of air pollution with SLE. A total of 682,208 individuals aged 18-70 years were retrieved from National Health Insurance Research Database. We applied 1-km resolution land use regression and satellite-based models to estimate air pollutant concentrations during 2001-2010. The mixed effect Cox models with time-dependent variables were performed to estimate the associations between air pollution and SLE, as hazard ratios (HRs) with 95% confidence interval (CI). We identified 1292 newly diagnosed SLE patients with average age of 43.26 ± 13.64 years, most of them were female. There were positive associations of SLE with exposure to a 9.76 ppb increase in nitrogen dioxide (NO 2 ), a 0.20 ppm increase in carbon monoxide (CO), and a 10.2 μg/m 3 increase in fine particles (PM 2.5 ) (HR = 1.21, 95% CI: 1.08-1.36, HR = 1.44, 95% CI: 1.31-1.59, and HR = 1.12, 95% CI: 1.02-1.23, respectively). Additionally, we observed negative associations with ozone (O 3 ) and sulfur dioxide (SO 2 ). According to the exposure-response relationships, exposure to NO 2 between 28 and 38 ppb, exposure to CO above 0.6 ppm, and exposure to PM 2.5 between 18 and 46 μg/m 3 were positively associated with SLE. The results suggested that long-term exposure to traffic-related gaseous air pollutants (NO 2 and CO) less than current National Ambient Air Quality Standards and PM 2.5 are significantly associated with the risk of SLE., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: Lung development is a multistage process from conception to the postnatal period, disruption of which by air pollutants can trigger later respiratory morbidity., Objective: We sought to evaluate the effects of weekly average fine particulate matter (particulate matter with an aerodynamic diameter less than 2.5 μm [PM 2.5 ]) exposure during pregnancy and infancy on asthma and identify vulnerable times to help elucidate possible mechanisms of the effects of PM 2.5 on asthma symptoms., Methods: A birth cohort study including 184,604 children born during 2004-2011 in Taichung City was retrieved from the Taiwan Maternal and Child Health Database and followed until 2014. A daily satellite-based hybrid model was applied to estimate PM 2.5 exposure for each subject. A Cox proportional hazard model combined with a distributed lag nonlinear model was used to evaluate the associations of asthma with PM 2.5 exposure during pregnancy and infancy., Results: The birth cohort contained 34,336 asthmatic patients, and the mean age of children given a diagnosis of asthma was 3.39 ± 1.78 years. Increased exposure to PM 2.5 during gestational weeks 6 to 22 and 9 to 46 weeks after birth were significantly associated with an increased incidence of asthma. The exposure-response relationship indicated that the hazard ratio (HR) of asthma increased steeply at PM 2.5 exposure of greater than 93 μg/m 3 during pregnancy. Additionally, the HRs remained significant with postnatal exposure to PM 2.5 between 26 and 72 μg/m 3 (range, 1.01-1.07 μg/m 3 ), followed by a sharp increase in HRs at PM 2.5 exposure of greater than 73 μg/m 3 ., Conclusion: Both prenatal and postnatal exposures to PM 2.5 were associated with later development of asthma. The vulnerable time windows might be within early gestation and midgestation and infancy., (Copyright © 2019 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Air pollution may cause specific genetic or epigenetic abnormalities and lead to the development of uterine fibroids (UFs). However, there have been limited studies evaluating the relationship between air pollutant exposure and the development of UFs., Methods: We conducted a 10-year cohort-based case-control study in Taiwan from 2001 to 2010 using National Health Institute Research Database (NHIRD) to assess the association between air pollution and the UFs development among Taiwanese women. The case group consisted of 11,028 women newly diagnosed with UFs during the study period and the control group was 44,112 women aged 25-45 years using density sampling with a 1:4 matching on the date of birth from 224,675 women in 2001-2010. The average age of onset was 36 ± 4.37 years old. Daily concentrations of PM 2.5 were estimated by linear mixed-effects model integrating aerosol optical depth (AOD) and meteorological variables; daily concentrations of O 3 , CO, NO 2 and SO 2 were calculated by the Inverse Distance Weighting (IDW). The annual cumulative exposure to air pollutants during the study period was calculated corresponding to residential zip codes., Results: In the conditional logistic regression adjusting for confounders, the adjusted odds ratio (aOR) for UFs per 10 μg/m 3 increase in PM 2.5 was 1.105 (95% confidence interval: 1.069, 1.141), per 10 ppb increase in O 3 was 1.075 (95% confidence interval: 1.039, 1.113), respectively., Conclusions: Our study suggests that exposure to PM 2.5 and O 3 may increase the risk of developing UFs. Further studies are needed to confirm this novel finding., (Copyright © 2019 Elsevier GmbH. All rights reserved.)

[This corrects the article DOI: 10.1371/journal.pone.0075510.].

Satellite-based aerosol optical depth (AOD) is now comprehensively applied to estimate ground-level concentrations of fine particulate matter (PM 2.5 ). This study aimed to construct the AOD-PM 2.5 estimation models over Taiwan. The AOD-PM 2.5 modeling in Taiwan island is challenging owing to heterogeneous land use, complex topography, and humid tropical to subtropical climate conditions with frequent cloud cover and prolonged rainy season. The AOD retrievals from the MODerate resolution Imaging Spectroradiometer (MODIS) onboard the Terra and Aqua satellites were combined with the meteorological variables from reanalysis data and high resolution localized land use variables to estimate PM 2.5 over Taiwan island from 2005 to 2015. Ten-fold cross validation was carried out and the residuals of the estimation model at various locations and seasons are assessed. The cross validation (CV) R 2 based on monitoring stations were 0.66 and 0.66, with CV root mean square errors of 14.0 μg/m 3 (34%) and 12.9 μg/m 3 (33%), respectively, for models based on Terra and Aqua AOD. The results provided PM 2.5 estimations at locations without surface stations. The estimation revealed PM 2.5 concentration hotspots in the central and southern part of the western plain areas, particularly in winter and spring. The annual average of estimated PM 2.5 concentrations over Taiwan consistently declined during 2005-2015. The AOD-PM 2.5 model is a reliable and validated method for estimating PM 2.5 concentrations at locations without monitoring stations in Taiwan, which is crucial for epidemiological study and for the assessment of air quality control policy., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

There have been few studies investigating interactions of G-protein beta3 subunit ( GNB3 ) C825T (rs5443) and dietary sodium intake on the risk of hypertension, i.e., BP salt sensitivity. The study aims to evaluate joint effects of GNB3 polymorphisms and sodium consumption on the development of hypertension. A cohort-based case-control study was conducted in 2014. There are 233 participants with newly diagnosed hypertension in the case group and 699 participants in the gender-matched control group. The primary outcome is the development of hypertension over a 10-year period. The determinants of hypertension were three genotypes of SNP in GNB3 (TT; CT; and CC) and two dietary salt categories on the basis of the level of sodium consumption representing high (>4800 mg/day) and low-sodium (.

