TOXICOLOGY OF ORGANOCHLORINE INSECTICIDES not seem to be mediated through oestrogenic or GABAegic actions but by some

38 TOXICOLOGY OF ORGANOCHLORINE INSECTICIDES not seem to be mediated through oestrogenic or GABAegic actions but by some

other anti-oestrogenic mechanism (Cooper et al., 1989; Uphouse, 1987; Uphouse and Williams, 1989).

Human toxicity Use experience Most documented experience of HCH is with lindane or the technical product,

HCH. Although HCH was explored as a possible anthelmintic agent it caused a burning sensation of the tongue (Klosa, 1950). Use against scabies has been stan- dard and generally trouble-free (Smith, 1991) but its use is now greatly restricted (Weinhold, 2001). It may soon end up being banned worldwide for environmental reasons as well as concern over long-term, low-level exposure of people. Perme- thrin cream rinse gave slightly better results against head lice than lindane with possibly fewer dermal reactions (Bowerman et al., 1987). However, lindane appears to be the better scabicide (Shacter, 1981). Because of the possible susceptibility of infants, pregnant women, and patients with highly excoriated skin other insecticides probably should be used in these circumstances. Lindane can be absorbed through the skin to an appreciable degree over a period of a few days (Feldmann and Maibach, 1970). In vitro experiments demonstrated that lindane in the epidermis was effectively extracted by human plasma protein (Menczel et al., 1984). The effectiveness of washing is variable and can actually aid absorption (Lange, Nitzsche, and Zesch, 1981; Nitsche, 1984).

Surveys of workers have revealed a moderate number of mild, acute intoxica- tions. However, the cases often show many of the elements found in occupational poisoning by dieldrin and aldrin (Smith, 1991). No significant neurophysiological, neuromuscular, or other poor health effects could be detected in a group of 60 workers producing lindane for 1–30 years (Baumann et al., 1981; Brassow, Baumann, and Lehnert, 1981) but abnormal EEG patterns in some workers exposed to HCH have been reported (Muller, Macholz, and Knoll, 1981). Toxic symptoms were observed in 90 per cent of workers engaged in the manufacture of technical HCH, some of whom showed evidence of cardiac effects (Kashyap, 1986).

The majority of effort to prevent poisoning by HCH and =or lindane focused on their use in vaporizing devices leading to low-level exposure. The unregulated sale of these devices led to their use in probably millions of homes.

Accidental and intentional poisoning Many accidental poisonings were of children who ate vaporizer pellets (Smith, 1991).

The clinical course of fatal poisoning occurred in as little as 2 h after ingestion. At the peak of its use, the number of recorded deaths from HCH was very small averaging less than one a year in the United States (Smith, 1991). Non-fatal cases

39 of illness occurred when HCH or lindane was accidentally added to food or food

CYCLODIENE AND RELATED INSECTICIDES

supply. Initial difficulty included malaise, faintness, and dizziness followed by collapse and convulsions, sometimes accompanied by foaming at the mouth and biting the tongue, nausea, vomiting, severe cyanosis of the face and extremities, facial pallor, and ocular defects (Bambov, Chomakov, and Dimitrova, 1966; Khare et al. , 1977). A moderate rise in temperature may be the consequence of the convulsions but a high fever has been reported and may be a direct toxic action of the pesticide especially in children (see Smith, 1991). Poisoned individuals eventually return to normal health, but in some cases this may take some weeks.

The amount of HCH ingested in fatal poisonings seems to have been approximately 200 mg =kg or above but reports of prompt vomiting in some cases and variation in the ages of patients confounds exact estimations (Jaeger et al., 1984; Smith, 1991). Con- vulsions may be observed at considerably lower doses (Klein-Natrop, Roder, and Kadner, 1970). Clinical chemistry, EEG patterns, and pathology following lindane poisoning or exposure are not diagnostic (Smith, 1991). A variety of the chlorinated phenols described under Metabolism and excretion, above, have been reported in the urine of acutely poisoned individuals or exposed workers and may be found as sul- phates, glucuronides, and mercapturates (Angerer, Maass, and Heinrich, 1983; Drummond, Gillanders, and Wilson, 1988; Starr and Clifford, 1972).