Carcinogen

What is a carcinogen

Carcinogen is any substance that causes cancer. Cancer is caused by changes in a cell’s DNA – its genetic “blueprint.” Some of these changes may be inherited from your parents. Others may be caused by outside exposures, which are often referred to as environmental factors. Environmental factors can include a wide range of exposures, such as:

  • Lifestyle factors (nutrition, tobacco use, physical activity, etc.)
  • Naturally occurring exposures (ultraviolet light, radon gas, infectious agents, etc.)
  • Medical treatments (radiation and medicines including chemotherapy, hormone drugs, drugs that suppress the immune system, etc.)
  • Workplace exposures
  • Household exposures
  • Pollution

Substances and exposures that can lead to cancer are called carcinogens. Some carcinogens do not affect DNA directly, but lead to cancer in other ways. For example, they may cause cells to divide at a faster than normal rate, which could increase the chances that DNA changes will occur.

Carcinogens do not cause cancer in every case, all the time. Substances labeled as carcinogens may have different levels of cancer-causing potential. Some may cause cancer only after prolonged, high levels of exposure. And for any particular person, the risk of developing cancer depends on many factors, including how they are exposed to a carcinogen, the length and intensity of the exposure, and the person’s genetic makeup.

Testing to see if something can cause cancer is often difficult. It is not ethical to test a substance by exposing people to it and seeing if they get cancer from it. That’s why scientists must use other types of tests, which may not always give clear answers.

Lab studies

Scientists get much of their data about whether something might cause cancer from lab studies in cell cultures and animals. There are far too many substances (both natural and man-made) to test each one in lab animals, so scientists use what is already known about chemical structures, results from other types of lab tests, the extent of human exposure, and other factors to select chemicals for testing. For example, they can often get an idea about whether a substance might cause a problem by comparing it to similar chemicals that have already been studied.

Although lab studies alone can’t always predict if a substance will cause cancer in people, virtually all known human carcinogens that have been adequately tested also cause cancer in lab animals. In many cases, carcinogens are first found to cause cancer in lab animals and are later found to cause cancer in people.

Most studies of potential carcinogens expose the lab animals to doses that are much higher than common human exposures. This is so that cancer risk can be detected in relatively small groups of animals. It is not always clear if the results from animal studies will be the same for people as they are normally exposed to a substance. For example, the effects seen in lab studies with very high doses of a substance may not be the same at much lower doses, or the effects of a substance when it is inhaled may not be the same as if it is applied to the skin. Also, the bodies of lab animals and humans don’t always process substances in the same way.

But for safety reasons, it is usually assumed that exposures that cause cancer at larger doses in animals may also cause cancer in people. It isn’t always possible to know how the exposure dose might affect risk, but it is reasonable for public health purposes to assume that lowering human exposure will reduce risk.

Studies in people

Another important way to identify carcinogens is through epidemiologic studies, which look at human populations to determine which factors might be linked to cancer. These studies also provide useful information, but they have their limits. Humans do not live in a controlled environment. People are exposed to many substances at any given time, including those they encounter at work, school, or home; in the food they eat; and in the air they breathe. It’s very unlikely they know exactly what they’ve been exposed to or that they would be able to remember all of their exposures if asked by a researcher. And there are usually many years (often decades) between exposure to a carcinogen and the development of cancer. Therefore, it can be very hard to definitely link any particular exposure to cancer.

By combining data from both types of studies, scientists do their best to make an educated assessment of a substance’s cancer-causing ability. When the evidence is conclusive, the substance is labeled as a carcinogen. When the available evidence is compelling but not felt to be conclusive, the substance may be considered to be a probable carcinogen. But in some cases there simply isn’t enough information to be certain one way or the other.

Who determines how carcinogens are classified?

Several national and international agencies are responsible for determining the cancer-causing potential of different substances.

International Agency for Research on Cancer

The International Agency for Research on Cancer (IARC) is part of the World Health Organization (WHO). One of its major goals is to identify causes of cancer. The most widely used system for classifying carcinogens comes from the IARC. In the past 30 years, the IARC has evaluated the cancer-causing potential of more than 900 likely candidates, placing them into one of the following groups:

  • Group 1: Carcinogenic to humans
  • Group 2A: Probably carcinogenic to humans
  • Group 2B: Possibly carcinogenic to humans
  • Group 3: Unclassifiable as to carcinogenicity in humans
  • Group 4: Probably not carcinogenic to humans

Perhaps not surprisingly, based on how hard it can be to test these candidate carcinogens, most are listed as being of probable, possible, or unknown risk. Only a little over 100 are classified as “carcinogenic to humans.”

