DDT

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.

MOLECULAR FORMULA

C14-H9-Cl5

ERG GUIDE NUMBER

151-SUBSTANCES - TOXIC (NON-COMBUSTIBLE)

SYNONYM REFERENCE

(Budavari, 1996; HSDB , 1999; Lewis, 1996; RTECS , 1999)

USES/FORMS/SOURCES

USES

Introduced in 1945, DDT was primarily used as a low-cost, broad-spectrum insecticide used in the tobacco and cotton industries. It was also an effective pesticide for tussock moths (Lewis, 1993; (Sittig, 1991). DDT was banned by the U.S. Environmental Protection Agency in December, 1972 due its long-term persistence in soil and water; its ability to be widely dispersed by erosion, runoff, and volatilization; its low-water solubility and high lipophilicity (resulting in accumulation in the fat of wildlife and humans); and its ability to induce eggshell thinning in predatory birds; its long-term per (Lewis, 1998; Sittig, 1991).
Until its ban in 1972, DDT was one of the most widely-used agricultural insecticides in the United States (registered for 334 agricultural commodities at its height) and around the world (HSDB , 1999). This compound is no longer allowed to be used in the U.S., except in public health emergencies. DDT is still produced in the U.S. for export for use in other countries (Lewis, 1993). DDT is still used extensively in tropical regions to control malaria because the use of a substitute such as malathion would be too expensive (Clayton & Clayton, 1994).
Primary uses included: control of malaria, typhus, some forest defoliators, spruce budworm, black headed budworm, hemlock looper, gypsy moth, pine tent caterpillar, douglas-fir tussock, pine tussock moth, pine butterfly, elm spanworm, sawflies; controlling mosquito larvae & adults, flies, body lice, bedbugs, and fleas, pests of livestock, farm crops, forest & shade trees, and stored products (HSDB , 1999).
Resistance is common among many insect species. This resistance is attributable to selection of naturally occurring genotypes that possess enhanced amount of enzyme DDT'ase which will detoxify DDT to inactive DDE (HSDB , 1999).
DDT can be used as a wettable powder, suspension, emulsion, or in solvent or aerosol form (OHM/TADS , 1999).

SOURCES

"DDT is a polychlorinated, lipophilic, environmentally persistent contact pesticide, larvicide, ectoparasiticide, and topical pediculicide that is toxic to many vertebrate animals. The p,p'-isomer is weakly estrogenic and has the greatest toxicity in insects; the o,p'-isomer is less toxic and more estrogenic" (Lewis, 1998).
DDT is derived by condensing chloral or chloral hydrate with chlorobenzene in the presence of sulfuric acid (Lewis, 1993).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

Human poisoning may occur by ingestion or by absorption through the skin or respiratory tract. The onset of symptoms usually occurs 2 or 3 hours after ingestion, and is characterized by paresthesias of the tongue, lips, and face. Patients soon develop tremor, a sense of apprehension, dizziness, confusion, malaise, headache, and fatigue.

Signs and symptoms of severe poisoning may include tonic and clonic seizures, cardiac or respiratory failure, and death.

Chronic exposure may cause liver damage, CNS degeneration, agranulocytosis, dermatitis, muscle weakness, seizures, coma, and death.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
Avoid any skin contact.
Effects of contact or inhalation may be delayed.
Fire may produce irritating, corrosive and/or toxic gases.
Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

ACUTE CLINICAL EFFECTS

DDT effects the central nervous system (CNS), causing both stimulation (seizures) and depression (coma) (Hathaway et al, 1996) HSDB, 1998). Ingestion of overdose amounts can cause paresthesias of the tongue and lips, tremors, confusion, anxiety, dizziness, malaise, headache, and seizures (Hathaway et al, 1996) HSDB, 1998). Coma, respiratory depression, vomiting, and diarrhea may occur (Baselt & Cravey, 1995; (Hathaway et al, 1996) Morgan, 1993; HSDB, 1998).

In severe poisonings, an irregular, slow pulse may be noted (HSDB, 1998). Noncardiogenic pulmonary edema is generally associated with pulmonary aspiration of the solvent vehicle (HSDB, 1998). Fatalities are generally only associated with ingestion and are due to respiratory arrest (HSDB, 1998).

Residual weakness of the hands has been reported in a few persons with acute DDT poisoning (Hathaway et al, 1996). Weakness, paralysis, or ataxia may persist for weeks following acute poisoning in some persons (HSDB, 1998).

Hepatotoxicity has been mentioned in only a few reported cases of acute DDT poisoning. Three men who ate DDT-contaminated pancakes developed jaundice 4 to 5 days later which persisted for 3 to 4 days (HSDB, 1998).

Exposure to high concentrations of DDT dust may cause eye and skin irritation (Hathaway et al, 1996). Dermal exposure has usually not resulted in irritation or systemic poisoning in humans (HSDB, 1998). DDT has generally not caused eye irritation, although direct contact with dust or powder may result in conjunctivitis (HSDB, 1998).

Focal and centrilobular necrosis of the liver has been noted in experimental animals fed large doses (Hathaway et al, 1996).

DDT is often formulated in organic solvents. Pulmonary aspiration of such solvents can result in potentially fatal lipoid pneumonitis (HSDB, 1998).

CHRONIC CLINICAL EFFECTS

Chronic DDT absorption results in fat storage of the compound and its metabolites (Hathaway et al, 1996). The long-term health implications of this in humans are unknown.

Rare cases of peripheral polyneuropathy and hypersensitivity dermatitis have been associated with chronic occupational DDT exposure (HSDB, 1998). The polyneuropathy is manifested by numbness, paresthesias, and asymmetrical weakness or paralysis, usually with spontaneous resolution if exposure ceases (HSDB, 1998). Other ingredients in commercial preparations may be responsible for these effects (HSDB, 1998).

Hepatotoxicity has NOT been found in workers with long-term chronic DDT exposure (HSDB, 1998; (Hathaway et al, 1996).

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance;give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet.
Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

FIRST AID

EYE EXPOSURE - Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Contact lenses should not be worn when working with this chemical.
DERMAL EXPOSURE - Promptly wash the contaminated skin with soap and water. If this chemical penetrates the clothing, promptly remove the clothing and wash the skin with soap and water. Get medical attention promptly.
INHALATION EXPOSURE - Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration . Keep the affected person warm and at rest. Get medical attention as soon as possible.
ORAL EXPOSURE - If this chemical has been swallowed, get medical attention immediately.
TARGET ORGANS - Eyes, skin, CNS, kidneys, liver, and peripheral nervous system [in animals: liver, lung and lymphatic tumors] (National Institute for Occupational Safety and Health, 2007).

GENERAL -

Move victims of inhalation exposure from the toxic environment and administer 100% humidified supplemental oxygen with assisted ventilation as required. Exposed skin and eyes should be copiously flushed with water. Because of the potential for rapid onset of CNS depression or seizures with possible aspiration of gastric contents, EMESIS SHOULD NOT BE INDUCED. Cautious gastric lavage followed by administration of activated charcoal may be of benefit if the patient is seen soon after the exposure.
The following treatment recommendations are for Chlorinated Hydrocarbon Insecticides in general.

INHALATION EXPOSURE -

INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.

DERMAL EXPOSURE -

DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

EYE EXPOSURE -

DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

ORAL EXPOSURE -

Because of the potential for CNS depression and seizures, DO NOT induce emesis.
GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.

CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.

ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).

Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.

