Ruth A. Etzel,
pediatrician
George Washington University School of Public Health and Health Services,
Dorr G. Dearborn
Send letter to journal:
Re: Importance of protecting infants from molds
retzel{at}earthlink.net Ruth A. Etzel, et al.
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We would like to compliment Drs. Lynnette Mazur and Janice Kim and the American Academy of Pediatrics Committee on Environmental Health for the technical report on the spectrum of noninfectious health effects from molds.(1, 2) The Committee summarized a difficult topic complicated by uncertainty and put together a generally fine review.
There are several points about which we would like to comment in a constructive way. Table 4 in the technical report (2) has multiple errors. For example, only some of the toxins listed are produced by Stachybotrys, only a few of the toxins in the column labeled ‘Macrocyclic Trichothecenes’ are that class of mycotoxins, only a few of the toxins in the column labeled ‘Enzymes’ are actually enzymes, and the major Stachybotrys proteinase, stachyrase A, a collagenolytic proteinase resistant to most mammalian host anti-proteinases, is not listed.(3) The Committee also could have listed the hemolytic toxin, stachylysin. Unfortunately, these factual errors detract from the validity of the remainder of the report. May we suggest an erratum?
It is also important to clarify on page e1916 of the technical report that the odds ratio (OR) dropped from 9.8 to 1.5 not just because of the omission of one infant’s data but primarily because a matched analysis was not performed by those who reanalyzed the data. Matched analysis is a key expectation when undertaking analysis of a study with a matched case-control design.(4)
There are several other errors. On page e1915 the technical report states that Stachybotrys only makes group D trichothecenes, i.e. macrocyclic trichothecenes. This is incorrect. About half of the Stachybotrys isolates only make the simple trichothecenes and atranones,(5) while the remainder produce the macrocylic trichothecenes. On page e1917 of the technical report there is a statement that experimental animal models of Stachybotrys mycotoxicosis in mice are limited. However, four different laboratories have published multiple papers on such models, mostly acute inhalation-type exposures and all found a hemorrhagic response.(6) These acute rodent models require rather high dose exposure and need to be extended to chronic low dose exposures (as is currently being designed by the National Toxicology Program).
There are a number of incorrect references in the policy statement and technical report. On page e1922 of the technical report,(2) the Committee cited a paper by Van Emon et al. (7) with regard to looking for antibodies to the hemolysin of Stachybotrys. Actually, this group used an immunassay to find the hemolysin itself, not antibodies against the hemolysin. On page 2583 of the policy statement,(1) the Committee stated that the first report suggesting a relationship between acute idiopathic pulmonary hemorrhage (AIPH) and the mold Stachybotrys came from Cleveland, Ohio in the 1990s, but they cite a reference that does not mention Stachybotrys. The correct reference is a Morbidity and Mortality Weekly Report published by the Centers for Disease Control and Prevention in 1997.(8)
We were disappointed to find no mention in the section of the technical report on Environmental Assessment and Sampling (page e1920) about quantitative polymerase chain reaction (QPCR), a new more versatile and more accurate fungal assessment tool that is commercially available. Recent experience in 140 visibly moldy homes in Cleveland demonstrated that tape lifts morphologically identified Stachybotrys in 56% of the homes, culturing settled dust on three different media only found it in 3.5 % of the homes, while QPCR on a parallel dust aliquot found it in 71% of the homes. Stachybotrys has a limited viability when dried out and does not compete well in mixed cultures. A much higher incidence of Stachybotrys will likely be found in homes as QPCR becomes more widely used.
A recent article from the Swetland Center for Environmental Health (9) described a new blood biomarker for Stachybotrys exposure and an abstract submitted for the 2007 American Thoracic Society meeting reported that these satratoxin protein adducts have been detected in the sera from the last two patients with AIPH at Rainbow Babies and Childrens Hospital and all of their four parents. This along with QPCR evidence of Stachybotrys in the tracheal secretions of 4 out of the previous 5 infants with AIPH indicates we are approaching a tighter etiologic connection. The 41st infant with AIPH was recently admitted to Rainbow Babies and Childrens Hospital. Stachybotrys has been documented in 88% of these infants’ homes.
Overall, we wish to thank the Committee on Environmental Health for adhering to the Precautionary Principle that states “We must act on facts, and on the most accurate interpretation of then, using the best scientific information. That does not mean we must sit back until we have 100% evidence about everything. Where the state of the health of the people is at stake, the risks can be so high and the costs of corrective action so great, that prevention is better than cure. We must analyze the possible benefits and costs of action and inaction. Where there are significant risks of damage to the public health, we should be prepared to take action to diminish those risks, even when the scientific knowledge is not conclusive, if the balance of likely costs and benefits justifies it”.(10) Fortunately, we often do not need to understand causal mechanisms in their entirety to put prevention measures in place. Knowing even one small component may allow significant degrees of prevention. Thus, the Committee’s recommendation to inquire about the presence of mold as part of a “healthy-home” inventory and to provide guidance to parents of all children about preventing and reducing mold exposure is well founded. Infants should not live in moldy homes.
In sum, the purpose of this letter is to compliment the Committee on Environmental Health and not to detract from the results of all the long hours and hard effort put into the policy statement and technical report. We applaud their fine efforts!
1. American Academy of Pediatrics Committee on Environmental Health. Spectrum of noninfectious health effects from molds. Pediatrics 2006;118:2582-2586.
2. Mazur LJ, Kim J, and the Committee on Environmental Health. Spectrum of noninfectious health effects from molds. Pediatrics 2006;118:e1909-e1926.
3. Kordula T, Banbula A, Macomson J, Travis J. Isolation and properties of stachyrase A, a chymotrypsin-like serine proteinase from Stachybotrys chartarum. Infect Immun. 2002;70:419-21.
4. Etzel RA. Stachybotrys. Current Opinion in Pediatr 2003;15:103-106.
5. Nielsen KF, Huttunen K, Hyvarinen A, Andersen B, Jarvis BB, Hirvonen MR. Metabolite profiles of Stachybotrys isolates from water-damaged buildings and their induction of inflammatory mediators and cytotoxicity in macrophages.
Mycopathologia. 2002;154:201-5.
6. Yike I, Dearborn DG. Pulmonary effects of Stachybotrys chartarum in animal studies. Adv Appl Microbiol. 2004;55:241-73.
7. Van Emon JM, Reed AW, Yike I, Vesper SJ, ELISA measurement of stachylysin in serum to quantify human exposures to the indoor mold Stachybotrys chartarum. J Occup Environ Med. 2003;45:582-591.
8. Centers for Disease Control and Prevention. Update: Pulmonary hemorrhage/hemosiderosis among infants--Cleveland, Ohio, 1993-1996. Morb Mort Weekly Report 1997;46:33-35.
9. Yike I, Distler AM, Ziady AG, Dearborn DG. Mycotoxin adducts on human serum albumin: biomarkers of exposure to Stachybotrys chartarum.
Environ Health Perspect. 2006;114:1221-6.
10. Horton R. The precautionary principle. London: UK Department of Environment (1990) In: Lancet 1998;352:252.
Conflict of Interest:
Dr. Dearborn has served as an expert witness for some of his patients. All proceeds went directly to his research. |
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