response relationship in a rat model of immunologic TMA disease (Zeiss et al., 1989). It is likely that such relationships also exist in humans, but there are no data to illuminate such linkages. (Quantitative exposure data from animal experiments may not necessarily translate to humans.)
Other than exposure, risk factors for the development of sensitization to a given chemical have not been defined. In studies of risk factors for development of sensitization to chemicals such as TDI, atopy and airway hyperreactivity were either not predictive or only weakly so (I. L. Bernstein, 1982; Chester and Schwartz, 1979; Nicholas, 1983).
Although some of the control measures used in industrial settings may not be directly applicable to the indoor air environment, the model of reduced exposure that results in reduced sensitization rates is applicable to indoor aeroallergens. Prospective studies of TMA workers (Grammer et al., 1991b; Zeiss et al., 1983, 1992) have reported that serial immunologic studies are useful in predicting which individuals are likely to develop immunologically mediated disease. With careful monitoring, those workers who develop specific antibody can be removed from exposure at the onset of any allergic symptoms. Alternatively, if the development of disease seemed very likely, the worker could be relocated at the onset of serologic positivity. In TMA workers, there is evidence that development of specific antibody is predictive of allergic disease, but this finding has not been confirmed in a definitive manner in populations of workers exposed to other chemical allergens.
The timing of removal from exposure relative to disease onset is important. Some data suggest that early removal of workers who develop asthma as a result of chemical exposure will allow most of them to return to normal pulmonary function. In contrast, asthma tends to persist among workers who have had the disease for several years before they are removed from exposure (Chan-Yeung, 1990). This is especially true for workers who already have abnormal pulmonary function.
With respect to reducing exposure, there is evidence that decreasing airborne concentrations of a chemical such as TMA reduces disease prevalence (Boxer et al., 1987; Chan-Yeung, 1990). As outlined earlier, other evidence in animals and in humans suggests the existence of environmental exposure concentration thresholds and environmental concentration exposure-immunologic response relationships. If these thresholds and relationships could be defined for chemical allergens, reducing exposure could be the best approach to preventing allergic disease caused by these substances. Exposure reduction measures would include improved ventilation, work practices, and protective equipment.