Handb Exp Pharmacol. 2010;(195):355-67. doi: 10.1007/978-3-540-79088-4_16.
Hormonal growth promoting agents in food producing animals.
Stephany RW1.
Author information
Abstract
In contrast to the use of hormonal doping agents in sports to enhance the performance of athletes, in the livestock industry hormonal growth promoters ("anabolics") are used to increase the production of muscle meat.
This leads to international disputes about the safety of meat originating from animals treated with such anabolics.
As a consequence of the total ban in the EU of all hormonal active growth promoters ("hormones") in livestock production, in contrast to their legal use [e.g. of five such hormones (17beta-estradiol, testosterone, progesterone, trenbolone and zeranol) as small solid ear implants and two hormones as feed additives for feedlot heifers (melengestrol acetate) and for swine (ractopamine) in the USA], the regulatory controls also differ sharply between the EU and the USA.
In the EU the treatment of slaughter animals is the regulatory offence that has to be controlled in inspection programs. In the USA testing for compliance of a regulatory maximum residue level in the edible product (muscle, fat, liver or kidney) is the purpose of the inspection program (if any).
The EU inspection programs focus on sample materials that are more suitable for testing for banned substances, especially if the animals are still on the farm, such as urine and feces or hair. In the case of slaughtered animals, the more favored sample materials are bile, blood, eyes and sometimes liver.
Only in rare occasions is muscle meat sampled.
This happens only in the case of import controls or in monitoring programs of meat sampled in butcher shops or supermarkets.
As a result, data on hormone concentrations in muscle meat samples from the EU market are very rare and are obtained in most cases from small programs on an ad hoc basis.
EU data for natural hormones in meat are even rarer because of the absence of "legal natural levels" for these hormones in compliance testing.
With the exception of samples from the application sites - in the EU the site of injection of liquid hormone preparations or the site of application of "pour on" preparations - the hormone concentrations observed in meat samples of illegally treated animals are typically in the range of a few micrograms per kilogram (ppb) down to a few tenths of a microgram per kilogram.
In the EU dozens of illegal hormones are used and the number of active compounds is still expanding. Besides estrogenic, androgenic and progestagenic compounds also thyreostatic, corticosteroidal and beta-adrenergic compounds are used alone or in "smart" combinations.An overview is given of the compounds identified on the EU black market. An estimate is also given of the probability of consumption in the EU of "highly" contaminated meat from the application sites in cattle.
Finally some data are presented on the concentration of estradiol in bovine meat from animals treated and not treated with hormone implants. These data are compared with the recent findings for estradiol concentrations in hen's eggs. From this comparison, the preliminary conclusion is that hen's eggs are the major source of 17alpha- and 17beta-estradiol in the consumer's daily "normal" diet.
lunes, 31 de agosto de 2015
Hormones In Food
Hormones In Food: Should You Worry?
Health.com | By Carina Storrs
Posted: 01/31/2011 8:11 am EST Updated: 05/25/2011 6:30 pm EDT
HORMONES IN FOOD
A salmon that grows to market size twice as fast as normal. Dairy cows that produce 15 percent more milk. Beef cows that grow 20 percent faster.
What do these hyper-productive animals have in common? Thanks to injections and implants (in the case of cows) or genetic engineering (in the case of salmon), they contain artificially high levels of sex or growth hormones.
Are these hormones dangerous to the humans who eat the food or drink the milk? The food industry says no -- and the Food and Drug Administration (FDA) agrees, at least when it comes to cows.
The FDA, which regulates the use of hormones in livestock, hasn't yet decided whether it will approve the sale of a genetically engineered salmon patented by the biotech company AquaBounty. If the salmon -- which is wired to produce growth hormone year-round, instead of just in the spring and summer -- gets an OK from the agency, it will be the first genetically engineered animal to wind up on your dinner plate. (Genetically engineered fruits and vegetables have been around for years.)
The FDA's stamp of approval isn't likely to reassure those who worry that excess hormones in the food supply are contributing to cancer, early puberty in girls, and other health problems in humans. For years, consumer advocates and public health experts have fought to limit the use of hormones in cows, and some support a ban on the practice similar to the one in place in Europe, where food regulations are generally more stringent than in the U.S.
But it's not clear if such hormones truly are bad for our health. Surprisingly little research has been done on the health effects of these hormones in humans, in part because it's difficult to separate the effects of added hormones from the mixture of natural hormones, proteins, and other components found in milk and meat. Buying organic may reassure shoppers, but there's little proof these products are indeed safer.
Growth Hormones
In 1993, the FDA approved recombinant bovine growth hormone (rBGH), a synthetic cow hormone that spurs milk production when injected into dairy cows, and consumer groups have been concerned about it ever since. The manipulation of growth hormone in the AquaBounty salmon has sparked similar concerns.
By itself, rBGH has no discernible effect in humans and is of little concern to your health, and the growth hormone in AquaBounty's salmon is expected to be inconsequential to your health as well. The actual fear is that manipulating growth hormones in cows -- or salmon -- may increase another hormone, insulin-like growth factor (IGF), which could mimic the effects of human growth hormone in harmful ways. In fact, research has found that milk from rBGH-treated cows contains up to 10 times more IGF than other milk.
Higher blood levels of IGF (regardless of what causes them) have been associated with an increased risk of breast, prostate, and other cancers in humans. In a 2004 study, patients with above-average IGF levels had nearly a 50 percent higher risk of prostate cancer and a 65 percent higher risk of hormone-dependent premenopausal breast cancer than people with below-average levels.
Many factors -- including genes, smoking, and fat intake -- contribute to these cancers, but "it's very likely that at least part of that [risk] is related to IGF levels," especially where prostate cancer is concerned, says Walter Willett, M.D., chairman of the department of nutrition at the Harvard School of Public Health, in Boston.
While consuming lots of milk and other dairy has been shown to raise blood levels of human IGF, the increase is probably not a direct effect of the animal's IGF level or the IGF found in these foods. That's because the amount of IGF in dairy products -- whether or not it's from rBGH-treated cows -- pales in comparison to what is naturally in your body.
"Just [to get] the amount of IGF secreted in your saliva and digestive tract in a day, you'd have to drink about 95 quarts of milk," says Terry Etherton, Ph.D., a professor of dairy and animal science at Pennsylvania State University and the author of a blog about food biotechnology.
And you'd have to eat at least 170 three-ounce servings of genetically modified salmon. (The IGF levels in the AquaBounty salmon and regular salmon are comparable, although consumer advocates say the studies that determined this are too small to be reliable.)
So if the amount of IGF in milk is negligible, how does milk consumption increase our IGF levels? Milk in general -- and the proteins, sugar, minerals, and non-IGF hormones it contains -- may somehow cause the human body to make more of its own IGF, Dr. Willett says.
Sex Hormones and Early Puberty
IGF isn't the only hormone found in the food supply. Ranchers have been fattening up cattle with sex hormones -- most notably estrogen -- since the 1950s. Today most beef cows in the U.S. -- except those labeled "organic" -- receive an implant in their ear that delivers a hormone, usually a form of estrogen (estradiol) in some combination with five other hormones. (These hormones are not given to chicken and pigs because they don't have the same growth-promoting effect in these animals, although antibiotics are given to all three species for similar growth-promoting reasons.)
One concern is that such hormones may spur earlier puberty in children, who are, on average, entering puberty at a younger age than they did a generation or two ago, for reasons that are unclear.
But Ann Macrina, Ph.D., a researcher in the Department of Dairy and Animal Science at Pennsylvania State University, says that the amount of estrogen found in meat is vanishingly small compared to the level in our bodies. A three-ounce serving of beef from an estrogen-treated cow contains less than a billionth of a gram of estrogen, a level around 400,000 times lower than estrogen in women and nearly 100,000 times lower than that in men.
However, even miniscule amounts of estrogen could affect prepubescent girls and boys, says Dr. Willett. "[For] a girl who's not producing hormones herself, they could be quite substantial."
A 2009 study found that children who consumed the most protein from animal sources entered puberty about seven months earlier than those who consumed the least. "It doesn't matter so much if it's milk, cheese, or meat -- all these animal proteins have a clear impact on [our] IGF system," says Thomas Remer, Ph.D., one of the authors of the study and a professor at the Research Institute of Child Nutrition, in Germany.
Still, hormones added to the food supply are probably not the biggest culprit behind early puberty. It's more likely that meat, milk, and similar foods help trigger earlier puberty because they are rich in protein, calories, and nutrients, says Marcia Herman-Giddens, an adjunct professor at the University of North Carolina School of Public Health, in Chapel Hill, and the lead author of an influential 1997 study on early puberty in girls.
