Dichlorodiphenyltrichloroethane
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DDT
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Names
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1,1'-(2,2,2-Trichloroethane-1,1-diyl)bis(4-chlorobenzene)
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Identifiers
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3D model (JSmol)
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PubChem CID
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Properties
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C14H9Cl5
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354.48 g·mol−1
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0.99 g/cm3
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108.5 °C
(227.3 °F; 381.6 K)
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260 °C
(500 °F; 533 K) (decomposes)
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Hazards
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Toxic, dangerous to
the environment, likely carcinogenic
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Danger
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H301, H351, H372, H410
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P201, P202, P260, P264, P270, P273, P281, P301+310, P308+313, P314, P321, P330, P391, P405
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Lethal dose or
concentration (LD, LC):
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PEL(Permissible)
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TWA 1 mg/m3 [skin]
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REL(Recommended)
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Ca TWA 0.5 mg/m3
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IDLH (Immediate danger)
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500 mg/m3
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Except where otherwise
noted, data are given for materials in their standard state (at 25 °C [77 °F],
100 kPa).
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Dichlorodiphenyltrichloroethane (DDT) is a colorless, tasteless, and almost
odorless crystalline organochlorine known for its insecticidal properties and
environmental impacts. First synthesized in 1874, DDT's insecticidal action was
discovered by the Swiss chemist Paul Hermann Müller in 1939. DDT was used in the second half of 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 as a contact poison against
several arthropods"
in 1948.[5]
By
October 1945, 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 was focused by the 1962 publication
of Rachel Carson's book Silent Spring. It cataloged
environmental impacts that coincided with widespread use of 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 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 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
[hide]
DDT is similar in structure to the insecticide methoxychlor and the acaricidedicofol. It is highly hydrophobic and nearly insoluble in water but has good solubility in most organic solvents, fats and oils. 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 has been marketed under trade names including Anofex, Cezarex, Chlorophenothane, Clofenotane, Dicophane, Dinocide, Gesarol, Guesapon, Guesarol, Gyron, Ixodex, Neocid, Neocidol and Zerdane.[12]
3CHO) and chlorobenzene (C
6H
5Cl), in the presence of an acidic catalyst. DDT has been marketed under trade names including Anofex, Cezarex, Chlorophenothane, Clofenotane, Dicophane, Dinocide, Gesarol, Guesapon, Guesarol, Gyron, Ixodex, Neocid, Neocidol and Zerdane.[12]
o,p' -DDT, a minor component in commercial DDT.
Commercial
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 (DDE)
and dichlorodiphenyldichloroethane (DDD)
make up the balance. DDE and DDD are the major metabolites and
environmental breakdown products.[12]
DDT
has been formulated in multiple forms, including solutions in xylene or petroleumdistillates, emulsifiable concentrates, water-wettable powders, granules, aerosols, smoke candles and charges for
vaporizers and lotions.[13]
From
1950 to 1980, 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 is the only country still manufacturing DDT and is the
largest consumer.[20] China ceased production in 2007.[21]
In
insects it 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 and similar insecticides. 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 revealed that
high level DDT resistance is polygenic, involving multiple resistance
mechanisms.[24]
Commercial product concentrate containing 50%
DDT, circa 1960s
Commercial product (Powder box, 50 g)
containing 10% DDT; Néocide. Ciba 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."
