Seasonal or perennial allergic rhinitis (inflammation of the nose) may be caused by pollens, hay, dust mites, molds, or animal dander, including that of cats, dogs, horses, cattle, rabbits, gerbils, guinea pigs, and hamsters. Allergic rhinitis may also be triggered by exposure to foods, such as milk, eggs, peanuts, tree nuts, wheat, soy, some spicy foods, shellfish, and fish, among others. Perennial nonallergic rhinitis is caused by any number of chemical sensitivities—cigarette smoke, wood smoke, perfumes, scented candles, air fresheners, household cleaning agents (Pinesol, Lysol, Clorox, and ammonia…), car exhaust, diesel fuel, gasoline, or freshly sprayed pesticides. Perennial nonallergic rhinitis may also be triggered by environmental exposure to cold air, humid air, dry air, or high barometric pressure.
Nonallergic rhinitis may follow an infection (acute and chronic sinusitis, Churg-Strauss Syndrome, influenza, RSV infection, or common cold) or be caused by use of certain medications (overuse of decongestant nasal sprays such as Oxymetazoline products, floral-scented steroid nasal sprays, blood pressure medications such as beta-blockers, or cocaine abuse). Nonallergic rhinitis may occur in patients with benign tumors in the nose. Examples are nasal polyps (a growth in the nasal passages), angiofibroma (a growth comprising fibrous tissue and blood vessels), fibrous dysplasia (abnormal growth of bony tissue), hemangioma (an abnormal growth of blood vessels), inverted papilloma (a one-sided, wart-like growth), or osteoma (tumor of the bony tissue of the nose), and structure abnormalities (deviated septum, enlarged adenoids, congestion due to pregnancy, foreign body in the nose). Herbicides such as alachlor, acetochlor, metolachlor, and metolachlor-s cause nasal turbinate tumors in animals and chronic allergy symptoms in humans. Lastly, and significantly, perennial nonallergic rhinitis may be caused by hormonal changes resulting from prolonged exposure to endogenous estrogens, phytoestrogens, xenoestrogens, or other endocrine-disrupting chemicals.
Food allergy trend diagrams show that 1996-1997 was a turning point in food allergy rates. What happened in 1996 that started an upward trend in food reactions? In agricultural production, the major change in 1996 was the widespread usage of glyphosate (the major ingredient in Roundup) on genetically modified plants. Glyphosate is estrogenic; acts like an antibiotic to kill good gut bacteria; is a mineral chelator; and causes tumors in animals, according to several published studies. Food reactions may be IgE-mediated, IgG- mediated, non-IgE- mediated or non-IgG- mediated (as occurs with reactions to pesticides), estrogen-mediated, Xenoestrogens-mediated, or acetylcholine-mediated. Most environmental chemicals can cause allergy symptoms.
When food was produced naturally, food allergies were rare. Large-scale, commercial food production—in which chemicals are used as pesticides, preservatives, and to serve other functions—has led to increased reaction to foods. Chemicals bound to foods yield chemopeptides (toxpetides or xenopeptides), and estrogens bound to foods yield estropeptides. Chemical contamination of foods causes food molecules to be designated by the body as allergens, which are attacked by antigen-presenting cells. Increase in pesticide load correlates with the increase in food allergy and environmental allergies.
Note: Adult Onset Allergies may be hormone related.
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