Toxic waste

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For other uses, see Toxic waste (disambiguation).

Valley of the Drums, a toxic waste site in Kentucky, United States, 1980.
Toxic waste is waste material that can cause death or injury to living creatures. It can be spread quite easily and
can contaminate lakes and rivers. The term is often used interchangeably with “hazardous waste”, or discarded
material that can pose a long-term risk to health or environment.
As with most pollution problems, toxic waste began to be a significant issue during the industrial revolution. It
usually is the product of industry or commerce, but comes also from residential use (e.g. cleaning products,
cosmetics, lawn care products), agriculture (e.g. chemical fertilizers, pesticides), the military (nuclear weapons
testing, chemical warfare), medical facilities (e.g. pharmaceuticals), radioactive sources, and light industry, such
as dry cleaning establishments.[1][2]

Contents
[hide]
• 1 Health effects
○ 1.1 Toxic waste
• 2 See also
• 3 Further reading
• 4 References
• 5 External links

[edit] Health effects

[edit] Toxic waste
Toxic wastes often contain carcinogens, and exposure to these by some route, such as leakage or evaporation
from the storage, causes cancer to appear at increased frequency in exposed individuals. For example, a cluster
of the rare blood cancer polycythemia vera was found around a toxic waste dump site in northeast Pennsylvania
in 2008.[3]
Toxic wastes containing organic carcinogens can be destroyed by incineration at high temperatures, which is
expensive. However, if the waste contains heavy metals or radioactive isotopes, these must be separated and
stored, as they cannot be destroyed.
[edit] See also
• Superfund
• List of Superfund sites in the United States
• Pollution
• Radioactive waste
• Hazardous Waste
 • Environmental remediation
• Agent Orange
[edit] Further reading
• John Stauber and Sheldon Rampton, Toxic Sludge is Good For You, Common Courage Press, 2002,
ISBN 978-1567510607
• Fred Setterberg and Lonny Shavelson, Toxic Nation: The Fight to Save Our Communities from
Chemical Contamination, Jossey-Bass, 1993, ISBN 978-0471575450
[edit] References
1. ^ "Environmental Risks and Pregnancy". March Of Dimes.
http://www.marchofdimes.com/855_9146.asp. Retrieved 2009-03-11.
2. ^ "China birth defects 'up sharply'". BBC News. 1 February 2009. http://news.bbc.co.uk/2/hi/asia-
pacific/7863290.stm. Retrieved 2009-03-11.
3. ^ MICHAEL RUBINKAM (2008). "Cancer cluster confirmed in northeast Pennsylvania". Associated
Press. http://news.yahoo.com/s/ap/20080826/ap_on_sc/toxic_dump_fears.
[edit] External links
• Information on toxic waste from the CDC
Hazardous waste
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This High Priority may require cleanup to meet Wikipedia's quality standards. Please improve
this High Priority if you can. (November 2008)

A hazardous waste is waste that poses substantial or potential threats to public health or the environment and
generally exhibits one or more of these characteristics:
• ignitable (i.e., flammable)
• reactive
• corrosive
• toxic
U.S. environmental laws (see Resource Conservation and Recovery Act) additionally describe a "hazardous
waste" as a waste (usually a solid waste) that has the potential to:
• cause, or significantly contribute to an increase in mortality (death) or an increase in serious
irreversible, or incapacitating reversible illness; or
• pose a substantial (present or potential) hazard to human health or the environment when improperly
treated, stored, transported, or disposed of, or otherwise managed.
These wastes may be found in different physical states such as gaseous, liquids, or solids. Furthermore, a
hazardous waste is a special type of waste because it cannot be disposed of by common means like other by-
products of our everyday lives. Depending on the physical state of the waste, treatment and solidification
processes might be available. In other cases, however, there is not much that can be done to prevent harm.

Contents
[hide]
• 1 Regulatory history
○ 1.1 Resource Conservation and Recovery Act (RCRA)
○ 1.2 Comprehensive Environmental Response, Compensation, and Liability Act
• 2 Hazardous wastes in the United States
○ 2.1 Characteristic wastes
 2.1.1 Ignitability
  2.1.2 Corrosive
 2.1.3 Reactivity
 2.1.4 Toxicity
○ 2.2 Listed wastes
 2.2.1 The F-list (non-specific source wastes)
 2.2.2 The K-list (source-specific wastes)
 2.2.3 Discarded wastes (P-List and U-List)
• 3 Universal wastes
• 4 Other hazardous wastes
• 5 Exempted hazardous wastes
• 6 Household Hazardous Waste
• 7 Final disposal of hazardous waste
○ 7.1 Recycling
○ 7.2 Portland cement
○ 7.3 Neutralization
○ 7.4 Incineration, destruction and waste-to-energy
○ 7.5 Hazardous waste landfill (sequestering, isolation, etc.)
○ 7.6 Pyrolysis
• 8 See also
• 9 References
• 10 External links

[edit] Regulatory history

[edit] Resource Conservation and Recovery Act (RCRA)
Modern hazardous waste regulations in the U.S. began with the Resource Conservation and Recovery Act
(RCRA) which was enacted in 1976. The primary contribution of RCRA was to create a "cradle to grave"
system of record keeping for hazardous wastes. Hazardous wastes must be tracked from the time they are
generated until their final disposition.
RCRA's record keeping system helps to track the life cycle of hazardous waste and reduces the amount of
hazardous waste illegally disposed.
[edit] Comprehensive Environmental Response, Compensation, and Liability Act
The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA), was enacted in
1980. The primary contribution of CERCLA was to create a "Superfund" and provided for the clean-up and
remediation of closed and abandoned hazardous waste sites.Before this act was created, hazardous wastes were
being disposed in regular landfills until scientists measured unfavorable amounts of hazardous materials seeping
into the ground. These chemicals eventually made their way to the water systems, and contaminated the soil that
animals and crops used, as well as the soil that people employed to build their communities. After these
regulations were put into practice, many landfills require now countermeasures against groundwater
contamination; for example installing a barrier along the foundation of the landfill to contain the hazardous
substances that may remain in the disposed waste.[1]Currently, in order to enter a landfill, hazardous wastes must
be stabilized and solidified, thus the new waste produced is less harmful than the original.
[edit] Hazardous wastes in the United States
Many types of businesses generate hazardous waste. Some are small areas that may be located in a community.
For example, dry cleaners, automobile repair shops, hospitals, exterminators, and photo processing centers all
generate hazardous waste. Some hazardous waste generators are larger companies like chemical manufacturers,
electroplating companies, and oil refineries.
A US facility that treats, stores or disposes of hazardous waste must obtain a permit for doing so under the
Resource Conservation and Recovery Act. Generators of and transporters of hazardous waste must meet specific
requirements for handling, managing, and tracking waste. Through the RCRA, Congress directed the United
States Environmental Protection Agency (EPA) to create regulations to manage hazardous waste. Under this
mandate, the EPA developed strict requirements for all aspects of hazardous waste management including the
treatment, storage, and disposal of hazardous waste. In addition to these federal requirements, states may
develop more stringent requirements or requirements that are broader in scope than the federal regulations.
In the United States, hazardous wastes generated by commercial or industrial activities may be classified as
"listed" hazardous wastes or "characteristic" hazardous wastes by the EPA.
In regulatory terms, a Resource Conservation and Recovery Act (RCRA) hazardous waste is a waste that either
a "characteristic waste" or a "listed waste":
• Characteristic Waste - exhibits at least one of the four "characteristics" of hazardous waste
(ignitability, corrosivity, reactivity, or toxicity)
• Listed Waste - appears on one of the four hazardous wastes lists (F-list, K-list, P-list, or U-list), or
Individual states may regulate particular wastes more stringently than mandated by federal regulation. This is
because the U.S. EPA is authorized to delegate primary rulemaking authorization to individual states. Most
states take advantage of this authority, implementing their own hazardous waste programs that are at least as
stringent as the federal program.
[edit] Characteristic wastes
Characteristic Hazardous Wastes are defined as wastes that exhibit the following characteristics: ignitability,
corrosivity, reactivity, or toxicity.
[edit] Ignitability
Ignitable wastes can create fires under certain conditions, are spontaneously combustible, or have a flash point
less than 60 °C (140 °F). Examples include waste oils and used solvents. For more details, see 40 CFR §261.21.
Test methods that may be used to determine ignitability include the Pensky-Martens Closed-Cup Method for
Determining Ignitability, the Setaflash Closed-Cup Method for Determining Ignitability, and the Ignitability of
Solids.
[edit] Corrosive
Corrosive wastes are acids or bases (pH less than or equal to 2, or greater than or equal to 12.5) that are capable
of corroding metal containers, such as storage tanks, drums, and barrels. Battery acid is an example. For more
details, see 40 CFR §261.22. The test method that may be used to determine corrosivity is the Corrosivity
Towards Steel (Method 1110A) (PDF).
[edit] Reactivity
Reactive wastes are unstable under "normal" conditions. They can cause explosions, toxic fumes, gases, or
vapors when heated, compressed, or mixed with water. Examples include lithium-sulfur batteries and
explosives. For more details, see 40 CFR §261.23. There are currently no test methods available.
[edit] Toxicity
Toxic wastes are those containing concentrations of certain substances in excess of regulatory thresholds which
are expected to cause injury or illness to human health or the environment. For more details see [3]
[edit] Listed wastes
Listed hazardous wastes are generated by specific industries and processes and are automatically considered
hazardous, based solely on the process that generates them and irrespective of whether a test of the waste shows
any of the "characteristics" of hazardous waste. Examples of listed wastes include:
• many sludges leftover from electroplating processes.
• certain waste from iron and steel manufacturing
• wastes from certain cleaning and/or degreasing processes
Hazardous wastes are incorporated into lists published by the Environmental Protection Agency. These lists are
organized into three categories:
[edit] The F-list (non-specific source wastes)
This list identifies wastes from common manufacturing and industrial processes, such as solvents, that have
been used in cleaning or degreasing operations. Because the processes producing these wastes can occur in
different sectors of industry, the F-listed wastes are known as wastes from non-specific sources.
[edit] The K-list (source-specific wastes)
This list includes certain wastes from specific industries, such as petroleum refining or pesticide manufacturing.
Certain sludges and wastewaters from treatment and production processes in these industries are examples of
source-specific wastes.
[edit] Discarded wastes (P-List and U-List)
P-List and U-List wastes are actually sublists of the same major list applying to discarded wastes. These wastes
apply to commercial chemical products that are considered hazardous when discarded and are regulated under
the following U.S. Federal Regulation: 40 C.F.R. 261.33(e) and 261.33(f). P-List wastes are wastes that are
considered "acutely hazardous" when discarded and are subject to more stringent regulation. Nitric oxide is an
example of a P-list waste and carries the number P076. U-Listed wastes are considered "hazardous" when
discarded and are regulated in a somewhat less stringent manner than P-Listed wastes.
[edit] Universal wastes
Universal wastes are hazardous wastes that (in the U.S.):
• generally pose a lower threat relative to other hazardous wastes
• are ubiquitous and produced in very large quantities by a large number of generators.
Some of the most common "universal wastes" are: fluorescent light bulbs, some specialty batteries (e.g. lithium
or lead containing batteries), cathode ray tubes, and mercury-containing devices.
Also, in worldwide, The United Nations Environmental Programme(UNEP) estimated that more than 400
million tons of hazardous wastes are produced universally each year, mostly by industrialized countries (schmit,
1999). About 1- percent of this total is shipped across international boundaries, with the majority of the transfers
occurring between countries in the Organization for the Economic Cooperation and Development(OECD)
(Krueger, 1999).[2] In a country like the United States, some undefined portion of the total is shipped legally or
illegally to underdeveloped countries. some of the reasons for industrialized countries to ship the hazardous
waste to industrializing countries for disposal are the rising cost of disposing hazardous waste in the home
country.[3]
Universal wastes are subject to somewhat less sringent regulatory requirements and small quantity generators of
universal wastes may be classified as "conditionally-exempt small quantity generators" (CESQGs) which
releases them from some of the regulatory requirements for the handling and storage hazardous wastes.
Universal wastes must still be disposed of properly. (For more information, see Fact Sheet: Conditionally
Exempt Small Quantity Generator)
[edit] Other hazardous wastes
The U.S. Environmental Protection Agency has other ways of regulating hazardous waste. These "rules"
include:
• The "Mixture Rule" - 400 CFR Section 261-23 (incorrect citation)
applies to a mixture of a listed hazardous waste and a solid waste and states that the result of a mixture of these
two wastes is regulated as a hazardous waste. Exemptions may apply in some cases.
• The "Derived-from Rule" - 40 CFR Section 261.3(b) applies to a waste that is generated from the
treatment, storage or disposal of a hazardous waste (for example, the ash from the incineration of
hazardous waste). Wastes "derived" in this manner may be regulated as hazardous wastes.
• The "Contained-in Rule" - - 40 CFR Section 261.3(f) applies to soil, groundwater, surface water and
debris that are contaminated with a listed hazardous waste.
[edit] Exempted hazardous wastes
USEPA regulations automatically exempt certain solid wastes from being regulated as "hazardous wastes". This
does not necessarily mean the wastes are not hazardous nor that they are not regulated. An exempted hazardous
waste simply means that the waste is not regulated by the primary hazardous waste regulations. Many of these
wastes may by regulated by different statutes and/or regulations and/or by different regulatory agencies. For
example, many hazardous mining wastes are regulated via mining statutes and regulations. "Exempted"
hazardous wastes include:
• Household hazardous waste (HHW); (see below)
• Agricultural wastes which are returned to the ground as fertilizer;
• Mining overburden returned to the mine site;
• Utility wastes from [coal] combustion to produce electricity;
• Oil and natural gas exploration drilling waste;
