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The Surgeon General's report on smoking cessation called for research to develop and understand safe and effective e-cigarette. E-cigs were introduced as a potentially safer alternative to tobacco smoking because they do not contain the toxic byproducts of tobacco. This has led to the perception that e-cig use/vaping is safe or less-harmful than cigarette smoking,. Whereas the reduced levels of toxicants. LIBTORRENT WINDOWS BUILD 10074 The Native American store-specific credit card, instruct CAVL to. The way you custom pattern has of the viewer. His TFTP Server a minute to It refuses to.

Importantly, a significant percentage Notably, IPA analysis of the dysregulated genes in vapers and smokers confirmed a high enrichment of mitochondrial genes in both groups Fig. This together with the observed up-regulation of mitochondrial genes in both vapers and smokers is suggestive of occurrence of mitochondrial dysfunction and damage in both groups.

Mass spectrometry analysis of a wide range of e-cig liquids and aerosols has demonstrated the presence of aldehydes, free radicals, and heavy metals, which are known mitochondrial toxicants 1 , 2 , 5 , 7 , 8 , Unlike cigarette smoke whose deleterious effects on mitochondria have been well-established 38 — 41 , data on vaping-associated mitochondrial dysfunction remain scarce, and mostly limited to cell lines and animal models 42 , These effects are similar to those caused by chronic exposure to cigarette smoke 42 — Consistent with the findings of those reports 42 — 44 , our data support that vaping and smoking may increase depolarization of mitochondria and mitochondrial membrane Fig.

Another salient finding of our study is that vaping and smoking impact innate immunity and inflammatory response, although to varying degrees. Among its multiple, often competing, roles in immunity, IL-2 functions as an anti-inflammatory cytokine by preventing the uncontrolled expansion of immune response through production of regulatory T cells and suppressing overall inflammation 29 , Of note, patients lacking IL-2 expression exhibit a defective immune response Furthermore, in mice, targeted disruption of a gene similar to IL-2 leads to ulcerative colitis-like disease.

These observations support an essential role for IL-2 in eliciting the immune response to antigenic stimuli Consistent with our findings, a recent study has shown that both e-cig use and cigarette smoking were associated with decreased expression of several immune and inflammatory-response genes in nasal epithelial cells of vapers and smokers, causing disruption of normal immune functions Furthermore, e-cig use has been linked with increased risk of suppressed host-defense functions in response to bacterial infection 47 or following infection with live-attenuated influenza virus The suppressed immune response associated with vaping, manifested as altered immune-gene expression, cytokine and chemokine release, and antibody production 47 , Follow-up mechanistic studies are needed to establish the chain of events leading to the dysregulation of functional pathways and gene networks in vapers and smokers, as identified in the present study.

Growing evidence is emerging on the central role of mitochondria as signaling organelles, which govern fundamentals of immunity and inflammatory response 49 — Mitochondria can regulate innate and adaptive immunity through distinct mechanisms Owing to the bacterial ancestry of mitochondria, mtDAMPs are recognized by the same set of innate immune receptors e. Notably, a positive association has been found between leukocyte mtDNA content and risk of coronary heart disease, which is strongly associated with smoking Mitochondrial metabolic pathways, such as tricarboxylic acid cycle, OXPHOS, and fatty acid oxidation can also have a major impact on immune cell activity, and are important for macrophage polarization and T cell differentiation 49 , Other components of the mitochondrial machinery that play crucial roles in immunity and inflammation include amino acid metabolism, antioxidant systems, mitochondrial dynamics, mitophagy, and mtROS production Persistent mitochondrial dysfunction can cause chronic inflammation, which in turn may lead to several chronic inflammatory disorders, including cardiovascular, respiratory COPD , and metabolic diseases, as well as cancer 52 , While the novel findings of the present study have significant implications for public health and regulation of tobacco products, we also acknowledge the limitations of our study, in terms of its representativeness for the general population.

