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PPS Cannabis and Biological Impurities


Results from biological and heavy tests performed by PPS on their own cannabis
- July 24th, 2003

If the safety of gamma irradiation in smoked product has never been established, why does the PPS gamma irradiate its cannabis?
The above test results of the PPS cannabis dated July 24th, 2003 shows that they have little choice; the biological impurities are so significant prior to gamma irradiation that they could never send it out "as is".  The numbers in pink show the level of biological impurities prior to irradiation: please note the Standard Plate Count of 125,000 CFU prior to gamma irradiation on page 1 of the PPS test results, and the high level of mold reported on page 2.  Of particular concern is the high level of aspergillus mold.  Aspergillus is a hyperallergenic mold, and certain types of aspergillus (parasiticus, flavus) produce dangerous mycotoxins that can have severe toxicological effects in humans (see Document 2 below).   Although gamma irradiation can kill aspergillus mold, it does not destroy the mycotoxins they produce (some studies even suggest an increase in mycotoxin production following gamma irradiation – see Document 4 below), and their ingestion can lead to mycotoxicoses, which is a series of diseases and conditions associated with exposure to these compounds.  
Because of their demonstrated carcinogenic properties and acute toxicological effect, aflotoxins are perhaps the best known and most commonly studied of all mycotoxins.  Produced by Aspergillus flavus and parasiticus, evidence of acute aflatoxicosis in humans have been reported from all over the world.  The syndrome is characterized by vomiting, abdominal pain. pulminary edema, convulsions, coma, and death with cerebral edema and fatty involvement of the liver, kidneys and heart.  In addition, in 1988, the IARC placed aflatoxin B1 on the list of human carcinogens. This is supported by a number of epidemiological studies done in Asia and Africa that have demonstrated a positive association between dietary aflatoxins and liver necrosis, cirrhosis, and carcinoma of the liver (see Document 1 and 3 below).

And what about other cannabis?  When the VICS had it's own organic cannabis analyzed alongside the PPS product, this is what we found:

Despite gamma irradiation, the PPS cannabis had a much higher plate count than the VICS (1400 vs 120 CFUs, or colony forming units).  So what does this all mean?  It means that Health Canada’s reassurances in regards to the safety of their cannabis appear overstated and unsubstantiated in the face of these justifiable patient concerns. Meanwhile, it is clear that well-grown organic cannabis like that produced by the Vancouver Island Compassion Society is not only stronger and of noticeably better quality, but also appears to be safer by any and all measures at our disposal.

Document 1
U.S. Food & Drug Administration
Center for Food Safety & Applied Nutrition
Foodborne Pathogenic Microorganisms
and Natural Toxins Handbook


1. Name of the Organism:

2. Nature of Acute Disease:

Aflatoxicosis is poisoning that results from ingestion of aflatoxins in contaminated food or feed. The aflatoxins are a group of structurally related toxic compounds produced by certain strains of the fungi Aspergillus flavus and A. parasiticus. Under favorable conditions of temperature and humidity, these fungi grow on certain foods and feeds, resulting in the production of aflatoxins. The most pronounced contamination has been encountered in tree nuts, peanuts, and other oilseeds, including corn and cottonseed. The major aflatoxins of concern are designated B1, B2, G1, and G2. These toxins are usually found together in various foods and feeds in various proportions; however, aflatoxin B1 is usually predominant and is the most toxic. When a commodity is analyzed by thin-layer chromatography, the aflatoxins separate into the individual components in the order given above; however, the first two fluoresce blue when viewed under ultraviolet light and the second two fluoresce green. Aflatoxin M a major metabolic product of aflatoxin B1 in animals and is usually excreted in the milk and urine of dairy cattle and other mammalian species that have consumed aflatoxin-contaminated food or feed.

3. Nature of Disease: 
  Aflatoxins produce acute necrosis, cirrhosis, and carcinoma of the liver in a number of animal species; no animal species is resistant to the acute toxic effects of aflatoxins; hence it is logical to assume that humans may be similarly affected. A wide variation in LD50 values has been obtained in animal species tested with single doses of aflatoxins. For most species, the LD50 value ranges from 0.5 to 10 mg/kg body weight. Animal species respond differently in their susceptibility to the chronic and acute toxicity of aflatoxins. The toxicity can be influenced by environmental factors, exposure level, and duration of exposure, age, health, and nutritional status of diet. Aflatoxin B1 is a very potent carcinogen in many species, including nonhuman primates, birds, fish, and rodents. In each species, the liver is the primary target organ of acute injury. Metabolism plays a major role in determining the toxicity of aflatoxin B1; studies show that this aflatoxion requires metabolic activation to exert its carcinogenic effect, and these effects can be modified by induction or inhibition of the mixed function oxidase system.

4. Diagnosis of Human Illness: Aflatoxicosis in humans has rarely been reported; however, such cases are not always recognized. Aflatoxicosis may be suspected when a disease outbreak exhibits the following characteristics:
  •   the cause is not readily identifiable
  •   the condition is not transmissible
  •   syndromes may be associated with certain batches of food
  •   treatment with antibiotics or other drugs has little effect
  •   the outbreak may be seasonal, i.e., weather conditions may affect mold growth.
The adverse effects of aflatoxins in animals (and presumably in humans) have been categorized in two general forms.

A. (Primary) Acute aflatoxicosis is produced when moderate to high levels of aflatoxins are consumed. Specific, acute episodes of disease ensue may include hemorrhage, acute liver damage, edema, alteration in digestion, absorption and/or metabolism of nutrients, and possibly death.

B. (Primary) Chronic aflatoxicosis results from ingestion of low to moderate levels of aflatoxins. The effects are usually subclinical and difficult to recognize. Some of the common symptoms are impaired food conversion and slower rates of growth with or without the production of an overt aflatoxin syndrome.

5. Associated Foods:
In the United States, aflatoxins have been identified in corn and corn products, peanuts and peanut products, cottonseed, milk, and tree nuts such as Brazil nuts, pecans, pistachio nuts, and walnuts. Other grains and nuts are susceptible but less prone to contamination.

6. Relative Frequency of Disease:
The relative frequency of aflatoxicosis in humans in the United States is not known. No outbreaks have been reported in humans. Sporadic cases have been reported in animals.

7. Course of Disease and Complications: In well-developed countries, aflatoxin contamination rarely occurs in foods at levels that cause acute aflatoxicosis in humans. In view of this, studies on human toxicity from ingestion of aflatoxins have focused on their carcinogenic potential. The relative susceptibility of humans to aflatoxins is not known, even though epidemiological studies in Africa and Southeast Asia, where there is a high incidence of hepatoma, have revealed an association between cancer incidence and the aflatoxin content of the diet. These studies have not proved a cause-effect relationship, but the evidence suggests an association.

One of the most important accounts of aflatoxicosis in humans occurred in more than 150 villages in adjacent districts of two neighboring states in northwest India in the fall of 1974. According to one report of this outbreak, 397 persons were affected and 108 persons died. In this outbreak, contaminated corn was the major dietary constituent, and aflatoxin levels of 0.25 to 15 mg/kg were found. The daily aflatoxin B1 intake was estimated to have been at least 55 ug/kg body weight for an undetermined number of days. The patients experienced high fever, rapid progressive jaundice, edema of the limbs, pain, vomiting, and swollen livers. One investigator reported a peculiar and very notable feature of the outbreak: the appearance of signs of disease in one village population was preceded by a similar disease in domestic dogs, which was usually fatal. Histopathological examination of humans showed extensive bile duct proliferation and periportal fibrosis of the liver together with gastrointestinal hemorrhages. A 10-year follow-up of the Indian outbreak found the survivors fully recovered with no ill effects from the experience.

