Is Your Apartment Killing You?

Is Your Apartment Killing You?	References
Introduction Timeline Discovery From Bad, to Worse Why Should I Be worried? Can Mold Cause Cancer? Summary FAQ Appendices	Institute for Inspection Cleaning and Restoration (IICRC) Standard S500 Standard and reference guide for professional water damage restoration Suggested Guidelines for Remediation of Damage from Sewage Backflow into Buildings Michael A, Berry, Ph.D., Jeff Bishop, Claude Blackburn, Eugene C. Cole, Dr.P.H., William C. Ewald, Terry Sniith, Nathan Suazo, and Steve Swan Abstract: Sewage backflows are serious health threats to humans indoors. The purpose of this paper is to summarize what is known about health effects associated with sewage backflow into indoor environments and to make technical recommendations for safe, effective restoration. Risks to human health from specific pathogens are considered, and the classes of disinfectants and their properties are discussed. The recommendations for remediation are based largely on the characteristics of the contaminated material and the length of time of the contamination. Journal of Environmental Health, October 1994 Cleanup Procedures for Flooded Houses, Canada Mortgage Housing Corporation OZONE GENERATORS THAT ARE SOLD AS AIR CLEANERS http://www.epa.gov/iaq/pubs/ozonegen.html An Insidious Mold http://www.cbsnews.com/now/story/0,1597,167069-412,00.shtml The Cleveland Outbreak http://gcrc.meds.cwru.edu/stachy/#THE CLEVELAND OUTBREAK Hypersensitivity Pneumonitis from Toxic Mold Exposure. Fungal Spores: Hazardous to Health? W.G. Sorenson Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, West Virginia USA Abstract Fungi have long been known to affect human well being in various ways, including disease of essential crop plants, decay of stored foods with possible concomitant production of mycotoxins, superficial and systemic infection of human tissues, and disease associated with immune stimulation such as hypersensitivity pneumonitis and toxic pneumonitis. The spores of a large number of important fungi are less than 5 µm aerodynamic diameter, and therefore are able to enter the lungs. They also may contain significant amounts of mycotoxins. Diseases associated with inhalation of fungal spores include toxic pneumonitis, hypersensitivity pneumonitis, tremors, chronic fatigue syndrome, kidney failure, and cancer. Key words: mold, fungi, mycotoxin, lung disease, toxic pneumonitis. Environ Health Perspect 107(suppl 3):469-472 (1999). Hypersensitivity lung disease presumptively due to Cephalosporium in homes contaminated by sewage flooding or by humidifier water. Patterson R, Fink JN, Miles WB, Basich JE, Schleuter DB, Tinkelman DG, Roberts M. Two cases of hypersensitivity lung disease apparently caused by home environment contamination with Cephalosporium have been identified. In one case repeated flooding of the home with sewer water appeared to be important in maintaining an environment contaminated with Cephalosporium, and in the other case a contaminated humidifier appeared to be the source. Both patients had chronic respiratory symptoms remitting during absence from the home, and both presented problems in diagnosis. In both cases cultures of the home environment or humidifier and serum antibody studies indicated Cephalosporium as the antigenic source responsible for the airway disease. An inhalation challenge in one case was positive, adding further evidence for Cephalosporium as the antigenic source and etiologic agent. In both cases complete remission followed moving from the home. Cephalosporium is reported as an apparent antigenic source for home contamination resulting in significant chronic pulmonary morbidity. J Allergy Clin Immunol 1981 Aug;68(2):128-32 SARCOIDOSIS AND EXPOSURE TO OCCUPATIONAL AND ENVIRONMENTAL AGENTS CAROL ORTIZ, M.P.H., MICHAEL HODGSON, M.D., M.P.H., DANIEL MCNALLY, M.D., EILEEN STOREY, MD, MPH Divisions of Occupational and Environmental Medicine and Pulmonary Diseases, Department of Medicine, University of Connecticut Health Center, Farmington, CT 06030-6210, address correspondence to: UCHC MC 6210, Farmington, CT 06030-6210, email: @nso.uchc.edu Supported in part by grants NIEHS. I K07-ES00305-01, and by EPA R825251 -01 -O ABSTRACT An index patient with sarcoidosis that appeared reversibly related to a school generated a case-control