Cadmium is a naturally occurring toxic metal with common exposure in industrial workplaces, plant soils, and from smoking. Due to its low permissible exposure in humans, overexposure may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposure. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. The primary use of cadmium is in the manufacturing of NiCd rechargeable batteries. The primary source for cadmium is as a byproduct of refining zinc metal.[1] Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, the construction industry, and the agricultural industry.[2]
Acute exposure to cadmium fumes may cause flu-like symptoms including chills, fever, and muscle ache sometimes referred to as "the cadmium blues." Symptoms may resolve after a week if there is no respiratory damage. More severe exposures can cause tracheobronchitis, pneumonitis, and pulmonary edema. Symptoms of inflammation may start hours after the exposure and include cough, dryness and irritation of the nose and throat, headache, dizziness, weakness, fever, chills, and chest pain.[citation needed]
Chronic
Complications of cadmium poisoning include cough, anemia, and kidney failure (possibly leading to death).[3] Cadmium exposure increases one's chances of developing cancer.[4] Similar to zinc, long-term exposure to cadmium fumes can cause lifelong anosmia.[citation needed]
Bone and joints
One of the main effects of cadmium poisoning is weak and brittle bones.[3] The bones become soft (osteomalacia), lose bone mineral density (osteoporosis), and become weaker. This results in joint and back pain, and increases the risk of fractures.[citation needed] Spinal and leg pain is common, and a waddling gait often develops due to bone deformities caused by the long-term cadmium exposure. The pain eventually becomes debilitating, with fractures becoming more common as the bone weakens. Permanent deformation in bones can occur.[3] In extreme cases of cadmium poisoning, mere body weight causes a fracture.[citation needed]
Renal
The kidney damage inflicted by cadmium poisoning is irreversible. The kidneys can shrink up to 30 percent. The kidneys lose their function to remove acids from the blood in proximal renal tubular dysfunction. The proximal renal tubular dysfunction causes hypophosphatemia, leading to muscle weakness and sometimes coma. Hyperchloremia also occurs. Kidney dysfunction also causes gout, a form of arthritis due to the accumulation of uric acid crystals in the joints because of high acidity of the blood (hyperuricemia). Cadmium exposure is also associated with the development of kidney stones.[citation needed]
Sources of exposure
Smoking is a significant source of cadmium exposure. Even small amounts of cadmium from smoking are highly toxic to humans, as the lungs absorb cadmium more efficiently than the stomach.[5] Cadmium is emitted to the electronic cigarette (EC) aerosol but, on currently available data, the lifetime cancer risk (LCR) calculated doesn't exceed the acceptable risk limit.[6][7]
Environmental
Buildup of cadmium levels in the water, air, and soil has been occurring particularly in industrial areas. Environmental exposure to cadmium has been particularly problematic in Japan where many people have consumed rice that was grown in cadmium-contaminated irrigation water. This phenomenon is known as itai-itai disease.[8]
People who live near hazardous waste sites or factories that release cadmium into the air have the potential for exposure to cadmium in air. However, numerous state and federal regulations in the United States control the amount of cadmium that can be released to the air from waste sites and incinerators so that properly regulated sites are not hazardous. The general population and people living near hazardous waste sites may be exposed to cadmium in contaminated food, dust, or water from unregulated or accidental releases. Numerous regulations and use of pollution controls are enforced to prevent such releases.[citation needed]
Some sources of phosphate in fertilizers contain cadmium in amounts of up to 100mg/kg,[9][10] which can lead to an increase in the concentration of cadmium in soil (for example in New Zealand).[11]
Food
Food is another source of cadmium. Plants may contain small or moderate amounts in non-industrial areas, but high levels may be found in the liver and kidneys of adult animals. The daily intake of cadmium through food varies by geographic region. Intake is reported to be approximately 8 to 30μg in Europe and the United States versus 59 to 113 μg in various areas of Japan.[12] A small study of premium dark chocolate samples found 48% had high levels of cadmium, the source commonly being the presence of cadmium in soil in which they were grown.[13]
Occupational exposure
In the 1950s and 1960s industrial exposure to cadmium was high, but as the toxic effects of cadmium became apparent, industrial limits on cadmium exposure have been reduced in most industrialized nations and many policy makers agree on the need to reduce exposure further. While working with cadmium it is important to do so under a fume hood to protect against dangerous fumes. Brazing fillers which contain cadmium should be handled with care. Serious toxicity problems have resulted from long-term exposure to cadmium plating baths.