National Toxicology Program

The National Toxicology Program (NTP) is formed from parts of several different US government agencies, including the National Institutes of Health (NIH), the Centers for Disease Control and Prevention (CDC), and the U.S. Food and Drug Administration (FDA). The National Toxicology Program (NTP) updates its Report on Carcinogens (RoC) every few years.

The Report on Carcinogens identifies 2 groups of agents:

  • “Known to be human carcinogens”
  • “Reasonably anticipated to be human carcinogens”

The current version of the Report on Carcinogens lists about 250 substances and exposures. Unlike the IARC’s list, the Report on Carcinogens does not list substances that have been studied and found not to be carcinogens.

Environmental Protection Agency

The US Environmental Protection Agency (EPA) maintains the Integrated Risk Information System (IRIS), an electronic database that contains information on human health effects from exposure to certain substances in the environment. The EPA uses a rating system similar to that of IARC when describing the cancer-causing potential of a substance:

  • Group A: Carcinogenic to humans
  • Group B: Likely to be carcinogenic to humans
  • Group C: Suggestive evidence of carcinogenic potential
  • Group D: Inadequate information to assess carcinogenic potential
  • Group E: Not likely to be carcinogenic to humans

Other agencies and groups

Other federal agencies, such as the CDC’s National Institute for Occupational Safety and Health (NIOSH), the U.S. Food and Drug Administration (FDA), and the National Cancer Institute (NCI) may comment on whether a substance or exposure may cause cancer and/or what levels of exposure to a particular substance might be considered acceptable.

Some state agencies also keep lists of known or probable carcinogens. For example, the California Environmental Protection Agency (CalEPA) maintains a list of “chemicals known to the state to cause cancer or reproductive toxicity.”

Does any exposure to a known carcinogen always result in cancer?

Any substance that causes cancer is known as a carcinogen. But simply because a substance has been designated as a carcinogen does not mean that the substance will necessarily cause cancer. Many factors influence whether a person exposed to a carcinogen will develop cancer, including the amount and duration of the exposure and the individual’s genetic background. Cancers caused by involuntary exposures to environmental carcinogens are most likely to occur in subgroups of the population, such as workers in certain industries who may be exposed to carcinogens on the job.

How can exposures to carcinogens be limited?

In the United States, regulations have been put in place to reduce exposures to known carcinogens in the workplace. Outside of the workplace, people can also take steps to limit their exposure to known carcinogens, such as testing their basement for radon, quitting smoking, limiting sun exposure, or maintaining a healthy weight.

How many cancers are caused by involuntary exposure to carcinogens in the environment?

This question cannot be answered with certainty because the precise causes of most cancers are not known. Some researchers have suggested that, in most populations, environmental exposures are responsible for a relatively small proportion of total cancers (less than 4 percent), whereas other researchers attribute a higher proportion (19 percent) to environmental exposures.

What is birth control carcinogen?

Oral contraceptives (birth control pills) are hormone-containing medications that are taken by mouth to prevent pregnancy. They prevent pregnancy by inhibiting ovulation and also by preventing sperm from penetrating through the cervix.

By far the most commonly prescribed type of oral contraceptive in the United States contains synthetic versions of the natural female hormones estrogen and progesterone. This type of birth control pill is often called a combined oral contraceptive. Another type of oral contraceptive, sometimes called the mini pill, contains only progestin, which is a man-made version of progesterone.

Nearly all the research on the link between oral contraceptives and cancer risk comes from observational studies, both large prospective cohort studies and population-based case–control studies. Data from observational studies cannot definitively establish that an exposure—in this case, oral contraceptives—causes (or prevents) cancer. That is because women who take oral contraceptives may differ from those who don’t take them in ways other than their oral contraceptive use, and it is possible that these other differences—rather than oral contraceptive use—are what explains their different cancer risk.

Overall, however, these studies have provided consistent evidence that the risks of breast and cervical cancers are increased in women who use oral contraceptives, whereas the risks of endometrial, ovarian, and colorectal cancers are reduced 1.

Breast cancer

An analysis of data from more than 150,000 women who participated in 54 epidemiologic studies showed that, overall, women who had ever used oral contraceptives had a slight (7%) increase in the relative risk of breast cancer compared with women who had never used oral contraceptives. Women who were currently using oral contraceptives had a 24% increase in risk that did not increase with the duration of use. Risk declined after use of oral contraceptives stopped, and no risk increase was evident by 10 years after use had stopped 2.

