How solid is the Academy position paper on mold exposure?
2006; Elsevier BV; Volume: 118; Issue: 3 Linguagem: Inglês
10.1016/j.jaci.2006.07.008
ISSN1097-6825
Autores Tópico(s)Air Quality and Health Impacts
ResumoTo the Editor:I disagree with much of the position paper by Bush et al.1Bush R.K. Portnoy J.M. Saxon A. Terr A.l. Wood R.A. The medical effects of mold exposure.J Allergy Clin Immunol. 2006; 117: 326-333Abstract Full Text Full Text PDF PubMed Scopus (310) Google Scholar There is much evidence supporting illness caused by water-damaged, moldy, or damp indoor spaces. Classic allergy accounts for only part of the problem. I am allotted only 500 words, and therefore the numbered statements lead to important references (see this article's additional references in the Online Repository at www.jacionline.org).1.Mycotoxin2Brasel T.L. Douglas D.R. Wilson S.C. Straus D.C. Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins on particulates smaller than conidia.Appl Environ Microbiol. 2005; 71: 114-122Crossref PubMed Scopus (103) Google Scholar, 3Brasel T.L. Martin J.M. Carriker C.G. Wilson S.C. Straus D.C. Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins in the indoor environment.Appl Environ Microbiol. 2005; 71: 7376-7388Crossref PubMed Scopus (107) Google Scholar, 4Cho S.-H. Seo S.-C. Schmechel D. Grinshpun S.A. Reponen T. Aerodynamic characteristics and respiratory deposition of fungal fragments.Atmos Environ. 2005; 39: 5454-5465Crossref Scopus (83) Google Scholar and allergen5Górny R.L. Reponen T. Willeke K. Schmechel D. Robine E. Boissier M. et al.Fungal fragments as indoor air biocontaminants.Appl Environ Microbiol. 2002; 68: 3522-3531Crossref PubMed Scopus (292) Google Scholar, Appendix have been documented in small fragments released by mold growth indoors. These particles are respirable and for Stachybotrys species can exceed spore counts by 500 times and spore deposition by 250 times in the respiratory tract.E4 These particles are unmeasured and uncharacterized in indoor evaluationsE2,E3,E5,E6 and are a vehicle for mycotoxin and allergen entry into the body.2.Personal monitoring and the determination of specific IgE sensitization to the individual's own environment through dual immunoassay has not been used routinely in exposure studies.E3 Personal monitoring should be preferred to area sampling alone.E7,E83.Germinating spores release more allergen than dormant spores in 8 of 11 molds studied, which is important in environments with active mold growth or when spores germinate or colonize the respiratory tract.E9,E104.Persons with environmental exposure to Stachybotrys species have had measurable stachylysinE11 and mycotoxinE12 in their serum.5.Inhaled mycotoxin is 10-fold more potent than ingested mycotoxin.E136.Common construction materials permit growth of toxigenic fungi and mycotoxin production.E14-E197.Mycotoxin can cause local mucosal damageE20-E22 independent of systemic toxicity. Some mycotoxins persist for many weeks in the body,E20 possibly permitting chronic toxicity.8.There are ciliostatic,E23-E26 cytotoxic,E25,E27 inflammatory,E20,E28-E40 and mutagenic,E41-E46 factors elaborated by fungi, even in the absence of mycotoxin production.E20,E47-E499.Water-damaged buildings have a distinct fungal ecology than outdoor moldsE50,E51 or non–water-damaged buildings. The human effects of these “water-indicator fungi”E52 might have overlap with outdoor fungal diseases yet are distinct.E5310.Molds have been shown to cause molecular mimicry and IgE- and T cell–mediated autoimmunity.E54-E5711.Molds cause a variety of immune effects,E58-E63 including diminishing TH1 reactivity while not diminishing or even stimulating TH2 reactivity.E64-E6712.Volatile organic compounds (VOCs) from Trichoderma virieae have been shown to trigger histamine release from human pulmonary mast cells.E6813.Preliminary studies (including studies for USC and Mt Sinai) have shown neuropsychologic aberrations in patients exposed to mold. These studies need replication.E69-E7414.Mold has been found to reside in the upperE59,E75-E81 and lowerE82 airways of many persons with chronic respiratory disease.15.Fungal intracellular proteinsE83 and proteaseE20,E83 and fungal surface proteinE84 have been shown to be allergenic.16.Alternaria species sensitization predicts polysensitization to a variety of fungi, some that are not routinely tested.E8517.Mold growth is accompanied by bacterial growth and potentially inflammatory bacterial products.E3,E86,E87 Amoebae have been found in these environments.New knowledge renders virtually every study of indoor mold exposure obsolete. I have mentioned some of the pieces of the puzzle that will have to be used to assemble the entire picture of indoor mold effects. New knowledge and new studies will solve this puzzle. To the Editor: I disagree with much of the position paper by Bush et al.1Bush R.K. Portnoy J.M. Saxon A. Terr A.l. Wood R.A. The medical effects of mold exposure.J Allergy Clin Immunol. 