Health and philanthropy—the tobacco connection

Author: Simon Chapman

On June 14, the world’s two richest men, Mexico’s Carlos Slim Helú and the USA’s Bill Gates, jointly announced that they would each contribute US$50 million to the Latam health project to increase vaccinations and improve child nutrition and natal health in central America.1 Slim already contributes reputedly $2·5 billion annually to his Instituto Carlos Slim de la Salud, which runs a large variety of health programmes in Latin America.2 The latest announcement will naturally attract widespread acclaim as an outstanding example of philanthropy. But it also invites important questions about consistency and competing interests.

Any assessment of Slim’s net contribution to public health must balance the impact of his philanthropic contributions as well as the indirect health consequences that flow from his wealth generation with a less appreciated source of his wealth. Descriptions of Slim’s vast fortune generally concentrate on his telecommunications empire.3 Relatively little is mentioned about his long-standing majority ownership of the Mexican tobacco company Cigatam,3 which has since 2007 been 80% owned by Philip Morris.4 Slim’s website acknowledges that Cigatam “turned out to be the first and most important because of its cash flow, providing the Group with sufficient liquidity to capitalize on available opportunities and thereby increase its acquisitions of big companies”.5 Nor is it as widely publicised that he has a continuing role as a non-executive director6 of the world’s largest tobacco company, Philip Morris International (PMI).

The company’s shareholders doubtless expect him—like all directors—to make a major contribution to maximise investment returns and the company’s bottom line. PMI’s website6 notes that Slim serves on its finance, product innovation, and regulatory affairs committees. The purposes of these committees include to “monitor the financial condition of the Company, oversee the sources and use of cash flow, capital structure and resulting financial needs”,7 to “monitor and review the development of new product strategies, key legislative, regulatory and public policy issues and trends affecting the Company”, and to “anticipate, respond to, and challenge where appropriate, regulatory and fiscal proposals”.8 This must include responding to international efforts at tobacco control. It is inconceivable that Slim would not have known of the action Philip Morris is currently taking against Uruguay in the International Centre for the Settlement of Industrial Disputes objecting (among other things) to that nation’s new requirement for large graphic health-warnings on cigarette packs.9

The tobacco industry has long suffered ethical bottom-feeder status with both the public and the corporate world. The Reputation Institute’s 2010 report,10 which involved over 80 000 respondents in 32 countries, saw the tobacco industry ranked a distant last of 25 industries on “reputation”. Why? This is an industry whose products kill over 5·5 million people each year, on average 15 years earlier than normal life expectancy.11 It is an industry which has engineered the chemistry and design of its products to, as one infamous 1984 Philip Morris internal memorandum put it, “make it harder for existing smokers to leave the product”.12 It is an industry whose product is responsible for the inexorable rise of lung cancer, the world’s leading cause of cancer death and a disease that was very uncommon before the mass production and marketing of cigarettes.13

Slim’s massive contributions to Latin American health undoubtedly do much good. But the consequences of his continuing history of high-level regional and global involvement in the tobacco industry are hardly trivial in any assessment of his public health footprint.

Gates’ philanthropy is unmatched this century. His commitment to reducing some of the world’s worst infectious diseases has poured unprecedented capital into health projects in many of the world’s poorest and unhealthiest nations. His contributions will have already saved uncounted lives.

Gates has recently begun to fund tobacco-control projects in low-income and middle-income nations, joining New York’s mayor Michael Bloomberg in injecting an estimated $500 million to try and curb tobacco use in the world’s poorest nations.14 In April this year,15 the Bill & Melinda Gates Foundation withdrew a grant of $5·2 million to Canada’s International Development Research Centre (IDRC), after it emerged that the IDRC’s chair, Barbara McDougall, was a very recent board member of Imperial Tobacco Canada.16 The Gates Foundation statement17 said: “The foundation was recently informed that the chair of the board of our partner, the International Development Research Centre (IDRC), has until recently also been a Director of Imperial Tobacco Canada, Ltd. We are deeply disappointed by this revelation and feel this conflict is unacceptable as we work to support meaningful tobacco control programs in Africa. Therefore, we are terminating our tobacco control grant to IDRC, effective immediately. We remain committed to tobacco control work and look forward to continuing to partner with the anti-tobacco community to reduce tobacco use in Africa.”

Gates’ decision just 2 months later to partner with Slim is plainly inconsistent. He apparently did not know of McDougall’s appointment when he funded the IDRC. He might well not have known about Slim’s tobacco connections when he joined with him in the Latam project. He must know now. His subsequent actions with IDRC were an outstanding example of principled philanthropy. Let us hope he makes the same call again.

Author: I declare that I have no conflicts of interest.

1 Anon. World’s richest want better health for Latam poors. Reuters. (accessed June 22, 2010).
2 Chapman S. International tobacco control should repudiate Jekyll and Hyde health philanthropy. Tob Control 2008; 17: 1. CrossRef | PubMed
3 Anon. Carlos Slim Helú: business activity. (accessed June 22, 2010).
4 Philip Morris International. Philip Morris International announces agreement in principle to acquire additional 30% stake in Mexican tobacco business from Grupo Carso. (accessed June 22, 2010).
5 Anon. Carlos Slim Helú: biography. (accessed June 22, 2010).
6 Philip Morris International. Board of Directors. (accessed June 22, 2010).
7 Philip Morris International. Finance Committee Charter. (accessed June 23, 2010).
8 Philip Morris International. Product Innovation and Regulatory Affairs Committee Charter. (accessed June 23, 2010).
9 Dias FC. Philip Morris initiates arbitration against Uruguay over new labeling requirements, taxes. (accessed June 22, 2010).
10 Reputation Institute. Global reputation PulseTM reports. (accessed June 22, 2010).
11 Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 2006; 3: e442. CrossRef | PubMed
12 Webb WH. Status of Marlboro Development Programme. (accessed June 22, 2010).
13 Oschner A. Bronchogenic carcinoma: a largely preventable lesion assuming epidemic proportions. Chest 1971; 59: 358-359. CrossRef | PubMed
14 Goldman H. Bloomberg, Gates set $500 million anti-tobacco fight (update1). (accessed June 22, 2010).
15 Anon. Gates Foundation pulls funding from IDRC due to ties to Big Tobacco. (accessed June 22, 2010).
16 Todkill A. Tobacco control and the collateral damage of conflict of interest. Open Med 2010; 4. (accessed June 22, 2010).
17 Bill & Melinda Gates Foundation. Statement regarding IDRC tobacco control grant. (accessed June 23, 2010). a School of Public Health, University of Sydney, Sydney, NSW 2006, Australia

January, 2011|Oral Cancer News|

Smoking may worsen pain for cancer patients

Author: Fran Lowry

Patients with cancer who continue to smoke despite their diagnosis experience greater pain severity than their counterparts who quit or who have never smoked, according to new research published in the January 2011 issue of Pain.

