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Adverse Health Effects of Indoor Molds

Authors:
  • Center for Environmental and Occupational Medicine
  • Environmental Health Center - Dallas

Abstract

Purpose: It has long been known that eating moldy food is hazardous, and airborne Aspergillus and other fungi can cause life‐threatening illnesses in immunocompromised patients. However, the possible health risks of indoor mold exposure in immunocompetent humans are controversial. This literature review examines the health effects of indoor airborne exposure to mold. Design: Literature review. Materials and Methods: This review was conducted by searching PubMed and other medical databases, as well as reading recent conference reports. Results: Many studies link exposure to damp or moldy indoor conditions to increased incidence and/or severity of respiratory problems such as asthma, wheezing and rhinosinusitis. Stachybotrys produces trichothecenes and other mycotoxins, which can inhibit protein synthesis and induce hemorrhaging disorders. Indoor mold exposure can alter immunological factors and produce allergic reactions. Several studies have indicated that indoor mold exposure can alter brain blood flow, autonomic nerve function, and brain waves, and worsen concentration, attention, balance and memory. Failure to perform the appropriate objective evaluations on patients may account for the commonly held belief that indoor mold exposure poses no significant health risks to immunocompetent humans. Conclusions: Exposure to high levels of indoor mold can cause injury to and dysfunction of multiple organs and systems, including respiratory, hematological, immunological, and neurological systems, in immunocompetent humans.
REVIEW
Adverse Health Effects of Indoor Molds
LUKE CURTIS MS, CIH,
1
ALLAN LIEBERMAN MD,
2
MARTHA STARK
MD,
3
WILLIAM REA MD
4
AND MARSHA VETTER MD, PHD
5
1
School of Public Health, University of Illinois at Chicago, Illinois,
2
Center for
Occupational and Environmental Health, North Charleston, South Carolina,
3
Harvard
University, Newton Center, Massachusetts,
4
Environmental Health Center, Dallas,
Texas,
5
Environmental Health Center, Hoffman Estates, Illinois, USA
Abstract
Purpose: It has long been known that eating moldy food is hazardous, and airborne
Aspergillus and other fungi can cause life-threatening illnesses in immunocompromised
patients. However, the possible health risks of indoor mold exposure in immunocompetent
humans are controversial. This literature review examines the health effects of indoor airborne
exposure to mold.
Design: Literature review.
Materials and Methods: This review was conducted by searching PubMed and other medical
databases, as well as reading recent conference reports.
Results: Many studies link exposure to damp or moldy indoor conditions to increased
incidence and/or severity of respiratory problems such as asthma, wheezing and rhinosinusitis.
Stachybotrys produces trichothecenes and other mycotoxins, which can inhibit protein
synthesis and induce hemorrhaging disorders. Indoor mold exposure can alter immunological
factors and produce allergic reactions. Several studies have indicated that indoor mold
exposure can alter brain blood flow, autonomic nerve function, and brain waves, and worsen
concentration, attention, balance and memory. Failure to perform the appropriate objective
evaluations on patients may account for the commonly held belief that indoor mold exposure
poses no significant health risks to immunocompetent humans.
Conclusions: Exposure to high levels of indoor mold can cause injury to and dysfunction of
multiple organs and systems, including respiratory, hematological, immunological, and
neurological systems, in immunocompetent humans.
Keywords: mold, fungi, mycotoxin, allergy, indoor air quality, asthma, neurotoxicity, lung hemorrhage,
Aspergillus, Penicillium, Cladosporium, Alternaria, Stachybotrys.
INTRODUCTION
In recent years, public attention has become increasingly focused on human health
concerns linked with mold (fungi) inside homes and workplaces. Indoor airborne mold
exposure has been associated with adverse human health effects in multiple organs and
body systems, including respiratory, nervous, immune, hematological and dermatological
systems. Indoor mold exposure can also lead to life-threatening systemic infections in
immunocompromised patients.
A qualitative systematic literature review was undertaken in order to examine and
Journal of Nutritional & Environmental Medicine (September 2004) 14(3), 261–274
ISSN 1359-0847 print/ISSN 1364-6907 online/04/030261-14
#
2004 Taylor & Francis Ltd
DOI: 10.1080/13590840400010318
appraise the current state of knowledge about indoor mold-linked health effects, and to
summarize the available evidence for use by health professionals. Physicians, in particular,
may encounter patients with common symptoms occurring in particular environments, and
understanding the potential for mold-related health effects is key to the complete
investigation of those environments. Physicians and industrial hygienists may be asked to
contribute reports to assist the courts in settling suits. In 2002, an estimated 10,000 mold-
related cases were pending in US courts [1]. Also in 2002, the insurance industry paid out
$2 billion in mold-related claims in Texas alone [2].
Literature was reviewed using the peer-reviewed database, and from recent conferences
on indoor molds. The levels of evidence available for each topic varied from level I (from at
least one properly randomized controlled trial) through level II (from trials without
randomization, exceptionally convincing uncontrolled experiments, cohort or case–control
studies), to level III (opinion of respected authorities based on clinical experience,
descriptive studies, or reports of expert committees) [3].
MOLDS IN THE INDOOR ENVIRONMENT
Fungi (or molds) are ubiquitous in both indoor and outdoor environments and are
frequently dispersed by airborne spores. Mold and mold spores require moisture and a
food source, such as cellulose or decaying food, to grow [4]. As mold spores swell with
water and grow, they elongate, forming balloon-like protuberances (hyphae), which secrete
digestive enzymes and mycotoxins. The fungi then digest the food source to support their
growth.
About 100,000 fungal species have already been identified; in fact, fungi are estimated to
comprise an astounding 25% of the world’s biomass [5]. Various surveys of homes in North
America and Europe have reported that visible mold and/or water damage are common,
found in 23–98% of all homes examined [6–9]. There are no official standards at this time
for indoor airborne fungi concentrations. However, indoor fungal levels above a range of
150–1000 colony-forming units per cubic meter of air (cfu m
23
) are considered to be
sufficient to cause human health problems [7, 10–12]. Numerous reports have documented
that indoor air can be contaminated with fungal spore levels well in excess of 1000 cfu m
23
[13–20]. The most common indoor fungal genera collected are Cladosporium, Aspergillus
and Penicillium [13–20]. Alternaria, Stachybotrys, Rhizopus, Mucor, Wallemia, Trichoderma,
Chaetonium, yeasts, Botrytis, Epicoccum and Fusarium species are often found indoors as
well [13–20].
MOLD-RELATED HEALTH SYMPTOMS
Patients have been reporting multiple ill health effects linked to exposures to mold. Studies
of more than 1600 patients suffering ill effects associated with fungal exposure were
presented at one meeting in Dallas in 2003 (21st Annual Symposium of Man and His
Environment, Dallas, Texas, 19–22 June 2003) [21–25].
To cite a few studies: Lieberman [21] examined 48 heavily mold-exposed patients who
had the following health problems: muscle and/or joint pain (71%), fatigue/weakness (70%),
neurocognitive dysfunction (67%), sinusitis (65%), headache (65%), gastrointestinal
problems (58%), shortness of breath (54%), anxiety/depression/irritability (54%), vision
problems (42%), chest tightness (42%), insomnia (40%), dizziness (38%), numbness/tingling
(35%), laryngitis (35%), nausea (33%), skin rashes (27%), tremors (25%) and heart
palpitations (21%). Rea et al.’s study [23] of 150 heavily indoor mold-exposed patients
found the following health problems: fatigue (100%), rhinitis (65%), memory loss and other
neuropsychiatric problems (46%), respiratory problems (40%), fibromyalgia (29%), irritable
L. CURTIS ET AL.262
bowel syndrome (25%), vasculitis (4.7%) and angioedema (4.0%). These clinical reports
suggest that there can be multisystem adverse effects of airborne mold. All reported cases
had environmental mold exposure consistent with toxic mold exposure.
MECHANISMS OF MOLD-RELATED HEALTH EFFECTS
Fungi can exert ill health effects by three major mechanisms: allergy, toxicity, and
infection.
Allergy and Irritation
At least 70 allergens have been well characterized from spores, vegetative parts and small
particles from fungi (0.3 mm and smaller) [26, 27]. A review of 17 studies revealed that
6–10% of the general population and 15–50% of atopics had immediate skin sensitivity to
fungi [28]. Fungi produce beta glucans, which have irritant properties [29].
Toxicity
Fungi produce a wide variety of toxic chemicals called mycotoxins [4, 30, 31]. Some
common mycotoxins include: aflatoxins—very potent carcinogens and hepatotoxins,
produced by some Aspergillus species; ochratoxins—nephrotoxic and carcinogenic,
produced by some Aspergillus and Penicillium; sterigmatocystin—immunosuppressive
and a liver carcinogen, produced by Aspergillus species, especially A. versicolor;
trichothecenes—produced primarily by Stachybotrys and Fusarium species and have
been reported to inhibit protein synthesis and cause hemorrhage and vomiting. Fungi also
produce beta glucans, which have immunological effects [32]. The smell of molds comes
primarily from volatile organic compounds [33].
