Coltsfoot

Coltsfoot (Tussilago farfara) is a small daisy-family plant whose bright yellow flowers are among the very first to appear in early spring, often pushing up through bare or frozen ground before the leaves. For more than two thousand years it was one of Europe's—and, as kuan dong hua, China's—most beloved cough herbs. Its very name says so: the genus Tussilago comes from the Latin for "cough dispeller." People took it as a tea, a syrup, a lozenge, and even smoked it to ease bronchitis, sore throats, and wheezing.

But this page has to be honest with you from the first paragraph, because coltsfoot carries a genuinely serious risk that is easy to miss behind its gentle, old-fashioned reputation: it naturally contains pyrrolizidine alkaloids, liver toxins that can cause cumulative, sometimes fatal liver damage and that are also linked to cancer. This is not a rare contaminant—it is part of the plant itself. That risk is real enough that several countries restrict or ban coltsfoot for internal use, and major health authorities advise against swallowing it. Below we cover what coltsfoot is and how it was traditionally used, the plausible reasons it soothes a cough, and then—front and center—the toxicity, who has been harmed, why "PA-free" products are hard to trust, and the safer herbs to reach for instead.

What Coltsfoot Is
Traditional Uses Through the Centuries
Why People Thought It Soothed Coughs
The Serious Problem: Pyrrolizidine Alkaloids
How These Alkaloids Injure the Liver
Documented Human Harm: An Infant Death and Beyond
Bans, Restrictions & Official Warnings
The "PA-Free" Cultivar Question, Honestly
The Honest Bottom Line
Gentler, Safer Options for a Cough
Who Must Absolutely Avoid Coltsfoot
Research Papers
Connections
Featured Videos

What Coltsfoot Is

Coltsfoot is a low-growing perennial in the daisy family (Asteraceae), the same broad botanical family as dandelions, chamomile, and ragweed. Its scientific name is Tussilago farfara. If you have walked a roadside, a clay bank, or a patch of waste ground in early spring, you have probably seen it: bright yellow, dandelion-like flower heads on short scaly stalks, appearing surprisingly early—sometimes while snow still lingers—and before the plant's leaves emerge. That habit earned it charming old names like "son-before-father." The broad, hoof-shaped leaves come later, and it is those leaves that give the plant its English name: coltsfoot, from their resemblance to a young horse's (a colt's) foot.

The Latin name is a small lesson in the plant's fame. Tussilago joins tussis, "cough," with agere, "to drive away"—literally a cough dispeller. In traditional Chinese medicine the dried flower buds are called kuan dong hua (款冬花), a name that reflects their appearance in the cold of winter. Native across Europe and much of Asia, coltsfoot has naturalized in North America and elsewhere. The parts used medicinally are the flowers (flower buds) and the leaves—which, as later sections explain, are also where the plant's toxins are found.

Traditional Uses Through the Centuries

Coltsfoot is one of the oldest recorded cough remedies in the Western world. The ancient Greek physician Dioscorides and the Roman naturalist Pliny both described it, and—remarkably—recommended smoking the dried leaves to relieve a stubborn cough, making coltsfoot one of the classic "medicinal smoke" herbs long before tobacco reached Europe. Through the medieval and early-modern herbal tradition it kept that reputation, prized above all for disorders of the chest and throat.

Its traditional list of uses centered squarely on the respiratory system:

Coughs of many kinds—dry, tickly, and productive.
Bronchitis, whooping cough, and asthma—to loosen phlegm and ease wheezing.
Sore throat, hoarseness, and laryngitis—as a soothing gargle or tea.

People took it in several forms: an infusion (tea) of the leaves or flowers, a sweet syrup, hard lozenges and boiled sweets (the old English confection "coltsfoot rock"), and dried-leaf herbal smoking mixtures such as the once-popular "British Herbal Tobacco." In traditional Chinese medicine, the honey-fried flower buds (kuan dong hua) were—and in some places still are—used for cough, wheezing, and phlegm, often combined with other herbs. It is worth being clear that all of this is traditional reputation, built on centuries of use rather than modern clinical trials. Longevity of use is a reason to take a herb seriously; it is not, by itself, proof that it works or that it is safe.

