Effects of smoking research paper

Rafael M, Zully K.

The habit of smoking. Causes and influences of the environment home-schooling high school students. Interdiscip J Contemp Res Bus ; This article has been cited by 1 Reasons for betel quid chewing amongst dependent and non-dependent betel quid chewing adolescents: a school-based cross-sectional survey Azmina Hussain,Sidra Zaheer,Kashif Shafique Substance Abuse Treatment, Prevention, and Policy. Reasons for smoking among the teenagers of age 14—17 years in Vikarabad town: A cross-sectional study.

Table 1: Opinions of the students regarding various reasons for smoking habit Click here to view. This article has been cited by. Reasons for betel quid chewing amongst dependent and non-dependent betel quid chewing adolescents: a school-based cross-sectional survey.

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Substance Abuse Treatment, Prevention, and Policy. Related articles Causes of smoking smoking social factors teenagers. Access Statistics. Seventy percent of smokers want to quit, but only percent will be successful on their own [16]. Long-term tobacco abstinence is extremely difficult and may require several attempts using multiple cessation strategies before a smoker achieves his or her ultimate goal. The average smoker has tried to quit six to nine times, and the quit rate only reaches percent with more effective interventions such as behavioral and pharmacological therapies [16].

It is imperative that physicians continue to work with patients on an ongoing basis to find cessation modalities that work for them. Nicotine replacement therapies such as the gum, patch or inhaler and Bupropion increase quit rates 1. Early results with Varenicline are also promising, with quit rates increased 2- to 3-fold over placebo. Bringing in social support systems such as friends and family may be effective as well. VitalSigns web site. Accessed December 3, Maugh TH. September 08, World Health Organization. The Tobacco Atlas. Office of the Surgeon General of the United States. The health consequences of smoking—nicotine addiction; The health consequences of smoking: a report of the surgeon general.


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Cigarette smoking increases colorectal cancer risk. December 3, Office of Surgeon General of the United States.

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Perceptions of health risks of cigarette smoking: A new measure reveals widespread misunderstanding

The effects of a smoking cessation intervention on Ann Intern Med. Cigarette smoking among adults—United States, Accessed December 15, Virtual Mentor.

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Consequences of Tobacco Use Fifty percent of smokers die of a smoking-related disease, and the life expectancy of one in four smokers is reduced by as much as years [5]. Areas of the body damaged by smoking include: Skin: Poor blood circulation due to chronic vascular insults leads to impaired oxygen delivery to the skin, causing lasting damage to collagen and epithelial tissue. This phenomenon also contributes to poor wound healing, making elective surgeries risky and emergency surgeries dangerous [7]. However, an appreciation of the neurotransmitter-related mechanisms involved in reward circuits in the human brain has suggested many candidate loci potentially associated with nicotine dependence The first genetic association studies in humans at dopaminergic loci 82 - 88 have reported statistically significant differences in the allele frequencies between smokers and nonsmokers at markers linked to the genes coding for the D1, D2, and D4 dopamine receptors and at the dopamine transporter, consistent with the dopaminergic reward hypothesis of nicotine dependence As in some previous studies of the D2 dopamine receptor in case-control studies of substance abuse 90 , the less frequent allele A1 at a genetic marker flanking the dopamine receptor D2 coding sequence DRD2 was found to be at a higher frequency in the collections of smokers versus nonsmokers 82 , In a sample of smokers undergoing a limited smoking cessation intervention, a protective association with a particular allele allele 9 at the dopamine transporter SLC6A3 was observed with smoking status, age at smoking initiation, and history of quitting, and the protective association with smoking status was stronger in those individuals with DRD2 A2 genotypes Since the DRD2 A1 allele has been found previously to be associated with lower D2 receptor densities 91 and the SLC6A3 allele 9 has been associated with excess dopamine after cocaine abuse 92 , this suggests that the protective association with smoking status observed may be due to normal densities of DRD2 receptors and increased synaptic dopamine that may provide some resistance to nicotine dependence At the D4 dopamine receptor locus, allele DRD4.

Smoking Causes Cancer, Heart Disease, Emphysema

In Caucasian-Americans, a statistically significant association of allele 4 of the DRD4 receptor not associated with novelty seeking with smoking for the regulation of mood in depressed smokers was observed 87 , suggesting that the DRD4 locus may affect smoking behavior in depressed individuals as well as increase vulnerability to nicotine dependence in some populations These preliminary candidate gene studies need to be repeated in larger samples, in samples with similar and different ethnic origins, and in family-based samples to confirm the effect of these alleles on vulnerability to nicotine dependence, to explore the effect in samples that differ in allele frequency and smoking prevalence, and to control for potential confounding in case-control samples.

