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Dichlorodiphenyltrichloroethane, commonly known as DDT, is a colorless, tasteless, and almost odorless crystalline chemical compound, an organochlorine, originally developed as an insecticide, and ultimately becoming infamous for its environmental impacts. First synthesized in 1874, DDT's insecticidal action was discovered by the Swiss chemist Paul Hermann Müller
Paul Hermann Müller
in 1939. DDT
DDT
was used in the second half of World War II
World War II
to control malaria and typhus among civilians and troops. Müller was awarded the Nobel Prize in Physiology or Medicine "for his discovery of the high efficiency of DDT
DDT
as a contact poison against several arthropods" in 1948.[5] By October 1945, DDT
DDT
was available for public sale in the United States. Although it was promoted by government and industry for use as an agricultural and household pesticide, there were also concerns about its use from the beginning.[6] Opposition to DDT
DDT
was focused by the 1962 publication of Rachel Carson's book Silent Spring. It cataloged environmental impacts that coincided with widespread use of DDT
DDT
in agriculture in the United States, and it questioned the logic of broadcasting potentially dangerous chemicals into the environment with little prior investigation of their environment and health effects. The book claimed that DDT
DDT
and other pesticides had been shown to cause cancer and that their agricultural use was a threat to wildlife, particularly birds. Its publication was a seminal event for the environmental movement and resulted in a large public outcry that eventually led, in 1972, to a ban on DDT's agricultural use in the United States.[7] A worldwide ban on agricultural use was formalized under the Stockholm Convention on Persistent Organic Pollutants, but its limited and still-controversial use in disease vector control continues,[8][9] because of its effectiveness in reducing malarial infections, balanced by environmental and other health concerns. Along with the passage of the Endangered Species Act, the United States ban on DDT
DDT
is a major factor in the comeback of the bald eagle (the national bird of the United States) and the peregrine falcon from near-extinction in the contiguous United States.[10][11]

Contents

1 Properties and chemistry

1.1 Isomers and related compounds 1.2 Production and use 1.3 Mechanism of insecticide action

2 History

2.1 Use in the 1940s and 1950s 2.2 United States ban 2.3 International usage restrictions

3 Environmental impact

3.1 Eggshell thinning

4 Human health

4.1 Acute toxicity 4.2 Chronic toxicity 4.3 Carcinogenicity

4.3.1 Breast cancer

5 Malaria
Malaria
control

5.1 Initial effectiveness 5.2 Mosquito resistance 5.3 Residents' concerns 5.4 Human exposure 5.5 Criticism of restrictions on DDT
DDT
use 5.6 Alternatives

5.6.1 Insecticides 5.6.2 Non-chemical vector control

6 See also 7 References 8 Further reading 9 External links

Properties and chemistry[edit] DDT
DDT
is similar in structure to the insecticide methoxychlor and the acaricide dicofol. It is highly hydrophobic and nearly insoluble in water but has good solubility in most organic solvents, fats and oils. DDT
DDT
does not occur naturally and is synthesised by a Friedel–Crafts hydroxyalkylation reaction between chloral (CCl 3CHO) and chlorobenzene (C 6H 5Cl), in the presence of an acidic catalyst. DDT
DDT
has been marketed under trade names including Anofex, Cezarex, Chlorophenothane, Clofenotane, Dicophane, Dinocide, Gesarol, Guesapon, Guesarol, Gyron, Ixodex, Neocid, Neocidol and Zerdane.[12] Isomers and related compounds[edit]

o,p' -DDT, a minor component in commercial DDT.

Commercial DDT
DDT
is a mixture of several closely–related compounds. The major component (77%) is the p,p' isomer (pictured above). The o,p' isomer (pictured to the right) is also present in significant amounts (15%). Dichlorodiphenyldichloroethylene
Dichlorodiphenyldichloroethylene
(DDE) and dichlorodiphenyldichloroethane (DDD) make up the balance. DDE and DDD are the major metabolites and environmental breakdown products.[12] Production and use[edit] DDT
DDT
has been formulated in multiple forms, including solutions in xylene or petroleum distillates, emulsifiable concentrates, water-wettable powders, granules, aerosols, smoke candles and charges for vaporizers and lotions.[13] From 1950 to 1980, DDT
DDT
was extensively used in agriculture – more than 40,000 tonnes each year worldwide[14] – and it has been estimated that a total of 1.8 million tonnes have been produced globally since the 1940s.[1] In the United States, it was manufactured by some 15 companies, including Monsanto,[15] Ciba,[16] Montrose Chemical Company, Pennwalt[17] and Velsicol Chemical Corporation.[18] Production peaked in 1963 at 82,000 tonnes per year.[12] More than 600,000 tonnes (1.35 billion pounds) were applied in the US before the 1972 ban. Usage peaked in 1959 at about 36,000 tonnes.[19] In 2009, 3,314 tonnes were produced for malaria control and visceral leishmaniasis. India
India
is the only country still manufacturing DDT
DDT
and is the largest consumer.[20] China ceased production in 2007.[21] Mechanism of insecticide action[edit] In insects DDT
DDT
opens sodium ion channels in neurons, causing them to fire spontaneously, which leads to spasms and eventual death.[22] Insects with certain mutations in their sodium channel gene are resistant to DDT
DDT
and similar insecticides. DDT
DDT
resistance is also conferred by up-regulation of genes expressing cytochrome P450 in some insect species,[23] as greater quantities of some enzymes of this group accelerate the toxin's metabolism into inactive metabolites. (The same enzyme family is up-regulated in mammals too, e.g., in response to ethanol consumption.) Genomic studies in the model genetic organism Drosophila melanogaster
Drosophila melanogaster
revealed that high level DDT resistance is polygenic, involving multiple resistance mechanisms.[24] History[edit]

Commercial product concentrate containing 50% DDT, circa 1960s

Commercial product (Powder box, 50 g) containing 10% DDT; Néocide. Ciba Geigy
Geigy
DDT; "Destroys parasites such as fleas, lice, ants, bedbugs, cockroaches, flies, etc.. Néocide Sprinkle caches of vermin and the places where there are insects and their places of passage. Leave the powder in place as long as possible." "Destroy the parasites of man and his dwelling". "Death is not instantaneous, it follows inevitably sooner or later." "French manufacturing"; "harmless to humans and warm-blooded animals" "sure and lasting effect. Odorless."

External audio

"Episode 207: DDT", Science History Institute

DDT
DDT
was first synthesized in 1874 by Othmar Zeidler under the supervision of Adolf von Baeyer.[25][26] It was further described in 1929 in a dissertation by W. Bausch and in two subsequent publications in 1930.[27][28] The insecticide properties of "multiple chlorinated aliphatic or fat-aromatic alcohols with at least one trichloromethane group" were described in a patent in 1934 by Wolfgang von Leuthold.[29] DDT's insecticidal properties were not, however, discovered until 1939 by the Swiss scientist Paul Hermann Müller, who was awarded the 1948 Nobel Prize in Physiology and Medicine
Nobel Prize in Physiology and Medicine
for his efforts.[5] Use in the 1940s and 1950s[edit]

An airplane spraying DDT
DDT
over Baker County, Oregon
Baker County, Oregon
as part of a spruce budworm control project, 1955

DDT
DDT
spray log in Bosa
Bosa
(Sardinia)

