Pathology – Epithilial cell proliferation Entry for November 09, 2007

This too is a photo of me. It was taken from an area where I had a significant number of the burning tingling bright red sores that I have been getting starting in 2002-2003 at a known exposure location. Recently I have started getting sores again that feel like they have glass slivers in them. They do not heal, and they do really hurt. Is this why?

According to my pathology report, this is why: Oxalate crystals produced by one of the more prevalantly present funguses found in my body, Aspergillus Niger. If you have ever had glass slivers or metal slivers under the skin, you would have an idea what this would feel like. The sores, as with any sliver, will not heal until the sliver comes out. In the interim you have soreness, inflammation, pressure pain, especially if the site is located on, at, or near a nerve. In addition, the skin will burn and tingle and discolour. I have many areas of scarring from these horrid things, and this photo shows what is going on at the microscopic level.

Although the Aspergillus Niger and it’s oxalate crystal production is not the entire explanation for my condition, and not all there is to the sores I get, it is one very active contributing factor. The oxalate crystals are proliferating my epithilial cells.

One of the many concerns I do have about my medical condition which is going untreated is what is happening to my organs and blood vessels. Amongst the many observations I am making in regard to my ongoing state of declining health is that my circulation is being affected. Definitely as well my breathing is being impacted, and my organs hurt severely. I think inflamation is causing some of the pain. These are just a few of some pretty profound observations and unnerving symptoms I cope with in a very solitary fashion each and every day of my life now.

Did you know: Staphylococcus aureus bacteria can co-colonize with fungus to create a potentially deadly, difficult to treat microbial cocktail which is often misdiagnosed.

Here is some info on this fungus and the oxalate crystals that it produces. This article states that Aspergillosis, caused by this fungus amongst others, is considered to affect only immunocompromised people with rare exceptions. This is not the general consensus amongst all familiar with this subject (no longer accurate). If you research it, you will find that, increasingly, more healthy people are falling victim to this condition. There are many immune system damaging substances in our modern environments and foods, which include toxins produced by many fungi, including this one, which attack your immune system, inevitably eventually rendering your immune system compromised, and thusly leaving you vulnerable to the threat posed to your health by such fungi.

Also, to consider, is the fact that fungi, in the presence of other toxic substances, has the tendency to mutate to survive the threat against it. In so doing, it then becomes more of a threat to you and I in it’s mutated form.

Keep this in mind when reading this article.

Jump to main content.

[logo] US EPA

Biotechnology Program Under Toxic Substances Control Act (TSCA)

Contact Us Search: All EPA This Area

Aspergillus niger Final Risk Assessment


Aspergillus niger

(February 1997)


Aspergillus niger is a member of the genus Aspergillus which includes a set of fungi that are generally considered asexual, although perfect forms (forms that reproduce sexually) have been found. Aspergilli are ubiquitous in nature. They are geographically widely distributed, and have been observed in a broad range of habitats because they can colonize a wide variety of substrates. A. niger is commonly found as a saprophyte growing on dead leaves, stored grain, compost piles, and other decaying vegetation. The spores are widespread, and are often associated with organic materials and soil.

History of Commercial Use and Products Subject to TSCA Jurisdiction

The primary uses of A. niger are for the production of enzymes and organic acids by fermentation. While the foods, for which some of the enzymes may be used in preparation, are not subject to TSCA, these enzymes may have multiple uses, many of which are not regulated except under TSCA. Fermentations to produce these enzymes may be carried out in vessels as large as 100,000 liters (Finkelstein et al., 1989). A. niger is also used to produce organic acids such as citric acid and gluconic acid.

The history of safe use for A. niger comes primarily from its use in the food industry for the production of many enzymes such as aamylase, amyloglucosidase, cellulases, lactase, invertase, pectinases, and acid proteases (Bennett, 1985a; Ward, 1989). In addition, the annual production of citric acid by fermentation is now approximately 350,000 tons, using either A. niger or Candida yeast as the producing organisms. Citric acid fermentation using A. niger is carried out commercially in both surface culture and in submerged processes (Berry et al., 1977; Kubicek and Rohr, 1986; Ward, 1989).

A. niger has some uses as the organism itself, in addition to its products of fermentation. For example, due to its ease of visualization and resistance to several antifungal agents, A. niger is used to test the efficacy of preservative treatments (Jong and Gantt, 1987). In addition, A. niger has been shown to be exquisitely sensitive to micronutrient deficiencies prompting the use of A. niger strains for soil testing (Raper and Fennell, 1965). There is also interest in using this fungus to performcertain enzymatic reactions that are very difficult to accomplish by strictly chemical means, such as specific additions to steroids and other complex rings (Jong and Gantt, 1987).


As is the case of many fungi, the taxonomy of Aspergillus is primarily based on morphological features, rather than the physiological, biochemical features and genetic characteristics often used to classify bacteria. The genus Aspergillus is usually defined as asexual saprophytic fungi that produce large black or brown conidia by phialides that are arranged in a globose head radiating from a vesicle or spherical conidiophore. This definition leads to inclusion of a complex assortment of organisms within the taxon. This is illustrated by the 132 species arranged in 18 groups by Raper and Fennell (1965) due to overlapping morphological or physiological characteristics. Aspergillus niger is both a species and a group within the genus Aspergillus.

The morphological approach to taxonomy has led to the existence of several synonyms for the genus Aspergillus. They are: Alliospora Pim; Aspergillonsis Spegazzini; Cladaspergillus Ritg; Cladosparum Yuill and Yuill; Euaspergilus Ludwig; Gutturomyces Rivolta; Raperia Subramaniam and Grove; Sceptromyces Corda; Spermatoloncha Spegazzini; Sphaeromyces Montagne; Sterigmatocystis Cramer; and Stilbothamnium Hennings (Bennett, 1985).

A.Definition of the Aspergillus niger Group

Raper and Fennell (1965) designated 15 species as comprising the Aspergillus niger group, which includes all of the aspergilli with black conidia. There have been suggestions to subdivide further (AlMusallam, 1980), but currently the concept of retention of the A. niger group based on black conidia seems dominant (Kustersvan Someren et al., 1990).

More sophisticated means of treating the classification of fungi have been attempted. Mullaney and Klich (1990) reviewed the molecular biological techniques for taxonomic classification studies of Aspergillus and Penicillium which include G + C molar percentage, DNA:DNA complementarity (measuring rate and extent of reassociation of single stranded DNA from two isolates), ribosomal RNA sequence comparison, and restriction fragment length polymorphism. One study of restriction digests of mitochondrial DNA indicated that all the Aspergillus groups examined are related. However, A. niger and A. awamori, both in the niger group, appear less related than would be expected for members in the same group (Kozlowski and Stepien, 1982). Work in the area of DNA homology and relatedness among the blackaspergilli is ongoing at the USDA Northern Regional Research Laboratory in Peoria, IL (Peterson, 1991). More exhaustive use of these and related techniques may give a clearer taxonomic system which will permit better separation of its members.

B.A. niger Species

While morphology provides a reasonable means of classification and assignment within the A. niger group, it is not a reliable means for identifying a given isolate from the field. The major distinction currently separating A. niger from the other species of Aspergillus is the production of carbon black or very dark brown spores from biseriate phialides (Raper and Fennell, 1965). Other features include the smooth and generally colorless conidiophores and spores that are ��5 ��m, globose, and have conspicuous ridges or spines not arranged in rows. A. niger isolates grow slowly on Czapek agar (Raper and Fennell, 1965). These physical characters such as spore color and rate of growth on a defined media are subject to change, especially under extended pure culture or selection and mutation. Though A. niger is relatively stable to spontaneous mutation compared to other aspergilli, variation in morphology may still be a problem with some strains (Raper and Fennell, 1965). Thus this species may be misidentified with other Aspergillus spp.

C. Potential Nomenclature Problems

Nomenclature problems of the genus Aspergillus arise from their pleomorphic life cycle. The newer findings show that this group of fungi has both a perfect (teleomorphic) and an imperfect (anamorphic) state. The International Code of Botanical Nomenclature provides a system of 76 mandatory rules (Articles), and also Recommendations, to promote nomenclature stability (Hawksworth, 1990). In a retrospective revision of the rules concerning fungi with pleomorphic life cycles, Art. 59, adopted by the 1981 International Botanic Congress (Voss et al., 1983), the decision was reached that “even if a species name was proposed under an anamorphic generic name, if the description and the type included the sexual ascosporic stage, then the name had to be applied to the teleomorph and was no longer available to the anamorph, the conidial state” (Hawksworth, 1990). Article 14 of the Code provides for conservation procedures to avoid disadvantageous changes in well-known family and generic names due to strict application of the code.

To avoid confusion, for economic or public health reasons taxonomists make exceptions to their rules. Thus, conservation of well-known names was also allowed for “species of major economic importance” (Art. 14.2) at the 1981 International Botanic Congress (Voss et al., 1983). Frisvad et al. (1990) pointed out that of the two obviously threatened names in the taxonomy of Aspergillus, A. niger van Tieghem is one of greatimportance. With this in mind Hawksworth (1990) recommended that the Aspergilli be included in a pilot study for the “List of Names in Current Use” initiative that could lead to formal adoption if sanctioned by the International Commission on the Taxonomy of Fungi.

If the rules for naming are rigorously applied, A. niger might disappear as a legitimate name, causing great commercial confusion. AlMusallam (1980) stated that there are two species described in the last century, A. phoenicus (Corda) Thom (1840) and A. ficuum (Reichardt) Hennings (1867) accepted as valid species by Thom and Raper (1945) and again by Raper and Fennel (1965) that are the same as A. niger, or that is a variety of one of them. However, Frisvad et al.(1990) believe that a clear case exists for conserving the name A. niger, because A. niger is “the source of commercial production of citric acid and other organic acids around the world, and clearly of major economic importance.” The earlier names have been used only rarely in modern publications. Thus, possible revision of the taxonomy of Aspergillus does not seem to include replacement of A. niger for the foreseeable future.

D. Conclusions on Taxonomy and Identification

Thus, while the name A. niger seems secure for now, the organisms to which it applies still represent a complex amalgam of morphologically related isolates. Those collections that take care to control conditions of culture and apply rigorous methods during identification should be able properly identify strains as belonging to this species. However, that does not guarantee that all strains properly called A. niger will share most physiological properties. The ones most likely to be well defined are those having long histories in culture, especially commercial culture, where the knowledge of these physiological properties is important to their maintenance. Since some features of concern for hazard may not be related to the morphological features used for classification, information on the physiology and biochemistry of A. niger strains maintained in culture, as well as their morphology, is useful for confirmation of identity.

E.Related Species of Concern

The taxonomy of Aspergillus has public health implications due to the production of potent mycotoxins by members of this genus. Most notable of these is the association of aflatoxins with members of the A. flavus group (Bennett, 1985b; Semeniuk et al., 1971). A. niger is not a member of that group, generally being distinguishable by color and structure of the conidial head (Raper and Fennel, 1965). Though proper separation among aspergilli requires a trained mycologist and care for proper culture conditions, when this is accomplished there should not beconfusion between A. niger strains and members of the A. flavus group.


A. Human Health Hazards

1. Colonization and Pathogenicity

The growth of the fungus Aspergillus in human tissue or within aircontaining spaces of the body, such as bronchus or pulmonary cavity, is termed aspergillosis (Bennett, 1979a). Exposure to Aspergillus must be nearly universal but disease is rare. The physiological condition of the exposed individual thus appears to be of paramount importance. Patients exhibiting aspergillosis are generally immunocompromised, and thus susceptible to otherwise common and usually harmless microorganisms. Factors that may lead to immunosuppression include an underlying debilitating disease (e.g., chronic granulomatous diseases of childhood), chemotherapy, and the use of supraphysiological doses of adrenal corticosteroids (Bennett, 1980).

Pulmonary aspergillosis is the most common clinical manifestation of aspergillosis. The most common symptoms of pulmonary aspergillosis are a chronic productive cough and hemoptysis (coughing up blood). According to a standard medical textbook, “Aspergillus can colonize ectatic bronchi, cysts, or cavities in the lung. Colonization is usually a sequel of a chronic inflammatory process, such as tuberculosis, bronchiectasis, histoplasmosis, or sarcoidosis. A ball of hyphae may form within an aircontaining space, particularly in the upper lobes, and is termed an aspergilloma. The fungus rarely invades the wall of the cavity, cyst, or bronchus in such patients” (Bennett, 1979a). It is not clear what role Aspergillus plays in non-invasive lung disease. Plugs of hyphae may obstruct bronchi. Perhaps allergic or toxic reaction to Aspergillus antigens could cause bronchial constriction and damage (Bennett, 1980).

Both the severity of aspergillosis and the patient’s prognosis are dependent on the physiologic status of the patient. Invasion of lung tissue in aspergillosis is almost entirely confined to immunosuppressive patients (Bennett, 1980). Roughly 90 percent of invasive pulmonary case patients will have two of these three conditions: severe immunosuppression (less than 500 granulocytes per cubic millimeter of peripheral blood), supraphysiological doses of adrenal corticosteroids, and a history of taking cytotoxic drugs such as azathioprine (Bennett,1980). In addition, the type of disease produced affects the patient’s chances for recovery. For example, simple colonization is treatable, but if the simple colonization becomes chronic or invades neighboring tissues, the infection becomes more difficult to treat (McGinnis, 1980). Surgical excision has been used successfully to treat invasive aspergillosis of the paranasal sinus as well as non-invasive sinus colonization. Intravenous amphotericin B has resulted in arrest or cure of invasive aspergillosis when immunosuppression is not severe (Bennett, 1980). Pleural aspergillosis often responds well to surgical drainage alone (Bennett, 1979b).

Although Aspergillus fumigatus is the usual cause of aspergillosis (Bennett, 1979b), there have been several recent case reports of pulmonary aspergillosis caused by A. niger. For example, Kierownik (1990) described a 66-year-old man who was admitted to the hospital with pulmonary lesions and cavitation of his lung. Fungi were cultured and the sputum contained fungal forms typical for A. niger complicating a pulmonary abscess in the course of a pneumonia. KorzeniowskaKosela et al. (1990) also describe a pulmonary aspergilloma caused by A. niger. Medina et al. (1989) reported on cases of bilateral maxillary sinusitis and a right pansinusitis.

A. niger was implicated in a case described by Louthrenoo et al. (1990), in which an amputation of the right foot had to be performed on a malnourished 70yearold man who presented with a painful black “gangrenous appearing” mass on the right foot. Tissue samples showed not only branching hyphae, but dark pigmented fungal fruiting heads with double sterigmata in which Aspergillus niger was identified.

Although Aspergillus niger is regarded as an opportunistic pathogen (Padhye, 1982; Walsh and Pizzo, 1988), an earlier report said that it can cause otomycosis in healthy, uncompromised persons who have no underlying disease (Austwick, 1965). Otomycosis is the name given to the growth of Aspergillus, often A. niger, on ceruman and desquamated debris in the external auditory canal. The condition is benign. Of 159 suspected cases of otomycosis in Nigeria, 36 were specifically confirmed on the basis of demonstrating microscopically fungal structures in epithelial debris plugs and a positive culture (Gugnani et al., 1989). Another 31 cases gave positive cultures but were negative microscopically, and thus were considered of doubtful fungal pathology. Again, A. niger was predominant.

2. Allergic Reactions to Aspergillus niger

Allergens produced by A. niger can produce allergic reactions in humans. When inhaled, A. niger can cause hypersensitivity reactions such as asthma and allergic alveolitis (Edwards and AlZubaidy, 1977). However, only a few instances ofasthma induced by A. niger have been reported. One such instance involved a manufacturing plant in which a specially selected strain of A. niger was being used to ferment molasses to produce citric acid. Both stirred tank and surface methods were being used. Eighteen workers were diagnosed as having occupational asthma; half had IgE antibody to A. niger based on skin and RAST tests. As determined by RAST inhibition experiments using a commercial extract of A. niger, the antigen that caused the sensitization appeared to be peculiar to the A. niger strain used for the fermentation (Topping et al., 1985).

In studies on 30 of 83 patients who showed symptoms of bronchial asthma, it was found that skin hypersensitivity to Aspergillus antigens with a high serum IgE to these antigens is indicative of Aspergillus sensitivity. In addition, levels of IgE protein and IgE antibodies specific for eight different allergenic extracts (including Aspergillus) were measured in the serum of persons infected with human immunodeficiency virus (HIV) and HIV negative subjects belonging to the same high risk group. Levels of IgE protein and antibodies were found to be definitively higher in the HIV infected patients (Maggi et al., 1989).

Massive inhalation of Aspergillus spores by normal persons can lead to an acute, diffuse, self-limiting pneumonitis. Spontaneous recovery taking several weeks is the usual course (Bennett, 1980). For example, Dykewicz et al. (1988) described the case of a 28-year-old man who developed fevers, cough, shortness of breath and other symptoms several hours after cutting live oak and maple trees. Fungal cultures of the wood chips yielded A. niger along with other Aspergillus species, three species of Penicillium, Paecilomyces sp., and Rhizopus sp. Several immunological techniques were used to show that the Penicillium sp. were probably responsible. Reports such as this illustrate that A. niger, while implicated by its isolation in association with some cases, is not necessarily the causative agent.

3. Toxin Production by A. niger

Aspergillus niger can produce a variety of fungal metabolites, termed mycotoxins, depending upon growth conditions and the strain of the organisms. The mycotoxins include oxalic acid crystals, kojic acid, and cyclic pentapeptides called malformins. The mycotoxins range from moderately to highly toxic in terms of acute toxicity.

A. niger produces oxalic acid and kojic acid abundantly. These two products have only a slight acute toxicity. Oxalic acid has an intraperitoneal LD50 of 150 mg/kg in rats and kojic acid has an intraperitoneal LD50 of 250 mg/kg in mice (Uen
o and Ueno, 1978).

Malformins produced by A. niger are more potent toxins, at least by the intraperitoneal route of administration. Malformin A has an intraperitoneal LD50 as low as 3.1 mg/kg in mice (Kobbe et al., 1977.) Pathologic signs accompanying fatality included dilatation with hemorrhage of the gastrointestinal tract and changes in the liver and kidney. Death occurred within four days. In contrast, oral doses up to 50 mg/kg failed to cause evidence of acute toxicity (Yoshizawa, 1975.)

In 1976, Anderegg et al. (1976) reported that a strain of A. niger collected from mold-damaged rice produced a highly toxic metabolite, Malformin C, which they established as the disulfide of cycloDcysteinylDcysteinylLvalylDleucylL-leucyl. When grown on white wheat in a fermentative process, malformin C was highly toxic to newborn rats (LD50 0.9 mg/kg; i.p.) and exhibited antibacterial activity against both gram positive and gram negative bacteria (Ciegler and Vesonder, 1987). Malformin C appears to have more mammalian toxicity than malformin A (Moss, 1977).

The production of malformins is related to the composition of the growth substrate and usually occurs in stationary phase cultures. While not always true, mycotoxins are generally produced on solid substrates with high carbon/nitrogen solid content (Ciegler and Kurtzman, 1970; Anderegg et al., 1976). For example, malformins are produced when A. niger is grown on onion bulbs (Curtis et al., 1974) and on fermenting grains (Kobbe et al.,1977). A strain of A. niger recovered from mold-damaged rice produced malformin A. A survey to define the number of strains in nature that are malformin producers appears not to have been made.

The use of radioactively labeled suspected precursors has helped clarify biosynthetic pathways for some mycotoxins. However, the specific enzymes involved in these transformations, their control and genetics are not always known even for well studied mycotoxins such as aflatoxin (Betina, 1989). The loci involved in mycotoxin biosynthesis have not been genetically mapped at present due to the difficulty of working with an asexual microorganism such as A. niger.

Aspergillus niger can interfere with the production of the potent mycotoxin aflatoxin by A. flavus under some conditions. Horn and Wicklow (1983) reported that when A. flavus and A. niger were co-cultured on autoclaved corn kernels, A. niger lowered the substrate pH sufficiently to suppress aflatoxin production.

4. Conclusions

A. niger is not a significant human pathogen. Throughout years of use and widespread exposure to A. niger in the environment, there are only several reports of aspergillosis withA. niger, and in Nigeria, one report of a number of cases of otomycosis. There have been only several reports of allergic reactions, which are not uncommon for aspergilli in general, and not unique to A. niger. A. niger is capable of producing several mycotoxins. However, mycotoxin production appears to be controlled by the conditions of fermentation.

B. Environmental Hazards

1. Hazards to Animals

Livestock ingesting A. niger contaminated feed have been shown to be adversely affected by mycotoxins. Calcium depletion and other physiological abnormalities including death can result from ingestion of A. niger colonized feed due to the fungal production of oxalic acid or malformins (Austwick, 1965). Chicks and mice were killed after being fed with moldy soybeans and mice died after eating contaminated wheat containing isolates of A. niger (Semeniuk, et al., 1971). The cause of death was assumed to be toxicosis, but pathogenicity was observed in some cases. Some of the malformins are currently under development for use as insecticidal compounds (Wicklow, 1991).

2. Hazards to Plants

A. niger has been isolated from 37 genera of plants (Farr et al., 1989). Often these reports involve coisolation with other perhaps more destructive microorganisms or isolation from a stored plant product. There are reports of A. niger being a plant pathogen in peanuts (Jackson, 1962). Apparently, A. niger can induce a crown rot of peanuts due to A. niger-infected seed under specific hot, humid growth conditions. The mycotoxins described above, namely oxalic acid, malformin A, and malformin C, have been shown to cause significant growth effects such as root curling and top deformation in plants (Anderegg et al., 1976).

A. niger can cause the rotting of numerous fruits, vegetables, and other food products, thus causing substantial economic losses due to spoilage. For example, black rot of onions associated with A. niger is responsible for serious losses of onion bulbs in the field and in storage. There are also reports of A. niger-induced spoilage of mangos (Prakash and Raoof, 1989), grapes (Sharma and Vir, 1986), and tomatoes (Sinha and Saxena, 1987).

3. Other Ecological Concerns

Members of the Aspergillus genus are well known as biodeteriogens (organisms that cause deterioration of materials). For example, A. niger causes discoloration and softening of the surface layers of wood, even in the presence of woodpreservatives. A. niger also causes damage to raw cotton fibers and other cellulosecontaining materials, as well as to tanning liquors used in the tanning of hides and leather. It can also attack plastics and polymers such as cellulose nitrate, polyvinyl acetate and polyester-type polyurethanes (Thomas, 1977). A. niger is also the major spoilage isolate on bakery products such as English style crumpets (Smith et al., 1988).

4. Conclusions

One set of major concerns for environmental hazard is, like that for human hazard, associated with mycotoxin production. Toxins from A. niger may affect other vertebrates and plants as well. There is one early report of crown rot of peanuts by A. niger under specific growth conditions. However, it is not a significant pathogen in the environment. In addition, A. niger is one of many commonplace spoilage-associated fungi, which can cause severe economic effects.


A. Worker Exposure

Aspergillus niger is considered a Class 1 Containment Agent under the National Institute of Health (NIH) Guidelines for Recombinant DNA Molecules (U.S. Department of Health and Human Services, 1986). In Europe, Aspergillus spp. are treated as low-risk-class microorganisms, i.e., category 2 of the European Federation of Biotechnology (Frommer et al., 1989) or category 1 on the OECD containment scale. Category 1 of the European Federation of Biotechnology scale includes organisms deemed harmless, which can be grown under good industrial large scale practices (GILSP), while category 2 organisms like Aspergillus require more stringent containment.

No data were available for assessing the release and survival specifically for fermentation facilities using A. niger. Therefore, the potential worker exposures and routine releases to the environment from large-scale, conventional fermentation processes were estimated on information available from eight premanufacture notices submitted to EPA under TSCA Section 5 and from published information collected from non-engineered microorganisms (Reilly, 1991). These values are based on reasonable worst-case scenarios and typical ranges or values are given for comparison.

During fermentation processes, worker exposure is possible during laboratory pipetting, inoculation, sampling, harvesting, extraction, processing and decontamination procedures. A typical site employs less than 10 workers/shift and o
perates 24 hours/day throughout the year. NIOSH has conducted walk-through surveys ofseveral fermentation facilities in the enzyme industry and monitored for microbial air contamination. These particular facilities were not using recombinant microorganisms, but the processes were considered typical of fermentation process technology. Area samples were taken in locations where the potential for worker exposure was considered to be potentially greatest, i.e., near the fermentor, the seed fermentor, sampling ports, and separation processes (either filter press or rotary drum filter). The workers with the highest potential average exposures at the three facilities visited were those involved in air sampling. Area samples near the sampling port revealed average airborne concentrations ranging from 350 to 648 cfu/m3. Typically, the Chemical Engineering Branch would not use area monitoring data to estimate occupational exposure levels since the correlation between area concentrations and worker exposure is highly uncertain. Personal sampling data are not available at the present time. Thus, area sampling data have been the only means of assessing exposures for previous PMN biotechnology submissions. Assuming that 20 samples per day are drawn and that each sample takes up to 5 minutes to collect, the duration of exposure for a single worker will be about 1.5 hours/day. Assuming that the concentration of microorganisms in the worker’s breathing zone is equivalent to the levels found in the area sampling, the worst-case daily inhalation exposure is estimated to range up to 650 to 1200 cfu/day. The uncertainty associated with this estimated exposure value is not known (Reilly, 1991).

B. Environmental and General Exposure

1. Fate of the Organism

Aspergilli are among the fungi most frequently isolated from soils and have been found to rapidly colonize and degrade easily available organic matter. The abundant asexual spores produced within the conidiophores are resistant to many environmental stresses which enables the organism to survive during inactive periods (Atlas and Bartha, 1981). Although no specific data comparing the survivability of industrial and wild type strains were available in the literature, the above characteristics indicate that released strains are likely to survive outside of containment (Versar, 1992).

2. Releases

Estimates of the number of A. niger organisms released during production are tabulated in Table 1 (Reilly, 1991). The uncontrolled/untreated scenario assumes no control features for the fermentor offgases, and no inactivation of the fermentation broth for the liquid and solid waste releases. The containment criteria required for the full exemption scenario assume the use of features or equipment that minimize the number of viable cellsin the fermentor off-gases. They also assume inactivation procedures resulting in a validated 6log reduction of the number of viable microorganisms in the liquid and solid wastes relative to the maximum cell density of the fermentation broth.


TABLE 1. Estimated Number of Viable A. niger

Organisms Released During Production

Uncontrolled/ Full

Release Media Untreated Exemption Release

(cfu/day) (cfu/day) (days/year)


Air Vents 2×108 – 1×1011 <2×108 – 1×1011 350

Rotary Drum Filter 250 250 350

Surface Water 7×1012 7×106 90

Soil/Landfill 7×1014 7×108 90


Source: Reilly, 1991

These are “worstcase” estimates which assume that the maximum cell density in the fermentation broth for fungi is 107 cfu/ml, with a fermentor size of 70,000 liters, and the separation efficiency for the rotary drum filter is 99 percent.

3. Air

Specific data which indicate the survivability of A. niger in the atmosphere after release are currently unavailable. Survival of vegetative cells during aerosolization is typically limited due to stresses such as shear forces, desiccation, temperature, and UV light exposure. As with naturally-occurring strains, human exposure may occur via inhalation as the organisms are dispersed in the atmosphere attached to dust particles, or lofted through mechanical or air disturbance.

Air releases from fermentor offgas could potentially result in nonoccupational inhalation exposures due to point source releases. To estimate exposures from this source, the sector averaging form of the Gaussian algorithm described in Turner (1970) was used. For purposes of this assessment, a release height of 3 meters and downward contact at a distance of 100 meters were assumed. Assuming that there is no removal of organisms by controls/equipment for offgases, potential human inhalation dose rates are estimated to range from 3.0 x 103 to 1.5 x 106 cfu/year for the uncontrolled/untreated scenario and less than that for systems with full exemptions. It should be noted that these estimates represent hypothetical exposures under reasonable worst case conditions (Versar, 1991).

4. Water

The concentrations of A. niger in surface water were estimated using stream flow values for water bodies receiving process wastewater discharges from facilities within SIC Code 283 (drugs, medicinal chemicals, and pharmaceuticals). The surface water release data (cfu/day) tabulated in Table 1 were divided by the stream flow values to yield a surface water concentration of the organism (cfu/l). The stream flow values for SIC Code 283 were based on discharger location data retrieved from the Industrial Facilities Dischargers (IFD) database on December 5, 1991, and surface water flow data retrieved from the RXGAGE database. Flow values were obtained for water bodies receiving wastewater discharges from 154 indirect (facilities that send their waste to a POTW) and direct dischargers facilities that have a NPDES permit to discharge to surface water). Tenth percentile values indicate flows for smaller rivers within this distribution of 154 receiving water flows and 50th percentile values indicate flows for more average rivers. The flow value expressed as 7Q10 is the lowest flow observed over seven consecutive days during a 10year period. The use of this methodology to estimate concentrations of A. niger in surface water assumes that all of the discharged organisms survive wastewater treatment and that growth is not enhanced by any component of the treatment process. Estimated concentrations of A. niger in surface water for the uncontrolled/untreated and the full exemption scenarios are tabulated in Table 2 (Versar, 1992).

TABLE 2. A. niger Concentrations in Surface Water


Flow Stream Flow Organisms

(MLD*) (cfu/l)


Mean 7Q10 Mean 7Q10



10th Percentile 156 5.60 4.5×104 1.25×106

50th Percentile 768 68.13 9.11×103 1.03×105

Full Exemption

10th Percentile 156 5.60 4.5×10-2 1.25×1000

50th Percentile 768 68.13 9.11×10-3 1.03×10-1


*MLD = million liters per day

Source: Versar, 1991

5. Soil

Since soil is the natural habitat for A. niger, long-term survival in the environment is expected. Human exposures via dermal contact and ingestion routes, and environmental exposures [i.e., to terrestrial, avian, and aquatic organisms (via runoff)] may occur at the discharge site because of the establishment of A. niger within the soil
(Versar, 1991).

6. Summary

Although direct monitoring data are unavailable, worst case estimates do not suggest high levels of exposure of A. niger to either workers or the public resulting from normal fermentation operations.


In the previous sections, information regarding the potential exposures and hazards to workers, the general public, animals, plants and the environment was reviewed. This section serves to integrate this information to evaluate the potential risks associated with the industrial use of Aspergillus niger.

A. Discussion

1. Risks to Humans and Animals

Reports associating A. niger with infectious diseases in healthy individuals are uncommon, although A. niger is a recognized opportunistic pathogen. Given the relative infrequency of anecdotal reports and the frequency with which all humans are exposed to A. niger, both by ingestion and inhalation, the probability of colonization in immunocompetent individuals must be quite small. The probability of colonization in immunosuppressed people, however, is relatively high. Nevertheless, given the already ubiquitous presence of A. niger, the increased environmental burden of A. niger due to release from commercial facilities under conditions imposed by exemption criteria is probably negligible. Thus, it may be concluded that the use of A. niger in fermentation facilities is unlikely to increase the baseline risk of infection by A. niger.

The primary hazard to humans and animals appears to be toxicity associated with the production of mycotoxins known as malformins. Concern is reduced due to available information on the relevant toxins. The higher values of toxicity formalformins A and C were determined by intraperitoneal injection, a route not considered to be environmentally relevant. Furthermore, data for toxicity via ingestion indicate that the toxicity is much lower by this route (Yoshizawa, 1975). This lower toxicity may be due to the destruction of the malformins, which are cyclic pentapeptides, in the gastrointestinal tract.

A. niger metabolites have caused adverse effects in livestock. The prevalence of strains that can produce these mycotoxins is unknown. Thus, it is uncertain whether the release, via waste disposal or air emissions, of A. niger strains capable of producing mycotoxins will add to the environmental burden of mycotoxin producing strains.

