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1.  Air Pollution and Newly Diagnostic Autism Spectrum Disorders: A Population-Based Cohort Study in Taiwan 
PLoS ONE  2013;8(9):e75510.
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 10 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.
doi:10.1371/journal.pone.0075510
PMCID: PMC3783370  PMID: 24086549
2.  Fine Particle, Ozone Exposure, and Asthma/Wheezing: Effect Modification by Glutathione S-transferase P1 Polymorphisms 
PLoS ONE  2013;8(1):e52715.
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 (O3) and particles with an aerodynamic diameter of 2.5 µm or less (PM2.5). The effect estimates were presented as odds ratios (ORs) per interquartile changes for PM2.5 and O3.
Findings
In a two-stage hierarchical model adjusting for confounding, the risk of asthma was negatively associated with PM2.5 (adjusted odds ratio (OR) 0.60; 95% confidence interval (CI) 0.45, 0.82) and O3 (OR 0.74; 95% CI 0.60, 0.90) among Ile105 homozygotes, but positively associated with PM2.5 (OR 1.52; 95% CI 1.01, 2.27) and O3 (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 PM2.5 and O3 and GSTP1 on wheezing was found.
Conclusion
Children who carried Ile105 variant allele and exposed to PM2.5 and O3 may be less likely to occurrence of asthma/wheezing.
doi:10.1371/journal.pone.0052715
PMCID: PMC3554722  PMID: 23357926
3.  DNA Polymorphisms and Biocontrol of Bacillus Antagonistic to Citrus Bacterial Canker with Indication of the Interference of Phyllosphere Biofilms 
PLoS ONE  2012;7(7):e42124.
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.
doi:10.1371/journal.pone.0042124
PMCID: PMC3407170  PMID: 22848728
4.  Risk of Stillbirth in the Relation to Water Disinfection By-Products: A Population-Based Case-Control Study in Taiwan 
PLoS ONE  2012;7(3):e33949.
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.
doi:10.1371/journal.pone.0033949
PMCID: PMC3311556  PMID: 22457804
5.  Pulmonary Function and Incident Bronchitis and Asthma in Children: A Community-Based Prospective Cohort Study 
PLoS ONE  2012;7(3):e32477.
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.
doi:10.1371/journal.pone.0032477
PMCID: PMC3311633  PMID: 22457716
7.  Air Pollution and Stillbirth: A Population-Based Case–Control Study in Taiwan 
Environmental Health Perspectives  2011;119(9):1345-1349.
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.
doi:10.1289/ehp.1003056
PMCID: PMC3230395  PMID: 21447454
air pollution; particle; stillbirth; sulfur dioxide
8.  Household environmental tobacco smoke and risks of asthma, wheeze and bronchitic symptoms among children in Taiwan 
Respiratory Research  2010;11(1):11.
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.
doi:10.1186/1465-9921-11-11
PMCID: PMC2828425  PMID: 20113468
9.  Ozone and Other Air Pollutants and the Risk of Oral Clefts 
Environmental Health Perspectives  2008;116(10):1411-1415.
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 ≤ 10 μm (PM10) during the first 3 months of pregnancy using inverse distance weighting method. We present the effect estimates as odds ratios (ORs) per 10-ppb change for SO2, NOx, and O3, 100-ppb change for CO, and 10-μg/m3 change for PM10.
Results
The risk of CL/P was increased in relation to O3 levels in the first gestational month [adjusted OR = 1.20; 95% confidence interval (CI), 1.02–1.39] and second gestational month (adjusted OR = 1.25; 95% CI, 1.03–1.52) in the range from 16.7 ppb to 45.1 ppb, but was not related to CO, NOx, SO2, or PM10.
Conclusions
The study provides new evidence that exposure to outdoor air O3 during the first and second month of pregnancy may increase the risk of CL/P. Similar levels of O3 are encountered globally by large numbers of pregnant women.
doi:10.1289/ehp.11311
PMCID: PMC2569104  PMID: 18941587
air pollution; cleft lip; ozone; traffic
10.  Water disinfection by-products and the risk of specific birth defects: a population-based cross-sectional study in Taiwan 
Environmental Health  2008;7:23.
Background
Recent findings suggest that exposure to disinfection by-products may increase the risk of birth defects. Previous studies have focused mainly on birth defects in general or groups of defects. The objective of the present study was to assess the effect of water disinfection by-products on the risk of most common specific birth defects.
Methods
We conducted a population-based cross-sectional study of 396,049 Taiwanese births in 2001–2003 using information from the Birth Registry and Waterworks Registry. We compared the risk of eleven most common specific defects 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 previous studies focusing on the same birth defects.
Results
In multivariate logistic regression analysis the risk of ventricular septal defects (adjusted odds ratio 1.81, 95% confidence interval: 0.98 3.35), cleft palate (1.56. 95% CI: 1.00, 2.41), and anencephalus (1.96, 95% CI: 0.94, 4.07) were elevated in the high exposure compared to the reference category. In the meta-analysis, the summary odds ratio for ventricular septal defects (1.59, 95% CI: 1.21, 2.07) was consistently elevated.
Conclusion
The present study suggests that prenatal exposure to disinfection by-products increases the risk of ventricular septal defects, cleft palate, and anencephalus. The evidence on ventricular septal defects is consistent in the three available studies.
doi:10.1186/1476-069X-7-23
PMCID: PMC2467412  PMID: 18518952
11.  Relation between air pollution and allergic rhinitis in Taiwanese schoolchildren 
Respiratory Research  2006;7(1):23.
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 μm 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 μg/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.
doi:10.1186/1465-9921-7-23
PMCID: PMC1420289  PMID: 16469096
12.  Home Dampness and Molds, Parental Atopy, and Asthma in Childhood: A Six-Year Population-Based Cohort Study 
Environmental Health Perspectives  2004;113(3):357-361.
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.
doi:10.1289/ehp.7242
PMCID: PMC1253765  PMID: 15743728
asthma; damp housing; effect modification; interaction; molds

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