LINDANE

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.

STCC NUMBER

4941150 (other than agricultural)
4941152 (other than liquid)
4941151 (liquid)

DESIGNATIONS

BEILSTEIN HANDBOOK REFERENCE:4-05-00-00058
BEILSTEIN REFERENCE NUMBER:1907337

MOLECULAR FORMULA

C6-H6-Cl6

ERG GUIDE NUMBER

151-SUBSTANCES - TOXIC (NON-COMBUSTIBLE)

SYNONYM REFERENCE

(HSDB, 2004; Lewis, 2000; RTECS , 2000; OHM/TADS , 2000; Budavari, 1996; Meister, 1996; EPA, 1988; EPA, 1985)Thompson, 1992

USES/FORMS/SOURCES

USES

Lindane is used as an insecticide in a wide variety of applications, although its use in the US is restricted (Clayton & Clayton, 1994). Restrictions may be State dependent. For instance, a complete ban on the use or sale of lindane-containing products for the treatment of lice or scabies took effect in California in January of 2002 (Forrester et al, 2004).
Some of the restricted applications include plant nurseries, livestock sprays, seed treatment, pet shampoos, household sprays, flea collars, and the treatment of hardwood logs. Treatment of food with lindane is limited to avocados and pecans (Clayton & Clayton, 1994).
Lotions, shampoos, and creams containing lindane can be used on humans to treat lice and scabies (Clayton & Clayton, 1994).
Lindane has been used on termites, lice, mosquitoes, and flies that can no longer be controlled by DDT (Clayton & Clayton, 1994).
As per the EPA, lindane may no longer be registered for use in vaporizers, on many food crops, and in the dairy industry. It is no longer produced in the US (ACGIH, 1991) Extoxnet, 2000).
Certain applications of lindane may only be conducted by certified applicators (ATSDR, 2003).
Lindane is used as a therapeutic scabicide/pesticide in humans and animals (ACGIH, 1991; Budavari, 1996).

FORMS

Lindane has been described as existing in the following forms: crystals, off-white powder, yellow to white crystalline powder, or as "needles from alcohol." Some sources report that the compound is odorless; others describe its odor as a slightly persistent musty or aromatic smell(HSDB, 2004; NIOSH , 2000; Budavari, 1996; Clayton & Clayton, 1994) .
Humans use lindane primarily as a scabicide and pediculocide. When lindane is used for the treatment of scabies, it is usually in a 1% cream or ointment form, but may also be formulated as an emulsion, solution, aerosol, lotion, cream, or shampoo. It is also used to treat human head and body lice (ATSDR, 2003; Hayes & Laws, 1991).

SOURCES

Lindane can be manufactured by selectively crystallizing or using chromatographic adsorption on crude benzene hexachloride treated with methanol or acetic acid (HSDB, 2004).
Methanol is the most common solvent used to extract lindane from HCH. Nitric acid is then used in the process for odor removal (HSDB, 2004).
Lindane can be produced by combining benzene with chlorine and using photochlorination/isomer separation (Ashford, 1994).

SYNONYM EXPLANATION

Lindane (CAS 58-89-9) is defined as not less than 99.5 percent of the pure gamma isomer of hexachlorocyclohexane (HCH). The 99 percent pure form is also called TECHNICAL LINDANE (ATSDR, 2003; Clayton & Clayton, 1994; Hayes & Laws, 1991).

Lindane is also known as benzene hexachloride (BHC) through common usage, although BHC is actually a complex mixture of six related isomers; BHC is a misnomer. There are seven other isomers of HCH, but non-gamma isomers can no longer be made or used in the USA (ATSDR, 2003; Hayes & Laws, 1991).

Technical grade HCH is a mixture of at least five isomers, including approximately 60 to 70 percent alpha-HCH, 5 to 12 percent beta-HCH, 10 to 15 percent gamma-HCH, 6 to 10 percent delta-HCH, and 3 to 4 percent epsilon-HCH. Technical grade HCH (or any of its isomers) are produced in the USA, -HCH is imported to the US from France, Germany, Spain, Japan and China, but the rate of imports has declined over the years (ATSDR, 2003).

CAS numbers for the different HCH forms are as follows (HSDB, 2004; Lewis, 1996; OHM/TADS , 2000; RTECS , 2000):

alpha-HCH           CAS 319-84-6
beta-HCH            CAS 319-85-7
delta-HCH           CAS 319-86-8
epsilon-HCH         CAS 6108-10-7
Technical HCH (or)
  HCH, mixed isomers CAS 608-73-1

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

USES: Lindane is an organochlorine insecticide most often used by topical application to treat body lice or scabies infestations, but has become second line treatment because safer, more effective agents have been developed.

PHARMACOLOGY: Presumably it is a CNS stimulant in arthropods causing seizures and death.

TOXICOLOGY: Lindane is believed to act as an indirect GABA antagonist, resulting in CNS stimulation and seizures.

EPIDEMIOLOGY: Uncommon exposure that can result in significant morbidity and death, especially in children.

WITH POISONING/EXPOSURE

MILD TO MODERATE TOXICITY: Vomiting, headache, nausea, dizziness, diarrhea, and tremor.
SEVERE TOXICITY: Seizures, CNS depression, agitation, ataxia, hypotension, respiratory depression, metabolic acidosis, and coma. Children appear to be more susceptible to the toxic effects of lindane and more likely to manifest severe effects.

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

SUMMARY

PHARMACOLOGY: Presumably it is a CNS stimulant in arthropods causing seizures and death.
TOXICOLOGY: Lindane is believed to act as an indirect GABA antagonist, resulting in CNS stimulation and seizures.
EPIDEMIOLOGY: Uncommon exposure that can result in significant morbidity and death, especially in children.
MILD TO MODERATE TOXICITY: Vomiting, headache, nausea, dizziness, diarrhea, and tremor.
SEVERE TOXICITY: Seizures, CNS depression, agitation, ataxia, hypotension, respiratory depression, metabolic acidosis, and coma. Children appear to be more susceptible to the toxic effects of lindane and more likely to manifest severe effects.

ACID-BASE

METABOLIC ACIDOSIS: Metabolic acidosis may be a consequence of seizures, and an immediate cause of death (Morgan, 1993).
LACTIC ACIDOSIS: Lactic acidosis has been reported after ingestions of lindane (Jaeger et al, 1984).
RESPIRATORY ACIDOSIS: Respiratory acidosis may develop in patients with significant CNS depression (Aks et al, 1995).

CARDIOVASCULAR

CARDIAC DYSRHYTHMIAS: High concentrations of organochlorine insecticides can cause cardiac dysrhythmias by increasing myocardial irritability (Morgan, 1993). Inhalation of lindane-hydrocarbon mixtures may result in ventricular dysrhythmias due to sensitization of the myocardium to circulating catecholamines; halogenated hydrocarbons have been most frequently implicated (Kulig & Rumack, 1981).
ECG ABNORMALITIES: Based on reports of occupational exposure to lindane, ECG abnormalities were reported in 15% of 45 workers manufacturing technical-grade HCH (ATSDR, 2003).
HYPOTENSION: Significant hypotension was reported following dermal (covering almost the entire body) application of lindane lotion (Sudakin, 2007).

DERMATOLOGIC

DERMATITIS: Extensive contact may result in dermatitis, irritation, and local hypersensitivity (Fiumara & Kahn, 1983; Budavari, 1996).
TOPICAL ABSORPTION: Percutaneous absorption may occur in patients with compromised epidermal barrier function (Friedman, 1987; Solomon et al, 1995).

ENDOCRINE

THYROID ENLARGEMENT: There was a report of a large number of patients presenting with palpable thyroid enlargement following ingestion of hexachlorobenzene-treated seed grain 25 years previously (Peters et al, 1982). No malignancies were seen.

GASTROINTESTINAL

VOMITING AND ABDOMINAL PAIN AND DIARRHEA: When ingested, lindane has caused abdominal pain, nausea, vomiting and diarrhea, especially when contained in petroleum solvents (Forrester et al, 2004; Lifshitz & Gavrilov, 2002; Jaeger et al, 1984); vomiting is common after ingestion (Nordt & Chew, 2000).
PANCREATITIS: Pancreatitis was reported 13 days after ingestion of 15 to 30 mL of lindane by a 35-year-old man (Munk & Nantel, 1977; Nantel et al, 1977).

GENITOURINARY

MYOGLOBINURIA: Myoglobinuria secondary to rhabdomyolysis has been described after ingestion of lindane (Jaeger et al, 1984; Rao et al, 1988; Hall & Hall, 1999).
RENAL INSUFFICIENCY: A man developed status epilepticus and myoglobinuria with subsequent acute renal insufficiency and generalized myolysis following ingestion of lindane-contaminated food (Nantel et al, 1977).

HEENT

Lindane can irritate the eyes, nose, and throat (EPA, 1985).
CONJUNCTIVITIS: Conjunctivitis has been caused by the use of ointments and lotions containing 0.1% to 1% lindane applied to eyelashes (Post & Juhlin, 1963).
AMBLYOPIA: Amblyopia has been reported (Lee et al, 1976).

HEMATOLOGIC

APLASTIC ANEMIA: Aplastic anemia has been reported in number of cases, both acutely and chronically, and a majority of the cases have involved concentrations of benzene hexachloride that exceed 1%. The chronic toxic effects were seen in patients with repeated exposure (Rauch et al, 1990; Morgan, 1993; Baselt, 1997; Woodliff et al, 1966; Loge, 1965). Pancytopenia occurred in a teenager following continuous use of 1% lindane lotion on 8 occasions to open lesions (Berry et al, 1987).
Isolated reports of other hematologic abnormalities (ie, leukopenia, leukocytosis, granulocytopenia, granulocytosis, eosinophilia, monocytosis, and thrombocytopenia) have occurred from occupational exposure to lindane; exposure levels were not specified (ATSDR, 2003).
PORPHYRIA: Mixed porphyria symptoms have been reported following an outbreak of accidental hexachlorobenzene ingestion from treated seed grain. Many patients had persistent abnormal porphyrin metabolism with significant neurologic, dermatologic, and orthopedic signs and symptoms (Peters et al, 1982).
IDIOPATHIC THROMBOCYTOPENIC PURPURA: ITP developed in a 17-year-old woman who worked formulating wood preservatives that included lindane (Hay & Singer, 1991).

HEPATIC

ABNORMAL LIVER ENZYMES: An important property of the chlorinated hydrocarbons, particularly lindane, is their capacity to induce the drug-metabolizing enzymes of the liver (Kolmodin-Hedman et al, 1971; Wells & Milhorn, 1983; Klaasen, 1985).
HEPATOMEGALY: Chronic absorption commonly induces liver damage and hepatomegaly (Budavari, 1996; Gosselin et al, 1984).

IMMUNOLOGIC

One study evaluated immunological alterations in the blood of 20 human lindane poisoning cases. Lindane exposure was associated with higher levels of serum IL-2, IL-4, and TNF-alpha and lower levels of IFN-gamma. However, serum immunoglobulin (IgG, IgM, IgA, IgE) levels did not change (Seth et al, 2005).

MUSCULOSKELETAL

RHABDOMYOLYSIS: Elevated creatine kinase with hemoglobinuria and myoglobinuria have been reported in patients exhibiting skeletal muscle damage from hexachlorobenzene toxicity (Peters et al, 1982; Munk & Nantel, 1977), with rhabdomyolysis reported in one 35-year-old man who ingested 15 to 30 mL of lindane (Jaeger et al, 1984).
MUSCLE WEAKNESS: In a case series analysis, a reported 73% of patients developed profound muscle weakness in the acute phase after a hexachlorobenzene ingestion epidemic(Peters et al, 1982).
ARTHRITIS: Arthritis, with and without gout, has been reported as an adverse sequelae to acute lindane and chlorinated hydrocarbon ingestions. Uric acid levels may be elevated (Peters et al, 1982; Wells & Milhorn, 1983).

NEUROLOGIC

HEADACHE: Severe headache may occur with exposure to lindane (Hathaway et al, 1996; Diaz, 1998).
NEUROTOXICITY: Mild drowsiness, somnolence or lethargy may develop in patients with mild toxicity. More severe CNS depression may develop following seizures (Aks et al, 1995).
SEIZURES: Lindane is a CNS excitant and convulsant, and can act as a neurotoxicant. Accidental ingestion has caused fatalities. Both topical exposure and ingestion have resulted in seizures. Young children and the elderly appear to be at a higher risk, and repeated case reports show the development of seizures in younger children postingestion (Sudakin, 2007; Aks et al, 1995; Anon, 2005; Bhalla & Thami, 2004; Lifshitz & Gavrilov, 2002; Nordt & Chew, 2000).
TREMORS: Tremors have been reported and often occur concomitantly with other adverse symptoms including seizures, agitation, sensory disturbances, peripheral neuropathy, and nervousness (Lifshitz & Gavrilov, 2002; Fischer, 1994; Czegledi-Janko & Avar, 1970).
ELECTROENCEPHALOGRAM ABNORMALITIES: Sensory disturbances, excitation with myoclonic jerking (Morgan, 1993), seizures, tremor, ataxia, agitation, nervousness, and amnesia may occur in association with EEG changes. EEG changes occurred in the absence of seizures in 15 of 17 persons occupationally exposed to lindane (Czegledi-Janko & Avar, 1970).
PERIPHERAL NEUROPATHY: Neuropathy can occur with lindane exposure and organochlorine poisoning. Presentation of these effects included hyperesthesia, paresthesia, and polyneuritis (Tolot, 1969; Morgan, 1993).
PSYCHOMOTOR AGITATION: Agitation, tremors, restlessness, muscle spasms, and nervousness can occur with lindane intoxication and are common (Lifshitz & Gavrilov, 2002; EPA, 1985; Fischer, 1994; Jaeger et al, 1984; Diaz, 1998; Zilker et al, 1999).

PSYCHIATRIC

HALLUCINATIONS: Hallucinations have been reported following acute poisonings (Diaz, 1998).
ALTERED MENTAL FUNCTION: Alterations in mental function occur as a result of the neurotoxicity of chlorinated hydrocarbon insecticides (Morgan, 1993).
Occupationally exposed persons experienced emotional changes with lindane exposure (Baselt, 1997).

RESPIRATORY

CHEMICAL PNEUMONITIS: Aspiration of insecticides containing petroleum distillates may result in chemical pneumonitis.
HYPOXEMIA: Pulmonary gas exchange may be reduced secondary to seizure development in some patients, and this reduced exchange can possibly lead to cyanosis and death (Morgan, 1993). Hypoventilation has also occurred necessitating mechanical ventilation (Nordt & Chew, 2000).
DYSPNEA: Dyspnea has been reported from ingestion of lindane (Lewis, 1996).
ACUTE LUNG INJURY: Pulmonary edema has occurred from lindane exposure, especially in children and where commercial formulations are in hydrocarbon solvents (Jaeger et al, 1984; EPA, 1985).
RESPIRATORY RATE: Respiratory depression secondary to seizures is common with severe lindane intoxications (Proctor et al, 1988; Aks et al, 1995; Nordt & Chew, 2000).

