Category Archives: Prevention

Can Aspirin Prevent Cancer and Cancer Deaths?

Nyedra W. Booker, PharmD, Tracy Rupp, PharmD, MPH, RD, Laura Gottschalk, PhD, and Danielle Shapiro, MD, MPH, Cancer Prevention and Treatment Fund

Doctors have prescribed aspirin to prevent heart attacks and stroke for many years. There is now good evidence that regular aspirin use can also prevent cancer. Experts already recommend an aspirin a day to prevent colon cancer, but aspirin may also “play a strong role in reducing death from cancer.”[1]  

Recommending Aspirin for Cancer Prevention

The U.S. Preventative Service Task Force (USPSTF), an independent group of medical experts, recommend  that people between the ages of 50 and 59 should take 81 mg of aspirin daily (which is the typical dosage of “baby” or low-dose aspirin) to prevent colon cancer. Since colon cancer develops slowly overtime, aspirin should be taken for at least 10 years.[2]

Daily aspirin is not for everyone between 50 and 59, however. For example, if you have an increased risk of bleeding because of other medication you are taking or because of a history of stomach or intestinal ulcers, kidney disease, or severe liver disease, the risks of taking aspirin daily may outweigh the benefits. 

The benefits of aspirin in preventing death from cancer are based in part on a 2016 study published in the prestigious Journal of the American Medical Association (JAMA), which looked at the rate of cancer in two large long-term studies.  The Nurse’s Health Study and the Health Professionals Follow-up study included almost 48,000 men and more than 88,000 women.[3] The study found that people who took aspirin regularly had a slightly lower risk for overall cancer and a 19% lower risk for colon cancer. These benefits were seen after just five years of use and are statistically significant, which means they are almost definitely due to the aspirin and not to other factors.

The new study results were presented at a national cancer conference in April 2017 and go beyond the results published in 2016.[1] Women in the studies who took aspirin regularly had a 7% lower chance of dying of any cause than women who did not take regular aspirin. Men who took aspirin regularly had an 11% lower chance of dying of any cause than men who did not take regular aspirin. Dying from cancer was 7% lower in women and 15% lower in men who regularly took aspirin. Women who regularly took aspirin had an 11% lower risk of dying from breast cancer. Men who regularly took aspirin had a 23% lower risk of dying from prostate cancer.  

Aspirin can have many benefits, but since it also has risks more studies are needed to examine who is most likely to benefit and who is most likely to be harmed. The study was observational, which means that it evaluated the health of people in the “real world,” rather than a randomized clinical trial.  Since it is not possible to know as much about all the health habits and other possible influences of the thousands of people in these huge studies as is possible in a clinical trial, the conclusions are considered less certain.

What You Need to do Before Starting Aspirin Therapy

Remember that aspirin is a drug, and it has risks even at low doses. You should talk about whether taking a daily aspirin is a good idea with your doctor, so that you can discuss:

  • Your medical history and all the medicines you are currently using, whether they are prescription or over-the-counter
  • Any allergies or sensitivities you may have to aspirin
  • Any vitamins or dietary supplements you are currently taking

Aspirin should not be taken with certain other over-the-counter pain medications such as ibuprofen (Motrin and Advil) and naproxen (Aleve) because they can increase the risk of internal bleeding. These medications are called NSAIDS.  Aspiring should also not be taken daily by those who regularly use herbs and nutritional supplements.  Vitamin E, fish oil (omega-3 fatty acids) and what’s known as the “four Gs”– garlic, ginger, gingko, and ginseng– can all increase your risk for bleeding when taken with aspirin and other blood thinners.[4]

If taking aspirin is not a safe option for you, there are other ways to reduce your chance of developing heart disease and cancer, without any side effects!  They include quitting smoking, eating a diet rich in fruits and vegetables, and getting up from your chair or couch regularly rather than sitting for hours without moving around. Walking or other exercising for at least 20-30 minutes each day is also helpful. However, for people at highest risk of heart disease or cancer, aspirin could truly be a lifesaver.

The Bottom Line

Regular aspirin use may prevent deaths from many causes including cancer, heart attacks, and strokes.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

Footnotes:

  1. American Association for Cancer Research News Release. Regular Aspirin Use in Associated with Lower Cancer Mortality. April 3, 2017. Available online: http://www.aacr.org/Newsroom/Pages/News-Release-Detail.aspx?ItemID=1036#.Wib80kqnGM9
  2. USPSTF. Final Update Summary: Aspirin Use to Prevent Cardiovascular Disease and Colorectal Cancer: Preventive Medication. April 2016. Available online: https://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/aspirin-to-prevent-cardiovascular-disease-and-cancer
  3. Cao Y, et al. Population-wide Impact of Long-term Use of Aspirin and the Risk for Cancer. JAMA Oncol. Published online March 03, 2016. DOI: 10.1001/jamaoncol.2015.6396
  4. U.S. National Library of Medicine. MedlinePlus: Drugs, Supplements, and Herbal Information. Accessed December 2017. https://medlineplus.gov/druginfo/herb_All.html

Pancreatic cancer: are you at risk?

Heidi Mallis, Cancer Prevention & Treatment Fund

Pancreatic cancer is the 3rd leading cause of cancer death among women and men in the U.S.[1]

Surprising Facts

  • The five-year survival rate is less than 8%. This figure has improved only slightly since 1975, when it was 3%.[2]
  • There is no reliable screening test for early detection of pancreatic cancer.[3]
  • Only about 2.5% of the National Cancer Institute’s federal research funding is currently allocated to pancreatic cancer.[4]
  • Pancreatic cancer has claimed the lives of several public figures including: actors Patrick Swayze and Alan Rickman, opera tenor Lucianno Pavarotti, and professor and bestselling author Dr. Randy Pausch.[5]

Risk Factors

Every year, more than 50,000 people are diagnosed with pancreatic cancer in the U.S., and more than 40,000 people die from the disease.[6] It is known as a “silent killer” because its symptoms (pain, jaundice, and weight loss) can easily be mistaken for other diseases. Diagnosis is often at an advanced stage when the cancer has spread to other parts of the body, making treatment more difficult. That is why new research is needed to help identify earlier warning signs that could lower the fatality rate for this disease.

Several risk factors are known. Most are common and can’t be changed. The following traits increase your risk of developing pancreatic cancer:

  • 60 years of age or older
  • African American
  • Male
  • Smoking:  Smokers are 2-3 times more likely to develop pancreatic cancer than nonsmokers, and smoking is responsible for 20-30% of all pancreatic cancer cases.
  • Type 2 diabetes:  Several studies show that people with diabetes are more likely to also develop pancreatic cancer and vice versa, but it is unclear whether diabetes causes pancreatic cancer or is caused by pancreatic cancer.[7][8]
  • Family history of pancreatitis (inflammation of the pancreas), ovarian, or colon cancer. If a person has an immediate family member who has any of these types of cancer, his or her chance of developing pancreatic cancer is tripled.[9]

Research has shown that family history or shared genes were a risk factor for pancreatic cancer. In 2009, new light was shed on the role of genes when a new study showed that people with blood type O may have a lower risk of pancreatic cancer than those with blood types A, B, or AB. The study was conducted by a group of researchers from several academic institutions that are part of the Pancreatic Cancer Cohort Consortium, which is affiliated with the National Cancer Institute (NCI).[10] The group hopes to further examine genetic risks, and future findings could help increase early detection and prevention of pancreatic cancer.

Regardless of blood type and other risk factors, individuals can reduce their risk of developing pancreatic cancer by lowering controllable risk factors. A study revealed that a diet rich in fresh fruit and vegetables, Vitamin C, and fiber might actually reduce the risk of developing pancreatic cancer.[11] Other risk factors, such as smoking or diabetes related to weight gain, can be reduced by quitting smoking and maintaining a healthy weight, which decreases a person’s risk of many other diseases as well. In addition, one study of 60,000 adults indicates that drinking fewer (non-diet) soft drinks may decrease the risk of pancreatic cancer.[12] The authors suggest that sugary drinks, by increasing insulin levels, help fuel pancreatic cancer cell growth. They also speculate that people who consume more soft drinks tend to be more likely to smoke and to eat red meat, all of which are considered potential risk factors for pancreatic cancer.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References

  1. Cancer Treatment Centers of America. (2016, October). What should you know about pancreatic cancer? http://www.cancercenter.com/~/media/Images/Others/Misc/10-2016-pancreatic-infographic.jpg
  2. National Cancer Institute. (2016, April). Cancer Stat Facts: Pancreas Cancer. https://seer.cancer.gov/statfacts/html/pancreas.html
  3. American Cancer Society (2017). Can cancer of the pancreas be found early? https://www.cancer.org/cancer/pancreatic-cancer/detection-diagnosis-staging/detection.html
  4. Office of Budget and Finance. Fiscal year 2015 fact book. National Cancer Institute. https://www.cancer.gov/about-nci/budget/fact-book/data/research-funding
  5. Pancreatic Cancer Action Network (2016). Public figures affected by pancreatic cancer. http://media.pancan.org/pdf/Public-Figures-affected-by-pancreatic-cancer.pdf
  6. American Cancer Society (2017). Key statistics for pancreatic cancer. https://www.cancer.org/cancer/pancreatic-cancer/about/key-statistics.html
  7. Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun MJ (2004). Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults. American Journal of Epidemiology, 159: 1160-1167.
  8. European Cancer Organisation. (2017, January). Diabetes or its rapid deterioration can be an early warning sign for pancreatic cancer. http://www.eccocongress.org/Global/News/ECCO2017-News/2017/01/ECCO2017-NEWS-Diabetes-or-its-rapid-deterioration-can-be-an-early-warning-sign-for-pancreatic-cancer
  9. National Cancer Institute (2017). Pancreatic cancer. U.S. National Institutes of Health. https://www.cancer.gov/types/pancreatic
  10. Amundadottir L, Kraft P, Stolzenberg-Solomon RZ, et al (2009, August 2). Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer. Nature Genetics, September 2009; 41(9): 986-990.
  11. Ghadirian P, Lynch HT, and Krewski D (2003). Epidemiology of pancreatic cancer: an overview. Cancer Detection and Prevention, 27(2): 87-93.
  12. Muelle NT, Odegaard A, Anderson A, Yuan J-M, Koh W-P, Pereira MA. Soft Drink and Juice Consumption and Risk of Pancreatic Cancer: The Singapore Chinese Health Study. Cancer Epidemiology, Biomarkers & Prevention. 2010.19(2);447-455.

 

Ovarian Cancer CA-125 Blood Test: Does It Work?

Stephanie Portes-Antoine, Brandel France de Bravo, MPH, and Laura Gottschalk, PhD, Cancer Prevention and Treatment Fund

Ovarian cancer is a deadly disease because it is rarely diagnosed early. There is not yet an effective, life-saving screening tool for the early diagnosis of ovarian cancer.

When ovarian cancer is diagnosed in the early stage—before the cancer has spread beyond the ovaries—chances of a woman’s survival are very good, with about 93% of women surviving at least 5 years.  Unfortunately, only 15% of cases are caught this early, because the symptoms of ovarian cancer are not obvious. For women diagnosed with advanced ovarian cancer, the chances of 5-year survival drop to less than 30%.[1] Given the dramatic differences in survival outcomes between advanced and early onset diagnosis, it is vitally important to detect ovarian cancer early.

Most women whose ovarian cancer is detected in the late stages will have a relapse (usually many times) following their initial treatment, requiring additional treatment.[2] The most widely used test to screen for the recurrence of ovarian cancer is the CA-125. This blood test measures a protein that tends to be higher in women with ovarian cancer. The test was approved for use on women who have already been diagnosed with ovarian cancer once. In 2008, Dr. Vladimir Nosov from UCLA Medical Center and his co-authors reported that elevated levels of the CA-125 biomarker are found in approximately 83% of women with advanced stage ovarian cancer and 50% of patients with stage I disease.[3]

Is testing for this “biomarker” an effective way to tell early on if a woman’s ovarian cancer has returned? And what about women who have never been diagnosed with ovarian cancer? Why can’t the CA-125 test be used to screen them?