Adverse human and animal effects from mycotoxin-contaminated foodstuffs have been
well recognized since the early twentieth century [30, 34], but the pathway of mycotoxin
injury through inhalation is questioned [35]. Because it is unethical to conduct controlled
studies on humans with inhaled mycotoxin exposure, only controlled animal exposures and
human cohort and case–control studies can be carried out. The literature reveals that
significant amounts of mycotoxins (including ochratoxin, sterigmatocystin and trichothe-
cenes) are present in indoor dust [36–39] and dust or fungal particles less than 10 mm
in diameter are respirable, thus allowing absorption of mycotoxins through the lungs
[31, 34, 40, 41].
Patients exposed to indoor Stachybotrys have been found to have measurable blood
levels of the Stachybotrys hemorrhagic toxin stachylysin [42]. Levels of trichothecene
mycotoxins in urine have also been found in significantly higher levels in patients exposed
to high indoor fungal levels as opposed to an unexposed control group [43].
Blood ochratoxin levels have been found to be significantly higher in food industry
workers exposed to airborne ochratoxin vs. unexposed controls [39]. These findings support
an inhalation pathway for entry of mycotoxins into the body.
Infection
Fungi such as Candida, Histoplasmosis, Cryptococcus, Blastomyces and Coccidioides can
infect immunocompetent people [44]. Fungi such as Trichophyton, Candida and Malasezia
commonly cause minor skin infections in immunocompetent humans [45].
Serious infections by such fungi as Candida, Aspergillus and Pneumocystis mostly involve
severely immunocompromised patients [45–47]. In recent years, the incidence of life-
threatening infections in immunocompromised patients from Aspergillus and other common
ADVERSE HEALTH EFFECTS OF INDOOR MOLDS 263
fungi has been growing rapidly [48, 49]. Invasive aspergillosis is very common among
immunocompromised patients, with the following reported incidence rates: lung
transplants: 17–26%; allogenic bone marrow transplants: 5–15%; acute leukemia: 5–24%;
heart transplants: 2–13% [50–51]. Even with strong anti-fungal drugs and intense hospital
treatment, mortality rates from invasive aspergillosis range from 50 to 99% in the
immunocompromised [52, 53].
SAMPLING FOR MOLD EXPOSURE
Indoor fungal sampling is most commonly performed by measuring airborne levels of
viable (culturable) or total (viable and non-viable) spores [54, 55]. Some of the airborne
viable sampling methods, such as Andersen samplers, collect air for only a few minutes.
Settle plates are an inexpensive method to obtain a semi-quantitative measure of indoor
airborne fungi levels. Viable and non-viable airborne spore counts can vary considerably
over a period of minutes, so air sampling over several periods of time may be necessary to
accurately characterize airborne fungal spore levels [54, 55]. However, airborne fungi
measurements fail to take into consideration mold contamination in dust or surfaces (often
visible to the naked eye) and mycotoxins in air, dust and on surfaces [54, 56]. Therefore,
testing settled dust for fungi and mycotoxins has been recommended [54, 55]. Other
techniques, such as polymerase chain reaction (PCR), enzyme-linked immunosorbent assay
(ELISA), and measurement of fungal volatile organic compounds, polysaccharides,
ergosterol and beta glucans, have also been found to be useful in assaying indoor
environments for molds, their allergens and mycotoxins [54].
INDOOR MOLD EXPOSURE AND HEALTH EFFECTS IN BODY SYSTEMS
Respiratory System
Many epidemiological studies have noted that residential exposure to molds and/or chronic
dampness can increase asthma/wheezing incidence or morbidity in both children and adults
[7–9, 57–70]. Asthma and related conditions are very common in the USA, with an overall
prevalence of about 5.4% among all age groups and incidences as high as 27% in inner city
children [71]. Studies with infants have reported that higher fungal exposures are associated
with more wheezing, coughing and respiratory illness [72, 73]. Higher indoor beta glucan
levels have been associated with significantly higher levels of chest tightness and joint pain
[74]. Non-industrial occupational mold exposure has been reported to be associated with
significantly higher levels of asthma, sinusitis, irritated skin and eyes, and chronic fatigue
[75–79]. One study found that patients exposed to high indoor fungal levels had
significantly lower lung function than unexposed controls [24]. Higher outdoor fungal
concentrations have been linked to higher asthma death rates [80] and higher asthma
incidence [81–83] in children or young adults. Challenge exposures with Penicillium and
Alternaria extracts equivalent to high outdoor levels of fungi were noted to severely lower
lung function in asthmatics [84]. Skin sensitivity to Alternaria has been linked to much
higher risk (odds ratio 190, 95% confidence interval 6.5–6.536, pv0.0001) of respiratory
arrest [85]. Various epidemiological studies have associated skin sensitivity to common
indoor fungi and higher asthma incidence or severity [86–90] and higher rates of sinusitis
[91].
Airborne fungal exposure is known to cause bronchopulmonary aspergillosis and
hypersensitivity pneumonitis, and can cause sinusitis [92, 93]. An estimated 14% of the US
population suffers from rhinosinusitis and related conditions [94]. Allergic fungal sinusitis
was diagnosed on the basis of fungal growth in nasal secretions and the presence of allergic
mucin in 93% of 101 consecutive patients undergoing sinus surgery [94]. Another study was
L. CURTIS ET AL.264
able to recover and culture fungi from the sinuses of 56% of 45 patients undergoing
endoscopic sinus surgery for chronic rhinosinusitis [95]. A long-term cohort study of 639
patients with allergic fungal sinusitis demonstrated that remedial steps taken to reduce
fungal exposure (by utilizing, for example, air filters, ionizers, moisture control and anti-
microbial nasal sprays) significantly reduced rhinosinusitis and improved nasal mucosa
morphology [22]. This study concluded that failure to reduce airborne fungi levels to less
than four per hour on a settle plate failed to resolve the sinusitis [22]. Although,
historically, anti-fungal drugs have generally not been recommended for the treatment of
fungal sinusitis [92, 93], recent observational studies have found beneficial effects of oral
and nasal medication for sinusitis patients [22, 96]. Several studies have linked residential
exposure to various fungi with hypersensitivity pneumonitis [97–99].
Hematological Effects
Exposure to high indoor levels of Stachybotrys, Aspergillus and other fungi has been
epidemiologically associated with infant lung hemorrhage [100–104]. Although questions
were raised after this association was discovered [105], it meets many epidemiological
criteria for causality [106]. Acute infant pulmonary hemorrhage can be rapidly fatal; when
the infant survives, lung blood vessel damage is present and deposits of hemosiderin will
remain in the lung macrophages and can be seen in tissue obtained during bronchoscopy
[101]. Stachybotrys fungi produce a wide range of trichothecene mycotoxins (including
satratoxins and T2), several roridin epimers, verrucarin J and B and hemolysin [31, 103]. A
hemorrhagic protein called stachylysin has been isolated from Stachybotrys collected from
homes of infants with lung hemorrhage [107, 108] and from serum of patients with
residential Stachybotrys exposure [42]. It is hypothesized that infants with their rapidly
growing lungs are more susceptible to the toxic effects of Stachybotrys mycotoxins [109].
Studies with Stachybotrys-exposed adults have noted a significantly higher incidence of
health conditions such as wheezing, skin and eye irritation, ’flu-like symptoms and chronic
fatigue [110]. Stachybotrys has been isolated from the lungs of a child with pulmonary
hemosiderosis [111].
A case study was presented of 16-month-old twins in a mold-infested home, one of whom
died of pulmonary hemosiderosis [112]. High levels of trichothecene mycotoxins were found
in the lungs and liver of the dead infant, while high IgG levels to Stachybotrys and IgM
levels to satratoxin and trichothecenes were found in the serum of the surviving infant.
Environmental sampling in the twins’ home found high levels of satratoxin as well as high
levels of spores from Stachybotrys, Aspergillus versicolor and Penicillium [112].
Immune System
Some studies have reported that indoor fungi-exposed patients have higher serum levels of
IgG, IgA and IgM antibodies to common fungi, trichothecenes and satratoxins [113–115].
IgG antibodies to nine common indoor fungi were significantly higher in subjects with
sinusitis vs. non-sinusitis subjects in a moldy school [116]. Other studies have noted no
significant increases in fungal IgG [117, 118] or fungal IgE [113] in fungi-exposed patients.
indoor fungal exposure has been associated with altered levels of T4, T8 and natural killer
cells and higher levels of autoantibodies [23, 25, 119, 120]. Occupants of homes with high
indoor glucan exposure had a lower proportion of cytotoxic t-cells (CD8zSF61z) and
higher secretion of tumor necrosis factor than occupants of homes with lower levels of beta
glucans [121]. Studies of animals given such common mycotoxins as aflatoxins, ochratoxins
and trichothecenes orally showed considerable immune impairment, including depression
of T cells, B cells and macrophages [122]. Human cell line studies have also found that
ADVERSE HEALTH EFFECTS OF INDOOR MOLDS 265
many mycotoxins can suppress T-cell, B-cell and natural killer cell activity at serum
concentrations similar to those found in indoor mold-exposed patients [123].
