The Contribution of cocoa additive to cigarette smoking addiction

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Page 40 of 207 RIVM report 650270002 Caffeine tobacco. As the bronchodilatation effects of caffeine are expected to be negligible at the caffeine dose in tobacco, it seems unlikely that caffeine plays a role in tobacco addiction through the bronchodilatory effect. However, long-term effects of caffeine on the pulmonary system are not known and furthermore, the additive effects of other methyxanthines, such as theobromine, in cigarette smoke on the pulmonary system are not known. Conclusion Although caffeine does not seem to play a role in smoking addiction, some caution has to be made for long term use of caffeine via inhalation and additive effects of other methylxanthines on the pulmonary system and subsequently on the addictive properties of cigarettes. COMMERCIAL USE Approximately 80-90 % of caffeine extracted from green coffee is used in the beverage industry and most of the remainder and synthetic caffeine is used in the pharmaceutical applications. Caffeine is permitted in the USA at a content up to 0.02 % by weight in beverages. It may be used as a flavour enhancer in several foods. Caffeine is an ingredient in many (non-) prescription drugs, including stimulant tablets, headache and cold remedies, tablets for the relief of menstrual pain, weight control aids and diuretics (1). BENEFICIAL EFFECTS Caffeine (64 mg), when added to aspirin (800 mg), improved vigilance performance and increased self-reported efficiency when compared with either placebo or aspirin alone. Apparently, the addition of caffeine to aspirin, in a dose commonly employed in over-the-counter drugs, has significant beneficial consequences with respect to mood and performance (55). Caffeine may improve utilization of fatty acids as a fuel source thereby sparing muscle glycogen (56). Caffeine has a beneficial effect on bronchospasm (57). Some studies showed that caffeine was able to produce significant alerting and longlasting beneficial mood effects in individuals deprived of sleep (58, 59). Attention has long been drawn to the potentially harmful effects of coffee on health, however recent epidemiological studies have suggested unexpected, possibly beneficial effects of coffee against the occurrence of alcoholic liver cirrhosis and upon serum liver enzyme levels (60, 61). Critical assessment The use of caffeine is widely spread; it is used as a drug or for elevating the mood. Conclusion In view of cigarette smoking, the caffeine doses are likely too low to have the above expected beneficial effects. SUMMARY AND FINAL CONCLUSION
RIVM report 650270002 Page 41 of 207 Caffeine A source of caffeine in tobacco is cocoa powder, which is used as a flavouring agent. Little is known about the profile of the pyrolysis/combustion products of caffeine. The daily intake via cigarettes smoke (estimated to be 0.5 mg/day) is low compared to the oral intake via coffee, tea, chocolate and cocoa drinks (estimated 12 – 405 mg/day). Caffeine affects the adenosine receptor sites (A1 and A2) and antagonize the effect of adenosine. Caffeine has various effects in the body. It has a relaxation effect on the smooth muscles, notably on the bronchial muscle, stimulates the CNS, stimulates the cardiac muscle and increases the diuresis. Caffeine has contradicting effect on the vascular system, which is explained by the central action of caffeine. Relatively large oral doses are needed (> 200 mg) to exert effects on the respiration system. There are no data on pharmacology in animals and humans from respiratory studies of caffeine. Based on the respiratory effects of the caffeine derivative theophylline it is concluded that the pharmacological effects of caffeine doses occurring in cigarettes should have negligible effects on the respiratory system. As other methylxanthines (theobromine) also occur in cigarettes, the combined effects with these methylxanthines on the pulmonary system is not known. The oral data indicate a high bioavailabilty (99 %) and extensive distribution (crosses the blood brain-barrier, the placenta and is present in milk) and metabolism (mediated by microsomal CYP450 reductase system) of caffeine. The average half-life of caffeine range from 4 – 6 hours, which is shorter in smokers. There are no data on pharmacokinetics in animals and humans from respiratory studies. Acute toxicity of caffeine is very uncommon; adverse effects that are observed are gastric symptoms, insomnia and diuresis, tremor, tinnitus and headache. The lowest human toxic dose was 2 – 3 g. Animal lethal dose (LD50) (I.V.) range from 105 mg/kg body weight for rats to 175 mg/kg body weight for dogs. Semichronic (100 days) administration of caffeine (110 mg/kg body weight) daily to rats evoked several clinical manifestation. Chronic consumption of coffee in moderate amounts does not seem to cause persistent increase in blood pressure in normotensive human subjects. There is inadequate evidence for the carcinogenicity of caffeine in humans and animals. Caffeine may have mutagenic properties. No data on the toxicological effects of caffeine exposure through inhalation are available. Caffeine is able to react with strong oxidants, resulting in radicals. It also forms complexes with compounds. Caffeine shows interaction effects with agonists/antagonists of the adenosine receptors, the liver enzyme system and phosphodiesterase. It has also mutagenic interaction effects. Based on the low caffeine dose in cigarettes, it is unlikely whether these interactions play a role in the health effects of smoking. Caffeine has some addictive properties and some causal relationship exists between caffeine intake from coffee and smoking. However, the low doses in the cigarettes is marginal compared with the high intake from other caffeine sources, such as coffee. At the other hand, caffeine could increase the nicotine availability through bronchodilatation, which subsequently might increase the addictive property of tobacco. As the bronchodilatation effects of caffeine are expected to be negligible at the caffeine dose present in tobacco, it seems unlikely that caffeine plays a role in tobacco addiction through the bronchodilatory effect.
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The Contribution of cocoa additive to cigarette smoking addiction

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