Health Effects of Toxin-Producing Indoor Molds in California
from: "California Morbidity", a monthly report from
Prevention Services, California Department of Health Services, April 1998
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 idopathic 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:
Sandra McNeel, D.V.M.; Debra Gilliss, M.D., M.P.H.;
Richard 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 Immunopathol. 1991.30: 73-87.
Croft WA, Jarvis BB, Yatawara CS. "Airborne outbreak of trichothecene
toxicoxix". Atmospheric Environment. 1986. 20(3):549-552.
Forgacs J. Stachybotrys toxicosis. In: Kadis S, Ciegler A, Aji SJ, eds.
Microbial Toxins: Volume VI-Fungal Toxins, New York: Academic Press:
1972:95-130.
Flannigan B, McCabe EM, McGarry F. "Allergenic and toxigenic
micro-organisms in houses". J Appl Bact Symp (Suppl) 1991; 70:61S-73S.
Hintikka EL. Human stachybotrytoxicosis. In: Wylie TD, Morehouse LG,
eds. Mycotoxigenic Fngi, Mycotoxins, Mycotoxicoses. New York: Marcel
Dekker; 1987:87-89.
Hodgson MJ, et. al. "Building-associated pulmonary disease from
exposure to Stachybotrys chartarum and Aspergillus versicolor.
J Occ Env Med. 1998. 40(3):241-249.
Jarvis BB, Yang C. Personal Communication. Discussion session. Fungi
and Bacteria in Indoor Air Environments. Saratoga Springs, NY. October
6-7, 1994.
Jarvis BB, Salemme J, Morais A. Stachybotrys toxins. Natural Toxins,
1995, 3:10-16.
Johanning E, Morey PR, Jarvis BB. "Clinical
epidemiological investigation of health effects caused by Stachybotrys
chartarum building contamination", Proceedings of Indoor Air, 1993;
Vol. 1: 225-230.
Johanning E, Biagini R, et. al. "Health and immunology
study following exposure to toxigenic fungi (Stachybotrys chartarum)
in a water-damaged office environment" Int Arch Occup Environ Health 1996,
68:207-218.
Kozak, PP, Gallup J, Cummins L.H., Gillman S.A.
"Currently available methods for home mold surveys". Ann Allergy 1979; 45:
167-176.
Montana 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):
Nikulin M, Reijula K, Jarvis BB, Hintikka E-L.
"Experimental lung mucotoxicosis in mice induced by Stachybotrys atra".
Int J Exp Path. 1996. 77:213-218.
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.
Ueno Y, editor. General toxicology. In: "Trichothecenes
- chemical, biological and toxicological aspects". Elsevier Science
Publishing Co., Inc.: New York, NY, 1983:135-146.
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