DDT
DDT
is the best-known of several chlorine-containing pesticides used in the 1940s and 1950s. With pyrethrum in short supply, DDT
DDT
was used extensively during World War II
World War II
by the Allies to control the insect vectors of typhus – nearly eliminating the disease in many parts of Europe. In the South Pacific, it was sprayed aerially for malaria and dengue fever control with spectacular effects. While DDT's chemical and insecticidal properties were important factors in these victories, advances in application equipment coupled with competent organization and sufficient manpower were also crucial to the success of these programs.[30] In 1945, DDT
DDT
was made available to farmers as an agricultural insecticide[12] and played a role in the final (for a time) elimination of malaria in Europe
Europe
and North America.[8][31][32] In 1955, the World Health Organization
World Health Organization
commenced a program to eradicate malaria in countries with low to moderate transmission rates worldwide, relying largely on DDT
DDT
for mosquito control and rapid diagnosis and treatment to reduce transmission.[33] The program eliminated the disease in "Taiwan, much of the Caribbean, the Balkans, parts of northern Africa, the northern region of Australia, and a large swath of the South Pacific"[34] and dramatically reduced mortality in Sri Lanka
Sri Lanka
and India.[35] However, failure to sustain the program, increasing mosquito tolerance to DDT, and increasing parasite tolerance led to a resurgence. In many areas early successes partially or completely reversed, and in some cases rates of transmission increased.[36] The program succeeded in eliminating malaria only in areas with "high socio-economic status, well-organized healthcare systems, and relatively less intensive or seasonal malaria transmission".[37] DDT
DDT
was less effective in tropical regions due to the continuous life cycle of mosquitoes and poor infrastructure. It was not applied at all in sub-Saharan Africa due to these perceived difficulties. Mortality rates in that area never declined to the same dramatic extent, and now constitute the bulk of malarial deaths worldwide, especially following the disease's resurgence as a result of resistance to drug treatments and the spread of the deadly malarial variant caused by Plasmodium falciparum. Eradication was abandoned in 1969 and attention instead focused on controlling and treating the disease. Spraying programs (especially using DDT) were curtailed due to concerns over safety and environmental effects, as well as problems in administrative, managerial and financial implementation.[36] Efforts shifted from spraying to the use of bednets impregnated with insecticides and other interventions.[37][38] United States ban[edit] By October 1945, DDT
DDT
was available for public sale in the United States, used both as an agricultural pesticide and as a household insecticide.[6] Although its use was promoted by government and the agricultural industry, US scientists such as FDA pharmacologist Herbert O. Calvery expressed concern over possible hazards associated with DDT
DDT
as early as 1944.[39][19][6] In 1947, Dr. Bradbury Robinson, a physician and nutritionist practicing in St. Louis, Michigan, warned of the dangers of using the pesticide DDT
DDT
in agriculture. DDT
DDT
had been researched and manufactured in St. Louis by the Michigan Chemical Corporation, later purchased by Velsicol Chemical Corporation,[40] and had become an important part of the local economy.[41] Citing research performed by Michigan State University[42] in 1946, Robinson, a past president of the local Conservation Club,[43] opined that:

... perhaps the greatest danger from D.D.T. is that its extensive use in farm areas is most likely to upset the natural balances, not only killing beneficial insects in great number but by bringing about the death of fish, birds, and other forms of wild life either by their feeding on insects killed by D.D.T. or directly by ingesting the poison.[44]

As its production and use increased, public response was mixed. At the same time that DDT
DDT
was hailed as part of the "world of tomorrow," concerns were expressed about its potential to kill harmless and beneficial insects (particularly pollinators), birds, fish, and eventually humans. The issue of toxicity was complicated, partly because DDT's effects varied from species to species, and partly because consecutive exposures could accumulate, causing damage comparable to large doses. A number of states attempted to regulate DDT.[6][12] In the 1950s the federal government began tightening regulations governing its use.[19] These events received little attention. Women like Dorothy Colson and Mamie Ella Plyler of Claxton, Georgia gathered evidence about DDT's effects and wrote to the Georgia Department of Public Health, the National Health Council in New York City, and other organizations.[45] In 1957 the New York Times
New York Times
reported an unsuccessful struggle to restrict DDT
DDT
use in Nassau County, New York, and the issue came to the attention of the popular naturalist-author Rachel Carson. William Shawn, editor of The New Yorker, urged her to write a piece on the subject, which developed into her 1962 book Silent Spring. The book argued that pesticides, including DDT, were poisoning both wildlife and the environment and were endangering human health.[7] Silent Spring was a best seller, and public reaction to it launched the modern environmental movement in the United States. The year after it appeared, President John F. Kennedy
John F. Kennedy
ordered his Science Advisory Committee to investigate Carson's claims. The committee's report "add[ed] up to a fairly thorough-going vindication of Rachel Carson’s Silent Spring
Silent Spring
thesis," in the words of the journal Science,[46] and recommended a phaseout of "persistent toxic pesticides".[47] DDT
DDT
became a prime target of the growing anti-chemical and anti-pesticide movements, and in 1967 a group of scientists and lawyers founded the Environmental Defense
Environmental Defense
Fund (EDF) with the specific goal of enacting a ban on DDT. Victor Yannacone, Charles Wurster, Art Cooley and others in the group had all witnessed bird kills or declines in bird populations and suspected that DDT
DDT
was the cause. In their campaign against the chemical, EDF petitioned the government for a ban and filed lawsuits.[48] Around this time, toxicologist David Peakall was measuring DDE levels in the eggs of peregrine falcons and California condors and finding that increased levels corresponded with thinner shells.[49] In response to an EDF suit, the U.S. District Court of Appeals in 1971 ordered the EPA to begin the de-registration procedure for DDT. After an initial six-month review process, William Ruckelshaus, the Agency's first Administrator rejected an immediate suspension of DDT's registration, citing studies from the EPA's internal staff stating that DDT
DDT
was not an imminent danger.[19] However, these findings were criticized, as they were performed mostly by economic entomologists inherited from the United States Department of Agriculture, who many environmentalists felt were biased towards agribusiness and understated concerns about human health and wildlife. The decision thus created controversy.[30] The EPA held seven months of hearings in 1971–1972, with scientists giving evidence for and against DDT. In the summer of 1972, Ruckelshaus announced the cancellation of most uses of DDT
DDT
– exempting public health uses under some conditions.[19] Immediately after the announcement, both EDF and the DDT
DDT
manufacturers filed suit against EPA. Industry sought to overturn the ban, while EDF wanted a comprehensive ban. The cases were consolidated, and in 1973 the United States Court of Appeals for the District of Columbia Circuit ruled that the EPA had acted properly in banning DDT.[19] Some uses of DDT
DDT
continued under the public health exemption. For example, in June 1979, the California Department of Health Services was permitted to use DDT
DDT
to suppress flea vectors of bubonic plague.[50] DDT
DDT
continued to be produced in the United States for foreign markets until 1985, when over 300 tons were exported.[1] International usage restrictions[edit] In the 1970s and 1980s, agricultural use was banned in most developed countries, beginning with Hungary in 1968[51] followed by Norway
Norway
and Sweden
Sweden
in 1970, West Germany
West Germany
and the US in 1972, but not in the United Kingdom until 1984. By 1991 total bans, including for disease control, were in place in at least 26 countries; for example Cuba in 1970, the US in the 1980s, Singapore in 1984, Chile in 1985 and the Republic of Korea in 1986.[52] The Stockholm Convention on Persistent Organic Pollutants, which took effect in 2004, put a global ban on several persistent organic pollutants, and restricted DDT
DDT
use to vector control. The Convention was ratified by more than 170 countries. Recognizing that total elimination in many malaria-prone countries is currently unfeasible absent affordable/effective alternatives, the convention exempts public health use within World Health Organization
World Health Organization
(WHO) guidelines from the ban.[53] Resolution 60.18 of the World Health Assembly commits WHO to the Stockholm Convention's aim of reducing and ultimately eliminating DDT.[54] Malaria
Malaria
Foundation International states, "The outcome of the treaty is arguably better than the status quo going into the negotiations. For the first time, there is now an insecticide which is restricted to vector control only, meaning that the selection of resistant mosquitoes will be slower than before."[55] Despite the worldwide ban, agricultural use continued in India,[56] North Korea, and possibly elsewhere.[20] As of 2013 an estimated 3,000 to 4,000 tons of DDT
DDT
were produced for disease vector control, including 2786 tons in India.[57] DDT
DDT
is applied to the inside walls of homes to kill or repel mosquitoes. This intervention, called indoor residual spraying (IRS), greatly reduces environmental damage. It also reduces the incidence of DDT
DDT
resistance.[58] For comparison, treating 40 hectares (99 acres) of cotton during a typical U.S. growing season requires the same amount of chemical as roughly 1,700 homes.[59] Environmental impact[edit]

Degradation of DDT
DDT
to form DDE (by elimination of HCl, left) and DDD (by reductive dechlorination, right)

