Biology Insights

Cotinine Level Chart: What Do Your Results Mean?

Understand your cotinine test results. Learn what different levels indicate about nicotine exposure and how various factors influence them.

By Lucie J. Kucerova

Cotinine is a byproduct your body produces when it breaks down nicotine, and its level in blood, urine, or saliva is the standard way researchers and clinicians gauge how much tobacco smoke or nicotine you have been exposed to. While older guidelines set the dividing line between smokers and nonsmokers at around 14 ng/mL in serum, more recent large-scale analyses have pushed that cutoff much lower, to roughly 3 ng/mL, which means a “chart” of cotinine values is not quite the fixed reference table many people expect. What your results actually mean depends on the sample type, your individual metabolism, and why the test was ordered in the first place.

Why Cotinine Instead of Nicotine

Nicotine itself disappears from your bloodstream quickly, with a half-life of about two hours. Your liver converts most of it into cotinine using a set of enzymes, the most important being one called CYP2A6. Cotinine sticks around much longer, averaging a half-life of about 16 hours in regular smokers and sometimes longer in nonsmokers exposed to secondhand smoke. That longer window makes cotinine far more practical as a marker: a single blood draw or urine sample can capture your exposure over the past few days rather than just the last couple of hours.

The Standard Cutoff Values and Why They Keep Shifting

For decades, most studies used a serum cotinine cutoff of 14 or 15 ng/mL to separate smokers from nonsmokers. A review of fourteen studies found that eight of them landed on that range, with sensitivity and specificity both exceeding 90 percent in most cases. That cutoff made sense when cigarette smoking was extremely common and environmental exposure was pervasive, because a higher threshold filtered out the background noise of secondhand smoke.

As smoking rates have dropped, so has the average person’s passive exposure, which means a lower cutoff now does a better job of catching light or occasional smokers who would slip through under the old threshold. An analysis of U.S. national survey data from 1999 to 2004 proposed new cutoffs of about 3 ng/mL for both adults and adolescents, with sensitivity above 86 percent and specificity above 93 percent at those levels. The old 14 ng/mL line, the study concluded, overestimates the number of nonsmokers compared to the proposed 3 ng/mL threshold.

A separate evaluation in a Korean population arrived at a somewhat higher optimal cutoff of about 13 ng/mL for distinguishing current smokers from nonsmokers, with sensitivity near 96 percent and specificity around 94 percent. The fact that different populations land on different numbers is not an error. It reflects real differences in smoking patterns, environmental exposure levels, and nicotine metabolism across groups.

How to Read Results by Sample Type

Your result’s meaning depends heavily on what was collected. Blood (serum or plasma), urine, saliva, and hair each measure cotinine differently, and the numbers are not directly interchangeable.

Why Two People With the Same Smoking Habit Can Get Different Numbers

Your cotinine level is not just a readout of how much nicotine went in. It is filtered through your body’s individual ability to break nicotine down, which varies more than most people realize.

The biggest driver of variation is genetics, specifically the CYP2A6 enzyme. People who carry certain gene variants that reduce CYP2A6 activity clear nicotine and cotinine more slowly, which means a given amount of smoking produces a higher cotinine reading in their blood. Conversely, people with faster-than-average CYP2A6 activity can smoke the same amount and show lower cotinine levels. One study found that slower metabolizers had cotinine levels that overestimate their actual tobacco exposure compared to faster metabolizers who smoke identically.

These genetic differences are not randomly distributed. CYP2A6 variants that slow nicotine metabolism are more common in certain populations, and this has measurable consequences. Data from the Third National Health and Nutrition Examination Survey found that Black smokers had substantially higher serum cotinine levels than white or Mexican American smokers at every level of cigarette consumption, with differences ranging from about 22 to 95 ng/mL higher depending on smoking intensity, even after controlling for the number of cigarettes smoked. A separate study confirmed the same pattern: the median cotinine level in Black smokers was 221 ng/mL compared to 170 ng/mL in white smokers, despite the white participants actually having higher estimated daily nicotine intake.

