What we know
The model runs: susceptibility plus an initiating event or exposure produces an altered high-gain environmental responsiveness, after which previously tolerated inputs produce disproportionate physiological responses. Different initiators — pesticide, solvent, mold, infection, injury — may lead into the same state; different inputs — chemicals, and possibly others — may then trigger it.
The systems that may interact: sensory nerves and TRPA1/TRPV1; central sensory processing; autonomic regulation; small-fiber biology; immune, inflammatory and mast-cell signaling; oxidative and metabolic regulation; genetics and epigenetics; and, after illness exists, learned or conditioned amplification. The order is unknown. Conditioning is not placed at the start of the chain unless evidence puts it there.