Dichlorodiphenyltrichloroethane (DDT) is a colorless, tasteless, and nearly odorless solid chemical, known as an organochloride. It was first created in 1874 by the Austrian chemist Othmar Zeidler. Later, in 1939, the Swiss chemist Paul Hermann Müller discovered that DDT could kill insects very effectively. During the second half of World War II, DDT was used to help prevent the spread of diseases like malaria and typhus, which are carried by insects. For this discovery, Müller received the Nobel Prize in Physiology or Medicine in 1948.
In the 1950s and 1960s, the World Health Organization (WHO) used DDT in its efforts to fight malaria. At first, these efforts were successful, but later, malaria returned in some developing countries.
After World War II, the widespread use of DDT raised environmental concerns. These concerns were highlighted in the United States by Rachel Carson’s 1962 book Silent Spring, which increased public awareness and led to a ban on DDT’s use in agriculture in the United States in 1972. Similar restrictions were later adopted worldwide due to evidence of harm to the environment, wildlife, and human health, as well as the development of insect resistance to DDT. These actions helped protect endangered species. In 2004, the Stockholm Convention on Persistent Organic Pollutants banned DDT’s agricultural use globally, though limited use for public health purposes, such as malaria control, is still allowed under WHO guidelines.
Today, DDT is still used in some programs to control mosquitoes that spread malaria because it is effective. However, its use is debated because of concerns about the environment and human health. DDT is one of several tools used to fight malaria, which remains a major health challenge in many countries. WHO guidelines require testing to ensure that mosquitoes are not resistant to DDT before it is used. Much of the resistance seen in mosquitoes is linked to the large amounts of DDT used in agriculture, which is far greater than what is needed for disease control.
Properties and chemistry
DDT has a similar structure to the insecticide methoxychlor and the acaricide dicofol. It does not mix well with water but dissolves easily in most organic solvents, fats, and oils. DDT is not found in nature and is made through a chemical process involving chloral (CCl₃CHO) and two parts of chlorobenzene (C₆H₅Cl), using an acidic catalyst. DDT has been sold under trade names such as Anofex, Cezarex, Chlorophenothane, Dicophane, Dinocide, Gesarol, Guesapon, Guesarol, Gyron, Ixodex, Neocid, Neocidol, and Zerdane. Its official name is clofenotane.
Commercial DDT is a mixture of several related compounds. The chemical process used to make DDT creates different combinations of substitution patterns on the molecule. The main component (77%) is the p,p′-isomer, which is the desired form. The o,p′-isomer is also present in large amounts (15%). Other impurities include dichlorodiphenyldichloroethylene (DDE) and dichlorodiphenyldichloroethane (DDD). DDE and DDD are also major breakdown products and metabolites of DDT. DDT, DDE, and DDD are sometimes grouped together as DDX.
- Components of commercial DDT
- p,p′-DDT (main compound)
- o,p′-DDT (impurity)
- p,p′-DDE (impurity)
- p,p′-DDD (impurity)
DDT has been made in various forms, including solutions in xylene or petroleum distillates, emulsifiable concentrates, water-wettable powders, granules, aerosols, smoke candles, and charges for vaporizers and lotions.
Between 1950 and 1980, DDT was widely used in agriculture, with over 40,000 tonnes produced annually worldwide. It is estimated that 1.8 million tonnes of DDT were made globally since the 1940s. In the United States, about 15 companies, including Monsanto, Ciba, Montrose Chemical Company, Pennwalt, and Velsicol Chemical Corporation, produced DDT. Production reached its highest level in 1963 at 82,000 tonnes per year. More than 600,000 tonnes were used in the U.S. before a 1972 ban. Use peaked in 1959 at about 36,000 tonnes.
China stopped making DDT in 2007, leaving India as the only country still producing it. India is also the largest user of DDT. In 2009, 3,314 tonnes were made for malaria control and visceral leishmaniasis. Recently, only India and seven other African countries continue to use DDT.
In insects, DDT opens channels in nerve cells that control electrical signals, causing them to fire uncontrollably. This leads to muscle spasms and death. Some insects are resistant to DDT due to changes in their sodium channel genes. Resistance can also occur when certain genes increase the production of enzymes that break down DDT into inactive substances. Studies on fruit flies (Drosophila melanogaster) show that high resistance to DDT involves multiple genes and mechanisms. Without genetic changes, insects may avoid DDT by behavior. A specific mutation called M918T makes insects resistant to pyrethroid insecticides but has no effect on DDT. Research by Scott in 2019 suggests this finding applies to other insect cells as well.