Do not give oils orally.
Do not administer adrenergic amines, which may further increase myocardial irritability and produce refractory ventricular arrhythmias.
CHOLESTYRAMINE - Oral administration may enhance the excretion of kepone and chlordane which are trapped in the enterohepatic circulation.
Hemodialysis is probably ineffective.
Exchange transfusion is probably ineffective.
Hemoperfusion is probably ineffective.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

GENERAL/SUMMARY

The lowest published lethal dose of DDT for humans (oral route) is 500 mg/kg (RTECS , 1999).
The lowest published lethal dose for man (unreported route) is 221 mg/kg (RTECS , 1999).
The lowest published lethal dose for an infant (oral route) is 150 mg/kg (RTECS , 1999).
Toxic doses of CHLORINATED HYDROCARBON INSECTICIDES vary enormously with route and rate of exposure. Acute hazard potential may be ranked (highest to lowest) approximately as: endrin, aldrin, dieldrin, chlordane, toxaphene, kepone, heptachlor, DDT, and methoxychlor.

MAXIMUM TOLERATED EXPOSURE

CASE REPORTS

" A dose of 20 grams has proved highly dangerous though not fatal to man. 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" (Lewis, 1996).
A single dose of 286 mg produced mild poisoning in a sick man weighing 47.5 kg (ACGIH, 1986).
A single ingestion at the rate of about 10 mg/kg produces moderate illness in some people (ACGIH, 1991).
A single dosage at the rate of 16 mg/kg frequently leads to convulsions (ACGIH, 1991).
Human volunteers have ingested up to 35 mg/day for 21 months of DDT with no ill effects: Another study reported no ill effects in workers exposed to up to 18 mg/day of DDT for 11 to 19 years (ACGIH, 1991; Lewis, 1996).
DDT and some of its degradation 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 unavailable, 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 (Lewis, 1996).

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 ppm of DDE and 648 ppm of DDT) was found in workers who had extensive exposure. Careful hospital examination of workers revealed no abnormality which could be attributed to DDT (Lewis, 1996).

Human volunteers who breathed 423 mg/m(3) of DDT for periods of one hour a day for six days reported eye irritation with no other ill effects (ACGIH, 1991).

Carcinogenicity Ratings for CAS50-29-3 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: DDT

A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.

EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: p,p'-Dichlorodiphenyltrichloroethane (DDT)

B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2B ; Listed as: DDT, p,p'-DDT

2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.

NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: DDT

Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).

MAK (DFG, 2002): Not Listed
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS50-29-3 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor: 3.4x10(-1) per mg/kg-day
RfD: 5x10(-4) mg/kg-day

Inhalation:

Unit Risk: 9.7x10(-2) per mg/m3
RfC:

Drinking Water:

Unit Risk: 9.7x10(-3) per mg/L

TOXICITY VALUES

References: ACGIH, 1991 Budavari, 1996 HSDB, 1999 ITI, 1995 Lewis, 1996 RTECS, 1999
- LD50- (ORAL)DOG:
- LD50- (ORAL)GOAT:
- LD50- (ORAL)GUINEA_PIG:
- LD50- (SKIN)GUINEA_PIG:
- LD50- (SUBCUTANEOUS)GUINEA_PIG:
- LD50- (ORAL)HAMSTER:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (INTRAVENOUS)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (ORAL)PRIMATE:
- LD50- (ORAL)RABBIT:
- LD50- (SKIN)RABBIT:
- LD50- (SUBCUTANEOUS)RABBIT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (INTRAVENOUS)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LD50- (SUBCUTANEOUS)RAT:
- LD50- (ORAL)SHEEP:
- LDLo- (INTRAVENOUS)CAT:
- LDLo- (ORAL)CAT:
- LDLo- (ORAL)CHICKEN:
- LDLo- (INTRAVENOUS)DOG:
- LDLo- (ORAL)DOG:
- LDLo- (ORAL)GOAT:
- LDLo- (ORAL)HUMAN:
- LDLo- (INTRAVENOUS)PRIMATE:
- LDLo- (INTRAVENOUS)RABBIT:
- LDLo- (INTRAPERITONEAL)RAT:
- LDLo- (INTRAVENOUS)RAT:
- LDLo- (ORAL)SHEEP:
- TD- (ORAL)MOUSE:
- TD- (ORAL)RAT:
- TDLo- (ORAL)DOG:
- TDLo- (ORAL)HAMSTER:
- TDLo- (ORAL)HUMAN:
- TDLo- (ORAL)MOUSE:
- TDLo- (SUBCUTANEOUS)MOUSE:
- TDLo- (ORAL)RABBIT:
- TDLo- (INTRAPERITONEAL)RAT:
- TDLo- (ORAL)RAT:

CALCULATIONS

AMBIENT CONVERSIONS

Conversion Factors: 1 mg/L (air) = 69 ppm; 1 ppm (air) = 14.5 mg/m(3) (at 25 degrees C, 760 mmHg) (Clayton & Clayton, 1994)

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS50-29-3 (American Conference of Governmental Industrial Hygienists, 2010):

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Adopted Value

TLV:

TLV-TWA: 1 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A3
Codes: Not Listed
Definitions:

A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.

TLV Basis - Critical Effect(s): Liver dam
Molecular Weight: 354.5

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS50-29-3 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS50-29-3 (National Institute for Occupational Safety and Health, 2007):

Listed as: DDT
REL:

TWA: 0.5 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
Skin Designation: Not Listed
Note(s): See Appendix A

IDLH:

IDLH: 500 mg/m3
Note(s): Ca

Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

OSHA PEL Values for CAS50-29-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Dichlorodiphenyltrichloroethane (DDT)
Table Z-1 for Dichlorodiphenyltrichloroethane (DDT):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 1

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: Yes
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS50-29-3 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS50-29-3 (U.S. Environmental Protection Agency, 2010):

Listed as: Benzene,1,1'-(2,2,2-trichloroethylidene) bis[4-chloro-
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:
Listed as: DDT
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:
Listed as: 4,4[prime]-DDT
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:
Listed as: DDT and metabolites

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS50-29-3 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS50-29-3 (U.S. Environmental Protection Agency, 2010b):

Listed as: Benzene, 1,1[prime]-(2,2,2-trichloroethylidene)bis[4-chloro-
P or U series number: U061
Footnote:
Listed as: DDT
P or U series number: U061
Footnote:
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS50-29-3 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS50-29-3 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS50-29-3 (49 CFR 172.101 - App. B, 2005):

Listed as DDT
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS50-29-3 (EPA, 2005):

Listed as: Benzene, 1,1'-(2,2,2-trichloroethylidene)bis[4-chloro-

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS50-29-3 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

DDT should be stored in a cool, dry, well-ventilated area. Iron storage containers should not be used (Sittig, 1991). DDT is incompatible with iron and aluminum salts, and alkaline substances (Budavari, 1996; Pohanish & Greene, 1997). The setting point of the technical grade is 88.6-91.4 degrees C (Budavari, 1996).

STORAGE

CONTAINER

DDT should be stored in a cool, dry, well-ventilated area. Iron storage containers should not be used (Sittig, 1991). Usual containers include bottles, tins, bags, and fiber drums (HSDB , 1999).

ROOM/CABINET RECOMMENDATIONS

DDT should be stored in a cool, dry, well-ventilated area. Iron storage containers should not be used (Sittig, 1991).

