Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

YONG SHUN UNSATURATED POLYESTER RESIN 157

NFPA

PRODUCT USE

The use of a quantity of material in an unventilated or confined space may result in
increased exposure and an irritating atmosphere developing.Before starting consider
control of exposure by mechanical ventilation. Used according to manufacturer' s
directions.

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

May form explosive peroxides.
Limited evidence of a carcinogenic effect.
HARMFUL - May cause lung damage if swallowed.
Harmful by inhalation and if swallowed.
Irritating to eyes and skin.
Flammable.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Swallowing of the liquid may cause aspiration into the lungs with the risk of chemical pneumonitis; serious consequences may result. (ICSC13733).  Accidental ingestion of the material may be damaging to the health of the individual.  Considered an unlikely route of entry in commercial/industrial environments.  

EYE

  The vapour when concentrated has pronounced eye irritation effects and this gives some warning of high vapour concentrations. If eye irritation occurs seek to reduce exposure with available control measures, or evacuate area.  There is evidence that material may produce eye irritation in some persons and produce eye damage 24 hours or more after instillation. Severe inflammation may be expected with pain. There may be damage to the cornea. Unless treatment is prompt and adequate there may be permanent loss of vision. Conjunctivitis can occur following repeated exposure.  

SKIN

  The material may cause moderate inflammation of the skin either following direct contact or after a delay of some time. Repeated exposure can cause contact dermatitis which is characterized by redness, swelling and blistering.  Skin contact with the material may damage the health of the individual; systemic effects may result following absorption.  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 vapors or aerosols (mists, fumes), generated by the material during the course of normal handling, may be harmful.  There is some evidence to suggest that the material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  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.  If exposure to highly concentrated vapor atmosphere is prolonged this may lead to narcosis, unconsciousness, even coma and unless resuscitated - death.  The use of a quantity of material in an unventilated or confined space may result in increased exposure and an irritating atmosphere developing.Before starting consider control of exposure by mechanical ventilation.  Acute effects from inhalation of high vapor concentrations may be chest and nasal irritation with coughing, sneezing, headache and even nausea.  

CHRONIC HEALTH EFFECTS

  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 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.  There has been concern that this material can cause cancer or mutations, but there is not enough data to make an assessment.