4,4'-DDT

Dichloro-diphenyl-trichloroethane (DDT) was first synthesised in 1873 by the German chemist Othmar Zeidler. Later in 1939, Paul Muller of Geigy Pharmaceutical in Switzerland discovered the effectiveness of DDT as an insecticide. For this discovery of DDT, Paul Muller was awarded the Nobel Prize in Medicine and Physiology in 1948. The use of DDT increased enormously on a worldwide basis after World War II, primarily because of its effectiveness against the mosquito that spreads malaria and lice that carry typhus. The World Health Organization (WHO) estimates that during the period of its use, approximately 25 million lives were saved.
DDT was extensively used during the World War II among Allied troops and certain civilian populations to control insect typhus and malaria vectors. By the 1970s, overuse and misuse of DDT became obviously associated with environmental and health effects. Eventually, in June of 1972, the U.S. EPA cancelled all use of DDT on crops except in certain cases of disease control where the U.S. EPA allowed a limited use of DDT. However, many tropical countries are still using DDT for the control of malaria.
Use of DDT was banned for use in Sweden in 1970 and in the United States in 1972. In view of its large-scale use over the decades, many insect pests may have developed resistance to DDT. It is no longer registered for use in the United States barring public health emergency, for example, outbreak of malaria.

DDT is a polychlorinated persistent chemical that exists as a solid under normal conditions.Even though DDT seemed to be a cheap and effective pesticide, enough was known in its early development to raise concerns. DDT is a persistent chemical that lasts a long time in the environment. DDT is fat-soluble and not readily metabolized by higher organisms. Th is meant that DDT accumulated in the fat tissues of higher organisms.

DDT was extensively used during World War II among the Allied troops and certain civilian populations to control insect typhus and malaria vectors. Application of DDT became extensive because of easy control of a large number of crop pests and vectors of human diseases. Humans are exposed to DDT because of different activities and many factors. These include, but are not limited to, (i) consumption of eating contaminated foods, such as root and leafy vegetable, fatty meat, fi sh, and poultry, but levels are very low; (ii) eating contaminated imported foods from countries that still allow the use of DDT to control pests; (iii) breathing contaminated air or drinking contaminated water near waste sites and landfi lls that may contain higher levels of these chemicals; (iv) infants fed on breast milk from mothers who have been exposed; and (v) breathing or swallowing soil particles near waste sites or landfi lls that contain these chemicals. By the 1970s, it was obvious that overuse and misuse of DDT was associated with environmental and health effects. Eventually, in June 1972, the US EPA cancelled all use of DDT on crops except in certain cases of disease control where the US EPA allowed a limited use of DDT. However, many tropical countries are still using DDT for the control of malaria. Use of DDT was banned in Sweden in 1970 and in the United States in 1972. In view of its large-scale use over the decades, many insect pests may have developed resistance to DDT. It is no longer registered for use in the United States barring a public health emergency, e.g., an outbreak of malaria. The latest group meeting by 110 countries on DDT met in Geneva (September 17, 1999) to phase out the production of DDT and impose a total ban on its use even for public health purposes. The conference agree on the conclusion for a global ban on DDT. Absence of a suitable substitute for DDT in the control of malaria and the absence of an antimalaria vaccine necessitates the continuing use of DDT for malaria control

DDT is a waxy solid or slightly off-white powder of indefinite melting point with a weak, chemical odor.

The technical p,p′-DDT is a waxy solid but in its pure form appears as colourless crystals. It is a mixture of three isomers, namely, p,p′-DDT isomer (about ca. 85%); o,p′-DDT; and o,o′-DDT (in smaller levels). DDT is very soluble in cyclohexanone, dioxane, benzene, xylene, trichloroethylene, dichloromethane, acetone, chloroform, diethyl ether, ethanol, and methanol.

Whites crystals or waxy solid, with a faint, fragrant, aromatic-like odor. Tasteless. Odor threshold concentration is 200 ppb (quoted, Keith and Walters, 1992) and in water, 350 μg/kg (Sigworth, 1964).

In 1939, the Swiss chemist Paul Müller (1899–1965), working for the Geigy chemical company, discovered that the compound dichlorodiphenyltrichloroethane (DDT) was an effective insecticide. DDT wasfirst synthesized in 1873 by an Austrian student, but it was Müller who discovered its efficacy as an insecticide. DDT was initially marketed in 1941 and found its first widespread use during World War II. During World War I several million deaths, including 150,000 soldiers, were attributed to typhus.there are several forms of typhus, but the most common form is due to bacteria carried by lice. During During World War II, fearing a repeat of World War I typhus outbreaks, the Allied forces used DDT to combat typhus in addition to malaria, yellow fever, and other diseases carried by insects. Soldiers liberally applied talcum powder containing 10% DDT to clothes and bedding to kill lice. America and its European allies were relatively free from typhus and other diseases, whereas the Germans, who did not use DDT, had many more noncombat deaths resulting from infectious diseases. DDT solutions were sprayed in areas of the Pacific theater to prevent malaria and yellow fever. In addition to its use in the war, DDT was used by civilians in tropical areas as a generic insecticide to prevent infectious diseases, especially malaria. Once the war ended, the use of DDT to advance public health in tropical developing countries was expanded for use in agriculture in developed countries. Paul Müller was awarded the Nobel Prize in physiology or medicine in 1948 for his discovery of the insecticide potential of DDT. By 1950, DDT and several related compounds were viewed as miracle insecticides that were inexpensive and that could be used indiscriminately.
the United Nations’ Stockholm Treaty on persistent organic pollutants calls for the phase out of DDT but recognizes its efficacy as a deterrent to vector-borne diseases such as malaria and typhus. According to the treaty, the continued use of DDT is discouraged, but until effective economical alternatives are found, DDT use will be continued in countries with high rates of vector diseases. A number of developing countries still use DDT. It is applied primarily in the interior of homes to prevent malaria. Currently DDT is produced only in India and China, and current production volumes are unknown.

The primary use of DDT is as a vector control for eradication of malaria-bearing mosquitoes. Less persistent insecticides have replaced DDT for control of insects on crops and in forests.

Use as an insecticide is now prohibited.

DDT belongs to a group of chemical insecticides know as organochlorides.these containhydrogen, carbon, and chlorine and kill by interfering with nerve transmission, making themneurotoxins. Organochlorides were the dominant type of chemical insecticide used from 1940to 1970. Some common organochlorides besides DDT are chlordane, heptachlor, aldrin, anddieldrin. Because of their problems and subsequent ban in many regions, numerous otherclasses of insecticides have been synthesized to replace organochlorides.

Contact insecticide.

4,4'-Dichlorodiphenyltrichloroethane is a synthetic organochlorine insecticide. 4,4'-Dichlorodiphenyltrichloroethane functions by opening sodium ion channels in the insects’neurons, causing them to f ire spontaneously which in turn leads to death. 4,4'-Dichlorodiphenyltrichloroethane is banned for agricultural use in North America, it is still commonly used in some countries and particularly as a means of malaria control.

ChEBI: A chlorophenylethane that is 1,1,1-trichloro-2,2-diphenylethane substituted by additional chloro substituents at positions 4 of the phenyl substituents. It is a commonly used organochlorine insecticide.

Odorless colorless solid. Sinks in water.

Insoluble in water.

4,4'-DDT may react with iron, aluminum, aluminum and iron salts, and alkalis. 4,4'-DDT is incompatible with ferric chloride and aluminum chloride. 4,4'-DDT can also react with strong oxidizing materials. .

