Dioxins

FIGURE 16.9 Tetrachlorodibenzo-p-dioxin (TCDD).

Liver lesions, adrenal atrophy, chloracne, and kidney abnormalities have been reported. Both skin and kidney effects appear in many species, which are likely targets for TCDD toxicity. In addition, TCDD is a promoter of carcinogenesis and is a carcinogen. Liver tumors and tumors of the mouth, nose, and lung have been found. TCDD may be three times more potent a carcinogen than is aflatoxin Bj. In addition, TCDD is a potent teratogen in mice and rabbits. Pregnancy ends in dose-dependent increased resorption and higher rates of postimplantation loss. TCDD is fetotoxic to the rhesus monkey, resulting in higher levels of abortion and death in pregnant females.

Based on the outcome of accidental TCDD exposures to humans, people seem to be less sensitive to the toxic effects of TCDD. Many hundreds of cases involving industrial accidents, and in one situation 37,000 residents of Seveso, Italy, had no fatalities. Documented toxic effects in humans include chloracne, fatigue, disturbances in the peripheral nervous system, and liver toxicity.

The most publicized health claim of neurological and particularly teratogenic effects made about TCDD was the exposure of Vietnam veterans to Agent Orange. Agent Orange was the military code name given to the fifty-fifty mixture of herbicides 2,4,5-T and 2,4-D. During the Vietnam War, Agent Orange was credited with saving many lives of the U.S. military by destroying enemy food crops. Dioxin was known to be a contaminant in 2,4,5-T, but dioxin has never been shown to be a human teratogen. In 1969, scientists reported a high rate of birth defects in laboratory animals exposed to 2,4,5-T and 2,4-D, which caused the suspension of the use of Agent Orange by the Department of Defense. In contrast to self-reported health problems by Vietnam veterans, studies by the National Cancer Institute and the American Cancer Society found no increased risk for most cancers and no links between birth defects and exposure to Agent Orange.

Heavy Metals Mercury

Mercury is a naturally occurring metal having several forms. Metallic mercury is a shiny, silver-white, odorless liquid. Mercury combines with other elements, such as chlorine, sulfur, or oxygen, to form inorganic mercury compounds or salts, which are usually white powders or crystals. Metallic mercury is used to produce chlorine gas and caustic soda, and is also used in thermometers, dental fillings, and batteries. Mercury also combines with carbon to make organic mercury compounds, such as methyl mercury, produced mainly by microscopic organisms in the water and soil. More mercury in the environment can increase the amounts of methyl mercury that the small organisms make.

The nervous system is very sensitive to all forms of mercury. Methyl mercury and metallic mercury vapors are more harmful than other forms, because more mercury in these forms reaches the brain. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Short-term exposure to high levels of metallic mercury vapors may cause lung damage, nausea, vomiting, diarrhea, increases in blood pressure or heart rate, skin rashes, and eye irritation. There is inadequate human cancer data for all forms of mercury. Mercuric chloride has caused increases in several types of tumors in rats and mice, and methyl mercury has caused kidney tumors in male mice. Thus, the EPA has concluded that mercuric chloride and methyl mercury are possible human carcinogens.

Children are more sensitive to mercury than are adults, and mercury in the mother's body passes to the fetus. Mercury can also pass to a nursing infant through breast milk. However, most scientists agree that the benefits of breast-feeding may be greater than the possible adverse effects of mercury in breast milk. Children poisoned by mercury may develop problems in their nervous and digestive systems and suffer from kidney damage.

The EPA has set a limit of 2 parts of mercury per billion parts of drinking water (2 ppb). The Food and Drug Administration (FDA) has set a maximum permissible level of 1 part of methyl mercury in a million parts of seafood (1 ppm). Three major scientific arms (fishing industry, government agencies, and scientific bodies) may also be on a collision course. Fish are a good low-cost, low-fat source of nutrition, rich in healthy omega-3 fatty acids. However, there is strong indication that children in utero are more sensitive than adult humans. This stance is supported by two large controlled longitudinal studies of effects of prenatal mercury exposure from seafood consumption on child neurodevelopment (Seychelles Islands in the Indian Ocean and Faroe Islands near Scotland). Large, long-lived predatory ocean fishes, such as tuna, swordfish, king mackerel, and shark, bioaccumulate methyl mercury in the edible portions.

Some local and state agencies have had regulatory programs in effect for more than 20 years. In Wisconsin, women of childbearing years, nursing mothers, and children below 15 years have been warned only to eat one meal per week of bluegill, sunfish, crappie, yellow perch, or bullheads and only one meal per month of pike, catfish, sturgeon, carp, and bass.

It is well established that the organic forms, such as methyl mercury, are the more toxic mercury compounds. Their effects on the nervous system follow a sharp dose-response curve. The mechanisms of action involve the property of lipid solubility and the affinity of such compounds for protein sites rich in sulfhydryl groups. These same sites are frequently responsible for the functional properties of many proteins, such as enzymic activity and redox reactions. Methyl mercury is toxic to cerebral and cerebellar cortices, causing focal necrosis of neurons and destruction of glial cells. In addition, methyl mercury is a known teratogen.

The paradox becomes more complicated when one considers that several nutrients have a profound effect on mercury and methyl mercury toxicity (selenium, zinc, vitamins C and E). For more than 30 years, the protective effects of selenium against mercury have been known. Many marine organisms that have high tissue levels of mercury also have high tissue levels of selenium, or a mercury-to-selenium tissue ratio of 1:1 stoichiometrically. Thus, the apparent survival of certain species in the conditions of mercury intoxication may be related to a detoxification mechanism involving interactions between mercury and selenium. An interaction between the two elements may involve sequestering and neutralizing the toxic effects of either ionic mercury or organic mercury. Selenite (SeO3) may act to both demethylate methyl mercury and form a molecular detoxification product of selenite and mercuric ion, which exhibits similarities to a synthetic Hg-Se-S species. Research in Europe has demonstrated the usefulness of a remediation process of adding selenium salts to mercury-contaminated lakes. The work has resulted in improving the ecology of such areas, including survival of endogenous aquatic organisms. However, U.S. agencies have not willingly grasped the concept of using a toxic element to remediate another toxic element.

Much more research is needed to develop a better understanding about the potential toxicant-dietary interactions and special susceptibilities. There are critical data gaps on exposure and neurological, immunological, and cardiovascular effects from toxicant-nutrient interactions. It is possible that such interactions result in overall better nutrition, health, and ecological stability.

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