Smoking chronic, effects

Inhaled nicotine is efficiently delivered to the brain (see chapter by Benowitz, this volume) where it selectively interacts with its central targets, the neuronal nicotinic acetylcholine receptors (nAChRs). The multiple subtypes of uAChR (see chapter by Collins et al, this volume) all bind nicotine but with different affinities, depending on the subunit composition of the uAChR. Binding may result in activation or desensitisation of uAChRs, reflecting the temporal characteristics of nicotine dehvery and local concentration of nicotine. Another level of complexity of the actions of nicotine reflects the widespread and non-uniform distribution of uAChR subtypes within the brain, such that nicotine can influence many centrally regulated functions in addition to the reward systems. In this chapter, we address the consequences of nicotine interactions with nAChRs at the molecular, cellular and anatomical levels. We critically evaluate experimental approaches, with respect to their relevance to human smoking, and contrast the acute and chronic effects of nicotine. 

Cannabis sativa plants contain at least 400 different compounds, of which as many as 60 are structurally related to 5 -tetrahydrocannabinol (5 -THC), the primary psychoactive constituent of cannabis. When cannabis is smoked, hundreds of additional compounds are produced by pyrolysis, which may contribute to both acute and chronic effects (Abood and Martin, 1992). The central nervous system actions of canna-binoids are mediated primarily through the CBj receptor. A second type of cannabinoid receptor, termed the CB2 receptor, is distributed primarily in the periphery (Gifford et ah, 1999). Activation of central cannabinoid receptors modulates neurotransmitter release at... 

Peak blood levels occur within 15 minutes after smoking. The effects last for approximately 4 hours, although it may take more than 24 hours for an individual to return to a normal state. The drugs are stored in fatty tissue and released slowly. PCP has a long half-life ranging from many hours to days, and the PCP glucuronide metabolite can be found in urine for several days or weeks. PCP is found in breast milk. The half-life of ketamine is three to four hours, and metabolites of ketamine are excreted in urine. PCP and ketamine cross the placental barrier, and infants of chronic abusers have been born with cerebral palsy, facial deformities, and behavioral abnormalities. 

Nicotine itself is the only common cause of this type of poisoning. (Varenicline toxicity is discussed elsewhere in this chapter.) The acute toxicity of the alkaloid is well defined but much less important than the chronic effects associated with smoking. In addition to tobacco products, nicotine is also used in insecticides. 

Block, R.I., Farinpour, R., and Braverman, K., Acute effects of marijuana on cognition relationships to chronic effects and smoking techniques, Pharmacol. Biochem. Behav., 43, 907, 1992. 

Consequences of the short-term effects of marijuana can greatly influence a teen s future life. Short-term acute effects describe a condition that is temporary and short-lived longterm chronic effects are cumulative and can last a lifetime. Many studies document the acute and chronic health consequences of smoking marijuana. For instance, there are consistent reports that marijuana temporarily impairs short-term memory and learning. This is confirmed by users of marijuana outside the... 

Studies indicate that both the acute and chronic effects from smoking marijuana often mirror the short-term and long-term effects associated with smoking tobacco. Smoke is made up of both solid and gas particles. The inhalation of hot gases combined with volatile tars (and other particulates) can be very harmful to the lungs, throat, and bronchial tubes. Short-term health effects from smoking marijuana can... 

The composition of tobacco smoke is complex (about 500 compounds have been identified) and varies with the type of tobacco and the way it is smoked. The chief pharmacologically active ingredients are nicotine (acute effects) and tars (chronic effects). 

This chapter is a review of nicotine and begins w ith some background information about its source and the ways that nicotine is consumed, followed by a history of tobacco use. We then discuss the prevalence of nicotine use and the mechanisms of its pharmacological action. We also review the acute and chronic effects of nicotine. The chapter concludes w ith a description of professional services available to help individuals stop smoking. 

Overall, the consequences of legal actions related to the chronic effects of cigarette smoking have been profound for the tobacco industry, for consumers of tobacco products, and for our principles of choice and personal responsibility. For example, if tobacco companies are held liable for diseases that can be traced to the use of their products, then what does that imply about liability for the public s use of alcohol—another legal drug that could have chronic detrimental effects Vt at would the companies liability imply about the principle that individuals have the freedom and responsibility for their actions ... 

Nondietary sources of cyanide include sodium nitro-prusside (a hypotensive agent), succinonitrile (an antidepressant agent), acrylonitrile (used in the plastic industry and as a fumigant to kill dry-wood termites), and tobacco smoke. Chronic exposure to cyanogenic compounds leads to toxic manifestations such as demyelination, lesions of the optic nerves, ataxia (failure of muscle coordination), and depressed thyroid functions. This last effect arises from accumulation of thiocyanate, the detoxified product of cyanide in the body (see below). Thiocyanate inhibits the active uptake of iodide by the thyroid gland and, therefore, the formation of thyroid hormones (Chapter 33). 

Weimer, J.T., Affleck, G.E., Farrand, R.L, Lee, F.K., and Pellerin, R.J., The acute and chronic effects of repeated exposure to United Kingdom red phosphoms screening smokes in rats, mice, guinea pigs, and rabbits. Technical Report ARCSL-TR-79053, Chemical Systems Laboratory, US Amiy Armament, Munitions and Chemical Command, Aberdeen Proving Ground, Edgewood, MD, 1980. 

In the studies of acute effects (1-5), marijuana was administered by smoking under double-blind conditions. The research assistant guided the subject in paced smoking procedures. Cigarettes that contained either 10 mg or 19 mg of A -tetrahydrocannabinol (THC) were compared with placebo cigarettes that contained inactive, cannabinoid-extracted marijuana with only trace amounts of THC. In the studies of chronic effects (6,7), chronic marijuana users were compared with nonusers, i.e., control subjects. In the initial study of chronic marijuana users (6), these users were also grouped according to frequency of marijuana use. 

Holt, P. G., and Keast, D. (1977) Ehvironmentally induced changes in immunological function acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals. Bacteriol. Rev. 41 205-216. 

Anbarasi K, Sabitha KE, Devi CS (2005) Lactate dehydrogenase isoenzyme patterns upon chronic exposure to cigarette smoke protective effect of bacoside A. Environ Toxicol Pharmacol 20 345-350... 

Substances toxic to all individuals are called toxic substances or toxins. Once a toxic substance has contacted the body it may have either acute (immediate) or chronic (long term) effects. Most of food-born toxins are substances with low acute toxicity (such as the pungent alkaloid piperine in black pepper), although some may present chronic effects, such as hepatotoxic pyrrohzidine alkaloids in plants (such as comfrey and coltsfoot species) or cause pathological changes to the respiratory system (e.g., tobacco smoke). 

The sources just discussed primarily, but not exclusively, produce acute health effects. Some indoor pollutants that are not acutely associated with SBS produce only chronic effects. Three of the most notable of these are radon, asbestos, and tobacco smoke. 

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