Interleukin-13(IL-13) might play an important role in driving aggregate bronchitic symptoms pathogenesis. However, none of the studies assessed the interaction between air pollutants exposure and IL-13 gene on the risk of aggregate bronchitic symptoms in non-asthma children. To assess the independent and joint effects of the exposure to air pollution and IL-13 haplotypes on the risk of aggregate bronchitic symptoms, we conducted a cross-sectional study and focused on non-asthma children. The study population consisted of 2944 children. The effect of each air pollutant on the risk of aggregate bronchitic symptoms was estimated as odds ratios per interquartile range (IQR) change. In the multiple logistic regressions, adjusted for confounding factors, the risk of chronic phlegm was associated with PM 2.5 exposure (aOR, 1.59; 95% CI, 1.07-2.37 per 12.51μg/m3 change), O 3 exposure (aOR, 1.54 95% CI, 1.05-2.27 per 8.28ppb change) and SO 2 exposure (aOR, 1.19; 95% CI, 1.02-1.39 per 0.98ppb change). Our study further provides the evidence that gene-environment interactions between IL-13 haplotype and O 3 exposure on chronic phlegm (95% CI for interaction, 1.01-1.38). Identifying children who are more sensitive to air pollution helps us to provide them an efficient prevention to avoid aggregate bronchitic symptoms., (Copyright © 2018. Published by Elsevier B.V.)

The effects of fine particles (PM 2.5 ) on asthma have been widely confirmed by epidemiological research studies. However, a limited number of studies have investigated the relationship between exposure to different PM 2.5 components and asthma. We characterized the PM 2.5 components in a suburban site of central Taiwan and conducted a time-stratified case-crossover study to elaborate the effects of daily concentration of each PM 2.5 component on asthma outpatient visits. We retrieved asthma outpatient claims for individuals less than 20 years old with a residential address in the Shalu district, Taiwan, from the National Health Insurance Research Database during 2000-2010. Multiple linear regression models were used to back extrapolate the historic concentration of individual components of PM 2.5 from 2000 through to 2010, including black carbon (BC) and eight ions, namely, sulfate, nitrate (NO 3 - ), ammonium, chloride, potassium (K + ), magnesium, calcium, sodium. The odds ratio (OR) with a 95% confidence interval (CI) of individual PM 2.5 components on asthma was estimated by conditional logistic regression. A total of 887 asthma outpatient visits with individuals who have an average age of 7.96±3.88 years were selected. After adjusting for confounders, we found an interquartile range (IQR) increase in BC level, an IQR increase in NO 3 - level, and an IQR increase in K + level that were all associated with the increased risk of asthma outpatient visits from the current day (OR = 1.18, 95% CI: 1.05-1.34; OR = 1.11, 95% CI: 1.01-1.21; and OR = 1.16, 95% CI: 1.04-1.30, respectively). The effects of these components on asthma were stronger in the cold season than in the warm season. However, we did not find any lagging effects. The results suggest that exposure to NO 3 - , BC, and K + derived from industry-related combustion or motor vehicles emission sources may increase the risk of asthma outpatient visits, particularly during the cold season., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: Allergic rhinitis (AR) is a highly prevalent chronic inflammatory disease affecting nearly 40% of the children in Taiwan. Genetic susceptibility may interact with specific environmental factors leading to allergic disease development., Methods: To assess the interactions between catalase gene promoter polymorphisms and environmental factors on the risk of AR, we conducted a case-control study in Taiwan. Data on AR and environmental factors were collected from 800 children using the ISSAC questionnaire. The case group consisted of 263 children with AR, and the control group consisted of =537 healthy children. Genotyping was performed for rs1001179 and rs769214 polymorphisms, and environmental exposure was assessed using four indicators including dwelling visible molds, mold odor, moisture on surfaces, and water damage., Results: We found that the presence of visible molds, mold odor, and moisture was associated with AR. An apparent joint effect of the GG genotype and mold odor, compared with the AA and AG combined genotypes and without any exposure indicator (adjusted odds ratio [OR] = 1.95 [95% confidence interval (CI) = 1.20, 3.18]; interaction adjusted odds ratio = 2.59 [95% CI = 1.27, 5.30]), was observed., Conclusions: Our findings suggest that gene-environment interactions between the catalase polymorphism rs769214 and mold odor may play an important role in childhood AR development.

Background: Limited studies have explored the relationship between air pollution and rheumatoid arthritis (RA), with the results being somewhat inconsistent., Methods: This was a retrospective cohort study that included 322,301 subjects aged 30-50 years, selected from the National Health Insurance Research Database in Taiwan, were followed from 2001 to 2010. We used a time-dependent extended Cox model and incorporated time-dependent variables to estimate the associations between the annual mean concentrations of air pollutants with RA, including carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), particles with an aerodynamic diameter less than 10 μm (PM10), and sulfur dioxide (SO2), and reported the hazard ratio (HR) and 95% confidence interval (CI)., Results: Newly diagnosed RA was positively associated with a 100-ppb increase in CO (adjusted HR = 1.17 [95% CI = 1.16, 1.18]), a 10-ppb increase in NO2 (1.54 [1.45, 1.64]), a 10-ppb increase in O3 (1.37 [1.33, 1.41]), and a 1 ppb in SO2 (1.02 [1.00, 1.04]). There was no association between a 10-μg/m increase in PM10 and RA (1.02 [0.99, 1.05])., Conclusions: Our finding suggests that O3 and traffic-related air pollutants (CO and NO2) may be positively associated with incident RA. This is an important finding given that many individuals are exposed to similar levels of O3 and NO2 globally.

Background: Kawasaki disease (KD) is an acute and multi-systemic vasculitis that occurs predominantly in infants and young children. Although the etiological agent of KD remains unclear, limited studies have reported that windborne environmental factors may trigger KD., Objectives: We conducted a time-stratified case-crossover study to assess the associations between air pollutants and KD in Taiwan., Methods: We identified children < 5 years old with a diagnosis of KD from the Longitudinal Health Insurance Database 2000 (LHID2000) between 2000 and 2010. We obtained data regarding carbon monoxide (CO), nitrogen dioxide (NO 2 ), ozone (O 3 ), particulate matter with aerodynamic diameter < 10 μm (PM 10 ), and sulfate dioxide (SO 2 ) from 70 monitoring stations and used inverse distance weighting to calculate average daily exposures for the residential postal code of each case. We performed conditional logistic regression to estimate associations between KD and each air pollutant according to interquartile range (IQR) increases and quartiles of exposure on the day of hospitalization versus 3-4 reference days during the same month for each case. Additionally, we estimated associations with single-day exposures lagged 1-2 days., Results: We identified 695 KD hospital admissions during the study period. An IQR increase (28.73 ppb) of O 3 was positively associated with KD after adjusting for temperature, humidity, northward wind, and eastward wind [adjusted odds ratio = 1.21; 95% confidence interval (CI): 1.01, 1.44]. There were no significant associations between KD and CO, NO 2 , PM 10 , or SO 2 . The association with O 3 was limited to exposure on the day of hospitalization and to exposure during the summer months (June-August)., Conclusions: Our results provide new evidence that exposure to O 3 may increase the risk of KD in children. However, further investigation is needed to confirm the association and identify a potential biological mechanism.

Previous epidemiologic studies have assessed the role of the exposure to ambient air pollution in the development of cardiac birth defects, but they have provided somewhat inconsistent results. To assess the associations between exposure to ambient air pollutants and the risk of cardiac defects, a population-based case-control study was conducted using 1087 cases of cardiac defects and a random sample of 10,870 controls from 1,533,748 Taiwanese newborns in 2001 to 2007.Logistic regression was performed to calculate odds ratios for 10 ppb increases in O3 and 10 μg/m increases in PM10. In addition, we compared the risk of cardiac defects in 4 categories-high exposure (>75th percentile); medium exposure (75th to 50th percentile); low exposure (<50th-25th percentile); reference (<25th percentile) based on the distribution of each pollutant. The risks of ventricular septal defects (VSD), atrial septal defects (ASD), and patent ductus arteriosus (PDA) were associated with 10 ppb increases in O3 exposure during the first 3 gestational months among term and preterm babies. In comparison between high PM10 exposure and reference category, there were statistically significant elevations in the effect estimates of ASD for all and terms births. In addition, there was a negative or weak association between SO2, NO2, CO, and cardiac defects.The study proved that exposure to outdoor air O3 and PM10 during the first trimester of gestation may increase the risk of VSD, ASD, and PDA.