Very large doses are followed promptly by vomiting, due to local gastric irritation; delayed emesis or diarrhea may occur. With smaller doses, symptoms usually appear 2-3 hours after ingestion. These include tingling of lips, tongue, and face; malaise, headache, sore throat, fatigue, coarse tremors of neck, head, and eyelids; apprehension, ataxia, and confusion. Convulsions may alternate with periods of coma and partial paralysis. Vital signs are essentially normal, but in severe poisoning the pulse may be irregular and abnormally slow; ventricular fibrillation and sudden death may occur at any time during acute phase. Pulmonary edema usually indicates solvent intoxication.

Acute toxicity: low to moderate; high dosescause headache, dizziness, confusion, sweating, tremor, and convulsions; may accumulate in body tissues, causing delayed ill effects after years of low-level exposure;chronic effects include liver damage, central nervous system degeneration, dermatitis, and convulsions; oral LD50 value (rats):～120 mg/kg; a teratogen causing adverseeffects on embryonic fetal development andadverse estrogenic activity; carcinogenicity:animal sufficient evidence, causing liver cancers; human inadequate evidence; exposurelimit: TLV-TWA 1 mg/m³ (ACGIH, MSHA,and OSHA); RCRA Waste Number U061
Tebourbi et al. (2006) have investigatedthe metabolism of DDT in different tissuesof rats. Rats were injected intraperitoneallydoses of DDT at 50 and 100 mg/kg bodyweight. After 10 days their adipose tissues,livers, brains, kidneys, thymus and testeswere examined. DDT was found to be accumulated in highest concentration in adiposetissue, however, in brain its concentrationwas low and remained unchanged at thehigher dose as well. The authors attributedsuch non-accumulation of DDT in brain tothe protective role of the blood–brain barrier limiting the access of xenobiotics in thecerebral compartment, and to the differentialtissue lipid composition. The concentrationof the metabolite, p, p’-DDD was greater inthe liver than in any other organs. In thebrain, however, the concentration of p, p’-DDE was greater than that of p, p’-DDD.This study indicated that the metabolismof DDT proceeded via more than onepathway.
Perez-Maldonado et al. (2005) studiedDDT-induced oxidative damage in humanblood mononuclear cells. They reported thatDDT and its metabolites, p, p’-DDD and p, p’-DDE induced apoptosis in human peripheral blood mononuclear cells which was preceded by increase in reactive oxygenspecies. N-Acetyl-L-cysteine inhibited suchinduction of apoptosis.

Exposures to high concentrations of DDT cause adverse health effects and poisoning among occupational workers. The symptoms of toxicity include, but are not limited to, tremors, diarrhea, dizziness, headache, vomiting, numbness, paresthesias, hyperexcitability, and convulsions. Chronic exposures to DDT caused adverse effects on the nervous system, liver, kidneys, and immune systems in experimental animals. Laboratory rats and mice given DDT (16–32 and 6.5–13 mg/kg for about 26 weeks and 80–140 weeks, respectively) experienced the tremors. Laboratory studies with non-human primates given DDT (10 mg/kg/ day over 100 days) showed changes in the cellular chemistry of the CNS and at higher doses (50 mg/kg/day) caused loss of equilibrium in animals. Prolonged exposures to DDT caused adverse effects in species of animals, i.e., rats, mice, hamsters, dogs, and monkeys, showing pathomorphological changes in the liver, kidney, CNS, and adrenal glands. Humans exposed to DDT have shown many adverse effects, i.e., nausea, diarrhea, increased liver enzyme activity, irritation of the eyes, nose and throat, disturbed gait, malaise and excitability; at higher doses, tremors and convulsions. It has been reported that the health effects of DDT in humans exposed to different doses and for different periods of poisoning include sweating, headache, nausea, and convulsions. It is very important to remember that earlier fi ndings on the toxicological effects of DDT in animals and humans, as reported above, require further confi rmatory data since the studies did not observe the GLP regulations. Therefore, the potential hazards of DDT to human health and environmental safety require careful evaluations.

This insecticide was formerly reported as a sensitizer in farmers or agricultural workers.

