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tent; for overexposure to chlorine, abnormalities were found to be rarely persistent. In a community study based on a population exposure to chlorine, subjects exposed during the derailment of a tank car were followed up six years after the accident. The rate of annual decline in FEV1 was found to be unrelated to the initial clinical status of the subjects (Jones et al., 1986).

Becklake concludes that none of the many case reports, nor the one community study, provides evidence to suggest that the pathophysiologic process induced by the exposure to an irritant gas was progressive. Persistent pulmonary damage did not appear to be determined by the degree of acute response at the time of the exposure, or by the extent of initial recovery that occurred during the several months following the exposure.

Exposures to cotton dust or components of the dust have been noted to cause both acute and chronic effects. The acute effects are represented by both a disabling respiratory syndrome (byssinosis) and a cross-shift decrement in FEV1. Chronic effects include both accelerated annual decrements in FEV1 and chronic bronchitis. The acute syndrome does not necessarily remit on removal from exposure, and there is a growing body of evidence to suggest a relationship between the acute effects and chronic airflow limitation. There is evidence that short-term exposures result in acute effects (Castellan et al., 1987; Martin and Higgins, 1976), but no evidence for whether such exposures, with or without an acute response, ultimately lead to chronic effects.

Isocyanates have been noted to cause several acute conditions, including chemical bronchitis and allergic bronchoconstriction (Axford et al., 1976; Brooks et al., 1985) and large dose-related cross-shift losses in FEV1 (Peters et al., 1968). The chronic respiratory effects caused by isocyanates include accelerated loss in pulmonary function over several years, suggesting the development of chronic airway limitation, and irreversible asthma (Peters and Wegman, 1975). There is also evidence that the presence of acute effects predicts both the development of chronic asthma and an accelerated rate of loss in lung function in nonasthmatics. Finally, there is evidence that short-term exposures to isocyanates can cause acute responses that are irreversible and progressive, but there is no evidence as to whether such short-term exposures without acute response result in irreversible respiratory effects.

Beryllium exposures have also been associated with both acute and chronic pulmonary disease, both of which have been shown to be disabling (AMA Archives of Industrial Health, 1959). Relevant to the present question, beryllium exposures, in one instance as brief as one week and in several instances occurring for less than ten weeks, have resulted in disease certified for inclusion in the registry of cases of



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