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Cotinine

Strip color for cotinine DOA test

Tobacco use is the most important preventable cause of premature morbidity and mortality in the United States. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer, emphysema, acute respiratory illness, cardiovascular disease, stroke, and various other disorders (U.S. DHHS, 2006). Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease; maternal exposure during pregnancy can result in lower birth weight. Children exposed to ETS are at increased risk for sudden infant death syndrome, acute respiratory infections, ear problems, and exacerbated asthma (U.S. DHHS, 2004). The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic, and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP, 2004).

Cigarettes contain about 1.5% nicotine by weight (Kozlowski et al., 1998), producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob, 1994; Hukkanen et al., 2005). Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al., 1975; Iwase et al., 1991). Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0.3 to 30 µg/m3, with higher levels measured in restaurants and bars. In homes with one or more smokers, mean air concentrations typically range from 2 to 14 µg/m3 (NTP, 2004). For an adult, the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. Children are primarily exposed to ETS by parents and caregivers who smoke.

Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff, chewing tobacco, or chewing gum, nasal sprays, or skin patches that contain nicotine. Workers who harvest tobacco can be exposed to nicotine and become intoxicated as a result of the transdermal absorption of nicotine contained in the plant. The tobacco plant, Nicotiana tabacum, contains nicotine in larger amounts than other nicotine-containing plants, which include potatoes, tomatoes, eggplants, and peppers. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms.

Once absorbed, nicotine has a half-life in blood plasma of several hours (Benowitz, 1996). Cotinine, the primary metabolite of nicotine, is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. Measuring cotinine is preferred over measuring nicotine because cotinine persists longer in the body with a plasma half-life of about 16 hours (Benowitz and Jacob, 1994). However, non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al., 1999; Perez-Stable et al., 1998). Cotinine can be measured in serum, urine, saliva, and hair. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL, with heavy exposure to ETS producing levels in the 1–10 ng/mL range. Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al., 2005).

Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. Acute tobacco or nicotine intoxication can produce dizziness, nausea, vomiting, diaphoresis, salivation, diarrhea, variable changes in blood pressure and heart rate, seizures, and death. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation, a process involved in the development of addiction. Symptoms of nicotine withdrawal include irritability, craving, cognitive and sleep disturbances, and increased appetite.

The IARC and the NTP consider tobacco smoke to be a human carcinogen. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration. The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. More information about the effects of smoking and nicotine can be found at: http://www.nida.nih.gov/researchreports/nicotine/nicotine.html .

Biomonitoring Information

Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al., 1996).

The serum cotinine levels seen in the NHANES 2003–2004 appear approximately similar to levels seen in the previous survey period (NHANES 2001–2002) for the total population estimates. Serum cotinine has been measured in many studies of nonsmoking populations, with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005; NCI, 1999). Over the previous decade, levels of exposure to ETS appeared to decrease since geometric mean cotinine serum concentrations in nonsmokers had fallen by approximately 70% and the rate of detectable cotinine in nonsmokers fell from 88% to 43% when NHANES 1988–1991 was compared to NHANES 1999–2002, (CDC, 2005; Pirkle et al., 2006). The overall decline in population estimates of serum cotinine likely reflects decreased ETS exposure among nonsmokers in locations with smoke-free laws (Pickett et al., 2006; Soliman et al., 2004). During each previous NHANES survey, the adjusted geometric mean serum cotinine was higher in children (aged 4–11 years) than in adults among both non-Hispanic blacks and non-Hispanic whites (Pirkle et al., 2006). Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al., 1998). Differences in cotinine concentrations among race/ethnicity and age groups may be influenced by pharmacokinetic differences as well as by ETS exposure (Benowitz et al., 1999; Hukkanen et al., 2005; Wilson et al., 2005).

Biomonitoring studies of serum cotinine will help physicians and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.

References

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Source: Centers for Disease Control and Prevention