Mechanism of Action

In the cockroach, lindane evokes synaptic after-discharges and excessive release of acetylcholine (Shankland, 1979; Uchida et al., 1975). However, the major target site of lindane in mammals and insects is the γ-aminobutyric acid (GABA) receptor. GABA is the major inhibitory neurotransmitter in the brain. Activation of the GABA receptor opens chloride-ion channels in neurons. The GABA-induced chloride uptake that results from the channel’s opening is inhibited by lindane (Ghiasuddin and Matsumura, 1982; Ogata et al., 1988). Lindane apparently interferes with binding to one subtype of GABA receptors, the GABAA receptors. Enhanced monoaminergic turnover has also been reported (Rivera et al., 1998), and central monoaminergic systems seem to have a role in lindane intoxication (Llorens et al., 1991).

Acute Human Exposures

Lindane has been used by humans to control scabies caused by mites and to combat lice in cream, ointment, emulsion, and aerosol formulations. Prescription products (Kwell® lotion and Kwell® shampoo) are available for human use (Facts and Comparions, 2001). Not many studies regarding lindane intoxication in humans have been published. A few cases of lindane intoxication following use for control of scabies were due largely to gross disregard of directions; it was applied to the entire body for many days or taken orally (Smith, 1991). A few deaths have been caused by accidental lindane ingestion, and there are many reports of nonfatal intoxication.

A large proportion of fatal and nonfatal lindane poisonings have been in children (Joslin et al., 1960; Savage et al., 1971). Accidental poisoning with lindane occurred when 11 people drank coffee prepared with lindane in place of sugar (Smith, 1991). Initial symptoms included malaise, faintness, and dizziness and were followed by collapse and convulsions, which were sometimes preceded by screaming and accompanied by foaming at the mouth and biting of the tongue. Nausea and vomiting occurred in many cases. The patients were unconscious during convulsions, and loss of consciousness lasted for 15 min to 3 h. Nine patients had retrograde amnesia. Most of the patients were discharged the next day.

Poisoning with lindane is often associated with the use of vaporizing devices. In two such cases, headache, nausea, and irritation of eyes, nose, and throat occurred shortly after exposure to vapors; the symptoms were reversible (AMA, 1952). Secondary effects seen following inhalation of lindane include blood dyscrasias, such as anemia, leukopenia, leukocytosis, granulocytopenia, granulocytosis, eosinophilia, thrombocytopenia, increased bone marrow megakaryocytes, and decreased bone marrow megaloblastoid of the erythroid series (Berry et al., 1987; Morgan et al., 1980), although Morgan and colleagues (1980) seriously questioned the role of lindane in blood dyscrasias.

Experimental Data

Neurotoxic Effects

Acute exposure of animals to lindane causes CNS stimulation, motor impairment, excitation, clonic (intermittent) and tonic (continuous) convulsions, increased respiratory rate or respiratory failure, pulmonary edema, and dermatitis (Drummer and Woolley, 1991;



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