Significant environmental release of the mycotoxins themselves is unlikely if the commercial production takes place in a submerged fermentation system, since mycotoxins tend to be elaborated when A. niger is grown on solid substrates. However, some production of citric acid does take place on surface cultures, and mycotoxins may be produced. In addition, malformins are more likely to be produced in cultures at stationary phase, so that production control could limit the elaboration of these toxins. Selection of recipient strains known to be incapable of mycotoxin production or direct toxicity testing of production strains can address the concerns of possible mycotoxin elaboration during commercial production. Inactivation of mycotoxins by physical or chemical means prior to release of either the final product or the fermentation wastes may be another mechanism for reducing risk. It should be noted, however, that methods used to reduce levels of the microbial organism may not inactivate the mycotoxin produced. Mycotoxin production also seems to be a strain specific phenomenon.

Incidents involving industrial strains associated with allergic reaction in workers are rare. The offending antigen also appears to be strain dependent. In general, A. niger has a documentable history of safe use. Additionally, exposure to workers and the public is limited with closed-system fermentation.

2. Risks to Plants

A. niger is generally regarded as a strict saprophyte (Farr et al., 1989, Commonwealth Mycological Institute, 1966). As with effects on animals, the rare adverse plant effects seen appear to be strain specific. Since A. niger is ubiquitous in the environment, and the use of this organism in fermentation systems will not increase the low potential for adverse effects.

3. Other Risks

Other problems with A. niger are related to its ability to grow on a variety of substrates, causing deterioration of materials on which it is growing. For example, A. niger causes economic losses due to spoilage of bakery, fruit and vegetable products. A. niger also damages surface layers of wood, raw cotton fibers and many other materials. However, because A. niger is already ubiquitous, the increased environmental burden of A. niger due to release from commercial facilities is probably negligible. Thus, the baseline risk of materials damage by A. niger will not be affected by the use of A. niger in commercial facilities.

4. Summary of Risk Integration

Aspergillus niger is worldwide in distribution and has been isolated from numerous habitats. Humans are continually exposed to A. niger spores and vegetative forms on foodstuffs and in the air. The vast majority of strains of A. niger, especially those used in industrial fermentation, have a history of safe use. While there are sporadic reports to the contrary, most isolates have not been documented to be serious pathogens of humans, animals or plants. Specific strains may produce certain mycotoxins or may elicit allergic responses among workers. Those limited instances of adverse effects seem to be associated with a limited number of strains. With proper characterization of industrial strains, use of those with potential for such effects can be avoided.

B. Recommendation

Aspergillus niger is recommended for the tiered exemption.VI. REFERENCES

A. Primary Sources

AIBS (American Institute of Biological Sciences). 1978. Report to the Environmental Protection Agency: Criteria and Rationale for Decision Making in Aquatic Hazard Evaluation (Contract No. 68012457). Office of Pesticide Programs, U.S. Environmental Protection Agency, Washington, D.C. (2)

AbdelHafez, S.I., A.A. Shoriet. 1985. Mycotoxin producing fungi and mycoflora of airdust from Taif, Saudi Arabia. Mycopathologia 92: 6571.

Anderegg, R.J., K. Biemann, G. Buechi and M. Cushman. 1976. Malformin C, a new metabolite of Aspergillus niger. Jour. Amer. Chem. Soc. 98: 3653370.

Atlas R. and Bartha R. 1981. Microbial ecology: Fundamentals and applications, pp. 216 and 231. Addison Wesley Publishing, Company, Inc., Phillipines. (3)

Austwick, P.K.C. 1965. Pathogenicity of Aspergillus species, pp. 82126. In K.B. Raper and D.I. Fennell,(eds.), The Genus Aspergillus. Williams and Wilkins, Baltimore, MD.

Barbesgaard, P. 1977. Industrial enzymes produced by members of the genus Aspergillus. In J.E. Smith and J.A. Pateman, (eds.), Genetics and physiology of Aspergillus. Academic Press, New York.

Beckwith, A., R. Vesonder, and A. Ciegler. 1976. Chemical methods investigated for detoxifying aflatoxin in foods and feeds, Chapter 4. In J. Roderick (ed.), Mycotoxins and other fungal related food problems, Advances in Chemistry Series #149. American Chemical Society, Washington, DC.

Bennett, J.E. 1979a. Aspergillosis, pp. 546-547. In P. Beeson, W. McDermott, and J. Wyngaarden, (eds.), Cecil textbook of medicine, 15th edition. W.B Saunders, Philadelphia.

Bennett, J.E. 1979b. Aspergillus species, pp. 2002-2008. In G. Mandell, R.G. Douglas, and J.E. Bennett, (eds.), Principles and Practices of Infectious Diseases, John Wiley and Sons, New York.

Bennett, J.E. 1980. Aspergillosis, pp. 742-744. In K.J. Isselbacher, R.D. Adams, E. Braunwald, R.G. Petersdorff, and J.D. Wilson (eds.), Harrison’s Principles of Internal Medicine, McGraw-Hill, New York.

Bennett, J.W. 1985a. Molds, manufacturing and molecular genetics. In W.E. Timberlake, (ed.), Molecular genetics of filamentous fungi. Alan R. Liss, Inc., NY.

Bennett, J.W. 1985b. Taxonomy of fungi and biology of the Aspergilli. In A.L. Demain and N.A. Solomon, (eds.), Biology of industrial microorganisms. Benjamin Cummings Publishing Co., Menlo Park, CA.

Berry, D., A. Chmiel, and Z. Al Obaidi. 1977. Citric acid production by Aspergillus niger. In J.E. Smith and J.A. Pateman, (eds.), Genetics and physiology of Aspergillus. Academic Press, NY.

Betina, V. 1989. Mycotoxins. In Bioactive Molecules, Volume 9. Elsevier American Publishers, Oxford.

Ciegler, A. and R.F. Kurtzman. 1970. Penicillic acid production by blue eye fungi on various agricultural commodities. App. Microbiol. 20:761764

Ciegler, A. and R.F. Vesonder. 1987. Microbial food and feed toxicants: fungal toxins, pp. 19126. In The CRC handbook of microbiology, Volume VIII. CRC Press, Boca Raton, FL.

Cole, R.J.. 1984. Screening for mycotoxins and toxinproducing fungi. In V. Betina (ed.), Mycotoxins: Production, isolation, separation and purification. Elsevier Scientific Publishers, Amsterdam.

Commonwealth Mycological Institute. 1966. Description #94. Aspergillus niger rot of onions.

Curtis, R.W., W.R. Stevenson, and J. Tuite. 1974. Malformin in Aspergillus niger infected onion bulbs (Allium cepa). Appl. Microbiol. 28: 362365.

Dykewicz, M.S., P. Laufer, R. Patterson, M. Roberts, and H.M. Sommers. 1988. Woodman’s disease: Hypersensitivity pneumonitis from cutting live trees. J. Allergy Clin. Immunol. 81:455460.

Edwards, J.H. and T.S. AlZubaidy. 1977. Medical aspects. In J. E. Smith and J. A. Pateman, (eds.), Genetics and physiology of Aspergillus. Academic Press, NY.

Farr, D.F., G.F. Bills, G.P. Chamuris, and A.Y. Rossman. 1989. Fungi on plants and plant products in the United States. APS Press, St. Paul, MN. (2)

Farringer, R. 1985. Hazard Evaluation Division Standard Evaluation Procedure: Wild Mammal Toxicity Test(EPA540/985004). Office of Pesticide Programs, U.S. Environmental Protection Agency, Washington, D.C. (2)

Finkelstein, D.B., et al. 1989. Protein secretion in Aspergillus niger. In C.L. Hershberger, S. Queener, and G. Hegeman, (eds), Genetics and molecular biology of industrial microorganisms. American Society for Microbiology, Washington, DC.

Frisvad, J.C., D.L. Hawksworth, Z. Kozakiewicz, J.I. Pitt, R.A. Samson, and A.C. Stolk. 1990. Proposals to conserve important species names in Aspergillus and Penicillium, pp. 8389. In R.A. Samson and J.I. Pitt, (eds.), Modern concepts in Penicillium and Aspergillus classification. Plenum Press, NY.(1)

Frommer, W., B. Ager, L. Archer, B. Brunius, C.H. Collins, R. Donakian, C. Frontali, S. Hamp, E.H. Houwink, M.T. Kuenzi, P. Kramer, H. Lagast, S. Lund, J.L. Mshler, F. Normand-Plessier, K. Sargeant, M.G. Tuijnenburg, S.P. Vranch and R.G. Werner. 1989. Safe biotechnology III. Safety precautions for handling microorganisms of different classes. Appl. Microbiol. Biotechnol. 30: 541-552

Gill, D.M.. 1982. Bacterial toxins: a table of lethal amounts. Microbiological Review 46:8694. (2)

Gugnani, A.C., B.C. Okafor, F. Nzelibe, and O.A. Njoku. 1989. Etiological agents of otomycosis in Nigeria. Mycoses 32: 224229. (1)

Hawksworth, D.L. 1990. Problems and prospects for improving the stability of names in Aspergillus and Penicillium. In R.A. Samson and J.I. Pitt, (eds.), Modern concepts in Penicillium and Aspergillus classification. NATO Advanced Science Institute Series, Series A: Life Sciences, Volume 185. Plenum Press, NY.(1)

Horn, B.W. and D.T. Wicklow. 1983. Factors influencing the inhibition of aflatoxin production in corn by Aspergillus niger. Can. J. Microbiol. 29:10871091.

Jackson, C.R. 1962. Aspergillus crown rot of peanuts in Georgia, seed treatment fungicides for control of seedborne fungi in peanut. Plant Disease Reporter 46:888892. (2)

Jong, S.C. and M.J. Gantt, (eds.) 1987. Catalogue of fungi and yeasts, 17th edition. American Type Culture Collection, Rockville, MD.

Kierownik. 1990. Pulmonary aspergillosis caused by Aspergillus niger. Pneumonol. Pol. 58: 328333.

Kobbe, B., M. Cushman, G.N. Wogan and A.L. Demain. 1977. Production and antibacterial activity of Malformin C, a toxic metabolite of Aspergillus niger. Appl. and Environ. Microbiol. 33: 996997. (1)

KorzeniowskaKosela, M., et al. 1990. Pulmonary Aspergillosis caused by Aspergillus. Pneumonol. Pol. 58:328333. (1)

Kozowski, M. and P.P. Stepien. 1982. Restriction analysis of mitochondrial DNA of members of the genus Aspergillus as an aid in taxonomy. Jour. Gen. Microbiol. 128:471476. (1)

Kubicek, C. and M. Rohr. 1986. Citric acid fermentation. CRC Critical Reviews in Biotechnology 3(4):331373.

Kubo, S. 1989. Changes in the specificity of blood groups induced by enzymes from soil fungi. Jour. Forensic Science 34(1):96104.

Kustersvan Someren, M.A., H.C.M. Kester, R.A. Samson, and J. Visser. 1990. Variations in pectolytic enzymes of the black Aspergilli: A biochemical and genetic approach. In R.A. Samson and J.I. Pitt, (eds.), Modern concepts in Penicillium and Aspergillus classification. NATO Advanced Science Institute Series, Series A: Life Sciences, Volume 185. Plenum Press, NY.(1)

Louthrenoo, W., Y.S. Park, L. Philippe, and H.R. Schumacher, Jr. 1990. Localized peripheral calcium oxalate crystal deposition caused by Aspergillus niger infection. Jour. Rheumatol. 17: 407412. (1)

Maggi, E., M. Mazzetti, A. Ravina, C. Simnelli, P. Parronchi, D. Macchia, P. Biswas, M. Di Pietro and S. Romagnani. 1989. Increased production of IgE protein and IgE antibodies specific for fungal antigens in patients with the acquired immunodeficiency syndrome. Ric. Clin. Lab. 19:4549. (1)

McGinnis, M.R. 1980. Laboratory handbook on medical mycology, pp. 475480. Academic Press, NY. (1)

Moss, M.D. 1977. Mycotoxins. In J.E. Smith and J.A. Pateman, (eds.), Genetics and physiology of Aspergillus. Academic Press, New York. (1)

Peterson, S. 1991. Phone conversation with John Kough, U.S. Environmental Protection Agency, Washington, D.C. (2)

Padhye, A.A. 1982. Fungi pathogenic to man and animals. In A. Laskin and H.A. Lechevalier, (eds.), CRC handbook of microbiology, Volume II. CRC Press, West Palm Beach, FL.

Palmas, F., S. Consentino and P. Cardia. 1989. Fungal airborne spores as health risk factors among workers in alimentary industries. Euro. Jour. Epidemiol. 5:239243. (1)

Pavlenko, S.A. 1990. Otomycoses in the Kuznetsk region and organization of medical services for this group of population. Vestn-Otorinolar. July-Aug(4):70-71. (1)

Prakash, O. and Raoof, M.A. 1989. Control of mango fruit decay with post harvest application of various chemicals against black rot, stem end rot and anthracnose disease. Int. J. Trop. Plant Dis. 6:99106.

Raper, K.B. and D.I. Fennell. 1965. The genus Aspergillus. Williams and Wilkins Company, Baltimore, MD.

Reilly,B. 1991. Analysis of environmental releases and occupational exposure in support of proposed TSCA 5(h)(4) exemption. Unpublished, U.S. Environmental Protection Agency, Washington, D.C.

Richard, J.L., J.R. Thurston, W.M. Peden, and C. Pinello. 1984. Recent studies on aspergillosis in Turkey poults. Mycopathologia 87:311. (2)

Sayre, P. 1991. Justification for TSCA biotechnology rule preamble criteria relevant to 5(h)(4) microorganisms. Unpublished, U.S. Environmental Protection Agency, Washington, D.C.

Semeniuk, G., G.S. Harshfield, C.W. Carlson, C.W
. Hesseltine and W.F. Kwolek. 1971. Mycotoxins in Aspergillus. Mycopathologia 43:137152.

Sharma, R.C. and D. Vir. 1986. Post harvest diseases of grapes and studies on their control with benzimidazole derivatives and other fungicides. Pesticides (Bombay) 20:1415.

Sinha, P. and Saxena, S.K. 1987. Effect of treating tomatoes with leaf extract of Lantana camara on development of fruit rot caused by A. niger in presence of Drosophila busckii. Indian J. Exp Biol. 25:143144.

Smith, J.P., S. Khanizadeh, F.R. van de Voort, et al. 1988. Use of response surface methodology in shelf life extension studies of a bakery product. Food Microbiol (Lond) 5:163176.

Thom, C. and K.B. Raper. 1945. A manual of the Aspergilli. Williams and Wilkins Company, Baltimore, MD. (1)

Thomas, A.R. 1977. The genus Aspergillus and biodeterioration. In J.E. Smith and J.A. Pateman, (eds.), Genetics and physiology of Aspergillus. Academic Press, NY.

Topping, M.D., D. Scarisbrick, C. Miucyzynska, E. Clarke, and E. Seaton. 1985. Clinical and immunological reactions to Aspergillus niger among workers at a biotechnology plant. Brit. Jour. Ind. Med. 42:312318.

Turner, B. 1970. Workbook of atmospheric dispersion estimates. U.S. Environmental Protection Agency, Research Triangle Park, NC. (3)

Ueno, Y. and I. Ueno. 1978. Toxicology and biochemistry of mycotoxins. In K. Uraguchi and M. Yamazaki, (eds.), Toxicology, bochemistry, and pathology of mycotoxins. John Wiley and Sons, Halstead Press, NY.

U.S. Department of Health and Human Services. 1986. Guidelines for research involving recombinant DNA molecules; Notice. 51 FR 16958, May 7, 1986.

U.S. Department of Health and Human Services. Undated. Proposed biosafety guidelines for microbial and biomedical laboratories. Office of Biosafety, Center for Disease Control.

Voss, E.G., et al. 1983. International code of botanical nomenclature adopted at the Thirteenth International Botanical Congress, Sydney, August 1981. Regnum Vegetabile 111:1472. (1)

Walsh, T.J. and P.A. Pizzo. 1988. Nosocomial fungal infections: A classification for hospitalacquired fungal infections and mycoses arising from endogenous flora or reactivation. Ann. Rev. Microbiol. 42:517545.

