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Mineral Toxicity


The term mineral toxicity refers to a condition in which the concentration in the body of any one of the minerals necessary for life is abnormally high, and which has an adverse effect on health.


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, fluorine, copper, zinc, chromium, manganese, iodine, selenium, and molybdenum. The last nine elements in this list are sometimes called trace minerals or micronutrients because humans need only small amounts of them in the diet. In high doses all nine trace minerals can be toxic in humans.

In general, mineral toxicity results when a person accidentally consumes too much of any mineral, as with drinking ocean water (sodium toxicity), or is overexposed to industrial pollutants, household chemicals, or certain drugs. Iron toxicity in children, for example, frequently results from accidental swallowing of dietary supplement tablets.

Mineral toxicity may also refer to toxic conditions resulting from certain diseases or injuries. For example, a disorder known as hemochromatosis leads to iron toxicity, while Wilson's disease results in copper toxicity. Severe trauma can lead to hyperkalemia or potassium toxicity.


Iron poisoning is the most common form of mineral toxicity in children in the United States and is one of the leading causes of fatal poisoning in children younger than six years of age. About 20,000 children are reported as accidentally swallowing iron tablets each year in the United States, although not all of these cases end in death. In one Indian study of 21 children treated for iron poisoning, four of the patients died.

With regard to diseases leading to mineral toxicity, about one person in ten in the United States has the genetic mutation that can lead to hemochromatosis; however, not everyone with this mutation necessarily develops the disease. It is thought that there are about 1 million persons in the United States with hemachromatosis as of the early 2000s. About one person in 30,000 has the genetic defect that causes Wilson's disease, while about 1.1 percent of the general population are carriers of the mutant gene. The incidence of Menkes disease, which primarily affects boys, is variously estimated at one in 50,000 to one in 250,000 persons. Wilson's disease and Menkes disease occur at the same rate in all races and ethnic groups.

Causes and symptoms

The causes and symptoms of mineral toxicity depend on the specific mineral in question:

The most common form of mineral toxicity for children and adolescents in the United States is accidental poisoning from iron supplements. Parents should take a child who is known to have swallowed iron tablets to the doctor or a hospital emergency room for treatment as soon as possible, as an iron overdose is potentially fatal.

Children born into families with a history of Wilson's disease should have a blood test for the disease at some point in their second year of life, before symptoms of the disease develop.


An initial diagnosis of mineral toxicity requires taking a careful history. The doctor asks the parents of a small child questions intended to identify any unusual aspects of the family's diet or intake of drugs and chemicals. An older teenager in the workforce may be asked about possible occupational exposure. The mineral content of the body may be measured by testing samples of body fluids, most commonly blood plasma, red blood cells from whole blood, and urine. Diagnosis of mineral toxicities also involves measuring the concentration of various metals in the plasma or urine. Concentrations that are above the normal range can confirm the initial suspected diagnosis.

Menkes disease may be diagnosed by the unusual appearance of the hair, skin, and facial features in male infants with the disorder as well as by their developmental problems.

In addition to a deficiency in blood plasma of a protein known as ceruloplasmin, Wilson's disease is characterized by gold or greenish-gold discolorations of the cornea of the eye known as Kayser-Fleischer rings. These rings may be detected by an ophthalmologist during a slit-lamp examination. The doctor may also suspect Wilson's disease in a child above the age of five with unexplained episodes of hepatitis or such symptoms of copper toxicity in the brain as drooling, loss of coordination, tremor, sudden drop in academic performance, or frank psychotic episodes. The clinical symptoms of Wilson's disease do not appear in young children; however, measurements of serum ceruloplasmin can be taken in children over 12 months of age if a family history of Wilson's disease is a risk factor.


Iron toxicity is treated by efforts to remove the remaining iron from the stomach by administering a solution of 5 percent sodium bicarbonate. Where plasma iron levels have risen 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 giving him or her lifelong doses of the drug L-dopa. The treatment is only partially successful. Treatment of nitrite or nitrate toxicity involves inhalation of 100 percent oxygen for several hours. If oxygen treatment is not effective, then a solution of 1.0 percent methylene blue may be injected in a dose of 1.0 mg methylene blue/kg body weight.

With regard to disorders of copper metabolism, Wilson's disease can be successfully controlled by lifelong treatment with d-penicillamine, trientine, and zinc acetate. 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. Patients with this disease must, however, comply with treatment for the rest of their lives, as untreated Wilson's disease is invariably fatal. Patients who develop liver failure as a result of the disease may be candidates for a liver transplant.

