It is widely known and accepted that grass pollen is a major outdoor cause of hay fever. Moreover, grass pollen is also responsible for triggering allergic asthma, gaining impetus as a result of the 1987/1989 Melbourne and 1994 London thunderstorm–associated asthma epidemics. However, grass pollen is too large to gain access into the lower airways to trigger the asthmatic response and micronic particles <5 μm are required to trigger the response. We have successfully shown that ryegrass pollen ruptures upon contact with water, releasing about 700 starch granules which not only contain the major allergen Lol p 5, but have been shown to trigger both in vitro and in vivo IgE–mediated responses. 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 particles 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 critical and mandatory for patient education and training in their allergen avoidance programs. More importantly, patients with serum IgE to group 5 allergens are at high risk of allergic asthma, especially those not protected by medication. Therefore, a system to determine the total atmospheric allergen load and devising of an effective asthma risk forecast is urgently needed and is subject to current investigation.