A second outbreak of aflatoxicosis was reported from Kenya in 1982. There were 20 hospital admissions with a 60% mortality; daily aflatoxin intake was estimated to be at least 38 ug/kg body weight for an undetermined number of days
In a deliberate suicide attempt, a laboratory worker ingested 12 ug/kg body weight of aflatoxin B1 per day over a 2-day period and 6 months later, 11 ug/kg body weight per day over a 14-day period. Except for transient rash, nausea and headache, there were no ill effects; hence, these levels may serve as possible no-effect levels for aflatoxin B1 in humans. In a 14-year follow-up, a physical examination and blood chemistry, including tests for liver function, were normal.

8. Target Populations:
Although humans and animals are susceptible to the effects of acute aflatoxicosis, the chances of human exposure to acute levels of aflatoxin is remote in well-developed countries. In undeveloped countries, human susceptibility can vary with age, health, and level and duration of exposure.

9. Food Analysis: Many chemical procedures have been developed to identify and measure aflatoxins in various commodities. The basic steps include extraction, lipid removal, cleanup, separation and quantification. Depending on the nature of the commodity, methods can sometimes be simplified by omitting unnecessary steps. Chemical methods have been developed for peanuts, corn, cottonseed, various tree nuts, and animal feeds. Chemical methods for aflatoxin in milk and dairy products are far more sensitive than for the above commodities because the aflatoxin M animal metabolite is usually found at much lower levels (ppb and ppt). All collaboratively studied methods for aflatoxin analysis are described in Chapter 26 of the AOAC Official Methods of Analysis.

10. Selected Outbreaks: Literature references can be found at the links below.

Very little information is available on outbreaks of aflatoxicosis in humans because medical services are less developed in the areas of the world where high levels of contamination of aflatoxins occur in foods, and, therefore, many cases go unnoticed.

Morbidity and Mortality Weekly Reports For more information on recent outbreaks see the CDC.

11. Education and Background Resources: Literature references can be found at the links below.

Loci index for genome Aspergillus flavus
Aspergillus parasiticus

   Available from the GenBank Taxonomy database, which contains the names of all organisms that are represented in the genetic databases with at least one nucleotide or protein sequence.

12. Molecular Structural Data: These structures were created by Fred Frye of the FDA.
Aflatoxin B1 and M1 
Aflatoxin G1

Document 2:


A L A B A M A    A & M    A N D    A U B U R N    U N I V E R S I T I E S


B.J. Jacobsen, Extension Plant Pathologist
K.L. Bowen, Department of Plant Pathology
R.A. Shelby, Department of Plant Pathology
U.L. Diener, Department of Plant Pathology
B.W. Kemppainen, Department of Physiology and Pharmacology
James Floyd, Extension Veterinarian

Mycotoxins are fungal metabolites that are toxic when consumed by animals, including human beings. The toxins can accumulate in maturing corn, cereals, soybeans, sorghum, peanuts, and other food and feed crops in the field and in grain during transportation. The toxins may occur in storage under conditions favorable for the growth of the toxin-producing fungus or fungi.

     Diseases in animals and human beings resulting from the consumption of mycotoxins are called mycotoxicoses. The effects in domestic animals include allergic reactions, reproductive failure, unthriftiness, loss of appetite, feed refusal, suppression of the immune system, decreased feed efficiency, and mortality (Table 1). For example, in 1934, in the Midwest, more than 5,000 horses died because of "moldy corn disease". In 1972, Gibberella ear rot caused extensive feed-refusal problems in swine in the Corn Belt. Aflatoxin has caused problems in several animal species in the southeastern United States for many years, and fescue toxicosis has been a common problem with fescue pastures in the South for many years.

     Human suffering from mycotoxicoses includes ergot poisoning associated with ingestion of rye flour contaminated with ergot (holy fire, St. Anthony's fire); cardiac beriberi associated with Penicillium molds in rice (yellow rice toxins); and alimentary toxic aleukia (ATA,) associated with Fusarium molds on overwintered wheat, millet, and barley. Several mycotoxins have been linked to increased incidence of cancer in human beings. These include aflatoxin, sterigmatocystin zearalenone, patulin, ochratoxin, and fumonisin.