However, Herman-Giddens cautions that more research is needed to untangle the many factors involved. For instance, she says, rising rates of overweight and obesity -- and the processed foods, high-calorie drinks, and lack of exercise driving them -- are "probably the biggest reason" for the trend toward earlier puberty. (Fat cells stimulate the body to produce estrogen.) Pesticides, flame-retardants, plastics, and other chemicals in the environment that can disrupt hormones may also be partly to blame.
Organic Or Not?
Organic beef and dairy products certified by the U.S. Department of Agriculture (USDA) come with the guarantee that the cows were not treated with rBGH or sex hormones. They also come with a much heftier price. Is the peace of mind worth the extra cash?
Probably not, says Dr. Willett, who advocates cutting back on meat in general. Most people should eat no more than two servings of red meat per week, Dr. Willett says, and "if you're [only] having a couple of servings a week, it doesn't make much difference whether it's organic or not."
Dr. Willett offers similar advice regarding organic dairy. On the other hand, experts like Herman-Giddens urge consumers to stay away from rBGH-treated milk because of its potentially higher IGF levels, and the fact that it does not have any added health benefits over regular milk. Instead of switching to organic milk, Dr. Willett recommends cutting back on dairy altogether, despite USDA recommendations that call for three servings a day of dairy.
Bruce Chassy, Ph.D., a professor of food microbiology at the University of Illinois at Urbana-Champaign, says "propaganda" from organic farming groups has created misconceptions about -- and resistance to -- rBGH among consumers. In fact, Chassy argues that manipulating growth hormones has benefits: rBGH-treated cows are better for the environment, not just the bottom line, since farmers can get the same amount of milk with fewer cows. Similarly, the AquaBounty salmon consumes 10 percent less feed during its lifecycle than a regular farmed salmon.
The most lasting effect of the fears surrounding hormones in the food supply may be the value of "organic" or "hormone free" as selling points, Chassy says.
"I think there are a lot of farms that are not using [rBGH] because they perceive that consumers do not want [rBGH]-treated milk," he says. He predicts that the AquaBounty salmon will likely inspire "marketing campaigns for 'hormone-free' fish." It's a ridiculous claim, he argues, since all fish -- and all meat and milk -- has hormones.
sábado, 29 de agosto de 2015
Food safety and Persistent organic pollutants (POPs) WHO
Food safety
Persistent organic pollutants (POPs)
About POPs
Persistent organic pollutants (POPs) are chemicals of global concern due to their potential for long-range transport, persistence in the environment, ability to bio-magnify and bio-accumulate in ecosystems, as well as their significant negative effects on human health and the environment. Humans are exposed to these chemicals in a variety of ways: mainly through the food we eat, but also through the air we breathe, in the outdoors, indoors and at the workplace. Many products used in our daily lives may contain POPs, which have been added to improve product characteristics, such as as flame retardants or surfactants. As a result, POPs can be found virtually everywhere on our planet in measurable concentrations.
The most commonly encountered POPs are organochlorine pesticides, such as DDT, industrial chemicals, most notably polychlorinated biphenyls (PCB), as well as unintentional by-products of many industrial processes, especially polychlorinated dibenzo-p-dioxins (PCDD) and dibenzofurans (PCDF), commonly known as 'dioxins'.
POPs bio-magnify throughout the food chain and bio-accumulate in organisms. The highest concentrations of POPs are thus found in organisms at the top of the food chain. Consequently, background levels of POPs can be found in the human body.
Human exposure - for some compounds and scenarios, even to low levels of POPs - can lead, among others, to increased cancer risk, reproductive disorders, alteration of the immune system, neurobehavioural impairment, endocrine disruption, genotoxicity and increased birth defects.
Biomonitoring of human milk for POPs
Since 1976 WHO through its GEMS/Food Programme has collected and evaluated information on levels of persistent organic pollutants in foods, including human milk.
Over the period 1987-2003, it has coordinated three international studies of human milk to assess the levels and trends of polychlorinated dibenzodioxins, polychlorinated dibenzofurans and dioxin-like polychlorinated biphenyls.
Analysis of human milk, maternal blood and adipose tissue are all relevant matrices for assessment of body burdens for persistent organic pollutants. However, human milk is recognized as the preferred matrix because has several important advantages.
Biomonitoring of human milk data can provide information on the exposure of the mother as well as the infants. Furthermore, such information provide guidance on the need for measures to reduce levels of this substances in food, which is the main source of exposures for most people.
More recently, it has been recognized that human milk is an ideal matrix to generally monitor levels of persistent organic pollutants in the environment.
In 2004, the Stockholm Convention on Persistent Organic Pollutants was ratified by governments to decrease environmental and human exposure to twelve priority substances in this class.
The revised WHO guidelines for developing a national protocol describe the basic study design that can be used to monitor human exposure over time in order to, among other things, see if the Stockholm agreement is actually effective in reducing the release of these chemicals into the environment.
These guidelines continue to support the monitoring of persistent organic contaminants for human health and food-chain contamination purposes.
The protocol was designed based on the advice of experts in the field (see ad hoc WHO Human Milk Survey Advisory Group) and on extensive experience of certain countries in undertaking similar surveys using human samples, including human milk.
In order to promote reliability and comparability, participating countries are encouraged to adhere as closely to this protocol as possible. Ethical issues, including informed consent of donors and confidentiality, are major considerations in this protocol.
Given that breastfeeding reduces child mortality and has health benefits that extend into adulthood, every effort has been made to protect, promote and support breastfeeding in the context of these studies.
PCBs and dioxins in salmon
A survey reported in the journal Science (09.01.04) compared the level of organochlorine contaminants, including PCBs and dioxins, in farmed versus wild salmon collected from around the world. Most organochlorine substances analysed in the study show a significantly higher level of contamination in farmed than in wild salmon.
This study is the largest conducted so far, in particular relating to the direct comparison between farmed and wild salmon. The results reported specifically for dioxins and PCBs are well within the range of previous studies. Dioxins and dioxin-like compounds are important substances that can affect human health.
They are persistent environmental pollutants that enrich via the food chain. Dioxins and PCBs are associated with industrial discharges, including discharges into the sea, and ocean fish have varying levels of these substances often directly related to the proximity of their habitat to discharge areas.
The level in farmed fish normally reflects the contamination level of the feed used, which has been also shown in above mentioned study by the detection of dioxins and PCBs in commercial fish feed.
WHO, in collaboration with FAO, has considered dioxins and dioxin-like compounds on several occasions. Most recently in June 2001, the Joint FAO/WHO Expert Committee on Food Additives (JECFA) examined new evidence on the toxicity of these chemicals and established a Provisional Tolerable Monthly Intake (PTMI) of 70 picograms of dioxins and dioxin-like PCBs.
When evaluating standard diets in different parts of the world the results indicated that the estimated intakes of these chemicals approach or exceed this PTMI.
Based on the mean contamination levels reported in above study, eating one or two portions per week of farmed salmon would result in a monthly intake below this level. However, an overall dietary risk assessment would require inclusion of other dietary sources of dioxins and dioxin-like PCBs.
In order to address these risks, several steps have been taken to reduce or eliminate emissions of dioxins, dioxin-like PCBs and other related persistent organic pollutants (often referred to as POPs). Many countries have now implemented the Stockholm Convention on POPs (2001), which suggests to end commercial use of 12 POPs and reduce or eliminate their emission into the environment.
To monitor reduction in human exposure WHO and UNEP run a monitoring program for POPs in breastmilk. A steady decline in levels has been observed since 1980 for most countries.
In regard to food contamination, the FAO/WHO Codex Alimentarius Commission, which is a risk management body comprised of 169 member countries, is developing a draft code of practice for dioxins and dioxin-like PCBs in food, which identifies source-directed measures to reduce their presence in food, including fish, as well as a position paper, which provides an evaluation of the need for possible regulatory measures, such as limits in food and feed.
The results of this new study in salmon and other studies should be used to maintain the focus on reducing the exposure of humans to dioxins and dioxin-like PCBs. Specifically, efforts to reduce the level of such substances in animals used for human consumption should be actively supported, in particular source-directed measures such as reduction of contamination levels in animal feed.
FAO and WHO consider fish to be an important component of a nutritious diet, and that the risk of consuming contaminated fish must be weighted in view of the beneficial nutritive effects of fish.
FAO and WHO plan to develop general guidance for such risk-benefit considerations, with the contamination of fish as case studies.
Toxic equivalency factors (TEFs) for dioxins and dioxin-like compounds
Dioxins occur as a complex mixture in the environment and in food. More than 90% of human exposure is through food, mainly meat and dairy products, fish and shellfish.
