only the IgE-mediated diseases. It is not clear why or under what conditions fungal particles can have this dual effect.
Research Agenda Item: Study the differences between fungal and other allergen-carrying particles that control the development of hypersensitivity pneumonitis as opposed to IgE-mediated asthma.
Many of the protein allergens have long been recognized, but a lengthening list of newly recognized allergenic chemicals is developing. Allergic diseases caused by these chemicals can differ from those caused by protein allergens in terms of symptoms, mechanisms of action, and appropriate treatment. The diseases can differ also in terms of etiology and exposure, i.e., often occurring at the work site. A better understanding of these differences will assist in the formulation of improved measures of prevention and treatment.
Research Agenda Item: Determine the types of allergic diseases caused by reactive allergenic chemicals, their prevalence rates, and the mechanisms responsible for the resulting airway reactions.
A body of knowledge about chemical allergens is available, but many areas have not been well studied. Other chemicals besides those already reported to cause allergic reactions may provoke responses. Thus, as new chemicals are introduced, the list of agents that elicit allergic reactions is likely to grow.
Research Agenda Item: Identify the risk factors, such as a specific immunologic response, that are predictive of the development of chemically induced sensitization or allergic disease, and as soon as possible after their introduction, determine the sensitizing potential of new chemical entities. This knowledge will facilitate the development of primary and secondary preventive strategies.
The allergic rhinitis, conjunctivitis, and asthma that arise from exposure to chemicals appear to be due to classic immunologic reactions. However, late respiratory systemic syndrome (LRSS) and immunologic hemorrhagic pneumonitis occur only in response to chemical exposures and are not the result of response to the usual protein allergens; the mechanisms of immunologic damage in these two cases are not entirely known. The mechanism of non-IgE-mediated isocyanate asthma is also unclear.
Research Agenda Item: Determine the disease mechanisms of chemically induced LRSS, of immunologic hemorrhagic pneumonitis, and of non-IgE-mediated isocyanate asthma. Appropriate in vitro or in vivo models should also be developed.