In Patients With Spinocerebellar Ataxia Type 3, Smoking Cessation Drug Improves Walking Function

Main Category: Neurology / Neuroscience
Also Included In: Smoking / Quit Smoking
Article Date: 24 Feb 2012 – 1:00 PST

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A nicotinic drug approved for smoking cessation significantly improved the walking ability of patients suffering from an inherited form of ataxia, reports a new clinical study led by University of South Florida researchers.

The randomized controlled clinical trial investigated the effectiveness of varenicline (Chantix®) in treating spinocerebellar ataxia type 3, or SCA3. The findings were published online earlier this month in Neurology, the journal of the American Academy of Neuroscience.

Lead author Dr. Theresa Zesiewicz and colleagues at the USF Ataxia Research Center collaborated with researchers from Beth Israel Deaconess Medical Center in Boston, MA, and from the David Geffen School of Medicine at UCLA in Los Angeles, CA.

Spinocerebellar ataxia impairs the brain and spinal cord causing progressive difficulty with coordination of movements, including walking. The uncoordinated movements, or ataxia, is a neurological symptom with no treatment or cure and can lead to serious fall-related injuries.

“This is the first clinical trial in patients with ataxia showing that nicotinic acetycholine agonists improve symptoms associated with the ability to stand straight and walk,” said Dr. Zesiewicz, professor of neurology and director of the USF Ataxia Research Center. “Patients receiving varenicline could walk with more ease, with less help and faster than those in the placebo group.”

The double-blind multicenter study evaluated 20 adult patients with genetically confirmed SCA3. Half the patients received 1 mg. of varenicline twice a day, and the other half received placebo. At the end of the eight-week study, patients taking varenecline performed significantly better on measures of gait, stance, rapid alternating movements and a timed 25-foot walk than those who did not. The drug was fairly well tolerated, with mild nausea being the most common side effect.

The study authors suggest that varenicline’s ability to improve ataxia may be associated with the drug’s ability to act at several different sites in the brain affected by nicotine.

Study co-author Lynn Wecker, PhD, a distinguished research professor at USF Health, is investigating the cellular and molecular mechanisms mediating the effects of varenicline and other nicotinic agonists. Dr. Wecker and colleagues, supported by a five-year grant funded by the National Institute of Neurological Disorders and Stroke, have shown that several drugs affecting neuronal nicotinic receptors improve gait and balance in an animal model of SCA3.

Further preclinical research is needed to understand how nicotinic acetylcholine agonists improve ataxia, and larger clinical studies with more patients are needed to identify other neurodegenerative diseases that may benefit from nicotinic medications, the authors conclude.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject. The study was supported by the National Ataxia Foundation and the Bobby Allison Ataxia Research Center.
Citation: “A randomized trial of varenicline (Chantix) for the treatment of spinocerebellar ataxia type 3,”T.A. Zesiewicz, MD, FAAN; P.E. Greenstein, MB, BCh; K.L. Sullivan, MSPH; L. Wecker, PhD; A. Miller, BS; I. Jahan, MD; R. Chen, MD and S.L. Perlman, MD, FAAN, Neurology, published online before print Feb. 8, 2012. DOI: 10.1212/WNL.0b013e318247cc7a.
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26 Feb. 2012. APA

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UK Quit Smoking Campaigns Come Under Fire

HomeNewsUK Quit Smoking Campaigns Come Under Fire

February 22, 2012   Two current UK government campaigns pull no punches about urging all smokers trying to quit to use drugs. One puts it bluntly: “Don’t go cold turkey”. Another poster on display in the nation’s waiting rooms says: “There are some people who can go cold turkey and stop smoking. But there aren’t many of them.” (See picture at bottom of this post.) That statement is manifestly incorrect and an enquiry should be undertaken into how such nonsense was approved for publication.  In 1986, just a few years after nicotine replacement therapies became available, the American Cancer Society stated: “Over 90% of the estimated 37 million people who have stopped smoking in this country since the Surgeon General’s first report linking smoking to cancer [1964] have done so unaided.”  How did they possibly manage to do it without drugs?

