The use of biologic fluid samples in assessing tobacco smoke consumption.

Nl, Benowitz

doi:10.1037/e475382004-001

Cited by 130 publications

(100 citation statements)

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“…Serum cotinine levels are clearly a consequence of tobacco exposure. These findings are in agreement with previous studies which concluded that cotinine can be reliably measured in blood, saliva and urine and all three sources are generally regarded as acceptable for monitoring nicotine exposure in people (Benowitz, 1983;Jarvis et al, 1988).…”

Section: Discussionsupporting

confidence: 83%

“…Nicotine, one of the most important components of tobacco, has a plasma life of approximately 30 min (Machacek and Jiang, 1986) and it is quickly converted to its metabolite, cotinine. The latter has been used as a biomarker of tobacco use (Cuff et al, 1989;Watts et al, 1990) and its plasma half-life is longer than that of nicotine, ranging from 10-30 h (Benowitz et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

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The Relationship between Serum Cotinine Levels and Periodontal Status

Al-Bayaty

Baharuddin

Abdulla

2010

OnLine Journal of Biological Sciences

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Problem statement:Smoking plays a significant role in the development of periodontal disease. Quantitative relation between smoking and increased severity of periodontal disease, by means of biochemical marker has not been described in Malaysian population. The present study was designed to apply serum cotinine measurement as a quantitative method to evaluate smoking levels in Malaysian patients and to correlate these levels with the severity of periodontal disease. Approach: The study group consisted of 80 healthy individuals (20-64) year, Current Smokers 26, Non Smokers 27 and Former Smokers 27. The subjects were then asked to complete a questionnaire including the demographic, socioeconomic status, medical history and history of cigarette smoking. The periodontal variables recorded were amount of Visible Plaque score, gingival bleeding Index and community periodontal index. Samples of blood "10 mL" were obtained in vacutainer tubes containing EDTA for quantitative analysis of serum levels of cotinine. The serum samples were analyzed for cotinine content by means of a competitive-inhibition ELISA technique. Results: Current smokers represent the highest mean cotinine serum level, 95.5 ng mL −1 , compared to former smokers, 35.5 ng mL −1 and non smokers, 22.9 ng mL −1 . The mean serum cotinine level in periodontally healthy patient showed the highest cotinine level (84 ng mL −1 ) followed by the gingivitis patients (68 ng mL −1 ) and (50 ng mL −1 ) for periodontitis patients. Conclusion: The present observations clearly indicate an association between smoking, periodontal disease clinical parameters "plaque, gingival bleeding scores" and cotinine serum levels in current smokers. Cotinine serum levels doesn't affected by the existence or the severity of periodontal disease.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

The Relationship between Serum Cotinine Levels and Periodontal Status

Al-Bayaty

Baharuddin

Abdulla

2010

OnLine Journal of Biological Sciences

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“…Nicotine is the major constituent of tobacco smoke but is difficult to measure or study because of its very short half-life. 17 Cotinine, the most abundant metabolite of nicotine, has been identified as a stable biomarker of smoke exposure and has been used in cell culture to mimic the affects of smoke exposure in vitro, reportedly signaling though the nicotinic acetylcholine receptor ␣-7 (nAChR␣Ϫ7). [17][18][19] Thus, to objectively address our hypothesis, we compared serum cotinine levels to PROKR expression in human Fallopian tube.…”

mentioning

confidence: 99%

“…17 Cotinine, the most abundant metabolite of nicotine, has been identified as a stable biomarker of smoke exposure and has been used in cell culture to mimic the affects of smoke exposure in vitro, reportedly signaling though the nicotinic acetylcholine receptor ␣-7 (nAChR␣Ϫ7). [17][18][19] Thus, to objectively address our hypothesis, we compared serum cotinine levels to PROKR expression in human Fallopian tube. We also examined the effects of cotinine on tubal PROKR expression in Fallopian tube in vitro and investigated whether this was mediated via nAChR␣Ϫ7.…”

mentioning

confidence: 99%

Cotinine Exposure Increases Fallopian Tube PROKR1 Expression via Nicotinic AChRα-7

Shaw

Oliver

Lee

et al. 2010

The American Journal of Pathology

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Tubal ectopic pregnancy (EP) is the most common cause of maternal mortality in the first trimester of pregnancy; however, its etiology is uncertain. In EP, embryo retention within the Fallopian tube (FT) is thought to be due to impaired smooth muscle contractility (SMC) and alterations in the tubal microenvironment. Smoking is a major risk factor for EP. FTs from women with EP exhibit altered prokineticin receptor-1 (PROKR1) expression, the receptor for prokineticins (PROK). PROK1 is angiogenic, regulates SMC, and is involved in intrauterine implantation. We hypothesized that smoking predisposes women to EP by altering tubal PROKR1 expression. Sera/FT were collected at hysterectomy (n ‫؍‬ 21). Serum levels of the smoking metabolite, cotinine, were measured by enzyme-linked immunosorbent assay. FTs were analyzed by q-RT-PCR , immunohistochemistry , and Western blotting for expression of PROKR1 and the predicted cotinine receptor, nicotinic acetylcholine receptor ␣-7 (AChR␣؊7). FT explants (n ‫؍‬ 4) and oviductal epithelial cells (cell line OE-E6/E7) were treated with cotinine and an nAChR␣؊7 antagonist. PROKR1 transcription was higher in FTs from smokers (P < 0.01). nAChR␣؊7 expression was demonstrated in FT epithelium. Cotinine treatment of FT explants and OE-E6/E7 cells increased PROKR1 expression (P < 0.05) , which was negated by cotreatment with nAChR␣؊7 antagonist. Smoking targets human FTs via nAChR␣؊7 to increase tubal PROKR1, leading to alterations in the tubal microenvironment that could predispose to EP.

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“…30 The other important limitation of the measurement is that the thiocyanate is present in several human diets and, therefore, there is always a chance of introducing false positive error in its measurement. 59 …”

Section: Salivary Thiocyanatementioning

confidence: 99%