A 2010 analysis of data from the Nurses’ Health Study 3, which has been following more than 116,000 female nurses who were 24 to 43 years old when they enrolled in the study in 1989, also found that participants who used oral contraceptives had a slight increase in breast cancer risk. However, nearly all of the increased risk was seen among women who took a specific type of oral contraceptive, a “triphasic” pill, in which the dose of hormones is changed in three stages over the course of a woman’s monthly cycle. An elevated risk associated with specific triphasic formulations was also reported in a nested case–control study that used electronic medical records to verify oral contraceptive use 4.

In 2017, a large prospective Danish study 5 reported breast cancer risks associated with more recent formulations of oral contraceptives. Overall, women who were using or had recently stopped using oral combined hormone contraceptives had a modest (about 20%) increase in the relative risk of breast cancer compared with women who had never used oral contraceptives. The risk increase varied from 0% to 60%, depending on the specific type of oral combined hormone contraceptive. The risk of breast cancer also increased the longer oral contraceptives were used.

Cervical cancer

Women who have used oral contraceptives for 5 or more years have a higher risk of cervical cancer than women who have never used oral contraceptives. The longer a woman uses oral contraceptives, the greater the increase in her risk of cervical cancer. One study found a 10% increased risk for less than 5 years of use, a 60% increased risk with 5–9 years of use, and a doubling of the risk with 10 or more years of use 6. However, the risk of cervical cancer has been found to decline over time after women stop using oral contraceptives 7.

Endometrial cancer

Women who have ever used oral contraceptives have a lower risk of endometrial cancer than women who have never used oral contraceptives. Risk is reduced by at least 30%, with a greater risk reduction the longer oral contraceptives were used 8. The protective effect persists for many years after a woman stops using oral contraceptives 7. An analysis of women participating in the prospective NIH-AARP Diet and Health Study found that the risk reduction was especially pronounced in those long-time users of oral contraceptives who were smokers, obese, or exercised rarely 8.

Ovarian cancer

Women who have ever used oral contraceptives have a 30% to 50% lower risk of ovarian cancer than women who have never used oral contraceptives 9. This protection has been found to increase with the length of time oral contraceptives are used 8 and to continue for up to 30 years after a woman stops using oral contraceptives 10. A reduction in ovarian cancer risk with use of oral contraceptives is also seen among women who carry a harmful mutation in the BRCA1 or BRCA2 gene 11, 12.

Colorectal cancer

Oral contraceptive use is associated with 15% to 20% lower risks of colorectal cancer 7.

How could oral contraceptives influence cancer risk?

Naturally occurring estrogen and progesterone stimulate the development and growth of some cancers (e.g., cancers that express receptors for these hormones, such as breast cancer). Because birth control pills contain synthetic versions of these female hormones, they could potentially also increase cancer risk.

In addition, oral contraceptives might increase the risk of cervical cancer by changing the susceptibility of cervical cells to persistent infection with high-risk HPV types (the cause of virtually all cervical cancers).

Researchers have proposed multiple ways that oral contraceptives may lower the risks of some cancers, including:

  • suppressing endometrial cell proliferation (endometrial cancer)
  • reducing the number of ovulations a woman experiences in her lifetime, thereby reducing exposure to naturally occurring female hormones (ovarian cancer)
  • lowering the levels of bile acids in the blood for women taking oral conjugated estrogens (colorectal cancer) 13

Human carcinogen list

Many people worry that substances or exposures in their environment may cause cancer. The lists below have been developed by two highly respected agencies – the International Agency for Research on Cancer (IARC) and the US National Toxicology Program (NTP). Some related information is included on how these and other agencies and groups test and classify possible carcinogens.

The International Agency for Research on Cancer (IARC) and the US National Toxicology Program (NTP) act independently but have studied many of the same agents, so many known or suspected carcinogens appear on both lists. But because an agent appears on one and not on the other does not necessarily mean there is a controversy, as one agency may not have evaluated it.

Unfortunately, many of the substances and exposures on the lists below can often go by different names. This can make it hard to find a particular substance on one or both of these lists, which are in alphabetical order and may not always use the most common term.

These lists include only those agents that have been evaluated by the agencies. These agencies tend to focus on substances and exposures most likely to cause cancer, but there are many others that have not been studied fully yet.

Most of the agents on the lists have been linked only with certain kinds of cancer, not all types. For more detailed information, refer to the specific monographs or reports published by the agencies (available on their websites).

The lists describe the level of evidence that something can cause cancer, not how likely it is that something will cause cancer in any particular person. For example, IARC considers there to be strong evidence that both tobacco smoking and eating processed meat can cause cancer, so both are listed as “carcinogenic to humans.” But smoking is much more likely to cause cancer than eating processed meat, even though both are in the same category.

