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STYRENE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Specific Substances

    1) Sytrene
    2) Styrene monomer
    3) Benzene, vinyl
    4) Cinnamene
    5) Cinnamenol
    6) Cinnamol
    7) Diarex HF 77
    8) Ethylene, phenyl
    9) NCI-c 02200
    10) Phenethylene
    11) Phenylethene
    12) Phenylethylene
    13) Stirolo (Italian)
    14) Styreen (Dutch)
    15) Styren (Czech)
    16) Styrol (German)
    17) Styrole
    18) Styrolene
    19) Styron
    20) Styropol
    21) Styropor
    22) Vinylbenzen (Czech)
    23) Vinylbenzene
    24) Vinylbenzol
    25) CAS 100-42-5
    26) References: RTECS, 1992; Sax, 1984
    1.2.1) MOLECULAR FORMULA
    1) C8-H8

Available Forms Sources

    A) FORMS
    1) Commercialized styrene is stabilized with up to 50 ppm of t-butylcatechol or a similar inhibitor (Ashford, 1994a; Zenz, 1994a).
    2) Styrene is available in a technical form, 99.2%, and a polymer, 99.6% (Lewis, 1997a).
    B) SOURCES
    1) Styrene is produced synthetically by dehydrogenating ethylbenzene, or by using the Arco SM-PO process and combining ethylbenzene, propylene, and oxygen (ACGIH, 1991a; Ashford, 1994a; Bingham et al, 2001a; Budavari, 2000; HSDB, 2002; Lewis, 1997a; Zenz, 1994a).
    2) The demethylation of cumene can also produce styrene (Bingham et al, 2001a).
    3) Other techniques for producing styrene are (HSDB, 2002):
    1) "Oxidation of ethylbenzene to ethylbenzene hydroperoxide, which reacts with propylene to five alpha-phenylethanol and proplene oxide, after which alcohol is dehydrated to styrene"
    2) "Oxidative conversion of ethylbenzene to alpha-phenylethanol by way of acetophenone and subsequent dehydration of the alcohol"
    3) "Side-chain chlorination of ethylbenzene followed by dehydrochlorination"
    4) "Side-chain chlorination of ethylbenzene, hydrolysis to the corresponding alcohols, followed by dehydration"
    5) "Pyrolysis of petroleum and recovery from various petroleum processes"
    4) Styrene can be found naturally in trace amounts in cinnamon and in the sap of styracaeous tree trunks (Bingham et al, 2001a; Harbison, 1998a).
    C) USES
    1) Styrene is widely used in the manufacture of polystyrene plastics, protective coatings, nitrile and butadiene rubber comonomer, electronic components, alkyd/epoxy ester resin modifier, paint, styrenated polyesters, copolymer resins with acrylonitrile and butadiene, and as a chemical intermediate. It is used as an insulator, floor waxes, adhesives, putty, metal cleaners, autobody fillers, dental filling component, in agricultural products, and as a diluent to reduce viscosity of uncured resin. Styrene is also an FDA-approved flavoring agent in foods, such as ice cream and candy (AAR, 2000; ACGIH, 1991a; Bingham et al, 2001a; Hathaway et al, 1996; HSDB, 2002; ILO , 1998; ITI, 1995; Lewis, 1997a).
    2) Packaging is the single largest use of styrene; it is used to make foams, and styrene resins (Harbison, 1998a).

Therapeutic Toxic Class

    A) Styrene is an alkenylbenzene compound produced by alkylation of benzene and ethylene to form ethylbenzene which is then submitted to catalytic dehydrogenation (Clayton & Clayton, 1994; Budavari, 1996). It also occurs naturally in the sap of the styracaceous tree, and may be an air pollutant (Clayton & Clayton, 1994).
    B) It is used in the manufacture of plastics, paints, other protective coatings, copolymer resins, and synthetic rubbers, as a chemical intermediate, as a dental filling component, in certain agricultural products, and as a stabilizing agent in some special products such as polymeric synthetic materials (Gosselin et al, 1984) ITI, 1985; (Student, 1981; Clayton & Clayton, 1994; ACGIH, 1991; Proctor & Hughes, 1978).
    C) Styrene is widely used in boat-building and boat repair (Brigham & Landrigan, 1985). After heating to 200 degrees, styrene monomer is converted to polystyrene, a clear plastic having excellent insulating properties which are maintained even at very high radio frequencies (Budavari, 1996).
    D) Styrene monomer can polymerize prematurely during storage (Finkel, 1983). Inhibitors such as butylcatechol or hydroquinone (both allergenic) are often added to control this premature polymerization (Finkel, 1983).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) Styrene may be irritating to the eyes, skin, and mucous membranes. It can be ototoxic, nephrotoxic and hepatotoxic, and is a CNS depressant. Signs and symptoms of exposure may include nausea, fatigue, headache, loss of coordination, muscle weakness, a feeling of drunkenness, dizziness, and unconsciousness.
    2) "Styrene sickness" with nausea, vomiting, and a sensation of drunkenness occurs with inhalation exposure.
    3) Liver damage may occur with substantial chronic exposure (over 5 years).
    4) Peripheral neuropathy and pulmonary edema may occur. Prolonged or repeated exposure may lead to defatting dermatitis. Fetotoxicity has been observed in experimental animals and genotoxicity has been observed in vitro.
    5) ACUTE: Central nervous system depression can occur in serious acute exposures. Following chronic exposure, styrene can disrupt amino acid transport across the blood-brain barrier. Effects of styrene on the nervous system include CNS depression and peripheral neuropathy.
    6) Irritation of the respiratory tract and occupational asthma may occur following acute exposure. Pulmonary edema has been reported in animals. Ongoing exposure to styrene can result in irritation or even obstructive lung disease.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) FEVER: Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Three (4%) residents experienced fever (Arnedo-Pena et al, 2003).
    0.2.20) REPRODUCTIVE
    A) There are several studies suggestive of potential reproductive effects in humans. Styrene has also been extensively studied for possible reproductive effects in experimental animals.
    0.2.21) CARCINOGENICITY
    A) Styrene is generally considered as metabolically toxic due to its metabolic conversion to styrene epoxide (Lewis, 1998).

Laboratory Monitoring

    A) Patients with acute exposure should have baseline liver and renal function tests, urinalysis, complete blood count, and amylase and lipase levels. Monitor arterial blood gases and chest x-ray if significant respiratory tract irritation occurs.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) AVOID INDUCED EMESIS. Gastric lavage is of questionable safety, and should be done only with caution.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) Administer 100% humidified supplemental oxygen with assisted ventilation as required. Central nervous system depression may make airway management including endotracheal intubation mandatory.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) A thorough ophthalmic examination should be done if visual symptoms are present.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) Styrene airborne concentrations of 10,000 parts per million are dangerous to life within 20 to 30 minutes. Concentrations of 2500 ppm are dangerous to life within 8 hours.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) Styrene may be irritating to the eyes, skin, and mucous membranes. It can be ototoxic, nephrotoxic and hepatotoxic, and is a CNS depressant. Signs and symptoms of exposure may include nausea, fatigue, headache, loss of coordination, muscle weakness, a feeling of drunkenness, dizziness, and unconsciousness.
    2) "Styrene sickness" with nausea, vomiting, and a sensation of drunkenness occurs with inhalation exposure.
    3) Liver damage may occur with substantial chronic exposure (over 5 years).
    4) Peripheral neuropathy and pulmonary edema may occur. Prolonged or repeated exposure may lead to defatting dermatitis. Fetotoxicity has been observed in experimental animals and genotoxicity has been observed in vitro.
    5) ACUTE: Central nervous system depression can occur in serious acute exposures. Following chronic exposure, styrene can disrupt amino acid transport across the blood-brain barrier. Effects of styrene on the nervous system include CNS depression and peripheral neuropathy.
    6) Irritation of the respiratory tract and occupational asthma may occur following acute exposure. Pulmonary edema has been reported in animals. Ongoing exposure to styrene can result in irritation or even obstructive lung disease.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) FEVER: Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Three (4%) residents experienced fever (Arnedo-Pena et al, 2003).

