1,1-ジクロロ-1-ニトロエタン

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

Use water spray, foam, powder, carbon dioxide. In case of fire: keep drums, etc., cool by spraying with water.

Fresh air, rest. Half-upright position. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Refer for medical attention .

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

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.

General First Aid:

(General first aid procedures)

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water if flooding quantities as fog. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use foam, dry chemical, or carbon dioxide. Keep run-off water out of sewers and water sources.

IN GENERAL, MATERIALS WHICH ARE TOXIC AS STORED OR WHICH CAN DECOMP INTO TOXIC COMPONENTS...SHOULD BE STORED IN A COOL, WELL-VENTILATED PLACE, OUT OF DIRECT RAYS OF THE SUN, AWAY FROM AREAS OF HIGH FIRE HAZARD, & SHOULD BE PERIODICALLY INSPECTED... INCOMPATIBLE MATERIALS SHOULD BE ISOLATED FROM EACH OTHER.

1. Remove all ignition sources. 2. Ventilate area of spill or leak. 3. For small quantities, absorb on paper towels. Evaporate in safe place (such as a fume hood). Allow sufficient time for evaporating vapors to completely clear the hood ductwork. Burn the paper in a suitable location away from combustible materials. Large quantities can be collected & atomized in a suitable combustion chamber equipped with an appropriate effluent gas cleaning device. 1,1-Dichloro-1-nitroethane should not be allowed to enter a confined space, such as a sewer, because of the possibility of an explosion.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

1,1-Dichloro-1-nitroethane may be disposed of by atomizing in a suitable combustion chamber equipped with an appropriate effluent gas cleaning device.

TERRESTRIAL FATE: Based on a suggested classification scheme(3), 1,1-dichloro-1-nitroethane will have high to very high mobility(SRC) in soil based on an estimated Koc values of 36 to 59(1,2,SRC). Insufficient data are available to predict the relative importance or rate of biodegradation in soil conditions(SRC). Volatilization of 1,1-dichloro-1-nitroethane is expected from dry soils(SRC) based on an experimental vapor pressure of 16.88 mm Hg(4,SRC), and may also be important from moist soils(SRC) based on an estimated Henry's Law constant of 0.00128 atm-cu m/mole(5,SRC).

AQUATIC FATE: Based on a suggested classification scheme(2), volatilization of 1,1-dichloro-1-nitroethane from water is not rapid but may be significant(SRC) based upon an estimated Henry's Law constant of 0.00128 atm-cu m/mol(1,SRC). Volatilization half-lives from a model river (1 m deep flowing 1 m/sec with a wind velocity of 3 m/sec) and a model lake (1 meter deep) can be estimated to be about 4 hours(1) and 5 days(1), respectively. Insufficient data are available to predict the relative importance or rate of biodegradation in natural waters(SRC).

ATMOSPHERIC FATE: Based on an experimental vapor pressure of approximately 16.88 mm Hg at 25 °C(1), 1,1-dichloro-1-nitroethane will exist primarily in the vapor phase in the atmosphere(SRC). Based on a suggested classification scheme(2), it will degrade in the ambient atmosphere by reaction with photochemically produced hydroxyl radicals with an estimated half-life of 107 days(3). Removal of atmospheric 1,1-dichloro-1-nitroethane may occur through wet deposition(SRC) because of the high water solubility(1).

The substance can be absorbed into the body by ingestion and by inhalation of its vapour.

inhalation, ingestion, skin and/or eye contact

Cough. Sore throat. Laboured breathing. Shortness of breath. Symptoms may be delayed.

Redness. Pain.

Watering of the eyes. Redness. Pain.

Burning sensation. Abdominal pain.

In Animals: irritation eyes, skin; liver, heart, kidney damage; pulmonary edema, hemorrhage

Using a structure estimation method based on molecular connectivity indexes(1), the Koc for 1,1-dichloro-1-nitroethane can be estimated to be about 36(SRC). The Koc for 1,1-dichloro-1-nitroethane can be estimated to be about 59(SRC) based on an estimated water solubility of 2500 mg/L(4) and a regression derived equation(2). According to a suggested classification scheme(3), these estimated Koc values suggest that 1,1-dichloro-1-nitroethane has high to very high soil mobility(SRC).

MAY PRODUCE SEVERE PULMONARY EDEMA EITHER BY INHALATION OF VAPOR OR INGESTION OF LIQUID. ALSO SKIN IRRITATION.

SYMPTOMATOLOGY: 2. ...VERY CONCN NITROUS FUMES PRODUCE PROMPT COUGHING, CHOKING, HEADACHE, NAUSEA, ABDOMINAL PAIN, & DYSPNEA... 3. SYMPTOM-FREE PERIOD FOLLOWS EXPOSURE & LASTS FOR 5 TO 72 HR. 4. FATIGUE, UNEASINESS, RESTLESSNESS, COUGH, HYPERPNEA, & DYSPNEA APPEAR INSIDIOUSLY, AS THE ADULT RESP DISTRESS SYNDROME GRADUALLY DEVELOPS. 5. INCREASINGLY RAPID & SHALLOW RESP, CYANOSIS, MILD OR VIOLENT COUGHING WITH FROTHY EXPECTORATION, & PHYSICAL SIGNS OF PULMONARY EDEMA... A SEROUS EXUDATE MAY DEVELOP IN THE PLEURAL CAVITY, BUT ITS VOLUME IS USUALLY SMALL. 6. ANXIETY, MENTAL CONFUSION, LETHARGY, & FINALLY LOSS OF CONSCIOUSNESS. 7. A WEAK, RAPID PULSE, DILATED HEART, VENOUS CONGESTION, INTENSE CYANOSIS &...HEMOCONCENTRATION. CIRCULATORY COLLAPSE IS SECONDARY TO ANOXIA & HEMOCONCENTRATION. 8. ASPHYXIAL DEATH DUE TO BLOCKADE OF GAS EXCHANGE IN LUNGS. DEATH...WITHIN FEW HR AFTER THE FIRST EVIDENCE OF PULMONARY EDEMA. 9. SOMETIMES A SECOND ACUTE PHASE FOLLOWS THE INITIAL PULMONARY REACTION AFTER A QUIESCENT PERIOD OF SEVERAL WK. ... 10. IN NONFATAL, CONVALESCENCE MAY BE COMPLICATED BY INFECTIOUS BRONCHITIS, BRONCHIOLITIS OBLITERANS, PNEUMONIA AND GENERAL ASTHENIA. RARELY DIFFUSE PULMONARY FIBROSIS MAY DEVELOP. /NITROGEN OXIDES/

