oral cancer

New cancer test isn’t ready for prime time

Author: H Gilbert Welch
Date: February 14, 2018
Source: http://www.cnn.com/2018/02/13/opinions/liquid-biopsy-opinion-welch/index.html

(CNN)- A simple blood test to detect cancer early. How great is that?

There has been enthusiasm about the so-called “liquid biopsy” for years. In mid-January, however, doctors learned more — both about this vision and its problems.

A widely reported study in the journal Science described a liquid biopsy test — CancerSEEK — which combined measuring eight tumor biomarkers with testing for pieces of DNA with cancer associated mutations in 16 genes.

It’s not one test; it’s a battery of tests. And while collecting the blood may be simple, the subsequent analysis is extraordinarily complex.

The task at hand is particularly challenging. We all have pieces of DNA in our blood. Distinguishing the tumor DNA from the background DNA requires finding the mutations specifically associated with cancer.

Adding to the complexity, healthy individuals can have mutations. To avoid labeling innocuous mutations as cancerous requires a bunch of statistical fine-tuning.

In other words, there are a lot of steps in a liquid biopsy and much potential for things to go awry.

To their credit, the CancerSEEK investigators were very forthright that the study conditions were ideal for the test to accurately detect cancer. The liquid biopsy simply had to discriminate between patients with known cancer (the majority of whom had symptoms) and healthy individuals. And the statistical fine-tuning was tailored to the study participants — with the knowledge of who had, and who did not have, cancer.

Although the test was able to detect most of the late-stage cancers, it detected less than half of the stage 1 cancers.

But doctors don’t screen to find advanced cancer, we screen to find early cancer. And we don’t screen people with symptoms of cancer, we screen people who don’t have symptoms of cancer.

There’s no doubt that there would be more detection errors in the less controlled environment of the real world.

Just how often was made clear in a recent JAMA-Oncology study. Forty patients with metastatic prostate cancer received liquid biopsies to tailor therapy in real time to the genetics of their spreading tumors. That’s the vision for precision medicine.

But the investigators added a little twist. They wanted to know whether it mattered which lab the liquid biopsies were sent to. So they sent each patient’s blood for two different commercial liquid biopsies: Guardant360 and PlasmaSELECT. Both tests were designed to detect mutations in the same genes.

Yet in over half of the 40 patients, the tests gave different answers about which mutations were present. Different liquid biopsy tests give different answers in a majority of patients? That’s not precision, that’s awful.

Sure, the analyses of liquid biopsies will improve. But if this much confusion exists about what mutations are present in the blood of patients with metastatic cancer (who have a lot of tumor DNA), imagine the uncertainty that will exist for asymptomatic individuals not known to have cancer — the very people who would be screened.

And then there is the question of what to do with a positive result. This is very different than detecting a concerning lung nodule on a screening chest CT scan or a concerning breast mass on a screening mammogram. In these cases, it’s clear what to do to get a definitive answer: surgically biopsy the nodule or the mass. But with a liquid biopsy, the anatomic location of a cancer can be a mystery. It may not even be clear what organ the cancer is in.

Imagine what this might mean for a patient: A doctor says, “It looks like you have cancer, but we are not sure where.”

Even if there is certainty that the cancer is in, say, the liver, doctors may not know where in the organ. What to do then? Randomly biopsy different parts of the liver?

This is doubly concerning when screening average-risk individuals, because most positive results are expected to be false alarms. We typically learn that a screening test is falsely positive because a surgical biopsy is normal. But absent the knowledge of where to biopsy, how can we ever be sure a positive liquid biopsy is wrong?

Doctors won’t know where to look, but we will keep looking. Liquid biopsies are a recipe for more health anxiety, more procedures, more complications and more overdiagnoses. Not to mention, more out-of-pocket costs for our patients.

Of course, we should continue to study liquid biopsies. The detection of circulating tumor DNA may ultimately prove useful in selected settings, such as tailoring therapy for aggressive cancers that are rapidly mutating. But the real enthusiasm is for screening average-risk individuals.

One reason is obvious: there is a lot of money to be made. A Goldman Sachs video estimated the potential liquid biopsy market to be $14 billion annually, adding “and we’re just at the beginning.” That kind of money doesn’t come from testing the few patients with aggressive cancer, that comes from screening millions of people.

And there is a less obvious reason: it is easier for a new test to pass regulatory muster than it is for a new drug. While the FDA has a longstanding mandate to protect us from snake oil treatments, this often doesn’t extend to snake oil testing.

The enthusiasm for finding things that might benefit people in the future ignores the fact that doing so can cause people to have problems now. In short, a bad test can do as much damage as a bad drug. Worrisome liquid biopsies will start a cascade of subsequent, not-so-simple tests and procedures. People will be hurt in the process.

February, 2018|Oral Cancer News|

CDHA Urges Hygienists to Remind Patients of Oral Cancer Screening

Author: Canadian Dental Hygienists Association
Date: January 29, 2018
Source: https://www.oralhealthgroup.com

World Cancer Day (February 4) is a perfect time for dental hygienists across Canada to remind the public of the importance of regular oral cancer screenings, not only during dental appointments, but also now at home.

The Canadian Cancer Society projected in 2017 that 4,700 Canadians would be diagnosed with oral cavity cancer, and that 1,250 Canadians would die.  In hopes of improving the long-term outcomes for people diagnosed with oral cancer, the Canadian Dental Hygienists Association (CDHA) has partnered with the Oral Cancer Foundation and the American Dental Hygienists Association on a “Check Your Mouth™” initiative to help individuals identify the early signs and symptoms of oral cavity cancers.  “Dental hygienists recognize that early detection has great potential to reduce the oral cancer burden in Canada,” states Sophia Baltzis, CDHA president. “Between dental visits, which usually include an oral cancer screening, our clients can and should examine their mouths for suspicious tissue changes.”

The Check Your Mouth™ campaign features an interactive website (www.checkyourmouth.org) that offers easy-to-use tools and tips for a quick visual and tactile examination of the oral cavity.  Individuals can learn to self-discover the early symptoms of disease and then seek further evaluation from a dental professional if necessary.  “Dental hygienists are your partners in prevention,” adds Baltzis. “We encourage all Canadians to maintain a healthy lifestyle, practice good oral hygiene habits, and spot the early signs of oral cancer. The Check Your Mouth™ website is a valuable resource that everyone should explore.”  By raising public awareness of oral cancer and its early signs and symptoms, dental hygienists are helping to meet the global challenge of saving lives. Together, we can make a difference!

Serving the profession since 1963, CDHA is the collective national voice of more than 28,495 registered dental hygienists working in Canada, directly representing 19,000 individual members including dental hygienists and students. Dental hygiene is the 6th largest registered health profession in Canada with professionals working in a variety of settings, including independent dental hygiene practice, with people of all ages, addressing issues related to oral health. For more information on oral health,

January, 2018|Oral Cancer News|

Study Identifies Potential Cause of Hearing Loss from Cisplatin

Author: NCI Staff
Date: January 26, 2018
Source: National Cancer Institute (https://www.cancer.gov/news-events)

Results from a new study may explain why many patients treated with the chemotherapy drug cisplatin develop lasting hearing loss.

