Indoor-related microbe damage induces complement system activation in building users.

In this comparative study, serum complement system antimicrobial activity was measured from 159 serum samples, taken from individuals from microbe-damaged (70 samples) and from reference buildings (89 samples). Antimicrobial activity was assessed using a probe-based bacterial Escherichia coli-lux bioluminescence system and comparison was made at a group level between the experimental and reference group. The complement activity was higher in users of microbe-damaged buildings compared with the reference group and the significant (P < 0.001) increase in activity was found in the classical reaction pathway. This study strengthens our notion that exposure to indoor-related microbe damage increases the risk for systemic subclinical inflammation and creates a health risk for building users.

[The sick building syndrome as a part of 'ASIA' (autoimmune/auto-inflammatory syndrome induced by adjuvants)].

The entity 'sick building syndrome' is poorly defined and comprises of a set of symptoms resulting from environmental exposure to a work or a living environment. The symptoms are mainly "allergic"-like and include nasal, eye, and mucous membrane irritation, dry skin as well as respiratory symptoms and general symptoms such as fatigue, lethargy, headaches and fever. The Autoimmune [Auto-inflammatory] Syndrome Induced by Adjuvants (ASIA) is a wider term which describes the role of various environmental factors in the pathogenesis of immune mediated diseases. Factors entailing an immune adjuvant activity such as infectious agents, silicone, aluminium salts and others were found in association with defined and non-defined immune mediated diseases. The sick building syndrome and ASIA share a similar complex of signs and symptoms and probably the same immunological mechanisms which further support a common denominator.

Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) 2013: Unveiling the pathogenic, clinical and diagnostic aspects.

In 2011 a new syndrome termed 'ASIA Autoimmune/Inflammatory Syndrome Induced by Adjuvants' was defined pointing to summarize for the first time the spectrum of immune-mediated diseases triggered by an adjuvant stimulus such as chronic exposure to silicone, tetramethylpentadecane, pristane, aluminum and other adjuvants, as well as infectious components, that also may have an adjuvant effect. All these environmental factors have been found to induce autoimmunity by themselves both in animal models and in humans: for instance, silicone was associated with siliconosis, aluminum hydroxide with post-vaccination phenomena and macrophagic myofasciitis syndrome. Several mechanisms have been hypothesized to be involved in the onset of adjuvant-induced autoimmunity; a genetic favorable background plays a key role in the appearance on such vaccine-related diseases and also justifies the rarity of these phenomena. This paper will focus on protean facets which are part of ASIA, focusing on the roles and mechanisms of action of different adjuvants which lead to the autoimmune/inflammatory response. The data herein illustrate the critical role of environmental factors in the induction of autoimmunity. Indeed, it is the interplay of genetic susceptibility and environment that is the major player for the initiation of breach of tolerance.

Dampness and moulds in workplace buildings: associations with incidence and remission of sick building syndrome (SBS) and biomarkers of inflammation in a 10 year follow-up study.

There are few longitudinal studies on health effects of dampness and moulds in workplace buildings. We studied associations between dampness and indoor moulds in workplace buildings and selected biomarkers as well as incidence and remission of sick building syndrome (SBS). The study was based on a ten-year prospective study (1992-2002) in a random sample of adults (N=429) from the Uppsala part of the European Community Respiratory Health Survey (ECRHS). The 10-year incidence (onset) of general, mucosal, dermal symptoms and any symptom improved when away from the workplace (work-related symptoms) was 7.2%, 11.6%, 6.4% and 9.4% respectively. The 10-year remission of general, mucosal, dermal symptoms and work-related symptoms was 71.4%, 57.1%, 70.4% and 72.2% respectively. Signs of dampness in the floor construction in any workplace building during follow up (cumulative exposure) was associated with incidence of mucosal symptoms (OR=2.43). Cumulative exposure to moldy odor was associated with incidence of work-related symptoms (OR=2.69). Cumulative exposure to dampness or moulds was associated with decreased remission of work-related symptoms (OR=0.20 for water leakage, OR=0.17 for floor dampness, and OR=0.17 for visible indoor mould growth). Working in a building repaired because of dampness (repaired building) or mould was associated with decreased remission of work-related symptoms (OR=0.32). Any dampness or moulds at baseline in the workplace building was associated with increased bronchial responsiveness (BR) and higher levels of Eosinphilic Cationic Protein (ECP) in serum and Eosinophilic counts in blood at baseline. Cumulative exposure to dampness and moulds, and work in a repaired building, was associated with increased BR at follow-up. In general, dampness and moulds in the workplace building is associated with increased incidence and decreased remission of SBS, as well as increased bronchial responsiveness and eosinophilic inflammation.

