Disease relevance of cotinine

• The presence of cotinine in urine was also independently associated with an increased risk of spontaneous abortion (odds ratio, 1.8; 95 percent confidence interval, 1.3 to 2.6) [1].
• Samples collected at enrollment from 292 persons in whom squamous-cell carcinoma of the head and neck developed, on average, 9.4 years after enrollment and from 1568 matched controls were analyzed for antibodies against HPV-16, HPV-18, HPV-33, and HPV-73 and for cotinine levels as a marker of smoking habits [2].
• The impact on infant birth weight and gestational age of cotinine-validated smoking reduction during pregnancy [3].
• OBJECTIVE: To examine the relationship between dental caries and serum cotinine levels [4].
• In the choriocarcinoma cell cultures, a supraphysiologic concentration of androstenedione (73 microM) in the culture medium blocked the inhibition of aromatase caused by nicotine, cotinine, and anabasine [5].

Psychiatry related information on cotinine

• Smoking cessation was measured by self-report after one year and validated using saliva cotinine measures [6].
• A dose-response relationship was observed with higher patch doses, which produced a higher percentage of cotinine replacement and better withdrawal symptom relief [7].
• The potential risk factors examined were alcohol consumption, physical activity, tobacco smoking, serum cotinine, serum lipids, body-mass index, blood pressure, prevalence of hypertension and non-insulin-dependent diabetes mellitus, and social class [8].
• The usefulness of cotinine as a marker of tobacco dependence is discussed [9].
• HPV 6, 11, 16, 18 and 33 seropositivity was used as a marker for the different HPV infections, and seropositivity for Chlamydia trachomatis and cotinine were used as markers for risk-taking sexual behavior and smoking respectively [10].

High impact information on cotinine

• RESULTS: After adjustment for cotinine levels, the odds ratio for squamous-cell carcinoma of the head and neck in subjects who were seropositive for HPV-16 was 2.2 (95 percent confidence interval, 1.4 to 3.4) [2].
• MAIN OUTCOME MEASURE: Risk for the development of cervical SCC by IgG antibodies to 10 different C trachomatis serotypes, adjusted for antibodies to HPV types 16, 18, and 33 and for serum cotinine levels [11].
• DESIGN: Nationally representative cross-sectional survey including questionnaire information from persons aged 2 months and older (n=16818) and measurements of serum cotinine (a metabolite of nicotine) from persons aged 4 years and older (n=10642) [12].
• DESIGN--Group analyses from a prospective, randomized smoking-cessation intervention trial using cotinine levels to assess smoking cessation and reduction [3].
• Users of ST did not differ from nonusers in blood pressure, pulse, total or high-density lipoprotein cholesterol level, or white blood cell count, but among users high-density lipoprotein cholesterol levels were inversely associated with serum cotinine levels [13].

Chemical compound and disease context of cotinine

• Higher smoking cessation rates were also observed in subjects assigned to the active patch who had lower serum levels of nicotine and cotinine at baseline, and withdrawal symptom relief was better in the active patch group compared with placebo [14].
• Withdrawal symptoms were measured using a daily diary, and smoking cessation was defined as self-reported abstinence, expired carbon monoxide of 9 ppm or less, and a 6-month urine cotinine level of less than 50 ng/mL [15].
• Analysis of variance was used to estimate the effect of caffeine on birth weight, gestational age at delivery, and birth weight ratio after accounting for the effects of other covariates, such as maternal sociodemographic characteristics, plasma cotinine, and pregnancy symptoms [16].
• Serum selenium level was significantly (P less than 0.05), but not strongly, correlated with a number of IHD risk factors: serum cotinine, tobacco smoking, social class, alcohol consumption, total cholesterol, hypertension, age and physical inactivity [17].
• Sperm samples from 44 cigarette smokers and 50 nonsmokers attending an infertility clinic were examined by high-performance liquid chromatography (HPLC) assay and HPLC-mass spectrometry for the presence of nicotine (NIC), cotinine (COT), and trans-3'-hydroxycotinine (THOC) in seminal plasma [18].

Biological context of cotinine

• Several compounds from cigarette smoke (nicotine and its major metabolite, cotinine) have been identified in cervical mucus, and the occurrence of smoking-related DNA damage in the cervical epithelium has been documented [19].
• We studied cotinine disposition kinetics in 28 healthy habitual cigarette smokers [20].
• The phenotype, as determined by plasma nicotine/cotinine ratios, had a descending rank order for these three genotype groups that did not reach significance [21].
• Nicotine and cotinine elimination pharmacokinetics in smokers and nonsmokers [22].
• The effect of fibrinogen on coronary heart disease and death was assessed through age-adjusted means and Cox proportional hazards regression models, accounting for age, cotinine (a measure of tobacco smoke inhalation) and 11 other major coronary risk factors [23].

Anatomical context of cotinine

• Cotinine in amniotic fluids from passive smokers [24].
• To examine possible mechanisms for the association between cigarette smoking and reduced fertility, we have measured the concentration of the nicotine metabolite cotinine in ovarian follicular fluid collected at the time of oocyte recovery during treatment for in-vitro fertilisation [25].
• Incubation of human liver microsomes with nicotine gave keto acid by using aminoketone as an intermediate; keto acid was not formed from cotinine [26].
• Nicotine and cotinine treatment resulted in reduction of CD44 surface expression on lung microvascular endothelial cell line (LEISVO) and bone marrow-derived (STR-12) endothelial cell line [27].
• This association was independent of maternal smoking or umbilical cord blood cotinine levels [28].

Associations of cotinine with other chemical compounds

• Cotinine, trans-nicotine-N'-oxide, and the mixture of cis- and trans-nicotine-N'-oxides were neither carcinogens nor promoters of urinary bladder tumors in rats initiated with FANFT [29].
• Both simple and multivariate analysis found a positive association of 4-aminobiphenyl-hemoglobin adducts with the quantity of tobacco smoked as determined by either urine cotinine or questionnaire data [30].
• Pretreatment blood cotinine levels, expired carbon monoxide levels, and self-reported cigarette consumption were evaluated as predictors of smoking treatment outcome in 114 patients [9].
• Ambulatory 24-hour daytime and nighttime heart rate and blood pressure values were determined for each treatment; plasma nicotine, cotinine, and carboxyhemoglobin levels and urinary catecholamines with aldosterone were measured on days 4 and 5 [31].
• However, elevation in natural killer cell cytotoxic activity appears not to be directly related to cessation-induced reductions in plasma nicotine, cotinine, or circulating cortisol levels [32].

Gene context of cotinine

• Although (S)-cotinine was observed to inhibit pig FMO1 (Ki = 675 microM), partially purified cDNA-expressed adult human liver FMO3 was not inhibited by (S)-cotinine [33].
• The polymorphism in the CYP2E1 5'-flanking region was related to the urinary cotinine level in intermediate smokers (who smoke 11-20 cigarettes/day; P < 0.01) [34].
• Nicotine and cotinine stimulate secretion of basic fibroblast growth factor and affect expression of matrix metalloproteinases in cultured human smooth muscle cells [35].
• Matrix metalloproteinase expression was determined in subconfluent cultures incubated in albumin with or without nicotine or cotinine at 10(-8) mol/L and 10(-7) mol/L for 6, 12, 18, 24 and 36 hours [35].
• CYP2A6 is the principle enzyme metabolizing nicotine to its inactive metabolite cotinine [36].

Analytical, diagnostic and therapeutic context of cotinine

• Racial and ethnic differences in serum cotinine levels of cigarette smokers: Third National Health and Nutrition Examination Survey, 1988-1991 [37].
• Plasma cotinine was analyzed by gas chromatography; PAH-albumin adducts in peripheral blood were analyzed by enzyme-linked immunosorbent assay [38].
• Smoking histories were taken at 3-monthly clinic visits and verified by measurement of salivary cotinine concentrations [39].
• Serum concentrations of nicotine were determined by using gas chromatography and mass spectrometry, and plasma concentrations of cotinine were measured by using high-performance liquid chromatography [40].
• We suggest that cotinine be measured to assess the influence of cigarette smoking in epidemiologic studies of blood pressure [41].

References