Peripheral neuropathy and inflammatory reactions of the central nervous system may accompany rheumatoid arthritis (RA). Inflammatory processes play a critical role in epilepsy. Therefore, we conducted this study to determine the risk of epilepsy in patients with RA.The RA cohort comprised patients ages 20 years and older who were newly diagnosed with RA between 2000 and 2011, with data obtained from the Registry of Catastrophic Illnesses Patient Database. Patients without RA were frequency matched with an RA cohort at a 1:1 ratio according to age, sex, and year of RA diagnosis.The overall crude hazard ratio (HR) for epilepsy was 1.27-fold higher in the RA cohort compared with that in the controls. After adjustment for age, sex, comorbidities, and medications, the patients with RA were associated with an increased risk of epilepsy compared with those without RA (adjusted HR [aHR] = 1.52, 95% confidence interval [CI] = 1.12-2.07). Compared with the RA patients with ≤ 560 days of nonsteroidal anti-inflammatory drug (NSAID) use, the RA patients with 1181 to 2145 and >2145 days of NSAID use had a significantly lower risk of epilepsy (aHR = 0.35, 95% CI = 0.24-0.52 and aHR = 0.15, 95% CI = 0.09-0.24, respectively).This study provides compelling evidence of an increased risk of epilepsy in patients with RA. The period of NSAID treatment is negatively associated with the risk of epilepsy in RA patients.

Several studies have indicated that air pollution induces systemic as well as tissue-specific inflammation. Chronic inflammatory diseases such as rheumatoid arthritis and chronic obstructive pulmonary disease reduce bone mineral density (BMD), leading to increased release of immune cells from the bone marrow. However, the association between air pollution and osteoporosis remains poorly defined. Therefore, we conducted this population-based retrospective cohort study to evaluate the risk of osteoporosis in Taiwanese residents exposed to air pollution.We combined 2 nationwide databases in this study. The National Health Insurance Research Database of Taiwan was available from 2000 to 2010. Detailed daily data on air pollution were collected by Taiwan Environmental Protection Agency (EPA) from 1998 to 2010. We calculated the yearly average concentrations of air pollutants from the study start to the date of osteoporosis occurrence, or withdrawal from the NHI program, or December 31, 2010. The yearly average concentrations of air pollutants were categorized into quartiles, and the risks of osteoporosis were evaluated among 4 stages of air pollutants.Among Q1, Q2, Q3, and Q4 of pollutants in all subjects, the adjusted hazard ratios (HRs) of osteoporosis in Q2, Q3, and Q4 were compared with Q1. For carbon monoxide (CO), the adjusted HRs were 1.05 (95% confidence interval [CI], 0.97-1.14), 1.78 (95% CI, 1.65-1.92), and 1.84 (95% CI, 1.71-1.98), respectively. For nitrogen dioxide (NO2), the adjusted HRs were 1.35 (95% CI, 1.25-1.45), 1.24 (95% CI, 1.15-1.35), and 1.60 (95% CI, 1.48-1.73), respectively, in all subjects.The findings of the present study show that CO and NO2 exposure is associated with an increased risk of osteoporosis in the Taiwanese population.

Objective: Noise exposure is associated with elevated blood pressure, but the effects on susceptible workers have not been reported. This repeated-measure study investigated the effects of noise exposure on 24-h ambulatory blood pressure among hypertensive, pre-hypertensive, and normotensive adults., Methods: We enrolled 113 volunteers in an occupational cohort in 2009. Individual noise exposure and personal blood pressure were measured simultaneously over 24 h on working and non-working days. Linear mixed-effects regressions were used to estimate the effects on SBP and DBP by controlling for potential confounders., Results: Each A-weighted decibel (dBA) increase in a 30-min time-lagged exposure was associated with transient elevations of work-time SBP [0.30 (95% confidence interval: 0.06, 0.54) mmHg] on working days as well as sleep-time SBP [0.39 (0.12, 0.66) mmHg] and DBP [0.33 (0.14, 0.51) mmHg] on non-working days among 19 hypertensive adults. In contrast, 46 normotensive workers had transient increases in work-time SBP [0.16 (0.03, 0.29) mmHg] and DBP [0.25 (0.15, 0.34) mmHg] on working days as well as sleep-time SBP [0.17 (0.06, 0.29) mmHg] and DBP [0.21 (0.14, 0.29) mmHg] on non-working days caused by a 1-dBA increase in the current exposure. All groups had sustained increases in 24-h average ambulatory SBP and DBP induced by noise exposure on 2 days, but the hypertensive workers had the most pronounced increase in SBP., Conclusion: Hypertensive adults are more susceptible to noise exposure with a greater effect on ambulatory SBP. These results suggest a need for more protection for this subpopulation.

Prenatal exposure to ambient air pollutants might cause adverse birth outcomes; however, there have been few studies in which the association between air pollution and preterm birth was examined after stratifying by pregnancy complications. We conducted a population-based case-control study of 1,510,064 singleton births from the Taiwanese birth registry during 2001-2007. Of the total of 1,510,064 births, we designated all 86,224 preterm births as the case group and then randomly selected an additional 344,896 from the remaining births (equivalent to 4 full-term births for every 1 preterm birth) as the control sample. We used an inverse distance weighting approach to calculate an average exposure parameter for air pollutants. The adjusted odds ratio for preterm birth per 10-ppb increase in ozone was 1.12 (95% confidence interval: 1.01, 1.23) for women with gestational diabetes mellitus who were exposed in the third trimester and 1.02 (95% confidence interval: 1.01, 1.03) for women without gestational diabetes (P for interaction <0.001). These findings suggest that exposure to ozone in pregnancy is associated with an increased risk of preterm birth, particularly for women who have gestational diabetes mellitus., (© The Author 2015. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: A limited number of studies have reported an association between long-term exposure to ambient air pollutants and lung function growth among children, with inconclusive results., Objectives: To assess the relationship between air pollutant exposure and lung function growth, and to examine potential sex differences in the susceptibility of lung function growth to air pollution., Methods: We conducted a two-year prospective cohort study of Taiwanese children aged 12 at baseline who were followed from October 1, 2007 to November 31, 2009. The study population comprised 2941 non-smoking children who completed pulmonary function tests at both baseline and follow-up surveys. We applied spatial modeling for individual-level exposure assessment to capture relevant exposures and also attempted to eliminate potential community-level confounding. The exposure parameters were annual averages and values calculated from 24-hourly PM2.5 and 8-hourly ozone (O3) concentrations, corresponding to the residential addresses over the study period. The effect estimates were presented as lung function growth deficits per interquartile range (IQR) for PM2.5 and O3., Results: In a multiple linear mixed effect model, adjusted for confounding, growth deficits in the forced vital capacity (FVC), forced expiration volume in 1s (FEV1), and forced expiratory flow between the 25th and 75th percentiles of the FVC were associated with increased exposure to PM2.5 and O3. For example, greater exposure to PM2.5 (IQR, 17.92μg/m(3)) was associated with an annual deficit in FVC growth of 75mL in boys and 61mL in girls (p for interaction <0.05). Similar associations were found for O3., Conclusions: The study provides evidence that long-term exposure to PM2.5 and O3 may have a detrimental effect on the development of lung function in children. The estimated deficits were generally larger in boys, compared to girls., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Several studies with animal research associate air pollution in Alzheimer's disease (AD) neuropathology, but the actual impact of air pollution on the risk of AD is unknown. Here, this study investigates the association between long-term exposure to ozone (O3) and particulate matter (PM) with an aerodynamic diameter equal to or less than 2.5 μm (PM2.5), and newly diagnosed AD in Taiwan. We conducted a cohort study of 95,690 individuals' age ≥ 65 during 2001-2010. We obtained PM10 and O3 data from Taiwan Environmental Protection Agency during 2000-2010. Since PM2.5 data is only accessible entirely after 2006, we used the mean ratio between PM2.5 and PM10 during 2006-2010 (0.57) to estimate the PM2.5 concentrations from 2000 to 2005. A Cox proportional hazards model was used to evaluate the associations between O3 and PM2.5 at baseline and changes of O3 and PM2.5 during the follow-up period and AD. The adjusted HR for AD was weakly associated with a raised concentration in O3 at baseline per increase of 9.63 ppb (adjusted HR 1.06, 95% confidence interval (CI) 1.00-1.12). Further, we estimated a 211% risk of increase of AD per increase of 10.91 ppb in O3 over the follow-up period (95% CI 2.92-3.33). We found a 138% risk of increase of AD per increase of 4.34 μg/m3 in PM2.5 over the follow-up period (95% CI 2.21-2.56). These findings suggest long-term exposure to O3 and PM2.5 above the current US EPA standards are associated with increased the risk of AD.