A longitudinal study of sick building syndrome among pupils in relation to microbial components in dust in schools in China.

There are few longitudinal studies on sick building syndrome (SBS), which include ocular, nasal, throat, and dermal symptoms, headache, and fatigue. We studied the associations between selected microbial components, fungal DNA, furry pet allergens, and incidence and remission of SBS symptoms in schools in Taiyuan, China. The study was based on a two-year prospective analysis in pupils (N=1143) in a random sample of schools in China. Settled dust in the classrooms was collected by vacuum cleaning and analyzed for lipopolysaccharide (LPS), muramic acid (MuA), and ergosterol (Erg). Airborne dust was collected in Petri dishes and analyzed for cat and dog allergens and fungal DNA. The relationship between the concentration of allergens and microbial compounds and new onset of SBS was analyzed by multi-level logistic regression. The prevalence of mucosal and general symptoms was 33% and 28%, respectively, at baseline, and increased during follow-up. At baseline, 27% reported at least one symptom that improved when away from school (school-related symptoms). New onset of mucosal symptoms was negatively associated with concentration of MuA, total LPS, and shorter lengths of 3-hydroxy fatty acids from LPS, C14, C16, and C18. Onset of general symptoms was negatively associated with C18 LPS. Onset of school-related symptoms was negatively associated with C16 LPS, but positively associated with total fungal DNA. In general, bacterial compounds (LPS and MuA) seem to protect against the development of mucosal and general symptoms, but fungal exposure measured as fungal DNA could increase the incidence of school-related symptoms.

Innate immunity and the pathogenicity of inhaled microbial particles.

Non-infectious inhaled microbial particles can cause illness by triggering an inappropriate immunological response. From the pathogenic point of view these illnesses can be seen to be related to on one hand autoimmune diseases and on the other infectious diseases.In this review three such illnesses are discussed in some detail. Hypersensitivity pneumonitis (HP) is the best known of these illnesses and it has also been widely studied in animal models and clinically. In contrast to HP Pulmonary mycotoxicosis (PM) is not considered to involve immunological memory, it is an acute self-limiting condition is caused by an immediate "toxic" effect. Damp building related illness (DBRI) is a controversial and from a diagnostic point poorly defined entity that is however causing, or attributed to cause, much more morbidity than the two other diseases.In the recent decade there has been a shift in the focus of immunology from the lymphocyte centered, adaptive immunity towards innate immunity. The archetypal cell in innate immunity is the macrophage although many other cell types participate. Innate immunity relies on a limited number of germline coded receptors for the recognition of pathogens and signs of cellular damage. The focus on innate immunity has opened new paths for the understanding of many chronic inflammatory diseases. The purpose of this review is to discuss the impact of some recent studies, that include aspects concerning innate immunity, on our understanding of the pathogenesis of inflammatory diseases associated with exposure to inhaled microbial matter.

The sick building syndrome as a part of the autoimmune (auto-inflammatory) syndrome induced by adjuvants.

Sick building syndrome (SBS) is a term coined for a set of clinically recognizable symptoms and ailments without a clear cause reported by occupants of a building. In the 1990s the term "functional somatic syndromes" was applied to several syndromes, including SBS, multiple chemical sensitivity, repetition stress injury, the side effects of silicone breast implants, the Gulf War syndrome (GWS), chronic fatigue syndrome, the irritable bowel syndrome, and fibromyalgia. Recently, Shoenfeld and Agmon-Levin suggested that four conditions--siliconosis, macrophagic myofascitis, the GWS, and post-vaccination phenomena--which share clinical and pathogenic resemblances, may be included under a common syndrome entitled the "autoimmune (auto-inflammatory) syndrome induced by adjuvants". Comparison of the clinical manifestations, symptoms, and signs of the four conditions described by Shoenfeld and Agmon-Levin with those described for SBS shows that nine out of ten main symptoms are present in all 5 conditions. Shoenfeld and Agmon-Levin further propose several major and minor criteria, which, although requiring further validation, may aid in the diagnosis of this newly defined syndrome. We propose here that SBS may also be included as a part of "Shoenfeld's syndrome".

Symptoms after mould exposure including Stachybotrys chartarum, and comparison with darkroom disease.