Workers can be exposed to cadmium in air from the smelting and refining of metals, or from the air in plants that make cadmium products such as batteries, coatings, or plastics. Workers can also be exposed when soldering or welding metal that contains cadmium. Approximately 512,000 workers in the United States are in environments each year where cadmium exposure may occur. Regulations that set permissible levels of exposure, however, are enforced to protect workers and to make sure that levels of cadmium in the air are considerably below levels thought to result in harmful effects.[citation needed]
Artists who work with cadmium pigments, which are commonly used in strong oranges, reds, and yellows, can easily accidentally ingest dangerous amounts, particularly if they use the pigments in dry form, as with chalk pastels, or in mixing their own paints.
Consumer products
Cadmium is used in nickel-cadmium batteries; these are some of the most popular and most common cadmium-based products.
In February 2010, cadmium was found in an entire line of Wal-Mart exclusive Miley Cyrus jewelry. The charms were tested at the behest of the Associated Press and were found to contain high levels of cadmium. Wal-Mart did not stop selling the jewelry until May 12 because "it would be too difficult to test products already on its shelves".[14]
On June 4, 2010, cadmium was detected in the paint used on promotional drinking glasses for the movie Shrek Forever After, sold by McDonald's Restaurants, triggering a recall of 12 million glasses.[15]
Inside cells, cadmium ions act as a catalytic hydrogen peroxide generator. This sudden surge of cytosolic hydrogen peroxide causes increased lipid peroxidation and additionally depletes ascorbate and glutathione stores. Hydrogen peroxide can also convert thiol groups on proteins into nonfunctional sulfonic acids and is also capable of directly attacking nuclear DNA. This oxidative stress causes the afflicted cell to manufacture large amounts of inflammatory cytokines.[18][19]
Toxicokinetics
Inhaling cadmium-laden dust quickly leads to respiratory tract and kidney problems which can be fatal (often from kidney failure). Ingestion of any significant amount of cadmium causes immediate poisoning and damage to the liver and the kidneys. Compounds containing cadmium are also carcinogenic.[20]
Diagnosis
Biomarkers of excessive exposure
Increased concentrations of urinary beta-2 microglobulin can be an early indicator of kidney dysfunction in persons chronically exposed to low but excessive levels of environmental cadmium. The urinary beta-2 microglobulin test is an indirect method of measuring cadmium exposure. Under some circumstances, the Occupational Health and Safety Administration requires screening for kidney damage in workers with long-term exposure to high levels of cadmium.[21] Blood or urine cadmium concentrations provide a better index of excessive exposure in industrial situations or following acute poisoning, whereas organ tissue (lung, liver, kidney) cadmium concentrations may be useful in fatalities resulting from either acute or chronic poisoning. Cadmium concentrations in healthy persons without excessive cadmium exposure are generally less than 1 μg/L in either blood or urine. The ACGIH biological exposure indices for blood and urine cadmium levels are 5 μg/L and 5 μg/g creatinine, respectively, in random specimens. Persons who have sustained kidney damage due to chronic cadmium exposure often have blood or urine cadmium levels in a range of 25-50 μg/L or 25-75 μg/g creatinine, respectively. These ranges are usually 1000-3000 μg/L and 100-400 μg/g, respectively, in survivors of acute poisoning and may be substantially higher in fatal cases.[22][23]
Treatment
A person with cadmium poisoning should seek immediate medical attention, both for treatment and supportive care.[24]
For long-term exposure, considerable evidence indicates that the traditional chelator EDTA can reduce a body's overall cadmium load. Co-administered antioxidants, including nephroprotective glutathione, appear to improve efficacy. For patients with extremely fragile kidneys, limited evidence suggests that saunasweat may differentially excrete the metal.[24]
Epidemiology
In a mass cadmium poisoning in Japan, a marked prevalence for skeletal complications has been noted for older, postmenopausal women, however, the cause of the phenomenon is not fully understood, and is under investigation. Cadmium poisoning in postmenopausal women may result in an increased risk for osteoporosis. Current research has pointed to general malnourishment, as well as poor calcium metabolism relating to the women's age.[26] Studies are pointing to damage of the mitochondria of kidney cells by cadmium as a key factor of the disease.[27]
History
An experiment during the early 1960s involving the spraying of cadmium over Norwich was declassified in 2005 by the UK government, as documented in a BBC News article.[28]
1 2 3 Yoshida F, Hata A, Tonegawa H (1999-09-01). "Itai-Itai disease and the countermeasures against cadmium pollution by the Kamioka mine". Environmental Economics and Policy Studies. 2 (3): 215–229. doi:10.1007/BF03353912. hdl:2115/53361. ISSN1867-383X. S2CID1902243.