study. All 59 patients seen between 1992 and 1997 in a pulmonary divi-sion, and unmatched controls from orthopedic surgeons, received two copies of a self-administered questionnaire inquiring about occupational and environmental histories. Thirty-one (52.2%) of the patients and ninety-four (32.4%) of the controls responded. Patients were significantly more likely to have been exposed to inorganic dusts (odds ratio [OR] 3.48; 95% confidence interval [95%CI]: 1.02- 11.80), molds (OR 9.8; 95%CJ: (0.98 - 98.40) and solvents or oils in the work place (OR: 9.8; 95%CI: (1.60 - 48.0) than controls. They described exposure at home through moldy basements (OR: 2.37; 95% CI: 1.0, 5.8) or mold on bathroom walls (OR: 5.69; 95% CI 1.3-25.6) more frequently than controls. Sarcoidosis may represent a disease at least in part attributable to occu-pational and environmental exposures. [Microbiological threat from buildings and rooms and its influence on human health (sick building syndrome)]. Ochmanski W, Barabasz W. I Katedra i Klinika Chorob Wewnetrznych Collegium Medicum, Uniwersytetu Jagiellonskiego w Krakowie. In buildings we can observe many different strains of bacteria, over 400 species of mould fungi, many strains of fungus causing the rotting of wood and wood like materials, many species of algae, aphids, and other types of growths and seed plants and also over 30 types of mites especially those seen in house dust. Buildings, especially their interiors have a very specific microclimate. Within it areas of so called ecological lows are formed in which conditions for settlement, growth and reproduction of these organisms take place. A building, which is a hazard to the health of its residents, is called a "sick building" from the term "sick building syndrome". The incidence and development of some types of mould fungus is associated with the production of very toxic metabolites which are called secondary metabolites i.e. mycotoxins. Long term human, especially in relation to children, contact with the species producing the most potent mycotoxins like aflatoxin--Apergillus flavus, ochratoxins--Aspergillus ochraceus, rubratoxins--Penicillium rubrum or strachybotrytoxins--Strachybotrys chartarum may even be the cause of death. Mould fungus or just mould is a saprophytic fungus derived from many different systemic groups (Mucor, Aspergillus, Penicillium, Fusarinum). Fungi can produce lethal mycotoxins such as: alternariol, aflatoxins, gliotoxins, ochratoxins, nivalenol, cytinine, dicumarol, rugulosine, trichoviridine and about 200 more which considering their mutagenicity are potentially dangerous to humans, animals, flora and microorganisms. Research which was begun by Prof. Julian Aleksandrowicz and Prof. Boleslaw Smyk in 1970 and 1971 showed that the so called "leukaemia houses" of leukaemia victims had an abundance of toxinogenic fungus in them, particularly the most potent fungus which turned out to be Aspergillus flavus. Toxinogenic funguses are abundant in many living spaces and cellars in older and also in new housing. Mycotoxins have been shown to be very toxic and harmful and it is no wonder that many inhabitants of these living spaces are constantly ill, mainly upper respiratory tract infections, lethargy, constant headaches, nausea and a general ill feeling. Inhabiting these living spaces for a considerable period may lead to cancer. Przegl Lek 2000;57(7-8):419-23 Tumor necrosis factor-alpha -308 promoter gene polymorphism and increased tumor necrosis factor serum bioactivity in farmer's lung patients. Schaaf BM, Seitzer U, Pravica V, Aries SP, Zabel P. Medical Clinic II, University of Lubeck, Lubeck, Germany. Bernhard.schaaf@medinf.mu-luebec.de Hypersensitivity pneumonitis (HP) represents an immunologic reaction of the pulmonary parenchyma to an inhaled agent. Since tumor necrosis factor (TNF)-alpha is thought to be involved in the pathogenesis of HP, and polymorphisms in the TNF genes have been associated with variations in the production of TNF-alpha, we investigated the serum bioactivity and genotype of TNF in HP. TNF bioactivity was measured after hay dust challenge in eight patients with farmer's lung (Group A) and in 12 healthy, sensitized (antibody-positive) controls (Group B). Genotyping for the -308 TNF-alpha promoter polymorphism and the TNF-beta intron 1 gene polymorphism was