Introduction
This topic covers the occupational poisonings and sensitisation caused by the monomers (building blocks) of synthetic polymer resins and plastics. Workers in plastics manufacture, moulding, extrusion, lamination, adhesive and coating production, and in the fabrication of composites are the main groups at risk. The key exam points are which monomer causes which organ effect, how the monomer enters the body, how the picture differs between thermoplastics and thermosets, and how the case is handled as an occupational disease.
Classification and sources of exposure
Synthetic polymer resins are large molecules built from repeating monomer units. Thermoplastics soften on heating and can be remoulded and recycled, while thermosets cure irreversibly into a heat-resistant network. Exposure to the free monomer is greatest during polymerisation, moulding, curing and heating or machining of the material, and when the material is burned or overheated, which releases thermal decomposition products.
Pathogenesis
The usual route is inhalation of vapour or aerosol, with a smaller contribution from dermal absorption of liquid resins and monomers and accidental oral intake. Many monomers are lipophilic and distribute widely, and several are biotransformed by cytochrome P450 enzymes (CYP2E1 in particular) to reactive epoxides. These are detoxified by glutathione conjugation; when glutathione is depleted, the epoxides bind to proteins and DNA, causing cell injury and, for some monomers, carcinogenesis. Separately, some reactive compounds act as haptens and trigger immune sensitisation, after which even very low exposures can cause allergic reactions.
- Inhalation: the main route, depending on volatility, concentration and ventilation.
- Dermal: important for epoxy components, acrylates and isocyanate-containing liquids.
- Metabolic activation: epoxide formation, then glutathione conjugation or macromolecular binding.
- Immune sensitisation: isocyanates, formaldehyde, epoxy components and acrylates can cause asthma or allergic dermatitis that persists after exposure is reduced.