BACKGROUND: Mould-attributed symptoms have included features which overlap with unexplained syndromes such as sick building syndrome. OBJECTIVES: We describe questionnaire and chart review findings in patients following exposure to moulds which include Stachybotrys and compare responses with two control groups. METHODS: Thirty-two patients presented with symptoms attributed to mould exposures. Exposure identification for 25 patients had reported S tachybotrys chartarum as well as other mould (Aspergillus, Penicillium), 88% at work. The remaining seven had professionally visualized or self-reported/photographic exposure evidence only. A chart review was performed and a follow-up with a questionnaire, including questions on current health status, and nonspecific symptoms. RESULTS: Cough, shortness of breath and chest tightness (at presentation) were reported in 79%, 70% and 64%, respectively, and persisted >6 weeks in 91%. Skin test(s) were positive to fungal extract(s) in 30%. Seventeen returned questionnaires were obtained 3.1 (SD 0.5) years after the initial clinic assessment. Among this subgroup, persisting asthma-like symptoms and symptoms suggestive of sick building syndrome were frequent, and similar to a group previously assessed for darkroom disease among medical radiation technologists. The mould-exposed group more commonly reported they were bothered when walking in a room with carpets, complained of a chemical or metallic taste in their mouth, and had problems in concentration when compared with a control physiotherapist group (P < 0.005). CONCLUSIONS: Although only a minority with health concerns from indoor mould exposure had demonstrable mould-allergy, a significant proportion had asthma-like symptoms. Other symptoms were also common and persistent after the initial implicated exposure.

Symptoms, complaints, ocular and nasal physiological signs in university staff in relation to indoor environment - temperature and gender interactions.

UNLABELLED: Symptoms, signs, perceptions, and objective measures were studied in university buildings. Two problem buildings with a history of dampness and complaints were compared with two control buildings. Health investigations among university staff were performed at the workplace (n = 173) including tear film stability [non-invasive break-up time (NIBUT) and self-reported break-up time (SBUT)], nasal patency (acoustic rhinometry), nasal lavage fluid analysis [NAL: eosinophil cationic protein (ECP), myeloperoxidase (MPO), lysozyme and albumin] and atopy by total serum IgE and IgE antibodies (Phadiatop). Exposure assessment included inspections, thermal and atmospheric climate at 56 points modelled for all work sites. Multiple regressions were applied, controlling for age and gender. Exposure differences between problem buildings and controls were small, and variations between rooms were greater. Workers in the problem buildings had more general and dermal symptoms, but not more objective signs than the others. Adjusted day NIBUT and SBUT increased at higher night air temperatures, with B (95% CI) 0.6 (0.04-1.2) and 1.3 (-0.02 to 2.5), respectively. Higher relative humidity at mean day air temperature <22.1 degrees C was associated with adjusted NIBUT and SBUT, with B (95% CI) 0.16 (0.03-0.29) and 0.37 (-0.01 to 0.75), respectively. Air velocity below recommended winter values and reduced relative humidity in the range of 15-30% were associated with dry air and too low temperature. PRACTICAL IMPLICATIONS: Thermal climate in university buildings may be associated with both perceptions and physiological signs. Reduced night time air temperature, increased difference in air temperature between day and night, and fast changes in air temperature might impair indoor environment. This may have implication for energy-saving policies. It might be difficult to identify the exposure behind, and find the reason why, some buildings are defined as 'problem buildings'.

Atopy, symptoms and indoor environmental perceptions, tear film stability, nasal patency and lavage biomarkers in university staff.

