Delayed hypersensitivity airway inflammation

Immediate responses to skin prick tests are often used as evidence of specific sensitisation to occupationally encountered agents implying this is the causal mechanism of airway disease. However when assessing occupational dermatoses, patch testing is considered far more useful indicating delayed type hypersensitivity. They are used for many agents, e.g.chrome and nickel which are also recognised as respiratory sensitisers. The interpretation (and possibly relevance) of immediate skin responses to these agents is unclear. Is it possible that the mechanism of airway disease in some cases of occupational asthma is delayed hypersensitivity rather than Type 1 reactions and should we therefore not try patch testing if immediate response is negative? If skin inflammation occurs via this mechanism is it not possible that airway inflammation also occurs by this mechanism?

Occupational Asthma, Specialist, 2/20/2006, 2/20/2006,

We have looked at patch testing to colophony workers with occupational asthma to colophony, the only positive (out of about 20) was in a lady with contact dermatitis as well. It seems that although the same agents can cause contact dermatitis and occupational asthma, those with positive patch tests generally have dermatitis rather than occupational asthma. Has anybody done similar studies with chrome, cobalt or nickel? The situation with epoxy resins is different, as the dermatitis is mostly due to the resin, rather than the acid anhydride cross linking agents, which are the usual cause of asthma, and produce positive skin prick tests (particularly when conjugated to albumin)

2/20/2006