     Although the adverse effects of feeding moldy feeds was long known by livestock and poultry producers, a specific mycotoxin was not implicated. An outbreak of "Turkey X disease" in Great Britain in 1960 was traced to contaminated peanut meal from Brazil. Aflatoxin was indicated as the cause of the death for more than 100,000 young turkeys and some 20,000 ducklings, pheasants, and partridge poults. This problem stimulated modem research on mycotoxins and the ecology of mycotoxin producing fungi. Some of the most common mycotoxins and associated fungi are found in Table 1.

     Aflatoxin Bl, which may be formed in corn, cereals, sorghum, peanuts, and other oil-seed crops, is one of the most potent naturally occurring animal carcinogens. If sensitive young animals regularly consume between 50 and 100 micrograms of aflatoxin B1 per kg of feed, the result can be fatal liver cancer; in older or mature animals, though, the effects may be only minor. All species of animals appear to be susceptible, although susceptibility varies greatly from species to species. Animals on a protein-deficient diet are more sensitive to aflatoxin injury than are those on a well-balanced ration.

     The toxic or carcinogenic effects of aflatoxin have been demonstrated experimentally in a wide variety of domestic and experimental animals and in human beings who inadvertently consumed contaminated corn, peanuts, or peanut meal. Field outbreaks of diseases have been observed in turkeys, ducks, chickens, swine, cattle, dogs, and trout.

     Aflatoxin has been implicated in primary liver cancer in human beings. An outbreak of aflatoxicosis in India was linked to moldy corn containing aflatoxin, killing more than 100 persons and affecting more than 400 dogs. Aflatoxin has been found in the tissues of children suffering from Reye's syndrome in the Orient and in colon cancer lesions. In 1977 and 1980, 60 percent or more of the corn grown in the southeastern United States contained 20 ppb or more of the aflatoxin B1 - the maximum level permitted by the U.S. Food and Drug Administration (FDA) in foods, feeds, or feed ingredients in interstate commerce. Some state agencies and foreign countries have established more restrictive limits (no more than 5 ppb) of permissible aflatoxin contamination in grains or other products in interstate or international commerce.


     Three genera of fungi -Aspergillus, Penicillium and Fusarium (Gibberella)- are the ones involved most frequently in cases of mycotoxin contamination in corn, small grains, and soybeans (Table 1). Aspergillus flavus produces aflatoxins in starchy cereal grains (for example, corn, wheat, sorghum, oats, barley, millet, and rice) starting at a moisture content of about 18 percent -that is, in equilibrium with 85-percent relative humidity (0.85 available water), and at temperatures of 54° to 108°F with an optimum at 81° to 86°F. The critical moisture content for soybeans is 15 to 15.5 percent and for peanuts 8 to 9 percent. The upper limit of moisture for growth of A. flavus for aflatoxin production is about 30 percent. A. flavus will grow slowly below 54°F and most rapidly at 98°F but will not produce aflatoxin at temperatures below 54°F or above 108°F. Under optimum conditions for growth, A. flavus can produce some aflatoxin within 24 hours and a biologically significant amount in a few days.

     Other toxin producing fungi grow on grain at moisture contents of 17 to 40 percent and over a wide range of temperatures, from below freezing for species of Penicillium and A. fumigatus to more than 131°F. The quality of the grain and its suitability for storage are adversely affected by (1) a high moisture content, (2) physical damage to the kernels, and (3) the extent to which storage fungi have invaded the seed.

     Fungi may grow well under a given set of conditions but not necessarily produce mycotoxins. Although A. flavus flourishes on many crop plants, it does not produce equal amounts of aflatoxin on all of them. For example, the fungus produces much more aflatoxin on peanuts than on soybeans, although it grows equally well on both crops. Aflatoxins are also much more likely to be formed in warm to hot, humid regions on drought-stressed plants, conditions most common in the southeastern United States.


     Aspergillus flavus and A. parasiticus are common in most soils and are usually involved in decay of plant materials. They commonly cause stored grams to heat and decay and, under certain conditions, invade grain in the field. The problem is serious in subtropical and tropical regions of the world where cereals, peanuts, corn, and copra are important in the human diet.