In order to assess the potential health risk of the whole mixture, the concept of toxic equivalence has been applied to this group of structurally and biologically related contaminants.
TCDD, the most toxic member of the family, is used as reference compound, and all other dioxins are assigned a toxic potency relative to TCDD, based on experimental studies.
These international TEFs have been developed for application in risk assessment and management, and have been adopted formally for regulatory purposes by a number of countries and regional bodies, including Canada, the European Union, Japan and the United States of America.
During the last 15 years, WHO, through the International Programme on Chemical Safety (IPCS), has established and regularly re-evaluated toxic equivalency factors (TEFs) for dioxins and related compounds through expert consultations.
WHO-TEF values have been established in 1998 which apply to humans, mammals, birds and fish. The last consultation was held in 2005 to update human and mammalian TEFs. Details on the process and outcome can be found through the links below.
International Programme on Chemical Safety
Persistent organic pollutants (POPs)
About POPs
Persistent organic pollutants (POPs) are chemicals of global concern due to their potential for long-range transport, persistence in the environment, ability to bio-magnify and bio-accumulate in ecosystems, as well as their significant negative effects on human health and the environment. Humans are exposed to these chemicals in a variety of ways: mainly through the food we eat, but also through the air we breathe, in the outdoors, indoors and at the workplace. Many products used in our daily lives may contain POPs, which have been added to improve product characteristics, such as as flame retardants or surfactants. As a result, POPs can be found virtually everywhere on our planet in measurable concentrations.
The most commonly encountered POPs are organochlorine pesticides, such as DDT, industrial chemicals, most notably polychlorinated biphenyls (PCB), as well as unintentional by-products of many industrial processes, especially polychlorinated dibenzo-p-dioxins (PCDD) and dibenzofurans (PCDF), commonly known as 'dioxins'.
POPs bio-magnify throughout the food chain and bio-accumulate in organisms. The highest concentrations of POPs are thus found in organisms at the top of the food chain. Consequently, background levels of POPs can be found in the human body.
Human exposure - for some compounds and scenarios, even to low levels of POPs - can lead, among others, to increased cancer risk, reproductive disorders, alteration of the immune system, neurobehavioural impairment, endocrine disruption, genotoxicity and increased birth defects.
Biomonitoring of human milk for POPs
Since 1976 WHO through its GEMS/Food Programme has collected and evaluated information on levels of persistent organic pollutants in foods, including human milk.
Over the period 1987-2003, it has coordinated three international studies of human milk to assess the levels and trends of polychlorinated dibenzodioxins, polychlorinated dibenzofurans and dioxin-like polychlorinated biphenyls.
Analysis of human milk, maternal blood and adipose tissue are all relevant matrices for assessment of body burdens for persistent organic pollutants. However, human milk is recognized as the preferred matrix because has several important advantages.
Biomonitoring of human milk data can provide information on the exposure of the mother as well as the infants. Furthermore, such information provide guidance on the need for measures to reduce levels of this substances in food, which is the main source of exposures for most people.
More recently, it has been recognized that human milk is an ideal matrix to generally monitor levels of persistent organic pollutants in the environment.
In 2004, the Stockholm Convention on Persistent Organic Pollutants was ratified by governments to decrease environmental and human exposure to twelve priority substances in this class.
The revised WHO guidelines for developing a national protocol describe the basic study design that can be used to monitor human exposure over time in order to, among other things, see if the Stockholm agreement is actually effective in reducing the release of these chemicals into the environment.
These guidelines continue to support the monitoring of persistent organic contaminants for human health and food-chain contamination purposes.
The protocol was designed based on the advice of experts in the field (see ad hoc WHO Human Milk Survey Advisory Group) and on extensive experience of certain countries in undertaking similar surveys using human samples, including human milk.
In order to promote reliability and comparability, participating countries are encouraged to adhere as closely to this protocol as possible. Ethical issues, including informed consent of donors and confidentiality, are major considerations in this protocol.
Given that breastfeeding reduces child mortality and has health benefits that extend into adulthood, every effort has been made to protect, promote and support breastfeeding in the context of these studies.
PCBs and dioxins in salmon
A survey reported in the journal Science (09.01.04) compared the level of organochlorine contaminants, including PCBs and dioxins, in farmed versus wild salmon collected from around the world. Most organochlorine substances analysed in the study show a significantly higher level of contamination in farmed than in wild salmon.
This study is the largest conducted so far, in particular relating to the direct comparison between farmed and wild salmon. The results reported specifically for dioxins and PCBs are well within the range of previous studies. Dioxins and dioxin-like compounds are important substances that can affect human health.
They are persistent environmental pollutants that enrich via the food chain. Dioxins and PCBs are associated with industrial discharges, including discharges into the sea, and ocean fish have varying levels of these substances often directly related to the proximity of their habitat to discharge areas.
The level in farmed fish normally reflects the contamination level of the feed used, which has been also shown in above mentioned study by the detection of dioxins and PCBs in commercial fish feed.
WHO, in collaboration with FAO, has considered dioxins and dioxin-like compounds on several occasions. Most recently in June 2001, the Joint FAO/WHO Expert Committee on Food Additives (JECFA) examined new evidence on the toxicity of these chemicals and established a Provisional Tolerable Monthly Intake (PTMI) of 70 picograms of dioxins and dioxin-like PCBs.
When evaluating standard diets in different parts of the world the results indicated that the estimated intakes of these chemicals approach or exceed this PTMI.
Based on the mean contamination levels reported in above study, eating one or two portions per week of farmed salmon would result in a monthly intake below this level. However, an overall dietary risk assessment would require inclusion of other dietary sources of dioxins and dioxin-like PCBs.
In order to address these risks, several steps have been taken to reduce or eliminate emissions of dioxins, dioxin-like PCBs and other related persistent organic pollutants (often referred to as POPs). Many countries have now implemented the Stockholm Convention on POPs (2001), which suggests to end commercial use of 12 POPs and reduce or eliminate their emission into the environment.
To monitor reduction in human exposure WHO and UNEP run a monitoring program for POPs in breastmilk. A steady decline in levels has been observed since 1980 for most countries.
In regard to food contamination, the FAO/WHO Codex Alimentarius Commission, which is a risk management body comprised of 169 member countries, is developing a draft code of practice for dioxins and dioxin-like PCBs in food, which identifies source-directed measures to reduce their presence in food, including fish, as well as a position paper, which provides an evaluation of the need for possible regulatory measures, such as limits in food and feed.
The results of this new study in salmon and other studies should be used to maintain the focus on reducing the exposure of humans to dioxins and dioxin-like PCBs. Specifically, efforts to reduce the level of such substances in animals used for human consumption should be actively supported, in particular source-directed measures such as reduction of contamination levels in animal feed.
FAO and WHO consider fish to be an important component of a nutritious diet, and that the risk of consuming contaminated fish must be weighted in view of the beneficial nutritive effects of fish.
FAO and WHO plan to develop general guidance for such risk-benefit considerations, with the contamination of fish as case studies.
Toxic equivalency factors (TEFs) for dioxins and dioxin-like compounds
Dioxins occur as a complex mixture in the environment and in food. More than 90% of human exposure is through food, mainly meat and dairy products, fish and shellfish.
In order to assess the potential health risk of the whole mixture, the concept of toxic equivalence has been applied to this group of structurally and biologically related contaminants.
TCDD, the most toxic member of the family, is used as reference compound, and all other dioxins are assigned a toxic potency relative to TCDD, based on experimental studies.
These international TEFs have been developed for application in risk assessment and management, and have been adopted formally for regulatory purposes by a number of countries and regional bodies, including Canada, the European Union, Japan and the United States of America.
During the last 15 years, WHO, through the International Programme on Chemical Safety (IPCS), has established and regularly re-evaluated toxic equivalency factors (TEFs) for dioxins and related compounds through expert consultations.
WHO-TEF values have been established in 1998 which apply to humans, mammals, birds and fish. The last consultation was held in 2005 to update human and mammalian TEFs. Details on the process and outcome can be found through the links below.
International Programme on Chemical Safety
Triple-Negative Breast Cancer and Checkpoint Inhibitors
Checkpoint Inhibitors Show Promise in Triple-Negative Breast Cancer | Page 1
Tony Hagen @oncobiz
Published Online: Friday, August 28, 2015
Rita Nanda, MD
Rita Nanda, MD
Immune checkpoint inhibitors can be of significant value in combatting recurrent and metastatic triple negative breast cancer (TNBC), Rita Nanda, MD, told physicians at the recent 14th Annual International Congress on the Future of Breast Cancer.