VITAL SIGNS

FEVER: Hyperthermia may occur with prolonged seizures, and fever occurred in a fatal case of endrin ingestion and may occur with lindane intoxications (Runhaar et al, 1985).

CHRONIC CLINICAL EFFECTS

WITH POISONING/EXPOSURE

Lindane is preferentially deposited in fat stores because it is lipophilic. Neurotoxic effects are more likely with repeated and frequent application of topical lindane for scabies treatment (Boffa et al, 1995).
From isolated case reports, chronic lindane exposure may cause decreased leukocyte counts (Brassow, 1981), pulmonary fibrosis (with mixed exposures) (Barthel, 1974), hepatic cirrhosis (with mixed exposures) (Bezuglyy, 1976), EEG abnormalities (Czegledi-Janko & Avar, 1970), kidney dysfunction (Loganovskii, 1971), and leukemia following development of aplastic anemia (one case with mixed exposure to lindane and DDT) (Hoshizaki et al, 1969). Elevated blood levels of HDL (alpha)-lipoprotein were found in some persons occupationally exposed to lindane (Hayes & Laws, 1991).
Long-term exposure to lindane, as used in wood-preserving chemicals, could be related to subjective complaints (attention, mood, and motivation) and to subtle alterations of neurobehavioral performance (memory) in women (Peper et al, 1998).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

SUMMARY

Prehospital oral decontamination should be avoided because of the risk of rapid onset CNS depression and seizures and subsequent aspiration.

EMESIS/NOT RECOMMENDED

Emesis is not recommended, since seizures commonly occur suddenly and without warning. Seizures have occurred as early as 15 minutes following ingestion (Jaeger et al, 1984). Death from ARDS and anoxia has occurred in an adult who seized during ipecac-induced vomiting (Kurt et al, 1986).

-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. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection.

Contact lens use is not recommended when working with this chemical. If contact lenses are worn, then appropriate eye and face protection devices must be used. OSHA emphasizes that dusty and/or chemical environments may represent an additional hazard to contact lens wearers.

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, respiratory system, central nervous system, blood, liver, and kidneys (National Institute for Occupational Safety and Health, 2007).(OSHA, 2000).

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.

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.
If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
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.

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).
Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
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.

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

Prehospital oral decontamination should be avoided because of the risk of rapid onset CNS depression and seizures and subsequent aspiration.
Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
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.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

ACUTE LETHAL STUDIES

Ingestion of 8 ounces of 20% lindane resulted in death in adults (Rao et al, 1988) Woolf et al, 1987).
The lethal dose of lindane is estimated to be 125 mg/kg (HSDB , 2000).
It is believed that 28 grams is the mean fatal dose of technical grade lindane in humans (Baselt, 1997).
An adult male died after ingesting 2 ounces of 1% lindane lotion (Baselt, 1997).
A man with scabies developed progressive severe neurotoxicity after a single application of a thin film of lindane (1%) to his skin from the neck to the toes. Prior to the lindane administration, fresh scratch marks were noted throughout the patient's body which might have increased dermal absorption of lindane significantly. In addition, the physician's order did not include instructions to wash lindane from the skin after its application. He experienced infectious complications and died 50 days after admission (Sudakin, 2007).
In a review article, 67 cases of severe adverse effects, including 20 death (including 7 children and 4 patients aged 65 and older) following the labeled use, excessive use, and ingestion of lindane were identified. Seizures and respiratory problems developed in the majority of patients using the labeled dose (defined as one 4-minute application of shampoo or one 8 to 12 hours of single total body application of lindane lotion 1%). Three patients ingested lindane. The most common adverse effects were tremor, vertigo, paresis, and aphasia. The following adverse effects were also reported: shortness of breath (n=3), visual changes (n=2), anaphylactic reaction (n=1), aplastic anemia (n=3), leukocytosis (n=1), tachycardia (n=1), alopecia (n=1), acute generalized exanthematous pustulosis (n=1) (Nolan et al, 2012).

CHRONIC LETHAL STUDIES

Lindane and other isomers of hexachlorocyclohexane may be reasonably anticipated to be carcinogens (ACGIH, 1991). The ACGIH places lindane in Category A3: confirmed animal carcinogen with unknown relevance to humans (ACGIH, 2000).
"NTP anticipated human carcinogen" (NTP, 2000).
Firm evidence does not exist linking lindane exposure in humans to development of aplastic anaemia or leukaemia (IARC , 1998). The IARC classifies Lindane in Group 2B: The agent (mixture) is possibly carcinogenic to humans.The exposure circumstance entails exposures that are possibly carcinogenic to humans (IARC, 1987).

In one study, workers involved in manufacturing lindane showed no evidence of chromosomal aberrations (IARC , 1998).

CHILDREN

ACUTE LETHAL STUDIES

Ingestion of 6 mg/kg in a child has resulted in death (Falk & Hinrichs, 1957).
A 2-month old died after total body application of 1 percent lindane that was left on for 18 hours (Davies et al, 1983).
Excessive application of a 1% lindane lotion resulted in death for a 2-month-old, 4.5 kg child. The lindane concentration in the brain was 110 ppb, which was 3 times the amount found in the blood (HSDB , 2000).
In a review article, 67 cases of severe adverse effects, including 20 death (including 7 children and 4 patients aged 65 and older) following the labeled use, excessive use, and ingestion of lindane were identified. Seizures and respiratory problems developed in the majority of patients using the labeled dose (defined as one 4-minute application of shampoo or one 8 to 12 hours of single total body application of lindane lotion 1%). Three patients ingested lindane. The most common adverse effects were tremor, vertigo, paresis, and aphasia. The following adverse effects were also reported: shortness of breath (n=3), visual changes (n=2), anaphylactic reaction (n=1), aplastic anemia (n=3), leukocytosis (n=1), tachycardia (n=1), alopecia (n=1), acute generalized exanthematous pustulosis (n=1) (Nolan et al, 2012).

MAXIMUM TOLERATED EXPOSURE

Toxic doses and the effects of lindane and related isomers vary with route and rate of absorption. Lindane, the gamma isomer of hexachlorocyclohexane, is more acutely toxic, while the beta and alpha isomers are retained in the body tissues longer and pose a greater chronic risk (Clayton & Clayton, 1994).

ACUTE NON-LETHAL STUDIES

An oral dose of 45 mg (approximately 0.65 mg/kg) has caused seizures (Lewis, 1996).
CASE REPORT: A 24-year-old man, found 20 minutes after ingesting 100 mL of a lindane hair shampoo (calculated amount of lindane 1035 grams), developed seizures. Following symptomatic therapy he recovered without sequelae (Zilker et al, 1999).
CASE REPORT: A 56-year-old man developed vomiting, seizures, cardiac dysrhythmias, and neurological abnormalities after ingesting about 12 ounces (about 355 mL) of an insecticide containing 20% lindane. Although he recovered following supportive care, he committed suicide 12 days after the initial presentation (Wiles et al, 2015).
Large ingestions of 1% lindane (unknown amount in Davies' (1983) case) and greater than 2 ounces in Kurt (1986) have resulted in significant toxicity.
In a review article, 67 cases of severe adverse effects (AE), including 20 death (including 7 children and 4 patients aged 65 and older) following the labeled use (47 patients) , excessive use (17 cases), and ingestion (3 cases) of lindane were identified. Seizures and respiratory problems developed in the majority of patients who developed severe AE after using the labeled dose (defined as one 4-minute application of shampoo or one 8 to 12 hours of single total body application of lindane lotion 1%). Three patients ingested lindane. The most common adverse effects were tremor, vertigo, paresis, and aphasia. The following adverse effects were also reported: shortness of breath (n=3), visual changes (n=2), anaphylactic reaction (n=1), aplastic anemia (n=3), leukocytosis (n=1), tachycardia (n=1), alopecia (n=1), acute generalized exanthematous pustulosis (n=1) (Nolan et al, 2012).

CHRONIC EXPOSURE STUDY

Humans tolerated purified gamma-lindane with no ill effects at 40 mg/man/day for 14 days, but the same dosage of the technical grade caused vertigo, headache, and diarrhea. In another study, lindane at 45 mg given three times per day for three days induced convulsions in one patient (ACGIH, 1991).

CHILDREN

ACUTE NON-LETHAL STUDIES

As little as two total body applications of 1% Kwell on successive days in an 18-month-old child have resulted in a seizure (Telch & Jarvis, 1982).
A 10-year-old patient suffered coma after a general total body application of 1% lindane (Lee & Groth, 1977).
CASE REPORT: A 3-year-old boy developed generalized seizures in his sleep with transient loss of sensorium about 1 hour after ingesting 10 mL of lindane lotion. He presented with drowsiness, a GCS (Glasgow coma score) of 10/15, and papular skin lesions. Following supportive care, he recovered 24 hours later (Ramabhatta et al, 2014).
One 4-month-old developed increased muscle tone, tonic posturing, and poor orientation to visual stimuli after a total body application of 1% lindane was left on for 24 hours (Pramanik & Hansen, 1979).
Ingestion of as little as 5 mL of 1% lindane has caused respiratory depression and/or seizures in children aged 1 to 4 years (Nordt & Chew, 1999; (Aks et al, 1995) Jaeger et al, 1983).
Seizures were reported in a 1-year-old child who was given one teaspoonful of 1% lindane (50 mg) in addition to topical application of 100 mg (Wheeler, 1977).
Oral doses of about 50 mg/kg have caused severe toxicity in young children who ingested lindane pellets (Stormont & Conley, 1955).

ANIMAL DATA

The maximally tolerated dose for rats fed lindane in the diet is 1500 ppm for 90 days (Proctor et al, 1988).
Minimal effects were seen in several species of laboratory animals exposed to an average concentration of 0.7 mg/m(3) of lindane, 7 hours per day, 5 days per week, for approximately 1 year. Rats exposed to 0.19 mg/m(3) continuously for 655 days, 24 hours per day, exhibited no abnormal pathology (ACGIH, 1991).
Oral doses of 60 mg/kg produced seizures in 17.6% of rats; 100 mg/kg in 69.4 percent, and 150 mg/kg in 95.5%. The lethality rate at the highest dose was 18 percent (Tusell et al, 1987).
Lindane is more toxic than DDT or dieldrin in some domestic animals, including calves (Lewis, 1996).
Lindane reduced the pregnancy rate in ewes through a diet of 1 mg/kg/day (Beard et al, 1999).

Carcinogenicity Ratings for CAS58-89-9 :

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

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): Not Assessed under the IRIS program. ; Listed as: gamma-Hexachlorocyclohexane (gamma-HCH)
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): Not Listed
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Lindane
MAK (DFG, 2002): Category 4 ; Listed as: Lindane

Category 4 : Substances with carcinogenic potential for which genotoxicity plays no or at most a minor part. No significant contribution to human cancer risk is expected provided the MAK value is observed. The classification is supported especially by evidence that increases in cellular proliferation or changes in cellular differentiation are important in the mode of action. To characterize the cancer risk, the manifold mechanisms contributing to carcinogenesis and their characteristic dose-time-response relationships are taken into consideration.

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 CAS58-89-9 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor:
RfD: 3x10(-4) mg/kg-day

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk:

TOXICITY VALUES

References: ACGIH, 1991 Budavari, 1996 CHRIS, 2000 Clayton & Clayton, 1994 ) (Extoxnet, 2000; Hayes & Laws, 1991 ITI, 1995 Lewis, 2000 RTECS, 2000 ) Tusell et al, 1987 Note: All values below are from RTECS (2000) unless otherwise specified.
- LCLo- (INHALATION)MOUSE:
- LD50- (ORAL)CAT:
- LD50- (ORAL)DOG:
- LD50- (ORAL)GUINEA_PIG:
- LD50- (SKIN)GUINEA_PIG:
- LD50- (SUBCUTANEOUS)GUINEA_PIG:
- LD50- (INTRAPERITONEAL)HAMSTER:
- LD50- (ORAL)HAMSTER:
- LD50- (INTRACEREBRAL)MOUSE:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (SKIN)MOUSE:
- LD50- (ORAL)RABBIT:
- LD50- (SKIN)RABBIT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LD50- (SUBCUTANEOUS)RAT:
- LDLo- (INTRAVENOUS)DOG:
- LDLo- (ORAL)HUMAN:
- LDLo- (INTRAPERITONEAL)MOUSE:
- LDLo- (INTRAVENOUS)RABBIT:
- LDLo- (INTRAPERITONEAL)RAT:
- TCLo- (INHALATION)CAT:
- TCLo- (INHALATION)MOUSE:
- TCLo- (INHALATION)RAT:
- TD- (ORAL)MOUSE:
- TDLo- (ORAL)DOG:
- TDLo- (ORAL)GUINEA_PIG:
- TDLo- (ORAL)HAMSTER:
- TDLo- (ORAL)HUMAN:
- TDLo- (SKIN)HUMAN:
- TDLo- (ORAL)MOUSE:
- TDLo- (SKIN)PIG:
- TDLo- (ORAL)RABBIT:
- TDLo- (INTRAPERITONEAL)RAT:
- TDLo- (INTRATESTICULAR)RAT:
- TDLo- (ORAL)RAT:

CALCULATIONS

AMBIENT CONVERSIONS

CONVERSION FACTORS

ppm X 4.96 = mg/m(3)
mg/m(3) X 0.20 = ppm

Conversion factors for lindane (gamma-hexachlorocyclohexane) in air at 20 degrees C (ATSDR, 1994) -

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS58-89-9 (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

Lindane

TLV:

TLV-TWA: 0.5 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A3
Codes: Skin
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.
Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.

TLV Basis - Critical Effect(s): Liver dam; CNS impair
Molecular Weight: 290.85

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 CAS58-89-9 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS58-89-9 (National Institute for Occupational Safety and Health, 2007):

Listed as: Lindane
REL:

TWA: 0.5 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: [skin]

Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.

Note(s):

IDLH:

IDLH: 50 mg/m3
Note(s): Not Listed

OSHA PEL Values for CAS58-89-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Lindane
Table Z-1 for Lindane:

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: 0.5

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 CAS58-89-9 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS58-89-9 (U.S. Environmental Protection Agency, 2010):

Listed as: Lindane (D013)
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity
Listed as: gamma-BHC
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:
Listed as: Cyclohexane, 1,2,3,4,5,6-hexachloro-,(1[alpha], 2[alpha], 3[beta]-, 4[alpha], 5[alpha], 6[beta])
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

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

1 (0.454)

Additional Information:
Listed as: Lindane (all isomers)
Final Reportable Quantity, in pounds (kilograms):

1 (0.454)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS58-89-9 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS58-89-9 (U.S. Environmental Protection Agency, 2010b):

Listed as: Cyclohexane, 1,2,3,4,5,6-hexachloro-, (1alpha,2alpha,3beta,4alpha,5alpha,6beta)-
P or U series number: U129
Footnote:
Listed as: Lindane
P or U series number: U129
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 CAS58-89-9 (U.S. Environmental Protection Agency, 2010):

Listed as: Lindane
Reportable Quantity, in pounds: 1

Only the statutory or final RQ is shown. For more information, see 40 CFR table 302.4.

Threshold Planning Quantity, in pounds:

1000/10,000
Amount necessary to be covered by this standard. See 40 CFR 355.30.

