Developments in the understanding of causes and natural history of asthma induced by isocyanates may allow improved preventive strategies for occupational asthma (OA), and may also lead to improved understanding of mechanisms involved in IgE-independent nonoccupational asthma. Studies of genetic markers in OA induced by isocyanates suggest that HLA class II genes, glutathione S-transferase and NAT1 genotypes may predispose to development of this type of OA. Specific IgE antibodies against isocyanates are not always found in subjects with OA caused by isocyanates, leading most researchers to consider this type of OA, as a model of IgE-independent asthma. Evidence for cell-mediated immunity in OA induced by isocyanates has been provided by bronchoalveolar lavage, bronchial biopsy and induced sputum studies. The pathology of this type of asthma is similar to that of nonoccupational asthma, with cells such as eosinophils and T lymphocytes that exhibit signs of activation, and with thickening of the reticular layer of the basement membrane. Animal studies have shown that isocyanate asthma is driven primarily by CD4+ T cells and is dependent upon the expression of Th2 cytokines. However, animal models are not always reflective of human responses. OA induced by isocyanates similarly to nonoccupational asthma, is a multifactorial condition, and it is likely that complex gene-environment interactions play a role. Better understanding of these interactions is important for affected workers, and also has potential relevance for nonoccupational asthma.
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