The potential for a wide variety of fungal toxins to cause adverse health effects from the ingestion of mycotoxin-contaminated foods and feeds is a well-documented and widely accepted health problem of global importance. Some of these fungal metabolites are extremely toxic even at very low concentrations and are included as possible bioterrorism agents. Consequently, detecting the presence of mycotoxins in food, and knowledge of its (their) concentration(s) is important in assessing the disease risk of ingesting fungal-contaminated foodstuffs. The documented hazard posed by mycotoxins ingested has caused some to postulate that other potential routes of exposure, e.g., inhalation of mold spores and mycotoxins, may lead to mycotoxicoses.
In the past decade, a number of studies have been published (Croft et al., 1986; Etzel et al., 1998; Hodgson et al., 1998; Johanning et al., 1996; Vesper et al, 2007a) that purport to describe the hazards of exposure to airborne fungi in indoor environments of homes and offices. In these studies, a wide variety of occupant symptoms, e.g., headaches, chronic fatigue syndrome, focal alopecia, neural and respiratory disorders and even deaths, have been attributed to exposure to airborne mycotoxins. These studies also have resulted in widely used and undefined lay terms, such as "toxic mold," to describe the fungi that produce mycotoxins and also appear commonly in indoor settings. These studies commonly are quoted by the media, and used to generate hypotheses advanced in court cases that leave scientific laymen with the impression that "toxic mold" is a scientifically well-documented and important public health problem. This is not the case.
A fundamental problem is that the studies evaluating "toxic mold" hypotheses are few in number and beset with major epidemiological shortcomings that undermine the reliability of their conclusions. The scientific literature for the past several years yields a nearly yearly review, e.g., Kuhn and Ghannoum (2003), Kelman et al. (2004) and Bush et al. (2006), that conclude that the widespread concern about indoor exposures to so-called "toxic mold" is unproven and not backed by convincing scientific evidence. In this chapter, we summarize our understanding of problems with "toxic mold" and whether these types of concerns are important in developing countries.
Typically, concentrations of fungi in outdoor air are higher than in indoor air (Shelton et al., 2002). Mold-related problems arise indoors when, because of water intrusions and dampness, environmental conditions favor fungal growth, reproduction and sporulation. In general, complaints re© CAB International 2008. Mycotoxins: Detection Methods, Management, Public Health - 317 -and Agricultural Trade (eds. J. F. Leslie et al.).
lated to mold occur, as expected, whenever visible fungal growth and sporulation has occurred indoors whether or not the indoor exposure levels exceed those typically encountered out of doors.
Several types of adverse outcomes can result from exposure to airborne fungi including allergic reactions, such as allergic rhinitis and sinusitis, e.g., Bush et al. (2006), that are well accepted by the medical community. (Note: Fungal sinusitis typically is rare and secondary to bacterial sinusitis; rhinitis by definition is not toxin mediated). There also is some evidence that asthma in asthmatics may be exacerbated following exposure to indoor airborne fungi. [Note: There are many more common triggers for asthma than indoor fungi including exposure to pets, insects, cold air and exercise (American Academy of Allergy, Asthma and Immunology, 2006). The fungal involvement in the exacerbation of asthma is not known to be toxin mediated.] Other potential outcomes also may occur, e.g., fungal infections and systemic mycoses, but serious fungal infections usually are rare and generally are limited to people with immune deficiencies.
A major question is whether mycotoxins occur in fungal spores that are the etiologic cause of adverse health effects from inhalation in indoor environments. Available studies usually are limited in scope and do not tie cultures from fungi purportedly responsible for an outbreak to toxic spores or fungal strains that produce spores carrying mycotoxins to any particular disease symptoms, e.g., Panaccione and Coyle (2005). Case studies and anecdotal reports are relatively common (see above), but well-designed epidemiological studies of this issue are needed. If mycotoxins are not carried in sufficient quantities by fungal spores, then any problems caused by airborne mycotoxins must result from their absorption from airborne dust or other particles into which the toxins were secreted by the fungi that produced them.
There is no known direct "dose-response" relationship between the concentrations of fungi and allergic health effects as there is with many industrial chemical exposures (NIOSH, 20056). This lack of a direct relationship is especially true of allergic reactions, as the idiosyncrasies of the individual's hypersensitivity to the fungal allergens is the primary determinant of whether an allergenic interaction would occur. In hypersensitive individuals, a very small amount of the right allergen can trigger an allergic reaction. If an illness is mediated by a mycotoxin, then similar interaction patterns to those seen for other chemical toxins should occur, making the presence of viable toxin-producing organisms less critical.