Carcinogens do not cause cancer at all times, under all circumstances. Some may only be carcinogenic if a person is exposed in a certain way (for example, swallowing it as opposed to touching it). Some may only cause cancer in people who have a certain genetic makeup. Some of these agents may lead to cancer after only a very small exposure, while others might require intense exposure over many years. Again, you should refer to the agencies’ reports for specifics.

Even if a substance or exposure is known or suspected to cause cancer, this does not necessarily mean that it can or should be avoided at all costs. For example, estrogen is a known carcinogen that occurs naturally in the body. Exposure to ultraviolet (UV) radiation from sunlight is also known to cause cancer, but it’s not practical (or advisable) to completely avoid the sun. These lists also include many commonly used medicines, particularly some hormones and drugs used to treat cancer. For example, tamoxifen increases the risk of certain kinds of uterine cancer but can be very useful in treating some breast cancers, which may be more important for some women. If you have questions about a medicine that appears on one of these lists, be sure to ask your doctor.

Looking at the list below can tell you whether or not something may increase your risk of cancer, but it is important to try to get an idea of how much it might increase your risk. It is also important to know what your risk is to begin with. Many factors can enter into this, including your age, gender, family history, and lifestyle factors (tobacco and alcohol use, weight, diet, physical activity level, etc.). As noted above, the type and extent of exposure to a substance may also play a role. You should consider the actual amount of increased risk when deciding if you should limit or avoid an exposure.

Known human carcinogens

International Agency for Research on Cancer

Group 1: Carcinogenic to humans

  • Acetaldehyde (from consuming alcoholic beverages)
  • Acheson process, occupational exposure associated with
  • Acid mists, strong inorganic
  • Aflatoxins
  • Alcoholic beverages
  • Aluminum production
  • 4-Aminobiphenyl
  • Areca nut
  • Aristolochic acid (and plants containing it)
  • Arsenic and inorganic arsenic compounds
  • Asbestos (all forms) and mineral substances (such as talc or vermiculite) that contain asbestos
  • Auramine production
  • Azathioprine
  • Benzene
  • Benzidine and dyes metabolized to benzidine
  • Benzo[a]pyrene
  • Beryllium and beryllium compounds
  • Betel quid, with or without tobacco
  • Bis(chloromethyl)ether and chloromethyl methyl ether (technical-grade)
  • Busulfan
  • 1,3-Butadiene
  • Cadmium and cadmium compounds
  • Chlorambucil
  • Chlornaphazine
  • Chromium (VI) compounds
  • Clonorchis sinensis (infection with), also known as the Chinese liver fluke
  • Coal, indoor emissions from household combustion
  • Coal gasification
  • Coal-tar distillation
  • Coal-tar pitch
  • Coke production
  • Cyclophosphamide
  • Cyclosporine
  • 1,2-Dichloropropane
  • Diethylstilbestrol
  • Engine exhaust, diesel
  • Epstein-Barr virus (infection with)
  • Erionite
  • Estrogen postmenopausal therapy
  • Estrogen-progestogen postmenopausal therapy (combined)
  • Estrogen-progestogen oral contraceptives (combined) (Note: There is also convincing evidence in humans that these agents confer a protective effect
  • against cancer in the endometrium and ovary)
  • Ethanol in alcoholic beverages
  • Ethylene oxide
  • Etoposide
  • Etoposide in combination with cisplatin and bleomycin
  • Fission products, including strontium-90
  • Fluoro-edenite fibrous amphibole
  • Formaldehyde
  • Haematite mining (underground)
  • Helicobacter pylori (infection with)
  • Hepatitis B virus (chronic infection with)
  • Hepatitis C virus (chronic infection with)
  • Human immunodeficiency virus type 1 (HIV-1) (infection with)
  • Human papilloma virus (HPV) types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 (infection with) (Note: The HPV types that have been classified as carcinogenic to humans can differ by an order of magnitude in risk for cervical cancer)
  • Human T-cell lymphotropic virus type I (HTLV-1) (infection with)
  • Ionizing radiation (all types)
  • Iron and steel founding (workplace exposure)
  • Isopropyl alcohol manufacture using strong acids
  • Kaposi sarcoma herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8) (infection with)
  • Leather dust
  • Lindane
  • Magenta production
  • Melphalan
  • Methoxsalen (8-methoxypsoralen) plus ultraviolet A radiation, also known as PUVA
  • 4,4′-Methylenebis(chloroaniline) (MOCA)
  • Mineral oils, untreated or mildly treated
  • MOPP and other combined chemotherapy including alkylating agents
  • 2-Naphthylamine
  • Neutron radiation
  • Nickel compounds
  • N’-Nitrosonornicotine (NNN) and 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK)
  • Opisthorchis viverrini (infection with), also known as the Southeast Asian liver fluke
  • Outdoor air pollution (and the particulate matter in it)
  • Painter (workplace exposure as a)
  • 3,4,5,3′,4′-Pentachlorobiphenyl (PCB-126)
  • 2,3,4,7,8-Pentachlorodibenzofuran
  • Phenacetin (and mixtures containing it)
  • Phosphorus-32, as phosphate
  • Plutonium
  • Polychlorinated biphenyls (PCBs), dioxin-like, with a Toxicity Equivalency Factor according to WHO (PCBs 77, 81, 105, 114, 118, 123, 126, 156, 157, 167, 169, 189)
  • Processed meat (consumption of)
  • Radioiodines, including iodine-131
  • Radionuclides, alpha-particle-emitting, internally deposited (Note: Specific radionuclides for which there is sufficient evidence for carcinogenicity to
  • humans are also listed individually as Group 1 agents)
  • Radionuclides, beta-particle-emitting, internally deposited (Note: Specific radionuclides for which there is sufficient evidence for carcinogenicity to humans are also listed individually as Group 1 agents)
  • Radium-224 and its decay products
  • Radium-226 and its decay products
  • Radium-228 and its decay products
  • Radon-222 and its decay products
  • Rubber manufacturing industry
  • Salted fish (Chinese-style)
  • Schistosoma haematobium (infection with)
  • Semustine (methyl-CCNU)
  • Shale oils
  • Silica dust, crystalline, in the form of quartz or cristobalite
  • Solar radiation
  • Soot (as found in workplace exposure of chimney sweeps)
  • Sulfur mustard
  • Tamoxifen (Note: There is also conclusive evidence that tamoxifen reduces the risk of contralateral breast cancer in breast cancer patients)
  • 2,3,7,8-Tetrachlorodibenzo-para-dioxin
  • Thiotepa
  • Thorium-232 and its decay products
  • Tobacco, smokeless
  • Tobacco smoke, secondhand
  • Tobacco smoking
  • ortho-Toluidine
  • Treosulfan
  • Trichloroethylene
  • Ultraviolet (UV) radiation, including UVA, UVB, and UVC rays
  • Ultraviolet-emitting tanning devices
  • Vinyl chloride
  • Wood dust
  • X- and Gamma-radiation

