carcinogen

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Any agent that produces cancer, e.g. tobacco smoke, certain industrial chemicals, and ionizing radiation (such as X-rays and ultraviolet rays).

For more information on carcinogen, visit Britannica.com.

A substance that can induce cancer; carcinogenesis is the process of induction of cancer.

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

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

Any substance capable of causing a cancer.

The ability or tendency to produce cancer.

A substance or agent that causes the development or increases the incidence of cancer.

• Diagnostic Terminology - carcinogen: substance that may produce cancer in living tissue

The hazard symbol for carcinogenic chemicals in the Globally Harmonized System.

A carcinogen is any substance, radionuclide, or radiation that is an agent directly involved in causing 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 carcinogens are inhaled asbestos, certain dioxins, and tobacco smoke. Although the public generally associates carcinogenicity with synthetic chemicals, it is equally likely to arise in both natural and synthetic substances.^[1]

Cancer is a disease in which damaged cells do not undergo programmed cell death. Carcinogens may increase the risk of 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.

Dioxins and dioxin-like compounds, benzene, kepone, EDB, and asbestos have all been classified as carcinogenic.^[2] 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 carcinogen.

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 carcinogenicity of benzo[a]pyrene in tobacco smoke, other aromatics, aflatoxin and mustard gas.

Contents 1 Radiation 2 Carcinogens in prepared food 3 Carcinogens in cigarettes 4 Circadian disruption 5 Mechanisms of carcinogenicity 6 Classification of carcinogens 6.1 International Agency for Research on Cancer 6.2 Globally Harmonized System 6.3 U.S. National Toxicology Program 6.4 American Conference of Governmental Industrial Hygienists 6.5 European Union 6.6 Safe Work Australia 7 Procarcinogen 8 Common carcinogens 8.1 Occupational carcinogens 8.2 Others 9 See also 10 Notes 11 External links

Radiation

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. Carcinogenicity 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 emitters 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.

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.

Low level ionizing radiation may induce irreparable DNA damage (leading to replicational and transcriptional errors needed for neoplasia or may trigger viral interactions) leading to pre-mature aging and cancer.^[3][4][5]

Substances or foods irradiated with electrons or electromagnetic radiation (such as microwave, X-ray or gamma) are not carcinogenic.^{[citation needed]} In contrast, non-electromagnetic neutron radiation produced inside nuclear reactors can produce secondary radiation through nuclear transmutation.

Carcinogens in prepared food

See also: Cooking#Cooking and carcinogens and Raw foodism

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).^[6] 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.^[7]

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).^[8] Studies are underway at the FDA and European regulatory agencies to assess its potential risk to humans.

Carcinogens in cigarettes

Main article: Tobacco and health

Tobacco smoke contains over 4000 chemical compounds, many of which are carcinogenic or otherwise toxic. One of these is a compound marketed as a rat poison.^[9]

Circadian disruption

"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).^[10] Multiple studies have documented a link between night shift work and the increased incidence of breast cancer.^{[11][12][13][14][15][16]} 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 antioxidant properties.^[17]

Mechanisms of carcinogenicity

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 (NMU) 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.^[18]

Classification of carcinogens

Approximate equivalences
between classification schemes

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

International Agency for Research on Cancer

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^[19] that have been highly influential in the classification of possible carcinogens.

• Group 1: the agent (mixture) is definitely carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans.
• Group 2A: the agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans.
• Group 2B: the agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans.
• Group 3: the agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans.
• Group 4: the agent (mixture) is probably not carcinogenic to humans.

Globally Harmonized System

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:

• Category 1: known or presumed to have carcinogenic potential for humans
  • Category 1A: the assessment is based primarily on human evidence
  • Category 1B: the assessment is based primarily on animal evidence
• Category 2: suspected human carcinogens

U.S. National Toxicology Program

The National Toxicology Program of the U.S. Department of Health and Human Services is mandated to produce a biennial Report on Carcinogens.^[20] As of June 2011, the latest edition was the 12th report (2011).^[2] It classifies carcinogens into two groups:

• Known to be a human carcinogen
• Reasonably anticipated to be a human carcinogen

American Conference of Governmental Industrial Hygienists

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.