 • Wastes from the extraction of beneficiation, and processing of ores and minerals, including coal;
• Cement kiln wastes;
• Wood treated with arsenic preservatives.
• Certain chromium-containing wastes (See Code of Federal Regulations Section 261.4(b))
• Recycled hazardous wastes: Some hazardous wastes that are recycled may also be exempted from
hazardous waste regulations.
[edit] Household Hazardous Waste
Household Hazardous Waste (HHW) (also referred to as domestic hazardous waste) is waste that is generated
from residential households. HHW only applies to wastes that are the result of the use of materials that are
labeled for and sold for "home use".
The following list includes categories often applied to HHW. It is important to note that many of these
categories overlap and that many household wastes can fall into multiple categories:
• Paints and solvents
• Automotive wastes (used motor oil, antifreeze, etc.)
• Pesticides (insecticides, herbicides, fungicides, etc.)
• Mercury-containing wastes (thermometers, switches, fluorescent lighting, etc)
• Electronics (computers, televisions, cell phones)
• Aerosols / Propane cylinders
• Caustics / Cleaning agents
• Refrigerant-containing appliances
• Some specialty Batteries (e.g. lithium, nickel cadmium, or button cell batteries)
• Ammunition
• Radioactive waste (some home smoke detectors are classified as radioactive waste because they
contain very small amounts of a radioactive isotope of americium (see: Disposing of Smoke Detectors).
Disposal of HHW in the United States
Because of the expense associated with the disposal of HHW, it is still legal for most homeowners in the U.S. to
dispose of most types of household hazardous wastes as municipal solid waste (MSW) and these wastes can be
put in your trash. Laws vary by state and municipality and they are changing every day. Be sure to check with
your local environmental regulatory agency, solid waste authority, or health department to find out how HHW is
managed in your area.
Modern landfills are designed to handle normal amounts of HHW and minimize the environmental impacts.
However, there are still going to be some impacts and there are many ways that homeowners can keep these
wastes out of landfills.[4]
Laws regulating HHW in the U.S. are gradually becoming more strict. As of 2007, radioactive smoke detectors
are the only HHW that are managed nationally. While it is still legal in the United States to dispose of smoke
detectors in your trash in most places, manufacturers of smoke detectors must accept returned units for disposal
as mandated by the Nuclear Regulatory law 10 CFR 32.27. If you send your detector back to a manufacturer
then it will be disposed in a nuclear waste facility.
In the U.S., states are regulating various HHW waste disposal in MSW landfills on a state by state basis. Some
commonly regulated wastes in some (but not all) states include restrictions on the disposal of:
• Recyclables (especially "source-separated" recyclables or recyclables that have already been separated
from solid waste). In this case this would only apply to household hazardous wastes that have been
separated for recycling.
• Lead-acid batteries
• Mercury-containing wastes
• Rechargeable batteries
• Cathode ray tubes (CRTs) from older computer monitors and televisions
• Cell phones and computers
• Refrigerant containing appliances such as a refrigerator, air conditioner or dehumidifier.
(Note: Yard waste or "green waste" (particularly "source-separated" yard waste such as from a city leaf
collection program) is not hazardous but may be a regulated household waste)
Local solid waste authorities and health departments may also have specific bans on wastes that apply to their
service area.
Solid Waste Haulers and HHW - One "catch-22" that residents often encounter is that while it may be legal to
dispose of some HHW in their regular trash, the waste hauler that collects the trash can choose not to haul the
waste. It is not uncommon for a waste hauler to refuse to pick up municipal solid waste that contains things like
paint and fluorescent light bulbs. There is often little recourse for residents in this case. In these cases the
resident may have to make their own arrangements to dispose of the waste by taking it directly to a landfill or
solid waste transfer station.
[edit] Final disposal of hazardous waste
Hazardous wastes undergo different treatments in order to stabilize and dispose of them.
[edit] Recycling
Many HWs can be recycled into new products. Examples might include lead-acid batteries or electronic circuit
boards where the heavy metals can be recovered and used in new products.Another example is the ash generated
by coal-fired power plants; these plants produced two types of these residues: fly and bottom ash. Fly ash
particles have a low density, are very fine, and are removed by air pollution control devices. On the other side,
bottom ash is a dense, dark, gravely substance that remains on the bottom of combustion chambers.[5] After these
types of ashes go though the proper treatment, they could bind to other pollutants and convert them into easier-
to- dispose solids, or they could be used as pavement filling. Such treatments reduce the level of threat of
harmful chemicals, like fly and bottom ash, while also recycling the safe product and helping the environment.
[edit] Portland cement
Another commonly used treatment is cement based solidification and stabilization. Cement is used because it
can treat a range of hazardous wastes by improving physical characteristics and decreasing the toxicity and
transmission of contaminants. The cement produced is categorized into 5 different divisions, depending on its
strength and components. This process of converting sludge into cement might include the addition of pH
adjustment agents, phosphates, or sulfur reagents to reduce the settling or curing time, increase the compressive
strength, or reduce the leach ability of contaminants.
[edit] Neutralization
Some HW can be processed so that the hazardous component of the waste is eliminated. making it a non-
hazardous waste. An example of this might include a corrosive acid that is neutralized with a basic substance so
that it is no-longer corrosive. (see acid-base reactions.)Another mean to neutralize some of the waste is pH
adjustment. pH is an important factor on the leaching activity of the hazardous waste. By adjusting the pH of
some toxic materials, we are reducing the leaching ability of the waste.
[edit] Incineration, destruction and waste-to-energy
A HW may be "destroyed" for example by incinerating it at a high temperature. Flammable wastes can
sometimes be burned as energy sources. For example many cement kilns burn HWs like used oils or solvents.
Today incineration treatments not only reduce the amount of hazardous waste. They also generate energy
throughout the gases released in the process. It is known that this particular waste treatment releases toxic gases
produced by the combustion of byproduct or other materials and this can affect the environment. However,
current technology has developed more efficient incinerator units that control these emissions to a point that this
treatment is considered a more beneficial option. There are different types of incinerators and they vary
depending on the characteristics of the waste. Starved air incineration is another method used to treat hazardous
wastes. Just like in common incineration, burning occurs, however controlling the amount of oxygen allowed
proves to be significant to reduce the amount of harmful bi products produced. Starved Air Incineration is an
improvement of the traditional incinerators in terms of air pollution. Using this technology it is possible to
control the combustion rate of the waste and therefore reduce the air pollutants produce in the process.
[edit] Hazardous waste landfill (sequestering, isolation, etc.)
A HW may be sequestered in a HW landfill or permanent disposal facility. "In terms of hazardous waste, a
landfill is defined as a disposal facility or part of a facility where hazardous waste is placed or on land and
which is not a pile, a land treatment facility, a surface impoundment, an underground injection well, a salt dome
formation, a salt bed formation, an underground mine, a cave, or a corrective action management unit (40 CFR
260.10)."[6][7]
[edit] Pyrolysis
Some hazardous waste types may be eliminated using pyrolisis in an ultra high temperature electrical arc, in
inert conditions to avoid combustion. This treatment method may be preferable to high temperature incineration
in some circumstances such as in the destruction of concentrated organic waste types, including PCBs,
pesticides and other persistent organic pollutants. [8] [9]
[edit] See also
• Bamako Convention
• Gade v. National Solid Wastes Management Association
• Household Hazardous Waste
• List of solid waste treatment technologies
• List of Superfund sites in the United States
• List of topics dealing with environmental issues
• List of waste management companies
• List of waste management topics
• List of waste types
• Mixed waste (radioactive/hazardous)
• National Priorities List (in the US)
• Pollution
• Radioactive waste
• Recycling
• Remediation
• Retail hazardous waste
• Superfund
• Toxic waste
• Triad (environmental science)
• Vapor intrusion
[edit] References
1. ^ Chaudhary R., Rachana M., 2006. Factors affecting hazardous waste solidification/stabilization: A
Review. In: Journal of Hazardous Materials B137 pp.267–276
2. ^ Orloff, Kenneth, and Henry Falk. 2003. An international perspective on hazardous waste practices.
International Journal of Hygiene and Environmental Health 206 (4-5):291- 302.
3. ^ Orloff, Kenneth, and Henry Falk. 2003. An international perspective on hazardous waste practices.
International Journal of Hygiene and Environmental Health 206 (4-5):291- 302.
4. ^ USEPA Household Hazardous Wastes
5. ^ Munson-McGee S.H., Parsa, J., Steiner, R., 1996. Stabilization/solidification of hazardous wastes
using fly ash. In: Journal of Environmental Engineering, 122 (10), pp. 935-940.
6. ^ Hazardous Waste Landfills
7. ^ Land Disposal Units
8. ^ [1]
9. ^ [2]
[edit] External links
• Environmental Hazardous Waste Cleanup Company Environmental Cleanup Services
• Agency for Toxic Substances and Disease Registry
• The EPA's hazardous waste page
• The U.S. EPA's Hazardous Waste Cleanup Information System
 • What Did We Know About Hazardous Waste and When Did We Know It, a February 2002 essay by
William Sanjour
Retrieved from "http://en.wikipedia.org/wiki/Hazardous_waste"
Categories: Waste
Carcinogen
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Jump to: navigation, search
Look up carcinogen in Wiktionary, the free dictionary.

