The discovery that a number of transient receptor potential (TRP) channels are expressed in a subpopulation of primary sensory neurons innervating the upper and lower airways, as well as in nonneuronal cells in the airways and lungs, has sparked an interest in understanding their role in respiratory tract physiology and pathophysiology. TRP vanilloid subfamily and TRP ankyrin 1 members promote airway neurogenic inflammation due to their localization in peptidergic sensory neurons. TRPA1, which is gated by oxidative and nitrative stress byproducts, has been identified to modulate inflammatory reactions caused by an unparalleled range of toxic and irritating chemicals caused by air pollution, cigarette smoke, and workplace accidents. The discovery that reactive chemicals endogenously generated in the airways/lungs of asthma, occupational asthma, and chronic obstructive pulmonary disease target TRPA1 emphasizes the TRPA1 channel’s major function in these disorders.

TRP channels, particularly TRPA1, have been identified as major targets of oxidative/nitrative stress and a variety of irritant environmental agents, lending support to the hypothesis that neurogenic inflammation plays an important role in work-related inflammatory diseases and that antagonists for such channels may be novel therapeutic options for the treatment of these diseases.