• Group A1: Confirmed human carcinogen
• Group A2: Suspected human carcinogen
• Group A3: Confirmed animal carcinogen with unknown relevance to humans
• Group A4: Not classifiable as a human carcinogen
• Group A5: Not suspected as a human carcinogen

European Union

The European Union classification of carcinogens is contained in the Dangerous Substances Directive and the Dangerous Preparations Directive. It consists of three categories:

• Category 1: Substances known to be carcinogenic to humans.
• Category 2: Substances which should be regarded as if they are carcinogenic to humans.
• Category 3: Substances which cause concern for humans, owing to possible carcinogenic effects but in respect of which the available information is not adequate for making a satisfactory assessment.

This assessment scheme is being phased out in favor of the GHS scheme (see above), to which it is very close in category definitions.

Safe Work Australia

Under a previous name, the NOHSC, in 1999 Safe Work Australia published the Approved Criteria for Classifying Hazardous Substances [NOHSC:1008(1999)].^[21] Section 4.76 of this document outlines the criteria for classifying carcinogens as approved by the Australian government. This classification consists of three categories:

• Category 1: Substances known to be carcinogenic to humans.
• Category 2: Substances that should be regarded as if they were carcinogenic to humans.
• Category 3: Substances that have possible carcinogenic effects in humans but about which there is insufficient information to make an assessment.

Procarcinogen

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]

Common carcinogens

Occupational carcinogens

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
Arsenic and its compounds	Lung Skin Hemangiosarcoma	Smelting byproduct Component of: Alloys Electrical and semiconductor devices Medications (e.g. melarsoprol) Herbicides Fungicides Animal dips Drinking water from contaminated aquifers.
Asbestos	Lungs Asbestosis Gastrointestinal tract Pleural Mesothelioma Peritoneal Mesothelioma	Not in widespread use, but found in: Constructions Roofing papers Floor tiles Fire-resistant textiles Friction linings (only outside Europe) Replacement friction linings for automobiles still may contain asbestos
Benzene	Leukemia Hodgkin lymphoma	Light fuel oil Former use as solvent and fumigant Printing Lithography Paint Rubber Dry cleaning Adhesives Coatings Detergents
Beryllium and its compounds	Lung	Missile fuel Lightweight alloys Aerospace applications Nuclear reactors
Cadmium and its compounds	Prostate	Yellow pigments Phosphors Solders Batteries Metal paintings and coatings
Hexavalent chromium(VI) compounds	Lung	Paints Pigments Preservatives
Ethylene oxide	Leukemia	Ripening agent for fruits and nuts Rocket propellant Fumigant for foodstuffs and textiles Sterilant for hospital equipment
Nickel	Nose Lung	Nickel plating Ferrous alloys Ceramics Batteries Stainless-steel welding byproduct
Radon and its decay products	Lung	Uranium decay Quarries and mines Cellars and poorly ventilated places
Vinyl chloride	Hemangiosarcoma Liver	Refrigerant Production of polyvinyl chloride Adhesive for plastics Former use in pressurized containers
Shiftwork that involves circadian disruption[10]	Breast
Involuntary smoking (Passive smoking)[23]	Lung
Unless else specified in boxes, then ref is:[24]

Others

• Gasoline (contains aromatics)
• Lead and its compounds
• Alkylating antineoplastic agents (e.g. mechlorethamine)
• Other alkylating agents (e.g. dimethyl sulfate)
• Ultraviolet radiation from the sun and UV lamps
• Alcohol (causing head and neck cancers)
• Other ionizing radiation (X-rays, gamma rays, etc.)