INCOMPATIBILITIES

DDT is incompatible with iron and aluminum salts, and alkaline substances (Budavari, 1996; Pohanish & Greene, 1997).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

Persons should wear appropriate protective equipment to prevent skin and eye contact with DDT. Workers should immediately wash contaminated skin with copious amounts of soap and water and promptly remove contaminated clothing (AAR, 1996; (NIOSH , 1999; Sittig, 1991). Work clothes should be changed before leaving the work site (NIOSH , 1999; Sittig, 1991). Contact lenses should not be worn when working with this chemical (HSDB , 1999).

RESPIRATORY PROTECTION

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 50-29-3.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.
- Containers may explode when heated.
- Runoff may pollute waterways.
Fires involving DDT should be extinguished using an agent suitable for the surrounding fire. DDT does not burn, or burns with difficulty. Fire fighting personnel should avoid breathing vapors and dusts and approach fire from upwind; toxic and irritating gas may be produced (AAR, 1996; (CHRIS , 1999). DDT melts and burns in a fire (CHRIS , 1999).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS50-29-3 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Dry chemical, CO2 or water spray.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Water spray, fog or regular foam.
Move containers from fire area if you can do it without risk.
Dike fire control water for later disposal; do not scatter the material.
Use water spray or fog; do not use straight streams.

TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Do not get water inside containers.
Cool containers with flooding quantities of water until well after fire is out.
Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.
For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

NFPA Extinguishing Methods for CAS50-29-3 (NFPA, 2002):

Not Listed

Fires involving DDT should be extinguished using water, dry chemical, foam, or carbon dioxide (CHRIS , 1999). Persons should avoid breathing vapors; runoff from fire control may produce poisonous gases or pollute water sources (HSDB , 1999).

COMBUSTION TOXICITY

DDT, when heated to decomposition, emits toxic chloride fumes (Lewis, 1996).

DUST/VAPOR HAZARD

DDT, when heated to decomposition, emits toxic chloride fumes (Lewis, 1996).

Heavy exposure to DDT dust may result in eye and skin irritation (Hathaway et al, 1996).

REACTIVITY HAZARD

DDT, when heated to decomposition, emits toxic chloride fumes (Lewis, 1996).

EVACUATION PROCEDURES

SUMMARY

Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 25 to 50 meters (80 to 160 feet) in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

If tank, rail car or tank truck 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.

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
As an 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.
Keep unauthorized personnel away.
Stay upwind.
Keep out of low areas.

AIHA ERPG Values for CAS50-29-3 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS50-29-3 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as DDT; (Dichlorodiphenyltrichloroethane)
TEEL-0 (units = mg/m3): 1
TEEL-1 (units = mg/m3): 1
TEEL-2 (units = mg/m3): 2
TEEL-3 (units = mg/m3): 500
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS50-29-3 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS50-29-3 (National Institute for Occupational Safety and Health, 2007):

IDLH: 500 mg/m3
Note(s): Ca

(Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.
- Stop leak if you can do it without risk.
- Prevent entry into waterways, sewers, basements or confined areas.
- Cover with plastic sheet to prevent spreading.
- Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers.
- DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
If spilled, DDT should be swept up and placed in a suitable container. Vermiculite or other inert material may be used to absorb liquids. The mixture should then be scooped into a suitable container (Sittig, 1991).
DDT should be kept out of water sources and sewers; it is harmful to aquatic life in very low concentrations (AAR, 1996; (CHRIS , 1999). Dikes can be used to contain flow. If DDT is spilled on land, pits, ponds, lagoons, or other holding areas can be used to contain liquid or solid material. A plastic sheet can be used to cover solids to prevent material from dissolving in rain or fire fighting water. Soil, sand bags, foamed polyurethane, or foamed concrete can be used to dike surface flow (AAR, 1996).
DDT is hydrophobic and will migrate to the shore where it is absorbed by the soil or co-distill with water (OHM/TADS , 1999). For a water spill, natural barriers and oil spill control booms can be used to limit spill travel. Natural deep water pockets, activated charcoal, excavated lagoons, or sand bag barriers can be used to trap material at the bottom of water source. Trapped material can then be removed with suction hoses or mechanical dredges (AAR, 1996; (HSDB , 1999).

WASTE TREATMENT OPTIONS

PHYSICAL TREATMENT

DDT can be successfully disposed of (over 99% efficiency) using an incinerator equipped with scrubbers (Sittig, 1991).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Releases of DDT occur through its manufacture and use as a pesticide and insecticide. In 1972, the United States banned DDT use. However, it is still used in other countries (HSDB, 2004).

Exposure may result from DDT's use as a polychlorinated, lipophilic, environmentally persistent contact pesticide, larvicide, ectoparasiticide, and topical pediculicide (Lewis, 1998).

DDT and some of its detoxification products, particularly dichlorodiphenyldichloroethlene (DDE) are stored in fat. This storage leads to magnified concentrations of DDT in the food chain (ACGIH, 1991; Lewis, 1996).

DDT is resistant to destruction by light and oxidation. This unusual stability creates difficulties in residue removal from water, soil, and food stuffs (Budavari, 1996).

ENVIRONMENTAL FATE AND KINETICS

In the atmosphere, DDT decomposes to form carbon dioxide and hydrochloric acid. It undergos direct photooxidation and reacts with photochemically-produced hydroxyl radicals (half-life of 2 days, estimate) (CD-ROM (1997); HSDB, 2004).
- Photooxidation is believed to be slow due to the presence of DDT in samples far from the area of use. Wet and dry deposition are expected to be significant removal mechanisms (HSDB, 2004).
- Laboratory studies indicate that, in the photochemically active ionosphere, DDT may be destroyed by solar irradiation (CD-ROM (1997)).
Half-life ranges from 17.7 hours to 177 hours (Howard, 1991).
The persistence of DDT in air samples in residential and rural environments was monitored during an 8 month period after application under a malaria control program in India. The DDT levels in air ranged from 1.0 to 14.6 millimicrograms/cubic meter, and after an initial decrease, rose to 5.9 millimicrograms/cubic meter in samples taken after 240 days of application. DDT was found mainly in the particulate phase up to 64 days after application (34 to 78%), and entirely in the vapor phase in subsequent samples (Singh et al, 1992).
During 1988 and 1989 air samples were collected at Sable Island off the coast of Scotland. Mean concentration of DDT and DDE was 4.5 pg/m(3). The results illustrate the importance of atmospheric transport in delivering contaminants to the Scotian Shelf (Bidleman et al, 1992).

WATER

SURFACE WATER
- In water, DDT is expected to strongly adsorb to sediments, significantly bioconcentrate in fish, and evaporate quickly (half-lives of several hours to 50 hours). DDT is subject to indirect photodegradation at the surface of the water body, but is not expected to hydrolyze. Ultimately, DDT is removed from aquatic environments by biotransformation, although studies indicate that indirect photolysis may also be significant (half-life approximately 1 week). Biodegradation may occur in waters and sediments where high populations of the proper microorganisms are present, but generally biodegradation in water is unlikely (HSDB, 2004).
- The half-life in water (25 degrees C; 1 m deep) is 74H, based on an evaporation rate of 9.34 x 10(-3)m/H (Verschueren, 2001).
- Hydrolysis is not a significant degradation process (half-life of 12 years at 207 degrees C and pH 3-5) (HSDB , 1999).
- Photooxidation by UV light in an aqueous medium at 90-95 degrees C formed CO2 (expressed as % of theoretical) at rates of 25% in 25.9 H; 50% in 66.5 H; and 75% in 120 H (Verschueren, 2001; HSDB , 1999).
- Direct photolysis is very slow (half-life >150 years). The presence of natural substances in some aquatic environments may cause indirect photolysis to be an important process for DDT transformation, with half-lives on the order of a few days or possibly hours for DDT loss. Half-lives for indirect photolysis of DDT are difficult to predict for general environmental assessments because of lack of information on the variability of waters (HSDB , 1999).
- Natural and distilled water (sterilized and unsterilized) with an initial concentration of 0.1 ppm was kept in darkness at 21 degrees C. The DDT persisted 95% in each scenario after 8W (Verschueren, 2001).
- The surface water half-life ranges from 7 to 350 days (Howard, 1991).
- Samples of water and suspended sediments were collected in the St. Lawrence River and analyzed for DDT. DDT was present in almost all the samples. The metabolite, p,p'-DDT, degraded faster in bottom sediment than in soils (Pham et al, 1993).
- Reductive dehalogenation did not occur after 3 months in anoxic sediment with 6% organic carbon incubated at 22 degrees C (Verschueren, 2001).
GROUND WATER
- The groundwater half-life ranges from 16 days to 31.3 years (Howard, 1991).

