The environmental contamination of food is a result of our modern, high-technology society. We produce and consume large volumes of a wide variety of substances, some of which are toxic.

Environmental contamination of food takes two forms; long-term low-level contamination resulting from gradual diffusion of persistent chemicals through the environment and relatively shorter term, higher level contamination stemming from industrial accidents and waste disposal.

An example of low-level contamination is polychlorinated biphenyls (PCBs). This group of substances was widely used in transformers and capacitors, as heat- transfer fluids and as an additive in dyes, carbon paper, pesticides and plastics.

An example of the second type of contamination is polybrominated biphenyls (PBBs) in dairy products and meat. PBBs, a fire retardant were accidentally mixed into animal feed. Dairy cattle that were fed the contaminated food produced contaminated milk. The distinctions between the two types of food contamination are not exclusive. For example, PBBs have now become a long-term, low-level contaminant in Michigan because they are very stable and resistant to decay. Animals raised on farms effected by the original feed contamination are now contaminated by the PBB residues remaining in the pastures and farm buildings.

HOW FOOD BECOMES CONTAMINATED: -

Chemicals contaminate foods through different routes depending on the chemical and its physical properties, its use, and the source or mechanism of contamination.

Organic substances that have contaminated food have been either industrial or agricultural chemicals. Pesticides are the only agricultural chemicals known to be environmental contaminants in food. A pesticide becomes an environmental contaminant when it is present in foods for which the application or use of the substance has not been approved. Livestock, poultry and fish can be contaminated when application or manufacturing of pesticides occurs in the vicinity or when residues are transported through the environment. Improperly fumigated railroaders, trucks, ships or storage of human food and animal food are also sources of environmental contamination. The interiers are sprayed or fumigated with pesticides and if not sufficiently aired contamination of the food or food occurs.

The manufacture of organic chemicals produces sludges, gases and liquid effluents or varying chemical complexities. The usual waste disposal methods (sewage systems, incineration, landfill) are unable to prevent organic residues from entering the environment in spite of several laws and corresponding regulations governing disposal. The routes include the atmosphere, soil and surface or ground water.

Metals can be released into the environment in several ways. The mining and refining processes produce dust and gases which enter the atmosphere. Metallic salts formed during recovery and refining processes can escape as waste products into surface and ground water. Sewage sludge used as fertilizer on agricultural land also poses a potential food contamination problem. Trace metals present in the sludge can be taken up by crops grown on treated soil. Cadmium is the trace metal in sludge that currently generates the greatest concern.

Radioactivity in food stems from three sources; natural radioactivity, releases from operation of nuclear reactors and processing plants and fallout from nuclear weapons tests. The primary route by which food becomes contaminated is the deposition of airborne material on vegetation or soil. The subsequent fate of the radionuclide is determined by its chemical and physical nature and whether it is absorbed and metabolized by piants or animals. Natural radioactivity may become a concern when ores containing radioactive substances are mined and processed. The products or wastes or slags from phosphorus production. Radium may enter the food chain when it dissolves in ground water and is taken up through plant roots.

Nuclear reactors normally release radioactive noble gases that do not contaminate foods. Reactors do contain large inventories of fission products, transuranies and other activation products. Accidental release can contaminate vegetation by deposition of particles on leaves and soil or through water. Gaseous releases would most likely involve the volatile elements such as iodine and tritium or those with volatile precursors, such as strontium 90 and cesium 137. Aqueous releases would follow failure of the onsite ionexchange cleanup system. Any of the water-soluble elements could be involved.

Nuclear waste-processing plants could also have either gaseous or aquecous release. In this case, the fission products are aged before processing and iodine and the gaseous procurser radionuclides are not released. Tritium and carbon 14 are the major airborne products, while the waterborne radionuclides are the same as for reactors.

Atmospheric nuclear weapons tests distribute their fission products globally. Local deposition depends on the size of the weapon and the conditions of firing (high altitude surface or underground.)

Some striking incidents :-

PCBs occur in food as the result of environment contamination leading to accumulation in the food chain, direct contact with food or animal feeds, or contact with food packaging materials made form recycled paper containing PCBs.

In the early part of 1968 the accidental contamination of edible rice-bran oil led to a poisoning epidemic among the Japanese families who consumed the oil. The disease became known as Yusho or rice-oil disease. Its chief symptoms were chloracne (a severe form of acne) and eye discharge; other symptoms include skin discoloration, headaches, fatigue, abdominal pain, menstrual changes and liver disturbances. Babies born to mothers who consumed the rice oil were abnormally small and had temporary skin discoloration. The first symptoms of Yusho disease were registered on June 7, 1968 and 1291 cases had been reported as of May 1975.