Ward, O.P. 1989. Fermentation biotechnology. Prentice Hall, Englewood Cliffs, NJ.

Wyllie, T.D. and L.G. Morehouse, (eds.) 1971. Mycotoxic fungi, mycotoxins, mycotoxicosis, Volume 3. (Russian) Vestn. Otorinolaringol. JulyAug. (4):7074. (1)

Yoshizawa, T., Y. Tsuchiya, N. Morooka and Y. Sawada. 1975. Malformin Al as a mammalian toxicant from Aspergillus niger. Agric. Biol. Chem. 39:13251326.

B. Secondary Sources

(1)Dynamac. 1991. Human health assessment of the possible risk for use Aspergillus niger as a recipient microorganism. Unpublished, U.S. Environmental Protection Agency, Washington, D.C.

(2)Kough, J. 1991. Environmental assessment for the use of A. niger as a recipient microorganism. Unpublished, U.S. Environmental Protection Agency, Washington, D.C.

(3)Versar. 1991. Screening level exposure assessment of Aspergillus species for 5(h)(4) exemption under the proposed biotech rule. Unpublished, U.S. Environmental Protection Agency, Washington, D.C.

(4)Dynamac. 1990. Organism Profile: A. niger. Unpublished, U.S. Environmental Protection Agency, Washington, D.C.

Jump to main content.


My opinion of Planet in Peril plus more on the lake Entry for October 24, 2007

This picture was also taken at the lake in my area last month. I can’t say for sure that there is any connection, but since making all these trips to this lake I have been brutally ill, and even landed in the emergency one night. Very out of character for me. I am still battling to try to get a grip on the problem. In keeping with my problems with the medical process; I had what looked like a very bad pneumonia, was coughing up large amounts of blood, had intense intra torsal and intracranial inflammation, nosebleeds, respiratory distress although lungs are apparently clear, and once again, all my test results came back negative. Nothing wrong with me. Absolutely ludicrous, but here I go again down the same repetitious “no answers” road.

Well, I watched CNN’s Planet in Peril. If you did not see it, it was a two part special on our planet’s declining condition that also delved into the Global Warming aspect, but was not limited to this. I agreed with what was said in general, but was disappointed by the lack of discussion around “what” is happening to our contaminated waters on the planet.

Although the program did make mention of contaminated water numerous times, the lack of detailed descriptions of what types of contaminants are threatening these waters was disappointing to me, but not a surprise. This always seems to get skipped over. It costs too much to test specific water bodies for so many of the potential contaminants.

More to the point, no publicly educating discussions are taking place around the domino effect set in motion by the presence or introduction of foreign contaminants to the threatened water and even soil ecosystems, and on into what then starts to be absent, what starts to become dominant, and how the surviving organisms evolve or mutate in the presence of all the foreign contaminants and absence of essential inhibiting organisms to the overgrowth of other organisms.

Through discussion of these issues can come a better understanding for the public at large of how normally present molds, algaes, bacteria, etc., can become threats to well health.

Contamination of water does not stop at the offending foreign substances such as chemicals that enter the water. It is likely that many would never even think of the multitude of foreign substances that find their way into our waters, or what the ripple effect really is, especially at the microscopic level.

Raw sewage or septic effluent is a big one. Raw sewage is not just a steaming pile of poo any more. In it are a cornucopia of pharmaceutical products, many of which have a direct interfacing effect on living organisms, vegetation, invertebrates, and wildlife that abide in the environment connected to the present water body. Examples of drugs which can interact with the life in any ecosystem including those with or in waterbodies are steroids, growth hormones, even birth control.

Raw sewage (septic effluent) can also contain all the waste from your tub, which would include soaps, shampoos, chemical cleaners for your tub, whatever you had in your mop bucket, etc.

Raw sewage (septic effluent) can include what you wash down the sink drain, which again includes chemicals. Did you know that high levels of teflon have been found in our environment? How did it get there? It came off your teflon pans when you washed them. Teflon is also coming off into what you are cooking, and has been found accumulating in people’s bodies as well. This fact remained a dirty little industry trade secret for many years.

Raw sewage (septic effluent) also includes what comes out of your washing machine. Again a lot of chemicals.

And then there is the water treatment chemicals themselves.

Just the stuff that raw sewage is made of these days is deadly to our waters. A lot of the world’s waters are contaminated with this modern day sewage cocktail, which has a devastating effect on the natural balance of water ecosystems from the most microscopic organisms on up to the largest consumers of this water.

One thing that shows up when the water is badly contaminated is algae that is not healthy for the lake ecosystem. These algaes will kill the lakes natural ecosystem.

The lake I have been photographing recently is a good example. Septic content is a known component in this lake. So is the runoff from a large plant nursery operation. The effect is clear.

In discussing the contents of my photographs with a soil scientist and a university professor, I confirmed that this is definitely not good news for this lake. In many of my photographs there is a film forming on top the water. I could literally see my jewellery in the reflection off this film in some of my photographs. This film to be acting as a mirror is a clear indication that the film is blocking the light from entering the water. This is very bad news for the water’s ecosystem needs. No light, and everything below the light blocking film will begin to die. The lake is in jeopardy of dying from this one aspect of a multi tiered threat process alone.

The sludge in my photographs is partly algae which would be harmful algae as it is a bi-product of the contaminants in the lake. But that is not all that is there.

What is in that water and other water bodies in this condition is what needs to become open discussion. It seems like the details of microbiological threats in our ambient environment is remaining a persistently elusive topic. It needs to be discussed…….. freely and openly.

Chemical contaminants are bad, no argument here, but they are dead things.

I am much more concerned about the living organisms that are emerging in this filthy world that are invading our bodies, especially given the fact that many of them are bi-products of the chemical insults to our environment. They have already survived the chemical insults delivered by us, thus making them chemical resistant.

If one or more species or strain(s) of these chemical resistant live organism(s) decides to invade your body and is a threat to your health……. exactly how would this problem be solved?

We are already in the midst of such a mess right here right now in North America right along with some other places on the planet.

Unconstrained, uncensored, open discussion on the microbiological threats to the living should be taking place and should be an accessible topic of discussion for each and every one of us at our request and/or in the case of relevance and the need to know.

This poorly publicized topic area needs much more attention in the public domain than it is presently getting. People need to know about these things, and have a right to know.

As it is a difficult topic for the average person to understand or make proper sense of, it would possibly take time for many to develop an understanding in these areas, and they should be starting that process already as it is relevant now.

The best minimizer of potential harm is education. There are so many who would educate if the information was there to access. It should be there. It should be there now.

Al Gore comes to a town near me. Entry for September 28, 2007

Vice President Al Gore
Live in Vancouver!

With Special Guest Dr. David Suzuki

One night with two of the world’s top environmentalists
Don’t miss this once-in-a-lifetime opportunity to catch the pioneering environmental leader in person .

Sounds pretty good so far doesn’t it. I was pretty excited about this, and would like to have attended. But from here a problem emerges. Herein lies the problem:


Choose your ticket type
General Admission Ticket – $250.00
Premium Seating Ticket – $500.00
Student Ticket – $99.00
*this ticket requires student ID
Associate Ticket
*this ticket requires a promotional code

Here is a link to the site for this event:

That excludes me, and anyone else of limited means. I would like to believe that these two gentlemen are indeed good men in the world, and I do. However, do they realize they are putting an unreachable to most price on a message that applies to each and every life upon this planet? Is there an issue of ethics here? I beleive there is.

This is not a special interest topic for those pursuing a specific career path. This is about life on this planet, all life, no matter of what financial means.

Although I realize that all things cost money, including this seminar, I am struggling with the fact that such an exorbitant amount of money is requested in order that one may get through the door to hear these people talk.

I am also aware that for the most part, the people with the means to be able to attend this seminar will be those who have more knowledge already than the population at large. Corporate and political representatives or entities have access to truths that the general public does not. If information seminars of this type are priced out of reach for the general public, then what is being accomplished in the way of educating the public?

I am especially annoyed by this as I do my part out of a room in a strangers house where one room acts as a living room, office, bedroom, bathroom, and kitchen, and literally juggle between providing for myself with the little money I have, or chasing leads and paying out of my own tiny income to investigate and document leads on the environmental and health front in the public interest. This state of struggle for me is as a result of my severe introduction to environmental contamination and the ensuing health insult. I have nothing, and my life is one of pure hell, yet I make my contribution without asking for anything. I know that these types of messages are for everyone, not just those with enough money to hear them. There are a lot of people with very little that I have met that want to learn more, but cannot afford to attend expensive seminars. Those are some of the people most likely to become participant in solutions on an individual basis. These people are just as important to the solutions as anyone else. They should not be excluded from any discussions, planning, or processes relative to the preservation of life on earth due to limited means.

An associate I met through my health-environmental work told me to remember this quote:

“Some of the most important work ever done in this world was done by people who had nothing”.

I said “point taken”, but I could do so much more if I had the resources to do so.

Should we not all be included and able to work together regardless of financial status, or does your message only have merit if you have the finances to back a very public display?

Does your message still have value if you are not of financial means? What do you think?

I would like to have met Mr. Gore and Mr. Suzuki simply to shake their hands as I support both their proclaimed agendas. I would also have liked to hear what these gentlemen had to say in it’s entirety, as I am sure would many others who have found the cost to be much to high. Unfortunately the reality for me personally is that attending this event is not an option due solely to the cost of attending.

This is really disappointing to me. I may not “have ” in financial stature, but without hesitation I can say that “I do have” something of value to contribute and a willingness to do so (because I care), and the intellect to carry it through. If I had their means I would still see things as I do now, I would just be able to do a much better job of what I am already doing. I would not lose sight however of the fact that all planetary environmental issues apply to and in fact you could even say “belong to” everyone, and to sit in a room full of people of all backgrounds and financial means to me would be much more enlightening than sitting in a room containing only those of specific means.

I should mention I am glad to see students being given a measurable break to enable them to attend.

What do you think? I would like to hear the opinions of others on this.

Conditions NOT exclusive to this region. Entry for September 24, 2007

This is a photo I took on September 03, 2007 at the lake in my area that I have been focused on recently. The murky appearance in the last two lake photos is caused by a film forming on top the water. This film gets thicker and increasingly more colourful as it thickens and comes to look like this. It is not oil or fuel as it mimics or resembles the appearance of. Given the right conditions it then starts to form bubbles and off gas as in the two previous posts relative to the bubbling sludge (Entries for January 22, 2007 entry 28, and 27).

I am particularly interested in this photo right now because I was researching algae, toxic algae, and warmer climate and it’s effect on algae. During this research I found one really cool website with pictures from a hotspring in Yellowstone national park where there are large pooling rings of multiple colors of algae. According to the photographer different temperatures cause different colors of algae to grow. I contacted the photographer and he sent me some links relevant to algae problems in other parts of the world. Another person who has done some research on what he has seen through the lens.

Next, I came across a website with several pictures fused together in a header bar. I couldn’t believe my eyes. Right there on that distant website was what looked like “my picture!” It was however not my picture, but nearly identical to this one I just took. There was a second picture on there that looked exactly like another one of mine as well. On this website it is being loosely referred to as “slime water” which I understand having seen this stuff up close. The other picture calls the other appearance brown algae. There is a brown algae, but there are also other things that can look like brown algae. The author of that website says that last year there was green algae where this new (never seen before) brown jelly like algae now is.

Part of the reason I wanted to bring this up is that this is a major break in my information seeking efforts. It puts this stuff, or something very similar and foreign in a location nowhere near this valley.

The other person’s pictures are from a canyon in Arizona. Higher and dryer than here. I am at sea level pretty much in a high water table region with a large amount of groundwater and it rains a lot here. Arizona’s climate is dryer, and the pictures from there were taken at 4500 feet above sea level. I believe our pictures were taken around the same time of year too, August /September. The Arizona author has not seen this before and instinctively did not want the dog near it. Perhaps the author should heed this instinctive caution for self too?

Common possible contributing factors that come to mind:

-People (there is a campground nearby)

-Migratory birds

-water treatment chemicals?

-chemical or biological forest initiatives?

-acid rain?

-Global warming

I said it would be in other places, and it will spread in those places like it is doing here. Yes, warmer weather instigates and escalates the rate of accumulation of this stuff, but the cold does not stop it either. In fact, this stuff melts ice!

Have a look and a read. Here are the links in the order I discussed them;

Yellowstone algae in hotspring :
Did you know: In biblical times; I beleive it was in excess of 500,000 people died from a toxic algae outbreak which contaminated the water in the Nile River. The cause was the disposal of their waste products into the Nile River.

How to Kill a Lake Entry for September 11, 2007

Taken by me September 03, 2007 at a nearby lake frequented by many.
Grab your towel, let’s go for a deadly dip!

This lake has a lot of history. It has been a very popular recreational destination for decades. There are many cottages on the lake that are summer retreats for those who can afford such luxuries. The lake has for years been photographed, painted, swam in, boated in, jet skiid in, and fished in. It was at one time a stunningly beautiful location to visit and enjoy.

But now as you visit the different vantage points on this fairly large lake, you see a filthy film on top most of the water. It has been noted throughout the summer that there was an eerie absence of insects here too. On the backside of the lake is a private access community with a sign posted upon entry stating that the piped water is neither safe to drink or to cook with. The screws on that sign are beginning to rust.

When you visit the community on the lake you hear that they have not had water to use out there for years, and most of the homes are only retreat use because of this. Everyone knows that this lake is drained once a year due to water quality issues, the details of which no one seems to be familiar with. There was a writeup in a newspaper a few years back about fish being found washed up dead on the banks, for which no satisfactory explanation has ever been obtainable by the residents of the lake. Hmmmmmmmm.

So why then do I go to a park on the lake and find people out on the sandbar in their swimsuits towing their children also in their swimsuits on their way to the water for a swim, as was the case on one of my recent trips to this lake, until they ventured out and saw what I was photographing on the recently exposed sandbar. No signs to say it is not safe to swim in this lake. No shortage of swimmers itch reports either. I don’t know,…….is it just me, or should there maybe be some signage at the very least warning of potential health effects of swimming in this filthy water? The sandbar that I have been photographing is only visible because the lake is being drained. It is usually under water. While under water, what you see in this picture was most likely just assumed to be sand oozing between people’s toes when wading through the water.

I also had a brief chat with a man who was on the sandbar with his two young boys , fishing@!


Did I mention that septic tanks have been draining into the lake for decades? I meant to. This is definitely a relevant piece of the history here. As is the the giant nursery operation on one side of the lake that not only uses the lake water for it’s massive operations, but also makes massive deposits back into the lake that are aiding in killing this lake, and threatening the health of anyone or anything that comes in contact with this lake water.

I got the attention of the Park officials one day out there in my white plastic bags over my boots with my camera and sample containers. One of the park officials told me they have been on well water up until this year. I was informed that every year about mid summer they had to shut down their well as the water was no longer usable, but this year they did not use the well. They shut it down and are on city water.

Okay, all this, but it seems to be okay to swim in and fish in this water. Is this making any sense to you? I sure hope not.

I know that some of what is in this photo is algae, some cyanobacteria, some molds, possibly yeast(s), and the film on the water that looks like oil slick is actually a byproduct of the microbial activity. The film on the water blocks the light from entering the water. If the light cannot enter the water, everything below the surface of the water will start to die. Another bit of bad news for an already greatly stressed lake ecosystem. I asked an environmental consultant what could be causing the layer of clear slime coating everything here. He says farm activity. Nitrates and phosphates from farming operations can cause this, although it is not confirmed at this time that this is the cause. It is never the less a possible cause.

Fact: One known cause of swimmers itch is toxic algae. Pfiesteria is of interest here, or dinoflagellates.

Fact: Raw sewage will cause algae to form. Algae formed as a result of raw sewage presence is harmful to your health.

