72-54-8Clc1ccc(C(c2ccc(Cl)cc2)C(Cl)Cl)cc1AHJKRLASYNVKDZ-UHFFFAOYSA-N72-54-8DTXSID4020373CHEMBL196590CHEBI:278411.385 (NTP, 1992) - Denser than water; will sink
Specific gravity: 1.476 at 20 °C (solid)
1.476 @ 20°C
Crystalline solid from petroleum ether
White solid
less than 1 mg/mL at 65.3 °F (NTP, 1992)
Solubility in water, 0.160 mg/L at 24 °C /99% purity/
Soluble in organic solvents; insoluble in water; not compatible with alkalies.
Slightly soluble in chloroform
In water, 0.09 mg/L at 25 °C
379 °F at 760 mmHg (NTP, 1992)
193 °C at 1 mm Hg
228 to 230 °F (NTP, 1992)
109-110 °C
109.5 °C
11 (NTP, 1992) - Heavier than air; will sink (Relative to Air)
11 (Air = 1)
This chemical does not meet GHS hazard criteria for 8.3% (1 of 12) of reports.
Danger
H301 (91.7%): Toxic if swallowed [Danger Acute toxicity, oral];H312 (91.7%): Harmful in contact with skin [Warning Acute toxicity, dermal];H351 (25%): Suspected of causing cancer [Warning Carcinogenicity];H400 (75%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard];H410 (75%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]
P203, P264, P270, P273, P280, P301+P316, P302+P352, P317, P318, P321, P330, P362+P364, P391, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 12 reports by companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.;Reported as not meeting GHS hazard criteria per 1 of 12 reports by companies.;There are 5 notifications provided by 11 of 12 reports by companies with hazard statement code(s).;Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.
Hazard Traits - Carcinogenicity; Neurotoxicity;Authoritative List - ATSDR Neurotoxicants; CWA 303(c); CWA 303(d); IRIS Carcinogens - B2; Prop 65;Report - regardless of intended function of ingredient in the product
Regulation (EC) No 178/2002 (amended)
Benzene, 1,1'-(2,2-dichloroethylidene)bis[4-chloro-: Does not have an individual approval but may be used under an appropriate group standard
The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)
... Following ... dosage of (60 mg/kg, iv), all of the isomers of TDE inhibited ACTH-induced steroid production in the dog, but the inhibition reached 50% of the control only 27 min after dosing with the m,p'-isomer compared with 87 min with the o,p'-isomer and 4-18 hr with the p,p'-isomer. There was marked temporal correlation between the percentage inhibition of adrenocorticotropic hormone (ACTH)-induced steroid production, the disruption of normal cellular structure of the fascicular and reticular zones of the adrenal cortex, and the severity of the damage to mitochondria in these zones caused by the three isomers.
In this study, we determined whether the DDT isomers p,p'-DDT [1,1,1,-trichloro-2,2-bis(p-chlorophenyl)ethane], o,p'-DDT [1,1,1-trichloro-2(p-chlorophenyl)-2-(o-chlorophenyl)ethane], and their metabolites p,p'-DDD [1,1-dichloro-2,2-bis(p-chlorophenyl)ethane], o,p'-DDD [1,1-dichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl)ethane], p,p'-DDE [1,1,-dichloro-2,2-bis(p-chlorophenyl)ethylene], o,p'-DDE [1,1-dichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl)ethylene], and p,p'-DDA [2,2-bis(p-chlorophenyl)acetic acid], could bind to and transcriptionally activate the human estrogen receptor (hER). Novel results from competitive binding assays showed that o,p'-DDD, o,p'-DDE, and p,p'-DDT, as well as the established environmental estrogen o,p'-DDT, were able to bind specifically to the hER with approximately 1000-fold weaker affinities for the hER than that of estradiol. In contrast, only o,p'-DDT, but not p,p'-DDT, bound to the rat estrogen receptor. Moreover, two yeast expression-reporter systems, constructed to test if the DDT isomers and metabolites could transcriptionally activate the hER, demonstrated that an o,p'-DDT metabolite could transactivate the hER or LexA-hER fusion protein with just a 140- to 300-fold weaker potency than that of estradiol. The DDT isomers and metabolites that bound the hER in vitro triggered estrogen receptor-mediated transcription of the lacZ reporter gene in the yeast systems. Furthermore, the DDT isomers and metabolites that transactivated the hER elicited an additive response when given together or with estradiol. The DDT isomers and metabolites that triggered transcription of the yeast expression-reporter systems also stimulated two estrogenic endpoints in estrogen-responsive MCF-7 cells: the induction of the progesterone receptor and the down-regulation of the hER. Thus, in MCF-7 cells and in yeast expression-reporter systems, certain DDT isomers and metabolites act directly as agonists and transactivate the hER at concentrations found in human
