Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

NAPHTHA PETROLEUM, MIDDLE, STEAM-CRACKED AROMATIC

NFPA

PRODUCT USE

Intermediate.

SYNONYMS

"naphtha petroleum, steam cracked middle aromatic C7-12", "medium steam cracked aromatic
naphtha, petroleum", "quench tower bottoms"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

May form explosive peroxides.
Causes severe burns.
Risk of serious damage to eyes.
HARMFUL - May cause lung damage if swallowed.
Harmful by inhalation and in contact with skin.
Highly flammable.
Toxic to aquatic organisms, may cause long- term adverse effects in the aquatic
environment.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  The material can produce severe chemical burns within the oral cavity and gastrointestinal tract following ingestion.  Ingestion of naphthalene and its congeners may produce abdominal cramps with nausea, vomiting, diarrhoea, headache, profuse perspiration, listlessness, confusion, and in severe poisonings, coma with or without convulsions. Irritation of the urinary bladder may also occur (presumably due to the excretory products of naphthalene metabolism) and produce urgency, dysuria, and the passage of brown or black urine with or without albumin or casts. These effects may disappear within a few days and have not been associated with haemolysis which is a prominent finding in naphthalene poisoning. Severe naphthalene poisoning in humans produces haemoglobinuria, methaemoglobinaemia, the production of Heinz bodies and death. Methaemoglobinemia produces a form of oxygen starvation (anoxia). Symptoms include cyanosis (a bluish discolouration skin and mucous membranes) and breathing difficulties. Symptoms may not be evident until several hours after exposure. At about 15% concentration of blood methaemoglobin there is observable cyanosis of the lips, nose and earlobes. Symptoms may be absent although euphoria, flushed face and headache are commonly experienced. At 25-40%, cyanosis is marked but little disability occurs other than that produced on physical exertion. At 40-60%, symptoms include weakness, dizziness, lightheadedness, increasingly severe headache, ataxia, rapid shallow respiration, drowsiness, nausea, vomiting, confusion, lethargy and stupor. Above 60% symptoms include dyspnea, respiratory depression, tachycardia or bradycardia, and convulsions. Levels exceeding 70% may be fatal. In those who survive haemotoxic effects, life-threatening acute renal failure, secondary to renal blockade, occurs. The acute lethal dose of naphthalene is estimated to be between 5 and 15 grams, although certain susceptible individuals have died after ingestion of a total dose of 2 grams. Hypersusceptibility, based on congenital deficiency of glucose-6-phosphate dehydrogenase activity, has been identified and is more common amongst Asians, Arabs, Caucasians of Latin ancestry and American and African blacks; males in particular are sensitive.  

EYE

  The material can produce severe chemical burns to the eye following direct contact. Vapors or mists may be extremely irritating.  If applied to the eyes, this material causes severe eye damage.  Exposure to naphthalene and its congeners has produced cataracts in animals and workers. In one study, eight of twenty-one workers, exposed to naphthalene for 5-years, showed opacities of the lens.  Direct eye contact with petroleum hydrocarbons can be painful, and the corneal epithelium may be temporarily damaged. Aromatic species can cause irritation and excessive tear secretion.  

SKIN

  Skin contact with the material may be harmful; systemic effects may resultfollowing absorption.  The material can produce severe chemical burns following direct contactwith the skin.  Workers sensitized to naphthalene and related compounds show an inflammation of the skin with scaling and reddening. Some individuals show an allergic reaction. Generally, absorption through the skin does not cause acute systemic reactions except in new-born babies. Photosensitization, sunburn-like responses or blisters have been reported. Animal testing revealed naphthalene can cause disease changes in a range of organs.  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 of aerosols (mists, fumes), generated by the material during the course of normal handling, may be harmful.  The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo.  Inhalation hazard is increased at higher temperatures.  Central nervous system (CNS) depression is seen at styrene exposures exceeding 50 ppm, whilst headache, fatigue, nausea and dizziness are reported consistently at exposures of 100 ppm.  Eye and throat irritation occurred in human volunteers exposed to 376 ppm styrene for 1 hour and was accompanied by increased nasal secretion at exposures of 800 ppm for 4 hours. At the end of an 8-hour workshift, workers exposed to 212 ppm styrene had higher urinary levels of alanine-aminopeptidase and N-acetyl-glucosaminidase than unexposed workers, indicating potential renal effects of styrene .  Evidence exists that 5% to 10% reductions in sensory nerve conduction occur at 100 ppm and that slowed reaction times occur after exposure to 50 ppm. Exposure at 370 ppm produces unpleasant subjective symptoms and signs of neurological impairment. High vapour concentrations may have a toxic and anaesthetic effect which may lead to unconsciousness or death. Exposure at 1000 ppm can rapidly lead to unconsciousness whilst exposure to 10000 ppm may cause death in less than one hour. Simple reaction times were increased and coordination decreased amongst volunteers inhaling 350 ppm (via mouth tube) for 30 minutes. Controlled inhalation studies with 300 ppm (via mouth tube) for one hour found reduced ocular tracking abilities but no changes in balance or coordination.  In humans exposed to styrene vapor, pulmonary retention is approximately 66% of the administered concentration.  Following inhalation exposure, styrene is preferentially distributed to adipose tissue. Fat levels in rats were 10-times greater than levels in observed organs after exposure to 50-2000 ppm for 5 hours.  Urinary excretion is the major route of elimination of styrene. In humans, the main urinary metabolites are mandelic acid and phenylglyoxylic acid; rats also excrete hippuric acid and glucuronide. Human volunteers exposed by inhalation to 50 to 200 parts per million (ppm) showed biphasic urinary elimination of mandelic acid with a half-life for the first phase of 4 hours and for the second phase of 25 hours. Urinary metabolite concentrations have been correlated with exposure concentrations in humans.  Headache, fatigue, lassitude, irritability and gastrointestinal disturbances (e.g., nausea, anorexia and flatulence) are the most common symptoms of xylene overexposure. Injury to the heart, liver, kidneys and nervous system has also been noted amongst workers. Transient memory loss, renal impairment, temporary confusion and some evidence of disturbance of liver function was reported in three workers overcome by gross exposure to xylene (10000 ppm). One worker died and autopsy revealed pulmonary congestion, oedema and focal alveolar haemorrhage. Volunteers inhaling xylene at 100 ppm for 5 to 6 hours showed changes in manual coordination reaction time and slight ataxia. Tolerance developed during the workweek but was lost over the weekend. Physical exercise may antagonise this effect. Xylene body burden in humans exposed to 100 or 200 ppm xylene in air depends on the amount of body fat with 4% to 8% of total absorbed xylene accumulating in adipose tissue.  Xylene is a central nervous system depressant.  Inhalation of naphthalene vapour has been associated with headache, loss of appetite and nausea. Other conditions associated with exposure to the vapour include optic neuritis, corneal injury and kidney damage. Animals exposed to aerosols of a refined commercial solvent mixture consisting primarily of mono-methylated naphthalenes, exhibited dyspnoea. When animals were exposed to this mixture for 27 daily one-hour exposures over a 35-day period, they showed dyspnoea, listlessness, prostration and marked salivation. Weight loss was evident in mice but not in other species. Pathological changes occurred in the lungs, liver and skin. Pulmonary changes consisted mainly of oedema, bronchopneumonia, emphysema, and thickening of the parabronchiolar alveolar septa. Haematology did not identify significant changes.  