Central Nervous System
Two case series of 48 and 150 mold-exposed patients found significant fatigue and
weakness in 70–100% of cases, and neurocognitive dysfunction including memory loss,
irritability, anxiety and depression in over 40% of the patients [21, 23]. Numbness, tingling
and tremor were also found in a significant number of patients [21, 23]. These signs and
symptoms have been described as classic manifestations of neurotoxicity [124].
A study of 43 mold-exposed patients found that they performed significantly worse than
202 controls on many neuropsychiatric tests, including balance sway speed, blinking reflex,
color perception, reaction times and left grip strength (pv0.0001) [125]. Quantitative
electroencephalogram (qEEG) studies in 182 patients with documented mold exposure also
noted significant alterations in brain waves, including hypoactivation of the frontal cortex
and narrowed frequency bands [126]. Higher levels of mold exposure (longer time in mold-
infested area, presence of Stachybotrys or higher cfu m
23
air) were associated with
significantly more abnormal qEEGs as well as significantly worse scores of concentration
and motor and verbal skills in these 182 patients [126]. A triple-headed SPECT brain scan
revealed neurotoxic patterns in 26 of 30 (87%) mold-exposed patients [127]. An iriscorder
study of autonomic nervous function in 60 mold-exposed patients found that 95% had
abnormal autonomic responses of the pupil compared with the population reference range
[23]. Visual contrast sensitivity studies were often abnormal in indoor mold-exposed
patients [23]. Additional studies have reported that mold-exposed patients do significantly
worse on tests of attention, balance, reaction time, verbal recall, concentration, memory,
and finger tapping compared with the general population reference range [24, 128, 129].
Most of these patients also experienced many health problems, including chronic fatigue,
headaches, insomnia and decreased balance, concentration and attention. Studies of indoor
mold-exposed children and adults found significantly more neurophysiological abnorm-
alities vs. controls, including abnormal EEGs and abnormal brainstem, visual and
somatosensory evoked potentials [25, 130, 131].
Lieberman [21] presented a case series of 12 patients who developed tremors following
documented heavy indoor mold exposure. Numerous articles have reported domestic dogs
developing tremors following ingestion of moldy food [132–134]. Territrem b, a mycotoxin
produced by the common fungus Aspergillus terreus, has been shown to be an irreversible
binder and inhibitor of acetylcholinesterase [135].
Renal System
It is known that ochratoxin-contaminated food is nephrotoxic [136, 137]. Indoor airborne
exposure to ochratoxin may also be nephrotoxic. In a case report of a family presenting
with increasing thirst/urination, lethargy, and skin rash, a considerable amount of
ochratoxin was found in their house dust. The family recovered after moving to another
home [36].
Reproductive System
The literature suggests a relationship between heavy airborne fungal exposure and
reproductive dysfunction. Kristensen et al. [138, 139] reported that airborne mycotoxin
exposures in Norwegian grain farmers were significantly related to higher rates of pre-
term deliveries, late-term miscarriages and higher rates of endometrial and ovarian
L. CURTIS ET AL.266
endocarcinoma. The veterinary literature finds a strong association between mycotoxtins in
feedstuffs and reproductive problems [140].
Diabetes
There is a great deal of evidence that links environmental factors to the triggering of type 1
diabetes. Exposure to viruses, bacteria and mycotoxins such as alloxan, streptozatocin and
L-asparginase has been linked to the development of type 1 diabetes in animals and
humans [141–143]. Lieberman [21] reported that in a single year, five of his patients
developed type 1 diabetes following documented heavy indoor mold exposure.
DIAGNOSIS AND MANAGEMENT OF POTENTIALLY MOLD-RELATED
HEALTH PROBLEMS
A careful medical and environmental history is an essential first step in evaluating a patient
for mold-related health problems [144–147]. Particular attention should be paid to any
history of exposure to visible mold and/or water damage at the home or workplace.
Environmental sampling for viable spores, total spores, and mycotoxins in the air and dust
can provide important exposure information. For a helpful overview of sampling methods,
see references [54, 148, 149]. For an informative guide to the classification, identification
and biology of common indoor fungi, see reference [4]. Several good guides exist for the
prevention and remediation of indoor fungi problems [144, 148–151].
For patients suspected of having substantial fungal exposure, a battery of sophisticated
laboratory tests has been developed:
(1) a basic metabolic panel to test for several important parameters (including
electrolytes, blood sugar, liver and kidney status)
(2) measurement of antibodies to molds and mycotoxins in serum [113, 114]
(3) immune tests for autoantibodies, complement, gamma globulins and lymphocyte
panels [120]
(4) urine and blood testing for mycotoxins [43]
(5) visual contrast sensitivity tests
(6) pupillometry and heart rate variation to assist in the evaluation of autonomic nervous
system function
(7) standard neuropsychological test batteries [23, 128–130]
(8) EEG and brain imaging techniques
(9) SPECT and magnetic resonance imaging (MRI) can be very helpful tools in
documenting neurological damage [25,125, 127, 131, 145]
(10) pulmonary function tests are also useful for patients with respiratory symptoms
[24, 124].
Failure to perform objective evaluations to access system or organ dysfunction account
for the presently accepted position that airborne mold exposures have no significant
adverse effects [35]. If end-stage organ damage is suspected, consultation with a specialist
may be useful.
Other common indoor environmental exposures should also be considered as a potential
source of health problems. Common non-fungal indoor environmental factors include poor
ventilation, carbon monoxide from faulty heat sources, leaking natural gas, pesticides,
wood smoke, second-hand tobacco smoke, petrochemicals, such as cleaners/building
materials/solvents, formaldehyde from outgassing carpets, building materials, bacteria, and
allergens from the fur, feathers, saliva and excrement of common household animals such
as cockroaches, dust mites, cats, dogs, mice, rats, caged birds, and pigeons. Exposure to
ozone, second-hand tobacco smoke, cockroach allergens, formaldehyde, and viral
ADVERSE HEALTH EFFECTS OF INDOOR MOLDS 267
infections have been noted to have a synergistic effect with fungal exposure to worsen
asthma and rhinitis [152–156].
The most important part of treatment for mold-exposed patients, symptomatic or not, is
avoidance of fungal exposure and remediation of mold contamination in the home and
workplace. Any water leaks and damage from flooded or damp areas should be rectified
immediately. Non-porous surfaces such as floors and walls that have visible mold growth
should be cleaned. Porous waterlogged materials like carpet and furniture should be
discarded. Control of humidity is important to control mold growth. The use of air
conditioners and dehumidifiers can significantly reduce summertime indoor airborne mold
concentrations [13, 157]. HEPA air filters can also significantly reduce indoor airborne
fungi concentrations [158]. For cleaning severe indoor water or mold problems, the use of
protective equipment like face masks and/or the use of a professional remediation firm may
be essential [148–151].
Environmental control plays a key role in preventing Aspergillus infections. Several
studies have linked hospital construction work to increased rates of invasive aspergillosis
[159–162]. Environmental controls such as using HEPA filters, sealing rooms, regular
cleaning of rooms, and using anti-fungal copper-8-quionolate paint have been shown to
both significantly reduce airborne levels of Aspergillus and significantly reduce rates of
invasive aspergillosis in immunocompromised hospital patients [158, 160–165]. Other recent
research has indicated that a large number of Aspergillus spores can spread through water
supplies [166] and that cleaning shower facilities can significantly lower airborne levels of
Aspergillus [167].
Use of sublingual or fungal immunotherapy by injection has been shown to be beneficial
to some patients sensitized to common indoor molds such as Alternaria and Cladosporium
herbarium [168, 169]. Some studies with laboratory animals suggest that a high-quality diet
with adequate antioxidant vitamins, selenium, phytochemicals, methionine and total
protein can reduce the harmful effects of food mycotoxins [170, 171].
SUMMARY
There is an accumulated weight of evidence linking indoor airborne mold and/or
mycotoxin exposures to multisystem adverse human health effects. A history of new
neurocognitive symptoms occurring in patients soon after heavy mold exposure,
accompanied by objective neuropsychological findings in such patients, adds considerably
to the weight of evidence from animal studies, epidemiological research, and case series.
Health care professionals, building managers, homeowners and the general public need
to be much more aware of the potential adverse health effects of high indoor fungal
exposures and the need for proper building construction, maintenance, and remediation of
dampness to prevent such effects. Potentially mold-related illnesses need to be considered in
differential diagnoses, and careful exposure histories taken. Prompt removal from exposure
to fungal contamination remains the treatment of choice, with some evidence that
immunotherapy and nutritional support are also useful. Indoor airborne mold particles can
be irritative to the respiratory tract, and fungal spores, antigens, volatile organic
compounds, and mycotoxins can be absorbed through the respiratory route to provoke
injury by the mechanisms of allergy, toxicity, and infection.