SOIL

TERRESTRIAL
- DDT released to soil is expected to strongly adsorb to the soil and is not expected to leach into groundwater. DDT will volatilize (half-life of 100 days). It is expected to photooxidize, but not hydrolyze (CD-ROM (1997)).
- DDT is expected to biodegrade in flooded soils or in anaerobic conditions as long as the required microorganisms are present at sufficient levels (CD-ROM (1997); HSDB, 2004).
- DDT will also be removed by plant absorption, water runoff, and chemical transformation. Under aerobic conditions, slow transformation to DDE normally occurs. Under anaerobic conditions, conversion to DDD results and is much more rapid than the aerobic conversion to DDE (CD-ROM (1997)).
- 75 - 100% disappearance from soils occurs in 4 - 30 years (Verschueren, 2001).
- Modification and stability of DDT in soils were the subjects of a study where three different soils were irradiated and flooded for 42 days. The volatilized organics contained large amounts of DDE under both flooding and non-flooding conditions. Flooding significantly increased binding of DDT, resulting in up to 33% remaining in nursery soils. Solar radiation and flood were more important than the type of soil in determining rate of volatilization (Nair & Pillai, 1992).
- Soil surveys were done during 1988 and 1989 to determine the persistence of DDT in a variety of agricultural soils in India. Higher DDT concentrations were found in upland soils, and lower concentrations were in paddy field soils. Large amounts of these pesticides are in use in India and have a persistent harmful effect on the Indian agricultural environment (Kawano et al, 1992).

ABIOTIC DEGRADATION

DDT likely adsorbs tightly to soil and sediments. Volatilization and photodegradation by indirect photolysis in water or by photooxidation in soil contribute to the removal of DDT. Presence of natural materials in an aquatic system may influence the importance of indirect photolysis as a transformation process in water. Removal from soil is further accomplished through plant uptake or biotransformation. Biodegradation in soil is effective, especially under anaerobic conditions and with adequate numbers of the appropriate microorganisms. Biodegradation in water may occur, but is generally not likely. It not expected to leach to groundwater. Hydrolysis is not a significant fate mechanism in soil or water (HSDB, 2004; CD-ROM (1997)).

DDT can exist as a vapor or in particulate phase in air. Atmospheric transport occurs, and it is primarily removed by wet and dry deposition. It may slowly decompose in the atmosphere by reaction with photochemically-produced hydroxyl radicals or direct photooxidation (CD-ROM (1997); Singh et al, 1992; HSDB, 2004).

BIODEGRADATION

DDT biodegrades by a number of isolated microorganisms from water, sediments, and soils. Under environmental conditions, biodegradation varies, especially in the presence of anaerobic conditions and high populations of the required microorganisms (HSDB, 2004).

The biodegradation half-life in soil ranges from 31 days to >15 years (Howard, 1991; HSDB, 2004).
A soil-water suspension at an initial concentration of approximately 0.1 mg/L and kept at 35 degrees C biodegraded under aerobic and anaerobic conditions. Percent mineralization to CO2 under aerobic conditions was 0.1% after 5D and 0.8% after 42D; 2.4% of the initial concentration remained after 42D. Percent mineralization under anaerobic conditions was 0.3% after 5D and 0.7% after 41D; 2% of the initial concentration remained after 42D (Verschueren, 2001).
Aerobic half-life: 2-15.6 years (Howard, 1991)
Anaerobic half-life: 16-100 days (Howard, 1991)

DDT in low concentrations (from 10 pg/mL to 100 pg/mL) was biodegraded by the soil bacterium, Bacillus species B75. Greater than 88% of the DDT was degraded after 2 weeks of incubation (Katayama et al, 1993).

BIOACCUMULATION

HUMANS

The concentrations of PCBs, DDT and other chlorinated insecticides were determined in human adipose tissue at two sites in Poland during 1979 and 1990. High concentrations of DDT were detected, with maximum values of about 50 mcg/g lipid weight. The results suggest that the Polish environment is still experiencing high contamination from agricultural and industrial activities (Tanabe et al, 1993).
The levels of blood lead and serum PCB and DDT were measured for 115 fish eaters from the Great Lakes region. Elevated serum PCB and DDT levels were observed in the fish eaters compared to non-fish eaters. Lead levels were higher in the fish eaters but did not correlate with the same consumption pattern (Hovinga et al, 1993).

FISH

Organochlorine pesticide (DDTs and the degradation products DDE and DDD) accumulation was examined in conjunction with accumulation of several heavy metals, polychlorinated biphenyls (PCBs), hexachlorobenzene (HCB), and hexachlorohexane isomers (HCHs) in marine species from the Ionian and Adriatic Seas. DDT and its metabolites were found in teleost and elasmobranch fish species and in bivalve and cephalopod mollusc species. Only alpha-DDT and p,p'-DDE were found in the crustaceans (Marcotrigiano & Storelli, 2003).

Levels of p,p'-DDT in Marine Species:

Fish Muscle: not detected-6.49 (average 0.79; standard deviation +/-1.04) ng/g wet weight
Fish Liver: not detected-63.33 (average 8.81; standard deviation +/-13.84) ng/g wet weight
Shark Muscle: not detected
Shark Liver: 32.0-274.0 (average 148.0; standard deviation +/-114.0) ng/g wet weight
Cephalopod Flesh: not detected
Cephalopod Digestive Gland: not detected-4.00 (average 2.00; standard deviation +/-1.29) ng/g wet weight
Bivalve Soft Body: not detected
Crustacean Flesh: not detected

Higher organochlorine pesticide, PCB, and HCB concentrations were in the liver and digestive gland tissue than in muscle tissue for all examined species. The accumulation order was PCBs = DDTs > HCB. This coordinated with the higher lipid content of the organs.
Organochlorine pesticide (DDTs) accumulation in fish liver and fish muscle tissue was similar to PCB accumulation in these tissues and greater than HCB accumulation.
The chemicals p,p'-DDT; o,p'-DDT; p,p'-DDD; and o,p'-DDD were not consistently detected in particular species of commercial interest (M. merluccius, S. smaris, P. blennoides, B. boops, L. caudatus, G. melastomus, and H. dactylopterus).
The only metabolite detected in shark muscle tissue among the DDTs was p,p'-DDE. Levels were similar to the low concentrations of PCBs found in the shark muscle tissue.
Shark liver concentrations were particularly high for all observed contaminants (PCBs, DDT, HCB). The accumulation trend was different from that in fish: DDTs > PCBs > HCB.
The cephalopod digestive gland had higher concentrations than the flesh with a similar accumulation order (PCBs > DDTs > HCB). The only DDT compound detected in cephalopod flesh was p,p'-DDE.
Bivalve molluscs had very low levels of PCBs, p,p'-DDE, and HCB.
PCBs and p,p'-DDE were also low in crustaceans. HCBs were below the reported detection limit.