OBJECTIVE: Study associations between airway symptoms, complaints on environmental perceptions, atopy definitions and biomarkers including tear film stability (BUT), nasal patency and nasal lavage (NAL). Personal predictors (gender, age, smoking, infections) for the biomarkers as well as associations between the biomarkers were also assessed. METHODS: A cross-sectional study of 173 employees in four university buildings, response rate 86%. Tear film break up time (BUT) was measured by a non-invasive method (NIBUT) and self-reported (SBUT). NAL-analysis included eosinophilic cationic protein (ECP), myeloperoxidase (MPO), lysozyme and albumin. Total serum IgE, and specific IgE using Phadiatop was measured. Data on subjective symptoms, environmental perceptions and background data were collected by use of a questionnaire. Multiple regression analyses were applied. RESULTS: Mean age was 43 years, 21% had weekly ocular, 21% nasal, and 17% laryngeal symptoms. Women had more complaints on environmental perceptions, shorter BUT and less nasal patency. Neither atopy (Phadiatop) nor Total IgE or allergy in the family, but asthma and hay fever was associated with mucosal symptoms or perceptions. Subjects with positive Phadiatop had higher levels of all NAL-biomarkers. Those with ocular symptoms had shorter BUT. Nasal symptoms were related to respiratory infections and laryngeal symptoms to NAL-lysozyme. Perceiving dry air was associated with lower BUT and reduced nasal volume difference before and after decongestion. Older subjects had greater nasal patency, and less atopy. All NAL-biomarkers were positively correlated. Higher lysozyme level was associated with less nasal patency and greater nasal decongestion. CONCLUSIONS: BUT and NAL-lysozyme was associated with ocular, nasal, laryngeal symptoms and indoor environmental perceptions. Ever having had asthma and ever having had hay fever were predictors for symptoms and perceived air quality, respectively. Phadiatop, Total IgE, familiar allergy and ever eczema were not associated to symptoms or perceived environments. Age, gender and Phadiatop were main predictors for ocular and nasal biomarkers.

Excess dampness and mold growth in homes: an evidence-based review of the aeroirritant effect and its potential causes.

Exposure to fungi produces respiratory disease in humans through both allergic and nonallergic mechanisms. Occupants of homes with excess dampness and mold growth often present to allergists with complaints of aeroirritant symptoms. This review describes the major epidemiological and biological studies evaluating the association of indoor dampness and mold growth with upper respiratory tract symptoms. The preponderance of epidemiological data supports a link between exposure to dampness and excess mold growth and the development of aeroirritant symptoms. In addition, biological and clinical studies evaluating potential causal substances for the aeroirritant effect, notably volatile organic compounds (VOCs), are examined in detail. These studies support the role of VOCs in contributing to the aeroirritant symptoms of occupants of damp and mold-contaminated homes.

[Clinical aspects of patients with MCS - from the standpoint of allergy].

BACKGROUND: "Sick House Syndrome" is thought to be an illness caused by indoor environments such as allergens, bacteria and chemical compounds. But it is not yet an established clinical entity. "Sick House Syndrome" overlaps in part with Multiple Chemical Sensitivity (MCS) whose symptoms are induced by very small amount of volatile chemical compounds. METHODS: We selected possible cases of MCS from patients who visited our specially built facility for"Sick House Syndrome" by tentative criteria as follow: (1)histories of chemical compounds exposure, (2)multi-organ symptoms, (3)exclusion of other disease(s) which may be responsible for symptoms, (4)chronic symptoms. Clinical aspects of the possible cases were examined. RESULTS: Fifty out of about 130 patients were the possible cases of MCS, 38 females and 12 males, aged 15 to 71 years old. Forty two out of 50 patients (84%) had a history and/or a complication of allergic diseases. This rate is much higher than the rate of prevalence of allergic diseases in Japanese population. Allergic rhinitis was the most popular allergic disease in the possible cases. Total IgE values were relatively low, 32 patients (64%) showed the IgE value below 200 IU/ml. No patients showed anti-formaldehyde IgE antibody. Decreased reactivity and decreased sensitivity of histamine release from peripheral blood were observed after challenge tests with chemical compounds. CONCLUSION: Allergic reactions can not be the causative mechanism(s) of the MCS, which is induced by multiple and different chemical compounds. Our results, however, suggest that patients having allergic diseases may be easily suffered from MCS or MCS may strengthen symptoms of allergic diseases.

Evaluation and a predictive model of airborne fungal concentrations in school classrooms.

Exposure to airborne fungal products may be associated with health effects ranging from non-specific irritation of the respiratory tract or mucus membranes to inflammation provoked by specific fungal antigens. While concentrations of airborne fungi are frequently measured in indoor air quality investigations, the significance of these measurements in the absence of visual mold colonization is unclear. This study was undertaken to evaluate concentrations of airborne fungal concentrations in school classrooms within a defined geographic location in British Columbia, Canada, and to build a model to clarify determinants of airborne fungal concentration. All elementary schools within one school district participated in the study. Classrooms examined varied by age, construction and presence or absence of mechanical ventilation. Airborne fungal propagules were collected inside classrooms and outdoors. Variables describing characteristics of the environment, buildings and occupants were measured and used to construct a predictive model of fungal concentration. The classrooms studied were not visibly contaminated by fungal growth. The data were evaluated using available guidelines. However, the published guidelines did not take into account significant aspects of the local environment. For example, there was a statistically significant effect of season on the fungal concentrations and on the proportional representation of fungal genera. Rooms ventilated by mechanical means had significantly lower geometric mean concentrations than naturally ventilated rooms. Environmental (temperature, outdoor fungal concentration), building (age) and ventilation variables accounted for 58% of the variation in the measured fungal concentrations. A methodology is proposed for the evaluation of airborne fungal concentration data which takes into account local environmental conditions as an aid in the evaluation of fungal bioaerosols in public buildings.