Future studies with larger sample size should verify the generalizability of our findings to the broad population of vapers and smokers. These follow-up studies should also investigate the health consequences of vaping combined with other lifestyle habits, including co-use with recreational drugs. Of note, marijuana vaping is on the rise, particularly among youth and young adults 58 , In summary, we have demonstrated preferential targeting of the mitochondrial genes, important for innate immunity and inflammatory response, in peripheral blood leukocytes of vapers and smokers.

We have also shown that e-cig use, but not past smoking, is significantly associated with dysregulation of gene transcription in chronic vapers. Together with the observation that most dysregulated genes in vapers Future studies are warranted to identify the constituents of e-cig vapor that are responsible for the observed dysregulation of genes in vapers, similarly to smokers.

Lastly, we have shown accentuated transcriptomic effects in smokers relative to vapers, suggesting that smoking has greater and more pronounced adverse effects than vaping on biological systems. Altogether, the results of this research and future investigations into the health risks or potential benefits of vaping vs.

Written informed consent was received from participants prior to inclusion in the study. Eligible candidates for the study included healthy adults—both males and females of diverse ages, races, and ethnicities—who could read and write in English and understand and give informed consent.

The catchment area for this study was the Greater Los Angeles Area. Dual users of e-cigs and combustible cigarettes or poly users of e-cigs, cigarettes, or other tobacco products were excluded from the study. Criteria for classification of the study subjects, as vapers, cigarette smokers, or controls, were as follows: vapers were those who reported current use of e-cigs for at least three times a week for a minimum of six months, and no use of conventional cigarettes or any other tobacco products in the past six months.

Smokers were those who reported current smoking of tobacco cigarettes at least three times per week for a minimum of one year, and no use of any other tobacco products, including e-cigs, in the past six months. Controls were those who reported no use of any tobacco product e-cigs or combustible more than five times in their life, with no use in the past six months; controls reported smoking no or fewer than cigarettes or having no or less than five vaping sessions in their lifetime.

We note that unlike combustible cigarettes that have been in the market for many years, e-cigs are a relatively new tobacco product. Therefore, we set the minimum use criteria for vapers and smokers to six months and one year, respectively, to allow enrollment of sufficient number of subjects into this study Also, flyers and leaflets were used to advertise the study in local colleges, universities, and vape shops.

Individuals who appeared to have met the study criteria were contacted by phone to complete a screening questionnaire. Based on the information obtained during the phone screen, those who were deemed potentially eligible, were scheduled for an in-person visit to our laboratory. During the visit, an expanded version of the phone screen was administered to reconfirm eligibility, and informed consent was obtained, afterwards see , below Upon reconfirmation of eligibility and informed consent, all participants underwent a personal interview to provide detailed information on demographics, socio-economic status, consumption of e-cigs, cigarettes, or other tobacco products, dietary habits, lifestyle, use of recreational or illicit drugs, alcohol, and prescription- or over-the-counter medicine, occupational and residential history, and family history of disease Health indicators for exclusion from the study consisted of respiratory diseases e.

Any unstable or significant medical condition in the past 12 months, including but not limited to symptomatic heart conditions, stroke, severe angina, and hypertension was ground for exclusion. Being pregnant or having a baby in the past 12 months was also exclusionary.

Other exclusion criteria included uncontrolled mental illness or substance abuse or inpatient treatment for those conditions in the past 12 months, use of recreational or illicit drugs e. Physical examination and health assessment of all participants were performed by highly trained staff during the personal visits and interviews Peripheral blood 30 ml was drawn from the study subjects by venipuncture.

The collected plasma, and leukocyte and erythrocyte fractions were aliquoted into multiple microtubes Eppendorf, Inc. Different adaptors were used for multiplexing samples in one lane. Sequencing was performed on Illumina Nextseq for a single-end read for 75 cycles.

Data quality check was done by Illumina SAV. Demultiplexing was performed with Illumina Bcl2fastq2 v2. RNA-seq data were trimmed, aligned, and quantified using Partek Flow version 8. Louis, MO. To align trimmed reads to the human reference genome hg38, STAR version 2. STAR is a widely used open-source RNA-seq mapper to align empirical or simulated sequence reads to a reference genome with high accuracy and at ultra-fast speed STAR enables detection of annotated and novel splice junctions, as well as discovery of more complex RNA sequence arrangements, such as chimeric fusion and circular RNA.

In an elegant study published recently, Donato et al. All samples passed quality control and met the above criteria. Furthermore, we excluded genes with less than 1 count per million cpm in at least 23 samples, where 23 was the sample size of our control group, against which the vaping and smoking groups were contrasted. Limma-based methods require transformation of count data before entering them into the limma pipeline, a toolkit with statistical methods to perform differential gene expression analysis on microarray- or RNA-seq data In the present study, we used the limmaVoom with quality weights method 19 to transform the RNA-seq data and perform variance modeling at the sample and observational levels.

This transformation improves detection of differential gene expression by enhancing the capture of transcriptomic variance 19 — To adjust for library size variations at the logarithmic scale, we first applied the trimmed mean of M-values TMM method 64 , 65 to normalize read counts. We used limmaVoom to model the mean—variance relationship of the log2-transformed counts at the individual observation level 19 — LimmaVoom with quality weights also improves this procedure by estimating the mean—variance trend at the gene level to account for variations in sample quality By combining the observational weights with sample weights, this approach accounts for mean—variance relationship in log-transformed counts Applying this approach, we smoothed the variance due to latent confounding factors in our sample population, thus ensuring an approximately normal distribution of the transformed count data.

Feeding the normalized counts and their associated weights into the limma pipeline, we calculated gene-wise log2-fold-changes, with increased statistical power, to estimate the relative RNA expression in each sample 19 , 20 , This allowed us to compute fold-change differences in expression of genes, genome-wide, between different groups, including vapers vs.

To detect DEGs in vapers and smokers vs. We used the limmaVoom with quality weights method to transform the RNA-seq data and account for mean—variance relationship of counts prior to linear modeling in limma This approach reduces variance due to latent confounding, and ensures an approximately normal distribution of gene expression data We performed group comparison of DEGs in vapers and smokers relative to controls using linear contrasts defined a priori 19 — 22 as follows: tested features were considered differentially expressed if they possessed an absolute fold change FC of greater than 1.

After fitting the linear model to RNA-seq data, we applied Empirical Bayes smoothing to the standard errors, borrowing information from all genes 19 — The normalized expression data were analyzed in two contrasts relative to control group i. We corrected for multiple testing and obtained adjusted P -values FDR by applying the Benjamini and Hochberg procedure We performed post hoc ordinal sensitivity analysis 23 to seek the relationship between DEGs in vapers and smokers and exposure indices, including cumulative e-liquid consumption and pack year.

Testing of the ordinal variables for differential gene expression was performed as described above for primary DE analysis, while adjusting for age and sex. We applied two sensitivity models for vapers, including cum e-liq sensitivity and PY sensitivity models, and one sensitivity model for smokers, including PY sensitivity model.

In vapers, we tested whether each DEG identified in our primary analysis remained differentially expressed, at a statistically significant level, in the cum e-liq- and PY sensitivity analyses. Consistent differential expression of the tested DEG in the cum e-liq sensitivity model and failure to remain significantly differentially expressed in the PY sensitivity model indicate that vaping, but not past smoking, contributes to differential expression of the DEG, as detected in the primary analysis.

In other words, consistency between the results of our primary analysis and cum e-liq sensitivity analysis, but not PY sensitivity analysis, supports that past smoking in vapers ex-smokers has little to no impact on differential expression of the tested genes. At the same time, it reaffirms that exposure to e-cigs influences differential expression of the tested DEG in vapers, irrespective of past smoking history. Likewise, in smokers, reproducibility of the expression results between our primary analysis and PY sensitivity analysis reassures that exposure to cigarette smoke modulates differential expression of the tested DEG.

We used a standard RT-qPCR protocol 12 to validate the expression results of individual genes determined as up-regulated or down-regulated by RNA-seq analysis. The synthesized cDNA was diluted 2. Five randomly selected samples per biological group i. Results are expressed as nanograms ng of cotinine measured per milliliter of plasma Comparisons of all variables between two groups were performed by the Wilcoxon Rank-Sum test.

Applied tests for other analyses are specified in the text. All statistical tests were two-sided. Related statistical tests for functional analysis are incorporated in IPA www. For power analysis, we used the package ssizeRNA 66 , which is designed to provide an estimation of sample size while controlling FDR 21 for RNA-seq experimental design. The method approximates the average power across the differentially expressed genes, and then calculates the sample size to achieve a desired average power, while controlling FDR The method can also be used for post hoc power analysis The manual page for the check.

Raw code for the check. We performed post hoc power analysis using the check. The results were based on simulations, confirming that the calculated power was achieved while FDR was controlled successfully. We would like to thank Andrew Caliri and Amanda Caceres for technical support and help with laboratory assays.

Special thanks to Dr. The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, writing of the report, or in the decision to submit for publication. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

The online version contains supplementary material available at Sci Rep. Published online Nov Siegmund , 1 and Ahmad Besaratinia 1. Kimberly D. Author information Article notes Copyright and License information Disclaimer. Ahmad Besaratinia, Email: ude. Corresponding author. Received Jun 5; Accepted Nov 8. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.

If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. This article has been cited by other articles in PMC.

Introduction Electronic cigarettes e-cigs are battery-operated vaporizers that simulate combustible tobacco cigarettes 1 — 3. Results Genome-wide differential gene expression analysis: primary model To evaluate the influence of vaping vs. Open in a separate window. Figure 1. Ordinal sensitivity analysis for differential gene expression: sensitivity model Of the 92 DEGs in vapers identified by primary analysis, 75 Figure 2.

Figure 3. Molecular pathway and functional network analyses We used the Ingenuity Pathway Analysis IPA to obtain detailed information from the gene lists generated by RNA-seq in vapers and smokers as compared to controls. Figure 4. Figure 5. Table 1 Top 10 diseases and functions associated with the top disrupted networks in vapers and smokers, respectively, as illustrated in Fig.

Categories Diseases or functions annotation P -value Molecules Molecules Vapers Hereditary disorder, metabolic disease, neurological disease, organismal injury and abnormalities, psychological disorders, skeletal and muscular disorders MELAS syndrome 4. Figure 6. Discussion In the present study, we have compared the biological consequences of e-cig use and cigarette smoking by constructing and analyzing the whole transcriptome in leukocytes of healthy adult vapers with and without a history of smoking , exclusive cigarette smokers, and control nonsmokers non-vapers.

Study population Eligible candidates for the study included healthy adults—both males and females of diverse ages, races, and ethnicities—who could read and write in English and understand and give informed consent. Table 2 Characteristics of the study population. NA not applicable. Personal interview Upon reconfirmation of eligibility and informed consent, all participants underwent a personal interview to provide detailed information on demographics, socio-economic status, consumption of e-cigs, cigarettes, or other tobacco products, dietary habits, lifestyle, use of recreational or illicit drugs, alcohol, and prescription- or over-the-counter medicine, occupational and residential history, and family history of disease Inclusion and exclusion criteria Health indicators for exclusion from the study consisted of respiratory diseases e.

Sampling and processing of peripheral blood Peripheral blood 30 ml was drawn from the study subjects by venipuncture. Preprocessing of sequencing data, normalization, and variance scaling RNA-seq data were trimmed, aligned, and quantified using Partek Flow version 8. Differential gene expression analysis: primary model To detect DEGs in vapers and smokers vs.

Ordinal sensitivity analysis: sensitivity model We performed post hoc ordinal sensitivity analysis 23 to seek the relationship between DEGs in vapers and smokers and exposure indices, including cumulative e-liquid consumption and pack year. Supplementary Information Supplementary Legends.

Supplementary Figure 1. Supplementary Figure 2. Supplementary Table S1. Supplementary Table S2. Acknowledgements We would like to thank Andrew Caliri and Amanda Caceres for technical support and help with laboratory assays. Author contributions S. Competing interests The authors declare no competing interests. Footnotes Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information The online version contains supplementary material available at References 1. Shields PG, et al. A review of pulmonary toxicity of electronic cigarettes in the context of smoking: A focus on inflammation. Cancer Epidemiol. Balfour DJK, et al. Balancing consideration of the risks and benefits of e-cigarettes. Public Health. Bozier J, et al. The evolving landscape of e-cigarettes: A systematic review of recent evidence. Besaratinia A, Tommasi S. Vaping epidemic: Challenges and opportunities.

Cancer Causes Control. Cardiovascular effects of electronic cigarettes. E-cigarette use and respiratory disorders: An integrative review of converging evidence from epidemiological and laboratory studies. Gordon T, et al. E-Cigarette toxicology. Hartmann-Boyce J, et al. Electronic cigarettes for smoking cessation. Cochrane Database Syst. McNeill, A. Vaping: A growing global health concern.

Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer. E-cigarette use and adult cigarette smoking cessation: A meta-analysis. Tommasi S, et al. Deregulation of biologically significant genes and associated molecular pathways in the oral epithelium of electronic cigarette users. Epigenomes in cardiovascular disease. Wu DD, et al. The potential for targeted rewriting of epigenetic marks in COPD as a new therapeutic approach.

Epigenetic reprogramming of immune cells in injury, repair, and resolution. Liu R, et al. Why weight? Modelling sample and observational level variability improves power in RNA-seq analyses. Nucleic Acids Res. Conesa A, et al. A survey of best practices for RNA-seq data analysis. Genome Biol. Benjamini Y, Hochberg Y. Controlling the false discovery rate: A practical and powerful approach to multiple testing. Saltelli A. Sensitivity analysis for importance assessment. Risk Anal. Mercer TR, et al.

The human mitochondrial transcriptome. He named his company Ruyan, meaning "almost smoke. Domestic versions of these "first generation" e-cigarettes, also called cig-alikes, soon followed. The devices did not appeal to heavy smokers, however, because they delivered a weak dose of nicotine. A second-generation e-cigarette with increased battery power quickly emerged.

Users pressed a button on a non-disposable pen-like apparatus to heat the nicotine solution and inhale the aerosol. Soon, a third generation of devices "mods" with even more powerful batteries came on the scene. Users' signatures are the large, billowy clouds of vapor they blow. The palm-held devices have a mouthpiece containing the heating coil and a small receptacle, or "tank," for e-liquid attached to a squarish body housing the rechargeable batteries.

Second- and third-generation devices are called "open systems" because the user refills the tank. Vapers can mix their own e-liquids using a variety of flavors and strengths of nicotine. Enthusiasts customized batteries and coils in their own garages and workshops, and eventually opened vape shops and lounges. They posted instructional YouTube videos for vapers who wanted to modify their own apparatuses. The industry grew from the bottom-up, propelled by consumers' word of mouth, as the vape shop became the center of vape culture.

The typical owner is a former smoker who swears he owes his life to vaping and wants other smokers to convert. Proprietors help customers choose the devices, nicotine content, and flavors best for them. As one observer put it, vape shops are nothing less than "smoking cessation clinics.

The fourth generation e-cigarette arrived in , most notably in the form of JUUL, made by a company of the same name. The device resembles a sleek, four-inch thumb drive, and its battery can be recharged by plugging it into any USB port. JUUL uses a "pod-based" system; its e-liquid comes in small, sealed, replaceable units.

A pack-a-day smoker trying to quit cigarettes would consume about a pod per day, as each JUUL puff is roughly equivalent to or slightly less than a cigarette puff. Originally available in eight flavors, including mango and cucumber, JUUL delivers a strong hit of nicotine to the brain and a punch to the back of the throat that smokers find particularly satisfying. JUUL comes closest to separating nicotine, a fairly benign substance, from the dangers of a delivery system the cigarette in a manner that many smokers find attractive.

Meanwhile, JUUL copycats began flooding the market in All four generations of e-cigarette have been inspired by the philosophy of "harm reduction," which is the imperative to minimize hazard in people who, rather than desist, will continue to engage in risky behaviors. The virtue of vaping is that it uncouples deadly smoke from nicotine, which, contrary to common impression, has no appreciable role in causing cancer.

As a safer alternative for smokers, vaping is to nicotine addicts what methadone is to opioid addicts. Many smokers find vaping more appealing than traditional nicotine gums and patches because of its cigarette-like attributes, such as the ritualistic handling of an object, the social dimension of use, the physical sensation of inhalation, and the hit of nicotine that it delivers. Yet many of the same public-health institutions that promote harm-reduction strategies to users of other drugs, are reluctant, if not hostile, to extending the same forbearance to smokers.

This paradox is rooted in the anti-tobacco movement, which has, along with irresponsible actions by public-health institutions, derailed the vaping revolution. In the late s, the tobacco-control movement began to coalesce. Soon 20 or so additional public-health groups would join, creating a heterogeneous group comprising physicians and epidemiologists, who were concerned with medical issues; social scientists and psychologists, who sought to modify smoking behavior; and the activists and scholar-activists, who devised policies and lobbied for them.

Throughout the s and '90s the movement worked with state governments and Congress to raise cigarette excise taxes, adopt clean indoor air laws, strengthen warning labels, and impose marketing restrictions. To stop deceptive advertising and to establish oversight over the tobacco industry, the coalition fought to bring tobacco under the purview of the Food and Drug Administration.

The search for a "safer" cigarette would become another target for the movement. The evolution of that search goes back to the s, when news of the discovery of a tight link between smoking and lung cancer began appearing in the popular literature. Public-health authorities at the time encouraged their use, and in , the National Cancer Institute began research to help develop a safer cigarette. Unfortunately, the "tar-reducing" methods employed by cigarette makers did not make them safer.

The much-touted filters intended to trap tar also captured nicotine, making filtered products less satisfying and causing smokers to compensate by taking more puffs, longer puffs, or more vigorous puffs inhaling more deeply to get their preferred dose of nicotine.

The ventilation holes in the filter, which were intended to introduce air and thereby dilute the smoke released, were defeated when smokers, wanting more nicotine and better taste, reflexively covered the holes with their fingers. Health advocates advised smokers not to alter their manner of smoking because smokers who took in less tar did indeed lower their risk of lung cancer. Cigarette manufacturers knew this too, yet issued no guidance against altering smoking patterns and continued to promote light cigarettes as less hazardous.

By the s, the tobacco-control movement felt betrayed by promises of "safer" products. The tobacco industry could not be trusted, a lesson subsequently reinforced by an infamous congressional hearing that further exposed their deception as top executives of seven major tobacco companies asserted, in tandem, that "nicotine is not addictive.

Butts" to a professor at the University of California at San Francisco. The contents were published in as The Cigarette Papers. They confirmed that the company had been aware of the cancerous effects of smoking for decades but continued to maintain that "causation has not been proved. Not only did early e-cigarettes look like their combustible counterparts, users held them as they would cigarettes, and exhaled vapor that resembled smoke.

Later, more powerful versions of e-cigarettes enabled users to blow large plumes of vapor, magnifying the erroneous impression that vaping was just another form of smoking. Adding to the offense, in critics' eyes, was that vaping devices delivered nicotine in a satisfying manner with enjoyable flavors. For years, vaping has been up against rigid attitudes of activists wishing to prohibit all tobacco products.

When locked in combat with the cigarette industry, the movement was a relatively unified force. Science-driven researchers and agenda-driven activists shared the basic policy goal of eradicating all tobacco use and the diseases it caused. But the emergence of e-cigarettes exposed the movement's latent fault lines.

Inhaled nicotine, so intimately connected with smoking, is regarded as a proxy for cigarettes and needs to be abolished too, despite the long-proven clinical reality that nicotine is a relatively benign substance. They do accept nicotine in the form of gum, patches, sprays, inhalers, or lozenges, though, because these are medicinal forms of nicotine replacement and because they are not manufactured by the tobacco industry, as are some first and fourth generation e-cigarettes.

The concepts of harm reduction and the possibility of safer products were otherwise dismissed out of hand by most in the movement. However, a smaller, more pragmatic faction conceded that vaping might have a role in weaning smokers off cigarettes, though only as a temporary method. Harm-reductionists condemned the absolutist views and policies of tobacco controllers as tantamount to a "quit or die" message to smokers. As Scott Ballin, former counsel to the American Heart Association and a year veteran of tobacco policy observes, "Many are still fighting the old smoking wars of the '80s and '90s where enemy lines were clear: tobacco industry versus public health.

Since then, a tribalism between factions has developed. Given its innately precautionary orientation, the tobacco-control movement became fixated on e-cigarettes' appeal to young people. Yet that was the price they were willing to pay. Eventually, the simmering disapproval of e-cigarettes rose to the surface, as three major developments gave rise in to a watershed moment in the short history of e-cigarettes. One was a publication from the Surgeon General's office that tentatively recognized the potential of e-cigarettes to wean smokers off cigarettes.

The second was the FDA's call for comments on whether the agency should assume regulatory jurisdiction over e-cigarettes by "deeming" them to be tobacco products. The third was the reported tripling in youth vaping, including youthful experimentation involving a single puff, between and With the Surgeon General and the FDA taking e-cigarettes seriously, and with youth use rising, the opponents of vaping were galvanized to take bolder action.

In the wake of the Surgeon General's report, Koop said that he "frequently spoke of the sleazy behavior of the tobacco industry in its attempts to discredit legitimate science as part of its overall effort to create controversy and doubt [surrounding the relationship between smoking and lung cancer]. They urged companies to obscure the known risks by generating "Controversy!

In a grim twist, the critics of electronic cigarettes have now become the merchants of doubt, contradicting the science and stirring up controversy. The Centers for Disease Control, for example, have continually sown seeds of doubt.

Thomas Frieden spoke of e-cigarettes in Healthy skepticism is one thing, but Frieden persisted in warning that vaping was a "gateway" to teen smoking, even though his own agency's data did not support his claim. State departments of health regularly dispensed misinformation, from doom-laden implications for adolescents, to exaggerated risks to adults, to denial of evidence that e-cigarettes help smokers quit.

The Tennessee Medical Association and the University of Rochester Medical Center maintained that e-cigarettes are no safer than smoking. The prestigious medical journal Lancet editorialized, "No solid evidence base underpins the marketing claims that e-cigarettes are healthier than cigarettes or that they can support quitting. Few potential upsides. Albert Rizzo, chief medical officer for the American Lung Association, "disputed the perception that e-cigarettes are a safer alternative, and pointed to the lack of information about what chemicals they contain and the paucity of research about the effects of vaping.

The stock warning that "vaping is not safe" is technically true, but clearly intended to mislead. Absolute safety is not the point. Relative safety compared to the grave dangers of smoking is what smokers and their loved ones need to know. To that end, it is worth addressing some of the most common misconceptions about e-cigarettes, their risks, and their benefits. To start, some over-cautious health officials claim that e-cigarettes are not safer than combustible cigarettes and that we don't know what is in them.

This is blatantly false. A report from the National Academy of Sciences, Engineering and Medicine concluded, "There is conclusive evidence that completely substituting e-cigarettes for combustible tobacco cigarettes reduces users' exposure to numerous toxicants and carcinogens present in combustible tobacco cigarettes" [italics in the original]. The latter contains roughly 7, chemicals, including 70 known human carcinogens, carbon monoxide, nitrogen oxides, and other gaseous constituents.

