Dictionary:
car·cin·o·gen (kär-sĭn'ə-jən, kär'sə-nə-jĕn') ![]() |
| 5min Related Video: carcinogen |
| Chemistry Dictionary: carcinogen |
Any agent that produces cancer, e.g. tobacco smoke, certain industrial chemicals, and ionizing radiation (such as X-rays and ultraviolet rays).
| Britannica Concise Encyclopedia: carcinogen |
For more information on carcinogen, visit Britannica.com.
| Food and Nutrition: carcinogen |
A substance that can induce cancer; carcinogenesis is the process of induction of cancer.
| Dental Dictionary: carcinogen |
A substance or agent that causes the development or increases the incidence of cancer.
| Encyclopedia of Public Health: Carcinogen |
A carcinogen is an agent that can cause cancer. Carcinogens can be chemicals, viruses, hormone, ionizing radiation, or solid materials. Carcinogens produce cancer by changing the information that cells receive from their DNA, causing immature cells to accumulate in the body rather than differentiate into normal functional cells. Carcinogens may be genotoxic, meaning that they interact physically with DNA to damage or change its structure. Ionizing radiation is a genotoxic carcinogen. Other carcinogens may change how DNA expresses its information without changing its structure directly, or may create a situation in a cell or tissue that makes it more susceptible to DNA damage from other sources. These are known as nongenotoxic carcinogens, or promoters. Arsenic and estrogen are nongenotoxic carcinogens. Still other carcinogens, such as nickel, may interfere with cell division, changing the number or structure of chromosomes in new cells after a cell divides.
Several changes in a cell's DNA are usually needed to transform a normal cell into a cancer cell. Such changes can accumulate over time, and can sometimes be repaired. Cells can also die before enough changes occur to turn them cancerous. The places that become altered in the DNA of cancer cells are called oncogenes and tumor suppressor genes. Oncogenes and tumor suppressor genes are particular locations on DNA that control a cell's ability to perform its biological functions and to control its growth.
Susceptibility to the action of carcinogens is very complex and is affected by genetic heritage, behavior, physiology, nutrition, external exposures, and other factors. For example, some chemicals are carcinogenic in their original form (direct carcinogens), while some must be metabolized in the body to their active form (indirect carcinogens). In such cases, individual susceptibility to a chemical carcinogen is affected by the rate at which the chemical metabolizes in the body into a cancer-causing form or into a harmless form. This rate varies from person to person.
Some carcinogens have been identified from studies of people exposed to various substances over time. These include cancer in cigarette smokers and leukemia in people breathing benzene in the workplace. Carcinogens have also been identified using laboratory animals exposed over time, usually to high doses. Saccharin was found to be a carcinogen through experiments to produce bladder cancer in rats, and aflatoxin was found to produce liver cancer in rats. Some substances that are carcinogens in laboratory animals, like saccharin, are not carcinogens in people because of differences in how they are metabolized or differences in how they produce cancer. The International Agency for Research on Cancer (part of the World Health Organization) and the U.S. National Toxicology Program publish documents listing chemicals and other exposures that they believe are known to be carcinogenic to humans and those that are suspected or likely to be carcinogens to humans.
(SEE ALSO: Ames Test; Cancer; Carcinogen Assessment Groups; Carcinogenesis; Toxicology)
Bibliography
Weinberg, R. A. (1996). Racing to the Beginning of the Road: The Search for the Origin of Cancer. New York: W. H. Freeman.
Zuddon, R. W. (1987). Cancer Biology. New York: Oxford University Press.
— GAIL CHARNLEY
| Genetics Encyclopedia: Carcinogens |
Carcinogens are agents that cause cancer, and include chemicals, radiation, and some viruses. While avoiding contact with carcinogenic agents is wise, it is virtually impossible to steer clear of them completely. Ultra-violet radiation from the sun, substances in food, and even oxygen can induce malignancies. In spite of the pervasive nature of carcinogens, however, not all individuals develop cancer, which suggests that mere contact with a carcinogenic agent is insufficient to produce this lethal disease. That is because organisms have evolved protective mechanisms to prevent cancer, and some of these defenses work by thwarting the potentially harmful effects of carcinogens.
