論文No2344
Association of asthma and smoking with lung function impairment in adolescence and early adulthood: the Isle of Wight Birth Cohort Study
S. Hasan Arshad, Claire Hodgekiss, John W. Holloway, Ramesh Kurukulaaratchy, Wilfried Karmaus, Hongmei Zhang, Graham Roberts
European Respiratory Journal 2020 55: 1900477; DOI: 10.1183/13993003.00477-2019
|
|
＜背景＞
我々は小児期から早期青年期にかけて、喘息と喫煙が肺機能、気道可逆性に及ぼす影響を検討した。
＜方法＞人口ベースの Isle of Wight Birth Cohort (n=1456)で出生時、１歳、２歳、４歳、１０歳、１８歳、２６歳時点を評価した。
喘息は医師による診断プラス現在の喘鳴and/or治療で定義した。
肺機能は１０歳（n=981)、18歳（n=839）、26歳（n=547）で施行した。
２６歳時点の喘息、喫煙状態にもとづいて、喘息のない非喫煙者、喘息のある非喫煙者、
喘息のない喫煙者、喘息のある喫煙者に分類した。
１０歳から２６歳の肺機能の軌跡を縦断モデルを使用して検討した。
＜結果＞
喘息のある非喫煙者はFEV1, FEF(25-75%) (forced expiratory flow at 25–75% of forced vital capacity (FVC))、
FEV1/FVCが喘息のない非喫煙者と比較して１０歳、１８歳時点で悪く、気管支拡張薬投与後はその差が減少した
(pre-bronchodilator FEV1 at 26 years 3.75 L versus 4.02 L, p<0.001; post-bronchodilator 4.02 L versus 4.16 L, p=0.08)。
この肺機能不足は１８歳以降は悪化しなかった。
喘息のない喫煙者は喘息のない非喫煙者よりも２６歳時点でのFEF25-75%、FEV1/FVCが低かった。
この差は１８歳以降に現れ、気管支拡張薬投与しても有意差があった
(for FEV1/FVC ratio at 26 years 0.80 versus 0.81, p=0.002; post-bronchodilator 0.83 versus 0.85, p=0.005)。
喘息のある喫煙者はほかの群よりも肺機能が悪かった。
＜感想＞
喘息、喫煙による肺機能悪化は青少年期から悪影響を及ぼしていたようです。
喘息だけだと気管支拡張薬に反応しますが、喫煙がからむと気管支拡張薬投与しても肺機能の改善はきびしかったようです。
|
|
We investigated associations of asthma and smoking with lung function and airway reversibility from childhood to early adulthood.
The population-based Isle of Wight Birth Cohort (n=1456) was assessed at birth, and at 1, 2, 4, 10, 18 and 26 years. Asthma was defined as physician diagnosis plus current wheeze and/or treatment. Spirometry was conducted at 10 (n=981), 18 (n=839) and 26 years (n=547). Individuals were subdivided into nonsmokers without asthma, nonsmokers with asthma, smokers without asthma and smokers with asthma, based on asthma and smoking status at 26 years. Their lung function trajectories from 10 to 26 years were examined using longitudinal models.
Nonsmokers with asthma had smaller forced expiratory volume in 1 s (FEV1), FEF25–75% (forced expiratory flow at 25–75% of forced vital capacity (FVC)) and FEV1/FVC ratio compared to nonsmokers without asthma at age 10 and 18 years, with differences reduced after bronchodilator (pre-bronchodilator FEV1 at 26 years 3.75 L versus 4.02 L, p<0.001; post-bronchodilator 4.02 L versus 4.16 L, p=0.08). This lung function deficit did not worsen after 18 years. Smokers without asthma had smaller FEF25–75% and FEV1/FVC ratio (but not FEV1) at 26 years compared to nonsmokers without asthma, with the deficit appearing after 18 years and persisting despite bronchodilator response (for FEV1/FVC ratio at 26 years 0.80 versus 0.81, p=0.002; post-bronchodilator 0.83 versus 0.85, p=0.005). Smokers with asthma had worse lung function compared to other groups.
Lung function deficits associated with asthma and smoking occur early in life. They are not fully responsive to bronchodilators, indicating a risk for long-term lung health, which highlights the need to institute preventive measures in adolescence and early adult life before irreversible damage occurs.