US EPA

15977 

Journal Article 

Review 

Neurogenic inflammation and particulate matter (PM) air pollutants 

Veronesi, B; Oortgiesen, M 

2001 

1 

NeuroToxicology
ISSN: 0161-813X
EISSN: 1872-9711 

22 

6 

795-810 

English 

11829413 

10.1016/S0161-813X(01)00062-6 

WOS:000173554300008 

http://linkinghub.elsevier.com/retrieve/pii/S0161813X01000626
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Exposure to a class of airborne pollutants known as particulate matter (PM) is an environmental health risk of global proportions. PM is thought to initiate and/or exacerbate respiratory disorders, such as asthma and airway hyperresponsiveness and is epidemiologically associated with causing death in the elderly and those with pre-existing respiratory or cardiopulmonary disease. Plausible mechanisms of action to explain PM inflammation and its susceptible subpopulation component are lacking. This review describes a series of published studies which indicate that PM initiates airway inflammation through sensory neural pathways, specifically by activation of capsaicin- sensitive vanilloid (e.g. VRI) irritant receptors. These acid-sensitive receptors are located on the sensory C nerve fibers that innervate the airways as well as on various immune and non-immune airway target cells. The activation of these receptors results in the release of neuropeptides from the sensory terminals that innervate the airways which subsequently interact with airway target cells to produce signs of inflammation (e.g. bronchoconstriction, vasodilation, histamine release, mucous secretion etc.). Our data have linked the activation of the VRI receptors to the surface charge carried on the colloidal particulates which constitute PM pollution. Related studies have examined how genetic and non-genetic factors modify the sensitivity of these irritant receptors and enhance the inflammatory responsiveness to PM. In summary, this review proposes a mechanism by which neurogenic elements initiate and sustain PM-mediated airway inflamnzation. Although neurogenic influences have been appreciated in normal airway homeostasis, they have not, until now, been associated with PM toxicity. The sensitivity of the sensory nervous system to irritants and its interactions with pulmonary target tissues, should encourage neuroscientists to explore the relevance of neurogenic influences to toxic disorders involving other peripheral target systems. 

particulate matter; neurogenic inflammation; tracheal epithelial cells; BEAS-2B; somatosensory neurons; vanilloid receptors; capsaicin receptors; acid-sensitive pathways