Chilmonczyk B A, Salmun L M, Megathlin K N, Neveux L M, Palomaki G E, Knight G J, Pulkkinen A J, Haddow J E
Foundation for Blood Research, Scarborough, ME 04070-0190.
N Engl J Med. 1993 Jun 10;328(23):1665-9. doi: 10.1056/NEJM199306103282303.
Exposure to environmental tobacco smoke, as reported by parents, has been linked to diminished pulmonary function and more frequent exacerbations of asthma in children with the disease. Further insight into this association might be gained by using urine cotinine levels to measure actual exposure.
We measured urine cotinine levels in 199 children with asthma; 145 also underwent pulmonary-function studies. A parent answered questions about each child's exposure to environmental tobacco smoke. Acute exacerbations of asthma during the preceding year were documented through blinded review of medical records. Possible confounding factors were accounted for by the use of multivariate analysis and by comparisons of serum theophylline levels in exposed and unexposed children.
The median urine cotinine levels were 5.6 ng per milliliter in the 116 children reported not to have been exposed to tobacco smoke, 13.1 ng per milliliter in the 53 children exposed to cigarette smoking by the mother or other persons, and 55.8 ng per milliliter in the 30 children exposed to cigarette smoking by the mother and other persons. Acute exacerbations of asthma increased with exposure, whether such exposure was reported by a parent or identified on the basis of the cotinine level; the relative risks for the highest as compared with the lowest exposure category were 1.8 (95 percent confidence interval, 1.4 to 2.2) for reported exposure and 1.7 (95 percent confidence interval, 1.4 to 2.1) for exposure indicated by cotinine levels. The forced expiratory volume in one second (FEV1), the forced expiratory flow between 25 and 75 percent of vital capacity, and the ratio of FEV1 to forced vital capacity also decreased with increases in both measures of exposure.
Measurement of urine cotinine levels provides further evidence of an association between exposure to environmental tobacco smoke and pulmonary morbidity in children with asthma. These data emphasize the need for systematic, persistent efforts to stop the exposure of children with asthma to environmental tobacco smoke.
据家长报告,儿童接触环境烟草烟雾与肺功能下降以及哮喘患儿哮喘发作更为频繁有关。通过使用尿可替宁水平来测量实际接触情况,可能会进一步了解这种关联。
我们测量了199名哮喘儿童的尿可替宁水平;其中145名儿童还进行了肺功能研究。一位家长回答了有关每个孩子接触环境烟草烟雾的问题。通过对医疗记录的盲法审查记录了前一年哮喘的急性发作情况。通过多变量分析以及比较接触和未接触儿童的血清茶碱水平来考虑可能的混杂因素。
在报告未接触烟草烟雾的116名儿童中,尿可替宁水平中位数为每毫升5.6纳克;在53名接触母亲或其他人吸烟的儿童中,为每毫升13.1纳克;在30名接触母亲和其他人吸烟的儿童中,为每毫升55.8纳克。无论这种接触是由家长报告还是根据可替宁水平确定,哮喘急性发作都随着接触增加而增多;与最低接触类别相比,最高接触类别的相对风险对于报告的接触为1.8(95%置信区间为1.4至2.2),对于可替宁水平表明的接触为1.7(95%置信区间为1.4至2.1)。一秒用力呼气量(FEV1)、肺活量25%至75%之间的用力呼气流量以及FEV1与用力肺活量的比值也随着两种接触测量值的增加而降低。
尿可替宁水平的测量为环境烟草烟雾接触与哮喘儿童肺部发病之间的关联提供了进一步证据。这些数据强调需要系统、持续地努力,使哮喘儿童避免接触环境烟草烟雾。