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ImportanceDrunk driving is a major cause of death in North America, yet physicians rarely counsel patients on the risks of drinking and driving.ObjectiveTo test whether the risks of a life-threatening alcohol-related traffic crash were further accentuated by adverse weather.DesignDouble matched case–control analysis of hospitalised patients.SettingCanada’s largest trauma centre between 1 January 1995 and 1 January 2015.ParticipantsPatients hospitalised due to a life-threatening alcohol-related traffic crash.ExposureRelative risk of a crash associated with adverse weather estimated by evaluating the weather at the place and time of the crash (cases) compared with the weather at the same place and time a week earlier and a week later (controls).ResultsA total of 2088 patients were included, of whom the majority were drivers injured at night. Adverse weather prevailed among 312 alcohol-related crashes and was significantly more frequent compared with control circumstances. The relative risk of a life-threatening alcohol-related traffic crash was 19% higher during adverse weather compared with normal weather (95% CI: 5 to 35, p=0.006). The absolute increase in risk amounted to 43 additional crashes, extended to diverse groups of patients, applied during night-time and daytime, contributed to about 793 additional patient-days in hospital and was distinct from the risks for drivers who were negative for alcohol.ConclusionsAdverse weather was associated with an increased risk of a life-threatening alcohol-related traffic crash. An awareness of this risk might inform warnings to patients about traffic safety and counselling alternatives to drinking and driving.

Chronic obstructive pulmonary disease (COPD) is characterized by fixed airflow limitation and progressive decline of lung function and punctuated by occasional exacerbations. The disease pathogenesis may involve activation of the bone marrow stimulating mobilization and lung-homing of progenitor cells. We investigated the hypothesis that lower circulating numbers of vascular endothelial progenitor cells (VEPCs) are a consequence of increased lung-sequestration in COPD. Nonatopic, current or ex-smokers with diagnosed COPD and nonatopic, nonsmoking normal controls were enrolled. Blood and induced sputum extracted primitive hemopoietic progenitors (HPCs) and VEPC were enumerated by flow cytometry. Migration and adhesive responses to fibronectin were assessed. In sputum, VEPC numbers were significantly greater in COPD compared to normal controls. In blood, VEPCs were significantly lower in COPD versus normal controls. There were no differences in HPC levels between the two groups in either compartment. Functionally, there was a greater migrational responsiveness of progenitors from COPD subjects to stromal cell-derived factor-1alpha (SDF-1α) compared to normal controls. This was associated with greater numbers of CXCR4+progenitors in sputum from COPD. Increased migrational responsiveness of progenitor cells may promote lung-homing of VEPC in COPD which may disrupt maintenance and repair of the airways and contribute to COPD disease pathogenesis.