Not only is their pain more severe, but it interferes more with their activities of daily living, lead author Joseph W. Ditre, PhD, a clinical psychologist at Texas A & M University in College Station, told Medscape Medical News.

“Many smokers, when they get cancer, feel that smoking is one of the only pleasures they have left to them and refuse to quit,” he said in an interview. “But our research suggests that quitting has definite benefits. It’s one more thing that doctors can tell their patients to help them stop smoking.”

Continued smoking has been associated with an increased risk of developing a second primary tumor, reduces the effectiveness of treatment, and is associated with poorer survival rates, Dr. Ditre said. “The subtext for this is that smoking can also worsen cancer-related symptoms and treatment side effects, such as pain and fatigue.”

“About 75% of people with advanced-stage cancer report moderate to very severe pain, so it is a very big factor in terms of the disease course, and yet there is surprisingly little research on this topic,” he added.

Dr. Ditre, who led this work while he was earning his doctorate at the University of South Florida and Moffitt Cancer Center in Tampa, told Medscape Medical News that the aim of his research was to examine the association with pain across diverse cancer types with regard to potential benefits of quitting smoking.

“Smoking is known to decrease oxygen, and there is also a possibility that tobacco smoke over time has some type of direct influence on the neurological processing of sensory information, and so may actually change the way pain receptors operate,” he said. “There are many potential mechanisms, and this is something that is under study.”

More Smoking, More Pain
In the current study, Dr. Ditre and colleagues looked at the association between multiple levels of smoking status and several pain-related outcomes in a sample of 224 patients who were about to begin chemotherapy for a variety of cancers, including breast, lung, bladder, ovarian, colon, head and neck, testicular, endometrial, prostate, and rectal/anal cancers; mesothelioma; and sarcoma.

The patients were part of a larger study investigating the efficacy of 2 interventions — stress management and exercise training — for improving quality of life during chemotherapy. Ten percent of patients had stage I disease, 26% had stage II, 30% had stage III, and 34% had stage IV.

The patients self-reported their smoking status and cigarette consumption at study entry. Patients who reported smoking more than 100 cigarettes in their lifetime were defined as smokers, and never-smokers were defined as smoking fewer than 100 cigarettes.

Smokers were further defined as former smokers (those who had quit smoking and had not smoked any cigarettes in the past month) and current smokers (those who reported having smoked in the past month). Current smokers were also asked how many cigarettes they currently smoked per day.

The patients used the Medical Outcomes Survey 36-item Short Form Body Pain subscale, rating their perceived severity of bodily pain on a scale of 1 to 6, where 1 indicated “none” and 6 indicated “very severe,” and the degree to which pain interfered with their daily routine on a scale of 1 to 5, where 1 indicated “not at all” and 5 indicated “extremely.”

They also rated their distress on the Memorial Symptom Assessment Scale-Short Form, where 0 indicated no distress at all and 4 indicated the most stress.

Current smokers reported experiencing significantly more severe pain than never-smokers and greater interference from pain than former smokers or never-smokers.

In addition, there was also an inverse relation between pain severity and the number of years since quitting: The longer it had been since a patient had quit smoking, the less pain that patient reported.

Dr. Ditre stressed that the findings are correlational and do not point to a direct cause between smoking and cancer pain. In fact, the direction of causality is unclear. “You cannot infer exactly what is causing what, only that they are connected in some way,” he said.

“Smoking may be increasing the pain that these cancer patients are experiencing, or another possibility is that their pain may have caused them to continue smoking. It could be one way or the other,” he noted. “In fact, we’ve done work with noncancer populations in which we have demonstrated that pain is a significant motivator of smoking behavior. People who experience pain have a greater desire to smoke and will be more motivated to smoke, and will smoke more.”

Whether or not there is a causal relationship, it is important for patients with cancer to realize that smoking appears to be worsening their pain, he said.

“Doctors can tell their patients that they now have information that suggests that if you stop smoking you may experience less pain than you would otherwise, although we are not 100% sure yet why that is,” Dr. Ditre said.

Research Needed to Understand Mechanisms
In an accompanying editorial, Lori Bastian, MD, from Duke University and Durham Veterans Affairs Medical Center in North Carolina, writes that the findings by Dr. Ditre and his team are consistent with those of other studies and that they have public health significance.

“Clinicians must do more to assist cancer patients to quit smoking after their diagnosis,” Dr. Bastian writes. “If pain increases the urge to smoke, a formal smoking cessation program for cancer patients should also include efforts to control pain severity.”

She concludes that more research is needed to understand the mechanisms that relate nicotine to pain and that prospective longitudinal studies should be performed to clarify “the issue of directionality, demonstrate no harm, and determine the impact of smoking cessation on pain severity among cancer patients.”

Pain. 2011;152:10-11, 60-65. Abstract

1. This study was supported by funding from the American Cancer Society and the National Institute on Drug Abuse. The study authors have disclosed no relevant financial relationships. Dr. Bastian is supported by grants from the Department of Veterans Affairs, Health Services Research and Development, and the National Institutes of Health/National Cancer Institute.

January, 2011|Oral Cancer News|

Californians continue to kick the cigarette habit

Author: Molly Hennessy-Fiske, Los Angeles Times

The percentage of California adults who smoke has continued to drop more than the national average, according to new data released Monday by state health officials. Still, deep disparities exist depending on gender, education, income, ethnicity and region.

Overall, Californians remain significantly less likely to smoke than people in the rest of the country, with 13.1% of adults surveyed statewide saying they smoked last year compared with 21% of adults nationwide.