Organic Dust Toxic Syndrome (ODTS)
The only "toxic" condition reported to result from exposure to airborne fungi, is the "Organic Dust Toxic Syndrome" a transient occupational disorder in agricultural workers resulting from intense exposures to extremely high levels of both fungal spores and bacteria from decaying organic material (Musgrave et al., 1994). The exposures that produce this syndrome are much higher than those found in indoor settings. ODTS has numerous names, including: (i) farmer's lung disease (Warren, 1977), (ii) pulmonary mycotoxicosis (Emanuel et al., 1975), (iii) grain fever in grain elevator workers (doPico et al., 1982), (iv) silo un-loader's syndrome (Pratt and May, 1984), (v) mill fever in cotton textile workers (Rylander et al., 1987), and (vi) inhalation fever (Rask-Andersen and Pratt, 1992).
The classic "toxic mold" case study
During the 1990s concerns emerged that exposure to toxigenic molds, particularly Stachy-botrys, in indoor air could cause severe illness.
Prior to 1993 investigators promoting the hypothesis that "toxic mold" was a health problem in indoor air were almost universally discounted. The hypothesis that airborne toxins associated with indoor mold cause serious illness got a major boost from preliminary reports of an investigation in Cleveland, Ohio in 1993 of infants who developed acute pulmonary hemorrhage/hemosiderosis and one of whom died. Investigators, including some from the Centers for Disease Control (CDC) in Atlanta, Georgia, concluded that Stachybo-trys atra (chartarum) in the homes of victims was the cause (Etzel et al., 1998; Montana et al., 1997). As some of the investigators were from CDC, these findings attracted attention and had instant credibility. These investigators hypothesized that toxins produced by Sta-chybotrys caused pulmonary hemorrhage. The resulting media coverage was incendiary and phrases such as "killer mold," "black mold" and "toxic mold" entered the vernacular. However, other epidemiologists at CDC were skeptical of the alleged association with Sta-chybotrys. Their skepticism increased when a similar "outbreak" of acute pulmonary hemorrhage occurred in infants in Chicago, but no Stachybotrys was found in any of the homes of the affected infants, even though the fungus was found in one of the control homes. This result prompted CDC to launch an internal review of its Cleveland study.
CDC conducted a rigorous internal scientific review of the Cleveland studies followed by an external review by a distinguished panel of experts. In June, 1999, CDC's internal scientific Work Group produced its report detailing methodological and statistical flaws (CDC, 1999a). The CDC External Panel on Acute Pulmonary Hemorrhage in Infants first met in August, 1999. They reviewed the report of the internal Work Group, the records from Cleveland, the relevant scientific literature, and interviewed the investigators. The report from the internal Work Group and the External panel (CDC, 1999b) caused CDC to back away from the initial conclusions of the Cleveland studies. This repudiation was published in March, 2000 and included the statement, "Conclusions regarding the possible association between cases of pulmonary hemorrhage/hemosiderosis in infants in Cleveland and household water damage or exposure to S. chartarum, are not substantiated adequately by the scientific evidence ... the association should be considered not proven ..." (DHHS/CDC, 2000). CDC followed up these reviews by forming expert advisory groups to establish a case definition for Acute Pulmonary Hemorrhage/Hemosiderosis in Infants (APHI), to facilitate nationwide surveillance of APHI and to identify opportunities for better studies.
Review by the American Industrial Hygiene Association (AIHA)
In 2000, one of us (BS) convened a panel of experts at the request of the Indoor Environmental Quality Committee of AIHA to review the epidemiologic literature most often cited to support the hypothesis that "toxic mold" causes toxic human illness. Four papers were selected for review: Croft et al. (1986), Johanning et al. (1996), Hodgson et al. (1998) and Etzel et al. (1998, the Cleveland studies). The question asked was, "Do toxins associated with these fungi in indoor settings result in increased frequency, severity, or a change in spectrum, of illness?" The panel presented their results at the 2000 annual AIHA meeting (Kirkland, 2001). Reported flaws in these studies include: (i) absence of clear and consistent case definitions, (ii) lack of consistent medical examinations, (iii) ignoring and not excluding other risk factors, (iv) non-blinded and inconsistent environmental assessment including biased sampling and flawed statistical analyses, (v) sample sizes insufficient to warrant conclusions, and (vi) the inability to combine and evaluate separate studies because they addressed different outcomes or different definitions of illness. Based on these shortcomings, the evaluators concluded that "... the evidence was insufficient to support the hypothesis that toxigenic fungi caused health complaints different from or worse than those associated with other common molds."
