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 toStachybotrys chartarum(a.k.a.S. atra), a toxigenic mold that has received
increasing attention recently among indoor air reseachers and the public. Within the last
12-18 months several scientific reports (and media attention) have focused onStachybotrys,
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 ofStachybotrys chartarumcan 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,
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 ofStachybotrys chartarumfor its ability to produce mycotoxins,in
vitroresults do not necessarily equate with thein vivosituation. 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, wheneverStachybotrys
chartarumis 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 inStachybotrys-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 activeStachybotryscolonies 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.
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. AfterStachybotryscontamination was removed the house was reoccupied and residents reported no recurrence of
Stachybotrysand 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 specificS. chartarumIgE and IgG levels were noted
between cases and controls.AlthoughStachybotrys chartarumspecific IgE
(RAST) and IgG (ELISA) tests are available, their sensitivity and specificity have not yet
A recent report describes identification of 10 likely or possible cases
of building-related asthma in a courthouse contaminated withStachybotrysandAspergillusspecies (Hodgson, 1998). Self-reported symptoms among co-workers included fever, headache,
rhinitis, coughing, dyspnea and chest tightness. Chest radiographs were negative andStachybotrys-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)). WhileSCwas
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, sinceStachybotrys
chartarumspores containingmycotoxins 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 cows
milk (Heiner syndrome) and its association with glomerulonephritis in Goodpastures
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
Sandra McNeel, D.V.M.; Debra Gilliss, M.D., M.P.H.; Richard Kreutzer,
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
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 toStachybotrys
chartarumandAspergillus 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 byStachybotrys chartarumbuilding
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 byStachybotrys atra". Int J Exp Path. 1996.
Nikulin M, Reijula K, Jarvis BB, Veijalainen P, Hintikka E-L.
"Effects of intranasal exposure to spores ofStachybotrys atrain 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.