Nicotine gum promoted cessation in this population of smokers unwilling to quit. Among reducers, the toxin intake correlated with reduced cigarette consumption although some compensatory smoking occurred.
Objective To evaluate the efficacy of using a nicotine patch for 5 months with a nicotine nasal spray for 1 year. Design Placebo controlled, double blind trial. Setting Reykjavik health centre. Subjects 237 smokers aged 22-66 years living in or around Reykjavik. Interventions Nicotine patch for 5 months with nicotine nasal spray for 1 year (n = 118) or nicotine patch with placebo spray (n = 119). Treatment with patches included 15 mg of nicotine for 3 months, 10 mg for the fourth month, and 5 mg for the fifth month, whereas nicotine in the nasal spray was available for up to 1 year. Both groups received supportive treatment. Main outcome measure Sustained abstinence from smoking. Results The log rank test for 6 years ( 2 = 8.5, P = 0.004) shows a significant association between abstinence from smoking and type of treatment. Sustained abstinence rates for the patch and nasal spray group and patch only group were 51% v 35% after 6 weeks (P = 0.011 ( 2 ), 95% confidence interval 1.17% to 3.32%), 37% v 25% after 3 months (P = 0.045, 1.01% to 3.08%), 31% v 16% after 6 months (P = 0.005, 1.27% to 4.50%), 27% v 11% after 12 months (P = 0.001, 1.50% to 6.14%), and 16% v 9% after 6 years (P = 0.077, 0.93% to 4.72%). Conclusions Short and long term abstinence rates show that the combination of using a nicotine patch for 5 months with a nicotine nasal spray for 1 year is a more effective method of stopping smoking than using a patch only. The low percentage of participants using the nasal spray at 1 year, and the few relapses during the second year, suggest that it is not cost effective to use a nasal spray for longer than 7 months after stopping a patch.
The present study examined the effect of smoking reduction and cessation on asthma regulation and biomarkers of exposure to cigarette smoke. In a prospective open design, we allocated 220 asthmatics among three groups: (a) Smoking reduction (reducers), with the aim of smoking fewer than seven cigarettes per day, (b) complete smoking cessation (abstainers), or (c) continuation of usual smoking (continuing smokers). Subjects used nicotine chewing gum or an oral nicotine inhaler to promote reduction and cessation. We monitored changes in the biomarkers carbon monoxide, cotinine, and thiocyanate, and in peak flow, medicine use, bronchial reactivity, and asthma symptoms. The analysis used the three outcome groups, regardless of original allocation to treatment groups. At 4 months, analysis of abstainers (n = 27), reducers (n = 33), and continuing smokers (n = 50) showed marked, statistically significant decreases in expired carbon monoxide of 17 ppm (abstainers) and 15 ppm (reducers); in plasma cotinine of 124 ng/ml (abstainers) and 122 ng/ml (reducers); and in plasma thiocyanate of 5.03 ng/ml (abstainers) and 3.74 ng/m (reducers). For abstainers, we observed improvements in the asthma-specific quality-of-life score, and reductions in self-reported day and night use of rescue beta2-agonists, in doses of inhaled corticosteroids, in daytime asthma symptoms, and in bronchial hyperreactivity. For reducers, smaller improvements occurred for night use of rescue beta2-agonists, doses of inhaled corticosteroids, and bronchial hyperreactivity. Smoking cessation resulted in a marked decrease in three biomarkers of cigarette smoke inhalation and improved asthma regulation, whereas smoking reduction had a less pronounced effect on biomarkers and only a small effect on asthma regulation.
This open study examined the effect of smoking reduction and smoking cessation on established cardiovascular risk factors. Fifty-eight healthy adult smokers (smoking >or=15 cigarettes/day for at least 3 years) were provided with nicotine nasal spray (to be used ad libitum) and asked to stop smoking. The primary goal during the first 8 weeks, however, was to reduce their daily smoking by at least 50%. Subjects were then followed for another 8 weeks; at this point, 33 participants had successfully stopped smoking. Cardiovascular risk factors including fibrinogen, hemoglobin, hematocrit, triglycerides, and cholesterol were measured at baseline and at 9 and 17 weeks. After 8 weeks of smoking reduction, the mean number of cigarettes smoked per day had decreased from 21.5 +/- 0.6 (baseline) to 10.8 +/- 0.6 (p < 0.001). This was accompanied by significant improvements in fibrinogen (from 2.9 +/- 0.1 g/l at baseline to 2.6 +/- 0.1 g/l, p = 0.011), white blood cells (from 7.0 +/- 0.4 to 6.2 +/- 0.3 x 10(9)/l, p = 0.005) and the high-density/low-density lipoprotein (HDL/LDL) ratio (0.33 +/- 0.03 to 0.37 +/- 0.03, p < 0.005). Following 8 weeks of abstinence from smoking, the mean white blood cell count was further reduced (to 6.1 +/- 0.3 x 10(9)/l, p = 0.026 vs. baseline) and there were also significant improvements in HDL (from 1.16 +/- 0.06 mmol/l at baseline to 1.32 +/- 0.06, p < 0.001) and LDL (from 3.78 +/- 0.16 mmol/l at baseline to 3.52 +/- 0.17, p = 0.015). In conclusion, 8 weeks of smoking reduction resulted in clinically significant improvements in established cardiovascular risk factors. These improvements were even greater after an additional period of abstinence from smoking.
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