read more at PAN UKs DDT section
|Table 1. Some countries which permit the import of DDT(47)|
DDT is moderately to slightly toxic to mammals. The acute oral LD50 ranges from 113-118 mg/kg in rats; 150-300 mg/kg in mice; 300 mg/kg in rabbits; 500-750 mg/kg in dogs; and >1,000 mg/kg in sheep and goats. DDT is less toxic to test animals exposed via the skin. The acute dermal LD50 for female rats is 2,510 mg/kg(10). DDT is categorised by the World Health Organisation as Class II "moderately hazardous"(11).
It mainly affects the central and peripheral nervous systems, and the liver. Acute effects in humans exposed to low to moderate levels may include nausea, diarrhoea, increased liver enzyme activity, irritation of the eyes, nose and/or throat. At higher doses, tremors and convulsions are possible(12). Deaths from exposure to DDT are rare. Even in developing countries there have been few reported cases, especially when compared with organophosphate insecticides (see PN34 pp20-21). In 1994, one fatal poisoning was reported in the US involving a child who ingested one ounce (28g) of a 5% DDT and kerosene solution(13).
DDT has caused chronic effects on the nervous system, liver, kidneys, and immune systems in experimental animals. Dose levels at which effects were observed are at very much higher levels than those which may be typically encountered in humans(14). However they may be at, or even below, levels found in body fat (see below).
DDT causes adverse reproductive effects in test animals. In one rat study, oral doses of 7.5 mg/kg/day for 36 weeks resulted in sterility. In rabbits, doses of 1 mg/kg/day administered on gestation days 4-7 resulted in decreased foetal weights. In mice, doses of 1.67 mg/kg/day resulted in decreased embryo implantation and irregularities in the oestrus cycle over 28 weeks(15). Many of these observations may be the result of disruptions to the endocrine (hormonal) system.
Available epidemiological studies involving exposure to DDT have not confirmed adverse effects in humans. One study did report a significant association between maternal DDT blood levels and miscarriage, but the presence of other organochlorines in maternal blood, make it difficult to attribute the effect solely to DDT(16).
Teratogenic effects (birth defects)
Again there is evidence that DDT causes teratogenic effects in test animals. In mice, maternal doses of 26 mg/kg/day DDT from gestation through to lactation resulted in impaired learning in maze tests(17). Epidemiological studies involving humans are unavailable(18).
The evidence relating to DDT and carcinogenicity provides uncertain conclusions. It has increased tumour production, mainly in the liver and lungs, in test animals such as rats, mice and hamsters in some studies, but not in others. In rats, liver tumours were induced in three studies at doses of 12.5 mg/kg/day over periods of 78 weeks to life, and thyroid tumours were induced at doses of 85 mg/kg/day over 78 weeks. Tests have shown laboratory mice were more sensitive to DDT. Life time doses of 0.4 mg/kg/day resulted in lung tumours in the second generation and leukaemia in the third generation, and liver tumours were induced at oral doses of 0.26 mg/kg/day in two separate studies over several generations(19).
The US Department of Health and Human Services (DHHS) has determined that 'DDT may reasonably be anticipated to be a human carcinogen'. DHHS has not classified DDE and DDD, but the US Environmental Protection Agency (EPA) has determined that they are probable human carcinogens(20).
Work carried out by the US National Cancer Institute correlates breast cancer in women with increased levels of DDE in blood serum. From 14,290 women monitored in the New York University Women's Health Study, researchers selected 58 women who had developed breast cancer and 171 matched controls without cancer. After adjusting for participants' childbearing and breast feeding histories, and for family history of breast cancer, researchers found a four-fold increase in relative risk of breast cancer for women with elevated levels of DDE in the blood(21).
Residues in food
DDT is very fat-soluble and is therefore found in fatty foods such as meat and diary products.
Even in countries across North America and Northern Europe, where its use has been banned for over a decade (see restrictions) DDT residues are still often found in food. This is because of environmental persistence, illegal use, or importation of contaminated food from regions where DDT is still used.
A range of analysis has been carried out in the UK, which is indicative of levels in the region. During 1996, the UK Working Party of Pesticide Residues (WPPR) found residues of DDT in butter, milk, eggs, lamb, potatoes, deep water fish and shell fish(22). The WPPR is trying to establish whether residues have originated from recent illegal use, or historical contamination.
In a survey of non-indigenous deep water fish and shell fish, low levels of DDT residues and metabolites were found in 16 (50%) of the deep water samples and three (19%) of the 16 shell fish samples analysed. Residues of DDE, TDE and DDT found indicated the pollution originated from countries where DDT is still approved (or has recently been approved) for use.
Eggs analysed as part of the Total Diet Survey in 1996 were found to contain residues as p,p'-DDT, o,p'-DDT, p,p-TDE and p,p'-DDE.
In another 1996 WPPR study which monitored geese for the first time, residues of DDT as p,p'-DDE and p,p'-DDT were found in 25% of samples, a residue profile similar to that found in ducks in a 1995 survey. The presence of p'p-DDT may indicate more recent DDT exposure to these animals(23).
