Background: Exercise-induced bronchoconstriction (EIB) is defined as a transient and reversible narrowing of the airways shortly after or during (vigorous) exercise. Often, harmful environmental conditions such as air pollution [diesel exhaust particles (DEP)] or cold dry air contribute to the development of symptoms.

Objectives: In an EIB mouse model, we investigated the exacerbating effects of cold air and DEP on acute respiratory responses and lung inflammation.

Methods: Sixty-four Balb/c mice were oropharyngeally challenged 5 days per week for 3 weeks with saline or 0.1 mg/ml DEP. Afterwards, they were exposed to a submaximal exercise protocol or resting period. Half of the animals were exposed to 4°C, whereas the other half stayed at room temperature. All animals were sacrificed to determine lung function, lung inflammation and immune mediated response.

Results: Submaximal exercise at 4°C induced acute changed breathing pattern and airway hyperreactivity to increasing concentrations of methacholine (with both saline and DEP exposure). Only when DEP exposure was added to exercise at 4°C, small airway resistance was significantly increased, neutrophilic airway inflammation was induced and type 2 dendritic cells were more abundantly present in the lungs. Pro-inflammatory cytokines (TNF-?, MCP-1, KC and GM-CSF) in bronchoalveolar lavage were significantly increased and leakage of surfactant protein D to serum was significantly enhanced in DEP-exposed animals, exercising at 4°C. In DEP-exposed mice, macrophages were more loaded with DEP at 4°C, exercise or both.

Conclusion: Combined exposure to cold air, DEP and exercise enhances respiratory adverse effects in an EIB mouse model.