Objective: The study investigates the association between active smoking, exposure to environmental tobacco smoke (ETS) and the development of bronchitis and bronchitic symptoms among adolescents., Methods: A prospective cohort study was conducted with 4134 adolescents aged 12-14 from the Taiwan Children Health Study in 14 communities in Taiwan since 2007. Parents or guardians completed written questionnaires regarding demographic information, household ETS and respiratory symptoms at baseline. The adolescents themselves completed identical questionnaires on respiratory outcomes in the 2009 survey. Associations between active smoking, exposure to ETS and the 2-year incidence of respiratory outcomes were analyzed by multiple Poisson regression models, taking overdispersion into account., Results: Active smoking was associated with an increased risk of developing chronic cough and chronic phlegm. We found significant dose-response associations between the duration of smoking, the numbers of cigarettes and the onset of bronchitic symptoms. Exposure to ETS was a significant risk factor for the development of chronic cough. Among asthmatic adolescents, exposure to ETS was associated with an additional risk for the onset of chronic phlegm., Conclusion: This study demonstrates that active smoking and exposure to ETS are associated with higher risks for developing bronchitic symptoms among adolescents., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Air pollution influences the development of limb defects in animals. There is little epidemiologic evidence on the effect of prenatal air pollution exposure on the risk of limb defects., Objective: To assess the relations between exposure to ambient air pollutants and the risk of limb defects., Methods: We conducted a matched-pairs case-control study in Taiwan from 2001 through 2007. The case group consisted of 1687 limb defects and the control group was density-sampling matched one to ten based on the month and year of conception from 1510,064 live singleton newborns in 2001-2007. Adjusted conditional logistic regression models were used to estimate odds ratios per 10 ppb change for O3, NO2, 1 ppb change for SO2, 10 µg/m(3) change for PM10, and 100 ppb change for CO during the first trimester and first three gestational months., Results: Of the specific limb defects, reduction deformities of limbs (adjusted OR=1.024, 95% CI: 1.000, 1.048) was associated with a 1 ppb increase in SO2 during weeks of 9-12 of gestation as well as the first trimester. Reduction deformities of limbs was also associated with a 10 ppb increase in O3 during weeks of 1-4 of gestation (adjusted OR=1.391, 95% CI: 1.064, 1.818) among preterm births., Conclusion: The present study provides evidence that exposure to outdoor air SO2 during the first trimester of pregnancy may increase the risk of limb defects. Exposure to O3 was associated with reduction deformities of limbs among preterm births. Similar levels of SO2 and O3 are encountered globally by large numbers of pregnant women., (Copyright © 2014 Elsevier Inc. All rights reserved.)

There is growing evidence that multiple genes and air pollutants are associated with asthma. By identifying the effect of air pollution on the general population, the effects of air pollution on childhood asthma can be better understood. We conducted the Taiwan Children Health Study (TCHS) to investigate the influence of gene-air pollution interactions on childhood asthma. Complete monitoring data for the ambient air pollutants were collected from Taiwan Environmental Protection Agency air monitoring stations. Our results show a significant two-way gene-air pollution interaction between glutathione S-transferase P (GSTP1) and PM10 on the risk of childhood asthma. Interactions between GSTP1 and different types of air pollutants have a higher information gain than other gene-air pollutant combinations. Our study suggests that interaction between GSTP1 and PM10 is the most influential gene-air pollution interaction model on childhood asthma. The different types of air pollution combined with the GSTP1 gene may alter the susceptibility to childhood asthma. It implies that GSTP1 is an important hub gene in the anti-oxidative pathway that buffers the harmful effects of air pollution., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

There is limited evidence that long-term exposure to ambient air pollution increases the risk of childhood autism spectrum disorder (ASD). The objective of the study was to investigate the associations between long-term exposure to air pollution and newly diagnostic ASD in Taiwan. We conducted a population-based cohort of 49,073 children age less than 3 years in 2000 that were retrieved from Taiwan National Insurance Research Database and followed up from 2000 through 2010. Inverse distance weighting method was used to form exposure parameter for ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and particles with aerodynamic diameter less than 10 µm (PM10). Time-dependent Cox proportional hazards (PH) model was performed to evaluate the relationship between yearly average exposure air pollutants of preceding years and newly diagnostic ASD. The risk of newly diagnostic ASD increased according to increasing O3, CO, NO2, and SO2 levels. The effect estimate indicating an approximately 59% risk increase per 10 ppb increase in O3 level (95% CI 1.42–1.79), 37% risk increase per 100 ppb in CO (95% CI 1.31–1.44), 340% risk increase per 10 ppb increase in NO2 level (95% CI 3.31–5.85), and 17% risk increase per 1 ppb in SO2 level (95% CI 1.09–1.27) was stable with different combinations of air pollutants in the multi-pollutant models. Our results provide evident that children exposure to O3, CO, NO2, and SO2 in the preceding 1 year to 4 years may increase the risk of ASD diagnosis.

The associations between occupational noise exposure and hypertension remain controversial because of the differences in study designs, exposure assessments, and confounding controls. This prospective study investigated the relationship between noise exposure and the 10-year risk of hypertension. A cohort of 578 male workers in Taiwan was followed from 1998 to 2008. All subjects were divided into high-, intermediate-, and low-exposure groups on the basis of noise exposure assessment. Cox regression models were used to estimate the relative risks of hypertension after adjustment for potential confounders. During the 7,805 person-years of follow-up, 141 hypertension cases were identified. Significant increases of 3.2 (95% confidence interval (CI): 0.2, 6.2) mm Hg in systolic blood pressure and 2.5 (95% CI: 0.1, 4.8) mm Hg in diastolic blood pressure between the baseline and follow-up measurements were observed in the high-exposure group. Participants exposed to ≥85 A-weighted decibels (dBA) had a 1.93-fold (95% CI: 1.15, 3.22) risk of hypertension compared with those exposed to <80 dBA. There was a significant exposure-response pattern (P = 0.016) between the risk of hypertension and the stratum of noise exposure. Prolonged exposure to noise levels ≥85 dBA may increase males' systolic and diastolic blood pressure levels. This association may translate into a higher incidence of hypertension.

