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Cigarette smoke and adverse health effects: An overview of research trends and future needs

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The frequency of investigations in the area of cigarette smoke composition and chemistry decreased during the last decade. Nonetheless, there are ample data to suggest that cigarette smoke is a highly complex mixture that contains approximately different compounds 8. The complex mixture also contains gases such as ozone, formaldehyde, ammonia, carbon monoxide, toluene and benzene, and about 10 10 particles of different sizes in each mL of mainstream smoke.

Many chemical and biological assays of smoke condensates have also documented the presence of potent inhibitors of carcinogenesis in smoke. Such a complex chemical composition of smoke has made it difficult to determine the active constituent s responsible for the tobacco-related health risks of smoking and has led to studies of individual constituents of smoke such as polycyclic aromatic hydrocarbons PAH , nitrosamines and nicotine.

Thus, over the years, various individual groups of smoke constituents have been the focus of research at different times.

For example, studies of PAH were in vogue during the s and s, followed by nitrosamines in the s. Tobacco alkaloids have long been studied because of their pharmacological activity and have attracted increased attention because of their suspected role in addiction, smoking behaviour and cessation.

However, it is also being realized now that the health effects of this complex mixture are likely to result from a combined effect of these chemicals through multiple mechanisms rather than as result of the effects of a single smoke constituent.

The mixture contains compounds belonging to almost every class of chemicals that are toxic and protective, agonist and antagonist, carcinogenic and anticarcinogenic, and exists in the gaseous as well as the particulate phase. Extensive studies on the chemical constituents of tobacco smoke and their relationship to disease were published by Hoffmann and Hoffmann of the American Health Foundation 8.

Newer studies have largely focused on the comparative chemistry of mainstream and sidestream smoke. Interest in the free radical chemistry of smoke has resurfaced due to the realization that smoke-induced oxidative injury may play an important role in the etiology of a variety of tobacco-related diseases.

Pioneering studies on the free radical chemistry of tobacco smoke, performed in the laboratory of William Pryor at the Louisiana State University 9 , identified short- and long-lived radicals in mainstream and sidestream cigarette smoke, and implicated them in various smoking-associated disease etiologies. Cardiovascular diseases, and atherosclerosis in particular, are the leading causes of death in industrial societies.

The predominant underlying cause of coronary artery disease CAD is atherogenesis, which also causes atherosclerotic aortic and peripheral vascular diseases. Cigarette smoking, independently and synergistically with other risk factors such as hypertension and hypercholesterolemia, contributes to the development and promotion of the atherosclerotic process.

Various studies have shown that the risk of developing CAD increases with the number of cigarettes smoked per day, total number of smoking years and the age of initiation, thus indicating a dose-related response. In contrast, cessation of smoking is reported to reduce mortality and morbidity from atherosclerotic vascular disease. The mechanisms through which smoking influences the development and progression of atherosclerosis are poorly understood at present, but recent studies point to an adverse effect of smoking on endothelial and smooth muscle cell functions as well as thrombotic disturbances produced by tobacco smoke 10 , With the use of modern ultrasonographic techniques, three independent studies performed in the United States, Europe and Australia have demonstrated that both active and passive smokers exhibit impaired endothelium-dependent vasoregulation 12 — Some degree of recovery of endothelial function in ex-passive smokers who have stayed away from smoke-contaminated environments further supported a secondary role of smoke in endothelial dysfunction Evidence has been presented that tobacco-related impairment of endothelial function may be related to its adverse effects on endothelial nitric oxide NO synthase 16 , An association between a genetic polymorphism of the endothelial NO synthase gene and the predisposition of smokers to CAD was reported 18 , Additionally, studies report that smoke interferes with L-arginine and NO metabolism, resulting in reduced NO formation Upregulation of the expression of endothelial cell adhesion molecules CAMs such as vascular CAM-1 and intercellular CAM-1 by smoke condensates, and stimulation of leukocyte and endothelium attachment by exposure to cigarette smoke was demonstrated Cigarette smoke extract has been shown to induce expression of CAMs However, the expression of a specific adhesion molecule is determined in vivo and the relationship between various events is poorly understood.

Exposure to tobacco smoke is known to increase oxidative stress in the body by various mechanisms, including depletion of plasma antioxidants such as vitamin C. At least two studies have been performed to determine the role of oxidative stress in increasing leukocyte-endothelial interactions that precede the development of atherosclerosis in smokers. One study showed that a high intake of vitamin C by smokers significantly reduced the adhesiveness of their monocytes to endothelial cells However, in a second study, sera from young smokers was collected before and after a single oral supplementation with vitamin C and L-arginine a substrate for NO production.

