Mineral Toxicity

views updated May 11 2018

Mineral toxicity

Definition

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.

Description

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.

Demographics

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:

Sodium: An increase in sodium concentration in the bloodstream can be toxic. The normal concentration of sodium in human 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 the cells in various body tissues, 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 when table salt (sodium chloride) was accidentally used to feed infants instead of sugar. Death due to sodium toxicity has also resulted when baking soda (sodium bicarbonate) was used to treat excessive diarrhea or vomiting . Although a variety of processed foods contain high levels of sodium chloride, the levels in these items are not enough to result in sodium toxicity.
Potassium: 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, 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 these 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: Iodine toxicity can result from an intake of 2.0 mg of iodide per day. Toxic levels of iodine inhibit the secretion of thyroid hormone, resulting in lower levels of thyroid hormone in the bloodstream. As a result, the thyroid gland becomes enlarged. This condition is known as goiter or hyperthyroidism . Goiter is usually caused by iodine deficiency. In addition to goiter, iodine toxicity produces a brassy taste in the mouth, excessive production of saliva, and ulcers on the skin. This skin condition has been called kelp acne because of its association with eating kelp, an ocean plant that contains high levels of iodine. Iodine toxicity occurs fairly frequently in Japan, where people consume large amounts of seaweed.
Iron: Iron toxicity is not unusual in small children due to the wide distribution of dietary supplements containing iron. A lethal dose of iron is in the range of 200—250 mg iron/kg body weight, meaning that a child who accidentally eats 20 or more iron tablets may die as a result of iron poisoning. Children are unfortunately likely to take large amounts of these pills because they look like candy. Within six hours of ingestion, iron toxicity can result in vomiting, diarrhea, abdominal pain , seizures, and possibly coma. In the second period of iron poisoning, the patient's symptoms appear to improve; however, this phase is followed by a terminal phase in which shock, low blood sugar levels, liver damage, convulsions, and death occur 12 to 48 hours after the fatal dose.
Nitrite: Nitrite poisoning should be considered along with iron toxicity, since nitrite produces its toxic effect by reacting with the iron atom in hemoglobin. Hemoglobin is an iron-containing protein that resides within the red blood cells. This protein is responsible for transporting nearly all of the oxygen acquired from the lungs to various tissues and organs of the body. Hemoglobin accounts for the red color of red blood cells. 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 percent 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: Nitrate is naturally present in green leafy vegetables and in the water supply. It is rapidly converted to nitrite by the bacteria that live in the mouth as well as in the intestines and then absorbed into the bloodstream. The amount of nitrate that is supplied by leafy vegetables and drinking water is generally about 100 to 170 mg/day. The amount of nitrite supplied by a typical diet is much lower, about 0.1 mg nitrite per 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 percent of the hemoglobin has been converted to methemoglobin. These symptoms include cardiac arrhythmias, headache , nausea and vomiting , and in severe cases, seizures.
Calcium and phosphate: 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 result from the 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 may result in the deposit of calcium phosphate crystals in various tissues of the body.
Zinc: Zinc toxicity is rare but is more likely to occur in adults than in children. It is usually related to occupational hazards and has been reported to occur in metal workers exposed to fumes containing zinc. A few instances of zinc toxicity have been reported in people who consumed acidic food or beverages that had been stored in galvanized zinc containers. Taking excessive supplemental 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.
Copper: Copper toxicity in humans is usually the result of disease. Severe alterations in copper metabolism occur in two genetic diseases, Wilson's disease and Menkes disease. These diseases are rare. They 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, which is caused by a mutation of the ATP7B gene on chromosome 13, first produces symptoms in teenagers and young adults. Copper accumulates in the liver, kidney, and brain, resulting in damage to the liver and nervous system. In Menkes disease, which is usually first noticed in infancy, impaired transport of copper from the digestive tract results in low levels of copper in the blood, while copper accumulates in the kidney, pancreas, and skeletal muscle. Children with Menkes disease have characteristic kinky hair, seizures, developmental failures, and progressive degeneration of the brain.
Selenium: Selenium toxicity occurs in a few regions of the world, most notably some parts of China where soils contain high levels of the mineral. A daily intake of 0.75 to 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. Continued intake of selenium results in changes in the fingernails, hair loss, and damage to the nervous system. The person's breath may acquire a characteristic garlic odor as a result of the increased production of dimethylselenide in the body and its release via the lungs.
Manganese: Manganese toxicity is most likely to affect adults rather than children. It occurs most commonly in workers in manganese mines who must breathe air containing high levels of manganese dust (in 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.

When to call the doctor

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.

Diagnosis

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.

Treatment

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.

Nutritional concerns

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.

Prognosis

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.

Prevention

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.

See also Heavy metal poisoning; Poisoning.

KEY TERMS

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.

Resources

BOOKS

"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.

PERIODICALS

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.

ORGANIZATIONS

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

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

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

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

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

WEB SITES

Chang, Celia H. "Menkes Disease." eMedicine, February 8, 2002. Available online at <www.emedicine.com/neuro/topic569.htm> (accessed November 29, 2004).

Spanierman, Clifford. "Toxicity, Iron." eMedicine, April 12, 2004. Available online at <www.emedicine.com/emerg/topic285.htm> (accessed November 29, 2004).

Tom Brody, PhD

Gale Encyclopedia of Children's Health: Infancy through Adolescence Brody, Tom

Mineral Toxicity

views updated May 21 2018

Mineral Toxicity

Definition

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.

Description

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 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.

Diagnosis

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.

Treatment

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.

Prognosis

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.

Prevention

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.