Rainbow trout in Lake Ontario, USA had a log bioaccumulation factor (log BAF) of 7.8 L/kg (lipid) (Verschueren, 2001).

DDT accumulates in the adipose tissue in fish. Brook trout accumulated a greater amount from food (10 times) than from water. In trout, DDT builds up in the liver and the intestines (OHM/TADS , 1999).

The concentration of DDT in sediment and water explained variability in fish contaminants when basin-specific ecological attributes were taken into account for the Great Lakes ecosystem (Rowan & Rasmussen, 1992).

Important factors determining the partitioning of organic contaminants were fish lipid content, trophic levels of the fish, and the trophic structure of the food chain (Rowan & Rasmussen, 1992).

Mercury and DDT were determined in the flesh of 1- to 12-year-old lake trout in central New York State. The concentration of DDT and mercury increased significantly (p <0.001) with age (Gutenmann et al, 1992).

DDT was shown to bioaccumulate and biomagnify in the Lake Kariba (Zimbabwe) ecosystem. The following DDT levels were found, with the highest levels found in the bottom living species (Berg et al, 1992):

Species	DDT Concentration
Tilapia rendalli(an algae feeder)	1900 ng/g fat
Hydrocynus forskahlii(predatory tigerfish)	5000 ng/g fat
Labeo altivelis(benthos feeding fish)	5700 ng/g fat
Corbicula africana(mussel)	10,100 ng/g fat

The concentration of DDT and other pesticide residuals was determined in cod-liver oil samples collected from the southern part of the Baltic between 1971 through 1989. These oil samples showed a general decline in residues, though present levels are higher than in western Europe. The higher level is thought to be a result of the continuous input of these chemicals from eastern Europe and a slower clearance rate in the Baltic ecosystem (Kannan et al, 1992).

Extremely high concentrations of polychlorinated biphenyls (PCBs) were found in the blubber of striped dolphins in the western Mediterranean in 1990. The concentrations ranged between 94 and 670 mcg/g (net weight) and contributed to the development of morbillivirus disease in these dolphins. Concentrations of DDT were also high, ranging from 22 to 230 mcg/g (Kannan et al, 1993).

Fish species in the rivers of an agriculturally and industrially developed area of Spain were measured to determine levels of organochlorine compounds (PCBs, DDTs, HCHs, and heptaclor epoxide). A clear geographical distribution of contamination was found with higher levels of the compounds located in the lower reaches of the rivers. PCBs were present in all analyzed samples while other analyzed compounds were present in more than 79% of the samples. While most observed levels fell within acceptable ranges for human consumption, biomagnification of the compounds may create a threat for sensitive species such as the otter (Lutra lutra) (Lopezmartin et al, 1995).

BIRDS

Birds of prey in the Netherlands had up to 1.6 ppm in the liver (OHM/TADS , 1999).
DDT residues in osprey eggs from Glenn L. Martin National Wildlife Refuge, Maryland, have significantly declined to undetectable levels since the 1970s (Audet et al, 1992).
DDT, or its metabolites DDD and DDE, was found in every sample of liver and visceral fat from 86 cormorants on Lake Kariba in 1986. The risk of mortality was minimal in full grown birds. Eggshell thinning and breeding failure were associated with DDE levels in a related species' adult females (Douthwaite et al, 1992).
Birds of prey act as targets in the food chain and accumulate DDT at high rates. Japanese quail kinetic studies show that DDT can be transferred from the maternal organism to the chicks. DDT is mainly associated with reproductive effects that greatly reduce the hatching success in contaminated birds (Burgatsacaze et al, 1993).
Fish eagle eggs were collected from nests at Lake Kariba, Zimbabwe in 1989 and 1990. Every egg showed some amount of unaltered DDT, and the metabolites DDD and DDE, in mean amounts from 14 to 49 mg/kg. At the eastern end of the lake the amounts were from 113 to 223 mg/kg dry weight. The shell thickness showed a decline of 115 compared to museum samples from 1036-41; while the eggshell at the eastern end of the lake showed thinning in excess of 20%. Chicks were seen in less than one half of the nests at the eastern end of the lake (Douthwaite, 1992).
A study reported the recovery of a sparrowhawk population in eastern England after a 20-year absence. The new population, starting in 1979, was correlated with a reduction in contamination by organochlorine pesticide residues, namely HEOD (derived from aldrin and dieldrin) and DDE (derived from DDT). The number of nests in 1979 was 3 and had increased to 84 by 1989 (Newton & Wyllie, 1992).

PLANTS

TERRESTRIAL
- Samples of pine needles (P. sylvestris) collected in 1986 were used to observe geographic and temporal patterns of atmospheric organic pollutants. DDT was found in Germany, as a result of a 1984 spraying event; while polychlorinated biphenyls were ubiquitous, with particularly high levels in southern France (Jensen et al, 1992).
- Certain plants accumulate DDT (OHM/TADS , 1999).

MAMMALS

DDT accumulates in the adipose tissue in mammals (OHM/TADS , 1999).
Crab-eater seals and penguins had 4-69 ppm DDT in fat (OHM/TADS , 1999).
The concentration of DDT in harbor seals was approximately four times higher in samples from the Baltic area than from the west coast of Sweden (Blomkvist et al, 1992).
Dolphins, porpoises and whales accumulate high concentrations of DDTs and transfer them to offspring during lactation. These animals have a small capacity to degrade these contaminants and are, therefore, vulnerable to long-term toxicity from hazardous chemicals (Tatsukawa, 1992).
Samples of adipose tissue were collected, in northern Poland in 1987-1988, from swine, cows, sheep, rabbits, ducks, geese, turkeys, wild boar, roe deer and stags and analyzed for DDT and other pesticides. All the samples contained detectable but low concentrations of organochlorine pesticides. Ducks and wild boar contained the highest levels of DDT in their fat, 400 and 440 mcg/kg of fat, respectively (Falandysz & Kannan, 1992).

OTHER

INVERTEBRATES
- The bioaccumulation factor for the Oligochaete worms Tubifex tubifex and Limnodrilus hoffmeisteri was 0.5 after 79D (8 degrees C and 0.092 mg/kg sediment concentration). The half-life was 74D (Verschueren, 2001).
- Squid of the northwest US Pacific ocean had a log bioaccumulation factor (log BAF) of 6.82 L/kg (lipid; sum DDT) (Verschueren, 2001).
- Oysters concentrate DDT more than 70,000-fold (OHM/TADS , 1999).
- The average mollusk concentrates in the range of 1210-9000 times (OHM/TADS , 1999).
OTHER
- A wide variety of animals are documented to contain DDT, even though their habitat areas were not sprayed with the material (OHM/TADS , 1999).