The dietary intake of DDT is considerably higher in developing countries. In 1996, the World Health Organisation (WHO) assessed the acceptable daily intake (ADI) for DDT from a number of countries (see table 2). ADIs are the amount of pesticide that can be consumed every day for a lifetime without harm. They do not take into account other pesticide exposures, other forms of DDT exposure, such as occupational, or residue levels already in body fat.
|Table 2. Relative DDT intakes|
|Country||Daily intake*||% of ADI|
Analysis of human fat has been carried out occasionally in the UK showing that DDT can persist for many years. Analysis of 203 samples of mostly renal fat showed 99% contained detectable residues of DDT (see table 3)(24). Many of the levels found are above effect-level exposures required to elicit a carcinogenic response in test animals (see mice studies above). They are also well above the life-time safety exposure limit ADI of 0.02 mg/kg body weight.
|Table 3. DDT* residues of in human fat (1995-1997) mg/kg (for UK)|
|No. of cases||level|
|47||1.0 - 9.3|
|135||0.1 - 0.9|
|19||0.01 - 0.09|
|* p,p'-DDT, o,p'-DDT, o,p'-TDE, and p,p'-DDE|
Once stored in fatty tissue, DDT residues are sequestrated and
stabilised unless they are mobilised either through lactation or significant
weight loss, which burns fat. Organochlorines appear to transfer freely across
the placenta from mother to foetus.
In one study involving humans, 17 people ate 35 mg/man daily (about 0.5 mg/kg daily) for 18 months suffering no ill-effect(25). In another study volunteers ate 0.31 to 0.61 mg/kg daily without any noticeable effects(26).
Residue values tend to be higher for older people. According to John Wargo of Yale University in the US, children under the age of 14 have roughly one-third the level of those over 45, and African-Americans experience levels roughly three times those of whites for corresponding age classes. It is unclear whether the differences for African-Americans are due to a variation in environmental exposure, or because of genetic differences(27).
DDT is excreted in human milk. A study carried out in Zimbabwe found high levels of DDE residues in breast milk commonly exceeded those required to cause hyporeflexia in infants(28).
Between 1950 and 1970 DDT was used over large areas of the Soviet Union. As a result, dangerously high residue levels were found in both food and human tissue(29).
DDT is found in the bodies of people living in the Arctic regions, where DDT has never been used. Along the west coast of Greenland, in Nunavik, Canada, and in Nikel on the Lola Peninsula of Russia, blood levels are only a factor of ten lower than the levels that are known to cause neurological effects in babies(30).
Levels of p,p-DDT in the UK have reduced significantly since the mid 1960s. This would be expected, as DDT has not been approved since 1984. Levels of the breakdown product p,p'-DDE are not coming down so quickly. Although the average figure has more than halved, the range has not changed much since the mid 1960's, and has even increased compared with the early 1970s and early 1980s figures(31).
DDT and its breakdown products have widespread persistence in the environment, and a high potential to bioaccumulate. It has a reported half-life in the environment of 2-15 years in most soils(32).
Many governmental and inter-governmental organisations regard DDT as a major hazard to the environment(33).
DDT is highly toxic to fish. The 96-hour LC50 (the concentration at which 50% of a test population die) ranges from 1.5 mg/litre for the largemouth bass to 56 mg/litre for guppy. Smaller fish are more susceptible than larger ones of the same species. An increase in temperature decreases the toxicity of DDT to fish(34).
DDT and its metabolites can lower the reproductive rate of birds by causing eggshell thinning which leads to egg breakage, causing embryo deaths. Sensitivity to DDT varies considerably according to species(35). Predatory birds are the most sensitive. In the US, the bald eagle nearly became extinct because of environmental exposure to DDT. According to research by the World Wildlife Fund and the US EPA, birds in remote locations can be affected by DDT contamination. Albatross in the Midway islands of the mid-Pacific Ocean show classic signs of exposure to organochlorine chemicals, including deformed embryos, eggshell thinning and a 3% reduction in nest productivity. Researchers found levels of DDT in adults, chicks and eggs nearly as high as levels found in bald eagles from the North American Great Lakes(36).
A recent overview of organochlorine use in Africa during the last 25 years concluded that continued use has led to serious problems for wildlife in terms of uptake into the tissues of many animals groups, particularly birds, with potential long-term adverse population effects(37).
DDT, DDD and DDE are all strongly suspected of being environmental endocrine disrupters (chemicals that affect the hormonal system). DDT can have reproductive endocrine effects (see above) and also has a major toxic effect on the adrenal glands. DDT-related deformities in birds include clubbed feet and crossed bills. There is also concern that it has the potential to disrupt the endocrine system of humans(38).
DDT is one of nine persistent organic pollutants (POPs) which bioaccumulate, and which are transported by air and water currents from warmer climates to temperate zones, where they have never been used. The process of degradation is dramatically slowed down in cooler climates. The global risk of adverse effects to human health and the environment has led the international community to mandate the UN Environment Programme (UNEP) to convene an intergovernmental negotiating committee (INC) for a POPs Convention to phase out production and use. The first INC meeting takes place in June 1998. This action endorses the recommendations of the Inter-governmental Forum on Chemical Safety (IFCS) Ad Hoc Working Group on POPs(41 ,42).
There is widespread global contamination of DDT. It is a hazard to the environment, both are areas where it is still used, and in many regions thousands of miles away where it is no longer, or never has been used. As a matter of urgency the use of DDT, a major POP, needs to be phased out.
Control actions to ban or severely restrict DDT have been taken by over 38 countries, that began in the early 1970s. In at least 26 countries, DDT is completely banned, and in 12 others it is severely restricted. In these latter cases, it is permitted for use by government agencies for special programmes, usually involving vector control programmes(43).
[This article first
appeared in Pesticides News No.40, June 1998, p18-20]