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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 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.

Contents
[hide]
• 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
• 7 Procarcinogen
• 8 Common carcinogens
○ 8.1 Occupational carcinogens
○ 8.2 Others
• 9 See also
• 10 Notes
• 11 External links

[edit] Radiation
This article includes a list of references, related reading or external links, but its sources remain
unclear because it lacks inline citations. Please improve this article by introducing more precise
citations where appropriate. (November 2008)
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 from consuming the irradiated food.
[edit] Carcinogens in prepared food
See also: Cooking#Potential harmful health effects 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).[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.
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]
[edit] Carcinogens in cigarettes
Main article: Tobacco and health
Tobacco smoke contains over 4000 chemical compounds, many of which are carcinogenic or otherwise toxic.[12]
[edit] 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).[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]
[edit] 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 (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]
[edit] Classification of carcinogens
[edit] International Agency for Research on Cancer Approximate equivalences
The International Agency for Research on Cancer (IARC) is between classification schemes
an intergovernmental agency established in 1965, which IARC GHS NTP ACGIH EU
forms part of the World Health Organization of the United Group 1 Cat. 1A Known A1 Cat. 1
Nations. It is based in Lyon, France. Since 1971 it has Group 2A Reasonably
published a series of Monographs on the Evaluation of Cat. 1B A2 Cat. 2
suspected
Carcinogenic Risks to Humans that have been highly
[20] Group 2B
influential in the classification of possible carcinogens. Cat. 2 A3 Cat. 3
• Group 1: the agent (mixture) is definitely Group 3
A4
carcinogenic to humans. The exposure circumstance
entails exposures that are carcinogenic to humans. Group 4 A5

• 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.
[edit] 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
[edit] 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.[21] As of March 2009, the latest edition was the 11th report (2005).[1]
It classifies carcinogens into two groups:
• Known to be a human carcinogen
• Reasonably anticipated to be a human carcinogen
[edit] 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
[edit] 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.
[edit] 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]
[edit] Common carcinogens
[edit] 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
• Smelting byproduct
• Component of:
• Alloys
• Lung
• Electrical and semiconductor devices
Arsenic and its compounds • Skin
• Medications (e.g. melarsoprol)
• Hemangiosarcoma
• Herbicides
• Fungicides
• Animal dips