Heent

    3.4.2) HEAD
    A) Volunteers exposed to 800 ppm for 3 hours described a metallic taste (Clayton & Clayton, 1994).
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Eye irritation is noted with exposures of 200 to 400 parts per million (Vainio & Hietanen, 1987). In one study of 345 styrene workers, 22% described conjunctival irritation (Clayton & Clayton, 1994; Triebig et al, 1989).
    2) Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Fifteen (18%) residents experienced eye irritations (Arnedo-Pena et al, 2003).
    3) CASE REPORT: One patient with styrene inhalation exposure developed retrobulbar optic neuritis and central scotomas, and a second developed central scotomas only from retinal vein occlusion (Grant, 1993; Clayton & Clayton, 1994).
    a) Evaluations of large groups of styrene exposed workers have detected no further cases of these effects (Clayton & Clayton, 1994).
    4) INCREASED INTRAOCULAR PRESSURE
    a) CASE REPORT/CHRONIC EXPOSURE: A 49-year-old man worked as a mold maker for a resin jewelry company and was regularly exposed to styrene for 7 years. In addition, he was exposed to 2 styrene spills in 2010 that occurred in an adjacent room. Protective equipment was not used. In 2010, he reported bilateral visual disturbances and dull eye pain, which improved when he was away from work. An eye examination showed bilaterally elevated intraocular pressure (36 mm Hg in the right eye; 38 mm Hg in the left eye). Other studies (disc assessment, Humphrey visual fields and retinal nerve) were within normal limits. He was started on a combination of latanoprost and timolol topically and his pressure improved within 2 weeks and remained within normal range. In 2011, he no longer worked in the same industry and he was successfully taken off of ocular antihypertensives with ongoing normal pressure readings (Inglis et al, 2014).
    5) ROTATORY NYSTAGMUS
    a) HUMANS: Volunteers exposed by inhalation to 300 ppm for one hour had mild disturbances in opticokinetic nystagmus (Tham et al, 1982).
    b) ANIMALS: Rats administered styrene by the intraarterial route developed a rotatory nystagmus response at arterial blood levels above 125 parts per million, but not at blood levels below 75 ppm (Tham et al, 1982).
    1) An excitation of the vestibulo-ocular reflex has also been demonstrated in rats with blood styrene levels of 80 parts per million (Tham et al, 1984).
    6) Changes in the standing potential and the electroretinogram noted in monkeys given intravenous infusions suggested a direct effect of styrene on the pigment epithelium of the eye (Skoog & Nilsson, 1981).
    7) COLOR VISION LOSS
    a) CASE SERIES: An investigation of 75 workers exposed to airborne styrene (3.2 to 549.5 milligrams/cubic meter) revealed a significant dose-related loss of color vision (Gobba et al, 1991).
    b) CASE SERIES: In 60 male shipbuilders exposed to average styrene concentrations of 24.3 ppm, there was a significant increase in blue-yellow and/or red-green color vision impairment compared to matched controls (Fallas et al, 1992).
    c) CASE SERIES: Chia et al (1994) demonstrated significant impairment in color vision in a study of 21 male shipbuilders exposed to estimated mean environmental styrene concentrations of 6 ppm.
    3.4.4) EARS
    A) WITH POISONING/EXPOSURE
    1) An occupational study of fiberglass and metal product plant workers suggested that workers exposed to low levels of styrene alone, or styrene and increased noise levels had significantly worse pure-tone thresholds at 2, 3, 4, and 6 kHz when compared to non-exposed or noise only exposed workers (Morata et al, 2002).
    2) The ototoxic effect of styrene was evaluated by reviewing seven occupational studies with various study designs on styrene and hearing. Three of the studies found modest correlations between hearing loss, styrene exposure and noise levels. Four of the studies found no relationship between styrene exposure and hearing loss. The review authors concluded that chronic low level styrene exposure and typical workplace noise may cause some degree of hearing loss. Further study was recommended(Lawton et al, 2006) .
    3) ANIMAL STUDIES: A study of ototoxicity in rats and guinea pigs exposed to styrene (1000 ppm) and toluene (600 ppm) 6 h/day for 5 consecutive days found that the rat model showed severe disruption of auditory function and cochlear pathology. The guinea pig model demonstrated no auditory or cochlear changes. The blood styrene concentration was four times higher in the rat than in the guinea pig. The authors suggested that this might be explained by differences between the species including:
    1) pharmacokinetic differences in the uptake of the solvents
    2) differences in metabolism
    3) a difference in glutathione concentrations within the sensory epithelium
    4) morphological differences of the lateral membranes of the outer hair cells
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Irritation of the mucosa of the nose and throat is noted with exposure to between 500 and 800 ppm (Vainio & Hietanen, 1987).
    2) Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Sixteen (19%) residents and nine (11%) residents experienced nasal irritations and nasal secretion, respectively (Arnedo-Pena et al, 2003).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Irritation of the mucosa of the nose and throat is noted with exposure to between 500 and 800 ppm (Vainio & Hietanen, 1987).
    2) Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Twenty-two (26%) residents experienced throat irritation (Arnedo-Pena et al, 2003).

Cardiovascular

    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DYSRHYTHMIA
    a) Cardiac dysrhythmias have been reported in experimental animals with inhalational exposure (Clayton & Clayton, 1994). This effect has not been reported in exposed humans.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) COUGH
    1) WITH POISONING/EXPOSURE
    a) Coughing occurs with exposure to between 500 and 800 ppm (Vainio & Hietanen, 1987).
    B) RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) Some workers in one group with chronic exposure had lower respiratory tract effects with decreases in FVC and in FEV(1)/FVC (Clayton & Clayton, 1994).
    C) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Two cases of occupational asthma have been reported, one accompanied by late development of an urticarial rash. Inhalation challenge with styrene concentrations equal to one-fourth the TLV (one-eighth the STEL) produced bronchospasm in these two patients (Moscato et al, 1987).
    b) CASE REPORT: A 30-year-old air frame technician developed chest tightness, wheezing, nocturnal dyspnea and decreased exercise tolerance while mixing styrene. The technician was relocated at work and treated with beclomethasone and salbutamol (by inhalation) for bronchospasm with subsequent resolution of his symptoms. The following year he returned to the area where he previously worked and required further treatment with beclomethasone and salbutamol. Inhalation testing was done (brush painting with 20 mL pure styrene; an equivalent of 12 ppm atmospheric styrene concentration). This provoked an immediate and late asthmatic response, with an associated reduction in histamine levels(Hayes et al, 1991).
    D) ASTHMA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Asthma symptoms including sneezing, nasal discharge, ocular itching, dyspnea, dry cough and wheezing developed in a 31-year-old man who handled paints containing hexamethylene diisocyanate and polyester resins and hardeners that included styrene at a concentration of 10% to 25%. He was evaluated 4 months after leaving his job because of these symptoms. His baseline PC20 methacholine was 2.3 mg/mL and 2.7 mg/mL 24 hours after a styrene inhalation challenge. The styrene challenge elicited an isolated asthmatic response with a maximum fall in FEV1 of 22% 11 hours after the test (Fernandez-Nieto et al, 2006).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY DISORDER
    a) MICE exposed to styrene alone by inhalation had significant bronchiolar and alveolar hyperplasia which was accentuated with exposure to both fibrous glass and styrene (Morisset et al, 1979).
    2) PULMONARY EDEMA
    a) Exposed experimental animals have developed severe respiratory tract irritation including pulmonary edema, especially after styrene aspiration (Gosselin et al, 1984). This effect has NOT been reported in exposed humans.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) CNS depression has been reported in cases of inhalational poisoning (Bakinson & Jones, 1985). Exposed humans have developed drowsiness, weakness, depression, inertia, and unsteadiness (Vainio & Hietanen, 1987; Lewis, 1998).
    B) ELECTROENCEPHALOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) An increased incidence of EEG abnormalities related to exposure levels has been noted in styrene-exposed workers (Vainio & Hietanen, 1987; Seppalainen & Harkonen, 1976; Harkonen et al, 1978; Seppalainen, 1978).
    C) FINE MOTOR IMPAIRMENT
    1) WITH POISONING/EXPOSURE
    a) Slight disturbances in psychomotor performance, visual-motor accuracy, and various neurasthenic and autonomic symptoms have been reported in workers exposed to styrene (Vainio & Hietanen, 1987; Flodin et al, 1989; Letz et al, 1990).
    D) SECONDARY PERIPHERAL NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A worker with several years of styrene inhalation exposure developed a sensory peripheral neuropathy involving a burning sensation of the feet and ankles, hypesthesia to pain and touch (but not vibration or positional sense) below the ankles, a moderately slow nerve conduction velocity in the lower extremities, and demyelination on sural nerve biopsy (Behari et al, 1986).
    b) Workers exposed to styrene have shown a reasonable incidence of peripheral dysesthesias, distal hypesthesias, and hypoactive or hyperactive deep tendon reflexes (Lilis et al, 1978; Rosen et al, 1978).
    c) CASE REPORT: A 52-year-old man developed progressive peripheral neuropathy of the extremities with loss of sensation in the hands and feet after two 8-hour days of inhalational exposure to a styrene-containing fiberglass resin. Laboratory tests showed a normal CBC and chemistry panel. Electrophysiologic tests revealed slowed motor nerve conduction velocities and prolonged distal latencies in sensory and motor nerves. One year after exposure, the patient continued to have lingering symptoms in his lower extremities (Fung & Clark, 1999).
    E) DYSFUNCTION OF VESTIBULAR SYSTEM
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 76-year-old man was admitted with a complaint of dizziness. He also reported recent episodes of postural vertigo and imbalance, weakness and headache over several months. The onset of symptoms coincided with the resurfacing of floors in his home following water damage. The patient noticed a distinct odor following the repair and the air quality was analyzed. The air concentration of styrene was 4-fold (1350 mcg/m(3)) higher than permitted by German air quality (300 mcg/m(3)) standards. The patient avoid further exposure and styrene was removed through mitigation efforts. During a physical exam, the vestibulospinal reflexes showed increased sway. He was diagnosed with transient isolated bilateral low frequency dysfunction of the vestibular ocular reflex and saccular dysfunction associated with transient styrene exposure. Eight months following cessation of exposure, the patient reported a significant improvement in symptoms and diagnostic studies were normal. At 2 year follow-up, his peripheral vestibular function remained normal (Fischer et al, 2014).
    F) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In 18 workers exposed to styrene levels below 110 milligrams/cubic meter for 6 to 15 years, disturbances in the central auditory pathways and the vestibulomotor-oculomotor reflex were noted (Moller et al, 1990).
    G) AMNESIA
    1) WITH POISONING/EXPOSURE
    a) Short term memory impairment has been reported following occupational exposures to styrene (Schoenhuber & Gentilini, 1989).
    H) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) In occupationally exposed workers, a slowing in sensory nerve conduction velocities was noted in 23% of those workers exposed to less than 50 ppm and 71% of workers exposed to more than 100 ppm (Cherry & Gautrin, 1990).
    I) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Workers exposed to styrene (mean TWA air concentration of 8.6 ppm) reported significantly more headache and fatigue than matched controls. No differences were observed between groups with respect to reaction time, color word vigilance, and symbol digit tests (Edling et al, 1993). The validity of the correlation between styrene exposure and symptoms in this study has been questioned (Nasterlack & Triebig, 1994).
    J) NEUROTOXICITY
    1) WITH POISONING/EXPOSURE
    a) In 11 styrene workers, V80 nerve conduction velocities and sensory conduction velocities were significantly decreased compared to matched controls. No difference was observed in somatosensory evoked potentials, motor conduction velocities, or heart rate between groups. Styrene exposure averaged 22 ppm and was estimated via urinary phenylglyoxylic acid excretion (Murata et al, 1991).
    b) A meta-analysis of long-term exposure to styrene reported increased choice reaction time in a dose-related manner, no significant effects on simple reaction time, and increased errors in performing a color arrangement/discrimination task. Eight work-years of exposure to 20 ppm was estimated to produce a 6.5% increase in choice reaction time (Benignus et al, 2005).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEUROPATHY
    a) RATS: Visual response speed and accuracy were influenced by styrene exposure in rats (Kulig, 1988).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Workers exposed by inhalation during manufacturing processes have been reported to have "styrene sickness" consisting of transient (few hours) nausea, appetite loss, fatigue, dizziness, unsteadiness, a feeling of drunkenness, vomiting, and general weakness (Clayton & Clayton, 1994; Gosselin et al, 1984).
    b) Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Six (7%) and one (1%) residents experienced nausea and vomiting, respectively (Arnedo-Pena et al, 2003).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Nine (11%) residents experienced abdominal pain (Arnedo-Pena et al, 2003).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Six (7%) residents experienced diarrhea (Arnedo-Pena et al, 2003).
    D) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) Human ingestions have not been reported. Experimental animals fed 2 grams per kilogram per day died in a few days and had severe irritation of the esophagus and stomach (Clayton & Clayton, 1994).
    E) INDIGESTION
    1) WITH POISONING/EXPOSURE
    a) One group of exposed workers had dyspepsia with reduction of gastric acid secretion (Clayton & Clayton, 1994).
    F) FINDING OF PANCREAS
    1) WITH POISONING/EXPOSURE
    a) Pancreatic changes were noted in one group of workers with chronic exposure (Clayton & Clayton, 1994).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In one group of exposed workers, mild changes in hepatic functions were noted. Another group of workers had normal liver function tests despite exposure to high concentrations (Clayton & Clayton, 1994).
    B) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Mildly elevated levels of gamma glutamyl transpeptidase (GGT), AST (SGOT), and ALT (SGPT) have been noted in some styrene exposed workers and did not correlate with reported ethanol consumption (Axelson & Gustavson, 1978).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) TOXIC NEPHROPATHY
    1) WITH POISONING/EXPOSURE
    a) Styrene is nephrotoxic (Lewis, 1998).
    b) Exposed experimental animals have developed renal injury (Gosselin et al, 1984). This effect has NOT been reported in exposed humans.
    B) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) A group of solvent-exposed workers (one-third of whom were exposed to styrene) had urinary excretion of more erythrocytes and leukocytes than an unexposed control group (Askergren, 1981).
    b) The exposed subjects also excreted more albumin than the controls, but beta-microglobulin excretion and concentrating capacity were not different (Askergren, 1981).
    c) No reduction in the glomerular filtration rate was found in the exposed group (Askergren et al, 1981).
    C) BLEEDING BETWEEN PERIODS
    1) WITH POISONING/EXPOSURE
    a) Women exposed to styrene were reported to have an increased incidence of menstrual cycle irregularities, (Barlow & Sullivan, 1982). These effects have not been confirmed by later studies (Lemasters et al, 1985).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMATOLOGY FINDING
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: One group of chronically exposed workers were found to have mild leukopenia, moderate anemia, reticulocytosis, decreased blood coagulability, and increased capillary permeability (Clayton & Clayton, 1994). A slight increase in levels of gamma globulin was observed in a different group of nine exposed workers (ACGIH, 1991).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Prolonged skin exposure may produce dermatitis with dry, rough, and fissured skin (Vainio & Hietanen, 1987; Conde-Salazar et al, 1989; Clayton & Clayton, 1994).
    b) Itching dermatitis and erythematous papular dermatitis have been reported (Vainio & Hietanen, 1987).
    c) Following the accidental contamination of a drinking-water tank in two buildings, 46 of 93 residents exposed to high styrene concentrations (up to 905 mcg/L) experienced symptoms. Twelve (14%) and five (6%) residents developed skin irritations and skin eruption, respectively (Arnedo-Pena et al, 2003).
    B) SKIN FINDING
    1) WITH POISONING/EXPOSURE
    a) Fair-skinned individuals appear to be more sensitive to the defatting and dehydrating action of styrene than dark-skinned persons (HSDB, 2000).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) DISORDER OF ENDOCRINE SYSTEM
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: A group of 30 styrene-exposed females had significantly higher serum prolactin levels and human growth hormone levels than unexposed controls. There were no differences between the two groups in thyroid stimulating hormone or gonadotropin levels (Mutti et al, 1984).
    b) CASE SERIES: A volunteer group of 16 styrene-exposed female workers had abnormally elevated increases in serum prolactin levels after intravenous injection of greater than physiological amounts of thyrotrophin-releasing hormone (Arfini et al, 1987).
    1) The authors speculated that styrene exposure somehow modifies dopaminergic modulation of neuroendocrine secretion (Arfini et al, 1987).
    B) HYPOPITUITARISM
    1) WITH POISONING/EXPOSURE
    a) Styrene-exposed women have been reported to have abnormal pituitary secretion, which may cause menstrual cycle irregularities (Brown, 1991).