Note(s): Not Listed

EPA SARA Title III, Community Right-to-Know for CAS58-89-9 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Lindane [Cyclohexane, 1,2,3,4,5,6-hexachloro-(1.alpha.,2.alpha.,3.beta.,4.alpha.,5.alpha.,6.beta.)-]
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS58-89-9 (49 CFR 172.101 - App. B, 2005):

Listed as Lindane
Severe Marine Pollutant: Yes
Listed as gamma-BHC
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS58-89-9 (EPA, 2005):

Listed as: Cyclohexane, 1,2,3,4,5,6-hexachloro-, (1.alpha.,2.alpha.,3.beta.,4.alpha.,5.alpha.,6.beta.)-

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 CAS58-89-9 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

Lindane should be properly handled and stored, and commercial solutions should be treated with special care as they contain liquids that are flammable or combustible (ITI, 1995).
Individuals working with lindane should wear proper protective equipment (ITI, 1995).

HANDLING

Personnel should wear rubber gloves, safety goggles, overalls, and self-contained breathing apparatus when handling lindane (ITI, 1995; OHM/TADS , 2000).

STORAGE

CONTAINER

Lindane is stored in bags or drums. Containers should be protected from damage (ITI, 1995; OHM/TADS , 2000).
The compound is stable in temperatures to 180 degrees C (Hartley & Kidd, 1987).

ROOM/CABINET RECOMMENDATIONS

Store in a cool, dry, well-ventilated place, preferably in outdoor, detached storage areas away from light, sources of fire, and other stored chemicals (ITI, 1995; Meister, 1996; Sittig, 1991).

INCOMPATIBILITIES

Lindane is incompatible with lime sulfur, lime, calcium arsenate, and other strong alkaline materials. It also is incompatible with iron, zinc, aluminum and other powdered metals. When in contact with ozone, lindane can become oxidized (HSDB , 2000) NTP, 2000; Thompson, 1992).

-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.

Safety goggles, rubber gloves, overalls, and a self-contained breathing apparatus should be worn when working with lindane (ITI, 1995). The use of protective clothing and respirators is required for certain applications (EPA, 1988).

Wash wet or contaminated skin immediately. Potentially contaminated clothing daily should be changed daily. If wet or contaminated, remove nonimpervious clothing at once. Ensure that personnel have access to emergency showers for quick body drenching (NIOSH , 2000; Sittig, 1991).

Before eating, smoking, or using restroom facilities, workers who handle lindane should wash their hands with a mild soap or detergent (HSDB , 2000).

EYE/FACE PROTECTION

Personnel should wear dust- and splash-proof goggles where lindane and liquids containing lindane have the potential to contact the eyes (HSDB , 2000).

Workers should not wear contact lenses when working with lindane (NIOSH , 2000).

Wash eyes that have come in contact with lindane with copious amounts of water. Lift upper and lower lids periodically while washing. Seek immediate medical attention (NIOSH , 2000).

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 58-89-9.

All data are compiled from published sources and are NOT recommended specifically by Truven Health Analytics. The appearance of specific manufacturers or products in this section does not represent an endorsement by Truven Health Analytics. No attempt has been made to verify the data presented. All product recommendations should be confirmed with the specific manufacturer for verification of product performance.
CLOTHING

Plastic Laminate

DuPont Personal Protection

Tychem 10,000

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid, saturated solution in acetone
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.02
Notes: liquid, saturated solution in methanol
Citation: (DuPont, 2002)

Tychem 7500

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid, saturated solution in acetone
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid, saturated solution in methanol
Citation: (DuPont, 2002)

Tychem 9400

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.06
Notes: liquid, saturated solution in acetone
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid, saturated solution in methanol
Citation: (DuPont, 2002)

Tychem BR

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.06
Notes: Not Listed
Citation: (DuPont, 2002)

Tychem LV

Degradation Rating: Not Listed
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.06
Notes: saturated solution in acetone
Citation: (DuPont, 2003)

Tychem QC

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: saturated solution in acetone
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: saturated solution in methanol
Citation: (DuPont, 2002)

Tychem SL

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid, saturated solution in acetone
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): Not Tested
Permeation Rate (mcg/cm2/min): Not Tested
Notes: liquid, saturated solution in methanol
Citation: (DuPont, 2002)

Tychem TK

Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.1
Notes: liquid, saturated solution in methanol
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.06
Notes: Not Listed
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.1
Notes: Not Listed
Citation: (DuPont, 2002)
Degradation Rating: No Degradation Rating provided
Breakthrough Time (minutes): >480
Permeation Rate (mcg/cm2/min): <0.06
Notes: liquid, saturated solution in acetone
Citation: (DuPont, 2002)

FOOTWEAR

Specific recommendations and test data for this product type were not found in the available manufacturers' product literature.

GLOVES

Specific recommendations and test data for this product type were not found in the available manufacturers' product literature.

GENERAL INFORMATION

This section provides a compilation of chemical resistance information and test data for specific protective clothing products. Chemical resistance information includes both degradation resistance ratings and permeation resistance data. This information is designed to assist in the selection of appropriate protective clothing. Only data on specific products and manufacturers are included. Generic information or recommendations are not provided since significant differences can exist in the chemical resistance for apparent similar product types.
Specific product information is organized by general product type (gloves, garments, and footwear), material type, and manufacturer. The category 'garments' may include totally encapsulating suits, splash suits, as well as other items (e.g., coveralls, jackets, and aprons). Specific manufacturers should be contacted to determine the features of available styles/models.
In addition to chemical resistance information, there are many critical variables in the selection of protective clothing which cannot be represented in this summary of the literature. Some factors to be considered in choosing protective clothing include, but are not limited to: overall clothing integrity, physical hazard resistance, durability, human factors, ease of decontamination, and cost. Overall clothing integrity refers to a specific design's ability to offer consistent protection for all clothing-covered areas of the body. Physical hazards include resisting the effects of abrasion, cuts, tears, and punctures. Human factors entail effects on wearer mobility, visibility, and hearing for garments; dexterity, tactility, and grip for gloves; ankle support and weight for footwear; and, any effect of the clothing on the function of the wearer. There are several variations in the design for gloves, garments, and footwear that affect these factors. Protective clothing must properly be sized and correctly fit the wearer to ensure its proper use and function.
As required in the U.S.A., protective clothing should be selected based on a risk assessment of the workplace. This risk assessment must account for the identification of existing as well as potential hazards and involve the recommendation of protective clothing appropriate for the identified hazards. Therefore, the recommendations in this section should not be used as the sole basis for decisions on choice of protective clothing, but rather should be used as a tool by qualified occupational health and safety professionals or other technically qualified persons in conjunction with a review of all mitigating factors. Consult the OSHA PPE Standard (29 CFR 1910.132 - 1910.138) for regulations and additional guidance regarding the selection and use of protective clothing and equipment. For general information on protective clothing selection, refer to the "PERSONAL PROTECTIVE EQUIPMENT - OSHA PUB 3077" document.
PROTECTIVE CLOTHING SELECTION

Determine the type of protective clothing item needed based on a risk assessment (e.g., gloves, garments, footwear).
For high risk situations, choose clothing that covers all parts of the body that may be exposed. In many cases, multiple clothing items will be required. Low risk situations may permit partial body protective clothing. Select protective clothing products that have reported chemical resistance data. High risk situations involving full body clothing or extended chemical contact often require permeation resistance data to determine the barrier effectiveness of materials used in the construction of clothing. Relatively low risk situations, where only splash or incidental exposure occur, may allow use of protective clothing based on degradation or penetration resistance data. Specifics on the interpretation of chemical resistance data are presented below.
Other factors must be considered in addition to chemical resistance. The selected chemical protective clothing item should offer the optimal combination of protection against identified hazards while allowing maximum function and comfort.

INTERPRETATION OF DEGRADATION RATINGS

Degradation refers to physical changes in a material as the result of chemical exposure. Degradation may become evident in visible changes, such as discoloration, swelling, delamination, deterioration, or disintegration. Degradation effects may also be measured by weight change or other changes in a material's physical properties (e.g., strength, elasticity, hardness).
Degradation resistance ratings are provided by manufacturers to rate the amount of degradation that occurs for a particular protective clothing material when contacted by a chemical. All degradation ratings are qualitative and include ratings, such as "EXCELLENT," "GOOD," "FAIR," "POOR," and "NOT RECOMMENDED." There is no standard test method for the measurement of chemical degradation resistance; therefore, manufacturer ratings may be based on different testing approaches. This makes comparison of degradation ratings between manufacturers unreliable.
The use of degradation resistance ratings alone to recommend protective clothing, particularly for high hazard situations, should be avoided. Degradation resistance testing does not directly assess the barrier quality of protective clothing, since materials can show relatively little degradation but still allow either permeation or penetration by a chemical. Degradation resistance ratings can be used to exclude protective clothing materials from consideration. Protective clothing materials with a "NOT RECOMMENDED" degradation resistance rating should never be used.
For some products, the rating "NO PENETRATION" is provided. This refers to penetration resistance test results that are based on a different procedure (American Society for Testing and Materials (ASTM) Standard Test Method F 903). Penetration resistance testing involves placing a material sample in a test cell, exposing the exterior side of the material to a chemical, and then observing the interior side of the material for visible signs of liquid penetration. Part of the test is conducted at an elevated pressure. Test results are reported as pass (no penetration) or fail (penetration detected). Unlike degradation testing, penetration testing provides an assessment of protective clothing material barrier performance. Since penetration resistance testing examines only observable amounts of liquid penetration, permeation may still occur. The use of penetration resistance data must be restricted to liquid chemicals, and should be limited to scenarios where there is no reasonable vapor exposure hazard under the conditions of exposure.

INTERPRETATION OF PERMEATION DATA

Permeation is the process of chemical movement through a material on a molecular level. Permeation resistance refers to the ability of a material to retard or prevent chemical movement through it. Permeation may occur without any visible signs of degradation.
Permeation resistance is measured using a test cell which is divided into two halves by a protective clothing specimen. Chemical is placed on the challenge side, while the collection side is periodically monitored for permeating chemical. Permeation data were obtained in accordance with the American Society for Testing and Materials (ASTM) Standard Test Method F 739 (Resistance of Materials Used in Protective Clothing to Permeation by Liquids and Gases), unless stated otherwise. In the case of chemicals that are classified as warfare agents, the data were obtained in accordance with the Military Standard 282 (MIL-STD-282) (Military Standard, Filter Units, Protective Clothing, Gas-Mask Components, and Related Products: Performance Test Methods).
Permeation rate is the amount of chemical that passes through a material for a measured surface area per unit time. In this section, permeation rate is expressed in micrograms per square centimeter per minute (mcg/cm(2)/min). The reported permeation rate is either the steady-state rate or the maximum rate observed during testing. In some cases, very large permeation rates exceed measurement techniques and are reported as ">" (greater than) or "HIGH."
Breakthrough time is the elapsed time, in minutes, from the time the chemical comes in contact with the material exterior surface, to the time that chemical is detected on the interior surface. When no breakthrough is detected, the breakthrough time is report as ">" the testing period. If permeation breakthrough is rapid, results are reported as "<" (less than) the earlier sampling time or as "IMMEDIATELY" (which usually means breakthrough in less than 4 minutes).
The breakthrough time should exceed the expected use period of the selected protective clothing. Additionally, there are several other factors that must be taken into account to provide appropriate protection.
Permeation testing is usually conducted with full strength, undiluted chemical for the duration of the test period. Actual exposures may involve diluted chemical for short or intermittent exposure periods.
Permeation testing is usually conducted at room temperature. Permeation occurs faster at elevated temperatures (short breakthrough times and higher permeation rates) and slower at reduced temperatures (long breakthrough times and lower permeation rates).
Permeation resistance of mixtures cannot usually be determined on the basis of the individual chemicals making up the mixture. Synergistic effects may occur and result in more rapid permeation than accounted for by the individual mixture chemicals.
Permeation rates may be used to calculate potential wearer exposure; however, several assumptions must be made about the extent of exposure and condition of clothing wear. Furthermore, there are few chemicals with dermal exposure limits, making it difficult to determine an acceptable skin exposure level.

COMPANY INFORMATION

DuPont Personal Protection P. O. Box 80705 Wilmington, DE 19880-0705 USA Phone: (302) 774-1000 Toll-Free: (800) 931-3456 Website: http://personalprotection.dupont.com Email: personalprotection@usa.dupont.com

REFERENCES

CHEMICAL PROTECTIVE CLOTHING CITATIONS

The following sources were consulted for chemical protective clothing data:

(Ansell-Edmont, 2001)
(Bata Shoe Company, 1995)
(Best Manufacturing, 2002)
(Best Manufacturing, 2004)
(Boss Manufacturing Company, 1998)
(ChemFab Corporation, 1993)
(Comasec Safety, Inc., 2003)
(Comasec Safety, Inc., 2003a)
(DuPont, 2002)
(DuPont, 2002)
(DuPont, 2003)
(Guardian Manufacturing Group, 2001)
(ILC Dover, Inc., 1998)
(Kappler Inc., 2001)
(Kimberly-Clark, 2002)
(LaCrosse-Rainfair, 1997)
(MAPA Professional, 2003)
(MAPA Professional, 2004)
(Mar-Mac Manufacturing, Inc, 1995)
(Marigold Industrial, 2003)
(Memphis Glove Company, 2001)
(Montgomery Safety Products, 1995)
(Nat-Wear, 2001)
(Neese Industries, Inc., 2003)
(North, 2002)
(North, 2002)
(Playtex, 1995)
(River City, 1995)
(Safety 4, 2002)
(Servus, 1995)
(Standard Safety Equipment, 1995)
(Tingley, 2002)
(Trelleborg-Viking, Inc., 2001)
(Trelleborg-Viking, Inc., 2002)
(Wells Lamont Industrial, 2002)
(Workrite, 1997)

-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.
Lindane in the form of solid/dry powder will not burn. However, it may be dissolved in a liquid or solvent that is flammable or combustible. Such commercial formulations have flash points of approximately 150 degrees F or higher; fires or explosions can occur if the formulation comes into contact with oxidizers (CHRIS , 2000; HSDB , 2000; Pohanish & Greene, 1997).
Lindane is "very stable to heat" (Hayes & Laws, 1991).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS58-89-9 (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 CAS58-89-9 (NFPA, 2002):

Not Listed

Water may not be effective in fighting fires involving lindane; foam, halon, dry chemical, and carbon dioxide are appropriate extinguishing media (Meister, 1996). Fires should be fought from the farthest distance possible (Sittig, 1991).

A water spray should be used to keep containers that may be exposed to fire cool (ITI, 1995). If no risk is involved, personnel should remove containers from area of fire (Sittig, 1991).

COMBUSTION TOXICITY

Very toxic fumes of chlorides, hydrogen chloride, and phosgene are released when lindane is heated to decomposition (Lewis, 2000).
Toxic concentrations of lindane vapors are formed at slightly elevated temperatures (HSDB , 2000).

EXPLOSION HAZARD

Under the category of explosion hazard, lindane is considered "stable" (OHM/TADS , 2000).

