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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. [ABSTRACT FROM AUTHOR]

In recent years, occupational asthma has become the most frequent occupational lung disease in many countries. Reports and statements on the frequency of occupational asthma due to isocyanates are quite contradictory. In order to clarify the issue, a critical review of the medical literature of the past half century worldwide has been performed, with special emphasis on toluene diisocyanate (TDI) as the main representative of the isocyanate family. Nine longitudinal workplace studies of 2,751 persons under risk allow calculation of incidences of occupational asthma due to toluene diisocyanate. Annual incidences had repeatedly been above five percent before 1980, and have decreased to zero to 0.7 percent since 1980. There is a downward trend during the last half century that clearly parallels the downward trend of toluene diisocyanate exposure in some studies. Prevalences of occupational asthma due to toluene diisocyanate can be estimated from 10 cross-sectional studies, based on 788 persons. Prevalences had repeatedly been above 10 percent before 1985, and have been mostly between zero and 10 percent in recent years. [ABSTRACT FROM AUTHOR]

Diisocyanates have been the most commonly identified cause for occupational asthma (OA) in industrialized areas. Asthma among diisocyanate workers may be true occupational asthma, caused by a high level of irritant exposure at work or by sensitization to diisocyanates. Alternatively, asthma may be coincidental to or may be aggravated by work exposures. A clear diagnosis usually requires a combination of investigations (serial peak expiratory flow recordings, methacholine challenges, and/or diisocyanate challenges), but it is important to provide the best management by identifying whether workplace changes are needed for the worker. Preventive measures to reduce the risk of occupational asthma from diisocyanates have not been prospectively evaluated. The introduction of a medical surveillance program (in Ontario, Canada) in 1983 was followed by retrospective assessments to determine benefits. Between 1980 and 1993, the proportion of all accepted compensation claims for OA that were attributed to diisocyanates, classified by year of symptom onset in the province with the program, rose to 64 percent by 1988, then fell significantly down to 29 percent in 1992 and 35 percent in 1993. Besides the medical surveillance program for diisocyanates, possible factors contributing to this reduction may include reduced diisocyanates exposures and better awareness of diisocyanate-induced asthma, both by workers and physicians. Compared with OA caused by other agents, those with OA due to diisocyanates had a significantly earlier onset of asthma after the start of the exposure (mean 5 yr vs. 7 yr), were younger and less likely to be atopic and to have smoked. The mean duration of asthma before the main medical assessment for compensation was significantly shorter among those with diisocyanate-induced asthma (mean 2 yr vs. 3 yr), and the severity was milder as assessed by medication use and pulmonary function. Those with diisocyanate-induced asthma were significantly less likely to be hospitalized for asthma. Among the subset whose outcome was determined at a mean of 2.1 years after the main medical assessment, the outcome severity was less for those with diisocyanate-induced OA. Among those with diisocyanate-induced OA, an earlier diagnosis and a trend to better outcome was found in workers from companies that were identified to be in compliance with surveillance measures. [ABSTRACT FROM AUTHOR]

Reviews the book "The Harvard Medical School Guide to Taking Control of Asthma: A Comprehensive Prevention and Treatment Plan for You and Your Family," by Christopher H. Fanta et al.

Even the asymptomatic asthmatic person with normal lung function may have peripheral airway obstruction and inflammation along with hyperresponsiveness to nonspecific challenges. The airway caliber change induced immediately following a deep inhalation (DI) appears to relate to the mechanism (inflammation vs. smooth muscle constriction) and site (peripheral vs. more central) of obstruction and the degree of hyperresponsiveness. Data are presented and reviewed that support the notion that relative hysteresis of parenchyma (including peripheral airways and alveolar ducts) and airways (more centrally located, conducting airways) can explain the magnitude and sign of airway caliber change that follow a DI in asthmatic subjects. [ABSTRACT FROM AUTHOR]

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