Mineral Toxicity

Mineral Toxicity



The term mineral toxicity means a condition where the concentration in the body of any one of the minerals is abnormally high, and where there is an adverse effect on health.


In general, mineral toxicity results when there is an accidental consumption of too much of any mineral, as with drinking ocean water (sodium toxicity) 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).
The mineral nutrients are defined as all the inorganic elements or inorganic molecules that are required for life. As far as human nutrition is concerned, the inorganic nutrients include water, sodium, potassium, chloride, calcium, phosphate, sulfate, magnesium, iron, copper, zinc, manganese, iodine, selenium, and molybdenum.
The mineral content of the body may be measured by testing samples of blood plasma, red blood cells, and urine.

Causes and symptoms

An increase in the concentrations of sodium in the bloodstream can be toxic. The normal concentration of sodium in the blood plasma is 136-145 mM, while levels over 152 mM can result in seizures and death. Increased plasma sodium, which is called hypernatremia, causes various cells of the body, including those of the brain, to shrink. Shrinkage of the brain cells results in confusion, coma, paralysis of the lung muscles, and death. Death has occurred where table 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 diarrhea or vomiting. Although a variety of processed foods contain high levels of sodium chloride, the levels used are not enough to result in sodium toxicity.
The normal level of potassium in the bloodstream is in the range of 3.5-5.0 mM, while levels of 6.3-8.0 mM (severe hyperkalemia) result in cardiac arrhythmias or even death due to cardiac arrest. Potassium is potentially 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 kidneys transferring the potassium ions from the blood to the urine. The body's regulatory mechanisms can easily be overwhelmed, however, when potassium chloride is injected intravenously, as high doses of injected potassium can easily result in death.
Iodine toxicity can result from an intake of 2.0 mg of iodide per day. The 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. In addition to goiter, iodine toxicity produces ulcers on the skin. This condition has been called "kelp acne," because of its association 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. A lethal 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. A latent period, where the symptoms appear to improve, may occur but it is followed by shock, low blood glucose, liver damage, convulsions, and death, occuring 12-48 hours after toxic levels of iron are ingested.
Nitrite poisoning should be considered along with iron toxicity, since nitrite produces its toxic effect by reacting with the iron atom of hemoglobin. Hemoglobin is an iron-containing protein that resides within the red blood cells. This protein is responsible for the transport of nearly all of the oxygen, acquired from the lungs, to various tissues and organs of the body. Hemoglobin accounts for the red color of our red blood cells. A very small fraction of our 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 accumulate in 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 the water supply is rapidly converted to nitrite by the naturally occurring bacteria residing on our tongue, as well as in the intestines, and then absorbed into the bloodstream. The amount of nitrate that is supplied by leafy vegetables and in drinking water is generally about 100-170 mg/day. The amount of nitrite supplied by a typical diet is much less, that is, than 0.1 mg nitrite/day. Poisoning by nitrite, or nitrate after its conversion to nitrite, results in the inability of hemoglobin to carry oxygen throughout the body. This condition can be seen by the blue color of the skin. 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 calcium phosphate in the soft tissues of the body. Phosphate toxicity can occur with overuse 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 of months, can result in the deposit of calcium phosphate crystals in various tissues of the body.
Zinc toxicity is rare, but it can occur in metal workers who are exposed to fumes containing zinc. Excessive dietary supplements of zinc can result in nausea, vomiting, and diarrhea. The chronic intake of excessive zinc supplements can result in copper deficiency, as zinc inhibits the absorption of copper.
Severe alterations in copper metabolism occur in two genetic diseases, Wilson's disease and Menkes' disease. Both of these diseases are rare and occur in about one in 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 and in young adults, and then remain for the lifetime. Copper accumulates in the liver, kidney, and brain, resulting in damage to the liver and nervous system. Wilson's disease can be successfully controlled by lifelong treatment with d-penicillamine. Treatment also involves avoiding foods that are high in copper, such as liver, nuts, chocolate, and mollusks. After an initial period of treatment with penicillamine, Wilson's disease may be treated with zinc (150 mg oral Zn/day). The zinc inhibits 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. A daily intake of 0.75-5.0 mg selenium may occur in these regions, due to the presence of selenium in foods and 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 a garlic odor, as a result of the increased production of dimethylselenide in the body, and its release via the lungs.
Manganese toxicity occurs in miners in manganese mines, where men breath air containing dust bearing manganese at a concentration of 5-250 mg/cubic meter. Manganese toxicity in miners has been documented in Chile, India, Japan, Mexico, and elsewhere. Symptoms of manganese poisoning typically occur within several months or years of exposure. These symptoms include a mental disorder resembling schizophrenia, as well as hyperirritability, violent acts, hallucinations, and difficulty in walking.


The initial diagnosis of mineral toxicity involves questioning the patient in order to determine any unusual aspects of the diet, unusual intake of drugs and chemicals, and possible occupational exposure. Diagnosis of mineral toxicities also involves measuring the metal concentration in the plasma or urine. Concentrations that are above the normal range can confirm the initial, suspected diagnosis.


Iron toxicity is treated by efforts to remove remaining iron from the stomach, by use of a solution of 5% sodium bicarbonate. Where plasma iron levels are above 0.35 mg/dL, the patient is treated with deferoxamine. Treatment of manganese toxicity involves removal of the patient from the high manganese environment, as well as lifelong doses of the drug L-dopa. The treatment is only partially successful. Treatment of nitrite or nitrate toxicity involves inhalation of 100% oxygen for several hours. If oxygen treatment is not effective, then methylene blue may be injected, as a 1.0% solution, in a dose of 1.0 mg methylene blue/kg body weight.


The prognosis for treating toxicity due to sodium, potassium, calcium, and phosphate is usually excellent. Toxicity due to the deposit of calcium phosphate crystals is not usually reversible. The prognosis for treating iodine toxicity is excellent. For any mineral overdose that causes coma or seizures, the prognosis for recovery is often poor, and death results in a small fraction of patients. For any mineral toxicity that causes nerve damage, the prognosis is often fair to poor.


When mineral toxicity results from the excessive consumption of mineral supplements, toxicity can be prevented by not using supplements. In the case of manganese, toxicity can be prevented by avoiding work in manganese mines. In the case of iodine, toxicity can be prevented by avoiding overconsumption of seaweed or kelp. In the case of selenium toxicity that arises due to high-selenium soils, toxicity can be prevented by relying on food and water acquired from a low-selenium region.



Brody, Tom. Nutritional Biochemistry. San Diego: Academic Press, 1998.
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