CLINICAL STUDY
Cardiovascular effects of carbon monoxide and cigarette smoking
Shoshana Zevin, MD*,
Sandra Saunders, MD ,
Steven G. Gourlay, MBBS, PhD  ,
Peyton Jacob, III, PhD and
Neal L. Benowitz, MD*,
* Department of Internal Medicine, Shaare Zedek Medical Center, Jerusalem, Israel
Division of Clinical Pharmacology and Experimental Therapeutics, Medical Service, San Francisco General Hospital Medical Center, and the Departments of Medicine, Psychiatry and Biopharmaceutical Sciences, University of California, San Francisco, San Francisco, California, USA
Pharmacological Sciences, Genentech Inc., South San Francisco, California, USA
Manuscript received October 31, 2000;
revised manuscript received June 26, 2001,
accepted August 10, 2001.
* Reprint requests and correspondence: Dr. Neal L. Benowitz, Chief, Division of Clinical Pharmacology and Experimental Therapeutics, University of California, San Francisco, Box 1220, San Francisco, California 94143-1220 USA
nbeno{at}itsa.ucsf.edu
OBJECTIVES
This study was designed to compare the effects of inhaled carbon monoxide (CO), administered to achieve concentrations similar to those found in cigarette smoking, with the effects of cigarette smoking and air inhalation on heart rate and blood pressure, catecholamine release, platelet activation and C-reactive protein (CRP), a marker of inflammation.
BACKGROUND
Carbon monoxide may contribute to smoking-induced cardiovascular disease. Exposure to environmental CO has been associated with increased cardiovascular morbidity and mortality. Animal and in vitro studies suggest that CO may contribute to atherosclerosis and endothelial injury. There is conflicting evidence about the hemodynamic consequences of exposure to CO and its role in platelet activation.
METHODS
In a single-blind, crossover design, 12 healthy smokers inhaled CO at 1,200 ppm to 1,500 ppm to simulate CO intake from cigarette smoking, inhaled air on a similar schedule and smoked 20 cigarettes per day, each for seven days. Mean carboxyhemoglobin was 5 ± 1% on CO treatment, 6 ± 1% while smoking and 0.4 ± 0.2% on air inhalations.
RESULTS
There was no difference in blood pressure between the treatments. Mean heart rate was higher during cigarette smoking compared with CO and air inhalations (75 beats/min vs. 66 beats/min; p < 0.05). Plasma levels of platelet factor 4 and CRP and urine epinephrine and norepinephrine were higher while smoking, with no effect of CO compared with air.
CONCLUSIONS
Carbon monoxide administered under conditions similar to those of cigarette smoking had no significant effect on blood pressure, heart rate, plasma catecholamines, platelet aggregation or CRP. The short-term chronotropic effect, adrenergic-activating, platelet-activating and CRP-increasing effects of smoking in healthy smokers are probably due to components of cigarette smoke other than CO.
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Abbreviations and Acronyms
| | AUC | = area under the concentration or response-time curve | | BTG | = beta thromboglobulin | | CO | = carbon monoxide | | COHb | = carboxyhemoglobin | | CRP | = C-reactive protein | | ELISA | = enzyme-linked immunosorbent assay | | NPD | = nitrogen phosphorus detection | | PF4 | = platelet factor 4 |
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