Smokers' behaviour and exposure according to cigarette yield and smoking experience

Hee, Jean; Callais, F.; Momas, Isabelle; Laurent, Anne Marie; Min, S.; Molinier, P.; Chastagnier, Madeleine; Claude, Jean; Festy, B.

doi:10.1016/0091-3057(95)00089-f

Cited by 40 publications

(26 citation statements)

References 28 publications

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“…The differences observed were not nearly as great as the differences in nominal yields of nicotine and CO, measured by the FTC method (8). Urinary mutagenicity did not correlate with tar yield (22). Our data, showing no differences in total cotinine, total NNAL, and 1-HOP among smokers of regular, light, and ultralight cigarettes, and no correlation of the biomarkers with FTC tar levels, are consistent with these reports.…”

Section: Discussionsupporting

confidence: 82%

Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Hecht

Murphy

Carmella

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

119

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Cigarette design has changed markedly over the past 60 years and sales-weighed levels of tar and nicotine have decreased. Currently, cigarettes are classified as regular (>14.5 mg tar), light (>6.5-14.5 mg tar), and ultralight (V V 6.5 mg tar), based on a Federal Trade Commission -specified machine-smoking protocol. Epidemiologic studies suggest that there is no difference in lung cancer risk among people who smoke light or ultralight cigarettes compared with regular cigarettes, but the uptake of lung carcinogens in smokers of these types of cigarettes has never been reported. We recruited 175 smokers, who filled out a tobacco use questionnaire in which their current brand was identified as regular, light, or ultralight. Urine samples were collected and analyzed for 1-hydroxypyrene (1-HOP), total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL plus its glucuronides) and total cotinine (cotinine plus its glucuronides). 1-HOP and total NNAL are biomarkers of uptake of polycyclic aromatic hydrocarbons and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, lung carcinogens in cigarette smoke. Total cotinine is a biomarker of nicotine uptake. There were no statistically significant differences in urinary levels of 1-HOP, total NNAL, and total cotinine in smokers of regular, light, and ultralight cigarettes, whether the results were expressed per mg urinary creatinine, per mL of urine, or per mg creatinine divided by cigarettes per day. Levels of machine measured tar were available for the cigarettes smoked by 149 of the subjects. There was no correlation between levels of tar and any of the biomarkers. These results indicate that lung carcinogen and nicotine uptake, as measured by urinary 1-HOP, total NNAL, and total cotinine is the same in smokers of regular, light, and ultralight cigarettes. The results are consistent with epidemiologic studies that show no difference in lung cancer risk in smokers of these cigarettes.

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Section: Discussionsupporting

confidence: 82%

Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Hecht

Murphy

Carmella

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

119

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“…In addition, we showed previously that CO also had antioxidative behavior 13) . Tobacco smoking is an important source of CO as a pollutant 15) . COHb commonly reaches a level of two or more percent in smokers and may even exceed 10 percent, compared to around one percent in nonsmokers 15) .…”

Section: Discussionmentioning

confidence: 99%

“…Tobacco smoking is an important source of CO as a pollutant 15) . COHb commonly reaches a level of two or more percent in smokers and may even exceed 10 percent, compared to around one percent in nonsmokers 15) . In this study, COHb was increased in the smoker patients who were influenced …”

Section: Discussionmentioning

confidence: 99%

“…Although the cytoprotective roles of CO has been investigated by in vitro studies using CO releasing molecules (11) and in vivo studies using high exogenous CO exposure 14) , the behavior of CO under pathophysiological conditions is still unknown. It has been widely reported that healthy smokers have high concentration levels of CO, which is measured by carboxyhemoglobin (COHb) (15), but the endogenous CO concentration levels of those with various pathophysiological conditions are unclear. In the present study, we clarified the behavior of CO in patients with acute coronary syndrome (ACS), and investigated whether CO could be a novel biomarker of ACS.…”

Section: Introductionmentioning

confidence: 99%

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Endogenous Carbon Monoxide Concentration in Blood Elevates in Acute Coronary Syndrome of Nonsmoker Population

Kobayashi

Mizukami

Sakamoto

et al. 2015

FJMS

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: Background : Carbon monoxide (CO) was previously only considered as a highly toxic pollutant since it binds to hemoglobin with high affinity. Recently, however, it has been recognized as a signaling molecule with regulatory roles in many physiological and pathophysiological processes within the cardiovascular system. The aim of this study was to clarify the behavior of CO in patients with acute coronary syndrome (ACS). Methods : We assessed 235 patients with suspected ACS, 98 smokers (88 male, 62 ± 14 years) and 137 nonsmokers (77 male, 72 ± 13 years), who had undergone emergent cardiac catheterization and blood sampling for calculation of carboxyhemoglobin (COHb). Patients were categorized into 4 groups : smoking patients with ACS (n=77), smoking patients without ACS (n=21), non -smoking patients with ACS (n=97), and non -smoker patients without ACS (n=40). We investigated whether biomarkers were related to COHb levels. Results : LogCOHb was significantly higher in the smoking patients compared to non -smoking patients (0.30 ± 0.12 vs. 0.45 ± 0.18, P < 0.01). Interestingly, among the non -smoking patients, COHb was increased in the ACS patients compared to the non ACS patients (0.31 ± 0.12 vs. 0.25 ± 0.12 P < 0.01). In contrast, among the smoking patients, there was no difference in COHb between the ACS and non -ACS patients (0.45 ± 0.18 vs. 0.44 ± 0.18, n.s.). There were no correlations between COHb and any of the biomarkers. Conclusions : These results suggest that endogenous CO may be useful to assess the risk of cardiovascular stress.

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“…Among the latter who are smokers, many patients who come to the ED smoke cigarettes immediately before checking into triage. This may lead to an elevation of their COHb concentrations (11,12). Alternatively, many patients who arrive in an ambulance do so while treated with oxygen.…”

mentioning

confidence: 96%

Non-Invasive Pulse CO-oximetry Screening in the Emergency Department Identifies Occult Carbon Monoxide Toxicity

Suner

Partridge

Sucov

et al. 2008

The Journal of Emergency Medicine

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Smokers' behaviour and exposure according to cigarette yield and smoking experience

Cited by 40 publications

References 28 publications

Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Endogenous Carbon Monoxide Concentration in Blood Elevates in Acute Coronary Syndrome of Nonsmoker Population

Non-Invasive Pulse CO-oximetry Screening in the Emergency Department Identifies Occult Carbon Monoxide Toxicity

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