Future studies involving neurobiologic candidate loci that potentially affect smoking behavior should also emphasize the analysis of functional genetic polymorphisms or of linkage disequilibrium structure to identify haplotypes potentially carrying functional polymorphisms Genetic epidemiologic studies using the twin-study design 95 , where multiple genetic and environmental risk factors and a threshold disease model are modeled by use of concordance data in monozygotic and dizygotic twins, have estimated the effects of genetic and environmental factors on current smoking, smoking initiation, and smoking persistence From the same studies, the mean additive genetic effect on the liability to smoking initiation i.

Thus, twin studies estimate that the majority of the liability to become and to remain a smoker is explained by additive genetic factors. A variable remaining portion of the risk is estimated to be related to specific environmental effects, but there is no consistent, statistically significant evidence for a shared or common environment effect. To assess whether the decline in smoking initiation in men and the increase in smoking initiation in women have led to a change in the interaction of genetic and environmental effects with birth cohort, three large twin studies were reanalyzed that covered birth cohorts from the early s to the mids Researchers tested heterogeneity of twin tetrachoric correlations across samples and across sex and found increased genetic effects in men in two of the samples compared with the third sample; however, there was no genetic heterogeneity by age cohort The modeling of age-related changes in the effects of genetic and environmental factors in smoking initiation in adolescent twin pairs showed that genetic effects increased with age; however, shared environmental effects, which explain the majority of variation in risk at early ages years , were not statistically significant in early adulthood Family studies of the relatives of substance-dependent individuals ascertained in treatment settings, with control subjects located via a random-digit-dialing protocol, suggest that there are both general factors increasing vulnerability to substance abuse and specific factors increasing vulnerability to specific drugs, including habitual smoking Only habitual smoking in the proband, but not other substance abuse, was a statistically significant predictor of habitual smoking in siblings, suggesting a specific risk factor for nicotine dependence.

Personality and behavioral studies have suggested why some people are more likely to smoke and what smokers perceive that they derive from smoking tobacco. Research in motives for smoking posits a limited number of factors based on responses to questions concerning hypothesized reasons for smoking - These factors have been constructed from psychosocial models of various motives for smoking, such as smoking to modify affect, smoking to relax, food substitution smoking, etc.

Investigation of the correlation structure among these hypothesized motives for smoking provided consistent and statistically significant support for six of these factors: addiction, automatic, stimulation, psychosocial, indulgent, and sensorimotor manipulation , Interfactor correlation analysis suggested that the first three factors loaded onto a second-order pharmacologic factor and the last three loaded onto a nonpharmacologic factor Smokers experience self-reported increases in arousal and decreases in stress after smoking cigarettes, with absolute levels of arousal and stress peaking in midday and in the morning, respectively Smokers experience stimulation and sedation simultaneously from each cigarette; however, they also experience lower equilibrium levels of arousal and higher equilibrium levels of stress than nonsmokers.

After smoking cessation, mean arousal and stress levels are increased and reduced, respectively, suggesting that smoking cigarettes may contribute to the increased stress observed in smokers Personality and temperament constructs that use questionnaires to measure heritable personality dimensions quantitatively, e. Novelty seeking, extraversion, impulsivity, and neuroticism have been identified as the personality factors found at higher levels among smokers than among nonsmokers - That both dependent and nondependent smokers exhibit similarly increased sensation-seeking scores relative to nonsmokers suggests that, while increased sensation-seeking may increase liability to smoking initiation, it may not be related to differences in nicotine dependence among smokers.

FTQ and FTND scores have been found to show statistically significant associations with biochemical measures related to the quantity of cigarettes smoked plasma nicotine, plasma or urinary cotinine, and expired CO and are also associated with cessation outcome in trials without nicotine replacement therapy , FTND scores from population-based samples of smokers are statistically significantly lower than scores from smokers seeking cessation help A small fraction of active cigarette smokers are known as chippers or nondependent smokers, defined as smoking five or fewer cigarettes per day Compared with regular smokers, chippers were found to extract similar amounts of nicotine per cigarette and to exhibit similar elimination half-lives of nicotine but to be statistically significantly less nicotine dependent and to have begun their smoking careers significantly more slowly - Regular smokers scored higher on pharmacologic smoking motive factors, and chippers scored higher on nonpharmacologic smoking motive factors Chippers and regular smokers both appear to smoke for affect management; however, unlike regular smokers, chippers do not crave cigarettes and exhibit lower levels of smoking for stimulation and smoking to relieve negative affect.

