A second type of irritant-induced asthma was not so sudden in onset and embodied features differing from RADS. The causative exposure persisted >24 h, was not brief, and asthma took longer to develop, sometimes days or weeks after repeated exposures.
The prevalence of atopy among subjects with the first type (sudden-onset irritant-induced asthma) who were considered to have RADS was 15 of 29 (52%), which though high was not statistically significant. Consistent with our findings is the rate of allergy/atopy reported for clinical facilities evaluating pulmonary patients with asthma Atopic prevalence might well be lower if other populations, such as orthopedic patients, were examined. Our investigation found that allergy/atopy prevalence was not increased among other asthma categories (38% for not occupational/environmental asthma and 9% for asthma due to sensitizer groups). The lower prevalence found for asthma due to an occupational sensitizer is in agreement with reported observations of asthma caused by low molecular weight chemical agents. emergency sepsis
Some subjects with new-onset irritant-induced asthma were actually in remission from a preexisting asthmatic state. Usually the remission had been present for years before the irritant exposure, during which time the person remained asymptomatic and did not require medications. It is reasonable to conclude that the irritant exposure exacerbated asthma in these individuals. We infer that such subjects, if studied prior to the occurrence of the irritant exposure, would manifest distinct pathologic airway changes, nonspecific airways hyperresponsiveness, and/or other biochemical abnormalities.
Persons with a history of asthma who were asymptomatic and considered themselves “normal” might demonstrate respiratory physiologic abnormalities that could become clinically evident as asthma after an irritant exposure. Nonspecific airway hyperresponsiveness has been found to be common among atopic persons with rhinitis, asymptomatic asthmatic subjects, and presumably, some “normal” persons. Individuals in this investigation, with preexisting asthma in remission, who developed a sudden-onset asthma after a high-level irritant exposure, would not be considered to have RADS or to have suffered newly acquired asthma.
For the not-so-sudden asthma cases, it is difficult to explain why a low-level, moderate-irritant exposure would provoke persistent airway inflammation and hyperresponsiveness. These irritant exposures were adjudged not to be of the magnitude described for subjects with RADS and there was a longer onset time (eg, >24 h) because the subjects could tolerate a lower-level exposure.