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Toxicologists tend to concentrate their efforts on hazardous chemicals such as polyaromatic hydrocarbons, heavy metals, and organic pesticides. Because they have devoted less effort to natural products, agriculturalists, chemists, microbiologists, and veterinarians who are often unfamiliar with the basic principles of toxicology have conducted most of the mycotoxin research. There has been a lot of reinventing of the wheel and sometimes an imprecise use of toxicology jargon.

For example, mycotoxicoses, like all toxicological syndromes, can be categorized as acute or chronic. Acute toxicity generally has a rapid onset and an obvious toxic response, while chronic toxicity is characterized by low-dose exposure over a long time period, resulting in cancers and other generally irreversible effects (128). Accepting that it is often difficult to distinguish between acute and chronic effects, many papers on mycotoxicoses blur this basic dichotomy entirely, and it is not always easy to interpret the published data on purported health effects. Almost certainly, the main human and veterinary health burden of mycotoxin exposure is related to chronic exposure (e.g., cancer induction, kidney toxicity, immune suppression). However, the best-known mycotoxin episodes are manifestations of acute effects (e.g., turkey X syndrome, human ergotism, stachybotryotoxicosis).

In order to demonstrate that a disease is a mycotoxicosis, it is necessary to show a dose-response relationship between the mycotoxin and the disease. For human populations, this correlation requires epidemiological studies. Supportive evidence is provided when the characteristic symptoms of a suspected human mycotoxicosis are evoked reproducibly in animal models by exposure to the mycotoxin in question (121). Human exposure to mycotoxins is further determined by environmental or biological monitoring. In environmental monitoring, mycotoxins are measured in food, air, or other samples; in biological monitoring, the presence of residues, adducts, and metabolites is assayed directly in tissues, fluids, and excreta (121).

In general, mycotoxin exposure is more likely to occur in parts of the world where poor methods of food handling and storage are common, where malnutrition is a problem, and where few regulations exist to protect exposed populations. However, even in developed countries, specific subgroups may be vulnerable to mycotoxin exposure. In the United States, for example, Hispanic populations consume more corn products than the rest of the population, and inner city populations are more likely to live in buildings that harbor high levels of molds (5)

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Ergotism is the effect of long term ergot poisoning, traditionally due to the ingestion of the alkaloids produced by the Claviceps purpurea fungus.

Convulsive symptoms include painful seizures and spasms, diarrhea, paresthesias, itching, mental effects including mania or psychosis, headaches, nausea and vomiting. Usually the gastrointestinal effects precede central nervous system effects.

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Fermented food and many alcoholic beverages can also contain significant amounts of acetaldehyde. Acetaldehyde, derived from mucosal or microbial oxidation of ethanol, tobacco smoke, and diet, appears to act as a cumulative carcinogen in the upper digestive tract of humans.[48]

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Dangers

Toxicity

Acetaldehyde is toxic when applied externally for prolonged periods, an irritant, and a probable carcinogen.[29] It is an air pollutant resulting from combustion, such as automotive exhaust and tobacco smoke. It is also created by thermal degradation of polymers in the plastics processing industry.[30] Acetaldehyde naturally breaks down in the human body[31] but has been shown to excrete in urine of rats.[32]

Irritation

Acetaldehyde is an irritant of the skin, eyes, mucous membranes, throat, and respiratory tract. This occurs at concentrations up to 1000 ppm. Symptoms of exposure to this compound include nausea, vomiting, headache. These symptoms may not happen immediately. The perception limit of acetaldehyde in air is in the range between 0.07 and 0.25 ppm.[10] At such concentrations, the fruity odor of acetaldehyde is apparent. Conjunctival irritations have been observed after a 15-minute exposure to concentrations of 25 and 50 ppm, but transient conjunctivitis and irritation of the respiratory tract have been reported after exposure to 200 ppm acetaldehyde for 15 minutes. It has a general narcotic action and large doses can even cause death by respiratory paralysis. It may also cause drowsiness, delirium, hallucinations, and loss of intelligence. Exposure may also cause severe damage to the mouth, throat, and stomach; accumulation of fluid in the lungs, chronic respiratory disease, kidney and liver damage, throat irritation, dizziness, reddening, and swelling of the skin.

Carcinogenicity

Acetaldehyde is a probable or possible carcinogen in humans.[29][33] In 1988 the International Agency for Research on Cancer stated, "There is sufficient evidence for the carcinogenicity of acetaldehyde (the major metabolite of ethanol) in experimental animals."[34] In October 2009 the International Agency for Research on Cancer updated the classification of acetaldehyde stating that acetaldehyde included in and generated endogenously from alcoholic beverages is a Group I human carcinogen.[35] In addition, acetaldehyde is damaging to DNA[36] and causes abnormal muscle development as it binds to proteins.[37]

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The World Health Organization has classified pickled foods as a possible carcinogen, based on epidemiological studies.[14] Other research found that fermented food contains a carcinogenic by-product, ethyl carbamate (urethane).[15][16] "A 2009 review of the existing studies conducted across Asia concluded that regularly eating pickled vegetables roughly doubles a person's risk for esophageal squamous cell carcinoma."[17]