Article excerpts about the
causes of Pollen allergy:
Plants produce microscopic round or oval pollen grains to reproduce. In some
species, the plant uses the pollen from its own flowers to fertilize itself.
Other types must be cross-pollinated; that is, in order for fertilization to
take place and seeds to form, pollen must be transferred from the flower of one
plant to that of another plant of the same species. Insects do this job for
certain flowering plants, while other plants rely on wind transport.
The types of pollen that most commonly cause allergic reactions are produced by the plain-looking plants (trees, grasses, and weeds) that do not have showy flowers. These plants manufacture small, light, dry pollen granules that are custom-made for wind transport. Samples of ragweed pollen have been collected 400 miles out at sea and 2 miles high in the air. Because airborne pollen is carried for long distances, it does little good to rid an area of an offending plant--the pollen can drift in from many miles away. In addition, most allergenic pollen comes from plants that produce it in huge quantities. A single ragweed plant can generate a million grains of pollen a day.
The chemical makeup of pollen is the basic factor that determines whether it is likely to cause hay fever. For example, pine tree pollen is produced in large amounts by a common tree, which would make it a good candidate for causing allergy. The chemical composition of pine pollen, however, appears to make it less allergenic than other types. Because pine pollen is heavy, it tends to fall straight down and does not scatter. Therefore, it rarely reaches human noses. (Source: excerpt from Something in the Air Airborne Allergens: NIAID)
As with all medical conditions, there may be many causal factors. Further relevant information on causes of Pollen allergy may be found in:
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The causes of anaphylactic reaction are ingestion of or other systemic exposure to a sensitizing drug or other substance.
Sensitizing substances include serums (usually horse serum), vaccines, allergen extracts, enzymes (such as l-asparaginase), hormones, penicillin and other antibiotics, sulfonamides, local anesthetics, salicylates, polysaccharides, diagnostic chemicals (sulfobromophthalein, sodium dehydrocholate, and radiographic contrast media), foods (legumes, nuts, berries, seafood, and egg albumin) and sulfite-containing food additives, and insect venom (honeybees, wasps, hornets, yellow jackets, fire ants, mosquitoes, and certain spiders).
A common cause of anaphylaxis is penicillin, which induces anaphylaxis in 1 to 4 of every 10,000 patients treated with it. Penicillin is most likely to induce anaphylaxis after parenteral administration or prolonged therapy and in atopic patients who are allergic to other drugs or foods.
An anaphylactic reaction requires previous sensitization or exposure to the specific antigen, resulting in the production of specific immunoglobulin (Ig) E antibodies by plasma cells. This antibody production takes place in the lymph nodes and is enhanced by helper T cells. IgE antibodies then bind to membrane receptors on mast cells (found throughout connective tissue, often near small blood vessels) and basophils.
On reexposure, the antigen binds to adjacent IgE antibodies or cross-linked IgE receptors, activating a series of cellular reactions that trigger degranulation — the release of powerful preformed chemical mediators (such as histamine, prostaglandins, and platelet activating factor) from mast cell stores. IgG or IgM enters into the reaction and activates the release of complement fractions.
This acute phase of the response occurs within minutes of exposure. Because of the systemic nature of the exposure, activation of mast cells is widespread, and the massive release of these powerful mediators near blood vessels leads to vascular collapse by stimulating contraction of certain groups of smooth muscles and by increasing vascular permeability. In turn, increased vascular permeability leads to decreased peripheral resistance and plasma leakage from the circulation to extravascular tissues (which lowers blood volume, causing hypotension, hypovolemic shock, and cardiac dysfunction).
In the later phase of this response (8 to 12 hours later), other mediators are synthesized and released, including chemokines, leukotrienes, and cytokines. These agents mediate the inflammatory response by recruiting eosinophils and lymphocytes. This delayed response may be less dramatic than the acute phase of anaphylaxis, but with a diffuse inflammatory response, further smooth-muscle contraction and edema can occur and progress to grave systemic symptoms.
Source: Handbook of Diseases, 2003
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