Health Effects of Toxin-Producing Indoor Molds in California

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from: " California Morbidity " , a monthly report from Prevention Services,

California Department of Health Services, April 1998

Health Effects of Toxin-Producing Indoor Molds in California

CA Department of Health Services

Environmental Health Investigations Branch

Due to excessive rainfall this winter many Californians are experiencing

increased exposure to indoor microorganisms. Several fungal species capable

of producing toxic substances have been found in water-damaged California

homes and offices. This article provides information about potential health

effects from exposure to Stachybotrys chartarum (a.k.a. S. atra), a

toxigenic mold that has received increasing attention recently among indoor

air researchers and the public. Within the last 12-18 months several

scientific reports (and media attention) have focused on Stachybotrys, a

ubiquitous saprophytic fungus that grows on nitrogen-poor, cellulose rich

materials such as hay, straw and building materials (ceiling tiles, wall

paper, paper covering on gypsum wallboard). The statewide prevalence of this

fungus in homes or work places is unknown, although one report found

Stachybotrys in 2-3% of a small survey of southern California homes (Kozak,

1979).

Mechanism of Action

Some strains of Stachybotrys chartarum can produce mycotoxins of the

trichothecene and spirolactone families. The trichothecene mycotoxins

satratoxins G and H are potent protein synthesis inhibitors and cause

immunosuppression in laboratory animals. In experimental animal studies, the

trichothecenes affect rapidly proliferating tissues such as skin and mucosa,

as well as lymphatic and hematopoietic tissues (Ueno, 1983). In laboratory

animals, acute exposure to large amounts of trichothecene toxins results in

a rapid release of sequestered white blood cells into circulation, while

repeated or chronic exposure destroys granulocytic precursor cells in bone

marrow leading to white cell depletion. Among the reported cellular effects

are: mitogen B/T lymphocyte blastogenesis suppression; decrease of IgM, IgG,

IgA; impaired macrophage activity and migration-chemotaxis; broad

immunosuppressive effects on the cellular and humoral-mediated immune

response leading to secondary infections; and, paradoxically, increased

spontaneous antibody producing cells in the spleen (Corrier, 1991).

Toxigenic strains of SC may also produce spirolactones (stachybotrylactone)

and spirolactams (stachybotrylactam), toxins which produce anticomplement

effects (Jarvis, 1995). Possible synergistic effects between the

trichothecenes and these mycotoxins have not yet been evaluated. Although

laboratories can test a sample of Stachybotrys chartarum for its ability to

produce mycotoxins, in vitro results do not necessarily equate with the in

vivo situation. Therefore, a fungus that produces toxins in the lab may not

do so in the field, or vice versa. It has been suggested that to assure the

safety of any exposed individual, whenever Stachybotrys chartarum is

identified, it should be considered as a potential mycotoxin-producing

organism (Jarvis, 1994).

Positive skin reactions to the fungus have been found in some asthmatics

living or working in Stachybotrys-contaminated rooms, suggesting a

hypersensitivity component in addition to the potential for mycotoxicosis.

Thus the fungal spores themselves or chemicals carried on the spores may

produce either allergenic or toxigenic effects (Flannigan, 1991).

Routes of Exposure

Due to its wet, slimy growth characteristics, it is unusual for spores from

active Stachybotrys colonies to become aerosolized. However, when colonies

of this fungus die and become dehydrated, there is increased risk for air

dispersion. Portals of possible entry into the body include inhalation and

dermal absorption when the fungus is found on walls or in carpets.

Case Reports

Historically, toxicologic effects from this fungus were reported in Europe,

where horses, sheep and cattle suffered fatal hemorrhagic disorders

following ingestion exposures (Forgacs,1972)). Human occupational exposures

to contaminated straw or hay resulted in nasal and tracheal bleeding, skin

irritation and alterations in white blood cell counts (Hintikka, 1987).

The first U.S. case of Stachybotrys-associated health effects from

inhalation exposure was reported in a suburban Chicago family (Croft, 1986).

