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Policy Statement - American Academy of Pediatrics - Toxic Effects of Indoor Molds (RE9736)

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http://www.aap.org/policy/re9736.html

Policy Statement

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Pediatrics Volume 101, Number 4 April 1998, pp 712-714

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Toxic Effects of Indoor Molds (RE9736)

AMERICAN ACADEMY OF PEDIATRICS

Committee on Environmental Health

ABSTRACT. This statement describes molds, their toxic properties, and their

potential for causing toxic respiratory problems in infants. Guidelines for

pediatricians are given to help reduce exposures to mold in homes of

infants. This is a rapidly evolving area and more research is ongoing.

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ABBREVIATIONS. SIDS, sudden infant death syndrome; CDC, Centers for Disease

Control and Prevention.

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The growth of molds is pervasive throughout the outdoor environment. Given

the proper conditions, molds may also proliferate in the indoor setting.

Because Americans spend 75% to 90% of their time indoors,1 they are exposed

to molds that are growing indoors.

Molds readily enter indoor environments by circulating through doorways,

windows, heating, ventilation systems, and air conditioning systems. Spores

in the air also deposit on people and animals, making clothing, shoes, bags,

and pets common carriers of mold into indoor environments. The most common

indoor molds are Cladosporium, Penicillium, Aspergillus, and Alternaria.2,3

Molds proliferate in environments that contain excessive moisture, such as

from leaks in roofs, walls, plant pots, or pet urine.4-6 Many building

materials are suitable nutrient sources for fungal growth. Cellulose

substrates, including paper and paper products, cardboard, ceiling tiles,

wood, and wood products, are particularly favorable for the growth of some

molds. Other substrates such as dust, paints, wallpaper, insulation

materials, drywall, carpet, fabric, and upholstery commonly support mold

growth.3 Molds also may colonize near standing water.7-9

Some indoor molds have the potential to produce extremely potent toxins

called mycotoxins.10-12 Mycotoxins are lipid-soluble and are readily

absorbed by the intestinal lining, airways, and skin.13 Species of

mycotoxin-producing molds include Fusarium, Trichoderma, and Stachybotrys.

In general, the presence of these molds indicates a long-standing water

problem.

DIRECT TOXIC EFFECTS FROM MOLD EXPOSURE

The toxic effects from mold exposure are thought to be associated with

exposure to toxins on the surface of the mold spores, not with the growth of

the mold in the body. Until recently, there was only one published report in

the United States linking airborne exposure to mycotoxins with health

problems in humans.14 This report described upper respiratory tract

irritation and rash in a family living in a Chicago home with a heavy growth

of Stachybotrys atra (also known as Stachybotrys chatarum). The

investigators documented that this mold was producing trichothecene

mycotoxins. The symptoms disappeared when the amount of mold was

substantially reduced.

More recently, molds that produce potent toxins have been associated with

acute pulmonary hemorrhage among infants in Cleveland, Ohio.15 In November

1994, physicians and public health officials in Cleveland reported a cluster

of eight cases of acute pulmonary hemorrhage and hemosiderosis that had

occurred during January 1993 through November 1994 among infants in

neighborhoods of eastern metropolitan Cleveland.16 Two additional cases were

identified in December 1994. Pulmonary hemorrhage recurred in five of the

discharged infants after they returned to their homes; of these infants, one

died from pulmonary hemorrhage.

A case-control study comparing those 10 infants who had acute pulmonary

hemorrhage and hemosiderosis with 30 age-matched control infants from the

same area in Cleveland[17] revealed that the infants with pulmonary

hemorrhage were more likely to have resided in homes with major water damage

from chronic plumbing leaks or flooding (95% confidence interval = 2.6 to

infinity). The quantity of molds, including the toxigenic fungus

Stachybotrys atra, was higher in the homes of infants with pulmonary

hemorrhage than in those of controls. Simultaneous exposure to environmental

tobacco smoke appeared to increase the risk of acute pulmonary hemorrhage

among these infants.