History
DDT was first created in 1874 by Othmar Zeidler, who worked under Adolf von Baeyer. In 1929, W. Bausch described it in a research paper, and two more papers were published in 1930. In 1934, Wolfgang von Leuthold wrote about the insect-killing abilities of certain chemicals in a patent. However, the insect-killing power of DDT was not discovered until 1939 by Paul Hermann Müller, a Swiss scientist. Müller received the 1948 Nobel Prize in Physiology and Medicine for his work.
DDT was one of several insect-killing chemicals containing chlorine that were used in the 1940s and 1950s. During this time, the United States used DDT to protect soldiers from diseases in tropical areas. Scientists in the United States and United Kingdom wanted to use DDT to stop the spread of malaria, typhus, dysentery, and typhoid fever among soldiers overseas. This was especially important because another insect-killing chemical called pyrethrum was hard to get, as it mostly came from Japan. Because DDT was very effective, the US War Production Board added it to military supply lists in 1942 and 1943 and encouraged its production for use abroad. The US government promoted DDT through posters showing soldiers fighting insects and Axis powers, and through media stories about its military uses. In the South Pacific, DDT was sprayed from planes to control malaria and dengue fever, with great success. While DDT’s chemical and insect-killing abilities were important, the success of these programs also depended on good equipment, organization, and enough workers.
In 1945, DDT became available to farmers as an insect-killing chemical. It helped reduce malaria in Europe and North America. Even though scientists had concerns, the FDA said it was safe in food up to 7 parts per million. There was strong financial motivation to sell DDT to farmers, governments, and individuals to control diseases and increase food production.
DDT also helped spread US influence abroad through spraying campaigns. In 1944, Life magazine featured a story about an Italian program, showing pictures of US public health workers spraying DDT on Italian families.
In 1955, the World Health Organization started a program to eliminate malaria in countries with low to moderate malaria rates. It relied heavily on DDT for mosquito control, along with quick diagnosis and treatment. The program successfully eliminated malaria in parts of North America, Europe, the former Soviet Union, Taiwan, much of the Caribbean, the Balkans, parts of northern Africa, northern Australia, and large areas of the South Pacific. It also greatly reduced deaths in Sri Lanka and India.
However, the program failed in some areas because mosquito populations became resistant to DDT, and the parasites that cause malaria also became more resistant. Early successes were sometimes lost, and in some places, malaria spread again. The program only succeeded in areas with strong economies, well-organized healthcare systems, and less intense or seasonal malaria.
DDT was less effective in tropical regions because mosquitoes had a constant life cycle and there was poor infrastructure. It was used in sub-Saharan Africa by colonial governments, but the global WHO program did not include this region. Malaria deaths in sub-Saharan Africa did not drop as much as in other areas. Today, this region has most of the world’s malaria deaths, partly because of resistance to drug treatments and the spread of a deadly form of malaria caused by Plasmodium falciparum. The malaria eradication program was stopped in 1969, and efforts shifted to controlling and treating the disease. DDT spraying was reduced due to safety and environmental concerns, as well as problems with management and funding. Instead, efforts focused on using insecticide-treated bednets and other methods.
By October 1945, DDT was sold to the public in the United States for use in farming and homes. While the government and agriculture industry promoted its use, scientists like Herbert O. Calvery, an FDA pharmacologist, raised concerns about possible dangers as early as 1944. In 1947, Bradbury Robinson, a doctor and nutritionist in St. Louis, Michigan, warned about the risks of using DDT in farming. DDT was produced in St. Louis by the Michigan Chemical Corporation, later bought by Velsicol Chemical Corporation, and became important to the local economy. Robinson cited research from Michigan State University in 1946 and said:
As DDT use grew, public reactions were mixed. While some praised it as part of the “world of tomorrow,” others worried it could harm harmless insects (like pollinators), birds, fish, and even humans. DDT’s effects varied between species, and repeated exposure could build up over time, causing harm similar to large doses. Some states tried to regulate DDT, and the federal government started stricter rules in the 1950s. These events received little attention. Women like Dorothy Colson and Mamie Ella Plyler in Claxton, Georgia, collected evidence about DDT’s effects and sent it to health organizations.
