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Water Hemlock Poisoning -- Maine, 1992

On October 5, 1992, a 23-year-old man and his 39-year-old brother were foraging for wild ginseng in the midcoastal Maine woods. The younger man collected several plants growing in a swampy area and took three bites from the root of one plant. His brother took one bite of the same root. Within 30 minutes, the younger man vomited and began to have convulsions; they walked out of the woods, and approximately 30 minutes after the younger man became ill, they were able to telephone for emergency rescue services.

Within 15 minutes of the call, emergency medical personnel arrived and found the younger man unresponsive and cyanotic with mild tachycardia, dilated pupils, and profuse salivation. Severe tonic-clonic seizures occurred and were followed by periods of apnea. He was intubated and transported to a local emergency department. Physicians performed gastric lavage and administered activated charcoal. His cardiac rhythm changed to ventricular fibrillation, and four resuscitative attempts were unsuccessful. He died approximately 3 hours after ingesting the root.

Although the older brother was asymptomatic when he arrived at the emergency department, he was treated prophylactically with gastric lavage and administered activated charcoal. He began to have seizures and exhibit delirium 2 hours after eating the root; he was stabilized and transferred to a tertiary-care center for observation. No additional adverse effects were reported.

The root ingested by the two brothers was identified as water hemlock (Cicuta maculata). In October 1993, postmortem samples of frozen liver tissue, blood, and gastric contents from the man were analyzed by high-pressure liquid chromatography for cicutoxin, a poisonous substance in water hemlock. Cicutoxin, a neurotoxin, was not detected; however, the toxin is labile and may have degraded during storage.

Reported by: K Sweeney, MD, Office of the Chief Medical Examiner; KF Gensheimer, MD, State Epidemiologist, Maine Dept of Human Svcs; J Knowlton-Field, Damariscotta, Maine. RA Smith, Livestock Disease Diagnostic Center, Dept of Veterinary Science, Univ of Kentucky, Lexington. Health Studies Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health, CDC.

Editorial Note

Editorial Note: Based on mortality data files maintained by CDC's National Center for Health Statistics, from 1979 through 1988 (the most recent national data available) at least 58 persons in the United States died after ingesting a poisonous plant that was misidentified as an edible fruit or vegetable; inadvertent ingestion of water hemlock, as in the two cases in this report, caused at least five of these deaths. During 1989-1992, the American Association of Poison Control Centers recorded four deaths attributed to ingestion of poisonous plants (1-4). Water hemlock -- also known as beaver poison, children's bane, death-of-man, poison parsnip, and false parsley -- is in the same family as parsley, parsnips, celery, and carrots. It is similar in appearance to parsnips, smells like fresh turnips, and tastes sweet, but it is the most toxic indigenous plant in North America (5).

Although cicutoxin is present in all parts of the water hemlock plant, the root contains the highest concentration. Ingestion of a 2-3-cm portion of the root can be fatal in adults (6), and use of toy whistles made from the water hemlock stem has been associated with deaths in children (7). The plant is poisonous at all stages of development and is most toxic in the spring. Poisonings typically result from ingestions; however, cicutoxin also may be absorbed through the skin.

Mild toxicity from water hemlock produces nausea, abdominal pain, and epigastric distress within 15-90 minutes. The early gastrointestinal response of vomiting may be somewhat protective as many persons regurgitate the undigested root. Diaphoresis, flushing, and dizziness also have been reported. In severe intoxications, profuse salivation, perspiration, bronchial secretion, and respiratory distress leading to cyanosis develop soon after ingestion. In fatal poisonings, severe seizures occur after the initial symptoms, and death results usually from status epilepticus. The case-fatality rate for poisonings reported from 1900 through 1975 was 30% (8). The last fatality attributed to ingestion of water hemlock in Maine occurred in the early 1970s. No antidotes exist, and treatment is supportive. Complications associated with serious poisonings include rhabdomyolysis with renal failure (transient hematuria, glycosuria, and proteinuria), severe metabolic acidosis, bradycardia, and hypotension (9).

This report underscores the need for persons who forage for edible wild plants to be aware of and able to recognize poisonous plants in their area. Water hemlock causes most of the fatalities attributed to misidentification of poisonous plants because the plant is lethal in small quantities, resembles edible plants, and is found throughout North America. Health-care providers who know that their patients eat wild plants should caution them about the potential adverse health effects.


  1. Litovitz TL, Holm KC, Clancy C, Schmitz BF, Clark LR, Oderda GM. 1992 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1993;11:494-555.

  2. Litovitz TL, Holm KC, Bailey KM, Schmitz BF. 1991 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1992;10:452-505.

  3. Litovitz TL, Bailey KM, Schmitz BF, Holm KC, Klein-Schwartz W. 1990 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1991;9:461-

  4. Litovitz TL, Schmitz BF, Bailey KM. 1989 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1990;8:394-442.

  5. Kingsbury JM. Poisonous plants of the United States and Canada. Englewood Cliffs, New Jersey: Prentice Hall, 1964:372.

  6. Dreisbach R. Handbook of poisoning. 8th ed. Los Altos, California: Lange Medical Publications, 1974:433.

  7. Miller MM. Water hemlock poisoning. JAMA 1933;101:852-3.

  8. Starreveld E, Hope MB. Cicutoxin poisoning (water hemlock). Neurology 1975;25:730-4.

  9. Carlton BE, Tufts E, Girard DE. Water hemlock poisoning complicated by rhabdomyolysis and renal failure. Clin Toxicol 1979;14:87-92.

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