Stachybotrys atra requires water-saturated cellulose-based materials for

growth in buildings. In studies conducted in North America, it has been

found in 2% to 3% of home environments sampled.8-18 Although Stachybotrys

atra has been associated with gastrointestinal hemorrhaging in animals that

had consumed moldy grain,19 the fungus previously had not been associated

with disease in infants. Infants may be particularly susceptible to the

effects of these inhaled mycotoxins because their lungs are growing very

rapidly. In an animal model, intranasal administration of toxic spores of

Stachybotrys atra to mice resulted in severe interstitial inflammation with

hemorrhagic exudates in the alveoli.20

The county coroner re-examined all infant deaths in Cleveland during January

1993 through December 1995 to determine whether pulmonary hemosiderin-laden

macrophages were present in the lung tissue. Postmortem examinations were

reviewed for all 172 infants who died during that period, including 117

deaths attributed to sudden infant death syndrome (SIDS). Pathologic lung

specimens were sectioned, stained with Prussian blue, and screened for the

presence of hemosiderin. The presence of hemosiderin-laden macrophages in

alveoli indicates alveolar bleeding at least 2 days before death.21

Hemosiderin-laden macrophages were abundantly present in the lung tissue of

nine (5%) infants. Of these nine deaths, two resulted from homicide, and one

had a recent history of child abuse. The other six deaths that were

accompanied by hemosiderin-laden macrophages in the lung thus may have been

misclassified as deaths from SIDS. All six infants had lived in the same

limited geographic area as the previously described cases of pulmonary

hemosiderosis.

The extent of this problem in other areas of the United States is still

unknown. Further investigation is needed to establish causation and prevent

further health effects if the findings in Cleveland are confirmed in other

areas.

CONCLUSION

Very little is currently known about acute idiopathic pulmonary hemorrhage

among infants. This is a newly recognized problem and knowledge is expected

to be evolving rapidly. In view of the severity of the problem,

environmental controls to eliminate water problems and to reduce the growth

of indoor molds are wise. Until more is known about the etiology of

idiopathic pulmonary hemorrhage, prudence dictates that pediatricians try to

ensure that infants under 1 year of age are not exposed to chronically

moldy, water-damaged environments.

Coroners and medical examiners should consider using the recently published

Guidelines for Death Scene Investigation of Sudden, Unexplained Infant

Deaths, which includes a question about dampness, visible standing water, or

mold growth.

Little is known about the prevalence of toxigenic molds in homes, nor is it

clear how extensive measures must be to achieve environments sufficiently

free of molds to avoid disease. Bulk mold must be removed, followed by a

thorough cleaning with soap and water. Caution must be used, because it is

possible that homeowners could actually increase the levels of mold spores

in the air by attempting extensive clean-up efforts without guidance from a

professional (a certified industrial hygienist or ventilation engineer).

These specialists can be found in the yellow pages in the telephone

directory under the listing for Industrial Hygiene Consultants. Additional

research is needed before the most appropriate recommendations for home

clean-up can be determined. Until then, interim guidelines have been

formulated.

RECOMMENDATIONS

In areas where flooding has occurred, prompt cleaning of walls and other

flood-damaged items with water mixed with chlorine bleach, diluted four

parts water to one part bleach, is necessary to prevent mold growth. Never

mix bleach with ammonia. Moldy items should be discarded.

Pediatricians should ask about mold and water damage in the home when they

treat infants with idiopathic pulmonary hemorrhage. If mold is in the home,

pediatricians should encourage parents to try to find and eliminate sources

of moisture. Testing the environment for specific molds is usually not

necessary. It appears to be important to clean up moldy conditions before

the infant is discharged from the hospital to prevent recurrent pulmonary

hemorrhage, although this needs further study. Interim clean-up guidelines

are available through the Centers for Disease Control and Prevention (CDC),

1600 Clifton Rd, Atlanta, GA 30333.

Infants with idiopathic pulmonary hemorrhage must not be exposed to

environments in which smoking occurs.

Pediatricians should report cases of idiopathic pulmonary hemorrhage and

hemosiderosis to state health departments. A reporting form is available

through the CDC.

Pediatricians should be aware that there is currently no method to test

humans for toxigenic molds such as Stachybotrys or mycotoxins.

Infants who die suddenly without known cause should have an autopsy done

including a Prussian blue stain of lung tissue to look for the presence of

hemosiderin.

COMMITTEE ON ENVIRONMENTAL HEALTH, 1997 to 1998

Ruth A. Etzel, MD, PhD, Chairperson

Sophie J. Balk, MD

F. Bearer, MD, PhD

Mark D. , MD

W. , MD, MPH

M. Shea, MD, MPH

LIAISON REPRESENTATIVES

Henry Falk, MD

Centers for Disease Control and Prevention

Lynn R. Goldman, MD

Environmental Protection Agency

W. , MD

National Cancer Institute

Walter Rogan, MD

National Institute of Environmental Health Sciences

SECTION LIAISON

Barbara Coven, MD

Section on Community Pediatrics

CONSULTANT

Holly J. Fedeyko, MPH

REFERENCES

Lebowitz MD. Health effects of indoor pollutants. Annu Rev Public Health.