BIOCONCENTRATION FACTOR

Algae (Chlorella fusca): 9350 (BCF, wet weight) (Verschueren, 2001)
Fathead minnow: 4.47 (log BCF) (Verschueren, 2001)
Fish (Gambusia): 84,500 (BCF radiolabeled DDT; 0.22 mcg/L water; after 33D in a model ecosystem) (Verschueren, 2001)
Mosquito larvae: 8200 (BCF radiolabeled DDT; 0.22 mcg/L water; after 33D in a model ecosystem) (Verschueren, 2001)
Mussel, freshwater (Anodonta grandis): 2400 (BCF) (Verschueren, 2001)
Mussel (Mytilus sp.): 40,000-690,000 (BCF) (Verschueren, 2001)
Mussel (Mytilus edulis): 4550-49,600 (BCF) (Verschueren, 2001)
Snails (Physa): 34,500 (BCF radiolabeled DDT; 0.22 mcg/L water; after 33D in a model ecosystem) (Verschueren, 2001)
Bioconcentration Factors (HSDB, 2004)
- Fish: 600-84,500
- Snail: 3660-34,500
- Mussel: 4550-690,000
- Oyster: 700-70,000
- Fathead Minnow: 51,000-100,000
- Ceratophyllum demersum (coontail): 1950 (30 days)
- Cladophora sp: 21,580 (30 days)
- Lemna minor (duckweed): 1210 (30 days)
- Myrolophyllum sp (water milfoil): 1870 (30 days)
- Potamogeton cripus (curly leaf pondweed): 14,280 (30 days)
- Potamogeton follosus (narrow-leaf pondweed): 781 (30 days)
- Potamogeton pectinatus (Sago pondweed): 6360 (30 days)
- Scirpus validus (soft stem bulrush): 495 (30 days)
- Sparganium eurycarpum (bur reed): 623 (30 days)
- Utricularia vulgaris (bladderwort): 2200 (30 days)
- Orconectes punctata (crayfish): 5060 (30 days)
- Tendipes sp (bloodworm): 4750 (30 days)
- Erpobdella punctata (red leach): 7520 (30 days)
An experimental study established the pharmacokinetic parameters and the rate-limiting process in polychlorinated biphenyl (PCB) uptake by Golden Shiners. C-14 labeled PCBs were used to monitor the process. The bioconcentration factor, K(b), was estimated to be 9059 mL water per gram fish, and the half-life of PCBs in solution with the fish to be 4.9 days (Karara & McFarland, 1992).

ENVIRONMENTAL TOXICITY

It is toxic to many vertebrate animals and highly toxic to fish. Widespread bird kills have resulted from the bioconcentration of DDT through the food chain (due to its presence in fish or earthworms). A major environmental problem has resulted from the specific effects of dichlorodiphenyldichloroethlene (DDE), a degradation product of DDT, on eggshell formation in raptorial birds where accumulation has caused decreases in shell thickness of 10-15%, resulting in widespread breakage (HSDB, 2004; Lewis, 1998).

In 1970, decreases in eggshell thickness were found in 15 of 22 species of aquatic birds, especially in those species that feed in fresh and brackish waters near agricultural areas. Brown pelican, reddish egret, white-faced ibis, laughing gull, and Forster's tern all experienced decreased populations (Clayton & Clayton, 1994).

Exposure to this compound has caused serious reproductive failure in birds and fish. DDT is very toxic to adult laboratory rats, but moderately toxic to newborn rats (Lewis, 1998).

DDT is toxic to a number of vertebrate animals. The p,p'-isomer is weakly estrogenic and has the greatest toxicity in insects. The o,p'-isomer is less toxic and more estrogenic (Lewis, 1998).

Freshwater Toxicity (concentrations in ppm) (CHRIS , 1999; OHM/TADS , 1999):

TLm - ACRONEURIA: 0.180 for 96H
TLm - PTERONAREYS CALIFORNIA: 0.100 for 96H
TLm - CLAASSENIA SUBULOSA: 0.010 for 96H
TLm - ARETOGISYCHE GRANDIS: 0.100 for 96H
TLm - DAPHNIA MAGNA: 0.001 for 96H
TLm - FATHEAD: 0.034 for 96H
TLm - SALMON: 0.047 for 24H
TLm - COHO: 0.013 for 96H
TLm - COHO: 0.024 for 48H
TLm - BLUEGILL: 0.016 for 96H
TLm - GOLDFISH: 0.027 for 96H
TLm - GUPPIES: 0.043 for 96H
TLm - FATHEAD: 0.032 for 96H
TLm - FATHEAD: 0.0155 for 96H
TLm - GAMMARUS LACUSTRIS: 0.009 for 96H -- TECH. IN ACETONE
TL50 - CATFISH: 0.016 for 96H
TL50 - BULLHEAD: 0.005 for 96H
TL50 - GOLDFISH: 0.021 for 96H
LC50 - MINNOW: 0.019 for 96H
TL50 - CARP: 0.010 for 96H
TL50 - SUNFISH: 0.005 for 96H
TL50 - BLUEGILL: 0.008 for 96H
TL50 - BASS: 0.002 for 96H
TL50 - RAINBOW: 0.007 for 96H
TL50 - BROWN: 0.002 for 96H
TL50 - COHO: 0.004 for 96H
TL50 - PERCH: 0.009 for 96H
TL50 - RAINBOW: 0.0096 for 24H
TL50 - RAINBOW: 0.0072 for 96H
TL50 - FATHEAD: 0.0246 for 24H
TL50 - FATHEAD: 0.0199 for 96H
TL50 - CATFISH: 0.0258 for 24H
TL50 - CATFISH: 0.0174 for 96H
TL50 - BLUEGILL: 0.0147 for 24H
TL50 - BLUEGILL: 0.0095 for 96H
TL50 - BASS: 0.0039 for 24H
TL50 - BASS: 0.0018 for 96H
TL50 - DAPHNIA MAGNA: 0.004 for 48H
TL50 - SEED SHRIMP: 0.054 for 48H
TL50 - SOWBUG: 0.0078 for 24H
TL50 - SOWBUG: 0.0047 for 48H
TL50 - GLASS SHRIMP: 0.0069 for 24H
TL50 - GLASS SHRIMP: 0.0042 for 48H
TL50 - DAMSELFLY: 0.060 for 24H
TL50 - DAMSELFLY: 0.0225 for 48H
TL50 - SCUD: 0.0104 for 24H
TL50 - SCUD 0.0036 for 48H
TL50 - BASS: 0.0039 ppm for 24H
TL50 - BASS: 0.0018 ppm for 96H
LC50 - RAINBOW: 0.008 for 24H
LC50 - BLUEGILL: 0.007 for 24H
LC50 - DAPHNIA MAGNA: 0.0014 for 50H
LC50 - MOSQUITOFISH: 0.01 for 72H
LC50 - BROOK TROUT: 0.0323 for 36H
LC50 - SALMON: 0.072
LC50 - SALMON: 0.08 for 36H
LC50 - GOLDFISH: 0.1 for 72H
LC50 - MOSQUITOFISH: 0.32 for 36H
LC50 - MOSQUITOFISH: 0.5 for 24H
LC50 - FATHEAD: 0.0074 for 48H
LC50 - FATHEAD: < 0.04 for 48H
LD50 - TUBIFEX AND LIMNADRILUS SP: 100 for 96H
LD50-LD100 - CARP EMBRYO: 5.0
LD - DACE: 0.01
LD - BASS: 9.01

Saltwater Toxicity (concentrations in ppm) (CHRIS , 1999; OHM/TADS , 1999):

TLm - SHRIMP LARVAE: 0.012 for 5H
TLm - SHRIMP, Adult: 0.142 for 5H
LD17 - BLUE CRABS: 0.2 LB/AC RE for 168H -- salt marsh stream
LD75 - MARSH FIDDLER CRAB: 0.2 LB/AC RE for 168H - salt marsh
LD36 - REDJNTDFIDDLER CRAB: 0.2 LB/AC RE for 168H -- salt marsh
LD50 - KILLIFISH: 0.0028 for 48H
LD50 - 0.0028 ppm for 48H (CHRIS, 1999)
EC50 - SHEEPHEAD MINNOW: 0.1 for 48H
EC50 - OYSTER: 0.03 for 96H
LD - OYSTER LARVAE: 1.0 for 96H
LD - BLUE CRAB: 0.001 for 192H

Waterfowl toxicity: 2240 mg/kg (CHRIS , 1999)

In rainbow trout (Pyloric caeca), dieldrin increased DDT's cumulative synergistic effect with 2,4-D. The presence of dieldrin decreases or inhibits elimination of DDT (OHM/TADS , 1999).