Immunologic

    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DISEASE OF IMMUNE SYSTEM
    a) In mice, styrene caused dose-dependent modulation of immunocompetence (Dogra et al, 1989).

Reproductive

    3.20.1) SUMMARY
    A) There are several studies suggestive of potential reproductive effects in humans. Styrene has also been extensively studied for possible reproductive effects in experimental animals.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) The Advisory Panel on Reproductive Hazards in the Workplace found no evidence that styrene is teratogenic to animals or humans (Council on Scientific Affairs, 1985).
    2) In one case, children born to a mother who was exposed to styrene (among a variety of agents) were noted to have some central nervous system effects (Clayton & Clayton, 1994).
    3) A Finnish study noted a possible clustering of central nervous system defects in children of women employed in the reinforced plastics industry, but there were no exposure estimates or other details (Holmberg, 1977; Kurppa, 1983). Styrene-exposed Finnish women also seemed to be at increased risk for spontaneous abortion (Hemminki, 1980), but this was not confirmed in a matched case-control study (Lindbohm, 1985).
    B) ANIMAL STUDIES
    1) Rats and rabbits exposed to these air concentrations did not exhibit teratogenic effects (Council on Scientific Affairs, 1985). Rats and rabbits administered 300 or 600 parts per million by gavage did not have increased teratogenicity rates or any adverse effect on fetal weight (Council on Scientific Affairs, 1985).
    2) Exposure of chick embryos produced a variety of malformations and embryolethality (Schreiner, 1983). An increase in resorptions and fetal bone defects (extra ribs, fused ribs) was seen in the offspring of pregnant mice exposed by inhalation to 250 parts per million (Kankaanpaa et al, 1980).
    3) One author feels that styrene, similar to benzene, may eventually prove to be a co-affective teratogen (Schreiner, 1983).
    4) In other experiments, pregnant rats exposed by either gavage or inhalation did not have malformations or increased resorptions, and rabbits with inhalation exposure during the period of organogenesis did not exhibit any fetal malformations (Schreiner, 1983).
    5) When administered by the inhalation route to rats or rabbits at 300 or 600 ppm, styrene was not embryotoxic, fetotoxic, or teratogenic, but there was some increase in normal skeletal variants (Barlow & Sullivan, 1982). It was not embryotoxic or teratogenic in rats exposed to a concentration of 200 mg/m(3) or 700 mg/m(3) (Vergiyeva, 1979).
    6) Rats exposed prenatally to styrene at airborne concentrations up to 300 ppm for 6 hours per day during days 7 to 21 of gestation had lower body weights and reduced levels of brain serotonin, suggesting that the offspring could have neurological defects despite the absence of overt structural malformations (Kishi et al, 1992). Functional neurological testing was not done in this study.
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) No adverse effect on human fertility is reported in the scientific literature (Council on Scientific Affairs, 1985).
    a) No adverse effects on number of births, spontaneous abortions, or pregnancies in styrene-exposed workers as compared with control groups have been reported, although documentation of the degree and duration of exposure has been poor (Council on Scientific Affairs, 1985).
    2) Lemasters et al (1989) investigated 1535 women working in the reinforced plastics industry with exposure to styrene during pregnancy and failed to demonstrate a significant dose-response trend in decreasing average birth weights.
    a) The majority of women were exposed to 30 ppm or less however, a small subgroup of 50 women were exposed to a mean styrene concentration of 82 ppm (as well as other solvents) and were associated with a 4% reduction in birth weight as compared to unexposed mothers (Lemasters et al, 1989).
    3) Some styrene does cross the placenta. Styrene has been found in fetal and umbilical cord blood at concentrations proportional to maternal blood levels (Dowty & Laseter, 1976).
    4) An increased incidence of toxemia of pregnancy was reported in a study of 67 styrene-exposed women (Zlobina, 1975), but there was no mention of birth defects. In a study of 2,209 workers (1,698 men and 511 women) in the reinforced plastics industry, there was no significant increase in birth defects (Harkonen, 1984). Styrene does seem to cross the placenta, and may concentrate in the fetus (Dowty & Laseter, 1976).
    B) ANIMAL STUDIES
    1) No adverse effects were seen in pregnant mice and rats with exposures as high as 250 parts per million (Council on Scientific Affairs, 1985).
    2) Increased embryo resorption rates were noted in mice at exposures of 250 parts per million and in hamsters at 1,000 parts per million (Council on Scientific Affairs, 1985).
    3) Styrene injected into chicken eggs at doses of 2 to 100 micromoles per egg produced a variety of malformations and some embryolethalities (Schreiner, 1983). Rats exposed by inhalation during pregnancy had an increased incidence of resorptions but no malformations (Schreiner, 1983).
    4) In experimental animals, styrene generally has resulted in increased pre-implantation loses or increased resorptions, but was not teratogenic.
    5) Styrene increased resorptions in mice at a concentration of 250 ppm and in hamsters exposed to 1,000 ppm (Kankaanpaa et al, 1980). Pre-implantation losses were increased in rats exposed to 11.8 ppm (Barlow & Sullivan, 1982), and there was damage to the ovaries (Bakhtizina, 1983).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) HUMANS
    1) At the time of this review, sufficient data were not found allowing an assessment of the potential effects of styrene exposure to an infant during lactation.
    2) Occupational exposure to styrene was reported to be linked with inhibition of lactation in women who worked at a glass-reinforced plastics factory (Izmerov, 1984).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS100-42-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Styrene
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.2) SUMMARY/HUMAN
    A) Styrene is generally considered as metabolically toxic due to its metabolic conversion to styrene epoxide (Lewis, 1998).
    3.21.3) HUMAN STUDIES
    A) SARCOMA
    1) One case of a lymphoblastic sarcoma has been reported in a worker exposed under conditions of poor ventilation (ACGIH, 1980).
    B) LEUKEMIA
    1) Danish reinforced plastics workers had a 2.5-fold increased risk for myeloid leukemia with clonal chromosome aberrations in a nested case-control study. Workers were employed during the 1960's, during which exposure to styrene may have been higher that at later dates. These results cannot distinguish between the possibilities that styrene may be a leukemogen through a clastogenic effect versus clonal selection of a particular subtype of leukemia which develops these types of chromosome aberrations (Kolstad et al, 1996) 1994).
    2) A large mortality study of workers in Germany found no increased deaths from cancer (Frentzel-Beyme, 1978), but another occupational mortality study reported increased lymphatic leukemias in one subgroup (Ott, 1980). These increased leukemias were not seen in a follow-up study of this group, but there was a persistent small excess of deaths from lymphatic cancers, especially multiple myelomas, in a subgroup which was also exposed to extrusion fumes, solvents, and colorants (Bond et al, 1992). Workers in the latter study were exposed primarily to styrene and were not exposed to 1,3-butadiene. Workers who produced styrene-butadiene latex did not have increased mortality from lymphatic and hematopoietic cancers (Bond et al, 1992).
    3) Excess deaths from leukemia occurred in a group of 15,649 styrene-butadiene rubber workers among hourly workers with 10 plus years worked and 20 plus years since hiring, and also among workers in polymerization, maintenance labor, and laboratories. The last three groups had the highest potential for exposure to styrene monomer, as well as 1,3-butadiene (Delzell et al, 1996).
    4) A follow-up study of 16,610 styrene-butadiene rubber workers developed quantitative estimates of exposure retrospectively. Risk of mortality from leukemia was less clear for cumulative styrene exposure than for cumulative 1,3-butadiene exposure (Macaluso et al, 1996).
    C) PANCREATIC CARCINOMA
    1) An increased incidence of pancreatic cancer was seen in a comprehensive study of 36,610 Danish reinforced plastics workers exposed from 1970 to 1990 (Kolstad et al, 1995).
    D) BREAST CARCINOMA