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External audio
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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 Medicinefor his efforts.[5]
An airplane spraying DDT over Baker County, Oregon as part of a spruce budworm control project, 1955
DDT
is the best-known of several chlorine-containing pesticides
used in the 1940s and 1950s. With pyrethrum in short supply,
DDT was used extensively during World War IIby 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 was made available to farmers as an agricultural insecticide[12] and played a role in the final elimination of malaria in
Europe and North America.[8][31][32]
In
1955, the World Health Organization commenced a program to eradicate malaria in countries with
low to moderate transmission rates worldwide, relying largely on 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 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
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.[citation needed]
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 bednetsimpregnated with insecticides and other
interventions.[37][38]
By
October 1945, 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 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 in
agriculture. 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 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 reported an unsuccessful struggle to restrict 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 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 thesis," in the words of the journal Science,[46] and recommended a phaseout of "persistent toxic
pesticides".[47]
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
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 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 condorsand finding that
increased levels corresponded with thinner shells.[citation needed]
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 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 – exempting public health uses under some
conditions.[19]Immediately after the announcement, both EDF and the 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 continued under the public health exemption. For example, in June
1979, the California Department of Health Services was permitted to use DDT to
suppress flea vectors of bubonic plague.[49] DDT continued to be produced in the United States for
foreign markets until 1985, when over 300 tons were exported.[1]
In
the 1970s and 1980s, agricultural use was banned in most developed countries,
beginning with Hungary in 1968[50] followed by Norway and Sweden in 1970, 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.[51]
The Stockholm Convention on Persistent Organic Pollutants, which took effect in 2004, put a global ban on several persistent organic
pollutants, and restricted 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 (WHO) guidelines
from the ban.[52]Resolution 60.18 of the World Health Assembly commits WHO to the Stockholm Convention's aim of reducing
and ultimately eliminating DDT.[53] 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."[54]
Despite
the worldwide ban, agricultural use continued in India,[55] North Korea, and possibly elsewhere as of 2008.[20] In 2010 about 3,000 to 4,000 tons of DDT were produced for disease vector control.[21][needs update] 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 resistance.[56] 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.[57]
Degradation of DDT to form DDE (by elimination
of HCl, left) and DDD (by reductive dechlorination, right)
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-lifecan 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 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 and its breakdown products are transported from warmer
areas to the Arctic by
the phenomenon of global distillation, where they then accumulate in the region's food web.[58]
Because
of its lipophilic properties,
DDT can bioaccumulate,
especially in predatory birds.[59] 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 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 in 2005, though their levels have
sharply declined since most uses were banned.[60] Estimated dietary intake has declined,[60] although FDA food tests commonly detect it.[61]
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][62][10][63][64][65] DDE-related eggshell thinning is considered a major reason
for the decline of the bald eagle,[10] brown pelican,[66] 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 that in turn
feed in the Palos Verdes Shelf area of the Montrose
Chemical Superfund site exhibited
continued thin-shell problems,[67][68] though DDT's role in the decline of the California condor is disputed.[65][64]
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][69][70][63] Other evidence indicates that o,p'-DDT disrupts female
reproductive tract development, later impairing eggshell quality.[71] Multiple mechanisms may be at work, or different
mechanisms may operate in different species.[1]
A U.S. soldier is demonstrating DDT
hand-spraying equipment. DDT was used to control the spread of typhus-carrying lice.
DDT
is an endocrine disruptor.[72][73] It is considered likely to be a human carcinogenalthough the majority of studies
suggest it is not directly genotoxic.[74][75][76] DDE acts as a weak androgen receptor antagonist, but not as an estrogen.[77] p,p'-DDT, DDT's main component, has little or no
androgenic or estrogenic activity.[78] The minor component o,p'-DDT has weak estrogenic activity.
DDT
is classified as "moderately toxic" by the US National Toxicology
Program(NTP)[79] and "moderately hazardous" by WHO, based on the
rat oral LD50 of 113 mg/kg.[80] Indirect exposure is considered relatively non-toxic for
humans.[81]
Primarily
through the tendency for DDT to buildup in areas of the body with high lipid
content, chronic exposure can affect reproductive capabilities and the embryo
or fetus.[81]
·
A review article
in The Lancet states, "research has shown that exposure to 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).[82]
·
Studies are
inconsistent on whether high blood DDT or DDE levels increase time to
pregnancy.[60] In mothers with high DDE blood serum levels, daughters may
have up to a 32% increase in the probability of conceiving, but increased DDT
levels have been associated with a 16% decrease in one study.[83]
·
Indirect exposure of
mothers through workers directly in contact with DDT is associated with an
increase in spontaneous abortions[81]
·
Other studies found
that DDT or DDE interfere with proper thyroid function in pregnancy and
childhood.[60][84]
In
2015, the International
Agency for Research on Cancer classifies DDT
