The common name “laurel” is applied to several botanically distinct plants, which complicates the question of toxicity. Many species widely referred to as laurel are indeed toxic to humans and pets, containing potent chemical compounds that can cause serious illness. The primary risk comes from the confusion in identification, as some varieties are harmless while others affect the cardiovascular and nervous systems.
Clarifying the “Laurel” Identity
The term “laurel” does not refer to a single species, leading to dangerous misidentification between toxic and non-toxic varieties. The true culinary laurel is the Bay Laurel (Laurus nobilis), an evergreen shrub whose leaves are widely used as a seasoning and are generally recognized as safe for human consumption. This species belongs to the Lauraceae family.
Conversely, two of the most common toxic varieties are the Mountain Laurel (Kalmia latifolia) and the Cherry Laurel (Prunus laurocerasus). Mountain Laurel, common in North America, is a member of the heath family (Ericaceae) and contains a potent class of toxins. Cherry Laurel, often used for hedging, is a member of the rose family (Rosaceae) and contains compounds found in the seeds of many stone fruits.
All parts of the Mountain Laurel are considered toxic. In Cherry Laurel, the leaves and the seeds inside the fruit contain the highest concentration of harmful compounds. The accidental confusion between these different plants poses the greatest danger to gardeners, children, and pets.
The Specific Toxins and Their Mechanism
The two main toxic laurel varieties contain distinct chemical compounds. Mountain Laurel is host to diterpenoid compounds known as grayanotoxins. These toxins operate by binding to voltage-gated sodium channels on the membranes of nerve and muscle cells.
Grayanotoxins prevent the sodium channels from closing, causing the cell membrane to remain in a continuously depolarized, or “open,” state. This leads to continuous firing of neurons and overstimulation of muscle tissue, particularly affecting the skeletal muscles and the heart. The action of these toxins can severely disrupt normal heart rate and blood pressure regulation.
Cherry Laurel contains cyanogenic glycosides, which are not toxic in their intact state. However, when the plant material is chewed, crushed, or digested, plant enzymes break down the glycosides. This process releases hydrogen cyanide, often referred to as prussic acid.
Hydrogen cyanide is a rapidly acting poison that inhibits cellular respiration. It binds to the ferric iron atom in cytochrome oxidase a3, a key enzyme within the mitochondria. This binding blocks the cell’s ability to use oxygen to produce cellular energy, leading to cell death and systemic failure.
Signs of Poisoning in Humans and Pets
The symptoms of laurel poisoning can manifest rapidly, typically within a few hours of ingestion. Grayanotoxin poisoning from Mountain Laurel often begins with gastrointestinal distress, including vomiting, excessive drooling, and abdominal pain. This is commonly followed by cardiovascular symptoms.
Grayanotoxins can cause a slow heart rate (bradycardia) and a drop in blood pressure (hypotension). Neurological signs include dizziness, weakness, loss of coordination, tremors, and a general stupor. In severe cases, the poisoning can lead to seizures, temporary blindness, and eventual cardiac failure.
Cyanide poisoning from Cherry Laurel ingestion presents with symptoms reflecting the body’s inability to utilize oxygen. Initial signs may include a scratchy throat, headache, and dizziness, coupled with vomiting and nausea. The skin may appear flushed or reddened.
As the poison takes hold, breathing becomes decreased and labored. In pets, signs may include rapid, shallow breathing, muscle weakness, and a decline in coordination. Without immediate intervention, severe cyanide poisoning can progress to convulsions, unconsciousness, and respiratory arrest.
Immediate Action and Emergency Care
Any suspected ingestion of a toxic laurel plant should be treated as a medical emergency requiring immediate professional intervention. The first step is to contact a poison control center (1-800-222-1222 in the US) or a veterinarian without delay. Rapid action significantly improves the prognosis.
Do not attempt to induce vomiting unless explicitly instructed by a medical or veterinary professional. They will assess the risk based on the type and amount of plant material consumed, as well as the time elapsed since ingestion. If possible, collect a sample or photograph of the plant to aid in accurate identification.
Medical treatment often involves gastric decontamination, typically through activated charcoal to bind remaining toxins in the digestive tract. Supportive care is then provided to stabilize vital signs, including intravenous fluids and medications to manage severe bradycardia or hypotension. The patient’s condition will be closely monitored until they are stable.