a) High concentrations of organochlorine insecticides can cause cardiac dysrhythmias by increasing myocardial irritability (Morgan, 1993).
b) 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).
c) CASE REPORT: A 56-year-old man vomited about 6 ounces (about 177 mL) of a white liquid about 30 minutes after ingesting about 12 ounces (about 355 mL) of an insecticide containing 20% lindane. Despite supportive therapy, including gastric lavage and activated charcoal, his mental status deteriorated, necessitating intubation about 75 minutes after ingestion. He experienced multiple seizures (a focal seizure followed by 3 brief generalized tonic-clonic seizures) from 3 to 14 hours postingestion and received diazepam, phenobarbital, and phenytoin. His arterial blood pH was 6.76 after the focal seizure and 7.05 after the first generalized seizure and he received sodium bicarbonate that corrected the pH to 7.34. He was extubated about 43 hours after ingestion, but he developed premature ventricular contractions and premature atrial contractions on day 3 and atrial fibrillation/flutter on day 5. Following supportive therapy, including IV lidocaine, digoxin, and IV verapamil, his condition resolved. On day 6, he developed ataxia, wide-based gait, slurred speech, paranoia, and depression with defects in higher mental functioning. On day 12, he still had neurological abnormalities (eg, poor memory, loss of task focus, inadequate mentation, and defects in fine motor coordination). At this time, he committed suicide by cutting his femoral artery. Toxicokinetics analysis revealed an estimated distribution half-life of 10.3 hours and a terminal half-life of 162.9 hours, which is much longer than the previously reported terminal half-life of 25 to 36 hours (Wiles et al, 2015).

a) Based on reports of occupational exposure to lindane, ECG abnormalities were reported in 15% of 45 workers manufacturing technical-grade HCH (ATSDR, 2003).

a) CASE REPORT: A 66-year-old man with scabies developed acute mental status changes, seizures, hypoxemia, severe respiratory acidosis, and hypotension (BP 73/48 mmHg; 11 hours after application) 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. All workup for bacteremia, sepsis, and meningitis were unremarkable. An EEG showed severe generalized cerebral dysfunction. He experienced infectious complications and died 50 days after admission. During autopsy, he was diagnosed with hypoxic ischemic encephalopathy from lindane poisoning (Sudakin, 2007).

a) Tachycardia has been reported following lindane use (Nolan et al, 2012).

a) Dyspnea has been reported from ingestion of lindane (Nolan et al, 2012; Lewis, 1996).

a) CASE REPORT - A 66-year-old man with scabies developed acute mental status changes, seizures, hypoxemia, severe respiratory acidosis, and hypotension approximately 8 hours 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. All workup for bacteremia, sepsis, and meningitis were unremarkable. An EEG showed severe generalized cerebral dysfunction. He experienced infectious complications and died 50 days after admission. During autopsy, he was diagnosed with hypoxic ischemic encephalopathy from lindane poisoning (Sudakin, 2007).

a) Severe seizures can limit pulmonary gas exchange, and this may be an immediate cause of death (Morgan, 1993).

a) Hypoventilation necessitating mechanical ventilation has been reported in a 4-year-old child following oral ingestion of 5 mL. No overt tonic-clonic activity was present, although brief eye deviation was noted. Pulse oximetry was measured at 90 percent (Nordt & Chew, 2000).

a) Pulmonary edema has occurred from lindane exposure, especially in children and where commercial formulations are in hydrocarbon solvents (Jaeger et al, 1984; EPA, 1985).

a) Aspiration of petroleum distillate solvent is likely to cause a hydrocarbon pneumonitis, which is potentially fatal.

