Molds may affect human health by three mechanisms: infection (by exposure of a susceptible

individual to mold spores; generally but not always a person who is immunocompromised),

hypersensitivity (allergy to mold spores, components, or toxins, including asthma and

hypersensitivity pneumonitis), or direct irritation (by mycotoxins, the toxins produced by mold).

In general, results from a large indoor air study 1 found that:

culturable airborne fungal concentrations in indoor air are lower than those in outdoor

air; fungal concentrations are highest in the fall and summer and lowest in the winter and

spring; geographically in the continental U.S., fungal concentrations are highest in the

southwest, far west, and southeast; and the most common culturable airborne fungi, both indoors and outdoors and in all

seasons and regions, were Cladosporium, Penicillium, nonsporulating fungi, and Aspergillus.

Considerable interest and controversy have been generated recently about searching for and

identifying specific molds in buildings. The Centers for Disease Control and Prevention (CDC)

currently state that determining what type of mold exists is unnecessary, and that all molds

should be treated the same with respect to potential health risks and removal.2

Mold may proliferate almost anywhere that has too much moisture. Even if renovation is done

properly, recurrence of moist conditions may cause mold regrowth. In one study, uninstalled

wallboard available from local distributors was found to contain a baseline bioburden, including

Stachybotrys chartarum. The authors noted that sanitation and preservation treatment of the

wallboard can markedly delay regrowth of certain fungi, particularly of S. chartarum.3

Mold has been considered as a causative agent of building related illness (BRI). Building related

illnesses are caused by known pathogens, have specific symptoms, and may be serious. Specific

diseases include those caused by Legionella species (Pontiac Fever, Legionnaire’s Disease) and

humidifier fever. Other airborne infectious diseases may have increased transmission when there

is inadequate ventilation4 (e.g., Tuberculosis 5, 6 Varicella,7 and Q fever8). Other symptoms

from indoor air contamination of offices where workers shared ventilation contaminated with

algal toxins (Pfiesteria piscicida, a dinoflagellate) are suspected to have occurred.9

Revised 7/18/03

Prudent health practice dictates limiting exposure of immunocompromised persons to excessive

levels of mold spores and limiting exposure of sensitized (allergic) individuals to airborne or

surface contamination of the specific mold to which the individual is sensitized.



The medical member of the indoor environmental quality (IEQ) investigative team can

contribute valuable expertise in advising what organisms the industrial hygienist (IH) should

sample for. If there is reason to suspect a particular species of mold - because of worker

concern, fungal infection, or identification by a worker’s health care provider (HCP) of allergy to

a specific mold - IH can be asked to direct sampling to recover and appropriately identify that

organism. Requesting IH to "sample for molds" because of non-specific symptoms in workers

will generally not be helpful, since simply the presence of molds may be insignificant with

respect to human health.

Communication between medical and other team members is important when trying to determine

if there is an exposure pathway. For example, discovery of mold on surfaces may be incidental

in a situation where airborne contamination is the problem (e.g., Legionella).


In general, it is preferable not to keep workers out of the work area, nor to advise workers to

avoid returning to a building unless: (1) a diagnosis of a building-related illness has been

established, or (2) a building-related diagnosis is suspected based on symptoms, disease patterns,

and findings consistent with a building-related illness.

If a worker is confirmed to have building-related mold or other allergy, the worker should not be

allowed back into the building until remediation has been completed and post-remediation

sampling documents confirm reduced levels of mold. After remediation, re-exposure should be

done with caution. It may be appropriate to have medical care immediately available in the case

of serious allergic reactions. If remediation has been adequate, there is reason to expect the

worker may successfully return to a building with few or no mold-related symptoms.48

The etiology of a worker’s condition may be unknown, but the worker’s condition is serious

enough that further exposure to any potential offending agent represents an unacceptable health

risk. In such cases, the prudent HCP may recommend against further exposure to a building until

the medical workup is complete. However, the HCP should complete the workup thoroughly

and accurately, being careful to avoid labeling the building a "health hazard" or stating that mold

in the building is the etiology until after the facts have established such a link. Incorrectly

identifying building mold as a source of health hazards can cause undue anxiety and loss of

income among workers, decreased productivity, increased operating costs, and decreased

readiness. Once a causal relationship has been established, however, relocation of affected

workers to a different building may be appropriate.

