Abstract

The study session discussion initially focussed on questions regarding the possible role of immunology in the pathophysiology of occupational asthma to toluene diisocyanate (TDI). Both the New Orleans group (as reported by Butcher and Salvaggio) and the Cleveland group (Gerblich et al.) performed skin testing on all their test subjects with TDI-induced asthma. Skin tests were performed with TDI conjugated with human serum albumin (TDI-HSA). When administered intradermally, the skin testing was generally negative. While a few of the tested subjects may have had a borderline skin response, the investigators interpreted these as negative, since the responses did not meet usually accepted criteria of positive allergic skin test reactivity. In fact, in extensive discussion of published and unpublished results it was agreed that most investigators have not been able to demonstrate good immunologic evidence for specific sensitization to TDI. However, a recent report from Pittsburgh suggests that antibodies have been demonstrated to TDI-HSA using a radioallergosorbent (RAST) assay. Unfortunately, this test is not widely available because of patents on the procedure to produce the RAST. One great problem in studying TDI asthma is the chemical nature of TDI, which is a highly reactive molecule that rapidly reacts or complexes with most compounds with which it comes into contact. The general concensus of opinion is that, at this time, TDI asthma has not been demonstrated to be an immunologically mediated disease. Further experimental work is now in progress and should be very helpful in understanding the pathogenesis of this disease. A discussion of host factors followed. It was pointed out that TDI is not usually detected by smell until it is present in an atmospheric concentration of about 2 ppm, which is well above the safety threshold limit value of 0.02 ppm. Thus, workers with TDI asthma can react to ambient concentrations well below levels detectable by smelling the TDI. The lowest dose

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