CHRONIC HEALTH EFFECTS

  There has been concern that this material can cause cancer or mutations, but there is not enough data to make an assessment.  Long-term exposure to respiratory irritants may result in disease of the airways involving difficult breathing and related systemic problems.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  There is limited evidence that, skin contact with this product is more likely to cause a sensitization reaction in some persons compared to the general population.  There is some evidence that human exposure to the material may result in developmental toxicity. This evidence is based on animal studies where effects have been observed in the absence of marked maternal toxicity, or at around the same dose levels as other toxic effects but which are not secondary non-specific consequences of the other toxic effects.  Exposure to styrene may aggravate central nervous system disorders, chronic respiratory disease, skin disease, kidney disease and liver disease.  Workers engaged in the manufacture of styrene polymers with exposure to generally <1 ppm for 1-36 years had low erythrocyte counts and altered liver enzyme profiles. Blood and liver effects do not appear to be of concern for human exposures to styrene. Occupational studies in humans show styrene to be a neurotoxicant.  Occupational styrene exposure causes central and peripheral nervous system effects. It causes a reversible decrease in colour discrimination and in some studies effects on hearing have been reported.  Neuro-optic pathways have been shown to be particularly vulnerable to organic solvent exposure and studies support the proposition that styrene exposure can induce dose-  dependent colour vision loss. In the fibre-glass reinforced plastics industry, visual colour impairment was detected were exposure was above 4 ppm. Campagna D. et al, Neurotoxicology, 17(2), pp 367-374, 1996  Studies of effects of styrene on the haematopoietic and immune systems, liver and kidney, in exposed workers, do not reveal consistent changes. Central nervous system effects of styrene in rats, guinea pigs and rabbits, have been reported. Styrene exposure causes liver and lung toxicity in mice and nasal toxicity in rats and mice.  Chromosomal abnormalities (micronucleii, chromosome gaps or breaks, nuclear bridges and unscheduled DNA synthesis in peripheral lymphocytes) have been recorded in workers exposed to styrene. Such aberrations however are not always apparent in epidemiological studies and the status of styrene as a DNA effector is equivocal.  Death due to cancers among workers exposed to styrene is statistically unremarkable.  The dominant first metabolite of styrene is styrene-7,8-epoxide which binds covalently to DNA and shows activity in various in-vitro and in-vivo assays for genetic effects where it induces dose-related responses of chromosomal damage at low concentrations. Styrene-7,  8-oxide is detected in the blood of workers exposed to styrene. Adducts in haemoglobin and DNA, DNA single-strand breaks/ alkali-labile sites as well as significant increases in the frequency of chromosomal damage have been found in workers exposed to styrene in the reinforced plastics industry.  In humans there is little evidence for an association between workplace exposure to styrene and spontaneous abortions, malformations or decreased male fecundity.  Spontaneous abortions amongst female worker, exposed to styrene, has been reported in some studies. This finding has not been substantiated in other studies. Increased congenital malformations, embryonic foetal deaths or reduced birth weights have also been reported but simultaneous exposure to other substances makes the link to styrene conjectural. In rats, there is some evidence for reduced sperm count and peripubertal animals may be more sensitive than adult animals. Styrene crosses the placenta in rats and mice. It increases prenatal death at doses levels causing decreased maternal weight gain. Decreased pup weight, postnatal developmental delays as well as neurobehavioral and neurochemical abnormalities have been reported in rats exposed to styrene during pre- or postnatal development. The potential for developmental toxicity appears to be much higher for styrene-7,8-oxide, a metabolite.  