Toxic mould syndrome--can the link be proved? Making a definitive link between fungal toxins and health outcomes remains difficult. Some people appear to have a greater sensitivity to these toxins than others.
As American doctor Abba Terr writes: "A suspicion of a 'new' disease affecting occupants of domestic and public buildings has been raised, in spite of the existence of fungi on earth for an estimated 550 million years. There have been sufficient published reports in both the professional literature and the popular press to arouse suspicion. It is now time for scientifically rigorous data to be used to answer the question about the effects of indoor mould exposure on human health." (1)
Symptoms of ill health
Sharon had worked atone in her office since 2002 and had been "unwell" since 2004. She had visited her local GP several times over several months, complaining of general fatigue, nausea and sleeplessness at night. She was prescribed anti-depressants, which she did not take as she felt she was not depressed. Omeprazole (losec) was prescribed for gastric reflux. Eventually, after a walk of minimal exertion, Sharon felt near to collapse from breathlessness and dizziness, and re-presented to the GP and blood tests were done. A haemoglobin (Hb) of 48g/L was found and a diagnosis of iron deficient anaemia of unknown origin was made. Sharon was immediately sent to hospital for four units of blood, after which she felt much improved. On discharge, her Hb was 105g/L. She began a course of iron tablets and the omeprazote was continued.
Further tests were arranged to establish if blood loss was the cause of the anaemia. A gastroscopy (and another a year later) showed mild gastritis, but no blood toss was found. In March 2005, a colonoscopy was performed, again with no blood loss found.
In 2006, a small bowel capsule endoscopy was performed and gastric inflammation was identified, consistent with gastric antral vascular ectasia (GAVE) or "water-melon stomach". GAVE is a condition whereby the lining of the stomach bleeds, causing it to look like the stripes of a watermelon when viewed on endoscopy. The cause of this bleeding is uncertain. However, it appears there are two distinct groups of GAVE patients: one related to immunologic disorders; the other to non-immune chronic liver disease and low platelets. (2)
The GAVE was treated with an argon plasma coagulator by gastroscopy. Sharon's liver function tests were only mildly abnormal at this time, showing mild cholestatic abnormality. Early primary biliary cirrhosis (PBC) was also considered, which has been linked to GAVE.
In 1997, Sharon suffered unexplained acute hepatitis (probable infection on top of an acute immune propensity was recorded in her notes). No cause for this was found, but the physician suggested it would be unusual for PBC to present with acute jaundice, though overlap syndromes with auto-immune hepatitis can occur. PBC is characterised by a T-cell mediated attack on the small intralobular bile ducts. If continued, the epithelial cells of the bile ducts are gradually destroyed, causing signs and symptoms of cholestasis and eventually cirrhosis and liver failure. (3)
"The precise cause of PBC is unknown, but appears to be related to genetic and environmental factors. A number of environmental causes have been implicated, including several bacteria and viruses and toxins." (3)
Following the treatment of the anaemia with iron tablets and infusions, Sharon continued to suffer a wide spectrum of symptoms, off and on, but not simultaneously, for approximately four years. These symptoms included: shortness of breath, chronic Fatigue, dizziness, headaches, sleep difficulties, nausea, acid reflux, jaw soreness, swallowing difficulties, sore tongue, coated tongue, dry mouth, slurred speech, production of oral mucous (sometimes bloodstained), generalised muscle and joint pains, feet and ankle oedema, dry and bloodshot eyes, face flushes and skin rashes, particularly on the face. There was no explanation for her illness.
In late 2006, a staff member at Sharon's place of work pointed to something on the wall in Sharon's office and accidentally poked her finger through the wall. The wall then crumbled away. Investigations were made as to the cause of the wall disintegration and laboratory sampling identified several fungi and spores (Aspergillus, Penicillium and others). However, the most significant finding was the abundant presence of the fungus Stachybotrys in the plaster board and carpet, and spores in the air, which is indicative of a long-term leak in the building. Stachybotrys is the most commonly cited fungus in the literature, concerning "sick building syndrome" and in "toxic mould" cases. (4)
Characteristics of Stachybotrys
Stachybotrys is a greenish-black mould that thrives in areas of high humidity, moisture and on cellulose materials (eg building paper, wood products and gib board) (5,6,7,1) Mould has the potential to grow wherever there is a chronic wet environment and cellulose materials. Mould spores may enter buildings through doors, windows, ventilation and air-conditioning systems, and where water leakage is present from sources such as roofs, pipes, walls, pot plants or sites of flooding. (4) In this building, roof flashings had not been installed when the building was renovated.
Stachybotrys, as with many moulds, can produce mycotoxins, which are fungal metabolites with the potential to cause harm to organisms. A commonly occurring mycotoxin from the Stachybotrys fungus is trichothecenes. (6,1) These inhibit protein synthesis. (7)
When trichothecenes are given to animals in low concentrations, acute toxicity can occur in varying degrees. Symptoms include gastrointestinal disturbances--vomiting, diarrhoea, inflammation and refusal of feed--skin irritations, abortion, anaemia and leukopenia. These trichothecenes can be acutely cytotoxic and strongly immunosuppressive. (8)
Depending on the amount of toxins, other symptoms of stachybotryotoxicosis in animals include eye and mucous membrane irritations, followed by necrosis, changes in blood parameters, haemorrhaging in many organs, severe disorders of the immune system and rapid death when exposed to high levels of toxins. Generally, ingestion of contaminated feed is the main source of this toxicity. (9) However, stachybotryotoxicosis in humans is generally acquired through either handling contaminated material or inhalation of airbourne toxins. (4,9,7)
Epidemiological studies of the effects of Stachybotrys trichothecenes suggest human symptoms are similar to those of animals. (7,10) Physical symptoms that may occur in humans as a result of exposure to these fungi include: Loss of steep and appetite, chronic fatigue, headaches, dizziness, vague aches and pains (joint ache), and respiratory problems including breathlessness, (5,9,11,1,10) rashes, conjunctivitis and diarrhoea, (7) nausea and vomiting, (1) cold and flu symptoms, sore throats, dermatitis, (9,6,10) haemoptysis (5) and pulmonary haemorrhages. (4,6,10) Psychological and cognitive symptoms include irritability, panic, anxiety, poor concentration and confusion, (11) and memory loss. (5,7) Abnormal blood cell levels, both red and white, are also reported. (5,9,6) However, there is no specific disease from these toxins; (1) rather, an excessive number of health complaints. Some people report an improvement in their condition when away from the building.
Sharon's excessive number of health complaints are consistent with the Literature. After the wall was exposed, her condition deteriorated rapidly--"The fatigue bowled me over; it just knocked me." Other symptoms to worsen particularly were: shortness of breath; bloodshot, dry irritated eyes; sore, coated tongue and a dry mouth. Her face became covered in a bright red rash, which was treated with oral steroids. However, after completion of the steroid treatment, a new rash appeared and Sharon has since been diagnosed with rosacea, a chronic, irreversible skin condition.
Sharon was unable to continue working in this condition and took three months' sick leave. Her condition began to improve and she returned to work part-time. Within two weeks, her symptoms reappeared--dry, itchy irritated eyes; dry mouth where her lips "stick" to her teeth and the rash on her face worsened. She was then transferred to another building. However, her general health continued to be poor and she was unable to perform the role as she once did, with memory losses making the job too difficult. After a period of sick leave, she resigned.
No test available
Unfortunately, "very few studies hove, however, established a causal relationship between mycotoxin exposure and building-related illnesses". (10) Currently, there is no test that proves a definitive link between Stachybotrys and particular symptoms. (4,6) Individuals with persistent symptoms are advised to seek medical advice and, if Stachybotrys or other moulds are found in a building, these moulds be removed. (4) Additionally, relocation of occupants from contaminated buildings has resulted in a significant decrease in symptoms. (7)
When investigating the negative health effects of Stachybotrys spores on humans, it is important to consider the exposure time, the concentration and toxicity of the spores, and the health status of the person being investigated. The very young, immuno-compromised and the hypersensitive (to mould) suffer more acute symptoms that others. (7) In view of the acute, unexplained hepatitis Sharon experienced before working in this building, it is possible she is immuno-compromised and therefore, hypersensitive to this mould.