DDT
DDT
is a persistent organic pollutant that is readily adsorbed to soils and sediments, which can act both as sinks and as long-term sources of exposure affecting organisms.[13] Depending on conditions, its soil half-life can range from 22 days to 30 years. Routes of loss and degradation include runoff, volatilization, photolysis and aerobic and anaerobic biodegradation. Due to hydrophobic properties, in aquatic ecosystems DDT
DDT
and its metabolites are absorbed by aquatic organisms and adsorbed on suspended particles, leaving little DDT dissolved in the water. Its breakdown products and metabolites, DDE and DDD, are also persistent and have similar chemical and physical properties.[1] DDT
DDT
and its breakdown products are transported from warmer areas to the Arctic
Arctic
by the phenomenon of global distillation, where they then accumulate in the region's food web.[60] Because of its lipophilic properties, DDT
DDT
can bioaccumulate, especially in predatory birds.[61] DDT
DDT
is toxic to a wide range of living organisms, including marine animals such as crayfish, daphnids, sea shrimp and many species of fish. DDT, DDE and DDD magnify through the food chain, with apex predators such as raptor birds concentrating more chemicals than other animals in the same environment. They are stored mainly in body fat. DDT
DDT
and DDE are resistant to metabolism; in humans, their half-lives are 6 and up to 10 years, respectively. In the United States, these chemicals were detected in almost all human blood samples tested by the Centers for Disease Control
Centers for Disease Control
in 2005, though their levels have sharply declined since most uses were banned.[62] Estimated dietary intake has declined,[62] although FDA food tests commonly detect it.[63] Eggshell thinning[edit] The chemical and its breakdown products DDE and DDD caused eggshell thinning and population declines in multiple North American and European bird of prey species.[1][64][10][65][66][67] DDE-related eggshell thinning is considered a major reason for the decline of the bald eagle,[10] brown pelican,[68] peregrine falcon and osprey.[1] However, birds vary in their sensitivity to these chemicals, with birds of prey, waterfowl and song birds being more susceptible than chickens and related species.[1][13] Even in 2010, California condors that feed on sea lions at Big Sur
Big Sur
that in turn feed in the Palos Verdes Shelf area of the Montrose Chemical Superfund
Superfund
site exhibited continued thin-shell problems,[69][70] though DDT's role in the decline of the California condor
California condor
is disputed.[67][66] The biological thinning mechanism is not entirely understood, but DDE appears to be more potent than DDT,[1] and strong evidence indicates that p,p'-DDE inhibits calcium ATPase in the membrane of the shell gland and reduces the transport of calcium carbonate from blood into the eggshell gland. This results in a dose-dependent thickness reduction.[1][71][72][65] Other evidence indicates that o,p'-DDT disrupts female reproductive tract development, later impairing eggshell quality.[73] Multiple mechanisms may be at work, or different mechanisms may operate in different species.[1] Human health[edit]

A U.S. soldier is demonstrating DDT
DDT
hand-spraying equipment. DDT
DDT
was used to control the spread of typhus-carrying lice.

Spraying hospital beds with DDT, PAIGC
PAIGC
hospital of Ziguinchor, 1973

DDT
DDT
is an endocrine disruptor.[74][75] It is considered likely to be a human carcinogen although the majority of studies suggest it is not directly genotoxic.[76][77][78] DDE acts as a weak androgen receptor antagonist, but not as an estrogen.[79] p,p'-DDT, DDT's main component, has little or no androgenic or estrogenic activity.[80] The minor component o,p'- DDT
DDT
has weak estrogenic activity. Acute toxicity[edit] DDT
DDT
is classified as "moderately toxic" by the US National Toxicology Program (NTP)[81] and "moderately hazardous" by WHO, based on the rat oral LD50 of 113 mg/kg.[82] Indirect exposure is considered relatively non-toxic for humans.[83] Chronic toxicity[edit] Primarily through the tendency for DDT
DDT
to buildup in areas of the body with high lipid content, chronic exposure can affect reproductive capabilities and the embryo or fetus.[83]

A review article in The Lancet
The Lancet
states, "research has shown that exposure to DDT
DDT
at amounts that would be needed in malaria control might cause preterm birth and early weaning ... toxicological evidence shows endocrine-disrupting properties; human data also indicate possible disruption in semen quality, menstruation, gestational length, and duration of lactation."[38] Other studies document decreases in semen quality among men with high exposures (generally from IRS).[84] Studies are inconsistent on whether high blood DDT
DDT
or DDE levels increase time to pregnancy.[62] In mothers with high DDE blood serum levels, daughters may have up to a 32% increase in the probability of conceiving, but increased DDT
DDT
levels have been associated with a 16% decrease in one study.[85] Indirect exposure of mothers through workers directly in contact with DDT
DDT
is associated with an increase in spontaneous abortions[83] Other studies found that DDT
DDT
or DDE interfere with proper thyroid function in pregnancy and childhood.[62][86]

