Antonio F. Hernández; Tesifón Parrón; Raquel Alarcón

Disclosures

Curr Opin Allergy Clin Immunol. 2011;11(2):90-96. 

In This Article

Abstract and Introduction

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.

Introduction

The respiratory tract is routinely exposed to low-molecular-weight chemicals and to a variety of many environmental chemical allergens whose inhalation is a leading cause of respiratory diseases, including asthma.[1] The increased pesticide exposure from occupational, environmental or residential usages over the past three decades may have contributed to the higher incidence of asthma, particularly in children from urban areas.[2,3]

Development of allergic respiratory diseases requires sensitization, which may be triggered by dermal or respiratory exposure to the sensitizing chemical.[4] Airways are also exposed to irritants which are noncorrosive chemicals that cause a reversible inflammatory change of the bronchial mucosa.[5•] Exposure to either sensitizing or irritant chemicals in the workplace may lead to work-related asthma, a recent term that encompasses both occupational asthma (e.g. asthma induced by sensitizer or irritant work exposures) and work-exacerbated asthma, that is pre-existing or concurrent asthma worsened by work factors, including irritant exposures.[6] When occupational asthma appears after exposure to an inhaled irritant at work, it is termed irritant-induced occupational asthma.[6]

Reactive airways dysfunction syndrome (RADS) can be considered a subset of irritant-induced asthma (IIA) that develops after an unintentional short-term high-level exposure to nonimmunogenic, highly irritating volatile substances. Pesticides are among the most common agents producing RADS.[7] Some of the clinical manifestations are very similar to those of asthma (e.g. inflammation, hyper-responsiveness and reversibility of the bronchial constriction), although this syndrome does not involve immunological mechanisms.[8] The pathomorphologic bronchial biopsies usually show neutrophilic and lymphocytic infiltrations without eosinophilia and some evidence of subepithelial thickening, fibrosis and destruction of the bronchial epithelium.[9] These histopathological findings are partially reversible and not sufficiently distinctive to be helpful in diagnosis.[10,11]

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