Chronic obstructive pulmonary disease (COPD) is a common disease characterized by airway obstruction caused by complex interactions between genes and environmental factors (1). Recently, there has been growing evidence showing that pesticide exposure is associated with poorer respiratory outcomes, such as chronic bronchitis and an impaired level of lung function compatible with airway obstruction (2, 3). Different types of pesticides have distinct physicochemical properties, and may cause direct damage to the cells of the bronchial mucosa, or may cause indirect damage via interaction with proinflammatory receptors, for example, transient receptor potential ion channels on airway chemosensory nerves (4). Genetic susceptibility to the adverse effects of pesticide exposure has been implicated in several diseases, such as cancer (5) and Parkinson’s disease (6). Whether genetic susceptibility is of importance for the effects of pesticide exposure in the lungs is largely unknown. Therefore, in the current study, we performed a genome-wide interaction study to assess genetic susceptibility to the effects of occupational pesticide exposure in relation to the FEV1, a measurement of lung function.