as Group 2A "probably carcinogenic to humans".[85] Previous assessments by the U.S. 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 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 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."[86]
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.[60]
The
question of whether 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 exposure and breast cancer risk.[87][88] The United States Institute of Medicine reviewed data on the
association of breast cancer with DDT exposure in 2012 and concluded that a
causative relationship could neither be proven nor disproven.[89]
A
2007 case control study[78] 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 levels in 1963. Reasoning that 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 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."[60][90] The National Toxicology Program notes that while the
majority of studies have not found a relationship between 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"[75]
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 as an endocrine
disruptor, a predictor of breast cancer, and a marker of high risk".[91]
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.[92] 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 to
the mosquitoes,"[93]to "toxic colonialism".[94]
Before
DDT, eliminating mosquito breeding grounds by drainage or poisoning with 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[95] 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 is one of 12
WHO–approved IRS insecticides.[37]
WHO's
anti-malaria campaign of the 1950s and 1960s relied heavily on 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][96] Resistance was largely fueled by unrestricted agricultural
use. Resistance and the harm both to humans and the environment led many
governments to curtail DDT use in vector control and agriculture.[36] In 2006 WHO reversed a longstanding policy against DDT by
recommending that it be used as an indoor pesticide in regions where malaria is
a major problem.[97]
Once
the mainstay of anti-malaria campaigns, as of 2008 only 12 countries used DDT,
including India and some southern African states,[95] though the number was expected to rise.[20]
When
it was introduced in World War II, DDT was effective in reducing malaria morbidity and mortality.[30] WHO's anti-malaria campaign, which consisted mostly of
spraying 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[98][99] 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 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][100]
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.[101] WHO reaffirmed its commitment to phasing out DDT, aiming
"to achieve a 30% cut in the application of 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 to achieve this
goal.[102]
South
Africa continues to use DDT under WHO guidelines. In 1996, the country switched
to alternative insecticides and malaria incidence increased dramatically.
Returning to DDT and introducing new drugs brought malaria back under control.[103] Malaria cases increased in 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 and achieved a 61%
reduction in malaria rates, while each of the other countries that gradually
decreased its DDT use had large increases.[57][104][105]
In
some areas resistance reduced DDT's effectiveness. WHO guidelines require that absence
of resistance must be confirmed before using the chemical.[106] 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 campaign, observed in 1956 that
"resistance has appeared after six or seven years."[34] Resistance has been detected in Sri Lanka, Pakistan, Turkeyand Central America and it has
largely been replaced by organophosphate or carbamate insecticides, e.g. malathion
or bendiocarb.[107]
In
many parts of India, DDT is ineffective.[108] Agricultural uses were banned in 1989 and its
anti-malarial use has been declining. Urban use ended.[109] One study concluded that "DDT is still a viable
insecticide in indoor residual spraying owing to its effectivity in well
supervised spray operation and high excito-repellency factor."[110]
Studies
of malaria-vector mosquitoes in KwaZulu-Natal Province, South Africa found
susceptibility to 4% 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."[111]
DDT
can still be effective against resistant mosquitoes[112] and the avoidance of DDT-sprayed walls by mosquitoes is an
additional benefit of the chemical.[110] For example, a 2007 study reported that resistant
mosquitoes avoided treated huts. The researchers argued that 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.[112] Others argue that the avoidance behavior slows
eradication.[113] 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."[107] In 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."[114]
IRS
is effective if at least 80% of homes and barns in a residential area are
sprayed.[106] Lower coverage rates can jeopardize program effectiveness.
Many residents resist DDT spraying, objecting to the lingering smell, stains on
walls, and the potential exacerbation of problems with other insect pests.[107][113][115] Pyrethroid insecticides
(e.g. deltamethrin and lambda-cyhalothrin) can overcome some of these issues, increasing participation.[107]
A
1994 study found that South Africans living in
sprayed homes have levels that are several orders of magnitude greater than others.[60] Breast milk from
South African mothers contains high levels of DDT and DDE.[60] 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.[107]
Most
studies of DDT's human health effects have been conducted in developed
countries where DDT is not used and exposure is relatively low.[38][60][116]
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 use is widespread
in Indian agriculture,[117] particularly mango production[118] and is reportedly used by librarians to protect books.[119] Other examples include Ethiopia, where DDT intended for
malaria control is reportedly used in coffee production,[120] and Ghana where it is used for fishing."[121][122] The residues in crops at levels unacceptable for export
have been an important factor in bans in several tropical countries.[107] Adding to this problem is a lack of skilled personnel and
management.[113]
A
few people and groups have argued that limitations on 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[123] and millions.[124] Robert Gwadz of the US National Institutes of
Health said in 2007, "The ban on DDT may
have killed 20 million children."[125] These arguments were rejected as "outrageous" by
former WHO scientist Socrates Litsios.[93]May Berenbaum, University of Illinois entomologist, says, "to blame environmentalists who
oppose DDT for more deaths than Hitler is worse than irresponsible."[93]
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?”