Carcinogenicity[edit] In 2015, the International Agency for Research on Cancer
Cancer
classifies DDT
DDT
as Group 2A "probably carcinogenic to humans".[87] Previous assessments by the U.S. National Toxicology Program
National Toxicology Program
classified it as "reasonably anticipated to be a carcinogen" and by the EPA classified DDT, DDE and DDD as class B2 "probable" carcinogens; these evaluations were based mainly on animal studies.[1][38] A 2005 Lancet review stated that occupational DDT
DDT
exposure was associated with increased pancreatic cancer risk in 2 case control studies, but another study showed no DDE dose-effect association. Results regarding a possible association with liver cancer and biliary tract cancer are conflicting: workers who did not have direct occupational DDT
DDT
contact showed increased risk. White men had an increased risk, but not white women or black men. Results about an association with multiple myeloma, prostate and testicular cancer, endometrial cancer and colorectal cancer have been inconclusive or generally do not support an association.[38] A 2017 review of liver cancer studies concluded that "organochlorine pesticides, including DDT, may increase hepatocellular carcinoma risk."[88] A 2009 review, whose co-authors included persons engaged in DDT-related litigation, reached broadly similar conclusions, with an equivocal association with testicular cancer. Case–control studies did not support an association with leukemia or lymphoma.[62] Breast cancer[edit] The question of whether DDT
DDT
or DDE are risk factors in breast cancer has not been conclusively answered. Several meta analyses of observational studies have concluded that there is no overall relationship between DDT
DDT
exposure and breast cancer risk.[89][90] The United States Institute of Medicine reviewed data on the association of breast cancer with DDT
DDT
exposure in 2012 and concluded that a causative relationship could neither be proven nor disproven.[91] A 2007 case control study[80] using archived blood samples found that breast cancer risk was increased 5-fold among women who were born prior to 1931 and who had high serum DDT
DDT
levels in 1963. Reasoning that DDT
DDT
use became widespread in 1945 and peaked around 1950, they concluded that the ages of 14–20 were a critical period in which DDT exposure leads to increased risk. This study, which suggests a connection between DDT
DDT
exposure and breast cancer that would not be picked up by most studies, has received variable commentary in third party reviews. One review suggested that "previous studies that measured exposure in older women may have missed the critical period."[62][92] The National Toxicology Program
National Toxicology Program
notes that while the majority of studies have not found a relationship between DDT
DDT
exposure and breast cancer that positive associations have been seen in a "few studies among women with higher levels of exposure and among certain subgroups of women"[77] A 2015 case control study identified a link (odds ratio 3.4) between in-utero exposure (as estimated from archived maternal blood samples) and breast cancer diagnosis in daughters. The findings "support classification of DDT
DDT
as an endocrine disruptor, a predictor of breast cancer, and a marker of high risk".[93] Malaria
Malaria
control[edit] Malaria
Malaria
remains the primary public health challenge in many countries. In 2015, there were 214 million cases of malaria worldwide resulting in an estimated 438,000 deaths, 90% of which occurred in Africa.[94] DDT
DDT
is one of many tools to fight the disease. Its use in this context has been called everything from a "miracle weapon [that is] like Kryptonite
Kryptonite
to the mosquitoes,"[95] to "toxic colonialism".[96] Before DDT, eliminating mosquito breeding grounds by drainage or poisoning with Paris green
Paris green
or pyrethrum was sometimes successful. In parts of the world with rising living standards, the elimination of malaria was often a collateral benefit of the introduction of window screens and improved sanitation.[34] A variety of usually simultaneous interventions represents best practice. These include antimalarial drugs to prevent or treat infection; improvements in public health infrastructure to diagnose, sequester and treat infected individuals; bednets and other methods intended to keep mosquitoes from biting humans; and vector control strategies[97] such as larvaciding with insecticides, ecological controls such as draining mosquito breeding grounds or introducing fish to eat larvae and indoor residual spraying (IRS) with insecticides, possibly including DDT. IRS involves the treatment of interior walls and ceilings with insecticides. It is particularly effective against mosquitoes, since many species rest on an indoor wall before or after feeding. DDT
DDT
is one of 12 WHO–approved IRS insecticides.[37] WHO's anti-malaria campaign of the 1950s and 1960s relied heavily on DDT
DDT
and the results were promising, though temporary in developing countries. Experts tie malarial resurgence to multiple factors, including poor leadership, management and funding of malaria control programs; poverty; civil unrest; and increased irrigation. The evolution of resistance to first-generation drugs (e.g. chloroquine) and to insecticides exacerbated the situation.[20][98] Resistance was largely fueled by unrestricted agricultural use. Resistance and the harm both to humans and the environment led many governments to curtail DDT
DDT
use in vector control and agriculture.[36] In 2006 WHO reversed a longstanding policy against DDT
DDT
by recommending that it be used as an indoor pesticide in regions where malaria is a major problem.[99] Once the mainstay of anti-malaria campaigns, as of 2008 only 12 countries used DDT, including India
India
and some southern African states,[97] though the number was expected to rise.[20] Initial effectiveness[edit] When it was introduced in World War II, DDT
DDT
was effective in reducing malaria morbidity and mortality.[30] WHO's anti-malaria campaign, which consisted mostly of spraying DDT
DDT
and rapid treatment and diagnosis to break the transmission cycle, was initially successful as well. For example, in Sri Lanka, the program reduced cases from about one million per year before spraying to just 18 in 1963[100][101] and 29 in 1964. Thereafter the program was halted to save money and malaria rebounded to 600,000 cases in 1968 and the first quarter of 1969. The country resumed DDT
DDT
vector control but the mosquitoes had evolved resistance in the interim, presumably because of continued agricultural use. The program switched to malathion, but despite initial successes, malaria continued its resurgence into the 1980s.[35][102] DDT
DDT
remains on WHO's list of insecticides recommended for IRS. After the appointment of Arata Kochi as head of its anti-malaria division, WHO's policy shifted from recommending IRS only in areas of seasonal or episodic transmission of malaria, to advocating it in areas of continuous, intense transmission.[103] WHO reaffirmed its commitment to phasing out DDT, aiming "to achieve a 30% cut in the application of DDT
DDT
world-wide by 2014 and its total phase-out by the early 2020s if not sooner" while simultaneously combating malaria. WHO plans to implement alternatives to DDT
DDT
to achieve this goal.[104] South Africa
South Africa
continues to use DDT
DDT
under WHO guidelines. In 1996, the country switched to alternative insecticides and malaria incidence increased dramatically. Returning to DDT
DDT
and introducing new drugs brought malaria back under control.[105] Malaria
Malaria
cases increased in South America
South America
after countries in that continent stopped using DDT. Research data showed a strong negative relationship between DDT residual house sprayings and malaria. In a research from 1993 to 1995, Ecuador increased its use of DDT
DDT
and achieved a 61% reduction in malaria rates, while each of the other countries that gradually decreased its DDT
DDT
use had large increases.[59][106][107] Mosquito resistance[edit] In some areas resistance reduced DDT's effectiveness. WHO guidelines require that absence of resistance must be confirmed before using the chemical.[108] Resistance is largely due to agricultural use, in much greater quantities than required for disease prevention. Resistance was noted early in spray campaigns. Paul Russell, former head of the Allied Anti- Malaria
Malaria
campaign, observed in 1956 that "resistance has appeared after six or seven years."[34] Resistance has been detected in Sri Lanka, Pakistan, Turkey
Turkey
and Central America
Central America
and it has largely been replaced by organophosphate or carbamate insecticides, e.g. malathion or bendiocarb.[109] In many parts of India, DDT
DDT
is ineffective.[110] Agricultural uses were banned in 1989 and its anti-malarial use has been declining. Urban use ended.[111] One study concluded that " DDT
DDT
is still a viable insecticide in indoor residual spraying owing to its effectivity in well supervised spray operation and high excito-repellency factor."[112] Studies of malaria-vector mosquitoes in KwaZulu-Natal Province, South Africa found susceptibility to 4% DDT
DDT
(WHO's susceptibility standard), in 63% of the samples, compared to the average of 87% in the same species caught in the open. The authors concluded that "Finding DDT resistance in the vector An. arabiensis, close to the area where we previously reported pyrethroid-resistance in the vector An. funestus Giles, indicates an urgent need to develop a strategy of insecticide resistance management for the malaria control programmes of southern Africa."[113] DDT
DDT
can still be effective against resistant mosquitoes[114] and the avoidance of DDT-sprayed walls by mosquitoes is an additional benefit of the chemical.[112] For example, a 2007 study reported that resistant mosquitoes avoided treated huts. The researchers argued that DDT
DDT
was the best pesticide for use in IRS (even though it did not afford the most protection from mosquitoes out of the three test chemicals) because the others pesticides worked primarily by killing or irritating mosquitoes – encouraging the development of resistance.[114] Others argue that the avoidance behavior slows eradication.[115] Unlike other insecticides such as pyrethroids, DDT requires long exposure to accumulate a lethal dose; however its irritant property shortens contact periods. "For these reasons, when comparisons have been made, better malaria control has generally been achieved with pyrethroids than with DDT."[109] In India
India
outdoor sleeping and night duties are common, implying that "the excito-repellent effect of DDT, often reported useful in other countries, actually promotes outdoor transmission."[116] Residents' concerns[edit] Main article: Indoor residual spraying
Indoor residual spraying
§ Residents' opposition to IRS IRS is effective if at least 80% of homes and barns in a residential area are sprayed.[108] Lower coverage rates can jeopardize program effectiveness. Many residents resist DDT
DDT
spraying, objecting to the lingering smell, stains on walls, and the potential exacerbation of problems with other insect pests.[109][115][117] Pyrethroid insecticides (e.g. deltamethrin and lambda-cyhalothrin) can overcome some of these issues, increasing participation.[109] Human exposure[edit] A 1994 study found that South Africans living in sprayed homes have levels that are several orders of magnitude greater than others.[62] Breast milk
Breast milk
from South African mothers contains high levels of DDT
DDT
and DDE.[62] It is unclear to what extent these levels arise from home spraying vs food residues. Evidence indicates that these levels are associated with infant neurological abnormalities.[109] Most studies of DDT's human health effects have been conducted in developed countries where DDT
DDT
is not used and exposure is relatively low.[38][62][118] Illegal diversion to agriculture is also a concern as it is difficult to prevent and its subsequent use on crops is uncontrolled. For example, DDT
DDT
use is widespread in Indian agriculture,[119] particularly mango production[120] and is reportedly used by librarians to protect books.[121] Other examples include Ethiopia, where DDT
DDT
intended for malaria control is reportedly used in coffee production,[122] and Ghana where it is used for fishing."[123][124] The residues in crops at levels unacceptable for export have been an important factor in bans in several tropical countries.[109] Adding to this problem is a lack of skilled personnel and management.[115] Criticism of restrictions on DDT
DDT
use[edit] A few people and groups have argued that limitations on DDT
DDT
use for public health purposes have caused unnecessary morbidity and mortality from vector-borne diseases, with some claims of malaria deaths ranging as high as the hundreds of thousands[125] and millions.[126] Robert Gwadz of the US National Institutes of Health
National Institutes of Health
said in 2007, "The ban on DDT
DDT
may have killed 20 million children."[127] These arguments were rejected as "outrageous" by former WHO scientist Socrates Litsios.[95] May Berenbaum, University of Illinois
University of Illinois
entomologist, says, "to blame environmentalists who oppose DDT
DDT
for more deaths than Hitler is worse than irresponsible."[95]

The question that ... malaria control experts must ask is not “Which is worse, malaria or DDT?” but rather “What are the best tools to deploy for malaria control in a given situation, taking into account the on-the-ground challenges and needs, efficacy, cost, and collateral effects—both positive and negative—to human health and the environment, as well as the uncertainties associated with all these considerations?”