2006; 117: 326-333Abstract Full Text Full Text PDF PubMed Scopus (310) Google Scholar There is much evidence supporting illness caused by water-damaged, moldy, or damp indoor spaces. Classic allergy accounts for only part of the problem. I am allotted only 500 words, and therefore the numbered statements lead to important references (see this article's additional references in the Online Repository at www.jacionline.org).1.Mycotoxin2Brasel T.L. Douglas D.R. Wilson S.C. Straus D.C. Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins on particulates smaller than conidia.Appl Environ Microbiol. 2005; 71: 114-122Crossref PubMed Scopus (103) Google Scholar, 3Brasel T.L. Martin J.M. Carriker C.G. Wilson S.C. Straus D.C. Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins in the indoor environment.Appl Environ Microbiol. 2005; 71: 7376-7388Crossref PubMed Scopus (107) Google Scholar, 4Cho S.-H. Seo S.-C. Schmechel D. Grinshpun S.A. Reponen T. Aerodynamic characteristics and respiratory deposition of fungal fragments.Atmos Environ. 2005; 39: 5454-5465Crossref Scopus (83) Google Scholar and allergen5Górny R.L. Reponen T. Willeke K. Schmechel D. Robine E. Boissier M. et al.Fungal fragments as indoor air biocontaminants.Appl Environ Microbiol. 2002; 68: 3522-3531Crossref PubMed Scopus (292) Google Scholar, Appendix have been documented in small fragments released by mold growth indoors. These particles are respirable and for Stachybotrys species can exceed spore counts by 500 times and spore deposition by 250 times in the respiratory tract.E4 These particles are unmeasured and uncharacterized in indoor evaluationsE2,E3,E5,E6 and are a vehicle for mycotoxin and allergen entry into the body.2.Personal monitoring and the determination of specific IgE sensitization to the individual's own environment through dual immunoassay has not been used routinely in exposure studies.E3 Personal monitoring should be preferred to area sampling alone.E7,E83.Germinating spores release more allergen than dormant spores in 8 of 11 molds studied, which is important in environments with active mold growth or when spores germinate or colonize the respiratory tract.E9,E104.Persons with environmental exposure to Stachybotrys species have had measurable stachylysinE11 and mycotoxinE12 in their serum.5.Inhaled mycotoxin is 10-fold more potent than ingested mycotoxin.E136.Common construction materials permit growth of toxigenic fungi and mycotoxin production.E14-E197.Mycotoxin can cause local mucosal damageE20-E22 independent of systemic toxicity. Some mycotoxins persist for many weeks in the body,E20 possibly permitting chronic toxicity.8.There are ciliostatic,E23-E26 cytotoxic,E25,E27 inflammatory,E20,E28-E40 and mutagenic,E41-E46 factors elaborated by fungi, even in the absence of mycotoxin production.E20,E47-E499.Water-damaged buildings have a distinct fungal ecology than outdoor moldsE50,E51 or non–water-damaged buildings. The human effects of these “water-indicator fungi”E52 might have overlap with outdoor fungal diseases yet are distinct.E5310.Molds have been shown to cause molecular mimicry and IgE- and T cell–mediated autoimmunity.E54-E5711.Molds cause a variety of immune effects,E58-E63 including diminishing TH1 reactivity while not diminishing or even stimulating TH2 reactivity.E64-E6712.Volatile organic compounds (VOCs) from Trichoderma virieae have been shown to trigger histamine release from human pulmonary mast cells.E6813.Preliminary studies (including studies for USC and Mt Sinai) have shown neuropsychologic aberrations in patients exposed to mold. These studies need replication.E69-E7414.Mold has been found to reside in the upperE59,E75-E81 and lowerE82 airways of many persons with chronic respiratory disease.15.Fungal intracellular proteinsE83 and proteaseE20,E83 and fungal surface proteinE84 have been shown to be allergenic.16.Alternaria species sensitization predicts polysensitization to a variety of fungi, some that are not routinely tested.E8517.Mold growth is accompanied by bacterial growth and potentially inflammatory bacterial products.E3,E86,E87 Amoebae have been found in these environments. New knowledge renders virtually every study of indoor mold exposure obsolete. I have mentioned some of the pieces of the puzzle that will have to be used to assemble the entire picture of indoor mold effects. New knowledge and new studies will solve this puzzle. Appendix. Supplementary data Download .pdf (.05 MB) Help with pdf files Download .pdf (.05 MB) Help with pdf files
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