This means that applying a single universal cutoff across all populations creates systematic errors. The U.S. national survey analysis noted that optimal cutoffs differed by race and ethnicity, ranging from about 0.84 ng/mL for Mexican Americans to about 5.92 ng/mL for non-Hispanic Black adults. Most clinical labs and insurance companies do not use race-specific cutoffs, so the published chart is an approximation at best.

Menthol, Pregnancy, and Other Metabolism Shifters

Genetics is the largest source of variation, but it is not the only one. Smoking menthol cigarettes slows the breakdown of nicotine, which results in higher cotinine levels per cigarette compared to non-menthol brands. A study comparing the same smokers on menthol versus non-menthol cigarettes found that menthol use reduced nicotine clearance by about 10 percent, through inhibition of both the oxidative pathway to cotinine and another elimination pathway. Lab work has confirmed the mechanism: menthol directly inhibits the CYP2A6 enzyme responsible for converting nicotine to cotinine.

Pregnancy pushes the metabolism in the opposite direction. Cotinine clearance roughly doubles during pregnancy, and its half-life drops from about 17 hours in non-pregnant women to about 9 hours. The practical consequence is that a pregnant woman who smokes the same number of cigarettes as a non-pregnant woman will show a lower cotinine level, which can lead to underestimation of her actual smoking if a standard chart is used.

Kidney function matters too. People with kidney failure eliminate cotinine more slowly than people with normal kidney function, which could produce higher readings for the same level of smoking. That said, research in people with chronic kidney disease found that urinary cotinine still correlated well with other measures of smoking exposure and was only minimally influenced by the degree of kidney impairment, so it remains a useful marker even in that population.

Secondhand Smoke and the Gray Zone

One of the most common reasons people are confused by a positive cotinine result is that they do not smoke themselves. Secondhand smoke exposure absolutely raises cotinine levels, and in heavy-exposure situations those levels can climb high enough to blur the line between passive and active smoking. Plasma cotinine in non-smokers with heavy secondhand exposure can reach up to about 25 ng/mL, which overlaps with the levels seen in light or occasional smokers. If you live with a heavy smoker or work in a poorly ventilated environment where smoking occurs, your cotinine result could be higher than you expect.

Even so-called thirdhand smoke, the residue left on surfaces and dust after smoking has stopped, appears to produce detectable cotinine in non-smokers. A study of non-smoking adults found that people exposed to thirdhand smoke at home had salivary cotinine levels about twice as high as those in unexposed homes, and people exposed to both secondhand and thirdhand smoke showed levels roughly triple those of the unexposed group.

E-Cigarettes and Nicotine Replacement Products

Cotinine tests do not distinguish between nicotine sources. If you vape, use nicotine patches, chew nicotine gum, or use snus, your cotinine level will reflect that nicotine intake. A review of e-cigarette studies found that cotinine levels after vaping are similar to those seen with traditional cigarettes. A separate study measuring saliva cotinine in e-cigarette users confirmed the same finding, noting that levels were comparable to those previously observed in smokers and higher than levels typically seen in people using nicotine replacement therapy like patches or gum.

This matters for anyone being tested for insurance or employment purposes. A cotinine test will flag a vaper or patch user the same way it flags a cigarette smoker. Where the difference shows up is in other biomarkers: e-cigarette-only users and nicotine-replacement-only users had much lower levels of cancer-causing compounds and toxic volatile chemicals than people who smoked cigarettes, even though their nicotine and cotinine levels were comparable. Cotinine tells you about nicotine, not about the harm profile of the delivery method.

Can Food Cause a Positive Result

Technically, yes, but the levels are tiny. Nicotine occurs naturally in plants from the nightshade family, including tomatoes, potatoes, and eggplant. One analysis found average nicotine concentrations of about 7 ng per gram in tomatoes and 15 ng per gram in potatoes, and estimated that normal dietary consumption of these foods could produce urinary cotinine levels somewhere between 0.6 and 6.2 ng/mL. A follow-up study confirmed that while nicotine is present in fresh nightshade vegetables at trace levels, cotinine itself was not detectable in those foods, meaning any cotinine that shows up in your body from dietary sources comes entirely from your own metabolism of the dietary nicotine.