The sera were tested for promotion of the adherence of human monocytes to human umbilical vein endothelial cell monolayers. It was shown that while oral L-arginine caused reduction in such leukocyte adherence, no reduction was seen with vitamin C supplementation This suggested that the NO levels may be important in smoking-induced leukocyte-endothelial interactions, at least during the early stages.

Neither NO nor any other markers of oxidative stress were measured in either of these studies. The levels of 8-hydroxydeoxyguanosine, an oxidized DNA product, and F2-isoprostane, an oxidative arachidonic acid product, were found to be elevated in passive smokers 25 , Oxidation of low-density lipoprotein LDL , which is a gold standard risk factor of the atherosclerotic process, was also found to be elevated in smokers, as determined by the presence of increased levels of autoantibodies against oxidized LDL.

Similarly, intake of a mixture of antioxidants was found to increase the resistance of smoker LDL to oxidative modification 28 and reduce the plasma levels of 8-hydroxydeoxyguanosine in passive smokers Relatively few studies related to cardiovascular effects of cigarette smoke have been performed in rodent models. Such animal studies are, however, needed to delineate the role of different mechanisms in promoting atherosclerotic disease and for developing appropriate interventions.

Tobacco carcinogenesis has remained a focus of research during the past 10 years, and various epidemiological and experimental studies have not only confirmed the major role of tobacco smoke exposure in lung and bladder cancers, but have also reported on its association with cancers of various other sites, such as the oral cavity, esophagus, colon, pancreas, breast, larynx and kidney.

It is also associated with leukemia, especially acute myeloid leukemia. In addition to the highly recognized role of cigarette smoking in lung cancer, it has been implicated in many other chronic diseases, including chronic bronchitis and pulmonary emphysema.

In the United States, the reduction in smoking has resulted in a decline in death due to lung cancer in men since the mid s. However, the incidence of lung cancer in women has surpassed that of breast cancer and continues to rise; it will likely be the focus of future studies 29 , Both active and passive smoking are implicated in this increase, and several studies of smoking behaviour and disease incidence in women suggest greater susceptibility of women to tobacco carcinogens Because of the antiestrogenic protective effects of smoking, the role of smoking in breast cancer is controversial.

However, recent studies suggest that both active and passive smoking may have a role in the occurrence of breast cancer. One example is a study that found an OR of 4. Women who were first exposed to passive smoke after 12 years of age had a lower, although still elevated, OR In both men and women, cancers of the head and neck are also on the rise, and this has been attributed to increased use of smokeless tobacco products.

Also, a synergistic interaction between cigarette smoking and radon exposure was confirmed in a large study that showed that lung cancer incidence due to an interaction between smoking and radon exposure exceeded incidence accounted for by additive effects and, therefore, indicated multiplicative effects Comparative toxicity studies have shown that in comparison with standard cigarettes, the new experimental cigarettes that heat tobacco have a relatively low toxicity One interesting observation relates to the nature of lung cancer, which has changed over the years with respect to the location and the types of lung tumours observed in smokers.

In the past, the primary tumours observed among smokers were the centrally located squamous cell carcinomas of the airways. Now, the predominant lung tumours in smokers are peripheral adenocarcinomas and other non-small-cell lung cancers.

This shift in tumour types has been attributed to changes in the composition of cigarettes and its effect on the smoking patterns of tobacco users over the past 30 years 8 , Significant reductions in cigarette tar and nicotine and increased levels of nitrates in cigarettes have markedly altered the manner in which cigarettes are smoked.

These changes in smoking patterns have promoted greater deposition of smoke constituents into the peripheral lungs, where adenocarcinomas develop.

Major advances are being made in the area of molecular epidemiology of tobacco-related cancers in human populations. Many recent epidemiological studies have focused on the differential susceptibility to tobacco-related cancers; they have employed polymerase chain reaction-based molecular assays that permit genotypic analysis of small human samples and supplement the information generated by enzymatic and immunological assays.

These assays are increasingly being used in human and experimental studies to examine various gene-gene and gene-environment interactions. One area that has received considerable attention in recent years is the role of polymorphic enzymes in the development of diseases.

It is now well recognized that genetic polymorphism strongly influences cancer susceptibility and incidence. The frequencies of mutated alleles of proto-oncogenes, tumour suppressor genes and xenobiotic bio-transformation genes vary significantly among different populations and impact substantially on their susceptibility to cancer. Some are even entirely absent in individuals, thereby influencing their susceptibility to disease development. The chemical complexity of tobacco smoke and the metabolic activation requirements for many of its carcinogenic constituents have drawn particular attention to genetic polymorphisms of biotransformation enzymes that metabolize tobacco smoke carcinogens.