a) 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 cases), excessive use (17 patients), and ingestion (3 cases) of lindane were identified. Seizures and respiratory problems developed in the majority of patients who developed severe AEs 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%) (Nolan et al, 2012).
b) CASE REPORT: A 38-year-old man with HIV, scabies, seborrheic dermatitis and tinea cruris developed status epilepticus 2 hours after 2 ounces of 1% lindane lotion was applied to his skin (Solomon et al, 1995). His HIV disease (potentially increased percutaneous absorption due to his skin disease) and coadministration of chlorpromazine were felt to have predisposed him to toxicity after therapeutic use.
c) CASE REPORT: A 66-year-old man with scabies developed acute mental status changes, repeated seizures, hypoxemia, respiratory acidosis, and hypotension approximately 8 hours 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. All workup for bacteremia, sepsis, and meningitis were unremarkable. An EEG showed severe generalized cerebral dysfunction. He experienced infectious complications and died 50 days after admission. During autopsy, he was diagnosed with hypoxic ischemic encephalopathy from lindane poisoning (Sudakin, 2007).

a) Lindane is a CNS excitant and convulsant. Accidental ingestion has caused fatalities. Both topical exposure and ingestion have resulted in seizures (Bhalla & Thami, 2004; Ryan et al, 1998; Zilker et al, 1999; Nordt & Chew, 2000). Effects in severe poisoning were repeated, violent, clonic seizures, sometimes superimposed on a continuous tonic spasm; onset can be rapid.
b) Respiratory difficulty and cyanosis secondary to seizures may occur; coma and respiratory depression may ensue (Morgan, 1993).
c) Most patients who survive recover completely over 1 to 3 days, usually within 24 hours (EPA, 1985); protracted illness is rare (Hathaway et el, 1996).
d) Persons at highest risk for development of seizures include young children and elderly patients, who may rarely develop neurotoxicity following therapeutic topical doses (Tenenbein, 1991). Most reports of seizures have involved ingestions or inappropriate topical use of lindane.
e) Grand mal seizures occurred in persons who had eaten benzene hexachloride-contaminated food (Nag et al, 1977; Nantel et al, 1977).
f) CASE REPORT: A 56-year-old man vomited about 6 ounces (about 177 mL) of a white liquid about 30 minutes after ingesting about 12 ounces (about 355 mL) of an insecticide containing 20% lindane. Despite supportive therapy, including gastric lavage and activated charcoal, his mental status deteriorated, necessitating intubation about 75 minutes after ingestion. He experienced multiple seizures (a focal seizure followed by 3 brief generalized tonic-clonic seizures) from 3 to 14 hours postingestion and received diazepam, phenobarbital, and phenytoin. His arterial blood pH was 6.76 after the focal seizure and 7.05 after the first generalized seizure and he received sodium bicarbonate that corrected the pH to 7.34. He was extubated about 43 hours after ingestion, but he developed premature ventricular contractions and premature atrial contractions on day 3 and atrial fibrillation/flutter on day 5. Following supportive therapy, including IV lidocaine, digoxin, and IV verapamil, his condition resolved. On day 6, he developed ataxia, wide-based gait, slurred speech, paranoia, and depression with defects in higher mental functioning. On day 12, he still had neurological abnormalities (eg, poor memory, loss of task focus, inadequate mentation, and defects in fine motor coordination). At this time, he committed suicide by cutting his femoral artery. Toxicokinetics analysis revealed an estimated distribution half-life of 10.3 hours and a terminal half-life of 162.9 hours, which is much longer than the previously reported terminal half-life of 25 to 36 hours (Wiles et al, 2015).
g) 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).
h) CASE REPORT: A 6-year-old girl developed generalized seizures lasting 5 to 10 minutes after ingesting an unknown amount of lindane lotion. Following supportive care, he recovered 24 hours later (Ramabhatta et al, 2014).
i) CASE REPORT: Starr & Clifford (1972) reported grand mal seizures and cyanosis in a 2-year-old female following ingestion of approximately 1.5 grams lindane from an insecticide pellet. Bilateral deep tendon reflexes were increased following seizure activity (Starr & Clifford, 1972).
j) CASE REPORT: A 13-month-old boy sustained two generalized tonic clonic seizures after ingesting an unknown amount of lindane lotion (Aks et al, 1995).
k) CASE REPORT: A 2-year-old boy developed what appeared to be petit mal seizures (staring blindly into space without responding to external stimuli) after ingesting one teaspoon of lindane lotion (Aks et al, 1995).
l) CASE REPORT: A 9-month-old infant developed seizures following accidental exposure to a 20% lindane insecticide which had been applied a day previously to a wooden deck where she was playing (Ryan et al, 1998).
m) CASE REPORT - A 3-year-old boy ingested approximately 1 teaspoon of 1% lindane shampoo. His mother induced vomiting in the boy twice. One hour after ingestion, he developed a tonic-clonic seizure lasting 4 to 5 minutes. He was discharged home from the ED after 3 hours of observation (Anon, 2005).
n) CASE REPORT: A 3.5-year-old boy developed lethargy, irritability, tremors, nausea, vomiting, mild metabolic acidosis, and general clonic-tonic seizures lasting about 2 minutes after ingesting an unknown quantity of 35% lindane solution. An EEG showed a typical 3/sec spike and generalized wave discharge. Following supportive treatment, his symptoms improved gradually; he was discharged home 42 hours post-ingestion (Lifshitz & Gavrilov, 2002).

