Self-titration by cigarette smokers

An 11-week crossover study was carried out in which 12 subjects smoked high-nicotine (1·84 mg standard yield) and low-nicotine (0·6 mg) cigarettes after an initial period of smoking their usual brands with a medium-nicotine yield (mean 1·4 mg). Plasma and urine nicotine concentrations, carboxyhaemoglobin (COHb) concentration, puffing behaviour, 24-hour cigarette consumption, and butt nicotine content were measured. The changes in plasma nicotine and blood COHb concentrations showed that the smokers compensated for about two-thirds of the difference in standard yields when switched to either high- or low-nicotine cigarettes. Thus, compared with the medium-nicotine brand, the intake of nicotine and carbon monoxide was only about 10% higher when subjects smoked the high-nicotine cigarettes, which had a standard yield 30-40% higher than the medium brands; and only about 15% lower when they smoked the low-nicotine cigarettes, which had a standard yield about 50% lower than the medium brands. But nicotine content and urine nicotine concentrations followed a similar pattern. Changes in puffing behaviour and in 24-hour cigarette consumption were only slight.The results show clear evidence of both upward and downward self-titration of nicotine and carbon monoxide (and tar) intakes when smokers change to cigarettes with standard yields that differ over the range studied.     

Metals in cigarette smoke

Metals are vital for a huge number of physiological processes in the human body, but can also destroy health when the concentration is not within the physiologically favourable range. Cigarette smoking interferes with the carefully controlled metal homeostasis of the human body. This review focuses on the consequences of metal delivery to the human body by cigarette smoking and discusses the body's responses. The metal content of tobacco plants, smoke, the circulation, and various organs is discussed. Finally, we link individual cigarette smoke contained metals to the genesis of human diseases.     

Using search query surveillance to monitor tax avoidance and smoking cessation following the United States' 2009 "SCHIP" cigarette tax increase

Smokers can use the web to continue or quit their habit. Online vendors sell reduced or tax-free cigarettes lowering smoking costs, while health advocates use the web to promote cessation. We examined how smokers' tax avoidance and smoking cessation Internet search queries were motivated by the United States' (US) 2009 State Children's Health Insurance Program (SCHIP) federal cigarette excise tax increase and two other state specific tax increases. Google keyword searches among residents in a taxed geography (US or US state) were compared to an untaxed geography (Canada) for two years around each tax increase. Search data were normalized to a relative search volume (RSV) scale, where the highest search proportion was labeled 100 with lesser proportions scaled by how they relatively compared to the highest proportion. Changes in RSV were estimated by comparing means during and after the tax increase to means before the tax increase, across taxed and untaxed geographies. The SCHIP tax was associated with an 11.8% (95% confidence interval [95%CI], 5.7 to 17.9; p<.001) immediate increase in cessation searches; however, searches quickly abated and approximated differences from pre-tax levels in Canada during the months after the tax. Tax avoidance searches increased 27.9% (95%CI, 15.9 to 39.9; p<.001) and 5.3% (95%CI, 3.6 to 7.1; p<.001) during and in the months after the tax compared to Canada, respectively, suggesting avoidance is the more pronounced and durable response. Trends were similar for state-specific tax increases but suggest strong interactive processes across taxes. When the SCHIP tax followed Florida's tax, versus not, it promoted more cessation and avoidance searches. Efforts to combat tax avoidance and increase cessation may be enhanced by using interventions targeted and tailored to smokers' searches. Search query surveillance is a valuable real-time, free and public method, that may be generalized to other behavioral, biological, informational or psychological outcomes manifested online.     

