there are well-documented acute and chronic non-specific airway effects from isocyanate exposures. Peters' studied workers exposed to very low levels of TDI. His work demonstrated significant change in FEV1 over the workshift.⁶⁷ A three year prospective study of these same workers demonstrated the losses were not just acute; exposed workers experienced accelerated losses over three years and there appeared to be a correlation between the magnitude of cross-workshift change and the accelerated functional loss.^68,69 My own work provided preliminary information on the relationship of acute and chronic losses to exposure level and that the effects persisted after controlling for cigarette smoking.^70,71 Epidemiology studies have also provided a preliminary estimate of a no-effect level⁷².

Work by Weill and his colleagues, in a prospective study of a new plant confirmed the broad population dose-related effects of chronic TDI exposure while directly accounting for healthy worker selection. ^73,74 Their work raised the possibility that peak exposures might be important not only for asthma⁷⁴ but for the non-asthma related chronic losses as well. These epidemiologic studies provided sufficient evidence that TDI was not a problem  for only a small population of sensitized workers, but that the agent was a risk for all TDI workers.

Finally no epidemiologic studies have yet examined the importance of the case reports of hypersensitivity pneumonitis as an exposure consequence.⁵⁵ As these are being reported with increasing frequency their relative importance as a risk from this chemical exposure is an important priority to determine.

In summary, isocyanates (a series of small molecular weight chemical compounds) have been noted to cause 1) several acute conditions: chemical bronchitis, allergic bronchoconstriction (after short-term high exposures as well as following longer-term lower exposures), and to cause large dose-related cross-shift loss in FEV₁; and 2) chronic respiratory effects including accelerated loss in pulmonary function over several years (suggesting the development of chronic airway limitation) and irreversible asthma. There is also evidence that the acute effects are related to the chronic effects both as asthma that does not remit and as cross-shift loss which is related to the rate of subsequent annual loss. Finally, there is evidence that short-term exposures can cause acute responses that are irreversible and progressive, but there is no evidence, either way, as to whether short-term exposures without acute response result in irreversible respiratory effects.

Beryllium exposures have been associated with both acute and chronic pulmonary disease.⁷⁵ Both acute and chronic conditions have