Vignette 3
Ms. C, age 34 and pregnant, is admitted to an outpatient treatment program for alcohol use disorder. She also has generalized anxiety disorder and tobacco use disorder. In addition to attending group therapy sessions and self-reporting any recent alcohol consumption, Ms. C also undergoes alcohol breathalyzer tests and urine studies of alcohol metabolites to monitor abstinence from alcohol. She says that the regular laboratory screening for alcohol use gives her a sense of accountability and tangible evidence of change that positively impacts her treatment. When the treating psychiatrist recommends that Ms. C also consider addressing her tobacco use disorder, she asks if there is some way to include laboratory testing to monitor her smoking cessation.
Cotinine as a predictor of smoking status
Smoking abstinence rates during pregnancy are lower than that for other substances, and pregnant women may not be aware of the impact of smoking on fetal development.30 Cotinine can be used to verify self-report of smoking status and severity.10,31,32
Salivary cotinine tests are commercially available, relatively economical, and convenient to use when frequent monitoring is required.32 In general, based on established cut-off values that are unique to the specimen collected, the overall high specificity and sensitivity of salivary testing allows clinicians to predict smoker vs nonsmoker status with confidence. For example, a 2008 study reported a salivary cotinine cut-off level of 12 ng/mL for smokers.21 The sensitivity and specificity of this cut-off value for distinguishing cigarette smokers from never smokers were 96.7% and 96.9%, respectively.21
Additionally, some studies suggest that cotinine levels may be predictive of treatment outcomes and retention in SUD treatment programs.33,34 One study of smoking cessation using nicotine replacement products found that compared with patients with lower baseline cotinine levels prior to treatment, patients with higher baseline cotinine plasma levels had lower smoking cessation success rates.34
A few caveats
There are several limitations to quantitative measures of cotinine (Box 221,23). These include (but are not limited to) potential errors related to sample collection, storage, shipping, and analysis.23 Compared with other methods, point-of-care cotinine measurement in saliva is noninvasive, simple, and requires less training to properly use.23
Box 2
Limitations of cotinine monitoring
Challenges in the collection of samples, storage, shipping, and instrumentation may limit cotinine consistency as a dependable biomarker in the clinical setting.23 Overall, quantitative measurements of cotinine have relative constructive utility in separating smokers from nonsmokers, because daily smokers typically have serum concentrations of 100 ng/mL or higher, in contrast to light/non-daily smokers, who have cotinine concentrations <10 ng/mL. Even heavy exposure to secondhand smoke typically yields plasma concentrations up to approximately 25 ng/mL. However, cotinine is a general metabolite found with the use of all nicotine products, which makes it extremely difficult to differentiate tobacco use from the use of nicotine replacement products, which are frequently used to treat tobacco use disorders.
One potential solution is to measure nicotine-derived nitrosamine ketone (NNK) and its metabolite 4-(methylnitrosamino)- 1-(3-pyridyl)-1-butanol (NNAL). Both NNK and NNAL are tobacco-specific lung carcinogens. NNAL can be measured in the urine. Although total NNAL represents only 15% of NNK dose intake, it has been quantified, with urine concentrations of ≥1,000 fmol/mL for daily smokers. NNAL also has an extremely high specificity to tobacco smoke, and thus allows differentiation of tobacco use from nicotine replacement treatment. Unfortunately, measurement for this biomarker requires specific chemical expertise and expensive equipment.
Another potential barrier to using cotinine in the clinical setting is the variable cut-off levels used in the United States, based on differences in race/ethnicity. This may be secondary to differences in smoking behaviors and/or differences in cotinine metabolism.21
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