Acute effects of passive smoking on blood pressure and heart rate in healthy females

OBJECTS 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. METHODS 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. RESULTS 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. CONCLUSION 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.

[1]  Thomas Eissenberg,et al.  Waterpipe tobacco and cigarette smoking: direct comparison of toxicant exposure. , 2009, American journal of preventive medicine.

[2]  G. Carrier,et al.  Determination of carboxyhaemoglobin in humans following low-level exposures to carbon monoxide , 2009, Inhalation toxicology.

[3]  C. Tsioufis,et al.  Association of passive smoking with masked hypertension in clinically normotensive nonsmokers. , 2009, American journal of hypertension.

[4]  F. Hu,et al.  Passive Smoking and Risk of Peripheral Arterial Disease and Ischemic Stroke in Chinese Women Who Never Smoked , 2008, Circulation.

[5]  Aruni Bhatnagar,et al.  Environmental Risk Factors for Heart Disease , 2008, Reviews on Environmental Health.

[6]  P. van de Borne,et al.  Acute Effects of Passive Smoking on Peripheral Vascular Function , 2008, Hypertension.

[7]  R. Redberg,et al.  Remote second-hand tobacco exposure in flight attendants is associated with systemic but not pulmonary hypertension. , 2008, Cardiology journal.

[8]  A. Balbarini,et al.  The Effects of Acute Passive Smoke Exposure on Endothelium-Dependent Brachial Artery Dilation in Healthy Individuals , 2007, Angiology.

[9]  O. Akpınar,et al.  Acute effects of smoking on right ventricular function. A tissue Doppler imaging study on healthy subjects. , 2007, Swiss medical weekly.

[10]  K. Node,et al.  Short-term passive smoking causes endothelial dysfunction via oxidative stress in nonsmokers. , 2006, Canadian journal of physiology and pharmacology.

[11]  S. Andreas,et al.  Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm. , 2006, European heart journal.

[12]  F. Verheugt.  [Passive smoking and the risk of coronary heart disease]. , 2004, Nederlands tijdschrift voor geneeskunde.

[13]  P. Joshi,et al.  Effect of passive smoking on endothelial function in: healthy adults. , 2004, The Journal of the Association of Physicians of India.

[14]  Azra Mahmud,et al.  Effects of passive smoking on blood pressure and aortic pressure waveform in healthy young adults--influence of gender. , 2003, British journal of clinical pharmacology.

[15]  P. Jacob,et al.  Cardiovascular effects of carbon monoxide and cigarette smoking. , 2001, Journal of the American College of Cardiology.

[16]  M. Yoshiyama,et al.  Acute effects of passive smoking on the coronary circulation in healthy young adults. , 2001, JAMA.

[17]  P. Whelton,et al.  Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies. , 1999, The New England journal of medicine.

[18]  M. Winniford,et al.  Cigarette Smoking Increases Sympathetic Outflow in Humans , 1998 .

[19]  C. Vlachopoulos,et al.  Unfavorable Effects of Passive Smoking on Aortic Function in Men , 1998, Annals of Internal Medicine.

[20]  K. Kugiyama,et al.  Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers. , 1996, Journal of the American College of Cardiology.

[21]  W. Kannel.  Blood pressure as a cardiovascular risk factor: prevention and treatment. , 1996, JAMA.

[22]  Sydney B. Miller,et al.  Estradiol, progesterone and cardiovascular response to stress , 1996, Psychoneuroendocrinology.

[23]  J. Deanfield,et al.  Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. , 1996, The New England journal of medicine.

[24]  C. Vlachopoulos,et al.  Effect of vasa vasorum flow on structure and function of the aorta in experimental animals. , 1995, Circulation.

[25]  K. Usadel,et al.  Elevated endothelin-1 levels after cigarette smoking. , 1994, Metabolism: clinical and experimental.

[26]  D. Penney,et al.  Is there a connection between carbon monoxide exposure and hypertension? , 1991, Environmental health perspectives.

[27]  N. Benowitz.  Drug therapy. Pharmacologic aspects of cigarette smoking and nicotine addiction. , 1988, The New England journal of medicine.

[28]  M. Winniford,et al.  Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone. , 1986, Circulation.

[29]  C. Hignite,et al.  Cigarette smoking--induced enhancement of platelet function: lack of prevention by aspirin in men with coronary artery disease. , 1985, The Journal of laboratory and clinical medicine.

[30]  L. Klein.  Cigarette smoking, atherosclerosis and the coronary hemodynamic response: a unifying hypothesis. , 1984, Journal of the American College of Cardiology.

[31]  J. Nadler,et al.  CIGARETTE SMOKING INHIBITS PROSTACYCLIN FORMATION , 1983, The Lancet.

[32]  D. Horrobin,et al.  The mechanism of coronary artery spasm: roles of oxygen, prostaglandins, sex hormones and smoking. , 1979, Medical hypotheses.

[33]  P. Cryer,et al.  Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events. , 1976, The New England journal of medicine.

[34]  S. Ayres,et al.  MYOCARDIAL AND SYSTEMIC RESPONSES TO CARBOXYHEMOGLOBIN * , 1970, Annals of the New York Academy of Sciences.

[35]  S. Ayres,et al.  Systemic and myocardial hemodynamic responses to relatively small concentrations of carboxyhemoglobin (COHB). , 1969, Archives of environmental health.