1 2 (IARC)International Agency for Research on Cancer. 1993. Beryllium, cadmium, mercury and exposures in the glass manufacturing industry, vol. 58. IARC, Lyon, France. 119238.
↑ Syers, J. Keith; MacKay, Alec D.; Brown, Michael W.; Currie, Lance D. (1986). "Chemical and physical characteristics of phosphate rock materials of varying reactivity". Journal of the Science of Food and Agriculture. 37 (11): 1057–64. Bibcode:1986JSFA...37.1057S. doi:10.1002/jsfa.2740371102.
↑ Trueman, N. A. (1965). "The phosphate, volcanic and carbonate rocks of Christmas Island (Indian Ocean)". Journal of the Geological Society of Australia. 12 (2): 261–283. Bibcode:1965AuJES..12..261T. doi:10.1080/00167616508728596.
↑ IPCS (International Programme on Chemical Safety) Cadmium–Environmental Health Criteria 134. Geneva: World Health Organization; 1992. Accessed 29 December 2009. Available: http://www.inchem.org/documents/ehc/ehc/ehc134.htm.
↑ ATSDR Toxicological Profile for Cadmium. Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services, Atlanta, GA (2012)
↑ Maret, Wolfgang; Moulis, Jean-Marc (2013). "The Bioinorganic Chemistry of Cadmium in the Context of Its Toxicity". Cadmium: From Toxicity to Essentiality. Metal Ions in Life Sciences. Vol.11. pp.1–29. doi:10.1007/978-94-007-5179-8_1. ISBN978-94-007-5178-1. PMID23430768.
↑ Nordberg, Gunnar F. (2010). "Biomarkers of exposure, effects and susceptibility in humans and their application in studies of interactions among metals in China". Toxicology Letters. 192 (1): 45–9. doi:10.1016/j.toxlet.2009.06.859. PMID19540908.
↑ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 212-214.
↑ Hamilton JW. "What is Itai-Itai disease". Access Science. McGraw-Hill Global Education Holdings, LLC. Archived from the original on 2013-11-13. Retrieved 2013-11-10.
"Cadmium and you"(PDF). Bootle, UK: Health and Safety Executive. March 2010. Retrieved January 29, 2011.
Shannon M. "Heavy Metal Poisoning", in Haddad LM, Shannon M, Winchester JF (editors): Clinical Management of Poisoning and Drug Overdose, Third Edition, 1998.
Cadmium is a chemical element; it has symbol Cd and atomic number 48. This soft, silvery-white metal is chemically similar to the two other stable metals in group 12, zinc and mercury. Like zinc, it demonstrates oxidation state +2 in most of its compounds, and like mercury, it has a lower melting point than the transition metals in groups 3 through 11. Cadmium and its congeners in group 12 are often not considered transition metals, in that they do not have partly filled d or f electron shells in the elemental or common oxidation states. The average concentration of cadmium in Earth's crust is between 0.1 and 0.5 parts per million (ppm). It was discovered in 1817 simultaneously by Stromeyer and Hermann, both in Germany, as an impurity in zinc carbonate.
A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts. The term has particular application to cadmium, mercury and lead, all of which appear in the World Health Organization's list of 10 chemicals of major public concern. Other examples include manganese, chromium, cobalt, nickel, copper, zinc, silver, antimony and thallium.
Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If arsenic poisoning occurs over a brief period of time, symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.
Toxicity is the degree to which a chemical substance or a particular mixture of substances can damage an organism. Toxicity can refer to the effect on a whole organism, such as an animal, bacterium, or plant, as well as the effect on a substructure of the organism, such as a cell (cytotoxicity) or an organ such as the liver (hepatotoxicity). By extension, the word may be metaphorically used to describe toxic effects on larger and more complex groups, such as the family unit or society at large. Sometimes the word is more or less synonymous with poisoning in everyday usage.
Berylliosis, or chronic beryllium disease, is a chronic allergic-type lung response and chronic lung disease caused by exposure to beryllium and its compounds, a form of beryllium poisoning. It is distinct from acute beryllium poisoning, which became rare following occupational exposure limits established around 1950. Berylliosis is an occupational lung disease.
Lead poisoning, also known as plumbism and saturnism, is a type of metal poisoning caused by lead in the body. Symptoms may include abdominal pain, constipation, headaches, irritability, memory problems, infertility, and tingling in the hands and feet. It causes almost 10% of intellectual disability of otherwise unknown cause and can result in behavioral problems. Some of the effects are permanent. In severe cases, anemia, seizures, coma, or death may occur.