For More Information:
http://blogs.crikey.com.au/croakey/2012/02/22/uk-quit-smoking-campaigns-come-under-fire/

Feb 24, 2012
Consumers Switching Between Tobacco Types
Read the full story Feb 24, 2012
Daytona Speedway to Ban Smoking
Read the full story Feb 23, 2012
More Troops on Smokeless Tobacco After Deployment
Read the full story Feb 23, 2012
Physicians Lack Confidence in Their Ability to Counsel Cancer Patients to Quit Smoking
Read the full story

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To Keep Research Funding, Texas Universities Consider Tobacco Ban

HomeNewsTo Keep Research Funding, Texas Universities Consider Tobacco Ban

February 21, 2012   University administrators around Texas are now considering campus-wide tobacco-free policies as a result of a new policy regarding grant funding. The new rules established by the Cancer Research Prevention Institute of Texas requires grant recipients to have policies prohibiting tobacco use in buildings and structures where financed research activities are occurring, as well as at the outdoor areas immediately adjacent to those buildings. The grant recipients must also provide smoking cessation services for community members who desire them. In 2007, the research institute was established and the state was authorized to issue $3 million in bonds over 10 years to finance cancer research and prevention efforts. Nearly $600 million in grants have been issued, primarily to academic institutions. For schools that pride themselves on their research function, there is a clear financial incentive to institute the changes.

For More Information:
http://www.texastribune.org/texas-education/higher-education/keep-research-funding-universities-mull-tobacco-ba/

Feb 24, 2012
Consumers Switching Between Tobacco Types
Read the full story Feb 24, 2012
Daytona Speedway to Ban Smoking
Read the full story Feb 23, 2012
More Troops on Smokeless Tobacco After Deployment
Read the full story Feb 23, 2012
Physicians Lack Confidence in Their Ability to Counsel Cancer Patients to Quit Smoking
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Daytona Speedway to Ban Smoking

HomeNewsDaytona Speedway to Ban Smoking

February 24, 2012   A smoking ban will prevent NASCAR fans from lighting up in the grandstands at Daytona International Speedway starting with the Coke Zero 400 in July. Fans will be required to use certain designated areas behind the grandstands once the ban takes effect. Joie Chitwood III, the Speedway’s president, said it’s a sign of the times and that no other venue in Florida allows smoking in the stands. In the meantime, smokers are being encouraged not to smoke in the seating areas during Speedweeks ahead of this Sunday’s Daytona 500. The ban, however, is not mandatory, said Chitwood, because smokers bought their tickets under the notion they could smoke.

For More Information:
http://www.clickorlando.com/news/Daytona-Speedway-to-ban-smoking/-/1637132/8815446/-/9d69b9z/-/index.html

Feb 24, 2012
Consumers Switching Between Tobacco Types
Read the full story Feb 24, 2012
Daytona Speedway to Ban Smoking
Read the full story Feb 23, 2012
More Troops on Smokeless Tobacco After Deployment
Read the full story Feb 23, 2012
Physicians Lack Confidence in Their Ability to Counsel Cancer Patients to Quit Smoking
Read the full story

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Fighting The Battle Of The Aortic Bulge – Abdominal Aortic Aneurysms

Main Category: Cardiovascular / Cardiology
Also Included In: Smoking / Quit Smoking;  GastroIntestinal / Gastroenterology
Article Date: 23 Feb 2012 – 1:00 PST

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When aortic walls buckle, the body’s main blood pipe forms an ever-growing bulge. To thwart a deadly rupture, a team of Stanford University School of Medicine researchers has found two tiny molecules that may be able to orchestrate an aortic defense.

A team led by cardiovascular scientists Philip Tsao, PhD, and Joshua Spin, MD, PhD, identified two microRNAs – small molecules that usually block proteins from being made – that work to strengthen the aorta during bulge growth. By tweaking the activity of each molecule, they could reduce abdominal aortic aneurysms in mice, which they believe is a promising step toward a new treatment for the disease.

Their findings were published in Science Translational Medicine and are a continuation of work the researchers published in the Journal of Clinical Investigation.

Abdominal aortic aneurysms affect thousands of people in the United States each year. The ballooning blood vessel – which looks more like a snake digesting a bowling ball than a central thoroughfare for oxygenated blood – is most likely to occur in people over age 65. For smokers, the chances are even greater.

“Ninety percent of people who get one of these are smokers,” said Spin, an instructor in cardiovascular medicine and a co-author of both papers.

These types of aortic aneurysms usually form below the kidneys, before the aorta branches into the legs. When they rupture, blood spills out into the abdomen, causing death in up to 90 percent of cases. Knowing you have an aortic aneurysm can be nerve-wracking.

