Occupational disease: Edited by Susan M. Tarlo and Piero MaestrelliPesticides and asthmaHernández, Antonio F; Parrón, Tesifón; Alarcón, RaquelAuthor Information aUniversity of Granada School of Medicine, Granada, Spain bUniversity of Almería, Spain cAndalusian Council of Health, Almería, Spain Correspondence to Dr Antonio F. Hernández, Department of Legal Medicine and Toxicology, University of Granada School of Medicine, Avda. Madrid 11, 18071-Granada, Spain Tel: +34 958 249927; fax: +34 958 246107; e-mail: [email protected] Current Opinion in Allergy and Clinical Immunology: April 2011 - Volume 11 - Issue 2 - p 90-96 doi: 10.1097/ACI.0b013e3283445939 Buy Metrics Abstract Purpose of review 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. Recent findings 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. Summary 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. Copyright © 2011 Wolters Kluwer Health, Inc. All rights reserved.