The establishment of nicotine dependence in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders DSM , third edition, represented the nosologic and diagnostic recognition of this drug dependency Specifically, nicotine is not considered to produce intoxication, and a diagnosis other than nicotine dependence would not be appropriate for maladaptive use of the substance Nicotine dependence is a model for drug dependence, where tobacco smoking fulfills the physiologic, behavioral, and social characteristics of a dependence syndrome, but it also acts as a gateway drug for other drugs of abuse However, the morbidity and mortality due to the direct effects of tobacco smoking exceed the direct or indirect effects of other drugs of abuse or, indeed, of any other single behavior on a population level 2 , While consumption and dependence are statistically significantly associated for all drugs of abuse, tobacco is similar to cocaine and the opiates in terms of its addiction liability; i.

Statistically significant associations have been found in different young adult and adult samples between smoking and depression, anxiety, and alcohol dependence. A randomized trial of clonidine in heavy smokers provided a provocative etiologic link between depression and smoking that led to a number of cross-sectional and prospective studies With the use of data from the St.

In a random-digit-dialing telephone study of Latinos, current smokers were found to have higher mean CES-D scores and were statistically significantly more likely to have experienced depressive symptoms than never smokers In a smoking-cessation study sample, statistically significantly more smokers scored over the CES-D cutoff for depression than in a general population sample; depressed smokers scored statistically significantly higher on the FTND than those below the CES-D cutoff These findings could result from a lack of power, since the prevalence of depression observed in the Durham survey was half that seen in the St.

Louis survey Furthermore, when adjusted for the presence of depression and anxiety disorders, moderate five to six of the criteria met but not mild three to four of the criteria met nicotine dependence was associated with a statistically significant increase in risk for all other drug dependencies compared with nondependent smoking Similarly, when adjusted for other drug dependencies, both mild nicotine dependence and moderate nicotine dependence significantly elevate risk for major depression, although not for any anxiety disorder In a month follow-up period in this young adult sample, the presence of major depression in current smokers resulted in an increased risk of becoming nicotine dependent or to progress from mild to moderate nicotine dependency An unresolved problem in the established association between depression and smoking is the issue of causality, since the potential for self-medication or precipitation of depression on cessation is inherent in the modulating effects of nicotine on neurotransmitter systems For example, tobacco smoke, but not nicotine administration, statistically significantly reduces levels of monoamine oxidases A and B, which are essential metabolic enzymes for many neurotransmitters , , suggesting that other components of tobacco smoke may have a substantial effect on synaptic dopamine concentrations Multiple methods were used in a sample of female twins to assess possible causal relationships between the statistically significant and reciprocally associated diagnoses of nicotine dependence and major depression in co-twins and in their families With the use of the co-twin control method that compares observed and expected rate differences between monozygotic and dizygotic twins, observed concordances rejected a causal model for one DSM-III-R diagnosis causing the other; in contrast, either a noncausal family environment or a noncausal genetic model fits the observed data.

Modeling of genetic and environmental factors indicated a statistically significant genetic correlation between the liabilities to smoking and major depression, with specific environmental factors affecting the liabilities independently and a common environmental factor influencing the liability to smoking only These data suggest that common genetic factors may contribute to both daily smoking and major depression. The relationship between tobacco and alcohol use and abuse has been the subject of comprehensive reviews ,, Smoking and alcoholism are statistically significantly associated in population samples; e.

DSM-III-R-defined nicotine dependence and alcohol dependence were statistically significantly associated with each other, with the association at the same level as that with major depression and anxiety, i. Modeling of the statistically significant associations between alcohol use disorders and nicotine dependence in a university-based sample followed prospectively for 7 years, with individual diagnostic data and family history interview data, supports both reciprocal influence and common vulnerability models Modeling of joint alcohol and tobacco use in a twin sample consisting of two age groups found that shared environmental factors are most important in early use ages years and that genetic factors are more important in later use ages years With the use of the NAS-NRC World War II Twin Registry to investigate the genetic effects on multiple substance use, a twin model with a common genetic pathway to tobacco, alcohol, and coffee use, with no environmental effects and separate pathways with both genetic and shared environmental effects for each substance, provided the best fit to the data Most of the genetic effect on tobacco consumption was found in the common genetic pathway, and most of the genetic effects on alcohol and coffee consumption were found in substance-specific pathways.

Smoking Habit and Nicotine Effects

Regression analysis of heavy consumers of the three substances in the NAS-NRC Twin Registry found two independent latent factors, one underlying heavy smoking and heavy alcohol use and one underlying heavy smoking and heavy coffee drinking Separate factors contributing to the comorbidity of alcohol and nicotine dependence and to the comorbidity of nicotine dependence and coffee drinking may reflect independent regulation of the multiple pharmacologic effects of nicotine and the paired substance Prevalence surveys indicate that some demographic variables—sex, age, ethnicity, and socioeconomic status SES —are consistently associated with cigarette smoking.