Why People Thought It Soothed Coughs

There is a plausible, physical reason coltsfoot feels soothing. Its leaves and flowers are rich in mucilage—a slippery, gel-forming carbohydrate that swells in water. Herbs high in mucilage are called demulcents: when you sip a mucilage-rich tea, it forms a thin, soothing film over the irritated lining of the throat and upper airway, which can calm the tickle that drives a dry cough. This is the same gentle mechanism at work in far safer demulcent herbs like marshmallow root, slippery elm, and mullein.

Coltsfoot also contains flavonoids (such as rutin and hyperoside) and distinctive sesquiterpene compounds, most notably tussilagone, which show anti-inflammatory activity in laboratory studies—for example, quieting inflammatory signaling in immune cells by switching on a protective enzyme called heme oxygenase-1 (Hwangbo 2009). Chen and colleagues' 2021 review catalogs well over a hundred compounds identified in the plant.

Here is the honest catch, though. Two things are true at once: the soothing demulcent effect is real and pleasant, and it is entirely ordinary—you can get the same coating comfort from herbs that carry no liver toxin at all. There is very little rigorous human-trial evidence that coltsfoot specifically outperforms those safer options. So the modest, unproven upside has to be weighed against a downside that is anything but modest, which is where the rest of this page turns.

The Serious Problem: Pyrrolizidine Alkaloids

This is the section that matters most. Coltsfoot naturally produces a group of compounds called pyrrolizidine alkaloids (PAs)—in coltsfoot's case chiefly senkirkine and senecionine. PAs are among the most significant natural poisons in the entire plant kingdom, and they are the plant's own chemical defense against insects. They are not a contaminant that careful farming can wash away; they are made by the coltsfoot plant, present in its leaves and, often in higher amounts, its flowers.

Coltsfoot is far from alone here. The same family of toxins is found in comfrey, borage, butterbur, and the ragworts and groundsels—all plants that toxicologists treat with caution. The dangerous members of this chemical group are the so-called 1,2-unsaturated pyrrolizidine alkaloids, and their reputation is well earned. Across many reviews they are described in the same three sober terms (Prakash 1999; Fu 2004; Edgar 2011; Moreira 2018):

Hepatotoxic—they poison the liver, and the damage can build up over time.
Genotoxic—they damage DNA, the blueprint inside cells.
Carcinogenic—in animals they cause cancer, and certain PAs are classed as possible human carcinogens.

The amount of PA in coltsfoot varies with the plant's genetics, where and when it grew, and which part is used—but "variable" is not the same as "safe." Because these toxins damage DNA, safety scientists generally assume there is no fully safe threshold: the sensible target is the lowest possible exposure, ideally none. That single fact reframes everything about how coltsfoot should be judged.

How These Alkaloids Injure the Liver

The way pyrrolizidine alkaloids harm you is a cruel biological irony: the coltsfoot alkaloid you swallow is fairly harmless on its own. The trouble starts when your liver tries to break it down. Liver enzymes (mainly a cytochrome called CYP3A) convert the alkaloid into highly reactive fragments known as pyrroles (Fu 2004; Ruan 2014). This step, called metabolic activation, is exactly what makes the liver the organ most in harm's way—it manufactures the poison inside itself.

Those reactive pyrroles then latch onto proteins and DNA and specifically attack the walls of the liver's smallest blood vessels, the sinusoids. The vessels swell and clog, blood cannot drain properly, and the liver becomes congested and injured. The medical name for this is hepatic sinusoidal obstruction syndrome (SOS), historically called hepatic veno-occlusive disease (VOD) (Chojkier 2003; Neuman 2015). It can come on quickly after a large dose, or—more insidiously—creep up after many small doses taken over weeks or months, because the injury is cumulative.

The warning signs are the kind people often blame on something else at first: pain and swelling in the upper-right belly, fluid buildup in the abdomen (ascites), an enlarged tender liver, jaundice (yellowing of the skin and eyes), nausea, and unexplained weight gain from retained fluid. In serious cases it progresses to liver failure and can be fatal. This is the heart of why coltsfoot deserves real caution: the damage can be silent until it is advanced, and by then it may not be reversible.