Naloxone reduces cigarette smoking

In a double-blind drug-placebo cross-over design, naloxone hydrochloride reduced the amount of cigarettes smoked by chronic smokers over a 3 hr period. The number of puffs was reduced by 32%, the weight of the amount smoked by 33%, and the number of trials in which cigarettes were smoked by 30%. The extent of the decreases in smoking was related to the amount of the decrease in the desire to smoke. There were no physiological differences or in side effects between the two conditions, and neither subjects nor experimenters were able to distinguish between the two. These findings are similar to the suppressive effects of naloxone on food, water and ethanol intake in animals and suggest that the endorphins are implicated. A heuristic theory of addiction is presented to explain these diverse effects.Naloxone hydrochloride (NAL) reduces the intake of nonintoxicating positive reinforcers, such as food and water, in animals (1–5), as well as ethanol (6). The reduction does not appear to be part of an abstinence syndrome (3), or of a general suppression of behavior (7), unless massive doses (i.e. 5 mg/kg or more) of the opiate antagonist are used (8). The mechanism for these effects is obscure, although it has been demonstrated that higher levels of Beta endorphin are associated with greater food intake, and that NAL suppresses food intake to a greater extent in genetically obese animals which have higher levels of Beta endorphin than their litter-mates of normal weight (4).Cigarette smoking has often been found to increase corticosteroid levels (9–12), which is considered presumptive evidence that there is an increase in ACTH production. Elevated levels of ACTH are associated with elevated levels of Beta endorphin in man (13–16). Assuming that smoking is another example of a nonintoxicating positive reinforcer, which also releases Beta endorphin because of ACTH release, we administered NAL to chronic smokers, with the expectation that the amount smoked, as well as the desire to do so, would be reduced. However, because of the possible addictive nature of nicotine (17–19), we were not sure whether these effects would be the result of a precipitated abstinence syndrome.     

Chemiluminescence of cigarette smoke.

Chemiluminescence from cigarette smoke (aerosol) and smoke "extracts" (suspensoids) are described. The emissons from aqueous and organic suspensoids persist for hours, are proportional to oxygen solubilities, possess energy of at least 1.8 electron volts, and display characteristics which suggest that the emissions may be partially sensitized by singlet oxygen.     

Malignant hypertension and cigarette smoking.

The smoking habits of 48 patients with malignant hypertension were compared with those of 92 consecutive patients with non-malignant hypertension. Thirty-three of the patients with malignant and 34 of the patients with non-malignant hypertension were smokers when first diagnosed. This difference was significant, and remained so when only men or black and white patients were considered separately. Results suggest that malignant hypertension is yet another disease related to cigarette smoking.     

Harmful health effects of cigarette smoking

This is a comprehensive review on the harmful health effects of cigarette smoking. Tobacco smoking is a reprehensible habit that has spread all over the world as an epidemic. It reduces the life expectancy among smokers. It increases overall medical costs and contributes to the loss of productivity during the life span. Smoking has been shown to be linked with various neurological, cardiovascular, and pulmonary diseases. Cigarette smoke not only affects the smokers but also contributes to the health problems of the non-smokers. Exposure to environmental tobacco smoke contributes to health problems in children and is a significant risk factor for asthma. Cigarette smoke contains several carcinogens that alter biochemical defense systems leading to lung cancer.     

Metabolic effects of cigarette smoking.

The inverse relationship between cigarette smoking and body weight, a potent obstacle to stopping smoking, may be due in part to effects of smoking on increasing whole body metabolism. Studies examining chronic and acute metabolic effects of smoking, as well as its constituent nicotine, are reviewed. Evidence suggests the absence of a chronic effect; most studies indicate that smokers and nonsmokers have similar resting metabolic rates (RMR) and that RMR declines very little after smoking cessation. Although an acute effect due to smoking is apparent, its magnitude is inconsistent across studies, possibly because of variability in smoke exposure or nicotine intake. In smokers at rest, the acute effect of smoking (and nicotine intake) appears to be significant but small (less than 10% of RMR) and transient (less than or equal to 30 min). However, the specific situations in which smokers tend to smoke may mediate the magnitude of this effect, inasmuch as smoking during casual physical activity may enhance it while smoking after eating may reduce it. Sympathoadrenal activation by nicotine appears to be primarily responsible for the metabolic effect of smoking, but possible contributions from nonnicotine constituents of tobacco smoke and behavioral effects of inhaling may also be important. Improved understanding of these metabolic effects may lead to better prediction and control of weight gain after smoking cessation, thus increasing the likelihood of maintaining abstinence.