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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.

Previous studies have shown that phthalate exposure in childhood is associated with the development of respiratory problems. However, few studies have assessed the relative impact of prenatal and postnatal exposure to phthalates on the development of asthma later in childhood. Therefore, we assessed the impact of prenatal and postnatal phthalate exposure on the development of asthma and wheezing using a Taiwanese birth cohort. A total of 430 pregnant women were recruited, and 171 (39.8%) of them had their children followed when they were aged 2, 5, and 8 years. The International Study of Asthma and Allergies in Childhood questionnaire was used to assess asthma and wheezing symptoms and serum total immunoglobulin E levels were measured at 8 years of age. Urine samples were obtained from 136 women during their third trimester of pregnancy, 99 children at 2 years of age, and 110 children at 5 years. Four common phthalate monoester metabolites in maternal and children's urine were measured using liquid chromatography-electrospray ionization-tandem mass spectrometry. Maternal urinary mono-benzyl phthalate [MBzP] concentrations were associated with an increased occurrence of wheezing in boys at 8 years of age (odds ratio [OR] = 4.95 (95% CI 1.08-22.63)), for upper quintile compared to the others) after controlling for parental allergies and family members' smoking status. Urinary mono-2-ethylhexyl phthalate [MEHP] levels over the quintile at 2-year-old were associated with increased asthma occurrence (adjusted OR = 6.14 (1.17-32.13)) in boys. Similarly, the sum of di-2-ethyl-hexyl phthalate [DEHP] metabolites at 5 years was associated with asthma in boys (adjusted OR = 4.36 (1.01-18.86)). Urinary MEHP in maternal and 5-year-old children urine were significantly associated with increased IgE in allergic children at 8 years. Prenatal and postnatal exposure to phthalate was associated with the occurrence of asthma in children, particularly for boys.

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: There is accumulating epidemiologic evidence that exposure to traffic-related air pollutants, including particulate matter (PM) and polyaromatic hydro carbons (PAHs), plays a role in etiology and prognosis of a large scale of illnesses, although the role of specific causal agents and underlying mechanisms for different health outcomes remains unknown., Objective: Our general objective was to assess the relations between personal exposure to traffic exhausts, in particular ambient PM(2.5) and PAHs, and the occurrence of DNA strand breaks by applying personal monitoring of PM and biomarkers of exposure (urinary 1-hydroxypyrene-glucuronide, 1-OHPG) and effect (urinary 8-hydroxydeoxyguanosine, 8-OHdG and DNA strand breaks)., Methods: We recruited 91 traffic conductors and 53 indoor office workers between May 2009 and June 2011 in Taipei City, Taiwan. We used PM(2.5) personal samplers to collect breathing-zone particulate PAHs samples. Spot urine and blood samples after work shift of 2 consecutive days were analyzed for 1-OHPG, 8-OHdG and DNA strand breaks, respectively. Statistical methods included linear regression and mixed models., Results: Urinary 8-OHdG levels and the occurrence of DNA strand breaks in traffic conductors significantly exceeded those in indoor office workers in mixed models. Particulate PAHs levels showed a positive association with urinary 1-OHPG in the regression model (β = 0.056, p = 0.01). Urinary 1-OHPG levels were significantly associated with urinary 8-OHdG levels in the mixed model (β = 0.101, p = 0.023). Our results provide evidence that exposure to fine particulates causes DNA damage. Further, particulate PAHs could be biologically active constituents of PM(2.5) with reference to the induction of oxidative DNA damages.

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: 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 carbon composition of fine particles (PM(2.5)) from traffic exhausts may play a role in adverse health effects. The objective of this study was to assess the concentrations of elemental and organic carbon in PM(2.5) in traffic exhausts from different types of vehicles in the booths of Taiwanese toll station workers and estimate the relations between traffic density and carbon concentrations. Tollbooth indoor monitoring samples were collected for 10 days to assess the 8 h integrated PM(2.5) concentration. Particle samples were analyzed for the content of total carbon, and elemental, and organic carbon. The mean carbon concentrations in the bus and truck lanes were [total: 167.7 microg/m(3) (SD 79.8 microg/m(3)); elemental: 131.7 (66.2); organic: 36.0 (25.8)], substantially higher compared with the car lanes with cash payment [39.2 (29.5); 20.2 (19.5); 19.2 (14.6)] and the car lanes with ticket payment [34.1 (26.1); 15.8 (17.6); 18.5 (12.2)]. The increase in elemental carbon concentration per vehicle in the bus and truck lane was 14 and 9 times greater than that of car lanes of ticket payment and car lanes of cash payment. The mass fraction of carbonaceous species in PM(2.5) accounted for 54% in bus and truck lanes, whereas the corresponding figure was 30-31% for car lanes. Elemental carbon is an important component of diesel exhaust. Workers in toll stations are exposed to high levels of both elemental and organic carbon.

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+ microg/L), medium (TTHMs 10-19 microg/L), low exposure (TTHMs 5-9 microg/L), and 0-4 microg/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.

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.

In this study, the authors assessed occupational exposure to PM2.5 among 47 highway toll station workers in Taipei, Taiwan. The subjects were monitored for 10 days to assess integrated 8-hr fine particulate matter (PM2.5) breathing zone concentration. Researchers constructed a microenvironment-time-concentration matrix and applied direct and indirect approaches to assess cumulative exposure. Mean PM2.5 concentration for workers in the truck and bus lanes was 308 microg/m3 (SD = 115.5 microg/m3), substantially higher compared with cash-payment car lanes (mean 115, SD = 41.8, p < 0.001) and ticket-payment car lanes (mean 109, SD = 48.7, p < 0.001). Concentration per vehicle in the truck and bus lanes was 6.4 and 3.7 times higher, respectively, than that of ticket- or cash-payment car lanes. Mean cumulative exposure for the 10-day period was 4,900-13,407 microg/m3.hr, with a mean of 8,019 microg/m3.hr (SD = 2,375.3). Indirect and direct concentrations were strongly correlated (r2 = .61, F(1,125); p = 0.000). The results of this study show that personal exposure to PM2.5 can be reliably estimated using indirect approaches.

In this cross-sectional study, the authors evaluated urinary 1-hydroxypyrene-glucuronide (1-OHP-gluc) as a potential biomarker of exposure to various traffic exhausts. Subjects were 47 female highway toll-station workers and 27 female office workers in training for toll-station employment in Taipei, Taiwan. The mean concentration of urinary 1 -OHP-gluc was 0.117 micromol/mol creatinine in the exposed group and 0.073 micromol/mol creatinine in the reference group (difference in mean concentrations: 0.044 micromol/mol creatinine [95% confidence interval [CI]: 0.015, 0.072). In the lanes where tolls were collected from passenger cars, there was a significant relationship between cumulative traffic and 1-OHP-gluc concentration (i.e., average increase of 0.015 micromol/mol creatinine [95% CI: 0.003, 0.027] per 1,000 vehicles). The average increase for truck/bus lanes was similar to that identified for the car lanes (i.e., average increase of 0.011 micromol/mol creatinine [95% Cl: -0.024, 0.045] per 1,000 vehicles). The authors determined that exposure to various traffic exhausts increased the urinary concentration of 1-OHP-gluc in a dose-response pattern, which suggests that this chemical may be a useful biomarker for exposure to vehicle exhausts.