Using a combination of in vitro assays we have evaluated whether DDT metabolites can interact with the progesterone receptor pathway in yeast expressing human progesterone receptor (hPR) and in T47D human breast cancer cells which express endogenous hPR. In transactivation assays using both yeast and T47D cells, o,p'-DDT and the metabolites p,p'-DDT, o,p'-DDD, p,p'-DDD, o,p'-DDE, p,p'-DDE, p,p'-DDA, and DDOH inhibited progesterone-induced reporter gene activity in a dose-dependent manner. None of the DDT metabolites functioned as hPR agonists. Whole cell competition binding assays using T47D cells indicated that the inhibitory effects of DDT metabolites on progesterone-dependent activites may occur through both hPR-dependent and hPR-independent pathways. Our results and previous reports of DDT metabolites interacting with estrogen and androgen receptors suggests that this class of environmental chemicals may interact with numerous hormone receptor signaling pathways.
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1e-06 mmHg at 86 °F (NTP, 1992)
0.00000135 [mmHg]
1.35X10-6 mm Hg at 25 °C
Dichlorodiphenyldichloroethane appears as a colorless crystalline solid. Insoluble in water and sinks in water. Toxic by inhalation, skin absorption or ingestion. Used as a pesticide.
Colorless to white solid; [HSDB]
2196;2196;2203;2203;2208;2208;2200;2199;2245.5;2211.5;2221;2243.1;2215.1;2240;2209.3;2213;2200;2212;2217.7;2200
2272;2256.9;2229;2259.6;2241.6;2261.4;2246.7;2265.2;2255.4;2265.3;2269.9;2252;2262.4;2261.9;2252.9;2259.4;2250.3;2240.6;2255.1
3310
SYMPTOMS: Symptoms of exposure to this compound may include anorexia, nausea, vomiting, diarrhea, dermatitis, apathy from mild dulling of interest to profound psychotic depression, gynecomastia, hematuria, leukopenia, thrombocytopenia and lassitude. It may cause slight irritation of the skin and lethargy. Chronic exposure may cause atrophy of the adrenal cortex and liver damage.;ACUTE/CHRONIC HAZARDS: This compound is toxic by skin absorption. It may cause slight irritation of the skin. When heated to decomposition this compound emits toxic fumes of chlorides, carbon monoxide, carbon dioxide and hydrogen chloride gas. (NTP, 1992)
Toxicity is similar to that of DDT; [Merck Index # 3061]
The major hazards encountered in the use and handling of DDD stem from its toxicologic properties as an organochlorine pesticide. Toxic effects may be exerted from all routes of exposure (ie, ingestion, inhalation, or dermal contact) and range from irritation of the skin, eyes, nose and throat, and liver damage, to possibly death in extreme exposure cases (estimated fatal oral dose for humans: 5 g/kg of body weight). These effects may be protected against by the wearing of rubber gloves, goggles or face shield or a self-contained breathing apparatus. Protect from exposure, individuals with liver disease. In cases where contact with the odorless, colorless dust of DDD is unavoidable, contaminated clothing and shoes should be removed and the affected areas of the body flushed with water. DDD will not ignite easily, but it will burn with the potential to emit irritating or poisonous gases. For small fires involving DDD, extinguish with dry chemical, CO2, water spray, or foam, and for large fires, use water spray, fog, or foam. Runoff from fire control water may give off poisonous gases or cause water pollution and should, therefore, be diked for later disposal. DDD should be stored at ambient temperature in containers that bear the label, "Keep Away From Food". All modes of transport are acceptable for DDD (ie, air, road, rail, and water). Small spills of DDD should be carefully shovelled into a container (liquid DDD is first absorbed by a non-combustible material, like sand) for later disposal. Large land spills are diked or deposited in excavated pits, ponds, or other holding areas (dry spills are covered with plastic sheeting) for later disposal. Large spills on water first may need to be trapped at the bottom with sand bag barriers or treated by an application of activated charcoal, then removed by suction hose or mechanical dredge. Before permanent land disposal of DDD, consult with environmental regulatory agencies. In addition to land disposal, DDD is a potentia
WHO; Environ Health Criteria: DDT and its Derivatives (1979). EHC publications are monographs designed for scientists and administrators responsible for the establishment of safety standards and regulations and provide basic scientific risk evaluations of a wide range of chemicals and groups of chemicals.