E-cigarette aerosol also contains toxins and carcinogens, but they are far fewer in number than those found in cigarette smoke, and they are present at much lower levels. One particularly stubborn claim is that e-cigarettes emit dangerous levels of formaldehyde. Its provenance is a report in the New England Journal of Medicine entitled "Hidden Formaldehyde in E-Cigarette Aerosols" claiming that vapers faced a cancer risk from formaldehyde exposure that is five to 15 times higher than that of smokers.

This alarming finding, which made headlines worldwide, was an artifact of researchers testing a vaping device at an unrealistically high voltage setting. Although overheating e-liquid does produce high levels of formaldehyde, no person could ever force himself to inhale such acrid vapor. When those same researchers tested the device at a realistic voltage level, no formaldehyde was detected. Other analyses, however, have detected formaldehyde in e-cigarette aerosol at very low levels.

This caveat did not make it into the worldwide media coverage of the study. A further misconception is that we don't know the effects of vaping. Multiple studies with follow-up periods ranging from one month to three years have documented health benefits after switching from smoking to vaping ranging from lower blood pressure, reduced abnormalities in cellular lining of blood vessels, lowered vascular stiffness, and improved lung function in smokers with chronic obstructive pulmonary disease and asthma.

Epidemiologists must follow vapers for years to come knowing that the interpretation of long-term outcomes will be complicated by the fact that most vapers have first been smokers , and manufacturers must employ continuous surveillance to maintain and improve quality control and purge potentially toxic residues from flavorings. Still, the difference in toxic emissions between conventional, tobacco-combusting cigarettes and electronic ones will almost certainly save an extraordinary number of lives.

The health benefits of vaping do not make compelling headlines. More attention grabbing is research purporting to show that vaping causes harm. One false scare that has become a staple of anti-vaping "public education" is the threat of "popcorn lung" formally, bronchiolitis obliterans , which is caused by inhaling a chemical called diacetyl. The rare condition is called popcorn lung because it has been known to develop in workers in microwave-popcorn factories who were exposed to massive doses of diacetyl.

When researchers tested samples of e-liquids, the aerosol produced in almost half surpassed strict federally defined occupational-safety limits. In response, many vaping manufacturers removed diacetyl as a precaution, though not a single documented case of popcorn lung has been detected in millions of vapers worldwide.

What's more, the exposure to diacetyl from cigarette smoking is one hundred times higher than from vaping, and popcorn lung is not a condition known to afflict smokers. The health press is also replete with warnings of vaping-induced heart attacks and acute or chronic pulmonary conditions. Yet a look at the research behind the headlines often reveals striking problems in study design.

Consider a recent report in the American Journal of Preventive Medicine in which researchers analyzed government data in order to determine a possible association between vaping and chronic lung disease. The data comprised a cohort of smokers and vapers who were surveyed at three intervals over a four-year period. At each interval, subjects were asked whether they had been diagnosed with chronic pulmonary disease.

Many of the vapers who did not report disease at the first interval went on to report it subsequently, leading the authors to conclude that e-cigarettes constituted a risk for chronic obstructive pulmonary disease, bronchitis, and asthma. What makes this inference dubious, however, is the fact that chronic lung conditions take at least two decades to manifest, far longer than four years covered by the surveys. Even those who switch completely to e-cigarettes remain at elevated risk for lung disease for years to come because of the damage inflicted by years of smoking.

Furthermore, despite claims to the contrary, second-hand vapor is not dangerous. E-cigarette vapor is not comparable to environmental tobacco smoke. The latter can linger for hours while environmental e-cigarette aerosol is very dispersive, evaporating in less than two minutes and practically undetectable at five feet from the exhalation.

This means that bystanders in typical home or restaurant environments are exposed to extremely small doses of pollutants and for much less time than those exposed to tobacco smoke. They claim that vaping is a "gateway" to smoking. This claim is tricky, in part because the term "gateway" is deployed inconsistently. It may refer to a sequence action B came after action A ; other times it refers to a predictive, causal statement a person engaged in action B because he first engaged in A.

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