In 1957, The New York Times reported a failed effort to limit DDT use in Nassau County, New York. This issue reached Rachel Carson, a writer and naturalist, when a friend, Olga Huckins, sent her an article about the harm DDT caused to birds in her area. William Shawn, editor of The New Yorker, encouraged Carson to write about the topic, which led to her 1962 book Silent Spring. The book argued that pesticides like DDT were harming wildlife, the environment, and human health. Silent Spring became a bestseller and started the modern environmental movement in the United States. The next year, President John F. Kennedy ordered a scientific committee to investigate Carson’s claims. The committee agreed with her, calling her book “a thorough vindication,” and recommended stopping the use of “persistent toxic pesticides.” In 1965, the US military removed DDT from its supply system because body lice became resistant to it, and it was replaced by lindane.
In the mid-1960s, DDT became a major focus of the growing environmental movement as concerns about its effects increased. In 1966, a fish die-off in Suffolk County, New York, was linked to a large DDT spill by the county’s mosquito control commission. A group of scientists and lawyers sued to stop further use of DDT. The following year, the group, led by Victor Yannacone and Charles Wurster, founded the Environmental Defense Fund (EDF) with scientists Art Cooley and Dennis Puleston. They filed several lawsuits against DDT use.
Environmental impact
DDT is a long-lasting chemical pollutant that sticks to soil and sediment, acting as both a place where it stays and a source of exposure for living things. Its time to break down in soil can vary from 22 days to 30 years, depending on the environment. Ways it can leave or break down include runoff, evaporation, sunlight breaking it apart, and being broken down by living things in both oxygen-rich and oxygen-poor conditions. Because DDT is not water-soluble, in water it is absorbed by aquatic animals and sticks to particles in the water, leaving very little in the water itself. However, its half-life in water is reported as 150 years. DDT’s breakdown products, DDE and DDD, are also long-lasting and have similar properties. DDT and its breakdown products move from warmer areas to the Arctic through a process called global distillation, where they build up in the food chain.
In 1974, medical researchers found a clear difference in the amount of DDT in human milk between mothers in New Brunswick and Nova Scotia, possibly because of past use of insecticide sprays in those areas.
Because DDT is fat-soluble, it builds up in the bodies of top predators, like birds of prey. DDT is harmful to many living things, including marine animals like crayfish, daphnids, sea shrimp, and many fish species. DDT, DDE, and DDD increase in concentration as they move up the food chain, with top predators like raptors having the highest levels. These chemicals are stored mainly in body fat. DDT and DDE are hard for the body to break down; in humans, they stay for about 6 years and up to 10 years, respectively. In the United States, these chemicals were found in nearly all human blood samples tested in 2005, though levels have dropped since their use was banned. People now eat less of these chemicals, though they are still sometimes found in food.
Even though DDT has been banned for many years, research in 2018 showed that DDT remains in European soils and Spanish rivers.
DDT and its breakdown products caused thin eggshells and population declines in many bird species in North America and Europe. Laboratory and field studies confirmed this. The first clear proof of this effect was found in the 1960s at Bellow Island in Lake Michigan during studies on American herring gulls. Thinning of eggshells due to DDE is considered a major reason for declines in bald eagles, brown pelicans, peregrine falcons, and ospreys. However, birds vary in how sensitive they are to these chemicals, with birds of prey, waterfowl, and songbirds being more affected than chickens and similar species. In 2010, California condors that eat sea lions near the Palos Verdes Shelf area still showed thin eggshells, though some debate whether DDT caused their decline.
The exact way DDT causes thin eggshells is not fully understood, but DDE seems to be more harmful than DDT. Strong evidence shows that p,p’-DDE stops a protein from moving calcium into the eggshell, making the shell thinner. Other evidence suggests that o,p’-DDT harms the development of the female reproductive system, later affecting eggshell quality. Different mechanisms may be at work in different species.
Human health
DDT is a chemical that can interfere with the body's hormone system. It is considered likely to cause cancer in humans, although most studies suggest it does not directly damage DNA. DDE, a breakdown product of DDT, weakly blocks a hormone receptor that helps with male traits but does not affect estrogen-related functions. The main component of DDT, p,p′-DDT, has little or no effect on male or female hormone activity. The smaller part, o,p′-DDT, has weak effects on female hormone activity.
