University of Granada School of Medicine, Granada, Spain.
Curr Opin Allergy Clin Immunol. 2011 Apr;11(2):90-6. doi: 10.1097/ACI.0b013e3283445939.
Several clinical and epidemiological studies have reported an association between exposure to pesticides, bronchial hyper-reactivity and asthma symptoms. This article reviews the mechanistic evidence lending support to the concept that either acute or chronic low-level inhalation of pesticides may trigger asthma attacks, exacerbate asthma or increase the risk of developing asthma.
Pesticide aerosols or gases, like other respiratory irritants, can lead to asthma through interaction with functional irritant receptors in the airway and promoting neurogenic inflammation. Cross-talk between airway nerves and inflammatory cells helps to maintain chronic inflammation that eventually damages the bronchial epithelium. Certain organophosphorus insecticides cause airway hyper-reactivity via a common mechanism of disrupting negative feedback control of cholinergic regulation in the lungs. These pesticides may interact synergistically with allergen sensitization rendering individuals more susceptible for developing asthma.
Many pesticides are sensitizers or irritants capable of directly damaging the bronchial mucosa, thus making the airway very sensitive to allergens or other stimuli. However, most pesticides are weakly immunogenic so that their potential to sensitize airways in exposed populations is limited. Pesticides may increase the risk of developing asthma, exacerbate a previous asthmatic condition or even trigger asthma attacks by increasing bronchial hyper-responsiveness.
几项临床和流行病学研究报告称，接触农药与支气管高反应性和哮喘症状之间存在关联。本文综述了支持以下概念的机制证据，即急性或慢性低水平吸入农药可能引发哮喘发作、加重哮喘或增加患哮喘的风险。
农药气溶胶或气体，与其他呼吸道刺激物一样，可通过与气道中的功能性刺激受体相互作用并促进神经源性炎症，导致哮喘。气道神经和炎症细胞之间的串扰有助于维持慢性炎症，最终损害支气管上皮。某些有机磷杀虫剂通过破坏肺部胆碱能调节的负反馈控制的共同机制引起气道高反应性。这些杀虫剂可能与过敏原致敏作用协同，使个体更容易患上哮喘。
许多农药是敏化剂或刺激物，能够直接损害支气管黏膜，从而使气道对过敏原或其他刺激物非常敏感。然而，大多数农药的免疫原性较弱，因此它们在暴露人群中使气道致敏的潜力有限。农药可能通过增加支气管高反应性来增加患哮喘的风险、加重先前的哮喘病情，甚至引发哮喘发作。