Cancer-Causing Chemicals
References to cancer have been found in the annals of human disease since ancient times, but the disease's association with carcinogen exposure is a relatively new concept. Sir Percival Potts, a British physician who lived in the eighteenth century, was the first to suggest that the induction of cancer might be linked to agents in the environment. Potts had observed high rates of scrotal and nasal cancer among England's chimney sweeps, men who were exposed to accumulated fireplace soot during their work. After some careful studies, Potts suggested correctly that exposure to soot caused the high cancer rates, providing the impetus for identifying other carcinogens present in the environment.
In retrospect, it was fortuitous that soot was acknowledged as one of the first carcinogenic agents. Soot is a complex mixture of chemicals that arises from the combustion of organic material. As scientists and physicians separated soot's individual components, it became clear that chemicals called polycyclic aromatic hydrocarbons (PAHs) were among its principal carcinogenic compounds. The story became even more intriguing when it was shown that many PAHs behave as procarcinogens. Procarcinogens do not cause cancer per se, but they can be converted to active carcinogens by enzymes located in organs like the liver and lung. The implications of this discovery are noteworthy. For example, cigarette smoke contains a wide variety of procarcinogenic PAHs that are turned into active carcinogens in lung cells. Since smokers draw these PAHs deep into their lungs with each inhale on a cigarette, one reason that cigarette smoking correlates so highly with the induction of lung cancer becomes very clear.
Oncogenes and Tumor Suppressors
How do carcinogens cause cancer? Answering this question still forms the core of much basic research, but a common feature of many carcinogens, particularly chemicals and radiation, is that they act as mutagens. Mutagens are agents that generate changes in DNA, sometimes by reacting with the DNA building blocks, guanine, adenine, thymine, and cytosine, which results in damaged DNA. When such damage remains in chromosomes, genes are often mutated in a way that impairs their normal function and enhances cancer induction. Cells try to prevent such mutations by repairing DNA damage, but they are not always successful. In fact, some individuals are susceptible to hereditary skin and colon cancers because they lack the ability to remove damaged DNA from chromosomes.
There are two general classes of genes that contribute to malignant tumor formation when they are mutated by carcinogens: oncogenes and tumor suppressor genes. Oncogenes (the prefix "onco-" meaning "tumor") are altered versions of normal genes called proto-oncogenes. Protooncogenes encode proteins that are often involved in regulating normal cell growth and division. When a proto-oncogene is mutated by exposure to a carcinogen, the protein it encodes may lose its ability to govern cell growth and division, often giving rise to the rapid, unrestrained cell proliferation that is characteristic of cancer. In such a case, the mutations in the protooncogene convert it into an actual oncogene.
While many oncogenes have been identified, numerous cancers are associated with mutations in one particular proto-oncogene, called ras, which is an abbreviation for "rat sarcoma." "Ras" is written as Ras when biologists refer to the protein, and as ras when they refer to the gene that encodes the protein. The ras gene encodes Ras protein, which acts to regulate cell growth. Normally, Ras protein cycles between an "off" and "on" form. Many carcinogens induce mutations in the ras proto-oncogene, converting it to a ras oncogene, which encodes a form of the Ras protein that is locked in the "on" state. By abolishing Ras protein's regulatory off/on cycle, the accumulated mutations in the ras gene contribute to the formation of malignancies.
Not all oncogenes arise from mutations in normal cellular protooncogenes. In the early twentieth century, Peyton Rous discovered a carcinogenic virus that now bears his name, the Rous sarcoma virus. This virus harbors a gene called v-src (viral-sarcoma) that is a mutant form of a normal cellular proto-oncogene called c-src (cell-sarcoma). Like Ras protein, c-Src protein helps to regulate cell growth. When cells are infected by Rous sarcoma virus, the v-src gene, which is classified as an oncogene, is expressed in those cells. High amounts of mutant v-Src protein encoded by the v-src oncogene are made in the cell, and they dominate the normal cellular c-Src protein, an event that contributes to abnormal cell growth and proliferation, eventually leading to cancer.
