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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 PM 2.5 and 8-hourly ozone (O 3 ) 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 PM 2.5 and O 3 . Results In a multiple linear mixed effect model, adjusted for confounding, growth deficits in the forced vital capacity (FVC), forced expiration volume in 1 s (FEV 1 ), and forced expiratory flow between the 25th and 75th percentiles of the FVC were associated with increased exposure to PM 2.5 and O 3 . For example, greater exposure to PM 2.5 (IQR, 17.92 μg/m 3 ) was associated with an annual deficit in FVC growth of 75 mL in boys and 61 mL in girls ( p for interaction 3 . Conclusions The study provides evidence that long-term exposure to PM 2.5 and O 3 may have a detrimental effect on the development of lung function in children. The estimated deficits were generally larger in boys, compared to girls.

Studies have reported an association between serum perfluoroalkyl substances (PFASs) and asthma. However, few studies have examined the possible associations between PFASs and the 16-kDa club cell secretory protein (Clara) (CC16) level, a prominent biomarker of asthma, among adolescents.We recruited a total of 231 asthmatic children and 225 non-asthmatic controls in the Genetic and Biomarkers study for Childhood Asthma (GBCA) in northern Taiwan from 2009 to 2010. Structured questionnaires were administered by face-to-face interview. Urine CC16 was determined by an enzyme-link immunoassay kit. Multiple general linear models were employed to examine the associations between PFASs and urinary CC16 levels.Asthmatic participants had significantly higher serum PFAS concentrations overall than the healthy controls. After adjusting for confounding factors, urinary CC16 was significantly, negatively associated with PFASs, especially PFOS, PFOA, PFDA and PFNA, and especially among males, as follows: PFOS (β = -0.003, 95% confidence interval [CI]: -0.004, -0.002), PFOA (β = -0.045, 95% CI: -0.086, -0.004), and PFHxA (β = -0.310, 95% CI: -0.455, -0.165) among asthmatic boys, and PFDA (β = -0.126, 95%CI: -0.241, -0.012) and PFNA (β = -0.329, 95% CI: -0.526, -0.132) among non-asthmatic boys. Among girls, PFDA (β = -0.088, 95% CI: -0.172, -0.004), was the only PFAS significantly associated with CC16. Significant interaction effects (p0.15) on CC16 levels were found between asthma and PFOS, PFOA, PFBS and PFHxA in all participants.Our overall results showed that serum PFASs were significantly, inversely associated with CC16 levels. Associations were stronger among males.

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/m3 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.

Introduction Environmental tobacco smoke (ETS) is a hazardous component of indoor air, and may increase the risk of respiratory diseases, atherosclerosis and otitis media in children. In this study, we explored the relationship between time inside the house, ETS exposure and urinary cotinine level, and also determined the association of time inside the house on asthma phenotypes when children exposed to ETS. Methods A total of 222 asthmatic children and 205 non-asthmatic controls were recruited in the Genetic and Biomarker study for Childhood Asthma (GBCA). Structured questionnaires and time–location pattern questionnaires were administered by face-to-face interview. Urinary cotinine was measured by liquid chromatography tandem mass spectrometry (LC/MS/MS). The level of household ETS exposure was assessed using the cotinine/creatinine ratio (CCR). Results In general, urinary cotinine and CCR were higher in subjects exposed to household ETS than those who never had ETS at home. A significant positive relationship was found between average time inside the house and urinary CCR in asthmatic children with current ETS at home (β=0.278, p=0.02). After adjustment for age and gender, average time inside the house was positively related to severe wheeze in asthmatic children with household ETS within 1 month (OR: 1.26, 95%: 1.02–1.64). Conclusions Our study suggests that the major source of ETS exposure for children is due to longer period of exposures among children living with adult smokers at home. Home-smoking restrictions that effectively prevent children from being exposed to ETS would be worthwhile.

Previous studies have demonstrated associations between serum levels of perfluoroalkyl substances (PFASs) and asthma or asthma related-biomarkers. However, no studies have reported a possible relationship between PFASs exposure and lung function among children. The objective of the present study is to test the association between PFASs exposure and lung function in children from a high exposure area by using a cross-sectional case-control study, which included 132 asthmatic children and 168 non-asthmatic controls recruited from 2009 to 2010 in the Genetic and Biomarkers study for Childhood Asthma. Structured questionnaires were administered face-to-face. Lung function was measured by spirometry. Linear regression models were used to examine the influence of PFASs on lung function. The results showed that asthmatics in our study had significantly higher serum PFAS concentrations than healthy controls. Logistic regression models showed a positive association between PFASs and asthma, with adjusted odds ratios (ORs) ranging from 0.99 (95% confidence interval [CI]: 0.80-1.21) to 2.76 (95% CI: 1.82-4.17). Linear regression modeling showed serum PFASs levels were significantly negatively associated with three pulmonary function measurements (forced vital capacity: FVC; forced expiratory volume in 1s: FEV1; forced expiratory flow 25-75%: FEF25-75) among children with asthma, the adjusted coefficients between lung function and PFASs exposure ranged from -0.055 (95%CI: -0.100 to -0.010) for FVC and perfluorooctane sulfonate (PFOS) to -0.223 (95%CI: -0.400 to -0.045) for FEF25-75 and perfluorooctanoic acid (PFOA). PFASs were not, however, significantly associated with pulmonary function among children without asthma. In conclusion, this study suggests that serum PFASs are associated with decreased lung function among children with asthma.

Background Dampness in the home is a strong risk factor for respiratory symptoms and constitutes a significant public health issue in subtropical areas. However, little is known about the effects of dampness and genetic polymorphisms on asthma. Methods In 2007, 6078 schoolchildren were evaluated using a standard questionnaire with regard to information about respiratory symptoms and environmental exposure. Multiple logistic regression analyses were performed to assess the effects of home dampness and beta-2-adrenergic receptor (ADRB2) gene polymorphisms on the prevalence of asthma and selected indicators of severity of asthma. Results The frequency of mildewy odor, the number of walls with water stamp, and the duration of water damage were all associated with being awakened at night due to wheezing. However, no other clear-cut associations were found for any of the other indicators of asthma. Children exposed to mildewy odor with ADRB2 Arg/Arg genotype were associated with being awakened at night due to wheezing (OR=1.95, 95% CI, 1.14–3.36), compared to those without exposure and with the ADRB2 Gly allele. ADRB2 Arg16Gly showed a significant interactive effect with home dampness on being awakened at night due to wheezing and current wheezing, but no significant effect on active asthma and medication use. Frequency and degree of home dampness were also associated with the prevalence of asthma and selected indicators of severity of asthma, in an exposure–response manner among children with ADRB2 Arg/Arg genotype. Conclusions Home dampness prevention is one of the important steps of asthma control, especially in children carrying ADRB2 Arg/Arg genotypes.