A factory making polyurethane foam uses toluene diisocyanate (TDI). Several workers develop asthma-like symptoms that worsen on work days and improve on weekends. The mechanism of TDI-induced occupational asthma DIFFERS from classical allergic asthma because:

• A TDI asthma is irreversible unlike classical atopic asthma
• B TDI acts purely via mast cell degranulation without T-cell involvement
• C TDI asthma does not show bronchial hyperresponsiveness on methacholine challenge
• D TDI can cause both IgE-mediated sensitisation and non-immunological pharmacological bronchoconstriction ✓

Explanation

TDI (toluene diisocyanate) is the most common cause of occupational asthma. Unlike classical allergic (atopic) asthma which is purely IgE-mediated, TDI causes asthma through both immunological (IgE-mediated sensitisation in ~5–10% of workers after latency period) and non-immunological mechanisms (direct pharmacological irritant effects and possible IgG-mediated mechanisms). Both T-cell and non-T-cell pathways are implicated. TDI asthma can become irreversible with continued exposure, but is potentially reversible if exposure ceases early — it is not always irreversible.

Reference: Park's Textbook of Preventive and Social Medicine, 27th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.