1983;4:203-221

JD. Fungi as contaminants in indoor air. Atmospheric Environ.

1992;26:2163-2172

Gravesen S, Frisvad JC, Samson RA. Microfungi. Copenhagen, Denmark:

Munksgaard Publishing; 1994

WR. Fungus aerosols arising from cold-mist vaporizers. J Allergy.

1974;54:222-228

Kozak PP, Gallup J, Cummins LH, et al. Currently available methods for home

mould surveys: II. examples of problem homes studied. Ann Allergy.

1980;45:167-176

Fergusson RJ, Milne LJ, Crompton GK. Penicillium allergic alveolitis: faulty

installation of central heating. Thorax. 1984;39:294-298

Kapyla M. Frame fungi on insulated windows. J Allergy. 1985;40:558-564

JD, Laflamme AM, Sobol Y, et al. Fungi and fungal products in some

Canadian houses. Int Biodeterioration. 1988;24:103-120

Pasanen P, Pasanen AL, Janunen M, et al. Water condensation promotes fungal

growth in ventilation ducts. Indoor Air. 1993;3:106-112

Burge HA. Toxigenic potential of indoor microbial aerosols. In: Sandu SS,

DeMarini DM, et al, eds. Short-term Bioassays in the Analysis of Complex

Environmental Mixtures. New York, NY: Plenum Press; 1987

Jarvis BB. Mycotoxins and indoor air quality. In: Morey PM, Feeley JC, Otten

JA, eds. Biological Contaminants in Indoor Environments. Philadelphia, PA:

American Society for Testing and Materials; 1990

Hendry KM, Cole EC. A review of mycotoxins in indoor air. J Toxicol Environ

Health. 1993;38:183-198

Kemppainen BW, Riley RT, Pace JG. Skin absorption as a route of exposure for

aflatoxin and trichothecenes. J Toxicol/Toxin Rev. 1988;7:95-120

Croft WA, Jarvis BB, Yatawara CS. Airborne outbreak of trichothecene

toxicosis. Atmos Environ. 1986;20:549-552

Centers for Disease Control and Prevention. Update: pulmonary

hemorrhage/hemosiderosis among infants--Cleveland, Ohio, 1993-1996. MMWR

Morb Mortal Wkly Rep. 1997;46:33-35

Centers for Disease Control and Prevention. Acute pulmonary

hemorrhage/hemosiderosis among infants-Cleveland, January 1993-November

1994. MMWR Morb Mortal Wkly Rep. 1994;43:881-883

Montaña E, Etzel RA, Allan T, Horgan TE, Dearborn DG. Environmental risk

factors associated with pediatric idiopathic pulmonary hemorrhage and

hemosiderosis in a Cleveland community. Pediatrics. 1997;99(1). URL:

http://www.pediatrics.org/cgi/content/full/99/1/e5

Kozak PP Jr, Gallup J. Endogenous mold exposure: environmental risk to

atopic and non-atopic patients. In: Gammage RV, Kay SV, eds. Indoor Air and

Human Health. Chelsea, MI: Publishers; 1985:149-167

Hintikka E-L. Stachybotryotoxicosis as a veterinary problem. In: Rodricks

JV, Hesseltine CW, Mehlman MA, eds. Mycotoxins in Human and Animal Health.

Park Forest, IL: Pathotox Publishers; 1977:277-284

Nikulin M, Reijula K, Jarvis BB, Veijalainen P, Hintikka E-L. Effects of

intranasal exposure to spores of Stachybotrys atra in mice. Fund Appl

Toxicol. 1997;35:182-188

S, Fawcett J, son W. Interstitial haemosiderin in the lungs of

sudden infant death syndrome: a histological hallmark of 'near-miss'

episodes? J Pathol. 1985;145:53-58

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The recommendations in this statement do not indicate an exclusive course of

treatment or serve as a standard of medical care. Variations, taking into

account individual circumstances, may be appropriate.

Copyright © 1998 by the American Academy of Pediatrics.

No part of this statement may be reproduced in any form or by any means

without prior written permission from the American Academy of Pediatrics

except for one copy for personal use.

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