     Aflatoxins B1, B2, G1, and G2 are produced by A. flavus and A. parasiticus in grains in both field and storage. Infection is most common after the kernels have been damaged by insects, birds, mites, hail, early frost, heat and drought stress, windstorms, and other unfavorable weather. Aflatoxins Ml and M2 are found in milk from animals fed aflatoxin-contaminated feeds. The presence of A. flavus or A. parasiticus in a given feed sample does not imply that the feed is unwholesome and will contain high levels of aflatoxin. Aflatoxin persists under extreme environmental conditions and is even relatively heat stable at temperatures above 212°F, the boiling point of water. Roasting, ammoniation at ambient temperatures, and some microbial treatments may sharply reduce but not eliminate the aflatoxin content. Ammoniation has been shown to be most effective in reducing aflatoxin levels. Currently, these treatments have limited application, with roasting being the least effective. Pelletizing feeds may eliminate fungi present in the stock but not reduce or eliminate aflatoxin present in any of the ingredients.


     All animal species are susceptible to aflatoxicosis, although sensitivity varies considerably from species to species. For example, birds, fish, dogs, and swine appear to be more susceptible than mature cattle. In poultry, besides fatty liver and kidney disorders, leg and bone problems can develop as well as outbreaks of coccidiosis. Aflatoxins may cause vaccines to fail, increase the birds' susceptibility to disease, and result in suppression of the natural immunity to infection. The animals become susceptible to infection by bacteria such as Salmonella and to various viruses and other infectious agents commonly found around the farm yard, feedlot, or poultry house that normal healthy animals ward off. Decreased blood clotting results in a greater downgrading and condemnation of the birds because of massive bleeding and bruises. .Less carcass pigmentation is exhibited and egg yolks are paler. The hatchability of eggs can drop, and reduced production may be noted as well as smaller eggs with shell problems. Growth is restricted and mortality increases, especially during the growing period.

     Regular or occasional consumption by farm animals of feed containing aflatoxin in the range of less than 100 ppb to a few hundred parts per million (ppm) results in decreased feed consumption, poor feed conversion, stunting, and decreased flesh growth. Decreased productivity may be accompanied by damage to the liver, hemorrhaging into the muscles or body cavities, and suppression of natural immunity to parasites and pathogens always present in the environment. Once the damage has been done, the animals will not fully recover, even if returned to a toxin-free ration.


     1. NovaSil, Englehard Corporation, Cleveland, Ohio (216-292-9200). NovaSil is available in Alabama through Fuller Supply Company, Birmingham (800-292-8567).
     2. Volclay and FD-181, American Colloid Company, Arlington Heights, Illinois. Volclay and FD-181 are available in Alabama through Agri Products, Incorporated, Birmingham (205-979-2474).
     3. Aflatoxins (B1 and M1), zearalenone, DON, and T2 toxin test kits are available from Neogen Corporation, Lansing, Michigan (800-234-5333). Other companies who have kits for aflatoxins and others are: Environmental Diagnostics, Burlington, North Carolina (800-334-1116); Vicam, Somerville, Maine (800-338-4381); Romer Labs, Washington, Missouri (314-239-3009), IDEXX Corporation, Portland, Maine (800-548-6733); and Rialdon Diagnostics, Bryan, Texas (409-846-6202). Mycotoxin analysis is available on a fee basis from the Department of Plant Pathology, Auburn University, AL 36849-5409 (334-844-5003).


