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PURPOSE: To assess the role of gene-environment interaction between interleukin (IL)-4 promoter and mold exposure on the development of asthma. METHODS: We conducted a cohort-based, incident, case-control study. The case group consisted of 188 children with new asthma and the control group (n = 376) was matched for age and gender. The outcome of interest was the development of asthma over the 6-year study period. The studied determinants were three polymorphisms of IL-4 promoter (TT, CT, and CC) and three indicators of exposure including histories of water damage, presence of visible molds, and perceived mold odor in the home. RESULTS: Apparent joint effects between IL-4 promoter and mold exposure were observed on both additive and multiplicative scales. Specially, the risk of asthma was significantly associated with children carrying the CT genotype and visible mold exposure comparing with those carrying the TT genotype without any exposure indicator (adjusted odds ratio [OR], 2.14; 95% confidence interval [CI], 1.05-4.34; modified Rothman synergy index for directly use of odds and OR [s] = 1.41; P for interaction = .03). A similar tendency was found (s = 1.30; P for interaction = .04) for children who were exposed to mold odor and carried CT genotype (adjusted OR, 1.99; 95% CI, 1.03-4.41). CONCLUSIONS: The results of this study suggest that gene-environment interactions between the IL-4 promoter and an indoor mold problem may play an important role in childhood asthma. [ABSTRACT FROM AUTHOR]

Objectives Previous studies on the effects of angiotensinogen (AGT) gene polymorphisms and chronic exposure to occupational noise on the risk of hypertension have mainly been cross-sectional or prevalent case-control studies, where temporality constitutes problems. The present study was to assess longitudinally both independent and joint effects of AGT gene polymorphisms and chronic exposure to occupational noise on occurrence of hypertension. Methods The authors conducted a 20-year prospective cohort study of 1301 aviation workers in Taiwan. The study population included 912 workers without hypertension at baseline. The outcome of interest was the development of hypertension during the study period. The studied determinants were three AGT genotypes (TT, TM and MM) and four exposure categories according to the levels of noise representing high (>80 dBA), medium (80-65 dBA), low exposure (64-50 dBA) and the reference level (49-40 dBA). Results In Poisson regression adjusting for confounders, AGT (TT vs MM adjusted incidence rate ratio (IRR) 1.77, 95% CI 1.24 to 2.51) and noise exposure (high and medium combined) during 3-15 years (adjusted IRR 2.35, 95% CI 1.42 to 3.88) were independent determinants of hypertension. Furthermore, the risk of hypertension increased with noise exposure (adjusted IRR 3.73, 95% CI 1.84 to 7.56) among TT homozygotes but not among those with at least one M allele (Rothman synergy index=1.05). Conclusions The results evidence further the independent effects of AGT gene polymorphisms and exposure to occupational noise. Our finding also suggests that workers carrying TT variant allele have higher risk of hypertension under chronic exposure to occupational noise. [ABSTRACT FROM AUTHOR]

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 byproducts 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. [ABSTRACT FROM AUTHOR]