a) Agitation, tremors, restlessness, muscle spasms, and nervousness can occur with lindane intoxication and are common (Nolan et al, 2012; Lifshitz & Gavrilov, 2002; EPA, 1985; Fischer, 1994; Jaeger et al, 1984; Diaz, 1998; Zilker et al, 1999).

a) Cogwheel rigidity with no other signs of extrapyramidal disease, other than weakness, occurred in persons exhibiting hexachlorobenzene-induced porphyria (Peters et al, 1982). Myotonia may also be seen (Peters et al, 1982).

a) 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).
b) ANIMAL STUDIES - In anaesthetized rats, lindane (20 mg/kg) elicited dose-dependent epileptic spikes in the hippocampus, along with rhythmic activity at 4 to 5 Hz (Nyitrai et al, 2002).

a) CASE REPORT - A 45-year-old man with a 30-year history of using 20 percent solutions of lindane developed a CSF pressure of 400 mm and pseudotumor cerebri. A direct cause-effect relationship could not be proven. Papilledema was seen in this patient as a result of the pseudotumor cerebri (Verderber et al, 1991).

a) Early signs of organochlorine poisoning involve hyperesthesia and paresthesia of the face and extremities, headache, dizziness, and incoordination (Morgan, 1993). Peters et al (1982) report a 60 percent incidence of sensory neuropathy in the acute phase of oral hexachlorobenzene toxicity.
b) Occasional reports have associated peripheral neuropathy with exposure to organochlorines. In one case, an agricultural worker developed polyneuritis of the sensory-motor type approximately two weeks after exposure to lindane in an unknown solvent (Tolot, 1969).

a) Severe headache may occur with exposure to lindane (Hathaway et al, 1996; Diaz, 1998).

a) Mild drowsiness, somnolence or lethargy may develop in patients with mild toxicity. More severe CNS depression may develop following seizures (Aks et al, 1995).
b) CASE REPORT: A 56-year-old man vomited about 6 ounces (about 177 mL) of a white liquid about 30 minutes after ingesting about 12 ounces (about 355 mL) of an insecticide containing 20% lindane. Despite supportive therapy, including gastric lavage and activated charcoal, his mental status deteriorated, necessitating intubation about 75 minutes after ingestion. He experienced multiple seizures (a focal seizure followed by 3 brief generalized tonic-clonic seizures) from 3 to 14 hours postingestion and received diazepam, phenobarbital, and phenytoin. His arterial blood pH was 6.76 after the focal seizure and 7.05 after the first generalized seizure and he received sodium bicarbonate that corrected the pH to 7.34. He was extubated about 43 hours after ingestion, but he developed premature ventricular contractions and premature atrial contractions on day 3 and atrial fibrillation/flutter on day 5. Following supportive therapy, including IV lidocaine, digoxin, and IV verapamil, his condition resolved. On day 6, he developed ataxia, wide-based gait, slurred speech, paranoia, and depression with defects in higher mental functioning. On day 12, he still had neurological abnormalities (eg, poor memory, loss of task focus, inadequate mentation, and defects in fine motor coordination). At this time, he committed suicide by cutting his femoral artery. Toxicokinetics analysis revealed an estimated distribution half-life of 10.3 hours and a terminal half-life of 162.9 hours, which is much longer than the previously reported terminal half-life of 25 to 36 hours (Wiles et al, 2015).
c) 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).
d) 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 cases), excessive use (17 patients), and ingestion (3 cases) of lindane were identified. Seizures and respiratory problems developed in the majority of patients who developed severe AEs 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 (Nolan et al, 2012).
e) Lindane-induced neurotoxicity (seizures, coma) occurred in a 10-month-old boy after he received repeated topical applications of 1% lindane (twice daily for 10 days) for the treatment of scabies. Laboratory results also revealed anemia and hypoproteinemia. Following the discontinuation of lindane and supportive treatment, his symptoms improved without further sequelae. The authors suggested that malnutrition may be a risk factor for developing neurotoxicity with lindane application. In addition, patients with reduced body fat may have higher lindane levels (Bhalla & Thami, 2004).

