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beryllium disease established at the Massachusetts General Hospital (Hall et al., 1959).

Silica exposures are generally considered important only for chronic disease production. However, the condition of acute silicosis is caused by relatively short-term, high-intensity exposures to very fine silica particulate (Jones et al., 1975). Exposures as brief as six months have been associated with acute silicosis. Yet even in the absence of such severe overexposures and acute clinical disease, there is evidence that low-level exposures, not associated with clinical symptoms or chest X-ray abnormality, can result in irreversible pathology (Craighead and Vallyathan, 1980).

Similarly, asbestos exposures are noted for causing chronic respiratory illness, as well as cancer. Brief high exposures are not recognized to cause respiratory complaints. However, relatively short-term exposures of less than four years have been associated with increased respiratory symptoms and decreased vital capacity (Rodriques-Roisin et al., 1986).

It should be noted that beryllium, asbestos, and silica are relatively insoluble particles that remain in the lungs for months to years following inhalation. Thus even a brief exposure results in a chronic exposure of lung tissue to the agent.

Based on this review, a set of answers has been suggested for the following key questions regarding sulfur mustard and Lewisite exposure and chronic nonmalignant pulmonary disease. However, it should be kept in mind that there is a striking absence of knowledge about the early stages of environmentally related pulmonary diseases and almost no knowledge on the natural (longitudinal) evolution of the clinical conditions. Thus, there is little to guide us towards the appropriate disease model or towards identification of the relevant pattern(s) of exposure for disease etiology.

Does the occurrence of an acute pulmonary reaction following exposure to toxic chemicals identify an individual at risk for long-term respiratory sequelae? Ample evidence has been provided for all of the agents reviewed that a significant portion of individuals who react acutely to short, high exposures (and even some to short, relatively low exposures) go on to develop a variety of long-term respiratory effects. The agents differ in the probability of long-term adverse outcomes, but none appear to be free of this risk. The literature reviewed does not allow identification of a minimum magnitude of acute response necessary in order for there to be long-term sequelae.

If acute pulmonary reactions can identify individuals at risk for long-term sequelae of chemical exposures, can the probability or degree of damage be predicted from  the magnitude of the acute

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