Tumor suppressor genes encode proteins that tend to repress cancer formation. When tumor suppressor genes are mutated by carcinogens, they often lose their ability to stem tumor formation, resulting in cancer. Some hereditary forms of breast cancer are linked to mutations in a tumor suppressor gene called BRCA-1. BRCA is derived from BReast CAncer. The BRCA-1 gene encodes BRCA-1 protein, which participates in controlling cell division, preventing cells from growing out of control, thus contributing to the suppression of tumor formation. Mutations in the BRCA-1 gene result in altered BRCA-1 protein that no longer functions correctly in cell-growth regulation, contributing to the formation of tumors, particularly in breast tissue.
Reducing Exposure
Decreased carcinogen contact along with improved methods for treating cancer provide two important means for curtailing the suffering, expense, and death associated with the disease. The documented existence of carcinogens has prompted a worldwide effort to detect additional cancer-causing agents. A variety of toxicological assessments, including the Ames test, are used to identify potential mutagens and carcinogens. When possible, established carcinogens, such as asbestos, are removed from the environment, home, and workplace.
Exposure can also be reduced if the population is provided with protective warnings, like those advising the use of sunblock to shield skin from the cancer-causing effects of ultraviolet radiation in sunlight. The cost and manpower of such efforts are enormous, but carcinogen identification is critical for ensuring that exposure is minimized. A great challenge is reducing exposure to the carcinogens to which people actively expose themselves, most notably cigarette smoke. Prolonged education programs have helped cut down the use of cigarettes, but continued education is needed for each new generation.
Bibliography
Lodish, Harvey, et al. Molecular Cell Biology, 4th ed. New York: W. H. Freeman, 2000.
Tomatis, Lorenzo. "The Identification of Human Carcinogens and Primary Prevention of Cancer." Mutation Research 462 (2000): 407-421.
Trichopoulos, Dimitrios, Frederick P. Li, and David J. Hunter. "What Causes Cancer?" Scientific American 275 (1996): 80-87.
Weinberg, Robert. "How Cancer Arises." Scientific American 275 (1996): 62-71.
—David A. Scicchitano
| Sports Science and Medicine: carcinogen |
Any substance capable of causing a cancer.
| Veterinary Dictionary: carcinogenicity |
The ability or tendency to produce cancer.
| Wikipedia: Carcinogen |
| Look up carcinogen in Wiktionary, the free dictionary. |
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A carcinogen is any substance, radionuclide or radiation that is an agent directly involved in the exacerbation of cancer or in the increase of its propagation. 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 carcinogens are inhaled asbestos, certain dioxins, and tobacco smoke.
Cancer is a disease where damaged cells of the patient's body do not undergo programmed cell death, but their growth is no longer controlled and their metabolism is altered. Carcinogens may increase the risk of getting cancer by altering cellular metabolism or damaging DNA directly in cells, which interferes with biological processes, and induces the uncontrolled, malignant division, ultimately leading to the formation of tumors. Usually DNA damage, if too severe to repair, leads to programmed cell death, but if the programmed cell death pathway is damaged, then the cell cannot prevent itself from becoming a cancer cell.
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 viruses 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.
Benzene, kepone, EDB, asbestos, and the waste rock of oil shale mining have all been classified as carcinogenic.[1] 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.
Co-carcinogens are chemicals that do not necessarily cause cancer on their own, but promote the activity of other carcinogens in causing cancer.
After the carcinogen enters the body, the body makes an attempt to eliminate it through a process called biotransformation. The purpose of these reactions is to make the carcinogen more water-soluble so that it can be removed from the body. But these reactions can also convert a less toxic carcinogen into a more toxic one.
DNA is nucleophilic, therefore soluble carbon electrophiles are carcinogenic, because DNA attacks them. For example, some alkenes are toxicated by human enzymes to produce an electrophilic epoxide. DNA attacks the epoxide, and is bound permanently to it. This is the mechanism behind the carcinogenity of benzo[a]pyrene in tobacco smoke, other aromatics, aflatoxin and mustard gas.