Background: There are limited studies on the role of interaction between exposure to ambient air pollution and glutathione-S-transferase (GST) P1 on the risk of asthma/wheezing among children, which provided suggestive, but inconclusive results., Methods: To assess the joint effect of air pollutants and GSTP1 on asthma/wheezing, we conducted a nationwide cross-sectional study of 3,825 children in Taiwan Children Health Study. The studied determinants were three GSTP1 Ile105Val (rs 1695) genotypes (Ile-Ile; Ile-Val and Val-Val) and expoure to ambient air pollutants. We used routine air-pollution monitoring data for ozone (O(3)) and particles with an aerodynamic diameter of 2.5 µm or less (PM(2.5)). The effect estimates were presented as odds ratios (ORs) per interquartile changes for PM(2.5) and O(3)., Findings: In a two-stage hierarchical model adjusting for confounding, the risk of asthma was negatively associated with PM(2.5) (adjusted odds ratio (OR) 0.60; 95% confidence interval (CI) 0.45, 0.82) and O(3) (OR 0.74; 95% CI 0.60, 0.90) among Ile105 homozygotes, but positively associated with PM(2.5) (OR 1.52; 95% CI 1.01, 2.27) and O(3) (OR 1.19; 95% CI 0.91, 1.57) among those with at least one val105 allele (interaction p value = 0.001 and 0.03, respectively). A similar tendency of effect modification between PM(2.5) and O(3) and GSTP1 on wheezing was found., Conclusion: Children who carried Ile105 variant allele and exposed to PM(2.5) and O(3) may be less likely to occurrence of asthma/wheezing.

Background: Few epidemiological studies that have assessed the relation between water disinfection by-products (DBPs) and the risk of stillbirth provide inconsistent results. The objective was to assess the relation between exposure to water disinfection by-products and the risk of stillbirth., Methods: We conducted a population-based case-control study of 3,289 cases of stillbirth and a random sample of 32,890 control subjects from 396,049 Taiwanese newborns in 2001-2003 using information from the Birth Registry and Waterworks Registry in Taiwan. We compared the risk of stillbirth in four disinfection by-product exposure categories based on the levels of total trihalomethanes (TTHMs) representing high (TTHMs 20+ µg/L), medium (TTHMs 10-19 µg/L), low exposure (TTHMs 5-9 µg/L), and 0-4 µg/L as the reference category. In addition, we conducted a meta-analysis of the results from the present and 5 previous studies focusing on stillbirth., Findings: In logistic regression analysis adjusting for gender, maternal age, plurality, conception of season and population density of the municipality where the mother lived during pregnancy, the odds ratio (OR) for stillbirth was 1.10 (95% CI 1.00-1.21) for medium exposure and 1.06 (95% 0.96-1.17) for high exposure compared to reference category. In the meta-analysis, the summary odds ratio for stillbirth (1.11, 95% CI: 1.03, 1.19) was consistently elevated., Conclusions: The present study is consistent with the hypothesis that the risk of stillbirth is related to prenatal exposure to disinfection by-products. This finding on stillbirth is consistent with previous epidemiologic studies, which strengthens the weight of evidence.

Background: Previous studies revealed that reduction of airway caliber in infancy might increase the risks for wheezing and asthma. However, the evidence for the predictive effects of pulmonary function on respiratory health in children was still inconsistent., Methods: We conducted a population-based prospective cohort study among children in 14 Taiwanese communities. There were 3,160 children completed pulmonary function tests in 2007 and follow-up questionnaire in 2009. Poisson regression models were performed to estimate the effect of pulmonary function on the development of bronchitis and asthma., Results: After adjustment for potential confounders, pulmonary function indices consistently showed protective effects on respiratory diseases in children. The incidence rate ratios of bronchitis and asthma were 0.86 (95% CI 0.79-0.95) and 0.91 (95% CI 0.82-0.99) for forced expiratory volume in 1 second (FEV₁). Similar adverse effects of maximal mid-expiratory flow (MMEF) were also observed on bronchitis (RR = 0.73, 95% CI 0.67-0.81) and asthma (RR = 0.85, 95% CI 0.77-0.93). We found significant decreasing trends in categorized FEV₁ (p for trend = 0.02) and categories of MMEF (p for trend = 0.01) for incident bronchitis. Significant modification effects of traffic-related air pollution were noted for FEV₁ and MMEF on bronchitis and also for MMEF on asthma., Conclusions: Children with high pulmonary function would have lower risks on the development of bronchitis and asthma. The protective effect of high pulmonary function would be modified by traffic-related air pollution exposure.

Citrus bacterial canker caused by Xanthomonas axonopodis pv. citri is a devastating disease resulting in significant crop losses in various citrus cultivars worldwide. A biocontrol agent has not been recommended for this disease. To explore the potential of bacilli native to Taiwan to control this disease, Bacillus species with a broad spectrum of antagonistic activity against various phytopathogens were isolated from plant potting mixes, organic compost and the rhizosphere soil. Seven strains TKS1-1, OF3-16, SP4-17, HSP1, WG6-14, TLB7-7, and WP8-12 showing superior antagonistic activity were chosen for biopesticide development. The genetic identity based on 16S rDNA sequences indicated that all seven native strains were close relatives of the B. subtilis group and appeared to be discrete from the B. cereus group. DNA polymorphisms in strains WG6-14, SP4-17, TKS1-1, and WP8-12, as revealed by repetitive sequence-based PCR with the BOXA1R primers were similar to each other, but different from those of the respective Bacillus type strains. However, molecular typing of the strains using either tDNA-intergenic spacer regions or 16S-23S intergenic transcribed spacer regions was unable to differentiate the strains at the species level. Strains TKS1-1 and WG6-14 attenuated symptom development of citrus bacterial canker, which was found to be correlated with a reduction in colonization and biofilm formation by X. axonopodis pv. citri on leaf surfaces. The application of a Bacillus strain TKS1-1 endospore formulation to the leaf surfaces of citrus reduced the incidence of citrus bacterial canker and could prevent development of the disease.

Unlabelled: To assess the independent and joint effects of parental atopy and exposure to molds on the development of asthma in childhood, the authors conducted a cohort-based, incident case-control study in 2008. The case group consisted of 188 children with new asthma, and the control group (n=376) was matched one to two for age and sex. The outcome of interest was the development of asthma during the study period. The studied determinants were parental atopy and three indicators of exposure including histories of water damage, presence of visible molds, and perceived mold odor in the home at baseline in 2002. In conditional logistic regression adjusting for confounding, parental atopy [adjusted odds ratio (aOR) 3.29, 95% CI 2.19-4.94] and the presence of mold odor (aOR 2.09, 95% CI 1.30-3.37) and visible mold (aOR 1.76, 95% CI 1.18-2.62) were independent determinants of incident asthma, and apparent interaction in additive scale was observed. Our finding suggests that the interaction between parental atopy and molds may play a role in the development of asthma in children., Practical Implications: Our study strengthens the evidence for the roles of indoor dampness problem and parental atopy as determinants of asthma in children. Furthermore, the interaction between parental atopy and exposure to molds suggests a role for the development of childhood asthma, i.e., the children whose parents had atopic disease and molds exposure are more susceptible to develop asthma., (© 2011 John Wiley & Sons A/S.)