    1) A suggestive association between occupational exposure to styrene and deaths from breast cancer was seen in a case-control study using mortality records from 24 US states from 1984 to 1989 (Cantor et al, 1995). Further studies are necessary to determine a cause and effect relationship.
    E) LYMPHOMA-LIKE DISORDER
    1) A NIOSH study of styrene-butadiene rubber workers found no significant increase in mortality, but there were some excess deaths from hematopoietic and lymphatic cancers (Meinhardt, 1980). Another NIOSH study found excess deaths from male genital cancers (Okun, 1981). Excess lymphomas were found in styrene workers (Hodgson & Jones, 1985).
    F) LACK OF EFFECT
    1) Studies of the possible carcinogenicity of styrene have been conflicting. It may be impossible to fully separate the effects due to styrene versus butadiene in these workers. As long as mixed exposures occurred, effects cannot be attributed to a single chemical.
    2) Case reports and some epidemiological studies have implied that an increased risk for development of hematopoietic and lymphatic malignancies may exist in workers exposed to styrene, styrene-butadiene rubber, and polystyrene, although presently available data do not allow a direct causal relationship to be established in humans (Vainio & Hietanen, 1987; Hodgson & Jones, 1985).
    3) An increased risk of mortality from cancer of the lymphatic and hematopoietic systems was found in a retrospective study of 40,688 workers exposed to styrene in the reinforced plastics industry (Kogevinas et al, 1994). This increased risk was not consistently associated with either cumulative styrene exposure or styrene exposure duration.
    4) CASE SERIES - A mortality study of a cohort of 5,021 styrene-exposed workers in a boat-building facility failed to disclose any excess deaths or cases of leukemia or lymphoma, although the power of the study to detect these tumors was low (Okun et al, 1985).
    5) CASE SERIES - A mortality study of 7,949 male and female workers exposed to styrene during manufacturing of glass-reinforced plastics failed to show either excess rates of cancer or deaths from any other source (Coggon et al, 1987).
    a) In particular, there was no excessive incidence of leukemias or lymphomas, which actually occurred less frequently than predicted (Coggon et al, 1987).
    b) The few hematopoietic tumors which did occur were not concentrated among employees with the longest or highest styrene exposures (Coggon et al, 1987).
    6) CASE SERIES - A mortality study of 13,920 male workers in the manufacture of styrene-butadiene rubber polymer failed to disclose any excess incidence of cancer or deaths from any cause, although cancers of the esophagus and large intestine and Hodgkin's disease occurred at slightly greater frequency than predicted by Standard Mortality Ratios (Matanoski & Schwartz, 1987).
    7) CASE SERIES - A cohort mortality study of 15,908 men and women exposed to styrene while working in the reinforced plastics and composites industry was unable to demonstrate any significant excess incidence of cancer or deaths from any specific cause (Wong, 1990).
    a) An additional 12 years of mortality data for this group of workers showed significant increases in all-cause mortality, death from all cancers, and death from other causes. However, when this data was analyzed for duration of styrene exposure and cumulative styrene exposure, no causality was established. The most likely confounding variables were socioeconomic class, smoking, and lifestyle factors (Wong et al, 1994).
    b) Another similar study did not find excess leukemia or lymphoma mortality among workers exposed to styrene in the reinforced plastic boat-building industry. Unanticipated excess urinary tract cancer (SMR 3.44; CI 1.26-7.50) and respiratory disease mortality (SMR 2.54; CI 1.31-4.44) were found; although presently available data do not allow a direct causal relationship to be established (Ruder et al, 2004).
    8) Some authors have cautioned against concluding prematurely that styrene is NOT a human carcinogen because published studies have involved young workers not followed for a long period of time (Kogevinas & Boffetta, 1991; Wong, 1991).
    3.21.4) ANIMAL STUDIES
    A) NEOPLASM
    1) RATS chronically exposed to 600 or 1,000 parts per million had a questionable increase in the rates of lymphoid and hematopoietic tumors (ACGIH, 1980).
    2) Styrene was not carcinogenic in mice or rats when given orally in corn oil, but there were "suggestive" increases in lung tumors in male B6C3F1 mice (ACGIH, 1991).
    3) Increased mammary tumors were seen in female rats exposed to 600 ppm for 6 hours/day, 5 days/week for 18 to 20 months, but there was no clear dose response (ACGIH, 1991). Mammary tumors were also seen in rats exposed to levels as high as 300 ppm for 52 weeks (ACGIH, 1991).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Patients with acute exposure should have baseline liver and renal function tests, urinalysis, complete blood count, and amylase and lipase levels. Monitor arterial blood gases and chest x-ray if significant respiratory tract irritation occurs.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Biological Exposure Indices (BEI) have been established for styrene exposure monitoring, including styrene blood levels at the end of a shift and prior to the shift (ACGIH, 2002).
    2) Styrene blood levels might be useful to confirm the diagnosis in patients with acute exposure.
    3) Levels of styrene in blood correlated better with exposure than urinary styrene (Ong et al, 1994).
    4) An exposure of 20 ppm TWA styrene produced a steady-state blood level of approximately 1 mcg styrene-7,8-oxide/L (Korn et al, 1994).
    5) Monitor liver and renal function tests and amylase and lipase levels in patients with significant acute exposure.
    B) HEMATOLOGIC
    1) Monitor complete blood count with significant exposure.
    C) ACID/BASE
    1) Patients with significant respiratory tract irritation should have baseline arterial blood gases.
    4.1.3) URINE
    A) OTHER
    1) Biological Exposure Indices (BEI) have been established for styrene exposure monitoring, including mandelic acid and phenylglyoxylic acid excretion in urine at the end of a shift, and mandelic acid urinary excretion at the end of the workweek. These may be corrected for urinary creatinine clearance (ACGIH, 2002). Their utility is limited by not being specific to styrene.
    a) The sum of urinary mandelic acid and phenylglycoxylic acid correlated better with styrene exposure than either metabolite alone (Ong et al, 1994).
    2) A study of 24 fiberglass boat workers with styrene inhalation exposure showed that in the actual conditions of use with large fluctuations in the air concentrations during the working day, the biologic measurement best correlated with the degree of exposure was a combination of the levels of mandelic and phenylglyoxylic acids in the urine collected at the end of the working day and corrected for creatinine clearance (Boiteau et al, 1987).
    a) An eight hour exposure to 50 ppm was correlated with a mean level of 714 plus or minus 35 milligrams of the combined styrene metabolites per gram of urinary creatinine (Boiteau et al, 1987).
    b) De Rosa et al (1988) confirm that the biologic measurement of metabolites (mandelic acid & phenylglyoxylic acid) in urine generally correlates to the degree of exposure. However, the authors believe that sequential samples covering the entire workshift may provide more accurate information.
    c) In a study of 214 styrene workers, end of shift urinary mandelic acid and phenylglyoxylic acid correlation coefficients to airborne styrene levels were 0.82 and 0.78, respectively, adding further evidence to the usefulness of urinary metabolite levels for biological monitoring of styrene exposure (Gobba et al, 1993).
    B) URINALYSIS
    1) Monitor urinalysis with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) BREATH ANALYSIS
    a) Biological Exposure Indices (BEI) have been established for styrene exposure monitoring, including styrene in mixed exhaled air prior to and during a shift (ACGIH, 2002).
    b) A study of 24 fiberglass boat workers with styrene inhalation exposure showed that in the actual conditions of use with large fluctuations in the air concentrations during the working day, expired air samples for styrene taken at the end of the working day did not correlate well with the degree of exposure (Boiteau et al, 1987).
    c) A study of 39 styrene exposed boat manufacturing workers (time weighted average, 40 ppm) showed that monitoring of mid-stream exhaled air at the end of the work shift correlated well with low level styrene exposure (Ong et al, 1994).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Patients with respiratory tract irritation should have a baseline chest x-ray.

