Prospective clinical studies have not clearly documented de novo induction of long standing AHR by moderate irritant exposures. A report of workers exposed to calcium oxide dust did not find an increase in new-onset buy asthma inhalers. However, recurrent exposures to high levels of chlorine have been associated with an increased prevalence of asthma and AHR. A spill of glacial acetic acid was reported to induce RADS in four exposed individuals with an apparent dose-response relationship. In that study, three of 14 subjects with high level exposure developed RADS compared with one of 30 with moderate exposure.
Because an animal model of RADS would allow better determination of the pathogenesis of this syndrome, the present study was designed to develop such a model. A previous report of the development of RADS following a high dose of acetic acid prompted the investigation of the effect of high dose inhaled acetic acid in an animal model. Fischer rats were chosen due to their relative baseline AHR. The short term effects of a single high dose exposure of inhaled methacholine (Mch) on airway responsiveness, lung resistance (Rl) and lung elastance (El) were assessed. It was hypothesized that this exposure would increase RL and airway responsiveness.