a) CASE REPORT: A 38-year-old man with HIV, scabies and seborrheic dermatitis and tinea cruris developed status epilepticus 2 hours after 2 ounces of 1 percent lindane lotion was applied to his skin (Solomon et al, 1995).
b) CASE REPORT - A 66-year-old man with scabies developed acute mental status changes, seizures, hypoxemia, respiratory acidosis, and hypotension approximately 8 hours 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. All workup for bacteremia, sepsis, and meningitis were unremarkable. An EEG showed severe generalized cerebral dysfunction. He experienced infectious complications and died 50 days after admission. During autopsy, he was diagnosed with hypoxic ischemic encephalopathy from lindane poisoning (Sudakin, 2007).

a) Following an acute poisoning after 3 applications of topical lindane, a 37-year-old female developed prolonged neurological and psychological symptoms for 20 months. Long-term effects included muscle spasm and extensor/flexor imbalance and myoclonic jerks, abdominal pain, urinary incontinence, and fecal incontinence. Long-term central effects included anxiety, depression, memory impairment, red/green visual changes, hallucinations, and incoordination (Hall & Hall, 1999).

a) When ingested, lindane has caused abdominal pain, nausea, vomiting and diarrhea, especially when contained in petroleum solvents (Lifshitz & Gavrilov, 2002; Jaeger et al, 1984). Vomiting is commonly reported after ingestion (Nordt & Chew, 2000).
b) CASE SERIES: Based on a five-year retrospective review of lindane exposures reported to six poison centers in Texas, the most frequent symptoms associated with inadvertent ingestion were nausea, vomiting, and throat irritation (Forrester et al, 2004).
c) Topical exposure to a 20% lindane insecticide has resulted in vomiting in an infant (Ryan et al, 1998).
d) CASE REPORT: A 47-year-old man developed vomiting after ingesting 1 ounce of lindane (concentration unknown) instead of a cough syrup (Anon, 2005).

a) CASE REPORT: 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).

a) An important property of the chlorinated hydrocarbons, particularly lindane, is their capacity to induce the drug-metabolizing enzymes of the liver (Wells & Milhorn, 1983; Klaasen, 1985).
b) CASE SERIES: Statistically significant increases in serum levels of lactate dehydrogenase (33%), and leucine aminopeptidase (45%), were reported in 19 individuals occupationally exposed (likely both inhalation and dermal exposure) to technical grade lindane for over 10 years in a lindane-formulating plant (ATSDR, 2003).
c) CASE REPORT: A single case report documents abnormal liver function tests in a patient who used 1% lindane twice a day for 3 weeks and subsequently developed aplastic anemia. No other cause was apparent for the abnormal liver function tests (Rauch et al, 1990).
d) Patients presenting with hexachlorobenzene-induced porphyria may develop elevated liver function tests (Peters et al, 1982).
e) CASE REPORT: Elevated LDH levels were found in a 14-year-old male following at least eight topical applications of lindane over a 6-week period (Berry et al, 1987).