If lindane is dissolved in a combustible solvent and that mixture is exposed to oxidizers, an explosion can result (Pohanish & Greene, 1997).

DUST/VAPOR HAZARD

Very toxic fumes of chlorides, hydrogen chloride, and phosgene are released when lindane is heated to decomposition (Lewis, 2000).

Toxic concentrations of lindane vapors are formed at slightly elevated temperatures (HSDB , 2000).

Irritation to the eyes, nose, and throat may result from exposure to lindane vapors (Budavari, 1996).

REACTIVITY HAZARD

Very toxic fumes of chlorides, hydrogen chloride, and phosgene are released when lindane is heated to decomposition (Lewis, 2000).

Carbon monoxide is listed as another decomposition product (HSDB , 2000).

When heated in steam at 102 degrees C, lindane produced 0.13% hydrogen chloride (HSDB , 2000).

Toxic concentrations of lindane vapors are formed at slightly elevated temperatures (HSDB , 2000).

Lindane is corrosive to aluminum and other metals (Thompson, 1992; (NIOSH , 2000).

It decomposes in the presence of alkalis at ambient temperature, forming trichlorobenzenes (HSDB , 2000).

Powdered iron, aluminum, and zinc will decompose lindane (HSDB , 2000).

Lindane is extremely stable to light, air, acids, and oxidation. It undergoes dehydrochlorination under alkaline conditions (Hartley & Kidd, 1987; HSDB , 2000).

Below 180 degrees C, lindane is stable. At pH 7 and 22 degrees C, 50% loss occurs in 191 days. At pH 9, 50% loss occurs in 11 hours (HSDB , 2000).

Lindane is incompatible with lime sulfur, lime, calcium arsenate, and other strong alkaline materials. It also is incompatible with iron, zinc, aluminum, and other powdered metals. When in contact with ozone, lindane can become oxidized (HSDB , 2000) NTP, 2000; Thompson, 1992).

If lindane is dissolved in a combustible solvent and that mixture is exposed to oxidizers, an explosion can result (Pohanish & Greene, 1997).

Lindane in the form of solid/dry powder will not burn. However, it may be dissolved in a liquid or solvent that is flammable or combustible. Such commercial formulations have flash points of approximately 150 degrees F or higher; fires or explosions can occur if the formulation comes into contact with oxidizers (CHRIS , 2000; HSDB , 2000; Pohanish & Greene, 1997).

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 CAS58-89-9 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS58-89-9 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Lindane (gamma-benzenehexachloride)
TEEL-0 (units = mg/m3): 0.5
TEEL-1 (units = mg/m3): 1.5
TEEL-2 (units = mg/m3): 50
TEEL-3 (units = mg/m3): 50
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 CAS58-89-9 (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 CAS58-89-9 (National Institute for Occupational Safety and Health, 2007):

IDLH: 50 mg/m3
Note(s): Not Listed

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.

SMALL LEAK/SPILL

Small spills may be absorbed with paper towels, the towels placed in a hood, and burned (ITI, 1988).
Spills of dry dust should be dampened with alcohol and the material placed into a suitable container. The area of the spill should then be wiped with absorbent paper dampened with alcohol, followed by a soap and water wash. All wastes should be placed in sealed plastic bags for eventual disposal (HSDB , 1996).

WASTE TREATMENT OPTIONS

CHEMICAL TREATMENT

Chemical treatment methods for lindane are ineffective. These include the application of alkalies, ozonization or other oxidation methods, and catalytic dehalogenation (HSDB , 1996).
Environmental regulatory agencies should be consulted for acceptable disposal practices before implementing land disposal of waste residue or waste sludge containing lindane (HSDB , 1996).
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.

BIOREMEDIATION

An anaerobic, expanded-bed granular activated carbon (GAC) reactor removed more than 90% of volatile organic compounds in a waste stream. Lindane was removed via biodegradation, while naphthalene was removed by adsorption on the activated carbon (Narayanan et al, 1993).
A new photocatalytic process involving titanium dioxide can remove as much as 99.9% gamma-lindane from water. Preliminary results from water operating in a parabolic trough concentrator have provided a better understanding of the photocatalytic process (Vidal, 1998).
Lindane involved in the organic chemical manufacturing process can be treated through neutralization and settling, followed by a "combined powdered carbon-biological process" (HSDB , 2000).

PHYSICAL TREATMENT

One method of disposing of excess lindane is incineration in a furnace with an afterburner and alkali scrubber. Lindane should first be dissolved in a flammable solvent to aid combustion (ITI, 1995).
Lindane may be a candidate for rotary kiln incineration with temperatures ranging from 820 to 1600 degrees C and residence times of seconds for liquids and gases, and hours for solids (HSDB , 2000).
Fluidized bed incineration may also be possible using a temperature range of 450 to 980 degrees C with residence times of seconds for liquids and gases, and longer for solids (HSDB , 2000).
In a trial burn, a destruction efficiency of 99.999% was achieved when lindane formulations of 12% emulsifiable concentrate with 71% aromatic petroleum, 12% xylene, and 5% emulsifier were burned in a liquid injection incinerator. The temperature was 1043 to 1265 degrees C with residence times of 0.132 to 1.77 seconds and 31 to 50% excess air (HSDB , 2000).
Destructive pyrolysis of lindane is possible when temperatures are 400-500 degrees C and the catalyst mixture contains 5-10% of either ferric chloride, zinc chloride, cupric chloride, or aluminum chloride on activated carbon (Sittig, 1991).
Another promising disposal technique involves several steps. First, soluble lindane is sorbed onto a demulsifying material such as peat moss, ground pine bark mulch, or steam-exploded wood fibers. These materials are readily available, inexpensive, and provide a beneficial environment for biodegradation. After sorption, the solid material is separated from the aqueous material through various filtration techniques. The liquid is then discarded or recycled and the solid matter is broken down by microorganisms in the composting process (ATSDR, 1994).
Adsorption on carbon or flocculation may be a possible method to remove lindane from effluent waters. However, the presence of methanol increases the solubility of lindane and other HCH isomers in water, and also elutes these isomers when they are adsorbed on activated carbon or similar materials (HSDB , 1996).
Use vermiculite, earth, dry sand, or like material to absorb liquids containing lindane (HSDB , 2000).
Use acetone to dampen solid spills and transfer material to appropriate containers. Absorb remaining material with acetone-dampened absorbent paper and seal this paper with any contaminated clothing in a plastic bag that is vapor tight for later disposal (NTP, 2000).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Lindane and other isomers of hexachlorocyclohexane (HCH) do not occur naturally in the environment (ATSDR, 1999).

Release of lindane to the environment occurs during its formulation and use as a pesticide/acaracide in a variety of applications (ATSDR, 1999; HSDB, 2004).

The HCH isomers, including lindane, have been detected in air, surface water, groundwater, sediment, soil, fish, and other aquatic organisms, wildlife, food, and humans, but they have not been found to be a major drinking water contaminant (ATSDR, 1999).

Lindane in soil may be a result of direct pesticide application or by direct or indirect releases during formulation, storage, or disposal (ATSDR, 1999).

The greatest releases to air were historically associated with agricultural pesticide applications, and to a lesser degree from manufacturing operations. Because of more strict controls on its use in the U.S. (i.e., aerial application prohibited and now restricted pesticide use), these sources are no longer expected to contribute to air levels. Concentrations in the atmosphere are associated with past use and disposal (ATSDR, 1999).

Agricultural activities, such as seeding with lindane-treated corn, have been shown to increase atmospheric levels of lindane. About 90 % of the released lindane is attributed to volatilization of the recently applied chemical, while the rest is from volatilization of the lindane still present in the soil from previous applications (Poissant & Koprivnjak, 1996).

Human exposure can occur in the workplace where it is produced, formulated into other products, or otherwise used; from inhalation of contaminated air near industries or areas where it is used or produced; by ingestion of plants, meat, milk, or water containing lindane; or from contact with contaminated soil or water (ATSDR, 1999).

Lindane's use in pharmacuetical medication for treatment of scabies or head lice presents direct human exposure to the material (ATSDR, 1999).

Human exposure to lindane likely occurs from ingestion of foods containing residual pesticide from its application to crops or from bioconcentraction. Some exposure from ingestion of drinking water containing lindane may also occur to a lesser extent. Workers involved in its use or manufacture may be exposed through inhalation or dermal contact (Howard, 1991).

Inhalation and eye or dermal contact are probable routes of occupational exposure. Lindane dusts may be inhaled and dermal contact with the material may occur while it is in use, after application, or during production. Exposure to the general public may occur from ingestion of contaminated food or drinking water, inhalation of ambient air, or dermal contact with medicinal products containing lindane. In addition, contaminated human breast milk may lead to infant exposure (HSDB, 2004).

An estimate of 9,509 U.S. workers (3,162 female) are potentially exposed to lindane as determined in a statistical survey by NIOSH. The National Occupation Exposure (NOES) Survey (1981-1983) estimate did not include farm workers (HSDB, 2004).

Metabolization by animals may preclude lindane's presence in meat or eggs, except where direct application to livestock or their feed has occurred (HSDB, 2004).

ENVIRONMENTAL FATE AND KINETICS

Airborne lindane may exist as vapor or sorbed to airborne particulate matter (ATSDR, 1999).
Modeling of gas/particle partitioning of semivolatile organic compounds in the atmosphere indicated that atmospheric lindane exists in both vapor and particulate phases (HSDB, 2004).
Based on its vapor pressure, lindane will likely exist almost completely in the vapor phase in ambient air. Reaction with photochemically produced hydroxyl radicals is potentially an important fate mechanism for atmospheric lindane (Howard, 1991).
Long-range atmospheric transport of lindane is reported and deposition is dependent on environmental conditions (ATSDR, 1999; Cleemann et al, 1995).
Lindane and other HCHs may be redistributed from the atmosphere, eventually resulting in equalization of concentrations in the environment based on the use of fugacity fractions and multicompartmental mass balance modeling (Breivik & Wania, 2002).
The broad global distribution of HCH isomers may signify that lindane is persistent in the atmosphere. Rain-out and dry deposition are likely to be important fate processes for particulate phase lindane (ATSDR, 1999; HSDB, 2004).
- The rates of removal are 2.5% per week for rainfall and 3.3% per week for dry deposition, with an estimated atmospheric residence time of 17 weeks (ATSDR, 1999; HSDB, 2004; Howard, 1991).
Photodegradation or other degradation processes are not important removal processes for lindane from air. However, photodegradation, forming two isomers of tetrachlorohexane and pentachlorohexane, was observed in a laboratory test, indicating that atmospheric transformation of lindane may occur (ATSDR, 1999).
Vapor-phase lindane is degraded through reaction with photochemically-produced hydroxyl radicals (HSDB, 2004).
- The calculated half-life is 28 days based on an estimated rate constant of 5.7 X 10(-13) cm(3)/molecule-sec (HSDB, 2004).
- A rate constant was estimated for this reaction to be 6.94 x 10(-12) cm(3)/molecule-sec at 25 degrees C. This corresponds to an atmospheric half-life of 2.3 days at atmospheric concentration of 5 x 10 (5) hydroxyl radicals per cm(3) (Howard, 1991).
Using a hydroxyl radical reaction rate constant in air of 6.9 x 10(-12) cm(3)/mol-sec and a 24-hour average hydroxyl radical concentration of 4 x 10(5) hydroxyl radicals/cm(3), the photooxidation lifetime may be estimated at 4 days (Poissant & Koprivnjak, 1996).
Photooxidation half-life in air (Howard et al, 1991):
- High: 92.4 hours (3.85 days)
- Low: 9.24 hours
- (Scientific judgement based upon estimated rate constant for reaction with hydroxyl radical in air)
Lindane may be re-released into the atmosphere in the gases generated from bacterial methanogenesis and denitrification processes in sediment. Approximately 85% of the lindane in these gases will be released to the atmosphere, with the remaining portion being dissolved in the water column (ATSDR, 1999).

WATER

SURFACE WATER

Lindane is likely to dissolve and remain in the surface water column (ATSDR, 1999).
Estimated lindane half-lives in river, lake, and groundwater were 3 to 30, 30 to 300, and greater than 300 days, respectively (Howard, 1991).
Volatilization is potentially an important fate process in surface water. Volatilization is expected to occur slowly, based on the Henry's Law constant of 3.5 x 10(-6) atm-m(3)/mole(HSDB, 2004).
Water depth substantially affects the evaporation half-life of lindane, based on estimated volatilization half-lives for lindane from water (Howard, 1991).

For a 1 m deep, stagnate body of water, lindane was estimated to have a volatilization half-life of 191 days (Howard, 1991).
A 3.2 day volatilization half-life was experimentally determined for still pure water, 4.5 cm deep at 24 degrees C, but with stirring (aeration introduced) the half-life was 1.5 days (Howard, 1991).
A 692 day half-life was predicted for a 1 m deep, stagnate water body, based on the experimental volatilization half-life of 3.2 days (from pure water at a 4.5 cm depth and 24 degrees C) and through the application of an equation relating water depth to volatilization half-life (Howard, 1991).

An estimated volatilization half-life of approximately 22 days was determined for a model river 1 meter deep flowing 1 m/sec, at a wind speed of 3 m/sec (Howard, 1991).
Based on the Henry's Law Constant, a volatilization half-life for a model river (1 m deep, flowrate 1 m/sec, and wind velocity of 3 m/sec) was estimated to be 18 days (HSDB, 2004).
Volatilization half-life for a model lake (1 m deep, flowing 0.05 m/sec) was estimated to be 140 days (HSDB, 2004).
A calculated half-life in water 1 m deep at 25 degrees C, based on an evaporation rate of 1.5 x 10(-4) m/hr: was 4590 hr (Verschueren, 2001).
Volatilization was recorded following a 24 hour incubation period as follows (HSDB, 2004):

16.4% volatilization from tap water;
11.5% volatilization from tap water containing suspended loam particles;
5.5% volatilization from tap water containing algae cells.

