Carcinogen

Common carcinogens; clockwise from top left: tobacco smoking, alcoholic beverages, asbestos, ultraviolet radiation

A carcinogen (/kɑːrˈsɪnəən/) is any substance, radionuclide, or radiation that promotes carcinogenesis (the formation of cancer). This may be due to the ability to damage the genome or to the disruption of cellular metabolic processes. Several radioactive substances are considered carcinogens, but their carcinogenic activity is attributed to the radiation, for example gamma rays and alpha particles, which they emit. Common examples of non-radioactive carcinogens are inhaled asbestos, certain dioxins, and tobacco smoke. Although the public generally associates carcinogenicity with synthetic chemicals, it is equally likely to arise from both natural and synthetic substances.[1] Carcinogens are not necessarily immediately toxic; thus, their effect can be insidious.

Carcinogens are agents in the environment capable of contributing to cancer growth. Carcinogens can be categorized into two different types: activation-dependent and activation-independent, and each nature impacts their level and type of influence when it comes to promoting cancer growth.[2] Activation-dependent carcinogens require metabolic activation or modification to induce cancer, while activation-independents ones do not. Examples of activation-dependent carcinogens[verification needed] range from certain viruses, such as HPV,[3] to consumed alcohol,[4] to excessive amounts of red and processed meats,[5] impacting a person's health in ways they may not immediately associate with cancer. Activation-independent carcinogens, such as ultraviolet rays or nitrosamines in tobacco products, possess characteristics enabling them to interact directly with DNA and other cellular components to cause harm. These include not requiring metabolic action or molecular changes to act, which complements their ability to be electrically excited, permitting them to interact with oxygen and nitrogen atoms in negatively charged cellular environments. This type of interaction leads to the alteration of DNA nucleotide bases, causing disarrangement of that genetic material. This disarrangement is also responsible for the formation of DNA adducts,[6] segments of DNA which bind to carcinogens, which furthers harm. Eventually, failure in DNA repair mechanisms will lead to a buildup of DNA damage and potentially the development of cancer.[6]

There are many natural carcinogens. Aflatoxin B1, which is produced by the fungus Aspergillus flavus growing on stored grains, nuts and peanut butter, is an example of a potent, naturally occurring microbial carcinogen. Certain viruses such as hepatitis B and human papilloma virus have been found to cause cancer in humans. The first one shown to cause cancer in animals is Rous sarcoma virus, discovered in 1910 by Peyton Rous. Other infectious organisms which cause cancer in humans include some bacteria (e.g. Helicobacter pylori[7][8]) and helminths (e.g. Opisthorchis viverrini[9] and Clonorchis sinensis[10]).

Dioxins and dioxin-like compounds, benzene, kepone, EDB, and asbestos have all been classified as carcinogenic.[11] As far back as the 1930s, industrial smoke and tobacco smoke were identified as sources of dozens of carcinogens, including benzo[a]pyrene, tobacco-specific nitrosamines such as nitrosonornicotine, and reactive aldehydes such as formaldehyde, which is also a hazard in embalming and making plastics. Vinyl chloride, from which PVC is manufactured, is a carcinogen and thus a hazard in PVC production.

  1. ^ Ames BN, Gold LS (January 2000). "Paracelsus to parascience: the environmental cancer distraction". Mutation Research. 447 (1): 3–13. doi:10.1016/S0027-5107(99)00194-3. PMID 10686303.
  2. ^ Poirier MC, ed. (28 September 2018). Carcinogens, DNA damage and cancer risk : mechanisms of chemical carcinogenesis. World Scientific. ISBN 978-981-323-719-3. OCLC 1086736058.
  3. ^ Cosper PF, Bradley S, Luo L, Kimple RJ (October 2021). "Biology of HPV Mediated Carcinogenesis and Tumor Progression". Seminars in Radiation Oncology. 31 (4): 265–273. doi:10.1016/j.semradonc.2021.02.006. PMC 8409095. PMID 34455982.
  4. ^ Rehm J, Shield KD, Weiderpass E (November 2020). "Alcohol consumption. A leading risk factor for cancer". Chemico-Biological Interactions. 331: 109280. doi:10.1016/j.cbi.2020.109280. PMID 33010221. S2CID 222154741.
  5. ^ Huang Y, Cao D, Chen Z, Chen B, Li J, Guo J, et al. (September 2021). "Red and processed meat consumption and cancer outcomes: Umbrella review". Food Chemistry. 356: 129697. doi:10.1016/j.foodchem.2021.129697. PMID 33838606.
  6. ^ a b Barnes JL, Zubair M, John K, Poirier MC, Martin FL (October 2018). "Carcinogens and DNA damage". Biochemical Society Transactions. 46 (5): 1213–1224. doi:10.1042/bst20180519. PMC 6195640. PMID 30287511.
  7. ^ Hatakeyama M, Higashi H (December 2005). "Helicobacter pylori CagA: a new paradigm for bacterial carcinogenesis". Cancer Science. 96 (12): 835–843. doi:10.1111/j.1349-7006.2005.00130.x. PMID 16367902.
  8. ^ González CA, Sala N, Rokkas T (September 2013). "Gastric cancer: epidemiologic aspects". Helicobacter. 18 (Supplement 1): 34–38. doi:10.1111/hel.12082. PMID 24011243. S2CID 22918077.
  9. ^ Sripa B, Kaewkes S, Sithithaworn P, Mairiang E, Laha T, Smout M, et al. (July 2007). "Liver fluke induces cholangiocarcinoma". PLOS Medicine. 4 (7): e201. doi:10.1371/journal.pmed.0040201. PMC 1913093. PMID 17622191.
  10. ^ Rustagi T, Dasanu CA (June 2012). "Risk factors for gallbladder cancer and cholangiocarcinoma: similarities, differences and updates". Journal of Gastrointestinal Cancer. 43 (2): 137–147. doi:10.1007/s12029-011-9284-y. PMID 21597894. S2CID 31590872.
  11. ^ Cite error: The named reference roc was invoked but never defined (see the help page).