- Adhesive industry
- Automotive industry
- Automotive indystry
- Chemical industry
- Foundry worker
- Joiner, Mechanic
- Plastics industry
1,3 bis cyclohexane pre-polymer, BIC, Diphenylmethane diisocyanate, HDI, Hexamethylene diisocyanate, IPDI, Isocyanates, Isophorone diisocyanate , MDI, Naphtalene diisocyanate, NDI, Polyurethane, TDI, TGIC, Toluene diisocyanate, Triglycylisocyanurate.
Incidence: Approximately 5% of exposed subjects.
Isocyanates are direct irritants to the respiratory tract. Their toxicity can result in fatality.
Atopy does not play a predisposing role.
Immunological mechanisms involving the anti-bodies IgE and IgG have been demonstrated. Other mechanisms involving bronchial beta-receptors or the inhibition of cholinesterase have also been suggested.
Bronchial response can be either immediate or delayed. Sensitized subjects may be intolerant to cruciferae. In the case of painters, sensitization results from mixtures of products (eczema may occur).
Sensitization: plastics (TDI and MDI), car paints (HDI and IPDI), polyurethanes (TDI), casting/melts and glues (MDI). Exposure; purely via the airways, may induce cutaneous sensitisation even in the absence of any contact with the skin. Isocyanate induced asthma (particularly TDI) is characterized by lymphocyte activation and secretion of pro-inflammatory cytokines. After exposure has ceased, a "remodelling" of the airways persists. The realisation of the problems associated with TDI, MDI and HDI, etc has led the industries to use oligomers with high molecular weights (BIC) with the aims of reducing the risks of sensitization. The norms for tolerable levels of these monomers are not sufficient to prevent work-related asthma. No norms have been fixed for polyisocyanates or polymer precursors. The response to TDI is regulated by the MHC class II loci DQA1 and DQB1. Fire retardants contain polyurethanes. A Swedish study performed in 2001 demonstrated that above 300 °C these polyurethanes degrade with the liberation of isocyanate-containing compounds (TDIs and monomers of TDI).
Asthma develops fairly quickly, however it is marked by its severity and persistence once established. Improvement is only observed several weeks after exposure to the risk has ceased. Asthma and hypersensitive lung disorders have been reported following exposure to polymer. As well as the classical clinical symptoms, myalgia, arthralgia and nausea have been reported (in approximativly 26% of cases). Toxic reactions can occur (0.5 ppm). One fatal case at the workplace has been reported following exposure to MDI in a pre-sensitized subject. Bronchial hyperreactivity often persists even after exposure has ceased. TGIC often results in contact skin dermatitis.
Skin prick test: 5 mg/ml TDI-HSA, 3.4 mg/ml TM-HSA (Na salt of TMA 1/200); these tests are no longer in widespread use. Immunological dosage: RAST/CAP RAST TDI, MDI and HDI. Bronchial provocation test (in Hospital).