a) Chronic exposure may induce liver damage and hepatomegaly, as reviewed in Gosselin (1984) and reported by Peters et al (1982).

a) Chronic exposure has caused hepatic damage in experimental animals (Budavari, 1996). Acute exposure has resulted in induction of liver microsomal drug-metabolizing enzymes (Kolmodin-Hedman et al, 1971).

a) Lindane produced some hepatomegaly in rats at 800 ppm in the diet (Clayton & Clayton, 1994), and changes at the cellular level were seen in rats given lindane at 50 ppm in the diet (Ortega et al, 1957).

a) Myoglobinuria secondary to rhabdomyolysis has been described after ingestion of lindane (Jaeger et al, 1984; Rao et al, 1988; Hall & Hall, 1999).

a) CASE REPORT: A 35-year-old man developed status epilepticus and myoglobinuria with subsequent acute renal insufficiency and generalized myolysis following ingestion of lindane-contaminated food (Nantel et al, 1977).

a) Renal degeneration has been reported in rodents exposed to lindane (Proctor et al, 1988). Fat deposits in the proximal convoluted tubule has been reported in a review by Solomon et al (1977).
b) Renal degeneration has been seen in rodents exposed chronically to lindane (Hathaway et al, 1996).

a) Lactic acidosis has been reported after ingestions of lindane (Jaeger et al, 1984).

a) Severe metabolic acidosis may be a consequence of severe convulsions (Morgan, 1993; Wiles et al, 2015), and the acidosis may be an immediate cause of death (Morgan, 1993).
b) CASE REPORT: A 35-year-old male presented with status epilepticus and severe metabolic acidosis following ingestion of lindane-contaminated food (Nantel et al, 1977).
c) CASE REPORT: A 3.5-year-old boy developed lethargy, irritability, tremors, nausea, vomiting, mild metabolic acidosis (pH 7.28, pCO2 41 mmHg, pO2 95 mmHg, HCO3 20 mmol/L), and general clonic-tonic seizures lasting about 2 minutes after ingesting an unknown quantity of 35% lindane solution. Following supportive treatment, his symptoms improved gradually; he was discharged home 42 hours postingestion (Lifshitz & Gavrilov, 2002).

a) CASE REPORT - A 66-year-old man with scabies developed acute mental status changes, seizures, hypoxemia, severe respiratory acidosis (pH=6.94; pCO2=84; pO2=196), and hypotension approximately 8 hours 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. All workup for bacteremia, sepsis, and meningitis were unremarkable. An EEG showed severe generalized cerebral dysfunction. He experienced infectious complications and died 50 days after admission. During autopsy, he was diagnosed with hypoxic ischemic encephalopathy from lindane poisoning (Sudakin, 2007).

a) Respiratory acidosis may develop in patients with significant CNS depression (Aks et al, 1995).

a) Large exposures to lindane have been associated with rare individual cases of aplastic anemia (Nolan et al, 2012; Morgan, 1993; Woodliff et al, 1966). At least eight cases have been reported for persons exposed to lindane from vaporizers (West, 1967; Loge, 1965; Baselt, 1997).
b) The association of aplastic anemia with exposure to lindane vapors generated from solid pellets in the absence of solvent excludes the possible contribution of benzene, which has been used as a solvent in some commercial preparations of lindane.
c) No evidence of pancytopenia with reticulopenia was found in persons occupationally exposed to lindane, however (Milby & Samuels, 1971).
d) CASE REPORT: A case of severe, reversible hypoplastic anemia was reported in a 2-year-old child from suspected exposure to lindane from a vaporizer (Morgan, 1980).
e) Acute leukemia has been reported from repeated topical exposures to related chlorinated hydrocarbon insecticides, namely chlordane and heptachlor, (Infante et al, 1978). Sidi et al (1983) report a case of a 66-year-old man with aplastic anemia following chronic exposure to lindane insecticide. He subsequently was diagnosed with acute myeloblastic leukemia and died soon thereafter from septicemia.
f) CASE REPORT: A 21-year-old man using 1% lindane lotion (applied twice a day to the body for 3 weeks) developed aplastic anemia 3 weeks later (Rauch et al, 1990).

