Ying-Chu Lin

Glutathione S‐transferase P1 gene polymorphism and air pollution as interactive risk factors for childhood asthma

Background Polymorphisms at the glutathione S‐transferase (GST) P1 locus were associated with asthma‐related phenotypes and bronchial hyper‐responsiveness.

Traffic related air pollution as a determinant of asthma among Taiwanese school 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 μm 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 μg/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.

Relation between air pollution and allergic rhinitis in Taiwanese schoolchildren

BackgroundRecent 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.MethodsWe 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.ResultsIn 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).ConclusionPersistent exposure to NOx, CO, and SO2 may increase the prevalence of allergic rhinitis in children.

Are maternal psychosocial factors associated with cord immunoglobulin E in addition to family atopic history and mother immunoglobulin E

Background Atopy in maternal and family histories is known to be a risk factor for elevated umbilical cord immunoglobulin E (cIgE). However, the association between cIgE and psychosocial factors remains under investigation.

Measurement of pulmonary status and surfactant protein levels during dexamethasone treatment of neonatal respiratory distress syndrome.

BACKGROUND: Early postnatal use of dexamethasone in infants with respiratory distress syndrome (RDS) has been shown effectively to improve pulmonary status and to allow early weaning off mechanical ventilation. However, the mechanisms to explain the beneficial effects of dexamethasone in ventilatory dependent preterm infants remain unclear. METHODS: A double blind, placebo controlled study was performed to determine the change in pulmonary ventilation of premature infants with RDS as a result of dexamethasone treatment, and to evaluate the effect of dexamethasone on the levels of surfactant-associated proteins A (SP-A) and D (SP-D) in the tracheal fluid from 34 premature infants with RDS and 29 control subjects. RESULTS: Dexamethasone treatment decreased fractional inspired oxygen concentration (FIO2), arterial carbon dioxide tension (PCO2), mean airway pressure (MAP), and facilitated successful weaning from mechanical ventilation. SP-A concentrations in the tracheal aspirates were increased at days 7 and 14, and SP-D concentrations were increased during the period from days 3 to 14 in the dexamethasone treated group compared with the control group. However, albumin levels in the tracheal aspirate samples were decreased after dexamethasone treatment over the period from days 3 to 14. There was an inverse correlation between PCO2 values and SP-A concentrations. CONCLUSIONS: These results suggest that early use of dexamethasone can improve pulmonary status and also increase SP-A and SP-D levels in the tracheal fluid in premature infants with RDS.

Time trend of asthma prevalence among school children in Taiwan: ISAAC phase I and III surveys

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.

Changing prevalence of asthma in Taiwanese adolescents: two surveys 6 years apart

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.

The association between tumor necrosis factor, HLA-DR alleles, and IgE-mediated asthma in Taiwanese adolescents

Background: Human leukocyte antigen (HLA) DR genes and the tumor necrosis factor (TNF) gene locus are associated with asthma and IgE production. TNFα‐308G/A frequencies between Japanese and Caucasians in the UK have been found to be different. The roles of HLA‐DRB1 and TNF genotypes are unknown in Taiwanese adolescents with IgE‐mediated asthma (I‐asthma).

Association between cord blood IgE and genetic polymorphisms of interleukin-4, the β-subunit of the high-affinity receptor for IgE, lymphotoxin-α, and tumor Necrosis factor-α

High cord blood immunoglobulin E (cbIgE) is known to be associated with increased risks of atopic diseases in childhood. The relationship between genetic polymorphisms and high cbIgE has not been well documented. A cross‐sectional study was conducted to assess the association between cbIgE and genetic polymorphisms of interleukin (IL)‐4 ‐590C/T, the β‐subunit of the high‐affinity receptor for IgE (FcɛRI‐β) E237G, lymphotoxin (LT)‐αNcoI alleles, and tumor necrosis factor (TNF)‐α ‐308G/A. A total of 320 mother–neonate pairs were recruited from four maternity hospitals from different locations of Taiwan. Cord blood was obtained and assayed for cbIgE. Polymerase chain reaction followed by restriction fragment length polymorphism was used to assess the genotypes. Three hundred pairs of mothers and neonates were included in the final analysis. Infants with IL‐4 ‐590 C allele were found to have higher risk of elevated cbIgE (≥0.35 IU/ml, 24.3%) (p = 0.004). After adjusting for gender, birth order, maternal age, and history of allergic disease in maternal and paternal families, odds ratios for CC and CT genotypes were 4.41 and 3.16 (95% confidence interval 0.78–22.67, and 1.66–6.13), respectively, using TT genotype as reference. The genotypes of FcɛRI‐β, LT‐α, and TNF‐α were not associated with cbIgE before or after the adjustment. Our finding suggested a significant association of cbIgE with genetic polymorphism of IL‐4 ‐590C/T, but not with the genotypes of FcɛRI‐β, LT‐α, and TNF‐α.

Roles of genotypes of β2-adrenergic receptor in the relationship between eosinophil counts and lung function in Taiwanese adolescents

To examine the roles of genetic polymorphism of the β2-adrenergic receptor (β2AR) in the relationship between eosinophil (EOS) counts and eosinophil cationic protein (ECP) counts and lung function, we recruited a random sample from the 1996 nationwide survey of asthma prevalence in middle school children. A total of 149 subjects—42 asthmatic children, 38 asthmatics in remission (no reported attack for more than 12 months), and 69 nonasthmatics—completed a physical evaluation, pulmonary function test, and determination of EOS, ECP, and β2AR genotypes at amino acids 16 and 27. Asthmatic children had higher EOS and ECP than did nonasthmatics. No association was found between asthma and β2AR genotypes. Lung function was significantly and inversely correlated with EOS but not with ECP in asthmatic children. By genotype, an inverse correlation between lung function and EOS was found in asthmatic children with Arg16Arg or Gln27Glu. A nonsignificant but similar inverse correlation was found in asthmatic children with Arg16Gly or Gln27Gln. However, a nonsignificant but positive correlation was found in asthmatic children with Gly16Gly. In conclusion, we suggest that EOS is a better clinical indicator of airway inflammation than ECP when children are not having an asthma attack. The association between an increase of EOS and lower lung function can be differentiated by β2AR genotypes at amino acid 16.