Based upon an estimated water solubility of 2500 mg/l(2), the BCF of 1,1-dichloro-1- nitroethane can be estimated to be approximately 7.5 from a regression-derived equation(1). This estimated BCF value suggests that bioconcentration in aquatic organisms may not be an important fate process(SRC).

The Henry's Law constant for 1,1-dichloro-1-nitroethane can be estimated to be 0.00128 atm-cu m/mole(SRC) using a structure estimation method(1,SRC). This value of Henry's Law constant indicates that volatilization from water is not rapid but possibly significant(SRC) based on a suggested classification scheme(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep flowing 1 m/sec with a wind velocity of 3 m/sec) can be estimated to be about 4.33 hours(2,SRC). The volatilization half-life from a model environmental lake (1 meter deep) can be estimated to be about 5 days(2,SRC).

The oral lethal dose of 1,1-dichloro-1-nitroethane for rabbits was found to lie between 150 and 200 mg/kg bw. Recovery from weight loss was reported to be quite slow. Animals exposed to these concentrations showed ulceration of the stomach wall and varying degrees of pulmonary edema. Several toxic effects were observed in the tissues of the fatally exposed animals. There was superficial erosion of the gastric mucosa with congestion, hemorrhage, and exudative inflammation; extensive, generalized, vascular damage with perivascular effusion and frequent venous clots; pulmonary edema, congestion, shrinkage, and desquamation of the alveolar cells; myocardial degeneration; severe hepatocellular degeneration and necrosis; and extensive glomerular tubular alteration.

Contact with the skin induced a marked reaction in rabbits. The skin became swollen and irritated. None of the animals died as the result of skin applications.

Observations of rabbits and guinea pigs were made ... through a series of 24 inhalation experiments. The duration of exposures varied from 10 minutes to 204 hours along with concentrations ranging from 144 mg/cu m (25 ppm) to 90,000 mg/cu m (15,600 ppm). Two rabbits and two guinea pigs were used for each experiment. The lowest lethal concentration for rabbits and guinea pigs was 300 mg/cu m (52 ppm) when the animals were exposed for 18.75 hours. In greater concentrations, the exposure was tolerated without lethal effect for shorter periods of time. Lower concentrations, 144 mg/cu m (25 ppm), were tolerated without lethal effect for 204 hours. In the highest concentration, 90,000 mg/cu m (15,600 ppm), all animals died within 12 hours after a 75-minute exposure period. The immediate physiologic effects observed following exposure were similar to other irritants. These effects included closed eyes, sneezing, coughing, and increased lacrimal and nasal secretions. In the longer exposure periods to fairly high air concentrations, there was excessive bronchial secretion, with coarse rales and rhonchi audible when the animals were removed from the exposure chamber. Other observations ... included weakness and appearance of illness, with no /SRP: no CNS depression/ or marked central nervous system (CNS) symptoms. At concentrations below 580 mg/cu m (100 ppm), the signs of irritation were definite but not severe and discharges were minimal. Neither irritation nor discharges were observed in animals exposed at 144 mg/cu m (25 ppm). The hematologic findings lacked any special significance. There was no distinct evidence of cellular destruction or stimulation of methemoglobin formation. In the case of animals exposed at high concentrations of 580 mg/cu m (100 ppm), there was some reduction in hemoglobin and the number of erythrocytes. During recovery, hemoglobin and erythrocytes returned to normal.

The most characteristic gross pathology occurred in the lungs of the rabbits and guinea pigs exposed to airborne concentrations in excess of 1.0 mg/l (170 ppm) for longer than 30 minutes. Edema, congestion, hemorrhage, and varying degrees of acute bronchitis were observed without inflammatory bronchitis like that following exposure to acid gases. The principal foci of damage from exposure at high concn were found in the heart, lungs, blood vessels, liver, and kidneys. The changes in the heart muscle consisted of acute myocardial degeneration with frequent rupture of the sarcolemma and fraying of the fibrils. The lungs showed congestion, focal hemorrhages, cellular infiltration with focal accumulations, pneumonitis, fibrinocellular exudation, alveolar degeneration, and necrosis. Vascular damage was apparent in all organs studied and consisted of perivascular and medial edema with cloudy swelling, necrosis of the medial muscle cells, and disruption and fragmentation of the vessel walls, along with other effects including thrombosis. In the liver, there were diffuse toxic changes of central configuration, cloudy swelling and degeneration, and nuclear damage and destruction (congestion and hemorrhage). These reported hepatic changes did not resemble those of highly chlorinated hydrocarbons. Most kidney damage occurred in the glomeruli and consisted of edema of the tufts, capsular tissue breakdown, occasional necrosis, and proliferation of the capsule. Tubular degeneration with granular casts and interstitial edema were also reported ... .