DDT is a nerve poison that affects the sodium channel of nerve membranes. It is a nonsystemic insecticide with contact and stomach action. The most important reactions of DDT (1) are dehydrochlorination to DDE (2) and reductive dechlorination to DDD (3). These reactions occur abiotically, in vivo and in soils. The products resemble DDT in their recalcitrance toward environmental degradation. The stability of DDT and its principal metabolites DDD and DDE, in combination with their lipid solubility and resistance to biological degradation, resulted in their bioconcentration in fish and other organisms exposed to extremely low levels of these compounds in water. Although metabolism of DDT in mammals may proceed via DDD to give 4,4- dichlorodiphenylacetic acid (5), DDE is also formed and stored in fat. It may be slowly depleted by oxidative reactions, and ringhydroxylated derivativeshave been detected in mammals and wildlife samples. Consumption of DDT residues in wildlife and fish by predators resulted in adverse effects.

Although DDT [1,1-(2,2,2-trichloroethylidene)bis(4-chlorobenzene)] has been banned in the United States since 1972, it remains one of the best-known synthetic pesticides. Because DDT is a very nonpolar molecule, it has high lipid solubility. Since DDT is also extremely stable, it accumulates in animal tissues and in the food chain. DDT is still one of the most abundant pesticide residues in food. During the 40 years following DDT s commercial introduction in the 1940s, more than 4 billion pounds were used to control insect-borne diseases. Until 1972, DDT was widely used in the United States, mostly on cotton, peanuts, and soybeans. As a result of its use, DDT residues are now ubiquitous in the environment, and at the present time, some level can be detected in almost all biological and environmental samples. In addition, due to its high lipid solubility, DDT concentrates in milk. When DDT was widely used, levels in human milk and adipose tissue were found to be higher than concentrations permitted in meat and dairy products. However, since its use has been prohibited, storage levels of DDT in human tissue have declined significantly. DDT is, however, still in use in other countries, largely to control insect-borne diseases that pose a substantial threat to public health.

Confirmed carcinogen with experimental carcinogenic, neoplastigenic, tumorigenic, and teratogenic data. Human poison by ingestion. Experimental poison by ingestion, skin contact, subcutaneous, intravenous, and intraperitoneal routes. Experimental reproductive effects. Human systemic effects by ingestion: anesthetic, convulsions, headache, analgesia, cardiac arrhythmias, nausea or vomiting, sweating, and unspecified pulmonary changes. Human mutation data reported. An insecticide. When heated to decomposition it emits toxic fumes of Cl-. See also CHLORINATED HYDROCARBONS, AROiWTIC. dangerous though not fatal to a human. This dose was taken by 5 persons who vomited an unknown portion of the material and even so recovered only incompletely after 5 weeks. Smaller doses produced less important symptoms with relatively rapid recovery. Experimental ingestion of 1.5 g resulted in great discomfort and moderate neurological changes including paresthesia, tremor, moderate ataxia, exaggeration of part of the reflexes, headache, and fatigue. Vomiting followed only after 11 hours. Recovery was complete on the following day. The fatal dose of DDT for humans is not known. Judgmg from the literature, no one has ever been killed by DDT in the absence of other insecticides and/or a variety of toxic solvents. However, these common solvent formulations are highly fatal when taken in small doses, partly because of the toxicity of the solvent, and perhaps because of the increased absorbabihty of the DDT; several fatal cases in humans have been reported. Little is known of the hazard of chronic DDT poisoning. Human volunteers have ingested up to 35 mg/day for 21 months with no dl effects. products, particularly DDE, are stored in fat. This storage effect leads to a concentration of DDT at higher levels of the food chain. DDT stored in the fat is at least largely inactive since a greater total dose may be stored in an experimental animal than is sufficient as a lethal dose for that same animal if given at one time. A study based on 75 human cases reported an average of 5.3 ppm of DDT stored in the fat. A higher content of DDT and its derivatives (up to 434 pprn of DDE and 648 ppm of DDT) was found in workers who had very extensive exposure. Without exception, the samples were taken from persons who were either asymptomatic or suffering from some disease completely unrelated to DDT. Careful hospital examination of workers who had been very extensively exposed and who had volunteered for examination revealed no abnormahty that could be attributed to DDT. Much higher levels have been found in humans than have been observed in the fat of experimental animals that were apparently asymptomatic. DDT stored in the fat is eluninated only very gradually when further dosage is discontinued. However, weight loss can speed the release of this stored DDT (and DDE) into the blood. After a single dose, the secretion of DDT in the milk and its excretion in the urine reach their height within a day or two and continue at a lower level thereafter.