“Immunology has arrived. It’s going to remain an important tool in the fight against cancer for a variety of tumors, and I think breast cancer is certainly going to be one of them,” said Nanda, a medical oncologist at University of Chicago Medical Center and the lead author on one of the studies involving pembrolizumab (Keytruda).
Nanda said her conclusion was justified by the results of two trials involving PD-L1 inhibitors: the KEYNOTE-012 trial, in which patients were treated with pembrolizumab, and a second trial involving atezolizumab (MPDL3280A) led by Leisha A. Emens, MD, PhD, of the Cancer Immunology and the Breast and Ovarian Cancer Programs at the Johns Hopkins Kimmel Cancer Center.1,2
The checkpoint inhibitors were used in heavily pretreated populations, and demonstrated safety and low toxicity while achieving good responses, Nanda said. “They certainly demonstrated single-agent activity, and I think the question now is what combinations can further build on this promise,” Nanda said.
TNBCs are associated with worse clinical outcomes and continue to represent an important clinical challenge, Nanda said. Lending support to the use of immunotherapy in TNBC is the fact that estrogen receptor (ER)–negative tumors have a higher density of tumor infiltrating lymphocytes (TIL) than ER positive tumors, Nanda said. TILs play an important role in killing tumor cells.
In addition, Vanderbuilt University researcher Brian D Lehmann and his colleagues have identified TNBC subtypes that may aid in guiding patients toward targeted therapies, Nanda said. Furthermore, TNBCs “are generally unstable, are prone to genetic mutations, and produce neoantigens, which in turn can stimulate immunity,” she said.
The high expression of PD-L1 in TNBC tumor cells leads to suppression of T-cell function. Pembrolizumab binds to PD-1 on inactive T cells and blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby enabling T cells to activate in the fight against tumor cells.
KEYNOTE-012 enrolled patients with a variety of different tumor types. Patients in the TNBC portion had metastatic or recurrent TNBC, an ECOG performance status of 0 or 1, and tumors testing positive for PD-L1 expression. Patients were not on systemic steroid therapy, and they did not have autoimmune disease or active brain metastases. They received intravenous pembrolizumab at 10 mg/kg every 2 weeks. Nanda originally reported on the phase 1b study in December at the 2014 San Antonio Breast Cancer Symposium.
Statistics on durability of response and survival were impressive, Nanda said, though the primary endpoints of the study were focused on safety, tolerability, and clinical activity. Secondary objectives included assessments of progression-free survival (PFS), overall survival, and response duration.
The trial enrolled 32 females with a mean age of 51.9 years. The prior treatment statistics were taxane, 93.8%; anthracycline, 78.1%; capecitabine, 65.6%; platinum, 59.3%; and eribulin, 21.9%. “Just under half of patients had had 3 or more prior lines of therapy for metastatic disease and almost 90% had previously received treatment in the early stage setting,” Nanda said.
The most common treatment-related adverse events of any grade included arthralgia, fatigue, myalgia, and nausea. “These were generally grade 1 to 2 and were very mild and easily managed,” Nanda said. Adverse events (AE) of a potentially immune-mediated nature, regardless of attribution, included pruritus (n = 3; all grade 1-2), hepatitis (n = 1; grade 3), and hypothyroidism (n = 1; grade 2).
There were four grade 3 events and one grade 4 event. There was one AE related to treatment that resulted in death, attributed to disseminated intravascular coagulation. “While it was certainly possible this was related to study-based therapy, I will mention that there are thousands of patients who received pembrolizumab for other tumor types. This hasn’t been a recurrent theme, so it’s certainly reassuring to us,” Nanda said.
Among 27 patients evaluable for response, the overall response rate was 18.5% (n = 5). The responses included 1 complete response, 4 partial responses (14.8%), 7 instances of stable disease (25.9%), and 12 instances of progressive disease (44.4%) at a median follow-up of 9.9 months.
“Responses were actually not limited to patients who had very few treatments,” Nanda said. “In fact, 4 of the 5 responders had had 3 or more lines of therapy for advanced breast cancer. Also the majority of these patients had also had neoadjuvant or adjuvant chemotherapy.”
The overall clinical benefit rate with pembrolizumab was 44%. The median progression-free survival (PFS) was 1.9 months. At 6 months, 23.3% of patients remained progression free. The median time to response was 18 weeks.
“You can see how durable these responses were,” Nanda said. “At the time of last data analysis, 3 of the patients who responded to study-based therapy remained on treatment, 2 had discontinued, and at the median follow-up of 10 months, the median duration of response had not yet been achieved.”
Nanda described the PFS in this very heavily pretreated patient population with a new checkpoint inhibition monotherapy as “quite impressive,” adding, “When we’re thinking about a relatively aggressive form of breast cancer in patients who have been heavily pretreated, that’s not generally what we see with chemotherapy in this setting.”
She said the trial of atezolizumab was similarly exciting. It demonstrated a 19% objective response rate, with 75% of responses ongoing in pretreated patients with metastatic TNBC, at the analysis. “Much like pembrolizumab, the goal of inhibition here was to stimulate the T cells to become active, to recognize cancer and to destroy it,” Nanda said.
In the multicenter phase Ia study, 54 patients with mTNBC received IV atezolizumab at 15 mg/kg, 20 mg/kg, or a flat 1200 mg dose every 3 weeks. At baseline, 69% of patients tested positive for PD-L1 expression.
The median age of patients enrolled in the study was 48 years. Patients had an ECOG PS of 0 or 1; 59% had visceral metastases; and 11% had bone metastases, according to the abstract. In addition, 85% received ≥4 prior systemic regimens, including taxanes (82%), anthracyclines (78%), carboplatin (41%), and cisplatin (15%).
Among 21 evaluable patients who were PD-L1¬–positive, 9.5% had complete responses, and 9.5% had partial responses. At the analysis, 75% of responses were ongoing, with a median not yet reached (range: 18-56+ weeks).
“Patients had an excellent performance, as approximately 70% had visceral disease, and again, we’re looking at a very heavily pretreated population,” Nanda said. “One in 10 patients did experience a grade 3 adverse event, and there were 2 deaths that occurred while on study therapy. The etiology of these deaths was ongoing at the time of the presentation [at the 2015 AACR annual meeting].”
Based on the durable responses and the safety and tolerability of the checkpoint inhibitors in these trials, Nanda said, the stage is set for further investigation.
“There are a lot of therapies that immune checkpoint inhibition can be combined with. You could potentially combine immune checkpoint inhibitors with each other or with chemotherapy, radiation therapy, and targeted therapies.”
She said vaccines up until now have been disappointments, but that in combination with other therapies, it may be possible to make vaccines work. - See more at: http://www.onclive.com/web-exclusives/checkpoint-inhibitors-show-promise-in-triple-negative-breast-cancer/2#sthash.HuhVxWVQ.dpuf
Tony Hagen @oncobiz
Published Online: Friday, August 28, 2015
Rita Nanda, MD
Rita Nanda, MD
Immune checkpoint inhibitors can be of significant value in combatting recurrent and metastatic triple negative breast cancer (TNBC), Rita Nanda, MD, told physicians at the recent 14th Annual International Congress on the Future of Breast Cancer.
“Immunology has arrived. It’s going to remain an important tool in the fight against cancer for a variety of tumors, and I think breast cancer is certainly going to be one of them,” said Nanda, a medical oncologist at University of Chicago Medical Center and the lead author on one of the studies involving pembrolizumab (Keytruda).
Nanda said her conclusion was justified by the results of two trials involving PD-L1 inhibitors: the KEYNOTE-012 trial, in which patients were treated with pembrolizumab, and a second trial involving atezolizumab (MPDL3280A) led by Leisha A. Emens, MD, PhD, of the Cancer Immunology and the Breast and Ovarian Cancer Programs at the Johns Hopkins Kimmel Cancer Center.1,2
The checkpoint inhibitors were used in heavily pretreated populations, and demonstrated safety and low toxicity while achieving good responses, Nanda said. “They certainly demonstrated single-agent activity, and I think the question now is what combinations can further build on this promise,” Nanda said.
TNBCs are associated with worse clinical outcomes and continue to represent an important clinical challenge, Nanda said. Lending support to the use of immunotherapy in TNBC is the fact that estrogen receptor (ER)–negative tumors have a higher density of tumor infiltrating lymphocytes (TIL) than ER positive tumors, Nanda said. TILs play an important role in killing tumor cells.
In addition, Vanderbuilt University researcher Brian D Lehmann and his colleagues have identified TNBC subtypes that may aid in guiding patients toward targeted therapies, Nanda said. Furthermore, TNBCs “are generally unstable, are prone to genetic mutations, and produce neoantigens, which in turn can stimulate immunity,” she said.
