Abstract
Aims Previous epidemiological investigations of the relationship between smoking and acute mountain sickness (AMS) risk yielded inconsistent findings. Therefore, a meta-analysis of observational studies was performed to determine whether smoking is related to the development of AMS. Methods Searches were performed on PubMed, Scopus, Embase, and Web of Science for relevant studies that were published before November 2016 reporting smoking prevalence and AMS. Two evaluators independently selected studies, extracted data, and assessed study quality. The pooled relative risks (RRs) and 95% confidence intervals (CIs) were obtained using random-effects models. Subgroup analyses were performed according to the type of participant, altitude, and study design. Results A total of 11 observational studies involving 7,106 participants, 2,408 of which had AMS, were eligible for inclusion in this meta-analysis. The summary RR for AMS comparing smokers to nonsmokers was 1.02 (95% CI: 0.83 to 1.26). Specific analyses for altitude, type of participant, and study design yielded similar results. There was significant heterogeneity for all studies (Q = 37.43; P < 0.001; I2 = 73%, 95% CI: 51% to 85%). No publication bias was observed (Egger's test: P = 0.548, Begg's test: P = 0.418). Conclusions The meta-analysis indicates that no difference was found in AMS risk with regard to smoking status.
Highlights
Climbers, trekkers, workers, and tourists who travel to highaltitude destinations are at risk of altitude illness due to hypoxia
Smoking causes an increase in carboxyhaemoglobin levels, resulting in a leftward shift of the oxyhaemoglobin dissociation curve when carbon monoxide is present in the blood
We conducted subanalyses by epidemiological study design, altitude [11], type of participant characteristics, and Newcastle-Ottawa Scale (NOS) (≥6 versus
Summary
Trekkers, workers, and tourists who travel to highaltitude destinations are at risk of altitude illness due to hypoxia. Smoking tobacco increases the carbon monoxide (CO) concentrations in the airways and the blood. Increased levels of carbon monoxide in the bloodstream have a negative ionotropic effect [10] and can limit the amount of oxygen transported in muscular capillaries, which adversely affects skeletal muscle performance. Smoking causes an increase in carboxyhaemoglobin levels, resulting in a leftward shift of the oxyhaemoglobin dissociation curve when carbon monoxide is present in the blood. Smokers exhibit a lower capacity to transport oxygen because of increased carboxyhaemoglobin and difficulties in breathing control and alterations in vascular tone, neurotransmission, and cellular metabolism due to carbon monoxide and lower vasodilatation in hypoxic environments than nonsmokers [11]. A metaanalysis of observational studies (cross-sectional studies, case-control or cohort studies) was performed to determine whether smoking was related to the development of AMS
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