Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

O-TOLUIDINE CHROMIUM TRICARBONYL

NFPA

PRODUCT USE

Catalyst. Fragrance

SYNONYMS

C10-H9-Cr-N-O3, C10-H9-Cr-N-O3, (CH3C6H4NH2)Cr(CO)3

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Harmful to aquatic organisms.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Accidental ingestion of the material may be damaging to the health of the individual.  Signs of intoxication in humans exposed to o-toluidine include methaemoglobinaemia, haematuria, marked renal and bladder irritation and physiological and psychological disturbances.  Daily gastric intubation of 225 mg o-toluidine/kg body weight to rats for 20 days produced cyanosis, splenic congestion with haemosiderosis and extramedullary haematopoiesis, hypercellularity in the bone marrow and mortalities. Rats given 35 mg/kg body weight daily for 2.5 months developed methaemoglobinaemia, erythropenia and reticulocytosis. A synthetic diet of a 7.5% solution in peanut oil (initial dose of 2 gm/rat reduced after 64 days to 1 gm/rat) produced bladder epithelial keratosis, metaplasia and a low incidence of papillomas. In a 7-week study, renal, hepatic and splenic pigmentation were observed in rats receiving 12500 ppm.  

EYE

  Although the material is not thought to be an irritant, direct contact with the eye may cause transient discomfort characterized by tearing or conjunctival redness (as with windburn). Slight abrasive damage may also result. The material may produce foreign body irritation in certain individuals.  Manifestations of severe visual disturbance can occur in cases of acute carbon monoxide poisoning associated with a period of unconsciousness. The types of disturbances that occur may be placed into three categories: (a.) amaurosis or hemianopsia, (b.) constriction of the visual fields, and (c.) visual abnormalities associated with optic nerve disturbances. Retinal venous engorgement and peripupillary hemorrhage have also been reported. All patients diagnosed with CO poisoning and exposed to CO for over 12 hours manifested retinal hemorrhages.  

SKIN

  The material is not thought to produce adverse health effects or skin irritation following contact (as classified using animal models). Nevertheless, 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.  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

  Inhalation may produce health damage*.  The material is not thought to produce respiratory irritation (as classified using animal models). Nevertheless inhalation of dusts, or fume, especially for prolonged periods, may produce respiratory discomfort and occasionally, distress.  Inhalation of dusts, generated by the material during the course of normal handling, may be damaging to the health of the individual.  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.  Clinical signs of intoxication in humans include methaemoglobinaemia and haematuria. An exposure of 40 ppm of toluidine (all isomers) in air for 60 minutes produces severe intoxication. Prolonged exposure to as little as 10 ppm was reported to cause symptoms of illness. A 1-hour exposure at 640 mg/kg p-toluidine, in air, cause ocular and upper respiratory tract irritation in rats.  Carbon monoxide poisoning results in breathing problems, diarrhea and shock. It combines with hemoglobin, the carrier of oxygen in the blood, much more easily than oxygen; the complex formed can disturb muscle function, especially the heart.  

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.  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.  Absorption across the placenta has produced foetal tumours in experimental animals. Bladder tumors have been produced in animals exposed to the substance by several routes.  When administered in the diet the hydrochloride increased the incidences of hepatocellular carcinomas or adenomas in female mice and haemangiosarcomas and haemangiomas of the abdominal viscera in both sexes of another strain; increased the incidences of sarcomas of multiple organs in rats of both sexes, subcutaneous fibromas and mesotheliomas in male rats, and sarcomas of the spleen, transitional cell papillomas and carcinomas of the urinary bladder, and mammary gland fibroadenomas and adenomas in the female rat. Although an excess of bladder cancers has often been found in workers exposed to varying combinations of dyestuffs and dyestuff intermediates, no population of workers exposed to o-toluidine alone has been described.  Chromium(III) is an essential trace mineral. Chronic exposure to chromium(III) irritates the airways, malnourishes the liver and kidneys, causes fluid in the lungs, and adverse effects on white blood cells, and also increases the risk of developing lung cancer. Chromium (VI) can irritate the skin, eyes and airways. Allergic reactions can involve both the skin and airways, and the compounds can diminish taste and smell, discolor the skin and eyes, cause blood disorders and damage the liver, kidneys, digestive tract and lungs. It predisposes humans to cancers of the respiratory tract and digestive system. Ulceration to the skin can occur, and, chromium(VI) is one of the most allergenic substances known.  Long-term (chronic) exposure to low levels of carbon monoxide may produce heart disease and damage to the nervous system. Exposure of pregnant animals to carbon monoxide may cause low birthweight, increased foetal mortality and nervous system damage to the offspring.  Carbon monoxide is a common cause of fatal poisoning in industry and homes. Non fatal poisoning may result in permanent nervous system damage. Carbon monoxide reduces the oxygen carrying capacity of the blood. Effects on the body are considered to be reversible as long as brain cell damage or heart failure has not occurred. Avoid prolonged exposure, even to small concentrations. A well-established and probably causal relationship exists between maternal smoking (resulting in carboxyhaemoglobin levels of 2-  7% in the foetus) and low birth weight. There also appears to be a dose-related increase in perinatal deaths and a retardation of mental ability in infants born to smoking mothers.  The foetus and newborn infant are considered to be very susceptible to CO exposure for several reasons:  · Foetal hemoglobin has a greater affinity for CO than maternal hemoglobin.  ·  Due to differences in uptake and elimination of CO, the fetal circulation is likely to have COHb  ·  levels higher (up to 2.5 times) than seen in the maternal circulation.  ·  The half-life of COHb in fetal blood is 3 times longer than that of maternal blood  ·  Since the fetus has a comparatively high rate of O2 consumption, and a lower O2 tension in the blood than adults, a compromised O2 transport has the potential to produce a serious hypoxia Carbon monoxide gas readily crosses the placenta and CO exposure during pregnancy can be teratogenic  Carbon dioxide at low levels may initiate or enhance deleterious myocardial alterations in individuals with restricted coronary artery blood flow and decreased myocardial lactate production. - Linde.