Background: There is limited evidence suggesting that prenatal exposure to ambient air pollutants may increase the risk of stillbirth, but previous epidemiological studies have not elaborated the most susceptible gestational period for the effects of air pollution exposure on stillbirth., Objectives: We estimated associations between exposure to ambient air pollutants and stillbirth, with special reference to the assessment of gestational periods when the fetus is most susceptible., Methods: We conducted a population-based case-control study in Taiwan. The case group consisted of 9,325 stillbirths, and the control group included 93,250 births randomly selected from 1,510,064 Taiwanese singleton newborns in 2001-2007. Adjusted logistic regression models were used to estimate odds ratios (ORs) per 10-ppb change for ozone and nitrogen dioxide, 1-ppb change for sulfur dioxide (SO2), 10-μg/m3 change for particulate matter with aerodynamic diameter ≤ 10 μm (PM10), and 100-ppb change for carbon monoxide during different gestational periods and according to term or preterm (< 37 weeks) birth status., Results: Stillbirth increased in association with a 1-ppb increase in first-trimester SO2 [adjusted OR = 1.02; 95% confidence interval (CI), 1.00-1.04], particularly among preterm births (adjusted OR = 1.04; 95% CI, 1.01-1.07). Stillbirth was also associated with a 10-μg/m3 increase in PM10 during the first (adjusted OR = 1.02; 95% CI, 1.00-1.05) and second (adjusted OR = 1.02; 95% CI, 1.00-1.04) month of gestation, and, as with SO2, associations appeared to be restricted to preterm births (first-trimester adjusted OR = 1.03; 95% CI, 1.00-1.07)., Conclusion: The study provides evidence that exposure to outdoor air SO2 and PM10 may increase the risk of stillbirth, especially among preterm births, and that the most susceptible time periods for exposure are during the first trimester of gestation.

Background: There were limited studies concerning ambient air pollution exposure on development of bronchitic symptoms among children. These studies provided suggestive but inconclusive results. Therefore, the objective of this study is to assess the association between air pollutants and the prevalence of bronchitic symptoms in the Taiwan Children Health Study., Methods: We conducted a nationwide cross-sectional study of 5,049 Taiwanese children in 2007. Routine air pollution monitoring data were used for sulfur dioxide (SO(2)), nitrogen dioxides (NO(2)), ozone (O(3)), carbon monoxide (CO), and particles with an aerodynamic diameter ≤ 2.5 μm (PM(2.5)). The exposure parameters were calculated using the between-community 3-year average concentration. The effect estimates were presented as odds ratios (ORs) per interquartile changes for SO(2), NO(2), O(3), CO, and PM(2.5)., Results: In the two-stage hierarchical model adjusting for confounding, the prevalence of bronchitic symptoms with asthma was positively associated with the between-community 3-year average concentrations of NO(2) (adjusted OR, 1.81 per 8.79 ppb; 95% CI, 1.14-2.86), and CO (OR, 1.31 per 105 ppb; 95% CI, 1.04-1.64). The prevalence of phlegm with no asthma was related to O(3) (OR, 1.32 per 8.77 ppb; 95% CI, 1.06-1.63)., Conclusions: The results suggest that long-term exposure to outdoor air pollutants, such as NO(2), CO, and O(3), may increase the prevalence of bronchitic symptoms among children.

The authors assessed the relation between exposure to dampness and molds in dwellings and the development of allergic rhinitis in childhood in a 6-year, population-based prospective cohort study of 1,863 children aged 1-7 years at baseline in 1991 (follow-up rate, 77%) from Espoo, Finland. The studied exposures were history of water damage, presence of moisture and visible mold, and perceived mold odor in the home, based on parent-administered questionnaire. A total of 246 (13.2%) children developed physician-diagnosed allergic rhinitis during the study period, resulting in an incidence rate of 440 cases per 10,000 person-years (95% confidence interval (CI): 387, 499). In logistic regression adjusting for confounding, any mold or dampness exposure indicator at baseline (adjusted odds ratio = 1.55, 95% CI: 1.10, 2.18), at follow-up (adjusted odds ratio = 1.62, 95% CI: 1.21, 2.18), or both (adjusted odds ratio = 1.96, 95% CI: 1.29, 2.98) was an important independent determinant of the risk of allergic rhinitis. Of the individual indicators, water damage and moisture on the surfaces were consistent determinants of allergic rhinitis. The results of this cohort study, which assessed exposure before the onset of allergic rhinitis, strengthen considerably the evidence of the role of indoor dampness problems as determinants of allergic rhinitis in children.

Background: Although studies show that maternal smoking during pregnancy increases the risks of respiratory outcomes in childhood, evidence concerning the effects of household environmental tobacco smoke (ETS) exposure remains inconsistent., Methods: We conducted a population-based study comprised of 5,019 seventh and eighth-grade children in 14 Taiwanese communities. Questionnaire responses by parents were used to ascertain children's exposure and disease status. Logistic regression models were fitted to estimate the effects of ETS exposures on the prevalence of asthma, wheeze, and bronchitic symptoms., Results: The lifetime prevalence of wheeze was 11.6% and physician-diagnosed asthma was 7.5% in our population. After adjustment for potential confounders, in utero exposure showed the strongest effect on all respiratory outcomes. Current household ETS exposure was significantly associated with increased prevalence of active asthma, ever wheeze, wheeze with nighttime awakening, and bronchitis. Maternal smoking was associated with the increased prevalence of a wide range of wheeze subcategories, serious asthma, and chronic cough, but paternal smoking had no significant effects. Although maternal smoking alone and paternal smoking alone were not independently associated with respiratory outcomes, joint exposure appeared to increase the effects. Furthermore, joint exposure to parental smoking showed a significant effect on early-onset asthma (OR, 2.01; 95% CI, 1.00-4.02), but did not show a significant effect on late-onset asthma (OR, 1.17; 95% CI, 0.36-3.87)., Conclusion: We concluded that prenatal and household ETS exposure had significant adverse effects on respiratory health in Taiwanese children.

Background/purpose: Congenital anomalies are important medical and public health conditions. However, the occurrence rates of congenital anomalies and their risk factors are unknown in Taiwan. We used the medical-practitioner-reported birth registry in 2002 to determine the occurrence of individual congenital anomalies and their associated risk factors, such as maternal age, fetal sex, and plurality., Methods: The birth registry was started in 2001 in Taiwan. We obtained the data for 2002 from the Department of Health, and translated the coding of congenital anomalies to International Classification of Diseases 9th revision-clinical modification (ICD-9-CM). The occurrence rates of individual congenital anomalies were calculated. The effects of maternal age, fetal sex, and plurality were calculated as odds ratios (ORs) by logistic regression analysis., Results: A total of 1775 infants were diagnosed as having congenital anomalies among 242,140 live and deceased newborn infants delivered in Taiwan in 2002.The occurrence rates of congenital anomalies of the nervous system, eyes and face, cardiovascular, digestive, urogenital, musculoskeletal and respiratory systems, and chromosomes were 0.67 per thousand, 1.86 per thousand, 1.47 per thousand, 0.62 per thousand, 0.71 per thousand, 2.05 per thousand, 0.07 per thousand and 0.79 per thousand, respectively. Sex chromosomal anomalies, Down syndrome, and trisomy 18 were associated with maternal age of > or = 35 years (OR, 15.9, 4.6, and 2.3, respectively). Such elevation was even more prominent for maternal age > or = 40 years (OR, 35.5, 22.2, and 11.62, respectively). A milder and borderline significant maternal age (> or = 40 years) effect was seen with cleft lip, with or without cleft palate (OR, 2.1). Female births had more cleft palates (OR, 1.6). There was no relationship between plurality and anomalies., Conclusion: The occurrence rates for individual congenital anomalies in Taiwan were reported. Older maternal age was a risk factor for the occurrence of chromosomal and orofacial anomalies. More active prenatal screening and further investigation of causal factors of congenital anomalies are of major importance.

