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Conium maculatum, commonly known as hemlock (British English) or poison hemlock (American English), is a highly poisonous flowering plant in the carrot family Apiaceae, native to Europe and North Africa. It is Herbaceous plant, with no woody parts, and has a Biennial plant lifecycle. Hemlock is a hardy plant capable of living in a variety of environments and is now widely naturalised in locations outside its native range, including parts of Australia, West Asia, and North and South America, to which it has been introduced. It is capable of spreading and thereby becoming an Invasive plant weed.
All parts of the hemlock plant are Toxic plant, particularly the seeds and roots, and especially when ingested. Under the right conditions, the plant grows quite rapidly during the growing season, and can reach heights of , with a long Taproot. The plant has a distinctive odour that is usually considered unpleasant and carries with the wind. The hollow stems are usually spotted dark maroon and turn dry and brown after the plant completes its Biennial plant lifecycle. The hollow stems of the plant remain deadly for up to three years after the plant has died.
A biennial plant, hemlock produces leaves at its base in its first year but no flowers. In its second year, it produces white flowers in umbrella-shaped clusters.
The plant should not be visually confused with the North American coniferous tree Tsuga, which is sometimes called hemlock, hemlock fir, or hemlock spruce due to a slight similarity in the leaf smell. The ambiguous shorthand term 'hemlock' for this tree is more common in US dialects than the plant it is actually named after. Similarly, the plant should not be confused with Cicuta (commonly known as water hemlock).
C. maculatum, also known as poison hemlock, was the first species within the genus to be described. It was identified by Carl Linnaeus in his 1753 publication, Species Plantarum. Maculatum means 'spotted', in reference to the purple blotches characteristic of the stalks of the species.
It exists in some woodland (and elsewhere) in most British Isles counties; (1968). 9780521046565, Cambridge University Press. ISBN 9780521046565 in Ulster, these are particularly County Down, County Antrim, and County Londonderry. (1992). 9780853894469, Institute of Irish Studies and The Queen's University of Belfast. ISBN 9780853894469
It has become naturalised in Asia, North America, Australia, and New Zealand. See also the substituent page: It is sometimes encountered around rivers in southeast Australia and Tasmania. Infestations and human contact with the plant are sometimes newsworthy events in the U.S. due to its extreme toxicity.
Conium contains the piperidine alkaloids coniine, N-methylconiine, conhydrine, , and gamma-coniceine (or g-coniceïne), which is the precursor of the other hemlock alkaloids.
Coniine has Pharmacology properties and a chemical structure similar to nicotine. Coniine acts directly on the central nervous system through inhibitory action on nicotinic acetylcholine receptors. Coniine can be dangerous to and livestock, and with its high potency, the ingestion of seemingly small doses can easily result in respiratory collapse and death.
The alkaloid content in C. maculatum also affects the Thermoregulation centre by a phenomenon called peripheral vasoconstriction, resulting in hypothermia in calves. In addition, the alkaloid content was also found to stimulate the sympathetic ganglia and reduce the influence of the parasympathetic ganglia in rats and rabbits, causing an increased heart rate.
Coniine also has significant toxic effects on the kidneys. The presence of rhabdomyolysis and acute tubular necrosis has been demonstrated in patients who died from hemlock poisoning. Some of these patients were also found to have acute kidney injury. Coniine is toxic for the kidneys because it leads to the constriction of the urinary bladder sphincter, eventually resulting in the accumulation of urine.
The onset of symptoms is similar to that caused by curare, with an ascending muscular paralysis leading to paralysis of the respiratory muscles and ultimately death by oxygen deprivation.
It has been observed that poisoned animals return to feed on the plant after initial poisoning. Chronic toxicity affects only pregnant animals when they are poisoned at low levels by C. maculatum during formation of the fetus's organs. In such cases, the offspring is born with , mainly palatoschisis and multiple congenital contractures (arthrogryposis). The damage caused to the fetus due to chronic toxicity is irreversible. Although arthrogryposis can sometimes be surgically corrected, most malformed animals die. Such losses may be underestimated, at least in some regions, due to the difficulty of associating malformations with maternal poisoning at a much earlier stage.
As there is no specific antidote available, prevention is the only way to deal with the production losses caused by the plant. The use of and grazing with less-susceptible animals (such as sheep) have been suggested as control methods. Contrary to popular belief, scientific studies have disproven the claim that C. maculatum alkaloids can enter the human food chain via milk and fowl.
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