Künzli N, Bridevaux P-O, Liu L-J S, Garcia-Esteban R, Schindler C, Gerbase M W, Sunyer J, Keidel D, Rochat T
Center for Research in Environmental Epidemiology, C Doctor Aiguader 88, Barcelona, Spain.
Thorax. 2009 Aug;64(8):664-70. doi: 10.1136/thx.2008.110031. Epub 2009 Apr 8.
Traffic-related pollution is associated with the onset of asthma in children. Its effect on adult-onset asthma is poorly investigated. The SAPALDIA cohort study was used to investigate associations between the 11-year change (1991-2002) in home outdoor traffic-related particulate matter up to 10 microm in diameter (TPM(10)) and the incidence of asthma.
Never-smokers without asthma at baseline aged 18-60 years in 1991 were eligible for inclusion in the study. Subjects reporting doctor-diagnosed asthma at follow-up were considered incident cases. TPM(10) at baseline and follow-up was predicted and interpolated to subjects' place of residence by dispersion models using emission and meteorological data. Cox proportional hazard models for time to asthma onset were adjusted (age, gender, baseline atopy, body mass index, bronchial reactivity, maternal allergies).
Of 2725 never-smokers, 41 reported asthma onset in 2002. Home outdoor TPM(10) concentrations improved during the interval (mean -0.6; range -9 to +7.2; IQR 0.6 microg/m(3)). The incidence of asthma was associated with a change in TPM(10). The hazard ratio (1.30; 95% CI 1.05 to 1.61) per 1 microg/m(3) change in TPM(10) (IQR) was not sensitive to further adjustments (education, workplace exposure, passive smoking, parental asthma or allergies, random area effects, lung function or co-pollutants such as regional, secondary, total PM(10) or proximity to busy roads).
The data suggest a role for traffic-related pollution in adult-onset asthma. Space, time and source-specific individual assignment of exposure to traffic-related pollution is a key strength of SAPALDIA. It may explain why findings were statistically significant despite the limited number of new cases. As traffic-related pollution prevails, the finding may be of substantial public health relevance.
与交通相关的污染与儿童哮喘的发病有关。其对成人哮喘发病的影响研究较少。采用瑞士成人肺部疾病队列研究（SAPALDIA）来调查1991年至2002年期间家庭室外直径达10微米的与交通相关的颗粒物（TPM(10)）的11年变化与哮喘发病率之间的关联。
1991年年龄在18 - 60岁、基线时无哮喘且不吸烟的人符合纳入该研究的条件。随访时报告医生诊断为哮喘的受试者被视为新发病例。使用排放和气象数据，通过扩散模型预测并内插基线和随访时受试者居住地的TPM(10)。对哮喘发病时间的Cox比例风险模型进行了调整（年龄、性别、基线特应性、体重指数、支气管反应性、母亲过敏情况）。
在2725名不吸烟者中，41人在2002年报告哮喘发病。在此期间家庭室外TPM(10)浓度有所改善（平均 -0.6；范围 -9至 +7.2；四分位间距0.6微克/立方米）。哮喘发病率与TPM(10)的变化有关。TPM(10)每变化1微克/立方米（四分位间距）的风险比为1.30（95%可信区间1.05至1.61），对进一步调整（教育程度、工作场所暴露、被动吸烟、父母哮喘或过敏、随机区域效应、肺功能或共同污染物如区域、二次、总PM(10)或靠近繁忙道路情况）不敏感。
数据表明与交通相关的污染在成人哮喘发病中起作用。SAPALDIA的一个关键优势在于对与交通相关污染的暴露进行空间、时间和源特异性的个体分配。这可能解释了尽管新病例数量有限但研究结果仍具有统计学意义的原因。鉴于与交通相关的污染普遍存在，该发现可能具有重大的公共卫生意义。
