AT, originally native to South America, is a widely cultivated ornamental shrub in Western Europe, Southeastern United States, Australia and Asia[1]. It has been naturalized in Korea as well. The plant stands 8–15 feet in height. Its leaves are shaped like lancets or eggs. The trumpet-shaped flowers come primarily in white, yellow or red colors, and measure 10–12 inches in diameter. These fragrant flowers hang straight down, endowing them with a unique appearance (Figure 1). The plant has been distributed widely and cultivated as a garden plant because of its low maintenance needs and beauty. However, it is not well known by the general public that AT is poisonous. Hence, poisoning by ingestion of AT is not uncommon.

AT contains tropane alkaloids such as scopolamine, hyoscyamine and atropine. They are embedded in virtually all parts of the plant. Any part of the plant could contain toxins but most are in the roots and seeds[1]. There is considerable variation in the concentration of these substances depending on the plant part tested, the season, the stage of maturation, and the state of hydration[2, 3].

The alkaloids contained in the plant (most notably scopolamine) cause post-synaptic competitive inhibition of cholinergic muscarinic receptors (in central and peripheral regions), resulting in the classic picture of anticholinergic poisoning seen in AT intoxication. Symptoms develop rapidly, sometimes as early as 5–10 minutes after ingestion[2]. In AT intoxication, patients initially experience salivation and sweating, followed by a dry mouth, mydriasis, and loss of accommodation and tachycardia. As the dose increases, urinary retention and hyperthermia ensue. At this point, confusion, agitation and anxiety can be witnessed as being due to acute anticholinergic poisoning by the plant. Neuropsychologic assessment of the patient can reveal impairment of orientation, affective lability, incoherent thoughts, flight of ideas, tangential thinking, and auditory or visual hallucinations[1]. Amnesia with regard to the events immediately after ingestion along with mydriasis may last for days even after remission of other neuropsychiatric symptoms. At even higher doses, convulsions, flaccid paralysis and delirium can occur[4]. If not recognized and treated promptly, severe intoxications may lead to death. In severe cases, the cholinesterase inhibitor physostigmine can be given via the intravenous route as an antidote. Gastric lavage and administration of activated charcoal are recommended ≤48 hours after ingestion[1]. Each blossom contains ≈ 0.65 mg scopolamine and 0.3 mg atropine. Fatalities have been reported at an atropine dose of 10 mg[2]. As such, ingestion with as few as 10 flowers can be not only toxic but also fatal.

Easy availability of AT has been suggested to be one reason behind its frequent abuse in western countries[1]. It was not until the 1970s in the USA when reports of intoxication by AT and Jimson weed increased as adolescents were poisoned inadvertently while consuming them for recreational purposes. In 1994 alone, in the state of Florida, USA, 85 cases of intentional ingestion of AT were reported[2]. Among the abusers of this plant, some chose to eat the blossoms while others smoked the leaves. The most popular method of ingestion has been steeping the blossoms and seeds in water to obtain a tea. This preparation is sometimes combined with alcohol or cannabis in the hope of amplifying its potential as a hallucinogen[2].