Hans Herren & Charles Mbogo[128]

Criticisms of a DDT
DDT
"ban" often specifically reference the 1972 United States ban (with the erroneous implication that this constituted a worldwide ban and prohibited use of DDT
DDT
in vector control). Reference is often made to Silent Spring, even though Carson never pushed for a DDT
DDT
ban. John Quiggin
John Quiggin
and Tim Lambert wrote, "the most striking feature of the claim against Carson is the ease with which it can be refuted."[129] Investigative journalist Adam Sarvana and others characterize these notions as "myths" promoted principally by Roger Bate
Roger Bate
of the pro-DDT advocacy group Africa Fighting Malaria
Malaria
(AFM).[130][131] Alternatives[edit] Insecticides[edit] Main article: Indoor residual spraying Organophosphate
Organophosphate
and carbamate insecticides, e.g. malathion and bendiocarb, respectively, are more expensive than DDT
DDT
per kilogram and are applied at roughly the same dosage. Pyrethroids such as deltamethrin are also more expensive than DDT, but are applied more sparingly (0.02–0.3 g/m2 vs 1–2 g/m2), so the net cost per house is about the same.[37] Non-chemical vector control[edit] Before DDT, malaria was successfully eliminated or curtailed in several tropical areas by removing or poisoning mosquito breeding grounds and larva habitats, for example by eliminating standing water. These methods have seen little application in Africa for more than half a century.[132] According to CDC, such methods are not practical in Africa because "Anopheles gambiae, one of the primary vectors of malaria in Africa, breeds in numerous small pools of water that form due to rainfall ... It is difficult, if not impossible, to predict when and where the breeding sites will form, and to find and treat them before the adults emerge."[133] The relative effectiveness of IRS versus other malaria control techniques (e.g. bednets or prompt access to anti-malarial drugs) varies and is dependent on local conditions.[37] A WHO study released in January 2008 found that mass distribution of insecticide-treated mosquito nets and artemisinin–based drugs cut malaria deaths in half in malaria-burdened Rwanda and Ethiopia. IRS with DDT
DDT
did not play an important role in mortality reduction in these countries.[134][135] Vietnam
Vietnam
has enjoyed declining malaria cases and a 97% mortality reduction after switching in 1991 from a poorly funded DDT-based campaign to a program based on prompt treatment, bednets and pyrethroid group insecticides.[136] In Mexico, effective and affordable chemical and non-chemical strategies were so successful that the Mexican DDT
DDT
manufacturing plant ceased production due to lack of demand.[137] A review of fourteen studies in sub-Saharan Africa, covering insecticide-treated nets, residual spraying, chemoprophylaxis for children, chemoprophylaxis or intermittent treatment for pregnant women, a hypothetical vaccine and changing front–line drug treatment, found decision making limited by the lack of information on the costs and effects of many interventions, the small number of cost-effectiveness analyses, the lack of evidence on the costs and effects of packages of measures and the problems in generalizing or comparing studies that relate to specific settings and use different methodologies and outcome measures. The two cost-effectiveness estimates of DDT
DDT
residual spraying examined were not found to provide an accurate estimate of the cost-effectiveness of DDT
DDT
spraying; the resulting estimates may not be good predictors of cost-effectiveness in current programs.[138] However, a study in Thailand found the cost per malaria case prevented of DDT
DDT
spraying (US$1.87) to be 21% greater than the cost per case prevented of lambda-cyhalothrin–treated nets (US$1.54),[139] casting some doubt on the assumption that DDT
DDT
was the most cost-effective measure. The director of Mexico's malaria control program found similar results, declaring that it was 25% cheaper for Mexico to spray a house with synthetic pyrethroids than with DDT.[137] However, another study in South Africa
South Africa
found generally lower costs for DDT spraying than for impregnated nets.[140] A more comprehensive approach to measuring cost-effectiveness or efficacy of malarial control would not only measure the cost in dollars, as well as the number of people saved, but would also consider ecological damage and negative human health impacts. One preliminary study found that it is likely that the detriment to human health approaches or exceeds the beneficial reductions in malarial cases, except perhaps in epidemics. It is similar to the earlier study regarding estimated theoretical infant mortality caused by DDT
DDT
and subject to the criticism also mentioned earlier.[141] A study in the Solomon Islands
Solomon Islands
found that "although impregnated bed nets cannot entirely replace DDT
DDT
spraying without substantial increase in incidence, their use permits reduced DDT
DDT
spraying."[142] A comparison of four successful programs against malaria in Brazil, India, Eritrea and Vietnam
Vietnam
does not endorse any single strategy but instead states, "Common success factors included conducive country conditions, a targeted technical approach using a package of effective tools, data-driven decision-making, active leadership at all levels of government, involvement of communities, decentralized implementation and control of finances, skilled technical and managerial capacity at national and sub-national levels, hands-on technical and programmatic support from partner agencies, and sufficient and flexible financing."[143] DDT
DDT
resistant mosquitoes have generally proved susceptible to pyrethroids. Thus far, pyrethroid resistance in Anopheles has not been a major problem.[109] See also[edit]

DDT
DDT
in Australia DDT
DDT
in New Zealand DDT
DDT
in the United States Mickey Slim, an alleged cocktail that combined gin with a pinch of DDT. Operation Cat Drop Biomagnification

References[edit]