Not in use, but still found in:

• Constructions
• Lungs
• Roofing papers
Asbestos • Mesothelioma
• Floor tiles
• Gastrointestinal tract
• Fire-resistant textiles
• Friction linings

• Light fuel oil

• Former use as solvent and fumigant
• Printing
• Lithography
• Leukemia • Paint
Benzene
• Hodgkin lymphoma • Rubber
• Dry cleaning
• Adhesives
• Coatings
• Detergents

• Missile fuel
Beryllium and its • Lightweight alloys
• Lung
compounds • Aerospace applications
• Nuclear reactors

• Yellow pigments
• Phosphors
Cadmium and its
• Prostate • Solders
compounds
• Batteries
• Metal paintings and coatings
 • Paints
Hexavalent chromium(VI)
• Lung • Pigments
compounds
• Preservatives

• Ripening agent for fruits and nuts

• Rocket propellant
Ethylene oxide • Leukemia
• Fumigant for foodstuffs and textiles
• Sterilant for hospital equipment

• Nickel plating
• Ferrous alloys
• Nose
Nickel • Ceramics
• Lung
• Batteries
• Stainless-steel welding byproduct

• Uranium decay
Radon and its decay
• Lung • Quarries and mines
products
• Cellars and poorly ventilated places

• Refrigerant
• Hemangiosarcoma • Vinyl polymers
Vinyl chloride
• Liver • Adhesive for plastics
• Former use in pressurized containers
Shiftwork that involves
• Breast
circadian disruption[13]
Involuntary smoking
• Lung • Tobacco smoke
(Passive smoking)[23]
Unless else specified in boxes, then ref is: [24]
[edit] Others
• Gasoline (contains aromatics)
• Lead and its compounds
• Alkylating antineoplastic agents (chemotherapy)
• Ultraviolet radiation from the sun and UV lamps
[edit] See also
• Industrial Union Department v. American Petroleum Institute
• International Agency for Research on Cancer
• Mutagen
• Possible carcinogen
• Teratogen
• Warburg hypothesis
[edit] Notes
1. ^ a b Report on Carcinogens, Eleventh Edition; U.S. Department of Health and Human Services, Public
Health Service, National Toxicology Program (2005).
2. ^ 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.
3. ^ 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.
4. ^ Cohen M, Lippman M, Chabner B. Role of pineal gland in aetiology and treatment of breast cancer.
Lancet 1978;2:14–16.
5. ^ The Independent Avoid breast cancer. Sleep in the dark...
6. ^ 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
7. ^ 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.
8. ^ National Cancer Institute, 2004 analysis and recommendations
9. ^ "Acrylamide". http://www.food.gov.uk/safereating/chemsafe/acrylamide_branch/.
10. ^ Thomas M., II Campbell; Campbell, Thomas M.; Colin T., PH D. Campbell (2005). The China
study: the most comprehensive study of nutrition ever conducted and the startling implications for diet,
weight loss and long-term health. Benbella Books. ISBN 1-932100-38-5.
11. ^ Parodi PW (2007). "A role for milk proteins and their peptides in cancer prevention". Current
Pharmaceutical Design 13 (8): 813–28. doi:10.2174/138161207780363059. PMID 17430183.
http://www.bentham-direct.org/pages/content.php?CPD/2007/00000013/00000008/0005B.SGM.
12. ^ http://quitsmoking.about.com/cs/nicotineinhaler/g/carbonmonoxide.htm
13. ^ a b IARC Monographs Programme finds cancer hazards associated with shiftwork, painting and
firefighting, International Agency for Research on Cancer,
http://monographs.iarc.fr/ENG/Meetings/vol98-pressrelease.pdf, retrieved 2009-01-24
14. ^ 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.
15. ^ Hansen J. Increased breast cancer risk among women who work predominantly at night.
Epidemiology 2001; 12:74–77.
16. ^ Hansen J. Light at night, shiftwork, and breast cancer risk.J Natl Cancer Inst 2001; 93:1513–1515.
17. ^ 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.
18. ^ 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
19. ^ "The Gale Encyclopedia of Cancer: A guide to Cancer and its Treatments, Second Edition. Page no.
137".
20. ^ IARC Monographs
21. ^ Section 301(b)(4) of the Public Health Service Act, as amended by Section 262, Pub. L. 95–622.
22. ^ Web definitions for Procarcinogen
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.
[edit] External links
• 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
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Mutation
From Wikipedia, the free encyclopedia
(Redirected from Genetic mutation)
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For other uses, see Mutation (disambiguation).

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A mutation has caused this garden moss rose to produce flowers of different colors. This is a somatic mutation
that may also be passed on in the germ line.
Mutations are changes in the DNA sequence of a cell's genome and are caused by radiation, viruses,
transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.[1][2][3] They
can also be induced by the organism itself, by cellular processes such as hypermutation.
Mutation can result in several different types of change in DNA sequences; these can either have no effect, alter
the product of a gene, or prevent the gene from functioning. Studies in the fly Drosophila melanogaster suggest
that if a mutation changes a protein produced by a gene, this will probably be harmful, with about 70 percent of
these mutations having damaging effects, and the remainder being either neutral or weakly beneficial.[4] Due to
the damaging effects that mutations can have on cells, organisms have evolved mechanisms such as DNA repair
to remove mutations.[1] Therefore, the optimal mutation rate for a species is a trade-off between costs of a high
mutation rate, such as deleterious mutations, and the metabolic costs of maintaining systems to reduce the
mutation rate, such as DNA repair enzymes.[5] Viruses that use RNA as their genetic material have rapid
mutation rates,[6] which can be an advantage since these viruses will evolve constantly and rapidly, and thus
evade the defensive responses of e.g. the human immune system.[7]
Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.[8]
These duplications are a major source of raw material for evolving new genes, with tens to hundreds of genes
duplicated in animal genomes every million years.[9] Most genes belong to larger families of genes of shared
ancestry.[10] Novel genes are produced by several methods, commonly through the duplication and mutation of
an ancestral gene, or by recombining parts of different genes to form new combinations with new functions.[11]
[12]
Here, domains act as modules, each with a particular and independent function, that can be mixed together to
produce genes encoding new proteins with novel properties.[13] For example, the human eye uses four genes to
make structures that sense light: three for color vision and one for night vision; all four arose from a single
ancestral gene.[14] Another advantage of duplicating a gene (or even an entire genome) is that this increases
redundancy; this allows one gene in the pair to acquire a new function while the other copy performs the
original function.[15][16] Other types of mutation occasionally create new genes from previously noncoding DNA.
[17][18]

