Gautier Clarisse, Charpin Denis
Department of Pulmonology and Allergy, North Hospital.
Department of Pulmonology and Allergy, North Hospital; Faculty of Medicine, Aix-Marseille University, Marseille, France.
J Asthma Allergy. 2017 Mar 7;10:47-56. doi: 10.2147/JAA.S121276. eCollection 2017.
Identifying asthma triggers forms the basis of environmental secondary prevention. These triggers may be allergenic or nonallergenic. Allergenic triggers include indoor allergens, such as house dust mites (HDMs), molds, pets, cockroaches, and rodents, and outdoor allergens, such as pollens and molds. Clinical observations provide support for the role of HDM exposure as a trigger, although avoidance studies provide conflicting results. Molds and their metabolic products are now considered to be triggers of asthma attacks. Pets, dogs, and especially cats can undoubtedly trigger asthmatic symptoms in sensitized subjects. Avoidance is difficult and rarely adhered to by families. Cockroach allergens contribute to asthma morbidity, and avoidance strategies can lead to clinical benefit. Mouse allergens are mostly found in inner-city dwellings, but their implication in asthma morbidity is debated. In the outdoors, pollens can induce seasonal asthma in sensitized individuals. Avoidance relies on preventing pollens from getting into the house and on minimizing seasonal outdoor exposure. Outdoor molds may lead to severe asthma exacerbations. Nonallergenic triggers include viral infections, active and passive smoking, meteorological changes, occupational exposures, and other triggers that are less commonly involved. Viral infection is the main asthma trigger in children. Active smoking is associated with higher asthma morbidity, and smoking cessation interventions should be personalized. Passive smoking is also a risk factor for asthma exacerbation. The implementation of public smoking bans has led to a reduction in the hospitalization of asthmatic children. Air pollution levels have been linked with asthmatic symptoms, a decrease in lung function, and increased emergency room visits and hospitalizations. Since avoidance is not easy to achieve, clean air policies remain the most effective strategy. Indoor air is also affected by air pollutants, such as cigarette smoke and volatile organic compounds generated by building and cleaning materials. Occupational exposures include work-exacerbated asthma and work-related asthma.
识别哮喘触发因素是环境二级预防的基础。这些触发因素可能是变应原性的或非变应原性的。变应原性触发因素包括室内变应原,如屋尘螨(HDM)、霉菌、宠物、蟑螂和啮齿动物,以及室外变应原,如花粉和霉菌。临床观察支持HDM暴露作为触发因素的作用,尽管避免接触研究结果存在矛盾。霉菌及其代谢产物现在被认为是哮喘发作的触发因素。宠物,尤其是狗和猫,无疑会在致敏个体中引发哮喘症状。避免接触很困难,家庭很少能坚持做到。蟑螂变应原会导致哮喘发病,避免接触策略可带来临床益处。小鼠变应原大多存在于市中心的住宅中,但其与哮喘发病的关系存在争议。在户外,花粉可在致敏个体中诱发季节性哮喘。避免接触依赖于防止花粉进入室内,并尽量减少季节性户外接触。室外霉菌可能导致严重的哮喘加重。非变应原性触发因素包括病毒感染、主动和被动吸烟、气象变化、职业暴露以及其他较少涉及的触发因素。病毒感染是儿童哮喘的主要触发因素。主动吸烟与较高的哮喘发病率相关,戒烟干预应个性化。被动吸烟也是哮喘加重的危险因素。实施公共禁烟已导致哮喘儿童住院人数减少。空气污染水平与哮喘症状、肺功能下降以及急诊室就诊和住院人数增加有关。由于难以实现避免接触,清洁空气政策仍然是最有效的策略。室内空气也受到空气污染物的影响,如香烟烟雾以及建筑和清洁材料产生的挥发性有机化合物。职业暴露包括工作加重型哮喘和与工作相关的哮喘。