See also

• Industrial Union Department v. American Petroleum Institute
• International Agency for Research on Cancer
• Carcinogenesis
• Mutagen
• Possible carcinogen
• Teratogen
• Warburg hypothesis
• Safe handling of carcinogens
• History of cancer
• Acrylamide
• Asian Dust

Notes

1. ^ Ames, Bruce N; Gold, Lois Swirsky (2000). "Paracelsus to parascience: The environmental cancer distraction". Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 447: 3. doi:10.1016/S0027-5107(99)00194-3. 
2. ^ ^{a b} Report on Carcinogens, Eleventh Edition; U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program (2011).
3. ^ Acharya, PVN; The Effect of Ionizing Radiation on the Formation of Age-Correlated Oligo Deoxyribo Nucleo Phospheryl Peptides in Mammalian Cells; 10th International Congress of Gerontology, Jerusalem. Abstract No. 1; January 1975. Work done while employed by Dept. of Pathology, University of Wisconsin, Madison.
4. ^ Acharya, PVN; Implicatons of The Action of Low Level Ionizing Radiation on the Inducement of Irreparable DNA Damage Leading to Mammalian Aging and Chemical Carcinogenesis.; 10th International Congress of Biochemistry, Hamburg, Germany. Abstract No. 01-1-079; July 1976. Work done while employed by Dept. of Pathology, University of Wisconsin, Madison.
5. ^ Acharya, PV Narasimh; Irreparable DNA-Damage by Industrial Pollutants in Pre-mature Aging, Chemical Carcinogenesis and Cardiac Hypertrophy: Experiments and Theory; 1st International Meeting of Heads of Clinical Biochemistry Laboratories, Jerusalem, Israel. April 1977. Work conducted at Industrial Safety Institute and Behavioral Cybernetics Laboratory, University of Wisconsin, Madison.
6. ^ Wei Zheng, Deborah R Gustafson, Rashmi Sinha, James R Cerhan, et al. "Well-done meat intake and the risk of breast cancer." Journal of the National Cancer Institute. Oxford: Nov 18, 1998.Vol. 90, Iss. 22; pg. 1724, 6 pgs.
7. ^ "National Cancer Institute, 2004 analysis and recommendations". Cancer.gov. 2004-09-15. http://www.cancer.gov/cancertopics/factsheet/Risk/heterocyclic-amines. Retrieved 2010-09-22. 
8. ^ "Acrylamide". http://www.food.gov.uk/safereating/chemsafe/acrylamide_branch/. 
9. ^ "Definition of Carbon Monoxide - Carbon Monoxide in Cigarette Smoke". Quitsmoking.about.com. http://quitsmoking.about.com/cs/nicotineinhaler/g/carbonmonoxide.htm. Retrieved 2010-09-22. 
10. ^ ^{a b} "IARC Monographs Programme finds cancer hazards associated with shiftwork, painting and firefighting, International Agency for Research on Cancer". http://www.iarc.fr/en/media-centre/pr/2007/pr180.html. Retrieved 2011-07-01 
11. ^ Schernhammer E, Schulmeister K. Melatonin and cancer risk: does light at night compromise physiologic cancer protection by lowering serum melatonin levels? Br J Cancer 2004;90:941–943.
12. ^ Hansen J. Increased breast cancer risk among women who work predominantly at night. Epidemiology 2001; 12:74–77.
13. ^ Hansen J. Light at night, shiftwork, and breast cancer risk.J Natl Cancer Inst 2001; 93:1513–1515.
14. ^ Schernhammer E, Laden F, Speizer FE et al. Rotating night shifts and risk of breast cancer in women participating in the nurses' health study. J Natl Cancer Inst 2001; 93:1563–1568.
15. ^ Scott Davis, Dana K. Mirick, Richard G. Stevens (2001). "Night Shift Work, Light at Night, and Risk of Breast Cancer". Journal of the National Cancer Institute 93 (20): 1557–1562. doi:10.1093/jnci/93.20.1557. PMID 11604479. http://jncicancerspectrum.oupjournals.org/cgi/content/full/jnci;93/20/1557?ijkey=e1472aefe9398c2c26bf8515391f5940acc05495. 
16. ^ Eva S. Schernhammer, Francine Laden, Frank E. Speizer, Walter C. Willett, David J. Hunter, Ichiro Kawachi, Graham A. Colditz (2001). "Rotating Night Shifts and Risk of Breast Cancer in Women Participating in the Nurses' Health Study". Journal of the National Cancer Institute 93 (20): 1563–1568. doi:10.1093/jnci/93.20.1563. PMID 11604480. http://jncicancerspectrum.oupjournals.org/cgi/content/full/jnci;93/20/1563?ijkey=c01d8ce29cb0ba35061db9c434a0c8e4816e70a9. 
17. ^ Navara KJ, Nelson RJ (2007) The dark side of light light at night: physiological, epidemiological, and ecological consequences. J. Pineal Res. 2007; 43:215–224
18. ^ "The Gale Encyclopedia of Cancer: A guide to Cancer and its Treatments, Second Edition. Page no. 137". 
19. ^ "IARC Monographs". Monographs.iarc.fr. http://monographs.iarc.fr/. Retrieved 2010-09-22. 
20. ^ Section 301(b)(4) of the Public Health Service Act, as amended by Section 262, Pub. L. 95–622.
21. ^ Safe Work Australia , NOHSC. (1999). Approved criteria for classifying hazardous substances [NOHSC:1008(1999)] §4.76. Accessed 21/05/2011
22. ^ "Web definitions for Procarcinogen". Lactospore.com. http://www.lactospore.com/glossary.htm. Retrieved 2010-09-22. 
23. ^ Tobacco Smoke and Involuntary Smoking, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 83 (2004).
24. ^ Table 6-2 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7.  8th edition.

External links

Look up carcinogen in Wiktionary, the free dictionary.

Wikimedia Commons has media related to: Carcinogens

• U.S. National Toxicology Program's Report on Carcinogens
• Recognized Carcinogens
• American Cancer Society
• Database of Rodent Carcinogens
• Comparing Possible Cancer Hazards from Human Exposures to Rodent Carcinogens

v t e Carcinogen—Cancer causing materials and agents Main articles Cancer · Cancer cells Major suspected carcinogens PFOA · Tobacco smoke · Xenoestrogen · Bisphenol A · Ionizing radiation · DDT · 1,3-Butadiene · List of breast carcinogenic substances · PAH IARC International Agency for Research on Cancer / IARC agent lists: Group 1 · Group 2A · Group 2B · Group 3 · Group 4 (Caprolactam) See also: Neoplasm · Oncology · Non-stick pan

v t e Pathology: Tumor, Neoplasm, Cancer, and Oncology (C00–D48, 140–239) Conditions Benign tumors Hyperplasia Cyst Pseudocyst Hamartoma Malignant progression Dysplasia Carcinoma in situ Cancer Metastasis Topography Head/Neck (Oral, Nasopharyngeal) Digestive system Respiratory system Bone Skin Blood Urogenital Nervous system Endocrine system Histology Carcinoma Sarcoma Blastoma Papilloma Adenoma Other Precancerous condition Paraneoplastic syndrome Staging/grading TNM Ann Arbor Prostate cancer staging Gleason Grading System Dukes classification Carcinogenesis Cancer cell Carcinogen Tumor suppressor genes/oncogenes Clonally transmissible cancer Oncovirus Cancer bacteria Misc. Research List of oncology-related terms History Cancer pain M: NEO tsoc, mrkr tumr, epon, para drug (L1i/1e/V03)

v t e Toxicology Toxinology · History of poison Fields Aquatic toxicology · Ecotoxicology · Entomotoxicology · Environmental toxicology · Forensic toxicology · In vitro toxicology · Toxicogenomics Concepts Poison · Venom · Toxicant (Toxin)  · Acceptable daily intake · Acute toxicity · Bioaccumulation · Biomagnification · Fixed Dose Procedure · Median lethal dose (LD50) · Lethal dose · Toxic capacity · Toxicity Class Treatments Antidote · Gastric lavage · Whole bowel irrigation · Activated carbon · Cathartic · Hemodialysis · Chelation therapy · Hemoperfusion Incidents Bradford · Minamata · Niigata · Alexander Litvinenko · Bhopal · 2007 pet food recalls · Seveso disaster · List of poisonings Related topics Hazard symbol · Carcinogen · Mutagen · List of extremely hazardous substances · Biological warfare · Food safety M: TOX gen / txn pto ant

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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

한국어 (Korean)
n. - 발암성 물질

日本語 (Japanese)
n. - 発癌物質

العربيه (Arabic)
‏(الاسم) مادة مسببه للسرطان‏

עברית (Hebrew)
n. - ‮חומר הגורם לסרטן, מסרטן, גורם סרטן‬

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