“There are no approved therapies, so the recommendation for many patients is just watchful waiting,” said Tsao, professor of cardiovascular medicine and the senior author of both papers. “When they reach a certain size, the risk of rupture outweighs the risks of surgical intervention.”

To repair the weak blood channel, doctors can either surgically replace the aneurysm with a graft, or use catheters to insert a self-expanding, cloth-covered tube that blocks off the ballooned region and restores blood flow to a straight path.

With such high stakes, Tsao and Spin set out to better understand why aneurysms form. All they knew was what happened in the aorta when they did: dissolution of muscle cells, inflammation, and thinning of supportive collagen and other fibers.

To understand the causes, the team compared cells in the vessel wall at the site of the aneurysm to unaffected cells nearby and to aortas without aneurysms. When they looked at genes that cells were turning on or off, they found differences in two microRNAs: miR-21and miR-29b.

MicroRNA is a special type of RNA, which usually functions as an intermediate step in the decoding of DNA into proteins for the cell to use. MicroRNAs, which get their names from being smaller than typical RNA, specifically clamp onto other RNA molecules and block the cell from making proteins.

From previous studies, the team knew that miR-21 – which the cells turned on during blood vessel ballooning – works to keep cells alive and dividing. MiR-29b, which works to keep collagen and other fibers from being made, was reduced.

“When you see something go up or down as disease is getting worse, you assume that what it’s doing is causing the disease,” Spin said. But appearances can be deceiving.

The team used human tissue, and mice that develop aortic aneurysms, to understand what these microRNA changes meant for aneurysm development. In each of the studies, they injected the mice with molecular mimics of the microRNAs, or other molecules that would specifically block either miR-21 or miR-29.

Because smoking is a large risk factor for the deadly aorta expansions, they also gave the mice nicotine injections to test whether it played a role.

Surprisingly, they found that when they gave the mice more miR-21, their aortas didn’t balloon as much or burst open. In contrast, knocking down the level of miR-21 in the cells had the opposite effect. Since the cells at the site of the aneurysm already had elevated levels of miR-21 compared to other cells, the team thinks the change is an attempt by the body to protect itself.

“This looks like a response of the body to the process; it’s trying to limit how fast the aneurysm is growing,” Spin said.

Interestingly, in the mice given nicotine, aneurysms grew even faster, suggesting that smoking, and more specifically nicotine, was a direct factor in aneurysm development. Additional miR-21 was also beneficial in this model of accelerated disease.

“Often one of the things that people try to use to stop smoking is nicotine therapy,” Spin said. “That may not be the best way to prevent an aneurysm from getting worse.”

When they looked at miR-29b, which the cells naturally turn down in aneurysms, they found that artificially knocking it down further slowed aneurysm development and prevented rupture. It too seems to be responding protectively to aneurysm development, rather than contributing.

While insights from the discoveries about the two microRNAs may lead to therapies for aortic aneurysms, the path is not without complications.

“Unfortunately, treatments that benefited aneurysms in the mice came with negative consequences on the heart and the liver,” Tsao said. “So one of the pressing matters would then be, ‘how can we get it only in that area or concentrated in the area?'”

They already have a collection of ideas of how to deliver the mini molecules, including using a balloon-like device at the location of the aneurysm that would directly inject microRNA mimics or inhibitors onto the cells.

It might be the case, Tsao said, that miR-29b or miR-21 might not be the best microRNAs to target. “Perhaps there are others that could work better,” he said. “But we hope this will establish a new way to approach the disease.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our cardiovascular / cardiology section for the latest news on this subject. The first author of both papers is postdoctoral scholar Lars Maegdefessel, MD, PhD. Other co-authors of the work reported in Science Translational Medicine are current and former postdoctoral scholars Junya Azuma, MD, PhD, Ryuji Toh, MD, Denis Merk, MD, Uwe Raaz, MD, and Azad Raiesdana, PhD; research assistants Alicia Deng and Anke Schoelmerich; Nicholas Leeper, MD, assistant professor of cardiovascular medicine; Michael McConnell, MD, professor of cardiovascular medicine; and Ronald Dalman, MD, professor of vascular surgery.
An additional co-author in the Journal of Clinical Investigation report was medical student Jocelyn Chin.
Maegdefessel, Spin and Tsao have applied for patents relating to miR-21 and miR-29b and protection from abdominal aortic aneurysm development.
The work reported in both publications was supported by research grants from the Stanford Cardiovascular Institute, the National Institutes of Health, the California Tobacco Related Disease Research Program of the University of California, the Deutsche Forschungsgemeinschaft, the American Heart Association and the Deutsche Herzstiftung e.V.
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Nicotine’s Role In Promoting Heart And Blood Vessel Disease – Invade And Conquer

