4,4'-DDT CAS 50-29-3
Introduction：Basic information about 4,4'-DDT CAS 50-29-3, including its chemical name, molecular formula, synonyms, physicochemical properties, and safety information, etc.
4,4'-DDT Basic informationHistory
| Product Name: | 4,4'-DDT |
| Synonyms: | 'LGC' (1112);1,1'-(2,2,2-trichloroethyliden)bis-(4-chlorobenzol);DDT (common name not adopted by ISO) clofenotane (INN) dicophane 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane dichlorodiphenyltrichloroethane;1,1,1-Trichloro-2,2-bis(4-chlorophenyl)ethane solution, 4,4μ-DDT solution;1,1,1-TRICHLORO-2,2-BIS(P-CHLOROPHENYL)ETHANE;1,1,1-TRICHLORO-2,2-DI(4-CHLOROPHENYL)ETHANE;1,1,1-TRICHLORO-2,2-BIS(4-CHLOROPHENYL)ETHANE;1,1-BIS(4-CHLOROPHENYL)-2,2,2-TRICHLOROETHANE |
| CAS: | 50-29-3 |
| MF: | C14H9Cl5 |
| MW: | 354.49 |
| EINECS: | 200-024-3 |
| Product Categories: | DA - DHPesticides;2000/60/EC;AcaricidesAlphabetic;D;European Community: ISO and DIN;Insecticides;Oeko-Tex Standard 100;OrganochlorinesMethod Specific;Pesticides;Pesticides&Metabolites;PesticidesMethod Specific;INSECTICIDE |
| Mol File: | 50-29-3.mol |
4,4'-DDT Chemical Properties
| Melting point | 107-110 °C(lit.) |
| Boiling point | 440.74°C (rough estimate) |
| density | 1.556 g/cm3 |
| vapor pressure | 0.5 at 25 °C (extrapolated from vapor pressures determined at higher temperatures, Tesconi andYalkowsky, 1998) |
| refractive index | 1.755 |
| Fp | 72 °C |
| storage temp. | APPROX 4°C |
| solubility | Chloroform: Slightly Soluble; Methanol: Heated |
| Water Solubility | Practically insoluble in water |
| Merck | 13,2861 |
| BRN | 1882657 |
| Henry's Law Constant | 0.188 at 5 °C, 0.513 at 15 °C, 0.681 at 20 °C, 0.957 at 25 °C, 2.76 at 35 °C:in 3% NaCl solution:1.15 at 5 °C, 1.88 at 15 °C, 3.36 at 25 °C, 5.43 at 35 °C (gas stripping-GC, Cetin et al., 2006) |
| Exposure limits | NIOSH REL: 0.5 mg/m3, IDLH 500 mg/m3; OSHA PEL: TWA 1mg/m3; ACGIH TLV: TWA 1 mg/m3. |
| Stability: | Stable. Combustible. Incompatible with strong oxidizing agents, iron and aluminium and their salts, alkalies. |
| Major Application | agriculture environmental |
| InChI | 1S/C14H9Cl5/c15-11-5-1-9(2-6-11)13(14(17,18)19)10-3-7-12(16)8-4-10/h1-8,13H |
| InChIKey | YVGGHNCTFXOJCH-UHFFFAOYSA-N |
| SMILES | Clc1ccc(cc1)C(c2ccc(Cl)cc2)C(Cl)(Cl)Cl |
| IARC | 2A (Vol. Sup 7, 53, 113) 2018 |
| EPA Substance Registry System | p,p'-DDT (50-29-3) |
Safety Information
| Hazard Codes | T,N,Xi,F,Xn |
| Risk Statements | 25-40-48/25-50/53-36/37/38-11-39/23/24/25-23/24/25-52/53-24-67-65-38 |
| Safety Statements | 22-36/37-45-60-61-36-33-26-16-7-62 |
| RIDADR | UN 2811 6.1/PG 3 |
| OEB | C |
| OEL | TWA: 0.5 mg/m3 |
| WGK Germany | 3 |
| RTECS | KJ3325000 |
| TSCA | TSCA listed |
| HazardClass | 6.1(b) |
| PackingGroup | III |
| Storage Class | 3 - Flammable liquids |
| Hazard Classifications | Aquatic Acute 1 Aquatic Chronic 1 Asp. Tox. 1 Flam. Liq. 2 Skin Irrit. 2 STOT SE 3 |
| Hazardous Substances Data | 50-29-3(Hazardous Substances Data) |
| Toxicity | LD50 in male, female rats (mg/kg): 113, 118 orally (Gaines, 1960) |
| IDLA | 500 mg/m3 |
| History | 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. |
| Description | 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 itsearly development to raise concerns. DDT is a persistent chemical that lasts a long time inthe environment. DDT is fat-soluble and not readily metabolized by higher organisms. Th ismeant that DDT accumulated in the fat tissues of higher organisms. |
| Chemical Properties | 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 |
| Chemical Properties | DDT is a waxy solid or slightly off-whitepowder of indefinite melting point with a weak, chemicalodor. |
| Chemical Properties | 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. |
| Physical properties | Whites crystals or waxy solid, with a faint, fragrant, aromatic-like odor. Tasteless. Odor thresholdconcentration is 200 ppb (quoted, Keith and Walters, 1992) and in water, 350 μg/kg (Sigworth,1964). |