Thus, genes for various activating enzymes such as cytochrome P CYP proteins, and deactivating enzymes such as glutathione S-transferase GST , N-acetyl transferase NAT and uridine diphosphate-glucose transferase have been the main target of many recent studies in the context of tobacco carcinogenesis. Two polymorphic variants that interact with smoking to modify lung cancer risk have been identified 47 , Thus, a homozygous minor allele combined with smoking was found to increase lung cancer risk.

Studies of the same gene in Western populations have, however, yielded negative or conflicting results 49 , although an interaction of CYP1A1 variants with the GST null genotype has been reported to significantly increase lung cancer risks in non-Japanese populations 50 , Depending on the presence or absence of a particular variant, individuals can be categorized as slow or fast acetylators, which in turn can influence the incidence of bladder cancer.

It was shown that slow acetylator NAT2 is an important modifier of the amount of aromatic amine-DNA adduct formation even at a low dose of tobacco smoke exposure Slow acetylator NAT2 genotype was also a significant risk factor for bladder cancer in moderate and heavy smokers, but had no effect in nonsmokers GSTs are another group of metabolic detoxification enzymes that have attracted a great deal of interest in recent years because of their association with risks for different types of cancers.

Based on their sequences, these enzymes are divided into five classes. Furthermore, the risk to individuals who carry homozygous deletions is generally small but increases significantly on interaction with cigarette smoking Among all metabolic cancer susceptibility genes, the association of GSTM1 deficiency with cancer risk is the most consistent and unidirectional. Various experimental and epidemiological observations support the role of this gene in tobacco-related cancers.

For example, it has been observed that the excretion of urinary mutagens and the number of lung tissue DNA adducts in GSTM1-deficient smokers is significantly greater than those carrying the wild-type allele 55 — Various epidemiological studies also support the premise that deficiency of this enzyme predisposes for lung and bladder cancers Furthermore, low activity alleles of GSTPi have been often found in association with different types of human cancers 59 , In addition to anomalies of biotransformation enzyme genes, inactivation of tumour suppressor genes such as p53 , and activation of the proto-oncogene K-ras are also involved in tobacco-related cancers.

Various mutated forms of tumour suppressor gene p53 have been commonly detected in lung tumours and it has been found that these mutations are predominantly located in exons 5 to 8. The nature of point mutations in this gene has been extensively investigated and studies show that the most common mutant allele of the p53 gene possesses a G: C transversion 61 , which is associated with tobacco use 62 , The above studies show that several genetically controlled polymorphic enzymes and enzyme systems are linked to tobacco carcinogen activation and deactivation.

Some of these genes have been identified and characterized, but others remain undiscovered. Not only the independent effects of single gene polymorphisms, but an interplay of multiple gene interactions appear to be involved. The complexity of epidemiological studies, which have many uncontrollable variables, makes it difficult to study such interactions and their control in human studies.

Additionally, many of the enzymes involved in tobacco carcinogen metabolism are also induced by other environmental factors such as alcohol use, dietary constituents, pesticide and xenobiotic exposure, hormonal status, etc, further complicating the interpretation of data.

The interaction of many of these genes with each other and the effect of environmental factors are just beginning to be examined.

The adverse effects of cigarette smoke on human health are widely recognized. It is the main etiological agent in chronic obstructive pulmonary disease and lung cancer, and is a known human carcinogen. While the risks to human health from active smoking are accepted, evidence supporting the risk of involuntary exposure to environmental tobacco smoke ETS has accumulated in recent years.

It is the main source of toxicant exposure by inhalation in nonsmokers. Despite recent regulations, smoking in public enterprises is not uncommon. However, despite an occasional report on the effect of secondhand smoke in nonsmokers, little attention was given to this aspect of smoking until about ETS is now regarded as a risk factor for development of lung cancer, cardiovascular disease and altered lung functions in passive smokers In general, children exposed to ETS show deterioration of lung function, more days of restricted activity, more pulmonary infections, more days in bed, more absences from school and more hospitalization than children living in nonsmoking homes Passive smoking is also implicated in increasing atherosclerosis in individuals 15 to 65 years of age.

Children exposed to ETS are at higher risk of developing cardiovascular disorders. Quantitative risk estimates were obtained by measuring the intimal-medial thickness of the carotid artery in a large longitudinal atherosclerosis risk study of 10, individuals.

A recent meta-analysis 67 of 18 epidemiological studies 10 cohort and eight case-control further showed an increased RR of CAD in ETS-exposed individuals. These investigators also identified a significant dose-response relationship between the intensity of smoke exposure and risk of CAD in passive smokers.

Cardiovascular health risks of smoke-exposed women are of particular concern. Although the exposure to ETS is a current topic of debate in tobacco-related cancers and other lung diseases, the limited research at the basic experimental level provides a strong argument for launching experimental studies to support human data and explore disease mechanisms.