However, while the negative association between educational attainment and smoking prevalence is consistently observed in diverse population samples in the United States , some non-U. In the United States, over the period from through , current smoking prevalence among adults less than 65 years of age has decreased in every demographic category except those with less than 12 years of education 9. In those adults greater than or equal to 65 years of age, stable to increased rates of current smoking are observed in those with less than 12 years of education, in women, and in African-Americans 9.

Combined with the postwar demographic bulge, the absolute number of older current smokers continues to increase despite a long-term decrease in smoking prevalence over the 30 years from through The relationship between SES and smoking is complex, involving a number of related factors. The statistically significantly increased risk of smoking prevalence in those below the poverty threshold 14 is concordant with a statistically significantly increased risk for the opportunity of exposure to tobacco products over the age period years because of neighborhood disadvantage, at least in Baltimore MD In this same city, reduced levels of parental monitoring [statistically significantly associated with male sex of the child, reduced educational achievement, and a history of psychiatric disorder in mothers ] are statistically significantly associated with increased risk of smoking initiation Cigarette acceptability and accessibility were the only school and neighborhood measures statistically significantly associated with cigarette smoking rates in a study of Midwestern elementary schools However, neighborhood disadvantage is not always associated with increased rates of cigarette smoking; adjusted for attitude toward substance use and availability including cigarettes , neighborhoods with lower population density, suggesting economic advantage, had higher rates of lifetime cigarette use in this Midwestern sample Intensive marketing of tobacco products has likely played an important role in establishing the prevalence of smoking observed today.

Targeted promotion may be responsible for a menthol cigarette brand being the most prevalent brand among African-American smokers and for brand recognition among adolescents 2, Publication of a cigar-oriented magazine, endorsement of cigar use by celebrities, and marketing to high SES consumers may have reversed a year decline in cigar consumption, the beginning of which coincided with advertising bans enacted in and There is evidence, however, that a number of social environmental factors, especially at the regulatory level, have been working to decrease the prevalence of smoking.

Increasing societal disapproval of smoking since the Surgeon General's Report has resulted in workplace regulation of smoking, among other antismoking sanctions However, a national survey of indoor workplace smoking policies reported by workers themselves observed statistically significantly different levels of workplace smoking restrictions by sex, age, smoking status, and occupation of the worker These differences found between these sociodemographic factors and workplace smoking restrictions parallel differences in smoking prevalence by sex, age, and educational attainment.

Recent U. Food and Drug Administration regulations and measures included in the first states' attorneys' general tobacco settlement were designed to modify the marketing behavior of the tobacco companies to susceptible youth populations and to contribute to smoking cessation programs , Analysis of media campaigns designed to reduce smoking initiation and to increase smoking cessation has demonstrated statistically significant associations between targeted media and reduced rates of smoking in adolescent females A combination of a large state tax increase and tobacco control measures that included prevention, cessation, and environmental tobacco smoke programs was associated with an increased average quarterly decline in cigarette sales, during a period in which average levels of educational attainment and income were decreasing The estimated number of worldwide current smokers of both sexes in exceeded one billion individuals Research into smoking behavior and pharmacology has established that most smokers are smoking to maintain nicotine levels 30 , Recent neurobiologic research 24 has established the proximate molecular neurobiologic substrate of the mechanism that maintains nicotine addiction.

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Nicotine dependence is significantly associated with substance abuse, anxiety disorders, and affective disorders ,, Twin-model analysis of the genetic and environmental factors affecting smoking initiation, current smoking, and persistence reveals that heritability is stable and more important than environmental factors However, major secular changes in smoking prevalence support strong effects of environmental determinants on smoking behavior , as do consistent demographic predictors such as educational attainment in the United States Nicotine dependence, major depression, and alcohol dependence are the three most prevalent specific psychiatric diagnoses in population samples in the United States, while substance abuse, anxiety disorders, and affective disorders are the three most prevalent diagnostic categories , Nicotine dependence is significantly associated with each of these three categories, an example of the striking concentration of psychiatric comorbidity in approximately one sixth of the U.

The increased severity of nicotine dependence within the U. While it is the contamination of the nicotine delivery device with carcinogens, carbon monoxide, and cytotoxic compounds that is the probable source of the attributable risk from smoking in cancer and cardiovascular and respiratory diseases, an improved understanding of the neurobiologic mechanisms that maintain nicotine dependence may provide the basis for reducing morbidity and mortality, through improved smoking cessation therapies.

Methods to incorporate covariates known to be significantly associated with smoking prevalence and behavior, including age, sex, SES, psychiatric history, and previously identified genetic loci, should be used in future candidate gene studies. Research sample design and future analyses of the smoking phenotype must address the consistent, statistically significant risks due to demographic, psychiatric, and genetic factors to improve our understanding of the socioeconomic, psychosocial, and neurobiologic bases of this behavior. Oxford University Press is a department of the University of Oxford.

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