Reviews by the Institute of Medicine (IOM)
IOM (2000) analyzed the evidence for a causal association between asthma and indoor exposures, including fungi. IOM concluded that the assertion that mold causes asthma must be qualified. In particular, the data available suffice only for conclusions that fungi can trigger exacerbation of asthma in asthmatics. The available data were not sufficient to support the conclusion that fungi cause the development of asthma. IOM added further that, ". fungal exposure ... is complex ... (which has) ... led to confusion, poorly constructed studies on the role of fungi, ... inconclusive results, and avoidance of the field by the best investigators."
In 2004, another IOM committee produced another report, Damp Indoor Spaces and Health (IOM, 2004). This committee reached very similar conclusions regarding asthma, and also concluded that there was "inadequate or insufficient evidence to determine whether an association exists" between the "presence of mold" and 15 other health effects as claimed by proponents of problems due to "toxic" fungal exposures including APHI, chronic fatigue, neuropsychiatric symptoms, cancer, reproductive effects, and rheumatologic and other immune disorders.
In most years since 2000 at least one major review of the scientific literature concerning the relationship of "toxic mold" to human illness has appeared. Page and Trout (2001) reviewed the literature indexed under "mycotoxins" and cross-referenced with "indoor air pollution" and/or "sick building syndrome." They concluded that "... there is inadequate evidence to support the conclusion that exposure to mycotoxins in the indoor (nonindustrial) environment is causally related to symptoms or illness among building occupants." These conclusions are consistent with those of CDC's internal and external reviews, and also with those of the AI-HA Forum. They further advised that, ". there is inadequate evidence to support recommendations for greater urgency in cases where mycotoxin-producing fungi have been isolated," as suggested in the AIHA Bioaerosol manual (Dillon et al., 1996, pp. 58-59).
Since then reviews have appeared approximately annually that reach the same consistent conclusion that there is a lack of scientific evidence for a relationship between toxigenic molds in indoor environments and human health problems, e.g., Hardin et al. (2002), Texas Medical Association (2002), Fung and Hughson (2003), Kuhn and Ghannoum
(2003), Lees-Haley (2003), Harbinson and Hillman (2004), Kelman et al. (2004) and Bush et al. (2006). In NIOSH (2005a) there is a description of a Health Hazard Investigation of an elementary school in California where the teachers had been diagnosed with "toxic encephalopathy" attributed to "toxic mold." NIOSH concluded that "none had evidence of toxic encephalopathy." While not a review article per se, this report restated the NIOSH conclusions that, "... there is currently no evidence of a link between mycotoxin exposure in the indoor environment and human illness" and specifically noted "insufficient evidence that mold, mycotoxins, or damp environments cause neuropsychiatry disease." Based on this steady accumulation of peer-reviewed scientific data, there is no scientifically valid reason to view "toxic mold," i.e., fungi that might be capable of producing mycotoxins, as a greater hazard than any other fungi in terms of nonindustrial indoor exposures.
The anecdotal studies of airborne exposure to "toxic mold" usually share the same limitations and violate basic epidemiologic principles. For example, the disease outcome usually is not pre-defined and medical ascertainment usually is not performed. Since no pre-defined disease definition is adhered to, subjects may be included (improperly) in the study based solely on symptoms that can vary to include whatever people complain about at the time of the study. Therefore the disease outcome can range from symptoms that are difficult to verify, e.g., headaches and chronic fatigue, to serious pulmonary hemorrhage. In short, the disease outcome is a moving target. The term "toxic mold" also often is poorly defined and may mean only a catch-all group of fungi and associated chemicals. There is no definitive list of "toxic molds" of concern in indoor air settings and no defined concentration threshold at which an adverse response would occur. The closest thing to such a list is that developed by Vesper et al. (2004), but this list includes many species regarded as non-toxigenic, e.g., species of Au-reobasidium, Chaetomium and Cladosporium, and excludes some important toxin producers, e.g., all Fusarium species. Without such a list, the specific fungi and mycotoxins of concern can be almost never-ending, with as yet unidentified toxins implicated as necessary. The "relative moldiness index" proposed by Vesper et al. (2007b) is similarly ill-defined both in terms of fungi analyzed and in the total number of fungal spores present. In short, without a pre-defined exposure of interest, the exposure variable is not only undefined but also can take on an effectively infinite number of possible outcomes. Studies in which both the exposure variable and/or the outcome variable are moving targets, are flawed. At their worst these studies document a building with complaining occupants in which "toxic" fungi are found and assume that the association of the two is meaningful. It is not surprising that these associations are found, but it is surprising that they are published as conclusions from "epidemiological" studies.
