Table 2

Non-allergen environmental asthma triggers, inflammatory markers, and clinical effects

Non-allergen environmental triggers
Tobacco↑/↓/↔ IL-4
↑/↓ IL-5
↑/↓ IL-6
↑/↔ TNF-α
↑/↓/↔ interferon (IFN)-γ
Varied and inconsistent data pattern of inflammatory response to tobacco smoke. Adults, children, men and women may demonstrate different responses.
Clinically, tobacco smoke exposure is well associated with increased frequency and severity of symptoms in patients with asthma.
Particulate matter 2.5 (PM2.5)
  • Diesel exhaust particles (DEPs)

  • Wildfire smoke

↑eosinophil cationic protein (ECP)
↑eotaxin
↑IL-5
↑/↔ IL-6
↑IL-4
↑IL-8
↓IL-12
↓IFN γ
↑TNF-α
↑IL-8
↑VEGF
DEP exposure stimulates type 2 inflammation and eosinophilic infiltration, mucus production and airway hyper-responsiveness.
Neutrophilic recruitment via IL-8, mucus hypersecretion, increased airway hyper-responsiveness.
Volatile organic compounds (VOC)
  • Toluene

  • Formaldehyde

  • Limonene

Hapten formation and IgE-mediated response
↓neuroendopeptidase and excess tachykinins
↑IL-4
↑IFN-γ
Oxidative stress and neurogenic pathway-mediated bronchospasm. Neutrophilic inflammation. Eosinophilic inflammation via recognition of hapten as an antigen and IL-4.
Associated with decline in spirometry and peak flow with increased dyspnea scores.