Fact: During my frequent trips to this location to document it, I suffered an incredibly profound decline in my respiratory function, developed a very sore throat, and the burning sensation in my organs and spine escalated severely, eventually (within 6 days) leading to a sensation of all my organs being bruised. Internal inflammation was in the reactions to me being in the presence of what is at this location. Because I have had previous long term high dose exposure to some or all of what is here, I have a clear reaction to re exposure.

A Lake full of Trouble September 02, 2007

I took this picture August 31, 2007.
“The stuff” in the water is just bordering on the stage where it starts to form bubbles and off gas. The strange thin film (like the skim on milk that has been sitting) is forming, and will thicken and begin to form bubbles. What organisms and/or processes are creating this strange film? Note the rust staining, or iron staining on the rocks that nearly always accompanies this process. It has been suggested to me that a process is taking place that is resulting in the iron being pulled out of the soil.
Thanks to Sarah for bringing this one to my attention. Good tip! Keep em’ comin’. We need more proactive young people in this world.

I mentioned in a previous post that I anticipated this stuff would show up in our lakes given time to accumulate enough mass. People have listened to me over the past 4+ years make my observations, and theorize as to what would happen next. I have had a whole raft of reactions from being viewed as a fatalist, to a nutcase, and/or troublemaker (got to include that one here as it comes up a lot), to a person with eerie insight into the potential impending health trends of humans, animals, and trees based in large part on environmental trend progressions which I have also been anticipating thus far accurately simply by observing and monitoring.
A biologist once commented that I had “an amazingly keen sense of observation. I was picking up on clues that a trained individual may well have missed” I was told. I considered that a very complimentary thing to be told. The more I observe, the more alarmed and concerned I become. Not only due to what is transpiring in the sense of environment and health, but the seeming lack of concern not only by those responsible for environmental management and human and animal health care, but by so many in the business community who see these types of issues only in the context of the threats to their bottom line that they do indeed in many cases have the potential to be.
This upset in our environment at the visible stage has been escalating and spreading for the more than 4 years that I have been actually paying attention. I don’t see it getting better, rather it is getting much, much worse.
This picture is now of part of the bank of a very large lake. There is a skim layer of the early stages of this process (surface level stage) starting to blanket and cover the lake’s water. I expected to see this occur in this very lake due in part to known history in the area that seems to have relevance to other like affected areas. I have said for several years now that this lake was going to go like the ditches were that I was photographing. However, when people demand water testing in this area, due in part to dead fish washing up on the lake shores over the years, any testing that has been done has shown no problem. An all too common conclusion around these parts.
It has been brought to my attention, by I might add, qualified individuals gainfully employed in relevant fields, that in many cases testing is done which does not begin to even remotely address the obvious presence requiring identification and/or analysis. This is in some instances due to ignorance (there’s that word again), and in some cases is a blatantly intentional deceptive stance. In the cases where improper/inadequate/inappropriate testing is done intentionally (as I have been informed is at times here the case), would one not be able to safely hypothesize that the problem, or a problem, is known to exist, and has at least to some degree been identified in full or in part, but that information is not being disclosed?
So if one were to look at the big picture from this angle: Why does the problem appear to be escalating out of control unchecked? Is anything being done at all? Can anything be done? What and/or who caused it?
The whole topic raises far more questions than answers. It seems clear to me that someone has at least some of the answers. So why then does no one want to answer or even discuss the questions?
I can tell you I took some pics of a drainage ditch several miles from here, and found myself being followed when I left, at 110 km hr. To me that says that someone did not like me standing on the shoulder of a public road taking pics of their farm field. Why not? It is just a field. This has happened to me on more than one occasion.
After taking these pictures and the ones at the lake, I became very lethargic, and have been struggling with a massive spike in respiratory difficulty since. My feet got a bit wet through my boots at the lake, and I now have burning skin all the way up to my knees. My organs are cramping up really badly. There are people who live in this area that fall into the pattern of the health trends of which I have become very familiar. Many small pets (dogs and cats) die, usually of cancer in areas where these conditions are found.
Again, no ground dwelling insects. Did see a flock of migratory birds, and a sick looking heron.
This is a nearly identical formation beginning to pick up steam in this lake to the one I found in a drainage ditch in a town a good hours drive away several years ago. It was not in this lake back then, or in any water body this large. At least not in visible mass quantities.
But it sure is now.
Fact: Did you know that fish can be autopsied and the findings used to assess or gauge the water’s affect on humans in the area from which they were collected. This is a practise in use today.

Mysterious honeybee deaths here too. Entry for August 30, 2007

This picture was taken by me recently in between the two towns mentioned in this article. There are what appear to be abandoned honeybee hive boxes in a field beside this spot. I was looking at them trying to figure out if I was right that there was no life in them there honeybee boxes because they looked abandoned.

Well, I had not planned this entry, but look what is in today’s paper. Now it is the bees right in the general vicinity of one of the areas I have been focused on since prior to 2003. So far, the avian influenza, over a million vanishing salmon, and now the bees, and then there is still the human and animal health trends. All right in my back yard metaphorically speaking while I keep getting told there is nothing wrong out here. Okay, is it just me, or is it lookin’ like I could be right and “they” could be lying, oops, I mean wrong.

I found an interesting little Science Teaser as it was called on one of our federal government agriculture related sights a few or four years back. It said that scientists were finding heat resistant fungus in blueberry soil. It is potentially possible to integrate this piece of information into some of the previous posts, including this one. Just thought I’d throw that in there.

Disappearing bees keep sweet industry guessing


Bees have disappeared from Jean-Marc Le Dorze’s hives.

By Kristine Thiessen
Mission Record

Aug 30 2007

Beekeeping is a high-risk business.

A spate of bad weather and a variety of mites can reduce Mission beekeeper Jean-Marc Le Dorze’s 2,000-plus hives by ten or 15 per cent each year.

Le Dorze is used to such losses, but for the first time in his 13 years running Golden Ear Apiaries, adult bees from a number of his hives just simply disappeared. Le Dorze is concerned, because he doesn’t know why. Not knowing “has never happened” to him before, he said.

Honeybees, those fuzzy, buzzing insects, could arguably be called the Fraser Valley’s unsung heroes.

“They’re the workhorse of American and Canadian bees on the pollination side,” said Le Dorze.

And for most consumers, it’s the pollination side that really matters. Honeybees are crucial to increasing berry crops like blueberries and cranberries.

“For blueberries, they can increase the crop by 50 per cent,” said Le Dorze. “They pollinate and then the fruit is larger, sweeter, and more uniform in size.”

To get a decent blueberry, each flower needs to be visited by a honeybee at least four times, explained John Gibeau, a vice president with the B.C. Honey Producer’s Association.

“There [are] about 7 million flowers per acre,” he said. “That’s about 28 million visits.”

In addition to the Fraser Valley’s berries, bees also pollinate pumpkins, zucchini, and “everything from alphalfa to seed oil production,” said Gibeau. “Honey production is probably about one-tenth of the value [compared to bees agricultural value].”

It’s not just Le Dorze’s critters that are dying off.

The Georgia Straight recently reported 23 per cent of B.C.’s colonies were wiped out last winter.

The unexplained disappearance of adult bees has been dubbed “colony collapse disorder,” or CCD.

“If you have a hive that’s collapsing and there’s not many bees . . . then that’s when they consider it CCD syndrome,” said Gibeau. “Bees will normally never abandon their brood.”

But while Le Dorze believes his bee disappearance is CCD, Gibeau chalks up this year’s bee losses in the Fraser Valley to the cool weather.

“The weather was just terrible this year for honeybees,” he said.

“They’re incapable of flying when the weather drops down to five or six degrees [Celcius]. Normally when it begins to cool, the bees come back home, where inside the hive is a nice and toasty 37 degrees.”

The Abbotsford beekeeper said it was the worst year he’s ever had in beekeeping.

Le Dorze agreed that the weather didn’t help.

“April was like this,” he said, gesturing at the cool and damp air one August morning.

However, while the weather played a role, Le Dorze speculates something inside the hives caused two to three per cent of his bees to disappear.

He pulled out trays of honeycomb and bees from the wooden crates that line the ground of his farm. Le Dorze pointed out the queen, the adults, the fuzzy young bees, and the antenna of a new bee emerging through a brown covering that caps the comb.

The brown coverings are the pupa, he explained. If the adults disappear from the hives and leave the brood, secondary pests will consume the pollen, the honey, and the wax.

This year, the pests didn’t enter the abandoned hives right away, and Le Dorze’s guess is that something in the hives discouraged them.

He’s anticipating an American study on CCD scheduled to come out in September, will link a pathogen to the collapse.Other guesses by scientists have ranged from viruses, to a group of pesticides, to a fungus, to new stresses like being trucked long distances.

A good Trichothecene Mycotoxin backgrounder Entry for August 30, 2007

My leg mid 2003
This is a picture of my leg (ankle) in mid 2003, when I lived at my known exposure sight. These are the sores I was getting. They were preceded by severe burning and tingling of the skin with no visible sign of any kind of a problem. This was followed within 2-3 days by bright red skin with increased burning, and the sores began to appear. I noted that the sores seemed to be located within hair follicles of the skin. At this time my hair was falling out in clumps, as it does for people undergoing chemotherapy treatment. I had a severe dry cough, dry mouth, tingling face and hands, very laboured breathing, and a knotting type pain in the area of the right liver lobe. I would wrap my feet in a quilt when I was sitting trying to watch television, listen to music, read, or do any idle activity as it felt like my feet and lower legs were being attacked by something, but I could see nothing there. At times, had visible signs of something going on not have been there, I may have been inclined to think I was going nuts. I noticed I was having involuntary tremoring, like Parkinson’s disease sufferers get. I was losing things. For reasons beyond my grasp, I was putting things where they did not belong, and could not find them. I was scared. I did not know what was happening to me, and no one in the government appointed relevant fields (public health officials, municipal inspectors, BCCDC), or the medical field was accommodating my pleas for answers. I was becoming convinced that I was going to die there.
These sores caused (or came with) an accumulation of clear fluid between the tissue layers that burned like lye.
I complained of blurry vision. Coordination problems, diarrhea, burning urine and stool, tooth pain, sharp chest pains, unexplained bruising with a strange trait,the bruises did not hurt, but these sores………oh my God!, did they burn!They also do something to the skin pigment. They were causing literal loss of pigment, where you would end up with a white scar where the sore was. Some of the sores actually ate away a bit of tissue and left little craters and purple or light brown scars, which are still there. As there were so many hazardous agents mixed together in my exposure, I was experiencing the effects of more than one thing happening to me. Can you imagine?! People still live there! I just stopped by there. Mistake. My feet are tingling like mad, and someone who has only been there a week has severe fatigue, runny nose, stuffed up, and burning tingling skin. This is more than 4 years after I left there. It is in the soil. You can smell it when you are standing in the yard. It is of coarse not only there, as it just does not work like that. It is however there in extremely high quantities. I could not stay inside the building as for one, it was very traumatising being there, and aside from that, I was having a severe reaction to the conditions there and could barely breathe.

This article has very good background summary on this topic.

Trichothecene Mycotoxins

Information on Trichothecene Mycotoxins

Trichothecene mycotoxins are produced by fungi (e.g., Fusaria, Trichoderma, Myrothecium, Stachybotrys); 60 are known. These were originally isolated as possible antifungal microbials or as antiplant agents. Analysis of trichothecene (and aflatoxin) exposures is complicated by their natural occurrence: Their presence alone does not prove a biological attack.

Iraq has admitted to possessing trichothecene mycotoxins and testing them in animals and has been accused of using them against Iran (UNSCOM, 1991, 1992, 1995; Zilinskas, 1997; Heyndrickx, 1984). The report of Iraqi possession of trichothecenes followed a considerable period of interest, attention, and controversy about their use in Southeast Asia (between 1974 and 1981, against Lao and Khmer populations by communist forces) and in Afghanistan (by Soviet forces) (Crocker, 1984; Haig, 1982; Schultz, 1982; Seagrave, 1981). Wannemacher and Wiener (1997), concluded that the Soviets and their clients have used trichothecenes, and the authors present a detailed review of the history of the subject and associated controversy. There may have been shortcomings in the epidemiological approaches (Hu et al., 1989). There were also many difficulties and inconsistencies in agent sampling, transport, and analysis.

These toxins, until discovered in Southeast Asian attack environments, had not been on the usual lists of potential toxin weapons (SIPRI, 1973). Analysts recognized that the toxins could produce the injuries encountered (Watson, Mirocha, and Hayes, 1984). Subsequent research identified properties of military significance, e.g., skin injury from nanogram amounts; eye injuries from micrograms; and serious central nervous system, respiratory, gastrointestinal, and hematological toxicity via multiple routes of exposure (Watson, Mirocha, and Hayes, 1984; Bunner et al., 1985; and Wannemacher and Wiener, 1997).


These mycotoxins have been poisoning people and animals for a long time. They grow well at low temperatures and frequently contaminate grain and other foodstuffs. They have been implicated in food-born illnesses on several continents (Ueno et al., 1984). A large disease outbreak in the Soviet Union during World War II, which involved thousands and had high mortality, was eventually traced to the consumption of grain contaminated by Fusaria molds, which had been left in the fields over the winter. The disease, alimentary toxic aleukia, resembled a severe radiation injury with nausea, vomiting, diarrhea, leukopenia, hemorrhagic diathesis, and sepsis.

These toxins are also hazardous via other routes. Domestic animals and farmers manifested skin and respiratory irritation and systemic malaise from exposure to contaminated dusts and hay. Human illnesses have arisen from trichothecene mycotoxin contamination of houses and ventilation systems, resulting in so-called “sick building” syndrome (Croft et al., 1986; Jarvis, 1985; Smoragiewicz et al., 1993). One family so exposed was affected with nonspecific symptoms whose cause was not identified for months (Myrothecium and Stachybotrys were identified). For a time, several trichothecene mycotoxins were tested as anticancer agents in clinical trials (Thigpen et al., 1981; Bukowski et al., 1982; Yap et al., 1979; Diggs et al., 1978; Murphy et al., 1978; Goodwin et al., 1981). Some laboratory accidents have added to experience with human exposure (Wannemacher and Wiener, 1997). In addition, there is considerable information on the effects of trichothecene mycotoxins on economically important animals (Ueno et al., 1984).

Reports of communist attacks on Lao tribal people, and later on the Khmer, began in 1974 with aircraft and helicopter delivery of colored smokes, dusts, and droplets. People near these attacks had signs and symptoms that did not resemble known chemical warfare agents. Later similar attacks were reported in Cambodia and Afghanistan. Symptoms included vomiting, dizziness, seizures, hematemesis, respiratory distress, hypotension, and blisters. Survivors were ill for a long time with rashes, joint pains, fatigue, and memory problems (Haig, 1982; Schultz, 1982; Crossland and Townsend, 1984).

Investigative teams in refugee camps were puzzled, identifying a t
oxic epidermolysis without other expected findings from known chemical agents (House, 1979), but intelligence analysts recognized the similarities to trichothecene intoxication. Later, clinical examinations, autopsies, laboratory tests, and tissue samples showed trichothecene mycotoxins (and a propylene-glycol carrier) together with tissue damage compatible with trichothecene effects (Crocker, 1984; Watson, Mirocha, and Hayes, 1984; Rosen and Rosen, 1982; Stahl et al., 1985).

Chinese analysts attributed a higher toxicity to trichothecene mycotoxins than to nerve agents. They alleged that, between 1975 and 1982, 6,000 Laotians; 1,000 Cambodians; and 3,000 Afghans had died from attacks with what came to be known as “yellow rain” (Fang, 1983).

During the Iran-Iraq War, especially in the fighting around Majoon Island, colored smokes and powders were used against Iranian forces, perhaps reflecting combinations of agents. Although controversial in the scientific community, Heyndrickx (1984) found trichothecene mycotoxins in Iranian casualties who appeared to have sustained mustard injuries. Although other laboratories did not confirm these findings from the same material, Professor Heyndrickx argued that biological tissues had degraded the toxin over time.[7]

It is not known if, during the Gulf War, any of the Iraqi chemical and biological facilities hit by Allied fire contained trichothecenes. Trichothecenes are very resistant to environmental degradation and resist heat below 500��F; hence, the production of effects after long-distance transport following explosive release is possible but unlikely because the chemical would be very diffuse by that time (U.S. Army, 1990; Wannemacher and Wiener, 1997; Trusal, 1985). However, no events described during the war closely correspond to known acute effects of trichothecene syndromes. Lethal effects require substantial doses (milligrams), but eye and skin irritation can occur at much lower levels (U.S. Army, 1990; Wannemacher and Wiener, 1997; Coulombe, 1993), raising the remote possibility that low-level exposures might have been misinterpreted as being due to some other cause.