Antibodies against molds and mycotoxins following exposure to toxigenic fungi in a water-damaged building.

Exposure to molds in water-damaged buildings can cause allergy, asthma, hypersensitivity pneumonitis, mucus membrane irritation, and toxicity--alone or in combination. Despite this, significant emphasis has been placed only on Type I allergy and asthma, but not on the other 3 types of allergies. In this study, we sought to evaluate simultaneous measurements of immunoglobulin (Ig) G, IgM, IgA, and IgE antibodies against the most common molds, and their mycotoxins, cultured from water-damaged buildings. Antibodies against 7 different molds and 2 mycotoxins were determined by enzyme-linked immunosorbent assay (ELISA) in the blood of 40 controls and 40 mold-exposed patients. The IgG antibody levels against all 7 of the molds used, as well as the 2 mycotoxins, were significantly greater in patients than in controls. The IgM antibody levels were significantly different in patients for only 6 of 9 determinations. Regarding IgA determinations, antibodies were elevated significantly against all antigens tested, except Epicoccum. However, the differences in IgE levels in controls and mold-exposed patients were significant only for Aspergillus and satratoxin. These differences implied that, overall, the healthy control group was different from the mold-exposed patients for IgG, IgM, and IgA antibodies, but not for the IgE anti-mold antibody. Most patients with high levels of antibodies against various mold antigens also exhibited elevated antibodies against purified mycotoxins, indicating that the patients had been exposed to mold spores and mycotoxins. Detection of high levels (colony-forming units per cubic meter) of molds--which, in this study, strongly suggested that there existed a reservoir of spores in the building at the time of sampling--along with a significant elevation in IgG, IgM, or IgA antibodies against molds and mycotoxins, could be used in future epidemiologic investigations of fungal exposure. In addition to IgE, measurements of IgG, IgM, and IgA antibodies should be considered in mold-exposed individuals.

Neural autoantibodies and neurophysiologic abnormalities in patients exposed to molds in water-damaged buildings.

Adverse health effects of fungal bioaerosols on occupants of water-damaged homes and other buildings have been reported. Recently, it has been suggested that mold exposure causes neurological injury. The authors investigated neurological antibodies and neurophysiological abnormalities in patients exposed to molds at home who developed symptoms of peripheral neuropathy (i.e., numbness, tingling, tremors, and muscle weakness in the extremities). Serum samples were collected and analyzed with the enzyme-linked immunosorbent assay (ELISA) technique for antibodies to myelin basic protein, myelin-associated glycoprotein, ganglioside GM1, sulfatide, myelin oligodendrocyte glycoprotein, alpha-B-crystallin, chondroitin sulfate, tubulin, and neurofilament. Antibodies to molds and mycotoxins were also determined with ELISA, as reported previously. Neurophysiologic evaluations for latency, amplitude, and velocity were performed on 4 motor nerves (median, ulnar, peroneal, and tibial), and for latency and amplitude on 3 sensory nerves (median, ulnar, and sural). Patients with documented, measured exposure to molds had elevated titers of antibodies (immunoglobulin [Ig]A, IgM, and IgG) to neural-specific antigens. Nerve conduction studies revealed 4 patient groupings: (1) mixed sensory-motor polyneuropathy (n = 55, abnormal), (2) motor neuropathy (n = 17, abnormal), (3) sensory neuropathy (n = 27, abnormal), and (4) those with symptoms but no neurophysiological abnormalities (n = 20, normal controls). All groups showed significantly increased autoantibody titers for all isotypes (IgA, IgM, and IgG) of antibodies to neural antigens when compared with 500 healthy controls. Groups 1 through 3 also exhibited abnormal neurophysiologic findings. The authors concluded that exposure to molds in water-damaged buildings increased the risk for development of neural autoantibodies, peripheral neuropathy, and neurophysiologic abnormalities in exposed individuals.

Analysis for mycotoxins: the chemist's perspective.