REFERENCES
[1] Umberger M. The start that upstaged the economy. Chicago Tribune, 13 January 2002, available
at WL 2612028, database ALLNEWS.
[2] Mold claims hit $4 billion in Texas, Insurance Journal, 27 May 2003 (http://insurancejournal.com).
L. CURTIS ET AL.268
[3] The Canadian Task Force on the Periodic Health Examination. The Canadian Guide to Clinical
Preventative Health Care. Ottawa: Supply and Services Canada, 1994.
[4] Samson R, Hoekstra E, Frisvad J, Filtenborg O. Introduction to Food and Airborne Fungi.
Utrecht: Centraalbureau voor Schimmelcultures, 2000.
[5] Miller JD. Fungi as contaminants of indoor air. Atmos Environ 1992; 26A(12): 2162–72.
[6] Presternon DR. Perceived moisture problems in Iowa homes. Technical note. Forest Products J
1991; 41(6): 47–48.
[7] Platt S, Martin C, Hunt S, Lewis C. Damp housing, mould growth and symptomatic health state.
Br Med J 1989; 298: 1673–8.
[8] Brunekreef B, Dockery D, Speizer FE. Home dampness and respiratory morbidity in children.
Am Rev Resp Dis 1989; 140: 1363–7.
[9] Dales R, Zwanenburg H, Burnett R, Franklin C. Respiratory health effects of home dampness
and molds among Canadian children. Am J Epidemiol 1991; 134(2): 196–203.
[10] Etzel R. Indoor air pollutants in homes and schools. Pediatr Clin North Am 2001; 48(5): 1153–65.
[11] Flannigan B, McCabe E, McGarry F. Allergic and toxigenic microorganisms in houses. J Appl
Bacteriol 1991; 70: 61S–73S.
[12] Dhillion M. Current status of mold immunotherapy. Ann Allergy 1991; 66: 385.
[13] Curtis L, Ross M, Persky V et al. Bioaerosol concentrations in the Quad Cities 1 year after the
1993 Mississippi River floods. Indoor Built Environ 2000; 9: 35–43.
[14] Shelton B, Kirkland K, Flanders WD, Morris G. Profiles of airborne fungi in buildings and
outdoor environments in the United States. Appl Environ Microbiol 2002; 68(4): 1743–53.
[15] Ren P, Jankun T, Leaderer B. Comparisons of seasonal fungal prevalence in indoor and outdoor
air and in house dwellings in one Northeast American county. J Exposure Anal Environ
Epidemiol 1999; 9: 560–8.
[16] Pei-Chih W, Huey-Jen S, Chia-Yin L. Characteristics of indoor and outdoor airborne fungi at
suburban and urban homes in two seasons. Sci Total Environ 2000; 253: 111–18.
[17] Li CS, Kuo YM. Characteristics of airborne microfungi in subtropical homes. Sci Total Environ
1994; 155(3): 267–71.
[18] Ebner E, Hasselwandter K, Frank A. Indoor and outdoor incidence of airborne fungal allergens
at low and high alpine environments. Mycol Res 1992; 97: 117–24.
[19] Solomon WR. A volumetric study of winter fungus prevalence in the air of midwestern homes.
J Allergy Clin Immunol 1976; 57(1): 46–55.
[20] Beaumont F, Kauffman HF, Sluiter HJ, DeVries K. A volumetric-aerobiological study of
seasonal fungus prevalence inside and outside dwellings of asthmatic patients living in northeast
Netherlands. Ann Allergy 1984; 53(6): 486–92.
[21] Lieberman A. Explosion of mold cases in homes, workplaces and occupational medicine
practices. Presented at the 21st Annual Symposium on Man and His Environment in Health and
Disease, Dallas, Texas, 19–22 June 2003.
[22] Dennis D. Chronic sinusitis: defective T-cells responding to superantigens, treated by reduction of
fungi in the nose and air. Arch Environ Health 2003; 58(7): 433–41.
[23] Rea WJ, Didriksen N, Simon TR, Pan Y, Fenyves EJ, Griffiths B. Effects of toxic exposure to
molds and mycotoxins in building-related illnesses. Arch Environ Health 2003; 58(7): 399–405.
[24] Kilburn KH. Indoor mold exposure associated with neurobehavioral and pulmonary impairment:
a preliminary report. Arch Environ Health 2003; 58(7): 390–8.
[25] Campbell A, Thrasher J, Madison R, Vojdani A, Gray M, Johnson A. Neural autoantibodies and
neurophysiologic abnormalities in patients exposed to molds in water damaged buildings. Arch
Environ Health 2003; 58(8): 464–78.
[26] Kurup V, Shen HD, Vijay H. Immunobiology of fungal allergens. Int Arch Allergy Immunol
2002; 129: 181–8.
[27] Gorny RL, Reponen T, Willeke K et al. Fungal fragments as indoor air contaminants. Appl
Environ Microbiol 2002; 68: 3522–31.
[28] Institute of Medicine. Clearing the Air. Asthma and Indoor Exposures. Institute of Medicine, 2000.
[29] Korpi A, Kasanen JP, Kosma VM, Rylander R, Pasanen AL. Slight respiratory irritation but not
inflammation in mice exposed to (1w3)-beta-D-glycan aerosols. Mediat Inflamm 2003; 12(3):
139–46.
[30] Etzel R. Mycotoxins. J Am Med Assoc 2002; 287(4): 425–7.
[31] Nielsen KF. Mycotoxin production by indoor molds. Fungal Genet Biol 2003; 39: 103–17.
[32] Rylander R. Indoor air-related effects and airborne (1w3)-beta-D-glucan. Environ Health
Perspect 1999; 107(Supplement 3): 501–3.
[33] Wilkins K, Larsen K, Simkus M. Volatile metabolites from mold growth on building materials
and synthetic media. Chemosphere 2000; 41(3): 437–46.
[34] Bennett J, Klich M. Mycotoxins. Clin Microbiol Rev 2003; 16(3): 497–516.
[35] Hardin B, Kelman B, Saxon A. ACOEM evidence base statement. Adverse health effects
associated with molds in the indoor environment. J Occup Environ Med 2003; 45(5): 470–8.
ADVERSE HEALTH EFFECTS OF INDOOR MOLDS 269
[36] Richard J, Plattner R, May J, Liska S. The occurrence of ochratoxin A in dust collected from a
problem household. Mycopathologica 1999; 146(2): 99–103.
[37] Smoragiewicz W, Cossette B, Boutard A, Krystyniak K. Trichothecene mycotoxins in the dust of
ventilation systems in office buildings. Int Arch Occup Environ Health 1993; 65(2): 113–17.
[38] Engelhart S, Loock A, Skutlarek D et al. Occurrence of toxigenic Aspergillus versicolor isolates
and sterigmatocystin in carpet dust from damp indoor environments. Appl Environ Microbiol
2002; 68(8): 3886–90.
[39] Iavacoli I, Brera C, Carelli G, Caputi R, Marinaccio A, Miraglia M. External and internal dose
in subjects occupationally exposed to ochratoxin A. Int Arch Occup Environ Health 2002; 75(6):
381–6.
[40] Fischer G, Dott W. Relevance of airborne fungi and their secondary metabolites for
environmental, occupational and indoor hygiene. Arch Microbiol 2003; 179: 75–82.
[41] Sorenson WG. Fungal spores: hazardous to health? Environ Health Perspect 1999; 107
(Supplement 3): 469–72.
[42] Van Emon J, Reed A, Yike I, Vesper S. ELISA measurement of stachylysin in serum to quantify
human exposures to the indoor mold Stachybotrys charatarum. J Occup Environ Med 2003; 45:
582–91.
[43] Croft W, Jastromski BM, Croft AL, Peters HA. Clinical confirmation of trichothecene
mycotoxicosis in patient urine. J Environ Biol 2002; 23(3): 301–20.
[44] Johnson P, Sarosi G. Community acquired fungal pneumonias. Semin Resp Infect 1989; 4(1):
56–63.
[45] Tierney L, McPhee S, Papadakis M. Current Medical Diagnosis and Treatment. New York:
Lange Medical Books, 2003.
[46] Nicod L, Pache J, Howarth N. Fungal infections in transplant recipients. Eur Resp J 2001; 17(1):
133–40.
[47] Garber G. An overview of fungal infections. Drugs 2001; 61(Supplement 1): 1–12.
[48] Groll AH, Shah PM, Mentzel C, Schneider M, Just-Nuebling G, Huebner K. Trends in
the postmortem epidemiology of invasive fungi at a university hospital. J Infect 1996; 33:
23–32.
[49] Husain S, Alexander BD, Munoz P et al. Opportunistic mycelial fungal infections in organ
transplant recipients: emerging importance of non-Aspergillus fungi. Clin Infect Dis 2003; 37(2):
221–9.
[50] Denning D. Report on a European Science Foundation Workshop on Invasive Aspergillosis,
21–22 October 1998, University of Manchester, Manchester.
[51] Kontoyiannis D, Bodey G. Invasive aspergillosis in 2002: an update. Eur J Clin Microbiol Infect
Dis 2002; 21: 161–72.