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spraying on malaria transmission in Bareilly District, Uttar Pradesh, India". Journal of Vector Borne Diseases. 42 (2): 54–60. PMID 16161701.  ^ Hargreaves K, Hunt RH, Brooke BD, Mthembu J, Weeto MM, Awolola TS, Coetzee M (December 2003). "Anopheles arabiensis and An. quadriannulatus resistance to DDT
DDT
in South Africa". Medical and Veterinary Entomology. 17 (4): 417–22. doi:10.1111/j.1365-2915.2003.00460.x. PMID 14651656.  ^ a b Grieco JP, Achee NL, Chareonviriyaphap T, Suwonkerd W, Chauhan K, Sardelis MR, Roberts DR (2007). Krishna S, ed. "A new classification system for the actions of IRS chemicals traditionally used for malaria control". PLoS ONE. 2 (8): e716. Bibcode:2007PLoSO...2..716G. doi:10.1371/journal.pone.0000716. PMC 1934935 . PMID 17684562.  ^ a b c Mabaso ML, Sharp B, Lengeler C (August 2004). "Historical review of malarial control in southern African with emphasis on the use of indoor residual house-spraying". Tropical Medicine & International Health. 9 (8): 846–56. doi:10.1111/j.1365-3156.2004.01263.x. PMID 15303988.  ^ Sharma VP (December 2003). "DDT: The fallen angel" (PDF). Current Science. 85 (11): 1532–37. Archived from the original (PDF) on May 18, 2005.  ^ In Malaria
Malaria
War, South Africa
South Africa
Turns To Pesticide
Pesticide
Long Banned in the West Archived October 13, 2007, at the Wayback Machine., Roger Thurow, Wall Street Journal, July 26, 2001 ^ Science Daily (May 9, 2009). "Unprecedented Use Of DDT
DDT
Concerns Experts". ScienceDaily.com. Retrieved May 30, 2009.  ^ Jayashree J (10 June 2009). " Pesticide
Pesticide
level in veggies, fruits rises". Economic Times. Retrieved June 10, 2009.  ^ Sanjana (June 13, 2009). "A Whole Fruit". Tehelka Magazine. 6 (23).  ^ Chakravartty A (8 June 2009). "State public libraries gasp for breath". Indian Express. Retrieved June 8, 2009.  ^ Katima J (June 2009). "African NGOs outline commitment to malaria control without DDT" (PDF). Pesticides News (84): 5. Archived from the original (PDF) on February 24, 2016.  ^ Ghana News Agency (November 17, 2009). "Ministry moves to check unorthodox fishing methods". Ghana News Agency. Archived from the original on November 18, 2010. Retrieved November 18, 2009.  ^ Appiah S (April 27, 2010). "Northern fisherfolks complain of committee's harassment". Joy Online. Archived from the original on April 29, 2010. Retrieved April 27, 2010.  ^ Kristof ND (March 12, 2005). "I Have a Nightmare". New York Times. A-15.  ^ Souder W (September 4, 2012). " Rachel Carson
Rachel Carson
Didn't Kill Millions of Africans". Slate. Retrieved September 5, 2012.  ^ Finkel M (July 2007). "Malaria". National Geographic.  ^ Herren HR, Mbogo C (July 2010). "The role of DDT
DDT
in malaria control". Environmental Health Perspectives. 118 (7): A282–3; author reply A283. doi:10.1289/ehp.1002279. PMC 2920925 . PMID 20601331.  ^ Quiggin J, Lambert T (May 2008). "Rehabilitating Carson". Prospect.  ^ Sarvana A (May 28, 2009). "Bate and Switch: How a free-market magician manipulated two decades of environmental science". Natural Resources New Service. Archived from the original on May 24, 2010. Retrieved June 2, 2009.  ^ Gutstein D (2009). Not a Conspiracy Theory: How Business Propaganda is Hijacking Democracy. ISBN 978-1-55470-191-9. . Relevant excerpt at Gutstein D (January 22, 2010). "Inside the DDT
DDT
Propaganda Machine". The Tyee. Retrieved January 22, 2010.  ^ Killeen GF, Fillinger U, Kiche I, Gouagna LC, Knols BG (October 2002). "Eradication of Anopheles gambiae from Brazil: lessons for malaria control in Africa?". The Lancet. Infectious Diseases. 2 (10): 618–27. doi:10.1016/S1473-3099(02)00397-3. PMID 12383612.  ^ "CDC – Malaria
Malaria
Malaria
Malaria
Worldwide – How Can Malaria
Malaria
Cases and Deaths Be Reduced? – Larval Control and Other Vector Control Interventions".  ^ Impact of long-lasting insecticidal-treated nets (LLINs) and artemisinin-based combination therapies (ACTs) measured using surveillance data in four African countries. Archived February 15, 2008, at the Wayback Machine. World Health Organization, January 31, 2008. ^ Malaria
Malaria
deaths halved in Rwanda and Ethiopia Better drugs, mosquito nets are the crucial tools, David Brown (Washington Post), SF Chronicle, A-12, February 1, 2008. ^ World Health Organization, "A story to be shared: The successful fight against malaria in Vietnam," November 6, 2000. Archived February 26, 2008, at the Wayback Machine. ^ a b " DDT
DDT
& Malaria" (PDF). Archived from the original (PDF) on May 21, 2010. Retrieved March 11, 2009.  ^ Goodman CA, Mills AJ (December 1999). "The evidence base on the cost-effectiveness of malaria control measures in Africa" (PDF). Health Policy and Planning. 14 (4): 301–12. doi:10.1093/heapol/14.4.301. PMID 10787646.  ^ Kamolratanakul P, Butraporn P, Prasittisuk M, Prasittisuk C, Indaratna K (October 2001). "Cost-effectiveness and sustainability of lambdacyhalothrin-treated mosquito nets in comparison to DDT
DDT
spraying for malaria control in western Thailand". The American Journal of Tropical Medicine and Hygiene. 65 (4): 279–84. PMID 11693869.  ^ Goodman CA, Mnzava AE, Dlamini SS, Sharp BL, Mthembu DJ, Gumede JK (April 2001). "Comparison of the cost and cost-effectiveness of insecticide-treated bednets and residual house-spraying in KwaZulu-Natal, South Africa". Tropical Medicine & International Health. 6 (4): 280–95. doi:10.1046/j.1365-3156.2001.00700.x. PMID 11348519.  ^ Corin S, Weaver S (2005). "A risk analysis model with an ecological perspective on DDT
DDT
and malaria control in South Africa" (PDF). Journal of Rural and Tropical Public Health. 4 (4): 21–32.  ^ Over M, Bakote'e B, Velayudhan R, Wilikai P, Graves PM (August 2004). "Impregnated nets or DDT
DDT
residual spraying? Field effectiveness of malaria prevention techniques in solomon islands, 1993–1999". The American Journal of Tropical Medicine and Hygiene. 71 (2 Suppl): 214–23. PMID 15331840.  ^ Barat LM (January 2006). "Four malaria success stories: how malaria burden was successfully reduced in Brazil, Eritrea, India, and Vietnam". The American Journal of Tropical Medicine and Hygiene. 74 (1): 12–16. PMID 16407339. 

Further reading[edit]

David Kinkela. DDT
DDT
and the American Century: Global Health, Environmental Politics, and the Pesticide
Pesticide
That Changed the World (University of North Carolina Press, 2011).

External links[edit]

Wikimedia Commons has media related to DDT.

Chemistry

DDT
DDT
at The Periodic Table of Videos
The Periodic Table of Videos
(University of Nottingham)

Toxicity

" DDT
DDT
Technical Fact Sheet" (PDF). National Pesticide
Pesticide
Information Center.  " DDT
DDT
General Fact Sheet" (PDF). National Pesticide
Pesticide
Information Center.  "DDT". Pesticide
Pesticide
Information Profiles. EXTOXNET.  Scorecard: The Pollution
Pollution
Information Site – DDT Interview with Barbara Cohn, PhD about DDT
DDT
and breast cancer Pesticide
Pesticide
residues in food 2000 : DDT "DDT". NIOSH Pocket Guide to Chemical Hazards. CDC. 

Politics and DDT

Bailey R (7 January 2004). "DDT, Eggshells, and Me". Reason magazine.  Swartz, Aaron (September–October 2007). "Rachel Carson, Mass Murderer?: The creation of an anti-environmental myth". Extra!. 

Malaria
Malaria
and DDT

Berenbaum M (4 June 2005). "If Malaria's the Problem, DDT's Not the Only Answer". Washington Post.  'Andrew Spielman, Harvard School of Public Health, discusses environmentally friendly control of Malaria
Malaria
and uses of DDT
DDT
Freeview video provided by the Vega Science Trust "Ugandan farmers push for DDT
DDT
ban". ABC News. Australian Broadcasting Commission. 31 May 2008. 

DDT
DDT
in Popular Culture

Examples of DDT
DDT
advertising in the United States.

v t e

Pest control: Insecticides

Carbamates

Aldicarb Bendiocarb Carbaryl Carbofuran Ethienocarb Fenobucarb Oxamyl Methomyl Propoxur

Inorganic compounds

Aluminium phosphide Boric acid Chromated copper arsenate Copper(II) arsenate Copper(I) cyanide Diatomaceous earth Lead hydrogen arsenate Paris Green Scheele's Green

Insect growth regulators

Benzoylureas Diflubenzuron Flufenoxuron Hydroprene Lufenuron Methoprene Pyriproxyfen

Neonicotinoids

Acetamiprid Clothianidin Dinotefuran Imidacloprid Nitenpyram Nithiazine Thiacloprid Thiamethoxam

Organochlorides

Aldrin Beta-HCH Carbon tetrachloride Chlordane Cyclodiene 1,2-DCB 1,4-DCB 1,1-DCE 1,2-DCE DDD DDE DDT Dicofol Dieldrin Endosulfan Endrin Heptachlor Kepone Lindane Methoxychlor Mirex Tetradifon Toxaphene

Organophosphorus

Acephate Azamethiphos Azinphos-methyl Bensulide Chlorethoxyfos Chlorfenvinphos Chlorpyrifos Chlorpyrifos-methyl Coumaphos Demeton-S-methyl Diazinon Dicrotophos Diisopropyl fluorophosphate Dimefox Dimethoate Dioxathion Disulfoton Ethion Ethoprop Fenamiphos Fenitrothion Fenthion Fosthiazate Isoxathion Malathion Methamidophos Methidathion Mevinphos Monocrotophos Naled Omethoate Oxydemeton-methyl Parathion Parathion-methyl Phenthoate Phorate Phosalone Phosmet Phoxim Pirimiphos-methyl Quinalphos Temefos Tebupirimfos Terbufos Tetrachlorvinphos Tribufos Trichlorfon

