Carbon monoxide (CO) is a colorless, odorless, and highly toxic gas that is a major component of cigarette smoke. This gas is produced through the incomplete combustion of tobacco during the burning process. Smoking is a significant source of CO exposure, introducing this dangerous chemical directly into the user’s bloodstream.
Quantifying Carbon Monoxide Exposure from Smoking
The amount of carbon monoxide (CO) delivered by a single cigarette, measured in the mainstream smoke, typically ranges from 5 to 20 milligrams (mg). This measurement is derived from standardized machine-smoking protocols used to compare different brands. However, these testing conditions are artificial and do not accurately reflect the actual exposure a human smoker receives.
The CO yield can vary significantly between different cigarette brands. The concentration of CO in cigarette smoke is extremely high, estimated to be nearly 600 times greater than the U.S. national ambient air quality standard. Actual exposure is more accurately reflected by the resulting carboxyhemoglobin (COHb) concentration in the blood, which ranges from 3% to 15% in chronic smokers, compared to 1% to 3% in non-smokers.
A substantial amount of carbon monoxide is also released into the environment as sidestream smoke, which is generated from the smoldering tip of the cigarette between puffs. Sidestream smoke contains a significantly higher concentration of CO than mainstream smoke. Analyses show that the ratio of CO in sidestream smoke to mainstream smoke can be as high as 6.8:1, resulting in yields up to 35 mg per cigarette released into the surrounding air.
Factors Influencing CO Delivery
The actual amount of carbon monoxide absorbed by a smoker can differ significantly from the machine-measured values due to both cigarette design and individual smoking behavior. One of the most important design factors is filter ventilation, where tiny holes in the filter dilute the smoke stream with air. Cigarette manufacturers can also manipulate paper porosity to allow more CO to diffuse out of the cigarette before it is inhaled.
However, a smoker’s behavior often negates the effect of these design features in a phenomenon known as compensatory smoking. Smokers often instinctively take deeper, more frequent, or larger-volume puffs to maintain their desired nicotine intake. They may also unknowingly block the filter ventilation holes with their fingers or lips, which concentrates the smoke and increases the final CO delivery.
Other factors influencing the CO yield include the tobacco’s moisture content and the number of puffs taken from a single cigarette. The concentration of CO increases as the cigarette is smoked down to the filter, meaning taking a cigarette to a shorter butt length increases overall CO exposure. These behavioral adjustments often mean that a smoker of a “low-yield” cigarette may absorb the same or greater amount of CO as a smoker of a “full-flavor” brand.
Immediate and Long-Term Physiological Effects of CO
The danger of carbon monoxide stems from its extremely high affinity for hemoglobin, the protein in red blood cells that carries oxygen. CO binds to hemoglobin to form carboxyhemoglobin (HbCO) with an affinity 200 to 300 times greater than that of oxygen. This strong bond displaces oxygen, reducing the blood’s capacity to transport oxygen to vital organs and tissues.
The resulting oxygen deprivation, known as cellular hypoxia, causes immediate strain on the cardiovascular system, leading to symptoms like headache, weakness, and dizziness. Even low COHb levels (2% to 5%) diminish the capacity for physical exercise because the heart and muscles lack sufficient oxygen. This sustained oxygen debt in chronic smokers accelerates the development of serious, long-term health conditions.
The continuous presence of carboxyhemoglobin contributes to accelerated atherosclerosis, increasing the risk of heart disease, stroke, and myocardial infarction. Carbon monoxide also directly disrupts cellular metabolism by binding to oxygen-using proteins in the mitochondria.
For pregnant smokers, CO freely crosses the placenta. Because fetal blood naturally has lower oxygen tension, CO exposure results in severe fetal hypoxia. This oxygen starvation is a major contributing factor to adverse outcomes, including low birth weight, premature delivery, and potential developmental issues.