Production using contemporary fermentation methods similar to those of brewing and antibiotic production is easy and inexpensive, and conventional bioreactors can readily produce tons of these agents (Wannemacher and Wiener, 1997). AD Little (1986, Ch. 4) described the conditions defining production. The large-scale production of Fusaria and trichothecenes for civil purposes in the former Soviet Union indicates the ease of large-scale production for other purposes (Buck et al., 1983). Formulations of T-2–one of the most potent trichothecenes–might also include polyethylene glycol, sodium lauryl sulfate, or dimethylsulfoxide (DMSO). These materials facilitate dispersal and handling of the toxin, possibly enhancing toxicity. Trichothecenes do not degrade to nontoxicity when exposed in the natural environment (for weeks at least) and are stable when stored. They can be delivered by mortars, artillery, free rockets, aerial bombs, and surface or aerial sprayers (Wannemacher and Wiener, 1997). Iraq possessed all the systems previously used to deliver trichothecenes.

T-2 is a skin-damaging agent of great potency (Bunner et al., 1985)–several hundred times more potent than mustards or lewisite (Wannemacher and Wiener, 1997). It is able to injure the eye in microgram amounts, which again indicates that it is more potent than mustards.

Toxicity by inhalation is comparable to mustards. NAS (1983) estimated that LC50 exposures of aerosols of 1 mg/m3 or surface contamination or LD50 of 1 g/m2 could readily be attained.

Trichothecenes readily result in vomiting, rather promptly at low concentrations, which might compromise the ability of exposed troops to use protective respirators. Other symptoms, including mild incapacitation, follow. Operationally, the persistence of trichothecenes makes them a threat even to military forces with protective equipment; Soviet troops in Afghanistan avoided operating in areas where these toxins were used (Fang, 1983). There are some indications that trichothecenes may have been used in combination with other agents in Southeast Asia and Afghanistan (Fang, 1983; Schultz, 1982).

Chemical and Physical Properties

The trichothecenes are classed as sesquiterpenes (Ueno, 1983). The members of this family of toxins vary depending on their side groups and include T-2, HT-2, nivalenol, deoxynivalenol, anguidine, diacetyoxyscirpenol (DAS), and crotocin.[8] When the toxins are extracted from fungal cultures, a yellow greasy residue remains. Had the various reported Asian attacks involved a crude extract containing some of that residue, the result might have been the yellow rain reported. The toxins are stable in air and light for weeks and can withstand heat; a temperature of 500��F is required to destroy T-2 (Trusal, 1985; Wannemacher and Wiener, 1997).

These toxins can be inactivated with 3- to 5-percent hypochlorite solutions (Wannemacher and Wiener, 1997). The toxins are relatively insoluble in water but are soluble in acetone, chloroform, DMSO, glycols, ethanol, and other organic solvents. They have a peppery odor and negligible vapor pressure. Detection

No military field detection systems currently deployed can detect trichothecenes, although laboratory techniques (e.g., antibody-ELISA, gas chromatography or mass spectroscopy, and thin-layer chromatography coupled to fluorimetry) have been used. Biological detection systems using animals are neither specific nor easy (Fontelo et al., 1983; Mirocha et al., 1984; Thompson and Wannemacher, 1984; Rosen and Rosen, 1982; NAS, 1983). Wannemacher and Wiener (1997), reviewing confirmatory procedures, indicated that mass spectroscopy is the procedure of choice, requiring little specimen “cleanup” and enabling detection of one part per billion (ppb) of toxin. More-complex systems being evolved may detect 0.1 ppb.

Toxicology and Toxicokinetics

Mechanisms of Action. The many mechanisms by which trichothecenes produce toxicity are varied, and their relative importance in producing illness is not fully understood (Coulombe, 1993). They include the following:

inhibition of protein synthesis, thought to be the most important effect (Ueno, 1983; Ueno et al., 1984; Tutelyan and Kravchenko, 1981)

inhibition of DNA synthesis (Thompson and Wannemacher, 1984), which might contribute to their radiomimetic properties

impairment of ribosome function (NAS, 1983; Coulombe, 1993; Tutelyan and Kravchenko, 1981)

inhibition of mitochondrial protein synthesis (Pace et al., 1985)

induction of reparable single strand breaks in DNA

immunosuppression, allowing secondary and opportunistic bacterial infections and possibly delayed hypersensitivity (Ueno, 1983; Yarom et al., 1984; Jagadeesan et al., 1982).

Trichothecenes react readily with thiol groups and, at low concentrations, inhibit thiol enzymes (e.g., creatine kinase, lactate dehydrogenase) (Tutelyan and Kravchenko, 1981; Ueno et al., 1984). They can be incorporated into lipid or protein elements of cell membranes. Tissue culture studies show alteration of membrane function (Coulombe, 1993; Pfeifer and Irons, 1985). Sulfhydryl effects in cell membranes are important in cell-to-cell interactions in the immune system. T-2 toxin induces cell membrane injury with hemolysis, apparently via a free-radical mechanism (Segal et al., 1983; Coulombe, 1993). Metabolism may be more important in detoxification than in producing toxicity.

Unlike the aflatoxins that require metabolic activation, the trichothecenes are directly toxic without activation, as their prompt effects on the gastrointestinal mucosa with epithelial cell necrosis suggest (Busby an
d Wogan, 1979).

T-2 and other trichothecene toxins are deacetylated in the liver.

Metabolites are also toxic but less so than T-2 (Ueno et al., 1984). Carboxyesterases (-SH serine esterases) in liver microsomes hydrolyze T-2 to the less potent HT-2. These enzymes may be clinically important. Inhibition of this enzyme by paraoxon (an organophosphate pesticide) in subclinical doses increases the toxicity of T-2 in mice (Johnsen et al., 1986). Other potent inhibitors of this enzyme are tri-o-cresyl phosphate (TOCP, an organophosphate), eserine (a carbamate), and diisopropyl fluorophosphate (DFP, a weak organophosphate nerve agent) (OSRD, 1946). These all inhibit hydrolysis of T-2 (Johnsen et al., 1986). This raises the strong possibility that similar compounds, such as PB; low levels of nerve agent; or other carbamate or organophosphate insecticides might enhance the toxicity of T-2 or other trichothecenes at low levels.

Exposure-Effect Relationships

T-2 toxin and other trichothecenes are absorbed slowly (12 to 24 hours) via the intact skin but rapidly through abraded skin. DMSO or similar penetrants can increase the rate of absorption, but even then the systemic toxicity appears slowly (Bunner et al., 1985; Schiefer, 1984; Kemppainen et al., 1986a, 1986b; Solberg et al., 1990).

The rapid appearance of symptoms after respiratory exposure in humans, along with the results of animal inhalation studies, indicates rapid absorption and high retention of aerosolized T-2 toxin, with the respiratory tree retaining small amounts (Creasia et al., 1987).[9] Tritium-labeled agent and immunoperoxidase studies have also been used to follow the distribution and disposition of T-2 toxin (Pace et al., 1985, Lee et al., 1984). Intramuscularly injected agent is distributed to liver, kidney, lung, and other tissues within 30 minutes. The plasma concentration has a biphasic course, with half-lives of 1.8 and 50 hours for the two phases. T-2 toxin and metabolites concentrate in bile with evidence of enterohepatic circulation. The liver and kidney are the main organs for detoxification. Oral intoxication showed T-2 toxin in the gastrointestinal tract and kidneys, but not in the liver, reflecting rapid hepatic metabolism. The brain showed a rapid uptake to levels higher than plasma but below many other tissues, with a rapid fall to levels similar to plasma in six hours. One would expect trichothecenes to enter the brain readily, since they are lipophilic (Wang, Wilson, and Fitzpatrick, 1992).

It has been shown, for example, that the effects of sustained low doses can accumulate to the clinical picture associated with alimentary toxic aleukia (Mayer 1953a, 1953 b; Lutsky et al., 1978). Or they can yield the more diffuse problems that Croft et al.(1986) and Jarvis (1985) reported: a case of ongoing illness for several years in a family of five, with recurring respiratory illness, flu syndromes, sore throats, diarrhea, cough, headaches, fatigue, and episodes of alopecia. One man had leg pains. Eventually, trichothecenes were identified in air ducts and ceiling material in the family’s house. Material extracted from these areas was toxic to rats and mice. Croft cited other reports by Forgacs (1972) of toxin exposures producing similar symptoms with central nervous system andneuropsychiatric manifestations.[10]

Respiratory is high and comparable to parenteral injections. Oral and dermal lethal toxicities are lower but produce similar systemic effects (Creasia et al., Dose Effect).


Skin Exposures

5-50 ng in liquid Min. erythema dose (guinea pig, rat) Ueno/Wannemacher et al. (1983)

209 ng/cm2 in liquid Min. erythema dose (monkey) Wannemacher/Bunner et al. (1983)

1 ��g/cm2 Irritation (guinea pig, rabbit) Fairhurst et al. (1987)

2 ��g Vesication, skin injury Bunner (1983)

0.25 mg/kg Severe illness, diarrhea (monkey) Bunner et al. (1983)

1.5 mg/kg in DMSO LD50 (rat; mean time to death, 19 hr.) Wannemacher (1983)

4.2 mg/kg in methanol LD50 (guin pigs; time to death 190 hr.) Wannemacher et al. (1983)


1 ��g Detectable corneal injury USAMRIID (1983)

2 ��g Severe corneal injury, conjunctivitis Bunner (1983)


0.24 mg/kg (abs) Mouse LD50 Creasia et al. (1987)

0.05 mg/kg (abs) Rat LD50 Bunner et al. (1985)

0.6-2.0 mg/kg (abs) Guinea pig LD50 Wieser (1997, p. 661)

5,479 mg-min/m3 Guinea pig LD50 AD Little (1986)

200-1,800 mg-min/m3 Estimated LCT50 U.S. Army (1990)

Systemic Toxicity

500 ��g/kg Estimated human LD50 U.S. Army (1990)

470 ��g/kg intram. Rat LD50 Bunner et al. (1985)

1.17 mg/kg Rat LD50 Bunner et al. (1985)

650 ��g/kgintram. Monkey LD20 Cosgriff et al. (1986)

790 ��g/kg intraven. Monkey LD50 AD Little (1986)

850 ��g/kgintram. Rat LD50 Chan and Gentry (1984)

111 mg/kgintram. Rabbit LD50 Chan and Gentry (1984)

Oral Toxicity

0.1-0.2 mg/kg Swine, emesis Busby and Wogan (79)

0.1-1.0 mg/kg Swine, diarrhea Ueno (1983a)

2.29 mg/kg Rat LD50 Bunner et al. (1985)

3.06 mg/kg Guinea pig LD50 AD Little (1986)

1.0 mg/kgb Male monkey LD100 Rukimi, Prasad, and Rao (1980)

1 5 mg/kg Estimated human LD50 U.S. Army (1990)

aNo primate data were located. bPer day for 15 days 1987; Bonomi et al., 1995; Wannemacher et al., 1993; Schiefer and Hancock, 1984).[11]

For less-than-lethal dosages and for all routes of administration, sequelae of leukopenia, thrombocytopenia, bleeding tendency, weakness, diarrhea, dyspnea, recurrent infections, vomiting, anorexia, and weight loss are expected. Other sequelae of acute exposures include prolonged rashes, joint pains and fatigue (Schultz, 1982), fever, chills, hypotension, confusion, somnolence, seizures, memory loss, hallucinations, and burning erythema (Belt et al., 1979; Murphy et al., 1978; Yap, et al., 1979; Diggs et al., 1978; Bukowski et al., 1982; Thigpen et al., 1981; Crossland and Townsend, 1984).

Pathology and Pathophysiology

The clinical manifestations of trichothecene intoxication are derived from several sources. They are summarized here prior to more detailed treatment of individual organ systems.

Known effects from evidence other than the yellow rain attacks are nausea, vomiting, seizures, central nervous system dysfunction, chills, fever, hypothermia, hypotension, epithelial necrosis, myelosuppression, and gastroenteritis with hematemesis and melena (bloody vomiting and stools). In the yellow rain attacks, the Hmong victims were probably exposed by several routes, including dermal, respiratory, and oral (the last from swallowing larger particles trapped in upper airways and returned to the oropharynx by ciliary action (Wannemacher and Wiener, 1997). Vomiting was induced and lasted several days. There was a feeling of intense heat, itching and burning of the skin, dizziness, tachycardia, chest pain, headache, and decreased vision. Within hours, victims reported intense eye pain, red eyes, bleeding gums, and hematemesis. Trembling was common, and some patients had seizures. Severe itching ensued with the formation of small hard blisters, some of which were hemorrhagic, occasionally progressing to large bullae. Abdominal pain and bloody diarrhea continued (Watson, Mirocha, and Hayes, 1984).

Khmer yellow rain ca
sualties had similar acute symptoms (Crossland and Townsend, 1984) with the following longer-term effects: intermittent weakness, anorexia, reduced memory and ability to concentrate, intermittent diarrhea, impotence, increased fatigue, cough and dyspnea, increased susceptibility to infection, and suspected increases in fetal abnormalities and spontaneous abortions (Haig, 1982; Schultz, 1982; Watson, Mirocha, and Hayes, 1984; Stahl et al., 1985; Crossland and Townsend, 1984). It must be noted that the Hmong cases with memory loss that Crossland described were not evaluated for the presence of toxins. These persons had undergone a harrowing experience, having been attacked, seen kinfolk die, fled, and become refugees. Severe apathy, confusion, and depression are common in survivors of natural or man-made disasters.

A limited autopsy was performed on a Kampuchean man injured in a toxic attack in February 1982, who died a month later having initially showed signs of recovery, then developing fever, jaundice, heoptysis, and anariax coma. Malaria was ruled out. The heart tissues showed interstitial myocardial hemorrhage and acute myocarditis, while the lungs showed only pulmonary edema. There was diffuse hepatitis with micronodular cirrhosis, as well as acute renal tubular necrosis. Tissues showed T-2 toxin in amounts ranging from 6.8 to 80 ppb, but there is little information with which to interpret the findings. The pathologist considered them to be compatible with mycotoxin poisoning (Stahl, Green, and Farnum, 1985).

Four stages were identified in the early Soviet Fusaria consumption incidents (a chronic oral exposure) (Mayer 1953a, 1953b):

Stage One begins within a few hours and lasts three to nine days. It consists of mild inflammation of the mouth and gastrointestinal tract, gastroenteritis, nausea, vomiting and diarrhea.

Stage Two is a quiet period of two weeks or more with few symptoms even while contaminated grain was still being ingested. There were laboratory abnormalities in some patients, but most appeared well.

Stage Three reveals the results of bone marrow aplasia with hemorrhagic diathesis, oral mucosal necrosis, and multiple infections.

Stage Four is a period of convalescence requiring several months after ingestion stopped.

Grain elevator workers are in a complex environment with dusts, plant products, and trichothecenes. They frequently experience coughing, breathlessness, wheezing, fever, and dermatitis (Kemppainen et al., 1986b); similar problems occur in “sick” buildings (Hendy and Cole, 1993; Jarvis, 1985).