Rats given weekly doses of styrene by gavage at 500 mg/kg for 102 weeks showed liver, kidney, and stomach lesions; no effects were seen in mice. Reduced weight gain and increased liver and kidney weights occurred in rats receiving 285 or 475 mg/kg/day for 185 days but no effects at 95 mg/kg/day . Male and female rats were given 0, 1000, or 2000 mg/kg and male and female mice were given 0, 150, or 300 mg/kg by gavage for 78 weeks . Reduced body weight occurred in both treated male rat groups, high-dose female rats, and both treated female mouse groups. In another study, male and female mice were treated weekly with 1350 mg/kg . At 20 weeks, mortality was 50% and 20% for males and females, respectively accompanied by liver necrosis, splenic hypoplasia, and lung congestion. Male and female mice were exposed to 0, 62.5, 125, 250, or 500 ppm styrene for 6 hours/day, 5 days/week for 13 weeks . In both sexes the liver to body weight ratio was increased at the two highest doses; histopathology of the respiratory tract revealed metaplasia and degeneration of the olfactory epithelium of the nasal cavity at the lowest dose, necrosis at higher concentrations, and bronchiolar regeneration at all concentrations. Male and female rats exposed to 0, 125, 500, 1000, or 1500 ppm on the same schedule had increased liver to body weight ratios at the three highest levels in males and the two highest levels in females; degeneration of the olfactory epithelium occurred in both sexes at around 1000 ppm. Pathological changes were observed in the respiratory mucosa of rats following exposure to 1000 ppm 4 hours/day, 5 days/week for 3 weeks  Chromosomal abnormalities (micronucleii, chromosome gaps or breaks, nuclear bridges and unscheduled DNA synthesis in peripheral lymphocytes) have been recorded in workers exposed to styrene. Such aberrations however are not always apparent in epidemiological studies and the status of styrene as a DNA effector is equivocal.  Death due to cancers among workers exposed to styrene is statistically unremarkable.  The dominant first metabolite of styrene is styrene-7,8-epoxide which binds covalently to DNA and shows activity in various in-vitro and in-vivo assays for genetic effects where it induces dose-related responses of chromosomal damage at low concentrations. Styrene-7,  8-oxide is detected in the blood of workers exposed to styrene. Adducts in haemoglobin and DNA, DNA single-strand breaks/ alkali-labile sites as well as significant increases in the frequency of chromosomal damage have been found in workers exposed to styrene in the reinforced plastics industry.  Prolonged or repeated contact with xylenes may cause defatting dermatitis with drying and cracking. Chronic inhalation of xylenes has been associated with central nervous system effects, loss of appetite, nausea, ringing in the ears, irritability, thirst anaemia, mucosal bleeding, enlarged liver and hyperplasia. Exposure may produce kidney and liver damage. In chronic occupational exposure, xylene (usually mix ed with other solvents) has produced irreversible damage to the central nervous system and ototoxicity (damages hearing and increases sensitivity to noise), probably due to neurotoxic mechanisms.  Industrial workers exposed to xylene with a maximum level of ethyl benzene of 0.06 mg/l (14 ppm) reported headaches and irritability and tired quickly. Functional nervous system disturbances were found in some workers employed for over 7 years whilst other workers had enlarged livers.  Xylene has been classed as a developmental toxin in some jurisdictions.  Small excess risks of spontaneous abortion and congenital malformation were reported amongst women exposed to xylene in the first trimester of pregnancy. In all cases, however, the women were also been exposed to other substances. Evaluation of workers chronically exposed to xylene has demonstrated lack of genotoxicity. Exposure to xylene has been associated with increased risks of haemopoietic malignancies but, again, simultaneous exposure to other substances (including benzene) complicates the picture. A long-term gavage study to mixed xylenes (containing 17% ethyl benzene) found no evidence of carcinogenic activity in rats and mice of either sex.  In a two-year inhalation study, groups of mice were exposed at 0, 10 or 30 ppm naphthalene, 6 hours/day, 5 days/week for 103 weeks. Female mice showed an increase of pulmonary alveolar/bronchiolar adenomas at 30 ppm. There was no increase in the incidence of tumours in male mice. Naphthalene inhalation was associated with an increase in the incidence and severity of chronic inflammation, metaplasia of the olfactory epithelium, and hyperplasia of the respiratory epithelium in the nose, and chronic inflammation of the lungs of both sexes.  Exposure to the material for prolonged periods may cause physical defects in the developing embryo (teratogenesis).