[52] Denning D. Therapeutic outcome in invasive aspergillosis. Clin Infect Dis 1996; 23(3): 608–15.
[53] Lin S, Schranz J, Teutsch S. Aspergillosis case-fatality rate: systemic review of the literature. Clin
Infect Dis 2001; 32(3): 358–66.
[54] Pasanen AL. A review: fungal exposure assessment in indoor environments. Indoor Air 2001; 11:
87–98.
[55] Dillon HK, Miller JD, Sorenson WG, Douwes J, Jacobs R. Review of methods applicable to the
assessment of mold exposure in children. Environ Health Perspect 1999; 107(Supplement 3):
473–80.
[56] Tiffany J, Bader H. Detection of Stachybotrys charatarum: the effectiveness of culturable-air
sampling and other methods. Environ Health 1999; 2000: 9–11.
[57] Gent J, Ren P, Belanger K et al. Levels of household mold associated with respiratory symptoms
in the first year of life in a cohort at risk for asthma. Environ Health Perspect 2002; 110(12):
A781–6.
[58] Dales R, Burnett R, Zwanenburg H. Adverse health effects among adults’ exposures to home
dampness and molds. Am Rev Resp Dis 1991; 143: 505–9.
[59] Ostro B, Lipsett M, Mann J, Braxton-Owens H, White M. Air pollution and exacerbation of
asthma in African-American children in Los Angeles. Epidemiology 2001; 12: 200–8.
[60] Zock J, Jarvis D, Lucynska G, Sunyer J, Burney P. Housing characteristics, reported mold
exposure, and asthma in the European Community Respiratory Health Survey. J Allergy Clin
Immunol 2002; 110(2): 285–92.
[61] Williamson I, Martin C, McGill G. Damp housing and asthma: a case control study. Thorax
1997; 52: 229–34.
[62] Verhoeff AP, Van Strien RT, Van Wijnen JH, Brunekreef B. Damp housing and household
respiratory symptoms: the role of sensitization to dust mites and molds. Am J Epidemiol 1995;
141: 103–10.
[63] Strachan DP, Flannigan B, McCabe E, McGarry F. Quantification of airborne moulds in the
homes of children with and without wheeze. Thorax 1990; 45: 382–7.
[64] Brunekreef B. Damp housing and adult respiratory symptoms. Allergy 1992; 47: 498–502.
L. CURTIS ET AL.270
[65] Waegemaekers M, Van Wageningen N, Brunekreef B, Boleij JS. Respiratory symptoms in damp
homes. A pilot study. Allergy 1989; 44: 192–8.
[66] Jedrychowski W, Flak E. Separate and combined effects of the indoor and outdoor air quality on
chronic respiratory symptoms adjusted for allergy among preadolescent children. Int J Occup
Med Environ Health 1998; 11: 19–35.
[67] Hu FB, Persky V, Flay BR, Richardson J. An epidemiological study of asthma prevalence and
related factors among young adults. J Asthma 1997; 34(1): 67–76.
[68] Jaakkola J, Jaakkola N, Ruotsalainen R. Home dampness and molds as determinants of
respiratory symptoms and asthma in pre-school children. J Exposure Anal Environ Epidemiol
1993; 3(Supplement 1): 126–42.
[69] Slezak J, Persky V, Kviz F, Ramakrishnan V, Byers C. Asthma prevalence and risk factors in
selected Head Start sites in Chicago. J Asthma 1998; 35(2): 203–12.
[70] Lee YL, Lin YC, Hsiue TR, Hwang BF, Guo YL. Indoor and outdoor environmental exposures,
parental atopy and physician diagnosed asthma in Taiwanese schoolchildren. Pediatrics 2003;
112(5): e389–95.
[71] Sly RM. Changing prevalence of allergic rhinitis and asthma. Ann Allergy Asthma Immunol
1999; 82(3): 233–48.
[72] Belanger K, Beckett W, Triche E et al. Symptoms of wheeze and persistent cough in the first year
of life: associations with indoor allergens, air contaminants, and maternal history of asthma. Am
J Epidemiol 2003; 158: 195–202.
[73] Stark PC, Burge HA, Ryan LM, Milton DK, Gold DR. Fungal levels in the home and lower
respiratory tract illness in the first year of life. Am J Resp Crit Care Med 2003; 168(2): 232–7.
[74] Thorn J, Rylander R. Airways inflammation and glucan in a rowhouse area. Am J Resp Crit Care
Med 1998; 157: 1798–803.
[75] Chao HJ, Schwartz J, Milton DK, Burge HA. The work environment and workers’ health in 4
large office buildings. Environ Health Perspect 2003; 111(9): 1242–8.
[76] Pirhonen I, Nevalainen A, Husman T. Home dampness, moulds and their influence on respiratory
infections in Finland. Eur Resp J 1996; 9: 2618–22.
[77] Koskinen OM, Husman TM, Meklin TM. The relationship between mould and moisture
observations in houses and state of health of their occupants. Eur Resp J 1999; 14: 1363–7.
[78] Ruotsalainen R, Jaakola N, Jaakola J. Dampness and molds in day-care centers as an
occupational health care problem. Int Arch Occup Environ Health 1995; 66: 369–74.
[79] Wan GH, Li CS. Dampness and airway inflammation and systemic conditions in office building
workers. Arch Environ Health 1999; 54: 58–63.
[80] Targonski P, Persky V, Ramakrishnan V. Effect of environmental molds on risk of death from
asthma during the pollen season. J Allergy Clin Immunol 1995; 95(5 Part 1): 955–61.
[81] Neas LM, Dockery DW, Burge H, Koutrakis P, Speizer FE. Fungus spores, air pollutants, and
other determinants of peak expiratory flow rates in children. Am J Epidemiol 1996; 143(8):
797–807.
[82] Delfino RJ, Zeiger RS, Seltzer JM et al. The effect of outdoor fungal spore concentrations on
daily asthma severity. Environ Health Perspect 1997; 105(6): 622–35.
[83] Dales RE, Cakmak S, Judek S et al. Influence of outdoor aeroallergens on hospitalization for
asthma in Canada. J Allergy Clin Immunol 2004; 113: 303–6.
[84] Liccorish K, Novey H, Kozak P, Fairshter R, Wilson A. Role of Alternaria and Penicillium spores
in the pathogenesis of asthma. J Allergy Clin Immunol 1985; 76(6): 819–25.
[85] O’Halloren M, Yungiger J, Offord K et al. Exposure to an aeroallergen as a possible precipitating
factor in respiratory arrest in young patients with asthma. N Engl J Med 1991; 324(6): 359–63.
[86] Zureik M, Neukirch C, Leynaert B, Laird R, Bousquet J. Sensitization to airborne moulds and
severity of asthma: cross sectional study from European Community Respiratory Health Survey.
Br Med J 2002; 325(7361): 411–14.
[87] Gergen PJ, Turkeltaub PC. The association of individual allergen reactivity with respiratory
disease in a national sample: data from the second National Health and Nutrition Examination
Survey, 1976–1980 (NHANES II). J Allergy Clin Immunol 1992; 90(4 Pt 1): 579–88.
[88] Tariq SM, Matthews SM, Stevens M, Hakim EM. Sensitization to Alternaria and Cladosporium
by the age of 4 years. Clin Exp Allergy 1996; 26(7): 794–8.
[89] Perzanowski MS, Sporik R, Squillance SP et al. Association of sensitization to Alternaria
allergens with asthma among school aged children. J Allergy Clin Immunol 1998; 101(5): 626–32.
[90] Nelson RP, DiNiccolo R, Fernandez-Caldas E, Seleznick MJ, Lockey R, Good RA. Allergen
specific IgE levels and mite allergen exposure in children with acute asthma first seen in an
emergency department and in nonasthmatic control subjects. J Allergy Clin Immunol 1996; 98(2):
382–8.
[91] 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; 50: 227–31.
ADVERSE HEALTH EFFECTS OF INDOOR MOLDS 271
[92] Schubert M. Medical treatment of allergic fungal sinusitis. Ann Allergy Asthma Immunol 2000;
85(2): 90–101.
[93] Greenberger P. Allergic bronchopulmonary aspergillosis, allergic fungal sinusitis and hypersensi-
tivity pneumonitis. Clin Allergy Immunol 2002; 16: 449–68.
[94] Ponikau JU, Sherris R, Kern EB. The diagnosis and incidence of allergic fungal sinusitis. Mayo
Clinic Proc 1999; 74: 877–84.
[95] Lebowitz R, Waltzman M, Jacobs J, Pearlman A, Tierno P. Isolation of fungi by standard
laboratory methods in patients with chronic rhinosinusitis. Laryngoscope 2002; 112(12): 2189–91.
[96] Rains BM, Mineck CW. Treatment of allergic fungal sinusitis with high-dose itraconazole. Am
J Rhinol 2003; 17(1): 1–8.
[97] Apostolakos M, Rossmore H, Beckett W. Hypersensitivity pneumonitis from ordinary residential
exposures. Environ Health Perspect 2001; 109(9): 979–81.