National Toxicology Program 14th Report on Carcinogens

Known to be human carcinogens

  • Aflatoxins
  • Alcoholic beverage consumption
  • 4-Aminobiphenyl
  • Analgesic mixtures containing phenacetin
  • Aristolochic acids
  • Arsenic and inorganic arsenic compounds
  • Asbestos
  • Azathioprine
  • Benzene
  • Benzidine
  • Beryllium and beryllium compounds
  • Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether
  • 1,3-Butadiene
  • 1,4-Butanediol dimethylsulfonate (also known as busulfan)
  • Cadmium and cadmium compounds
  • Chlorambucil
  • 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (MeCCNU)
  • Chromium hexavalent compounds
  • Coal tar pitches
  • Coal tars
  • Coke oven emissions
  • Cyclophosphamide
  • Cyclosporin A
  • Diethylstilbestrol (DES)
  • Dyes metabolized to benzidine
  • Epstein-Barr virus (EBV)
  • Erionite
  • Estrogens, steroidal
  • Ethylene oxide
  • Formaldehyde
  • Hepatitis B virus
  • Hepatitis C virus
  • Human immunodeficiency virus type 1 (HIV-1)
  • Human papilloma viruses: some genital-mucosal types
  • Human T-cell lymphotropic virus type 1 (HTLV-1)
  • Kaposi sarcoma-associated herpesvirus (KSHV) (also know as human herpesvirus 8, or HHV-8)
  • Melphalan
  • Merkel cell polyomavirus (MCV)
  • Methoxsalen with ultraviolet A therapy (PUVA)
  • Mineral oils (untreated and mildly treated)
  • Mustard gas
  • 2-Naphthylamine
  • Neutrons
  • Nickel compounds
  • Oral tobacco products
  • Radon
  • Silica, crystalline (respirable size)
  • Solar radiation
  • Soots
  • Strong inorganic acid mists containing sulfuric acid
  • Sunlamps or sunbeds, exposure to
  • Tamoxifen
  • 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); “dioxin”
  • Thiotepa
  • Thorium dioxide
  • Tobacco smoke, environmental
  • Tobacco, smokeless
  • Tobacco smoking
  • o‑Toluidine
  • Trichloroethylene (TCE)
  • Vinyl chloride
  • Ultraviolet (UV) radiation, broad spectrum
  • Wood dust
  • X-radiation and gamma radiation