Methods

    A) CHROMATOGRAPHY
    1) Gas chromatographic methods are the most valid for tissue or blood samples (Vainio & Hietanen, 1987).
    2) Gas-liquid chromatographic methods have been used to measure expired air samples (Boiteau et al, 1987).
    3) High performance liquid chromatography and gas chromatography/mass spectrometry methods have been used for measuring styrene urinary metabolites (Arnedo-Pena et al, 2003; Boiteau et al, 1987). A fluormetric method has also been described (Chakrabarti, 1979).
    4) Gas chromatographic methods are most often used for measuring styrene levels in atmospheric air, waste water, manufacturing processes, etc. A sensitive colorimetric method has been described for atmospheric air measurements (Vainio & Hietanen, 1987).
    5) Concomitant ingestion of ethanol or other solvents may produce a delay in the urinary excretion of mandelic acid after styrene exposure.
    a) A gas chromatographic procedure for the identification of the intermediate metabolites which accumulate in blood in such a setting (phenylethyleneglycol enantiomers and phenylethanol isomers), has been developed and suggested for use in monitoring workers who drink ethanol to avoid underestimating styrene exposure (Korn et al, 1985).
    B) SAMPLING
    1) A personal sampling technique using a Perkin-Elmer tube containing Tenax and usually worn on the worker's lapel has been described. Using this technique in field trials, it was found that samples could be stored at room temperature for up to 6 months without appreciable styrene loss (Brown et al, 1987).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Symptomatic patients should probably be admitted to the hospital until all symptoms have cleared.
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Patients with respiratory tract irritation or central nervous system depression should be admitted until all symptomatology has cleared.

Monitoring

    A) Patients with acute exposure should have baseline liver and renal function tests, urinalysis, complete blood count, and amylase and lipase levels. Monitor arterial blood gases and chest x-ray if significant respiratory tract irritation occurs.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) Avoid induced emesis due to the potential for esophageal irritation.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Induced emesis should be avoided because of the potential for esophageal irritation.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    B) IRRITATION SYMPTOM
    1) Although not reported in humans, significant gastric and esophageal irritation could occur with ingestion of large amounts. Observe carefully for signs of serious complications such as perforation, bleeding, or mediastinitis.
    2) If signs of serious esophageal irritation are present, endoscopy may be considered for evaluation and monitoring. A possible late sequelae of serious esophageal irritation could be stricture formation, requiring consultation and evaluation.
    C) MONITORING OF PATIENT
    1) Monitor EKG, liver and renal function tests, urinalysis, complete blood count, and amylase and lipase in serious ingestions.
    D) AIRWAY MANAGEMENT
    1) If central nervous system depression occurs, airway patency and oxygenation must be carefully evaluated and airway protective measures including endotracheal intubation undertaken if indicated.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) OXYGEN
    1) Administer 100% humidified supplemental oxygen with assisted ventilation as required.
    B) AIRWAY MANAGEMENT
    1) If central nervous system depression occurs, airway patency and oxygenation must be carefully evaluated and airway protective measures including endotracheal intubation undertaken if indicated.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) MONITORING OF PATIENT
    1) Neuropsychiatric testing may be useful as a measurement of psycho-organic impairment in significant, especially chronic, exposures.
    E) GENERAL TREATMENT
    1) Patients who develop occupational asthma should be precluded from further styrene exposure (Moscato et al, 1987).
    F) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) A thorough ophthalmic examination including funduscopy should be done in any patient with complaints involving the eyes.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Dermal irritation should be treated with standard topical therapy.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) No studies have addressed the use of extracorporeal elimination procedures in styrene poisoning. Pharmacokinetic data would argue against their effectiveness.