DDT is a low-cost broad-spectrum insecticide. However, following an extensive review of health and environmental hazards of the use of DDT, United States Environmental Protection Agency decided to ban further use of DDT in December 1972. This decision was based on several properties of DDT that had been well evidenced : DDT and its metabolites are toxicants with long-term persistence in soil and water ; it is widely dis- persed by erosion, runoff, and volatization ; and the low- water solubility and high lipophilicity of DDT result in concentrated accumulation of DDT in the fat of wildlife and humans which may be hazardous.

If this chemical gets into the eyes, remove anycontact lenses at once and irrigate immediately for at least15 min, occasionally lifting upper and lower lids. Seek medical attention immediately. If this chemical contacts theskin, remove contaminated clothing and wash immediatelywith soap and water. Speed in removing material from skinis of extreme importance. Shampoo hair promptly if contaminated. Seek medical attention immediately. If thischemical has been inhaled, remove from exposure, beginrescue breathing (using universal precautions, includingresuscitation mask) if breathing has stopped and CPR ifheart action has stopped. Transfer promptly to a medicalfacility. When this chemical has been swallowed, get medical attention. Give large quantities of water and inducevomiting. Do not make an unconscious person vomit.

Dichlorodiphenyltrichloroethane (DDT) is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in experimental animals.

Biological. In four successive 7-day incubation periods, p,p′-DDT (5 and 10 mg/L) was recalcitrant to degradation in a settled domestic wastewater inoculum (Tabak et al., 1981).
The white rot fungus Phanerochaete chrysosporium degraded p,p′-DDT yielding the following metabolites: 1,1-dichloro-2,2-bis(4-chlorophenyl)ethane (p,p′-DDD), 2,2,2- trichloro-1,1-bis(4-chlorophenyl)ethanol (dicofol), 2,2-dichloro-1,1-bis(4-chlorophenyl) e
Mineralization of p,p′-DDT by the white rot fungi Pleurotus ostreatus, Phellinus weirri and Polyporus versicolor was also demonstrated (Bumpus and Aust, 1987). Aerobacter aerogenes degraded p,p′-DDT under aerobic conditions to p,p′-DDD, p,p′-DDE, 1-chloro
Under aerobic conditions, the amoeba Acanthamoeba castellanii (Neff strain ATCC 30.010) degraded p,p′-DDT to p,p′-DDE, p,p′-DDD and dibenzophenone (Pollero and dePollero, 1978).
Incubation of p,p′-DDT with hematin and ammonia gave p,p′-DDD, p,p′-DDE, bis(pchlorophenyl) acetonitrile, 1-chloro-2,2-bis(p-chlorophenyl)ethylene, 4,4′-dichlorobenzophenone and the methyl ester of bis(p-chlorophenyl)acetic acid (Quirke et al., 1979).

Upon UV irradiation with methyl oleate, DDT is extensively added to the carbon ? carbon double bond of methyloleate via radical mechanisms. Besides chlorinated stearic acids, several addition products are formed, offering new possibilities to produce bound residues in plants. A mixture of hemin and excess cysteine (the hemin ? cysteine model system) is able to degrade DDT partially and the major degradation products are three water-soluble, non-toxic conjugates of DDT metabolites with cysteine which lose two or three of the five chlorine atoms of DDT. In the presence of a designed 24-residue polypeptide or b-casein, two DDT-binding proteins, an additional fourfold increase in the rate of DDT degradation is observed. Although the concentrations of DDT and cysteine occurring in an organism would be expected to be lower than those in the experiments described, the formation of water-soluble conjugates of DDT with cysteine (and other amino acids) could also play a role in metabolism and excretion of DDT in vivo.