Mercury poisoning is a type of metal poisoning due to exposure to mercury. Symptoms depend upon the type, dose, method, and duration of exposure. They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. High-level exposure to methylmercury is known as Minamata disease. Methylmercury exposure in children may result in acrodynia in which the skin becomes pink and peels. Long-term complications may include kidney problems and decreased intelligence. The effects of long-term low-dose exposure to methylmercury are unclear.
Itai-itai disease was the name given to the mass cadmium poisoning of Toyama Prefecture, Japan, starting around 1912. The term "itai-itai disease" was coined by locals for the severe pains people with the condition felt in the spine and joints. Cadmium (Cd) poisoning can also cause softening of the bones and kidney failure. Effective treatments involve the use of chelators to promote urinary excretion of Cd. The cadmium was released into rivers by mining companies in the mountains, which were successfully sued for the damage. Remediation efforts in the affected region have been ongoing since 1972 and were mostly complete as of 2012. Monetary costs of the cleanup have been paid for in part by Japan's national government, Mitsui Mining, and the Gifu and Toyama prefectural governments. Itai-itai disease is known as one of the Four Big Pollution Diseases of Japan.
Fumonisin B1 is the most prevalent member of a family of toxins, known as fumonisins, produced by several species of Fusarium molds, such as Fusarium verticillioides, which occur mainly in maize (corn), wheat and other cereals. Fumonisin B1 contamination of maize has been reported worldwide at mg/kg levels. Human exposure occurs at levels of micrograms to milligrams per day and is greatest in regions where maize products are the dietary staple.
An environmental hazard is a substance, state or event which has the potential to threaten the surrounding natural environment or adversely affect people's health, including pollution and natural disasters such as storms and earthquakes. It can include any single or combination of toxic chemical, biological, or physical agents in the environment, resulting from human activities or natural processes, that may impact the health of exposed subjects, including pollutants such as heavy metals, pesticides, biological contaminants, toxic waste, industrial and home chemicals.
Abrin is an extremely toxic toxalbumin found in the seeds of the rosary pea, Abrus precatorius. It has a median lethal dose of 0.7 micrograms per kilogram of body mass when given to mice intravenously. The median toxic dose for humans ranges from 10 to 1000 micrograms per kilogram when ingested and is 3.3 micrograms per kilogram when inhaled.
Blood lead level (BLL), is a measure of the amount of lead in the blood. Lead is a toxic heavy metal and can cause neurological damage, especially among children, at any detectable level. High lead levels cause decreased vitamin D and haemoglobin synthesis as well as anemia, acute central nervous system disorders, and possibly death.
The four big pollution diseases of Japan were a group of man-made diseases all caused by environmental pollution due to improper handling of industrial wastes by Japanese corporations. The first occurred in 1912, and the other three occurred in the 1950s and 1960s.
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. In the case of lead, any measurable amount may have negative health effects. 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.
Environmental toxicology is a multidisciplinary field of science concerned with the study of the harmful effects of various chemical, biological and physical agents on living organisms. Ecotoxicology is a subdiscipline of environmental toxicology concerned with studying the harmful effects of toxicants at the population and ecosystem levels.
Acute beryllium poisoning is acute chemical pneumonitis resulting from the toxic effect of beryllium in its elemental form or in various chemical compounds, and is distinct from berylliosis. After occupational safety procedures were put into place following the realization that the metal caused berylliosis around 1950, acute beryllium poisoning became extremely rare.
Animal lead poisoning is a veterinary condition and pathology caused by increased levels of the heavy metal lead in animal's body.
Nitrogen dioxide poisoning is the illness resulting from the toxic effect of nitrogen dioxide. It usually occurs after the inhalation of the gas beyond the threshold limit value. Nitrogen dioxide is reddish-brown with a very harsh smell at high concentrations, at lower concentrations it is colorless but may still have a harsh odour. Nitrogen dioxide poisoning depends on the duration, frequency, and intensity of exposure.
Chronic kidney disease of unknown etiology (CKDu) is an increasing health concern in Sri Lanka. CKDu is recognized as chronic kidney disease without the usual associated causative factors. The first cases of CKDu were reported in Sri Lanka's North Central Province (NCP). Chronic kidney disease, was identified as the 8th leading cause of in-hospital mortality in Sri Lanka, and the leading cause of death in Anuradhapura and Polonnaruwa in 2016. This rise in mortality coincided with the increasing cases of CKDu seen across the country. Studies have shown an estimated 70,000 CKDu patients in high risk areas. Various possible causes for CKDu in Sri Lankans have been investigated, including poisoning from metals, cyanobacteria toxins, agrochemicals, and heat stress, but no definite causes have been identified.
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