The high expression of PD-L1 in TNBC tumor cells leads to suppression of T-cell function. Pembrolizumab binds to PD-1 on inactive T cells and blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby enabling T cells to activate in the fight against tumor cells.
KEYNOTE-012 enrolled patients with a variety of different tumor types. Patients in the TNBC portion had metastatic or recurrent TNBC, an ECOG performance status of 0 or 1, and tumors testing positive for PD-L1 expression. Patients were not on systemic steroid therapy, and they did not have autoimmune disease or active brain metastases. They received intravenous pembrolizumab at 10 mg/kg every 2 weeks. Nanda originally reported on the phase 1b study in December at the 2014 San Antonio Breast Cancer Symposium.
Statistics on durability of response and survival were impressive, Nanda said, though the primary endpoints of the study were focused on safety, tolerability, and clinical activity. Secondary objectives included assessments of progression-free survival (PFS), overall survival, and response duration.
The trial enrolled 32 females with a mean age of 51.9 years. The prior treatment statistics were taxane, 93.8%; anthracycline, 78.1%; capecitabine, 65.6%; platinum, 59.3%; and eribulin, 21.9%. “Just under half of patients had had 3 or more prior lines of therapy for metastatic disease and almost 90% had previously received treatment in the early stage setting,” Nanda said.
The most common treatment-related adverse events of any grade included arthralgia, fatigue, myalgia, and nausea. “These were generally grade 1 to 2 and were very mild and easily managed,” Nanda said. Adverse events (AE) of a potentially immune-mediated nature, regardless of attribution, included pruritus (n = 3; all grade 1-2), hepatitis (n = 1; grade 3), and hypothyroidism (n = 1; grade 2).
There were four grade 3 events and one grade 4 event. There was one AE related to treatment that resulted in death, attributed to disseminated intravascular coagulation. “While it was certainly possible this was related to study-based therapy, I will mention that there are thousands of patients who received pembrolizumab for other tumor types. This hasn’t been a recurrent theme, so it’s certainly reassuring to us,” Nanda said.
Among 27 patients evaluable for response, the overall response rate was 18.5% (n = 5). The responses included 1 complete response, 4 partial responses (14.8%), 7 instances of stable disease (25.9%), and 12 instances of progressive disease (44.4%) at a median follow-up of 9.9 months.
“Responses were actually not limited to patients who had very few treatments,” Nanda said. “In fact, 4 of the 5 responders had had 3 or more lines of therapy for advanced breast cancer. Also the majority of these patients had also had neoadjuvant or adjuvant chemotherapy.”
The overall clinical benefit rate with pembrolizumab was 44%. The median progression-free survival (PFS) was 1.9 months. At 6 months, 23.3% of patients remained progression free. The median time to response was 18 weeks.
“You can see how durable these responses were,” Nanda said. “At the time of last data analysis, 3 of the patients who responded to study-based therapy remained on treatment, 2 had discontinued, and at the median follow-up of 10 months, the median duration of response had not yet been achieved.”
Nanda described the PFS in this very heavily pretreated patient population with a new checkpoint inhibition monotherapy as “quite impressive,” adding, “When we’re thinking about a relatively aggressive form of breast cancer in patients who have been heavily pretreated, that’s not generally what we see with chemotherapy in this setting.”
She said the trial of atezolizumab was similarly exciting. It demonstrated a 19% objective response rate, with 75% of responses ongoing in pretreated patients with metastatic TNBC, at the analysis. “Much like pembrolizumab, the goal of inhibition here was to stimulate the T cells to become active, to recognize cancer and to destroy it,” Nanda said.
In the multicenter phase Ia study, 54 patients with mTNBC received IV atezolizumab at 15 mg/kg, 20 mg/kg, or a flat 1200 mg dose every 3 weeks. At baseline, 69% of patients tested positive for PD-L1 expression.
The median age of patients enrolled in the study was 48 years. Patients had an ECOG PS of 0 or 1; 59% had visceral metastases; and 11% had bone metastases, according to the abstract. In addition, 85% received ≥4 prior systemic regimens, including taxanes (82%), anthracyclines (78%), carboplatin (41%), and cisplatin (15%).
Among 21 evaluable patients who were PD-L1¬–positive, 9.5% had complete responses, and 9.5% had partial responses. At the analysis, 75% of responses were ongoing, with a median not yet reached (range: 18-56+ weeks).
“Patients had an excellent performance, as approximately 70% had visceral disease, and again, we’re looking at a very heavily pretreated population,” Nanda said. “One in 10 patients did experience a grade 3 adverse event, and there were 2 deaths that occurred while on study therapy. The etiology of these deaths was ongoing at the time of the presentation [at the 2015 AACR annual meeting].”
Based on the durable responses and the safety and tolerability of the checkpoint inhibitors in these trials, Nanda said, the stage is set for further investigation.
“There are a lot of therapies that immune checkpoint inhibition can be combined with. You could potentially combine immune checkpoint inhibitors with each other or with chemotherapy, radiation therapy, and targeted therapies.”
She said vaccines up until now have been disappointments, but that in combination with other therapies, it may be possible to make vaccines work. - See more at: http://www.onclive.com/web-exclusives/checkpoint-inhibitors-show-promise-in-triple-negative-breast-cancer/2#sthash.HuhVxWVQ.dpuf
Intravesical Immunotherapy for Bladder Cancer with MCNA
FDA Grants Intravesical Immunotherapy Priority Review for Bladder Cancer
Silas Inman @silasinman
Published Online: Friday, August 28, 2015
Michael J. Berendt
Michael J. Berendt, PhD
The FDA has assigned a priority review designation to the intravesical immunotherapy MCNA as a treatment for patients with high-risk non-muscle invasive bladder cancer following first-line bacillus Calmette-Guérin (BCG) therapy, according to a statement from the drug's developers, Telesta Therapeutics.
The priority review was based on findings from an open-label phase III trial, which demonstrated significant activity with MCNA, an immunotherapy that is comprised of mycobacterial cell wall fragments complexed with nucleic acids. Under this review program, the FDA will make a decision on the application for the treatment by February 27, 2016. Prior to this date, the agency announced plans to hold an advisory meeting to discuss the application.
In the pivotal open-label phase III study, 25% of patients treated with MCNA remained disease-free at 1-year, which met the criteria established for the primary endpoint of the study. At 2-years, the disease-free survival (DFS) rate was 19%. In patients with papillary only tumors, the DFS rate was 35.1% and 32.2% at 1 and 2 years, respectively.
Telesta submitted the biologics license application (BLA) for MCNA to the FDA in June 2015. At this time, the FDA waived $2.3 million in user fees associated with the application. Certain waivers for fees exist under the Prescription Drug User Fee Act, specifically for small companies filing their first new drug application. A new treatment has not been approved for patients with high-risk bladder cancer since 1998.
"Today is a historic day for Telesta Therapeutics and for all of our staff and collaborators who have worked so diligently to advance our new treatment for non-muscle invasive bladder cancer towards potential regulatory approval early next year," Michael J. Berendt, PhD, chief executive officer and chief scientist at Telesta, said in a statement. "While we recognize that the FDA must complete its full review of our BLA filing before rendering its ultimate decision, we are working extremely hard, at all levels, to prepare for commercial launch in the United States."
In the phase III study, 129 patients were treated with an induction dose of MCNA at 8 mg weekly. After 3 months of induction therapy, those who remained disease-free went on to receive a maintenance dose from months 3 to 24. In this portion of the study, MCNA was given in 3 weekly installments every 3 months.
Of the patients enrolled, 91 had carcinoma in situ with or without papillary disease and 38 had papillary only tumors. Most patients had high-risk disease, 107 were BCG-refractory, and 68 patients had received 2 or more prior BCG induction courses. The primary endpoint of the study was DFS rate at 1 year.
At a median 34.7-month follow-up, the median disease-free duration in responders was 32.7 months. The progression-free survival (PFS) rate at 1-year was 87.3%. At year 2 and 3, the PFS rate with MCNA was 79.8% and 77.7%, respectively.
Adverse events (AEs) experienced by patients in the trial were mild to moderate in severity and did not frequently lead to treatment discontinuation. Only 2 serious AEs were considered to be treatment-related (hematuria and urinary tract infection).
Findings from the phase III study exploring MCNA were initially presented at the 2011 AUA Annual Meeting. At the time of this presentation, Endo Pharmaceuticals and Bioniche Life Sciences were developing the treatment. In 2012, Endo returned global rights for the medication to Bioniche, which later rebranded itself as Telesta in 2014.