Main Category: Smoking / Quit Smoking
Also Included In: Heart Disease;  Cardiovascular / Cardiology
Article Date: 24 Feb 2012 – 4:00 PST

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Cigarette smoke has long been considered the main risk factor for heart disease. But new research from Brown University in Providence, R.I., shows that nicotine itself, a component of cigarette smoke, can contribute to the disease process by changing cell structure in a way that promotes migration and invasion of the smooth muscle cells that line blood vessels. In particular, invading cells can remodel structures called podosomes, and this leads to further degradation of vessel integrity.

Ultimately, this cellular migration and invasion process gives rise to the formation of vessel-clogging fatty deposits known as plaque – the hallmark of heart and blood vessel disease. The results on the nicotine-podosome link will be presented at the 56th Annual Meeting of the Biophysical Society (BPS), held Feb. 25-29 in San Diego, Calif.

If confirmed in further studies, the finding that nicotine itself promotes vessel damage by changing podosomes appears to question the health benefits of helping people quit smoking through smokeless nicotine delivery agents such as gum or patches.

“The finding that nicotine is as effective as cigarette smoke in enhancing cellular structural changes, and breakdown of scaffold proteins by vascular smooth muscle cells, suggests that replacing cigarette smoking by nicotine treatment may have limited beneficial effects on atherosclerosis,” notes lead researcher Chi-Ming Hai, professor of medical science in the department of molecular pharmacology, physiology, and biotechnology at Brown University.

Hai’s research illuminates the multistep process of plaque formation, and suggests that a new powerful player, nicotine, may be involved. The plaque formation process begins as a response to cellular injury, and progresses to destructive and chronic inflammation of the vessel walls that attracts mobs of white blood cells, further inflaming the vessels. This damage-causing inflammation can be triggered by chemical insults from high blood sugar, modified low-density lipoproteins (LDL, the “bad cholesterol“), physical stress from high blood pressure, or chemical insult from tobacco smoke. Now nicotine itself appears to remodel key structures in a way that primes and enhances the invasion of smooth muscle lining the vessel wall.

Identifying a possible nicotine-posodome link in the invasion step of plaque formation process suggests a new means of intervening in the process: targeting the cell structures that are changed by nicotine and that promote invasion of the smooth muscle lining the vessel wall. If a therapy could prevent, slow, or reverse that step, it would likely interrupt the plaque-production cycle.

Fatty deposits accumulate in blood vessels beginning as young as age 10 and progress over a person’s lifetime. Heart disease results if the deposits continue to build and harden into vessel-clogging plaque. When plaque ruptures, it can block blood flow, starving the heart or brain of oxygen and leading to a heart attack or stroke.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our smoking / quit smoking section for the latest news on this subject. The presentation, “Cigarette smoke and nicotine-induced remodeling of actin cytoskeleton and extracellular matrix by vascular smooth muscle cells,” is at 1:45 p.m. on Sunday, Feb. 26, 2012, in the San Diego Convention Center, Hall FGH. ABSTRACT: http://tinyurl.com/73e836j
Meeting Home Page: http://www.biophysics.org/2012meeting/Main/tabid/2386/Default.aspx
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Smokeless Tobacco Substitutes Save Lives

Main Category: Smoking / Quit Smoking
Also Included In: Cancer / Oncology;  Public Health
Article Date: 21 Feb 2012 – 0:00 PST

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Substituting smokeless tobacco products can save smokers’ lives, and there is a scientific foundation that proves it.

That is the message Brad Rodu, D.D.S., professor of medicine at the University of Louisville (UofL) School of Medicine and the Endowed Chair in Tobacco Harm Reduction at UofL’s James Graham Brown Cancer Center, delivered at the Annual Meeting of the American Association for the Advancement of Science. Rodu spoke at the session, “Harm Reduction: Policy Change to Reduce the Global Toll of Smoking-Related Disease.”