Page 2 of 11

A case report of office-related Alternaria allergy supports the following as "considerations" for

concluding an association exists between IEQ-related mold exposure and illness in an

occupational setting: symptoms and signs consistent with a medical diagnosis; either in vitro or

in vivo evidence of exposure; environmental evidence of plausible biological exposure; and

substantial improvement or resolution of the illness after appropriate building remediation.49


Successful remediation can result in a building that can be reoccupied without recurrent related

illness, even in a subtropical climate.48

If sampling reveals pathogens suspected because of the symptoms or signs exhibited by building

occupants, remediation effectiveness should be confirmed by clearance sampling before building

reoccupation. Building processes (for example, heating, ventilation, and air-conditioning

(HVAC) and humidification systems or decorative fountains) that may be similar in other

buildings may warrant preventive attention as a public health measure. Building engineers,

inspectors, or public health officials may be appropriate points of contact in such situations.


Molds are usually opportunistic pathogens, causing clinically significant infections only in cases

of overwhelming exposure or in individuals who are immune compromised (i.e., debilitated by

extremes of age, underlying infection, poor sanitation, inadequate nutrition, wounds); immune

suppressed (chemotherapy, severe stress, pregnancy); or immune deficient (human

immunodeficiency virus). Mold infection diagnoses will be made by appropriate microbial

identification studies or clinical courses (which are beyond the scope of this document).


Respiratory or skin (allergic contact dermatitis) allergy symptoms are the most likely symptoms

encountered from building-related mold allergy. Sensitivity to mold allergens is an important

risk factor for adenoid hypertrophy in children with allergic rhinitis.10 Adult-onset asthma is

associated with self-reported mold exposures in the home.11 Other organ system involvement,

such as gastrointestinal hypersensitivity-related complaints, may be a clue that the offending

exposure may not be indoor environment related, but rather related to an ingested allergen.

Allergens are common in most environments. Certain classes of allergens are especially

pertinent to an indoor environmental quality investigation. Again, the history given by those

affected can be the most helpful information in determining the source of the problem. In

addition to potential for infectious disease, molds can cause allergic problems. Buildings that

have been water damaged for several days or more - whether from flood, leaking roofs or walls,

broken plumbing, improperly installed or adjusted humidifiers, or condensation on cold surfaces

- may become culture media for any of a number of molds and fungi.

Page 3 of 11

Specific IEQ-associated illnesses with an allergic (sensitization) basis include asthma,

hypersensitivity pneumonitis, rhinitis or sinusitis, bronchitis or tracheitis (usually associated with

sinusitis), and humidifier fever (HF). HF is thought to be allergic, as patients have shown

sensitivity and symptoms with exposure to specific antigens in humidifiers.15 HF has been

associated with contamination of humidifiers by biologicals including amoeba, 16 fungi,17, 18

Bacillus subtilis,19 endotoxins,20 flavobacterium,20 and Pseudomonas species.21 It is also

possible that not all etiologies of IEQ-related allergic complaints are biologicals, as one report

noted HVAC "dust and mud."22

Spirometry may help document involvement of the lower respiratory tract. A peak flow meter

may be the simplest way to document expiratory impairment or exacerbation of asthma with

building exposure.12 A significant association was found between basophil histamine release

showing serum IgE specific to one or more indoor molds, and building-related symptoms in

individuals working in damp and moldy buildings.13 Skin testing (skin prick test) may be more

sensitive than blood testing (radioallergosorbent test, commonly called RAST) in detecting

sensitization to molds.14 However, determining a specific mold to which someone is allergic in a

given situation may be difficult, as sensitized individuals often react to more than one species.14


Stachybotrys mycotoxins are biologically active,23 and it is thought that they act as irritants.

Respiratory irritation has been documented to occur in rodents exposed to Stachybotrys.24

Special conditions may be necessary for mycotoxins produced by surface Stachybotrys in a

building to reach sufficient concentrations to cause such effects, according to the results of one

experimental study.25 The controversy is noted previously as to whether documentation is

sufficient that direct irritation from mycotoxins, rather than a hypersensitivity-related response to

molds or mycotoxins, has occurred in humans exposed to mold in indoor air.

