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13.1.6 Aflatoxin. What Is It?


This article is from the Food Preserving FAQ, by Eric Decker ericnospam@getcomputing.com with numerous contributions by others.

13.1.6 Aflatoxin. What Is It?

Food dehydrators have another set of toxic pests to worry about. While
bacteria need free water to reproduce, molds can grow and spread, and de-
velop their toxins under much drier conditions. The most famous mold is
that of ergot, which when ingested causes hallucinations. The molds of
most concern here are those of _Aspergillus_, which produces aflatoxin.
The Bad Bug MO of aflatoxin is listed below.

U S Food & Drug Administration Center for Food Safety & Applied
Nutrition Foodborne Pathogenic Microorganisms and Natural Toxins 1992
(Bad Bug Book)

1. Name of Toxin: Aflatoxins
2. Name of Acute Disease: Aflatoxicosis

Aflatoxicosis is poisoning that results from ingestion of aflatoxins in
contaminated food or feed. The aflatoxins are a group of structurally re-
lated 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 encoun-
tered in tree nuts, peanuts, and other oilseeds, including corn and cotton-

2. Aflatoxins:
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 pro-
portions; 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. [Could a black light be useful to monitor dried
items?--LEB]. 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

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, expo-
sure level, and duration of exposure, general 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 aflatoxin requires meta-
bolic activation to exert its carcinogenic effect, and these effects can be
modified by induction or inhibition of the mixed function oxidase system.

4. Normal Course of Disease:
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 carcin-
ogenic potential. Therelative 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

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 out-
break, 397 persons were affected and 108 persons died. In this outbreak,
contaminated corn was the major dietary constituent, and aflatoxin levels of
0.25 to15 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 pe-
culiar and very notable feature of the outbreak: the appearance of signs of
disease in one village population was preceded by a similar disease in domes-
tic 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 bodyweight for an undetermined number of

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 control 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.

5. Diagnosis of Human Illnesses:
Aflatoxicosis in humans has rarely been reported; however, such cases are
not always recognized. Aflatoxicosis may be suspected when a disease out-
break 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 into 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 dif-
ficult to recognize. Some of the common symptoms are impaired food conver-
sion and slower rates of growth with or without the production of an overt
aflatoxin syndrome.

6. Associated Foods:
In the United States, aflatoxins have been identified in corn and corn pro-
ducts, 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.

7. 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.

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

9. Analysis of Foods:
Many chemical procedures have been developed to identify and measure afla-
toxins 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 anal-
ysis are described in Chapter 26 of the AOAC Official Methods of Analysis.

10. History of Recent Outbreaks:
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.

Text last edited: 21 Jan 92
Hypertext last edited: 19 Apr 95 mow@vm.cfsan.fda.gov


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