performed in 20 patients with farmer's lung, 25 patients with pigeon breeder's lung, and 216 controls. TNF bioactivity increased in Group A at 4 to 10 h after hay dust challenge, but not in Group B (p < 0.05). The frequency for the TNFA2 allele, a genotype associated with high TNF-alpha production in vitro, was significantly higher in farmer's lung patients (frequency [f] = 0.43, p = 0.0012) than in controls (f = 0.19) or patients with pigeon breeder's lung (f = 0.16). Genotyping for TNF-beta revealed no significant abnormalities. Thus, increased production of TNF-alpha after hay contact, and a genetic predisposition to TNF-alpha production, are implicated in the pathogenesis of alveolitis in farmer's lung. Am J Respir Crit Care Med 2001 Feb;163(2):379-82 Tumor necrosis factor plays an essential role in determining hypersensitivity pneumonitis in a mouse model. Denis M, Cormier Y, Fournier M, Tardif J, Laviolette M. Unite de recherche, Centre de Pneumologie, Hopital Laval, Sainte-Foy, Quebec, Canada. We examined the importance of the cytokine tumor necrosis factor-alpha (TNF-alpha) in a mouse model of hypersensitivity pneumonitis (HP). Mice of the C57BL/6 strain were instilled intranasally 3 days/wk for 3 wk with 150 micrograms of the actinomycete Faenia rectivirgula (Micropolyspora faeni) to induce HP as a model of farmer's lung. This experimental model was associated with a progressive inflammation in the lungs of challenged mice, seen histologically as cellular infiltrates of large quantities of macrophages and lymphocytes and some neutrophils. The disease in challenged mice treated with a control rabbit serum was also associated with a substantial release of tumor TNF-alpha (up to 80 U/ml of TNF-alpha in the bronchoalveolar lavage [BAL] at 3 wk after beginning of treatment) and interleukin-1, which peaked at 1 wk (approximately 300 U/ml) and diminished thereafter. A very large increase in BAL cell number (11-fold increase versus saline controls) and an enhanced release potential for TNF-alpha by alveolar macrophages was also seen. Lung fibrosis was also evident in challenged animals, as demonstrated by a 2-fold increase in hydroxyproline levels. Infusion of challenged mice with a rabbit polyclonal antibody against TNF-alpha (2 mg/wk) completely abrogated the disease, as mice so treated had normal lung histology. Anti-TNF-alpha blocked cellular recruitment in the lungs (only a 2-fold increase at week 3); it also completely abolished TNF-alpha secretion in the BAL and drastically reduced interleukin-1 levels in this fluid. Anti-TNF-alpha also abolished lung index increases and lung fibrosis, with both parameters similar to that of saline-instilled mice.(ABSTRACT TRUNCATED AT 250 WORDS) Am J Respir Cell Mol Biol 1991 Nov;5(5):477-83 Tumour necrosis factor alpha promoter gene polymorphism in sarcoidosis. Seitzer U, Swider C, Stuber F, Suchnicki K, Lange A, Richter E, Zabel P, Muller-Quernheim J, Flad HD, Gerdes J. Forschungszentrum Borstel, Parkallee 22, Borstel, D-23845, Germany. Biallelic polymorphisms in the promoter region of the TNF-alpha gene (TNFA) and in the first intron of the TNF-beta gene (TNFB) have been associated with variation in TNF-alpha production and with susceptibility to severe diseases. Among other functions, TNF-alpha plays a pivotal role in regulatory aspects of granuloma formation and sustenance. In sarcoidosis, a systemic granulomatous disorder of unknown aetiology, the clinical course of the disease has been associated with the patient's individual capacity of spontaneous TNF-alpha production by alveolar macrophages. We determined the TNFA and TNFB polymorphisms in 101 patients with pulmonary sarcoidosis and 216 healthy blood donors. A highly significant shift to the more uncommon TNFA2 allele was found in the Lofgren syndrome patient group, which represents the acute form of the disease with frequent spontaneous remission. The results show that gene frequencies of the TNFA gene variation are significantly different within the clinical forms of sarcoidosis, indicating that genetic predisposition for TNF-alpha production may play a role in the pathogenesis of the disease. Copyright 1997 Academic Press Limited. Cytokine 1997 Oct;9(10):787-90 Circulating levels of TNF alpha and TNF receptor superfamily members in lymphoid neoplasia. Metkar SS, Naresh KN, Manna PP, Srinivas