Documented Human Harm: An Infant Death and Beyond

This is not a theoretical worry dreamed up in a laboratory. The harm has been documented in people.

The most sobering case was published in The Journal of Pediatrics in 1988. A newborn developed fatal hepatic veno-occlusive disease after the mother had regularly drunk an herbal tea during pregnancy—a tea intended to contain coltsfoot (Roulet 1988). Pyrrolizidine alkaloids were identified as the cause, and the case carries a double lesson. First, these toxins cross the placenta and can devastate a developing baby's liver. Second, when the plant material was examined, the "coltsfoot" was thought to have been misidentified or mixed with a related, even more PA-rich look-alike—a stark illustration of how unreliable and dangerous loose herbal material can be. Either way, a baby died from pyrrolizidine-alkaloid liver disease traced to a coltsfoot tea.

Beyond that single tragedy, PA-containing plants have a long and grim public-health record. Outbreaks of pyrrolizidine poisoning—sometimes from contaminated grain, sometimes from herbal medicines—have caused hundreds of cases of veno-occlusive liver disease and many deaths in various parts of the world (Prakash 1999; Chen & Huo 2010; Edgar 2011). Coltsfoot itself has been tested directly: in a classic experiment, rats fed coltsfoot developed liver tumors, showing that the whole herb—not just an isolated chemical—is carcinogenic in animals (Hirono 1976). The same has been shown for its cousin comfrey (Mei 2010), and international cancer agencies list certain pyrrolizidine alkaloids as possibly carcinogenic to humans. Put plainly: the risks attached to coltsfoot are documented in human liver disease, in an infant death, and in animal cancers—not merely predicted.

Bans, Restrictions & Official Warnings

Regulators have taken this evidence seriously, and the trend across the world runs in one direction: away from swallowing coltsfoot.

Germany has long restricted it. German authorities set strict limits on how much pyrrolizidine alkaloid a person may receive from herbal products—limits measured in the low micrograms per day and only for short-term use—which effectively rules out ordinary, unpurified coltsfoot for internal consumption.
The European Union, through its food-safety and herbal-medicine bodies, treats pyrrolizidine alkaloids as contaminants to be driven as low as possible and has set very low tolerable exposures. European herbal regulators have not supported traditional-use approval for internal coltsfoot on safety grounds, and a number of European countries restrict or ban PA-containing herbs taken by mouth.
The United States permits coltsfoot to be sold as a dietary supplement, but U.S. authorities and independent experts flag it as a plant of concern and caution against internal use; reputable references list it among herbs to avoid swallowing.

The common thread is unmistakable: where governments have looked closely at coltsfoot, they have restricted it, banned it for internal use, or capped the tolerable alkaloid dose so tightly that everyday herbal preparations cannot meet it. When multiple independent health authorities land in the same cautious place, it is worth heeding.

The "PA-Free" Cultivar Question, Honestly

Because coltsfoot has real traditional standing, plant breeders tried to solve its poison problem at the source. They developed low-PA and so-called "PA-free" cultivars—selectively bred coltsfoot clones that produce little or no detectable pyrrolizidine alkaloid—and in a few countries these are the only forms officially tolerated. In principle, that is a genuine step forward.

In practice, though, "PA-free" is a promise a shopper can rarely verify, and the honesty this page owes you means laying out why:

The label seldom proves the batch was tested. A package can say "PA-free" without any accessible certificate showing that this lot was actually assayed and cleared.
Wild-harvested and imported material is uncontrolled. Cheaper products, bulk dried herb, and homegrown or foraged coltsfoot are not the special low-PA clones—they are ordinary, PA-containing plants.
Content swings with part, place, and season. Flowers, young leaves, growing region, and harvest timing all change the alkaloid load, so even genuine coltsfoot is a moving target.
Look-alikes and adulteration are a real hazard. Coltsfoot can be confused with, or mixed with, other PA-rich plants such as butterbur or Adenostyles—precisely the kind of mix-up implicated in the infant-death case above.
"Low" is not "zero," and zero is the goal. Because these alkaloids are genotoxic carcinogens with no assumed safe threshold, even a low-PA product is not the same as a risk-free one.

