PPS Cannabis and Biological
Results from biological and
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
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.
Food & Drug Administration
Center for Food Safety &
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
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
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
rarely been reported; however, such cases
are not always recognized. Aflatoxicosis may be suspected when a
disease outbreak exhibits the following characteristics:
The adverse effects of aflatoxins in animals (and presumably in humans)
have been categorized in two general forms.
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
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
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,
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
|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
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
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
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
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:
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
information on recent outbreaks see the CDC.
|11. Education and Background
references can be found at the links below.
|Loci index for genome
Available from the GenBank Taxonomy database, which
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
Fred Frye of the FDA.
|Aflatoxin B1 and M1
A L A B A M
A & M A N
D A U B U R N U N I V E R S I T I E
B.J. Jacobsen, Extension Plant
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.
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.
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
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
have been observed in turkeys, ducks, chickens, swine, cattle, dogs,
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
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
Three genera of fungi -Aspergillus,
Penicillium and Fusarium (Gibberella)
- are the ones involved
frequently in cases of mycotoxin contamination in corn, small grains,
and soybeans (Table 1). Aspergillus
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
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
They commonly cause stored grams to heat and decay
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.
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
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
Meronuck, R. A. 1987. Molds in grain storage.
St. Paul, Minnesota: University of Minnesota Extension Service Folder
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.
Occurrence and Health
Aflatoxins are toxic
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
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
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
. Moreover, these studies also revealed that there are
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
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
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
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
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
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