DDT decomposed very slowly in sunlight, and 93% was recovered unchanged from the surface of an apple after 3 months. DDE decomposed more rapidly than DDT in sunlight. Other reports indicate that DDT was photolyzed under field conditions to give products, including DDE, 4,4- dichlorobenzophenone (6), 4-chlorobenzoyl chloride, 4- chlorobenzoic acid, and 4-chlorophenyl 4-chlorobenzoate. Irradiation of DDT at shorter wavelengths under laboratory conditions gave a variety of products that arose from reactions of photolytically generated radicals.

In g/L: Benzyl benzoate (420), carbon tetrachloride (450), chlorobenzene (740), cyclohexanone(1,160), gasoline (100), isopropanol (30), kerosene (80–100), morpholine (750), peanut oil (110), pine oil (100–160), tetralin (610), tributyl phosphate (500) (Windholz et al., 1983). 95.4 g/kg in triolein at 25 °C (Chiou and Manes, 1986)
In wt %: acetone (21.2 at 0 °C, 27.3 at 7.2 °C, 40.3 at 24.0 °C, 59.0 at 48.0 °C); benzene (6.8 at 0 °C, 27.1 at 7.2 °C, 44.0 at 24.0 °C, 59.3 at 48.0 °C; carbon tetrachloride (9.0 at 0 °C, 10.5 at 7.2 °C, 18.0 at 24.0 °C, 34.8 at 45.0 °C); chloroform (18.2 at 0 °C, 21.9 at 7.2 °C, 31.0 at 24.0 °C, 47.4 at 45.0 °C); 1,4-dioxane (8 at 0 °C, 29 at 7.2 °C, 46 at 24.0 °C, 61 at 48 °C); ethyl ether (15.0 at 0 °C, 18.9 at 7.2 °C, 27.5 at 24.0 °C); 95% ethanol (0.8 at 0 °C, 1.0 at 7.2 °C, 2.2 at 24.0 °C, 3.9 at 48.0 °C); pyridine (21 at 0 °C, 36 at 7.2 °C, 51 at 24.0 °C, 62 at 48.0 °C) (Gunther, 1945)

In g/L: Benzyl benzoate (420), carbon tetrachloride (450), chlorobenzene (740), cyclohexanone(1,160), gasoline (100), isopropanol (30), kerosene (80–100), morpholine (750), peanut oil (110), pine oil (100–160), tetralin (610), tributyl phosphate (500) (Windholz et al., 1983). 95.4 g/kg in triolein at 25 °C (Chiou and Manes, 1986)
In wt %: acetone (21.2 at 0 °C, 27.3 at 7.2 °C, 40.3 at 24.0 °C, 59.0 at 48.0 °C); benzene (6.8 at 0 °C, 27.1 at 7.2 °C, 44.0 at 24.0 °C, 59.3 at 48.0 °C; carbon tetrachloride (9.0 at 0 °C, 10.5 at 7.2 °C, 18.0 at 24.0 °C, 34.8 at 45.0 °C); chloroform (18.2 at 0 °C, 21.9 at 7.2 °C, 31.0 at 24.0 °C, 47.4 at 45.0 °C); 1,4-dioxane (8 at 0 °C, 29 at 7.2 °C, 46 at 24.0 °C, 61 at 48 °C); ethyl ether (15.0 at 0 °C, 18.9 at 7.2 °C, 27.5 at 24.0 °C); 95% ethanol (0.8 at 0 °C, 1.0 at 7.2 °C, 2.2 at 24.0 °C, 3.9 at 48.0 °C); pyridine (21 at 0 °C, 36 at 7.2 °C, 51 at 24.0 °C, 62 at 48.0 °C) (Gunther, 1945)

Color Code—Blue: Health Hazard/Poison: Storein a secure poison location. Prior to working with DDT youshould be trained on its proper handling and storage. Storein tightly closed containers in a cool, well-ventilated areaaway from strong oxidizers, strong bases, and heat. Shouldnot be stored in iron containers. A regulated, marked areashould be established where this chemical is handled, used,or stored in compliance with OSHA Standard 1910.1045

UN2761 Organochlorine pesticides, solid, toxic, Hazard Class: 6.1; Labels: 6.1-Poisonous materials.

