Mayo Clinic

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mayo clinic study

mold fast facts a 1999 mayo clinic study cites molds as the cause of most of the chronic sinus infections that inflict 37 million americans each year. recent studies also link molds to the soaring asthma rate. molds have been an under recognized health problem, but that is changing. healthcare professionals now know that molds can cause allergies, trigger asthma attacks and increase susceptibility to colds and flu. anyone with a genetic predisposition can become allergic if exposed repeatedly to high enough levels. last year dr. david sherris at the mayo clinic performed a study of 210 patients with chronic sinus infections and found that most had allergic fungal sinusitis. the prevailing medical opinion has been that mold accounted for 6 to 7 percent of all chronic sinusitis. the mayo clinic study found that it was 93 percent - the exact reverse. newsweek, 12/4/00 there are over 100,000 known living species of fungus, some of which are beneficial to mankind. mycologists estimate that there may be as many as 200,000 more unidentified species of fungus. yeasts, molds, mildews, rusts, and mushrooms are types of fungus. mold spores cause illness, other than allergy and/or infections. it is the mycotoxins released when the molds' food source (moisture) is severed. to help comprehend how small mycotoxins are, one common housefly could carry about 7.35 billion attached to its external body hairs. consequently, if 50,000 constitute a theoretically lethal dose, a housefly could carry a lethal dose for over 100,000 individuals. when the stachybotrys mold dries, the mycotoxin production increases up to 40,000 times. outdoor spores are not a usual cause of toxicity, (except for allergies and infection), but when growing inside, molds produce toxins, which are in much higher concentration and can cause illness. indoor mold spores indicate mold growth, which indicates mycotoxin production. currently, we can measure spores, identify spores, but it is difficult to measure mycotoxins. stachybotrys produces at least 170 known mycotoxins, and probably more that have not been identified. the trick with mold is control the moisture and excessive food sources. if there are no structure defects that allows moisture in then get a cheap hygrometer / thermometer ($25) and monitor it. don't let the humidity climb above 60% for two days or more. pay attention to basements. humidity sinks to the basement in the summer. if you have a little more money, get a humidistat or a dehumidifier installed on your "balanced" hvac system. new abstract of their recent study presented to the : american academy of allergy, asthma and immunology : (at the 2001 annual meeting) : http://www.harcourthealth.com/scripts/om.dll/serve?action=searchdb&searchdbf

or=art&arttype=misc&id=aai011072b3ab0536 abnormal immunologic responses to fungal antigens in patients with chronic rhinosinusitis : (seung-heon shin & hirohito kita @ mayo clinic foundation, rochester, mn) background: chronic rhinosinusitis (crs) is one of the most frequent chronic diseases in the u.s.; however, the etiology is not well understood. sinus mucosae of patients with crs are characterized by the presence of inflammatory cells, especially eosinophils and il-5 producing t cells. because nasal and sinus cavities of humans are colonized with fungi, we tested the hypothesis that immunologic responses to these fungal antigens are involved in the pathophysiologic mechanisms of crs. methods: peripheral blood mononuclear cells (pbmc) were isolated from 18 crs patients (10 allergic, 8 nonallergic) and 15 normal volunteers and were stimulated with extracts from 5 common fungal species (alternaria, aspergillus, candida, cladosporium, and penicillium). after 72 hours of incubation, pbmc proliferation responses were examined, and supernatants were analyzed for the amounts of cytokines produced (il-4, il-5, il-13, and ifn-). results: when cultured with fungal antigens, pbmc from normals, as well as those from crs patients, proliferated; there was no significant difference in the increased proliferative responses between normals and patients. interestingly, pbmc from almost all the crs patients produced il-5 and il-13 when stimulated with alternaria or candida antigens; there were no differences in the amounts of these cytokines between allergic and nonallergic crs patients. in contrast, no or minimal il-5 and il-13 were produced by pbmc from normal volunteers when stimulated with these fungal antigens. furthermore, in response to alternaria and candida antigens, crs patients' pbmc produced approximately 10-times more ifn- compared to normal volunteers' pbmc; il-4 was undetectable. aspergillus, cladosporium and penicillium extracts minimally stimulated cytokine production by patients' pbmc. conclusions: lymphocytes from crs patients are activated by alternaria and candida antigens and produce large quantities of il-5, il-13, and ifn-, irrespective of allergic status. by continuously stimulating lymphocytes, fungi colonized in the nasal and sinus cavities of crs patients may play important roles in the pathogenesis of the disease, resulting in persistent cytokine production and eosinophilic inflammation of the upper airways. useful links for mayo clinic include the original study, : as well as the abstract for their latest study. -------------------------------------------------------------------------- from original study and related informaton from september 99 - mayo clinic news-- fungus as cause of chronic sinusitis : http://www.mayo.edu/comm/mcr/news/news_773.html mayo clinic proceedings-- allergic fungal sinusitis http://www.mayo.edu/proceedings/1999/7409a1.pdf (300+kb) - mayo clinic-- antifungal therapy in chronic rhinosinusitis http://www.mayo.edu:80/sinusinfo/early.html - mayo clinic's distribution list for chronic sinusitis studies... : http://www.mayo.edu:80/sinusinfo/index.html