[98] Kita T, Nishi K, Fujimura M et al. A case of hypersensitivity pneumonitis caused by Humicola
fuscoatra. Respirology 2003; 8: 95–8.
[99] Ando M, Yoshida K, Soda K, Araki S. Specific bronchoalveolar lavage IgA antibody in patients
with summer type hypersensitivity pneumonitis induced by Trichosporon cutaneum. Annu Rev
Resp Dis 1986; 134: 177–9.
[100] Centers for Disease Control (CDC): Pulmonary hemorrhage/hemosiderosis among infants,
Cleveland, Ohio, 1993–6. MMWR 1997; 46: 33–5.
[101] Montana E, Etzel R, Allan T, Horgan T, Dearborn D. Environmental risk factors associated with
pediatric idiopathic pulmonary hemorrhage and hemosiderosis in a Cleveland community.
Pediatrics 1997; 99: 117–24.
[102] Etzel R, Montana E, Sorenson W et al. Acute pulmonary hemorrhage in infants associated with
exposure to Stachybotrys atra and other fungi. Arch Pediatr Adolesc Med 1998; 152: 757–62.
[103] Vesper S, Dearborn D, Yike I, Sorenson W, Haugland R. Hemolysis, toxicity and randomly
amplified polymorphic DNA analysis of Stachybotrys chartarum strains. Appl Environ Microbiol
1999; 65(7): 3175–81.
[104] Dearborn D, Smith P, Dahms B et al. Clinical profile of 30 infants with acute pulmonary
hemorrhage in Cleveland. Pediatrics 2002; 110(3): 627–37.
[105] Center for Disease Control and Prevention (CDC). Update: Pulmonary hemorrhage/hemosi-
derosis among infants, Cleveland, Ohio 1993–6. MMWR 2000; 49: 180–184.
[106] Etzel T. Stachybotrys. Curr Opin Pediatr 2003; 15(1): 103–6.
[107] Vesper S, Magnuson M, Dearborn D, Yike I, Haugland R. Initial characterization of the
hemolysin stachylysin from Stachybotrys chartarum. Infect Immun 2001; 69(2): 912–16.
[108] Vesper S, Vesper MJ. Stachylysin may be a cause of hemorrhaging in humans exposed to
Stachybotrys chartarum. Infect Immun 2002; 70(4): 2065–9.
[109] Yike I, Allan T, Sorenson W, Dearborn D. Highly sensitive protein translation assay for
trichothecene toxicity in airborne particulates: comparison with cytotoxicity assays. Appl Environ
Microbiol 1999; 65(1): 88–94.
[110] Johanning E, Biagini R, Hull D, Morey P, Jarvis B, Landsbergis P. Health and immunology
study following exposure to toxigenic fungi (Stachybotrys chartarum) in a water-damaged office
environment. Int Arch Environ Health 1996; 68: 207–18.
[111] Elidemir O, Colasurdo G, Rossmann S, Fan L. Isolation of Stachybotrys from the lung of a child
with pulmonary hemosiderosis. Pediatrics 1999; 104(4 Part1): 964–6.
[112] Hooper D. Molecular evaluation for autopsy and clinical tissue in patients. Presented at the 22nd
Annual Symposium on Man and His Environment in Health and Disease, Dallas, Texas, 27 June
2004.
[113] Vojdani A, Campbell A, Kashanian A, Vojdani E. Antibodies against molds and mycotoxins
following exposure to toxigenic fungi in water-damaged building. Arch Environ Health 2003;
58(6): 324–36.
[114] Vojdani A, Thrasher J, Madison R, Gray M, Heuser G, Campbell A. Antibodies to molds
and satratoxin individuals in a water-damaged building. Arch Environ Health 2003; 58(7):
421–32.
[115] Savilahti R, Uitti J, Laippala P, Hussman T, Reiman M. Immunoglobulin G antibodies of
children exposed to microorganisms in a water-damaged school. Pediatr Allergy Immunol 2002;
13(6): 438–42.
[116] Patovirta RL, Reiman M, Husman T, Haverinen U, Toivola M, Nevalainen A. Mould specific
IgG antibodies connected with sinusitis in teachers of a mould damaged school: a 2 year follow up
study. Int J Occup Med Environ Health 2003; 16(3): 221–30.
[117] Taskinen TM, Laitinen S, Nevalainen A et al. Immunoglobulin G antibodies to moulds in school-
children from moisture problem schools. Allergy 2002; 57(1): 9–16.
[118] Malkin R, Martinez K, Marinovich V, Wilcox T, Wall D, Biagini R. The relationship between
symptoms and IgG and IgE antibodies in an office environment. Environ Res 1998; 76(2): 85–93.
[119] Dales R, Miller D, White J, Dulberg C, Lazarovitis A. Incidence of residential fungal
L. CURTIS ET AL.272
contamination on peripheral blood lymphocyte populations in children. Arch Environ Health
1998; 53(3): 190–5.
[120] Vojdani A. Health effects and immunotoxicology of toxigenic molds and mycotoxins. Presented
at the 21st International Symposium of Man and His Environment in Health and Disease, Dallas,
Texas, 20 June 2003.
[121] Beijer L, Thorn J, Rylander R. Mould exposure at home relates to inflammatory markers in
blood. Eur Resp J 2003; 21(2): 317–22.
[122] Bondy G, Pestka J. Immunomodulation by fungal toxins. J Toxicol Environ Health B 2000; 3(2):
109–43.
[123] Berek L, Petri IB, Msterhazy A, Teren J, Molnar J. Effects of mycotoxins on human immune
functions in vitro. Toxicol In Vitro 2001; 15(1): 25–30.
[124] Singer R. Neurotoxicity Guidebook. New York: Van Nostrand Reinold, 1990.
[125] Gray M, Kilburn K, Crago R. Molds, mycotoxins and public health: summary of 195 patients
treated collaboratively. Presented at the American Public Health Association (APHA) Meeting,
Philadelphia, Pennsylvania, 11 November 2002.
[126] Crago BR, Gray M, Nelson L, Davis M, Arnold L, Thrasher J. Psychological, neuropsycho-
logical and electrocortical effects of mixed mold exposure. Arch Environ Health 2003; 58(8):
452–63.
[127] Simon T. Neurotoxicity—mold exposure versus all causes. Presented at the 21st Annual
Symposium on Man and His Environment in Health and Disease, Dallas, Texas, 19–22 June
2003.
[128] Gordon W, Johanning E, Haddad L. Cognitive impairment associated with exposure to toxigenic
fungi. Presented at the 3rd International Conference on Fungi, Mycotoxins and Bioaerosols,
Saratoga Springs, New York, 23–25 September 1998. In: Bioaerosols, Fungi and Mycotoxins:
Health Effects. Assessments, Prevention and Control. Albany, New York: Eastern New York
Center for Environmental and Occupational Health, 1999.
[129] Didricksen N. Neurocognitive deficits in individuals exposed to toxigenic molds. Presented at the
21st Annual Symposium on Man and His Environment in Health and Disease, Dallas, Texas,
19–22 June 2003.
[130] Baldo JV, Ahmad L, Ruff R. Neuropsychological performance of patients following mold
exposure. Appl Neuropsychol 2002; 9(4): 193–202.
[131] Anyanwu E, Campbell A, Vojdani A. Neurophysiological effects of chronic indoor environmental
toxic mold exposure on children. Sci World J 2003; 3(4): 281–90.
[132] Boysen SR, Rozanski EA, Chan DL, Grobe TL, Fallon MJ, Rush J. Tremorgenic mycotoxicosis
in four dogs from a single household. J Am Vet Med Assoc 2002; 221(10): 1441–4.
[133] Young DL, Villar D, Carson TL, Ierman PM, Moore RA, Bottoff MR. Tremorgenic mycotoxin
intoxication with penitrem A and roquefortine in two dogs. J Am Vet Med Assoc 2002; 222(1):
52–3.
[134] Naude TW, O’Brien OM, Rundberget T, McGregor AD, Roux C, Flaoyen A. Tremorogenic
neuromycotoxicosis in 2 dogs ascribed to ingestion of penitrem A and possibly roquefortine in
rice contaminated with Penicillium crustosum. J S Afr Vet Assoc 2002; 73(4): 211–15.
[135] Chen JW, Luo YL, Hwang MJ, Peng FC, Ling KH. Territrem B. a tremorgenic mycotoxin that
inhibits acetylcholinesterase with a noncovalent yet irreversible binding mechanism. J Biol Chem
1999; 274(49): 34916–23.
[136] Krogh P, Hald B, Pedersen J. Occurrence of ochratoxin A and citrinin in cereals associated with
mycotoxic porcine nephropathy. Acta Path Micro Scand 1973; 81 Sect B: 689–95.
[137] Castegnaro M, Plestina R, Dirheimer O, Chernosemsky IN, Barsch H. Mycotoxins, endemic
nephropathy and urinary tract tumors. IARC Sci Pub 1991; 115: 1–340.
[138] Kristensen P, Irgens L, Andersen A, Bye AS, Sundheim L. Gestational age, birth weight, and
perinatal death among births to Norwegian farmers, 1967–1991. Am J Epidemiol 1997; 146:
329–38.
[139] Kristensen P, Andersen A, Irgens L. Hormone-dependent cancer and adverse reproductive
outcomes in farmers families—effects of climatic conditions favoring fungal growth in grain.
Scand J Work Health 2000; 26(4): 331–7.
[140] Diekman M, Green M. Mycotoxins and reproduction in domestic livestock. J Anim Sci 1992; 70:
1615–27.
[141] Cotran RS. Robbins Pathologic Basis of Disease, 5th edn. New York: WB Saunders, 1994, p. 914.
[142] Cheta D. Animal models of type 1 (insulin-dependent) diabetes mellitus. J Pediatr Endocrinol
Metab 1998; 11(1): 11–19.
[143] Hoffmeister PA, Storer BE, Sanders JE. Diabetes mellitus in long-term survivors of pediatric
hematopoietic cell transplantation. J Pediatr Hematol Oncol 2004; 26(2): 81–90.
[144] Eggleston PA. Environmental control for fungal allergen exposure. Curr Allergy Asthma Rep
2003; 3(5): 424–9.
[145] Heuser G, Axelrod P, Heuser S. Defining chemical injury: a diagnostic protocol and profile of
ADVERSE HEALTH EFFECTS OF INDOOR MOLDS 273
chemically injured civilians, industrial workers and Gulf War veterans. Int Perspect Public Health
2002; 13: 1–16.
[146] Marshall L, Weir E, Abelsohn A, Sanborn MD. Identifying and managing adverse environmental
effects: 1) taking an exposure history. Can Med Assoc J 2002; 166(8): 1049–55.
[147] Dales RE, Miller D, McMullen E. Indoor air quality and health: validity and determinants of
reported home dampness and molds. Int J Epidemiol 1997; 26: 120–4.
[148] Macher J (ed.) Bioaerosols: Assessment and Control. American Conference of Governmental and
Industrial Hygienists (ACGIH), Cincinnati, Ohio, 1999.
[149] Portnoy JM, Barnes CS, Kennedy K. Sampling for indoor fungi. J Allergy Clin Immunol 2004;
113: 189–98.
[150] Institute of Medicine Committee on the Health Effects of Indoor Allergens: Engineering Control
Strategies. Allergens: Assessing and Controlling Adverse Health Effects. Engineering Control
Strategies. Washington, DC: National Academy Press, 1993, 206–32.
[151] Institute for Inspection, Cleaning and Restoration. IICRC S520 Standard and reference guide for
professional mold remediation. Vancouver, Washington: IICRC Press, 2003.
[152] Higgins BG, Francis HC, Yates G et al. Environmental exposure to air pollution and allergens
and peak flow changes. Eur Resp J 2000; 16(1): 61–6.
[153] Thorn J, Brisman J, Toren K. Adult-onset asthma is associated with self-reported mold or
environmental tobacco smoke in the home. Allergy 2001; 56: 287–92.
[154] Chen WY, Tseng HI, Wu MT et al. Synergistic effect of multiple indoor allergen sources on
atopic symptoms in primary school children. Environ Res 2003; 93(1): 1–8.
[155] Skoner DP. Viral infection and allergy: lower airway. Allergy Asthma Proc 2002; 23(4): 229–32.
[156] Fireman P. Virus-provoked rhinitis in patients who have allergies. Allergy Asthma Proc 2002;
23(2): 99–102.
[157] Hirsch D, Hirsch R, Kalbfleish S. Effect of central air-conditioning and meterological factors on
indoor spore counts. J Allergy Clin Immunol 1978; 62(1): 22–6.
[158] Sheretz RJ, Belani A, Kramer BS et al. Impact of air filtration on nosocomial Aspergillus
infections. Am J Med 1987; 83(4): 709–18.
[159] Panackal A, Dahlman A, Keil K et al. Outbreak of invasive aspergillosis among renal transplant
patients. Transplantation 2003; 75(7): 1050–3.
[160] Oren I, Haddad N, Finkelstein R, Rowe J. Invasive pulmonary aspergillosis in neutropenic
patients during hospital construction: before and after chemoprophylaxis and institution of
HEPA filters. Am J Hematol 2001; 66(4): 257–62.
[161] Loo V, Betrand C, Dixon C et al. Control of construction-associated nosocomial aspergillosis in
an antiquated hematology unit. Infect Control Hosp Epidemiol 1996; 17(6): 360–4.
[162] Iwen P, Davis J, Reed EC, Winfield BA, Hinrichs SH. Airborne fungal spore monitoring in a
protective environment during hospital construction, and correlation with outbreak of invasive
aspergillosis. Infect Control Hosp Epidemiol 1994; 15(5): 303–6.
[163] Hahn T, Cummings K, Michalek AM, Lipman B, Segel B, McCarthy P. Efficacy of high-
efficiency particulate air filtration in preventing aspergillosis in immunocompromised patients
with hematologic malignancies. Infect Control Hosp Epidemiol 2002; 23(9): 525–31.
[164] Cornet M, Levy V, Fleury L et al. Efficacy of prevention by high-efficiency particulate air
filtration or laminar airflow against Aspergillus airborne contamination during hospital
renovation. Infect Control Hosp Epidemiol 1999; 20(7): 508–13.
[165] Withington S, Chambers ST, Beard ME et al. Invasive aspergillosis in severely neutropenic
patients over 18 years: impact of intranasal amphotericin B and HEPA filtration. J Hosp Infect
1998; 38(1): 11–18.
[166] Annaisie EJ, Stratton SL, Dignani MC et al. Pathogenic Aspergillus species recovered from a
hospital water system: a 3 year prospective study. Clin Infect Dis 2002; 34(6): 780–9.
[167] Annaisie EJ, Stratton SL, Dignani MC et al. Cleaning patient shower facilities: a novel approach
to reducing patient exposure to aerosolized Aspergillus species and other opportunistic molds.
Clin Infect Dis 2002; 35(8): E86–8.
[168] Bernardis P, Agnoletto M, Puccinelli P, Parmiani S, Pozzan M. Injective versus sublingual
immunotherapy in Alternaria tenuis allergic patients. J Invest Allergol Clin Immunol 1996; 6(1):
55–62.
[169] Helbling A, Reimers A. Immunotherapy in fungal allergy. Curr Allergy Asthma Rep 2003; 3(5):
447–53.
[170] Galvano F, Piva A, Ritieni A, Galvano G. Dietary strategies to counteract the effects of
mycotoxins: a review. J Food Protect 2001; 64(1): 120–31.
[171] Atroshi F, Rizzo A, Westermarck, Ali-Vehmas T. Antioxidant nutrients and mycotoxins.
Toxicology 2002; 180(2): 151–67.
L. CURTIS ET AL.274
... Mould can cause damage to a building and initiate chemical emissions from building materials, which are prone to microbial growth and health hazards for the residents [13]- [15]. Most commonly the moulds found in homes belong to the species Penicillium, Cladosporium, Aspergillus [16]; [17], Alternaria, Fusarium, and Trichoderma [18]. ...
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The objective of this study was to determine mould resistance of the plaster made from waste paper. To study the plaster quality, two laboratory tests were conducted. First, mould resistance of a dry plaster was studied, and second, mould resistance of a wet plaster was tested. Since wet plaster mix must be used for plastering, the resulting surfaces are extremely wet. The plaster placed on the wall would dry for at least two weeks under favourable conditions (sufficient ventilation and temperature). During this period, there is a great risk that the plaster might become mouldy. Another risk of becoming mouldy occurs when an already plastered wall receives moisture (e.g., water damage). The experiments carried out under laboratory conditions showed that in an environment with high relative humidity the plaster did not become mouldy.
... They may include limb weakness or numbness, loss of memory, vision, and/or intellect, uncontrollable obsessive and/or compulsive behaviors, delusions, headache, cognitive and behavioral problems and sexual dysfunction. Chronic mold exposure in homes can lead to neurotoxicity which may not appear for months to years of exposure (Curtis et al., 2004). All symptoms listed above are consistent with mold mycotoxin accumulation (Kilburn et al., 2004). ...
... The hot and humid climate in this region provides ideal conditions for mold proliferation, leading to frequent exposure of residents to indoor mold [4,13]. These molds can not only trigger allergic reactions such as rhinitis and asthma but may also lead to more severe respiratory infections and immune-related disorders [14][15][16][17][18]. Especially during the wet and rainy seasons in the southern region, humidity management and mold control in buildings are crucial to ensuring the health of residents [5]. ...
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To address the challenges of indoor mold in southern China, this study designed and constructed an innovative experimental system to investigate mold growth in buildings under the combined influence of multiple factors. Using Fluent simulation (Ansys Fluent 19.0), we designed a suitably sized experimental chamber to realistically replicate the effects of factors such as temperature, humidity, and air velocity on mold growth. After establishing and fine-tuning the experimental system, we conducted two preliminary experiments, successfully validating the feasibility of our setup. Additionally, we observed that in a high-temperature, high-humidity environment of 28 °C and 80% relative humidity, the mold growth rate in the experimental chamber increased with the rise in inlet air velocity. This experimental system will serve as the foundation for future studies on indoor mold growth in building spaces in southern China.
... Straws, like other natural bio-based materials (Koh et al., 2022), are prone to mould growth when exposed to humid environments, leading to deterioration. The well-established negative health effects of indoor moulds (Koskinen et al., 1999;Portnoy et al., 2005;Curtis et al., 2004) necessitate the prevention of straw becoming a source of fungal proliferation. Freshly harvested wheat and barley straws are naturally contaminated with several fungi species such as Aspergillus and Penicillium spp. ...
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This study investigates the potential of wheat and barley straws as sustainable alternatives to conventional insulation materials. The focus is on evaluating the risk of mould growth in straw-filled wall assemblies across different climate types, while comparing the physical, thermal, hygroscopic, and durability properties of wheat and barley straws. Additionally, the effectiveness of boric acid as an antifungal treatment on straws is assessed. The findings reveal that both barley and wheat straws exhibit low thermal conductivity, ranging from 45 and 65 mW·m-1·K-1 for bulk density of 60 to 100 kg·m-3. Notably, barley straws demonstrate lower sorption capacity, higher vapour diffusion, lower thermal conductivity, and reduced mould growth intensity, rendering them more suitable as insulation material. The application of boric acid treatment effectively enhances the mould resistance of straw without adversely affecting their hygric and thermal properties. Consequently, boric acid treatment is recommended for wheat straw under unfavourable climatic conditions.
... 5 Mould exposure has been linked to adverse health reactions. [6][7][8][9][10][11][12] and as such effective monitoring of mould is an important task. ...
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Surface sampling techniques for non-viable fungi in building environments are useful tools for investigators in determining hazards to occupants. However, data regarding capture efficiency in this context is limited. Our data demonstrates that collection efficiency of Bio-Tape surface capture medium on paper-faced gypsum board only captures between half and three-quarters of mould present on the surface. Surface sampling using a dry-swab technique showed similar efficiency of capture to tape lift samples. ‘Surface air’ samples had poor collection efficiency and should be avoided where possible in preference to other sampling options. Finally, we propose a sampling strategy based on non-viable microscopy techniques followed by molecular analysis for validation and speciation of samples of interest. Improvements in sampling and data analysis techniques for mould sampling of buildings will aid in providing meaningful results to help building inspectors evaluate health hazards.
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Determining the etiology of episodic abdominal pain, nausea and vomiting with and without pseudo-obstruction and implementing effective treatment can be challenging. Mycotoxins activate mast cells which rapidly degranulate releasing pro-inflammatory cytokines. Mast cells commonly reside in the gastrointestinal mucosa and adjacent to nerves. Aberrant mast cells with loss of control due to genetic abnormalities are present in mast cell activation syndrome, a common, yet often unrecognized multisystemic disorder. Mold exposure with consequent toxicity by its mycotoxins can present with complex multisystem disorders along with abdominal pain, nausea, and vomiting. A 63-year-old man presented with episodic attacks of abdominal pain, nausea and vomiting when he was exposed to dwellings with mold. Over a 4-year period he was admitted and there was radiographic evidence of dilation of the stomach and small intestine during three admissions and dilation of the colon in the other admission. When the patient was subsequently diagnosed and treated for underlying mast cell activation syndrome, the attacks ceased, and he has been healthy for the last three years. Recognition that mycotoxins can act as triggering factors is essential to effectively treat patients with and without mast cell activation syndrome who have these gastrointestinal attacks and episodic gastrointestinal pseudo-obstruction.
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The effects of pressurized hot water extraction (HWE) treatment on the mould resistance of wood have not been extensively investigated yet. The activity of the mould fungi is dependent on the availability of nutrients. Therefore, the soluble degradation products produced during HWE treatment could affect the wood’s susceptibility to mould growth. Scots pine ( Pinus sylvestris L.) sapwood specimens were treated with HWE at 140 °C for 1–5 h. Afterwards, the degradation products were either removed via leaching or the wood was dried without applying the leaching procedure. The surface layer (1.5 mm) was removed from half of the leached and non-leached specimens. The resistance of the specimens against mould growth was tested in an incubation chamber. HWE treated wood showed a higher susceptibility to mould growth when it was neither leached nor subjected to surface removal. The susceptibility of wood to mould fungi depended on the availability of hemicellulose-based degradation products produced during HWE treatment. These degradation products were removable via a leaching procedure, but also by removing the outermost layer of the wood. The results show the relevance of removing HWE degradation products located on the wood surface in improving resistance against mould growth.
Conference Paper
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In this study, the author used endoscopic sinus photography to study the effects of reduction of fungi in the nose, and in environmental air, on the sinus mucosa of 639 patients diagnosed with chronic rhinosinusitis. Sinus mucosal photographs were taken before and after reduction of fungal load in the nose and air, to determine if there was an optimum environmental air fungal load associated with sinus mucosal recovery to normal appearance. Systemic symptoms associated with fungal exposure, which resolved when fungus was removed from the patient and the environmental air and reappeared with recurrent environmental fungal exposure, are also discussed and are termed systemic fungal symptoms. Interventions consisted of nasal fungal load reduction with normal saline nasal irrigations and antimicrobial nasal sprays, and environmental air fungal load reduction with high-efficiency particulate air (HEPA) filtration in combination with ionizers or evaporation of a solution of botanical extract. Main outcome measures were obtained with environmental air 1-hr gravity-plate fungal colony counts, laser air particle counts, and endoscopic sinus photography. Blood levels of immunoglobulins IgG and IgE for 7 common molds were also determined. After intervention, 94% of patients who used antimicrobial nasal sprays and who reduced their environmental fungal air count to 0-4 colonies per 1-hr agar gravity-plate exposure (n = 365) exhibited normal sinus mucosa by endoscopic exam. Environmental air fungal counts that exceeded 4 colonies resulted in sinus mucosal abnormalities ranging from edema, to pus and/or nasal polyps at higher counts. Neutralization of allergy, and/or surgery, were used as appropriate following implementation of environmental measures. On the basis of these observations, as well as detailed clinical experience and a review of the current literature, the author hypothesizes that the pathogenesis of chronic rhinosinusitis, allergic fungal sinusitis, and systemic fungal symptoms is a genetic defect at the variable beta chain helper T-cell receptor (TCR Vbeta) site which requires the presence of an antigen (fungus). Chronic sinusitis patients who have recurring exposure to environmental air that contains fungal concentrations in excess of 4 colonies per 1-hr agar plate exposure appear to have an increased risk of persistent chronic sinusitis and/or systemic symptoms, regardless of the medical treatment provided.
Conference Paper
Recently, patients who have been exposed indoors to mixed molds, spores, and mycotoxins have reported asthma, airway irritation and bleeding, dizziness, and impaired memory and concentration, all of which suggest the presence of pulmonary and neurobehavioral problems. The author evaluated whether such patients had measurable pulmonary and neurobehavioral impairments by comparing consecutive cases in a series vs. a referent group. Sixty-five consecutive outpatients exposed to mold in their respective homes in Arizona, California, and Texas were compared with 202 community subjects who had no known mold or chemical exposures. Balance, choice reaction time, color discrimination, blink reflex, visual fields, grip, hearing, problem-solving, verbal recall, perceptual motor speed, and memory were measured. Medical histories, mood states, and symptom frequencies were recorded with checklists, and spirometry was used to measure various pulmonary volumes and flows. Neurobehavioral comparisons were made after individual measurements were adjusted for age, educational attainment, and sex. Significant differences between groups were assessed by analysis of variance; a p value of less than 0.05 was used for all statistical tests. The mold-exposed group exhibited decreased function for balance, reaction time, blink-reflex latency, color discrimination, visual fields, and grip, compared with referents. The exposed group's scores were reduced for the following tests: digit-symbol substitution, peg placement, trail making, verbal recall, and picture completion. Twenty-one of 26 functions tested were abnormal. Airway obstructions were found, and vital capacities were reduced. Mood state scores and symptom frequencies were elevated. The author concluded that indoor mold exposures were associated with neurobehavioral and pulmonary impairments that likely resulted from the presence of mycotoxins, such as trichothecenes.
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In-depth microbial investigations were performed in four commercial buildings from the Mid-Atlantic region of the United States. The samples from each building were analyzed for the presence of Stachybotrys chartarum. Samples were collected with bioaerosol, swab, and bulk-sampling methods. In each building, S. chartarum was present, with more than 2.8 square meters of visible mold contamination; elevated levels (more than 30 colonies) were detected in the swab and/or bulk samples. The culturable-air (bioaerosol) samples, however, rarely showed detectable levels of S. chartarum. Thus, the use of culturableair sampling for the detection of S. chartarum often will result in a false negative finding. Investigators should use bioaerosol methods in conjunction with visual inspections, spore trap, swab, and bulk sampling.