Probable human carcinogens

International Agency for Research on Cancer

Group 2A: Probably carcinogenic to humans

  • Acrylamide
  • Adriamycin (doxorubicin)
  • Androgenic (anabolic) steroids
  • Art glass, glass containers, and press ware (manufacture of)
  • Azacitidine
  • Biomass fuel (primarily wood), emissions from household combustion
  • Bischloroethyl nitrosourea (BCNU), also known as carmustine
  • Captafol
  • Carbon electrode manufacture
  • Chloral
  • Chloral hydrate
  • Chloramphenicol
  • alpha-Chlorinated toluenes (benzal chloride, benzotrichloride, benzyl chloride) and benzoyl chloride (combined exposures)
  • 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU)
  • 4-Chloro-ortho-toluidine
  • Chlorozotocin
  • Cisplatin
  • Cobalt metal with tungsten carbide
  • Creosotes
  • Cyclopenta[cd]pyrene
  • DDT (4,4′-Dichlorodiphenyltrichloroethane)
  • Diazinon
  • Dibenz[a,j]acridine
  • Dibenz[a,h]anthracene
  • Dibenzo[a,l]pyrene
  • Dichloromethane (methylene chloride)
  • Diethyl sulfate
  • Dimethylcarbamoyl chloride
  • 1,2-Dimethylhydrazine
  • Dimethyl sulfate
  • Epichlorohydrin
  • Ethyl carbamate (urethane)
  • Ethylene dibromide
  • N-Ethyl-N-nitrosourea
  • Frying, emissions from high-temperature
  • Glycidol
  • Glyphosate
  • Hairdresser or barber (workplace exposure as)
  • Human papillomavirus (HPV) type 68 (infection with)
  • Indium phosphide
  • IQ (2-Amino-3-methylimidazo[4,5-f]quinoline)
  • Lead compounds, inorganic
  • Malaria (caused by infection with Plasmodium falciparum)
  • Malathion
  • Merkel cell polyomavirus (MCV)
  • 5-Methoxypsoralen
  • Methyl methanesulfonate
  • N-Methyl-N´-nitro-N-nitrosoguanidine (MNNG)
  • N-Methyl-N-nitrosourea
  • Nitrate or nitrite (ingested) under conditions that result in endogenous nitrosation
  • 6-Nitrochrysene
  • Nitrogen mustard
  • 1-Nitropyrene
  • N-Nitrosodiethylamine
  • N-Nitrosodimethylamine
  • 2-Nitrotoluene
  • Non-arsenical insecticides (workplace exposures in spraying and application of)
  • Petroleum refining (workplace exposures in)
  • Pioglitazone
  • Polybrominated biphenyls (PBBs)
  • Procarbazine hydrochloride
  • 1,3-Propane sultone
  • Red meat (consumption of)
  • Shiftwork that involves circadian disruption
  • Silicon carbide whiskers
  • Styrene-7,8-oxide
  • Teniposide
  • Tetrachloroethylene (perchloroethylene)
  • Tetrafluoroethylene
  • Trichloroethylene
  • 1,2,3-Trichloropropane
  • Tris(2,3-dibromopropyl) phosphate
  • Very hot beverages (above 65 degrees Celsius)
  • Vinyl bromide (Note: For practical purposes, vinyl bromide should be considered to act similarly to the human carcinogen vinyl chloride.)
  • Vinyl fluoride (Note: For practical purposes, vinyl fluoride should be considered to act similarly to the human carcinogen vinyl chloride.)

