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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.

  1. If acute pulmonary reactions can identify individuals at risk for long-term sequelae, can the probability or degree of damage be predicted from  the magnitude of the acute response? The second question has generally not been studied. The fact that an association of dose is found with the acute as well as the chronic responses, provides support for the association, but not for a relationship between the magnitude of the acute response and the magnitude of the chronic response. Only in the case of the non-asthma-like isocyanate effects has the question been directly addressed. Here the acute cross-shift change in FEV1 has several times been significantly correlated with accelerated decrement in function. This association, however, is not invariant since the highly significant correlations were still under 0.5. Furthermore, the acute symptomatic response has not been a reliable predictor of accelerated functional losses.

    If the disease model invoked requires the acute exposure to cause acute irreversible damage one might propose that it is likely the magnitude of acute response would predict the magnitude of the chronic. However, if the model invoked is that the acute exposure resulted in or led to an alteration in individual risk factors, then it is quite likely that the magnitude of the acute and chronic responses would be unrelated.

  2. What assurance is there that the absence of an acute pulmonary reaction identifies individuals who will not develop long-term sequelae? This may be the most important question to ask and, unfortunately, the one for which no direct evidence could be found. The indirect evidence reported, however, would suggest that it would have to be an unusual disease model which would need to be invoked that could exclude the possible mechanism of change in individual risk factors so that the absence of an acute reaction would eliminate the possibility of a chronic effect related to the acute exposure.

LITERATURE CITED

1. Somani SM, Babu SR. Toxicodynamics of sulfur mustard. Int J Clin Pharm Therapy Tox (1989) 27:419-435.

2. World Health Organization. 1984 report of the specialists appointed by the Secre-



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