Pyrethroids

Acrinathrin Allethrins Bifenthrin Bioallethrin Cyfluthrin Cyhalothrin Cypermethrin Cyphenothrin Deltamethrin Empenthrin Esfenvalerate Etofenprox Fenpropathrin Fenvalerate Flumethrin Imiprothrin Metofluthrin Permethrin Phenothrin Prallethrin Pyrethrin
Pyrethrin
(I, II; chrysanthemic acid) Pyrethrum Resmethrin Silafluofen Tefluthrin Tetramethrin Tralomethrin Transfluthrin

Ryanoids

Chlorantraniliprole Cyantraniliprole Flubendiamide Ryanodine Ryanodol

Other chemicals

Afoxolaner Amitraz Azadirachtin Buprofezin Chlordimeform Chlorfenapyr Cyromazine Fenazaquin Fenoxycarb Fipronil Fluralaner Hydramethylnon Indoxacarb Limonene Lotilaner Pyridaben Pyriprole Ryanodine Sarolaner Sesamex Spinosad Sulfluramid Tebufenozide Tebufenpyrad Veracevine Xanthone Metaflumizone

Metabolites

Oxon Malaoxon Paraoxon TCPy

Biopesticides

Bacillus thuringiensis Baculovirus Beauveria bassiana Beauveria brongniartii Metarhizium acridum Metarhizium anisopliae Nomuraea rileyi Lecanicillium lecanii Paecilomyces fumosoroseus Paenibacillus popilliae Purpureocillium
Purpureocillium
lilacinum

v t e

Cancer-causing materials and agents (carcinogens)

Cancer Cancer
Cancer
cells

Prominent human carcinogens

Acetaldehyde Arsenic Asbestos Bacteria

Helicobacter Pylori

Benzo[a]pyrene Bisphenol
Bisphenol
A 1,3-Butadiene Diethylstilbestrol Formaldehyde Ionizing radiation
Ionizing radiation
(e.g., from isotopes of plutonium and radium) Tobacco smoke Ultraviolet light Viruses

Epstein–Barr Hepatitis B Hepatitis C Human papillomavirus

IARC lists

Group 1 Group 2A Group 2B Group 3 Caprolactam
Caprolactam
(Group 4)

#WHO-EM ‡Withdrawn from market Clinical trials:

†Phase III §Never to phase III

v t e

Food safety

Adulterants, food contaminants

3-MCPD Aldicarb Cyanide Formaldehyde Lead poisoning Melamine Mercury in fish Sudan I

Flavorings

Monosodium glutamate
Monosodium glutamate
(MSG) Salt Sugar

High-fructose corn syrup

Microorganisms

Botulism Campylobacter jejuni Clostridium perfringens Escherichia coli O104:H4 Escherichia coli O157:H7 Hepatitis A Hepatitis E Listeria Norovirus Rotavirus Salmonella

Parasitic infections through food

Amoebiasis Anisakiasis Cryptosporidiosis Cyclosporiasis Diphyllobothriasis Enterobiasis Fasciolopsiasis Fasciolosis Giardiasis Gnathostomiasis Paragonimiasis Toxoplasmosis Trichinosis Trichuriasis

Pesticides

Chlorpyrifos DDT Lindane Malathion Methamidophos

Preservatives

Benzoic acid Ethylenediaminetetraacetic acid
Ethylenediaminetetraacetic acid
(EDTA) Sodium benzoate

Sugar
Sugar
substitutes

Acesulfame potassium Aspartame Saccharin Sodium cyclamate Sorbitol Sucralose

Toxins, poisons, environment pollution

Aflatoxin Arsenic
Arsenic
contamination of groundwater Benzene in soft drinks Bisphenol
Bisphenol
A Dieldrin Diethylstilbestrol Dioxin Mycotoxins Nonylphenol Shellfish poisoning

Food contamination incidents

Devon colic Swill milk scandal 1858 Bradford sweets poisoning 1900 English beer poisoning Morinaga Milk arsenic poisoning incident Minamata disease 1971 Iraq poison grain disaster Toxic oil syndrome 1993 Jack in the Box E. coli outbreak 1996 Odwalla E. coli outbreak 2006 North American E. coli outbreaks ICA meat repackaging controversy 2008 Canada listeriosis outbreak 2008 Chinese milk scandal 2008 Irish pork crisis 2008 United States salmonellosis outbreak 2011 Germany E. coli outbreak 2011 Taiwan
Taiwan
food scandal 2011 United States listeriosis outbreak 2013 Bihar school meal poisoning 2013 horse meat scandal 2013 Taiwan
Taiwan
food scandal 2014 Taiwan
Taiwan
food scandal 2017 Brazil weak meat scandal 2017–18 South African listeriosis outbreak Food safety
Food safety
incidents in China Foodborne illness

outbreaks death toll United States

Regulation, standards, watchdogs

Acceptable daily intake E number Food labeling regulations Food libel laws International Food Safety Network ISO 22000 Quality Assurance International

Institutions

Centre for Food Safety European Food Safety Authority Institute for Food Safety and Health International Food Safety Network Ministry of Food and Drug Safety

v t e

Androgen receptor
Androgen receptor
modulators

AR

Agonists

Testosterone
Testosterone
derivatives: 4-Androstenediol 4-Dehydroepiandrosterone
4-Dehydroepiandrosterone
(4-DHEA) 4-Hydroxytestosterone 5-Androstenedione 11-Ketotestosterone 11β-Hydroxyandrostenedione Adrenosterone
Adrenosterone
(11-ketoandrostenedione, 11-oxoandrostenedione) Androstenediol (5-androstenediol)

Androstenediol 3β-acetate Androstenediol 17β-acetate Androstenediol diacetate Androstenediol dipropionate

Androstenedione (4-androstenedione) Atamestane Boldenone

Boldenone
Boldenone
undecylenate

Boldione
Boldione
(1,4-androstadienedione) Clostebol

Clostebol
Clostebol
acetate Clostebol
Clostebol
caproate Clostebol
Clostebol
propionate

Cloxotestosterone

Cloxotestosterone
Cloxotestosterone
acetate

Dehydroandrosterone DHEA (androstenolone, prasterone; 5-DHEA)

DHEA enanthate (prasterone enanthate) DHEA sulfate

Exemestane Formestane Plomestane Quinbolone Silandrone Testosterone# (+dutasteride)

Testosterone
Testosterone
esters Polytestosterone phloretin phosphate

Dihydrotestosterone
Dihydrotestosterone
derivatives: 1-Androstenediol 1-Androstenedione 1-Androsterone
1-Androsterone
(1-andro, 1-DHEA) 1-Testosterone 3α-Androstanediol 5α-Androst-2-en-17-one 7β-Hydroxyepiandrosterone 11-Ketodihydrotestosterone Androsterone Bolazine

Bolazine
Bolazine
capronate

Dihydrofluoxymesterone Dihydrotestosterone
Dihydrotestosterone
(DHT) (androstanolone, stanolone)

Dihydrotestosterone
Dihydrotestosterone
esters

Drostanolone

Drostanolone
Drostanolone
propionate

Epiandrosterone Epitiostanol Mepitiostane Mesabolone Mesterolone

Mesterolone
Mesterolone
cipionate

Methyldiazinol Nisterime

Nisterime
Nisterime
acetate

Prostanozol Stenbolone

Stenbolone
Stenbolone
acetate

Testifenon
Testifenon
(testiphenon, testiphenone)

19-Nortestosterone derivatives: 7α-Methyl-19-norandrostenedione
7α-Methyl-19-norandrostenedione
(MENT dione, trestione) 11β-Methyl-19-nortestosterone

11β-Methyl-19-nortestosterone
11β-Methyl-19-nortestosterone
dodecylcarbonate

19-Nor-5-androstenediol 19-Nor-5-androstenedione 19-Nordehydroepiandrosterone Bolandiol