DDT is classified as "moderately toxic" by the US National Toxicology Program (NTP) and "moderately hazardous" by WHO, based on the dose that kills half of test animals when given orally (LD₅₀ of 113 mg/kg). Exposure to DDT through the environment is considered relatively safe for humans. High-dose exposure to DDT can cause effects in animals, such as headaches, tremors, and convulsions. In laboratory tests, animals given a single dose of about 50 mg DDT per kilogram of body weight showed tremors, hyperactivity, or a hunched posture at doses as low as 27 mg/kg. Similar effects were observed in multiple species, including humans. In controlled studies, humans exposed to 6 mg DDT/kg orally did not show illness but experienced sweating, headaches, and nausea. At doses of 16 mg/kg or higher, convulsions occurred. At about 22 mg/kg, symptoms such as dizziness, confusion, tremors, headaches, and fatigue appeared within 10 hours of exposure. These symptoms usually resolved within 24 hours.
DDT tends to accumulate in body parts with high fat content, which can lead to long-term exposure affecting reproductive health and the development of embryos or fetuses.
A review in The Lancet reported that exposure to DDT at levels used for malaria control might increase the risk of preterm birth and early weaning. Toxicological evidence shows DDT can interfere with hormone systems, and human studies suggest possible effects on semen quality, menstrual cycles, pregnancy length, and breastfeeding duration. Other studies found lower semen quality in men with high DDT exposure, often from indoor spraying. Research on whether high DDT or DDE levels increase time to pregnancy is inconsistent. In some studies, high DDE levels in mothers were linked to a 32% higher chance of daughters conceiving, but high DDT levels were associated with a 16% lower chance. Indirect exposure through workers handling DDT was linked to increased spontaneous abortions. Studies also found that DDT or DDE may disrupt thyroid function during pregnancy and childhood. Mothers with high DDT levels during pregnancy were more likely to have children who later developed autism.
In 2015, the International Agency for Research on Cancer classified DDT as Group 2A, "probably carcinogenic to humans." Earlier assessments by the US National Toxicology Program labeled it "reasonably anticipated to be a carcinogen," and the EPA classified DDT, DDE, and DDD as Class B2 "probable" carcinogens, based mainly on animal studies.
A 2005 The Lancet review found that occupational DDT exposure was linked to higher pancreatic cancer risk in some studies but not in others. Results about liver and biliary tract cancer are conflicting. Some studies showed increased risk in workers without direct DDT contact, while others found no clear link. Evidence about DDT and cancers such as multiple myeloma, prostate, testicular, endometrial, and colorectal cancer is inconclusive. A 2017 review suggested that organochlorine pesticides, including DDT, may increase the risk of liver cancer.
A 2009 review, including authors involved in DDT-related legal cases, found similar results, with unclear links to testicular cancer. Studies did not support a connection between DDT and leukemia or lymphoma.
The link between DDT or DDE and breast cancer remains unclear. Most studies found no overall relationship between DDT exposure and breast cancer risk. In 2012, the US Institute of Medicine concluded that a cause-and-effect relationship could not be proven or disproven. A 2007 study using blood samples found a fivefold increase in breast cancer risk among women born before 1931 with high DDT levels in 1963. Researchers suggested that exposure during ages 14–20 (when DDT use was high) might be critical. This study, which highlights a potential link not seen in other research, received mixed responses. The US National Toxicology Program noted that while most studies found no link, a few studies in women with high exposure or specific groups showed positive associations.
A 2015 study found a link (odds ratio 3.4) between in-utero DDT exposure (measured through maternal blood samples) and breast cancer in daughters. The findings support classifying DDT as an endocrine disruptor, a predictor of breast cancer, and a marker of high risk.
Malaria control
Malaria continues to be the biggest public health challenge in many countries. In 2015, there were 214 million malaria cases worldwide, leading to about 438,000 deaths. Ninety percent of these deaths occurred in Africa. DDT is one tool used to fight malaria. Its use has been described in many ways, including as a "miracle weapon" that is very effective against mosquitoes and as "toxic colonialism."
Before DDT, people tried to stop mosquitoes by draining water where they breed or using chemicals like Paris green or pyrethrum. In areas where living standards improved, malaria often decreased because of better sanitation and the use of window screens. The best way to control malaria includes several actions at the same time. These include using antimalarial drugs to prevent or treat infections, improving public health systems to find and treat infected people, using bednets to keep mosquitoes away, and controlling mosquito populations through methods like spraying insecticides indoors, adding fish to water to eat larvae, or draining mosquito breeding areas.
