Styrene Toxicity

Styrene toxicity is injury from inhaling or absorbing styrene, an aromatic solvent and monomer. Acute exposure irritates mucosa and depresses the central nervous system. Chronic exposure causes neurobehavioural change, colour vision loss and hearing loss.

Exposure. Fibreglass reinforced plastic and boat building, polystyrene and resin manufacture, synthetic rubber, and lamination work. Skin absorption adds to inhaled dose.

Epidemiology. Workplace limits are about 20 ppm as an eight hour average in many regions, and lower in some. Effects on colour vision and reaction time are reported at low exposures, and hearing loss is greater when noise is also present.

Cancer. Evidence for lymphohaematopoietic cancer is inconclusive, and styrene is regarded as a probable human carcinogen.

Metabolism. Styrene is oxidised to styrene-7,8-oxide, a reactive epoxide, and excreted mainly as mandelic acid and phenylglyoxylic acid.

Pathophysiology.

Styrene is lipophilic and accumulates in the brain and fat. Styrene oxide forms DNA and protein adducts and causes oxidative stress.

Dopaminergic disturbance is proposed to underlie colour vision and psychomotor effects, and cochlear hair cell injury explains the ototoxicity.

• Acute: eye, nose and throat irritation, headache, nausea, dizziness, drowsiness and ataxia; unconsciousness at very high levels.
• Chronic: fatigue, poor concentration, memory complaint, mood change, slowed reaction time, and acquired blue yellow colour vision loss.
• Hearing loss and tinnitus, especially with noise.
• Skin: irritant dermatitis with defatting and fissuring.

Red flags.

• Reduced consciousness, respiratory depression or pulmonary oedema after high acute exposure.

• Exposure history with resin tasks, ventilation, skin contact and respiratory protection.
• Urinary mandelic plus phenylglyoxylic acid at the end of the shift: about 400 mg/g creatinine is the usual workplace reference. Blood or exhaled styrene reflects recent exposure.
• Colour vision testing with a desaturated panel test or hue test.
• Audiometry, neuropsychological testing and liver function when symptoms persist.

Differential diagnosis. Other solvent toxicity, inherited colour vision defect, noise induced hearing loss, depression, alcohol related impairment.

• Remove from exposure; improve ventilation, enclose processes and substitute low emission resins; respirators as an adjunct.
• Acute exposure: fresh air, oxygen, removal of contaminated clothing, skin washing, and eye irrigation with water for at least 15 minutes. No antidote exists; supportive care and observation for 6 hours after heavy exposure.
• Headache: paracetamol 1 g orally every 6 hours as needed, maximum 4 g in 24 hours (3 g if under 50 kg, chronic alcohol excess or liver disease), for the shortest period that controls pain. Reduce dose in hepatic impairment; extend dosing interval when eGFR is under 30.
• Hearing protection and annual audiometry; counsel on alcohol, which increases effects.
• Colour vision and cognitive deficits often improve over months after exposure ends, but may persist.

Monitoring. Colour vision, audiometry and urinary metabolites yearly in exposed workers.

Referral and escalation. Occupational physician for exposure review and fitness assessment; neurology or neuropsychology for persistent cognitive deficit; ophthalmology for colour vision loss; notification and compensation where required.