Albumin-isocyanate conjugates

There are several possible routes whereby such responses can be affected. First, there is a neural response, as evidenced by the analogous symptoms of the cardiac and pulmonary chemoreflexes. Second, mediators released from the inflammatory cells in the lungs are carried by the blood directly to the heart. Of note, C3a and C5a which are released during anaphylaxis activate cardiac, but not limg mast cells (62). Third, antigens may penetrate the airway and alveolar epithelium and enter into the vasculature and directly interact with cardiac mast cells and basophils. This latter pathway is likely important when small molecules, such as sodium diisocyanate, are inhaled, as these molecules form albumin-isocyanate conjugates that may be related to the induction of toluene diisocyanate hypersensitivity (69). 

Isocyanate-induced asthma and hypersensitivity pneumonitis in humans have been reviewed (Baur, 1995 Bernstein, 1996). A case of fatal asthma of a 4,4 -mcthylcncdiphcnyl diisocyanate-scnsitized subject has been described (Carino et al., 1997). Exposure to 4,4 -methylenediphcnyl diisocyanate is a frequent cause of occupational asthma (Liss et al., 1988 Vogelmcicr et al., 1991 Bernstein et al., 1993) but may also induce hypersensitivity pneumonitis (Malo Zeiss, 1982 Vandenplas et al., 1993) and inflammatory upper respiratory tract diseases (Liss et al., 1988 Littorin et al., 1994). Most patients with 4,4 -methylenediphcnyl diisocyanate-induced asthma have elevated levels of IgG-class antibodies towards 4,4 -methylenediphenyl diisocyanate-albumin conjugates in the plasma, while IgE-class antibodies are rare (Liss et al., 1988). 

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