V, Advani SH, Nadkarni JJ. Immunology Division, Cancer Research Institute, Tata Memorial Center, Parel,Mumbai, India. We have correlated the serum levels of TNF alpha and soluble TNF receptor superfamily members with clinico-pathologic parameters in patients of Hodgkin's disease (HD, N = 26) and non-Hodgkin's lymphoma (NHLs, N = 35). HD patients had significantly higher levels of TNF alpha, sTNFRI, and sTNFRII in serum while NHL patients had significantly higher levels of sTNFRI, sTNFRII, sCD27, and sFas as compared to controls. In NHL patients the levels of sCD27 correlated directly and significantly with the high-stage disease, bone marrow involvement, lymph nodal presentation, and serum LDH levels. Similarly in NHL patients, levels of sFas also correlated directly and significantly with the presence of high stage disease. HD patients with B symptoms had significantly higher levels of sTNFRII. Arch Environ Health 1997 Nov-Dec;52(6):426-32 Serum levels of tumour necrosis factor-alpha in patients with B-cell chronic lymphocytic leukaemia. Adami F, Guarini A, Pini M, Siviero F, Sancetta R, Massaia M, Trentin L, Foa R, Semenzato G. Department of Clinical Medicine, Padua University School of Medicine, Italy. Serum levels of tumour necrosis factor-alpha (TNF-alpha) have been evaluated in the peripheral blood of 91 patients with B-cell chronic lymphocytic leukaemia (B-CLL), and have been correlated with the clinical stage (according to Rai's staging system) and relevant haematological and immunological data. Increased values were detected, compared to 36 normal age-matched controls (36 pg/ml +/- 5 versus 0.11 pg/ml +/- 0.08; P < 0.05). An increase of TNF-alpha serum levels was observed in all stages including stage 0, with a progressive increase in relation to the stage of the disease. A significant relationship between serum TNF-alpha levels and the number of circulating monocytes (P < 0.002) and an inverse correlation with the level of the haemoglobin (P < 0.001) was established, as defined by the Pearson's correlation test. In contrast, no correlation was observed between TNF-alpha serum levels and the other parameters taken into account, including the white blood cell and platelet counts, the absolute number of peripheral blood (PB) lymphocytes, CD5+ B lymphocytes, CD57+ lymphocytes, serum levels of lactic dehydrogenase, total serum immunoglobulins and the serum levels of IgG, IgA and IgM. These data suggest that, in addition to the B-CLL neoplastic cells, the PB monocytes may be involved in the release of TNF-alpha. Eur J Cancer 1994;30A(9):1259-63 Nitric oxide and proinflammatory cytokines in nasal lavage fluid associated with symptoms and exposure to moldy building microbes. Hirvonen MR, Ruotsalainen M, Roponen M, Hyvarinen A, Husman T, Kosma VM, Komulainen H, Savolainen K, Nevalainen A. Division of Environmental Health, National Public Health Institute, Kuopio, Finland. Maija-Riitta.Hirvonen@ktl.fi Epidemiological data indicate that living or working in a moldy building is associated with increased risk of respiratory symptoms and disease related to inflammatory reactions, but biochemical evidence linking cause and effect is still scarce. The staff working in a mold-contaminated school, and a reference group without such exposure, were studied. Nasal lavage was performed and health data were collected with a questionnaire at the end of the spring term, after a 2.5-mo summer vacation, and at the end of the fall term. Here we show that concentrations of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and nitric oxide (NO) in nasal lavage fluid were significantly higher in the exposed than in the control subjects at the end of the first exposure period. These inflammatory mediators decreased to reference group concentrations during the period when there was no exposure and the production of NO and IL-6 increased again during the reexposure in the fall term. Reports of cough, phlegm, rhinitis, eye irritation, and fatigue paralleled the changes in the measured inflammatory markers. These results point to an association between inflammatory markers in the nasal lavage fluid, the high prevalence of respiratory symptoms among the occupants, and chronic exposure to molds in the indoor environment. Am J Respir Crit Care Med 1999 Dec;160(6):1943-6
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