Inhalation of chlorine causes lung inflammation and airway hyperresponsiveness in a rat model of chemical-induced lung injury

We investigated acute and late inflammatory changes after exposure to chlorine (Cl 2 ) with the aim to identify biomarkers of adverse inflammatory responses. Such biomarkers would be of value to diagnose whether an exposed individual would be at risk for persistent lung injuries.This study compares changes in pulmonary function (AHR),selected endpoints in serum, and bronchoalveolar lavage fluid (BALF) following a single, 15-min nose-only exposure of rats to 200 ppm Cl 2 . The time-course of lung injury was locally and systematically examined up to 14 days post exposure with the objective to identify early diagnostic biomarkers suitable to guide countermeasures to accidental exposures. One exposure to Cl 2 was non-lethal and all rats (female Sprague-Dawley) displayed signs of anorexia and lethargy up to 24 h post exposure. Cl 2 -exposed rats displayed elevated numbers of total leukocytes with a significant increase of neutrophils (p 2 induced increased lung weight (p 2 -exposed rats as compared to the control group at 24 h post exposure. On day 14, there were signs of lung fibrosis as indicated by increased collagen deposition in tissue. By the use of this model,there is a potential for understanding the mechanisms by which exposure to chemical compounds, such as Cl 2 , causes long-term effects. These results provide a foundation for future studies aimed at identification of biomarkers for adverse inflammatory responses, as well as for evaluation of new concepts for treatment of chemical-induced lung injury.