Table 1.
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.