Evidence needed to substantiate the claim that mycotoxins in indoor air cause disease(s) include: (i) defining the airborne inhalation dose needed to elicit defined symptoms for each mycotoxin, (ii) data showing that the specific mycotoxin was present at or above the dose level by inhalation in the indoor air in the disease setting, and (iii) a link between criteria (i) and (ii) in terms of sick people with specific pre-defined symptoms. Without such supporting evidence, the associations may be coincidental rather than causal, and those who publicize them may appear to be on a crusade rather than providing a public service.
A typical problematic study of "toxic mold" is that of Auger et al. (1994). This short two-page report summarizes three different case studies and concludes that toxic mold is linked to both upper respiratory infections and a chronic fatigue-like syndrome. The basic epidemiological parameters of exposure and medical ascertainment are inadequately defined in this study. Hence, both the disease outcomes and the exposures of interest are moving targets in this study. That "toxic mold" might cause a chronic fatigue-like syndrome is perhaps the ultimate irony for this study, as it concludes that an epidemiologically undefined exposure agent can cause a vague and medically undefined disease with a sample size of n < 3. Current studies of "toxic mold" are at the anecdotal stage. Going beyond the anecdotes requires rigorously defined studies to determine what risks, if any, airborne fungal mycotoxins pose in a nonindustrial setting.
In developing countries, the situation will not be the same as that found in the developed countries of Europe and North America. As detailed elsewhere in this book, mycotoxin exposure by ingestion may be high and all but unavoidable in many developing countries. In most parts of Africa, the major threats will be the aflatoxins and fumonisins associated with maize and peanuts (Marasas et al., Chapter 4). African diets consisting primarily of more traditional cereals, e.g. sorghum and millet, should be safer in terms of lower levels of mycotoxin exposure (Bandyopadhyay et al., 2007). Airborne exposure to mycotoxins is probably much less than that encountered in foods. Fungal growth and degradation of thatch roofing material, bedding and grain stored in houses could result in spores and dust carrying mycotoxins that could potentially be absorbed following inhalation.
In terms of exposure to airborne fungi, problems that parallel ODTS observed in agrarian portions of the United States and Western Europe seems a much more likely problem. ODTS results from exposure to large numbers of spores and high levels of dust. Such conditions are common in agrarian settings in developing countries, where there might be no paved surface in an entire village. Hand-harvesting of crops and drying and storing the harvest in the indoor family living areas would increase the exposure to dust and fungal spores even further.
Health problems associated with ODTS are readily detected in Western Europe and the United States. Reports to a physician in a developed country of recurring symptoms such as shortness of breath, coughing, wheezing and fever, although not life-threatening in-and-of-themselves, would elicit follow-up examinations and treatment to reduce symptom severity. In a rural agrarian setting in a developing country, an individual with such symptoms, if they contacted a physician at all, would be unlikely to receive more than a cursory examination and the symptoms probably would be attributed to one or more tropical diseases or to general poor health. Thus, a problem viewed as a significant occupational hazard for farmers in Western Europe and the United States is probably ignored and untreated in most developing countries.
Problems attributable to airborne fungal spores, especially in an agrarian setting, are well known and well documented. Dangers due to airborne exposure to mycotoxins and to "toxic mold" in indoor air in developed countries have been claimed, but the claims have not been substantiated through epidemiological studies. Good scientific process demands evi dence, proof, verification and reproducibility, all of which are available for ODTS, but almost none of which are available for the currently claimed "toxic mold" cases. Without the establishment of causation, e.g., a defined toxic dose of a specific toxin, confirmation of the toxin in the environment at or above the threshold, and reliable, verified symptoms in exposed individuals consistent with the exposure chemical and level, problems with "toxic mold" are questionable in developed countries and are probably negligible in developing countries. Instead the lung and other health problems clearly associated with agriculture in Western Europe as far back as at least the early 1700s (Warren, 1977) need to be given more attention as regards their role in reducing economic output and quality of life in current developing countries.
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Institutional Issues in Mycotoxin Management
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