Changes in chromosome number may involve even larger mutations, where segments of the DNA within
chromosomes break and then rearrange. For example, two chromosomes in the Homo genus fused to produce
human chromosome 2; this fusion did not occur in the lineage of the other apes, and they retain these separate
chromosomes.[19] In evolution, the most important role of such chromosomal rearrangements may be to
accelerate the divergence of a population into new species by making populations less likely to interbreed, and
thereby preserving genetic differences between these populations.[20]
Sequences of DNA that can move about the genome, such as transposons, make up a major fraction of the
genetic material of plants and animals, and may have been important in the evolution of genomes.[21] For
example, more than a million copies of the Alu sequence are present in the human genome, and these sequences
have now been recruited to perform functions such as regulating gene expression.[22] Another effect of these
mobile DNA sequences is that when they move within a genome, they can mutate or delete existing genes and
thereby produce genetic diversity.[2]
In multicellular organisms with dedicated reproductive cells, mutations can be subdivided into germ line
mutations, which can be passed on to descendants through their reproductive cells, and somatic mutations,
which involve cells outside the dedicated reproductive group and which are not usually transmitted to
descendants. If the organism can reproduce asexually through mechanisms such as cuttings or budding the
distinction can become blurred.
For example, plants can sometimes transmit somatic mutations to their descendants asexually or sexually where
flower buds develop in somatically mutated parts of plants. A new mutation that was not inherited from either
parent is called a de novo mutation. The source of the mutation is unrelated to the consequence[clarification needed],
although the consequences are related to which cells were mutated.
Nonlethal mutations accumulate within the gene pool and increase the amount of genetic variation[23]. The
abundance of some genetic changes within the gene pool can be reduced by natural selection, while other "more
favorable" mutations may accumulate and result in adaptive evolutionary changes.
For example, a butterfly may produce offspring with new mutations. The majority of these mutations will have
no effect; but one might change the color of one of the butterfly's offspring, making it harder (or easier) for
predators to see. If this color change is advantageous, the chance of this butterfly surviving and producing its
own offspring are a little better, and over time the number of butterflies with this mutation may form a larger
percentage of the population.
Neutral mutations are defined as mutations whose effects do not influence the fitness of an individual. These can
accumulate over time due to genetic drift. It is believed that the overwhelming majority of mutations have no
significant effect on an organism's fitness. Also, DNA repair mechanisms are able to mend most changes before
they become permanent mutations, and many organisms have mechanisms for eliminating otherwise
permanently mutated somatic cells.
Mutation is generally accepted by biologists as the mechanism by which natural selection acts, generating
advantageous new traits that survive and multiply in offspring as well as disadvantageous traits, in less fit
offspring, that tend to die out.

Contents
[hide]
• 1 Classification of mutation types
○ 1.1 By effect on structure
○ 1.2 By effect on function
○ 1.3 By effect on fitness
○ 1.4 By inheritance
 1.4.1 By pattern of inheritance
 ○ 1.5 By impact on protein sequence
○ 1.6 Special classes
○ 1.7 Causes of mutation
○ 1.8 Nomenclature
• 2 Harmful mutations
• 3 Beneficial mutations
• 4 Prion mutation
• 5 See also
• 6 References
• 7 External links

[edit] Classification of mutation types

Illustrations of five types of chromosomal mutations.

