THUNDERSTORM ASTHMA DUE TO GRASS-POLLEN

It is widely known and accepted that grass pollen is a major outdoor c ause of hay fever, Moreover, grass pollen is also responsible for trig gering allergic asthma, gaining impetus as a result of the 1987/1989 M elbourne and 1994 London thunderstorm-associated asthma epidemics. How ever, grass pollen is too large to gain access into the lower airways to trigger the asthmatic response and micronic particles <5 mu m are r equired to trigger the response. We have successfully shown that ryegr ass pollen ruptures upon contact with water, releasing about 700 starc h granules which not only contain the major allergen Lol p 5, but have been shown to trigger both in vitro and in vivo IEE-mediated response s. Furthermore, starch granules have been isolated from the Melbourne atmosphere with 50-fold increase following rainfall. Free grass pollen allergen molecules have been recently shown to interact with other pa rticles including diesel exhaust carbon particles, providing a further transport mechanism for allergens to gain access into lower airways. In this review, implication and evidence for grass pollen as a trigger of thunderstorm-associated asthma is presented. Such information is c ritical and mandatory for patient education and training in their alle rgen avoidance programs. More importantly, patients with serum IgE to group 5 allergens are at high risk of allergic asthma, especially thos e not protected by medication. Therefore, a system to determine the to tal atmospheric allergen load and devising of an effective asthma risk forecast is urgently needed and is subject to current investigation.