In summary and in the words of Canadian doctor Richard Weber: "There are well-defined problems that people can get into with mould exposures, however, are mould toxins as big a problem as we think they may be? The problem is we just don't know. There is not enough information and there ore also not enough good ways of assessing the impact of some of these toxins on patients. Specific toxicity due to inhaled moulds, including Stachybotrys in building-related illness, has not been scientifically established by any published study." (11)
To establish a case toward a mould claim, it has been suggested the following must be demonstrated:
* the presence of mould;
* the cause of the mould (to demonstrate who is responsible);
* actual exposure to the mould;
* an exposure dose significant enough to cause health effects; and * a medical link between the type of mould and the claim injury. (4)
In Sharon's case, two questions remain unanswered. Is the toxicity exposure significant enough to be causing these health problems and is there a medical link between the mould and a claim for injury? Sharon is currently unemployed, has been left with ongoing health concerns and the possibility of a shorter life expectancy.
This case study has presented a number of "health complaints" that Sharon has been experiencing, in varying degrees, over the last four years. Her condition deteriorated rapidly when the office wall became exposed and Stachybotrys fungus and spores (and therefore the mycotoxin tricothecenes) were detected through laboratory samples. Her symptoms are consistent with those of animal toxicity when exposed to tricothecenes and also with those of human toxicity identified in the literature. However, a review of the literature regarding the role of mycotoxins and building-related illness found case definitions are inconclusive. (6) Further research is required to make a definitive link between fungal toxins and the hearth outcomes of people.
This article was reviewed by Kai Tiaki Nursing New Zealand's practice article review committee in February 2008. Carol Ashcroft did not take part in this review.
(1) Terr, A. I. (2004) Are indoor moulds causing a new disease? Journal of Allergy and Clinical Immunology; 113: 2, 221-226.
(2) Chaves, D. M., Sakai, P. & Oliveira, C. V. et al (2006) Watermelon stomach: Clinical aspects and treatment with argon plasma coagulation, http://www.ncbi.nlm.nih.gov.helicon.vuw.ac.nz/entrez/query. fcgi?db=pubmed&cmd=. Retrieved 3/03/06.
(3) Kaplan, M. M. (2006) Pathogenesis of primary biliary cirrhosis. UpToDate. www.uptodate.com. Retrieved 13/01/07.
(4) Babcock, D. W. (2006) The legal implications of "toxic" mold exposure. Journal of Environmental Health; 68: 8, 50-51.
(5) McBride, D. (2002) Toxic fungus found in damp dwellings. New Zealand Doctor, May, p25.
(6) Page, E. H. & Trout, D. B. (2001) The role of Stachybotrys mycotoxins in building-related illness. American Industrial Hygiene Association Journal; 62: 5, 644-649.
(7) Scheel, C. A., Rosing, W. C. & Farone, A, L. (2001) Possible sources of sick building syndrome in a Tennessee middle school. Archives of Environmental Health; 56: 5, 413-417.
(8) European Mycotoxin Awareness Network (n.d.). Basic fact sheet 8 trichothecene, http://www.leatherheadfood.com/emanJ/fsheet8.asp. Retrieved 10/02/07.
(9) Nikulin, M., Pasanen, A., Berg, S., & Hintikka, E. (1994) Stachybotrys atra growth and toxin production in some building materials and fodder under different relative humidities. Applied and Environmental Microbiology; 60: 9, 3421-3424.
(10) Tuomi, T., Reijula, K., Johnsson, T. & Hemminki, K. et al (2000) Mycotoxins in crude building materials from water-damaged buildings. Applied Environmental Microbiology; 66: 5, 1899-1904.
(11) Schieszer, J. (2005) Data lacking on toxic mould syndrome. Medical Post Toronto; 41: 43, 18.
Carol Ashcroft, RN, BHSc, MEd, is an associate clinical manager, theatre services, at Whanganui District Health Board and a member of Kai Tiaki Nursing New Zealand's practice article review committee.
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|Publication:||Kai Tiaki: Nursing New Zealand|
|Article Type:||Case study|
|Date:||May 1, 2009|
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