Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

WILD CHERRY BARK EXTRACT

NFPA

PRODUCT USE

Ant- tussive, expectorant, astringent, nervine, anti- spasmodic. In cosmetics. Extract of
the bark from young plants; the outer bark is stripped off and the inner bark is carefully
dried in the shade. Upon maceration with water it develops a distinct bitter- almond
odour. The dried and powdered alcoholic extract known as the " concentration" , " prunin"
or " cerasin" is an inefficient agent, seldom used. Due to its powerful sedative action on
the cough reflex used mainly in the treatment of irritating coughs and thus has a role in
the treatment of bronchitis and whooping cough. Also used as a bitter where digestion is
sluggish. The cold infusion of the bark is used in eye washes to treat inflammation.
Regeant

SYNONYMS

"oils, cherry laurel", "wildcherry, tree oil", "prunus serotina, extract", prunin,
"The Concentration", cerasin

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Contact with acids liberates very toxic gas.
May cause long- term adverse effects in the environment.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Accidental ingestion of the material may be damaging to the health of the individual.  At sufficiently high doses the material may be hepatotoxic(i.e. poisonous to the liver).  Central nervous system (CNS) depression may include general discomfort, symptoms of giddiness, headache, dizziness, nausea, anaesthetic effects, slowed reaction time, slurred speech and may progress to unconsciousness. Serious poisonings may result in respiratory depression and may be fatal.  Cyanide intoxication, from cyanogenic glycosides, is common in tropical regions and is associated with motor-neuron diseases such as "konzo" and "mantekassa". Toxic effects are especially evident when foods or treatments, containing these cyanogens, are taken concurrently with foods containing high levels of the beta-glucosidase enzymes (such as the seeds of apples and pears). The potential toxicity of a cyanogenic plant depends primarily on its capacity to produce hydrogen cyanide at concentrations toxic to humans and animals. The release of hydrogen cyanide can occur either maceration of the plant material - this activates the intracellular beta-glucosidase which in turn hydrolyses glycoside - or by hydrolysis of glycoside by the microflora of the gut. Intestinal microflora, in the rat, are capable of releasing cyanide from cyanogenic glycosides such as amygdalin (and other mandelonitrile glycosides), and it is probable that this mechanism accounts for the (up to) 40-fold toxic effect when these substances are administered by mouth (or other enteral routes - per os, enemas, suppositories) compared to the intravenous route. Symptoms of cyanide poisoning may be delayed compared to that of in organic cyanides.  Tannic acid causes failure of breathing, inflammation of the stomach, tissue death of the liver, and kidney inflammation.  

EYE

  There is some evidence to suggest that this material can causeeye irritation and damage in some persons.  This material can cause eye irritation and damage in some persons.  

SKIN

  This material can cause inflammation of the skin oncontact in some persons.  The material may accentuate any pre-existing dermatitis condition.  Skin contact with the material may damage the health of the individual; systemic effects may result following absorption.  Open cuts, abraded or irritated skin should not be exposed to this material.  Entry into the blood-stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected.  

INHALED

  The material is not thought to produce either adverse health effects or irritation of the respiratory tract following inhalation (as classified using animal models). Nevertheless, adverse effects have been produced following exposure of animals by at least one other route and good hygiene practice requires that exposure be kept to a minimum and that suitable control measures be used in an occupational setting.  

CHRONIC HEALTH EFFECTS

  There has been some concern that this material can cause cancer or mutations but there is not enough data to make an assessment.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  There is some evidence that inhaling this product is more likely to cause a sensitization reaction in some persons compared to the general population.  Long term exposure to high dust concentrations may cause changes in lung function i.e. pneumoconiosis; caused by particles less than 0.5 micron penetrating and remaining in the lung. Prime symptom is breathlessness; lung shadows show on X-ray.  There are grounds to suspect that cyanogenic glycoside-contaminated foodstuffs, such as cassava and pulses, are directly implicated in acute and chronic cyanide toxicity.  Symptoms of chronic cyanide poisoning include headache, vertigo, tinnitus, nausea, vomiting and tremors. These symptoms tend to be transitory and exposure to fresh air generally results in recovery.  On the basis of epidemiological observations, associations have been made between chronic exposure to cyanogenic glycosides and diseases such as goitre, spastic paraparesis,and tropical ataxic neuropathy. However these observations are confounded by nutritional deficiencies, and causal relationships have not been definitely established.  It appears that chronic cyanide intoxication, resulting from intake of foods containing these glycosides, in combination with deficient intake of riboflavin and/ or a poor quality of protein, and hence methionine deficiency is/ are responsible.  Epidemiological and experimental studies show that cyanogenic glycosides in food products play an important role in the development of goitre. Thiocyanate, the detoxification product of hydrogen cyanide derived from cyanogenic products, is responsible for interference with thyroid function. Studies on endemic goitre in Africa have identified iodine deficiency and the antithyroid activity of cyanogenic cassava diets, as major etiological factors of the disease. Cretinism has also been identified amongst the off-  spring of women exposed to a diet of insufficiently processed cassava. This effect is also caused by metabolic thiocyanate. Such findings occur in individuals who are also subject to low dietary intake of iodine - this is a common dietary constraint in many Africans.  Another study which evaluates the possible association of high cyanide and low sulfur intake in cassava-induced spastic paraparesis (SP) was conducted in Mozambique. The study concluded that where dietary intake of sulfur-containing amino acids was low, the incidence of SP was high in those individuals whose diet was largely cassava-based. Sulfur-containing amino acids are essential for the detoxification of cyanide.  In Nigeria, chronic cyanide intoxication is caused by the consumption of a cassava diet. A lack of dietary riboflavin (Vitamin B2) has been associated with the development of tropical (ataxia) neuropathy (TAN) amongst individuals whose diet is largely cassava dependent. The essential neurological components of the disease are myelopathy, bilateral optic atrophy, perceptive deafness and polyneuropathy. The initial and most common symptoms consist of various forms of paraesthesia and dysaethesia, usually starting in the distal portion of the lower limbs. In about a third of patients, stomatoglossitis is present. Additionally symptoms include motor neurone disease, Parkinson's disease, cerebellar degeneration, psychosis and dementia. A high prevalence of goitre is also seen in populations with a high incidence of TAN.  Tannic acid produced liver tumors in rats following subcutaneous injection.