In practice, this is unlikely to cause you problems on a typical screening test. The upper end of the dietary estimate, around 6 ng/mL in urine, is well below the 200 ng/mL cutoff used by most standard immunoassay test strips. However, it could be enough to produce a faint signal at the lower 10 ng/mL cutoff, and it could theoretically push a serum cotinine reading into the ambiguous zone near the 3 ng/mL threshold that some researchers now advocate. If you are a non-smoker with a very low positive result and eat a lot of potatoes or tomatoes, diet is worth mentioning to whoever ordered the test.

How Long Cotinine Stays Detectable

In regular smokers, cotinine’s half-life in blood and urine averages roughly 16 hours, meaning the concentration drops by half every 16 hours after the last cigarette. After about four to five half-lives, levels drop below most detection thresholds, which puts the practical detection window for blood and urine at roughly three to four days after the last exposure for a daily smoker. Non-smokers exposed to secondhand smoke seem to clear cotinine more slowly, with one study finding a mean half-life of about 27 hours in never-smokers exposed to environmental tobacco smoke, compared to about 17 hours in smokers.

Newborns process cotinine differently as well. In neonates, cotinine’s elimination half-life averaged about 16 hours based on blood data and about 23 hours based on urine data, comparable to the adult range or slightly longer. Hair testing, as mentioned earlier, operates on a completely different timescale, potentially capturing months of cumulative exposure.

Insurance and Employment Screening

If your cotinine test was ordered by a life insurance company, the stakes are different than in a clinical setting. Insurance underwriters commonly use a urine cotinine cutoff of 25 ng/mL or lower to classify applicants as nonsmokers. A positive result above that line typically means you will be offered smoker premium rates, which assume a mortality risk more than 25 percent higher than for nonsmokers. This is one area where e-cigarette users and nicotine replacement therapy users often get caught off guard, since their cotinine levels will trigger the same classification as a pack-a-day smoker even though their health risk profile is different.

Employment screening is less standardized. Some employers test for cotinine as part of broader drug panels, particularly in healthcare and fire service settings. The cutoff levels and consequences vary by employer, and there is no single federal standard governing tobacco testing in the workplace (unlike drug testing, which has regulated cutoffs for federal employees). If your employer is testing you, the cutoff they use and what happens if you test positive should be spelled out in the company policy you signed.

Prenatal and Newborn Testing

Cotinine testing in pregnant women and newborns serves a different purpose than adult screening. The goal is usually to assess how much tobacco smoke a fetus was exposed to during development, since maternal smoking is linked to a range of complications. Cord blood cotinine levels are sometimes measured immediately after delivery, with one commonly used classification scheme sorting newborns into categories: below 1 ng/mL as unexposed, 1 to 14 ng/mL as low exposure, 14 to 50 ng/mL as medium exposure, and above 50 ng/mL as high exposure.

Umbilical cord tissue and meconium (the first stool a newborn passes) can also be tested for nicotine metabolites. Either specimen can detect third-trimester exposure to nicotine, though the specific patterns of metabolites differ between the two sample types. Meconium cotinine has also been studied as a predictor of early respiratory problems in infancy. The accelerated cotinine metabolism during pregnancy described earlier means that a mother’s blood level at delivery may understate her actual smoking during pregnancy, making cord blood or meconium testing a more reliable window into fetal exposure.

Immunoassay Versus Lab-Confirmed Results

Not all cotinine tests are equally precise. The cheapest and fastest method is a lateral-flow immunoassay strip, similar in format to a home pregnancy test. These strips are widely used in point-of-care and insurance screening. At a 200 ng/mL cutoff, one evaluation found they achieved about 96 percent accuracy compared to the gold-standard laboratory method, with sensitivity near 100 percent and specificity around 92 percent. A more sensitive 10 ng/mL strip had about 93 percent accuracy, but its positive predictive value dropped to about 85 percent, meaning roughly one in seven positive results at that lower cutoff was a false alarm.

If a quick screening test comes back positive and you believe it is wrong, you can request confirmation by a laboratory method that directly measures cotinine concentration rather than relying on an antibody reaction. This is especially worth doing if your result is near the cutoff, if you have secondhand smoke exposure that might explain a low positive, or if there are financial consequences like higher insurance premiums riding on the outcome. A confirmed quantitative result also gives you and your doctor an actual number to interpret, rather than just a yes/no classification.

Related Content

More in Tests