The half-life of lindane determined for estuarine water in a model mudflat ecosystem composed of estuarine water, sediment, and cockles (Anadara granosa) was 21.9 hours under aerated conditions and 43.0 hours without aeration (Abdullah & Shanmugam, 1995).
Lindane may undergo adsorption and desorption processes with sediments and materials in the water. This is influenced by the organic content of the sediment and the natural characteristics of the system (ATSDR, 1999).
Adsorption to sediments or suspended solids in the water column is likely, based on the sediment Koc values (range from 2164 to 4800) and a particular classification scheme (HSDB, 2004).
Lindane partitions from the water column to suspended and bottom sediments. This process is expected to be slow. Data from field experiments led to the determination that particle transport to sediment (settling) was small compared to diffusion(Howard, 1991).
Sorption to suspended sediment and biota is not great, but sorption serves as a means of transport of lindane to anaerobic sediments where it may undergo transformation (HSDB, 2004).
A half-life of 3.2 days (at 22 degrees C) was reported for lindane where reductive halogenation in anoxic sediment with 6% organic carbon content was evaluated (Verschueren, 2001).
Adsorbed lindane in sediments may be re-released in gas bubbles from bacterial methanogenesis and denitrification processes. The majority is released to the atmosphere, but approximately 15% dissolves into the water column as the bubbles rise (ATSDR, 1999).
The fate of lindane was evaluated in an extremely oligotrophic, lentic lake system. Lindane and DDE were introduced in equal concentrations in late May to a flooded limestone quarry, and monitoring of water, sediment, and biota concentrations was completed for one year. Seasonal effects such as thermal stratification, turnover, and runoff inflow were reported. Results and conclusions are listed below (HSDB, 2004):

Lindane concentrations decreased 32% (averaged over the entire water column) after 102 days.
Lindane concentrations decreased 50% (averaged over the entire water column) after 123 days.
Most of the substance was retained in the epilimnion until fall turnover of the lake after 123 - 144 days.
After fall turnover, remaining concentrations were generally homogeneous in the water column.
No lindane concentrations were detected in suspended sediments, compared to high levels of DDE, an indication that sorption and sedimentation were not significant for lindane.
Lindane underwent rapid diffusion to lower layers of the bottom mud, possible due to its solubility in the interstitial water in mud.
Zooplankton had peak concentrations after 5 days, but the levels decreased with the decreasing water concentrations. Concentrations factors were from 170 to 488.
Lindane in bluegill was at equilibrium with water after 5 days, with concentration factors from 0.42 to 1470.

Biodegradation is believed to be the most important factor for the breakdown of lindane in an aquatic environment, although hydrolysis and photolysis can also occur (ATSDR, 1999).
Lindane underwent biosorption with the fungus Rhizopus arrhius and activated sludge. Equilibrium was reached in 1 hour for the fungus and 4 hours for the sludge material. Rapid desorption (zero-order kinetics) occurred with death of the biomass, perhaps indicating that adsorbed lindane can be re-released (ATSDR, 1999).
Hydrolysis and photolysis of lindane are slow at environmental pH levels in natural waters (HSDB, 2004).

Under alkaline conditions, lindane is hydrolyzed fairly quickly, but hydrolysis becomes much less important in neutral or acidic waters (ATSDR, 1994).
The importance of photolysis as a fate process for lindane in water is unclear (ATSDR, 1999).
Hydrolysis and photolysis in an aquatic environment were studied, examining three different types of surface water. Temperature was maintained at 25 degrees C and first order kinetics were observed. Results are provided below (Howard, 1991; HSDB, 2004):

Surface Water Sample Type	Hydrolysis Rate Constant [hr(-1)]	Hydrolysis Half-Life (hr)	pH
1. eutrophic pond (TX), pH 9.3	7.5 X 10(-3)	92 (approx. 3 days)	9.3
2. dystrophic reservoir (LA), pH 7.3	8.99 X 10(-4)	771 (approx. 32 days)	7.3
3. oligotrophic rock quarry (IN), pH 7.8	1.07 X 10(-3)	648 (27 days)	7.8

The same study conducted direct sunlight photolysis experiments and observed first order aqueous photolysis of lindane. The higher pH, or more alkaline conditions, of the Texas water sample influenced the rates of reaction for hydrolysis and photolysis. Results are as follows (Howard, 1991; HSDB, 2004):

Surface Water Sample Type	Photolysis Rate Constant[hr(-1)]	Photolysis Half Life(hr)	pH
1. eutrophic pond (TX)	4.1 x 10(-3)	169 (approx. 7 days)	9.3
2. dystrophic reservoir (LA)	3.9 x 10(-4)	1791 (approx. 74 days)	7.3
3. oligotrophic rock quarry (IN)	4.5 x 10(-4)	1540 (approx. 64 days)	7.8

Additional results from this particular study were identified, providing more insight to the hydrolysis of lindane. The data are summarized as follows(Howard, 1991; HSDB, 2004):
Hydrolysis Rate Constant [hr(-1)] Hydrolysis Half-Life (hr) pH Temperature (degrees C)
7.3 x 10(-3) 95 9 25
1.6 x 10(-4) 4331 7 25
7.4 x 10(-4) 936 5 25
Water Sample Type Photolysis Rate Constant[hr(-1)] Photolysis Half Life(hr) pH
Milli-Q water 8.9 X 10(-4) 779; and adjusted mid-winter half-life is 1560 hr 6.98
The photolysis reaction was faster in the more alkaline natural water sample from Texas than in the Milli-Q (pure) water; this was attributed to the hydrolysis reaction products in the more alkaline scenario having undergone photolysis more receptively than lindane in the pure sample. On the other hand, the slower rates in the natural water samples at pH 7.2 and 7.8 may be a result of association of lindane with the natural water matrix (Howard, 1991; HSDB, 2004).

A hydrolysis half-life of 42 years was determined at pH 8 and 5 degrees C(HSDB, 2004).
A hydrolysis half-life of 240 days at pH 7 and 25 degrees C was determined using a neutral rate constant of 1.2 x 10(-4)/hr (HSDB, 2004).
Half-life in surface water (based on hydrolysis half-life) (Howard et al, 1991):

High: 5765 hours (240 days)
Low: 330 hours (13.8 days)
First order hydrolysis half-life (pH 7 and 25 degrees C; based on measured neutral and base catalyzed hydrolysis rate constants): 4957 hours (207 days)

Hydrolysis Degradation (Howard et al, 1991):

First-order hydrolysis half-life - 4957 hours (207 days) (based on measured neutral and base catalyzed hydrolysis rate constants);
Acid rate constant - No data [using t1/2 = 5765 hours (240 days) at pH 5 and 25 degrees C and based on measured neutral and base catalyzed rate constants;
Base rate constant - 198 [M(OH-)-hr](-1) [using t1/2 = 330 hours (13.8 days) at pH 9 and 25 degrees C and based on measured neutral and base catalyzed hydrolysis rate constants]

A study where lindane in purified water was exposed to sunlight noted decreased concentrations after a 50 day exposure time. The results were reported to indicate that lindane in aqueous solution may isomerize to alpha-HCH in the presence of sunlight (HSDB, 2004; Howard, 1991).
A study of photooxidation of lindane by UV light in an aqueous medium at 90 to 95 degrees C produced the following results (Verschueren, 2001):

Time for CO2 formation (% theoretical, gamma):
- 25% --- 3 hours
- 50% --- 17 hours
- 75% --- 46 hours

Lindane persistence in river water was measured with an initial concentration of 10 mcg in a sealed glass container placed under sunlight and artificial fluorescent light. After 8 weeks, 100% of the material remained (Verschueren, 2001).
Lindane half-lives were 64.98 hours and 69.41 hours for tap water and unfiltered natural water (pH 9), respectively. Chemical breakdown was the primary removal mechanism and biodegradation was secondary (HSDB, 2004).

GROUND WATER

Leaching to groundwater from soil may occur. However, because of the sorptive properties of lindane this is not expected to be an important fate mechanism. Migration to groundwater is influenced by lindane's solubility as well as the organic content of the soil. Should lindane exist in an aquifer, adsorption to groundwater sediments is not sufficient to prevent groundwater contamination. This is because groundwater sediments are generally low in organic carbon content (ATSDR, 1999).
A study examining sorption and desorption of lindane from aquifer sand showed 30% to 40% adsorption at 5 degrees C after a 3-100 hour equilibrium time (Verschueren, 2001).
Half-life in ground water (based on hydrolysis half-life) (Howard et al, 1991):

High: 5765 hours (240 days)
Low: 142 hours (5.9 days)
First order hydrolysis half-life (pH 7 and 25 degrees C; based on measured neutral and base catalyzed hydrolysis rate constants): 4957 hours (207 days)

SOIL

TERRESTRIAL

Lindane is not very mobile in soil systems. It will generally bind to soil particulates, but can also leach to groundwater or volatilize to the ambient atmosphere. Migration to groundwater is influenced by lindane's solubility as well as the organic content of the soil. Releases to the atmosphere can occur through volatilization from treated agricultural soils and plant foliage or wind erosion of impacted surface soil (ATSDR, 1999).
Lindane residue persistence in soil is influenced not only by soil type, but also by the presence of crops. Half-lives of 107 and 62.1 days were reported for lindane on cropped and uncropped plots, respectively (ATSDR, 1999).
Biotransformation is an important degradation process for lindane in soil and sediment, but volatilization is the principal soil removal mechanism for lindane. This is possibly more pronounced in warm climates (ATSDR, 1999).
It may volatilize to the atmosphere from soil, with this process influenced by soil water content. Volatilization is more likely from moist soils than dry soils, considering lindane's Henry's Law Constant and vapor pressure (HSDB, 2004).

After a 24-hour incubation period, moist loam soil showed 0.92% lindane volatilization(HSDB, 2004).
Application to moist and dry soil surfaces led to the following results (HSDB, 2004):

Moist Soil: decrease by 10% after 6 hours, and decrease by 50% after 6 days.
Dry Soil: decrease of 22% after 50 hours.

Tests in a model laboratory system were reported (Verschueren, 2001):

Temperature	Volatilization Half Life(1)	Volatilization Half Life(1)	Volatilization Half Life(1)
Degrees C	Peat Soil	Sandy Soil	Plant Surfaces (turnip, bean, and oats)
10	12-22 days	5-22 days	0.6-0.7 days (11 degrees C)
20	6-16 days	3-7 days	0.3-0.7 days (20 degrees C)

(1) >98% air humidity and 0.05 m/sec wind velocity

Volatilization half-lives at 10 degrees C and 20 degrees C from oat plant surfaces were 0.29-0.73 days, respectively (ATSDR, 1999).
Volatilization half lives were 2.3 days and 24.8 days from the surface of a sandy soil and peat soil, respectively (20 degrees C) (HSDB, 2004).

A volatilization rate of >20% from soil surfaces was determined in 24 hour wind tunnel test (ATSDR, 1999).
A 54% evaporation loss was recorded within 24 hours after application to sunflower and sugarbeet fields (ATSDR, 1999).
Fields planted with lindane-treated canola (Brassica napus L.) seed were evaluated to measure volatilization and estimate atmospheric losses of the material. Summary information is provided below (Waite et al, 2001):

Data showed that the seeded field was the primary source of lindane in atmospheric samples, as the highest atmospheric concentrations were measured in ambient air samples collected closest to the ground above the field. Highest overall concentrations were found the second week of sampling. Variability in the data was attributed to influences of the soil water content.
Horizontal atmospheric transport was examined and an estimated 12 - 30% of lindane applied to the seed volatilized to the atmosphere for each of two 5- and 6-week examination periods in 1997 and 1998, respectively. This was estimated to create an atmospheric loading of 66.4 to 188.8 Mg for a 6-week period following planting.
During the dryer year of 1998, measured dry atmospheric deposition of lindane at the test area ranged from 853 to 2203 ng/m(2)-day for the first 3 weeks following planting, and less than the quantitation level for the final 3 weeks of sampling.
Measured rain or wet deposition concentrations were similar at the test area as the control area.

Seasonal trends were found for atmospheric levels of lindane and alpha-HCH in studies of air and water gas exchange. Net deposition of lindane was reported in air-sea gas exchange determinations (Sundqvist et al, 2004; Wiberg et al, 2001).
Lindane will adsorb to soil particulates and can slowly leach to groundwater. Leachability is influenced by the organic carbon content of the soil, based on evaluations of different soil types (HSDB, 2004).

Using a classification method, Koc values determined for various soil types indicated low soil mobility (HSDB, 2004):

Sandy loam soil (1.3% organic carbon) - 204;
Muck soil (30.5% organic carbon) - 46.2;
Mineral soil (1.26% organic carbon) - 830;
Sediment near sugar cane area - 2164.

Adsorption to soil particulates is an important fate mechanism. In soil, this may inhibit leaching to groundwater. However, groundwater sediments, which are generally low in organic carbon content, will not adsorb lindane sufficiently to prevent groundwater contamination (ATSDR, 1999).

Laboratory soil column leaching studies examining different levels of organic content as well as municipal refuse found that lindane has low mobility in soil. It was also found to be highly adsorptive to sediments under aerobic and anaerobic conditions when evaluated in a laboratory system at pH 7.42 and 18% organic carbon (ATSDR, 1999).

Leaching from soil to groundwater is expected to be slow, based on a mean Koc of 1081 from three soils and the material's solubility in water (Howard, 1991).
A decrease of lindane residues by 40 to 80% each year from eight varieties of soil was observed. The substance's half-life was 4-6 weeks, when sprayed on the soil surface; in 30-40 weeks, only 10% remained. Lindane's half-life was 15-20 weeks when worked into soil; in 2-3 years, 10% remained. A 400-day half-life is "typical" for lindane (Extoxnet, 2000).
Disappearance of 75 to 100% of lindane from soils was reported over a range of 3 to 10 years (Verschueren, 2001).
Abiotic degradation processes are not considered significant fate processes for lindane in soil (ATSDR, 1999).
Half-life of lindane in soil (based upon hydrolysis half-life) (Howard et al, 1991):

High: 5765 hours (240 days);
Low: 330 hours (13.8 days).

OTHER

OTHER
- One study examined lindane residues found on leaves and stems of carnation plants (Dianthus caryophyllus L.) used as animal feed. The samples were divided into three groups: one exposed to open air, another washed with tap water, and one in an enclosed container simulating feed storage conditions. After 49 days, lindane residues had dropped below 1 mg/kg in all samples except the one in the enclosed container. Residues remaining for this group after 48 days were 12.81 mg/kg (dry weight) and 10.67 mg/kg (green weight). None of the values of lindane residues in samples 49 days after spraying were below the USA maximum residue levels for lindane in stockfeed (0.1 mg/kg). Lindane residues found on samples immediately after washing were reduced by only 23% from the original levels, probably due to lindane's low solubility in water (Ceron et al, 1995).
- Some studies have indicated that alpha-HCH may be a decomposition product of lindane, while other research has indicated instead that lindane is rapidly dechlorinated to form pentachlorocyclohexenes and tetrachlorocyclohexene (Poissant & Koprivnjak, 1996).
- Dechlorination, co-oxidation, and/or translocation appear to be possible mechanisms for breakdown of lindane in the environment (Poissant & Koprivnjak, 1996).

ABIOTIC DEGRADATION

Lindane is not particularly mobile in soil systems. It will adsorb to soil particulates and can slowly leach into groundwater. Leachability is influenced by the organic carbon content of the soil, based on evaluations of different soil types. It may volatilize to the atmosphere from soil, and volatilization is more likely from moist soils than dry soils, considering lindane's Henry's Law Constant and vapor pressure (HSDB, 2004).

Lindane in soil can be released to groundwater from soil leachate. Atmospheric levels may result from particulate wind erosion of treated soil or volatilization from treated soil and plants. Lindane may also enter the air from contaminated soil and plants at spill and dump sites. It can migrate to surface water from soil erosion or surface runoff of dissolved material washed by rain from the soil or plants, or from atmospheric (wet) deposition (ATSDR, 1999).

Lindane released to a water environment will dissolve and remain in the water column. It may slowly volatilize from water surfaces based on the Henry's Law Constant, but evaporative losses from water are not significant because of its solubility. It will likely undergo some adsorption to sediment and suspended matter based on Koc values, or it will slowly diffuse into bottom sediments where it may undergo transformation. Settling of lindane is not as important as diffusion in its transport to bottom sediments. Hydrolysis and photolysis of lindane can occur, but will be slow. Hydrolysis is particularly slow at environmental pHs (natural waters), and photolysis is not considered to be an important fate process for lindane in water (ATSDR, 1999; HSDB, 2004; Howard, 1991).

