Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

LINAMARIN

NFPA

PRODUCT USE

Intermediate. Extracted from seed skins or embryos of flax, white clover, cassava (Manihot
esculenta), lima beans

SYNONYMS

C10-H17-N-O6, C10-H17-N-O6, "propanenitrile, 2-(beta-D-glucopyranosyloxy)-2-methyl-",
"propanenitrile, 2-(beta-D-glucopyranosyloxy)-2-methyl-", 2-(beta-D-
glucopyranosyloxy)isobutyronitrile, 2-(beta-D-glucopyranosyloxy)isobutyronitrile, 2-(beta-
D-glucopyranosyloxy)-2-methylpropanenitrile, 2-(beta-D-glucopyranosyloxy)-2-
methylpropanenitrile, phaseolunatin, "cyanogenic glycosides"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Contact with acids liberates very toxic gas.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Although ingestion is not thought to produce harmful effects, the material may still be damaging to the health of the individual following ingestion, especially where pre-  existing organ (e.g. liver, kidney) damage is evident. Present definitions of harmful or toxic substances are generally based on doses producing mortality (death) rather than those producing morbidity (disease, ill-health). Gastrointestinal tract discomfort may produce nausea and vomiting. In an occupational setting however, ingestion of insignificant quantities is not thought to be cause for concern.  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.  Cyanide poisoning can cause increased saliva output, nausea without vomiting, anxiety, confusion, vertigo, dizziness, stiffness of the lower jaw, convulsions, spasm, paralysis, coma and irregular heartbeat, and stimulation of breathing followed by failure. Often the skin becomes cyanosed (blue-gray), and this is often delayed. Doses which are not lethal are eventually excreted in the urine.  

EYE

  Although the material is not thought to be an irritant, direct contact with the eye may produce transient discomfort characterized by tearing or conjunctival redness (as with windburn).  

SKIN

  Skin contact with the material may damage the health of the individual; systemic effects may result following absorption.  The material is not thought to be a skin irritant (as classified using animal models). Temporary discomfort, however, may result from prolonged dermal exposures. Good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting.  Open cuts, abraded or irritated skin should not be exposed to this material.  Toxic effects may result from skin absorption.  

INHALED

  Inhalation may produce health damage*.  The material is not thought to produce respiratory irritation (as classified using animal models). Nevertheless inhalation of the material, especially for prolonged periods, may produce respiratory discomfort and occasionally, distress.  Persons with impaired respiratory function, airway diseases and conditions such as emphysema or chronic bronchitis, may incur further disability if excessive concentrations of particulate are inhaled.  

CHRONIC HEALTH EFFECTS

  Principal routes of exposure are by accidental skin and eye contact andinhalation of generated dusts.  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.  Chronic exposure to cyanides and certain nitriles may result in interference to iodine uptake by thyroid gland and its consequent enlargement. This occurs following metabolic conversion of the cyanide moiety to thiocyanate. Thyroid insufficiency may also occur as a result of metabolic conversion of cyanides to the corresponding thiocyanate. Exposure to small amounts of cyanide compounds over long periods are reported to cause loss of appetite, headache, weakness, nausea, dizziness, abdominal pain, changes in taste and smell, muscle cramps, weight loss, flushing of the face, persistent runny nose and irritation of the upper respiratory tract and eyes. These symptoms are not specific to cyanide exposure and therefore the existence of a chronic cyanide toxicity remains speculative. Repeated minor contact with cyanides produce a characteristic rash with itching, papules (small, superficial raised spots on the skin) and possible sensitization. Concerns have been expressed that low-level, long term exposures may result in damage to the nerves of the eye.