those exposed to what appear to be comparable levels are affected. This points to a role of individual susceptibility. In turn, the key factor which makes an individual susceptible may well be the capacity of his or her airways to become reactive to inhaled materials.
Different patterns of asthmatic reactions have been noted in response to high and low molecular weight agents. The former (proteins, polysaccharides and peptides) produce specific IgE (sometimes IgG) antibodies, generally have a positive immediate skin test to extracts, and produce results in isolated immediate or biphasic (immediate and late) reactions, but generally do not show isolated late reactions. These appear not to differ in mechanism from asthma due to common allergens such as house dust.
The latter, low molecular weight agents appear to be of two types. Some (e.g., the anhydrides or platinum salts) act as haptens and show asthma patterns similar to the high molecular weight agents. Others, best exemplified by the isocyanates, do not produce IgE in most responders. The asthma associated with isocyanates affects 5-10% of the exposed, and is associated predominantly with a late phase (isolated or part of a biphasic reaction) response to inhalation challenge studies. The asthma persists after removal in many and appears to affect atopic and non-atopic individuals equally.
Immunologically active substances can cause occupational asthma in some exposed workers while exposure to nonimmunogenic substances (i.e., irritants) may cause reactive airway dysfunction (RADS) or irritant induced occupational asthma in a wider population. Asthma and airway hyperresponsiveness typically occur together although they are not synonymous, so irritant-induced asthma is not necessarily caused through an acquired airway hyperreactivity mechanism. Documentation of the mechanism, however, would be strongly suggestive.
Hyperresponsiveness is an amplification of the normal physiologic response to irritant stimulation. It is a characteristic of asthma, but is not always associated with overt asthma or with respiratory symptoms. It can be an inherent characteristic of the person or an acquired one, and it can be either temporary or permanent. Distribution of hyperresponsiveness in population studies is skewed, possibly bimodal. It has been hypothesized that it may lead to, or may be a predisposing factor in, subsequent chronic obstructive lung disease. This is a candidate for