Ecotoxicity Values (HSDB , 1999):

LC50 - (ORAL) COLINUS VIRGINIANUS (Bobwhite Quail), 2 weeks old: 611 ppm for 5D (ad libitum) - 95% confidence limit 514-724 ppm
LC50 - (ORAL) COTURNIX JAPONICA (Japanese Quail), 2 weeks old: 568 ppm for 5D (ad libitum) - 95% confidence limit 470-687 ppm
LC50 - (ORAL) COTURNIX JAPONICA (Japanese Quail), 14 days old: 416 ppm for 5D (ad libitum) - 95% confidence limit 341-509 ppm
LC50 - (ORAL) PHASIANUS COLCHICUS (Pheasant), 2 weeks old: 311 ppm for 5D (ad libitum) -- 95% confidence limit 256-374 ppm
LC50 (ORAL) ANAS PLATYRHYNCHOS (Mallard Duck), 2 weeks old: 1869 ppm for 5D ad libitum -- 95% confidence limit 1500-2372 ppm
LC50 - ASELLUS BREVICAUDUS (SOWBUGS), mature: 4.0 mcg/L for 96H - at 21 degrees C; 95% confidence limit 1.2-6.5 mcg/L
LC50 - GAMMARUS LACUSTRIS (SCUDS), mature: 1.0 mcg/L for 96H -- at 21 degrees C; 95% confidence limit 0.7-1.5 mcg/L; static bioassay
LC50 - PALAEMONETES KADIAKENSIS (GLASS SHRIMP), mature: 2.3 mcg/L for 96H -- at 21 degrees C; 95% confidence limit 1.3-4.9 mcg/L; static bioassay
LC50 - PTERONARCYS CALIFORNICA (STONEFLIES), second year class: 7.0 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 4.9-9.9 mcg/L; static bioassay
LC50 - ISOPERLA SP (STONEFLIES), juvenile: 1.2 mcg/L for 96H -- at 15 degrees C; 95% confidence limit 0.3-4.9 mcg/L; static bioassay
LC50 - PENTANEURA SP (MIDGES), juvenile: 1.5 mcg/L for 96H -- at 21 degrees C; static bioassay
LC50 - CHAOBORUS SP (PHANTOM MIDGES), juvenile: 7.4 mcg/L for 96H -- at 15 degrees C; static bioassay
LC50 - ONCORHYNCHUS KISUTCH (COHO SALMON): 4.0 mcg/L for 96H -- 1.0g; at 13 degrees C (95% confidence limit 3.0-6.0 mcg/L); static bioassay
LC50 - SALMO GAIRDNERI (RAINBOW TROUT): 8.7 mcg/L for 96 H -- 1.0g; at 13 degrees C (95% confidence limit 6.8-11.4 mcg/L); static bioassay
LC50 - ESOX LUCIUS (NORTHERN PIKE): 2.7 mcg/L for 96H -- 0.7g; at 18 degrees C; static bioassay
LC50 - PIMEPHALES PROMELAS (FATHEAD MINNOW): 12.2 mcg/L for 96H -- 1.2g; at 18 degrees C (95% confidence limit 10.0-15.4 mcg/L); static bioassay
LC50 - ICTALURUS MELAS (BLACK BULLHEAD): 4.8 mcg/L for 96H -- 1.2g; at 18 degrees C (95% confidence limit 3.4-6.8 mcg/L); static bioassay
LC50 - ICTALURUS PUNCTATUS (CHANNEL CATFISH): 21.5 mcg/L for 96H -- 1.5g; at 18 degrees C (95% confidence limit 17.7-26.1 mcg/L); static bioassay
LC50 - LEPOMIS MACROCHIRUS (BLUEGILL): 8.6 mcg/L for 96H -- 1.5g; at 18 degrees C (95% confidence limit 6.2-12.0 mcg/L); static bioassay
LC50 - MICROPTERUS SALMOIDES (LARGEMOUTH BASS): 1.5 mcg/L for 96H -- 0.8g; at 18 degrees C (95% confidence limit 0.9-2.4 mcg/L); static bioassay
LC50 - PERCA FLAVESCENS (YELLOW PERCH): 9.0 mcg/L for 96H --1.4 g, at 18 degrees C (95% confidence limit 7.0-11.0 mcg/L); static bioassay
LC50 - STIZOSTEDION VITREUM VITREUM (WALLEYE): 2.9 mcg/L for 96H --1.4g; at 18 degrees C (95% confidence limit 2.4-3.5 mcg/L); static bioassay
LC50 - ORCONECTES NAIS (CRAYFISH), juvenile: 0.18 mcg/L for 96H -- at 21 degrees C; well water (95% confidence limit 0.12-0.30 mcg/L); static bioassay
LD50 - (ORAL) PHASIANUS COLCHICUS (RING-NECKED PHEASANTS), females 3-4M: 1334 mg/kg -- (95% confidence limit 894-1990 mg/kg); purity >99%; set point, 105.5 deg C
LD50 - (ORAL) GRUS CANADENSIS (SANDHILL CRANE), adult female: >1200 mg/kg -- purity >99%; set point, 105.5 deg C
LD50 - (ORAL) GRUS CANADENSIS (SANDHILL CRANE), adult male: >1200 mg/kg --purity >99%; set point, 105.5 deg C
LD50 - (ORAL) RANA CATESBEIANA (BULLFROG), female: >2000 mg/kg -- purity 77.2%
LD50- (ORAL) ANAS PLATYRHYNCHOS (MALLARD DUCK), female 3M: >2240 mg/kg -- purity 77.2%
LD50 - (ORAL) COTURNIX JAPONICA (JAPANESE QUAIL), male 2M: 841 mg/kg -- 95% confidence limit 607-1170 mg/kg; purity 77.2%
LD50 - (ORAL) COLUMBA LIVIA (ROCK DOVE, DOMESTIC PIGEON), female: >4000 mg/kg -- purity 77.2%
LD50 - (ORAL) COLUMBA LIVIA (ROCK DOVE, DOMESTIC PIGEON), male: >4000 mg/kg -- purity 77.2%
LD50 - (ORAL) CALLIPEPLA CALIFORNICA (CALIFORNIA QUAIL), male 6M: 595 mg/kg -- 95% confidence limit 430-825 mg/kg; technical grade
LC50 - PTERONARCELLA BADIA (STONEFLIES): 1.9 mcg/L for 96H -- conditions of bioassay not specified
LC50 - CHIRONOMUS RIPARIUS, fourth instar larvae: 4.7 mcg/L for 24H -- conditions of bioassay not specified
LC50 - ASELLUS BREVICAUDUS (SOWBUG): 4.7 mcg/L for 48H -- conditions of bioassay not specified
LC50 - GAMMARUS FASCIATUS (SCUD): 3.6 mcg/L for 48H -- conditions of bioassay not specified
LC50 - ISCHNURA VERTICALIS (DAMSELFLY): 22.5 mcg/L for 48H -- conditions of bioassay not specified
LC50 - ACRONEURIA PACIFICA (STONEFLY) (NAIAD): 72 mcg/L for 30D -- conditions of bioassay not specified
LC50 - PTERONARCYS CALIFORNICA (STONEFLY) (NAIAD): 265 mcg/L for 30D -- conditions of bioassay not specified
LC50 - NOTEMIGONUS CRYSOLEUCAS (GOLDEN SHINER): 29.9 mcg/L for 36H -- conditions of bioassay not specified
LC50 - LEPOMIS CYANELLUS (GREEN SUNFISH): 23.5 mcg/L for 36H -- conditions of bioassay not specified
LC50 - LEPOMIS MACROCHIRUS (BLUEGILL): 28.7 mcg/L for 36H -- conditions of bioassay not specified
LC50 - BUFO WOODHOUSEI FOWLERI (TOAD): 560,000 mcg/L for 36H -- conditions of bioassay not specified
LC50 - ICTALURUS PUNCTATUS (CHANNEL CATFISH) FINGERLING: > 2000 mcg/L for 96H -- 50% DDT dust; conditions of bioassay not specified
LC50 - BUFO WOODHOUSEI FOWLERI (TOAD) tadpole 4-5W: 1000 mcg/L for 96H; -- conditions of bioassay not specified
LC50 - BUFO WOODHOUSEI FOWLERI (TOAD) tadpole 6W: 100 mcg/L for 96H -- conditions of bioassay not specified
LC50 - BUFO WOODHOUSEI FOWLERI (TOAD) tadpole 7W: 30 mcg/L for 96H -- conditions of bioassay not specified
LC50 - PSEUDACRIS TRISERIATA (FROG) TADPOLE: 400 mcg/L for 96H -- conditions of bioassay not specified
LC50 - LEIOSTOMUS XANTHURUS (SPOT): 1.8 mcg/L for 2D -- conditions of bioassay not specified
LC50 - MUGIL CEPHALUS (STRIPED MULLET): 0.4 mcg/L for 2D -- conditions of bioassay not specified