The primary indicator that symptoms among workers may be caused by building-related mold is

that there is a temporal relationship of the symptoms to building exposure. Mold allergy may

involve both IgG and IgE immunoglobulins.26 Thus, an allergic reaction may occur immediately

on entering a building, after several hours of exposure, or even 2 to 8 hours after leaving the

building. A clear worker history of a temporal association of allergy symptoms with building

exposure should alert the health care provider to the possibility of building-related allergy.

It is unknown how much exposure time is required before sensitivity to mold develops. As many

molds are commonly found outside of the workplace, it is expected that some individuals have

been sensitized prior to any occupational exposure. Further, since development of allergy to

some substances may take over 30 years of exposure,27 it is probable that in certain individuals,

sensitization develops only after many years.

Page 4 of 11


Aspergillus species molds are commonly found. Inhalation of Aspergillus conidia or mycelium

fragments may result in airway colonization, which may subsequently cause infections in

susceptible hosts.28 A significant relationship was found between the incidence of invasive

nosocomial aspergillosis and the degree of fungal contamination of air and surfaces in patient

rooms in a bone marrow transplantation unit and two hematology wards.29 As an antigen,

hypersensitivity to A. fumigatus may cause Aspergillus asthma and allergic bronchopulmonary

aspergillosis (ABPA).28 Specific IgE and IgG may be detected in ABPA. X-ray studies are

characterized by fleeting pulmonary infiltrates that are often confused with pulmonary

tuberculosis on chest x-ray, and by central bronchiectasis on chest CT (computerized

tomography). Early diagnosis and therapy may alter the course of the disease and prevent the

development of end-stage lung fibrosis.26

Aspergillus candidus, common in grain dust, has been suggested to be an etiologic factor in

organic dust toxic syndrome30 and to pose an important occupational hazard for grain handling

workers through its immunomodulating properties.31

Aspergillus versicolor has been found in an investigation of building-related complaints, but no

association was seen between IgE or IgG antibodies and the presence of disease.32


Stachybotrys chartarum (also called Stachybotrys atra) has been known as an animal pathogen,

and has recently attracted attention as possibly having a role in human IEQ-related disease.23 It

is a toxigenic fungus frequently found in water-damaged buildings.33 In one study, S. chartarum

was identified in the indoor air in 6% of the buildings studied and in the outdoor air of 1% of the

buildings studied.1 S. chartarum has been found to produce volatile organic compounds that are

quite different from those produced by Aspergillus.33

S. chartarum produces trichothecene mycotoxins, which are biologically active and can produce

a variety of physiological and pathologic changes in humans and animals, including modulation

of inflammation and altered alveolar surfactant phospholipid concentrations.23 Sensitivity to

Stachybotrys has been found to involve both immunoglobulin IgE and IgG against antigenic

proteins of S. chartarum.34 Effects of S. chartarum may be related to direct irritant as well as

immunologic properties. Inhalation of S. chartarum extract aerosols was observed to provoke

sensory irritation in the airways of both naive and immunized mice.24 Alveolar type II cells are

sensitive to exposure to S. chartarum spores and mycotoxin (isosatratoxin-F, a trichothecene).35

S. chartarum has been associated with nasal bleeding in adults. Stachylysin, a mycotoxin, may

be one chemical responsible for the hemorrhagic effects.36 Stachyrase A, a chymotrypsin-like

proteinase from S. chartarum, has been isolated from a child with pulmonary hemorrhage.37 A

possible association between S. chartarum and pulmonary hemorrhage/hemosiderosis in infants

has been reported, but further review of evidence by the CDC and other experts concluded that

the association was unproven.38

Page 5 of 11

Articles are not consistent as to the significance of Stachybotrys in relation to human health.

Two reviews have found inadequate evidence to clearly establish the place of Stachybotrys in

human disease.39, 40


Thermophilic Actinomyces and Aspergillus fumigatus have been suggested as possibly having a

causative antigenic role in stipatosis, a hypersensitivity pneumonitis found in Mediterranean-area

stucco workers exposed to those organisms in esparto grass (Stipa tenacissima).41 Note that

although the name Actinomyces suggests a fungus, actinomycosis is a bacterial infection.

Cladosporium cladosporioides was found to be the etiologic agent of hypersensitivity

pneumonitis associated with a hot tub.42 Skin sensitization to C. cladosporioides was the most

commonly found mold skin sensitization in a small population in Toronto, Canada.43

Fusarium species infections in a hospital led to an investigation that identified the water

distribution system of the hospital as the reservoir of Fusarium. Aerosolization of Fusarium

species was documented after running the showers.44

IgG to Sporobolomyces salmonicolor was the most commonly detected anti-mold

immunoglobulin associated with exposure in a Finnish military hospital building with severe,

repeated, and enduring water and mold damage. Rhinitis, asthma, and alveolitis were noted

among personnel reacting positively to S. salmonicolor provocation tests.45

Streptomyces albus was found to be responsible for a biopsy-proven case of hypersensitivity


An increased risk of developing asthma in adulthood has been found to be significantly related to

IgG antibodies to Trichoderma citrinoviride (but not to other molds).47

For more information on IEQ medical guidance, contact Occupational Medicine at (757) 953-

0769 or

Page 6 of 11


PMID numbers are linked to article abstracts available at National Center for Biotechnology

Information, U.S. National Library of Medicine, PubMed query at

1 Shelton BG, Kirkland KH, Flanders WD, Morris GK. Profiles of airborne fungi in buildings

and outdoor environments in the United States. Appl Environ Microbiol. 2002 Apr;68(4):1743-

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2 CDC. Questions and Answers on Stachybotrys chartarum and other molds. U.S. Department

of Health and Human Services. Centers for Disease Control and Prevention. National Center for

Environmental Health. June 06, 2002. Available at

3 Price DL, Ahearn DG. Sanitation of wallboard colonized with Stachybotrys chartarum. Curr

Microbiol. 1999 Jul;39(1):21-6. PMID 10387112

4 Brundage JF, Scott RM, Lednar WM, Smith DW, Miller RN. Building-associated risk of

febrile acute respiratory diseases in Army trainees. JAMA. 1988 Apr 8;259(14):2108-12. PMID


5 Burge HA. Risks associated with indoor infectious aerosols. Toxicol Ind Health. 1990

Mar;6(2):263-74. Review. PMID 2192480


Nolan CM, Elarth AM, Barr H, Saeed AM, Risser DR. An outbreak of tuberculosis in a shelter

for homeless men. A description of its evolution and control. Am Rev Respir Dis. 1991

Feb;143(2):257-61. PMID 1990937


Tsujino G, Sako M, Takahashi M. Varicella infection in a children's hospital: prevention by

vaccine and an episode of airborne transmission. Biken J 1984 Sep;27(2-3):129-32. PMID


8 Carrieri MP, Tissot-Dupont H, Rey D, Brousse P, Renard H, Obadia Y, Raoult D.

Investigation of a slaughterhouse-related outbreak of Q fever in the French Alps. Eur J Clin

Microbiol Infect Dis. 2002 Jan;21(1):17-21. PMID 11913496

9 Schmechel DE, Koltai DC. Potential human health effects associated with laboratory

exposures to Pfiesteria piscicida. Environ Health Perspect. 2001 Oct;109 Suppl 5:775-779.

PMID 11677188

10 Huang SW, Giannoni C. The risk of adenoid hypertrophy in children with allergic rhinitis.

Ann Allergy Asthma Immunol. 2001 Oct;87(4):350-5. PMID 11686429

Page 7 of 11

11 Thorn J, Brisman J, Toren K. Adult-onset asthma is associated with self-reported mold or

environmental tobacco smoke exposures in the home. Allergy. 2001 Apr;56(4):287-92. PMID


12 National Institutes of Health. Clinical practice guidelines expert panel report 2 guidelines for

the diagnosis and management of asthma. National Asthma Education and Prevention Program.

National Heart, Lung, and Blood Institute. National Institutes of Health. NIH Publication No. 97-

4051:July 1997. Available at

13 Lander F, Meyer HW, Norn S. Serum IgE specific to indoor moulds, measured by basophil

histamine release, is associated with building-related symptoms in damp buildings. Inflamm Res.

2001 Apr;50(4):227-31. PMID 11392611

14 Mabry RL, Marple BF, Mabry CS. Mold testing by RAST and skin test methods in patients

with allergic fungal sinusitis. Otolaryngol Head Neck Surg. 1999 Sep;121(3):252-4. PMID


15 Edwards JH, Cockcroft A. Inhalation challenge in humidifier fever. Clin Allergy. 1981

May;11(3):227-35. PMID 7249338

16 Finnegan MJ, Pickering CA, Davies PS, Austwick PK, Warhurst DC. Amoebae and

humidifier fever. Clin Allergy. 1987 May;17(3):235-42. PMID 3301062

17 Mamolen M, Lewis DM, Blanchet MA, Satink FJ, Vogt RL. Investigation of an outbreak of

"humidifier fever" in a print shop. Am J Ind Med. 1993 Mar;23(3):483-90. PMID 8503466

18 Baur X, Behr J, Dewair M, Ehret W, Fruhmann G, Vogelmeier C, Weiss W, Zinkernagel V.

Humidifier lung and humidifier fever. Lung. 1988;166(2):113-24. PMID 3130530

19 Parrott WF, Blyth W. Another causal factor in the production of humidifier fever. J Soc

Occup Med. 1980 Apr;30(2):63-8. PMID 6782372

20 Rylander R, Haglind P, Lundholm M, Mattsby I, Stenqvist K. Humidifier fever and endotoxin

exposure. Clin Allergy. 1978 Sep;8(5):511-6. PMID 709796

21 Forsgren A, Persson K, Ursing J, Walder M, Borg I. Immunological aspects of humidifier

fever. Eur J Clin Microbiol. 1984 Oct;3(5):411-8. PMID 6499837

22 Lebedev SV, Aleksandrovskii VG, Chekhonin VP. Humidifier fever [Russian]. Ter Arkh.

1988;60(11):90-3. PMID 3238588

23 Mahmoudi M, Gershwin ME. Sick building syndrome. III. Stachybotrys chartarum. J Asthma.

2000 Apr;37(2):191-8. PMID 10805208

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24 Korpi A, Kasanen JP, Raunio P, Kosma VM, Virtanen T, Pasanen AL. Effects of aerosols

from nontoxic Stachybotrys chartarum on murine airways. Inhal Toxicol. 2002 May;14(5):521-

40. PMID 12028806

25 Wilkins CK, Larsen ST, Hammer M, Poulsen OM, Wolkoff P, Nielsen GD. Respiratory

effects in mice exposed to airborne emissions from Stachybotrys chartarum and implications for

risk assessment. Pharmacol Toxicol. 1998 Sep;83(3):112-9. PMID 9783329

26 Shah A, Panjabi C. Allergic bronchopulmonary aspergillosis: a review of a disease with a

worldwide distribution. J Asthma. 2002 Jun;39(4):273-89. PMID 12095177

27 Tarvainen K, Jolanki R, Estlander T. Occupational contact allergy to unsaturated polyester

resin cements. Contact Dermatitis. 1993 Apr;28(4):220-4. PMID 8508632

28 Tomee JF, van der Werf TS. Pulmonary aspergillosis. Neth J Med. 2001 Nov;59(5):244-58.

PMID 11705644

29 Alberti C, Bouakline A, Ribaud P, Lacroix C, Rousselot P, Leblanc T, Derouin F.

Relationship between environmental fungal contamination and the incidence of invasive

aspergillosis in haematology patients. J Hosp Infect. 2001 Jul;48(3):198-206. [PMID 11439007

30 Krysinska-Traczyk E. Microflora of the farming work environment as an occupational risk

factor [Polish]. Med Pr. 2000;51(4):351-5. PMID 11059408

31 Krysinska-Traczyk E, Dutkiewicz J. Aspergillus candidus: a respiratory hazard associated

with grain dust. Ann Agric Environ Med. 2000;7(2):101-9. PMID 11153039

32 Hodgson MJ, Morey P, Leung WY, Morrow L, Miller D, Jarvis BB, Robbins H, Halsey JF,

Storey E. Building-associated pulmonary disease from exposure to Stachybotrys chartarum and

Aspergillus versicolor. J Occup Environ Med. 1998 Mar;40(3):241-9. PMID 9531095

33 Gao P, Martin J. Volatile metabolites produced by three strains of Stachybotrys chartarum

cultivated on rice and gypsum board. Appl Occup Environ Hyg. 2002 Jun;17(6):430-6. PMID


34 Barnes C, Buckley S, Pacheco F, Portnoy J. IgE-reactive proteins from Stachybotrys

chartarum. Ann Allergy Asthma Immunol. 2002 Jul;89(1):29-33. PMID 12141716

35 Rand TG, Mahoney M, White K, Oulton M. Microanatomical changes in alveolar type II cells

in juvenile mice intratracheally exposed to Stachybotrys chartarum spores and toxin.Toxicol Sci.

2002 Feb;65(2):239-45. PMID 11812928

36 Vesper SJ, Vesper MJ. Stachylysin may be a cause of hemorrhaging in humans exposed to

Stachybotrys chartarum. Infect Immun. 2002 Apr;70(4):2065-9. PMID 11895972

Page 9 of 11

37 Kordula T, Banbula A, Macomson J, Travis J. Isolation and properties of stachyrase A, a

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Jan;70(1):419-21. PMID 11748212

38 CDC. Update: Pulmonary hemorrhage/hemosiderosis among infants--Cleveland, Ohio, 1993-

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39 Terr AI. Stachybotrys: relevance to human disease. Ann Allergy Asthma Immunol. 2001

Dec;87(6 Suppl 3):57-63. PMID 11770686

40 Page EH, Trout DB. The role of Stachybotrys mycotoxins in building-related illness. AIHAJ.

2001 Sep-Oct;62(5):644-8. PMID 11669391

41 Hinojosa M, Fraj J, De la Hoz B, Alcazar R, Sueiro A. Hypersensitivity pneumonitis in

workers exposed to esparto grass (Stipa tenacissima) fibers. J Allergy Clin Immunol. 1996

Nov;98(5 Pt 1):985-91. PMID 8939163

42 Jacobs RL, Thorner RE, Holcomb JR, Schwietz LA, Jacobs FO. Hypersensitivity pneumonitis

caused by Cladosporium in an enclosed hot-tub area. Ann Intern Med. 1986 Aug;105(2):204-6.

PMID 3729202

43 Tarlo SM, Fradkin A, Tobin RS. Skin testing with extracts of fungal species derived from the

homes of allergy clinic patients in Toronto, Canada. Clin Allergy. 1988 Jan;18(1):45-52. PMID


44 Anaissie EJ, Kuchar RT, Rex JH, Francesconi A, Kasai M, Muller FM, Lozano-Chiu M,

Summerbell RC, Dignani MC, Chanock SJ, Walsh TJ. Fusariosis associated with pathogenic

fusarium species colonization of a hospital water system: a new paradigm for the epidemiology

of opportunistic mold infections. Clin Infect Dis. 2001 Dec 1;33(11):1871-8. PMID 11692299

45 Seuri M, Husman K, Kinnunen H, Reiman M, Kreus R, Kuronen P, Lehtomaki K, Paananen

M. An outbreak of respiratory diseases among workers at a water-damaged building--a case

report. Indoor Air. 2000 Sep;10(3):138-45. PMID 10979195

46 Kagen SL, Fink JN, Schlueter DP, Kurup VP, Fruchtman RB. Streptomyces albus: a new

cause of hypersensitivity pneumonitis. J Allergy Clin Immunol. 1981 Oct;68(4):295-9. PMID


47 Jaakkola MS, Laitinen S, Piipari R, Uitti J, Nordman H, Haapala AM, Jaakkola JJ.

Immunoglobulin G antibodies against indoor dampness-related microbes and adult-onset asthma:

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48 Jarvis JQ, Morey PR. Allergic respiratory disease and fungal remediation in a building in a

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Page 10 of 11

49 Fung F, Tappen D, Wood G. Alternaria-associated asthma. Appl Occup Environ Hyg. 2000

Dec;15(12):924-7. PMID 11141604

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