50-29-3 Usage
History
Different sources of media describe the History of 50-29-3 differently. You can refer to the following data:
1. 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.
2. 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.
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 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.
Chemical Properties
Different sources of media describe the Chemical Properties of 50-29-3 differently. You can refer to the following data:
1. 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.
2. 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
3. DDT is a waxy solid or slightly off-white
powder of indefinite melting point with a weak, chemical
odor.
Physical properties
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).
Uses
Different sources of media describe the Uses of 50-29-3 differently. You can refer to the following data:
1. 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.
2. Use as an insecticide is now prohibited.
3. 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.
4. 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.
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
Different sources of media describe the Health Hazard of 50-29-3 differently. You can refer to the following data:
1. 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.
2. 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.
3. 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 U061Tebourbi 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.
Contact allergens
This insecticide was formerly reported as a sensitizer in farmers or agricultural workers.
Pharmacology
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.
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.
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.
Potential Exposure
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.
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 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)
eMineralization 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-chloroUnder 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).
Metabolic pathway
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.
Metabolism
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.
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 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)
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 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)
Purification Methods
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.
Toxicity evaluation
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.
Degradation
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).
Incompatibilities
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
Waste Disposal
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.
Check Digit Verification of cas no
The CAS Registry Mumber 50-29-3 includes 5 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 2 digits, 5 and 0 respectively; the second part has 2 digits, 2 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 50-29:
(4*5)+(3*0)+(2*2)+(1*9)=33
33 % 10 = 3
So 50-29-3 is a valid CAS Registry Number.
InChI:InChI=1/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