Follow-up of news stories, and local and state ordinances, leads to the conclusion that more communities and states are restricting exposure to secondhand smoke. The results are summarized below. A total of hits were obtained and a careful review of the abstracts provided the following distribution:. A similar search of the NIH database from to revealed grants in all award categories.

The grant distribution by category was as follows:. All the remaining grants generally supported behavioural and epidemiological studies in humans or other systems. Thus, it is clear that the need for basic experimental research in the field of smoking-associated diseases and the mechanisms through which tobacco smoke causes various diseases remain as important as they ever were. The escalation of health care costs makes it even more necessary to find ways to protect the health of smokers and smoke-exposed individuals with any dietary or therapeutic interventions that hold promise.

The most benefit is likely to result from detailed epidemiological studies complemented by specific molecular genotyping of various populations. Ideally, studies of this type will re-evaluate the prevalence of smoking and tobacco use and determine the exact nature of tobacco-related disease incidence, the role of contributory factors such as dietary habits, exposure to other substances and the genetic composition of subpopulations most at risk.

Various biochemical and molecular assays will need to be applied to screen nonsmoker and smoker populations for a variety of health risks. Analysis of the results from such studies will help identify the main interacting factors for various health risks and define relationships among various epidemiological parameters.

It would appear necessary to assemble teams of multidisciplinary investigators to perform these coordinated human studies in the field and in the laboratory. By nature, such studies are expensive and will involve commitment of resources, time and substantial amounts of funds to obtain meaningful results. Given the limited resources and competing priorities for research funding, it is not easy to undertake such human studies.

Hence, the experimental studies in animal models using inhalation exposure to whole smoke, and not individual constituents of smoke, is probably the next best approach for smoking and health programs. The human epidemiological studies described in the present review have identified a number of genes that appear to have a distinct role in various tobacco-related diseases, and cancers in particular.

Inability to control all the different variables in human studies has made it difficult to clearly define the contribution of various suspect genes in tobacco carcinogenesis. With the recent commercial availability of a variety of transgenic and knock-out animals for research, it would be most desirable, as a first step, to use these animals to establish experimental models of various tobacco-related diseases which can then be used for determining the contribution of different genes to disease processes and for elucidation of the mechanism s of disease development.

Furthermore, these animal models can be used to identify various agents possessing protective and therapeutic potential. Research efforts in the area of smoking and health would benefit by focusing on studies of the in vivo effects of inhaled whole cigarette smoke in animal models of known specific genetic composition.

Selection of the genetic composition would also require a thorough consideration of the information available from human molecular epidemiological studies. As indicated earlier, there are a number of genes that clearly influence the development of smoke-related diseases. In this context, many relevant transgenic and knock-out animals that can be effectively used for the study of tobacco-related diseases are now becoming available.

Tobacco abuse is a major public health problem and includes secondhand smoke exposure. Continued efforts to control and eliminate this abuse are a medical necessity. National Center for Biotechnology Information , U. Journal List Int J Angiol v. Telephone , fax , e-mail ude. We are a team of professional native English speaking writers and students, working day and night to create a helpful academic guide for current students.

In our posts, we will uncover the secrets of writing essays, research papers, term papers and dissertations. Sometimes we would take on homework assignments from students and assist them in completing their tasks free of charge. Tobacco has remained to be the most widely used drug all over the world despite its negative effects to human health.

It is used by both male and females. According to several researches it has been noted that tobacco smoking is responsible for more deaths annually than any other related hazards such as illicit brews and road accidents. Smoking of tobacco affects the body both internally and externally.

Some of the effects of occur after one has started smoking while others occur in the long term life of the smoker. Amongst young people who engage in smoking at early age it leads to addiction hence the youngsters cannot easily leave the smoking.

As a result of addiction, most young people continue to use tobacco that eventually lowers the functioning of lung and its growth rate. Furthermore; in adults it causes heart disease such as heart attack and stroke. Scientists suggest that someone who smokes a pack of cigarettes each day lives less 7 years of his life expectancy and to the early smokers it increase the risk of lung cancer infection.

Lung cancer is the most common ailment risk that smokers have to endure with as they smoke in their day to day life. Recent studies have suggested that the level of psychological distress is more in smokers than in non-smokers adults thus it indicates that smoke leads to exposure of high levels of mental stress.

Moreover,it was found out that smoking is a cause for most divorce in many couples. It suggested that smokers have a 54 per cent greater chance of divorcing their wives than nonsmokers.


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Tobacco Usage - Research Paper Sample. Tobacco has remained to be the most widely used drug all over the world despite its negative effects to human health. It is used by both male and females.

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