Remote second-hand tobacco exposure in flight attendants is associated with systemic but not pulmonary hypertension.
ABSTRACT Second-hand tobacco smoke has been associated with cardiopulmonary dysfunction. We sought to examine the residual effects of remote second-hand smoke exposure on resting and exercise cardiopulmonary hemodynamics. We hypothesized that remote secondhand smoke exposure results in persistent cardiopulmonary hemodynamic abnormalities.
Participants were non-smoking flight attendants who worked in airline cabins prior to the in-flight tobacco ban. Participants underwent clinical evaluations and completed smoke exposure questionnaires. We used Doppler echocardiography to measure pulmonary artery systolic pressure (PASP) and pulmonary vascular resistance (PVR) at rest and during supine bicycle ergometer exercise, using the validated formula TRV/VTIRVOT x 10 + 0.16, where VTIRVOT is the velocity time integral at the right ventricular outflow tract and TRV is the tricuspid regurgitation velocity. The group was divided into quartiles according to the degree of smoke exposure. Analysis of variance was used to determine the differences in hemodynamic outcomes.
Seventy-nine flight attendants were included in our analysis. Baseline characteristics among participants in each quartile of smoke exposure were similar except for history of systemic hypertension, which was more prevalent in the highest quartile. Peak exercise PASP rose to the same degree in all test groups (mean PASP 44 mm Hg, p = 0.25), and PVR increased by approximately 27% in all quartiles. There was no significant difference in pulmonary artery systolic pressure or pulmonary vascular resistance among quartiles of smoke exposure.
We found that remote heavy second-hand smoke exposure from in-flight tobacco is associated with systemic hypertension but does not have demonstrable pulmonary hemodynamic consequences.
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ABSTRACT: BackgroundThe aim of this study was to analyze the influence of active and passive smoking on cardiorespiratory responses in asymptomatic adults during a sub-maximal-exertion incremental test.MethodsThe participants (n = 43) were divided into three different groups: active smokers (n = 14; aged 36.5 ± 8 years), passive smokers (n = 14; aged 34.6 ± 11.9 years) and non-smokers (n = 15; aged 30 ± 8.1 years). They all answered the Test for Nicotine Dependence and underwent anthropometric evaluation, spirometry and ergospirometry according to the Bruce Treadmill Protocol.ResultsVO2max differed statistically between active and non-smokers groups (p < 0.001) and between non-smokers and passive group (p=0.022). However, there was no difference between the passive and active smokers groups (p=0.053). Negative and significant correlations occurred between VO2max and age (r = - 0.401, p = 0.044), percentage of body fat (r = - 0.429, p = 0.011), and waist circumference (WC) (r = - 0.382, p = 0.025).ConclusionVO2max was significantly higher in non-smokers compared to active smokers and passive smokers. However, the VO2max of passive smokers did not differ from active smokers.Multidisciplinary respiratory medicine 06/2014; 9(1):34. DOI:10.1186/2049-6958-9-34 · 0.15 Impact Factor
- Cardiovascular Effects of Inhaled Ultrafine and Nanosized Particles, 03/2011: pages 317 - 350; , ISBN: 9780470910917
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ABSTRACT: Carbon monoxide (CO) is suspected of playing a major role in cigarette smoke-induced cardiovascular diseases. Hypertension is one of the common chronic cardiovascular diseases that lead to heart attacks, strokes, chronic heart failure, and chronic renal failure. We aimed to investigate the immediate effects of passive smoking on blood pressure and heart rate during and after exposure in healthy females. In addition, we examined that whether carboxyhemoglobin (COHb) levels were correlated with heart rate and blood pressure measurements. Thirty healthy nonsmoker female volunteers (mean age: 26±5 years) were prospectively enrolled in the study. Systolic and diastolic blood pressure and heart rate were obtained at baseline, 5th, 10th, 15th, 30th minute of exposure and at 5th, 15th, and 30th minute after exposure. Blood samples for measuring COHb were taken at baseline and after spending 30 min in the smoking room from all volunteers. Difference between baseline and second measurements of COHb were described as ΔCOHb. Mean COHb level was significantly higher at the end of exposure when compared with baseline values (COHb 0.5±0.1 vs. 1.8±0.4%, P<0.05). Heart rate and systolic blood pressure measurements at 15th and 30th minute of exposure were higher than at baseline and 5th minute of exposure (88±3.2 and 90±3.7 vs. 76±3.9 and 78±4.5 beats/min, P<0.05; 135±1.1 and 136±4.0 vs. 113±5.7 and 115±3.5 mmHg, P<0.05). They elevated significantly at the same time interval. Diastolic blood pressure was significantly increased at 30th minute of exposure when compared with earlier measurements (90±5.1 vs. 74±2.2, 72±3.2 vs. 71±4.5 mmHg, P<0.05). Heart rate and systolic blood pressure decreased notably at 15th minute and returned to baseline values at 30th minute after exposure (80±1.2 and 76±3.2 vs. 88±4.5 beats/min, P<0.05; 120±4.4 and 115±1.9 vs. 135±2.2 mmHg, P<0.05). Diastolic blood pressure decreased significantly at 30th minute and returned to baseline values at 60th minute after exposure (75±3.6 and 70±2.5 vs. 89±4.3 mmHg, P<0.05). Heart rate and diastolic blood pressure measurements were moderately correlated and systolic blood pressure measurements were closely correlated with ΔCOHb values at the end of the exposure. Our results suggested that passive smoking has remarkable acute effect on heart rate and blood pressure in young healthy females. Beside this, we found that ΔCOHb level is closely correlated with systolic blood pressure and moderately correlated with heart rate and diastolic blood pressure measurements.Blood pressure monitoring 10/2010; 15(5):251-6. DOI:10.1097/MBP.0b013e32833e439f · 1.18 Impact Factor