Objectives: Independent exposure to noise or organic solvents is reported to be associated with cardiovascular effects, but the effect of joint exposure is unclear. The present study aimed to investigate effects of noise, a mixture of organic solvents (N,N-dimethylformamide (DMF) and toluene) and their interaction on hypertension., Methods: We recruited 59 volunteers working in a synthetic leather manufacturing company during 2005-2006. Both personal noise exposure and airborne co-exposure to DMF and toluene at work were measured and used to calculate the mixed hazard index (HI). Multivariate logistic regressions were conducted to estimate between-group differences of hypertension by controlling for potential confounders., Results: We found that 18 co-exposure workers (82.22 +/- 2.70 dBA and a mixed HI of 0.53 +/- 0.20) had the highest prevalence of hypertension (55.6%) compared to 15 solvent-exposure workers (a mixed HI of 0.32 +/- 0.18; 46.7%), 9 noise-exposure workers (84.13 +/- 2.30 dBA; 44.4%) and 17 low-exposure workers (11.8%). The adjusted odds ratio (OR) of hypertension compared to low-exposure workers increased from 7.9 times (95% confidence interval (CI)=0.9-66.3; p=0.06) in solvent-exposure workers and 9.1 times (OR=9.1, 95% CI=1.0-81.1; p<0.05) in noise-exposure workers to 13.5 times (95% CI=1.5-117.8; p<0.05) in co-exposure workers., Conclusions: Our findings suggest that co-exposure to noise, DMF and toluene is associated with hypertension in synthetic leather workers. Simultaneous exposure to noise and a mixture of organic solvents may have a sub-additive effect on the risk of hypertension.

Background: Air pollution influences the development of oral clefts in animals. There are few epidemiologic data on the relation of prenatal air pollution exposure and the risk of oral clefts., Objectives: Our goal in this study was to assess the relations between exposure to ambient air pollution and the risk of cleft lip with or without cleft palate (CL/P)., Methods: We conducted a population-based case-control study of all 653 cases of CL/P and a random sample of 6,530 control subjects from 721,289 Taiwanese newborns in 2001-2003. We used geographic information systems to form exposure parameters for sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, and particulate matter with an aerodynamic diameter

The standardized International Study of Asthma and Allergies in Childhood (ISAAC) is a valid tool in assessing prevalence of asthma indices. In order to determine the time trends of childhood asthma in Taiwan, we compared data from nationwide ISAAC surveys from a very large sample of Taiwanese 12- to 15-year-old school children, using ISAAC core written and video questionnaires. The number of participants was 44,104 in 1995-96 (phase I) and 11,048 in 2001 (phase III). We found a general tendency towards an increase in lifetime prevalence of physician-diagnosed asthma and asthma symptoms between two surveys, more marked for girls than for boys. Most of the 12-month prevalence of asthma symptoms decreased among boys but stabilized among girls. When comparing different severity levels, we also noted that the decreasing trends of current symptoms were more marked with regard to severe symptoms than mild symptoms in both sexes. A combination of both improved awareness and management of asthma might in part explain this circumstance. Over the past decade in Taiwan, the lifetime prevalence of childhood asthma was increasing, more marked among girls; however, the 12-month prevalence of asthma symptoms was decreasing, mostly among boys. The exact reasons for such trends remain to be explored.

Background: Recent findings suggest that exposure to outdoor air pollutants may increase the risk of allergic rhinitis. The results of these studies are inconsistent, but warrant further attention. The objective of the study was to assess the effect of relation between exposure to urban air pollution and the prevalence allergic rhinitis among school children., Methods: We conducted a nationwide cross-sectional study of 32,143 Taiwanese school children. We obtained routine air-pollution monitoring data for sulphur dioxide (SO2), nitrogen oxides (NOx), ozone (O3), carbon monoxide (CO), and particles with an aerodynamic diameter of 10 microm or less (PM10). A parent-administered questionnaire provided information on individual characteristics and indoor environments (response rate 92%). Municipal-level exposure was calculated using the mean of the 2000 monthly averages. The effect estimates were presented as odds ratios (ORs) per 10 ppb change for SO2, NOx, and O3, 100 ppb change for CO, and 10 microg/m3 change for PM10., Results: In two-stage hierarchical model adjusting for confounding, the prevalence of allergic rhinitis was significantly associated with SO2 (adjusted odds ratio (OR) = 1.43, 95% confidence interval (CI): 1.25, 1.64), CO (aOR = 1.05, 95% CI: 1.04, 1.07), and NOx (aOR = 1.11, 95% CI: 1.08, 1.15). Contrary to our hypothesis, the prevalence of allergic rhinitis was weakly or not related to O3 (aOR = 1.05, 95% CI: 0.98, 1.12) and PM10 (aOR = 1.00, 95% CI: 0.99, 1.02)., Conclusion: Persistent exposure to NOx, CO, and SO2 may increase the prevalence of allergic rhinitis in children.

Background: There is evidence that long term exposure to ambient air pollution increases the risk of childhood asthma, but the role of different sources and components needs further elaboration. To assess the effect of air pollutants on the risk of asthma among school children, a nationwide cross sectional study of 32 672 Taiwanese school children was conducted in 2001., Methods: Routine air pollution monitoring data for sulphur dioxide (SO2), nitrogen oxides (NOx), ozone (O3), carbon monoxide (CO), and particles with an aerodynamic diameter of 10 microm or less (PM10) were used. Information on individual characteristics and indoor environments was from a parent administered questionnaire (response rate 93%). The exposure parameters were calculated using the mean of the 2000 monthly averages. The effect estimates were presented as odds ratios (ORs) per 10 ppb changes for SO2, NOx, and O3, 100 ppb changes for CO, and 10 microg/m3 changes for PM10., Results: In a two stage hierarchical model adjusting for confounding, the risk of childhood asthma was positively associated with O3 (adjusted OR 1.138, 95% confidence interval (CI) 1.001 to 1.293), CO (adjusted OR 1.045, 95% CI 1.017 to 1.074), and NOx (adjusted OR 1.005, 95% CI 0.954 to 1.117). Against our prior hypothesis, the risk of childhood asthma was weakly or not related to SO2 (adjusted OR 0.874, 95% CI 0.729 to 1.054) and PM10 (adjusted OR 0.934, 95% CI 0.909 to 0.960)., Conclusions: The results are consistent with the hypothesis that long term exposure to traffic related outdoor air pollutants such as NOx, CO, and O3 increases the risk of asthma in children.

Previous studies of how parental atopy and exposure to dampness and molds contribute to the risk of asthma have been mainly cross-sectional or prevalent case-control studies, where selection and information bias and temporality constitute problems. We assessed longitudinally the independent and joint effects of parental atopy and exposure to molds in dwellings on the development of asthma in childhood. We conducted a population-based, 6-year prospective cohort study of 1,984 children 1-7 years of age at the baseline in 1991 (follow-up rate, 77%). The study population included 1,916 children without asthma at baseline and complete outcome information. The data collection included a baseline and follow-up survey. The outcome of interest was development of asthma during the study period. The studied determinants were parental allergic diseases and four indicators of exposure at baseline: histories of water damage, presence of moisture and visible molds, and perceived mold odor in the home. A total of 138 (7.2%) children developed asthma during the study period, resulting in an incidence rate of 125 cases per 10,000 person-years [95% confidence interval (CI), 104-146]. In Poisson regression adjusting for confounding, parental atopy [adjusted incidence rate ratio (IRR) 1.52; 95% CI, 1.08-2.13] and the presence of mold odor in the home reported at baseline (adjusted IRR 2.44; 95% CI, 1.07-5.60) were independent determinants of asthma incidence, but no apparent interaction was observed. The results of this cohort study with assessment of exposure before the onset of asthma strengthen the evidence on the independent effects of parental atopy and exposure to molds on the development of asthma.

This study compared the prevalence of asthma among Taiwanese adolescents with individual-level risk factors and municipal-level air pollution and meteorology data to determine whether changes in these factors could explain the observed change in prevalence. We conducted two national surveys of respiratory illness and symptoms in Taiwanese middle-school students in 1995-96 and 2001. The effects of personal and environmental factors were assessed and temporal changes of outdoor monitoring data were also compared with asthma prevalence difference. A total of 44,104 children from the 1995-96 survey and 11,048 children from the 2001 survey attended schools located within 1 km of 22 monitoring stations. Lifetime prevalences of physician-diagnosed and questionnaire-determined asthma increased during this period. After adjustment for potential risk factors, the prevalence differences were statistically unchanged. Although parental education level contributed most, changes in investigated personal and environmental factors might not explain the observed changes in asthma prevalence. Municipalities with higher temperature increase were significantly associated with prevalence difference in questionnaire-determined asthma. We concluded that correlates of the investigated individual-level factors, which have changed over time, still underlie changes in asthma prevalence. Increasing temperature might be the main reason for the rising trends of asthma in Taiwanese adolescents., (Copyright (c) 2005 Blackwell Munksgaard)

Objective: Parental atopy and environmental exposures are recognized risk factors for childhood asthma. However, the relative contributions of specific risk factors and the overall contributions of indoor and outdoor exposures remain unexplored. This study was undertaken to identify risk factors, estimate the population attributable risk of each exposure, and compare the data for boys versus girls for physician-diagnosed asthma in Taiwanese schoolchildren., Methods: During a February to June 2001 cross-sectional national survey, 35 036 6- to 15-year-old schoolchildren were chosen from 22 elementary and 22 middle schools located within 1-km catchment areas of 22 air-monitoring stations in Taiwan. The main outcome measure was physician-diagnosed asthma, as reported by the parents. We investigated hereditary and indoor and outdoor environmental factors for childhood asthma by questionnaire. The adjusted prevalences of questionnaire-determined outdoor indicators were also compared with air-monitoring data., Results: Outdoor air pollutants were associated with parent-reported perceived ambient air pollution. Physician-diagnosed asthma was reported for 8.1% of the boys (1330 of 16 441) and 5.6% of the girls (894 of 16 056). The risk of physician-diagnosed asthma was significantly associated with parental atopy and perceived ambient air pollution in both sexes. The presence of visible cockroaches (odds ratio [OR]: 1.30; 95% confidence interval [CI]: 1.07-1.59), mold on walls at home (OR: 1.20; 95% CI: 1.01-1.41), and water damage (OR: 1.33; 95% CI: 1.02-1.70) were also associated with asthma in girls; however, only visible mold on walls at home was related to asthma in boys. Mutually adjusted analytical models produced statistically significant associations between any indoor factor and asthma in girls (OR: 1.24; 95% CI: 1.00-1.56) but not in boys (OR: 1.04; 95% CI: 0.87-1.25). For all hereditary and environmental factors, the total population attributable risk was 44.31% in boys and 60.61% in girls., Conclusions: Parental atopy contributed more to childhood asthma than indoor or outdoor environmental factors. Girls may be more susceptible to indoor factors than boys.

The authors used the Medline data retrieval system for 1966-2001 to identify and synthesize the epidemiological evidence for adverse effects of prenatal exposure to chlorination byproducts on birth defects. For 5 studies that provided estimates of the effect of exposure on 1 or several birth defects, the authors calculated summary odds ratios and 95% confidence intervals using the Mantel-Haenszel method for a fixed-effects model, and the DerSimonian-Laird method for a random-effects model. The results of this meta-analysis provide evidence for an effect of exposure to chlorination byproducts on the risk of any birth defect, and of neural tube and urinary system defects. The results for respiratory system, major cardiac, and oral cleft defects were heterogeneous and inconclusive. Differences in the susceptibility of populations, and different approaches in exposure assessment, may explain the heterogeneity of the results.

To assess the effect of water chlorination by-products on specific birth defects, the authors conducted a nationwide cross-sectional study of 285,631 Norwegian births in 1993-1998. Risks of birth defects according to four chlorination by-product exposure categories were compared on the basis of chlorination (yes/no) and level of water color (mg Pt/liter), representing the amount of natural organic matter: high (chlorination, < or =20), medium (chlorination, 10-19.9), and low (chlorination, <10) exposure, with no chlorination and low color (<10) as the reference category. In logistic regression analysis, the risks of any birth defect (adjusted odds ratio (OR) = 1.13, 95% confidence interval (CI): 1.01, 1.25) and of cardiac (adjusted OR = 1.37, 95% CI: 1.00, 1.89), respiratory system (adjusted OR = 1.89, 95% CI: 1.00, 3.58), and urinary tract (adjusted OR = 1.46, 95% CI: 1.00, 2.13) defects were significantly associated with exposure (medium and high combined). Regarding risk of specific birth defects, only that for ventricular septal defects was significantly elevated, with an exposure-response pattern, yielding adjusted odds ratios of 1.63 (95% CI: 1.02, 2.58) for the medium and 1.81 (95% CI: 1.05, 3.09) for the high exposure categories. Furthermore, risk of neural tube defects was related to high color (adjusted OR = 2.60, 95% CI: 1.30, 5.26).

Objective: To assess the effect of exposure to chlorination byproducts during pregnancy on foetal growth and duration of pregnancy., Methods: A population based study was conducted of 137,145 Norwegian children born alive in 1993--5. Information was obtained from the Norwegian medical birth registry, waterwork registry, and social science data service. The outcomes of interest were birth weight, low birth weight (<2500 g), small for gestational age, and preterm delivery (gestational age <37 weeks). The exposure assessment was based on quality of drinking water in the municipality where the mother lived during pregnancy. Municipal exposure was calculated with information on chlorination and the amount of natural organic matter in raw water measured as colour in mg precipitate/l. The main exposure category was high colour and chlorination, which was contrasted with the reference category of low colour and no chlorination., Results: In logistic regression analysis adjusting for confounding, the risks of low birth weight (odds ratio (OR) 0.97, 95% confidence interval (95% CI) 0.89 to 1.06) and small for gestational age (OR 1.00, 95% CI 0.91 to 1.10) were not related to exposure. Contrary to the hypothesis, the risk of preterm delivery was slightly lower among the exposed than the reference category (OR 0.91, 95% CI 0.84 to 0.99). The risks of the studied outcomes were similar in newborn infants exposed to high colour drinking water without chlorination and chlorinated drinking water with low colour compared with the reference category., Conclusions: The present study did not provide evidence that prenatal exposure to chlorination byproducts at the relatively low concentrations encountered in Norwegian drinking water increases the risk of the studied outcomes.