Mineral toxicity
Mineral toxicity is a condition in which the concentration in the body of anyone of the minerals is abnormally high and results in an adverse effect on health. Mineral nutrients are the inorganic elements or inorganic molecules that are required for life. The inorganic nutrients in human nutrition includewater, sodium, potassium, chloride, calcium, phosphate, sulfate, magnesium, iron, copper, zinc, manganese, iodine, selenium, and molybdenum.
In general, mineral toxicity results when there is an accidental consumptionof too much of a mineral, as with drinking ocean water (sodium toxicity); taking too much of a mineral supplement (available in most drug and health stores); or with overexposure to industrial pollutants, household chemicals, or certain drugs. Mineral toxicity may also apply to toxicity that can be the result of certain diseases or injuries. For example, hemochromatosis leads to iron toxicity; Wilson's disease results in copper toxicity; severe trauma can lead to hyperkalemia (potassium toxicity).
Depending on the mineral, the effects vary and toxicity occurs at different levels of the mineral in the body. An increase in the concentrations of sodiumin the bloodstream can result in seizures and death. Increased plasma sodium, which is called hypernatremia, causes various cells of the body, includingthose of the brain, to shrink. Shrinkage of the brain cells results in confusion, coma, paralysis of the lung muscles, and death. Death has occurred wheretable salt (sodium chloride) was accidently used, instead of sugar, for feeding infants. Death due to sodium toxicity has also resulted when baking soda(sodium bicarbonate) was used during attempted therapy of excessive diarrheaor vomiting. Although a variety of processed foods contain high levels of sodium chloride, the levels used are not enough to result in sodium toxicity.
Excessive levels of potassium in the bloodstream (severe hyperkalemia) can result in cardiac arrhythmias or even death due to cardiac arrest. Potassium ispotentially quite toxic, however toxicity or death due to potassium poisoning is usually prevented because of the vomiting reflex. The consumption of food results in mild increases in the concentration of potassium in the bloodstream, but levels of potassium do not become toxic because of the uptake of potassium by various cells of the body, as well as by the action of the kidneystransferring the potassium ions from the blood to the urine. The body's regulatory mechanisms can easily be overwhelmed, however, when potassium chlorideis injected intravenously, and high doses of injected potassium can result indeath.
Iodine toxicity results in impairment of the creation of thyroid hormone, resulting in lower levels of thyroid hormone in the bloodstream. The thyroid gland enlarges, as a consequence, and goiter is produced. This enlargement is also called hyperthyroidism. (Goiter is usually caused by iodine deficiency.) Iodine toxicity produces ulcers on the skin called "kelp acne" because of itsassociation with eating kelp, an ocean plant which contains high levels of iodine. Iodine toxicity occurs in Japan, where large amounts of seaweed are consumed.
Iron toxicity is not uncommon, due to the wide distribution of iron pills. Alethal dose of iron is in the range of 200-250 mg iron/kg body weight. Hence,a child who accidently eats 20 or more iron tablets may die as a result of iron toxicity. Within six hours of ingestion, iron toxicity can result in vomiting, diarrhea, abdominal pain, seizures, and possibly coma. Although symptoms may appear to improve, this improvement can be followed by shock, low bloodglucose, liver damage, convulsions, and death within 12-48 hours after toxiclevels of iron are ingested.
Nitrite poisoning occurs during a reaction with the iron atom of hemoglobin,an iron-containing protein that resides within the red blood cells. This protein is responsible for the transport of nearly all of the oxygen from the lungs to various tissues and organs of the body. A very small fraction of hemoglobin spontaneously oxidizes per day, producing a protein of a slightly different structure, called methemoglobin. Normally, the amount of methemoglobin constitutes less than 1% of the total hemoglobin. Methemoglobin can accumulatein the blood as a result of nitrite poisoning. Infants are especially susceptible to poisoning by nitrite.
Nitrate, which is naturally present in green leafy vegetables and in water israpidly converted to nitrite by the naturally occurring bacteria residing onthe tongue, as well as in the intestines, and then absorbed into the bloodstream. Poisoning by nitrite, or nitrate after its conversion to nitrite, results in the inability of hemoglobin to carry oxygen throughout the body, identifited by a bluish skin color. Adverse symptoms occur when over 30% of the hemoglobin has been converted to methemoglobin, and these symptoms include cardiac arrhythmias, headache, nausea and vomiting, and in severe cases, seizures.
Calcium and phosphate are closely related nutrients. Calcium toxicity is rare, but overconsumption of calcium supplements may lead to deposits of calciumphosphate in the soft tissues of the body. Phosphate toxicity can occur withoveruse of laxatives or enemas that contain phosphate. Severe phosphate toxicity can result in hypocalcemia, and in various symptoms resulting from low plasma calcium levels. Moderate phosphate toxicity, occurring over a period ofmonths, can result in the deposit of calcium phosphate crystals in various tissues of the body.
Zinc toxicity is rare but can occur in metal workers who are exposed to fumescontaining zinc. Excessive dietary supplements of zinc can result in nausea,vomiting, and diarrhea, and copper deficiency because zinc inhibits the absorption of copper.
Severe alterations in copper metabolism occur in two genetic diseases, Wilson's disease and Menkes' disease, both of which are rare and occur in about onein 100,000 births. Both diseases involve mutations in the proteins that transport copper, that is, in special channels that allow the passage of copper ions through cell membranes. Wilson's disease tends to occur in teenagers andin young adults and usually lasts throughout their lives. Copper accumulatesin the liver, kidney, and brain, resulting in damage to the liver and nervoussystem. Wilson's disease can be successfully controlled by lifelong treatment with d-penicillamine. Treatment also involves avoiding foods that are highin copper, such as liver, nuts, chocolate, and mollusks. After an initial period of treatment with penicillamine, Wilson's disease may be treated with zinc supplements to inhibit the absorption of dietary copper.
Selenium toxicity occurs in regions of the world, including some parts of China, where soils contain high levels of selenium that are then found in foodsand water. Early signs of selenium toxicity include nausea, weakness, and diarrhea. With continued intake of selenium, changes in fingernails and hair loss results, and damage to the nervous system occurs. The breath may acquire agarlic odor.
Manganese toxicity occurs in manganese mine workers, where men breath air containing dust bearing manganese. It has been documented in Chile, India, Japan, Mexico, and elsewhere. Symptoms of manganese poisoning can occur within several months or years of exposure and include a mental disorder resembling schizophrenia, as well as hyperirritability, violent acts, hallucinations, and difficulty in walking.
The prognosis for treating toxicity due to sodium, potassium, calcium, iodineand phosphate is usually excellent. Toxicity due to the deposit of calcium phosphate crystals is not usually reversible. For any mineral overdose that causes coma, seizures, or nerve damage the prognosis for recovery is often poor, and death results in a small fraction of patients.
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