“Quit or die: That’s been the brutal message delivered to 45 million American smokers, and it has helped contribute to 443,000 deaths per year, according to statistics from the Centers for Disease Control and Prevention,” Rodu said. “The truth, however, is that total nicotine and tobacco abstinence is unattainable and unnecessary for many smokers.”

Rodu’s presentation, “Transforming Tobacco Use: The Potential of Tobacco Harm Reduction,” was based on his almost 20 years of research. His work shows that smokers can greatly reduce their risk of disease and death by replacing smoking products with e-cigarettes or modern, spit-free smokeless tobacco. These products provide a much safer alternative for those smokers who are unable or unwilling to quit smoking because they continue to deliver nicotine without the harmful effect of smoking.

“Nicotine is addictive, but it is not the cause of any smoking-related disease. Like caffeine, nicotine can be used safely by consumers,” Rodu said.

Decades of epidemiologic research bear out Rodu’s findings. While no tobacco product is completely safe, smokeless products have been shown to be 98 percent safer than cigarettes. In the United Kingdom, the Royal College of Physicians reported in 2002 that smokeless tobacco is up to 1,000 times less hazardous than smoking, and in 2007, further urged world governments to seriously consider instituting tobacco harm reduction strategies as a means to save lives.

To see the proof of what tobacco harm reduction can do, look to Sweden, Rodu said. “Over the past 50 years, Swedish men have had Europe’s highest per capita consumption of smokeless tobacco as well as Europe’s lowest cigarette use. During the same time, they also have the lowest rate of lung cancer than men in any other European country.”

In the United States, steps have been made to document the value of tobacco harm reduction. In 2006, a National Cancer Institute-funded study estimated that if tobacco harm reduction was “responsibly communicated” to smokers, 4 million would switch to smokeless tobacco. The American Council on Science and Health – which organized Rodu’s session at the AAAS Annual Meeting – concluded in the same year that tobacco harm reduction “shows great potential as a public health strategy to help millions of smokers.”

Rodu is well aware of the controversy his research findings generate. Opponents of any use of nicotine delivery products maintain that smokeless tobacco puts the user at great risk for oral cancer, a position not supported by research.

“The risk of mouth cancer among smokeless tobacco users is extremely low – certainly lower than the risk of smoking-related diseases among smokers,” he said. “The annual mortality rate among long-term dry snuff users is 12 deaths per 100,000 and the rate among users of more popular snus, moist snuff and chewing tobacco is much lower. For perspective, the death rate among automobile users is 11 per 100,000 according to a 2009 report from the National Highway Traffic Safety Administration. Compare those to the rate among smokers: more than 600 deaths per 100,000 every year”

“The data clearly show that smokeless tobacco users have, at most, about the same risk of dying from mouth cancer as automobile users have of dying in a car wreck.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our smoking / quit smoking section for the latest news on this subject. Rodu earned his dental degree from The Ohio State University. After an oral pathology residency program at Emory University, he completed fellowships at the University of Alabama at Birmingham sponsored by the American Cancer Society and the National Cancer Institute. He was on the UAB faculty from 1981 to 2005 with appointments in several departments in the schools of Medicine, Public Health and Dentistry. He joined the UofL faculty in 2005. His research is supported by unrestricted grants from tobacco manufacturers to the University of Louisville and by the Kentucky Research Challenge Trust Fund.
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Physicians Lack Confidence in Their Ability to Counsel Cancer Patients to Quit Smoking

HomeNewsPhysicians Lack Confidence in Their Ability to Counsel Cancer Patients to Quit Smoking

February 23, 2012   Less than one-fifth (18.1%) of healthcare providers reported high levels of confidence in their ability to counsel patients with cancer to quit smoking, a survey published in The Oncologist found. These results suggest “outpatient oncology providers may not be using the ‘teachable moment’ of cancer diagnosis to provide smoking-cessation assistance,” the investigators noted. Of the 74 physicians and midlevel providers surveyed, 82.4% frequently or always assessed smoking in new patients, but rates declined at subsequent visits. Rates of advising patients to quit smoking were also high, but <30% of providers reported frequently or always providing intervention to patients who smoked, and only 30% reported following up with patients to assess progress with quitting. Additional training and clinic-based interventions may help improve adherence to tobacco-cessation practice guidelines in the outpatient oncology setting. The most important barrier to smoking cessation was a patient’s lack of motivation.