The Yusho study, nevertheless had two important results; first the information established that PCBs can be transferred from mother to fetus and from mother to child through breast feeding and second highly chlorinated PCB compounds are excreted more slowly from the body than less chlorinated ones.

More recent experiments in animals have demonstrated a variety of toxic effects. Cancers have been produced in mice and rats fed PCBs equivalent to the amounts consumed bu Yush patients developed similar reproductive disorders. Young monkeys nursing on mothers consuming feed containing PCB developed toxic effects and behavieral abnormalities.

Foods are the major source of human exposure to mercury. The mercury concentration in food is dependent on the type of food, the environmental level of mercury in the area where the food is produced, and the use of mercury containing compounds in the agricultural and industrial production of the food. All living organisms have the ability to concentrate mercury. Therefore, all animal and vegetable tissues contain at least trace amounts.

In the Minamata Bay tragedy in Japan the effects of chronic exposure to methyl mercury have been well-documented. It has been observed that a factory nearby Minamata Bay used to discharge its effluent in that bay. The effluent contained considerable amount of mercury. This mercury was converted to methyl mercury by different microorganisms present in the underground soil of the bay. This methyl mercury accumulates in the fishes of the bay and the people were seriously effected by consuming those fishes. Many people died and some developed paralysis.

Mercury readily accumulated within the central nervous system and clearence of mercury back into the bloodstream is slow. Consequently, the central nervous system is considered to be the critical target in chronic mercury exposure. The clinical symptoms of Central nervous system involvement include headache, vertige, vasomotor disturbance, ataxia, and pain and numbness in the extromities.

In evaluating the teratogenic hazards of mercury exposure to man, the placental transfer of mercury is particularly significant. Levels that are not toxic to pregnant women are sufficient to produce birth defects in their offspring.

In human, the most widely reported fetal risk associated with maternal exposure to mercury is brain damage. The placental transfer of mercury and its effects on the human fetus were first recognized in the 1950's with the well-known outbreak of congenital Minamata disease in the towns of Minamata and Niigata, Japan. By 1959, 23 infants suffering from mental retardation and motor to mothers exposed to methylmercury during their pregnancies. The clinical symptoms of the infants resembled those of severe cerebral palsy or cerebral disfunction syndrome. They included disturbance of coordination, speech and hearing constriction of visual field; impairment of chewing and swallowing; enhanced tendon reflex; pathological reflexes; involuntary movement; primitive reflexes; superficial sensation; salivation; and forced laughing. Only 1 of the 23 mothers exhibited any symptoms of mercury poisoning.

Ionizing radiation (X-rays, gamma rays, or beta particles with sufficient energy to strip electrons from molecules and produce ions can produce birth defects, mutations, and cancers. These adverse health effects are usually associated with high dose levels delivered at high dose rates.

Such a combination is not ordinarily encountered in food Previous radioactive contamination of foods has involved relatively small quantities of radioactive elements which have delivered low dose rates.

In these situations, the effects of the radiation exposure on health are extremely difficult to evaluate. High does rates (100 million to 1 billion times background) are estimated to produce 2,6000 ionization events per second in cells. Background radiation levels are estimated to produce less than one ionization in the cell nucleus per day. Because cells have the capacity to repair of ionization damage may occur at low radiation exposure. Higher exposures may overwhelm the cell's repair capacity. Whether any effects are observed in such cases depends on several factors. These include the dose delivered to the tissues, the nature of the emissions, and the metabolism of the cell. The following examples, illustrate these points:

Strontium 90 in food arouses most concern not only because of its long half-life but also because it behaves in the body in a manner somewhat similar to calcium. The replacement of bone calcium with strontium 90 exposes tissues and cells covering the bone to radiation. In addition bone marrow is subject to the ionizing radiation from the strontium 90. Thus, cancer of the bone-forming and bone-covering tissue as well as leukemias of the bone marrow blood-forming cell can possibly result.

Iodine is concentrated by the thyroid gland. Radioiodines produced in atmospheric nuclear detonations or released from nuclear power stations are also taken up and concentrated by the thyroid, increasing the risk of thyroid cancer.

Tritium, or radioactive hydrogen, combines chemically with oxygen to form water. Tritium derived from food would be widely distributed throughout the body exposing all tissues to radiation.

The uncertainties surrounding the repair capacities of cells and the irreversible nature of the possible health effects have led to the adoption in the United States of a prudent policy towards low level ionizing radiation. Since any amount of radiation is potentially harmful, unnecessary exposure should be avoided.