Range Of Toxicity

Summary

    A) Styrene airborne concentrations of 10,000 parts per million are dangerous to life within 20 to 30 minutes. Concentrations of 2500 ppm are dangerous to life within 8 hours.

Minimum Lethal Exposure

    A) The minimum lethal human dose to this agent has not been delineated.
    B) There have been no reported deaths from styrene exposure; based on animal data, styrene is expected to be low to moderately toxic to humans via oral, dermal, and inhalation exposure routes (ATSDR, 1992; (Bingham et al, 2001; Lewis, 2000; Lewis, 1998).
    C) ANIMAL DATA:
    1) Rats died after ingesting high doses of styrene at 1000 to 2000 mg/kg over 28 days (ACGIH, 1991).
    2) 2000 ppm of styrene in air is lethal to rats (OHM/TADS , 2002).
    3) Guinea pigs and rats inhaled 10,000 ppm of styrene and died 30 to 60 minutes later (ACGIH, 1991; Hathaway et al, 1996a).
    4) Some animals, species and route of exposure was not reported, died following an exposure to 2500 ppm within 8 hours (ACGIH, 1991; Hathaway et al, 1996a).

Maximum Tolerated Exposure

    A) HUMAN DATA
    1) Styrene is irritating to the eyes, skin, mucous membranes, and respiratory tract. High exposure levels may cause anesthesia and other effects of central nervous system depression (ATSDR, 1992; (Bingham et al, 2001; Harbison, 1998).
    2) Following the accidental contamination of a drinking-water tank in two buildings, 93 residents were exposed to high styrene concentrations (up to 905 mcg/L) and low levels of toluene and other dissolved hydrocarbons. Overall, 46 (26 children and 20 adults) of the 84 persons interviewed experienced symptoms after drinking tap water, exposure to vapors from the basement, bathing and showering, or eating foods prepared with tap water. The following symptoms were reported by the residents: throat irritation (26%); nasal irritation (19%); eye irritation (18%); skin irritation (14%); nasal secretion (11%); abdominal pain (11%); diarrhea (7%); nausea (7%); skin eruption (6%); fever (4%); vomiting (1%) (Arnedo-Pena et al, 2003).
    3) Some people experienced vapor exposures at 100 ppm caused mild irritation of the eyes and throat within 20 minutes. After 15 minutes at 375 ppm, not all volunteers experienced eye irritations but all reported nasal irritations (ACGIH, 1991; Grant, 1993; Zenz, 1994).
    4) Concentrations of styrene at 400 to 500 ppm could be tolerated, but all volunteers experienced eye and nose irritation. At 1300 ppm, extreme irritation was noted (Grant, 1993).
    5) Humans exposed to 50 ppm for 90 minutes reported subjective complaints such as headache, fatigue, and difficulty concentrating. The level of styrene in alveolar air varied with the level of exercise (Bingham et al, 2001; Hathaway et al, 1996a).
    6) Eyes and nasal irritation were reported at 376 ppm within 15 minutes of exposure. Headache, nausea, decreased dexterity and coordination, and other signs of transient neurologic impairment were experienced after one hour (ACGIH, 1991; Bingham et al, 2001; Hathaway et al, 1996a).
    7) Inhalation studies showed persons could tolerate 300 ppm (via mouth tube) of styrene for 1 hour. The volunteers had difficulty with visual tracking, but did not experience diminished coordination or balance (ACGIH, 1991).
    8) Liquid and vapor styrene may be absorbed through the skin. The absorption rate of liquid styrene through hand and forearm skin was 9-15 mg/cm(2)/hour. Prolonged or repeated exposure caused dermatitis and fissured skin. Fair-skinned individuals are more susceptible to the dehydration and defatting effects of styrene (ATSDR, 1992; (Bingham et al, 2001; Hathaway et al, 1996a).
    B) OCCUPATIONAL EXPOSURE
    1) ACUTE
    a) CASE REPORT: A 24-year-old man was inadvertently exposed to a single high dose of styrene during the transfer of styrene monomer from a tank to a container. Exposure was approximately 30 seconds and witnessed by several of his coworkers. Following recovery from acute intoxication, he complained of headache, dyspnea and decreased responsiveness to stimuli. He also displayed anxiety and unpredictable behavior. He developed significant cognitive and psychotic symptoms (ie, elevated mood, grandiosity, a belief he could communicate telepathically and paranoid delusions) that lasted for more than 3 months. Clinical neuroimaging including a brain MRI and toxicology screening were normal. Symptoms improved with quetiapine (700 mg) therapy. However, he developed chronic deterioration and his symptoms returned due to poor compliance with therapy which led to frequent readmissions (Moon et al, 2015).
    2) CHRONIC
    a) Workers in polystyrene plants have been found to have liver damage after exposure to concentrations of 20 to 150 ppm for over 5 years (Sittig, 1991).
    C) LACK OF EFFECT
    1) Volunteers exposed to 50 ppm of styrene for one hour did not report any subjective symptoms nor were there any abnormal objective clinical findings (ACGIH, 1991).
    D) ANIMAL DATA
    1) ACUTE
    a) Mice experienced 50% respiratory rate reduction after inhaling 160 ppm for 3 minutes (ACGIH, 1991).
    b) Applications to the skin of rats at 500 or 300 mg/kg/day for 7 days did not cause changes in hepatic cytochrome P-450 content (ACGIH, 1991).
    c) Animals did not develop any serious systemic effects after 8 hours at 1300 ppm (Bingham et al, 2001).
    d) Animals exposed to 2500, 5000, or 10,000 ppm had nasal and eye irritations. After 10 hours at 2500 ppm, 1 hour at 5000 ppm, and a few minutes at 10,000 ppm the animals became unconscious (Bingham et al, 2001).
    E) CHRONIC
    1) Rats and rabbits developed eye and nasal irritations after exposures to styrene at 1300 ppm for 7 to 8 hours/day for 7 days/week for 26 weeks (OHM/TADS , 2002).
    2) Styrene exposures at 1 g/kg/day affected organ growth and weight and some mortalities occurred. Severe irritation to the stomach and esophagus at 2 g/kg/day, caused death to follow quickly (Bingham et al, 2001).
    3) Concentrations of styrene at 200 to 400 ppm had an irritating effect on the eyes and nose of rats. Rats and guinea pigs had definite signs of irritation at 1300 ppm, but no permanent injury was noted after repeated doses for 7 to 8 hours/day for 5 days/week for 6 months. Rabbits and rhesus monkeys did not show adverse effects at the same concentration (ACGIH, 1991; Bingham et al, 2001; Grant, 1993; Hathaway et al, 1996a).
    F) LACK OF EFFECT:
    1) Guinea pigs had no observed effects at 650 ppm (ACGIH, 1991).
    2) The no effect level was 133 to 667 mg/kg/day, animal species was not specified (Bingham et al, 2001).
    3) Subacute and chronic exposures to styrene with no level of effect (Bingham et al, 2001):
    1) NOAEL (ORAL) RAT: 66.7 mg/kg/day for 5 days/week for 185 days
    2) NOAEL (ORAL) RAT: 100 mg/kg/day for 5 days/week for 28 days
    3) NOAEL (ORAL) RAT: 133 mg/kg/day for 5 days/week for 185 days
    4) NOAEL (INHL) RABBIT: 1300 ppm for 7H/day at 264 exposures over 12 months
    5) NOAEL (INHL) RABBIT: 2000 ppm for 7H/day at 126 exposures over 5 months
    6) NOAEL (INHL) GUINEA PIG: 650 ppm for 7H/day at 130 exposures over 6 months
    7) NOAEL (INHL) RHESUS MONKEY: 1300 ppm for 7H/day at 264 exposures over 12 months

