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STOP-EXPOSURE STUDIES OF INHALED CHLORINE PROVIDE IMPORTANT INSIGHTS ON PATHOGENESIS
Citation:
JARABEK, A. M., J. MCKEE, G. A. Wilson, M. H. George, R. H. JASKOT, D. G. ROSS, T. MOORE, AND T. S. Peay. STOP-EXPOSURE STUDIES OF INHALED CHLORINE PROVIDE IMPORTANT INSIGHTS ON PATHOGENESIS. Presented at Society of Toxicology 49th Annual Meeting, Salt Lake City, UT, March 07 - 11, 2010.
Impact/Purpose:
As part of a project to inform approaches for risk assessment of inhaled irritants of interest to homeland security, a set of acute (Peay et aI., SOT 2010) and subacute (George et aI., SOT 2010) studies of inhaled chlorine (CI2) in female F344 rats was performed.
Description:
As part of a project to inform approaches for risk assessment of inhaled irritants of interest to homeland security, a set of acute (Peay et aI., SOT 2010) and subacute (George et aI., SOT 2010) studies of inhaled chlorine (CI2) in female F344 rats was performed. The exposure design included equivalent exposure levels when calculated based on a daily "C x til product (ppm-hr). Additionally, stop-exposure studies were included that allowed for comparison across different study durations: the recovery period for the stop-exposure study after the 6-hr exposure coincided with the necropsy of the 5-day (6 hid, 5 d/w) exposure, and the recovery period of the stop-exposure study after the 5-day exposure coincided with the necropsy of the 14-day (6 hid, 5 d/w) exposure. A third stop-exposure study sacrificed animals 2 weeks after the 14-day exposure. The concentrations at which recovery was evaluated in these studies were 0, 1.0 and 10 ppm; O. 1.0 and 2.5; and 0, 0.1 and 1.0 ppm respectively. The "C x r equivalent levels were 0, 0.6,6.0, and 15 ppm-hr. Noses were sectioned transversely to provide six standard section levels for histopathology. Biochemical analyses of nasal lavage and bronchoalveolar lavage fluids included lactate dehydrogenase, N-acetyl-13D- glucosaminidase, and total protein. Inflammation in the nose tip and in the 1st two standard sections of the respiratory epithelium on the lateral wall (LAT RE) was the only persistent lesion after these stop exposures. After the 2-week recovery period, the LAT RE was the only region involved, and a significant proximal to distal pattern with both concentration and duration persisted. These results will be useful to a modeling effort mapping the trajectory of epithelial lesions due to inhaled CI2 across