Lindane is not stable in an alkaline environmental system and will decompose to trichlorobenzenes and hydrochloric acid (Verschueren, 2001).

BIODEGRADATION

Biodegradation is expected to be a very important fate process for the degradation of lindane in water and soil (ATSDR, 1999).

SOIL

A biologically rich, anaerobic environment is most beneficial to biotransformation of lindane (ATSDR, 1999).
Seventy-one of 147 microorganisms isolated from loamy sand soil were able to use lindane solution as the sole carbon source (ATSDR, 1999).

Formation of the chloride ion was noted in this study. The extent to which lindane biodegraded was not explored (Howard, 1991).
Metabolites isolated from 13 of the 71 microorganisms included gamma-2,3,4,5,6-pentachloro-1-cyclohexene; alpha-, beta, and gamma-3,4,5,6-tetrachloro-1-cyclohexene; and pentachlorobenzene (HSDB, 2004).
Pure cultures were used so any biodegradation rates would not be relevant to soil or water environments (HSDB, 2004).

Aerobic pure culture laboratory testing examined white rot fungus degradation of lindane. Approximately 35% degradation was observed over a 60-day test period in a silt loam soil/corncob matrix and 53.5% degradation in liquid cultures over a 30-day test period. Other studies support these results (ATSDR, 1999).
The following lindane-degrading bacterium was isolated from contaminated soil: Sphingomonas paucimobilis. A Pseudomonas species was also isolated from pre-treated soil, and it effectively degraded lindane under aerobic and anaerobic conditions (ATSDR, 1999).
Anaerobic degradation of lindane is more extensive than aerobic degradation, based on evaluation of anaerobic and aerobic soil suspensions of lindane. After 3 weeks incubation, 63% of the applied lindane disappeared from anaerobic suspensions, versus 0% from the aerobic suspensions (Howard, 1991).

Soil-water suspension biodegradation testing at 35 degrees C and an initial concentration of 0.1 mg/l (Verschueren, 2001):

Test Conditions	Percent Mineralization to CO2
aerobic	0.4% after 5 days2% after 42 daysNote: 3% of the initial concentration remained in the water after 42 days.
anaerobic	0.4% after 5 days 3% after 42 daysNote: 2% of initial concentration remained in the water after 42 days

Eighty-seven percent of lindane was degraded in 24 hours under anaerobic conditions by a Clostriduim species isolated from a lindane-amended and flooded soil system (Howard, 1991).
Mixed flora from soils enriched anaerobically produced accelerated dechlorination and degradation. The effective species were Clostridium, several Bacillus species, and Enterobacteriaceae. Propionibacterium and Lactobacillaceae were not active in the process. Metabolites were partially volatile and practically free of chlorine while organic bound chlorine was released as chloride. Gamma-tetrachlorocyclohexene was formed in an intermediate phase, but later was also dechlorinated (HSDB, 2004).
Clay soil containing lindane had 60% degradation under anaerobic conditions after 15 days, while aerobic conditions showed no biodegradation (HSDB, 2004).
Lindane biodegradation in anaerobic clay loam soil and in sewage sludge produced benzene (HSDB, 2004).
E. coli will metabolize lindane, producing gamma-2,3,4,5,6-pentachloro-1-cyclohexene (HSDB, 2004).
In a study involving two types of Egyptian soils, lindane was determined to significantly inhibit microbial activity at 10 mg lindane/kg soil (Farghaly, 1998).

WATER

The water-related fate of lindane includes biodegradation (HSDB, 2004):

Biologically rich anaerobic conditions will encourage biodegradation of lindane (ATSDR, 1999).
Clostridium sphenoicles metabolizes lindane to gamma-3,4,5,6-tetrachloro-1-cyclohexane (HSDB, 2004).

An in-vitro persistence study was completed using 2 ppm initial lindane concentration in capped bottles kept in darkness. Percent remaining after 8 weeks: 90% in sterilized natural water, sterilized distilled water, and distilled water, while 40% remained in natural water (Verschueren, 2001).

After 16 weeks: <30% remained in the unsterilized natural water. Biodegradation was determined to be the cause of reduced concentrations in the natural water, but involvement of hydrolysis or possible adsorption to the glass bottles was not clear (ATSDR, 1999; Howard, 1991).

Aqueous Biodegradation Rates (Unacclimated) (Howard et al, 1991):

Aerobic half-life (based on aerobic soil die-away study data) :

High: 9912 hours (413 days)
Low: 744 hours (31 days)

Anaerobic half-life (based on anaerobic flooded soil die-away study data):

High: 734 hours (30 days)
Low: 142 hours (5.9 days)

Removal/secondary treatment (based on data from a continuous activated sludge biological treatment simulator):

High: 25%

Nitrogen-fixing blue-green algae biodegrade lindane, reducing its toxic effects after repeated inoculations (ATSDR, 1999).
Dechlorination to gamma-pentachlorocyclo-hexene resulted with fungi in aqueous suspensions and in algal cultures (ATSDR, 1999).

SLUDGES

Lindane was 98% degraded after 120 days in bench-scale anaerobic digestion testing of contaminated sludges. Sorption to solids accounted for 2% of initial feed, no volatilization losses occurred (ATSDR, 1999).
Live activated sludge testing initially underwent reversible biosorption and was the dominant removal process. Then, after a 10-hour acclimation period, aerobic biodegradation increased. Hydrolytic dechlorination was noted followed by subsequent ring cleavage and then partial or full mineralization (ATSDR, 1999).
Biological adaptation of sewage sludge may be slow (1-2 months), but once acclimated, 70-80% biodegradation of lindane can occur (ATSDR, 1999).

Likely degradation mechanisms are co-oxidation or reductive dechlorination (ATSDR, 1999).

At 35 degrees C, lindane biodegraded quickly in thick anaerobic digested wastewater sludge. At applications of 10 ppm and 1 ppm, and after 2 and 4 days, respectively, less than 10% of applied lindane remained. An anaerobic biodegradation rate at 20 degrees C was slower at approximately 0.1 mcg/ml/D (HSDB, 2004).
Anaerobic sludge digesters degraded 98% of lindane (HSDB, 2004).
A degradation half-life of 20 days was reported for lindane in sewage sludge under stable anaerobic conditions (HSDB, 2004).

OTHER

Biodegradation studies identify products of transformation as tetrachlorohexene; tri-, tetra-, and pentachlorinated benzenes; penta- and tetracyclohexanes; other HCH isomers; and other related chemicals. The variation was due to differences in the organisms, analyzation method and timing of the analysis (ATSDR, 1999).
Isomerization of lindane to alpha-HCH was observed in a mixed culture containing Pseudomonas aeruginosa as the primary component. Metabolites were gamma-2,3,4,5,6-pentachlorocyclohexane (PCCH), tetrachlorobenzene (TeCB), and unknown nonpolar metabolites (Verschueren, 2001).

BIOACCUMULATION

HUMANS

A dermal bioavailability analysis estimated 0.45% to 2.35% dermal absorption depending on the soil loading (ATSDR, 1999).

FISH

Hexachlorohexane isomers (HCHs) accumulation was examined in conjunction with accumulation of several heavy metals, polychlorinated biphenyls (PCBs), hexachlorobenzene (HCB), and organochloride pesticide (DDTs) in marine species from the Ionian and Adriatic Seas. Teleost and elasmobranch fish species, bivalve and cephalopod mollusc species, and crustaceans were examined. Concentrations of HCHs were below instrument detection limits in all species (Marcotrigiano & Storelli, 2003).
RAINBOW TROUT BAF: 12600 L/kg(lp), Lake Ontario (Verschueren, 2001)

PLANTS

TERRESTRIAL
- In terrestrial organisms and plants, uptake from soils and bioconcentration of lindane are limited (ATSDR, 1999)
- Grain, maize, and rice plants accumulated 0.95%, 0.11%, and 0.04% bound lindane residues after 14 to 20 days growth in sandy loam soil. Extractable residues were taken up more readily (4-10 times higher concentrations) when both bound and extractable residues of lindane were added to the test soil (ATSDR, 1999).
- log BCF for vegetation: -0.41 (Verschueren, 2001)

MAMMALS

Limited data suggest lindane is metabolized, rather than biomagnified much in the terrestrial food chain. Exposure to lindane from ingestion of contaminated soil or foliage can lead to transfer of the material to animal tissue (ATSDR, 1999).
- Lindane was found in cow adipose tissue at concentrations 10 times greater than the levels in their feed (ATSDR, 1999).
- Lindane residues were at lower concentrations in the tissues of herbivorous animals, such as chicken, sheep, and pigeons which feed wholly on plant material, than in carnivores (ATSDR, 1999).
Biotransfer Factors (Verschueren, 2001):
- in beef (log Bb): -1.78
- in milk (log Bm): -2.60

OTHER

INVERTEBRATES
- Tubificide oligochaetes maintained in a static sediment/water system bioaccumulated lindane (ATSDR, 1999).
- Earthworms exposed to 5 ppm lindane for up to 8 weeks in treated humus soil bioconcentrated the material by a factor of 2.5. Transformation of more than 50% of the accumulated material was observed with the primary degradation product beng gamma-2,3,4,5,6-pentachlorocyclohex-1-ene (ATSDR, 1999).

BIOCONCENTRATION FACTOR

- AQUATIC ORGANISMS
- AQUATIC PLANTS

ENVIRONMENTAL TOXICITY

Lindane is highly toxic to honeybees, aquatic life, and some beneficial parasites and predacious insects. Lindane is also toxic to birds and other wildlife (Thompson, 1992) (EPA, 1988).

Very low concentrations may be harmful to aquatic life (CHRIS, 2004).

LC48 - SIMOCEPHALUS, first instar: 520 mcg/L for 48 hours at 15 degrees C -- 95% confidence limit, 340 to 790 mcg/L (HSDB, 2004)
LC48 - DAPHNIA PULEX, first instar: 460 mcg/L for 48 hours at 15 degrees C -- 95% confidence limit, 386 to 547 mcg/L (HSDB, 2004)
LC50 - AMERICAN EEL (Anguilla rostrata): 56 ppb for 96H -- static lab bioassay (HSDB, 2004)
LC50 - ASELLUS, mature: 10 mcg/L for 96H at 15 degrees C -- 95% confidence limit, 7 to 14 mcg/L (HSDB, 2004)
LC50 - BLUEGILL, 1.5 g: 68 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 60 to 78 mcg/L (HSDB, 2004)
LC50 - BLACK BULLHEAD, 1.2 g: 64 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 49 to 81 mcg/L (HSDB, 2004)
LC50 - (ORAL) BOBWHITE QUAIL, 9 days: 882 ppm for 5D ad libitum -- 95% confidence limit, 755 to 1041 ppm (HSDB, 2004)
LC50 - BROWN TROUT, 1.7 g: 1.7 mcg/L for 96 hours at 13 degrees C -- 95% confidence limit, 1.2 to 2.4 mcg/L (HSDB, 2004)
LC50 - CARP, 0.6 g: 90 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 75 to 120 mcg/L (HSDB, 2004)
LC50 - CHANNEL CATFISH, 1.5 g: 44 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 37 to 52 mcg/L (HSDB, 2004)
LC50 - COHO SALMON, 0.6 g: 23 mcg/L for 96H at 12 degrees C -- 95% confidence limit, 19 to 28 mcg/L (HSDB, 2004)
LC50 - CYPRIDOPSIS, mature: 3.2 mcg/L for 96H at 21 degrees C -- 95% confidence limit, 2.2 to 4.6 mcg/L(HSDB, 2004)
LC50 - DAPHNIA PULEX: 1250 mcg/L for 24H; 460 mcg/L for 48H (HSDB, 2004)
LC50 - FATHEAD MINNOW, 1.2 g: 87 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 69 to 101 mcg/L (HSDB, 2004)
LC50 - GAMMARUS FASCIATUS, mature: 10 mcg/L for 96H at 15 degrees C -- 95% confidence limit, 7 to 14 mcg/L (HSDB, 2004)
LC50 - GAMMARUS LACUSTRIS, mature: 88 mcg/L for 96H at 21 degrees C -- 95% confidence limit, 57 to 136 mcg/L (HSDB, 2004)
LC50 - GASTROPOD (Lymnea stagnalis): 7.3 ppm for 48H (HSDB, 2004)
LC50 - GOLDFISH, 0.9 g: 131 mcg/L for 96H hours at 18 degrees C -- 95% confidence limit, 92 to 187 mcg/L (HSDB, 2004)
LC50 - GREEN SUNFISH, 1.1 g: 83 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 47 to 149 mcg/L (HSDB, 2004)
LC50 - INSECT LARVAE (chaoborus): 0.008 ppm for 48H (HSDB, 2004)
LC50 - INSECT LARVAE (colean): 0.092 ppm for 48H (HSDB, 2004)
LC50 - (ORAL) JAPANESE QUAIL, 7 days: 425 ppm for 5D ad libitum -- 95% confidence limit, 347 to 520 ppm (HSDB, 2004)
LC50 - LAKE TROUT, 0.7 g: 32 mcg/L for 96H hours at 12 degrees C -- 95% confidence limit, 24 to 42 mcg/L (HSDB, 2004)
LC50 - LARGEMOUTH BASS, 0.9 g: 32 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 27 to 38 mcg/L (HSDB, 2004)
LC50 - (ORAL) MALLARD DUCK, 15 days: >5000 ppm for 5D ad libitum (HSDB, 2004)
LC50 - MUMMICHOG (Fundulus heteroclitus): 20 ppb for 96H (HSDB, 2004)
LC50 - PALAEMONETES PUGIO: 4.44 mcg/L for 96H -- flow-through bioassay (HSDB, 2004)
LC50 - PTERONARCYS, second year class: 4.5 mcg/L for 96H at 15 degrees C -- 95% confidence limit, 3.6 to 5.7 mcg/L (HSDB, 2004)
LC50 - RAINBOW TROUT, 1 g: 27 mcg/L for 96H at 12 degrees C -- 95% confidence limit, 20 to 36 mcg/L (HSDB, 2004)
LC50 - RAINBOW TROUT (Salmo gairdneri), fry: 0.037 mg/L for 24H; 0.023 mg/L for 48H; 0.022 mg/L for 96H. Test parameters: temperature, 20 degrees C; pH, 8.1; Hardness, 20 mg CaCO3/L(HSDB, 2004)
LC50 - (ORAL) RING-NECKED PHEASANT, 10 days: 561 ppm for 5D ad libitum -- 95% confidence limit, 445 to 690 ppm (HSDB, 2004)
LC50 - SPHAEROIDES MACULATIS: 35 ppb for 96H -- static lab bioassay (HSDB, 2004)
LC50 - YELLOW PERCH, 1.4 g: 68 mcg/L for 96H at 18 degrees C -- 95% confidence limit, 60 to 76 mcg/L (HSDB, 2004)
LC50 - CHIRONOMUS RIPARIUS, fourth instar larva: 3.6 mcg/L for 24H (HSDB, 2004)
LD50 - (ORAL) MALLARD DUCK, Male, 3-4 months: >2000 mg/kg -- acute (HSDB, 2004)
Libitum--12 percent mortality to 1500 ppm, 17 percent at 5000 ppm (HSDB, 2004)
TL50 - KOREAN SHRIMP (Palaemon macrodactylus): 4.7 - 32.7 ppb for 96H -- static bioassay (HSDB, 2004)
TL50 - KOREAN SHRIMP (Palaemon macrodactylus): 5.8 - 15.0 ppb for 96H -- flowing bioassay (HSDB, 2004)
TLm - EASTERN OYSTER (Crassostrea virginica), egg: 9100 ppb for 48H -- static lab bioassay (HSDB, 2004)
LC10 - RAINBOW TROUT (Salmo gairdneri), fry: 0.026 mg/L for 24H; 0.02 mg/L for 48H; 0.018 mg/L for 96H. Test parameters: temperature, 20 degrees C; pH, 8.1; Hardness, 20 mg CaCO3/L (HSDB, 2004)
TC - MICROCYSTIS AERUGINOSA: 0.3 mg/L -- inhibition of cell multiplication (HSDB, 2004)