USEPA; Ambient Water Quality Criteria Doc: DDT (1980) EPA 440/5-80-038
DHEW/NCI; Bioassay of DDT, TDE, and p,p'-DDE for Possible Carcinogenicity Technical Report Series No. 131 (1978) NIH Pub. 78-1386
DHHS/ATSDR; Toxicological Profile for DDT, DDE, and DDD (PB/2002/100137) (September 2002). The ATSDR toxicological profile identifies and reviews the key literature that describes a hazardous substance's toxicologic properties. Other pertinent literature is also presentedin less detail.
For more Special Reports (Complete) data for DDD (6 total), please visit the HSDB record page.
U060; As stipulated in 40 CFR 261.33, when DDD, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).
Cancellations issued prior to Rebuttable Presumption Against Registration/Special Review Process. Pesticide and review criteria possibly met or exceeded: carcinogenicity, bio-accumulation, hazard to wildlife and other chronic effects.
Cancelled, all products containing DDD, a metabolite of DDT. Criteria of concern: Carcinogenicity, bioaccumulation, and hazard to wildlife and other chronic effects. (PR Notice 71-5 (3/18/71)).
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.;SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment.;INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.;INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)
Storage temperature: ambient
PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/
... Store in a cool, dry place. Where possible, automatically transfer material from drums or other storage containers to process containers. Sources of ignition such as smoking and open flames are prohibited where this chemical is handled, used, or stored. Metal containers involving the transfer of this chemical should be grounded and bonded. Wherever this chemical is used, handled, manufactured, or stored, use explosion-proof electrical equipment and fittings.
SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a POTW is acceptable only after review by the governing authority. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must meet Hazardous Material Criteria for disposal.
For land spill: Dig a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water.
For water spill: Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. If dissolved, apply activated carbon at ten times the spilled amount in region of 10 ppm or greater concentration. Remove trapped material with suction hoses. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.
The applicability of carbon to remove toxicants on EPA's published list and fish kill due to influent and effluent from five industrial plants currently using adsorption as a treatment method are examined. In the laboratory, activated carbon can achieve levels of less than 1 mg/l of aldrin, dieldrin, endrin, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethene, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane, toxaphene, and Aroclor 1254. In operating plants, the toxicity of wastes to fish due to unknown constituents is significantly reduced or totally removed by activated carbon treatment.
For more Cleanup Methods (Complete) data for DDD (6 total), please visit the HSDB record page.
SMALL SPILLS AND LEAKAGE: If a spill of this chemical occurs, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with acetone and transfer the dampened material to a suitable container. Use absorbent paper dampened with acetone to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.;STORAGE PRECAUTIONS: You should store this chemical under ambient temperatures, and keep it away from oxidizing materials. (NTP, 1992)
Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U060, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
DDD is a potential candidate for incineration by rotary kiln with a temperature range of 820-1600 °C and a residence time of seconds for liquid or gas and hours for solid. /SRP: Control acid mist from exhaust gases./
Group I Containers: Combustible containers from organic or metallo-organic pesticides (except organic mercury, lead, cadmium, or arsenic compounds) should be disposed of in pesticide incinerators or in specified landfill sites. /Organic or metallo-organic pesticides/
Group II Containers: Noncombustible containers from organic or metallo-organic pesticides (except organic mercury, lead, cadmium, or arsenic compounds) must first be triple-rinsed. Containers that are in good condition may be returned to the manufacturer or formulator of the pesticide product, or to a drum reconditioner for reuse with the same type of pesticide product, if such reuse is legal under Department of Transportation regulations (eg 49 CFR 173.28). Containers that are not to be reused should be punctured ... and transported to a scrap metal facility for recycling, disposal, or burial in a designated landfill. /Organic or metallo-organic pesticides/
For more Disposal Methods (Complete) data for DDD (10 total), please visit the HSDB record page.
SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.
SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.
Stop discharge if possible. Keep people away. Avoid contact with solid and dust. Isolate and remove dischaged material. Notify local health and pollution control agencies.
Remove contaminated clothing and shoes. Flush affected areas /of body/ with plenty of water.
For more Preventive Measures (Complete) data for DDD (13 total), please visit the HSDB record page.
Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:;IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.;SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.;FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)
0.80 [mg/m3]
83 [mg/m3]
500 [mg/m3]
Dust mask; goggles or face shield; rubber gloves (USCG, 1999)
Wear goggles, or face shield, dust mask, rubber gloves, or self contained breathing apparatus.
PRECAUTIONS FOR "CARCINOGENS": ... dispensers of liq detergent /should be available./ ... Safety pipettes should be used for all pipetting. ... In animal laboratory, personnel should ... wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. ... gowns ... /should be/ of distinctive color, this is a reminder that they are not to be worn outside the laboratory. /Chemical Carcinogens/
DDD was detected in 84% of 37 human female adipose tissue samples taken from ethnic Chinese residents of Hong Kong between June 1999 and July 2000, with a mean (range) concn of 45 (0-27) ng/g fat(1). Thirty-two samples were taken and analyzed in a study conducted from 2002-2003 in Chiba and Yamanashi, Japan, where DDD was detected in maternal serum at a mean concn (standard deviation) of 766 pg/g lipid (982), ranging from no detection to 3,800 pg/g lipid; in the umbilical cord it had a detection rate of 15% with a mean concn of 215 pg/g lipid (527) and a maximum concn of 1600 pg/g lipid(2); DDD was not detected in any samples of umbilical cord serum. DDD was detected in the blood serum of residents of Nainital, India at a mean concn of 0.91 mg/L with a range of no detection to 2.82 mg/L(3).
DDD was detected in whole mothers milk at an avg concn of 17 ppb (rural India) and 8.4 (suburban India)(1). DDD was detected in US human blood at concns of 5.7-44.8 ppb (males) and <0.1-15.0 ppb (females)(2). DDD was detected in 5 out of 65 human blood samples in females residing in Veracruz, Mexico during 1998 at a mean concn of 0.3 ng/mL(3).
Residues in Canadian human milk avg 4 ng/g whole milk (1967) and avg 3 ng/g whole milk (1970).
Human adipose storage decreases in the order DDE > p,p'-DDT > DDD.
... At a dosage of 50 mg/kg/day for 14 days, o,p'-DDD caused a gradually progressive hypotensive failure in dogs injected with epinepherine or norepinepherine, while leaving unchanged the cardioaccelerator and immediate pressor response of these drugs. The hypotensive failure was associated with weakening of the contractile force of the heart and with a reduction in plasma volume. The latter may have been caused by loss of fluid from the intravascular compartment and was not caused by release of histamine. The hypotensive state could be prevented to a significant degree by pretreatment with prednisolone.
If cortisol is taken ... DDD ... increased the formation of hydroxylated metabolites, and cause changes in patterns of excretion from glucuronides to other conjugates. ... With testosterone, DDD again gives rise to increased formation of hydroxylated metabolites ...
DDT has been shown to cause mild anemia. Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted. (T10)
LC50; Species: Colinus virginianus (Bobwhite quail, 23 days old) oral 5-day diet ad libitum 2178 ppm for 5 days (95% confidence limit 1835-2584 ppm) /Technical grade, purity >95%/
LC50; Species: Coturnix japonica (Japanese quail, 7 days old) oral ad libitum 3165 ppm for 5 days (95% confidence limit 2534-3978 ppm) /Technical grade, purity >95%/
LC50; Species: Coturnix japonica (Japanese quail) oral ad libitum 2,636 ppm for 5 days (95% confidence limit: 2,225-3,122 ppm) /Technical grade, 100% AI/
LC50; Species: Phasianus colchicus (Ring-necked pheasant, 10 days old) oral ad libitum 445 ppm for 5 days (95% confidence level 402-494 ppm) /Technical grade, purity >95%/
For more Ecotoxicity Values (Complete) data for DDD (35 total), please visit the HSDB record page.