The rate was even lower in several Southern California counties, including Los Angeles (10.4%), Orange (10.9%), Ventura (11.8%), Riverside and San Bernardino (each12.7%), according to a 2008 telephone survey.

“We have saved billions of dollars in healthcare costs that have been averted,” Kimberly Belshé, the state’s secretary of Health and Human Services, said Monday at a news conference near downtown Los Angeles to release the figures and display the state’s latest anti- smoking advertisements.

Still, she said, “these prevalence rates also tell us we have more work to be done.”

As of last year, California had seen a 38% decrease in smokers since 1990, when public health officials created the California Tobacco Control Program, funded by Proposition 99. The smoking rate is expected to decrease to 12.6% this year, close to the national goal of 12% by 2020. Only Utah reports a lower rate of smokers.

The downward trend in California is moving faster than the nation’s, which has seen a smaller decrease in the smoking rate, down to 21% from 26% in 1990, according to the Centers for Disease Control and Prevention.

But rates within the state vary, in some cases widely. Many rural counties had rates of 17% or higher, including Lake (31.6%), Tehama (22.8%), Tuolomne (21.9%) and Humboldt (17.7%). Northern and eastern parts of the state have seenthe least decline in smoking since 1990.

Men still smoke at higher rates than women, 14.9% compared to 8.4% as of 2008.

College graduates smoked at less than half the rate of those without college degrees, about 6%. Among households with an income of $150,000 or more, about 8% smoked, while about 20% living in households earning less than $20,000 smoked as of 2008.

About 12.7% of whites smoked as of 2008, compared to 14.2% of African Americans, 10.2% of Latinos and 8.1% of Asians as of 2008.

Asian and Latino men smoked at nearly three times the rate of female counterparts. Among women, African Americans had the highest smoking rate (12.1%), followed by whites (10.8%), Latinos (5.3%) and Asians (3.8%).

“There are just unacceptable disparities across racial groups in the prevalence of smoking,” said Dr. Mark Horton, the state’s public health director. “We think we can really target some of those disparities as we move forward.”

Belshé said public health officials also plan to work with counterparts in local communities to better understand what prevents certain ethnic groups from smoking, particularly Latinos.

Two of the four state-sponsored ads unveiled Monday featured Debi Austin, 60, a former smoker and emphysema survivor from Canoga Park. Austin, who spoke Monday, rose to fame in the 1990s after a state anti-smoking ad showed her smoking through the laryngectomy hole in her throat.

Austin said she hopes people will see her and think twice about lighting up, especially young people.

“I am the worst case scenario that your mother told you about,” Austin said. “I am the walking dead, the cast-off of the tobacco industry that they can’t fix, they can’t heal.”

In addition to those ads, which will begin airing next month, state officials plan to release ads next spring in Spanish, Korean, Mandarin and Vietnamese.

Some ads will emphasize the environmental effect of smoking. Cigarette butts are not biodegradable and account for 34% of litter collected statewide, polluting beaches, clogging storm drains and igniting wildfires, according to officials.

“We want everyone who smokes to rethink their practice of flicking it out the window and onto the ground,” Horton said. “It’s bad for them and bad for the environment.”

Horton said he was hopeful that Californians will kick the habit in the New Year. According to the latest survey, 60% of those smoking statewide said they have tried to quit during the last year, including 76% of smokers age 18 to 24.

December, 2010|Oral Cancer News|

Electronic nicotine delivery systems: is there a need for regulation?

Author: Anna Trtchounian, Prue Talbot

Electronic nicotine delivery systems (ENDS) purport to deliver nicotine to the lungs of smokers. Five brands of ENDS were evaluated for design features, accuracy and clarity of labeling and quality of instruction manuals and associated print material supplied with products or on manufacturers’ websites.

ENDS were purchased from online vendors and analyzed for various parameters.

While the basic design of ENDS was similar across brands, specific design features varied significantly. Fluid contained in cartridge reservoirs readily leaked out of most brands, and it was difficult to assemble or disassemble ENDS without touching nicotine-containing fluid. Two brands had designs that helped lessen this problem. Labeling of cartridges was very poor; labelling of some cartridge wrappers was better than labelling of cartridges. In general, packs of replacement cartridges were better labelled than the wrappers or cartridges, but most packs lacked cartridge content and warning information, and sometimes packs had confusing information. Used cartridges contained fluid, and disposal of nicotine-containing cartridges was not adequately addressed on websites or in manuals. Orders were sometimes filled incorrectly, and safety features did not always function properly. Print and internet material often contained information or made claims for which there is currently no scientific support.

Design flaws, lack of adequate labeling and concerns about quality control and health issues indicate that regulators should consider removing ENDS from the market until their safety can be adequately evaluated.

Authors affiliation:
Department of Cell Biology and Neuroscience, University of California, Riverside, California, USA

December, 2010|Oral Cancer News|

U.S. cigarette brands tops in cancer causing chemicals

Source: CNN
Author: Miriam Falco

Smokers of U.S. brand cigarettes may get more bang for their buck in the worst way according to a small study conducted by the Centers for Disease Control and Prevention.

Researchers found U.S. made cigarettes contain more cancer-causing chemicals than some cigarettes brands made elsewhere around the world.

“Not all cigarettes are made alike” says Dr. Jim Pirkle, deputy director for science at the CDC’s National Center for Environmental Health. He says this is the first study to show that “U.S. cigarettes have more of the major carcinogen [TSNAs] than foreign made cigarettes.” TSNAs are “tobacco-specific nitrosamines,” the major cancer-causing substance in tobacco.

126 smokers in five cities – Waterloo, Ontario; Melbourne, Victoria (Australia); London, England, Buffalo, New York, and Minneapolis, Minnesota – were recruited for this study.

They were between the ages of 18 and 55 and smoked at least 10 cigarettes a day for the past year and had been brand loyal for at least three months. The cigarettes smoked by the study recruits represented some of the more popular brands for each country including: Players light and DuMaurier in Canada; Marlboro, Newport Light, Camel Light in the U.S.; Peter Jackson and Peter Stuyvesant in Australia; and Benson & Hedges and Silk Cut Purple in the United Kingdom.

Scientists analyzed more than 2,000 cigarette butts to get the data they are reporting today, says Pirkle.