a) Leukocytosis has been reported following the use of lindane (Nolan et al, 2012).

a) CASE REPORT: Pancytopenia was reported in a 14-year-old boy who applied 1% lindane lotion on 8 occasions to open lesions, and left the lotion on for 48 hours after the final application (Berry et al, 1987).

a) CASE REPORT: Disseminated intravascular coagulation (DIC) was described 8 hours postingestion in a 43-year-old woman who ingested 8 ounces of 20% lindane. The coagulopathy reversed following a decline in lindane serum levels (Rao et al, 1988).

a) 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).

a) CASE REPORT: Idiopathic thrombocytopenic purpura developed in a 17-year-old woman who worked formulating wood preservatives (Hay & Singer, 1991). Her exposures included lindane, pentachlorophenol, tributyl-tin oxide, permethrin and petroleum based solvents.

a) Extensive contact may result in dermatitis and local hypersensitivity reactions (Fiumara & Kahn, 1983; Budavari, 1996).

a) Acute generalized exanthematous pustulosis has been reported following lindane use (Nolan et al, 2012).

a) CASE REPORT: A 9-year-old boy developed Henoch-Schonlein (anaphylactoid) purpura 2 days following therapeutic topical application of 1% lindane shampoo (Fagan, 1981).

a) Percutaneous absorption may occur in patients with compromised epidermal barrier function (Friedman, 1987; Solomon et al, 1995).

a) Some skin irritation results from extensive contact with these agents or with petroleum distillates in which they are contained.
b) CASE REPORT: Scattered small papules and wheal lesions with itching were reported on the extremities of a 24-year-old woman after daily applications of lindane for 24 consecutive days (Diaz, 1998). No areas of blistering, cracking, scaling, or excoriation were noted.

a) 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. She 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).

a) There was a report of an outbreak of accidental hexachlorobenzene ingestions in persons consuming treated seed grain. Persistent abnormal porphyrin metabolism was seen 25 years later with significant porphyria cutanea tarda present in many patients. A syndrome called "pembe yara" or "pink sore", related to porphyria, was noted in the form of pigmented patches on the skin resembling a ringworm rash (Peters et al, 1982).

a) CASE REPORT: Rhabdomyolysis, muscle weakness and myoglobinuria were reported in a 35-year-old man who ingested 15 to 30 mL of lindane. Seizures were present for 2 hours (Munk & Nantel, 1977). Elevated creatine kinase with hemoglobinuria and myoglobinuria have been reported in patients exhibiting skeletal muscle damage from hexachlorobenzene toxicity (Peters et al, 1982).
b) CASE SERIES: After a hexachlorobenzene ingestion epidemic, a reported 73% of patients developed profound muscle weakness in the acute phase (Peters et al, 1982).
c) CASE REPORT: Rhabdomyolysis with increased creatine kinase levels developed 3 days after ingestion of a lindane-solvent mixture in one case (Jaeger et al, 1984).

a) 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).

a) 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.

a) 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).

a) Anaphylactic reaction has been reported following lindane use (Nolan et al, 2012).

a) RABBITS - Lindane given at 10 mg/kg/d for 90 days was not immunosuppressive in rabbits (Roszkowski, 1978).

a) Lindane increased postimplantation deaths in rats (Mametkuliev, 1976). It has also caused stillbirths in dogs (Earl, 1973) and rabbits (Khamidov, 1984).

a) Female CD-1 mice were given lindane orally (15 or 25 mg/kg) prior to mating or immediately after mating, and the results indicated that lindane exposure of developing oocytes in vivo led to an increase of irreversible damage (ie, lysis, fragmentation) in two-cell embryos. Based on the experimental doses used in this study (approximately 1000 to 10000 times the measured concentration of lindane in the general human population), the authors suggested that there appears to be an ample margin of safety for human embryonic development (Scascitelli & Pacchierotti, 2003).

a) The average daily intake of lindane for persons living in the US was 5.6 mcg from 1965 to 1970. During this time, levels of lindane in body fat ranged from 0.2 to 0.6 ppm. Levels in Japanese, Formosans, and Argentinians have been higher (Clayton & Clayton, 1994).