Rats, mice, and guinea pigs die rapidly from large respiratory exposures (1 to 12 hours) but show little sign of pulmonary injury, unlike direct effects on gastrointestinal mucosa (Creasia et al., 1987; Wannemacher and Wiener, 1997; Bunner et al., 1985). At low levels of respiratory exposure, coughing and upper respiratory irritation occur. Higher exposures produce pulmonary edema, collapse, hypoxia, and death within a few hours, or more indolent symptoms with later pulmonary hemorrhage, hypotension and shock, edema, or infections (Rukmini, Prasad, and Rao, 1980; Lutsky et al., 1978; Bunner, 1983; Bunner et al. 1985). Fifty Hmong survivors reported the following: smell of gunpowder or pepper (14 percent), rhinorrhea (28 percent), nasal itching (14 percent), sore throat (40 percent), aphonia (26 percent), cough (60 percent), dyspnea (52 percent), severe chest pain (52 percent), and hemoptysis (18 percent). Systemic signs (vomiting, tachycardia, hypotension, etc.) follow. Oral or intravenous exposures result in pulmonary edema, hemorrhage, consolidation, and secondary pulmonary infection.

Toxicity by the respiratory route may be influenced by the material used to suspend the toxin (Creasia et al., 1987). Fibrinous exudate may be seen, and pulmonary fibrosis was a late complication in some of the trichothecene cancer trials (Goodwin et al., 1981). In contrast to inhaled ricin, where effects are confined to the lungs, respiratory exposure produces much less pulmonary change and pronounced systemic toxicity.


Conjunctivitis begins several hours after exposure, although the mechanism of the immediate visual disturbances is unclear. Corneal changes begin at 12 hours, with the peak effect in 24 to 48 hours. Blurred vision continues, with recovery from mild injuries in three to seven days. Hmong yellow rain victims reported eye pain and burning (68 percent), blurred vision (58 percent), and tearing (47 percent). Eyelid edema and scleral inflammation are associated with more-intense exposures. Corneal thinning can follow toxin exposure, with irregularities lasting up to six months (Bunner, 1983).


The skin responds to nanogram amounts of toxin with edema and inflammation. T-2 administered with DMSO to animals produced almost no local reaction (Bunner et al., 1985), but the systemic effects were substantial, although delayed, and cutaneous LD50s were elevated, compared to application without DMSO.

Dermal application can produce the same effects as oral administration: bone marrow, thymus, and lymphatic changes and gastrointestinal effects (Schiefer, 1984; Wannemacher et al., 1983).

Despite decontamination, a burning sensation developed from 4 to 24 hours in the contact area, followed by numbness. In cancer trials, erythema, burning stomatitis, and alopecia were common (Schiefer and Hancock, 1984; Murphy et al., 1978; Bukowski et al., 1982; Diggs et al., 1978; Belt et al., 1979; Yap et al., 1979; Thigpen et al., 1981; Goodwin et al., 1981). Hmong survivors reported persistent burning sensations, with tingling, itching, and pain lasting several hours. Some numbness lasted two days to several months in some victims. Scattered erythema was noted after a few hours, but only 23 percent reported blisters. In some cases, large hemorrhagic bullae occurred, with underlying necrosis. Necrotic areas sloughed easily when corpses were moved (Wannemacher and Wiener, 1997). Sequelae include secondary infections, hyperpigmentation, and recurrent rashes.


T-2 and other trichothecenes readily injure the rapidly dividing cells of the gastrointestinal tract. Tissue responses include edema, cytolysis, and sloughing, with loss of gastric epithelium and villus tips (Lee et al., 1984; Rukmini, Prasad, and Rao, 1980). The trichothecene DAS given intravenously showed marked gastrointestinal tract necrosis (Coppock et al., 1985) and pancreatic damage resulting in hyperglycemia. Some jaundice was seen in yellow rain victims. The liver is involved in detoxification, but liver failure is rare (Lutsky et al., 1978). Liver enzymes and amylase rise initially but return to normal in three to seven days (Bunner et al., 1985). As a later consequence, the bowel may become less resistant to bacterial penetration, which can increase susceptibility to infection (Lutsky et al., 1978).

Nervous System

The central nervous system effects are striking. Animals and humans exposed via the respiratory route show early central nervous system signs and symptoms. Symptoms reported from cutaneous exposures–burning pain followed by numbness–suggest that these toxins may directly affect the peripheral nerves.

The early and sustained vomiting suggests direct central nervous system effects involving chemotactic and vomiting centers. Hallucinations are a distinctive feature of trichothecene intoxications. Headaches, drowsiness, anxiety, confusion, and seizures occur, but their mechanisms have not been studied (Yap et al., 1979; Thigpen et al., 1981; Bukowski et al., 1982).

There are
few autopsy reports. DAS-poisoned swine showed cerebral hemorrhages (Coppock et al., 1985), while other animal studies showed meningeal bleeding and scattered petechial hemorrhages (Ueno et al., 1984). Experimental studies show alterations in levels of hydroxyindoleacetic acid and seratonin in the brain, with regional norepinephrine increases. Trichothecenes make the blood-brain barrier permeable to mannitol, although not dextran (Wang, Wilson, and Fitzpatrick, 1992). Intracerebral administration of T-2 decreased learning in mice, and intraperitoneal administration disturbed both learning ability and memory (Umeuchi et al., 1996).

The descriptions of chemotherapy patients (Thigpen et al., 1981; Yap et al., 1979), home exposures (Croft et al., 1986), and yellow rain cases (Watson, Mirocha, and Hayes, 1984; Crossland and Townsend, 1984) convey a picture of neurotoxicity, with somnolence, confusion, tremors, depression, weakness, malaise, and memory problems (some of which resemble findings in some Gulf veterans). In the cases just cited, however, symptoms appeared promptly, and there were other conspicuous indications of exposure.

Cardiovascular, Lymphatic, Hematologic

Among yellow rain victims reported chest pain, sometimes crushing, along with weakness. Animals poisoned with T-2 develop tachycardia and later bradycardia. Hypotension occurs early and may persist for several days, sometimes proceeding to shock. Hypotension and orthostatic hypotension were common in chemotherapy patients (7 to 40 percent) (Yap et al., 1979; Thigpen et al., 1981; Murphy et al., 1978; Bukowski et al., 1982). Mucous membranes are bright red, reflecting vasodilation. Commonly, hemorrhagic foci are found throughout the myocardium (Ueno et al., 1984; Stahl et al., 1985), and the electrocardiogram may show a prolonged P-R interval and prolongation of the QRS and QT intervals, reflecting conduction system abnormalities and increased risk of arrhythmias.

Beginning with the alimentary toxic aleukia diagnoses, bone marrow and lymphatic system injury has been a consistent finding (Mayer 1953a, 1953b; Ueno et al., 1984). Cell culture studies show stem cells to be sensitive to T-2 toxin. Mycotoxins produce profound alterations in hemostasis, as noted in yellow-rain cases and documented by primate studies (Cosgriff et al., 1986). Prothrombin and activated partial thromboplastin times are increased early in intoxication from decreased coagulation factors. Lethal hemorrhage risk is greater because T-2 inhibits platelet aggregation (Yarom et al., 1984).


There are clinical signs of muscle involvement. The among complained of weakness, fatigability, tremors, and cramps. Animals show flaccid weakness after T-2 poisoning. The early elevation of serum creatine kinase could reflect muscle or cardiac injury, or both. Isoenzyme studies have not been reported (Bunner, 1983).

Impaired immunity and infection resistance is another effect of these toxins. The ability of leukocytes to kill bacteria is impaired (Yarom et al., 1984); immunoglobulin levels are depressed; and cell-mediated immunity is suppressed (Jagadeesan et al., 1982; Schiefer, 1984; Ueno et al., 1984).

Renal output decreases after T-2 intoxication, and the toxin is found in substantial amounts in the kidney. Observed tubular necrosis could be related to hypotension and liver disorders

The endocrine effects of T-2 and other trichothecenes are not prominent. Adrenal cortical necrosis from T-2 exposure has been reported in rats (Thurman et al., 1986). Decreased spermatozoa production has been seen in several species.


The literature on trichothecene interactions is limited. Combining aflatoxins and trichothecenes may increase toxicity (Schultz, 1982; U.S. Army, 1990). No reports emerged of studies examining combined inhalation exposures. There were indications of synergism in feeding studies of chickens (Huff et al., 1988). (However, a study of DAS and aflatoxin in lambs did not show any enhanced toxicity from combined oral exposures of these toxins (Harvey et al., 1995). There is a strong possibility that the severity of trichothecenes could be potentiated by exposure even to low levels of organophosphate pesticides, carbamate pesticides or pretreatments, or low levels of nerve agent, through inhibition of carboxyesterases involved in detoxification (Johnson and Read, 1987). Drugs inducing the increase of detoxifying enzymes, such as epoxide hydrolase or cytochrome P450, may favorably interact to decrease toxin severity. Such drugs as phenobarbital, metoclopramide, metochlopramide carbamazepine, metyrapone, and clofibrate have shown beneficial effects in animal models (Fricke, 1993; Wannemacher and Wiener, 1997).

What to Look for in the Gulf Context

Because of the high sensitivity of the skin and eyes to trichothecenes, injuries to these organs should be looked for in unit medical records. Conjunctivitis, erythema, burning skin, and blurred vision were followed by nausea, vomiting, and diarrhea might increase suspicion of trichothecene exposure.[12]

Summary and Recommendations

The trichothecenes are credible biological warfare toxins for some purposes. However, there is no proof or even a strong indication of their use against U.S. forces in the Gulf. With more concentrated exposure, hematological changes, seizures and other serious sequelae might have been expected.

Current information arises from clinically recognized exposures or laboratory research. Trichothecenes have multiple toxic effects with potential long-term consequences, such as central nervous system injury, immune suppression, and prolonged disability. The sequelae noted in the Hmong, e.g., long-term memory problems; the animal memory studies; and the story of the household exposure may resemble some features of the illnesses in Gulf War veterans, but the expected hematological alterations have not been reported among Gulf War patients. Furthermore, the Hmong effects resulted from substantial exposures with major short-term consequences. Little is known about the behavioral effects of sustained low-level exposures. The extreme sensitivity of the skin and eyes to T-2 and other trichothecenes makes it unlikely that delayed systemic illnesses in Gulf veterans represent a late effect of exposure to toxin “fallout.” One would have expected an “epidemic” of painful dermatitis and conjunctivitis, as well as a number of other symptoms, which would have drawn attention to the exposure.

As in other cases, the AFIP should be consulted. The tests for trichothecenes are not routine, but have been used enough to be considered more than experimental. The AFIP might be consulted about the possibility of detecting trichothecene metabolites in tissue specimens obtained from the Gulf and immediately after. If used protective mask filters from the war period become available, it might be possible to analyze them for the presence of trichothecenes, which are very stable molecules. Had trichothecenes been used, it is possible that their toxicity might have been increased by interactions with nerve agents or PB, although this has not been studied explicitly.

To see actual article go here:

Pathology of Trichothecene Mycotoxins on and/or in Man Entry for August 28, 2007

The above photo is taken from my own pathology report. In the report the caption below the photo reads:

In Sub-Dermis please note fat cells with some evidence of increased staining indicating Fibrinous Inflamation of the fat cell membranes as observed in these lipomas. This is a large artery that demonstrates severe fibrinous inflamation of lumenal surface leading to almost occlusion of the vessel. This is consistently observed with Trichothecene Mycotoxin Exposure and places this patient into high Stage 2 and early Stage 3 of Trichothecene Mycotoxicosis. 150X

My pathology workup and report was done by the man in the following article (William A. Croft, D.V.M., PhD.), as was this photo. This article explains the stages of progression of the health effects of such exposure, and I hope it will be read by many as this stuff is far more widespread in the environment than any of us might like to believe. I am a living example of it’s harmful deadly effect. For some it brings about a very rapid death, and for others it is slow and extremely painful. I had produced a list of my own symptoms before meeting Dr. Croft. It was an almost identical list. It took a long time to find a medical professional that saw a recognizable pattern to my strange (complex as it is termed) set of symptoms. A lot of time was wasted. Time is a killer with this type of undiagnosed condition. Although this is only one of a battery of microbiological insults found ravaging my system, this one is key. It is of the most harmful and would prevent solutions to the other invaders from being of any usefulness, which I will discuss in separate entries here.So here is the article from the man who recognized my complex symptoms pattern when no one else did:

Abstract Information & Notes

William A. Croft, D.V.M., Ph.D. Date of talk: Thursday, June 19, 2003, 2:00pm

Environmental Diagnostic Group Inc. Phone: 715/757-3756

521 Hilltop Dr. Fax: 715/757-9302

Madison, WI 53711 E-mail:

Veterinary School Attended: University of Minnesota

Medical School Attended: University of Wisconsin, Madison, Wisconsin

Major and date of Graduation: Ph.D. in Medical Pathology from the University of Wisconsin, Madison, Wisconsin.

Current Job Description: Study Human diseases within the environment from outbreak of human disease as a Medical Pathologist.

Other Information: Was on Faculty of the University of Wisconsin as Medical Pathologist, was accepted by the National Institute of Health as a Medical Pathologist, qualified to research human diseases. Obtain over $900,000 of highly competitive research grants from the national Institute of Health while at the University of Wisconsin.

Disclosure Statement: None

SPEECH TITLE: ���Pathology of Trichothecene Mycotoxins in Man���

The speaker has provided the information below.

1.) Goals and objectives: To demonstrate the pathologic changes in the primary target organs after inhalation verses ingestion exposure to Trichothecene Mycotoxins in man.

2.) Outline of talk/abstract: A. History of Mycotoxicosis, B. Detection of “Sick Buildings��� ingestion verses inhalation exposure. Signs and Symptoms expressed by over 6,000 patients exposed to Trichothecene Mycotoxins, attempting to establish diagnosis. C. The pathologic changes associated with inhalation exposure to trichothecene mycotoxins. D. The primary organs involved with inhalation Mycotoxicosis.

3.) Conclusion of what is to be learned: The primary target organs of this disease and how this mycotoxin affects every cell in the body.

4.) References:

a. Croft, W.A., Jarvis, B.B., and Yatawara, C.S.,: Airborne Outbreak of Trichothecene Toxicosis, In: Atmospheric Environ, 20(3), 549-552 (1986).

b. Croft, W.A., Jastromski, B.M., Croft, A.L., and Peters, H.A., “Clinical Confirmation of Trichothecene Mycotoxicosis In Patient Urine,” In: Journal of Environmental Biology 23(3), 301-320 (2002).

The Pathology of Trichothecene Mycotoxicosis In Humans

1. The Fingerprint of the Agent Causing the Disease is Displayed Within the Cells or Tissue of The Body.

2. Degeneration and Necrosis of The Entire Central Nervous System, Cardiovascular, lung, Digestive Tract, Spleen, Liver, Kidney, Pancreas, Immune, Skin, Reproductive, Eye, Urinary Bladder and Prostate.

3. The Signs and Symptoms Described For Trichothecene Mycotoxicosis Match the Pathology Observed.

4. Every Cell in The Body is Affected or Susceptible to Trichothecene Mycotoxins When Exposed.

5. The Exposed Cells Are Not Allowed to Grow and Make Cellular Products in The Rough Endoplasm Reticulum Represents of First Mechanism of Action on The Cells.

6. The Burning or Denaturation of Tissue From the Epoxide Molecule is Another Mechanism of Action on The Cells of The Body Causing Intense Scarring of Organs. (Like Phenol)

7. The Rapidly Turnover Organs Systems Are Affected The Most Severe, G.I. Tract, Immune System and Reproductive, (like radiation damage)

8. The Central Nervous System is Severely Affected and is A Primary Target Organ. The Neurons in the Cerebral Hemispheres, White and Grey Matter, Brain Stem and even the Ependymal Cells. The Purkinje Cells of The Cerebellum Are Severely Affected That Affect Motion and Balance. The Dorsal and Ventral Motor Neurons Are Destroyed Causing Amyotrophic Lateral Sclerosis. Peroxidation of Peripheral Nerves is Also Observed. The Central Nervous System is The Organ Most Affected as Reported By People Exposed to Toxic Mold.

9. Lack of Cellular Production, Epoxide- Peroxidation of Lipid Membranes, Loss of Vessels, Loss of Oxygen From Severe Lung Scarring, and Loss of Proper Nutrients Due Loss of Functional Absorption of Intestine Affect the Brain and All Organs of The Body.