Bolandiol
Bolandiol
dipropionate

Bolandione
Bolandione
(19-nor-4-androstenedione) Bolmantalate
Bolmantalate
(nandrolone adamantoate) Dienedione Dienolone Dimethandrolone

Dimethandrolone
Dimethandrolone
buciclate Dimethandrolone
Dimethandrolone
dodecylcarbonate Dimethandrolone
Dimethandrolone
undecanoate

LS-1727
LS-1727
(nandrolone 17β-N-(2-chloroethyl)-N-nitrosocarbamate) Methoxydienone
Methoxydienone
(methoxygonadiene) Nandrolone

Nandrolone
Nandrolone
esters

Norclostebol

Norclostebol
Norclostebol
acetate

Normethandrone
Normethandrone
(methylestrenolone, normethisterone) Oxabolone

Oxabolone
Oxabolone
cipionate (oxabolone cypionate)

Trenbolone

Trenbolone
Trenbolone
acetate Trenbolone
Trenbolone
enanthate Trenbolone
Trenbolone
hexahydrobenzylcarbonate Trenbolone
Trenbolone
undecanoate

Trendione Trestolone
Trestolone
(MENT)

Trestolone
Trestolone
acetate

Dihydrotestosterone
Dihydrotestosterone
and 19-nortestosterone derivatives: 5α-Dihydrolevonorgestrel 5α-Dihydronandrolone 5α-Dihydronorethandrolone 5α-Dihydronorethisterone 5α-Dihydronormethandrone 19-Norandrosterone

17α-Alkylated testosterone derivatives: Bolasterone Calusterone Chlorodehydromethylandrostenediol
Chlorodehydromethylandrostenediol
(CDMA) Chlorodehydromethyltestosterone
Chlorodehydromethyltestosterone
(CDMT) Chloromethylandrostenediol
Chloromethylandrostenediol
(CMA) Enestebol Ethyltestosterone Fluoxymesterone Formebolone Hydroxystenozole Metandienone
Metandienone
(methandrostenolone) Methandriol
Methandriol
(methylandrostenediol)

Methandriol
Methandriol
bisenanthoyl acetate Methandriol
Methandriol
diacetate Methandriol
Methandriol
dipropionate Methandriol
Methandriol
propionate

Methylclostebol
Methylclostebol
(chloromethyltestosterone) Methyltestosterone
Methyltestosterone
(+esterified estrogens)

Methyltestosterone
Methyltestosterone
3-hexyl ether

Oxymesterone Penmesterol Tiomesterone

17α-Alkylated dihydrotestosterone derivatives: Androisoxazole Desoxymethyltestosterone Furazabol Mebolazine
Mebolazine
(dimethazine) Mestanolone Metenolone

Metenolone
Metenolone
acetate Metenolone
Metenolone
enanthate

Methasterone Methyl-1-testosterone Methylepitiostanol Methylstenbolone Oxandrolone Oxymetholone Stanozolol

17α-Alkylated 19-nortestosterone derivatives: Bolenol Dimethyldienolone Dimethyltrienolone Ethyldienolone Ethylestrenol Methyldienolone Methylhydroxynandrolone
Methylhydroxynandrolone
(MOHN, MHN) Metribolone Mibolerone Norboletone Norethandrolone Propetandrol RU-2309 Tetrahydrogestrinone

17α- Vinyltestosterone
Vinyltestosterone
derivatives: Norvinisterone (vinylnortestosterone) Vinyltestosterone

17α-Ethynyltestosterone derivatives: Δ4-Tibolone Danazol Desogestrel Ethisterone
Ethisterone
(ethynyltestosterone) Etonogestrel Etynodiol Etynodiol
Etynodiol
diacetate Gestodene Gestrinone Levonorgestrel Levonorgestrel
Levonorgestrel
butanoate Lynestrenol Norethisterone

Norethisterone
Norethisterone
acetate Norethisterone
Norethisterone
acetate oxime Norethisterone
Norethisterone
enanthate

Norgestrel Norgestrienone Quingestanol Quingestanol
Quingestanol
acetate Tibolone

Progesterone derivatives: Medroxyprogesterone acetate Megestrol acetate

Others/unsorted: 3-Keto-5α-abiraterone 5α-Androstane Alternariol Cl-4AS-1 Drupanol ZM-182345

Mixed (SARMs)

Nonsteroidal: 198RL26 ACP-105 AC-262536 Acetothiolutamide Andarine
Andarine
(acetamidoxolutamide, androxolutamide, GTx-007, S-4) BMS-564929 DTIB Enobosarm
Enobosarm
(ostarine, MK-2866, GTx-024, S-22) FTBU-1 GSK-4336A GSK-8698 LG-121071
LG-121071
(LGD-121071) LGD-2226 LGD-2941 (LGD-122941) LGD-3303 LGD-4033 JNJ-26146900 JNJ-28330835 JNJ-37654032 ORM-11984 R-1 RAD140 RU-59063 S-1 S-23 S-40503 S-101479 Triclosan

Steroidal: MK-0773 TFM-4AS-1 YK-11

Antagonists

Steroidal: 7α-Thioprogesterone 7α-Thiospironolactone 7α-Thiomethylspironolactone 9,11-Dehydrocortexolone 17α-butyrate
9,11-Dehydrocortexolone 17α-butyrate
(CB-03-04) 11α-Hydroxyprogesterone 15β-Hydroxycyproterone acetate Abiraterone Abiraterone
Abiraterone
acetate Allyltestosterone Benorterone BOMT Canrenoic acid Canrenone Chlormadinone acetate Clometerone Cortexolone 17α-propionate
Cortexolone 17α-propionate
(CB-03-01) Cyproterone Cyproterone
Cyproterone
acetate Delanterone Delmadinone acetate Dicirenone Dienogest Drospirenone Edogestrone Epitestosterone Galeterone Guggulsterone Medrogestone Megestrol acetate Mespirenone Metogest Mexrenone Mifepristone Nomegestrol acetate Nordinone Osaterone Osaterone
Osaterone
acetate Oxendolone Potassium canrenoate Promegestone Prorenone Rosterolone SC-5233
SC-5233
(spirolactone) Spironolactone Spirorenone Spiroxasone Topterone Trimegestone Trimethyltrienolone
Trimethyltrienolone
(R-2956) Zanoterone

Nonsteroidal: 5N-Bicalutamide AA560 Antarlides Arabilin Apalutamide Atraric acid AZD-3514 Bakuchiol BAY-1024767 Bicalutamide Bisphenols (e.g., BADGE, BFDGE, bisphenol A, bisphenol F, bisphenol S) BMS-641988 Cimetidine Cioteronel Darolutamide DDT
DDT
(via metabolite p,p’-DDE) Dieldrin DIMP Endosulfan Enzalutamide EPI-001 Fenarimol Flutamide Hydroxyflutamide Inocoterone Inocoterone
Inocoterone
acetate Ketoconazole Lavender oil LG-105 LG-120907 Linuron Methiocarb N-Butylbenzenesulfonamide N-Desmethylapalutamide N-Desmethylenzalutamide Nilutamide ONC1-13B ORM-15341 Pentomone PF-998425 Phenothrin Prochloraz Procymidone Proxalutamide Ralaniten
Ralaniten
(EPI-002) Ralaniten
Ralaniten
acetate (EPI-506) RD-162 Ro 2-7239 Ro 5-2537 RU-22930 RU-56187 RU-57073 RU-58642 RU-58841 Seviteronel Thalidomide Topilutamide
Topilutamide
(fluridil) Valproic acid Vinclozolin YM-580 YM-92088 YM-175735

GPRC6A

Agonists

Cations (incl. aluminum, calcium, gadolinium, magnesium, strontium, zinc) Dehydroandrosterone Dihydrotestosterone Estradiol L-α-Amino acids (incl. L-arginine, L-lysine, L-ornithine) Osteocalcin SHBG Testosterone

See also Receptor/signaling modulators Androgens and antiandrogens Estrogen
Estrogen
receptor modulators Progesterone receptor modulators List of androgens/anabolic steroids

Authority control

LCCN: sh85035995 GND: 4148933-0 N

.