Children with Menkes disease are sometimes helped temporarily by intravenous injections of copper supplements. There is, however, no cure for the disease as of the early 2000s, and most children with the disorder live only a few years.

Families consuming a well-balanced diet without overuse of dietary supplements are unlikely to have problems with mineral toxicity. Children or adolescents diagnosed with Wilson's disease must observe the dietary limitations described earlier.


The prognosis for mineral 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. Wilson's disease is fatal, usually before age 30, unless the patient complies with continual lifelong treatment to prevent brain or liver disease. Children diagnosed with Menkes disease rarely live past their third birthday.


When mineral toxicity results from the excessive consumption of mineral supplements, toxicity can be prevented by minimizing the use of dietary supplements and keeping iron tablets in particular out of the reach of children. Zinc toxicity may be prevented by not storing food or beverages in zinc containers. In the case of iodine, toxicity can be prevented by avoiding overconsumption of seaweed or kelp. In the case of selenium toxicity resulting from high-selenium soils, toxicity can be prevented by relying on food and water acquired from a low-selenium region.

Such genetic diseases as Wilson's disease and Menkes disease cannot be prevented as of the early 2000s.

Parental concerns

Parental concerns about mineral toxicity in most children should be directed toward preventing accidental consumption of iron and other mineral supplements in young children and in monitoring the adoption of fad diets in teenagers.

In the case of children with hemachromatosis or Wilson's disease, parents will need to make sure that the affected child complies with all aspects of necessary treatment. In the case of a child with Menkes disease, parents should seek genetic counseling, as the grim prognosis of this illness places a heavy emotional as well as economic burden on a family.


Arrhythmia —Any deviation from a normal heart beat.

Goiter —Chronic enlargement of the thyroid gland.

Hemochromatosis —An inherited blood disorder that causes the body to retain excessive amounts of iron. This iron overload can lead to serious health consequences, including painful joints, diabetes, and liver damage, if the iron concentration is not lowered.

Hyperkalemia —An abnormally high level of potassium in the blood.

Hypernatremia —An abnormally high level of sodium in the blood.

Hypocalcemia —A condition characterized by an abnormally low level of calcium in the blood.

Menkes disease —A genetic disease caused by a mutation on the X chromosome and resulting in impaired transport of copper from the digestive tract. It was first identified in 1962.

Methemoglobin —A compound formed from hemoglobin by oxidation of its iron component. Methemoglobin cannot carry oxygen.

Micronutrient —An organic compound such as vitamins or minerals essential in small amounts and necessary to the growth and health of humans and animals.

Trace element —An element that is required in only minute quantities for the maintenance of good health. Trace elements are also called micronutrients.

Wilson's disease —A rare inherited disease in which excessive amounts of copper accumulate in the liver or brain. It is fatal unless the patient complies with lifelong treatment with penicillamine and zinc oxidase. Wilson's disease is also known as inherited copper toxicosis.


"Mineral Deficiency and Toxicity." Section 1, Chapter 4 in The Merck Manual of Diagnosis and Therapy , edited by Mark H. Beers and Robert Berkow. Whitehouse Station, NJ: Merck Research Laboratories, 2002.

Dunn, A. M., C. Burns, and B. Sattler. "Environmental Health of Children." Journal of Pediatric Health Care 17 (September-October 2003): 223–31.

Singhi, S. C., and A. K. Baranwal. "Acute Iron Poisoning: Clinical Picture, Intensive Care Needs, and Outcome." Indian Pediatrics 40 (December 2003): 1177–82.

U.S. Preventive Services Task Force. "Screening for Presence of Deficiency, Toxicity, and Disease." Nutrition in Clinical Care 6 (October-December 2003): 120–22.

American Academy of Emergency Medicine (AAEM). 555 East Wells Street, Suite 1100, Milwaukee, WI 53202. Web site:

American Academy of Family Physicians (AAFP). 11400 Tomahawk Creek Parkway, Leawood, KS 66211–2672. Web site:

National Institute of Child Health and Human Development (NICHD). 31 Center Drive, Room 2A32, Bethesda, MD 20892–2425.

National Organization for Rare Disorders Inc. (NORD). 55 Kenosia Avenue, Danbury, CT 06813–1968. Web site:

Wilson's Disease Association International (WDA). 1802 Brookside Drive, Wooster, OH 44691. Web site:

Chang, Celia H. "Menkes Disease." eMedicine , February 8, 2002. Available online at (accessed November 29, 2004).

Spanierman, Clifford. "Toxicity, Iron." eMedicine , April 12, 2004. Available online at (accessed November 29, 2004).

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