Table 1.

Aspects of mechanisms and pathophysiology

Nonoccupational Asthma	Occupational Asthma
	Immunological OA	Irritant-induced OA
For some agents/some patients an IgE-dependent response, for others unknown initiating mechanisms.	IgE-dependent response for high-molecular-weight agents; variable or unknown for the rest of agents.	Acute phase: “toxic reaction”; chronic phase: inflammation and remodeling.
Th2 lymphocyte mechanism with or without participation of IgE.	Th2 lymphocyte mechanism with or without participation of IgE (low-molecular weight agents).
Th17 activation associated with neutrophilic response.	Th17 activation associated with neutrophilic response.	Oxidative stress, role of neurogenic inflammation (substance P).
Inflammation and remodeling.	Inflammation and remodeling.	Mainly remodeling.
Genes related to atopy and antigenic recognition.	Genetic variants in antioxidant, catenin-control genes, genes related to Th2 and remodeling responses. Genes related to Th2 response. Genes related to remodeling. For diisocyanates, hypermethylation of IFN-γ gene promoter.
Genes related to the epithelium.
Genes related to remodeling.
Non-IgE–related mechanisms are unclear, and hypothetically some may be similar to those of low-molecular-weight sensitizer–induced OA.	For low-molecular-weight agents, some may induce IgE-mediated responses. Others may resemble a delayed hypersensitivity response similar to contact dermatitis (e.g., persulfates).	Role of alarmins. Stimulation of epithelium with production of chemoattractant substances, toll-like receptors. General airway sensory hyperreactivity.

Definition of abbreviations: OA = occupational asthma.

Similarities are printed in bold. Features that differ or have only been only evaluated for one condition are not bold.