TERRESTRIAL FATE: Based on a classification scheme(1), measured Koc values ranging from 130,600(2) and 131,800(3), indicate that DDD is expected to be immobile in soil(SRC). Volatilization of DDD from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 6.60X10-6 atm-cu m/mole(4). However, adsorption to soil is expected to attenuate volatilization(SRC). DDD is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.35x10-6 mm Hg at 25 °C(5). DDD was described as persistent in Nixon sandy loam soil(6), and a half-life in anaerobic soil microcosms was reported as 160 days(7). Based on these data, biodegradation is not an important environmental fate process in soil(SRC).
AQUATIC FATE: Based on a classification scheme(1), measured Koc values ranging from 130,600(2) and 131,800(3), indicate that DDD is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(4) based upon a Henry's Law constant of 6.6X10-6 atm-cu m/mole(5). Estimated volatilization half-lives for a model river and model lake are 10 days and 79 days, respectively(4). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 134 years if adsorption is considered(6). According to a classification scheme(7), BCF values ranging from of 2,710(8) to 51,000(9), suggests that bioconcentration in aquatic organisms is very high(SRC). 100% of the original DDD (initial concn = 10 ug/L) in river water remained after 8 weeks in a sealed glass jar under sunlight and artificial fluorescent light(8), indicating that DDD is not susceptible to direct photolysis in sunlight(SRC). No degradation of DDD was observed in aerobic ocean sediments(10), domestic wastewater inoculum(11), and raw stream water(12), indicating that biodegradation is not an important environmental fate process in aquatic environments(SRC).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), DDD, which has a vapor pressure of 1.35X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase DDD is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 7.4 days(SRC), calculated from its rate constant of 4.3X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase DDD may be removed from the air by wet or dry deposition(SRC). 100% of the original DDD (initial concentration = 10 ug/L) in river water remained after 8 weeks in a sealed glass jar under sunlight and artificial fluorescent light(4), indicating that DDD is not susceptible to direct photolysis in sunlight(SRC).
DDD was identified, not quantified, in food products from the US at the following rates of detection: 42 out of 216 (1964-65); 80 out of 312 (1965-66); 104 out of 360 (1966-67); 113 out of 360 (1967-68); and 101 out of 360 (1968-69)(1). DDD was identified, not quantified, in food composites in the US at the following rates of detection: 90 out of 360 (1971); 157 of 420 (1972); 48 of 360 (1973); 37 of 360 (1974); 9 of 240 (1975); and 7 of 240 (1976)(2). From Aug 1976 to Sept 1977, DDD was detected in 6 of 300 adult total diet composites at concns ranging from 2-11 ppb(3); from Oct 1977-Sept 1978, DDD was detected in 3 of 240 adult total diet composites at 2-7 ppb(4). DDD was detected in the following foods (mean concn, ppm): 31 of 780 domestic cheese samples (0.001); 624 of 5,471 imported cheese samples (0.018); 32 of 2,303 eggs (0.005); 75 of 3,281 domestic large fruits (0.003); and in 28 of 1,048 imported large fruits (0.004)(2). DDD was detected in 9 out of 14 alfalfa samples from Mexico at a max concn of 0.05 ug/g(8).
DDD was identified at mean concns in the following food items: 0.0060 ppm, 1 pan-cooked pork chop; 0.0016 ppm, 5 pan-cooked pork sausages; 0.0004 ppm, 1 pan-cooked pork bacon; 0.0004 ppm, 1 pan-cooked lamb chop; 0.0022 ppm, 12 boiled fresh/frozen spinach; 0.0022 ppm, 3 boiled fresh/frozen collards; 0.0008 ppm, 3 raw celery sticks; 0.0010 ppm, 1 boiled fresh/frozen summer squash; 0.0006 ppm, 2 raw radishes; 0.0004 ppm, 1 heated frozen french fries; 0.0003 ppm, 1 white potato baked with skin; 0.0009 ppm, 1 commercial chocolate chip cookie; 0.0011 ppm, 14 plain milk chocolate candy bars; 0.0004 ppm, 1 boiled shrimp; 0.0006 ppm, 3 boiled fresh/frozen turnips; 0.0010 ppm, 1 boiled frozen mixed vegetables sample; 0.0005 ppm, 1 sweet cucumber pickles; 0.0002 ppm, 2 yellow mustard samples; 0.0010 ppm, 2 olive/safflower oil samples; 0.0030 ppm, 12 baked fresh or frozen salmon steaks or filets; 0.0002 ppm, 1 strained/junior squash(1).