Researchers found that, in both mice and humans, cisplatin can be found in the cochlea—the part of the inner ear that enables hearing—months and even years after treatment. By contrast, the drug is eliminated from most organs in the body within days to weeks after being administered.

The study, led by researchers from the National Institute on Deafness and other Communication Disorders (NIDCD), part of the National Institutes of Health, was published November 21 in Nature Communications.

Cisplatin, a platinum-based chemotherapy drug, is commonly used for the treatment of many cancers, including bladder, ovarian, and testicular cancers. But cisplatin and other similar platinum-containing drugs can damage the cochlea, leaving 40%–80% of adults, and at least 50% of children, with significant permanent hearing loss, a condition that can greatly affect quality of life.

“This study starts to explain why patients who receive the drug sustain hearing loss,” said Percy Ivy, M.D., associate chief of NCI’s Investigational Drug Branch, who was not involved in the study. “This is very important, because as we come to understand how cisplatin-related hearing loss occurs, over time we may figure out a way to block it, or at least diminish its effects.”

A New Approach to Researching Cisplatin-Induced Hearing Loss

The new study differs from previous research because it is a comprehensive look at the pharmacokinetics, or concentration, of the drug in the inner ear, explained study investigator Andrew Breglio, of NIDCD.

The research team primarily used a technique called inductively coupled plasma mass spectrometry (ICP-MS) to quantify the amount of platinum left in inner ear tissue following cisplatin treatment in mice.

Lisa Cunningham, Ph.D., of NIDCD, who led the research team, noted that instead of using one high dose of cisplatin with mice as other studies have, they developed a treatment protocol like those used in everyday care, in which the drug is given in cycles.

Testing done following each cisplatin cycle showed increasingly progressive hearing loss in the mice. The researchers also measured platinum levels in various organs throughout the drug cycles and found that, whereas other organs eliminated the drug relatively quickly, the cochlea retained the cisplatin, showing no significant loss of platinum 60 days after the last administration of the drug.

The researchers also conducted postmortem analysis of inner ear tissue of human patients who had received cisplatin, and found that platinum was retained in cochleae at least 18 months after the last treatment. In addition, they found that in the cochlea of one pediatric patient (the only one available for study), significantly more platinum was retained than in adult patients, consistent with the fact that children’s ears are known to be more susceptible to cisplatin-induced hearing loss.

In both the mouse model and in studies of human tissue, the researchers determined that the platinum accumulates in a part of the cochlea called the stria vascularis, which, Breglio explained, regulates the makeup of the fluid that bathes the sensory hair cells in the ear “and is critical to their proper function.”

This lengthy retention in the cochlea could explain why this drug is damaging the inner ear, Breglio said. Furthermore, these findings, demonstrating the accumulation of the drug and identifying where it is retained, mean that future studies need to “look beyond hair cells” to explain cisplatin-induced hearing loss, the researchers wrote.

Findings That Could Lead to Hearing Loss Treatment and Prevention

The finding that cisplatin is retained in the cochlea indefinitely is important for patient care, Dr. Ivy said.

Hearing loss from cisplatin “is not a static injury, it doesn’t stay the same. It can progress over time and it can occur late,” she added. “That suggests that a long-term survivor needs ongoing monitoring of their hearing.”

She said it will be up to practitioners to continue this monitoring and to rapidly intervene with devices that assist in hearing, such as hearing aids.

Hearing loss can have a particularly negative impact on children, she said.

“If adults develop hearing loss, they’re more acutely aware of it, and are more likely to seek assistance, whereas younger children who develop hearing loss might not notice it as much or be unable to explain the problem,” she explained. “Since they can’t hear very well, they may have trouble paying attention and that could be misconceived as a learning disability or a behavior problem. And yet, if they get the appropriate intervention, they perform at the same level they did prior to receiving platinum.”

This is why researchers on Dr. Cunningham’s team are trying to find ways to block cisplatin from entering the inner ear. They are looking at the cellular mechanism by which cisplatin is taken up by the cells of the stria vascularis to find ways to block uptake, as well as identify drugs that might “target cisplatin itself, and bind it or sequester it” before it can get into the inner ear, Breglio said.

“[Cisplatin] is one of the most widely used anticancer drugs on the planet, and it’s saving a lot of lives,” Dr. Cunningham said. But the hearing loss is permanent. “So these patients are surviving and they have this hearing loss for the rest of their lives. What we’d like to be able to do is develop a therapy that will allow patients to take the life-saving drug, but preserve their hearing.”

 

January, 2018|Oral Cancer News|

Anti-smoking plan may kill cigarettes–and save Big Tobacco

Date: January 19, 2018
Author: Matthew Perrone
Source: www.apnews.com

WASHINGTON (AP) — Imagine if cigarettes were no longer addictive and smoking itself became almost obsolete; only a tiny segment of Americans still lit up. That’s the goal of an unprecedented anti-smoking plan being carefully fashioned by U.S. health officials.

But the proposal from the Food and Drug Administration could have another unexpected effect: opening the door for companies to sell a new generation of alternative tobacco products, allowing the industry to survive — even thrive — for generations to come.

The plan puts the FDA at the center of a long-standing debate over so-called “reduced-risk” products, such as e-cigarettes, and whether they should have a role in anti-smoking efforts, which have long focused exclusively on getting smokers to quit.

“This is the single most controversial — and frankly, divisive — issue I’ve seen in my 40 years studying tobacco control policy,” said Kenneth Warner, professor emeritus at University of Michigan’s school of public health.

The FDA plan is two-fold: drastically cut nicotine levels in cigarettes so that they are essentially non-addictive. For those who can’t or won’t quit, allow lower-risk products that deliver nicotine without the deadly effects of traditional cigarettes.

 

US health officials are pushing ahead with an unprecedented plan to make cigarettes less addictive and provide lower-risk alternative products to US smokers. (Jan. 19)

This month the government effort is poised to take off. The FDA is expected to soon begin what will likely be a years-long process to control nicotine in cigarettes. And next week, the agency will hold a public meeting on a closely watched cigarette alternative from Philip Morris International, which, if granted FDA clearance, could launch as early as February.

The product, called iQOS (pronounced EYE-kose), is a penlike device that heats Marlboro-branded tobacco but stops short of burning it, an approach that Philip Morris says reduces exposure to tar and other toxic byproducts of burning cigarettes. This is different from e-cigarettes, which don’t use tobacco at all but instead vaporize liquid usually containing nicotine.

For anti-smoking activists these new products may mean surrendering hopes of a knockout blow to the industry. They say there is no safe tobacco product and the focus should be on getting people to quit. But others are more open to the idea of alternatives to get people away from cigarettes, the deadliest form of tobacco.

Tobacco companies have made claims about “safer” cigarettes since the 1950s, all later proven false. In some cases the introduction of these products, such as filtered and “low tar” cigarettes, propped up cigarette sales and kept millions of Americans smoking. Although the adult smoking rate has fallen to an all-time low of 15 percent, smoking remains the nation’s leading preventable cause of death and illness, responsible for about one in five U.S. deaths.

Anti-smoking groups also point to Big Tobacco’s history of manipulating public opinion and government efforts against smoking: In 2006, a federal judge ruled that Big Tobacco had lied and deceived the American public about the effects of smoking for more than 50 years. The industry defeated a 2010 proposal by the FDA to add graphic warning labels to cigarette packs. And FDA scrutiny of menthol-flavored cigarettes — used disproportionately by young people and minorities — has been bogged down since 2011, due to legal challenges.

“We’re not talking about an industry that is legitimately interested in saving lives here,” said Erika Sward of the American Lung Association.

But some industry observers say this time will be different.

“The environment has changed, the technology has changed, the companies have changed — that is the reality,” said Scott Ballin, a health policy consultant who previously worked for the American Heart Association.

Under a 2009 law, the FDA gained authority to regulate certain parts of the tobacco industry, including nicotine in cigarettes, though it cannot remove the ingredient completely. The same law allows the agency to scientifically review and permit sales of new tobacco products, including e-cigarettes. Little has happened so far. Last year, the agency said it would delay the deadline for manufacturers to submit their vapor-emitting products for review until 2022.

The FDA says it wants to continue to help people quit by supporting a variety of approaches, including new quit-smoking aids and opening opportunities for a variety of companies, including drugmakers, to help attack the problem. As part of this, the FDA sees an important role for alternative products — but in a world where cigarettes contain such a small amount of nicotine that they become unappealing even to lifelong smokers.

“We still have to provide an opportunity for adults who want to get access to satisfying levels of nicotine,” but without the hazards of burning tobacco, said FDA Commissioner Dr. Scott Gottlieb. He estimates the FDA plan could eventually prevent 8 million smoking-related deaths.

“SMOKE-FREE FUTURE”

Philip Morris International and its U.S. partner Altria will try to navigate the first steps of the new regulatory path next week.

At a two-day meeting before the FDA, company scientists will try and convince government experts that iQOS is less-harmful than cigarettes. If successful, iQOS could be advertised by Altria to U.S. consumers as a “reduced-risk” tobacco product, the first ever sanctioned by the FDA.

Because iQOS works with real tobacco the company believes it will be more effective than e-cigarettes in getting smokers to switch.

Philip Morris already sells the product in about 30 countries, including Canada, Japan and the United Kingdom.

iQOS is part of an elaborate corporate makeover for Philip Morris, which last year rebranded its website with the slogan: “Designing a smoke-free future.” The cigarette giant says it has invested over $3 billion in iQOS and eventually plans to stop selling cigarettes worldwide — though it resists setting a deadline.

Philip Morris executives say they are offering millions of smokers a better, less-harmful product.

Matthew Myers of the Campaign for Tobacco-Free Kids still sees danger. He says FDA must strictly limit marketing of products like iQOS to adult smokers who are unable or unwilling to quit. Otherwise they may be used in combination with cigarettes or even picked up by nonsmokers or young people who might see the new devices as harmless enough to try.

“As a growing percentage of the world makes the decision that smoking is too dangerous and too risky, iQOS provides an alternative to quitting that keeps them in the market,” Myers says.

It’s unclear whether existing alternatives to cigarettes help smokers quit, a claim often made by e-cigarette supporters. Research from the Centers for Disease Control and Prevention suggests about 60 percent of adult e-cigarette users also smoke regular cigarettes.

THE CASE FOR LOWER NICOTINE

Experts who study nicotine addiction say the FDA plan is grounded in the latest science.

Several recent studies have shown that when smokers switch to very low-nicotine cigarettes they smoke less and are more likely to try quitting. But they also seek nicotine from other sources, underscoring the need for alternatives. Without new options, smokers would likely seek regular-strength cigarettes on the black market.

Crucial to the FDA proposal is a simple fact: nicotine is highly addictive, but not deadly. It’s the burning tobacco and other substances inhaled through smoking that cause cancer, heart disease and bronchitis.

“It’s hard to imagine that using nicotine and tobacco in a way that isn’t burned, in a non-combustible form, isn’t going to be much safer,” said Eric Donny, an addiction researcher at the University of Pittsburgh.

A study of 800 smokers by Donny and other researchers showed that when nicotine was limited to less than 1 milligram per gram of tobacco, users smoked fewer cigarettes. The study, funded by the FDA, was pivotal to showing that smokers won’t compensate by smoking more if nicotine intake is reduced enough. That was the case with “light” and “low-tar” cigarettes introduced in the 1960s and 1970s, when some smokers actually began smoking more cigarettes per day.

Still, many in the anti-smoking community say larger, longer studies are needed to predict how low-nicotine cigarettes would work in the real world.

LEGAL RISKS

Key to the FDA plan is the assumption that the two actions will happen at the same time: as regulators cut nicotine in conventional cigarettes, manufacturers will provide alternative products.

But that presumes that tobacco companies will willingly part with their flagship product, which remains enormously profitable.

Kenneth Warner, the public policy professor, said he would be “astonished” if industry cooperates on reducing nicotine levels.

“I don’t think they will. I think they will bring out all of their political guns against it and I’m quite certain they will sue to prevent it,” he said.

In that scenario, the FDA plan to make cigarettes less addictive could be stalled in court for years while companies begin launching FDA-sanctioned alternative products. Tobacco critics say that scenario would be the most profitable for industry.

“It’s like Coke, you can have regular Coke, Diet Coke, Coke Zero, we’ll sell you any Coke you like,” said Robin Koval, president of the Truth Initiative, which runs educational anti-tobacco campaigns.

But the FDA’s Gottlieb says the two parts of the plan must go together. “I’m not going to advance this in a piecemeal fashion,” he said.

When pressed about whether industry will sue FDA over mandatory nicotine reductions, tobacco executives for Altria and other companies instead emphasized the long, complicated nature of the regulatory process.

“I’m not going to speculate about what may happen at the end of a multiyear process,” said Jose Murillo, an Altria vice president. “It will be science and evidence-based and we will be engaged at every step of the way.”

 

January, 2018|Oral Cancer News|

HPV vaccine is safe, effective after 10 years: study

Author: AFP/RelaxNews
Date: November 30, 2017
Source: Globalnews.ca

New research looking into the long-term effects of the human papillomavirus (HPV) vaccine has found it to be both safe and effective in protecting against the most virulent strains of the virus.

Led by Dr. Daron G. Ferris, professor in the Department of Obstetrics and Gynecology at the Medical College of Georgia and at the Georgia Cancer Center at Augusta University, the study is the longest followup to date on the vaccine, looking at data from 1,661 male and female participants who were followed for just under 10 years.

Of these participants, around two-thirds received a three-dose regimen of the vaccine when they were ages nine to 15 and sexually inactive.

Initially about one-third received a placebo — not a vaccine — however, the placebo group also received the vaccine 30 months into the study, meaning that these individuals were followed a shorter period of time.

Ferris found that the vaccine was virtually 100 per cent effective in preventing the disease, although vaccinating earlier produced the most robust initial and long-term antibody response, the proteins found in the blood which help fight infection.

“We needed to answer questions like if we vaccinate earlier in life, will it last,” explained Ferris, “The answer is yes, this cancer prevention vaccine is working incredibly well 10 years later. A booster vaccine likely will not be needed by these young people. I think now we have come full circle.”

The new finding also supports previous research which suggests that a more widespread and earlier administration of the HPV vaccine, before teens and preteens are exposed to the infection, is the preferred option.

Although the disease can be cleared in around two-thirds of infected individuals, the virus can persist in the remaining one-third, potentially causing a wide range of further health problems.

The quadrivalent vaccine, which protects against HPV types 6, 11, 16 and 18, is designed to better arm the immune system to eliminate the virus.

According to the National Cancer Institute, HPV types 16 and 18 account for essentially all cervical cancer and for most other HPV-related cancers such as penile and anal cancers. Types 6 and 11 account for about 90 per cent of genital warts as well as non-cancerous tumour growths in the respiratory tract.

 

HPV is the most sexually transmitted infection in the U.S.A. Around 79 million Americans, most in their late teens and early 20s, are infected according to the Centers for Disease Control and Prevention (CDC). HPV is also the most common cause of cervical cancer.

The Food and Drug Administration approved the first quadrivalent vaccine, Gardasil, in June 2006, with the vaccine currently approved for patients ages nine to 26.

 

Although the CDC reports that around 43 per cent of U.S. teens are up to date on recommended doses of the HPV vaccine, Ferris added that, “Now we need to push for more young people to get vaccinated. We are doing miserably in the United States.”

The HPV researchers added that the vaccine can be given along with the meningococcal and tetanus, diphtheria and pertussis vaccines, to 11- and 12-year-olds.

The results can be found published online in the journal Pediatrics.

November, 2017|Oral Cancer News|

Understanding personal risk of oropharyngeal cancer: risk-groups for oncogenic oral HPV infection and oropharyngeal cancer

Author: G D’Souza, T S McNeel, C Fakhry
Date: October 19, 2017
Source: Academic.oup.com

Abstract

Background

Incidence of human papillomavirus (HPV)-related oropharyngeal cancer is increasing. There is interest in identifying healthy individuals most at risk for development of oropharyngeal cancer to inform screening strategies.

Patients and methods

All data are from 2009 to 2014, including 13 089 people ages 20–69 in the National Health and Nutrition Examination Survey (NHANES), oropharyngeal cancer cases from the Surveillance, Epidemiology, and End Results (SEER 18) registries (representing ∼28% of the US population), and oropharyngeal cancer mortality from National Center for Health Statistics (NCHS). Primary study outcomes are (i) prevalence of oncogenic HPV DNA in an oral rinse and gargle sample, and (ii) incident oropharyngeal squamous cell cancer.

Results

Oncogenic oral HPV DNA is detected in 3.5% of all adults age 20–69 years; however, the lifetime risk of oropharyngeal cancer is low (37 per 10 000). Among men 50–59 years old, 8.1% have an oncogenic oral HPV infection, 2.1% have an oral HPV16 infection, yet only 0.7% will ‘ever’ develop oropharyngeal cancer in their lifetime. Oncogenic oral HPV prevalence was higher in men than women, and increased with number of lifetime oral sexual partners and tobacco use. Men who currently smoked and had ≥5 lifetime oral sexual partners had ‘elevated risk’ (prevalence = 14.9%). Men with only one of these risk factors (i.e. either smoked and had 2–4 partners or did not smoke and had ≥5 partners) had ‘medium risk’ (7.3%). Regardless of what other risk factors participants had, oncogenic oral HPV prevalence was ‘low’ among those with only ≤1 lifetime oral sexual partner (women = 0.7% and men = 1.7%).

Conclusions

Screening based upon oncogenic oral HPV detection would be challenging. Most groups have low oncogenic oral HPV prevalence. In addition to the large numbers of individuals who would need to be screened to identify prevalent oncogenic oral HPV, the lifetime risk of developing oropharyngeal caner among those with infection remains low.

Introduction

Human papillomavirus (HPV) is the most commonly sexually transmitted infection in the United States. HPV now causes ∼70% of all oropharyngeal squamous cell cancer (OPC) in the United States [1] and the incidence of HPV-related OPC (HPV-OPC) among men has more than doubled over the past 20 years [2]. Indeed, OPC is projected to be more common than cervical cancer in the United States by 2020 [3]. Given the ‘epidemic’ of HPV-OPC, there is interest in identifying specific groups that could benefit from screening, if effective tests were developed.

Sexual behaviors responsible for exposure to oral HPV infection are common (80% of the US population reports ever performing oral sex) [4]. Given the ubiquitous exposure to HPV infection and resulting anxiety [5], there is interest in identifying healthy individuals most at risk for development of OPC. As oncogenic oral HPV infection is the precursor to malignancy, identification of individuals with oncogenic oral HPV infection may point to individuals with premalignant disease. Such risk triage could both inform screening approaches and assist the public in understanding personal risk. This analysis therefore aims to understand how common HPV16, oncogenic HPV and HPV-OPC are in groups of people with different risk factor profiles.

Methods

Study population

This study included 13 089 people ages 20–69 years old who participated in National Health and Nutrition Examination Survey (NHANES) between 2009 and 2014 and had oral HPV DNA testing. Analyses involving number of oral sex partners were limited to ages 20–59, with data for number of oral sex partners, resulting in a sample size of 9425. Incidence and incidence-based mortality data from SEER 18 registries between 2009 and 2014 [6] were used with NCHS mortality data for projections of OPC risk.

HPV measurement

As previously described [7, 8] oral HPV DNA was tested in exfoliated cells collected from an oral rinse and gargle sample using PCR amplification using PGMY 09/11 consensus primers and line blot for the detection of 37 specific HPV types. Oncogenic oral HPV was defined as detection of any of the following 12 types: HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 [9].

Analytic methods

Analyses of NHANES oral HPV data were weighted by Mobile Examination Center (MEC) exam sampling weights, and conducted using SUDAAN software (release 11.0.1, Research Triangle Institute) to account for survey sample design. Projected OPC risk was calculated using DevCan software [10].

To better understand subgroup risk, prevalence of oncogenic HPV and HPV16 were explored stratifying by multiple factors including sex, sexual behavior, age, and current smoking. Groups with similar prevalence were combined to create parsimonious risk stratification of people with similar prevalence.

Results

Oncogenic oral HPV and oral HPV16 infection are rare in the general US population. As expected, prevalence of infection is higher among men than women of every age group (oncogenic HPV; 6.0% versus 1.1%, P < 0.001; Table 1). Prevalence of oncogenic oral HPV is contrasted with risk of OPC in Table 1 by sex and age groups. While oncogenic oral HPV is detected in 3.5% of all adults age 20–69, the lifetime risk of OPC is low (37 per 10 000). For example, among men 50–59 years old, 8.1% have an oncogenic oral HPV infection, 2.1% have an oral HPV16 infection, yet 0.7% will ‘ever’ develop OPC in their lifetime; and risk of developing OPC in the next 10 (0.2%) or 20 (0.4%) years is even lower (Table 1).

Table 1.

Oral HPV prevalence by sex and age, compared with the risk of developing oropharyngeal cancer (OPC) in each group

    Risk spectrum: infection to cancer

 

NHANESa (prevalence)

 

SEERb (OPC risk: cases/100 people) 

 

Sex  Age  Oncogenic Oral HPV (%)  Oral HPV16 (%)  Lifetime (%)  Next 20 years (%)  Next 10 years (%) 
Men
20–29 4.8 1.1 0.7 0.01 <0.01
30–39 4.7 1.5 0.7 0.07 0.01
40–49 6.2 2.3 0.7 0.3 0.06
50–59 8.1 2.1 0.7 0.4 0.2
60–69 6.1 2.4 0.5 0.4 0.3
Total 6.0 1.9 0.7
Women
20–29 1.4 0.3 0.2 <0.01 <0.01
30–39 1.0 0.3 0.2 0.01 <0.01
40–49 0.8 0.1 0.2 0.05 0.01
50–59 1.6 0.5 0.2 0.08 0.03
60–69 0.7 0.1 0.1 0.10 0.05
Total 1.1 0.3 0.2
Men and women All 3.5 1.1 0.4

a- Weighted prevalence accounting for NHANES study design weights to reflect the general US population.

b- Estimates of OPC risk combine data on cancer occurrence from SEER with population data. OPC is shown as risk per 100 people to contrast with HPV prevalence. For reference in interpretation, 0.6% risk represent that 0.6 people out of the 100 (or 6 out of 1000, or 600 out of 100 000) would develop OPC.

While prevalence of oncogenic oral HPV infection is low, the distribution of infections is not representative of the population (supplementary Table S1, available at Annals of Oncologyonline). Indeed 84% of oncogenic oral HPV infections in 20- to 69-year olds were among men. To elucidate why oncogenic oral HPV was more concentrated among certain groups, behavioral characteristics were considered. Performing oral sex and smoking are each strongly associated with detection of oncogenic oral HPV (Table 2) and HPV16 (supplementary Table S2, available at Annals of Oncology online). Oncogenic oral HPV prevalence is low (<2.5%) among both men and women who never performed oral sex. Prevalence of oncogenic oral HPV increased with number of lifetime oral sexual partners, up to 14.4% in men age 20–59 years old with ≥10 lifetime oral sexual partners (Table 2).

 

Table 2.

Oncogenic oral HPV prevalence by participant characteristics and behaviors

    Oncogenic oral HPV prevalencea(%)

 

 
Men  Women  All 
Characteristics (among those 20–69 years old)  No. of people  N = 6420  N = 6669  N = 13 089  P-valueb 
Sex
Women 6669 1.1 1.1 <0.0001
Men 6420 6.0 6.0
Currently smoke
No 10 041 4.5 0.9 2.6 <0.0001
Yes 3044 10.5 2.1 6.7
Age, in years
 20–29 2738 4.8 1.4 3.1 0.13
 30–39 2668 4.7 1.0 2.8
 40–49 2699 6.2 0.8 3.4
 50–59 2494 8.1 1.6 4.8
 60–69 2490 6.1 0.7 3.3
Race/ethnicity
 White non-Hispanic 5135 6.3 1.1 3.7 0.008
 Black non-Hispanic 2931 7.5 1.4 4.2
 Any race Hispanic 3347 4.5 1.3 2.9
 Other 1676 3.7 0.7 2.1
Ever oral sex (or man or woman)
 No 2453 2.3 0.2 1.1 <0.0001
 Yes 9272 6.5 1.4 4.0
Ever oral sex on a woman
 No 6660 3.6 1.0 1.4 <0.0001
 Yes 5095 6.4 3.5 6.2
Ever oral sex on a man
 No 7054 5.8 0.2 4.9 <0.0001
 Yes 4693 10.2 1.4 1.8
Number of partners performed oral sex on in lifetimec
 0 1661 2.4 0.2 1.2 <0.0001
 1 1877 1.2 1.0 1.1
 2–4 3165 4.8 0.7 2.5
 5–9 1363 3.9 2.5 3.3
 10+ 1359 14.4 3.0 11.1

a- Weighted prevalence accounting for NHANES study design weights to reflect the civilian non-institutionalized US population.

b-Wald F test (based on transforming the Wald χ2) for independence of row variable and oral HPV16, not accounting for sex (except where sex is the row variable).

C- Data on number of lifetime oral sex partners was not collected consistently in those 60 and older so is only presented among those 20–59 years old.

 

 

Oncogenic oral HPV prevalence was explored by sex, sexual behavior, and tobacco use to better understand groups that have higher and lower prevalence (Figure 1). Regardless of what other risk factors participants had, oncogenic oral HPV prevalence was low among those with only ≤1 lifetime oral sexual partner (women = 0.7% and men = 1.7%). Oncogenic oral HPV prevalence doubled among women with ≥2 versus 0–1 lifetime oral sexual partners (1.5% versus 0.7%, P = 0.02), but remained low among women with higher number lifetime oral sexual partners (Table 2). Oncogenic oral HPV prevalence was highest among men who currently smoked and had ≥5 lifetime oral sexual partners (14.9%, 95% CI = 11.4–19.1). Men with only one of these risk factors (i.e. either smoked and had two to four partners or did not smoke and had ≥5 partners) had ‘medium risk’, with 7.3% (95% CI = 5.8–9.1) oncogenic oral HPV prevalence (Figure 1). Findings were similar when considering oral HPV16 infection specifically.

 

What is my risk of oral HPV? Prevalence of oral HPV16 and any oncogenic oral HPV infection by risk group. In the ‘very low-risk’ group (among women with 0–1 lifetime oral sexual partners), oncogenic oral HPV was similar among smokers and nonsmokers (1.8% versus 0.5%, P = 0.26). In the ‘low-risk’ group of women, oncogenic oral HPV prevalence was 1.5% among women with two or more lifetime oral sexual partners. In the ‘low-risk’ group of men, oncogenic oral HPV prevalence was 1.7% among men with 0–1 lifetime oral sexual partners and was higher among men who did not smoke and had 2–4 lifetime oral sexual partners (4.1%, P = 0.0042). In the ‘medium risk’ group, oral HPV16 prevalence was 7.1% among men who smoke and had 2–4 partners and 7.4% among men who do not smoke and had 5+ partners (P = 0.87).

 

Discussion

This analysis highlights that the yield of oncologic oral HPV screening would be limited in most groups in the United States. With the increasing incidence of OPC, there is a need to understand how to identify individuals at risk of OPC. Oncogenic oral HPV detection is attractive as it samples the relevant epithelium in a non-invasive method, has relatively low cost and serves as a biomarker for HPV-OPC. However, for screening to succeed, a high prevalence population is needed to limit false positives, and balance the psychologic and physical harms of screening with the benefits.

From this analysis, it is clear that screening based upon oncogenic oral HPV detection would be challenging. Women across all categories have low prevalence of infection and low risk of OPC and therefore benefits of screening are unlikely to outweigh harms in this group. The higher prevalence of oncogenic oral HPV in men than women is thought be due to both a higher per partner risk of acquisition when performing oral sex [11, 12], and decreased clearance among men than women [11, 13]. While there are specific risk groups of men enriched for oncogenic oral HPV, most men have low prevalence of infection. Even among the elevated risk group, the majority of men do not have a prevalent oncogenic oral HPV. In addition to the large numbers of individuals who would need to be screened to identify prevalent oncogenic oral HPV, the lifetime risk of developing OPC among those with infection remains low [11, 14].

These characteristics suggest that other tests will need to be combined or supplant present methods to accurately identify those with the greatest risk of OPC in the population. Serum HPV oncoprotein antibody tests are specific [15], but are even rarer than oral HPV16 infection [16], so may be impractical to use in most groups. An additional challenge for screening is that precursor lesions for HPV-OPC have not been found and the ability to detect lesions early in an ‘elevated-risk’ group is unknown.

With growing appreciation of the relationship between oral sex, infection, and cancer, some individuals have questions about their risk of having oncogenic oral HPV infection. To address concerns about infection among individuals with high number of oral sex partners or others concerned about their cancer risk, the infographic can be used to reassure that oncogenic oral HPV prevalence is low among most groups. This analysis has several imitations. Data on oral HPV infection were cross-sectional, with no information linking HPV and SEER data used for cancer risk. Comparing oncogenic oral HPV prevalence and OPC risk in this way informs potential future screening studies, and personal risk assessment. In summary, this analysis shows that screening based upon oncogenic oral HPV infection will not be useful and presents data to communicate to the layperson the low risk of infection and cancer.

Acknowledgements

The authors acknowledge Maura Gillison who led the testing for oral HPV in NHANES provided in the publicly available dataset. This dataset has provided investigators the opportunity to better understand the epidemiology of oral HPV infection in the United States. We also acknowledge the contributions of the Oral Cancer Foundation.

Funding

National Institute of Dental and Craniofacial Research (NIDCR) (R35 DE026631).

Disclosure

The authors have declared no conflicts of interest.

 

References

1 Saraiya M, Unger ER, Thompson TD et al. US assessment of HPV types in cancers: implications for current and 9-calent HPV vaccines. J Natl Cancer Inst 2015; 107(6): djv086

 

2 Jemel A, Simard EP, Dorell C et al. Annual Report to the Nation on the Status of Cancer, 1975-2009, featuring the burden and trends in human papillomavirus(HPV)-associated cancers and HPV vaccination coverage levels. J Natl Cancer Inst 2013; 105(3): 175-201.

 

3 Chaturvedi AK, Engels EA, Pfeiffer RM et al. Human papillomavirus and rising oropharyngeal cancer incidence in the United States. J Clin Oncol 2011;29(32): 4294-4301

 

4 D’Souza G, Cullen K, Bowie J et al. Differnece in oral sexual behaviors by gender, age, and race explain observed difference in prevalence or oral human papillomavirus infection. PLoS One 2014; 9(1): e86023

 

5 D’Souza G, Zhang Y, Merritt S et al. Patient experience and anxiety during and after treatment for and HPV-related oropharyngeal cancer. Oral Oncol 2016; 60: 90-95.

 

6 SEER Incidence and Incidence-Based Mortality Date, SEER 18 Regs (Excl Lousiana) 1973-2014; http://seer.cancer.gov/date/ (8 May 2017, date last accessed).

 

7 Gillison ML, Broutain T, Pickard RKL et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA 2012;307(7): 693-703.

 

8 NHANES 2013-2014: Human Papillomavirus (HPV)- Oral Rinse Data Documentation, Codebook, and Frequencies:

https://wwwn.cdc.gov/Nchs/Nhanes/2013-2014/ORHPV_H.htm (2 May 2017, date last accessed).

 

9 IARC. Human Papillomavirus; http://monographs.iarc.fr/ENG/Monographs/vol100B/mono100B-11.pdf (23 May 2017, date last accessed)

 

10 Devcan: Probability of Developing or Dying of Cancer- Surveillance Research Program; https://surveillance.cancer.gov/devcan/ (8 May 2017, date last accessed).

 

11 D’Souza G, Wentz A, Kluz N et al.   Sex differnces in risk factors and natural history of oral human papillomavirus (HPV) infection. J Infect Dis 2016;213(12):1893-1896.

 

12 Chaturvedi AK, Graubard Bl, Broutian T et al. NHANES 2009-2012 findings: association of sexual behaviors with higher prevalence of oral oncogenic human papillomavirus infections in U.S. men. Cancer Res 2015; 75(12): 2468-2477.

 

13 Beachler DC, Sugar EA, Margolick JB et al. Risk Factors acquisition and clearance or oral human papillomavisur infection among HIV-infected and HIV-uninfected adults. Am J Epidemiol 2015; 181(1): 40-53.

 

14 Pierce Campbell CM, Kreimer AR, Lin H-Y et al. Long-term persistence of oral human papillomavirus type 16: the HPV infection in men (HIM) Study. Cancer Pres Res Phila Pa 2015; 8(3): 190-196.

 

15 Holzinger D, Wichmann G, Baboci L et al. Sensitivity and specificity of antibodies against HPV16 E6 and other early proteins for the detection of HPV16-driven oropharyngeal squamous cell carcinoma. Int J Cancer 2017; 140(12):2748-2757.

 

16 Beachler DC, Waterboer T, Pierce Campbell CM et al. HPV16 E6 seropositivity among cancer-free men with oral, anal or genital HPV16 infection. Papillomavirus res 2016; 2: 141-144.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

October, 2017|Oral Cancer News|

Lindsey Stirling Honors Her Late Father with Moving Routine on Dancing with the Stars: ‘I Felt Like I Was Dancing with My Dad’

Author: Karen Mizoguchi
Source: People.com
Date: October 9, 2017

Lindsey Stirling has had an incredibly tragic year. The violinist is mourning the loss of her father, Stephen, who died of throat cancer. And on Monday night’s episode of Dancing with the Stars, she honored him with her routine for Most Memorable Year Week, choosing 2017.

“I am the woman I am today because of you and I love you so much,” she said on the reality dancing competition series.

To celebrate her dad’s life, Stirling and pro partner Mark Ballas — who wore her father’s hat and scarf as part of his costume — performed a touching Viennese Waltz. “I felt like I was dancing with my dad,” said Stirling, who was awarded a 26/30 by judges.

“I feel like I got to thank my dad in a way I’ve never been able to before. I was really looking forward to this dance, I was terrified to do it and I’m really happy,” she said. “When you’re dancing about something that is so important that means so much to you doing something I’ve never done before, I just wanted it to be so special. And I feel like it was.”

In January, the YouTube star announced the sad news on Facebook, Twitter and Instagram, writing, “My dad passed away early this morning. There is nothing to say that could express my gratitude for this amazing, selfless man.”

She added, “But I love you daddy. I’m the woman I am today because of you.”

Along with the loving message, the America’s Got Talent alum shared a childhood photo of herself and her father.

In June 2016, Stirling’s father, a religious educator and author, detailed his battle with cancer on his website.

“The pain in my throat persists. (That pain is likely the residual result of radiation and chemotherapy. In other words, I now suffer from the cure, now that the disease has fled.  Ironic.),” he wrote about his illness, which he was diagnosed for in late 2015.

The father of five wrote his final Facebook post. “As I prepare to write the next chapter of my life, I am not afraid. God be with you ’til we meet again,” he said.

October, 2017|Oral Cancer News|

Treatment That’s Easy to Swallow in HPV+ Throat Cancer

Source: Medscape.com
Author: Nick Mulcahy
Date: September 27, 2017

SAN DIEGO, California ― Daniel Ma, MD, of the Mayo Clinic in Rochester, Minnesota, treats a lot of relatively young patients with human papillomavirus (HPV)-related oropharyngeal cancers who are cured by various standard combinations of surgery, radiation therapy and chemotherapy and then have “another 30 to 40 years of life ahead of them.”

But that life expectancy can be marred by the “potentially life-altering side effects” of standard treatment, including dry mouth, loss of taste, and, in about one half of patients, difficulty swallowing, he said.
These patients inspired the genesis of Dr. Ma’s phase 2 study of an “aggressive dose de-escalation” of adjuvant radiation in this setting, he said.

The investigators evaluated experimental radiation doses of 30 to 36 Gy, which is a 50% reduction from the current standard of 60 to 66 Gy.

At a median of 2 years’ follow-up among 80 patients, the treatment de-escalation has resulted in locoregional control rates comparable to historical controls, low toxicity, and, perhaps most notably, no decrement in swallowing function or quality of life, Dr. Ma reported here at the American Society for Radiation Oncology (ASTRO) 2016 Annual Meeting.

The toxicity and swallowing results are “the most exciting data,” Dr. Ma told a standing-room-only crowd at a meeting session today.

“It’s the first clinical trial in head and neck cancer to demonstrate no injury to swallowing function after radiation,” he told Medscape Medical News. In other words, patients’ ability to swallow was no worse post treatment. In fact, patients’ ability to swallow improved slightly at 1 year following radiation therapy compared to pretreatment (P = .03).

“It’s an exciting concept. Everyone’s going to want to hear more about it,” said Thomas Galloway, MD, of Fox Chase Cancer Center in Philadelphia, Pennsylvania, who was asked for comment about the trial.

The answer is not yet known, but the 2-year results from Dr. Ma are encouraging.

Two-year data indicate that after de-escalated treatment, the rate of locoregional tumor control was 95%, which is comparable to results with standard radiation (60 Gy) from the Radiation Therapy Oncology Group (RTOG) 0234 trial.

In the Mayo Clinic trial, three patients experienced local recurrence, and one patient experienced a nodal recurrence.

Fox Chase’s Dr. Galloway also observed that, in the new trial, patients received 30 Gy delivered in 1.5 Gy twice a day over 12 days (along with weekly docetaxel, 15 mg/m2, days 1 and 8). Twelve days is a lot shorter than the standard 6 weeks for 60-Gy therapy, but the twice-daily schedule may not be suitable for all patients, he pointed out.

De-escalation radiation therapy is experimental, but a phase 3 study that seeks to confirm the approach, known as the DART-HPV trial, is now underway.

“This is not incremental change,” he told Medscape Medical News. “It’s a stark change from the current standard of care.”

Dr. Galloway and Dr. Ma both said that HPV-positive head and neck cancers are necessitating change, because patients with these cancers are younger and healthier than patients without the virus, whose cancers are typically caused by smoking and alcohol consumption.

Some HPV-positive patients are now being treated without surgery. “What the perfect recipe for treatment is, no one knows for sure,” Dr. Galloway told Medscape Medical News about treatment combinations.

Paul Harari, MD, of the University of Wisconsin, Madison, said the HPV-positive head and neck cancers, including oropharyngeal cancers, “warrant different treatment approaches.” Standard treatment is toxic ― “make no mistake about it,” Dr Harari commented while acting as moderator at a press conference featuring the dose de-escalation trial.

However, cutting the radiation therapy dosage, he said, prompts a “tense question: can you maintain the cure rate?”

 

More Study Details, Including Toxicity

About half of the study patients, all of whom had oropharynx squamous cell carcinoma, had the above-described 2-week-long treatment schedule. But 43 patients had extracapsular extension, a marker of aggressive disease, and thus received an additional radiation boost to the affected areas, for a total dose of 36 Gy.

Data for both groups of patients were combined in the statistical tallies.

All of the study patients had no evidence of residual disease following surgery and a minimal smoking history (eg, less than one pack per day for 10 years or less). The median patient age was 60.5 years. All patients had stage III or IV disease.

There was also a “very dramatic reduction” in side effects, compared with standard treatment, said Dr. Ma. No patients required percutaneous endoscopic gastrostomy (PEG); by contrast, with traditional radiation therapy, one fifth to one third of patients undergo PEG.

The PEG feeding tube is inserted through the abdomen into the stomach. Typically, one fifth to one third of patients will receive such a feeding tube during standard treatment for oropharyngeal cancers, he said.

The rate of grade ≥2 toxicities 2 years post radiation therapy was 10%. Again, this compared favorably with 55% rate reported in RTOG 0234.

No patients had grade 3+ toxicity at 1 or 2 years following treatment.

All 14 patients (18%) who experienced cumulative grade 3+ toxicity did so within 3 months of treatment, and all cases resolved by 6 months post treatment. One patient experienced acute grade 4 toxicity related to a chemotherapy reaction, which quickly resolved.

Patient quality of life either improved or did not change following treatment, except with regard to xerostomia. Patients reported worse salivary flow following treatment (P < .0001).

Dr. Ma, his coinvestigators, Dr Galloway, and Dr. Harari have disclosed no relevant financial relationships.

American Society for Radiation Oncology (ASTRO) 2017 Annual Meeting. Abstract LBA-14, presented September 26, 2017.

 

 

 

 

September, 2017|Oral Cancer News|

Don’t start, be smart: Local, Reno Rodeo competitor advocates being tobacco-free

Source: mynews4.com
Author: Kenzie Bales
Date: June 13th, 2017

RENO, Nev. (News 4 & Fox 11) — As a country phenomenon, Garth Brooks once said, “It’s bulls and blood, it’s dust and mud, it’s the roar of a Sunday crowd. It’s the white in his knuckles, the gold in the buckle, he’ll win the next go ’round. It’s boots and chaps, it’s cowboy hats, it’s spurs and latigo, it’s the ropes and the reins, and the joy and the pain and they call the thing rodeo.”

2017 Reno Rodeo competitor Cody Z Kiser has been riding and roping for as long as he can remember.

Born and raised to Carrie and P.D. Kiser in Carson City, Nevada, Cody started riding bulls as a Dayton High School student.

A horrific injury would set Kiser back, but by no means did it keep him from chasing his dreams.

Kiser says a bull stepped on his face and crushed all the bones in the left side of his face. After recovering, Kiser transitioned from bull riding to bareback bucking horses and hasn’t looked back since.

If traveling to rodeos all the time wasn’t enough to keep someone completely preoccupied, Cody competed while pursuing a Bachelor’s Degree in Civil Engineering at the University of Nevada, Reno.

After testing the waters in the engineering field for awhile, Kiser decided it was time to chase his lifelong dream and give rodeo his full attention.

During his endeavors as a cowboy, Cody was fortunate enough to establish a partnership with the Oral Cancer Foundation.

Everyone knows it is terrible for you, yet they still do it.

He says that being tobacco-free is something he advocates for because he understands the huge health risks that come along with it.

I have seen the impact it can have on a human’s health and it is something that I want no part of, and if I can help others from starting it, then I am happy.

Kiser says he is always willing to answer questions pre-existing tobacco users may have, but by no means is he trying to tell people how to live their life.

A big goal of his: to show people that you don’t have to smoke or chew to be a real cowboy or to be successful in the sport you love. Primarily focusing on kids, Kiser hopes to spread the movement to younger generations who haven’t picked up the bad habit yet.

The sport is hard enough on your body, no sense in making in harder on yourself.

Kiser says he strays away from just throwing facts and statistics at people, but rather making a positive, memorable impact and associating with people without the use of tobacco.

After partnering with the OCF three years ago, the cowboy says that he has had nothing but positive feedback and calls himself the “luckiest guy in the world.”

If you are interested in watching Cody Kiser compete in the 2017 Reno Rodeo, you can catch him on Father’s Day, Sunday, June 18 (making his dad, a former bucking horse rider proud) or Monday, June 19.

June, 2017|Oral Cancer News|

Study reveals high environmental cost of tobacco

Source: www.cnn.com
Date: May 31st, 2017
Author: Jacopo Prisco

Details of the environmental cost of tobacco are revealed in a study released Wednesday by the World Health Organization, adding to the well-known costs to global health, which translate to a yearly loss of $1.4 trillion in health-care expenses and lost productivity.

From crop to pack, tobacco commands an intensive use of resources and forces the release of harmful chemicals in the soil and waterways, as well as significant amounts of greenhouse gases. Its leftovers linger, as tobacco litter is the biggest component of litter worldwide.

“Tobacco not only produces lung cancer in people, but it is a cancer to the lungs of the Earth,” said Dr. Armando Peruga, who previously coordinated the WHO Tobacco Free Initiative and now works as a consultant. He reviewed the new report for the WHO.

Commercial tobacco farming is a worldwide industry that involves 124 countries and occupies 4.3 million hectares of agricultural land. About 90% of it takes place in low-income countries, with China, Brazil and India as the largest producers.

Because tobacco is often a monocrop — grown without being rotated with other crops — the plants and the soil are weak in natural defenses and require larger amounts of chemicals for growth and protection from pests.

“Tobacco also takes away a lot of nutrients from the soil and requires massive amounts of fertilizer, a process that leads to degradation of the land and desertification, with negative consequences for biodiversity and wildlife,” Peruga said.

The use of chemicals directly impacts the health of farmers, 60% to 70% of whom are women. This is especially prominent in low- and middle-income countries, where some compounds that are banned in high-income countries are still used.

300 cigarettes = one tree

Farming also uses a surprisingly large amount of wood, rendering tobacco a driver of deforestation, one of the leading causes of climate change.

About 11.4 million metric tonnes of wood are utilized annually for curing: the drying of the tobacco leaf, which is achieved through various methods, including wood fires. That’s the equivalent of one tree for every 300 cigarettes, or 1.5 cartons.

This adds to the impact of plantations on forest land, which the study describes as a significant cause for concern, citing “evidence of substantial, and largely irreversible, losses of trees and other plant species cause by tobacco farming.”

Deadly gases

In 2012, 967 million daily smokers consumed approximately 6.25 trillion cigarettes worldwide, the WHO estimates.”That means about 6,000 metric tones of formaldehyde and 47,000 metric tonnes of nicotine are released into the environment,” Peruga said.

Tobacco smoke contains about 4,000 chemicals, at least 250 of which are known to be harmful. It also contains climate-warming carbon dioxide, methane and nitrous oxides. “The combination of greenhouse gases from combustion is equivalent to about 1.5 million vehicles driven annually,” Peruga said.

Secondhand smoke is particularly deadly: It contains twice as much nicotine and 147 times more ammonia than so-called mainstream smoke, leading to close to 1 million deaths annually, 28% of them children.

Some of these pollutants remain in the environment (and our homes) as “third-hand smoke,” accumulating in dust and surfaces indoors, and in landfills. Some, like nicotine, even resist treatment, polluting waterways and potentially contaminating water used for consumption, the study notes.

Non-biodegradable litter

Tobacco litter is the most common type of litter by count worldwide.

“We calculate that two-thirds of every cigarette ends up as litter,” Peruga said.

The litter is laced with chemicals including arsenic and heavy metals, which can end up in the water supply. Cigarette butts are not biodegradable, and tossing one on the ground is still considered a socially acceptable form of littering in many countries.

The WHO estimates that between 340 million and 680 million kilograms of tobacco waste are thrown away every year, and cigarette butts account for 30% to 40% of all items collected in coastal and urban clean-ups.

“In addition to that, there are 2 million tons of paper, foil, ink and glue used for the packaging,” Peruga said.

A way forward?

Even though smoking is declining globally, it is increasing in some regions, such as the eastern Mediterranean and Africa. China is a world leader both in production (44%) and consumption, with 10 times more cigarettes smoked than in any other nation.

Every stage of the production of a cigarette has negative effects on the environment and the people who are involved in manufacturing tobacco products, even before the health of smokers and non-smokers is affected.

Although governments worldwide already collect $270 billion in tobacco taxes a year, the WHO suggests that increasing tax and prices is an effective way of reducing consumption and help development priorities in each country, adding that by collecting 80 cents more per pack, the global tax revenue could be doubled.

“Tobacco threatens us all,” WHO Director-General Margaret Chan said in a note. “It exacerbates poverty, reduces economic productivity, contributes to poor household food choices, and pollutes indoor air.”

May, 2017|Oral Cancer News|