As part of the submission process for MCNA, Telesta completed a number of upgrades and improvements to its manufacturing facility and operating procedures. These upgrades were completed in February 2015, prior to an FDA pre-approval inspection under their formal review process.
In June 2015, Telesta, which is based in Canada, received a patent for MCNA in the United States, providing intellectual property (IP) protection for the immunotherapy for 16 years.
"We are extremely pleased with the issuance of this US composition of matter patent, which provides strong IP coverage in the largest and most important commercial market for MCNA," Berendt said. "This patent is a key component of our IP portfolio and will provide intellectual property protection for at least 16 years, which is a major advantage as we look forward to commercial approval in 2016.”
- See more at: http://www.onclive.com/web-exclusives/fda-grants-intravesical-immunotherapy-priority-review-for-bladder-cancer#sthash.iCABNURl.dpuf
Silas Inman @silasinman
Published Online: Friday, August 28, 2015
Michael J. Berendt
Michael J. Berendt, PhD
The FDA has assigned a priority review designation to the intravesical immunotherapy MCNA as a treatment for patients with high-risk non-muscle invasive bladder cancer following first-line bacillus Calmette-Guérin (BCG) therapy, according to a statement from the drug's developers, Telesta Therapeutics.
The priority review was based on findings from an open-label phase III trial, which demonstrated significant activity with MCNA, an immunotherapy that is comprised of mycobacterial cell wall fragments complexed with nucleic acids. Under this review program, the FDA will make a decision on the application for the treatment by February 27, 2016. Prior to this date, the agency announced plans to hold an advisory meeting to discuss the application.
In the pivotal open-label phase III study, 25% of patients treated with MCNA remained disease-free at 1-year, which met the criteria established for the primary endpoint of the study. At 2-years, the disease-free survival (DFS) rate was 19%. In patients with papillary only tumors, the DFS rate was 35.1% and 32.2% at 1 and 2 years, respectively.
Telesta submitted the biologics license application (BLA) for MCNA to the FDA in June 2015. At this time, the FDA waived $2.3 million in user fees associated with the application. Certain waivers for fees exist under the Prescription Drug User Fee Act, specifically for small companies filing their first new drug application. A new treatment has not been approved for patients with high-risk bladder cancer since 1998.
"Today is a historic day for Telesta Therapeutics and for all of our staff and collaborators who have worked so diligently to advance our new treatment for non-muscle invasive bladder cancer towards potential regulatory approval early next year," Michael J. Berendt, PhD, chief executive officer and chief scientist at Telesta, said in a statement. "While we recognize that the FDA must complete its full review of our BLA filing before rendering its ultimate decision, we are working extremely hard, at all levels, to prepare for commercial launch in the United States."
In the phase III study, 129 patients were treated with an induction dose of MCNA at 8 mg weekly. After 3 months of induction therapy, those who remained disease-free went on to receive a maintenance dose from months 3 to 24. In this portion of the study, MCNA was given in 3 weekly installments every 3 months.
Of the patients enrolled, 91 had carcinoma in situ with or without papillary disease and 38 had papillary only tumors. Most patients had high-risk disease, 107 were BCG-refractory, and 68 patients had received 2 or more prior BCG induction courses. The primary endpoint of the study was DFS rate at 1 year.
At a median 34.7-month follow-up, the median disease-free duration in responders was 32.7 months. The progression-free survival (PFS) rate at 1-year was 87.3%. At year 2 and 3, the PFS rate with MCNA was 79.8% and 77.7%, respectively.
Adverse events (AEs) experienced by patients in the trial were mild to moderate in severity and did not frequently lead to treatment discontinuation. Only 2 serious AEs were considered to be treatment-related (hematuria and urinary tract infection).
Findings from the phase III study exploring MCNA were initially presented at the 2011 AUA Annual Meeting. At the time of this presentation, Endo Pharmaceuticals and Bioniche Life Sciences were developing the treatment. In 2012, Endo returned global rights for the medication to Bioniche, which later rebranded itself as Telesta in 2014.
As part of the submission process for MCNA, Telesta completed a number of upgrades and improvements to its manufacturing facility and operating procedures. These upgrades were completed in February 2015, prior to an FDA pre-approval inspection under their formal review process.
In June 2015, Telesta, which is based in Canada, received a patent for MCNA in the United States, providing intellectual property (IP) protection for the immunotherapy for 16 years.
"We are extremely pleased with the issuance of this US composition of matter patent, which provides strong IP coverage in the largest and most important commercial market for MCNA," Berendt said. "This patent is a key component of our IP portfolio and will provide intellectual property protection for at least 16 years, which is a major advantage as we look forward to commercial approval in 2016.”
- See more at: http://www.onclive.com/web-exclusives/fda-grants-intravesical-immunotherapy-priority-review-for-bladder-cancer#sthash.iCABNURl.dpuf
miércoles, 26 de agosto de 2015
Chemical Farming and Planned Obsolescence
Designed to Fail: GMOs, Chemical Farming and Planned Obsolescence
Designed to fail
Barbara H. Peterson
Farm Wars
One of the most important things to remember when dealing with companies such as Monsanto, Dow, DuPont, etc., is that they are first and foremost chemical manufacturing companies.
The genetically engineered seeds (GMO) they produce are designed to increase pesticide usage, not decrease it. Their own pesticides, that is. Sold by companies that are… remember… first and foremost, chemical manufacturing companies, with profit as their sole reason for existence.
Feeding the starving world? Marketing strategy, nothing more. These companies exist to sell chemicals, and pesticides are a mainstay.
Planned Obsolescence
Our society is based on unlimited consumption and planned obsolescence. This is by design, and it all started with the light bulb.
Planned Obsolescence Documentary
Did you know that the lifetime of light bulbs once used to last for more than 2500 hours and was reduced on purpose to just 1000 hours? Did you know that nylon stockings once used to be that stable that you could even use them as tow rope for cars and its quality was reduced just to make sure that you will soon need a new one? Did you know that you might have a tiny little chip inside your printer that was just placed there so that your device will break after a predefined number of printed pages thereby assuring that you buy a new one? Did you know that Apple originally did not intend to offer any battery exchange service for their iPods/iPhones/iPads just to enable you to continuously contribute to the growth of this corporation?
This strategy was maybe first thought through already in the 19th century and later on for example motivated by Bernhard London in 1932 in his paper Ending the Depression Through Planned Obsolescence.
The intentional design and manufacturing of products with a limited lifespan to assure repeated purchases is denoted as planned/programmed obsolescence and we are all or at least most of us upright and thoroughly participating in this doubtful endeavor.
Or did you not recently think about buying a new mobile phone / computer / car / clothes / because your old one unexpectedly died or just because of this very cool new feature that you oh so badly need?
We are conditioned to want the latest and greatest gadget, a new car every year, and to have the mega-mart down the street supply us with groceries. These goods are shipped around the world, with little regard for the ultimate cost to our health or the environment that such a long distance mentality causes.
The food is irradiated, chemically lobotomized, and made to withstand long periods of travel. The fruit and veggies you get at the market most likely have come from a cold storage unit across the country, or even across the globe. Fresh? Good luck with that.
Chemical Agriculture Designed to Fail
Our agricultural system is designed to fail just like the light bulb. Why? Because it is much more profitable for chemical companies to continue to sell “new and improved” chemicals to solve the problems that the original chemicals caused due to resistance. They know it will happen, and plan ahead for it.
Resistance is a given, so a system based on increased chemical resistance and the necessity to purchase new chemicals to combat it is designed to fail so that the companies can reap more profit from new products when it does.
Just as the truth is that chemical companies exist primarily to sell chemicals, another inconvenient truth is that chemical usage breeds resistance. This is a known issue.
No matter how “new and improved” your product is, resistance will build up, and more, stronger chemicals will need to be used down the road to manage it.
Planned Obsolescence.
Throw the old away, get the new, improved, stronger chemical, and don’t worry, in a couple of years, when resistance builds up to that one, we will be sure and have another in the works to solve your problem. Only the problem is never really solved.
For farmers this means that weeds are building resistance to Roundup just as bacteria build up a resistance to antibiotics, and equine worms have built a resistance to chemical de-wormers.
Any “new and improved” chemicals will only succumb to the same resistance, and while it may be a bad thing for you and me, the chemical companies are laughing all the way to the bank. Planned Obsolescence. It can’t go on indefinitely, and you will pay through the nose for patented seeds and proprietary chemicals that will only get more expensive and more toxic unless you ditch the practice of chemical farming.
As for the people eating these polluted creations of the chemical giants? Well, they will just keep making the doctors and lawyers rich beyond measure as they limp towards an early grave.
The solution? Local, non-GMO, fresh food grown at home and at the neighbor’s place.