Between 1970-1973, overall residue levels of DDD in all classes of food decreased 89%.
ENVIRONMENTAL: From 1970 to 1976, DDD was detected in 255 of 4,638 whole milk samples from the US at an avg concn of 0.003 ppm(1). From 1964 to 1969, DDD was detected in 2,143 of 12,989 domestic milk samples at an avg concn of 0.02 ppm(2). DDD was identified, not quantified, in 2,114 out of 31,548 samples of milk in the US during 1961-62(3). p,p'-DDD was detected in 49 of 59 milk samples from Alberta, Canada, (1966-70) at an avg concn of 0.151 ppm and in 16 of 33 samples (1977-78), at an avg concn of 0.023 ppm(4).
ENVIRONMENTAL: Whole mothers milk, avg ppb/samples, rural, 17.0/13, urban, 8.4/12(1). Residues in Canadian human milk avg 4 ng/g whole milk (1967) and avg 3 ng/g whole milk (1970).
DDD toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDD reduces potassium transport across the membrane. DDD inhibits the inactivation of voltaged-gated sodium channels. The channels activate (open) normally but are inactivated (closed) slowly, thus interfering with the active transport of sodium out of the nerve axon during repolarization and resulting in a state of hyperexcitability. DDD inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDD also inhibits the ability of calmodulin, a calcium mediator in nerves, to transport calcium ions that are essential for the release of neurotransmitters. All these inhibited functions reduce the rate of depolarization and increase the sensitivity of neurons to small stimuli that would not elicit a response in a fully depolarized neuron. DDD is also believed to adversely affect the reproductive system by mimicking endogenous hormones and binding to the estrogen and adrogen receptors. (T10, L85)
Hazard Traits - Carcinogenicity; Neurotoxicity;Authoritative List - ATSDR Neurotoxicants; CWA 303(c); CWA 303(d); IRIS Carcinogens - B2; Prop 65;Report - regardless of intended function of ingredient in the product
Regulation (EC) No 178/2002 (amended)
Benzene, 1,1'-(2,2-dichloroethylidene)bis[4-chloro-: Does not have an individual approval but may be used under an appropriate group standard
The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)
U060; As stipulated in 40 CFR 261.33, when DDD, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).
Cancellations issued prior to Rebuttable Presumption Against Registration/Special Review Process. Pesticide and review criteria possibly met or exceeded: carcinogenicity, bio-accumulation, hazard to wildlife and other chronic effects.
Cancelled, all products containing DDD, a metabolite of DDT. Criteria of concern: Carcinogenicity, bioaccumulation, and hazard to wildlife and other chronic effects. (PR Notice 71-5 (3/18/71)).
Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1 lb or 0.454 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).
Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /DDT and metabolites/
DDD is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.
(MN) MINNESOTA 1 ug/L
(FL) FLORIDA 0.1 ug/L
The mechanisms of action of o,p'-DDD on adrenal steroidogenesis were investigated in vitro in rainbow trout (Oncorhynchus mykiss). Acute exposures to o,p'-DDD inhibited ACTH-stimulated cortisol secretion while cell viability decreased significantly only at the highest concentration tested (200 microM o,p'-DDD). Stimulation of cortisol secretion with a cAMP analogue (dibutyryl-cAMP) was inhibited at a higher concentration than that needed to inhibit ACTH-stimulated cortisol synthesis in cells exposed to o,p'-DDD. Forskolin-stimulated cortisol secretion and cAMP production, and NaF-stimulated cAMP production were inhibited in a concentration-dependent manner by o,p'-DDD. In contrast, basal cortisol secretion was stimulated while basal cAMP production was unaffected by o,p'-DDD. Pregnenolone-stimulated cortisol secretion was enhanced by o,p'-DDD at a physiologically relevant pregnenolone concentration, while o,p'-DDD inhibited cortisol secretion when a pharmacological concentration of pregnenolone was used. /These/ results suggest that the cAMP generation step is a target in o,p'-DDD-mediated disruption of ACTH-stimulated adrenal steroidogenesis in rainbow trout but that other downstream targets such as steroidogenic enzymes responsible for cortisol synthesis might also be affected.