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

354.50

DESCRIPTION/PHYSICAL STATE

DDT exists as a white, colorless, odorless, waxy, crystals or white to slightly off-white powder (Lewis, 1998) Lewis, 1993; (Sittig, 1991). This compound has also been reported as having a weak chemical-like odor or slight aromatic odor (Lewis, 1993; (Sittig, 1991).

VAPOR PRESSURE

5.5x10(-6) mmHg (at 20 degrees C) (ACGIH, 1991)

1.5x10(-7) mmHg (at 20 degrees C) (Budavari, 1996)

2.0x10(-7) mmHg (at 20 degrees C) (NIOSH , 1999)

1.6x10(-7) mmHg (at 20 degrees C) (HSDB , 1999)

SPECIFIC GRAVITY

OTHER TEMPERATURE AND/OR PRESSURE

0.99 (at 20/4 degrees C) (NIOSH , 1999)

TEMPERATURE AND/OR PRESSURE NOT LISTED

0.98 (ACGIH, 1991)
0.98-0.99 (HSDB , 1999)
SOLID: 1.56 (at 15 degrees C) (CHRIS , 1999)

FREEZING/MELTING POINT

FREEZING POINT

108 degrees C; 226 degrees F; 381 degrees K (CHRIS , 1999)
227 degrees F (NIOSH , 1999)

MELTING POINT

107-109 degrees C (Sittig, 1991)
108.5-109 degrees C (Budavari, 1996)
108-109 degrees C (ACGIH, 1991)
109 degrees C (OHM/TADS , 1999)
108.5 degrees C (HSDB , 1999)

BOILING POINT

260 degrees C (ACGIH, 1991; HSDB , 1999)

230 degrees F (NIOSH , 1999)

110 degrees C; decomposes (OHM/TADS , 1999)

FLASH POINT

72-75 degrees C (Sittig, 1991)

72-77 degrees C (ACGIH, 1991)

162 degrees F (CHRIS , 1999)

171 degrees F (closed cup) (CHRIS , 1999)

EXPLOSIVE LIMITS

LOWER

Unknown (NIOSH , 1999)

UPPER

Unknown (NIOSH , 1999)

SOLUBILITY

IN WATER

DDT is insoluble in water (Lewis, 1993).
DDT is practically insoluble in water (Budavari, 1996)
0.002 ppm (at 25 degrees C) (OHM/TADS , 1999)
1.0 x 10(-7) g/100 mL (at 27 degrees C) (HSDB , 1999)
0.0031-0.0034 mg/L (at 25 degrees C) (HSDB , 1999)

IN ORGANIC SOLVENTS

Solubilities (Budavari, 1996):

Acetone (58 g/100 mL)
Alcohol (95%) (2 g/100 mL)
Benzene (78 g/100 mL)
Benzyl benzoate (42 g/100 mL)
Carbon tetrachloride (45 g/100 mL)
Chlorobenzene (74 g/100 mL)
Cyclohexanone (166 g/100 mL)
Ethyl Ether (28 g/100 mL)
Gasoline (10 g/100 mL)
Isopropanol (3g/100 mL)
Kerosene (8-10 g/100 mL)
Morpholine (75 g/100 mL)
Peanut oil (11 g/100 mL)
Pine oil (10-16 g/100 mL)
Tetralin (61 g/100 mL)
Tributyl phosphate (50 g/100 mL)

Solubility (at 27 degrees C) (HSDB , 1999):

Dibutyl phthalate (33 g/100 mL)
o-Dichlorobenzene (68 g/100 mL)
Dichlorodifluoromethane (2 g/100 mL)
Dioxane (100 g/mL)
Kerosene (crude) (8 g/100 mL)
Kerosene (refined) (4 g/100 mL)
Methylated naphthalenes (40-60 g/100 mL)
Mineral oil (5 g/100 mL)
Xylene (60 g/100 mL)

DDT is freely soluble in dioxane and pyridine; it is practically insoluble in other dilute acids and alkalies (Budavari, 1996) Lewis, 1993). Its solubility in organic solvents increases sharply with a rise in temperature (Budavari, 1996). In organic solvents, DDT dehydrochlorinates in organic or alkali bases (HSDB , 1999).

OTHER

DDT is highly soluble in lipids (HSDB , 1999)

OCTANOL/WATER PARTITION COEFFICIENT

log Kow = 6.91 (HSDB, 2004)

log Kow = 6.36 (HSDB , 1999)

log Kow = 6.38 (high pressure liquid chromatography) (HSDB , 1999)

log Kow = 6.19 (Clayton & Clayton, 1994)

SPECTRAL CONSTANTS

15542 (Sadtler Research Laboratories Prism Collection) (HSDB , 1999)

4655 (Sadtler Research Laboratories Spectral Collection) (HSDB , 1999)

OTHER/PHYSICAL

ODOR THRESHOLD

Not pertinent (CHRIS , 1999)
High: 5.0725 mg/m(3) (HSDB , 1999)
Low: 5.0725 mg/m(3) (HSDB , 1999)

ORGANIC CARBON PARTITION COEFFICIENT

238,000 (experimental) (HSDB , 1999)
146,000 (calculated) (HSDB , 1999)
1.13x10(5) to 3.5x10(5) (HSDB, 2004)
129 (Dragun, 1988)
239,883 (Dragun, 1988)
150,000 (Dragun, 1988)

NUCLEAR MAGNETIC RESONANCE

620 (Varian Associates NMR Spectra Catalogue) (HSDB , 1999)

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Classification | Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents