Why Is Smoking Bad For You?

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Smoking is responsible for several diseases, such as cancer, long-term (chronic) respiratory diseases, and heart disease, as well as premature death. Over 480,000 people in the USA and 100,000 in the UK die because of smoking each year. According the US CDC (Centers for Disease Control and Prevention), $92 billion are lost each year from lost productivity resulting from smoking-related deaths.

Of the more than 2.4 million deaths in the USA annually, over 480,000 are caused by smoking.1

Smoking is the largest cause of preventable death in the world. Recent studies have found that smokers can undermine the health of non-smokers in some environments.

In an article published online in Medical News Today on 30 May 2013, we presented data demonstrating that, on average, smokers die ten years sooner than non-smokers.

Smoking causes cancer

Lung cancer is one of the most common causes of cancer deaths in the world. According to the American Lung Association, 90% of male lung cancer patients develop their disease because of smoking. In addition, male smokers are 23 times more likely to develop lung cancer than those who have never smoked. Female smokers are 13 times more likely to develop lung cancer than those who have never smoked.2

In addition to lung cancer, smokers also have a significantly higher risk of developing:

Cigarette on ash tray
Smoking contributes to 80% of lung cancer deaths in women and 90% of lung cancer deaths in men (American Lung Association).

According to Cancer Research UK, one person dies every 15 minutes in Great Britain from lung cancer.

Smoking also raises the risk of cancer recurrences (the cancer coming back).

Why does smoking raise cancer risk?

Scientists say there are over 4,000 compounds in cigarette smoke. A sizeable number of them are toxic – they are bad for us and damage our cells. Some of them cause cancer – they are carcinogenic.

Tobacco smoke consists mainly of:

  • Nicotine – this is not carcinogenic. However, it is highly addictive. Smokers find it very hard to quit because they are hooked on the nicotine. Nicotine is an extremely fast-acting drug. It reaches the brain within 15 seconds of being inhaled. If cigarettes and other tobacco products had no nicotine, the number of people who smoke every day would drop drastically. Without nicotine, the tobacco industry would collapse.Nicotine is used as a highly controlled insecticide. Exposure to sufficient amounts can lead to vomiting, seizures, depression of the CNS (central nervous system), and growth retardation. It can also undermine a fetus’ proper development.
  • Carbon Monoxide – this is a poisonous gas. It has no smell or taste. The body finds it hard to differentiate carbon monoxide from oxygen and absorbs it into the bloodstream. Faulty boilers emit dangerous carbon monoxide, as do car exhausts.If there is enough carbon monoxide around you and you inhale it, you can go into a coma and die. Carbon monoxide decreases muscle and heart function, it causes fatigue, weakness, and dizziness. It is especially toxic for babies still in the womb, infants and individuals with heart or lung disease.
  • Tar – consists of several cancer-causing chemicals. When a smoker inhales cigarette smoke, 70% of the tar remains in the lungs. Try the handkerchief test. Fill the mouth with smoke, don’t inhale, and blow the smoke through the handkerchief. There will be a sticky, brown stain on the cloth. Do this again, but this time inhale and the blow the smoke through the cloth, there will only be a very faint light brown stain.

We have published another article containing a longer list of harmful chemicals found in cigarette smoke and how they can harm you.

Smoking and heart/cardiovascular disease

Smoking causes an accumulation of fatty substances in the arteries, known as atherosclerosis, the main contributor to smoking-related deaths. Smoking is also a significant contributory factor in coronary heart disease risk. People with coronary heart disease are much more likely to have a heart attack.

Tobacco smoke raises the risk of coronary heart disease by itself. When combined with other risk factors, such as hypertension (high blood pressure), obesity, physical inactivity, or diabetes, the risk of serious, chronic illness and death is huge.

Smoking also worsens heart disease risk factors. It raises blood pressure, makes it harder to do exercise, makes the blood clot more easily than it should. People who have undergone bypass surgery and smoke have a higher risk of recurrent coronary heart disease.

According to the American Heart Association:

“Cigarette smoking is the most important risk factor for young men and women. It produces a greater relative risk in persons under age 50 than in those over 50.”

A female smoker who is also on the contraceptive pill has a considerably higher risk of developing coronary heart disease and strokecompared to women using oral contraceptives who don’t smoke.

If you smoke your levels of HDL, also known as good cholesterol will drop.

If you have a history of heart disease and smoke, your risk of having such a disease yourself is extremely high.

A much higher percentage of regular smokers have strokes compared to other non-smokers of the same age. The cerebrovascular system is damaged when we inhale smoke regularly.

Those who smoke run a higher risk of developing aortic aneurysm and arterial disease.

Recent developments on smoking from MNT news

Smoking during pregnancy may lower your child’s reading scores

Research has suggested that babies born to mothers who smoke more than a pack of cigarettes a day while pregnant have lower reading scores and a harder time with reading tests, compared with children whose mothers do not smoke.

Smoking causes half of all deaths from 12 cancers, estimate shows

Researchers estimating the number of deaths from 12 smoking-related cancers have found that 48.5% of the 346,000 deaths in the US in 2011 were attributable to cigarettes.

Does cigarette smoking contribute to schizophrenia?

A meta-analysis published in the journal Lancet Psychiatry reports that people who smoke are more than three times more likely to suffer from psychosis, compared with nonsmokers.

Tooth decay risk doubles in children exposed to secondhand smoke

Exposure to secondhand smoke at 4 months of age is associated with an increased risk of tooth decay at age 3 years, concludes a study published in The BMJ.

We’re not just blowing smoke

 BY MICHAEL ROIZEN, M.D., AND MEHMET OZ, M.D.

Time to quit smoking — period

 BY MICHAEL ROIZEN, M.D., AND MEHMET OZ, M.D.

Classification Tree Analysis as a Method for Uncovering Relations Between CHRNA5A3B4 and CHRNB3A6 in Predicting Smoking Progression in Adolescent Smokers

<span class=”paragraphSection”><div class=”boxTitle”>Abstract</div><div class=”boxTitle”>Introduction:</div>Prior research suggests the <span style=”font-style:italic;”>CHRNA5A3B4</span> and <span style=”font-style:italic;”>CHRNB3A6</span> gene clusters have independent effects on smoking progression in young smokers. Here classification tree analysis uncovers conditional relations between these genes.<div class=”boxTitle”>Methods:</div>Conditional classification tree and random forest analyses were employed to predict daily smoking at 6-year follow-up in a longitudinal sample of young smokers (<span style=”font-style:italic;”>N</span> = 480) who had smoked at least one puff at baseline and were of European ancestry. Potential predictors included gender, lifetime smoking, Nicotine Dependence Syndrome Scale (NDSS), and five single nucleotide polymorphisms (SNPs) tagging <span style=”font-style:italic;”>CHRNB3A6</span> and <span style=”font-style:italic;”>CHRNA5A3B4</span> Haplotypes A, B, and C. Conditional random forest analysis was used to calculate variable importance.<div class=”boxTitle”>Results:</div>The classification tree identified NDSS, the <span style=”font-style:italic;”>CHRNB3A6</span> SNP rs2304297, and the <span style=”font-style:italic;”>CHRNA5A3B4</span> Haplotype C SNP rs6495308 as predictive of year 6 daily smoking with the baseline NDSS identified as the strongest predictor. The <span style=”font-style:italic;”>CHRNB3A6</span> protective effect was contingent on a lower level of baseline NDSS, whereas the <span style=”font-style:italic;”>CHRNA5A3B4</span> Haplotype C protective effect was seen at a higher level of baseline NDSS. A <span style=”font-style:italic;”>CHRNA5A3B4</span> Haplotype C protective effect also was observed in participants with low baseline NDSS who had no <span style=”font-style:italic;”>CHRNB3A6</span> rs2304297 minor allele.<div class=”boxTitle”>Conclusions:</div>The protective effects of <span style=”font-style:italic;”>CHRNA5A3B4</span> Haplotype C and <span style=”font-style:italic;”>CHRNB3A6</span> on smoking progression are conditional on different levels of baseline cigarette use. Also, duplicate dominant epistasis between SNPs indicated the minor allele of either SNP afforded comparable protective effects in the absence of a minor allele at the other locus. Possible mechanisms underlying these conditional relations are discussed.<div class=”boxTitle”>Implications:</div>The substantive contributions of this paper are the demonstration of a difference in the protective effects of <span style=”font-style:italic;”>CHRNB3A6</span> and <span style=”font-style:italic;”>CHRNA5A3B4</span> Haplotype C in young smokers attributable to level of cigarette use, as well as observation of duplicate dominant epistasis between the two markers. The methodological contribution is demonstrating that classification tree and random forest statistical methods can uncover conditional relations among genetic effects not detected with more common regression methods.</span>

Examination of the Involvement of Cholinergic-Associated Genes in Nicotine Behaviors in European and African Americans

<span class=”paragraphSection”><div class=”boxTitle”>Abstract</div><div class=”boxTitle”>Introduction:</div>Cigarette smoking is a physiologically harmful habit. Nicotinic acetylcholine receptors (nAChRs) are bound by nicotine and upregulated in response to chronic exposure to nicotine. It is known that upregulation of these receptors is not due to a change in mRNA of these genes, however, more precise details on the process are still uncertain, with several plausible hypotheses describing how nAChRs are upregulated. We have manually curated a set of genes believed to play a role in nicotine-induced nAChR upregulation. Here, we test the hypothesis that these genes are associated with and contribute risk for nicotine dependence (ND) and the number of cigarettes smoked per day (CPD).<div class=”boxTitle”>Methods:</div>Studies with genotypic data on European and African Americans (EAs and AAs, respectively) were collected and a gene-based test was run to test for an association between each gene and ND and CPD.<div class=”boxTitle”>Results:</div>Although several novel genes were associated with CPD and ND at <span style=”font-style:italic;”>P</span> < 0.05 in EAs and AAs, these associations did not survive correction for multiple testing. Previous associations between <span style=”font-style:italic;”>CHRNA3, CHRNA5</span>, <span style=”font-style:italic;”>CHRNB4</span> and CPD in EAs were replicated.<div class=”boxTitle”>Conclusions:</div>Our hypothesis-driven approach avoided many of the limitations inherent in pathway analyses and provided nominal evidence for association between cholinergic-related genes and nicotine behaviors.<div class=”boxTitle”>Implications:</div>We evaluated the evidence for association between a manually curated set of genes and nicotine behaviors in European and African Americans. Although no genes were associated after multiple testing correction, this study has several strengths: by manually curating a set of genes we circumvented the limitations inherent in many pathway analyses and tested several genes that had not yet been examined in a human genetic study; gene-based tests are a useful way to test for association with a set of genes; and these genes were collected based on literature review and conversations with experts, highlighting the importance of scientific collaboration.</span>

Resting-State Functional Connectivity of the Basal Nucleus of Meynert in Cigarette Smokers: Dependence Level and Gender Differences

<span class=”paragraphSection”><div class=”boxTitle”>Abstract</div><div class=”boxTitle”>Introduction:</div>Numerous studies have characterized impaired cerebral functioning in nicotine-addicted individuals. Whereas nicotine interacts with multiple neurotransmitters in cortical and subcortical circuits, it directly targets the cholinergic system, sourced primarily from the basal nucleus of Meynert (BNM). However, no studies have examined how this cholinergic system is influenced by cigarette smoking. Here, we addressed this gap of research.<div class=”boxTitle”>Methods:</div>Using a dataset from the Functional Connectome Projects, we investigated this issue by contrasting seed-based BNM connectivity of 40 current smokers and 170 age- and gender-matched nonsmokers. We followed our data analytic routines in recent work and examined differences between smokers and nonsmokers in men and women combined as well as separately.<div class=”boxTitle”>Results:</div>Compared to nonsmokers, female but not male smokers demonstrated greater positive BNM connectivity to the supplementary motor area, bilateral anterior insula, and right superior temporal/supramarginal gyri as well as greater negative connectivity to the posterior cingulate cortex and precuneus. Further, BNM connectivity to the supplementary motor area is negatively correlated to the Fagerström Test for Nicotine Dependence score in male but not female smokers.<div class=”boxTitle”>Conclusions:</div>Along with a previous report of upregulated nicotinic acetylcholine receptor in male but not female smokers, these new findings highlight functional changes of the cholinergic systems in cigarette smokers. The results suggest sex-specific differences in cholinergic dysregulation and a need for multiple imaging modalities to capture the neural markers of nicotine addiction.<div class=”boxTitle”>Implications:</div>Nicotine influences cognition via cholinergic projections of the basal forebrain to the cerebral cortex. This study examined changes in resting-state whole-brain functional connectivity of the BNM in cigarette smokers. The new findings elucidate for the first time sex differences in BNM–cerebral connectivity in cigarette smoking.</span>

Smokers’ Perspectives on Texting for Tobacco Dependence Treatment: A Qualitative Analysis

<span class=”paragraphSection”><div class=”boxTitle”>Abstract</div><div class=”boxTitle”>Background:</div>Numerous evidence-based pharmacologic and behavioral approaches exist for the treatment of tobacco dependence. Short-message service texting is a newer modality which shows promise, but smokers’ perspectives on texting have not been widely explored.<div class=”boxTitle”>Objective:</div>To use a qualitative research approach to elicit from a sub-sample of participants in a pilot clinical trial their perspectives concerning the feasibility, acceptability, and personal relevance of a publicly available texting program for smoking cessation.<div class=”boxTitle”>Methods:</div>Adult smokers enrolled in the intervention arm in a randomized trial of tobacco treatment were interviewed by telephone. Consenting subjects engaged in a 15–30min semi-structured interview with a trained research assistant, discussing their experience with and attitudes about the texting program and how it affected their tobacco use. Interviews were audio-recorded, transcribed verbatim, and analyzed thematically. Descriptive statistics were calculated for the 16 Likert-formatted items.<div class=”boxTitle”>Results:</div>Of 30 subjects in the intervention arm, 25 (83%) agreed to participate in the qualitative interviews. In general subjects found the program helpful. Common themes were that the texts served as a form of social support, provided useful strategies to reduce tobacco use, validated subjects’ attempts to quit, and offered welcome distractions from cravings. Subjects were satisfied with the frequency, timing, and number of texts, although some improvements were suggested.<div class=”boxTitle”>Conclusions:</div>Texting was perceived as feasible, acceptable, and helpful in smokers’ attempts to abstain from tobacco.<div class=”boxTitle”>Implications</div>The major themes identified included the program being a valued source of external support that provided useful strategies to reduce tobacco use. Subjects were satisfied with the frequency, timing, and number of texts. Texting was perceived as feasible, acceptable, and helpful in smokers’ attempts to abstain from tobacco. Suggestions to improve the program primarily concerned increasing customizable options and using simple, declarative sentences.</span>

Access to Subsidized Smoking Cessation Medications by Australian Smokers Aged 45 Years and Older: A Population-Based Cohort Study

<span class=”paragraphSection”><div class=”boxTitle”>Abstract</div><div class=”boxTitle”>Introduction:</div>The principal aim of this study was to assess the accessibility of subsidized cessation medications to socioeconomically disadvantaged smokers, including smokers living in regional and remote communities.<div class=”boxTitle”>Methods:</div>Analyses used baseline questionnaire and linked Pharmaceutical Benefits Scheme data for 18 686 regular smokers participating in the 45 and Up Study, a large-scale Australian cohort study of people aged 45 years and older. Participants who were dispensed nicotine replacement therapy, varenicline, or bupropion were identified from the Pharmaceutical Benefits Scheme data, which provide an essentially complete record of participants’ access to subsidized pharmaceuticals. Associations between the supply of each pharmacotherapy and a range of sociodemographic and health-related variables were evaluated using multiple logistic regression.<div class=”boxTitle”>Results:</div>The odds that participants were supplied with a cessation medication declined markedly with increasing age for participants older than 60 years and were substantially higher for participants who smoked 20 or more cigarettes/day than for participants who smoked fewer than 10 cigarettes/day. Participants with no formal qualification and those residing in socioeconomically disadvantaged areas had higher odds of receiving nicotine replacement therapy or varenicline than university-educated participants and participants living in the least disadvantaged areas. There was no evidence that participants residing in regional and remote communities had lower odds of receiving a cessation medication than participants residing in major cities.<div class=”boxTitle”>Conclusions:</div>Older Australian smokers’ access to cessation pharmacotherapies is determined predominantly by age and daily cigarette consumption and does not appear to be limited by educational achievement, socioeconomic disadvantage, or remoteness.<div class=”boxTitle”>Implications:</div>Promoting the use of cessation medications is a principal measure proposed to achieve Australia’s <span style=”font-style:italic;”>National Tobacco Strategy 2012−2018</span> goal of reducing cigarette consumption among socioeconomically disadvantaged smokers. The results of this large-scale cohort study indicate that access to cessation pharmacotherapies is determined primarily by age and daily cigarette consumption, and is not limited by socioeconomic circumstances, providing some reassurance that existing government subsidies are sufficient to ensure that pharmaceutical aids are accessible to all Australian smokers.</span>

Study identifies two additional carcinogens not previously reported in e-cigarette vapor

While previous studies have found that electronic cigarettes emit toxic compounds, a new study from Lawrence Berkeley National Laboratory (Berkeley Lab) has pinpointed the source of these emissions and shown how factors such as the temperature, type, and age of the device play a role in emission levels, information that could be valuable to both manufacturers and regulators seeking to minimize the health impacts of these increasingly popular devices.

Caffeine Concentrations in Coffee, Tea, Chocolate, and Energy Drink Flavored E-liquids

<span class=”paragraphSection”><div class=”boxTitle”>Abstract</div><div class=”boxTitle”>Introduction:</div>Most electronic cigarettes (e-cigarettes) contain a solution of propylene glycol/glycerin and nicotine, as well as flavors. E-cigarettes and their associated e-liquids are available in numerous flavor varieties. A subset of the flavor varieties include coffee, tea, chocolate, and energy drink, which, in beverage form, are commonly recognized sources of caffeine. Recently, some manufacturers have begun marketing e-liquid products as energy enhancers that contain caffeine as an additive.<div class=”boxTitle”>Methods:</div>A Gas Chromatography-Mass Spectrometry (GC-MS) method for the quantitation of caffeine in e-liquids was developed, optimized and validated. The method was then applied to assess caffeine concentrations in 44 flavored e-liquids from cartridges, disposables, and refill solutions. Products chosen were flavors traditionally associated with caffeine (ie, coffee, tea, chocolate, and energy drink), marketed as energy boosters, or labeled as caffeine-containing by the manufacturer.<div class=”boxTitle”>Results:</div>Caffeine was detected in 42% of coffee-flavored products, 66% of tea-flavored products, and 50% of chocolate-flavored e-liquids (limit of detection [LOD] – 0.04 µg/g). Detectable caffeine concentrations ranged from 3.3 µg/g to 703 µg/g. Energy drink-flavored products did not contain detectable concentrations of caffeine. Eleven of 12 products marketed as energy enhancers contained caffeine, though in widely varying concentrations (31.7 µg/g to 9290 µg/g).<div class=”boxTitle”>Conclusions:</div>E-liquid flavors commonly associated with caffeine content like coffee, tea, chocolate, and energy drink often contained caffeine, but at concentrations significantly lower than their dietary counterparts. Estimated daily exposures from all e-cigarette products containing caffeine were much less than ingestion of traditional caffeinated beverages like coffee.<div class=”boxTitle”>Implications:</div>This study presents an optimized and validated method for the measurement of caffeine in e-liquids. The method is applicable to all e-liquid matrices and could potentially be used to ensure regulatory compliance for those geographic regions that forbid caffeine in e-cigarette products. The application of the method shows that caffeine concentrations and estimated total caffeine exposure from e-cigarette products is significantly lower than oral intake from beverages. However, because very little is known about the effects of caffeine inhalation, e-cigarette users should proceed with caution when using caffeine containing e-cigarette products. Further research is necessary to determine associated effects from inhaling caffeine.</span>