Tobacco smoke sensitivity: a result of allergy?

In summary, we know that IgE antibodies against crude tobacco leaf are present in smokers, nonsmokers, and ex-smokers and that atopic individuals are far more likely to show such responses than nonatopic individuals. It has also been established that IgE antibodies can be detected against at least three specific tobacco leaf allergens, namely CIE antigens 19, 23, and 30, but these IgE antibodies do not correlate with any type of clinical smoke sensitivity. To date, there is no concrete evidence for the presence of IgE antibodies in man against smoke extract. Finally, there is at least preliminary evidence that smoke challenge under controlled conditions in an environmental chamber does not induce significant decreases in FEV1 or peak flow in smoke-sensitive subjects, even though they complain of symptoms. In essence, we know that tobacco leaf is immunogenic in rabbits, but it is not known if any tobacco incineration products per se are immunogenic in man. One can visualize many possible future extensions of this study. We should, for example, learn more about other immunoglobulin class-specific antibody responses in man to tobacco leaf antigens, and we should make an effort to identify those antigens that are collected in extract and condensate from unlit cigarettes. We should also undertake larger studies involving further inhalation challenge tests in patients, and employing more sensitive tests of airways obstruction. The problem of shared antigens between tobacco and many other members of the Solanaceae family and the possible clinical relevance of antibody responses to foods as they relate to inhalant allergens should also be studied. The increased interest in tobacco smoke and its relationship to putative immunologically mediated tobacco smoke hypersensitivity has necessitated further studies of clinical smoke sensitivity. To date, the role of hypersensitivity responses in tobacco smoke sensitivity is as yet undefined. In spite of the considerable number of previous studies and their supporting evidence of an allergic response to tobacco smoke, the obvious pitfalls of these studies (undefined study populations, inappropriate antigens, and inadequate documentation of smoke sensitivity) undermine any significant conclusions. In view of the lack of information relating to tobacco smoke hypersensitivity in man, it is difficult to recommend specific diagnostic or therapeutic strategies. Clearly, skin test and RAST studies have proved invaluable in studies of many IgE-mediated allergic disease syndromes related to certain environmental allergens.(ABSTRACT TRUNCATED AT 400 WORDS)