Small, organic neighborhood mini-farms designed to take care of the community and the family.
We can either choose to continue throwing our money into a system that was designed to fail from the start through planned obsolescence and make the chemical companies rich in the process, or begin to take responsibility for our own food supply, and not some faceless corporation that relies on our ignorance to lead us all the way to the grave with chemicalized, radiated, genetically engineered foodstuffs that are designed to fail and make those who eat them fail, one disease at a time, as doctors shove “new and improved” chemical concoctions down the throats of those who have succumbed to the onslaught.
©2014 Barbara H. Peterson
Designed to fail
Barbara H. Peterson
Farm Wars
One of the most important things to remember when dealing with companies such as Monsanto, Dow, DuPont, etc., is that they are first and foremost chemical manufacturing companies.
The genetically engineered seeds (GMO) they produce are designed to increase pesticide usage, not decrease it. Their own pesticides, that is. Sold by companies that are… remember… first and foremost, chemical manufacturing companies, with profit as their sole reason for existence.
Feeding the starving world? Marketing strategy, nothing more. These companies exist to sell chemicals, and pesticides are a mainstay.
Planned Obsolescence
Our society is based on unlimited consumption and planned obsolescence. This is by design, and it all started with the light bulb.
Planned Obsolescence Documentary
Did you know that the lifetime of light bulbs once used to last for more than 2500 hours and was reduced on purpose to just 1000 hours? Did you know that nylon stockings once used to be that stable that you could even use them as tow rope for cars and its quality was reduced just to make sure that you will soon need a new one? Did you know that you might have a tiny little chip inside your printer that was just placed there so that your device will break after a predefined number of printed pages thereby assuring that you buy a new one? Did you know that Apple originally did not intend to offer any battery exchange service for their iPods/iPhones/iPads just to enable you to continuously contribute to the growth of this corporation?
This strategy was maybe first thought through already in the 19th century and later on for example motivated by Bernhard London in 1932 in his paper Ending the Depression Through Planned Obsolescence.
The intentional design and manufacturing of products with a limited lifespan to assure repeated purchases is denoted as planned/programmed obsolescence and we are all or at least most of us upright and thoroughly participating in this doubtful endeavor.
Or did you not recently think about buying a new mobile phone / computer / car / clothes / because your old one unexpectedly died or just because of this very cool new feature that you oh so badly need?
We are conditioned to want the latest and greatest gadget, a new car every year, and to have the mega-mart down the street supply us with groceries. These goods are shipped around the world, with little regard for the ultimate cost to our health or the environment that such a long distance mentality causes.
The food is irradiated, chemically lobotomized, and made to withstand long periods of travel. The fruit and veggies you get at the market most likely have come from a cold storage unit across the country, or even across the globe. Fresh? Good luck with that.
Chemical Agriculture Designed to Fail
Our agricultural system is designed to fail just like the light bulb. Why? Because it is much more profitable for chemical companies to continue to sell “new and improved” chemicals to solve the problems that the original chemicals caused due to resistance. They know it will happen, and plan ahead for it.
Resistance is a given, so a system based on increased chemical resistance and the necessity to purchase new chemicals to combat it is designed to fail so that the companies can reap more profit from new products when it does.
Just as the truth is that chemical companies exist primarily to sell chemicals, another inconvenient truth is that chemical usage breeds resistance. This is a known issue.
No matter how “new and improved” your product is, resistance will build up, and more, stronger chemicals will need to be used down the road to manage it.
Planned Obsolescence.
Throw the old away, get the new, improved, stronger chemical, and don’t worry, in a couple of years, when resistance builds up to that one, we will be sure and have another in the works to solve your problem. Only the problem is never really solved.
For farmers this means that weeds are building resistance to Roundup just as bacteria build up a resistance to antibiotics, and equine worms have built a resistance to chemical de-wormers.
Any “new and improved” chemicals will only succumb to the same resistance, and while it may be a bad thing for you and me, the chemical companies are laughing all the way to the bank. Planned Obsolescence. It can’t go on indefinitely, and you will pay through the nose for patented seeds and proprietary chemicals that will only get more expensive and more toxic unless you ditch the practice of chemical farming.
As for the people eating these polluted creations of the chemical giants? Well, they will just keep making the doctors and lawyers rich beyond measure as they limp towards an early grave.
The solution? Local, non-GMO, fresh food grown at home and at the neighbor’s place.
Small, organic neighborhood mini-farms designed to take care of the community and the family.
We can either choose to continue throwing our money into a system that was designed to fail from the start through planned obsolescence and make the chemical companies rich in the process, or begin to take responsibility for our own food supply, and not some faceless corporation that relies on our ignorance to lead us all the way to the grave with chemicalized, radiated, genetically engineered foodstuffs that are designed to fail and make those who eat them fail, one disease at a time, as doctors shove “new and improved” chemical concoctions down the throats of those who have succumbed to the onslaught.
©2014 Barbara H. Peterson
Planned obsolescence
Planned obsolescence The Economist
Mar 23rd 2009 | Online extra
Planned obsolescence is a business strategy in which the obsolescence (the process of becoming obsolete—that is, unfashionable or no longer usable) of a product is planned and built into it from its conception. This is done so that in future the consumer feels a need to purchase new products and services that the manufacturer brings out as replacements for the old ones.
Consumers sometimes see planned obsolescence as a sinister plot by manufacturers to fleece them. But Philip Kotler, a marketing guru (see article), says: “Much so-called planned obsolescence is the working of the competitive and technological forces in a free society—forces that lead to ever-improving goods and services.”
A classic case of planned obsolescence was the nylon stocking. The inevitable “laddering” of stockings made consumers buy new ones and for years discouraged manufacturers from looking for a fibre that did not ladder. The garment industry in any case is not inclined to such innovation. Fashion of any sort is, by definition, deeply committed to built-in obsolescence. Last year's skirts, for example, are designed to be replaced by this year's new models.
The strategy of planned obsolescence is common in the computer industry too. New software is often carefully calculated to reduce the value to consumers of the previous version. This is achieved by making programs upwardly compatible only; in other words, the new versions can read all the files of the old versions, but not the other way round. Someone holding the old version can communicate only with others using the old version. It is as if every generation of children came into the world speaking a completely different language from their parents. While they could understand their parents' language, their parents could not understand theirs.
The production processes required for such a strategy are illustrated by Intel. This American semiconductor firm is working on the production of the next generation of PC chips before it has begun to market the last one.
A strategy of planned obsolescence can backfire. If a manufacturer produces new products to replace old ones too often, consumer resistance may set in. This has occurred at times in the computer industry when consumers have been unconvinced that a new wave of replacement products is giving sufficient extra value for switching to be worth their while.
As the life cycle of products has increased—largely because of their greater technical excellence—firms have found that they need to plan for those products' obsolescence more carefully. Take, for instance, the example of the automobile. Its greater durability has made consumers reluctant to change their models as frequently as they used to. As the useful life of the car has been extended, manufacturers have focused on shortening its fashionable life. By adding styling and cosmetic changes to their vehicles, they have subtly attempted to make their older models look outdated, thus persuading consumers to trade them in for new ones.
Planned obsolescence is obviously not a strategy for the luxury car market. Marques such as Rolls-Royce rely on propagating the idea that they may (like antiques) one day be worth more than the price that was first paid for them; Patek Philippe advertises its watches as being something that the owner merely conserves for the next generation. At the same time as the useful life of consumer goods becomes shorter, consumers hanker after goods that endure.
Further reading
Slade, G., “Made to Break: Technology and Obsolescence in America”, Harvard University Press, 2006
martes, 25 de agosto de 2015
Food additives, safety, and organic foods ACS.
ACS Guidelines on Nutrition and Physical Activity for Cancer Prevention
Food additives, safety, and organic foods
The previous sections point to food choices that might lower a person's risk of cancer. Many people are also interested in other aspects of food intake and their potential impact on cancer risk.
Food additives and contaminants
Many substances are added to foods to prolong shelf and storage life and to enhance color, flavor, and texture. The possible role of food additives in cancer risk is an area of great public interest.
New food additives must be cleared by the US Food and Drug Administration (FDA) before being allowed into the food supply, and thorough testing is done in lab animals to determine any effects on cancer as part of this process. Additives are usually present in very small quantities in food, and some are nutrients that may have beneficial effects (for example, vitamins C and E are sometimes added to food products as a preservative).
Other compounds find their way into the food supply through agricultural use, animal farming, or food processing, even if their use is not directly intended for human consumption. Examples include growth hormones or antibiotics used in animal farming, small amounts of pesticides and herbicides in plant-based foods, and compounds such as bisphenol A (BPA) or phthalates that enter food from packaging. Some of these compounds are not known to directly cause cancer, but they may influence cancer risk in other ways – for example, by acting as hormone-like substances in the body.