     Christensen, C. M., ed. 1982. Storage of cereal grains and their products. St. Paul, Minnesota: American Association of Cereal Chemists, Inc.
     Christensen, C. M., and H. H. Kaufmann. 1969. Grain storage: The role of fungi in quality loss. Minneapolis, Minnesota: The University of Minnesota Press.
     Christensen, C. M., and R. A. Meronuck. 1986. Maintenance of quality in stored grains and seeds. Minneapolis, Minnesota: The University of Minnesota Press.
     Christensen, C. M., C. J. Mirocha, and R A. Meronuck. 1988. St. Paul, Minnesota: University of Minnesota Extension Service Folder AG-FO-3538.
     Hesseltine, C. W, and M. E. Mehlman, eds. 1977. Mycotoxins in human and animal health. Park Forest South, Illinois: Pathotox Publishers.
     Lacey, J. 1985. Trichothecenes and other mycotoxins. New York, New York: John Wiley & Sons.
     Marasas, W R O., and P. E. Nelson. 1987. Mycotoxicology. Univeristy Park, Pennsylvania: The Pennsylvania State University Press.
     Meronuck, R. A. 1987. Molds in grain storage. St. Paul, Minnesota: University of Minnesota Extension Service Folder AG-FO-0564.
     Rodricks, J. V., ed. 1976. Mycotoxins and other fungal related food problems. Advances in Chemistry Series 149. Washington, D.C.: American Chemical Society.
     Shotwell, 0. L. 1977. Aflatoxin in Corn.Joumal of American Oil Chemists Society 54:216A-224A.
     Wyflie, T D., and L. G. Morehouse, eds. 1977-1978. Mycoto3dc fungi, mycotoxins, mycotoxicoses: An encyclopedic handbook. 3 vols. New York, New York: Marcel Dekker, Inc.

Document 3:


Occurrence and Health Risks


Aflatoxins are toxic metabolites produced by certain fungi in/on foods and feeds. They are probably the best known and most intensively researched mycotoxins in the world. Aflatoxins have been associated with various diseases, such as aflatoxicosis, in livestock, domestic animals and humans throughout the world. The occurence of aflatoxins is influenced by certain environmental factors; hence the extent of contamination will vary with geographic location, agricultural and agronomic practices, and the susceptibility of commodities to fungal invasion during preharvest, storage, and/or processing periods.  Aflatoxins have received greater attention than any other mycotoxins because of their demonstrated potent carcinogenic effect in susceptible laboratory animals and their acute toxicological effects in humans . As it is realized that absolute safety is never achieved , many countries have attempted to limit exposure to aflatoxins by imposing regulatory limits on commodities intended for use as food and feed.


In the 1960 more than 100,000 young turkeys on poultry farms in England died in the course of a few months from an apparently new disease that was termed "Turkey X disease". It was soon found that the difficulty was not limited to turkeys. Ducklings and young pheasants were also affected and heavy mortality was experienced.

A careful survey of the early outbreaks showed that they were all associated with feeds, namely Brazilian peanut meal . An intensive investigation of the suspect peanut meal was undertaken and it was quickly found that this peanut meal was highly toxic to poultry and ducklings with symptoms typical of Turkey X disease.

Speculations made during 1960 regarding the nature of the toxin suggested that it might be of fungal origin. In fact, the toxin-producing fungus was identified as Aspergillus flavus (1961) and the toxin was given the name Aflatoxin by virtue of its origin (A.flavis--> Afla).

This discovery has led to a growing awareness of the potential hazards of these substances as contaminants of food and feed causing illness and even death in humans and other mammals. Studies that are summarized in the following sections revealed that aflatoxins are produced primarily by some strains of A. Flavus and by most, if not all, strains of A. parasiticus, plus related species, A. nomius and A. niger . Moreover, these studies also revealed that there are four major aflatoxins : B1, B2, G1, G2 plus two additional metabolic products, M1 and M2, that are of significance as direct contaminants of foods and feeds. The aflatoxins M1 and M2 were first isolated from milk of lactating animals fed aflatoxin preparations ; hence, the M designation. Whereas the B designation of aflatoxins B1 and B2 resulted from the exhibition of blue fluorescence under UV-light, while the G designation refers to the yellow-green fluorescence of the relevant structures under UV-light . These toxins have closely similar structures and form a unique group of highly oxygenated, naturally occuring heterocyclic compounds . Their molecular formulas as established from elementary analyses and mass spectrometric determinations are:

  •   B1 : C17 H12 O6
  •   B2 : C17 H14 O6
  •   G1 : C17 H12 O7
  •   G2 : C17 H14 O7

Aflatoxins B2 and G2 were established as the dihydroxy derivatives of B1 and G1 , respectively . Whereas , aflatoxin M1 is 4-hydroxy aflatoxin B1 and aflatoxin M2 is 4-dihydroxy aflatoxin B2 .

