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Toxicology of Industrial Compounds

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Table 10.1 Chemicals identified as human respiratory allergens<br />

I.KIMBER 139<br />

inhalation <strong>of</strong> the chemical allergen, it is likely that this is an important<br />

route <strong>of</strong> exposure in the occupational setting.<br />

It is well established that respiratory sensitization caused by protein<br />

aeroallergens is effected by IgE antibody. This class <strong>of</strong> antibody in man is<br />

homocytotropic and is able to associate, via specific membrane receptors,<br />

with mast cells, including mast cells in the respiratory tract. Following<br />

subsequent exposure <strong>of</strong> the sensitized individual to the same allergen, mast<br />

cell-bound IgE is cross-linked and this, in turn, results in mast cell<br />

degranulation and the release <strong>of</strong> both preformed and newly-synthesized<br />

mediators which provoke acute inflammatory reactions. In the case <strong>of</strong><br />

sensitization <strong>of</strong> the respiratory tract caused by chemicals, however, an<br />

invariable association with the presence <strong>of</strong> specific IgE antibody has failed<br />

to emerge. Although IgE antibody specific for all recognized chemical<br />

respiratory allergens has been demonstrated, it is not uncommonly the case<br />

that individuals displaying symptoms <strong>of</strong> pulmonary hypersensitivity have<br />

been reported to lack demonstrable IgE. This may suggest that<br />

immunological processes independent <strong>of</strong> IgE antibody may play a decisive<br />

role in the induction <strong>of</strong> respiratory sensitization. An alternative explanation<br />

is that inappropriate or insensitive techniques have been employed for<br />

serological analysis and that IgE antibody may be associated more<br />

commonly than suspected previously with chemical respiratory allergy. In<br />

this context it is relevant that it has been found that positive skin prick<br />

tests can be provoked in patients sensitized to acid anhydrides who, on the<br />

basis <strong>of</strong> radioallergosorbent tests (RAST), were found to lack measurable<br />

levels <strong>of</strong> serum IgE antibody (Drexler et al., 1993). Despite the absence <strong>of</strong><br />

formal confirmation that there exists a universal causal relationship<br />

between specific IgE and pulmonary hypersensitivity induced by chemicals,

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