Crystallise DDT from n-propyl alcohol (5mL/g), then dry it in air or an air oven at 50-60o. Alternatively crystallise it from 95% EtOH, and the purity is checked by TLC. [Beilstein 5 III 1833.] TOXIC INSECTICIDE.

DDT decomposes thermally with elimination of hydrogen chloride in alkaline solution and at temperatures above its melting point (the technical product has m.p. 108.5-109 °C) to form DDE (2). When dissolved in a proton donor solvent, such as methanol, DDT decomposes thermally (e.g. in a heated metal gas chromatographic inlet) to give products that include DDD (3).
In sunlight, decomposition of DDT was slow and 93% could be recovered unchanged from the surface of an apple after three months. DDE decomposed more rapidly in sunlight. Other reports have indicated that DDT is susceptible to photolysis under field conditions and products included DDE (2), 4,4'-dichlorobenzophenone (5), 4-chlorobenzoyl chloride, 4-chlorobenzoic acid and 4-chlorophenyl4-chlorobenzoate (see Scheme 1).
Although DDT is resistant to photolysis at longer wavelengths, at shorter wavelengths it gives a variety of products that arise from the reactions of photolytically-generated radicals. The identity of products and the composition of the product mixture depend on the solvent and the presence or absence of oxygen. Scheme 1 also shows some of the many compounds that have been isolated or detected after irradiation of DDT in solvents by energetic ultraviolet irradiation (less than 260 nm).
Irradiated at around 260 nm in methanol, DDT yields a complex mixture of products. In methanol under nitrogen, major products were DDD (3) and 1,1-bis(4-chlorophenyl)-2-chloroethylene(DDMU, 4).

The acute oral gavage LD₅₀ of p,p- DDT in the rat is about 150 mg/kg. The dermal toxicity is approximately 10-fold lower. The o,p-DDT isomer is over 20-fold less toxic by oral ingestion than is p,p-DDT. The hamster appears to be resistant to acute and chronic toxic effects. Following a single dose, young rats are less susceptible than are adults to the toxic effects of p,p-DDT, but this difference is not apparent with repeated doses. Amongseveral possible explanations, it has been suggested that young rats are less susceptible than are adults to DDTinduced hyperthermia.

Contact with strong oxidizers may cause fire and explosion hazard. Incompatible with salts of iron or aluminum, and bases. Do not store in iron containers

Incineration has been success- fully used on a large scale for several years; huge incinera- tor equipment with scrubbers to catch HCl, a combustion product, are in use at several facilities, such as Hooker Chemical, Dow Chemical and other producers of chlori- nated hydrocarbon products. One incinerator operates @ 900 C 1400 C with air and steam added which precludes formation of Cl2. A few companies also constructed incinerator-scrubber combinations of smaller size, e.g., a system built by Garver-Davis, Inc., of Cleveland, Ohio, for the Canadian government, can handle 200 500 lb DDT/ day as a kerosene solution. In accordance with 40CFR165, follow recommendations for the disposal of pesticides and pesticide containers. Must be disposed properly by follow- ing package label directions or by contacting your local or federal environmental control agency, or by contacting your regional EPA office. Consult with environmental regulatory agencies for guidance on acceptable disposal practices. Generators of waste containing this contaminant (≥100 kg/mo) must conform with EPA regulations govern- ing storage, transportation, treatment, and waste disposal.