The fungus had contaminated the ventilation system and ceilings of the

house. Health effects reported by the family included chronic recurring cold

and flu-like symptoms, sore throat, diarrhea, headache, fatigue, dermatitis,

intermittent focal alopecia and generalized malaise. Workers who cleaned and

removed contaminated material from this house also experienced skin

irritation and respiratory symptoms. After Stachybotrys contamination was

removed the house was reoccupied and residents reported no recurrence of

clinical symptoms.

Stachybotrys and satratoxin H (one of the trichothecene mycotoxins) were

subsequently identified in a water-damaged office building in New York City.

A small case-control study showed workers exposed to the fungus were at

statistically significant higher risk for nonspecified disorders of the

lower airways, eyes and skin; fevers and flu-like symptoms, and chronic

fatigue (Johanning, 1993, 1996). No significant differences in specific S.

chartarum IgE and IgG levels were noted between cases and controls. Although

Stachybotrys chartarum specific IgE (RAST) and IgG (ELISA) tests are

available, their sensitivity and specificity have not yet been determined.

A recent report describes identification of 10 likely or possible cases of

building-related asthma in a courthouse contaminated with Stachybotrys and

Aspergillus species (Hodgson, 1998). Self-reported symptoms among co-workers

included fever, headache, rhinitis, coughing, dyspnea and chest tightness.

Chest radiographs were negative and Stachybotrys-specific serology was

uninformative.

Stachybotrys chartarum, along with other fungi and environmental tobacco

smoke, was recently postulated to have an association with pulmonary

hemosiderosis in a cluster of Cleveland, Ohio infants (Montana, 1997; MMWR,

1997)). While SC was found more frequently in the homes of case infants

compared to controls, exposure of case infants to mycotoxins in the home

could not be determined. Because there is no field test for airborne

mycotoxins, it is not currently possible to determine if toxins were

actually present in the living space of case infants, and if so, at what

levels. However, since Stachybotrys chartarum spores containing mycotoxins

have been shown to produce pulmonary alveolar and intra-bronchiolar

inflammation and hemorrhage in mice (Nikulin, 1996, 1997), more research

into the inhalation effects of these toxins, especially on immature alveoli

and pulmonary vascular walls, is critically needed.

Pulmonary hemosiderosis is a condition characterized by recurrent alveolar

hemorrhage resulting in clinical signs of cough, wheeze, hemoptysis,

tachypnea, low grade fever, and microcytic hypochromic anemia. Chest

radiographs typically show patchy infiltrates and sputum specimens,

laryngeal swabs or gastric aspirates reveal hemosiderin-laden macrophages.

The association of some cases with allergy to cow's milk (Heiner syndrome)

and its association with glomerulonephritis in Goodpasture's syndrome

suggests an immunologic etiology but immunologic findings in idiopathic

cases have been inconsistent. Some familial case reports also suggest a

genetic component.

California Department of Health Services staff reviewed statewide hospital

discharge data for 1989-1995 (last year for which data is available) and

identified a total of eight hospitalizations and no deaths during these

years for hemosiderosis in infants less than one year of age. There were no

more than 3 cases in any year and no geographic clustering.

American Academy of Pediatrics

On April 6, 1998, the American Academy of Pediatrics (AAP) Committee on

Environmental Health released a statement concerning toxic effects of indoor

molds and acute idiopathic pulmonary hemorrhage in infants. They recommend

that until more information is available on the etiology of this condition,

pediatricians should try to ensure that infants under 1 year of age are not

exposed to chronically moldy, water-damaged environments (AAP, 1998).

Sources of Additional Information/Assistance:

California Department of Health Services, Environmental Health

Investigations Branch:

McNeel, D.V.M.; Debra Gilliss, M.D., M.P.H.; Kreutzer, M.D.

(510) 622-4500

REFERENCES

American Academy of Pediatrics. " Toxic Effects of Indoor Molds " . Pediatrics.

1998. 101(4):712-714.

CDC. " Update: pulmonary hemorrhage/hemosiderosis among infants - Cleveland,

Ohio. 1993-1996 " . MMWR 1997,46:33-35.

Corrier DE. " Mycotoxicosis: mechanism of immunosuppression " . Vet Immunol

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Flannigan B, McCabe EM, McGarry F. " Allergenic and toxigenic micro-organisms

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