| 摘要: | 氣喘是一種很常見的呼吸道疾病，且氣喘盛行率在各國逐年增加，而個體的抗氧化能力較低可能會增加氣喘的風險。環境中的汙染物例如臭氧(O3)、氮氧化物(NOX)等，還有室內二手菸或空氣中的各種過敏原都可能造成氣喘的產生，但是氣喘和二手菸之間的關係仍然需要釐清，因此本研究透過問卷及基因型分析，欲探討氣喘、和解毒酵素有關的NAD(P)H dehydrogenase, quinone 1(NQO1)、glutathione S-transferase M1 (GSTM1)基因及環境中二手菸暴露之間的關係。
本研究使用橫斷式研究設計，分別在2006年4月到2008年4月從台灣的北部、中部及南部地區收集922位國小兒童樣本，排除掉沒有口腔細胞的樣本以及基因型無法判定者，最後使用的樣本總共為772個，經由卡方檢定、邏輯斯迴歸了解NQO1、GSTM1基因型和環境因子中二手菸與兒童氣喘之間的關係。
家人抽菸、住家空氣污染、家中燒香、使用蚊香以及家中會聞到發霉氣味都會增加氣喘風險，但只有家中會聞到發霉氣味有達統計顯著(P=0.04)。在基因型方面，攜帶NQO1 C609T TT或CT基因型者相較於攜帶NQO1 C609T CC基因型者有1.2倍氣喘風險(95%CI=0.7-2.0)；攜帶GSTM1 null基因型相對於攜帶GSTM1 present基因型者無顯著氣喘風險。具有NQO1 C609T TT或CT基因型者並且家人每天抽11支菸以上者相對於攜帶NQO1 C609T CC基因型並且家人沒有抽菸者會有2.2倍的氣喘風險(95%CI=0.8-6.2)，但是並沒有達到統計上的顯著差異。
我們的研究結果發現，當GSTM1 基因型為null時，攜帶NQO1 TT或CT基因型者，會有較高的氣喘風險；更進一步發現當攜帶GSTM null基因型和NQO1 TT或CT基因型者暴露在較高劑量二手菸中可能會增加氣喘的風險，雖然皆沒有達到統計上的顯著差異，但符合我們當初的假設，當攜帶NQO1 TT或CT基因型會減少NQO1的酵素活性，而GSTM1 null基因型會缺乏GSTM1酵素活性，同時攜帶NQO1 TT或CT基因型以及GSTM1 null基因型者，並且暴露在二手菸的情況之下，會有較高的氣喘風險，而我們的結果可以提供未來研究的一個方向。
Asthma is a common respiratory disease and the prevalence is increasing around the world. Individuals with a lower antioxidant capacity may increase asthma risk. The environment pollution, including O3, NOX , environment tobacco smoke (ETS), and allergens may induce asthma, but the association of inflammatory path way of asthma and ETS is not clear. We used a structured questionnaire and genotypes to research the association of NAD(P)H dehydrogenase, quinone 1(NQO1), glutathione S-transferase M1 (GSTM1), and environment factors with childhood asthma.
We used a cross-sectional study design to recruit elementary schoolchildren from the northern, central, and southern areas in Taiwan during April, 2006 and April, 2008. Among 922 participants with questionnaire data, we excluded 150 subjects for no buccal cell samples or no genotyping results, and the rest 772 individuals were used for the data analysis. The associations between NQO1, GSTM1, and environment factors were examined by Chi-square tests and logistic regression models.
Household tobacco exposures, air pollution of the residence area, burning joss sticks in the house, and moldy smell at home increased asthma risk. We found that, relative to children carrying a NQO1 CC genotype, children with a NQO1 C609T TT or CT genotype were at a 1.2 fold higher risk of asthma (95%CI=0.7-2.8). There was no statistically significant difference in asthma risk between children carrying GSTM1 null and GSTM1 present genotypes. If children’s family member smoked 11 tobacco cigarettes or more inside the house and children carried a NQO1 C609T CT or TT genotype, they had 2.2 times higher of asthma risk compared to children with a NQO1 CC genotype and without household tobacco exposure (95%CI=0.8-6.2).
Our results showed children with a GSTM1 null genotype and a NQO1 C609T TT/CT genotype would increase asthma risk. We also found that children carrying a GSTM1 null genotype, a NQO1 C609T TT/CT genotype, and exposed to a higher dose of ETS were at a higher risk of asthma. Although our results were not statistically significant, our findings could support the hypothesis that the NQO1 enzyme activity is reduced if children carry a NQO1 C609T TT/CT genotype. Our findings can suggest that children carrying at least one NQO1 T allele, a GSTM1 null genotype, and exposed to ETS would increase asthma risk. |