Criticisms
of a 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 in vector control). Reference is often made to Silent
Spring, even though Carson never pushed for a DDT ban. John Quiggin and Tim Lambert
wrote, "the most striking feature of the claim against Carson is the ease
with which it can be refuted."[127]
Investigative
journalist Adam Sarvana and others characterize these notions as
"myths" promoted principally by Roger Bate of the pro-DDT
advocacy group Africa Fighting
Malaria (AFM).[128][129]
Organophosphate
and carbamate insecticides, e.g. malathion and bendiocarb, respectively, are more expensive
than 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]
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.[130] 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."[131]
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 did not play an
important role in mortality reduction in these countries.[132][133]
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.[134]
In
Mexico, effective and affordable chemical and non-chemical strategies were so
successful that the Mexican DDT manufacturing plant ceased production due to
lack of demand.[135]
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 residual spraying
examined were not found to provide an accurate estimate of the
cost-effectiveness of DDT spraying; the resulting estimates may not be good
predictors of cost-effectiveness in current programs.[136]
However,
a study in Thailand found the cost per malaria case prevented of DDT spraying (US$1.87) to be 21% greater than the cost per case prevented
of lambda-cyhalothrin–treated nets (US$1.54),[137] casting some doubt on the assumption that 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.[135] However, another study in South Africa found generally
lower costs for DDT spraying than for impregnated nets.[138]
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 and subject to
the criticism also mentioned earlier.[139]
A
study in the Solomon Islands found that "although impregnated bed nets cannot
entirely replace DDT spraying without substantial increase in incidence, their
use permits reduced DDT spraying."[140]
A
comparison of four successful programs against malaria in Brazil, India,
Eritrea and 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."[141]
DDT
resistant mosquitoes have generally proved susceptible to pyrethroids. Thus
far, pyrethroid resistance in Anopheles has not been a major
problem.[107]
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DDT
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Names
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1,1'-(2,2,2-Trichloroethane-1,1-diyl)bis(4-chlorobenzene)
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Identifiers
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3D model (JSmol)
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PubChem CID
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Properties
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C14H9Cl5
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354.48 g·mol−1
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0.99 g/cm3
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108.5 °C
(227.3 °F; 381.6 K)
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260 °C
(500 °F; 533 K) (decomposes)
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Hazards
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Toxic, dangerous to
the environment, likely carcinogenic
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Danger
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H301, H351, H372, H410
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P201, P202, P260, P264, P270, P273, P281, P301+310, P308+313, P314, P321, P330, P391, P405
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Lethal dose or
concentration (LD, LC):
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PEL(Permissible)
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TWA 1 mg/m3 [skin]
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REL(Recommended)
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Ca TWA 0.5 mg/m3
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IDLH (Immediate danger)
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500 mg/m3
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Except where otherwise
noted, data are given for materials in their standard state (at 25 °C [77 °F],
100 kPa).
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Dichlorodiphenyltrichloroethane (DDT) is a colorless, tasteless, and almost
odorless crystalline organochlorine known for its insecticidal properties and
environmental impacts. First synthesized in 1874, DDT's insecticidal action was
discovered by the Swiss chemist Paul Hermann Müller in 1939. DDT was used in the second half of 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 as a contact poison against
several arthropods"
in 1948.[5]
By
October 1945, 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 was focused by the 1962 publication
of Rachel Carson's book Silent Spring. It cataloged
environmental impacts that coincided with widespread use of 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 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 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
[hide]
DDT is similar in structure to the insecticide methoxychlor and the acaricidedicofol. It is highly hydrophobic and nearly insoluble in water but has good solubility in most organic solvents, fats and oils. 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 has been marketed under trade names including Anofex, Cezarex, Chlorophenothane, Clofenotane, Dicophane, Dinocide, Gesarol, Guesapon, Guesarol, Gyron, Ixodex, Neocid, Neocidol and Zerdane.[12]
3CHO) and chlorobenzene (C
6H
5Cl), in the presence of an acidic catalyst. DDT has been marketed under trade names including Anofex, Cezarex, Chlorophenothane, Clofenotane, Dicophane, Dinocide, Gesarol, Guesapon, Guesarol, Gyron, Ixodex, Neocid, Neocidol and Zerdane.[12]
o,p' -DDT, a minor component in commercial DDT.
