1-chloro-4-[2,2-dichloro-1-(4-chlorophenyl)ethenyl]benzene

Pesticide Ecotoxicity Data from EPA: 3

ATMOSPHERIC FATE: A photolysis half-life of 0.9 days in summer and 6.1 days in winter by direct sunlight at 40 deg latitude was observed.

... DDE in sediment remained in the top 1.5 cm layer and did not move into lower sediment layers.

PURE CULTURE: Under aerobic conditions, the ring cleavage of DDT by Alcaligenes eutrophus A5 and of DDE by biphenyl grown cells of Psudomonas acidovorans M3GY occur via pathways similar to those for biphenyl degradation. Under anaerobic conditions, DDE was reductively dechlorinated to DDMU [1-chloro-2,2-bis-(p-chlorophenyl)ethene] in marine sediment slurries(1).

There have been but a few studies on the alteration of pesticide toxicity in saline waters. ... /It has been/ reported that young mosquitofish accum significantly lesser amounts of DDT, DDE, and DDD in 15% saline waters than in freshwater.

... DDE volatilized from distilled water and natural water solutions five times faster than DDT under identical conditions.

When DDT and DDE in pyrex tubes were exposed to UV-irradiation (lambda greater than 290 nm) as solids in an oxygen stream, mineralization products (carbon dioxide and hydrogen chloride) were observed in small amt after 7 days. DDE yielded dichlorobenzophenone and trichlorobenzophenone.

... The amount of insecticide in restaurant meals in Wenatchee, Washington, USA indicated an average intake of ... 0.102 mg/man per day of DDE (1954). Most of the DDT was in food of animal origin, and persons who abstained from eating meat but obtained the food they ate from regular, commercial sources received an average of only ... 0.027 mg/man per day of DDE.

In aquatic vascular plants in Lake Paijanne, Finland: mean: 2 ug/kg dry weight (1972-1973).

DDE was detected in 14 out of 45 effluent samples at a median concn of 0.010 ppb(1). DDE was detected in wastewater from foundries (5-20 ppb), metal finishing plants (10-53 ppb) and aluminum forming facilities (<0.01-7 ppb)(2). DDE was detected in agricultural drainage systems in northwest Mexico at concns of 0.006-1.266 ug/L(3). From 2002-2003, DDE was detected in 24 of 36 crop soils, 15 of 36 ditch sediments, and 10 of 36 water samples flowing from farm areas to salmon streams of the Fraser River in British Columbia, Canada, at mean concns (ranges) of 0.22 (<0.02-0.71) mg/kg dry weight, 0.14 (<0.02-0.40) mg/kg dry weight, and 0.04 (<0.01-0.14) ug/L, respectively(4).

RURAL REMOTE: In marine atmosphere in the Northwest Gulf of Mexico, March-April 1977: avg: 0.049 ng/cu m; range: 0.009-0.180 ng/cu m. Atmospheric levels in agricultural areas: not detected-14.2 ng/cu m.

In nature, DDE and not DDD constitutes the major component of the sum of DDT ... /and it has been/ reported /that/ DDE is the principal constituent of the sum of DDT in Great Lakes fish; therefore, uptake through food alone cannot explain the increase in the sum of DDT levels of Great Lakes fish. If the uptake of residues is through water, then given an environment with a stable contaminant situation, the fat in all species should accumulate a given pesticide or chemical approx to the same level, depending on the water solubility and partitioning of that chemical into the lipid phase. Such a situation, if observed in nature, would support the conclusion that accumulation is mainly through water.

DDE, (2,2-bis(p-chlorophenyl)-1,1-dichloroethene) is an impurity and a degradation product of the formerly manufactured and used pesticide DDT, (2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane)(1); therefore, DDE has been directly released to the environment as a result of the use of DDT as an insecticide(SRC). The use of DDT in the US has been banned since 1972(2).