| History | In 1939, the Swiss chemist Paul Müller (1899–1965), working for the Geigy chemical company,discovered that the compound dichlorodiphenyltrichloroethane (DDT) was an effectiveinsecticide. DDT wasfirst synthesized in 1873 by an Austrian student, but it was Müller whodiscovered its efficacy as an insecticide. DDT was initially marketed in 1941 and found itsfirst widespread use during World War II. During World War I several million deaths, including150,000 soldiers, were attributed to typhus.there are several forms of typhus, but themost common form is due to bacteria carried by lice. During During World War II, fearing a repeatof World War I typhus outbreaks, the Allied forces used DDT to combat typhus in additionto malaria, yellow fever, and other diseases carried by insects. Soldiers liberally applied talcumpowder containing 10% DDT to clothes and bedding to kill lice. America and its Europeanallies were relatively free from typhus and other diseases, whereas the Germans, who didnot use DDT, had many more noncombat deaths resulting from infectious diseases. DDTsolutions were sprayed in areas of the Pacific theater to prevent malaria and yellow fever. Inaddition to its use in the war, DDT was used by civilians in tropical areas as a generic insecticideto prevent infectious diseases, especially malaria. Once the war ended, the use of DDT toadvance public health in tropical developing countries was expanded for use in agriculture indeveloped countries. Paul Müller was awarded the Nobel Prize in physiology or medicine in1948 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 usedindiscriminately. the United Nations’ Stockholm Treaty on persistent organic pollutants calls for the phaseout of DDT but recognizes its efficacy as a deterrent to vector-borne diseases such as malariaand typhus. According to the treaty, the continued use of DDT is discouraged, but until effectiveeconomical alternatives are found, DDT use will be continued in countries with high ratesof vector diseases. A number of developing countries still use DDT. It is applied primarilyin the interior of homes to prevent malaria. Currently DDT is produced only in India andChina, and current production volumes are unknown. |
| Uses | 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. |
| Uses | Use as an insecticide is now prohibited. |
| Uses | The primary use of DDT is as a vector control for eradication ofmalaria-bearing mosquitoes. Less persistent insecticides have replacedDDT for control of insects on crops and in forests. |
| Uses | 4,4'-Dichlorodiphenyltrichloroethane is a synthetic organochlorine insecticide. 4,4'-Dichlorodiphenyltrichloroethane functions by opening sodium ion channels in the insects’neurons, causing them to fire 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. |
| Uses | Contact insecticide. |
| Definition | 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. |
| General Description | Odorless colorless solid. Sinks in water. |
| Air & Water Reactions | Insoluble in water. |
| Reactivity Profile | 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. . |
| Health Hazard | 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. |
| Health Hazard | 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. |
| Health Hazard | 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. |
| Contact allergens | This insecticide was formerly reported as a sensitizer in farmers or agricultural workers. |
| Pharmacology | DDT is a nerve poison that affects thesodium channel of nerve membranes. It is a nonsystemicinsecticide with contact and stomach action.The most important reactions of DDT (1) are dehydrochlorinationto DDE (2) and reductive dechlorinationto DDD (3). These reactions occur abiotically, in vivo andin soils. The products resemble DDT in their recalcitrancetoward environmental degradation. The stability of DDTand its principal metabolites DDD and DDE, in combinationwith their lipid solubility and resistance to biologicaldegradation, resulted in their bioconcentration infish and other organisms exposed to extremely low levelsof these compounds in water. Although metabolismof DDT in mammals may proceed via DDD to give 4,4-dichlorodiphenylacetic acid (5), DDE is also formed andstored in fat. It may be slowly depleted by oxidative reactions,and ringhydroxylated derivativeshave been detectedin mammals and wildlife samples. Consumption of DDTresidues in wildlife and fish by predators resulted inadverse effects. |
| Safety Profile | 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. |
| Toxicology | 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. |