1) Therefore, any toddler or child who ingests a product containing any amount of lindane should be referred to a medical facility for evaluation.
2) Children who sustain a dermal exposure to lindane products should have the skin immediately washed well with soap and water. Children who develop signs of lethargy or CNS excitation, and young children/infants (less than 1 year old) with prolonged dermal exposure should be referred for medical evaluation and treatment.

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 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 (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 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 (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

a) If seizures are not controlled by the above measures, patients will require endotracheal intubation, mechanical ventilation, continuous EEG monitoring, a continuous infusion of an anticonvulsant, and may require neuromuscular paralysis and vasopressor support. Consider continuous infusions of the following agents:
b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required (Brophy et al, 2012) and consultation with a neurologist is strongly advised.
c) Neuromuscular paralysis (eg, rocuronium bromide, a short-acting nondepolarizing agent) may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis. If rhabdomyolysis is possible, avoid succinylcholine chloride, because of the risk of hyperkalemic-induced cardiac dysrhythmias. Continuous EEG monitoring is mandatory if neuromuscular paralysis is used (Manno, 2003).

a) ANIMALS - Pretreatment with phenytoin appeared to enhance the convulsive effects of lindane in rats (Tilson et al, 1985).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) Osmotic diuretic used in the management of rhabdomyolysis and myoglobinuria (Zimmerman & Shen, 2013).

a) ADULT: TEST DOSE: (for patients with marked oliguria or those with inadequate renal function) 0.2 g/kg IV as a 15% to 25% solution infused over 3 to 5 minutes to produce a urine flow of at least 30 to 50 mL/hr; a second test dose may be given if urine flow does not increase within 2 to 3 hours. The patient should be reevaluated if there is inadequate response following the second test dose (Prod Info MANNITOL intravenous injection, 2009). TREATMENT DOSE: 50 to 100 g IV as a 15% to 25% solution may be used. The rate should be adjusted to maintain urinary output at 30 to 50 mL/hour (Prod Info mannitol IV injection, urologic irrigation, 2006) OR 300 to 400 mg/kg or up to 100 g IV administered as a single dose (Prod Info MANNITOL intravenous injection, 2009).
b) PEDIATRIC: Dosing has not been established in patients less than 12 years of age(Prod Info Mannitol intravenous injection, 2009). TEST DOSE (for patients with marked oliguria or those with inadequate renal function): 0.2 g/kg or 6 g/m(2) body surface area IV as a 15% to 25% solution infused over 3 to 5 minutes to produce a urine flow of at least 30 to 50 mL/hr; a second test dose may be given if urine flow does not increase; TREATMENT DOSE: 0.25 to 2 g/kg or 60 g/m(2) body surface area IV as a 15% to 20% solution over 2 to 6 hours; do not repeat dose for persistent oliguria (Prod Info MANNITOL intravenous injection, 2009).

a) Fluid and electrolyte imbalance, in particular sodium and potassium; expansion of the extracellular fluid volume leading to pulmonary edema or CHF exacerbations(Prod Info MANNITOL intravenous injection, 2009).

a) Contraindicated in well-established anuria or impaired renal function not responding to a test dose, pulmonary edema, CHF, severe dehydration; caution in progressive oliguria and azotemia; do not add to whole blood for transfusions(Prod Info Mannitol intravenous injection, 2009); enhanced neuromuscular blockade observed with tubocurarine(Miller et al, 1976).

a) Renal function, urine output, fluid balance, serum potassium, serum sodium, and serum osmolality (Prod Info Mannitol intravenous injection, 2009).