Workplace Standards

    A) ACGIH TLV Values for CAS100-42-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Styrene, monomer
    a) TLV:
    1) TLV-TWA: 20 ppm
    2) TLV-STEL: 40 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: BEI
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
    c) TLV Basis - Critical Effect(s): CNS impar; URT irr; peripheral neuropathy
    d) Molecular Weight: 104.16
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS100-42-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Styrene
    2) REL:
    a) TWA: 50 ppm (215 mg/m(3))
    b) STEL: 100 ppm (425 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 700 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS100-42-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Styrene, monomer
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Styrene
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2B ; Listed as: Styrene
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Styrene
    5) MAK (DFG, 2002): Category 5 ; Listed as: Styrene
    a) Category 5 : Substances with carcinogenic and genotoxic effects, the potency of which is considered to be so low that, provided the MAK and BAT values are observed, no significant contribution to human cancer risk is to be expected. The classification is supported by information on the mode of action, dose dependence and toxicokinetic data pertinent to species comparison.
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS100-42-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Styrene
    2) Table Z-1 for Styrene:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3:
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed
    3) Table Z-2 for Styrene (Z37.15-1969):
    a) 8-hour TWA:100 ppm
    b) Acceptable Ceiling Concentration: 200 ppm
    c) Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:
    1) Concentration: 600 ppm
    2) Maximum Duration: 5 min. in any 3 hrs
    d) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Bingham et al, 2001 Budavari, 2000 HSDB, 2002 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 660 mg/kg
    b) 615.7-704.3 mg/kg (Budavari, 2000; HSDB, 2002)
    2) LD50- (ORAL)MOUSE:
    a) 316 mg/kg
    b) 4920 mg/kg (OHM/TADS, 2002)
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 898 mg/kg
    4) LD50- (ORAL)RAT:
    a) 1 g/kg (HSDB, 2002)
    b) 1-5 g/kg (Bingham et al, 2001)
    c) 5 g/kg (Bingham et al, 2001)
    d) 5000 mg/kg (HSDB, 2002; Lewis, 2000)
    e) 2650 mg/kg -- somnolence and changes to the liver
    5) LD50- (SUBCUTANEOUS)RAT:
    a) 2650 mg/kg
    6) TCLo- (INHALATION)HUMAN:
    a) 376 ppm for 1H -- change in motor activity and flaccid paralysis without anesthesia
    b) 600 ppm -- changes to sense organs
    c) 20 mcg/m(3) -- sense organs effected
    7) TCLo- (INHALATION)MOUSE:
    a) 250 ppm for 6H/5D-intermittent -- dehydrogenases, changes in liver weight, and death
    b) 250 ppm for 6H/14D- intermittent -- hepatitis and changes in liver weight, and death
    c) 500 ppm for 6H/22D- intermittent -- changes in blood serum, hepatitis, and other transferases
    d) 500 ppm for 90D-intermittent -- changes to trachea and bronchi stucture or function, hepatitis, and death
    e) 160 ppm for 6H/2Y-intermittent -- respiratory tumors and carcinogenic by RTECS criteria
    f) Female, 500 ppm for 6H at 6-16D of pregnancy -- post-implantation mortality
    8) TCLo- (INHALATION)RAT:
    a) 50 mg/m(3) for 24H/70D- continuous -- true cholinesterase, changes in erythrocyte and leukocyte count
    b) 6 g/m(3) for 8H/26W-intermittent -- changes to sense organs
    c) 300 ppm for 6H/2W-intermittent -- change to liver and respiratory system; structural or functional changes in bronchi or trachea
    d) 1500 ppm for 6H/13W-intermittent -- affected fluid intake and sense organs
    e) 2000 ppm/8H for 32W-intermittent -- changes to peripheral nerve, weight loss, or decreased weight gain
    f) Female, 293 ppm for 6H at 7-21D of pregnancy -- changes to behavior
    g) Female, 50 ppm for 6H at 7-12D of pregnancy -- affected growth statics
    h) Female, 1500 mcg/m(3) for 24H at 1-22D of pregnancy - fetotoxicity and fetal death
    i) Female, 1500 mcg/m(3) for 24H at 1-7D of pregnancy - pre- and post-implantation mortality
    j) 100 ppm for 4H for 5D/1Y- intermittent -- skin and appendage tumors, leukemia, and carcinogenic by RTECS criteria
    k) Female, 5 mg/m(3) for 24H at 1-22D of pregnancy -- affected weaning or lactation index and stillbirths

Pharmacology Toxicology

Toxicologic Mechanism

    A) Styrene is a direct irritant of the conjunctiva and mucous membranes (Clayton & Clayton, 1994).
    B) Styrene produces dermatitis by a defatting and dehydrating action (Clayton & Clayton, 1994).
    C) The oxidative metabolite, styrene oxide, is conjugated to glutathione and may bind covalently to hepatocyte macromolecules in conditions of glutathione depletion (Vainio & Hietanen, 1987).
    1) In rats, styrene administration produces dose-dependent decreases in hepatic glutathione levels, decreased activity of hepatic glutathione-S-transferase activity, and increased hepatic lipid peroxidation (Srivastava et al, 1983).

Physicochemical

Physical Characteristics

    A) At room temperature, styrene is a colorless to light yellow, or a clear, colorless to dark-colored, oily liquid. At 15 degrees C and 1 atm styrene is a liquid and is described as viscous, solventy and rubbery. At low concentrations styrene has a sweet, floral or balsamic-like odor; it can be penetrating, sharp, pungent, and disagreeable in high concentrations. It is very refractive and lighter than water. Styrene can spontaneously polymerize or it can react when exposed to heat; light and air, or a peroxide catalyst can cause it to polymerize, oxidize, and form explosive peroxides. It will form a slick on the water's surface and slowly dissolve (AAR, 2000; (ACGIH, 1991; Ashford, 1994; Bingham et al, 2001; Budavari, 2000; CHRIS , 2002; Harbison, 1998; HSDB , 2002; ILO , 1998; ITI, 1995; Lewis, 1997; Lewis, 2000; NFPA, 1997; NIOSH , 2002; OHM/TADS , 2002).
    1) If styrene is pure, it is sweet and pleasant, but it usually contains aldehydes which cause it to have a sharp, penetrating, sweet and unpleasant odor (Verschueren, 2001).

Molecular Weight

    A) 104.15

References

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