The World Health Organization (WHO) used DDT heavily in its anti-malaria campaigns during the 1950s and 1960s. This helped reduce malaria in some places, but the effects were not long-lasting in developing countries. Experts say malaria returned because of poor leadership, lack of funding, poverty, civil unrest, and more irrigation. Mosquitoes also became resistant to early drugs and insecticides. This resistance was partly caused by using DDT in farming. Because of the harm to people and the environment, many governments stopped using DDT. In 2006, WHO changed its policy and allowed DDT to be used indoors in areas where malaria is common.
As of 2019, only five countries used DDT for indoor spraying. During World War II, DDT helped reduce malaria cases and deaths. WHO’s anti-malaria program, which included spraying DDT and treating infected people quickly, was successful at first. For example, in Sri Lanka, cases dropped from about one million per year before spraying to 18 in 1963 and 29 in 1964. The program stopped later to save money, and malaria cases rose again. When DDT was used again, mosquitoes had already become resistant, likely because of continued use in farming. The program then switched to another insecticide, but malaria cases still increased in the 1980s.
DDT is still on WHO’s list of approved insecticides for indoor spraying. In 2006, WHO changed its policy to recommend using DDT in areas where malaria is constantly present, not just in areas where it occurs seasonally. WHO plans to reduce DDT use worldwide by 30% by 2014 and stop using it completely by the early 2020s if possible, while finding alternatives.
South Africa uses DDT under WHO guidelines. In 1996, the country stopped using DDT, and malaria cases increased. When DDT was used again and new drugs were introduced, malaria cases decreased. In South America, malaria cases rose after countries stopped using DDT. Studies show that using DDT indoors is strongly linked to lower malaria rates. For example, Ecuador reduced malaria by 61% after increasing DDT use, while other countries that reduced DDT use saw large increases in cases.
In some areas, mosquitoes became resistant to DDT, making it less effective. WHO requires testing to confirm that mosquitoes are not resistant before using DDT. Resistance is mainly caused by using DDT in farming, where it is used in much larger amounts than needed for malaria control.
Resistance to DDT was noticed early in spray campaigns. In 1956, a leader of the Allied Anti-Malaria campaign said resistance appeared after six to seven years. Resistance has been found in Sri Lanka, Pakistan, Turkey, and Central America. These areas now use other insecticides, like malathion or bendiocarb.
In many parts of India, DDT is not effective. Farming use of DDT was banned in 1989, and its use for malaria control has decreased. One study said DDT can still work well in indoor spraying if used carefully.
Studies in South Africa found that 63% of mosquitoes tested were still susceptible to DDT, compared to 87% of the same species found outside. Researchers said the discovery of DDT resistance in mosquitoes near areas where other insecticides are also resistant shows the need for better strategies to manage insecticide resistance in malaria control programs.
DDT can still work against resistant mosquitoes. Mosquitoes avoid walls sprayed with DDT, which helps reduce their ability to bite humans. A 2007 study found that resistant mosquitoes avoided treated homes. Researchers said DDT was the best pesticide for indoor spraying, even though it did not protect people as well as other chemicals, because other pesticides kill or irritate mosquitoes, encouraging resistance. Some people say the avoidance behavior makes it harder to eliminate malaria. Unlike other insecticides, DDT needs long exposure to kill mosquitoes, but its irritant property makes mosquitoes leave quickly. Studies show that pyrethroid insecticides, like deltamethrin, usually work better for malaria control than DDT. In India, where people often sleep outdoors or work at night, DDT’s ability to repel mosquitoes may actually increase malaria transmission.
Indoor residual spraying (IRS) is most effective when at least 80% of homes and barns in an area are sprayed. Lower coverage can reduce the success of the program. Some people refuse DDT spraying because of the strong smell, stains on walls, or problems with other insects. Pyrethroid insecticides can help with these issues and increase participation.
A 1994 study found that South Africans living in homes sprayed with DDT had much higher levels of DDT in their bodies than others. Breast milk from South African mothers also had high levels of DDT and DDE. It is unclear if these levels came from home spraying or food. Evidence suggests these levels may be linked to problems with infant brain development.
Most studies on DDT’s effects on human health have been done in developed countries where DDT is not used. Exposure in these countries is usually much lower than in areas where DDT is sprayed indoors.