SOILS: DDE was detected in soil samples from 5 US cities in 1971 at concns of 0.01-7.86 ppm(1). DDE was detected in soil samples from 8 US cities at avg concns of 0.11-52.73 ppm(2). DDE was detected in soils from India at concns of 0.020-0.024 ug/g in 1992-1994(3). p,p'-DDE and o,p'-DDE were detected in soils from 37 states around the US at concns of 0.01-7.16 and 0.01-0.09 ppm, respectively in 1971(4). DDE was detected in soil samples in Ontario, Canada apple orchards from 1972-75 at the following concns: 0.78-33.3 ppm (0-15 cm); 0.24-5.5 ppm (15-30 cm)(5). DDE was detected in soil samples in Ontario, Canada sour cherry orchards from 1972-75 at the following concns: 0.02-2.13 ppm 0-15 cm); 0.02-0.90 ppm (15-30 cm)(5). DDE was detected in the Rhizosphere and bulk soils from 2 sites in T...

Tissue storages of DDE in the general population originate almost entirely from dietary DDE rather than DDT conversion.

The concn of p,p'-DDE in cigarettes manufactured between 1961 and 1979 and between 1983 and 1994 were 58-959 ng/g and 6.6-15.8 ng/g(1).

DDE, (2,2-bis(p-chlorophenyl)-1,1-dichloroethene) is an impurity and a degradation product of the formerly manufactured and used pesticide DDT, (2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane); therefore, DDE has been directly released to the environment as a result of the use of DDT as an insecticide. If released to air, a vapor pressure of 6X10-6 mm Hg at 25 °C indicates DDE will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase DDE will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 2 days. Particulate-phase DDE will be removed from the atmosphere by wet and dry deposition. DDE may undergo direct photolysis in the environment since it absorbs light greater...

Acute signs of DDT poisoning include paresthesia after oral ingestion. Studies have shown that a mammal poisoned with DDT-type agents displays periodic persistent tremoring and/or convulsive seizures that are suggestive of repetitive discharges in neurons. These repetitive tremors and seizures can be initiated by tactile and auditory stimuli. (T10)

Treatment of DDT exposure should be primarily directed towards decontamination and supportive care, as there is no specific antidote. The use of gastric lavage and activated charcoal for large ingestions may be effective. (L140)

Hepatic

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)

IARC Carcinogen - Class 3: Chemicals are not classifiable by the International Agency for Research on Cancer.

Oral (L85)

DDE toxicity occurs via at least four mechanisms, possibly all functioning simultaneously. DDE reduces potassium transport across the membrane. DDE 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. DDE inhibits neuronal adenosine triphosphatases (ATPases), particularly Na+K+-ATPase, and Ca2+-ATPase which play vital roles in neuronal repolarization. DDE 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 depolariz...

The AVDI of DDE in the US in units of mg/kg body weight was reported as follows: 0.0003 (1964-1965); 0.0003 (1965-1966); 0.0002 (1966-1967); 0.0002 (1967-1968); 0.0002 (1968-1969)(1). The AVDI of DDE for the US population from 1979-1980 was reported as 2.14 ug, with the majority of intake due to consumption of dairy products and meat, poultry and fish(2).

Oral Slope Factor Reference: IRIS Current

0.005 MG/KG (FAO/WHO, 1973) /FROM TABLE/

Not directly listed by IARC, but carcinogenicity studies of this DDT metabolite are discussed in connection with DDT (L2151).

LD50 Mouse oral 700 mg/kg

... Individuals with /diseases/ of the nervous system, liver, or blood /should be protected from exposure to/ organochlorine pesticides. /Organochlorine pesticides/

Fraction of Contaminant Absorbed in Gastrointestinal Tract: 1

Classification of carcinogenicity: 1) evidence in humans: inadequate; 2) evidence in animals: sufficient. Overall summary evaluation of carcinogenic risk to humans is Group 2B: The agent is possibly carcinogenic to humans. / Based on former classification system. /From table/

Fraction of Contaminant Absorbed in Gastrointestinal Tract: 1

Reference: Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP