The dose-response relationship between cigarette consumption, biochemical markers and risk of lung cancer

Law, Malcolm; Morris, Joan K.; Watt, Hilary; Wald, Nicholas

doi:10.1038/bjc.1997.287

Cited by 94 publications

(71 citation statements)

References 17 publications

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“…In the correlation analysis, urinary cotinine levels were associated with both the number of cigarettes smoked per day and the FTND scores, which was consistent with previous studies (Heatherton et al, 1991;Payne et al, 1994;Law et al, 1997;Caraballo et al, 1998;Park et al, 2004;Blackford et al, 2006). In contrast to previous reports that showed that the duration of smoking was not associated with the FTND scores (John et al, 2003;Park et al, 2004), the degree of nicotine dependence increased according to the total smoking period in our study.…”

Section: Discussionsupporting

confidence: 91%

“…How quickly to smoke after awakening in the morning has been regarded as a strong marker of nicotine dependence, because highly dependent smokers have lower tolerability to depleted plasma nicotine levels on waking (Heatherton et al, 1991;Baker et al, 2007). Other reports showed a dose-dependent relationship between cotinine levels and the number of cigarettes smoked per day, another measure of the FTND (Law et al, 1997;Blackford et al, 2006;Fu et al, 2012). Moreover, several previous reports showed a significant relationship between the degree of nicotine dependence (as assessed by the total FTND score) and cotinine levels (Heatherton et al, 1991;Payne et al, 1994;Pomerleau et al, 1994).…”

Section: Introductionmentioning

confidence: 94%

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Can Urinary Cotinine Predict Nicotine Dependence Level in Smokers?

Jung

Kim²,

Son³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Although nicotine dependence plays a role as a main barrier for smoking cessation, there is still a lack of solid evidence on the validity of biomarkers to determine nicotine dependence in clinical settings. This study aimed to investigate whether urinary cotinine levels could reflect the severity of nicotine dependence in active smokers. Materials and Methods: Data regarding general characteristics and smoking status was collected using a self-administered smoking questionnaire. The Fagerström test for nicotine dependence (FTND) was used to determine nicotine dependence of the participants, and a total of 381 participants were classified into 3 groups of nicotine dependence: low (n=205, 53.8%), moderate (n=127, 33.3%), and high dependence groups (n=49, 12.9%). Stepwise multiple linear regression model and receiver operating characteristic (ROC) curves analyses were used to determine the validity of urinary cotinine for high nicotine dependence. Results: In correlation analysis, urinary cotinine levels increased with FTND score (r=0.567, P<0.001). ROC curves analysis showed that urinary cotinine levels predicted the high-dependence group with reasonable accuracy (optimal cut-off value=1,000 ng/mL; AUC=0.82; P<0.001; sensitivity=71.4%; specificity=74.4%). In stepwise multiple regression analysis, the total smoking period (β=0.042, P=0.001) and urinary cotinine levels (β=0.234, P<0.001) were positively associated with nicotine dependence, whereas an inverse association was observed between highest education levels (>16 years) and nicotine dependence (β=-0.573, P=0.034). Conclusions: The results of this study support the validity of using urinary cotinine levels for assessment of nicotine dependence in active smokers.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 94%

Can Urinary Cotinine Predict Nicotine Dependence Level in Smokers?

Jung

Kim²,

Son³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…1D), and that this relationship seemed to be influenced mainly by the two extreme groups (0-5 and >30 CPD), suggesting that the heaviest smokers inhale each cigarette with less intensity compared with those smoking the least CPD. This has also been seen in the relationship between daily cigarette consumption and carboxyhemoglobin levels measured in plasma (45). Our results indicated that plasma cotinine showed the strongest correlation with CO levels.…”

Section: Discussionsupporting

confidence: 66%

CYP2A6 Genotype, Phenotype, and the Use of Nicotine Metabolites as Biomarkers during Ad libitum Smoking

Malaiyandi

Goodz

Sellers³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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CYP2A6 inactivates nicotine to cotinine and cotinine to 3-hydroxycotinine. We investigated which of plasma nicotine and metabolites were most related to CYP2A6 genotype and smoking levels. We assessed demographic and smoking histories in 152 Caucasian ad libitum smokers, measured breath carbon monoxide (CO) levels, and determined plasma nicotine, cotinine, and 3-hydroxycotinine by highperformance liquid chromatography and CYP2A6 genotypes by PCR. Cigarettes per day was most closely related to CO (r = 0.60, P < 0.001) followed by plasma cotinine (r = 0.53, P < 0.001), whereas plasma cotinine was most strongly correlated with CO levels (r = 0.74, P < 0.001), confirming that cotinine is a good indicator of smoking levels; this was not limited by CYP2A6 variants. 3-Hydroxycotinine/cotinine is reported to be a good marker of CYP2A6 activity, and we found that the 3-hydroxycotinine/(cotinine + nicotine) ratio was most correlated with CYP2A6 genotype (r = 0.38, P < 0.001). Inclusion of the CYP2A6*12A allele strengthened the correlation (r = 0.46, P < 0.001), suggesting that the identification of novel alleles will continue to improve this relationship. Nicotine metabolism is slower in smokers, and we have shown that CYP2A6 is reduced by nicotine treatment in monkeys. Here, we found that plasma nicotine levels were inversely correlated with CYP2A6 activity (3-hydroxycotinine/cotinine, r = À0.41, P < 0.001) among those without CYP2A6 variants, suggesting a reduction in metabolism with higher nicotine levels. Together, these findings (a) confirm the use of plasma cotinine and CO as indicators of Caucasians' smoking levels, and that this is not limited by CYP2A6 genetic variation; (b) indicate that 3-hydroxycotinine/cotinine and 3-hydroxycotinine/(cotinine + nicotine) are moderately good indicators of the CYP2A6 genotype; and (c) support that nicotine exposure may reduce its own metabolism. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1812 -9)

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“…The values of COHb found in northern elephant seals from this study are higher than values in humans that smoke ≥40 cigarettes per day (Law et al, 1997) and comparable to the highest recorded endogenous values (9.7% COHb) found in a critically ill human patient with hemolytic anemia (Hampson, 2007) (Fig. 2).…”

Section: Discussionmentioning

confidence: 78%

Elevated carboxyhemoglobin in a marine mammal, the northern elephant seal

Tift

Ponganis

Crocker

2014

Journal of Experimental Biology

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Low concentrations of endogenous carbon monoxide (CO), generated primarily through degradation of heme from hemeproteins, have been shown to maintain physiological function of organs and to exert cytoprotective effects. However, high concentrations of carboxyhemoglobin (COHb), formed by CO binding to hemoglobin, potentially prevent adequate O 2 delivery to tissues by lowering arterial O 2 content. Elevated heme-protein concentrations, as found in marine mammals, are likely associated with greater heme degradation, more endogenous CO production and, consequently, elevated COHb concentrations. Therefore, we measured COHb in elephant seals, a species with large blood volumes and elevated hemoglobin and myoglobin concentrations. The levels of COHb were positively related to the total hemoglobin concentration. The maximum COHb value was 10.4% of total hemoglobin concentration. The mean (±s.e.m.) value in adult seals was 8.7±0.3% (N=6), while juveniles and pups (with lower heme-protein contents) had lower mean COHb values of 7.6±0.2% and 7.1±0.3%, respectively (N=9 and N=9, respectively). Serial samples over several hours revealed little to no fluctuation in COHb values. This consistent elevation in COHb suggests that the magnitude and/or rate of heme-protein turnover is much higher than in terrestrial mammals. The maximum COHb values from this study decrease total body O 2 stores by 7%, thereby reducing the calculated aerobic dive limit for this species. However, the constant presence of elevated CO in blood may also protect against potential ischemia-reperfusion injury associated with the extreme breath-holds of elephant seals. We suggest the elephant seal represents an ideal model for understanding the potential cytoprotective effects, mechanisms of action and evolutionary adaptation associated with chronically elevated concentrations of endogenously produced CO. KEY WORDS: Calculated aerobic dive limit, Carbon monoxide, Hemoglobin absorption spectra, Marine mammal, Oxygen stores INTRODUCTIONCarbon monoxide (CO) is often classified as a strictly toxic gas, depriving the body of oxygen (O 2 ) by binding to heme-proteins such as hemoglobin and forming carboxyhemoglobin (COHb) (Weaver, 2009). Deleterious symptoms (e.g. headache, nausea and shortness of breath) of CO-driven hypoxia are typically seen when COHb values reach ≥20% of total hemoglobin concentration, and death is associated with values of 50-80% (Stewart, 1975;Weaver, 2009 storage capacity (decreased arterial O 2 content), thus limiting mitochondrial respiration. However, CO is also generated endogenously in low concentrations, and functions in neurotransmission and in protection of tissues and cells against inflammation, apoptosis and ischemia-reperfusion injuries (Snyder et al., 1998; Kevin and Laffey, 2008;Mustafa et al., 2009; Kajimura et al., 2010;Prabhakar, 2012). Therefore, low concentrations of CO can provide beneficial and therapeutic effects up to a specific concentration, at which elevated CO then leads to detrimental effects from reduce...

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The dose-response relationship between cigarette consumption, biochemical markers and risk of lung cancer

Cited by 94 publications

References 17 publications

Can Urinary Cotinine Predict Nicotine Dependence Level in Smokers?

Can Urinary Cotinine Predict Nicotine Dependence Level in Smokers?

CYP2A6 Genotype, Phenotype, and the Use of Nicotine Metabolites as Biomarkers during Ad libitum Smoking

Elevated carboxyhemoglobin in a marine mammal, the northern elephant seal

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