| Synthesis | DDT, 2,2-bis-(p-chloro-phenyl)-1,1,1-trichloroethane can be obtained by reactingone mol of chloral with two mols of chlorobenzene in the presence of sulfuric acid: All operations were carried out under a hood Fifteen and five-tenths grams (0.105 mol) of chloral was obtained by mixing the required amount of U. S. P. chloral hydrate with twice its weight d sulfuric acid, and distilling the chloral layer which readily separates. The chloral was dissolved in 22.5 Gm. (0.2 mol) of chlorobenzene (Eastman, Practical grade) and the solution was cooled to 5℃. under constant stirring. A temperature of from 5 to 10℃. was maintained, and to the solution, under constant stirring, were added dropwise twelve 1-cc. portions of chlorosulfonic acid (Eastman, Practical grade) at ten-minute intervals. The acid can be added safely with the use of a 5-cc. pipette. After about 8 cc. of the acid was added a solid began to separate, and within a few minutes the entire mixture became pasty. After the last portion of acid was added the stirring was continued for one hour at 10-15' C., and then for two hours at room temperature. At the end of this period the reaction mixture was mixed with chipped ice, and the crude DDT was filtered off with suction. The crude product was stirred into ten times its weight of boiling water to remove occluded acid. The product was again collected on a Biichner funnel, and washed with an equal weight of cold methanol or recrystallized once from a mixture of three parts of methanol and one part of diethyl ether. The washed product melted at 106-107℃. (uncorr.) and the recrystallized product melted at 107-108℃. (uncorr.). The yield of the purified compound was 65-70%.[1] |
| Potential Exposure | DDT is a low-cost broad-spectruminsecticide. However, following an extensive review ofhealth and environmental hazards of the use of DDT,United States Environmental Protection Agency decided toban further use of DDT in December 1972. This decisionwas based on several properties of DDT that had been wellevidenced: DDT and its metabolites are toxicants withlong-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 inconcentrated accumulation of DDT in the fat of wildlifeand humans which may be hazardous. |
| First aid | 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. |
| Carcinogenicity | Dichlorodiphenyltrichloroethane (DDT) is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in experimental animals. |
| Environmental Fate | 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 thefollowing 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 weirriand Polyporus versicolor was also demonstrated (Bumpus and Aust, 1987). Aerobacteraerogenes 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 ATCC30.010) degraded p,p′-DDT to p,p′-DDE, p,p′-DDD and dibenzophenone (Pollero anddePollero, 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′-dichlorobenzophenoneand the methyl ester of bis(p-chlorophenyl)acetic acid (Quirke et al., 1979). |
| Metabolic pathway | Upon UV irradiation with methyl oleate, DDT isextensively added to the carbon ? carbon double bondof methyloleate via radical mechanisms. Besideschlorinated stearic acids, several addition products areformed, offering new possibilities to produce boundresidues in plants. A mixture of hemin and excesscysteine (the hemin ? cysteine model system) is able todegrade DDT partially and the major degradationproducts are three water-soluble, non-toxic conjugatesof DDT metabolites with cysteine which lose two orthree of the five chlorine atoms of DDT. In thepresence of a designed 24-residue polypeptide orb-casein, two DDT-binding proteins, an additionalfourfold increase in the rate of DDT degradation isobserved. Although the concentrations of DDT andcysteine occurring in an organism would be expected to be lower than those in the experiments described,the formation of water-soluble conjugates of DDT withcysteine (and other amino acids) could also play a rolein metabolism and excretion of DDT in vivo. |
| Metabolism | DDT decomposed very slowly insunlight, and 93% was recovered unchanged from thesurface of an apple after 3 months. DDE decomposed morerapidly than DDT in sunlight.Other reports indicate that DDT was photolyzed underfield 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 underlaboratory conditions gave a variety of products thatarose from reactions of photolytically generated radicals. |
| Solubility in organics | 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 at24.0 °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) |
| Solubility in water | 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 at24.0 °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) |
| storage | 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
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