Objective: We have previously shown that acute passive smoking impaired left ventricular diastolic function in healthy volunteers. The aim of this study was to determine whether length of exposure and/or ambient smoke concentration is the key determinant of this outcome.
Methods: We measured blood carboxyhemoglobin (COHb)and lactate level to investigate the acute effects of passive smoking on tissue oxygenation. A total of 90 healthy nonsmoker volunteers were prospectively enrolled into the study. Each of 30 subjects were exposed to carbon monoxide (CO) less than 5.0 ppm smoke in group A for 30 minutes, to CO 5 to 10 ppm smoke in group B for 30 minutes, and to CO less than 5.0 ppm smoke in group C for 60 minutes. Hemodynamic parameters were obtained, blood samples for measuring COHb and lactate levels were taken and echocardiographic examinations were performed at baseline and after exposure to passive smoking.
Results: Mean ± SD CO levels in groups A, B, and C were 4.2 ± 0.5 ppm, 9.2 ± 0.3 ppm, and 4.1 ± 0.8 ppm, respectively. There was no change in left ventricular systolic functions in all groups. Left ventricular diastolic functions were impaired in groups B and C, whereas no change was observed in group A. Carboxyhemoglobin and lactate levels increased after passive smoking in groups B and C. However, group B had significantly higher COHb and lactate levels compared to group C (P < 0.001).
Conclusions: Our results suggested that passive smoking at a certain dose in relation with length of exposure and ambient smoke concentration seems to cause relative left ventricular diastolic dysfunction.