Metal toxicity or metal poisoning is the
toxic effect of certain
metals in certain forms and doses on
life. Some metals are toxic when they form
poisonous soluble compounds. Certain metals have no biological role, i.e. are not essential minerals, or are toxic when in a certain form.[1] In the case of
lead, any measurable amount may have negative health effects.[2] It is often thought that only
heavy metals can be toxic, but lighter metals such as
beryllium and
lithium may also be in certain circumstances. Not all heavy metals are particularly toxic, and some are essential, such as
iron. The definition may also include
trace elements when abnormally high doses may be toxic. An option for treatment of metal poisoning may be
chelation therapy, a technique involving the administration of
chelation agents to remove metals from the body.
Toxic metals sometimes imitate the action of an essential element, interfering with the metabolic processes resulting in
illness. Many metals, particularly
heavy metals are toxic, but some are essential, and some, such as
bismuth, have a low toxicity. Metals in an oxidation state abnormal to the body may also become toxic:
chromium(III) is an essential trace element, but
chromium(VI) is a
carcinogen.
Only soluble metal-containing compounds are toxic. Soluble metals are called
coordination complexes, which consist of a metal ion surrounded by
ligands. Ligands can range from water in
metal aquo complexes to methyl groups as in
tetraethyl lead. Usually metal complexes consist of a mixture of ligands.
Toxic metal complexes can be detoxified by conversion to insoluble derivatives or (ii) by encasing in rigid molecular environments using chelating agents. Alternatively, when very dilute, metal complexes are often innocuous.[3] This method uses plants to extract and lower the concentration of toxic heavy metals in the soil.[3] An aspirational method of decontamination of heavy metals is
phytoremediation or
bioremediation, but these approaches have solved few real world problems.
Toxic metals can
bioaccumulate in the body and in the
food chain.[4] Therefore, a common characteristic of toxic metals is the chronic nature of their toxicity. This is particularly notable with radioactive heavy metals such as
radium, which imitates
calcium to the point of being incorporated into human bone, although similar health implications are found in
lead or
mercury poisoning.
A dominant kind of metal toxicity is arsenic poisoning. This problem mainly arises from
ground water that naturally contains high concentrations of arsenic. A 2007 study found that over 137 million people indicates that more than 70 countries may be affected by arsenic poisoning from drinking water.[5]
Lead poisoning, in contrast to arsenic poisoning, is inflicted by industry. Most lead on the planet is immobilized as minerals, which are relatively harmless. Two major sources of lead poisoning are leaded gasoline and lead leached from plumbing (from Latin, plumbus for lead). Use of
leaded gasoline has declined precipitously since the 1970s.[6][7] One lead-containing pigments is
lead chromate (the yellow-orange of U.S. school buses), but this material is so stable and so insoluble that little evidence exists for its toxicity.
No evidence for biological action in mammals, but essential in some lower organisms. (In the case of the
lanthanides, the definition of an essential nutrient as being indispensable and irreplaceable is not completely applicable due to their extreme similarity. The stable early lanthanides La–Nd are known to stimulate the growth of various lanthanide-using organisms, and Sm–Gd show lesser effects for some such organisms. The later elements in the lanthanide series do not appear to have such effects.)[13]
Many metal ions are required for life. Even in these cases, a large excess of these ions can prove toxic.
Selenium poisoning has been observed even though Se is an essential
trace element. The
Tolerable Upper Intake Level is 400 micrograms per day. Additional Se intake can lead to selenosis.[15] Signs and symptoms of selenosis include a garlic odor on the breath, gastrointestinal disorders, hair loss,
sloughing of nails, fatigue, irritability, and neurological damage.
Zinc toxicity has been seen to occur at ingestion of greater than 225 mg of zinc.[16] Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish.[17][18][19]
Toxicities from nonessential metals
No global mechanism exists for the toxicities of these metal ions. Excessive exposure, when it occurs, typically is associated with industrial activities.
Beryllium poisoning is attributed to the ability of Be2+ to replace Mg2+ in some enzymes.[20] Be has been classified by one agency as a carcinogen.[21]
Cadmium poisoning came into focus with the discovery of the
Itai-itai disease due to cadmium contaminated waters resulting from mining in the
Toyama Prefecture starting around 1912.[22] The term refers to the severe
pains (Japanese: 痛い itai) people with the condition felt in the spine and joints. Cd2+ is thought to accumulate in the kidneys, where it tightly binds to the sulfur in
cysteine-containing proteins.[23]
Mercury poisoning came into sharp focus with the discovery of
Minamata disease, named for the Japanese city of
Minamata. In 1956, a factory in that city released of
methylmercury in the
industrial wastewater resulting in thousands of deaths and many other health problems.[25] This incident alerted the world to the phenomenon of
bioaccumulation. While all mercury compounds are toxic,
organomercury compounds are especially dangerous because they are more mobile.
Methyl mercury and related compounds are thought to bind to the sulfur of cysteinyl residues in proteins.[26]
Thallium poisoning has been observed on several occasions, and it is well known that
thallium compounds are highly toxic. Nonetheless, incidents of thallium poisoning are few.[30] Tl is located on the periodic table near two other highly toxic metals, mercury and lead.
Chelation therapy is a medical procedure that involves the administration of
chelating agents to remove or deactivate heavy metals from the body. Chelating agents are molecules that form particularly stable
coordination complexes with metal ions. Complexation prevents the metal ions from reacting with molecules in the body, and enable them to be dissolved in blood and eliminated in urine. It should only be used in people who have a diagnosis of metal intoxication.[32] That diagnosis should be validated with tests done in appropriate biological samples.[33]
Other conditions
This section needs to be updated. Please help update this article to reflect recent events or newly available information.(May 2024)
It is difficult to differentiate the effects of low level metal poisoning from the environment with other kinds of environmental harms, including nonmetal pollution.[34] Generally, increased exposure to heavy metals in the environment increases risk of developing cancer.[35]
^Ultratrace minerals. Authors: Nielsen, Forrest H. USDA, ARS Source: Modern nutrition in health and disease / editors, Maurice E. Shils ... et al. Baltimore: Williams & Wilkins, c1999., p. 283-303. Issue Date: 1999 URI:
[1]
^Muyssen, Brita T.A.; De Schamphelaere, Karel A.C.; Janssen, Colin R. (2006). "Mechanisms of chronic waterborne Zn toxicity in Daphnia magna". Aquatic Toxicology. 77 (4): 393–401.
doi:
10.1016/j.aquatox.2006.01.006.
PMID16472524.
^Zhiguang, Xiao; Wedd, Anthony G.; "Coping with Toxic Metals", pp 271-298 in "Metals, Microbes and Minerals: The Biogeochemical Side of Life" (2021) pp xiv + 341. Walter de Gruyter, Berlin. "Metals, Microbes and Minerals: . Walter de Gruyter, Berlin. Editors Kroneck, Peter M.H. and Sosa Torres, Martha.
Gruyter.com/document/doi/10.1515/9783110589771-009 DOI 10.1515/9783110589771-009
^Tabrez, Shams; Priyadarshini, Medha; Priyamvada, Shubha; Khan, Mohd Shahnawaz; NA, Arivarasu; Zaidi, Syed Kashif (2014). "Gene–environment interactions in heavy metal and pesticide carcinogenesis". Mutation Research/Genetic Toxicology and Environmental Mutagenesis. 760: 1–9.
doi:
10.1016/j.mrgentox.2013.11.002.
PMID24309507.