International Notes Acute Convulsions Associated with Endrin Poisoning -- Pakistan

Between July 14, and September 26, 1984, an outbreak of acute convulsions occurred in Talagang, a wheat-growing subdistrict of the Punjab province of Pakistan. At least one case was reported in 21 (32%) of 65 villages in the subdistrict. Altogether, 192 cases, with 19 deaths, were reported. Sixty percent of the cases occurred among persons between 1 year and 9 years of age, and 80% occurred among persons under 15 years of age. Males and females were equally affected. None of the patients interviewed had a prior history of seizures.

Young children had no prodromal symptoms before the onset of seizures. They were observed to be engaged in routine activities when they collapsed suddenly, with bilateral jerking of the upper extremities followed by generalized tonic, clonic contractions and frothing or vomiting. Older patients reported having headaches and/or nausea and minor muscular spasms approximately half an hour before collapsing. Among untreated patients, seizures continued intermittently for 15 minutes to more than 2 hours. Repeated attacks were associated with hypoxia, pulmonary congestion, and death. Axillary temperatures of 37.8 C (100 F) were recorded in some patients immediately after the seizures ceased. More severely ill patients did not vomit as frequently as mildly affected patients, and they had higher temperatures. The combination of diazepam, phenobarbital, and atropine (to control secretions) was an effective therapeutic regimen in controlling symptoms. More severely affected patients were also given general anesthesia. For most patients, seizures were controlled within 1-2 hours, and patients remained sleepy for 24-48 hours, then recovered completely. Afterwards, patients did not remember the seizures.

Sera from 12 of 21 patients with convulsions had measurable levels of endrin. Values for all 21 ranged from 0 parts per billion (ppb) to 254 ppb (mean 17.10 ppb; median 1 ppb). Stomach contents from one of the 12 patients whose sera were positive had 307 ppb endrin. Autopsy tissues from another person contained endrin levels consistent with fatal acute exposures. Food samples collected from case homes were negative for endrin. Although 1,1,-trichloro-2,2-dis(4-chlorophenyl)ethane and benzene hexachloride (BHC) were found in the homes of many Talagang residents, there was no evidence that endrin was being used by local farmers, nor was it available in the local market.

A case-control study (25 cases, 21 and 23 from two sets of controls) did not implicate causative food or environmental factors. Nevertheless, available data suggested that a common food product (sugar) could have been contaminated during transport to a wholesale depot in the subdistrict capital--the only commercial food distribution point in Talagang--then distributed to the villages. Cases clustered in villages located near the main road to the subdistrict capital. There was little to no communication between villages, but shopkeepers and village residents frequently traveled to the subdistrict capital to purchase supplies. Cotton and sugar-cane growers in the southern part of the Punjab use endrin. Several independent truckers reported delivering chemicals to these growers, then picking up loads of food in the same trucks for transport to Talagang. However, there were no records with which to verify these reports. Additional environmental and food samples from patients' homes and the wholesale food depots are still being analyzed, and results may clarify the source and route of exposure. Reported by National Institutes of Health, Pakistan; World Health Organization, Geneva, Switzerland; Toxicology Br, Clinical Chemistry Div, Special Studies Br, Chronic Diseases Div, Center for Environmental Health, CDC.

Editorial Note

Editorial Note: Endrin is a chlorinated hydrocarbon pesticide, one of the group that includes DDT, BHC, chlordane, heptachlor, dieldrin, and aldrin. Endrin, chlordane, heptachlor, dieldrin, and aldrin are structurally similar. All have a cyclodien ring, but endrin is the most toxic. The minimum dose needed to produce a single convulsion in humans and the dose necessary for repeated nonfatal convulsions have been estimated to be 0.2-0.25 mg/kg and 1 mg/kg, respectively (1). Endrin is no longer commercially available in the United States. In Pakistan, it is imported for use in the early growth stages of cotton and sugar cane.

Animal studies have found that endrin is rapidly absorbed, metabolized, and excreted in feces, with a half-life in rats ranging from 2 to 6 days. In contrast, dieldrin is redistributed in body organs, particularly fat (2). Endrin is not persistent in animals or humans. Unlike DDT, BHC, dieldrin, and some of the other chlorinated hydrocarbons, endrin has not been found in fat samples taken from general surveys of humans exposed to chlorinated hydrocarbons, including endrin (4), nor has it been found in the blood of endrin workers, except in association with recent gross accidental exposure (1,3). Previously reported blood levels of patients poisoned by ingestion of endrin have ranged from 4 ppb to 53 ppb within the first day of consuming contaminated food (5,6). No endrin was detected 29-31 days after exposure (6). The presence of endrin in 57% of seizure patients tested in Pakistan suggests that endrin was the cause of this most recent outbreak.

Previous outbreaks of endrin poisoning have been associated with consumption of contaminated flour. Bread and rolls from the outbreaks contained 126-180 parts per million of endrin (5,7). The first reported outbreak was in Great Britain, where endrin was spilled on the floor of a box car; 1 month later, bags of flour stacked on the floor of the car became contaminated (8). In the Middle East, over 800 cases of endrin poisoning occurred in four outbreaks after contaminated flour was used in several bakeries (7). The flour had been imported aboard ships that were also transporting endrin. Endrin spilled from the upper decks of the ships onto the sacks of flour. As a result of the investigation, the governments of Qatar and Saudi Arabia required that ships transporting foodstuffs identify the type and location of all toxic chemicals and that the ships be inspected before food was unloaded for delivery (7).

In the Pakistan episode, circumstances of endrin use and food and chemical transport suggest that food products could have been contaminated during transport. Whether further analysis of environmental samples and epidemiologic data can document the source(s) and route(s) of exposure remains to be seen.

References

1. Hayes WJ Jr. Clinical handbook on economic poisons. Emergency information for treating poisoning. Atlanta, Georgia: Public Health Service publication no. 476, revised 1963.

2. Jager KW. Aldrin, dieldrin, endrin and telodrin. An epidemiological and toxicological study of long-term occupational exposure. Amsterdam, The Netherlands: Elsevier Publishing Company, 1970.

3. Hayes WJ Jr, Curley A. Storage and excretion of dieldrin and related compounds. Effect of occupational exposure. Arch Environ Health 1968;16:155-62.

4. Hayes WJ Jr, Dale WE, Burse VW. Chlorinated hydrocarbon pesticides in the fat of people in New Orleans. Life Sciences 1965;4:1611-5.

5. Coble Y, Hildebrant P, Davis J, Raasch F, Curley A. Acute endrin poisoning. JAMA 1967;202:489-93.

6. Curley A, Jennings RW, Mann HT, Sedlak V. Measurement of endrin following epidemics of poisoning. Bull Environmental Contam Toxicol 1970;5:24-9.

7. Weeks DE. Endrin food-poisoning. A report on four outbreaks caused by two separate shipments of endrin-contaminated flour. Bull WHO 1967;37:499-512.

8. Davies GM, Lewis I. Outbreak of food-poisoning from bread made of chemically contaminated flour. Br Med J 1956;2:393-8.

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