Commercial
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 (DDE)
and dichlorodiphenyldichloroethane (DDD)
make up the balance. DDE and DDD are the major metabolites and
environmental breakdown products.[12]
DDT
has been formulated in multiple forms, including solutions in xylene or petroleumdistillates, emulsifiable concentrates, water-wettable powders, granules, aerosols, smoke candles and charges for
vaporizers and lotions.[13]
From
1950 to 1980, 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 is the only country still manufacturing DDT and is the
largest consumer.[20] China ceased production in 2007.[21]
In
insects it 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 and similar insecticides. 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 revealed that
high level DDT resistance is polygenic, involving multiple resistance
mechanisms.[24]
Commercial product concentrate containing 50%
DDT, circa 1960s
Commercial product (Powder box, 50 g)
containing 10% DDT; Néocide. Ciba 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."
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External audio
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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 Medicinefor his efforts.[5]
An airplane spraying DDT over Baker County, Oregon as part of a spruce budworm control project, 1955
DDT
is the best-known of several chlorine-containing pesticides
used in the 1940s and 1950s. With pyrethrum in short supply,
DDT was used extensively during World War IIby 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 was made available to farmers as an agricultural insecticide[12] and played a role in the final elimination of malaria in
Europe and North America.[8][31][32]
In
1955, the World Health Organization commenced a program to eradicate malaria in countries with
low to moderate transmission rates worldwide, relying largely on 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 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
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.[citation needed]
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 bednetsimpregnated with insecticides and other
interventions.[37][38]
By
October 1945, 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 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 in
agriculture. 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 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 reported an unsuccessful struggle to restrict 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 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 thesis," in the words of the journal Science,[46] and recommended a phaseout of "persistent toxic
pesticides".[47]
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
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 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 condorsand finding that
increased levels corresponded with thinner shells.[citation needed]
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 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 – exempting public health uses under some
conditions.[19]Immediately after the announcement, both EDF and the 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 continued under the public health exemption. For example, in June
1979, the California Department of Health Services was permitted to use DDT to
suppress flea vectors of bubonic plague.[49] DDT continued to be produced in the United States for
foreign markets until 1985, when over 300 tons were exported.[1]
In
the 1970s and 1980s, agricultural use was banned in most developed countries,
beginning with Hungary in 1968[50] followed by Norway and Sweden in 1970, 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.[51]
The Stockholm Convention on Persistent Organic Pollutants, which took effect in 2004, put a global ban on several persistent organic
pollutants, and restricted 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 (WHO) guidelines
from the ban.[52]Resolution 60.18 of the World Health Assembly commits WHO to the Stockholm Convention's aim of reducing
and ultimately eliminating DDT.[53] 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."[54]
Despite
the worldwide ban, agricultural use continued in India,[55] North Korea, and possibly elsewhere as of 2008.[20] In 2010 about 3,000 to 4,000 tons of DDT were produced for disease vector control.[21][needs update] 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 resistance.[56] 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.[57]
Degradation of DDT to form DDE (by elimination
of HCl, left) and DDD (by reductive dechlorination, right)
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-lifecan 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 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 and its breakdown products are transported from warmer
areas to the Arctic by
the phenomenon of global distillation, where they then accumulate in the region's food web.[58]
Because
of its lipophilic properties,
DDT can bioaccumulate,
especially in predatory birds.[59] 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 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 in 2005, though their levels have
sharply declined since most uses were banned.[60] Estimated dietary intake has declined,[60] although FDA food tests commonly detect it.[61]
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][62][10][63][64][65] DDE-related eggshell thinning is considered a major reason
for the decline of the bald eagle,[10] brown pelican,[66] 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 that in turn
feed in the Palos Verdes Shelf area of the Montrose
Chemical Superfund site exhibited
continued thin-shell problems,[67][68] though DDT's role in the decline of the California condor is disputed.[65][64]
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][69][70][63] Other evidence indicates that o,p'-DDT disrupts female
reproductive tract development, later impairing eggshell quality.[71] Multiple mechanisms may be at work, or different
mechanisms may operate in different species.[1]
DDT
is an endocrine disruptor.[72][73] It is considered likely to be a human carcinogenalthough the majority of studies
suggest it is not directly genotoxic.[74][75][76] DDE acts as a weak androgen receptor antagonist, but not as an estrogen.[77] p,p'-DDT, DDT's main component, has little or no
androgenic or estrogenic activity.[78] The minor component o,p'-DDT has weak estrogenic activity.