National Toxicology Program 14th Report on Carcinogens

Reasonably anticipated to be human carcinogens

  • Acetaldehyde
  • 2-Acetylaminofluorene
  • Acrylamide
  • Acrylonitrile
  • Adriamycin® (doxorubicin hydrochloride)
  • 2-Aminoanthraquinone
  • o-Aminoazotoluene
  • 1-Amino-2,4-dibromoanthraquinone
  • 1-Amino-2-methylanthraquinone
  • 2-Amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ)
  • 2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx)
  • 2-Amino-3-methylimidazo[4,5-f]quinoline (IQ)
  • 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)
  • Amitrole
  • o-Anisidine and its hydrochloride
  • Azacitidine (5-Azacytidine®, 5-AzaC)
  • Basic Red 9 Monohydrochloride
  • Benz[a]anthracene
  • Benzo[b]fluoranthene
  • Benzo[j]fluoranthene
  • Benzo[k]fluoranthene
  • Benzo[a]pyrene
  • Benzotrichloride
  • 2, 2-bis-(bromoethyl)-1,3-propanediol (technical grade)
  • Bromodichloromethane
  • 1-Bromopropane
  • Butylated hydroxyanisole (BHA)
  • Captafol
  • Carbon tetrachloride
  • Ceramic fibers (respirable size)
  • Chloramphenicol
  • Chlorendic acid
  • Chlorinated paraffins (C12, 60% chlorine)
  • Chloroform
  • 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea
  • Bis(chloroethyl) nitrosourea
  • 3-Chloro-2-methylpropene
  • 4-Chloro-o-phenylenediamine
  • Chloroprene
  • p-Chloro-o-toluidine and p-chloro-o-toluidine hydrochloride
  • Chlorozotocin
  • Cisplatin
  • Cobalt and cobalt compounds that release cobalt ions in vivo
  • Cobalt-tungsten carbide: powders and hard metals
  • p-Cresidine
  • Cumene
  • Cupferron
  • Dacarbazine
  • Danthron (1,8-dihydroxyanthraquinone)
  • 2,4-Diaminoanisole sulfate
  • 2,4-Diaminotoluene
  • Diazoaminobenzene
  • Dibenz[a,h]acridine
  • Dibenz[a,j]acridine
  • Dibenz[a,h]anthracene
  • 7H-Dibenzo[c,g]carbazole
  • Dibenzo[a,e]pyrene
  • Dibenzo[a,h]pyrene
  • Dibenzo[a,i]pyrene
  • Dibenzo[a,l]pyrene
  • 1,2-Dibromo-3-chloropropane
  • 1,2-Dibromoethane (ethylene dibromide)
  • 2,3-Dibromo-1-propanol
  • Tris (2,3-dibromopropyl) phosphate
  • 1,4-Dichlorobenzene
  • 3,3′-Dichlorobenzidine and 3,3′-dichlorobenzidine dihydrochloride
  • Dichlorodiphenyltrichloroethane (DDT)
  • 1,2-Dichloroethane (ethylene dichloride)
  • Dichloromethane (methylene chloride)
  • 1,3-Dichloropropene (technical grade)
  • Diepoxybutane
  • Diesel exhaust particulates
  • Diethyl sulfate
  • Diglycidyl resorcinol ether
  • 3,3′-Dimethoxybenzidine
  • 4-Dimethylaminoazobenzene
  • 3,3′-Dimethylbenzidine
  • Dimethylcarbamoyl chloride
  • 1,1-Dimethylhydrazine
  • Dimethyl sulfate
  • Dimethylvinyl chloride
  • 1,6-Dinitropyrene
  • 1,8-Dinitropyrene
  • 1,4-Dioxane
  • Disperse blue 1
  • Dyes metabolized to 3,3′-dimethoxybenzidine
  • Dyes metabolized to 3,3′-dimethylbenzidine
  • Epichlorohydrin
  • Ethylene thiourea
  • Ethyl methanesulfonate
  • Furan
  • Glass wool fibers (inhalable)
  • Glycidol
  • Hexachlorobenzene
  • Hexachlorocyclohexane isomers
  • Hexachloroethane
  • Hexamethylphosphoramide
  • Hydrazine and hydrazine sulfate
  • Hydrazobenzene
  • Indeno[1,2,3-cd]pyrene
  • Iron dextran complex
  • Isoprene
  • Kepone® (chlordecone)
  • Lead and lead compounds
  • Lindane, hexachlorocyclohexane
  • 2-Methylaziridine (propylenimine)
  • 5-Methylchrysene
  • 4,4′-Methylenebis(2-chloroaniline)
  • 4-4′-Methylenebis(N,N-dimethyl)benzenamine
  • 4,4′-Methylenedianiline and its dihydrochloride salt
  • Methyleugenol
  • Methyl methanesulfonate
  • N-methyl-N’-nitro-N-nitrosoguanidine
  • Metronidazole
  • Michler’s ketone [4,4′-(dimethylamino) benzophenone]
  • Mirex
  • Naphthalene
  • Nickel, metallic
  • Nitrilotriacetic acid
  • o-Nitroanisole
  • Nitrobenzene
  • 6-Nitrochrysene
  • Nitrofen (2,4-dichlorophenyl-p-nitrophenyl ether)
  • Nitrogen mustard hydrochloride
  • Nitromethane
  • 2-Nitropropane
  • 1-Nitropyrene
  • 4-Nitropyrene
  • N-nitrosodi-n-butylamine
  • N-nitrosodiethanolamine
  • N-nitrosodiethylamine
  • N-nitrosodimethylamine
  • N-nitrosodi-n-propylamine
  • N-nitroso-N-ethylurea
  • 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone
  • N-nitroso-N-methylurea
  • N-nitrosomethylvinylamine
  • N-nitrosomorpholine
  • N-nitrosonornicotine
  • N-nitrosopiperidine
  • N-nitrosopyrrolidine
  • N-nitrososarcosine
  • o-Nitrotoluene
  • Norethisterone
  • Ochratoxin A
  • 4,4′-Oxydianiline
  • Oxymetholone
  • Pentachlorophenol and by-products of its synthesis
  • Phenacetin
  • Phenazopyridine hydrochloride
  • Phenolphthalein
  • Phenoxybenzamine hydrochloride
  • Phenytoin and phenytoin sodium
  • Polybrominated biphenyls (PBBs)
  • Polychlorinated biphenyls (PCBs)
  • Polycyclic aromatic hydrocarbons (PAHs)
  • Procarbazine and its hydrochloride
  • Progesterone
  • 1,3-Propane sultone
  • beta-Propiolactone
  • Propylene oxide
  • Propylthiouracil
  • Reserpine
  • Riddelliine
  • Safrole
  • Selenium sulfide
  • Streptozotocin
  • Styrene
  • Styrene-7,8-oxide
  • Sulfallate
  • Tetrachloroethylene (perchloroethylene)
  • Tetrafluoroethylene
  • Tetranitromethane
  • Thioacetamide
  • 4,4′-Thiodianaline
  • Thiourea
  • Toluene diisocyanates
  • Toxaphene
  • 2,4,6-Trichlorophenol
  • 1,2,3-Trichloropropane
  • Tris(2,3-dibromopropyl) phosphate
  • Ultraviolet A radiation
  • Ultraviolet B radiation
  • Ultraviolet C radiation
  • Urethane
  • Vinyl bromide
  • 4-Vinyl-1-cyclohexene diepoxide
  • Vinyl fluoride
  1. Bassuk SS, Manson JE. Oral contraceptives and menopausal hormone therapy: relative and attributable risks of cardiovascular disease, cancer, and other health outcomes. Annals of Epidemiology 2015; 25(3):193-200[]
  2. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53,297 women with breast cancer and 100,239 women without breast cancer from 54 epidemiological studies. Lancet 1996; 347(9017):1713–1727[]
  3. Bhupathiraju SN, Grodstein F, Stampfer MJ, et al. Exogenous hormone use: Oral contraceptives, postmenopausal hormone therapy, and health outcomes in the Nurses’ Health Study. American Journal of Public Health 2016; 106(9):1631-1637[]
  4. Beaber EF, Buist DS, Barlow WE, et al. Recent oral contraceptive use by formulation and breast cancer risk among women 20 to 49 years of age. Cancer Research 2014; 74(15):4078-4089[]
  5. Mørch LS, Skovlund CW, Hannaford PC, et al. Contemporary hormonal contraception and the risk of breast cancer. New England Journal of Medicine 2017; 377(23):2228-2239[]
  6. Smith JS, Green J, Berrington de Gonzalez A, et al. Cervical cancer and use of hormonal contraceptives: a systematic review. Lancet 2003; 361(9364):1159-1167[]
  7. Iversen L, Sivasubramaniam S, Lee AJ, Fielding S, Hannaford PC. Lifetime cancer risk and combined oral contraceptives: The Royal College of General Practitioners’ Oral Contraception Study. American Journal of Obstetrics and Gynecology 2017; 216(6):580.e1-580.e9[][][]
  8. Michels KA, Pfeiffer RM, Brinton LA, Trabert B. Modification of the associations between duration of oral contraceptive use and ovarian, endometrial, breast, and colorectal cancers. JAMA Oncology 2018; doi:10.1001/jamaoncol.2017.4942[][][]
  9. Wentzensen N, Poole EM, Trabert B, et al. Ovarian cancer risk factors by histologic subtype: An analysis from the Ovarian Cancer Cohort Consortium. Journal of Clinical Oncology 2016; 34(24):2888-2898[]
  10. Havrilesky LJ, Moorman PG, Lowery WJ, et al. Oral contraceptive pills as primary prevention for ovarian cancer: a systematic review and meta-analysis. Obstetrics and Gynecology 2013; 122(1):139-147[]
  11. Friebel TM, Domchek SM, Rebbeck TR. Modifiers of cancer risk in BRCA1 and BRCA2 mutation carriers: systematic review and meta-analysis. Journal of the National Cancer Institute 2014; 106(6):dju091[]
  12. Moorman PG, Havrilesky LJ, Gierisch JM, et al. Oral contraceptives and risk of ovarian cancer and breast cancer among high-risk women: a systematic review and meta-analysis. Journal of Clinical Oncology 2013; 31(33):4188-4198[]
  13. Murphy N, Xu L, Zervoudakis A, et al. Reproductive and menstrual factors and colorectal cancer incidence in the Women’s Health Initiative Observational Study. British Journal of Cancer 2017; 116(1):117-125[]
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