Ecotoxicity Values (Freshwater):

IMMOBILIZED - DAPHNIA MAGNA: 1.1 ppm for 64H; Test environment: 78 degrees F (OHM/TADS, 2004)
LC50 - BLACK BULLHEAD: 0.064 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - BLUEGILL: 0.061 ppm for 24H (OHM/TADS, 2004)
LC50 - BLUEGILL: 0.068 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - BLUEGILL: 0.160 ppm for 24H; Test environment: 45 degrees F (OHM/TADS, 2004)
LC50 - BLUEGILL: 0.088 ppm for 48H; Test environment: 45 degrees F (OHM/TADS, 2004)
LC50 - BLUEGILL: 0.065 ppm for 96H; Test environment: 45 degrees F (OHM/TADS, 2004)
LC50 - BROWN TROUT: 0.002 ppm for 96H; Test environment: static(OHM/TADS, 2004)
LC50 - P. CALIFORNICA: 0.012 ppm for 24H; Test environment: 15.5 degrees C(OHM/TADS, 2004)
LC50 - P. CALIFORNICA: 0.008 ppm for 48H; Test environment: 15.5 degrees C (OHM/TADS, 2004)
LC50 - P. CALIFORNICA: 0.0045 ppm for 96H; Test environment: 15.5 degrees C (OHM/TADS, 2004)
LC50 - CARP: 0.09 ppm for 96H; Test environment: static(OHM/TADS, 2004)
LC50 - CHANNEL CATFISH: 0.044 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - COHO SALMON: 0.041 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - FATHEAD MINNOW: 0.087 ppm for 96H; Test environment: static(OHM/TADS, 2004)
LC50 - GOLDEN SHINER (Resistant): 3.14 ppm for 48H; Test environment: static (OHM/TADS, 2004)
LC50 - GOLDEN SHINER (Susceptible): 0.15 ppm for 48H; Test environment: static (OHM/TADS, 2004)
LC50 - GOLDFISH: 0.131 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - GREEN SUNFISH (Resistant): 1.9 ppm for 48H; Test environment: static (OHM/TADS, 2004)
LC50 - GREEN SUNFISH (Susceptible): 0.05 ppm for 48H; Test environment: static (OHM/TADS, 2004)
LC50 - GUPPY (.2 g): 0.05 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - HARLEQUIN FISH: 0.045 ppm for 48H; Test environment: static flow-through gamma BHC (OHM/TADS, 2004)
LC50 - LARGEMOUTH BASS: 0.083 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - MOSQUITO FISH (1.9 g): 0.13 ppm for 96H; Test environment: static(OHM/TADS, 2004)
LC50 - PALEAMONETES KADIAKENSIS (Resistant): 0.014 - 0.0373 ppm for 24H; Test environment: static (OHM/TADS, 2004)
LC50 - PALEAMONETES KADIAKENSIS (Susceptible): 0.0051 ppm for 24H; Test environment: static (OHM/TADS, 2004)
LC50 - RAINBOW: 0.030 ppm for 24H (OHM/TADS, 2004)
LC50 - RAINBOW: 0.022 ppm for 48H (OHM/TADS, 2004)
LC50 - RAINBOW: 0.022 ppm for 96H (OHM/TADS, 2004)
LC50 - RAINBOW TROUT: 0.027 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - SMALLMOUTH BASS: 0.032 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - STRIPED BASS FINGERLINGS: 0.4 ppm for 96H; Test environment: static (OHM/TADS, 2004)
LC50 - TILAPIA MOSSAMBICA: 0.06 ppm for 96H; Test environment: static
LC50 - YELLOW PERCH: 0.068 ppm for 96H; Test environment: static(OHM/TADS, 2004)
TL50 - BASS: 0.032 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - BLUEGILL:0.068 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - BROWN TROUT: 0.002 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - BULLHEAD: 0.064 ppm for 96H; Test environment: predicted(OHM/TADS, 2004)
TL50 - CARP: 0.090 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - CATFISH: 0.044 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - COHO:0.041 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - GOLDFISH: 0.131 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - MINNOW: 0.087 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - PERCH: 0.068 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - RAINBOW: 0.027 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TL50 - SUNFISH: 0.083 ppm for 96H; Test environment: predicted (OHM/TADS, 2004)
TLM - BLUEGILL: 0.077 ppm for 96H (OHM/TADS, 2004)
TLM - FATHEAD: 0.062 ppm for 96H (OHM/TADS, 2004)
TLM - FISH: 0.063 ppm for 96H (OHM/TADS, 2004)
TLM - GOLDFISH: 0.152 ppm for 96H (OHM/TADS, 2004)
TLM - GUPPIES: 0.138 ppm for 96H (OHM/TADS, 2004)
TLM - MINNOW: 0.056 ppm for 96H(OHM/TADS, 2004)

Ecotoxicity Values (Saltwater):

EC50 - OYSTER: 0.36 - 1 ppm for 96H (OHM/TADS, 2004)
LC - COHO FRY: 0.034 ppm for 10H(OHM/TADS, 2004)
LC50 - SAND SHRIMP: 0.014 ppm for 24H(OHM/TADS, 2004)
LC50 - HERMIT CRAB: 0.038 ppm for 24H(OHM/TADS, 2004)
LC50 - GRASS SHRIMP: 0.062 ppm for 24H (OHM/TADS, 2004)
35% LETHAL - SHEEPSHEAD MINNOW: 0.1 ppm for 168H; Test environment: salt marsh(OHM/TADS, 2004)
35% LETHAL - SPOT: 0.1 ppm for 168H; Test environment: salt marsh (OHM/TADS, 2004)
35% LETHAL - STRIPED MULLET: 0.1 ppm for 168H; Test environment: salt marsh (OHM/TADS, 2004)
35% LETHAL - RJ FIDDLER CRAB: 0.1 ppm for 168H; Test environment: salt marsh(OHM/TADS, 2004)
10% LETHAL - BLUE CRAB: 0.1 ppm for 168H; Test environment: salt marsh (OHM/TADS, 2004)
80% LETHAL - M FIDDLER CRAB: 0.1 ppm for 168H; Test environment: salt marsh
RETARDED GROWTH - MARINE PLANKTON: 7.5 - 9 ppm for unspecified time

Ecotoxicity Values:

ALGAE

ALGAE (Microcystis aeroginosa): inhibition of cell multiplication starts at 0.3 mg/L (Verschueren, 2001)
LC25 - ALGAE (Protococcus sp.): 5000 ppb for 10D (Verschueren, 2001)
LC43 - ALGAE (Chlorella sp.): 5000 ppb for 10D (Verschueren, 2001)
LC40 - ALGAE (Dunaliella): 9000 ppb for 10D (Verschueren, 2001)
LC70 - ALGAE (Phaeodactylum): 5000 ppb for 10D (Verschueren, 2001)
LC0 - ALGAE (Monochrysis lutheri): 5000 ppb for 10D (Verschueren, 2001)

BACTERIA

EC20 - BACTERIA (Photobacterium phosphoreum): 12 mg/L for 5M; Biotox(TM) test (Verschueren, 2001)
EC50 - BACTERIA (Photobacterium phosphoreum): 61 mg/L for 5M; Biotox(TM) test (Verschueren, 2001)
EC50 - BACTERIA (Photobacterium phosphoreum): 6360 mg/L for 5M; Microtox(TM) test (Verschueren, 2001)
EC50 - BACTERIA (Vibrio fisheri): 11 mg/L for 5M; Microtox(TM) test (Verschueren, 2001)

BIRDS

LD50 - COMMON CROW: >100 mg/kg (Verschueren, 2001)
LD50 - COMMON GRACKLE: >100 mg/kg (Verschueren, 2001)
LD50 - HOUSE SPARROW: 56 mg/kg (Verschueren, 2001)
LD50 - MOURNING DOVE: 350-400 mg/kg (Verschueren, 2001)
LD50 - REDWINGED BLACKBIRD: 100 mg/kg (Verschueren, 2001)
LD50 - STARLING: 75 mg/kg (Verschueren, 2001)

CRUSTACEANS

LC50 - CRUSTACEAN (Daphnia magna): 0.46 mg/L for 48H (Verschueren, 2001)
LC50 - CRUSTACEAN (Asellus brevicaudus): 10 mcg/L for 96 H (Verschueren, 2001)
LC50 - CRUSTACEAN (Daphnia magna): 1250 mcg/L for 24H (Verschueren, 2001)
LC50 - CRUSTACEAN (Daphnia pulex): 460 mcg/L for 48 H (Verschueren, 2001)
LC50 - CRUSTACEAN (Gammarus fasciatus): 10 mcg/L for 96 H (Verschueren, 2001)
LC50 - CRUSTACEAN (Gammarus lacustris): 48 mcg/L for 96 H (Verschueren, 2001)
LC50 - CRUSTACEAN (Gammarus pulex): 0.03 ppm for 48 H (Verschueren, 2001)
LC50 - CRUSTACEAN (Simocephalus serrulatus): 520 mcg/L for 48 H (Verschueren, 2001)
LC50 - BROWN SHRIMP (Penaeus aztecus): 400 ppb for 96H, static bioassay (Verschueren, 2001)
LC50 - GRASS SHRIMP (Palaemonetes vulgaris): 10 ppb for 96H, static bioassay (Verschueren, 2001)
LC50 - GREEN NEON SHRIMP (Neocaridina denticulata): 9.36 ng/L for 96H (95%CL = 8.00-10.96) -- test conditions: pH = 7.4-7.8, DO >7.3 mg/L, hardness = 38-45 mg CaCO3/L. Also reported: 100% mean mortality at 30 mcg/L (Huang & Chen, 2004).
LC50 - KOREAN SHRIMP (Palaemon macrodactylus): 9.2 (5.8-15) ppb for 96 H, flow-through bioassay(Verschueren, 2001)
LC50 - KOREAN SHRIMP (Palaemon macrodactylus): 12 (4.7-33) ppb for 96 H, static bioassay(Verschueren, 2001)
LC50 - SAND SHRIMP (Crangon septemspinosa): 5 ppb for 96H, static bioassay (Verschueren, 2001)

FISH

LC10 - RAINBOW TROUT (Salmo gairdneri Richardson), fry: 0.026 mg/L for 24H at 20 degrees C, pH 8.1, and 20 mg CaCO3/L hardness(Verschueren, 2001)
LC10 - RAINBOW TROUT (Salmo gairdneri Richardson), fry: 0.02 mg/L for 48H at 20 degrees C, pH 8.1, and 20 mg CaCO3/L hardness(Verschueren, 2001)
LC10 - RAINBOW TROUT (Salmo gairdneri Richardson), fry: 0.018 mg/L for 96H at 20 degrees C, pH 8.1, and 20 mg CaCO3/L hardness(Verschueren, 2001)
LC50 - FISH (Brachydanio rerio): 0.12 mg/L for 96H (Verschueren, 2001)
LC50 - FISH (Colisa fasciatus): 0.64 mg/L for 96H at 18 degrees C, static bioassay (Verschueren, 2001)
LC50 - FISH (Colisa fasciatus): 0.41 mg/L for 96H at 33 degrees C, static bioassay (Verschueren, 2001)
LC50 - FISH (Colisa fasciatus): 0.87 mg/L for 12H at 18 degrees C, static bioassay (Verschueren, 2001)
LC50 - FISH (Colisa fasciatus): 0.60 mg/L for 12H at 33 degrees C, static bioassay (Verschueren, 2001)
LC50 - FISH (Cyprinodon variegatus): 104 mcg/L for 96H, flow-through bioassay (Verschueren, 2001)
LC50 - FISH (Ictalurus melas): 64 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Ictalurus punctatus): 44 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Lagadon rhomboides): 86 mcg/L for 96H, flow-through bioassay (Verschueren, 2001)
LC50 - FISH (Lagadon rhomboides): 31 mcg/L for 96H, flow-through bioassay (Verschueren, 2001)
LC50 - FISH (Lepomis macrochirus): 68 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Lepomis microlophus): 83 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Micropterus salmoides): 32 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Oncorhynchus kisutch): 41 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Perca flavescens): 68 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Pimephales promelas): 87 mcg/L for 96H (Verschueren, 2001)
LC50 - FISH (Pteronarcys): 4.5 mcg/L for 48H (Verschueren, 2001)
LC50 - AMERICAN EEL (Anguilla rostrata): 56 ppb for 96H (Verschueren, 2001)
LC50 - ATLANTIC SILVERSIDE (Menidia menidia): 9 ppb for 96H (Verschueren, 2001)
LC50 - BASS: 32 mcg/L for 96H (Verschueren, 2001)
LC50 - BLUEGILL: 68 mcg/L for 96H (Verschueren, 2001)
LC50 - BLUEGILL: 0.062 ppm for 96H (Verschueren, 2001)
LC50 - BLUEGILL: 0.03 mg/L for 2Y at 27 degrees C, flow-through (Verschueren, 2001)
LC50 - BLUEHEAD (Thalossoma bifasciatum): 14 ppb for 96H (Verschueren, 2001)
LC50 - BROOK TROUT: 0.026 mg/L for 1.3y at 9-16 degrees C, flow-through (Verschueren, 2001)
LC50 - BROWN TROUT: 2 mcg/L for 96H (Verschueren, 2001)
LC50 - BULLHEAD: 64 mcg/L for 96H (Verschueren, 2001)
LC50 - CARP: 90 mcg/L for 96H (Verschueren, 2001)
LC50 - CARP (Cyprinus carpio): 0.32 mg/L for 48H (Verschueren, 2001)
LC50 - CATFISH: 44 mcg/L for 96H (Verschueren, 2001)
LC50 - COHO SALMON: 41mcg/L for 96H (Verschueren, 2001)
LC50 - GOLDFISH: 131 mcg/L for 96H (Verschueren, 2001)
LC50 - GUPPY: 0.8 mg/L for 48H at 24 degrees C, static bioassay (Verschueren, 2001)
LC50 - MINNOW (unspecified): 87 mcg/L for 96H (Verschueren, 2001)
LC50 - MUMMICHOG (Fundulus heteroclitus): 20; 60 ppb for 96H (Verschueren, 2001)
LC50 - NORTHERN PUFFER (Sphaeroides maculatis): 35 ppb for 96H (Verschueren, 2001)
LC50 - PERCH: 68 mcg/L for 96H (Verschueren, 2001)
LC50 - RAINBOW TROUT: 27 mcg/L for 96H (Verschueren, 2001)
LC50 - RAINBOW TROUT: 0.060 ppm for 96H (Verschueren, 2001)
LC50 - RAINBOW TROUT: 0.051 mg/L for 24H at 20-25 degrees C, flow-through bioassay (Verschueren, 2001)
LC50 - RAINBOW TROUT: 0.032 mg/L for 96H at 20-25 degrees C, flow-through bioassay (Verschueren, 2001)
LC50 - RAINBOW TROUT: 1.05 mg/L for 48H at 12 degrees C, static bioassay (Verschueren, 2001)
LC50 - RAINBOW TROUT (Salmo gairdneri Richardson), fry: 0.037 mg/L for 24H at 20 degrees C, pH 8.1, and 20 mg CaCO3/L hardness(Verschueren, 2001)
LC50 - RAINBOW TROUT (Salmo gairdneri Richardson), fry: 0.023 mg/L for 48H at 20 degrees C, pH 8.1, and 20 mg CaCO3/L hardness(Verschueren, 2001)
LC50 - RAINBOW TROUT (Salmo gairdneri Richardson), fry: 0.022 mg/L for 96H at 20 degrees C, pH 8.1, and 20 mg CaCO3/L hardness(Verschueren, 2001)
LC50 - RAINBOW TROUT (Salmo gairdneri Richardson), fry: 0.01 mg/L extrapolated for 3mo at 20 degrees C, pH 8.1, and 20 mg CaCO3/L hardness(Verschueren, 2001)
LC50 - RAINBOW TROUT (Salmo gairdneri): 27 mcg/L for 96H (Verschueren, 2001)
LC50 - RAINBOW TROUT (Salmo gairdneri): 13 mcg/L for 96H (Verschueren, 2001)
LC50 - STRIPED KILLIFISH (Fundulus majalis): 28 ppb for 96H (Verschueren, 2001)
LC50 - STRIPED MULLET (Mugil cephalus): 66 ppb for 96H (Verschueren, 2001)
LC50 - SUNFISH: 83 mcg/L for 96H (Verschueren, 2001)
LC50 - THREESPINE STICKLEBACK (Gasterosteus aculeatus): 50 ppb for 96H (Verschueren, 2001)