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CERCLA identifies all radionuclides as carcinogens, although the nature of the emitted radiation (alpha, beta, gamma, or neutron and the radioactive strength), its consequent capacity to cause ionization in tissues, and the magnitude of radiation exposure, determine the potential hazard. Carcinogenity of radiation depends of the type of radiation, type of exposure and penetration. For example, alpha radiation has low penetration and is not a hazard outside the body, but are carcinogenic when inhaled or ingested.
For example, Thorotrast, a (incidentally-radioactive) suspension previously used as a contrast medium in x-ray diagnostics, is a potent human carcinogen known because of its retention within various organs and persistent emission of alpha particles. Marie Curie, one of the pioneers of radioactivity, died of cancer caused by radiation exposure during her experiments.
Not all types of electromagnetic radiation are in fact carcinogenic. Low-energy waves on the electromagnetic spectrum are generally not, including radio waves, microwave radiation, infrared radiation and visible light. Higher-energy radiation, including ultraviolet radiation (present in sunlight), x-rays, and gamma radiation, generally is carcinogenic, if received in sufficient doses.
Several published studies suggest a link between exposure to light at night and risk of breast cancer, due to suppression of the normal nocturnal production of melatonin.[2][3] In 1978 Cohen et al. proposed that reduced production of the hormone melatonin might increase the risk of breast cancer and citing "environmental lighting" as a possible causal factor.[4] Researchers at the National Cancer Institute (NCI) and National Institute of Environmental Health Sciences have concluded a study that suggests that artificial light during the night can be a factor for breast cancer.[5] A good review of current knowledge of the health consequences of exposure to artificial light at night and an explanation of the causal mechanisms has been published in the Journal of Pineal Research in 2007.[6]
Substances or foods irradiated with electrons or electromagnetic radiation (such as microwave, X-ray or gamma) are not carcinogenic. No "radiation" remains, just like no light remains in room after you turn out the light. (In contrast, non-electromagnetic neutron radiation produced inside nuclear reactors can produce secondary radiation by making bombarded substances radioactive.)
In other words, there is no possibility of getting cancer if the food is consumed.
Cooking food at high temperatures, for example grilling or barbecuing meats, can lead to the formation of minute quantities of many potent carcinogens that are comparable to those found in cigarette smoke (i.e., benzo[a]pyrene).[7] Charring of food resembles coking and tobacco pyrolysis, and produces similar carcinogens. There are several carcinogenic pyrolysis products, such as polynuclear aromatic hydrocarbons, which are converted by human enzymes into epoxides, which attach permanently to DNA. Pre-cooking meats in a microwave oven for 2–3 minutes before grilling shortens the time on the hot pan, and removes heterocyclic amine (HCA) precursors, which can help minimize the formation of these carcinogens.[8]
Reports from the Food Standards Agency have found that the known animal carcinogen acrylamide is generated in fried or overheated carbohydrate foods (such as french fries and potato chips).[9] Studies are underway at the FDA and European regulatory agencies to assess its potential risk to humans. The charred residue on barbecued meats has been identified as a carcinogen, along with many other tars.
Dr. T. Colin Campbell argues in The China Study that the milk protein casein, found in milk and many prepared foods, is also a carcinogen.[10] However, independent studies report that casein and other milk proteins protect against cancer.[11]
Tobacco smoke contains over 4000 chemical compounds, many of which are carcinogenic or otherwise toxic.[12]
"Shiftwork that involves circadian disruption" was listed, in 2007, as a probable carcinogen by the World Health Organization's International Agency for Research on Cancer. (IARC Press release No. 180).[13] Multiple studies have documented a link between night shift work and the increased incidence of breast cancer.[14][15][16][17] Circadian disruption by exposure to light at night suppresses the production of the hormone melatonin which leads to reduction in cellular immune defense and surveillance necessary for protection from development of cancers. Melatonin also seems to have a direct protective effect against cancer possibly in part because of its strong anti oxidant properties.[18]
Carcinogens can be classified as genotoxic or nongenotoxic. Genotoxins cause irreversible genetic damage or mutations by binding to DNA. Genotoxins include chemical agents like N-nitroso-N-methylurea (MNU) or non-chemical agents such as ultraviolet light and ionizing radiation. Certain viruses can also act as carcinogens by interacting with DNA.
