Hassanzad Maryam, Khalilzadeh Soheila, Eslampanah Nobari Shabnam, Bloursaz Mohammadreza, Sharifi Hooman, Mohajerani Seyed Amir, Tashayoie Nejad Sabereh, Velayati Ali Akbar
Pediatric Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Disease, Masih Daneshvari Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Tobacco Prevention Control Research Center, National Research Institute of Tuberculosis and Lung Disease, Masih Daneshvari Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Iran J Allergy Asthma Immunol. 2015 Feb;14(1):67-73.
Asthma environmental triggers play important roles in severity of disease. Passive smoking could exacerbate asthma symptoms and enhance the decrease in lung function. Cotinine levels could be a reflection of passive exposure to the cigarette both in adults and pediatrics. The aim of this study was to determine degree of association of asthma severity and cotinine level as a marker of passive smoking. In a cross-sectional study, 100 pediatric patients (under 10 years old) with asthma were enrolled, 50 of whom, had been exposed to passive smoking and 50 others included as controls. A complete clinical history, lab exam, and spirometry were performed. A sample of urine, serum and saliva was collected from all attendant patients and controls in the study after confirmation of diagnosis and determination of severity of asthma. The results revealed that age, sex, age of onset of asthma, family history and allergic history were not significantly different between two groups of patients. According to GINA classification, percentage of patients with severe asthma was significantly higher in passive smoker group (p=0.001). Cotinine was significantly higher in passive smoker group compared to control group in serum (p=001), saliva (p=0.001), and urine (p=0.0014). In passive smoker group, cotinine levels were significantly higher in serum (p=0.001), urine (p=0.007), and saliva (p=0.01) of patients with severe asthma than moderate and mild asthma. Serum cotinine (OR: 1.81, 95% CI: 1.35-2.32, p=0.024), urine cotinine (OR: 3.56,95% CI = 1.29-5.53, p=0.01) and saliva cotinine (OR: 1.66, 95% CI: 1.23-1.98, p=0.031) were also significantly associated with higher risk of severe asthma. Cotinine levels were higher in passive smokers compared to non-passive smokers. Besides, cotinine was a predictive risk factor for severe asthma.
哮喘的环境触发因素在疾病严重程度中起重要作用。被动吸烟会加重哮喘症状并加剧肺功能下降。可替宁水平可反映成人和儿童被动接触香烟的情况。本研究的目的是确定哮喘严重程度与作为被动吸烟标志物的可替宁水平之间的关联程度。在一项横断面研究中，纳入了100名10岁以下的哮喘儿童患者，其中50名曾接触过被动吸烟，另外50名作为对照。进行了完整的临床病史、实验室检查和肺功能测定。在确诊哮喘并确定其严重程度后，从研究中的所有患者和对照中采集了尿液、血清和唾液样本。结果显示，两组患者在年龄、性别、哮喘发病年龄、家族史和过敏史方面无显著差异。根据全球哮喘防治创议（GINA）分类，重度哮喘患者在被动吸烟组中的比例显著更高（p = 0.001）。与对照组相比，被动吸烟组血清（p = 0.01）、唾液（p = 0.001）和尿液（p = 0.0014）中的可替宁水平显著更高。在被动吸烟组中，重度哮喘患者血清（p = 0.001）、尿液（p = 0.007）和唾液（p = 0.01）中的可替宁水平显著高于中度和轻度哮喘患者。血清可替宁（比值比：1.81，95%置信区间：1.35 - 2.32，p = 0.024）、尿液可替宁（比值比：3.56，95%置信区间 = 1.29 - 5.53，p = 0.01）和唾液可替宁（比值比：1.66，95%置信区间：1.23 - 1.98,p = 0.031）也与重度哮喘的较高风险显著相关。与非被动吸烟者相比，被动吸烟者的可替宁水平更高。此外，可替宁是重度哮喘的预测风险因素。