DDT
is classified as "moderately toxic" by the US National Toxicology
Program(NTP)[79] and "moderately hazardous" by WHO, based on the
rat oral LD50 of 113 mg/kg.[80] Indirect exposure is considered relatively non-toxic for
humans.[81]
Primarily
through the tendency for DDT to buildup in areas of the body with high lipid
content, chronic exposure can affect reproductive capabilities and the embryo
or fetus.[81]
·
A review article
in The Lancet states, "research has shown that exposure to 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).[82]
·
Studies are
inconsistent on whether high blood DDT or DDE levels increase time to
pregnancy.[60] In mothers with high DDE blood serum levels, daughters may
have up to a 32% increase in the probability of conceiving, but increased DDT
levels have been associated with a 16% decrease in one study.[83]
·
Indirect exposure of
mothers through workers directly in contact with DDT is associated with an
increase in spontaneous abortions[81]
·
Other studies found
that DDT or DDE interfere with proper thyroid function in pregnancy and
childhood.[60][84]
In
2015, the International
Agency for Research on Cancer classifies DDT
as Group 2A "probably carcinogenic to humans".[85] Previous assessments by the U.S. 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 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 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."[86]
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.[60]
The
question of whether 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 exposure and breast cancer risk.[87][88] The United States Institute of Medicine reviewed data on the
association of breast cancer with DDT exposure in 2012 and concluded that a
causative relationship could neither be proven nor disproven.[89]
A
2007 case control study[78] 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 levels in 1963. Reasoning that 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 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."[60][90] The National Toxicology Program notes that while the
majority of studies have not found a relationship between 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"[75]
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 as an endocrine
disruptor, a predictor of breast cancer, and a marker of high risk".[91]
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.[92] 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 to
the mosquitoes,"[93]to "toxic colonialism".[94]
Before
DDT, eliminating mosquito breeding grounds by drainage or poisoning with 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[95] 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 is one of 12
WHO–approved IRS insecticides.[37]
WHO's
anti-malaria campaign of the 1950s and 1960s relied heavily on 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][96] Resistance was largely fueled by unrestricted agricultural
use. Resistance and the harm both to humans and the environment led many
governments to curtail DDT use in vector control and agriculture.[36] In 2006 WHO reversed a longstanding policy against DDT by
recommending that it be used as an indoor pesticide in regions where malaria is
a major problem.[97]
Once
the mainstay of anti-malaria campaigns, as of 2008 only 12 countries used DDT,
including India and some southern African states,[95] though the number was expected to rise.[20]
When
it was introduced in World War II, DDT was effective in reducing malaria morbidity and mortality.[30] WHO's anti-malaria campaign, which consisted mostly of
spraying 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[98][99] 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 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][100]
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.[101] WHO reaffirmed its commitment to phasing out DDT, aiming
"to achieve a 30% cut in the application of 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 to achieve this
goal.[102]
South
Africa continues to use DDT under WHO guidelines. In 1996, the country switched
to alternative insecticides and malaria incidence increased dramatically.
