Tar is a complex residue generated when tobacco burns, consisting of solid and liquid particles suspended in the smoke aerosol. It is not a substance added to cigarettes but is created through the combustion process. This residue is formally defined as the total particulate matter of the smoke minus the weight of water and nicotine. Its presence is quantified to gauge potential exposure from smoking and understand its physical impact on the body.
Quantifying Tar Exposure in a Pack
The tar content cited for commercially sold cigarettes is an estimate based on standardized machine testing. Most commercially available cigarettes are reported to yield between 7 and 15 milligrams (mg) of tar per cigarette when tested. This reported number allows for calculating the potential exposure from a full pack of twenty cigarettes.
If a single cigarette yields 15 mg of tar, a 20-cigarette pack would contain 300 mg of deposited tar, roughly the weight of a small paperclip. Brands with lower reported yields, such as 6 mg, still contribute 120 mg of tar per pack. This range of 120 to 300 mg per pack represents the calculated weight of residue deposited into the lungs over the course of smoking one package.
Standardized Measurement Versus Real-World Intake
The tar yields displayed on packaging are the result of machine-smoking protocols, such as those established by the International Organization for Standardization (ISO) or the former Federal Trade Commission (FTC) method. These regulatory tests use a smoking machine calibrated to take a fixed-volume puff, usually 35 milliliters, over two seconds, once every minute. The purpose of these tests is to provide a consistent, comparative measure between different cigarette brands, not an accurate assessment of human exposure.
The limitation of these standardized methods is that human smokers do not smoke like a machine. People tend to adjust their smoking behavior to compensate for lower nicotine delivery in “low-tar” or “light” cigarettes, a phenomenon known as compensatory smoking. This adjustment includes taking deeper, more frequent, or longer puffs, and often involves instinctively blocking the ventilation holes present on the filter. These behavioral changes cause a smoker to inhale significantly more tar and nicotine than the machine test indicates, meaning the reported numbers underestimate the true intake.
The machine-generated numbers are therefore more a regulatory tool for comparison than a reliable measure of actual exposure. Recognizing the misleading nature of these figures, organizations like the European Union have stated that tar ratings are not an appropriate metric for consumers to identify a product’s level of harm. More intensive machine-smoking regimens, which account for the blocking of filter ventilation and harder puffing, have been developed by some governments to provide a less misleading estimate of the actual yield.
The Physical Impact of Tar on the Lungs
Once the tar residue is inhaled, it travels into the airways and interacts with the respiratory system. The residue coats the hair-like structures called cilia that line the bronchial tubes. The cilia’s normal function is to beat rhythmically, sweeping mucus, debris, and foreign particles out of the lungs in a process known as mucociliary clearance.
The tar paralyzes and eventually destroys these cilia, impairing the lungs’ natural cleaning system. When the cilia cannot move, mucus and trapped particles accumulate in the airways, leading to the characteristic “smoker’s cough” as the body attempts to clear the buildup. This interference contributes to chronic conditions like bronchitis, where the airways become inflamed, and emphysema, which involves the destruction of the lungs’ air sacs.
Tar is not a single chemical but a complex mixture containing thousands of chemical compounds, including many known carcinogens, such as polycyclic aromatic hydrocarbons. When the tar residue settles and becomes trapped in the lung tissue, it exposes the cells to these toxic substances. This prolonged exposure creates the conditions that contribute to long-term cellular damage and the development of smoking-related diseases.