10. The Trichothecene Mycotoxins are Cumulative in Their Health Effects on Organ Systems.

11. Trichothecene Mycotoxins are ���Hit and Run��� Poisons and are not Stored in The Body.

12. Inhalation of Trichothecene Mycotoxins Are More Poisonous As Observed by The Intense Scarring of The Alveolar Tissue Than Consumption Due To The Neutralization of Mycotoxin by Bacteria.

13. Depression of the Immune System Allows for Increase Infections by Bacteria, Viral, Fungal and Cancer to Form.

14. Yeasts are allowed to Colonize the Intestine Tract Because They Are Resistant to Trichothecene Mycotoxins.

15. Yeast Can Cause Diabetes Mellitus, Gout and Prevent Proper Liver Function to Detoxify Xenobiotics.

16. Trichothecene Mycotoxins are Released Within the Urine and Feces as Evidenced by The Pathology Observed Within Those Tissues.

17. Children Exposed to Trichothecene Mycotoxins are 100 to 1000 X more suscep
tible because stems are killed not allowing for additional growth within the individual.

18. There is No Safe Level of Exposure to Trichothecene Mycotoxins.

19. The third Mechanism For Trichothecene Mycotoxicosis is To Develop Anaphylaxis to Mold Allergens When Mycotoxin Leaves The Body.

Dr. William Croft, (Medical Pathologist)

Stages of Mycotoxicosis: For Inhalation of Mycotoxin

The three Stages (1-3) ranging from lower to higher severity of poisoning were modified according to exposure via the air as opposed to ingestion already established (Forgacs et al., 1962; Joffe, 1971). A separate Stage of convalescence occurs when a patient is completely removed from the contaminated premises and the source of mycotoxin or mold spores.

Stage 1: The primary changes are in the brain, respiratory and immune systems, mucus membranes and gastrointestinal tract. Signs and symptoms may include burning sensation in the mouth, tongue, throat, palate, esophagus, and stomach, which is a result of the action of the toxin on the mucous membranes and skin in the exposed areas. Moist areas of the body armpits, under breasts, belt line and groin are more sensitive or first affected. Patients may report burning within the eyes, ears and nose. Patients also reported that their tongues felt swollen and stiff. Mucosa of the oral cavity may be hyperemic. Mild gingivitis, stomatitis, glositis, and esophagitis developed. Inflammation, in addition to gastric and (small and large) intestinal mucosal, resulted in vomiting, diarrhea and abdominal pain. Excessive salivation, headache, dizziness, weakness, fatigue and tachycardia were also present.

There may be fever and sweating. The respiratory system develops burning sensations and congestion. Severe exposure to mycotoxin within the lungs may lead to congestion, edema and failure, due to caustic action. Body temperature remains normal and controllable by the patient. The poisoning appears and disappears relatively quickly in this Stage with the exception of, lungs and central nervous system. Initially (Stage 1), the patient���s symptoms are very uncomfortable or painful. As the poisoning continues and the patient progress toward Stage 2, he or she becomes accustomed to the presence of the mycotoxin and a quiescent period follows due to lack of nerve sensation. Depending on exposure levels, the first Stage may last from 3 – 9 days. In scoring the 50 signs and symptoms listed in Tables-1 and 2, an average score range of 20-45 represents Stage 1.

Stage 2 : This Stage is often called the latent Stage or incubation period because the patient feels apprehensive, but is capable of normal activity in the beginning of this Stage. Every organ of the body is affected by degeneration and necrosis with continued exposure. The primary target organs for an individual become evident over time, due to biological variation. These are disturbances in the central and autonomic nervous systems resulting in headaches, mental depression, loss of short-term memory, loss of problem-solving ability, various neuropsychiatric manifestations, meningism, severe malaise and fatigue, narcolepsy, loss of temperature control, hyperesthesia or numbness of body areas, and cerebellar dysfunction including hypotonia, attitude and gait, dysmetria, asthenia, vertigo, disturbances of speech, and loss of balance (Best, 1961). Spinal cord degeneration may also be observed in gait and reflex abnormalities, such as the ability to drive vehicles, ride bicycles or pass sobriety tests (inability to tolerate ethyl alcohol). Attention deficient disorder may be observed in children. Various systems may include: Eyes: visual disturbances, floating objects, light sensitive, lack of tears, burning and itching. Ears: burning, itching, and loss of hearing. Immune and hematopoietic: progressive loss of white and red cells including a decrease of platelets and hemoglobin, and high susceptibility to bacterial, mycotic and viral infections, debilitating chemical and allergies. Gastrointestinal: metallic taste in mouth, tooth loss, gum problems, stomatitis, sores in gums and throat, nausea, vomiting, diarrhea or constipation, excessive flatulence, abdominal distention, hepatitis, pancreatitis, and diabetes mellitus. Respiratory : burning and bleeding from nasal membranes, respiratory difficulty, asthma, extreme susceptibility to cold, flu and pneumonia. Skin: thinning of hair on head, burning on face, rashes, irritation, and edema. Renal: proteinuria, possible hematuria. Reproductive: irregular ovarian cycles, increased menstrual flow, fibroid growths in uterus, cystic development in mammary glands, and tumors of mammary and prostate glands. Musculoskeletal : somatitis, muscle weakness, spasms, cramps, joint pain, enlargement of joints in hand, and clubbing of fingers. Cardiovascular: chest pain, palpitations, ruptures of atrial walls, myocardial infection and aneurysm of arteries.

The skin and mucous membranes may be icteric, pupils dilated, the pulse soft and labile, and blood pressure may decrease or increase. The body temperature does not exceed 38 degree C and the patient may be afebrile, or chilled. Visible hemorrhagic spots may appear on the skin. Thoughts of suicide may be prominent in the person���s mind at this time or anytime in Stage 2. Human bonding is very important for survival.

Degeneration and hemorrhages of the vessels marks the transition from the second to the third Stage of the disease and may not be consistently observed. The degeneration of the
vital organs including serious respiratory insufficiency or asthma and CNS degeneration will take the patient into Stage three along with development of necrotic angina. If exposure continues, depending on exposure levels, Stage 2 may continue from weeks to months or even years until the symptoms of the third Stage develop. Evaluating the 50 signs and symptoms (Table-1 and 2) by assigning a score (0-least intense to 5-most intense or severe) to each symptom, we have determined that an average score range of 45-180 represents Stage 2.

Stage 3: Severe degeneration of the vital organs. The transition from the second to the third Stage is sudden. In this Stage, the patient���s resistance is already low, and violent severe symptoms are present, especially under the influence of stress, or associated with physical exertion and fatigue. The first visible sign of this Stage may be lung, brain or heart failure (heart attack), with or without the appearance of petechial hemorrhage on the skin of the trunk, the axillary and inguinal areas, the lateral surfaces of the arms and thighs, the face and head, and in serious Cases, the chest. The petechial hemorrhages vary from a few millimeters to a few centimeters in diameter. There is increased capillary fragility and any slight trauma may cause the hemorrhages to increase in size.

Aneurysms of the brain or aorta may be observed by angiography. Hemorrhages may also be found on the mucous membranes of the mouth and tongue, and on the soft palate and tonsils. There may be severe interstitial thickening or scarring of the lungs, or respiratory failure. Nasal, gastric and intestinal hemorrhages and hemorrhagic diathesis may occur. Necrotic angina begins in the form of catarrhal symptoms and necrotic changes soon appear in the mouth, throat, and esophagus with difficulty and pain on swallowing. Severe degeneration of the skin on the face, eyelids, and loss of lashes is also often present.

Necrotic lesions may extend to the uvula, gums, buccal mucosa, larynx, vocal cords, lungs, stomach, and intestines and other internal organs such as the liver and kidneys and are usually contaminated with a variety of avirulent bacteria. Bacteria infection causes an unpleasant odor from the mouth due to the enzymatic activity of bacteria on proteins. Areas of necrosis may also appear on the lips and on the skin of the fingers, nose, jaws, and eyes. Regional lymph nodes are frequently enlarged. Esophageal lesions may occur and involvement of the epiglottis may cause laryngeal edema and aphonia (loss of voice). Death may occur by strangulation.

Patients may suffer an acute parenchymatous hepatitis accompanied by jaundice. Bronchopneumonia, pulmonary hemorrhages, and lung abscesses are frequent complications. Tumors may develop of various organs, including skin, urinary bladder, brain, mammary gland, bone, immune, liver, prostate, possibly resulting in death. The most common cause of death is brain failure due to both direct effects of the mycotoxin on the central nervous system and indirect effects due to respiratory failure or lack of oxygen to the brain caused by the severe caustic inflammation (fibrinous exudation) reaction with the lung tissue, rendering it non-functional. Again, using the scoring system represented in Tables-1 and 2, an average score of greater or equal 180 represents Stage 3.

Stage of Convalescence: The course and duration of this Stage 3 depends on the intensity of the poisoning and complete removal of the patient from the premises or source of mycotoxin. Therefore, the duration of the recovery period is variable. There is considerable cellular necrosis and scarring to all major organs of the body in which cells will not regenerate, including the brain, spinal cord, eyes, lung, heart, liver, pancreas, kidney, adrenal, and blood vessels. If the disease is diagnosed during the first Stage, hospitalization is usually unnecessary, but allergies and asthma should be monitored closely. If the disease is diagnosed during the second Stage and even at the transition from the second to third Stages, early hospitalization may preserve the patient���s life. If however, the disease is only detected during the third Stage, death cannot be prevented in most Cases.

1. Croft, W. A., Jastromski, B. M., Croft, A. L., and Peters, H. A., ���Clinical

Confirmation of Trichothecene Mycotoxicosis in Patients Urine���, In: Journal of

Environmental Biology 23(3), 301-320 (2002)

2. .Forgacs, J., and W. T. Carll : Mycotoxicoses. In : Advances in Veterinary

Science. Academic Press, New York and London, pp 273-372 (1962).

Toxic Black Mold & Air Quality Experts

Global Warming and Inland Water August 20, 2007

This picture is of a large creek out here that I remember being able to see the bottom of. Like so many of the water bodies here and elsewhere this is no longer the case. What is happening to our inland waters?

I went on a little tour of some of the spots I have been watching for the past 4+ years. I was not surprised at what I saw. I had predicted that what is now happening in our waterways was coming. I said it was just a matter of time. Now here it is. I used to find the strange multicoloured waterborne microbial masses in small (meaning narrow and relatively shallow) waterways where the water either moved very slowly to not at all, or where water flow had become impeded by a buildup of branches or other obstacles. In 2004, I predicted that this visible mass of microbial soup would eventually start accumulating in visible quantities in larger bodies of water. I suspected it was already there but would take longer in the larger water bodies to accumulate enough mass to become visible.

Well, here we are. Unfortunately, I was right. It is now showing up in large waterways such as creeks and next will be our lakes and rivers, and of coarse our watersheds. It first builds visible mass along the banks, and if the water does not keep the accumulation moving it will become visible throughout the waterbodies. While at a location a good two miles from here that looks exactly like this one, two ladies walking a dog and myself got talking. They never saw this before. I explained that it was only in the ditches last year. Now it is filling up the creeks. They asked if it could make the birds sick. I said very possibly. I know why they asked me that. The Avian Influenza hot zone is adjacent to the waterway where I met these ladies, and the one in the above photo snakes right through it. No one was ever completely satisfied with the explanation(s) given around the officially named Avian Influenza event. Perhaps it was, perhaps it was not, and then again, perhaps it was, plus more. There remains some discontentment in relation to the explanation(s) pertaining to that event to this day. No one feels the “whole story” was ever revealed in regard to this occurrence. I have to agree with the skeptics on this one, literally based on events within my own journey here that had relevance to the so named Avian Influenza event.

Someone came up with a novel way to prevent photographing the ditches I used to monitor. They no longer cut the grass in the ditches making it impossible without some intentional clearing effort to see clearly what is there, and virtually impossible to get a useful pic of same.

This won’t work with the large creeks though.

In the area where I find the most profound accumulation of this stuff there are several key factors. There is the geography. This is all land near a world famous fish bearing river, and high inland water table. There are quite a few creeks in the area.

The use of the land is in my opinion not practical or wise. There is a military base, a lot of farms, including factory farms and massive greenhouse operations, our dump, and the sewage treatment plant which also grows trees in this area fertilized with treated sewage.

There is a small island on the river, right across from the sewage treatment plant outflow which is a bird sanctuary. There was a lot of sawmill operations along this stretch of the river as well.

All this within a roughly 5 mile radius.

In the past recent years some of the sawmill or timber operations in this vicinity have moved their operations back from the river’s shore, which is of specific interest to me.

This after the Avian influenza outbreak in this area, followed by the disappearance of over a million fish also in this vicinity.

Our missing fish have never been officially accounted for to the best of my knowledge, and the salmon stocks have never recovered.

I have to include Global Warming here, as I have been watching and observing the recent hot weather’s effect on the waterborne microbial soup.

What I have seen is a huge surge in it’s cumulative visible mass during the hot spell. There are two possible contributors to this event that I am familiar with. It’s growth appears to be aided by heat, like yeast rises in the oven. It even reaches a stage of bubbling up and off gassing. The other contributor that I realize to be relevant is that with no rain falling the water has not been moving much if at all, thus aiding the accumulating masses without separation of the individual microbial entities. I noted that there is a nearly total absence of ground dwelling insects in areas where this is occurring in the water. This would be a serious concern as well, as the insects aerate (oxygenate) the soil.

I noted that myself and my dog have been battling respiratory difficulties accompanied by chest, lung, and sinus infection.

In discussion with others, the health trends out here are consistent in that whatever symptoms you have, others as well as animals are having them at the same time. On mass; back pain, leg pain, respiratory and sinus infections, headaches, excessive fatigue or full body weakness, nausea, burning tingling skin.

In talking with people around town, I also stumbled upon a pattern with the animals that is of interest here. The animals are searching for rain water. They do not want to drink the tap water. Nor do they want to drink water coming from people’s private wells. This is significant. There is a problem with the water out here if the animals do not want to drink it. One person I know tells me they have had to resort to buying bottled water for their pig, as the pig will not drink the well water or municipal tap water. My own dog seeks rain water accumulation. In lieu of this, I have two water bowls for him to choose from. One has municipal tap water. The other has municipal tap water with activated charcoal in it. He will only drink the one with the activated charcoal in it, and in so doing began to show some visible signs of improvement in his condition. So my question, and concern is: “Why is no problem being detected with this water when tested? Are “they” missing something, or………………..?” I say “or…………….”

Did you know?…

Algae induced by raw sewage is a health threat.

Toxic Algae produces neurotoxins which can do serious harm and cause extremely painful conditions. As well, with toxic algae exposure to yourself comes the risk of exposure to pfiesteria organisms also researchable under the term dinoflagellates. Incredibly nasty looking little invaders.

Then there is the fungus. Under normal climactic temperatures, nature destroys excess fungi in the environment once a year via freezing conditions. Freezing weather causes a natural once yearly die off of fungi, helping keep the quantity of fungi in the environment under control. With Global Warming this will cease to occur, and the quantities of potentially mycotoxin and neurotoxin producing fungi will be able to accumulate to reach health threatening levels present in the ambient, recreational, and agricultural environment, and you will get sick like me.

Do you know that heat resistant fungus has been detected in blueberry soil? Our bodies use heat as one of their primary defenders against invaders in our system. Get too much heat resistant fungus in your system, and you will have a problem as it will be able to survive at your body temperature. Heat resistant fungus is resistant to most chemical insults, therefore rendering most pharmaceutical interventions useless. This is a very real problem that already has a foothold in this polluted world. Global Warming will not bother it either, until we run out of water. Fungus needs moisture to grow. Not a problem here, as it doesn’t care if the water is clean or dirty. It will mutate (adjust or alter itself) to survive what ever conditions exist, as long as
it has moisture and some nutrients. When you think about it, fungus is in a position to outlive us as it will not be killed by the contamination that is causing Global Warming, but we surely will if we keep it up. We already have populations on mass that are in poor health as a result of our planetary conditions.

« Older entries Newer entries »