Women with No Symptoms or Who Have Never Been Diagnosed with Ovarian Cancer

Other studies have confirmed that CA-125 by itself is not sensitive enough to diagnose ovarian cancer in the very early stage of the disease, before there are symptoms. Dr. Saundra S. Buys is co-director of the Family Cancer Assessment Clinic at the Huntsman Cancer Institute in Salt Lake City, Utah. According to Dr. Buys, CA125 testing “may be appropriate to screen for ovarian cancer in women who have abdominal symptoms, but for women who have no medical symptoms, doing screening for ovarian cancer results in a lot of false-positives.”[4] False positives are test results that inaccurately show the person might have cancer. Dr. Buys based her conclusions on data for women ages 55 to 75 who were participating in a large study called the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial.[5]

In 2011, Dr. Buys and her colleagues published more results from that trial which involved more than 78,000 women. They concluded that using the CA-125 blood test to screen for ovarian cancer doesn’t prevent women from dying from the disease, it actually is harmful.[6] False positives resulted in many women having unnecessary surgery: 3,285 women received false positives and 1080 of these women underwent biopsy surgery. In 15% of cases, the unnecessary surgery caused serious complications. At the same time, there was no benefit in terms of survival for the women who took the test as compared with those who did not.

Women Who Have Previously Had Ovarian Cancer

CA-125 by itself is clearly not reliable at detecting early ovarian cancer in women of low or average risk—women who have never before been diagnosed with ovarian cancer, and women who have no symptoms. Is it at least effective at detecting a recurrence of ovarian cancer?  In 2010, Dr. Gordon Rustin of the Mount Vernon Cancer Centre in England published the results of a study done with women who had already been diagnosed with and treated for ovarian cancer. He found  that women who started chemotherapy early, based on a CA125 test result indicating relapse of ovarian cancer, did not live any longer than women who did not begin treatment until symptoms of relapse appeared.[7]

The Future of Ovarian Cancer Screening

Research is underway to evaluate whether the CA-125 test can be used more reliably, either by administering it only to women with other biomarkers that indicate increased risk (such as elevated levels of the protein HE4) or combined with other screening tests such as vaginal ultrasound.

Dr. Karen Lu from the MD Anderson Center at the University of Texas has had success correctly identifying postmenopausal women at high risk for ovarian cancer by measuring CA-125 at regular intervals and relying on a mathematical model. Only women whose CA-125 levels went up over time were given a vaginal ultrasound, and only those with suspicious findings on the ultrasound had surgery. This two-staged approach seemed potentially effective .[8] However, when this approach was studied on more than 200,00 women, it did not significantly prevent death from ovarian cancer.[9]

The Bottom Line:

The CA-125 test by itself is not a good screening tool for ovarian cancer. When used alone on women with no symptoms or previous history of ovarian cancer, it leads to many false positives. Among women who have already been treated for ovarian cancer once, it doesn’t seem to matter whether they get treatment for their ovarian cancer recurrence based on CA-125 results or based on their symptoms. Either way, women who relapsed and got treatment lived about the same amount of time.

References:

  1. The National Cancer Institute. Surveillance Epidemiology and End Results. SEER Stat Fact Sheets. Cancer: Ovary. http://seer.cancer.gov/statfacts/html/ovary.html
  2. NCI Cancer Bulletin. Early Chemo to Prevent Ovarian Cancer Recurrence Fails to Increase Survival. June 2, 2009. Volume 6/Number 11. http://www.cancer.gov/ncicancerbulletin/060209/page2
  3. Nosov V., et al. The early detection of ovarian cancer: from traditional methods to proteomics. Can we really do better than serum CA-125? American Journal of Obstetrics and Gynecology. September 2008: 199(3): 215-223.
  4. Reinberg, S. Ovarian screening Methods Inaccurate. National Women’s Health Resource Center. November 7, 2005. http://www.healthywomen.org/resources/womenshealthinthenews/dbhealthnews/ovariancancerscreeningmethodsinaccurate
  5. Buys S.S., et al. Ovarian cancer screening in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial: Findings from the initial screening of a randomized trial. American Journal of Obstetrics and Gynecology. November 2005: 193(5): 1630-1639.
  6. Buys S.S., et al. Effects of Screening on Ovarian Cancer Mortality: The Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Randomized Controlled Trial. The Journal of the American Medical Association. July 2011; 2011 (616):1.
  7. Rustin, G.J. and van der Burg. Early versus delayed treatment of relapsed ovarian cancer (MRC OV05/EORTC 55955): a randomized trial. Lancet. October 2010
  8. Lu, Karen et al. A 2-Stage Ovarian Cancer Screening Strategy Using the Risk of Ovarian Cancer Algorithm (ROCA) Identifies Early-Stage Incident Cancers and Demonstrates High Positive Predictive Value. Cancer. September 2013; 2013 (119):17.
  9. Jacobs  IJ, Menon  U, Ryan  A,  et al.  Ovarian cancer screening and mortality in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomised controlled trial . Lancet. doi:10.1016/S0140-6736(15)01224-6.

Colon Cancer: Who Is at Risk, and How Can It Be Prevented?

Noy Birger and Brandel France de Bravo, MPH, Cancer Prevention & Treatment Fund

When cancer begins in the colon (large intestine) or rectum, it is called colorectal cancer or colon cancer.

In the early stages, this cancer begins with small polyps, which are shaped like little mushrooms growing on the wall of the colon. Polyps are very common, especially as people get older. Not all polyps develop into cancer but all colorectal cancer begins with polyps. Certain kinds of polyps are more likely to lead to cancer than others, but the doctor can’t tell if a polyp is precancerous just by looking at it. This is why doctors prefer to remove and analyze any polyp found during screening. Polyps can be identified and removed by colonoscopy, in which a small camera on a flexible tube is inserted into the rectum.[1]

Thanks to more screening, the number of people diagnosed with colon cancer has decreased, but it is still the 4th most common cancer for both men and women.[2][3] The death rate is high because many people who are at risk for colon cancer do not get screened for the disease.[4]

A study published in February 2012 in New England Journal of Medicine found that patients who received colonoscopies and had noncancerous or pre-cancerous growths (polyps) removed, were half as likely to die from colon cancer than people in the general population who were not screened or used less effective screening methods. [5]

Men and women are equally likely to die from colon cancer,[6] but men are more likely to be diagnosed with colon cancer than women of the same age. [7] Black men and black women are at higher risk for developing colon cancer and dying from it than are white men and white women of the same age.[8][9] Being overweight or obese increases men’s risk of colon cancer more than it does women’s (see Weight and Cancer: What You Should Know).  In the U.S., nearly one in ten cases of colon cancer is estimated to be caused by excess body fat.[10]

Risk Factors for Developing Colon Cancer

In addition to your sex and race, your age and genes are important risk factors you can’t do anything about. Your chances of developing colon cancer increase as you get older: 90% of cases are in people over 50. Having a family member with colon cancer also increases your chances of developing it. About 20% of people with colon cancer have a first-degree relative (parents, siblings or children) or second-degree relative (aunts, uncles, grandparents, grandchildren, nieces, nephews, or half-siblings) who also had colon cancer. [11]

In addition to people with pre-cancerous polyps, people who suffer from ulcerative colitis or Crohn’s disease are more likely to develop colon cancer.[12] Ulcerative colitis and Crohn’s disease cause inflammation of the colon, which is why they are both also referred to as Inflammatory Bowel Disease (IBD). Chronic inflammations in the body seem to increase the risk of various types of cancer.

Less is known about what you can do to prevent colon cancer. People who eat too much fat in their diet or too little fiber or too little calcium, smoke, drink alcohol, don’t exercise enough, or are overweight are more likely to be diagnosed with colon cancer. However, scientists do not know whether people can lower their risks of getting colon cancer if they change one or more of those behaviors.  For example, several large research studies show that eating a high-fiber diet does not decrease your chances of getting colon cancer.[13][14][15] On the other hand, there is clear evidence that fiber, calcium, exercising, maintaining a healthy weight, and avoiding smoking and alcohol is generally good for your health, whether it reduces your chances of colorectal cancer or not.

So, What Can You Do to Lower Your Risk?

  • Get screened regularly from age 50 to 75. If you have a relative with colon cancer, your doctor may want to screen you earlier than age 50. The recommended screening tests are:
    • High Sensitivity Fecal Occult Blood Test (FOBT), which involves providing stool samples and should be done once every year
    • Colonoscopy (mentioned above), which requires anesthesia and is more expensive, and the doctor can remove polyps if found. It is only needed every 10 years unless a close relative developed colon cancer; and
    • Flexible sigmoidoscopy is similar to a colonscopy. It can be used to find polyps but not to remove them. It is recommended every 5 years

A “virtual colonoscopy,” which is done with a Computed Tomography (CT) scan, is more expensive than the other screening tools and is not recommended by the U.S. Preventive Services Task Force. As with any CT scan, it exposes you to relatively high levels of radiation (see Everything You Ever Wanted to Know about Radiation and cancer, But Were Afraid to Ask).

The advantage to a regular colonoscopy (not a virtual one) over the other methods is that polyps can be removed during the screening process. The disadvantage is that you need to take a day off from work, fast for about 12 hours and purge with large quantities of an unpleasant laxative drink. The advantage of the FOBT is that it is easier and less expensive. However, the FOBT and CT scan only detect potential problems or polyps – you would still need the colonscopy to have them removed if the results are abnormal. [16]

  • Quit smoking. Cigarette smoking doubles your chances of getting polyps and long-term smoking increases the risk of colon cancer. It also increases your chances of dying from colon cancer.[17][18][19]
  • Maintain a healthy weight. Extra pounds mean extra risk for all kinds of cancer, including colorectal cancer. Fat cells appear to trigger chronic inflammation of the body, which stresses the immune system.[20]
  • Eat a balanced diet. Be sure to include plenty of fruits and vegetables (especially ones from the cabbage family, like broccoli, cauliflower, cabbage, Brussels sprouts, and collard greens), limit the amount of red meat you eat (particularly well-done) and stay active. At least some of the research supports this kind of diet, and since eating this way offers so many different health benefits, why not try it? [21][22]
  • Get more Vitamin D through sunlight and supplements, since few foods are naturally rich in Vitamin D. Recent studies of doses higher than the 400 IU/day that is in standard multiple vitamins, show that Vitamin D can reduce the risk of colon cancer.[23] Blacks, who are at the highest risk for colon cancer, and people living in the northern half of the U.S., typically have too little Vitamin D in their bodies because they are exposed to less sun, and darker skin benefits less from sunshine.  And since Vitamin D is good for your health in many ways (see http://ods.od.nih.gov/factsheets/vitamind.asp),[24] it makes sense to give this a try if you are concerned about colon cancer. Vitamin D is in milk and fortified breakfast cereals and in fatty fish such as tuna, salmon, and sardines, or you might consider a Vitamin D supplement.  Experts agree that adults can take up to 4,000 IU/day of Vitamin D without harming their health, and they recommend getting 5-30 minutes of sun at least twice a week. This means sun exposure to your face, arms or legs (preferably all three) without sun screen and between 10:00 a.m. to 3:00 p.m. However, too much Vitamin D can be dangerous.  The best way to make sure you are getting enough Vitamin D, but not too much, is to get your Vitamin D levels checked the next time you visit your doctor.
  • Low-dose aspirin. The U.S. Preventive Services Task Force found that taking low-dose aspirin can help prevent colorectal cancer and heart disease in some adults, depending on age and other factors. For more information, see: Aspirin Use for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer: Consumer Guide. [PDF-212K]. Despite some early studies, there is no clear evidence that other types of anti-inflammatory products help prevent colorectal cancer, such as ibuprofen or fish oil tablets.

All articles on our website are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

Related Content:

Have colon cancer? Skip the hot dogs, deli, and burgers
Colon cancer screening
Can aspirin prevent both heart disease and cancer?

References

  1. Basic Information About Colorectal Cancer. Centers for Disease Control and Prevention. http://www.cdc.gov/cancer/colorectal/basic_info/index.htm.
  2. “Cancer Among Women.” Centers for Disease Control and Prevention; 2015 http://www.cdc.gov/cancer/dcpc/data/women.htm.
  3. “Cancer Among Men.” Centers for Disease Control and Prevention; 2015 http://www.cdc.gov/cancer/dcpc/data/men.htm.
  4. Swan J, Breen N, Coates RJ, Rimer BK, Lee NC. Progress in cancer screening practices in the United States: results from the National Health Interview Survey.
  5. Zauber AG, Winawer SJ, O’Brien M.J, Lansdorp-Vogelaar I, van Ballegooijen M, Hankey BF, et al. Colonoscopic polypectomy and long-term prevention of colorectal-cancer deaths. New  EnglandJournal of Medicine. 2012; 366(8), 687-696.
  6. Fuchs CS, Giovannucci EL, Colditz GA, et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. New England Journal of Medicine. 1999; 340:169-176.
  7. Jemal A, Siegal R, Ward E, Hoa Y, Xu J, Thun MJ. Cancer Statistics 2009.  CA:A Cancer Journal for Clinicians.. 2009;59:225-249.
  8. Lieberman D, Holub J, Moravec M, Eisen G, Peters D, Morris C. Prevalence of colon polyps detected by colonoscopy screening in asymptomatic black and white patients. Journal of American Medical Association. 2008;300:1417-1422.
  9. Colorectal Cancer Rates by Race and Ethnicity. Centers for Disease Control and Prevention. http://www.cdc.gov/cancer/colorectal/statistics/race.htm.
  10. American Institute for Cancer Research. Researchers present data linking obesity/overweight to higher cancer risk, poorer cancer survival. November 2009. www.aicr.org.
  11. Castels A, Castellvi-Bel S, Balaguer F. Concepts in familial colorectal cancer: where do we stand and what is the future? Gastroenterology. 2009; 137:404-409.
  12. Jia Q, Lupton JR, Smith R, Weeks BR, Callaway E, Davidson LA, et al. Reduced Colitis-Associated Colon Cancer in Fat-1 (n-3 Fatty Acid Desaturase) Transgenic Mice. Cancer Research. 2008; 68: (10).
  13. Fuchs CS, Giovannucci EL, Colditz GA, et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. New England Journal of Medicine. 1999; 340:169-176.
  14. Park Y, Hunter DJ, Speigelman D, Bergkvist L, Berrino F, van den Brandt PA, et al. Dietary Fiber Intake and Risk of Colorectal Cancer: A Pooled Analysis of Prospective Cohort Studies. Journal of American Medical Association. 2005; 294:2849-2857.
  15. Schatzkin A, Mouw T, Park Y, Subar AF, Kipnis V, Hollenbeck A, et al. Dietary fiber and whole-grain consumption in relation to colorectal cancer in the NIH-AARP Diet and Health Study. American Journal of Clinical Nutrition, 2007; 85. 5:1353-1360.
  16. Edwards BK, Ward E, Kohler BA, Eheman C, Zauber AG, Anderson RN, Jemal A, Schymura MJ, Lansdorp-Vogelaar I, Seeff LC, van Ballegooijen M, Goede SL, Ries LA. Annual report to the nation on the status of cancer, 1975-2006, featuring colorectal cancer trends and impact of interventions (risk factors, screening, and treatment) to reduce future rates. Cancer 2010;116(3):544-573.
  17. Botteri E, Iodice S, Raimondi D, Maisonneuve P, Lowenfels AB. Smoking and Adenomatous Polyps: a Meta-analysis. Gastroenterology. 2008;134(2):388-395.e3
  18. Hannan LM, Jacobds EJ, Thun MJ. The association between cigarette smoking and risk of colorectal cancer in a large prospective cohort from the United States. Cancer Epidemiology, Biomarkers & Prevention.2009;18(12):3362-3367.
  19. Botteri E, Iodice S, Bagnard V, Raimondi S, Lowenfels AB, Maisonneuve P. Smoking and colorectal cancer: a meta-analysis. Journal of American Medical Association.2008;300(23):2765-2778.
  20. American Institute for Cancer Research. Researchers present data linking obesity/overweight to higher cancer risk, poorer cancer survival. November 2009. www.aicr.org.
  21. Cotterchio M, Boucher BA, Manno M, Gallinger S, Okey AB, Harper PA. Red meat intake, doneness, polymorphisms in genes that encode carcinogen-metabolizing enzymes, and colorectal cancer risk.Cancer Epidemiology, Biomarkers & Prevention. 2008;17:3098-3107.
  22. Cheng J, Ogawa K, Kuriki K, Yokoyama Y, Kamiya T, Seno K. Increased intake of n-3 polyunsaturated fatty acids elevates the level of apoptosis in the normal sigmoid colon of patients polypectomized for adenomas/tumors. Cancer Letters, Volume 193, Issue 1,10 April 2003; 1: 17-24
  23. “Vitamin D and Cancer Prevention.” National Institutes of Health. National Cancer Institute; 2013 http://www.cancer.gov/about-cancer/causes-prevention/risk/diet/vitamin-d-fact-sheet.
  24. “Dietary Supplement Fact Sheet: Vitamin D.” National Institutes of Health. Office of Dietary Supplements. http://dietary-supplements.info.nih.gov/factsheets/vitamind.asp.

Phthalates and Children’s Products

Paul Brown, Keris Krenn Hrubec, Dana Casciotti, PhD, Brandel France de Bravo, MPH, Stephanie Fox-Rawlings, PhD, Cancer Prevention & Treatment Fund

Phthalates are synthetic chemicals found in every home, in plastic toys, personal care products such as shampoos and lotions, vinyl floors, and shower curtains. They are also found in some medical products, such as saline bags, feeding tubes and catheters. They are used to make plastic flexible and to add fragrances to soap and other personal products.  Unfortunately, these chemicals don’t stay inside the products. Based on recent research on ants, scientists have concluded that the high levels of phthalates in the bodies of insects around the world are the result of phthalates in the air.[1] Because phthalates are released into the air and dust around us, they are found in human urine, blood, and breast milk.[2] Levels are highest in women and children ages 6 to 11. Young children may have higher levels of phthalates in their bodies because their hands find their way into their mouths more frequently: they touch objects made with phthalates and surfaces covered with phthalate dust, and then their hands touch their mouths.

Phthalates are called “endocrine disruptors” because they affect the body’s hormones by mimicking them or blocking them. They interfere with the body’s natural levels of estrogen, testosterone, and other hormones, which is why they are called “disruptors.” Endocrine disruptors are hard to study for several reasons: 1) we are exposed to very small quantities from many different sources every day, 2) researchers have proved that, unlike other chemicals, these appear to have more serious effects at lower levels than at higher levels.[3] Usually, we assume that the higher the dose or exposure, the greater the harm, but endocrine disruptors play by different rules. The director of the National Institute of Environmental Health Sciences, Linda Birnbaum, says that chemical manufacturers are asking “old questions” when they test for safety even though “science has moved on.”[4]

Hormones can increase the risk of some cancers, whether those hormones are natural or synthetic. Too much or too little of a hormone can be harmful. Is a child who is exposed to phthalates more likely to develop cancer as an adult?  No one knows for sure but animals exposed to phthalates are more likely to develop liver cancer, kidney cancer, and male reproductive organ damage.[5]

Phthalates are believed to also affect girls’ hormones, but the health impact is not yet known. Studies also show associations between children’s exposure to phthalates and the risk of asthma, allergies and bronchial obstruction.[6][7][8]

Researchers at Mount Sinai also found a link between obesity and phthalates.[9] They found that among overweight girls ages 6 to 8, the higher the concentration of certain phthalates (including low molecular weight phthalates) in their urine, the higher their body mass index (BMI).  BMI takes height and weight into account when determining if someone is overweight. A study among Danish children ages 4 to 9 found that the higher the concentration of phthalates (all of them), the shorter the child. This was true for girls and boys.[10] More research is needed to determine the impact of phthalates on height and BMI.

Even short-term exposure has now been linked to developmental deficits.[11] Researchers found that children in intensive care units were exposed to the phthalate DEHP through plastic tubing and catheters. The children had 18 times (!)  as much DEHP in their blood compared to children who had not spent time in the ICU. Four years later, the children who had been exposed to DEHP had more problems with attention and motor coordination. The researchers found that the DEHP caused these problems regardless of medical complications or treatments.

Prenatal Exposure to Phthalates

Childhood exposure to phthalates begins in the womb. Several studies that have tested phthalate levels in women in their third trimester of pregnancy have found health effects in the infants, toddlers, and older children of the mothers with the highest levels. There are many different types of phthalates. Most studies look at several types, and the effects tend to vary by type.  A 2011 study found that six-month-old boys whose mothers had the highest phthalate levels scored lower on brain and motor development tests.[12] The same effect was not true for female infants.

Research indicates that boys exposed to phthalates while in the womb may be more likely to develop smaller genitals and incomplete descent of the testicles.[13] Boys who are born with undescended testicles are 2-8 times more likely to develop testicular cancer later on than men born with both testicles descended[14] (their risk is lessened if they get corrective surgery before age 13.[15]). Studies by Harvard researchers have shown phthalates may alter human sperm DNA and semen quality.[16][17][18][19]

Columbia University researchers discovered that three-year olds with high prenatal exposure to two types of phthalates were more likely to have motor delays.[20] They also reported that three phthalates were linked to certain behavior problems in three-year olds, such as social withdrawal.  One phthalate in the study was linked to lower mental development in girls.

Other studies have also linked increased prenatal phthalate exposure to behavior problems. Researchers in Taiwan found an association with aggressive and disobedient behaviors in eight-year-olds of both sexes.[21][22] Similarly, researchers from Icahn School of Medicine at Mount Sinai found that higher levels of exposure to phthalates during gestation were associated with aggression, rule-breaking, and conduct problems for males only.[23]

Researchers at Mount Sinai School of Medicine studied the impact of prenatal exposure to “low molecular weight” phthalates—the kind often found in personal care products and the coatings of some medications—on the social behavior of children ages 7 to 9. Children who were exposed to higher levels of these phthalates, which include DEP and DBP, had worse scores for social learning, communication, and awareness.  This means they were less able to interpret social cues, use language to communicate, and engage in social interactions.[24]

What Is Being Done to Limit Children’s Exposure?

As of February, 2009, children’s toys and child care products sold in the U.S (such as teething rings and plastic books) cannot contain certain phthalates.  The ban on those phthalates is the result of a law passed in 2008, the Consumer Product Safety Improvement Act.  The law permanently bans certain kinds of phthalates (BBP, DBP and DEHP) from toys and child care products, and temporarily bans other phthalates (DIDP, DINP and DnOP) until a scientific board (the Chronic Hazard Advisory Panel) determines for the Consumer Product Safety Commission (CPSC) whether or not they are safe. In 2014 the Chronic Hazard Advisory Panel determined that stricter regulations were appropriate.[25] It stated that the permeant bans should remain on BBP, DBP and DEHP, and that DINP should be added to this list. Furthermore, because a large component of exposure to these chemicals comes from food and other products, it recommended increased regulation. The panel was less concerned about DIDP and DnOP, but recommended additional study. Finally, the panel recommended permanently banning DIBP, DPENP, DHEXP, and DCHP, and putting an interim ban on DIOP.

A few months before the 2008 bill passed, major retailers such as Wal-Mart, Target, and Babies “R” Us promised to remove or severely restrict children’s products containing phthalates by the end of 2008.[26] That provided added incentives for major companies making teething rings and other soft plastic products to stop using phthalates.

The ban in the U.S.followed similar bans in other countries.  In 2006, the European Union banned the use of 6 phthalates in toys that may be placed in the mouth by children younger than 3 years old.[27] The banned phthalates are DINP, DEHP, DBP, DIDP, DNOP, and BBzP.  Fourteen other countries, including Japan, Argentina, and Mexico, had also banned phthalates from children’s toys prior to the U.S.

Phthalate Exposure Continues

A 2014 study looking at data over a ten-year period (2001– 2010) found that exposures to some phthalates have declined while others have increased. Americans’ exposure to three substances permanently banned in toys and children’s products—DEHP, DBP and BBP—has declined. But exposure to other phthalates such as DiNP and DiBP, as measured in urine, has increased. The higher  levels of DiBP and other phthalates “suggest that manufacturers may be using them as substitutes for other phthalates even though the US EPA has expressed concern about their use.”[28] It is surprising that DiNP exposure has gone up since it was banned on an interim basis from children’s toys and children’s products.  Additionally, in 2013, California declared DiNP a carcinogen.[29]

Even with the ban on phthalates in children’s toys, children, and adults, too, continue to be exposed because these chemicals are in many products, including food packaging, pharmaceuticals, medical devices and tubing, soap, lotions, and shampoos.[30] Johnson & Johnson recently reformulated its baby shampoo to remove harmful chemicals,[31] and Proctor & Gamble has promised to eliminate the phthalate DEP from fragrances used in its products by the end of 2014.[32] DEP is used in personal care products  and “reductions in DEP exposures have been the most pronounced,” according to the 2014 study.[33] Ten years ago, more than a thousand companies pledged to remove “chemicals of concern from personal care products,” however, it is unclear how many have done so. The U.S. Food and Drug Administration (FDA) regulates many of these products, including baby shampoo and baby lotion.  If the FDA does not decide to ban phthalates from these products, legislation would be required to do so.

The U.S. Environmental Protection Agency (EPA) developed an “action plan” in 2010 for eight phthalates “because of their toxicity and the evidence of pervasive human and environmental exposure.” [34] The phthalates are being studied for health effects and for alternatives. The EPA developed two new rules for these chemicals. However, the rules were delayed and then withdrawn in 2013.[35] In 2014, seven of these phthalates were included in the Toxic Substances Control Act work plan, because of their potential for harm and the frequency of exposure.[36] The eighth phthalate (DnPP) was not included because it is no longer being used in new products. The chemicals on the work plan are to be assessed for additional study or regulation, but it is unclear when that assessment will occur.

While other government agencies are concerned about phthalates in specific products, the EPA’s job is to focus on the chemicals for use in any kind of product and establish safety standards for each phthalate.  A challenge for the EPA is to set safety standards that make sense given that people may be exposed to several phthalates from many different sources. Teenage girls, for instance, have been found to use up to 17 personal care products a day.[37] Setting safety standards for phthalates individually or for individual products without considering their interactions and cumulative effects could underestimate the real-world risks of phthalates to the health of children and adults.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References

  1. Rudel RA, Brody JG, Spengler JD, Vallarino J, Geno PW, Sun G, Yau A (2001). Identification of selected hormonally active agents and animal mammary carcinogens in commercial and residential air and dust samples. Journal of Air and Waste Management Association 51(4):499-513.
  2. Kato K, Silva MJ, Reidy JA, Hurtz D, Malek NA, Needham LL, Nakazawa H, Barr DB, Calafat AM (2003). Mono(2-ethyl-5-hydroxyhexyl) phthalate and mono-(2-ethyl-5-oxhexyl) phthalate as biomarkers for human exposure assessment to di-(2-ethylhexyl) phthalate. Environmental Health Perspectives 112: 327-330.
  3. Vandenberg et al. (2012). Hormones and Endocrine Disrupting Chemicals: Low-dose Effects and Nonmonotonic Dose Responses. Endocrine Reviews.  First published ahead of print March 14, 2012 as doi:10.1210/er.2011-1050.
  4. Cone, Marla and Environmental Health News. Low Doses of Hormone-Like Chemicals May Have Big Effects. Scientific American.march 15, 2012. http://www.scientificamerican.com/article.cfm?id=low-doses-hormone-like-chemicals-may-have-big-effects.
  5. Vastag, B., (2001). CDC Unveils First Report on Toxins in People, JAMA 285(14): 1827-1828.
  6. Jaakkola JJ, Knight TL (2008 July). The Role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: a systematic review and meta-analysis. Environ Health Perspect, 116(7): 845-53.
  7. Kanazawa A, Kishi R (2009 May). Potential risk of indoor semivolatile organic compounds indoors to human health. Nippon Eiseigaku Zasshi, 64(3): 672-82.
  8. Hsu NY, Lee CC, Wang JY, et al. (2012). Predicted risk of childhood allergy, asthma, and reported symptoms using measured phthalate exposure in dust and urine. Indoor Air. 22(3): 189-99.
  9. Teitelbaum SL, Mervish N, L Moshier E, Vangeepuram N, Galvez MP, Calafat AM, Silva MJ, L Brenner B, Wolff MS. (2012, January).Associations between phthalate metabolite urinary concentrations and body size measures in New York City children. Environmental Research 112:186-193.
  10. Boas M, Frederiksen H, Feldt-Rasmussen U, Skakkebaek NE, Hegedus L, Hilsted L, et al. (2010). Childhood exposure to phthalates: associations with thyroid function, insulin-like growth factor I, and growth. Environmental Health Perspectives 118:1458-1464.
  11. Verstraete S, Vanhorebeek I, Covaci A, Güiza F, Malarvannan G, Jorens PG, Van den Berghe G. (2016). Circulating phthalates during critical illness in children are associated with long-term attention deficit: a study of a development and a validation cohort. Intensive Care Med 42(3):379-92.
  12. Yeni Kim Y, Eun-Hee Ha, Eui-Jung Kim, et al. (2011). Prenatal Exposure to Phthalates and Infant Development at Six Months: Prospective Mothers and Children’s Environmental Health (MOCEH) Study, Environmental Health Perspectives. 119(10): 1495-500.
  13. Main KM, Skakkebaek NE, Virtanen HE, Toppari J (2010). Genital anomalies in boys and the environment. Best Pract Res Clin Endocrinol Metab.Apr;24(2):279-89.
  14. Toppari J, Kaleva M. Maldescendus testis. Horm Res 1999;51:261-9.
  15. Pettersson A et al. (2007) Age at surgery for undescended testis and risk of testicular cancer. New England Journal of Medicine 356:1835-41.
  16. Duty, S. M., M. J. Silva, et al., (2003). Phthalate exposure and human semen parameters. Epidemiology 14(3): 269-77.
  17. Duty, S. M., N. P. Singh, et al., (2003). The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay. Environ Health Perspect 111(9): 1164-9.
  18. Duty, S. M., A. M. Calafat, et al., (2004). The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. J Androl 25(2): 293-302.
  19. Duty, S. M., A. M. Calafat, et al., (2005). Phthalate exposure and reproductive hormones in adult men. Hum Reprod 20(3): 604-10.
  20. Whyatt RM, Liu X, Rauh, VA, Calafat AM, Just AC, Hoepner L, Diaz D, et al. (2012). Maternal prenatal urinary phthalate metabolite concentrations and child mental, psychomotor and behavioral development at age three years.  Environmental Health Perspectives 120(2):290-5.
  21. Lien YJ, Ku HY, Su PH, Chen SJ, Chen HY, Liao PC, Chen WJ, & Want SL (2015). Prenatal Exposure to Phthalate Esters and Behavioral Syndromes in Children at 8 Years of Age: Taiwan Maternal and Infant Cohort Study. Environ Health Perspect 123(1): 95–100.
  22. Prenatal Phthalate Exposures and Neurobehavioral Development Scores in Boys and Girls at 6–10 Years of Age. Environ Health Perspect 122(5): 521–528.
  23. Kobrosly RW, Evans S, Miodovnik A, Barrett ES, Thurston SW, Calafat AM, & Swan SH (2014).
  24. Miodovnik A, Engel SM, Zhu C, et al. (2011). Endocrine disruptors and childhood social impairment.  Neurotoxicology Mar;32(2):261-7.
  25. CPSC. Chronic Hazard Advisory Panel on Phthalates and Phthalate Alternatives. 2014. http://www.cpsc.gov/PageFiles/169902/CHAP-REPORT-With-Appendices.pdf
  26. Pereira, J. and Stecklow, S. (2008, May). Wal-Mart Raises Bar on Toy-Safety Standards, The Wall Street Journal.
  27. Sathyanarayana S, Swan SH et al., (2008, February). Baby Care Products: Possible Sources of Infant Phthalate Exposure, Pediatrics, Vol. 121, No. 2.
  28. Zota AR, Calafat AM, & Woodruff TJ (Advance on-line publication January 15, 2014) Temporal Trends in Phthalate Exposures: Findings from the National Health and Nutrition Examination Survey, 2001-2010.
  29. Lee SM, (January 15, 2014). Banned chemicals replaced by worrisome ones, UCSF study shows. SFgate.com (San Francisco Chronicle).
  30. U.S. Food and Drug Administration (2008). Phthalates and Cosmetic Products. Retrieved November 4, 2009 at http://www.fda.gov/Cosmetics/ProductandIngredientSafety/SelectedCosmeticIngredients/ucm128250.htm
  31. Thomas K (January 17, 2014). The ‘No More Tears’ Shampoo, Now With No Formaldehyde. The New York Times. http://www.nytimes.com/2014/01/18/business/johnson-johnson-takes-first-step-in-removal-of-questionable-chemicals-from-products.html.
  32. Prcoter & Gamble Web site: What are Phthalates?  Accessed January 22, 2014. http://www.pg.com/en_US/sustainability/safety/ingredients/phthalates.shtml.
  33. Zota AR, Calafat AM, & Woodruff TJ (Advance on-line publication January 15, 2014) Temporal Trends in Phthalate Exposures: Findings from the National Health and Nutrition Examination Survey, 2001-2010.
  34. EPA. Phthalates Action Plan Summary. http://www.epa.gov/assessing-and-managing-chemicals-under-tsca/phthalates.
  35. Sheppard Kate (September 6, 2013). EPA Quietly Withdraws Two Proposed Chemical Safety Rules. Huffington Post. http://www.huffingtonpost.com/2013/09/06/epa-chemical-safety_n_3882262.html.
  36. EPA. TSCA Work Plan for Chemical Assessments: 2014 Update. https://www.epa.gov/sites/production/files/2015-01/documents/tsca_work_plan_chemicals_2014_update-final.pdf
  37. Environmental Working Group. 2008. Sutton R. Adolescent exposures to cosmetic chemicals of concern. http://www.ewg.org/research/teen-girls-body-burden-hormone-altering-cosmetics-chemicals.

Stomach Cancer and Diet: Can Certain Foods Increase Your Risk?

Laura Gottschalk, PhD, Cancer Prevention & Treatment Fund

There is growing evidence that the foods we eat can increase the chances of developing certain types of cancer. A new report by the World Cancer Research Fund International says that stomach cancer is one of them.

Stomach cancer is the fifth most common cancer worldwide and the third most common cause of death from cancer.[1] Older adults are more at risk to develop stomach cancer with most people in the U.S. being diagnosed over the age of 70.[2] Men are twice as likely to develop stomach cancer compared to women.[2]

You can’t control how old you are or whether you are a man or woman, but what you eat can either increase or decrease your chances of developing stomach cancer. The World Cancer Research Fund looked at all the scientific research that was available discussing diet, weight, physical activity, and the risk of stomach cancer.[3] After looking at 89 studies that examined nearly 77,000 cases of stomach cancer, the report concluded that each of the following can increase a person’s risk for developing stomach cancer.

  • Drinking three or more alcoholic drinks per day.
  • Eating foods preserved by salting, such as pickled vegetables and salted or dried fish, as traditionally prepared in East Asia.
  • Eating processed meats that have been preserved by smoking, curing or salting, or by the addition of preservatives. Examples: ham, bacon, pastrami, salami, hot dogs, and some sausages
  • Being overweight or obese, as measured by body mass index (BMI).

Based on their findings, the WCFR has made several recommendations to reduce your risk of stomach cancer:

  • Maintain a healthy weight
  • Be physically active
  • Eat a healthy diet that avoids processed meat and limits salt
  • Limit your alcohol consumption

These recommendations are good ones for preventing cancer in general, not just stomach cancer.

Still not convinced to give up your 6-packs, kimchi, and bacon just yet? This is just the latest of many studies showing that being overweight and eating processed meats increases your risk of cancer. And, previous research has also shown that drinking more alcohol increases your chances of developing cancer.[4] However, this is probably the most comprehensive study showing the link between a range of eating and drinking habits and stomach cancer.

In addition to what you eat, there are other aspects of your life that increase the risk of stomach cancer.

  • Smoking: It is estimated that 11% of stomach cancer cases are due to smoking.
  • Infection: A bacteria called pylori is known to cause chronic inflammation of the stomach which can lead to stomach cancer. Fortunately, food sanitation in developed countries dramatically cuts down on risk of infection.
  • Industrial chemicals: Exposure to dust and high-temperature environments in the workplace increases the risk of stomach cancer.

If you can’t reduce the risks of smoking, infection or industrial chemicals, changing your diet is the best option for reducing your chances of stomach cancer. Eating fresh vegetables and meats is better than preserved and processed ones. That doesn’t mean you should never eat another hot dog or slice of bacon, but it does mean trying to eat them only rarely. As with most things, moderation is key. Try and balance your diet:  don’t just decrease the amount of unhealthy foods you eat, but also increase the amount of healthy foods. Studies have shown that eating lots of fresh fruits and vegetables, especially citrus fruit,[5] may even reduce your chances of developing stomach cancer![3]

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References

  1. end Centers for Disease Control and Prevention. “Global Cancer Statistics.”  Department of Health and Human Services. 02 Feb. 2015. Accessed: 05/04/2016. http://www.cdc.gov/cancer/international/statistics.htm
  2. end National Cancer Institute. “What you need to know about stomach cancer.” NIH Publication No. 09-1554. Printed September 2009. Brochure.
  3. end World Cancer Research Fund International/American Institute for Cancer Research. Continuous “Update Project Report: Diet, Nutrition, Physical Activity and Stomach Cancer.” 2016. Available at: wcrf.org/stomach-cancer-2016.
  4. end IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. “Personal habits and indoor combustions. Volume 100 E. A review of human carcinogens. Exit Disclaimer.” IARC Monographs on the Evaluation of Carcinogenic Risks in Humans. 2012: 100(Pt E):373-472.
  5. end Bae JM, Lee EJ, et al. “Citrus fruit intake and stomach cancer risk: a quantitative systematic review.” Gastric Cancer. 2008;11(1):23-32.

Are E-Cigarettes Safer Than Regular Cigarettes?

Brandel France De Bravo, MPH, Sarah Miller, Jessica Becker, and Laura Gottschalk, PhD, Cancer Prevention & Treatment Fund

Electronic cigarettes, or e-cigarettes, are being marketed as the “safe” new alternative to conventional cigarettes. But are e-cigarettes safe?  What does the FDA think about them?  Are e-cigarettes going to reverse the decline in smoking—giving new life to an old habit—or can they help people quit smoking? Here is what you need to know before picking up an e-cigarette.

What Are E-Cigarettes?

E-cigarettes are battery-operated devices shaped like cigarettes that provide a way to get nicotine. Nicotine is an addictive drug (it stimulates and relaxes) that is naturally found in tobacco. The most popular way for people to take in nicotine is to inhale it by smoking cigarettes. E-cigarettes also allow nicotine to be inhaled, but they work by heating a liquid cartridge containing nicotine, flavors, and other chemicals into a vapor. Because e-cigarettes heat a liquid instead of tobacco, what is released is considered smokeless.[1]

Are E-Cigarettes Safer Than Traditional Cigarettes?

The key difference between traditional cigarettes and e-cigarettes is that e-cigarettes don’t contain tobacco.  But, it isn’t just the tobacco in cigarettes that causes cancer. Traditional cigarettes contain a laundry list of chemicals that are proven harmful, and e-cigarettes have some of these same chemicals.

Since 2009, FDA has pointed out that e-cigarettes contain “detectable levels of known carcinogens and toxic chemicals to which users could be exposed.”[2] For example, in e-cigarette cartridges marketed as “tobacco-free,” the FDA detected a toxic compound found in antifreeze, tobacco-specific compounds that have been shown to cause cancer in humans, and other toxic tobacco-specific impurities.[3] Another study looked at 42 of these liquid cartridges and determined that they contained formaldehyde,  a chemical known to cause cancer in humans.[4] Formaldehyde was found in several of the cartridges at levels much higher than the maximum EPA recommends for humans.

The body’s reaction to many of the chemicals in traditional cigarette smoke causes long-lasting inflammation, which in turn leads to chronic diseases like bronchitis, emphysema, and heart disease.[5f] Since e-cigarettes also contain many of the same toxic chemicals, there is no reason to believe that they will significantly reduce the risks for these diseases.

There are no long-term studies to back up claims that the vapor from e-cigarettes is less harmful than conventional smoke. Cancer takes years to develop, and e-cigarettes were only very recently introduced to the United States. It is almost impossible to determine if a product increases a person’s risk of cancer or not until the product has been around for at least 15-20 years. Despite positive reviews from e-cigarette users who enjoy being able to smoke them where regular cigarettes are prohibited, very little is known about their safety and long-term health effects.

Can E-Cigarettes Be Used to Cut down or Quit Smoking Regular Cigarettes?

If a company makes a claim that its product can be used to treat a disease or addiction, like nicotine addiction, it must provide studies to the FDA showing that its product is safe and effective for that use. On the basis of those studies, the FDA approves or doesn’t approve the product. So far, there are no large, high-quality studies looking at whether e-cigarettes can be used to cut down or quit smoking long-term. Most of the studies have been either very short term (6 months or less) or the participants were not randomly assigned to different methods to quit smoking, including e-cigarettes. Many of the studies are based on self-reported use of e-cigarettes. For example, a study done in four countries found that e-cigarette users were no more likely to quit than regular smokers even though 85% of them said they were using them to quit.[6] Another year-long study, this one in the U.S., had similar findings.[7] People may believe they are smoking e-cigarettes to help them quit,  but 6-12 months after being first interviewed, nearly all of them are still smoking regular cigarettes.

Until there are results from well-conducted studies, the FDA has not approved e-cigarettes for use in quitting smoking.[8]

Teenagers, Children, and E-Cigarettes

The percentage of teenagers who have tried e-cigarettes has almost quadrupled in just four years, from 5% in 2011 to 19% in 2015.  Three million U.S. students in middle school and high school tried e-cigarettes in 2015, according to the National Youth Tobacco Survey.  And, 1 in 5 middle schoolers who said they had tried e-cigarettes also said they had never smoked conventional cigarettes.[9]

E-cigarette use by young people is worrisome for a number of reasons:

1) The younger people are when they begin smoking, the more likely it is they will develop the habit: nearly 9 out of 10 smokers started before they were 18.[10]

2) Nicotine and other chemicals found in e-cigarettes might harm brain development in younger people.[11]

3) E-cigarettes may introduce many more young people to smoking who might otherwise never have tried it, and once they are addicted to nicotine, some may decide to get their “fix” from regular cigarettes. Whether e-cigarettes end up being a “gateway” to regular cigarettes or not, young people who use them risk becoming addicted to nicotine and exposing their lungs to harmful chemicals.

The sharp rise in young e-cigarette users highlights the need to stop manufacturers from targeting teenagers with candy-like flavors and advertising campaigns.

Even children who are too young to smoke have been harmed by e-cigarettes. The liquid used in e-cigarettes is highly concentrated, so absorbing it through the skin or swallowing it is far more likely to require an emergency room visit than eating or swallowing regular cigarettes. In 2012, less than 50 kids under the age of six were reported to poison control hotlines per month because of e-cigarettes. In 2015, that number had skyrocketed to about 200 children a month, almost half of which were under the age of two![12]

How Are E-Cigarettes Regulated?

The FDA was given the power to regulate the manufacturing, labeling, distribution and marketing of all tobacco products in 2009 when President Obama signed into law the Family Smoking Prevention and Tobacco Control Act and in 2010 a court ruled that the FDA could regulate e-cigarettes as tobacco products.[13]

It wasn’t until 2016 that the FDA finally announced a rule to regulate e-cigarettes.[14] Under the final rule, the FDA plans to ban the sale of e-cigarettes to anyone under the age of 18.  The rule also requires all makers of e-cigarettes sold after February 15, 2007 to go through a “premarket review.” This is the process that the FDA uses to determine whether potentially risky products are safe. However, companies are allowed to have anywhere from 18 months to two years to prepare their applications. And it will take another year for the FDA to actually approve these applications. So don’t expect e-cigarettes currently on the market to be officially allowed to be sold by the FDA for another couple of years.

In the meantime, individual states have always had the power to pass laws restricting the sale and use of e-cigarettes. For example, in May 2013, the California state senate proposed a law making all e-cigarettes subject to the same regulations and restrictions as traditional cigarettes and tobacco products.  However, that did not become law.

The Bottom Line

E-cigarettes have not been around long enough to determine if they are harmful to users in the long run.  Unfortunately, many people, including teenagers, are under the impression that e-cigarettes are safe or that they are effective in helping people quit smoking regular cigarettes.  Neither of these assumptions has yet been proven. Studies by the FDA show that e-cigarettes contain some of the same toxic chemicals as regular cigarettes, even though they don’t have tobacco.  The big three tobacco companies—Lorillard, Reynolds American, and Altria Group—all have their own e-cigarette brands, so it’s not surprising that e-cigarettes are being marketed and advertised much the way regular cigarettes used to be.  Here are the 7 Ways E-Cigarette Companies Are Copying Big Tobacco’s Playbook.

Unless you want to be a guinea pig, hold off on e-cigarettes until more safety information is available.  And if you need help quitting or reducing the number of cigarettes you are smoking, check out the smokefree.gov website.

Related Content:

Quitting smoking: women and men may do it differently
Third-hand smoke
Smoking cessation products

All articles on our website have been approved by Dr. Diana Zuckerman and other senior staff. 

References

  1. Richard J. O’Connor Non-cigarette tobacco products: What have we learned and where are we headed? Tob Control. Author manuscript; available in PMC 2013 July 19. Published in final edited form as: Tob Control. 2012 March; 21(2): 181–190. doi: 10.1136/tobaccocontrol-2011-050281.
  2. “Summary of Results: Laboratory Analysis of Electronic Cigarettes Conducted By FDA.” FDA News & Events. FDA, 22 July 2009. http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm173146.htm.
  3. “Summary of Results: Laboratory Analysis of Electronic Cigarettes Conducted By FDA.” FDA News & Events. FDA, 22 July 2009. Web. 09 Aug. 2013. http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm173146.htm.
  4. Varlet et al. (2015) Toxicity of refill liquids for electronic cigarettes. International Journal for Environmental Research and Public Health. 12:4796-4815.
  5. Stoller, JK & Juvelekian, G; Chronic Obstructive Pulmonary Disease; 2010 Cleveland Clinic Center for Continuing Education. https://my.clevelandclinic.org/departments/respiratory/depts/chronic-obstructive-pulmonary-disease.
  6. Adkison SE, O’Connor RJ, Bansal-Travers M, et al. Electronic nicotine delivery systems: international tobacco control four-country survey. Am J Prev Med. 2013;44(3):207-215.
  7. Grana RA, Popova L, Ling PM. A Longitudinal Analysis of Electronic Cigarette Use and Smoking Cessation. JAMA Internal Medicine, published online March 24, 2014
  8. “Electronic Cigarettes” FDA News & Events. FDA, 25 July 2013. http://www.fda.gov/newsevents/publichealthfocus/ucm172906.htm
  9. Singh T, Arrazola RA, Corey CG, et al. Tobacco Use Among Middle and High School Students – United States, 2011-2015. CDC Morbidity and Mortality Weekly Report. April 15, 2016. 65(14);361-367.
  10. Centers for Disease Control and Prevention. Fact sheets: Youth and tobacco use.  http://www.cdc.gov/tobacco/data_statistics/fact_sheets/youth_data/tobacco_use/.
  11. US Department of Health and Human Services. Preventing tobacco use among youth and young adults. Atlanta, GA: US Department of Health and Human Services, CDC; 2012. http://www.cdc.gov/tobacco/data_statistics/sgr/2012/index.htm.
  12. Kamboj A, Spiller HA, Casavant MJ, et al. Pediatric Exposure to E-Cigarettes, Nicotine, and Tobacco Products in the United States. Pediatrics. May 2016. In Press.
  13. “Regulation of E-Cigarettes and Other Tobacco Products.” FDA News & Events. FDA, April 25, 2011. http://www.fda.gov/newsevents/publichealthfocus/ucm252360.htm.
  14. Deeming Tobacco Products To Be Subject to the Federal Food, Drug, and Cosmetic Act, as Amended by the Family Smoking Prevention and Tobacco Control Act; Restrictions on the Sale and Distribution of Tobacco Products and Required Warning Statements for Tobacco Products. 21 CFR Parts 1100, 1140, and 1143 (2016).

Prostate Cancer: Diet and Dietary Supplements

Stephanie Portes-Antoine, Brandel France de Bravo, MPH, Caitlin Kennedy, PhD, Anna E. Mazzucco, PhD, and Laura Gottschalk, PhD, Cancer Prevention & Treatment Fund

Prostate cancer is the most common cancer in men in North America. In 2008, approximately 186,000 men in the United States and 25,000 men in Canada were diagnosed with prostate cancer, which accounts for 25% of all cancers in men.[1][2]

Compared to most cancers, prostate cancer usually progresses very slowly, and many men live with it for years and even decades. Once diagnosed, some men decide to undergo treatment to halt the progression of the disease, and others refrain from treatment, preferring instead to closely monitor the cancer’s progression. Those who choose “watchful waiting” do this because the medical and surgical treatments for prostate cancer can cause debilitating side effects, and because most men with prostate cancer will die from something else. This strategy is especially likely for older men in the earliest stage of the disease.

At one time, it was unheard of to suggest that diet might have a role to play in battling prostate cancer. But there is now evidence that certain foods and dietary supplements have an impact on prostate health—both positive and negative. Some foods or supplements appear to promote prostate health and prevent cancer cells from developing, but others should not necessarily be taken by men who already have prostate cancer.

The role of diet drew researchers’ attention when they noticed that prostate cancer rates vary greatly from one country to another, with the highest rates appearing in countries where people tend to eat a lot of fat. Studies also show that men who are obese or have a high fat diet are more likely to have prostate cancer.[2] Diets high in saturated fats, such as the animal fats found in red meat, may pose the greatest risk. The lowest rates of prostate cancer are found in Asian countries where men eat a lot of soy foods, a rich source of naturally occurring phytoestrogens. It was hoped that by increasing men’s intake of phytoestrogens, they might reduce their risk of prostate cancer, slow its progression, or reduce the risk of prostate cancer recurring, but at least three studies have failed to find any protective benefit from phytoestrogens.[4][5][6]

As more and more people take dietary supplements containing antioxidants, studies have been conducted to determine their effect on reducing the risk and growth of cancers, including prostate cancer. Three antioxidants that have received attention with regard to prostate health are vitamin E, selenium, and vitamin D.

Studies comparing men who live in areas of the country with high levels of selenium to men in areas with low levels suggest that this mineral protects against prostate cancer. Selenium is believed to reduce the risk of developing prostate cancer because it keeps cells from proliferating or dying off in a rapid or unusual way. An analysis in 2002 of the Nutritional Prevention of Cancer Trial revealed that the men who took selenium supplements daily were half as likely to be diagnosed with prostate cancer.[7] However, in 2008, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) indicated that neither selenium nor vitamin E, alone or in combination, was effective for the primary prevention of prostate cancer.[8][9]  In fact, a 2014 report showed that after several more years of observing the men from the SELECT trial, taking vitamin E supplements actually increased the risk of prostate cancer by 17%.[10]  This result led the researchers to discourage men over 55 from taking amounts of vitamin E higher than the recommended dietary allowance (RDA), which is 15 mg of alpha-tocopherol, especially for supplements which contain only the alpha-tocopherol type of vitamin E.

So do antioxidants prevent prostate cancer or not? The case of selenium is an interesting one that helps shed light on this question. Based on the newest research by Philip Kantoff, June Chan, and their colleagues at the Dana-Farber Cancer Institute in Boston, it seems that higher selenium levels in the blood may worsen prostate cancer in many men who already have the disease.[11]

In his earlier research, Dr. Kantoff had found that the risk of developing prostate cancer was modified by a strong interaction between a mitochondrial enzyme (SOD2) and selenium.[12] In his most recent study published in 2009, Dr. Kantoff and his research team measured selenium in the blood of men with prostate cancer and determined which of the two forms of SOD2 the men had: AA or V.9 Among the men with the AA genotype, those with a higher level of selenium in their blood had a lower risk of aggressive prostate cancer. In contrast, the men with the much more common V genotype who had higher levels of selenium in their blood were at an increased risk for aggressive prostate cancer. Unless a man knows which of the two genotypes he has, he may want to avoid taking supplements with selenium, particularly if he has already been diagnosed with prostate cancer.

But what about men who don’t have prostate cancer—should they take selenium?  In 2014, the SELECT trial  found that for men who already had high levels of selenium, taking selenium supplements increased their risk of prostate cancer by 91%.10 Clearly, men should avoid having too much selenium.  As a result of this trial, the researchers have encouraged men over 55 to limit their intake of selenium to the recommended dietary allowance (RDA) of 55 mcgs.

The SELECT findings on selenium don’t mean that antioxidants have no role to play in preventing cancer or slowing its spread. Scientists still have much to learn about antioxidants. Some antioxidants may be helpful and yet some may actually encourage small cancers to grow larger.  A 2013 study by researchers at the Bedford and Addenbrooke’s Hospitals in the U.K. tested the effect of Pomi-T, a supplement that contains broccoli, pomegranate, green tea, and turmeric on the health of men with prostate cancer. After six months, they found that the men taking Pomi-T had a smaller increase or sometimes even a decrease in PSA, a protein that becomes elevated with prostate cancer, as compared to men with prostate cancer who didn’t take Pomi-T. Also, fewer supplement-taking men went on to receive treatment or surgery than non-supplement-taking men. The researchers suggest that the unique blend of polyphenols and antioxidants in the supplement had a beneficial effect on health of these prostate cancer patients.[13]

A study published in 2016 brought yet another antioxidant, vitamin D, into the prostate cancer discussion. Vitamin D is well known for its role in helping build strong bones and teeth, but it may also contribute to the fight against cancer. Higher levels of vitamin D have previously been linked to better breast cancer outcomes (read more here). The prostate cancer study looked at the levels of vitamin D in men who had their prostates removed due to cancer. They found that men who had the most aggressive forms of prostate cancer had lower levels of vitamin D in their blood compared to men with less aggressive forms of cancer.[14] It is not yet known whether higher levels of vitamin D prevent more aggressive forms of prostate cancer or if aggressive prostate cancer lowers levels of vitamin D. Since it is impossible to know if low levels of vitamin D is a cause or effect of aggressive prostate cancer, and since high levels of vitamin D can be dangerous, more research is needed before experts will know if men diagnosed with prostate cancer should try to take more vitamin D.

More studies are needed in order to determine exactly how diet and dietary supplements can be used to prevent prostate cancer and slow its spread. Meanwhile, men should reduce saturated fats as much as possible. While the jury is still out on phytoestrogens, men may benefit from eating more soy products—especially if they are eating them in place of red meat!

For more on cancer and antioxidants, read here.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References

  1. American Cancer Society: Statistics for 2008. Available at http://www.cancer.org. Accessed July 31, 2009.
  2. Canadian Cancer Society: Canadian Cancer Statistics 2008. Available at http://www.cancer.ca
  3. Ma R, Chapman K. A systematic review of the effect of diet in prostate cancer prevention and treatment. Journal of Human Nutrition and Dietetics. Vol (22)2009:187-199.
  4. Ganry O. Phytoestrogens and prostate cancer risk. Preventive Medicine. Vol (41) 2005:1-6.
  5. Ward H, Chapelais G, Kuhnle GC, Luben R, Khaw KT, Bingham S. Lack of Prospective Associations between Plasma and Urinary Phytoestrogens and Risk of Prostate or Colorectal Cancer in the European Prospective into Cancer-Norfolk Study. Cancer Epidemiology Biomarkers & Prevention Vol (17) 2008: 2891-2894.5
  6. Bosland MC, Kato I, Zeleniuch-Jacquotte A, Schmoll J, Rueter EE, Melamed J, Kong MX, Macias V, Kajdacsy-Balla A, Lumey LH, Xie H, Gao W, Walden P, Lepor H, Taneja SS, Randolph C, Schlicht MJ, Meserve-Watanabe H, Deaton RJ, & Davies JA. Effect of soy protein isolate supplementation on biochemical recurrence of prostate cancer after radical prostatectomy. JAMA 2013; 310(2): 170-178. doi: 10.1001/jama.2013.7842
  7. Duffield-Lillico AJ, et al. Baseline characteristics and the effect of selenium supplementation on cancer incidence in a randomized clinical trial: A summary report of the Nutritional Prevention of Cancer Trial.Cancer Epidemiology, Biomarkers, and Prevention. Vol (11) 2002: 630-639.
  8. Lippman SM, et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: The Selenium and Vitamin E Cancer Prevention Trial (SELECT). Journal of American Medical Association. Vol (301)2008: 39-51.
  9. Klein EA, et al. SELECT: The next prostate cancer prevention trial-Selenium and Vitamin E Cancer Prevention Trial. Journal of Urology. Vol (166) 2001:1311-1315.
  10. Kristal AR, et al., Baseline Selenium Status and Effects of Selenium and Vitamin E Supplementation on Prostate Cancer Risk.  Journal of the National Cancer Institute, 2014.
  11. Chan JM et al. Plasma Selenium, Manganese Superoxide Dismutase, and Intermediate-or High-Risk Prostate Cancer. Journal of Clinical Oncology. Vol (27) 2009: 3577-3583.
  12. Li H, et al. Manganese superoxide dismutase polymorphism, pre-diagnostic antioxidant status, and risk of clinical significant prostate cancer. Cancer Research. Vol (65)2005:2498-2505.
  13. Thomas RJ, Williams MMA, Sharma H, Chaudry A, & Bellamy P. A double-blind, placebo RCT evaluating the effect of a polyphenol-rich whole food supplement on PSA progression in men with prostate cancer: The U.K. National Cancer Research Network (NCRN) Pomi-T study. Results presented at the 2013 Annual Meeting of the American Society of Clinical Oncology. Abstract retrieved on July 12, 2013 from: http://meetinglibrary.asco.org/content/112921-132
  14. Nyame Ya, et al. Associations between serum vitamin D and adverse pathology in men undergoing radical prostatectomy. J Clin Oncol. 2016 Feb 22.

Breast implants and mammography: what we know and what we don’t know

Elizabeth Santoro, RN, MPH and Dr. Diana Zuckerman

There has been a lot of attention given to mammography screening in recent years. Some of this information has been confusing to women—at what age should I first have a mammogram, how frequently should I have repeat mammograms, and are mammograms even effective? These are questions that women both with and without breast implants have been trying to understand. Despite this confusion, experts continue to recommend that the average woman have mammograms every two years starting at age 50, while women with a great risk consider having mammograms every year or two starting at age 40.1 But, what does this mean for women who have breast implants? Are women with breast implants faced with different risks when undergoing a mammogram? Will women with implants require special considerations during the procedure?

Delayed Breast Cancer Detection

Breast implants can interfere with the detection of breast cancer, because the implants can obscure the mammography image of a tumor. Implants therefore have the potential to delay the diagnosis of breast cancer. Although mammography can be performed in ways that minimize the interference of the implants, as described below, Miglioretti and her colleagues found that even so, 55% of breast tumors were missed, compared to 33% of tumors for women without implants.2  They also found that among newly diagnosed breast cancer patients who did not have any symptoms, the augmented women had larger tumors than those who did not have implants.

What is the impact of this possible delay in diagnosis?  Research findings have been inconsistent, but a 2013 Canadian systematic review of 12 studies found that women with breast cancer who had breast implants are diagnosed with later-stage cancers than women with breast cancer who did not have implants.3

A delay in diagnosis could result in the woman needing more radical surgery or the delay could be fatal.  A 2013 Canadian meta-analysis of five studies found that if women who had breast augmentation later developed breast cancer, they were more likely to die from it than women diagnosed with breast cancer who did not have breast augmentation.3

These studies indicate that for an individual woman, a delay in diagnosis could potentially result in death, and more research is needed to determine how often that happens, and under what circumstances. From a public health perspective, delays in diagnosis could potentially necessitate more radical surgery: a cancer that could have been treated at an earlier stage with breast-sparing treatments, such as lumpectomy, may instead require a mastectomy.4,5

What are the other possible problems that implants can cause regarding mammography?

A study by FDA scientist Dr. S. Lori Brown and colleagues describes problems that were reported to the FDA related to breast implants and mammography screening.6 The authors found 66 adverse events that were reported as either occurring during the mammogram or involving breast implants interfering with the mammogram. Forty-one reports of either silicone or saline breast implants- – almost two out of three reports– pertained to ruptures that were suspected as happening during mammography. The other 25 reports included delayed breast cancer detection, inability to perform the mammogram due to capsular contracture or because of fear that the implant would rupture, and pain/soreness during and after the procedure.

Description of the FDA Study

This study examined data from the Manufacturer and User Facility Device Experience (MAUDE) database. This FDA database collects mandatory or voluntary reports of medical device adverse events from physicians, breast implant manufactures, consumers, and others. The reports were received between June 1992 and October 2002 for events that occurred between June 1972 and June 2002. The mean age of the implant was 14.5 years, and ranged from 2-29 years.

The use of the MAUDE database has limitations. The FDA does not verify the information that is provided. Therefore, the FDA cannot guarantee that the information is accurate and complete. In addition, in some cases, a doctor and a patient could potentially report the same problem.  On the other hand, most problems are not reported even once, since patient and physician reporting is voluntary. It is well-documented that the vast majority of problems arising from medical products are not reported to the FDA. As a result of these shortcomings, these data cannot be used to calculate the number of new adverse events expected for a given number of people in a defined time period.

Key Implications of the Studies on Implants and Mammograms

Potential Implant Rupture

The FDA warns that all implants will eventually break, and research shows that most women who have implants for ten years or longer will have at least one broken implant.7 The risk of breast implant rupture is known to increase as the implant ages. A study by Holmich and colleagues suggested that during the first ten years a woman has implants, most implants do not break, between 11-20 years most will break, and by the time they are more than 20 years almost all have broken.8 Women with implants have been told that mammography is safe for them, but the results of the Brown study suggest that the risk of rupture can be exacerbated by mammography.

Brown and her colleagues also reviewed the published research on implant rupture during mammography and found an additional 17 cases reported in medical journals. According to the American Society of Plastic Surgery, approximately half of the women who get breast implants are in their 20′s or early 30′s,9 which means that the implants are already broken or vulnerable by the time these women are old enough for screening mammograms.

Mammography may therefore increase the risk of a rupture earlier in the typical lifespan of implants, and the squeezing involved in mammography probably increases the risk of leakage in implants that are already ruptured. The potential risk of rupture or leakage needs to be weighed against the benefits of mammography by each individual woman. For women who are concerned about breast cancer, knowledge of mammography problems might discourage women from getting breast implants, or encourage them to have their implants removed and not replaced. Current guidelines encourage women with breast implants to have regular mammograms provided that the technician knows the woman has implants prior to the procedure and that special techniques are utilized.6 In light of this new research, those guidelines need to be reconsidered, especially for women with silicone gel breast implants, where leakage can cause permanent disfigurement and has unknown health risks.

Avoidance of Mammography

The Brown study also found that implants sometimes make it impossible to perform a mammogram. This can happen for two reasons. First, conditions such as capsular contracture, where the scar tissue around the implant tightens and causes the breast to become hard and misshapen, can make it very difficult or even impossible to perform the mammogram.10, 11 The compression of the breast that is required in order to perform the mammogram can be extremely painful if there is capsular contracture, and in some cases the hardness of the breast makes it impossible to compress the breast for the mammogram. Some women avoid getting mammograms because they are afraid of rupture and the latest research indicates that this is a reasonable concern.

Biomaterials testing of breast implants indicates that implants should only break under the most traumatic circumstances, and yet implants break for no apparent reason, as well as under pressure from mammograms.12 It is difficult to know how much risk a mammogram increases the risk of rupture since so little is understood about why implants break and under what circumstances.

What Does this Mean for Women?

Women considering breast implants and women with breast implants need to be informed consumers, and that includes knowing about the problems that arise from having mammograms with breast implants. This is true for all women, but especially breast cancer patients who may use implants on a healthy breast so that it will match the reconstructed breast after a mastectomy. (Detection of cancer in the reconstructed breast is unlikely to be a problem because mammography is not used after a mastectomy. Since breast cancer survivors are at greater risk for breast cancer in the breast that was not removed, compared to women who have not had breast cancer, survivors should have regular mammograms of the surviving breast, and need to know the risks.

Women with breast implants and those considering breast implants need to know that they will have a different mammography experience than women without implants, to try to improve the accuracy. The special techniques used will push the implant back to try to move it out of the way, and extra views will be taken. Even so, as reported earlier in this article, mammograms performed on women with implants will still miss more tumors than is typical of mammograms for women who do not have implants.7, 13 In addition, women with implants should expect that mammography will require more views and take longer, thus costing more and exposing them to increased levels of radiation. Unfortunately, the most common problem, capsular contracture, can make mammography more painful, less accurate, or even impossible to perform. In such cases other, more expensive tests, such as an MRI or ultrasound, may be required.

Women also need to understand that even if breast implants do not cause contracture or other problems, they will still interfere with mammography and mammograms might still cause rupture and leakage.

The bottom line is that women considering breast implants and those who already have them need to be informed about potential problems with mammography so that they can make the decisions that will help them reduce the risk of breast cancer and avoid the problems that arise with implant breakage and leakage.

For more information on breast implants, see www.breastimplantinfo.org.


Related Content:
What you need to know: Breast cancer, suicide, mastectomy, and breast implants
Summary of: Breast Implants, Self-Esteem, Quality of Life, and the Risk of Suicide
2016 Update: When should women start regular mammograms? 40? 50? And how often is “regular”?

 

Lung cancer: who is at risk and can they be screened?


By Tiffanie L. Hammond and Amrita Ford, MA

Risk Factors for Lung Cancer
The Face of Lung Cancer
Symptoms of Lung Cancer
Screening for Lung Cancer
Biomarker Tests for Diagnosis
What We Still Need to Know and Change

Lung cancer is the second most commonly diagnosed cancer in both men and women in the U.S., but it is the #1 cancer killer. In 2012, it was estimated that approximately 226,160 men and women would be diagnosed with lung cancer and about 160,340 men and women would die from it.14 That is more deaths than from breast, prostate, colon, and cervical cancers combined. One of the reasons for the disproportionate death rate is that while these other cancers have screening guidelines issued by U.S. public health agencies aimed at increasing early diagnosis, no such formal guidelines exist for the early diagnosis of lung cancer. The most common causes of lung cancer are well known, and changes in behavior can reduce the risk, but many men and women without risk factors are diagnosed with lung cancer every year.

Risk Factors for Lung Cancer

Smokers

Smoking is the leading cause of lung cancer. It is responsible for 90% of lung cancer deaths in men and 80% in women. Today, there are over 90 million current and former smokers living in the U.S. Most are men, but while the number of new cases of men diagnosed with lung cancer is declining every year, the number of new diagnoses among women was increasing annually until very recently.15 The percentage of women who smoke began to increase in the 1940s during World War II and peaked in the 1960s.16 Decades later, lung cancer cases began rising in women, and stayed high, due to the long delay between starting to smoke and being diagnosed with lung cancer. Over the last few decades, smoking declined in popularity among women and men, resulting in a gradual decline in new cases of lung cancer.

Non-smokers

About 15% of lung cancer cases occur among nonsmokers, and each year about 20,000 people who never smoked die of lung cancer.17 Non-smoking women are at higher risk for lung cancer than non-smoking men: one in five women who develop lung cancer are non-smokers whereas only one in twelve men with lung cancer are non-smokers.18  Other causes of lung cancer in non-smokers include exposure to second-hand smoke, radon, asbestos, benzene or other cancer-causing agents, air pollution, and genetic vulnerability.

It is unclear why non-smokers develop lung cancer. One study found that about 30% of non-smokers who developed lung cancer had the same rare variation in a tumor-suppressor gene. This variation limits the gene’s ability to protect certain cells from cancer.19  Several molecular and genetic markers are thought to predispose some people to lung cancer but more research is needed to understand precisely how these markers influence the development of the disease.

The Face of Lung Cancer

Lung cancer patients are typically former or current smokers over the age of 65.  Most are men. African-American men are 37% more likely than Caucasian men to be diagnosed with lung cancer and 22% more likely to die from lung cancer, despite similar smoking rates.20 Research studies have examined smoking behavior, workplace and environmental exposures, biological and genetic differences, and cultural influences as potential causes for increased susceptibility and mortality of African Americans to lung cancer without a definitive answer.

Women accounted for 46% of new lung cancer cases in 2009, the most recent statistics available.21  Studies indicate that biological and genetic differences between men and women may play a role in differences in susceptibility to lung cancer and risk of dying from lung cancer.  Some research shows that estrogen, a hormone found in men and women that is much higher in women, may cause certain lung cancer cells to grow and spread throughout the lungs.  For example, a 2009 study based on the Women’s Health Initiative showed that post-menopausal women who took combined estrogen and progesterone replacement therapy (HRT) had an increased risk of dying from lung cancer, although they were not more likely to be diagnosed with lung cancer.22  In contrast, a 2010 study indicated that HRT may also increase the risk of developing lung cancer.23 In 2011, a study showed that women who take tamoxifen or other estrogen-blocking hormones to prevent breast cancer are at reduced risk for lung cancer death.24 For more on women’s risk of lung cancer, see Lung Cancer is a Women’s Health Issue.

Symptoms of Lung Cancer

One of the reasons why lung cancer is so deadly is that symptoms usually appear during the later stages, when treatment is least effective. General symptoms include:

  • a persistent cough that may worsen over time, including coughing up blood
  • breathing trouble, such as shortness of breath
  • chest pain
  • raspy or hoarse voice
  • frequent lung infections, such as pneumonia
  • extreme and constant fatigue
  • unintentional weight loss

Most lung cancers are detected by accident when testing for other health problems, or when the lung cancer is so advanced that symptoms are relatively obvious. The majority of lung cancer patients are diagnosed with late-stage lung cancer, when the cancer has usually already spread to other parts of the body, and at this point the 5-year survival rate is only 3.7%.25

Screening for Lung Cancer

The purpose of screening for cancer is to diagnose it early before symptoms appear. Cancer screening is only recommended when there is a method that is low-risk and accurate, and when the cancer can be detected early on.

There is currently no approved screening test for lung cancer.

Because of this, only 16% of lung cancer patients are diagnosed before their cancer has metastasized (spread to other parts of the body) compared to over 60% of breast cancer patients and over 90% of prostate cancer patients whose cancers are detected early-on through screening.26

Three major clinical trials in the 1970s evaluated two potential screening methods: chest x-ray and sputum cytology, an examination of cells found in the mucus of the lungs. The Johns Hopkins Lung Project, the Memorial Sloan-Kettering Lung Study, and the Mayo Lung Project evaluated men screened annually with only a chest x-ray (control group) against men screened with an annual chest x-ray plus sputum cytology (an analysis of their spit) every four months (intervention group). The studies found that screening men more often and with both screening tests resulted in more lung cancer diagnoses in one of the projects (the Mayo Lung Project), but there was no difference in the rate of lung cancer deaths.27  28
In 1992 the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial evaluated nearly 155,000 men and women, comparing those who got an annual chest x-ray screening for 4 years to those who did not undergo any screening. More lung cancer cases were detected in the screening group, but after 13 years of follow-up the study found that annual chest x-ray screening did not reduce lung cancer deaths.29

In 1999, the Early Lung Cancer Action Project found that low-dose computerized tomography scans (low-dose CT) were four times more likely than chest x-rays to detect a cancerous tumor. Most of the cancers detected (85%) were very early lung cancers (Stage I).30

In 1999, Stephen J. Swensen and his colleagues at the Mayo Clinic found that having a low-dose CT scan every year for 5 years increased survival times, but it did not reduce mortality rates. Survival is a measure of how long a person lives once cancer is diagnosed. If mortality does not change, it means a person might be aware of his or her diagnosis for a longer period of time than someone who did not undergo screening, but he or she does not live any longer.31

The National Lung Screening Trial (NLST), which started in 2002, evaluated the use of chest x-rays and low-dose CT scans in men and women who were heavy smokers. Each randomized group was screened annually for three years. Researchers found that using low-dose CT scans could reduce lung cancer deaths by 20%. Based on a 2011 report of the trial,32 low-dose CT screening could potentially increase the 5-year lung cancer survival rate to 70% if it allowed lung cancer to be detected in its earliest stage (stage 1A), when the tumor is still relatively small, still in the lung, and can be removed easily through surgery.17 18
33

Low-Dose CT Scans

Prior to these most recent low-dose CT scan findings, the U.S. Preventive Services Task Force, which is the government agency that reviews scientific evidence and makes recommendations on health care services, had concluded that there was insufficient evidence to recommend for or against screening people who do not have symptoms with low-dose CT, chest x-ray, sputum cytology, or any combination of these tests. 34 It is expected that the Task Force will re-visit their conclusions.

Who is recommending them?

Although no U.S. public health agency has recommended screening for lung cancer, in January 2013 the American Cancer Society (ACS) did so for the first time, saying that annual screening with low dose CT scans “could save many lives.”35  ACS has recommended that people at highest risk for lung cancer, as defined by the National Lung Screening Trial, have a discussion with their doctor about the benefits and risks of annual screening. They advised doctors to have this conversation only with patients who match the profile of the people who were enrolled in the National Lung Cancer Screening Trial: current and former smokers who are 55 to 74 years old and have a 30-pack-year history of smoking (20 cigarettes a day for 30 years, 40 cigarettes a day for 15 years, and so on. To calculate your pack years, visit http://smokingpackyears.com/). If the patients are former smokers, they should have quit within the last 15 years.  Doctors should discuss screening with patients only if low dose CT scans and high quality treatment are available in their area, and only if the patient seems healthy and able to undergo treatment in the event that cancer is found.  For all other patients, “there is too much uncertainty regarding the balance of benefits and harms …”

In 2012, the American Lung Association became the first national lung organization—devoted to lung health as opposed to lung cancer—to endorse low dose CT scans for lung cancer screening. Three other organizations have issued guidelines for lung cancer screening on the basis of the National Lung Screening Trial results. Most of the guidelines are fairly similar but there are some key differences. The National Comprehensive Cancer Network (NCCN), a group of the nation’s major cancer centers, for instance, has a broader definition of high risk. Unlike the American Cancer Society, the NCCN allows people to skip annual screenings for an unspecified period of time if they have had 3 years in a row of normal results. The NCCN uses the same definition of high risk as the American Cancer Society but they also have a second definition that includes people as young as 50 and as old as 79 with only a 20-pack-year history—provided they have one other risk factor for lung cancer such as a family history, Chronic Obstructive Pulmonary Disease (COPD), or exposure to radon.  Given the close link between COPD and lung cancer, the Network’s screening criteria could potentially find more cases of lung cancer than the 30-pack criteria. (For more on COPD, read: Chronic Obstructive Lung Disease and Lung Cancer). The American College of Chest Physicians and the American Society of Clinical Oncology also have guidelines.  Only time will tell which guidelines work best, but any of these guidelines make it more likely that insurance companies will pay for screening. As a result of the National Lung Cancer Screening Trial, the U.S. Department of Veterans Affairs is starting to implement a screening program using CT scans for veterans at high risk.  However, most government health programs, such as Medicare and Medicaid, do not usually reimburse for lung cancer screening and might not do so until a public health agency has issued guidelines.

In the past, the lung cancer screening debate focused on the lack of evidence that screening reduced lung cancer deaths. Since the NLST trial, the debate is focusing on the benefits, risks, and cost of low-dose CT scans. Some of the risks include radiation exposure, a high rate of false-positive test results, and over-diagnosis (diagnosis of tumors that are not cancerous or not threatening to the patient).

False Positives

Chest x-rays report fewer false positives than low-dose CT scans, but they usually find large, aggressive tumors that are typical of later stages of lung cancer when treatment is usually not effective. When the men and women who had abnormal findings on either low-dose CT scans or x-rays underwent biopsies, approximately 96% did not have lung cancer. Biopsies can cause serious complications for patients. Since the low-dose CT scans found three times as many abnormal findings compared to x-rays, it resulted in many more false positives, biopsies, and complications. The approximately 1% of smokers screened with the CT scan who were found to have lung cancer would have an improved chance of survival. In contrast, the approximately one in four people screened who had false positive results would be at risk for complications, and those numbers would increase the more often people were screened.18
Computer-aided detection (CAD) methods may enhance the accuracy of CT screening and are being investigated. A European study which incorporated CAD into CT screening found a sensitivity of 95% in accurately detecting lung cancer. This means that out of 100 people at high risk for lung cancer with detected abnormalities, 95 really have lung cancer and 5 people have false-positive results. This same screening method was found to have a specificity of 99% in accurately ruling out disease in patients at high risk for lung cancer, which means that out of 100 people determined not to have lung cancer, only 1 person really does (a “false negative”).36

Over-Diagnosis

Over-diagnosis is the identification of a disease in a person who would never have any symptoms or be harmed by the disease. Over-diagnosis can result in the treatment of pre-cancerous lesions with radiation therapy, hormone therapy, or surgery even though the lesions will never develop into lung cancer.

There are numerous reasons to be concerned about over-diagnosis of lung cancer. Those most likely to be screened are elderly, current or former smokers who may have co-existing medical conditions such as heart disease or emphysema. Scarring in the lungs from years of smoking and related respiratory illnesses can lead to a misdiagnosis of lung cancer, which will require further evaluation.

The testing can itself cause health problems. Radiologic imaging examinations, such as chest x-rays, chest CTs, and FDG-PET scans (fluorodeoxyglucose positron emission tomography), are the most common follow-up measures that are used to determine if additional invasive diagnostic procedures are needed. Radiologic imaging has little short-term risk, but it exposes patients to unnecessary radiation that can be harmful later in life. Invasive procedures, such as needle biopsies, are inserted into the lung to remove tissue samples and determine if there is cancer. This procedure can puncture the lung and cause it to collapse. Bleeding can also occur in the tumor or at the site of the needle insertion. Although very serious complications are rare (less than one in 1,000), they can occur.

Surgery may be necessary for diagnostic evaluation. It is also the preferred treatment for early-stage lung cancer. As with any invasive procedure, there are risks. Age and co-existing medical conditions increase the risk of death or complications from surgery. If a section of the lung is removed to reduce the chance of cancer spreading outside of the lung, then the patient will have reduced respiratory function. This could make breathing more difficult, especially for current and former smokers who already have respiratory issues.

Unnecessary treatment can also lead to pain, lost time at work, increased medical costs, and a reduction in the quality of life.

Radiation Exposure

Low-dose CT scans might result in earlier diagnosis of lung cancer, but radiation exposure from the screening test might actually increase a person’s risk of lung cancer, especially with repeated screenings. Although low-dose CT releases one tenth of the radiation of standard diagnostic CTs, the radiation that is released may act together with smoking to increase the risk of lung cancer. More research is needed to accurately measure the potential risk from exposure to radiation.

The frequency and dose of radiation exposure could affect risk, in addition to smoking history and age. The impact of frequency, dose, and age are still being determined, but risk modeling suggests that the risk of cancer caused by annual low-dose CT screening decreases with age.

Dr. David J. Brenner of Columbia University suggests that there is up to a 5.5% increase in the risk for lung cancer between the ages of 50 and 75 from annual low-dose CT screening of smokers or others at high risk for lung cancer during those 25 years. That risk would be reduced by half if screening was done every 2 years instead. He concludes that the screening method chosen for lung cancer must reduce lung cancer deaths by more than 5.5% to compensate for the potential risk of cancer caused by the CT radiation.37

Costs, Benefits, and Insurance Coverage

On average, low-dose CT scans cost about $300 per screening, making them more expensive than mammograms for breast cancer ($80-$150) and pap smears for cervical cancer ($25-$75). No private insurance agencies (except for WellPoint) cover lung cancer screening with CT scans because it is not currently recommended by the U.S. Preventive Services Task Force. Medicare will cover low-dose CT scans for individuals who meet the following criteria:

  • Age 55-77 years
  • Has a tobacco smoking history of at least 30-pack years
  • Is a current smoker or quit within the past 15 years
  • Receives a written order for a low-dose CT scan from a qualified individual such as a doctor

A 2012 study conducted by actuaries (people trained to calculate the cost of risk and uncertainty) and published in Health Affairs, concluded that CT screening for lung cancer could save thousands of lives at a relatively low cost if it were covered by insurance companies.38 The study examined the costs and benefits of providing high-risk individuals—smokers and long-term former smokers ages 50 to 64—with lung cancer screening using low-dose CT. Most private insurers do not currently cover the screening because evidence of the screening’s cost effectiveness has been scarce or conflicting until now. The researchers found that the screening would cost insurance companies about $247 per member screened annually, and when the total expense of screening was spread over the commercially insured population, the cost was under $1 per insured member per month. According to the study if the screening had been in place for the last 15 years, 130,000 more people under the age of 65 would be alive today, and the cost per life-year saved would be lower than screening for both cervical and breast cancers. The authors acknowledged that actual costs could be higher and the benefits lower if the screenings are not conducted according to best practice guidelines for pricing and follow-up of patients. The study is the first to show that low-dose CT screening is potentially cost-effective and could actually save insurance companies money since lung cancer would often be detected earlier and therefore require less expensive treatment. More importantly, detecting lung cancer early could save lives and improve the quality of life for people diagnosed with lung cancer.

Biomarker Tests for Diagnosis

Biomarker tests, which examine urine, blood, sputum (spit), tissue samples, and even exhaled air, for abnormal levels of certain proteins, antibodies or other substances, are being investigated as another type of diagnostic tool for detecting lung cancer.39  Used together with low-dose CT scans, biomarker tests could potentially result in fewer misdiagnoses and less unnecessary treatment.

What We Still Need to Know and Change

The latest research suggests that lung cancer deaths can be reduced with low-dose CT screening in people who are at increased risk for lung cancer due to heavy smoking, and that annual chest x-rays are not effective regardless of smoking history. Questions remain about who else would benefit from screening (such as non-smokers who live with smokers or have had substantial radon exposure), at what age different groups should begin screening, and how often they should get screened. For now, low-dose CT appears to be the screening method with the most favorable ratio of benefit to harm, but the number of people harmed is quite large compared to the number of people who would benefit. Researchers will continue to search for other less risky and more accurate methods for lung cancer screening.

Funding and Legislation

Lung cancer research has not been a priority at the National Cancer Institute. Research dollars for lung cancer investigations continue to lag far behind other cancers that are less fatal. In fiscal year 2010, the National Cancer Institute spent $631 million for breast cancer research and $300 million for prostate cancer research. Lung cancer, the #1 cancer killer for women and men, received only $282 million. In fact in 2009, lung cancer research funding at NCI was actually reduced from the previous year, while breast and prostate cancer research funding continued to grow. Breast and prostate cancers have benefited from vigorous federal funding, and as a result, have made great strides in the early detection and treatment of the cancers.40

Increased funding is needed to understand gender and racial differences in lung cancer and to continue research at the cellular and molecular levels for targeted, individualized, and less invasive detection and treatment of lung cancer. For more on lung cancer treatments, read here (Lung Cancer is a Women’s Health Issue).

In a 2010 report, the Institute of Medicine recommended that the NCI increase reimbursement from $2000 to $6000 per patient in their studies to encourage investigators in large cooperative groups to increase their involvement in lung cancer research. This reimbursement level has remained unchanged for over 10 years and the IOM report found that investigators limit their involvement in cancer research based on reimbursement concerns. Study participants would also benefit from increased funds. Patients in under-represented groups such as racial and ethnic minorities may be more likely to participate in trials that include reimbursement costs for patient care during the duration of the trial.41

As policy-makers continue to debate about federal research funding, some are proposing that the tobacco industry help underwrite the costs of screening smokers. Most of the state funding for lung cancer prevention activities comes from the 1998 tobacco industry lawsuit. States will collect $25.3 billion this year from the tobacco lawsuit and state taxes from the sale and distribution of tobacco products. However, only about 2% of that revenue will go toward smoking cessation programs. The distribution of settlement money from the lawsuit is at the discretion of states, most of which are using the funding for unrelated state projects because of economic problems that they face. Unfortunately, most states have now reduced funding for prevention and smoking cessation programs to 1999 levels. Although the lawsuit did not stipulate that the settlement money go towards lung cancer prevention, treatment, or early detection programs, progress in finding more effective screening is less likely unless funding from the law suit is used to improve lung cancer screening, diagnosis, and treatment activities.42

There is some pending legislation that may help persuade the federal government to fund more lung cancer research. The Lung Cancer Mortality Reduction Act of 2011 is a bipartisan bill currently in Congress which aims to reduce lung cancer mortality by 50% by 2020.43 The bill, first introduced in 2008, calls on the cooperation of the Department of Health and Human Services, the Department of Defense, and Veterans Affairs to meet that goal and develop a coordinated plan that addresses the prevention, early detection, and treatment of lung cancer. It would require the National Cancer Institute to review and prioritize research grants related to lung cancer, the Food and Drug Administration to establish quality standards and guidelines for facilities that screen for lung cancer using low-dose CT scans, and the Centers for Disease Control and Prevention to establish a Lung Cancer Early Detection Program which would provide low-income, uninsured, and underserved populations at high risk for lung cancer with access to early detection services. For more information and to support this important legislation in the fight against lung cancer, visit http://www.opencongress.org/bill/112-h1394/show.

As lung cancer continues to take lives, increased funding for lung cancer research will be critical for ensuring better screening, earlier diagnosis, more effective treatment, longer survival, and an overall lower mortality for patients diagnosed with the disease. New research will not only benefit smokers and former smokers, but nonsmokers as well who make up 15% of lung cancer cases.