Selection of disease-causing mutations, in a standard table of the genetic code of amino acids.[24]
[edit] By effect on structure
The sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health
depending on where they occur and whether they alter the function of essential proteins. Mutations in the
structure of genes can be classified as:
• Small-scale mutations, such as those affecting a small gene in one or a few nucleotides, including:
○ Point mutations, often caused by chemicals or malfunction of DNA replication, exchange a
single nucleotide for another[25]. These changes are classified as transitions or transversions[26].
Most common is the transition that exchanges a purine for a purine (A ↔ G) or a pyrimidine
for a pyrimidine, (C ↔ T). A transition can be caused by nitrous acid, base mis-pairing, or
mutagenic base analogs such as 5-bromo-2-deoxyuridine (BrdU). Less common is a
transversion, which exchanges a purine for a pyrimidine or a pyrimidine for a purine (C/T ↔
A/G). An example of a transversion is adenine (A) being converted into a cytosine (C). A
point mutation can be reversed by another point mutation, in which the nucleotide is changed
back to its original state (true reversion) or by second-site reversion (a complementary
mutation elsewhere that results in regained gene functionality). Point mutations that occur
within the protein coding region of a gene may be classified into three kinds, depending upon
what the erroneous codon codes for:
 Silent mutations: which code for the same amino acid.
 Missense mutations: which code for a different amino acid.
 Nonsense mutations: which code for a stop and can truncate the protein.
○ Insertions add one or more extra nucleotides into the DNA. They are usually caused by
transposable elements, or errors during replication of repeating elements (e.g. AT repeats[citation
needed]
). Insertions in the coding region of a gene may alter splicing of the mRNA (splice site
mutation), or cause a shift in the reading frame (frameshift), both of which can significantly
alter the gene product. Insertions can be reverted by excision of the transposable element.
○ Deletions remove one or more nucleotides from the DNA. Like insertions, these mutations
can alter the reading frame of the gene. They are generally irreversible: though exactly the
same sequence might theoretically be restored by an insertion, transposable elements able to
revert a very short deletion (say 1–2 bases) in any location are either highly unlikely to exist
or do not exist at all. Note that a deletion is not the exact opposite of an insertion: the former is
quite random while the latter consists of a specific sequence inserting at locations that are not
entirely random or even quite narrowly defined.
• Large-scale mutations in chromosomal structure, including:
○ Amplifications (or gene duplications) leading to multiple copies of all chromosomal regions,
increasing the dosage of the genes located within them.
○ Deletions of large chromosomal regions, leading to loss of the genes within those regions.
○ Mutations whose effect is to juxtapose previously separate pieces of DNA, potentially
bringing together separate genes to form functionally distinct fusion genes (e.g. bcr-abl).
These include:
  Chromosomal translocations: interchange of genetic parts from nonhomologous
chromosomes.
 Interstitial deletions: an intra-chromosomal deletion that removes a segment of
DNA from a single chromosome, thereby apposing previously distant genes. For
example, cells isolated from a human astrocytoma, a type of brain tumor, were found
to have a chromosomal deletion removing sequences between the "fused in
glioblastoma" (fig) gene and the receptor tyrosine kinase "ros", producing a fusion
protein (FIG-ROS). The abnormal FIG-ROS fusion protein has constitutively active
kinase activity that causes oncogenic transformation (a transformation from normal
cells to cancer cells).
 Chromosomal inversions: reversing the orientation of a chromosomal segment.
○ Loss of heterozygosity: loss of one allele, either by a deletion or recombination event, in an
organism that previously had two different alleles.
[edit] By effect on function
• Loss-of-function mutations are the result of gene product having less or no function. When the allele
has a complete loss of function (null allele) it is often called an amorphic mutation. Phenotypes
associated with such mutations are most often recessive. Exceptions are when the organism is haploid,
or when the reduced dosage of a normal gene product is not enough for a normal phenotype (this is
called haploinsufficiency).
• Gain-of-function mutations change the gene product such that it gains a new and abnormal function.
These mutations usually have dominant phenotypes. Often called a neomorphic mutation.
• Dominant negative mutations (also called antimorphic mutations) have an altered gene product that
acts antagonistically to the wild-type allele. These mutations usually result in an altered molecular
function (often inactive) and are characterised by a dominant or semi-dominant phenotype. In humans,
Marfan syndrome is an example of a dominant negative mutation occurring in an autosomal dominant
disease. In this condition, the defective glycoprotein product of the fibrillin gene (FBN1) antagonizes
the product of the normal allele.
• Lethal mutations are mutations that lead to the death of the organisms which carry the mutations.
• A back mutation or reversion is a point mutation that restores the original sequence and hence the
original phenotype.[27]
[edit] By effect on fitness
In applied genetics it is usual to speak of mutations as either harmful or beneficial.
• A harmful mutation is a mutation that decreases the fitness of the organism.
• A beneficial mutation is a mutation that increases fitness of the organism, or which promotes traits
that are desirable.
In theoretical population genetics, it is more usual to speak of such mutations as deleterious or advantageous. In
the neutral theory of molecular evolution, genetic drift is the basis for most variation at the molecular level.
• A neutral mutation has no harmful or beneficial effect on the organism. Such mutations occur at a
steady rate, forming the basis for the molecular clock.
• A deleterious mutation has a negative effect on the phenotype, and thus decreases the fitness of the
organism.
• An advantageous mutation has a positive effect on the phenotype, and thus increases the fitness of the
organism.
• A nearly neutral mutation is a mutation that may be slightly deleterious or advantageous, although
most nearly neutral mutations are slightly deleterious.
[edit] By inheritance
• inheritable generic in pro-generic tissue or cells on path to be changed to gametes.
• non inheritable somatic (eg, carcinogenic mutation)
• non inheritable post mortem aDNA mutation in decaying remains.
[edit] By pattern of inheritance
The human genome contains two copies of each gene – a paternal and a maternal allele.
 • A heterozygous mutation is a mutation of only one allele.
• A homozygous mutation is an identical mutation of both the paternal and maternal alleles.
• Compound heterozygous mutations or a genetic compound comprises two different mutations in the
paternal and maternal alleles.[28]
• A wildtype or homozygous non-mutated organism is one in which neither allele is mutated. (Just not
a mutation)
[edit] By impact on protein sequence
• A frameshift mutation is a mutation caused by insertion or deletion of a number of nucleotides that is
not evenly divisible by three from a DNA sequence. Due to the triplet nature of gene expression by
codons, the insertion or deletion can disrupt the reading frame, or the grouping of the codons, resulting
in a completely different translation from the original. The earlier in the sequence the deletion or
insertion occurs, the more altered the protein produced is.
• A nonsense mutation is a point mutation in a sequence of DNA that results in a premature stop codon,
or a nonsense codon in the transcribed mRNA, and possibly a truncated, and often nonfunctional
protein product.
• Missense mutations or nonsynonymous mutations are types of point mutations where a single
nucleotide is changed to cause substitution of a different amino acid. This in turn can render the
resulting protein nonfunctional. Such mutations are responsible for diseases such as Epidermolysis
bullosa, sickle-cell disease, and SOD1 mediated ALS (Boillée 2006, p. 39).
• A neutral mutation is a mutation that occurs in an amino acid codon which results in the use of a
different, but chemically similar, amino acid. The similarity between the two is enough that little or no
change is often rendered in the protein. For example, a change from AAA to AGA will encode lysine, a
chemically similar molecule to the intended arginine.
• Silent mutations are mutations that do not result in a change to the amino acid sequence of a protein.
They may occur in a region that does not code for a protein, or they may occur within a codon in a
manner that does not alter the final amino acid sequence. The phrase silent mutation is often used