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 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 (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 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 (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

a) If seizures are not controlled by the above measures, patients will require endotracheal intubation, mechanical ventilation, continuous EEG monitoring, a continuous infusion of an anticonvulsant, and may require neuromuscular paralysis and vasopressor support. Consider continuous infusions of the following agents:
b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required (Brophy et al, 2012) and consultation with a neurologist is strongly advised.
c) Neuromuscular paralysis (eg, rocuronium bromide, a short-acting nondepolarizing agent) may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis. If rhabdomyolysis is possible, avoid succinylcholine chloride, because of the risk of hyperkalemic-induced cardiac dysrhythmias. Continuous EEG monitoring is mandatory if neuromuscular paralysis is used (Manno, 2003).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 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 (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 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 (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

a) If seizures are not controlled by the above measures, patients will require endotracheal intubation, mechanical ventilation, continuous EEG monitoring, a continuous infusion of an anticonvulsant, and may require neuromuscular paralysis and vasopressor support. Consider continuous infusions of the following agents:
b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required (Brophy et al, 2012) and consultation with a neurologist is strongly advised.
c) Neuromuscular paralysis (eg, rocuronium bromide, a short-acting nondepolarizing agent) may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis. If rhabdomyolysis is possible, avoid succinylcholine chloride, because of the risk of hyperkalemic-induced cardiac dysrhythmias. Continuous EEG monitoring is mandatory if neuromuscular paralysis is used (Manno, 2003).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) CASE REPORTS

a) In a study of occupational exposure, whole blood lindane levels of greater than 0.02 part per million (20 nanograms/mL) correlated with clinical symptoms of toxicity and EEG changes (Czegledi-Janko & Avar, 1970).

a) The threshold-blood concentration for initiation of seizures in rats was 1.3 to 1.7 mcg/mL (Tusell et al, 1987).

1) Lindane

a) TWA: 0.5 mg/m(3)
b) STEL:
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: [skin]
f) Note(s):

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

a) 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.

a) 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.

a) 8-hour TWA:

a) 125 mg/kg

a) 44 mg/kg
b) 86 mg/kg (Hayes & Laws, 1991)
c) 340-562 mg/kg (Hayes & Laws, 1991)
d) 59-246 mg/kg (Extoxnet, 2000)

a) 300 mg/kg (Hayes & Laws, 1991)

a) 35 mg/kg

a) 76 mg/kg
b) Male, 88 mg/kg (Budavari, 1996)
c) 88 mg/kg (Hayes & Laws, 1991)
d) Female, 91 mg/kg (Budavari, 1996)
e) 80-125 mg/kg (Tusell et al, 1987)
f) 88-200 mg/kg (ACGIH, 1991)
g) 88-270 mg/kg (Extoxnet, 2000)
h) 50-500 mg/kg (CHRIS, 2000)
i) 125 mg/kg (Hayes & Laws, 1991)
j) 190 mg/kg (Hayes & Laws, 1991)
k) 200 mg/kg (Hayes & Laws, 1991)

a) 414 mg/kg
b) 900 mg/kg (Hayes & Laws, 1991)
c) 1000 mg/kg (Hayes & Laws, 1991)
d) 500 mg/kg (Hayes & Laws, 1991; Lewis, 2000)
e) 500-1000 mg/kg (ACGIH, 1991)

a) 50 mg/kg (Hayes & Laws, 1991)

a) 1 mg/m(3) for 80D intermittent -- bone marrow changes

a) 1700 mcg/m(3) for 17W intermittent -- serum composition changes; phosphatases; dehydrogenases

a) Gastric lavage and administration of activated charcoal were used to decontaminate the gut and prevent further absorption of a seed dressing containing lindane and phenylmercury acetate (Shaw, 1988).

1) Symptomatic treatment was effective in allowing recovery from acute gamma-hexachlorocyclohexane toxicity in a 9-year-old border collie (Shaw, 1988).

1) Copious washing of the exposed external surfaces may help prevent percutaneous absorption (Shaw, 1988).

1) GENERAL TREATMENT