So the PA-free cultivar is a real and well-intentioned idea, but for the average person standing in a shop or ordering online, it is a weak guarantee resting on trust you usually cannot check.

The Honest Bottom Line

Lay the two sides of the scale side by side. On one side: a mild, pleasant, largely unproven soothing effect—the kind of demulcent comfort you can get from several other herbs. On the other side: a cumulative liver toxin that can cause serious and sometimes fatal veno-occlusive disease, that damages DNA, that is carcinogenic in animals, that crosses the placenta, and for which no fully safe dose can be assumed.

Weighed honestly, that is not a close call. Because there are effective coughs remedies that are far safer, most herbal-safety authorities and toxicologists recommend avoiding internal coltsfoot altogether. This page reaches the same conclusion. If someone chooses to use it anyway, the only defensible version is a certified, tested, PA-free product, used briefly, and never by anyone in the high-risk groups below—but the genuinely simple and safe choice is to skip swallowing coltsfoot and reach for a gentler herb. That is not fear for its own sake; it is straightforward risk-versus-benefit arithmetic, and the arithmetic points clearly one way.

Gentler, Safer Options for a Cough

The good news is that the soothing effect people seek from coltsfoot is easy to find without the liver risk. Reasonable, far safer choices include:

Demulcent herbs with no pyrrolizidine problem—marshmallow root, slippery elm, and mullein leaf give the same soothing, throat-coating comfort.
Traditional cough herbs with a better safety record—thyme, elecampane, horehound, plantain leaf, and licorice (mind licorice's own blood-pressure caution).
Simple home soothers—honey has good evidence for easing cough, especially in children over one year old (never give honey to a baby under twelve months, because of botulism risk), along with warm fluids, steam, and rest.

And a practical reminder: a cough that lasts more than about three weeks, or that comes with coughing up blood, breathlessness, chest pain, or a persistent fever, deserves a visit to a clinician rather than any herb.

Who Must Absolutely Avoid Coltsfoot

Some people should not take coltsfoot internally under any circumstances—PA-free label or not:

Anyone who is pregnant. Pyrrolizidine alkaloids cross the placenta and can cause fatal liver disease in the baby, as the documented infant death shows. This is the single most important warning on this page.
Anyone breastfeeding. The alkaloids can pass into breast milk and reach the infant.
Infants and children. Smaller, developing livers are especially vulnerable; coltsfoot should never be given to a baby or young child.
Anyone with liver disease—hepatitis, cirrhosis, fatty liver, or any liver condition—or who is taking medications that stress the liver.
Heavy drinkers and people on many medications, whose livers already carry an added burden.
Anyone already using other pyrrolizidine-containing herbs such as comfrey or borage, since the liver toll from these toxins adds up across sources.

For everyone else, the honest guidance from the sections above still stands: given how good and how safe the alternatives are, the wisest move is simply not to swallow coltsfoot at all. If you are considering it despite this, talk it through with a doctor or pharmacist first—especially if you take prescription medicines or have any liver concern.

Research Papers

Chen S, Dong L, Quan H, et al. A review of the ethnobotanical value, phytochemistry, pharmacology, toxicity and quality control of Tussilago farfara L. (coltsfoot). Journal of Ethnopharmacology. 2021;267:113478. doi:10.1016/j.jep.2020.113478 — A comprehensive modern review of coltsfoot's traditional uses, its many compounds, its pharmacology, and—importantly—its pyrrolizidine-alkaloid toxicity and the resulting quality-control problem.
Roulet M, Laurini R, Rivier L, Calame A. Hepatic veno-occlusive disease in newborn infant of a woman drinking herbal tea. The Journal of Pediatrics. 1988;112(3):433–436. doi:10.1016/s0022-3476(88)80330-5 — The landmark case report: a newborn died of hepatic veno-occlusive disease traced to pyrrolizidine alkaloids in a coltsfoot herbal tea drunk during pregnancy.
Chen Z, Huo JR. Hepatic veno-occlusive disease associated with toxicity of pyrrolizidine alkaloids in herbal preparations. Netherlands Journal of Medicine. 2010;68(6):252–260. PubMed: 20558855 — Reviews how pyrrolizidine-alkaloid herbal products cause veno-occlusive liver disease in people, including diagnosis and outcomes.
Hirono I, Mori H, Culvenor CC. Carcinogenic activity of coltsfoot, Tussilago farfara L. Gann (Japanese Journal of Cancer Research). 1976;67(1):125–129. PubMed: 1269853 — The classic feeding study in which rats given coltsfoot developed liver tumors, direct evidence that the whole herb is carcinogenic in animals.
Prakash AS, Pereira TN, Reilly PE, Seawright AA. Pyrrolizidine alkaloids in human diet. Mutation Research. 1999;443(1–2):53–67. doi:10.1016/s1383-5742(99)00010-1 — A key review of how people are exposed to pyrrolizidine alkaloids (including herbal teas and remedies) and the liver disease and genotoxicity that follow.
Fu PP, Xia Q, Lin G, Chou MW. Pyrrolizidine alkaloids — genotoxicity, metabolism enzymes, metabolic activation, and mechanisms. Drug Metabolism Reviews. 2004;36(1):1–55. doi:10.1081/DMR-120028426 — Explains how the liver converts these alkaloids into reactive pyrroles that damage DNA and liver tissue.
Chojkier M. Hepatic sinusoidal-obstruction syndrome: toxicity of pyrrolizidine alkaloids. Journal of Hepatology. 2003;39(3):437–446. doi:10.1016/s0168-8278(03)00231-9 — A focused account of how pyrrolizidine alkaloids clog the liver's small vessels to cause sinusoidal-obstruction (veno-occlusive) disease.
Ruan J, Yang M, Fu P, Ye Y, Lin G. Metabolic activation of pyrrolizidine alkaloids: insights into the structural and enzymatic basis. Chemical Research in Toxicology. 2014;27(6):1030–1039. doi:10.1021/tx500071q — Details the metabolic-activation step that turns a swallowed alkaloid into the reactive pyrrole responsible for liver injury.
Edgar JA, Colegate SM, Boppré M, Molyneux RJ. Pyrrolizidine alkaloids in food: a spectrum of potential health consequences. Food Additives & Contaminants: Part A. 2011;28(3):308–324. doi:10.1080/19440049.2010.547520 — Surveys the full range of harm from dietary pyrrolizidine alkaloids, from acute liver disease to cancer risk.
Moreira R, Pereira DM, Valentão P, Andrade PB. Pyrrolizidine alkaloids: chemistry, pharmacology, toxicology and food safety. International Journal of Molecular Sciences. 2018;19(6):1668. doi:10.3390/ijms19061668 — A wide-ranging review covering the chemistry of these alkaloids, their toxicity, and the food-safety limits regulators have set.
Neuman MG, Cohen L, Opris M, Nanau RM, Jeong H. Hepatotoxicity of pyrrolizidine alkaloids. Journal of Pharmacy & Pharmaceutical Sciences. 2015;18(4):825–843. doi:10.18433/j3bg7j — Reviews the mechanisms and clinical picture of pyrrolizidine-alkaloid liver toxicity, including herbal sources.
Wiedenfeld H, Edgar J. Toxicity of pyrrolizidine alkaloids to humans and ruminants. Phytochemistry Reviews. 2011;10(1):137–151. doi:10.1007/s11101-010-9174-0 — Summarizes the human and animal toxicity of these alkaloids and why exposure should be minimized.
Mei N, Guo L, Fu PP, Fuscoe JC, Luan Y, Chen T. Metabolism, genotoxicity, and carcinogenicity of comfrey. Journal of Toxicology and Environmental Health, Part B. 2010;13(7–8):509–526. doi:10.1080/10937404.2010.509013 — A parallel case in a closely related pyrrolizidine herb, reinforcing the DNA-damaging and cancer-causing potential of this class of plant toxins.
Hwangbo C, Lee HS, Park J, Choe J, Lee JH. The anti-inflammatory effect of tussilagone, from Tussilago farfara, is mediated by the induction of heme oxygenase-1 in murine macrophages. International Immunopharmacology. 2009;9(13–14):1578–1584. doi:10.1016/j.intimp.2009.09.016 — A laboratory study of tussilagone, a coltsfoot compound behind the plant's traditional soothing, anti-inflammatory reputation.

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