In pigeons (Columba liva) ... feeding of DDD ... /gave/ rise to small residues of DDE. The DDD was rapidly metabolized exclusively to 2,2-bis(p-chlorophenyl-1-chloroethylene.
... DDD ... in peanut oil ... was injected into fertile leghorn eggs or fed in the diet to chicks hatched from untreated eggs. No significant differences ... between two treatments were observed. ... p,p'-DDD gave rise to o,p'-DDD, 2,2-bis(p-chlorophenyl)-1-chloroethylene (DDMU), 2,2-bis(p-chlorophenyl)-1-chloroethane (DDMS), 2,2-bis(p-chlorophenyl)ethylene (DDNU), 2,2-bis(p-chlorophenyl)ethanol (DDOH), bis(p-chlorophenyl)-acetic acid (DDA), DDM, and dichlorobenzophenone (DBP).
The mexican bean beetle, Epilachna varivestis muls, contained DDT-dehydrochlorinase activity in its tissues and was able to dehydrochlorinate DDD.
After ingestion of ... DDD by adult volunteers, bis(p-chlorophenyl)-acetic acid (DDA) was excreted in urine ... DDD readily degrades ... through a series of intermediates to DDA and is rarely found as a stored metabolite in the general population.
For more Metabolism/Metabolites (Complete) data for DDD (15 total), please visit the HSDB record page.
DDD is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDD occurs mainly via cytochrome P-450 enzymes in the liver and kidney. Its metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), are excreted in the urine. (L85)
In chronic feeding experiments DDD, like DDT, is stored in body fat, but it is mobilized and excreted faster than DDT when a normal diet is resumed.
Sheep were orally dosed for 28 consecutive days with ... DDD ... DDE appeared as a metabolite of DDD ... in fat. ... DDD showed 2 maxima /in blood; one occurring/ at 8 hr and /the other at/ 32 hr after dosing.
Tetrachlorodiphenyl ethane (p,p-DDD) ... was found in urine of New Zealand red rabbits ... exposed to cigarette smoke containing labeled TDE. In fat, vital organs, and other tissues, tetrachlorodiphenyl ethane and TDEE were found.
DDD was quantified in specimens of maternal blood, placenta, and umbilical cord blood from women experiencing stillbirth and live birth. Specimens of stillbirth cases had higher organochlorine insecticide contents as compared to matched controls.
For more Absorption, Distribution and Excretion (Complete) data for DDD (15 total), please visit the HSDB record page.
Used as an insecticide in the U.S. in the past; [HSDB]
For DDD (USEPA/OPP PC Code: 029101) there are 0 label matches. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./
Cancelled, all products containing DDD, a metabolite of DDT. Criteria of concern: Carcinogenicity, bioaccumulation, and hazard to wildlife and other chronic effects. (PR Notice 71-5 (3/18/71)).
Insecticide /Former US/
Dusts, emulsions, and wettable powders for contact control of leaf rollers and other insects /Former use/
... Does not have the broad-spectrum insecticidal activity of DDT but has equal or greater potency against larvae of some mosquitoes and lepidoptera.
(1977) Not produced commercially in US
(1972) Probably greater than 4.54x10+5 g
(1973) Probably greater than 4.54x10+5 g
Prepared by condensing dichloroacetaldehyde with chlorobenzene
Ethanol may be chlorinated to give 2,2-dichlorovinylethyl ether. ... This is the condensed with 2 mols of chlorobenzene to give TDE.
Chlorination of ethanol and condensation of chlorobenzene.
The commercial preparation of TDE from the ethyl acetal of dichloroacetaldehyde and chlorobenzene usually gives a technical product consisting mainly of the para,para'-isomer, with 7-8% of the ortho,para'-isomer.
TDE is avail as technical grade product containing mostly p,p'-TDE, with setting-point not less than 86 °C. ... TDE is also formulated into WP, EC, and dusts.
The technical product consists largely of the p,p'-isomer & 7-8% of the o,p'-isomer.
Grade: Technical
The WHO Recommended Classification of Pesticides by Hazard identifies DDD as an active ingredient believed to be obsolete or discontinued for use as a pesticide.
Cancellation issued prior to RPAR/Special Review Process
DDD use in the USA has been banned since the early 1970's.
Formulators' trade name: Rothane (Rohm and Haas Co.)
A component of technical grade DDT