Karadag B, Karakoç F, Ceran O, Ersu R, Inan S, Dagli E
Marmara University, Division of Pediatric Pulmonology, Istanbul, Turkey.
Allergol Immunopathol (Madr). 2003 Nov-Dec;31(6):318-23. doi: 10.1016/s0301-0546(03)79205-2.
The relationship between asthma and passive smoking has been well established. However, it is still not clear whether an acute asthma attack can be induced by acute smoke exposure. The specific aims of this study were: 1- To assess the degree of smoke exposure through urinary cotinine levels in asthmatic children during and 4 weeks after asthma attacks and, 2- To evaluate the reliability of parental questionnaires in asthmatic children by comparing the data obtained from cotinine measurements and parental reports. Thirty-two consecutive asthmatic children who were admitted to the emergency clinic were included in the study. Parents were asked to complete a questionnaire about their smoking habits and housing conditions. Urinary cotinine and creatinine levels were measured in children during and 4 weeks after the acute asthma attack. The mean age of the patients was 5.7 +/- 3.2 years. The mean attack rate was 3.5 +/- 3.8 per year. Thirty-eight percent of the patients were taking no preventive treatment. In 80 % of patients, urinary cotinine and creatinine ratios (CCR) were significantly above the non-exposed, non-smoker levels. However, CCR levels during acute asthma attacks were not higher than those measured 4 weeks after the acute attack (314.6 +/- 299.1 vs. 203.8 +/- 165.2 ng/mg respectively, p > 0.05). Although parental reports of passive smoke exposure was 71 %, CCR levels revealed that 81 % and 97 % of children were exposed to passive smoke during acute attacks and asymptomatic periods, respectively. In conclusion, although the proportion of children with acute asthma attacks who were exposed to passive smoking was high, the degree of passive smoke exposure was not higher during acute attacks. Parental questionnaires were found to be unreliable in reporting passive smoke exposure in asthmatic children during acute attacks.
哮喘与被动吸烟之间的关系已得到充分证实。然而,急性烟雾暴露是否会诱发急性哮喘发作仍不明确。本研究的具体目的是:1. 通过哮喘儿童在哮喘发作期间及发作后4周的尿可替宁水平评估烟雾暴露程度;2. 通过比较可替宁测量数据与家长报告数据,评估哮喘儿童家长问卷的可靠性。本研究纳入了32名连续入住急诊诊所的哮喘儿童。要求家长填写一份关于他们吸烟习惯和居住条件的问卷。在急性哮喘发作期间及发作后4周测量儿童的尿可替宁和肌酐水平。患者的平均年龄为5.7±3.2岁。平均发作率为每年3.5±3.8次。38%的患者未接受预防性治疗。80%的患者尿可替宁与肌酐比值(CCR)显著高于未暴露、不吸烟人群的水平。然而,急性哮喘发作期间的CCR水平并不高于急性发作后4周测量的水平(分别为314.6±299.1与203.8±165.2 ng/mg,p>0.05)。尽管家长报告的被动吸烟暴露率为71%,但CCR水平显示,在急性发作期和无症状期,分别有81%和97%的儿童暴露于被动吸烟环境。总之,虽然急性哮喘发作儿童中暴露于被动吸烟的比例较高,但急性发作期间的被动吸烟暴露程度并不更高。研究发现,家长问卷在报告哮喘儿童急性发作期间的被动吸烟暴露情况时不可靠。