When researchers compared cigarette brands in the U.S. to those in Canada and Australia, they found three times higher levels of the cancer causing substance in the U.S. smokers’ mouths. The mouth levels are important because they give an indication of what levels if carcinogens are going into the lungs. (Smoking tobacco is a major cause of lung cancer).

“If you want to stop exposure to these things, you have to stop smoking.”

They also found twice as much TSNA in the urine samples of U.S. smokers compared to those in Canada and Australia, an indication that cancer-causing substance has traveled throughout the body.

There is no one group that speaks for the tobacco institute anymore, according to Darryl Jason, a spokesman for the Tobacco Merchants Association (TMA), which is why he couldn’t comment on the study. The TMA was founded in 1915 to “manage information of vital interest to the worldwide tobacco industry according to their website. Jason did point out that cigarettes manufactured in the U.S. contain a different blend of tobacco from cigarettes made elsewhere.

The study acknowledges that there are different types of tobacco depending where the cigarettes are made. But that’s only one factor says Pirkle: “The TSNA levels largely come from the way tobacco is cured.” The heating process, humidity and the type of the ferlizer used to grow the tobacco also contribute to the levels of cancer causing substances, says Pirkle.

Editor’s Note: Medical news is a popular but sensitive subject rooted in science. We receive many comments on this blog each day; not all are posted. Our hope is that much will be learned from the sharing of useful information and personal experiences based on the medical and health topics of the blog. We encourage you to focus your comments on those medical and health topics and we appreciate your input. Thank you for your participation.

June, 2010|Oral Cancer News|

Oral Cancer Foundation donates screening devices to West Virginia Free Clinics

Author: press release

In 2009 the Oral Cancer Foundation initiated a program of donating VELscope® Oral Cancer Screening Systems to free clinics. The most recent recipients of this program are two West Virginia clinics: WV Health Right in Charleston, and the Susan Dew Hoff Memorial Clinic in West Milford.

“Our intent is to identify free clinics in areas that have a high concentration of people who are both at risk for oral cancer and without the financial means to pay for comprehensive oral exams,” said Oral Cancer Foundation founder and executive director Brian Hill. “It is difficult to think of an area that better fits those criteria than West Virginia.” The state ranks highest in the country in tobacco usage, and next-to-last in per capita income. In identifying free clinics to be potential recipients of the device which identifies loss of tissue auto-fluorescence, an indicator of abnormal tissues, the Oral Cancer Foundation is careful to ensure that each candidate clinic has at least one dentist on staff who can be trained to use the device and can train other staff members.

Oral cancer belongs to the head and neck cancer group, and is often referred to by other names such as; tongue cancer, mouth cancer, tonsil cancer, lip cancer, and throat cancer. While some people think this is a rare cancer, it is not. Approximately 100 people in the U.S. will be newly diagnosed with oral cancer each day, and it takes a life in the U.S. every hour of every day.

WV Health Right was founded in 1982 by a small group of physicians and nurses who recognized the need for a source of ongoing health care for Charleston’s low-income uninsured. The clinic has grown so much since its’ founding that it is now in its third location. In 2001, it added a three-unit dental operatory, making it West Virginia’s first free dental clinic. It now serves almost 20,000 patients per year thanks to over 180 medical and dental professional volunteers.

According to WV Health Right executive director Patricia White, “West Virginia has some of the worst oral health statistics in the country, in large part because of the relatively high percentage of residents who are spit tobacco users and smokers.” Because of the well-established connection between tobacco usage and oral cancer, WV Health Right’s dental clinic has always insisted on giving all patients a conventional oral cancer examination regardless of their reason for visiting the clinic. The conventional exam is a manual palpation and visual inspection of the oral cavity and the neck. “Now,” says Ms. White, “our clinicians can also view the oral cavity using fluorescence visualization technology, which will enhance our ability to detect cancerous and pre-cancerous lesions that might be hard to see with the naked eye.”

The Susan Dew Hoff Memorial Clinic serves over 1,800 active patients in West Virginia’s Harrison County. Volunteers include five dentists, five dental assistants, and one hygienist. Roughly half of the patients are employed but without health insurance, while the other half are elderly and rely largely on Medicare.

“A high percentage of our patients use chewing tobacco, smoking tobacco or both,” said clinic director Sister Mary Rebecca Fidler, Ph. D., RSM. “If patients have cancer or any other serious condition, they will want to know about it at the earliest possible time, when survival rates are the highest, and treatment related morbidity the lowest,” she said. She added, “Up until now, we’ve discovered oral lesions on several patients merely by having our clinicians examine them using a visual and tactile conventional screening. Now, with this technology, we look forward to doing not only a better job of detecting early stage oral cancer, but even pre-cancerous tissues changes.”

In the words of the Oral Cancer Foundation’s Hill, “The key to reducing the death rate of oral cancer is earlier detection, and the key to that is for all adults to receive opportunistic oral cancer examinations at least once a year.” Mr. Hill pointed out that tobacco users, heavy alcohol users, and those with a prior history of cancer should be examined more frequently Even people who do not share those traits should be examined annually in light of the mounting evidence of a link between oral cancer and the sexually-transmitted human papilloma virus.

Peter Whitehead, founder and chief executive officer of VELscope manufacturer LED Dental, said, “When we started our company, our goal was to help achieve a significant reduction in the incidence of oral cancer, by elucidating pre-malignant tissue abnormalities. Unfortunately, many times the people who are most at risk for the disease are also the people who cannot afford the regular dental exams that can allow us to discover these early or pre-malignant changes.” According to Mr. Whitehead, “Now, thanks to the efforts of the Oral Cancer Foundation, our potentially life-saving technology is able to reach people we otherwise would likely have missed. Our relationship with OCF in this effort speaks to the core reasons that most of us at LED worked in the arena of adapting high technologies to enable better outcomes in the area of oral cancer. We could not be more pleased to see our technology end up in these underserved areas.”

About the Oral Cancer Foundation: The Oral Cancer Foundation, founded by oral cancer survivor Brian R. Hill, is a non-profit 501(c)(3) public service charity that provides information, patient support, sponsorship of research, and advocacy related to this disease. It maintains a Web site at, which receives millions of hits per month. At the forefront of this year’s agenda is the drive to promote solid awareness in the minds of the American public about the need to undergo an annual oral cancer screening, and an outreach to the dental community to provide this service as a matter of routine practice. Supporting the foundation’s goals is a scientific advisory board composed of leading cancer authorities from varied medical and dental specialties, and from prominent educational, treatment, and research institutions in the United States.

Source: Oral Cancer Foundation

HPV-linked head and throat cancers easier to treat unless patient is a smoker, University of Michigan study finds

Author: Tina Reed

A growing incidence of head and throat cancers have been traced back to the human papillomavirus, or HPV, rather than smoking. With that in mind, University of Michigan researchers recently decided to examine the difference in outcomes between smokers with HPV-linked head and throat cancer and those who had never smoked.

Turns out, the HPV-linked tumors were easier to treat than non-HPV associated cancers. That is, unless the patient was a smoker. Those with HPV-linked cancers who smoked were six times as likely to recur than those who had never smoked.

According to a Los Angeles Time health blog, treatments for head and neck cancers include harsh treatments such as radiation, chemotherapy and surgery. The researchers from U-M’s Comprehensive Cancer Center said they planned to begin a clinical trial to milder treatments later this year.

February, 2010|Oral Cancer News|

Quitting cigarettes completely or switching to smokeless tobacco: do US data replicate the Swedish results?

Source: Tob Control 2009;18:82-87 doi:10.1136/tc.2008.028209
Authors: S-H Zhu et al.

Swedish male smokers are more likely than female smokers to switch to smokeless tobacco (snus) and males’ smoking cessation rate is higher than that of females. These results have fuelled international debate over promoting smokeless tobacco for harm reduction. This study examines whether similar results emerge in the United States, one of few other western countries where smokeless tobacco has long been widely available.

US data source: national sample in Tobacco Use Supplement to Current Population Survey, 2002, with 1-year follow-up in 2003. Analyses included adult self-respondents in this longitudinal sample (n = 15 056). Population-weighted rates of quitting smoking and switching to smokeless tobacco were computed for the 1-year period.

Among US men, few current smokers switched to smokeless tobacco (0.3% in 12 months). Few former smokers turned to smokeless tobacco (1.7%). Switching between cigarettes and smokeless tobacco, infrequent among current tobacco users (<4%), was more often from smokeless to smoking. Men quit smokeless tobacco at three times the rate of quitting cigarettes (38.8% vs 11.6%, p<0.001). Overall, US men have no advantage over women in quitting smoking (11.7% vs 12.4%, p = 0.65), even though men are far likelier to use smokeless tobacco.

The Swedish results are not replicated in the United States. Both male and female US smokers appear to have higher quit rates for smoking than have their Swedish counterparts, despite greater use of smokeless tobacco in Sweden. Promoting smokeless tobacco for harm reduction in countries with ongoing tobacco control programmes may not result in any positive population effect on smoking cessation.

S-H Zhu1, J B Wang1, A Hartman2, Y Zhuang1, A Gamst1, J T Gibson3, H Gilljam4, M R Galanti4

Author Affiliations
1University of California, San Diego, California, USA
2National Cancer Institute
3Information Management Services, Rockville, Maryland, USA
4Karolinska Institutet, Stockholm, Sweden

December, 2009|Oral Cancer News|

U.S. smoking rates remain steady, but vary widely by state

Source: Medical News
Author: John Gever

National rates of cigarette smoking showed little change in 2008 from a year earlier, the CDC reported, though states vary widely both in rates of current smoking and exposures of nonsmokers to secondhand smoke.

Some 20.6% of Americans were current smokers in 2008 (95% CI 19.9% to 21.4%), not significantly different from the 19.8% found in 2007 (95% CI 19.0% to 20.6%) according to the the government’s ongoing National Health Interview Survey, detailed by Shanta R. Dube, PhD, and other CDC researchers in the Nov. 13 issue ofMorbidity and Mortality Weekly Report.

But analysis of a another data set in MMWR — the 2008 results from the Behavioral Risk Factor Surveillance System (BRFSS) — revealed a twofold variation in rates among states.

Utah had by far the lowest rate of current cigarette smoking, at 9.2%, followed by California (14.0%), New Jersey (14.8%) and Maryland (14.9%), according to Ann M. Malarcher, PhD, and CDC colleagues.

West Virginia led the other end of the list at 26.6%. Other states with current smoking rates of 25% or more included Indiana, Kentucky, and Missouri.

West Virginia had several other smoking distinctions.

It was the only state in which the current smoking rate was higher among women than men — 27.1% versus 26.1% — although the difference was not statistically significant.

The BRFSS data showed the Mountain State had the highest rate of home exposure to secondhand smoke among 12 states and territories for which data were available.

Some 10.6% of West Virginia adults said there was secondhand smoke in their homes (95% CI 9.2% to 12.0%), while the lowest rate was in Arizona (3.2%, 95% CI 2.3% to 4.1%). The national median was 7.8%

West Virginia respondents were also least likely to report that smoking was banned inside their homes, at 68.8% (95% CI 67.0% to 70.6%).

The U.S. Virgin Islands sported the highest home smoking ban figure, 85.7% (95% CI 83.8% to 87.6%), a statistical tie with Arizona’s 85.6%. The national median was 78.1%.

Similar variation in workplace exposure to secondhand smoke was apparent in the result, though with a different pattern of highs and lows.

Tennessee had the lowest rate, with 6.0% of survey respondents saying there was secondhand smoke at work (95% CI 4.0% to 8.0%). Mississippi had the highest, at 15.8% (95% CI 13.7% to 17.9%). The national median was 8.6%.

As in previous surveys, the 2008 National Health Interview data showed that smoking rates were markedly higher among individuals with a high school education or less (27.5%, 95% CI 25.5% to 29.6%) compared with those with more education.

People with “some college” had a 2008 smoking rate of 22.7% (95% CI 21.3% to 24.2%) while just 5.7% of those holding graduate degrees were current smokers (95% CI 4.6% to 7.1%).

Dube and colleagues also found substantial racial-ethnic differences in 2008 smoking rates, similar to those seen in previous years:

  • Non-Hispanic whites: 22.0%
  • Non-Hispanic blacks: 21.3%
  • Hispanics: 15.8%
  • American Indian/Alaska native: 32.4%
  • Asian: 9.9%

In an unsigned commentary, MMWR editors noted that the national prevalence of smoking has declined significantly since 1998, when 24.1% of adults smoked. That was the year when the “master settlement agreement” with tobacco companies began limiting their marketing activities, the editors said.

But year-to-year decreases have been sporadic, they added.

“Although comprehensive tobacco control programs have been effective in decreasing tobacco use in the U.S., they remain underfunded,” the editors wrote.

The editors added that state-level tobacco control programs “need to continue to encourage the public to make their homes smoke-free.”

More states also need to legislate smoking bans in restaurants, bars, and other workplaces, they said, as the patchwork nature of such bans appears to be a major factor in the state-to-state variation in exposure to secondhand smoke on the job.

No external funding for the CDC studies was reported.

No potential conflicts of interest were reported.

November, 2009|Oral Cancer News|

Understanding the link between HPV and oropharyngeal cancers

Source: (Journal of the American Academy of Physician Assistants, October, 2009)
Authors: Denise Rizzolo, PA-C, PhD, Mona Sedrak, PA-C, PhD

Head and neck cancer is diagnosed in approximately 650,000 patients each year worldwide.1 The term head and neck cancer refers to a group of biologically similar cancers originating from the upper aerodigestive tract, including the lip, oral cavity (mouth), nasal cavity, paranasal sinuses, pharynx, and larynx. Oropharyngeal refers to all the structures of the mouth and pharynx, including the tonsils and tongue. Oral squamous cell carcinoma (OSCC) is the most common form of head and neck cancer.2 Seventy-five percent of all OSCCs are attributable to tobacco and alcohol use.3 People who smoke cigarettes are 4 times more likely to develop oral cancer than nonsmokers. Furthermore, individuals who consume alcohol are 3 times more likely than nondrinkers to develop oral cancer.3 According to the Substance Abuse and Mental Health Services Administration, the prevalence of cigarette smoking has decreased among Americans, and alcohol use has also declined since the 1970s.4,5 However despite this, the incidence of oropharyngeal cancers, including cancer of the base of the tongue and tonsils, has increased, especially in younger patients. These trends have led researchers to investigate other potential risk factors.6-8

New studies suggest that there may be an alternative pathway for the development of oropharyngeal cancers. The high-risk types of human papillomavirus (HPV), especially type 16 (HPV-16), are now thought to be potential etiologic agents.2,3 The concept that HPV plays a role in head and neck cancers is not new. This link has been under investigation for at least 20 years.6 This is a worrisome public-health concern because patients with HPV-positive OSCC are 3 to 5 years younger at diagnosis than those with HPV-negative OSCC, and they have a history of high-risk sexual behavior.9-12 Interestingly, patients with HPV-positive OSCC are also less likely to have a history of alcohol and tobacco abuse.3 Therefore, educating patients regarding the disturbing trend of HPV-positive oropharyngeal cancer is important.

Incidence and Prevalence
In the United States alone, an estimated 34,360 people received a diagnosis of oropharyngeal cancer in 2007; of these, 7,550 (5,180 men and 2,370 women) died.13 On average, more than 25% of people who develop oropharyngeal cancer will die of the disease, with only 60% surviving for more than 5 years.14 In fact, oropharyngeal cancer is as common as leukemia and claims more lives than either melanoma or cervical cancer.13

Since the mid 1970s, oropharyngeal cancer rates have increased approximately 15%, with significant disparities in some population groups. For instance, oropharyngeal cancer prevalence is significantly higher in males than in females.14 Prevalence is also higher in Hispanic and black males than it is in white males.14 The risk of oropharyngeal cancer increases with age, and occurrence is highest in persons older than 50 years and peaks between ages 60 and 70 years.14 However, there has been a startling 5-fold increase in the incidence of oral cancer in patients younger than 40 years, many of whom have no known risk factors.4

HPV is associated with 15% to 35% of head and neck cancers worldwide.11 Fifty percent to 90% of OSCCs in the pharynx, tonsil, and tongue are HPV-positive.11 Chaturvedi and colleagues investigated the impact of HPV on the epidemiology of OSCCs in the United States.9 These researchers reported that HPV-positive OSCCs were diagnosed at younger ages than HPV-negative OSCCs (mean age at diagnosis was 61.0 and 63.8 years, respectively) and the incidence increased significantly for HPV-positive OSCC from 1973 to 2004, particularly among younger white men.

Kreimer and colleagues conducted a systematic review of 60 studies and determined that 25.9% of the 5,046 patients with head and neck squamous cell carcinoma (HNSCC) were HPV-positive.2 Furthermore, these researchers noted that HPV-16 was the most prevalent genotype in these cancers, accounting for 86.7% of cases.

Although there is research that supports the association between HPV and oropharyngeal cancers, some studies dispute that relationship. Specifically, controversy exists over the prevalence and significance of HPV in oral tongue cancers (cancer of the anterior two-thirds of the tongue). In a 2008 Mayo Clinic study, researchers examined fresh-frozen tissues from 51 patients with oral tongue cancers.15 Their findings suggest that the incidence of oral HPV in oral tongue cancer was low and was unlikely to play a significant role in the etiology, pathogenesis, and clinical outcomes of oral tongue cancers.15 The authors admit the study was limited by a small sample size and that more research is needed.

The oropharyngeal sites that are most often associated with the HPV infection are the tonsils and the tongue.16,17 Reasons why the oropharynx is more susceptible to the HPV infection remain unclear; however, the similarity in accessibility to infection between the tonsillar tissue and the uterine cervical mucosa is believed to make the oropharyngeal area more vulnerable. Another explanation is that tonsillar tissue contains deep invaginations that may capture the virus and facilitate it into the basal cells.

The mechanism of HPV carcinogenesis was first characterized in cervical cancer. Ninety percent of cervical cancer cases are related to HPV infection, predominantly HPV-16 and HPV-18.18 The viral oncoproteins E6 and E7 of the high-risk HPV types are associated with the malignant process in both anogenital and head and neck cancers.17 These oncoproteins inactivate the p53 and pRb tumor suppressor pathways, which is important to the genetic progression of head and neck cancers. HPV infection may therefore represent an alternate but functional pathway for HNSCC pathogenesis. Yet, despite recent literature confirming that HPV is a risk factor associated with oropharyngeal cancers, the HPV infection is not necessary nor is it sufficient for oropharyngeal carcinoma to develop. Therefore, more research is needed to closely define the link between the acquisition of the virus and the progression to cancer.

The major prognostic factors for head and neck cancer are the presence of local and regional metastasis, vascular or lymphatic invasion, positive surgical margins, and extracapsular spread of tumor cells from the lymph nodes into the soft tissue of the head and neck.19 Thus, understanding the mechanism of tumor progression may help to identify new prognostic and predictive markers that will aid in the development of new therapeutic agents for the treatment of HPV-positive cancer.20

Incidence of HPV Transmission
The association between high-risk sexual behavior and transmission of HPV is well-established.10,21 Certain sexual behaviors are associated with a significantly increased risk of HPV transmission, including engaging in casual sex, young age at first intercourse, and infrequent use of condoms. Specifically, a high number of lifetime sex partners (26 or more vaginal-sex partners, 6 or more oral-sex partners) is associated with an increased risk of oropharyngeal cancer. A study conducted from 2000 to 2006 positively correlated HPV-16-positive cancer of the head and neck with number of oral-sex partners, as well as with marijuana use.22

Diffuse white area on the buccal mucosa

Diffuse white area on the buccal mucosa

The onset of the HIV epidemic has resulted in an increase in oral sex practices among teenagers and young adults, which may be contributing to the increase in the incidence of HPV-positive cancers.23 A common belief among people in these age-groups is that oral sex represents a form of “safe sex,” leading to a worry-free behavior that precludes them from contracting sexually transmitted diseases. These findings emphasize a significant implication to public health. The increase in the incidence of tonsillar and base-of-tongue cancers in the United States may be a result of a higher incidence of oral-sex practices.7,8

Clinical Signs and Symptoms
HPV-positive oropharyngeal cancer manifests in the same manner as HPV-negative oropharyngeal cancer. Therefore, clinicians should be aware of the signs and symptoms that suggest OSCC. Patients present with a variety of signs and symptoms depending on the site of origin, including a sore throat, dysphagia, odynophagia, and hoarseness14 (Table 1). The two precursor lesions clinicians should look for are leukoplakia, white lesions (Figure 1), and erythroplakia, red lesions. Although leukoplakia lesions are more common, erythroplakia and lesions with erythroplakic components have a much greater potential for becoming cancerous. Any white or red lesion that does not resolve within 2 weeks should be reevaluated and considered for biopsy to obtain a definitive diagnosis.14 The following are the four basic steps to early detection and prevention of disease:

• Take a thorough history
• Perform a detailed examination of the head and neck
• Educate patients on the risk factors associated with oral cancers
• Provide adequate follow-up to ensure a definitive diagnosis of any suspicious lesions.14


A thorough history and physical examination of the head and neck should be a routine part of each patient’s general medical examination. Clinicians should be particularly vigilant when examining patients who have a history of tobacco use or drink excessive amounts of alcohol. The examination is conducted with the patient seated. The patient should remove any intraoral prostheses before beginning the examination. The extraoral assessment includes inspection of the face, head, and neck; note any asymmetry or skin pathology, such as crusts, fissuring, growths, and/or color changes. The regional lymph node areas are bilaterally palpated to detect any enlarged nodes.14 The perioral and intraoral examination follows a detailed, seven-step systematic assessment14 (Table 2).


Recent data suggests a better prognosis for those patients with HPV-positive HNSCC than for those with HPV-negative HNSCC; however, there is still intense debate over this theory.20 Treatment is the same for patients, regardless of whether they have HPV-positive or HPV-negative HNSCC. Traditional therapy for patients with stage I or II head and neck cancer consists of radiation and/or surgery, and prognosis is excellent. Unfortunately, most patients present with stage III or IV disease, and treatment consists of a combination of chemotherapy, radiation, and surgery.20 Survival rates are greatly diminished when the disease is diagnosed at a later stage.

An interesting note is that research suggests that HPV-positive tumors behave in a different fashion, have a different response to therapy, and are more sensitive to radiation-based therapies; therefore, HPV-positive HNSCCs may require a different therapeutic approach compared with HPV-negative HNSCCs.24 Fakhry and colleagues found that patients with HPV-positive HNSCC had better overall and progression-free survival rates than did patients with HPV-negative HNSCC.24 These findings raise the question of whether traditional therapy is the best option for HPV-positive disease. Even when HNSCC is diagnosed early, treatment still consists of removal of the diseased tissue and/or weeks of radiation therapy that may leave some patients disfigured or with permanent negative sequela (dry mouth, loss of taste, alteration of speech patterns, etc). If HPV-positive cancers are more sensitive to traditional therapy, can less aggressive and extensive treatment be used thereby minimizing the side effects of current therapeutic regimens on this subset of patients? The study authors interpret their results cautiously, suggesting that more research is needed on treatment response and subsequent survival patterns of patients with HPV-positive cancers. Until further research is conducted, therapeutic treatment strategies are the same for HPV-positive and HPV-negative HNSCC.24

Patient Education: Prevention and Detection
The best way to prevent oropharyngeal cancer is to avoid tobacco and alcohol use. In addition, regular dental checkups, including an examination of the entire mouth, are essential for early detection of cancerous and precancerous conditions. Red or white lesions often precede the development of oropharyngeal cancer; therefore, if patients notice any new lesions in their mouths, they should have them evaluated by their clinicians. Lesions that do not resolve after 2 weeks should be biopsied. Detection of oropharyngeal carcinoma while the disease is still localized can dramatically increase survival rates. The 5-year survival rate for patients with localized disease at diagnosis is 82%, compared with only 28% for those whose cancer has spread to other parts of the body.14

Clinicians should take the time to educate young patients regarding HPV infection, its correlation to oropharyngeal cancer, and safe-sex practices. Some discussions in the literature suggest that the HPV vaccine could be considered for the prevention of HPV-positive HNSCC.6,10,20 The HPV vaccine has become an important strategy in the prevention of cervical cancer because HPV has been shown to cause nearly all cases of female cervical cancer. Ninety-five percent of patients with HPV-positive HNSCC are positive for HPV-16; therefore, researchers are exploring whether the vaccine could provide the same prophylactic effect against HPV-positive HNSCC as it does for HPV-associated anogenital cancers.25 D’Souza and colleagues argue that a rationale for HPV vaccination in both boys and girls is that oropharyngeal cancers occur in both men and women.10 They also suggest that if the vaccine prevents oral disease as effectively as it prevents cervical disease, a substantial reduction in the incidence of oropharyngeal cancer in vaccinated populations would provide the ultimate evidence of causality. However, no definitive recommendations to use the HPV vaccine to prevent HPV-positive HNSCC have been made.


Cancers of the head and neck are a worldwide concern. The incidence of HPV-related head and neck cancer is increasing. Clinicians should be aware of the risk factors as well as the clinical signs and symptoms of oropharyngeal cancers. The best way to prevent oropharyngeal cancer is to avoid tobacco and alcohol use. However, consistent safe-sex practices are also effective preventive measures because of the strong correlation between HPV infection and oropharyngeal cancers. This association has researchers considering the potential effectiveness of the HPV vaccine in the prevention of HPVpositive head and neck cancers. JAAPA

Authors’ affiliations
Mona Sedrak is an associate professor in the PA program at Seton Hall University, South Orange, New Jersey. Denise Rizzolo works at the Care Station, Springfield, New Jersey, and is faculty assistant professor in the PA program at Seton Hall University. They have indicated no relationships to disclose relating to the content of this article.

1. Boyle P, Ferlay J. Cancer incidence and mortality in Europe, 2004. Ann Oncol. 2005;16(3):481-488.
2. Kreimer AR, Clifford GM, Boyle P, Franceschi S. Human papillomavirus types in head and neck squamous cell carcinomas worldwide: a systematic review. Cancer Epidemiol Biomarkers Prev. 2005;14(2):467-475.
3. Mork J, Lie K, Glattre E, et al. Human papillomavirus infection as a risk factor for squamous-cell carcinoma of the head and neck. N Engl J Med. 2001;344(15):1125-1131.
4. Schantz SP, Yu GP. Head and neck cancer incidence trends in young Americans, 1973-1997, with a special analysis for tongue cancer. Arch Otolaryngol Head Neck Surg. 2002;128(3):268-274.
5. Substance Abuse and Mental Health Services Administration. Results from the 2006 National Survey on Drug Use and Health: National Findings. Rockville, MD: Substance Abuse and Mental Health Services Administration, US Dept of Health and Human Services; 2006. DHHS publication SMA 07-4293.
6. Syrjanen S. Human papillomaviruses in head and neck carcinomas. N Engl J Med. 2007;356(19):1993-1995.
7. Frisch M, Hjalgrim H, Jaeger AB, Biggar RJ. Changing patterns of tonsillar squamous cell carcinoma in the United States. Cancer Causes Control. 2000;11(6):489-495.
8. Shiboski CH, Schmidt BL, Jordan RC. Tongue and tonsil carcinoma: increasing trends in the U.S. population ages 20-44 years. Cancer. 2005;103(9):1843-1849.
9. Chaturvedi AK, Engels EA, Anderson WF, Gillison ML. Incidence trends for human papillomavirus-related and -unrelated oral squamous cell carcinomas in the United States. J Clin Oncol. 2008;26(4):612-619.
10. D’Souza G, Kreimer AR, Viscidi R, et al. Case-control study of human papillomavirus and oropharyngeal cancer. N Engl J Med. 2007;356(19):1944-1956.
11. Saraiya M, Kawaoka K. Incidence of human papillomavirus (HPV)-related head and neck cancers in the US from 1998-2003: Pre-HPV vaccine licensure. [ASCO abstract 6003] J Clin Oncol. 2007;25(suppl):299s.
12. Schwartz SM, Daling JR, Doody DR, et al. Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection. J Natl Cancer Inst. 1998;90(21):1626-1636.
13. American Cancer Society. Cancer Facts & Figures 2007. Atlanta, GA: American Cancer Society; 2007.
14. National Institute of Dental and Craniofacial Research. Detecting oral cancer: A guide for health care professionals. NIDCR Web site.
15. Liang XH, Lewis J, Foote R, et al. Prevalence and significance of human papillomavirus in oral tongue cancer: the Mayo Clinic experience. J Oral Maxillofac Surg. 2008;66(9):1875-1880.
16. Gillison ML, Koch WM, Capone RB, et al. Evidence for a causal association between human papillomavirus and a subset of head and neck cancers. J Natl Cancer Inst. 2000;92(9):709-720.
17. Haddad RI. Human papillomavirus infection and oropharyngeal cancer. Medscape CME Web site. Accessed September 4, 2009.
18. Muñoz N, Bosch FX, de Sanjosé S, et al; International Agency for Research on Cancer Multicenter Cervical Cancer Study Group. Epidemiologic classification of human papillomavirus types associated with cervical cancer. N Engl J Med. 2003;348(6):518-527.
19. Forastiere A, Koch W, Trotti A, Sidransky D. Head and neck cancer. N Engl J Med. 2001;345(26):1890-1900.
20. Haddad RI, Shin DM. Recent advances in head and neck cancer. N Engl J Med. 2008;359(11):1143-1154.
21. Gillison ML, Shah KV. Chapter 9: Role of mucosal human papillomavirus in nongenital cancers. J Natl Cancer Inst Monogr. 2003;(31):57-65.
22. Gillison ML, D’Souza G, Westra W, et al. Distinct risk factor profiles for human papillomavirus type 16-positive and human papillomavirus type 16-negative head and neck cancers. J Natl Cancer Inst. 2008;100(6):407-420.
23. Mosher WD, Chandra A, Jones J. Sexual behavior and selected health measures: men and women 15-44 years of age, United States, 2002. Adv Data. 2005;(362):1-55.
24. Fakhry C, Westra WH, Li S, Cmelak A, et al. Improved survival of patients with human papillomavirus—positive head and neck squamous cell carcinoma in a prospective clinical trial. J Natl Cancer Inst. 2008;100(4):261-269.
25. Devaraj K, Gillison ML, Wu TC. Development of HPV vaccines for HPV-associated head and neck squamous cell carcinoma. Crit Rev Oral Biol Med. 2003;14(5):345-362.

October, 2009|Oral Cancer News|