Returning to DDT and introducing new drugs brought malaria back under control.[103] Malaria cases increased in 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 and achieved a 61%
reduction in malaria rates, while each of the other countries that gradually
decreased its DDT use had large increases.[57][104][105]
In
some areas resistance reduced DDT's effectiveness. WHO guidelines require that absence
of resistance must be confirmed before using the chemical.[106] 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 campaign, observed in 1956 that
"resistance has appeared after six or seven years."[34] Resistance has been detected in Sri Lanka, Pakistan, Turkeyand Central America and it has
largely been replaced by organophosphate or carbamate insecticides, e.g. malathion
or bendiocarb.[107]
In
many parts of India, DDT is ineffective.[108] Agricultural uses were banned in 1989 and its
anti-malarial use has been declining. Urban use ended.[109] One study concluded that "DDT is still a viable
insecticide in indoor residual spraying owing to its effectivity in well
supervised spray operation and high excito-repellency factor."[110]
Studies
of malaria-vector mosquitoes in KwaZulu-Natal Province, South Africa found
susceptibility to 4% 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."[111]
DDT
can still be effective against resistant mosquitoes[112] and the avoidance of DDT-sprayed walls by mosquitoes is an
additional benefit of the chemical.[110] For example, a 2007 study reported that resistant
mosquitoes avoided treated huts. The researchers argued that 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.[112] Others argue that the avoidance behavior slows
eradication.[113] 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."[107] In 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."[114]
IRS
is effective if at least 80% of homes and barns in a residential area are
sprayed.[106] Lower coverage rates can jeopardize program effectiveness.
Many residents resist DDT spraying, objecting to the lingering smell, stains on
walls, and the potential exacerbation of problems with other insect pests.[107][113][115] Pyrethroid insecticides
(e.g. deltamethrin and lambda-cyhalothrin) can overcome some of these issues, increasing participation.[107]
A
1994 study found that South Africans living in
sprayed homes have levels that are several orders of magnitude greater than others.[60] Breast milk from
South African mothers contains high levels of DDT and DDE.[60] 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.[107]
Most
studies of DDT's human health effects have been conducted in developed
countries where DDT is not used and exposure is relatively low.[38][60][116]
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 use is widespread
in Indian agriculture,[117] particularly mango production[118] and is reportedly used by librarians to protect books.[119] Other examples include Ethiopia, where DDT intended for
malaria control is reportedly used in coffee production,[120] and Ghana where it is used for fishing."[121][122] The residues in crops at levels unacceptable for export
have been an important factor in bans in several tropical countries.[107] Adding to this problem is a lack of skilled personnel and
management.[113]
A
few people and groups have argued that limitations on 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[123] and millions.[124] Robert Gwadz of the US National Institutes of
Health said in 2007, "The ban on DDT may
have killed 20 million children."[125] These arguments were rejected as "outrageous" by
former WHO scientist Socrates Litsios.[93]May Berenbaum, University of Illinois entomologist, says, "to blame environmentalists who
oppose DDT for more deaths than Hitler is worse than irresponsible."[93]
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?”
Criticisms
of a 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 in vector control). Reference is often made to Silent
Spring, even though Carson never pushed for a DDT ban. John Quiggin and Tim Lambert
wrote, "the most striking feature of the claim against Carson is the ease
with which it can be refuted."[127]
Investigative
journalist Adam Sarvana and others characterize these notions as
"myths" promoted principally by Roger Bate of the pro-DDT
advocacy group Africa Fighting
Malaria (AFM).[128][129]
Organophosphate
and carbamate insecticides, e.g. malathion and bendiocarb, respectively, are more expensive
than 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]
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.[130] 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."[131]
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 did not play an
important role in mortality reduction in these countries.[132][133]
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.[134]
In
Mexico, effective and affordable chemical and non-chemical strategies were so
successful that the Mexican DDT manufacturing plant ceased production due to
lack of demand.[135]
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 residual spraying
examined were not found to provide an accurate estimate of the
cost-effectiveness of DDT spraying; the resulting estimates may not be good
predictors of cost-effectiveness in current programs.[136]
However,
a study in Thailand found the cost per malaria case prevented of DDT spraying (US$1.87) to be 21% greater than the cost per case prevented
of lambda-cyhalothrin–treated nets (US$1.54),[137] casting some doubt on the assumption that 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.[135] However, another study in South Africa found generally
lower costs for DDT spraying than for impregnated nets.[138]
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 and subject to
the criticism also mentioned earlier.[139]
A
study in the Solomon Islands found that "although impregnated bed nets cannot
entirely replace DDT spraying without substantial increase in incidence, their
use permits reduced DDT spraying."[140]
A
comparison of four successful programs against malaria in Brazil, India,
Eritrea and 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."[141]
DDT
resistant mosquitoes have generally proved susceptible to pyrethroids. Thus
far, pyrethroid resistance in Anopheles has not been a major
problem.[107]vvv
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