Occupational asthma, lung function decrement, and toluene diisocyanate (TDI) exposure: a critical review of exposure-response relationships.

An extensive amount of clinical/epidemiological literature exists regarding the effects of toluene diisocyanate (TDI) exposure on respiratory health. This review presents an evaluation and synthesis of that literature with an emphasis on assessing exposure-response relationships in the workplace. The key respiratory disorders examined are bronchial asthma and an accelerated decline in lung function. In the early years of the industry, annual incidence rates of TDI-induced occupational asthma (OA) were as high as 5-6 percent. In settings where mean TDI concentrations have been maintained below 5 ppb based on 8-hr personal samples, OA incidence rates have declined to < 1 percent annually. Recent data also suggest that overexposure incidents may play an important role in inducing OA, particularly in work environments engineered to minimize routine ambient air concentrations. Fourteen studies were reviewed that examined lung function decrement. Early studies from the 1960s and 1970s provided evidence of transient or fixed lung function loss (measured as a decline in forced expiratory volume in one second [FEV1]) during periods of ongoing exposure among employees experiencing high rates of work-related symptoms of OA. Such findings would not be unexpected in that modest FEV1 declines have been demonstrated in general population studies of persons with bronchial hyperresponsiveness or persistent non-occupational asthma. More recent workplace studies have provided no consistent evidence of accelerated FEV1 loss among employees exposed up to 5 ppb TDI (8-hr TWA) even with documented routine short-term TDI concentrations exceeding 20 ppb TDI.