GSTP1 is a hub gene for gene-air pollution interactions on childhood asthma.

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.

Molds, parental atopy and pediatric incident asthma.

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.

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 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.

Foetal growth and duration of gestation relative to water chlorination.

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.

Chronic low-dose gamma-radiation exposure and the alteration of the distribution of lymphocyte subpopulations in residents of radioactive buildings.

PURPOSE: To elucidate the immunological change incurred in a human population by protracted gamma-radiation exposure at home environment. MATERIALS AND METHODS: An examination on the CD3+, CD4+, CD8+ and HLA-DR+ lymphocyte subsets was arranged for 196 exposed subjects with mean excess cumulative dose of 169 mSv during 2-13 years of exposure. Another 55 close relatives of the exposed subjects were recruited as the non-exposed reference population. RESULTS: The mean percentages of CD4+ T-lymphocytes, HLA-DR+ lymphocytes and the CD4+ /CD8+ ratios in the exposed subjects (35.5, 19.9 and 1.51 respectively) were significantly lower than those of reference individuals (38.0, 22.6 and 1.72; p= 0.02, 0.003, and 0.03 respectively), while the CD8+ in total counts of the exposed was moderately increased above that of the reference populations (p=0.1). By ANOVA analysis, the percentages of CD4+ and HLA-DR+ subsets were significantly associated with radiation dose (p=0.0046, 0.003), while CD4+/CD8+ ratios were moderately associated with dose (p=0.073). HLA-DR+ counts were significantly and positively associated with duration of relocation from radioactive apartments (p = 0.029). CONCLUSIONS: Significant immunological effects were observed in those who had received chronic low-dose radiation exposure.

Change in centromeric and acentromeric micronucleus frequencies in human populations after chronic radiation exposure.

Acute radiation exposure of humans was observed to induce various forms of cytogenetic damage, including increased frequencies of micronuclei and chromosomal aberrations. However, the cytogenetic effects of chronic low dose radiation exposure in vivo needs further characterization. Sixteen subjects with chronic low dose rates of gamma-radiation exposure from 60Co-contaminated steel in radioactive buildings were compared with seven non-exposed reference subjects for micronucleus frequencies after they relocated. By in situ hybridization using a digoxigenin-labeled anti-alpha all human centromere probe, the exposed subjects were shown to have a significant increase in cytochalasin B-modulated micronucleus (CBMN) frequencies, as well as a significant increase in centromere-positive (C+) CBMN, centromere-negative (C-) CBMN, total C+signals, single C+ MN signals and multiple C+ signals/1000 binucleated cells (BN). However, decreases in the ratios C+MN/C- MN and C+MN/total CBMN (%) were also noted in the exposed subjects. By mixed effects analysis, considering individuals from the same families, the C- MN and single C+ MN/1000 BN were both positively and moderately associated with previous cumulative exposure. When the time period of relocation post-exposure (relocation time or RT) was considered, total C+MN and multiple C+MN/1000 BN were negatively and significantly associated with RT. Moreover, the C+MN, C- MN, C+MN/C- MN ratio and single C+MN/1000 BN were all negatively and moderately associated with RT, but not with exposure dose. This suggested that acentromeric and single or multiple centromeric CBMN cytogenetic damage seems to disappear differentially in human subjects post chronic low dose radiation exposure.

Cytogenetic effect of chronic low-dose, low-dose-rate gamma-radiation in residents of irradiated buildings.

BACKGROUND: Many people in Taiwan have been living in buildings constructed with cobalt-60-contaminated steel rods. To study the biological effects of chronic low-dose ionising radiation on the residents of one such building, micronucleus formation in these individuals was compared with that in controls. METHODS: The 73 residents had 77 age-and-sex-matched controls: 31 had 31 close relatives as controls (group A controls); eight of the 31 had a second set of close relatives; and the other controls were 38 residents in neighbouring buildings. Two micronucleus assays were used-a cytochalasin B (CBMN) assay and another involving incubation with cytarabine (CBMNA). Assay results are given as "frequency", or the number of binucleate cells containing one micronucleus per 1000 randomly examined binucleate cells. FINDINGS: The CBMN and CBMNA mean (SD) frequencies for 31 exposed individuals (0.016 [0.009] and 0.025 [0.013] respectively) were greater than those for their group A controls (0.009 [0.004] and 0.016 [0.009], respectively) (p = 0.0006 and 0.0002, respectively). The mean CBMN and CBMNA frequencies for all the exposed individuals (0.017 [0.011] and 0.030 [0.014], respectively) were significantly greater than those for all controls (0.011 [0.008] and 0.019 [0.01]; p = 0.0001 for both comparisons). The ranges of the differences in CBMN or CBMNA frequencies between 31 exposed individuals and their group A controls were 0.003 to 0.020 and 0.001 to 0.032, respectively. After adjustment for age, sex, and cigarette smoking, the adjusted relative risks of micronucleus formation from radiation exposure in all 73 residents was 1.58 (95% CI 1.42-1.71; p = 0.0001) by the CBMN assay and 1.64 (1.53-1.77; p = 0.0001) by the CBMNA assay. INTERPRETATION: These findings suggest that chronic low-dose and low-dose-rate gamma-ray environmental exposure may induce cytogenetic damage in human beings.