Nongenotoxins do not directly affect DNA but act in other ways to promote growth. These include hormones and some organic compounds.[19]
| IARC | GHS | NTP | ACGIH | EU |
|---|---|---|---|---|
| Group 1 | Cat. 1A | Known | A1 | Cat. 1 |
| Group 2A | Cat. 1B | Reasonably suspected |
A2 | Cat. 2 |
| Group 2B | ||||
| Cat. 2 | A3 | Cat. 3 | ||
| Group 3 | ||||
| A4 | ||||
| Group 4 | A5 |
The International Agency for Research on Cancer (IARC) is an intergovernmental agency established in 1965, which forms part of the World Health Organization of the United Nations. It is based in Lyon, France. Since 1971 it has published a series of Monographs on the Evaluation of Carcinogenic Risks to Humans[20] that have been highly influential in the classification of possible carcinogens.
The Globally Harmonized System of Classification and Labelling of Chemicals (GHS) is a United Nations initiative to attempt to harmonize the different systems of assessing chemical risk which currently exist (as of March 2009) around the world. It classifies carcinogens into two categories, of which the first may be divided again into subcategories if so desired by the competent regulatory authority:
The National Toxicology Program of the U.S. Department of Health and Human Services is mandated to produce a biennial Report on Carcinogens.[21] As of March 2009, the latest edition was the 11th report (2005).[1] It classifies carcinogens into two groups:
The American Conference of Governmental Industrial Hygienists (ACGIH) is a private organization best known for its publication of threshold limit values (TLVs) for occupational exposure and monographs on workplace chemical hazards. It assesses carcinogenicity as part of wider assessment of the occupational hazards of chemicals.
The European Union classification of carcinogens is contained in the Dangerous Substances Directive and the Dangerous Preparations Directive. It consists of three categories:
This assessment scheme is being phased out in favor of the GHS scheme (see above), to which it is very close in category definitions.
A procarcinogen is a precursor to a carcinogen. One example is nitrites when taken in by the diet. They are not carcinogenic themselves, but turn into nitrosamines in the body, which are carcinogenic.[22]
Occupational carcinogens are agents that pose a risk of cancer in several specific work-locations:
| Carcinogen | Associated cancer sites or types | Occupational uses or sources |
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| Arsenic and its compounds |
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| Asbestos |
Not in use, but still found in:
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| Benzene |
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| Beryllium and its compounds |
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| Cadmium and its compounds |
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| Hexavalent chromium(VI) compounds |
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| Ethylene oxide |
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| Nickel |
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| Radon and its decay products |
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| Vinyl chloride |
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| Shiftwork that involves
circadian disruption[13] |
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| Involuntary smoking (Passive smoking)[23] |
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This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
| Translations: Carcinogen |
Dansk (Danish)
n. - kræftfremkaldende stof
Nederlands (Dutch)
carcinogeen
Français (French)
n. - substance cancérigène
Deutsch (German)
n. - (med.) Krebserreger
Ελληνική (Greek)
n. - καρκινογόνος ουσία
Italiano (Italian)
agente cancerogeno
Português (Portuguese)
n. - carcinógeno (m) (Med.), cancerígeno (m) (Med.)
Русский (Russian)
канцерогенное вещество
Español (Spanish)
n. - agente carcinógeno o cancerígeno
Svenska (Swedish)
n. - karcinogent ämne
中文(简体)(Chinese (Simplified))
致癌物质
中文(繁體)(Chinese (Traditional))
n. - 致癌物質
العربيه (Arabic)
(الاسم) مادة مسببه للسرطان
עברית (Hebrew)
n. - חומר הגורם לסרטן, מסרטן, גורם סרטן
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