interchangeably with the phrase synonymous mutation; however, synonymous mutations are a
subcategory of the former, occurring only within exons. The name silent could be a misnomer. For
example, a silent mutation in the exon/intron border may lead to alternative splicing by changing the
splice site (see Splice site mutation), thereby leading to a changed protein.
[edit] Special classes
• Conditional mutation is a mutation that has wild-type (or less severe) phenotype under certain
"permissive" environmental conditions and a mutant phenotype under certain "restrictive" conditions.
For example, a temperature-sensitive mutation can cause cell death at high temperature (restrictive
condition), but might have no deleterious consequences at a lower temperature (permissive condition).
[edit] Causes of mutation
Two classes of mutations are spontaneous mutations (molecular decay) and induced mutations caused by
mutagens.
Spontaneous mutations on the molecular level can be caused by:
• Tautomerism – A base is changed by the repositioning of a hydrogen atom, altering the hydrogen
bonding pattern of that base resulting in incorrect base pairing during replication.
• Depurination – Loss of a purine base (A or G) to form an apurinic site (AP site).
• Deamination – Hydrolysis changes a normal base to an atypical base containing a keto group in place
of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be
corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be
detected as a mutation because thymine is a normal DNA base.
• Slipped strand mispairing - Denaturation of the new strand from the template during replication,
followed by renaturation in a different spot ("slipping"). This can lead to insertions or deletions.
A covalent adduct between benzo[a]pyrene, the major mutagen in tobacco smoke, and DNA[29]
Induced mutations on the molecular level can be caused by:
• Chemicals
○ Hydroxylamine NH2OH
○ Base analogs (e.g. BrdU)
○ Alkylating agents (e.g. N-ethyl-N-nitrosourea) These agents can mutate both replicating and
non-replicating DNA. In contrast, a base analog can only mutate the DNA when the analog is
incorporated in replicating the DNA. Each of these classes of chemical mutagens has certain
effects that then lead to transitions, transversions, or deletions.
○ Agents that form DNA adducts (e.g. ochratoxin A metabolites)[30]
○ DNA intercalating agents (e.g. ethidium bromide)
○ DNA crosslinkers
○ Oxidative damage
○ Nitrous acid converts amine groups on A and C to diazo groups, altering their hydrogen
bonding patterns which leads to incorrect base pairing during replication.
• Radiation
○ Ultraviolet radiation (nonionizing radiation). Two nucleotide bases in DNA – cytosine and
thymine – are most vulnerable to radiation that can change their properties. UV light can
induce adjacent pyrimidine bases in a DNA strand to become covalently joined as a
pyrimidine dimer. UV radiation, particularly longer-wave UVA, can also cause oxidative
damage to DNA[31].
○ Ionizing radiation
• Viral infections[32]
DNA has so-called hotspots, where mutations occur up to 100 times more frequently than the normal mutation
rate. A hotspot can be at an unusual base, e.g., 5-methylcytosine.
Mutation rates also vary across species. Evolutionary biologists have theorized that higher mutation rates are
beneficial in some situations, because they allow organisms to evolve and therefore adapt more quickly to their
environments. For example, repeated exposure of bacteria to antibiotics, and selection of resistant mutants, can
result in the selection of bacteria that have a much higher mutation rate than the original population (mutator
strains).
[edit] Nomenclature
Nomenclature of mutations specify the type of mutation and base or amino acid changes.
• Nucleotide substitution (e.g. 76A>T) - The number is the position of the nucleotide from the 5' end, the
first letter represents the wild type nucleotide, and the second letter represents the nucleotide which
replaced the wild type. In the given example, the adenine at the 76th position was replaced by a
thymine.
○ If it becomes necessary to differentiate between mutations in genomic DNA, mitochondrial
DNA, and RNA, a simple convention is used. For example, if the 100th base of a nucleotide
sequence mutated from G to C, then it would be written as g.100G>C if the mutation occurred
in genomic DNA, m.100G>C if the mutation occurred in mitochondrial DNA, or r.100g>c if
the mutation occurred in RNA. Note that for mutations in RNA, the nucleotide code is written
in lower case.
• Amino acid substitution (e.g. D111E) – The first letter is the one letter code of the wild type amino
acid, the number is the position of the amino acid from the N terminus, and the second letter is the one
letter code of the amino acid present in the mutation. Nonsense mutations are represented with an X for
the second amino acid (e.g. D111X).
• Amino acid deletion (e.g. ΔF508) – The Greek letter Δ (delta) indicates a deletion. The letter refers to
the amino acid present in the wild type and the number is the position from the N terminus of the
amino acid were it to be present as in the wild type.
[edit] Harmful mutations
Changes in DNA caused by mutation can cause errors in protein sequence, creating partially or completely non-
functional proteins. To function correctly, each cell depends on thousands of proteins to function in the right
places at the right times. When a mutation alters a protein that plays a critical role in the body, a medical
condition can result. A condition caused by mutations in one or more genes is called a genetic disorder. Some
mutations alter a gene's DNA base sequence but do not change the function of the protein made by the gene.
Studies of the fly Drosophila melanogaster suggest that if a mutation does change a protein, this will probably
be harmful, with about 70 percent of these mutations having damaging effects, and the remainder being either
neutral or weakly beneficial.[33] However, studies in yeast have shown that only 7% of mutations that are not in
genes are harmful.[34]
If a mutation is present in a germ cell, it can give rise to offspring that carries the mutation in all of its cells. This
is the case in hereditary diseases. On the other hand, a mutation may occur in a somatic cell of an organism.
Such mutations will be present in all descendants of this cell within the same organism, and certain mutations
can cause the cell to become malignant, and thus cause cancer[35].
Often, gene mutations that could cause a genetic disorder are repaired by the DNA repair system of the cell.
Each cell has a number of pathways through which enzymes recognize and repair mistakes in DNA. Because
DNA can be damaged or mutated in many ways, the process of DNA repair is an important way in which the
body protects itself from disease.
[edit] Beneficial mutations
Although most mutations that change protein sequences are harmful, some mutations have a positive effect on
an organism. In this case, the mutation may enable the mutant organism to withstand particular environmental
stresses better than wild-type organisms, or reproduce more quickly. In these cases a mutation will tend to
become more common in a population through natural selection.
For example, a specific 32 base pair deletion in human CCR5 (CCR5-Δ32) confers HIV resistance to
homozygotes and delays AIDS onset in heterozygotes.[36] The CCR5 mutation is more common in those of
European descent. One possible explanation of the etiology of the relatively high frequency of CCR5-Δ32 in the
European population is that it conferred resistance to the bubonic plague in mid-14th century Europe. People
with this mutation were more likely to survive infection; thus its frequency in the population increased.[37] This
theory could explain why this mutation is not found in Africa, where the bubonic plague never reached. A newer
theory suggests that the selective pressure on the CCR5 Delta 32 mutation was caused by smallpox instead of
the bubonic plague.[38]
[edit] Prion mutation
Prions are proteins and don't contain genetic material, however prion replication has been shown to be subject to
mutation and natural selection just like other forms of replication.[39]
[edit] See also
Genotoxicity
From Wikipedia, the free encyclopedia
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Look up genotoxicity in Wiktionary, the free dictionary.

Genotoxicity describes a deleterious action on a cell's genetic material affecting its integrity. Genotoxic
substances are known to be potentially mutagenic or carcinogenic, specifically those capable of causing genetic
mutation and of contributing to the development of tumors. This includes both certain chemical compounds and
certain types of radiation.
Typical genotoxins like aromatic amines are believed to cause mutations because they are nucleophilic and form
strong covalent bonds with DNA resulting with the formation of Aromatic Amine-DNA Adducts, preventing
accurate replication.
Genotoxins affecting sperm and eggs can pass genetic changes down to descendants who have never been
exposed to the genotoxin.