Cadmium poisoning

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]

Cadmium poisoning
SpecialtyToxicology

Sources

Cadmium is used in nickel-cadmium batteries; these are some of the most popular and most common cadmium-based products.

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.

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.[3]

Long-term use of cadmium-contaminated water can lead to osteomyelitis.

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.[4]

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]

Aside from smokers, 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.

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.

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.

Some sources of phosphate in fertilizers contain cadmium in amounts of up to 100 mg/kg,[6][7] which can lead to an increase in the concentration of cadmium in soil (for example in New Zealand).[8] Cadmium can be removed from soil using nanopolymers.[9]

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.[10]

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".[11] On June 4 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.[12]

Mechanism

Cadmium is an extremely toxic industrial and environmental pollutant classified as a human carcinogen: Group 1, according to the International Agency for Research on Cancer;[13] Group 2a, according to Environmental Protection Agency (EPA); and a 1B carcinogen as classified by European Chemical Agency [14][15]

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.

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.[16]

The bones become soft (osteomalacia), lose bone mineral density (osteoporosis) and become weaker. This causes pain in the joints and the back, and also increases the risk of fractures. In extreme cases of cadmium poisoning, mere body weight causes a fracture.

The kidneys lose their function to remove acids from the blood in proximal renal tubular dysfunction. The kidney damage inflicted by cadmium poisoning is irreversible. The proximal renal tubular dysfunction creates low phosphate levels in the blood (hypophosphatemia), causing muscle weakness and sometimes coma. The 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). Another side effect is increased levels of chloride in the blood (hyperchloremia). The kidneys can also shrink up to 30 percent. Cadmium exposure is also associated with the development of kidney stones.

Similar to zinc, long-term exposure to cadmium fumes can cause life long anosmia.

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.[17][18]

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.[19] 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.[20][21]

Treatment

For a single exposure by ingestion, gastric decontamination by emesis or gastric lavage may be beneficial soon after exposure. Administration of activated charcoal has not been proven effective. Chelation therapies to remove cadmium are not effective, so the most important action is to prevent additional exposure. [22]

See also

References
  1. USGS (2018). Cadmium. Retrieved from https://minerals.usgs.gov/minerals/pubs/commodity/cadmium/mcs-2018-cadmi.pdf
  2. "Safety and Health Topics | Cadmium". Osha.gov. Retrieved 2013-07-08.
  3. "Itai-itai disease". Kanazawa-med.ac.jp.
  4. Elinder CG. Uses, occurrence and intake. In:Cadmium and Health: An Epidemiologic and Toxicological Appraisal, Friberg L, Elinder CG, Nordberg GF et al, CRC press, Boca Raton, FL 1985. Vol 1, p.23
  5. Järup, Lars; Berglund, Marika; Elinder, Carl Gustaf; Nordberg, Gunnar; Vahter, Marie (1998). "Health effects of cadmium exposure – a review of the literature and a risk estimate". Scandinavian Journal of Work, Environment & Health. 24 (Suppl 1): 1–51. JSTOR 40967243. PMID 9569444.
  6. 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. doi:10.1002/jsfa.2740371102.
  7. 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. Bibcode:1965AuJES..12..261T. doi:10.1080/00167616508728596.
  8. Taylor, M.D. (1997). "Accumulation of cadmium derived from fertilisers in New Zealand soils". Science of the Total Environment. 208 (1–2): 123–6. Bibcode:1997ScTEn.208..123T. doi:10.1016/S0048-9697(97)00273-8. PMID 9496656.
  9. Boparei. (2010). Kinetics and thermodynamics of cadmium ion removal by adsorption onto nanozerovalent iron particles. Retrieved from http://www.eng.uwo.ca/research/grc/pdfs/2011/Boparai_et_al_Kinetics.pdf
  10. "BBC News - Enquiry into spray cancer claims". 2005-12-07.
  11. Pritchard, Justin (2010). "AP IMPACT: Wal-Mart pulls jewelry over cadmium - Yahoo! News". Cite journal requires |journal= (help)
  12. Gelles, Jeff (2010). "McDonald's Recalls Cadmium-Tainted Shrek Glasses - Made in NJ". Huffington Post.
  13. (IARC)International Agency for Research on Cancer. 1993. Beryllium, cadmium, mercury and exposures in the glass manufacturing industry, vol. 58. IARC, Lyon, France. 119238.
  14. 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.
  15. ATSDR Toxicological Profile for Cadmium. Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services, Atlanta, GA (2012)
  16. "Safety and Health Topics | Cadmium - Health Effects". Osha.gov. Retrieved 2013-07-08.
  17. 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. 11. pp. 1–29. doi:10.1007/978-94-007-5179-8_1. ISBN 978-94-007-5178-1.
  18. "Cadmium (Cd) Toxicity: How Does Cadmium Induce Pathogenic Changes? | ATSDR - Environmental Medicine & Environmental Health Education - CSEM". Atsdr.cdc.gov. Retrieved 2013-07-08.
  19. ATSDR. Case Studies in Environmental Medicine (CSEM) Cadmium Toxicity Clinical Assessment - Laboratory Tests Archived 2017-09-08 at the Wayback Machine Retrieved on 2010-09-10.
  20. 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. PMID 19540908.
  21. R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 212-214.
  22. CDC. (2017). Cadmium Toxicity How Should Patients Exposed to Cadmium Be Treated and Managed? retrieved from https://www.atsdr.cdc.gov/csem/csem.asp?csem=6&po=16#tocbookmark3

Footnotes
  • Shannon M. Heavy Metal Poisoning, in Haddad LM, Shannon M, Winchester JF(editors): Clinical Management of Poisoning and Drug Overdose, Third Edition, 1998.
  • "Cadmium and you" (PDF). Redgrave Court, Merton Road, Bootle, Merseyside, L20 7HS, United Kingdom: Health and Safety Executive. March 2010. Retrieved January 29, 2011.CS1 maint: location (link)
  • Hartwig, Andrea (2013). "Cadmium and Cancer". Cadmium: From Toxicity to Essentiality. Metal Ions in Life Sciences. 11. pp. 491–507. doi:10.1007/978-94-007-5179-8_15. ISBN 978-94-007-5178-1.
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