This Article Full Text Full Text (PDF) Online Supplement All Versions of this Article: 200201-021OCv1 168/5/568    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Martin, J. G. Articles by Maghni, K. Search for Related Content PubMed PubMed Citation Articles by Martin, J. G. Articles by Maghni, K.

Chlorine-induced Injury to the Airways in Mice

Meakins-Christie Laboratories, Department of Medicine, McGill University; and Respiratory Division, Hôpital Sacre Coeur, University of Montreal, Montreal, Quebec, Canada

Correspondence and requests for reprints should be addressed to James G. Martin, M.D., Meakins-Christie Laboratories, 3626 St Urbain, Montreal, PQ, H2X 2P2 Canada. E-mail: james.martin{at}mcgill.ca

Exposure to chlorine gas (Cl₂) causes occupational asthma that we hypothesized occurs through the induction of airway inflammation and airway hyperresponsiveness by oxidative damage. Respiratory mechanics and airway responsiveness to methacholine were assessed in A/J mice 24 hours after a 5-minute exposure to 100, 200, 400, or 800 ppm Cl₂ and 2 and 7 days after inhalation of 400 ppm Cl₂. Airway responsiveness was higher 24 hours after 400 and 800 ppm Cl₂. Responsiveness after inhalation of 400 ppm Cl₂ returned to normal by 2 days but was again elevated at 7 days. Airway epithelial loss, patchy alveolar damage, proteinaceous exudates, and inflammatory cells within alveolar walls were observed in animals exposed to 800 ppm Cl₂. Macrophages, granulocytes, epithelial cells, and nitrate/nitrite levels increased in lung lavage fluid. Increased inducible nitric oxide synthase expression and oxidation of lung proteins were observed. Epithelial cells and alveolar macrophages from mice exposed to 800 ppm Cl₂ stained for 3-nitrotyrosine residues. Inhibition of inducible nitric oxide synthase with 1400W (1 mg/kg) abrogated the Cl₂-induced changes in responsiveness. We conclude that chlorine exposure causes functional and pathological changes in the airways associated with oxidative stress. Inducible nitric oxide synthase is involved in the induction of changes in responsiveness to methacholine.

Key Words: chlorine • inducible nitric oxide synthase • nitric oxide • oxidative injury

This article has been cited by other articles:

				R. V. Babu, V. Cardenas Jr, and G. Sharma Acute Respiratory Distress Syndrome From Chlorine Inhalation During a Swimming Pool Accident: A Case Report and Review of the Literature J Intensive Care Med, July 1, 2008; 23(4): 275 - 280. [Abstract] [PDF]

				G. Bonetto, M. Corradi, S. Carraro, S. Zanconato, R. Alinovi, G. Folesani, L. Da Dalt, A. Mutti, and E. Baraldi Longitudinal Monitoring of Lung Injury in Children after Acute Chlorine Exposure in a Swimming Pool Am. J. Respir. Crit. Care Med., September 1, 2006; 174(5): 545 - 549. [Abstract] [Full Text] [PDF]

				J.-L. Malo Future advances in work-related asthma and the impact on occupational health Occup. Med., December 1, 2005; 55(8): 606 - 611. [Abstract] [Full Text] [PDF]

				C. E. Mapp, P. Boschetto, P. Maestrelli, and L. M. Fabbri Occupational Asthma Am. J. Respir. Crit. Care Med., August 1, 2005; 172(3): 280 - 305. [Abstract] [Full Text] [PDF]

				G. Zhan, P. Fenik, D. Pratico, and S. C. Veasey Inducible Nitric Oxide Synthase in Long-term Intermittent Hypoxia: Hypersomnolence and Brain Injury Am. J. Respir. Crit. Care Med., June 15, 2005; 171(12): 1414 - 1420. [Abstract] [Full Text] [PDF]

				M. J. Tobin Asthma, Airway Biology, and Nasal Disorders in AJRCCM 2003 Am. J. Respir. Crit. Care Med., January 15, 2004; 169(2): 265 - 276. [Full Text] [PDF]