For More Information:
http://www.chemotherapyadvisor.com/teachable-moments-for-smoking-cessation-in-patients-diagnosed-with-cancer-underutilized/article/227993/  

Feb 24, 2012
Consumers Switching Between Tobacco Types
Read the full story Feb 24, 2012
Daytona Speedway to Ban Smoking
Read the full story Feb 23, 2012
More Troops on Smokeless Tobacco After Deployment
Read the full story Feb 23, 2012
Physicians Lack Confidence in Their Ability to Counsel Cancer Patients to Quit Smoking
Read the full story

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Man’s Face Burns From Exploding Electronic Cigarette

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Main Category: Smoking / Quit Smoking
Article Date: 16 Feb 2012 – 10:00 PST

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A Florida man’s electronic cigarette exploded while he was using it, knocking out some front teeth and causing severe burns on his face, according to officials from North Bay Fire Department. Joseph Parker, Fire Department Chief, said he believes the device’s battery blew up while he was inhaling from it. Parker said it was as if a rocket had ignited in the victim’s mouth.

According to reports in local media, it appears the man, who had been using the electronic cigarette to give up tobacco smoking also lost part of his tongue.

The fire chief, who added that the device’s battery seemed to be faulty, said that the victim thanked them yesterday and said he would probably be leaving a hospital in Mobile, Ala. Today.

No details have yet been released regarding the electronic cigarette brand, and what type of battery it contained. Parker believes it is a rechargeable lithium battery, because they found a recharging station.

The victim’s name has not been released. However, local media point towards a Tom Holloway (57) Facebook page which has filled up with get-better messages from friends commenting on a very similar incident – both addresses match, the one in the fire report and the other in the social media page.

The electronic cigarette explosion also burned the man’s carpet, chair, pictures and cushions – he was at his office at home when the incident occurred. Officials found a burnt battery care surrounded by melted carpet. Other members of his household, on hearing the explosion, came to his rescue and tried to extinguish the fire with salt.

Electronic cigarettes, also known as e-cigarettes, and vaporizer cigarettes are devices that mimic the movements and sensations of tobacco cigarette smoking – they emit vaporized nicotine which is inhaled. The mechanism is driven by a battery, and the device can also emit hundreds of other non-nicotine vaporized solutions, such as menthol, cola, coffee and even strawberry.

E-cigarette manufacturers and sellers say that their devices do not contain the more than 4,000 different harmful chemicals contained in cigarette smoke.

Device makers, as well as a growing number of users, say the e-cigarette really does provide a very similar sensation to tobacco smoking, but without the combustion (without the smoke).

E-cigarettes are long tube-shaped devices, many of which look similar to the tobacco products the user used to smoke (or perhaps still does) – some look like ballpoint pens. Some are reusable, while others are throw-away ones.

Electronic cigarettes RN4072 CT-M401
Examples of two electronic cigarettes and their spare detatchment batteries (picture used for illustration pusporses only; the brand of the exploding device has not yet been revealed)

Other related articles:

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our smoking / quit smoking section for the latest news on this subject. Medical News Today archives, CBS, Please use one of the following formats to cite this article in your essay, paper or report:

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19 Feb. 2012. APA

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posted by Bingham on 16 Feb 2012 at 4:33 pm

I think this guy is a lied, or he was trying to smoke crack from it. These been millions of electronic cig out there and this is the first. Also what cig company was it? The guy even wanted to hide is identity knowing this is another, “ballon boy” fibber story. I have been smoking electronic cigs for over 5 years. The best I have found was cige. Battery life last almost forever and it only takes 15 minutes to charge. I have tried everything out there and cige has been the best bet. Go to cige.co not dot com and read about em. Best taste and design for the average smoker. This one is small and I’m sure if it blows up it wouldn’t hurt lol. I almost 100 percent sure this guy did something to the cig to make it blow. What a crock.

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posted by Chris on 16 Feb 2012 at 4:40 pm

Every reputable E-Cigarette vendor, will recommend protected Batteries. The type pictured contains a protected battery. These protected batteries contain a circuit that stops the battery from functioning in order to prevent such incidents.

My guess is that he was using a low grade custom E-Cig,with no vent holes, and did not put protected batteries, turning the tube into a pipe bomb.

Quality ECigaretts even include electronic circuitry to prevent things like this from happening

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