INSECTS

LC50 - INSECT (Chaoborus), larvae: 8 mcg/L for 48H (Verschueren, 2001)
LC50 - INSECT (Chironomus riparius), fourth instar larval: 3.6 mcg/L for 24H (Verschueren, 2001)
LC50 - INSECT (Cloeon): 92 mcg/L for 48H (Verschueren, 2001)
LC50 - INSECT (Pteronarcys californica): 4.5 mcg/L for 96H (Verschueren, 2001)

MOLLUSCS

LC50 - DECAPODS (Palaemonetes pugio): 4.4 mcg/L for 96 H, flow-through bioassay(Verschueren, 2001)
LC50 - DECAPODS (Panaeus duorarum): 0.17; 0.34 mcg/L for 96 H, flow-through bioassay(Verschueren, 2001)
LC50 - EASTERN OYSTER (Crassostrea virginica), egg: 9100 ppb for 48H, static bioassay(Verschueren, 2001)
LC50 - GASTROPODA (Lymnaea stagnalis): 7.3 ppm for 48 H -- at 2 ppm there was a decrease in growth rate from the third month and a 60% decrease in fecundity (Verschueren, 2001)
LC50 - HARD CLAM (Mercenaria mercenaria), egg: >10,000 ppb for 48H, static bioassay(Verschueren, 2001)
LC50 - HARD CLAM (Mercenaria mercenaria), larvae: >10,000 ppb for 12D, static bioassay(Verschueren, 2001)
LC50 - MYSIDACEA (Mysidopsis bahia): 6.3 mcg/L for 96 H, flow-through bioassay(Verschueren, 2001)

Lymnaea stagnalis L.: 2 mg/L -- rearing of larvae impossible (Verschueren, 2001)
MUD SNAIL (Nassa obsoletea): 10 ppm for 96H, static lab bioassay -- egg case deposition reduction from 1473 (control) to 749 (133D post exposure in clean water) (Verschueren, 2001)

Lowest NOECs by species (Verschueren, 2001):

Cyanophyta: 150 mcg/L (Verschueren, 2001)
Chlorophyta: 250; 500; 950 mcg/L (Verschueren, 2001)
Protozoa: 440 mcg/L (Verschueren, 2001)
Gastropoda: 330 mcg/L (Verschueren, 2001)
Branchiopoda: 11 mcg/L (Verschueren, 2001)
Malacostraca: 4.3 mcg/L (Verschueren, 2001)
Diptera: 2.2 mcg/L (Verschueren, 2001)
Pisces: 2.9; 8.8; 9.1 mcg/L (Verschueren, 2001)

Ecotoxicity Values (Ferrando et al, 1995; Hartley & Kidd, 1987):

LC50 - DAPHNIA MAGNA: 1.64 mg/L for 24H -- static
LC50 - GUPPY: 0.16-0.3 mg/L for 48H
LD50 - BOBWHITE QUAIL: 120-130 mg/kg

Water pollution of pesticides was assessed in an experimental study to evaluate the impacts of the insecticides lindane and deltamethrin. The insecticides were used in four ponds, with lindane at a concentration of 321 mcg/L and deltamethrin at 13 mcg/L. The microzooplankton (rotifera and copepod nauplii) were highly susceptible to both insecticides. The original zooplankton population recovered after two months, and had a new and dominant species: Ceriodaphnia reticulata (Tidou et al, 1992).

Pupation and adult emergence were the most sensitive stages to lindane in the life cycle of the diptera, Chironomus riparius meigen. The no observed effect concentration (NOEC) and lowest observed effect concentration (LOEC) for lindane were 1.1 and 9.9 mcg/L, respectively (Taylor et al, 1993).

Many abnormal behaviors were observed in the dragonfly, Pantala flavescens Fabr. (Libellulidae, Odonata), under lindane toxicity stress. The abnormalities were due to neuroapoplexy and were dose dependent (Bhardwaj & Tyagi, 1993).

After being exposed to sunlight for 6 days, lindane emulsion became 50% less toxic to mosquito larvae, and after 11 days' exposure was completely non-toxic (HSDB, 2004).

Impacts to differential white blood cell (WBC) counts in African catfish (Clarias albopunctatus) were seen in an evaluation of the effects of sublethal lindane concentrations on total and differential leucocyte counts. A static bioassay sytem was used for lindane exposure at five levels (0 mcg/L for the control and 0.25 -1.0 mcg/l for testing). Results indicated adaptive response for protection from lindane intoxication and related infection. Details follow(Mgbenka et al, 2003):

Total WBC counts increased significantly with increased lindane concentrations.
Monocytes were significantly lower in the exposed fish, and were absent in the blood of the 0.75 mcg/L and 1.0 mcg/L level fish at day 21.
Neutrophils decreased significantly in in the exposed fish, except the 0.5 mcg/L treatment group. The neutrophils decreased with increasing concentration up to day 14, but then increased significantly an all groups. Athough the levels increased, they remained lower than the control.
Leucocytosis was observed.
Fish treated with lindane underwent monocytopenia.

Acute toxicity in male mallard ducks given a lethal oral dose included regurgitation, polydipsia, tremors, circling, reflex slowing, and opisthotonos (HSDB, 2004).

Lindane residues were found in the tissue and eggs of laying hen pheasants administered radiolabeled lindane in capsules and feed. Chick tissue contained 1,2-DCB; 1,2,4-TCB, 1,2,3,4-TeCB; 1,2,3,5-/or 1,2,4,5-TeCB; gamma-PCCH. PCB was also found in the tissue. Egg yolk contained the same metabolites as found in the tissue as well as 1,3,5-TCB and 1,2,3-TCB (HSDB, 2004).

Lindane poisoning in trout (Salmo trutta) produces similar cause of death as that which occurs with hypoxia (HSDB, 2004).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

290.85

DESCRIPTION/PHYSICAL STATE

Lindane is a colorless or white to yellow crystalline powder or monoclinic prism. CHRIS (2000) reports that the solid is "light to dark brown." It has a bitter taste and may have a slightly musty or aromatic odor. Pure lindane is odorless (HSDB, 2005; NIOSH, 2005; ATSDR, 1994) NTP, 2000). Lindane has more vapor activity than most organochlorine insecticides (HSDB , 2000).

Lindane in its liquid form floats on water; the solid sinks (CHRIS , 2000).

Lindane is the gamma isomer of 1,2,3,4,5,6-hexachlorocyclohexane (HCH). There are seven other isomers of HCH, but non-gamma isomers can no longer be made or used in the United States (ACGIH, 1991; ATSDR, 1994; Hayes & Laws, 1991).

VAPOR PRESSURE

9.4 x 10(-6) mmHg (at 20 degrees C) (Budavari, 1996; Clayton & Clayton, 1994)

5.57 X 10(-5) mmHg (at 25 degrees C) (Howard, 1991)

4.20 X 10(-5) mmHg (at 20 degrees C) (HSDB, 2005)

0.03 mmHg (at 20 degrees C) (NTP, 2000)

0.0000094 mmHg (at 20 degrees C)(NTP, 2000)

SPECIFIC GRAVITY

OTHER TEMPERATURE AND/OR PRESSURE

1.891 (at 19 degrees C) (CHRIS , 2000)
1.87 (20/4 degrees C) (NTP, 2000)

TEMPERATURE AND/OR PRESSURE NOT LISTED

1.89 (Clayton & Clayton, 1994)
1.85 (NIOSH, 2005)

DENSITY

OTHER TEMPERATURE AND/OR PRESSURE

1.89 g/cm(3) (at 19 degrees C) (ATSDR, 1994)
1.87 g/mL (at 20 degrees C) (NTP, 2000)

FREEZING/MELTING POINT

FREEZING POINT

235 degrees F (NIOSH, 2005)

MELTING POINT

112.5 degrees C (Clayton & Clayton, 1994; Howard, 1991)
112-113 degrees C (NTP, 2000)

BOILING POINT

323.4 degrees C (at 760 mmHg) (HSDB, 2005; Howard, 1991)

614 degrees F (NIOSH, 2005)

176.2 degrees C at 10 mmHg (NTP, 2000)

288 degrees C (ITI, 1995) NTP, 2000)

FLASH POINT

Not Applicable (NIOSH, 2005)

The dry powder will not burn. Commercial solutions normally contain flammable or combustible liquids with flash points of approximately 150 degrees F or higher (HSDB , 2000).

AUTOIGNITION TEMPERATURE

Not Flammable (ATSDR, 1994)

EXPLOSIVE LIMITS

LOWER

Not Applicable (NIOSH, 2005)

UPPER

Not Applicable (NIOSH, 2005)

SOLUBILITY

IN WATER

Lindane is insoluble in water (Budavari, 1996).
17 ppm in water (Clayton & Clayton, 1994)
7.3 mg/L; 2 mg/L (Howard, 1991)
7 mg/L (Extoxnet, 2000)
0.001% (NIOSH, 2005)
7.52 ppm (HSDB, 2005)
The solubility in water varies with temperature:

7.3 ppm (at 25 degrees C) (HSDB, 2005)
12 ppm (at 35 degrees C) (HSDB, 2005)
14 ppm (at 45 degrees C) (HSDB, 2005)
<1 mg/mL (at 24 degrees C) (NTP, 2000)

IN ORGANIC SOLVENTS

It is moderately soluble in benzene, acetone, and chlorinated hydrocarbons. Lindane is only slightly soluble in kerosene (Clayton & Clayton, 1994) and soluble in acid (NTP, 2000).
>5 g/100 g in benzene, ethanol, acetone, and ethyl acetate (Extoxnet, 2000)
Lindane solubility in various solvents:

DMSO: 50-100 mg/mL (at 23 degrees C) (NTP, 2000)
95% Ethanol: 1-5 mg/mL (at 23 degrees C) (NTP, 2000)
Methanol: 7.4% (NTP, 2000)
Acetone: greater than or equal to 100 mg/mL (at 23 degrees C)(NTP, 2000)
Toluene: >50 g/L (NTP, 2000)
Petroleum ether: 2.9% (NTP, 2000)
Chloroform: 24% (NTP, 2000)
Ethyl acetate: >50 g/L (NTP, 2000)
Ether: >50 g/L (NTP, 2000)
Benzene: >50 g/L (NTP, 2000)
Acetic acid: 12.8% (NTP, 2000)
Carbon tetrachloride: 6.7% (NTP, 2000)
Cyclohexanone: 36.7% (NTP, 2000)
Dioxane: 31.4% (NTP, 2000)
Kerosene: 2-3.2% (NTP, 2000)
Xylene: 24.7% (NTP, 2000)
In g/L (at 20 degrees C) (HSDB, 2005):

Acetone: 43.5
Ethanol: 6.4
Benzene: 28.9
Toluene: 27.6
Diethyl ether: 20.8
Petroleum ether: 2.9
Ethyl acetate: 35.7
Cyclohexanone: 36.7
Dioxane: 31.4

OTHER

Rat fat: 12.55% (NTP, 2000)

OCTANOL/WATER PARTITION COEFFICIENT

log Kow = 3.72 (HSDB, 2005)

log Kow = 3.61 (Howard, 1991)

log Kow = 3.3 (Clayton & Clayton, 1994)

HENRY'S CONSTANT

7.8 x 10(-6) atm-m(3)/mol (ATSDR, 1994)

3.2 x 10(-6) atm-m(3)/mol (ATSDR, 1994)

2.92 x 10(-6) atm-m(3)/mol (at 25 degrees C) (Howard, 1991)

2 x 10(-6) cm(3)/mol-sec (at 23 degrees C) (HSDB, 2005)

3.50 x 10(-6) atm-m(3)/mol (at 25 degrees C) (HSDB, 2005)

SPECTRAL CONSTANTS

574 (Sadtler Research Laboratories IR Grating Collection) (HSDB, 2005)

MASS

4774 (National Bureau of Standards EPA-NIH Mass Spectra Data Base, NSRDS-NBS-63) (HSDB, 2005)

OTHER/PHYSICAL

ODOR THRESHOLD

Lower: 0.33 ppm (OHM/TADS, 2005)
Medium: 1.8 ppm (OHM/TADS, 2005)

INDEX OF REFRACTION

1.644 at 20 degrees C/D (Budavari, 1996)

IONIZATION POTENTIAL

Unknown (NIOSH, 2005)

TASTE THRESHOLD

Lower: 0.8 ppm (OHM/TADS, 2005)
Medium: 0.2 ppm (OHM/TADS, 2005)

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Information to evaluate chemical incidents