Mycotoxins are fungal metabolites that pose a health risk to exposed animals and humans. In recent years, concern has mounted regarding human exposure to mycotoxins via inhalation of mold spores produced in damp buildings and homes. Although mycotoxins can be detected in such buildings, reliable means for measuring an occupant's level of exposure to most mycotoxins are lacking. The author briefly reviews the chemical methods currently available for mycotoxin analysis, outlining accepted practices and discussing the limitations of these measurements.

Mixed mold mycotoxicosis: immunological changes in humans following exposure in water-damaged buildings.

The study described was part of a larger multicenter investigation of patients with multiple health complaints attributable to confirmed exposure to mixed-molds infestation in water-damaged buildings. The authors present data on symptoms; clinical chemistries; abnormalities in pulmonary function; alterations in T, B, and natural killer (NK) cells; the presence of autoantibodies (i.e., antinuclear autoantibodies [ANA], autoantibodies against smooth muscle [ASM], and autoantibodies against central nervous system [CNS] and peripheral nervous system [PNS] myelins). A total of 209 adults, 42.7 +/- 16 yr of age (mean +/- standard deviation), were examined and tested with (a) self-administered weighted health history and symptom questionnaires; (b) standardized physical examinations; (c) complete blood counts and blood and urine chemistries; (d) urine and fecal cultures; (e) thyroid function tests (T4, free T3); (f) pulmonary function tests (forced vital capacity [FVC], forced expiratory volume in 1 sec [FEV1.0], and forced expiratory flow at 25%, 50%, 75%, and 25-75% of FVC [FEF25, FEF50, FEF75, and FEF2(25-75)]); (g) peripheral lymphocyte phenotypes (T, B, and NK cells) and mitogenesis determinations; and (h) a 13-item autoimmune panel. The molds-exposed patients reported a greater frequency and intensity of symptoms, particularly neurological and inflammatory symptoms, when compared with controls. The percentages of exposed individuals with increased lymphocyte phenotypes were: B cells (CD20+), 75.6%; CD5+CD25+, 68.9%; CD3+CD26+, 91.2%; CD8+HLR-DR+, 62%; and CD8+CD38+, 56.6%; whereas other phenotypes were decreased: CD8+CD11b+, 15.6% and CD3-CD16+CD56+, 38.5%. Mitogenesis to phytohemagglutinin was decreased in 26.2% of the exposed patients, but only 5.9% had decreased response to concanavalin A. Abnormally high levels of ANA, ASM, and CNS myelin (immunoglobulins [Ig]G, IgM, IgA) and PNS myelin (IgG, IgM, IgA) were found; odds ratios for each were significant at 95% confidence intervals, showing an increased risk for autoimmunity. The authors conclude that exposure to mixed molds and their associated mycotoxins in water-damaged buildings leads to multiple health problems involving the CNS and the immune system, in addition to pulmonary effects and allergies. Mold exposure also initiates inflammatory processes. The authors propose the term "mixed mold mycotoxicosis" for the multisystem illness observed in these patients.

Antibodies to molds and satratoxin in individuals exposed in water-damaged buildings.

Immunoglobulin (Ig)A, IgM, and IgG antibodies against Penicillium notatum, Aspergillus niger, Stachybotrys chartarum, and satratoxin H were determined in the blood of 500 healthy blood donor controls, 500 random patients, and 500 patients with known exposure to molds. The patients were referred to the immunological testing laboratory for health reasons other than mold exposure, or for measurement of mold antibody levels. Levels of IgA, IgM, and IgG antibodies against molds were significantly greater in the patients (p < 0.001 for all measurements) than in the controls. However, in mold-exposed patients, levels of these antibodies against satratoxin differed significantly for IgG only (p < 0.001), but not for IgM or IgA. These differences in the levels of mold antibodies among the 3 groups were confirmed by calculation of z score and by Scheffé's significant difference tests. A general linear model was applied in the majority of cases, and 3 different subsets were formed, meaning that the healthy control groups were different from the random patients and from the mold-exposed patients. These findings indicated that mold exposure was more common in patients who were referred for immunological evaluation than it was in healthy blood donors. The detection of antibodies to molds and satratoxin H likely resulted from antigenic stimulation of the immune system and the reaction of serum with specially prepared mold antigens. These antigens, which had high protein content, were developed in this laboratory and used in the enzyme-linked immunosorbent assay (ELISA) procedure. The authors concluded that the antibodies studied are specific to mold antigens and mycotoxins, and therefore could be useful in epidemiological and other studies of humans exposed to molds and mycotoxins.