Aflatoxins and Human Health
Humans are exposed to aflatoxins by consuming foods contaminated with products of fungal growth . Such exposure is difficult to avoid because fungal growth in foods is not easy to prevent. Even though heavily contaminated food supplies are not permitted in the market place in developed countries, concern still remains for the possible adverse effects resulting from long-term exposure to low levels of aflatoxins in the food supply.

Evidence of acute aflatoxicosis in humans has been reported from many parts of the world, namely the Third World Countries, like Taiwan, Ouganda, India, and many others. The syndrome is characterized by vomiting, abdominal pain, pulmonary edema, convulsions, coma, and death with cerebral edema and fatty involvment of the liver, kidneys, and heart.

Conditions increasing the likelihood of acute aflatoxicosis in humans include limited availability of food, environmental conditions that favor fungal development in crops and commodities, and lack of regulatory systems for aflatoxin monitoring and control.

Because aflatoxins, especially aflatoxin B1, are potent carcinogens in some animals, there is interest in the effects of long-term exposure to low levels of these important mycotoxins on humans. In 1988, the IARC placed aflatoxin B1 on the list of human carcinogens. This is supported by a number of epidemiological studies done in Asia and Africa that have demonstrated a positive association between dietary aflatoxins and Liver Cell Cancer (LCC).  Additionally , the expression of aflatoxin-related diseases in humans may be influenced by factors such as age, sex, nutritional status, and/or concurrent exposure to other causative agents such as viral hepatitis (HBV) or parasite infestation.



1. Anon.1989.Mycotoxins , Economic and Health Risks.Council for Agricultural science and Technology, Report No.116 pp91.
2. Eaton,D.L. and Groopman,J.D.1994.The Toxicology of Aflatoxins. Academic Press, New York.pp383-426.
3. Finley,J.W.,Robinson,S.F. and Armstrong ,D.J.1992.Food Safety Assessment. American Chemical Society,Washington ,D.C. pp261-275.
4. Goldbatt, L.A.1969.Aflatoxin.Academic Press,New York. pp1-40.
5. Heathcote,J.G. and Hibbert,J.R. 1978. Aflatoxins : Chemical and biological aspect. Elsevier, New York.pp.173-186.
6. Liener,I.E.1969.Toxin constituents of plant foodstuffs. Academic Press , New york.pp392-394.
7. Wyllie,T.D. and Morchause,L.G. 1978.Mycotoxin Fungi, Mycotoxins, Mycotoxicoses-An Encyclopedic Handbook.Vols.1,2, and 3.Marcel Dekker,Inc.New york.


Document 4:

Effect of Graded Doses of Gamma-Irradiation on Aflatoxin Production by Aspergillus parasitucus in Wheat


Effect of Graded Doses of Gamma-Irradiation on Aflatoxin Production by Aspergillus parasitucus in Wheat


E. Priyadarshini and P. G. Tulpule*
(* National Institute of Nutrition, Indian Council of Medical Research, Jamai-Osmania P. O., Hyderabad-500007, India.)


Fd. cosmet. Toxicol., Vol. 17, 1979, 505-507


The use of gamma-irradiation can extend the storage life of certain foods, but following irradiation, some foods have been found, under laboratory conditions, to support a greater production of aflatoxin B1. Wheat irradiated at different dose levels up to 250 krad showed a dose-dependent susceptibility to aflatoxin production, both toxin production and the free acid levels of the wheat grains following an exponential pattern as the irradiation dosage increased from 50 to 250 krad. However, no correlation was observed between the degree of irradiation and the growth of the fungus.

Jacobsen et al.  (1993) Mycotoxins and Mycotoxicoses.  Circular ANR-767, 02/93.  Alabama A&M and Auburn Universities.