Unintended contamination of food may also result in exposure to chemicals that are a cause of concern and may be related to cancer risk. Examples include heavy metals such as cadmium or mercury. These metals may enter the food supply if they build up the food chain, such as from fish, or they may enter through contamination or their natural presence in soil or water.
For many other compounds for which the effects on cancer risk are not clear, there may be other good reasons to limit exposure. But at the levels that these are found in the food supply, lowering cancer risk is unlikely to be a major reason to justify this.
Food processing
Food processing may also alter foods in ways that might affect cancer risk. An example is the refining of grains, which greatly lowers the amount of fiber and other compounds that may reduce cancer risk.
The processing of meat, by adding preservatives such as salt or sodium nitrite to prevent the growth of germs, or smoking the meat to preserve or enhance color and flavor, may add compounds that might increase the potential of these foods to cause cancer. Studies have linked eating large amounts of processed meats with an increased risk of colorectal cancer. This may be due to nitrites, which are added to many lunch meats, hams, hot dogs, and other processed meats.
Some food processing, such as freezing and canning vegetables and fruits, can preserve vitamins and other components that may decrease cancer risk. Cooking or heat-treating (such as when canning) vegetables breaks down the plant cell walls and may allow the helpful compounds in these foods to be more easily digested. But some of these methods may also lower the content of some heat-sensitive vitamins, such as vitamin C and some B vitamins.
Irradiated foods
Irradiation of food products is one way to limit the risk of germ contamination and food poisoning. In the United States, some foods, such as spices, are routinely irradiated. Irradiated meats and other foods are also widely available. Because radiation is known to cause cancer, there has been concern that food irradiation may present a cancer risk. However, radiation does not remain in foods that have been irradiated.
Organic foods
Concern about the possible effects of food additives on health, including cancer, is one reason that many people are now interested in organic foods. Organic foods are often promoted as an alternative to foods grown with conventional methods that use chemical pesticides and herbicides, hormones, or antibiotics. These compounds cannot be used for foods labeled as "organic." Organic foods, as defined by the US Department of Agriculture (USDA), also exclude genetically modified foods or foods that have been irradiated.
Whether organic foods carry a lower risk of cancer because they are less likely to be contaminated by compounds that might cause cancer is largely unknown.
Several studies have looked at the nutrient content of organic versus conventionally grown fruits or vegetables, and while some studies suggest a higher nutrient content, others suggest no difference. It is not known if the nutritional differences that have been reported would result in health benefits such as a reduced cancer risk.
Vegetables, fruits, and whole grains should form the central part of a person's diet, regardless of whether they are grown conventionally or organically.
Last Medical Review: 01/11/2012
Last Revised: 04/09/2015
Endocrine Disruptors and Plastics.
Dangerous Plastics, Safe Plastics
From toys to water bottles, we're all surrounded by dangerous plastics. Here’s how to choose safe plastics.
By Linda B. White, M.D.
August/September 2009
You’ve been out — working, exercising, shopping. You open the car door and slip into the ovenlike interior. Throat dry, you reach for the water bottle that’s been sitting in the cup holder all day. It’s warm. But at least it’s water, right? Water, yes, albeit water potentially spiked with chemicals that migrated out of the plastic — chemicals that aren’t good for your health.
The latest scientific research has given us a lot of good reasons to think carefully about how we use plastics. The main concern with several types of plastic is that they contain endocrine disruptors — substances that, when taken into our bodies, alter normal hormonal function. Over the past several years, scientists and the media have struggled to find answers to mysteries such as precocious puberty, declining fertility rates in otherwise healthy adults, hyperactivity in kids, the fattening of America, and the persistent scourges of prostate cancer and breast cancer.
Although multiple factors play a role in all of these conditions, one recurrent theme is the brew of endocrine disruptors infiltrating our lives.
Effects of Endocrine Disruptors
Endocrine disruptors (which are now widespread in food, water, soil and even the air we breathe) include a long list of chemicals such as dioxins, cadmium, parabens, bisphenol A, phthalates, polychlorinated biphenyls (PCBs), agricultural chemicals, polybrominated flame retardants, and some of the active ingredients in sunscreens.
Many of these chemicals cause problems because they can mimic the action of natural estrogen.
These foreign estrogens (also known as xenoestrogens) can upset normal hormonal balance, stimulate the growth and development of reproductive tumors (breast, uterine, prostate), impair fertility, and disrupt pregnancy. Worse, many can cross the placenta to affect the fetus and get into breast milk.
Chemicals such as phthalates have an antiandrogenic effect, meaning they interfere with testosterone and other hormones responsible for male sex characteristics. Exposure to these agents during fetal life and early childhood can derail normal sexual development and heighten the risk for diseases that don’t become apparent until adulthood, such as cancer.
Problems with BPA
One of the most troubling endocrine disruptors is a common ingredient in plastic called bisphenol A (commonly called BPA). According to Laura N. Vandenberg, who holds a doctorate in cell, molecular and developmental biology and works at the Center for Developmental and Regenerative Biology at Tufts University, “BPA is one of the highest volume chemicals produced worldwide, with over 6 billion pounds produced each year.”
Used to produce polycarbonate plastics and epoxy resins, BPA is found in many drinking containers, the lining of most food and beverage cans (including soda cans), bottle caps, plastic cutlery, plastic food storage containers, toys, dental sealants, some dental composites, water pipes, eyeglass lenses, and more.
Polycarbonate is often blended with other plastics to create products such as mobile phone cases, car parts, electronic equipment, medical equipment, and household items. Because BPA is in printer ink, newspapers, and carbonless receipts, most recycled paper contains it, including paper towels and paper used to contain food.
The problem is that BPA migrates from the plastic into neighboring substances such as food, water, and saliva. Heat, contact with acidic (think vinegar or soda), and alkaline (think baking soda) substances, and repeated washing of polycarbonate plastics accelerate the process. BPA also leaches into groundwater from plastics piled in landfills.
Although most of our intake is dietary, BPA can also be inhaled, and can move across the skin into our blood by means of bath water.
Because it is so pervasive, we all have BPA on board.
One study by the Centers for Disease Control and Prevention found BPA in 95 percent of urine samples.
It’s also present in blood, amniotic fluid, fetal tissues, ovarian fluid, and breast milk.
Infants and small children take in more BPA than adults because — relative to their size — they breathe, drink and eat more, put everything within reach into their mouths, and don’t clear the chemical from their bodies as fast as adults.
Information on the potential dangers of BPA comes mostly from animal research. In lab rats and mice, even low doses during early development alter the reproductive hormone cycles in males and females. Specifically, females have earlier puberty, increased mammary (breast) development, prolonged estrous cycles (the equivalent of menstrual cycles), chromosomal abnormalities in their eggs, and other fertility problems.
Males have decreased testosterone levels, fewer and less motile sperm, more abnormal sperm, increased prostate size, and changes reflecting a heightened risk for prostate cancer. In some studies, both males and females tend to weigh more and have more body fat. Exposure during fetal development can alter brain structure and function, and lead to subsequent behavioral changes, such as increased aggressiveness, impaired motor activity, anxious behavior, and impaired learning.
Risk assessment reports before 2004 — particularly those funded by groups such as the American Plastics Council — dismissed the dangers to humans on the grounds that levels in humans fell short of the concentrations that caused ill effects in test-tube and animal studies.
However, Frederick vom Saal, who holds a doctorate in neurobiology and is a prominent researcher and professor at the University of Missouri, notes that of the 115 low-dose BPA studies published by the end of 2004, 94 found estrogen-like effects in animals. More pointedly, he says, “No industry funded studies have reported significant effects of low doses of BPA, although more than 90 percent of government funded studies have reported significant effects.”
In 2007, the University of North Carolina’s Chapel Hill Bisphenol A Expert Panel, which included Vandenberg and 38 other experts, published a report stating that human exposure levels are well within the range that has proven harmful to rats and mice.
Furthermore, these adverse effects in lab animal studies mirror health conditions that have been on the rise in humans over the past 50 years: infertility, breast and prostate cancer, type-2 diabetes, obesity, attention deficit disorder, cardiovascular diseases, autism, and abnormal development of the penis. More research is needed to confirm these correlations.
Despite the Panel’s report, the U.S. National Toxicology Program’s (NTP) Center for the Evaluation of Risks to Human Reproduction issued a brief in April 2008 that fell short of sounding the alarm. In June 2008, the NTP Board of Scientific Counselors further downgraded some of the potential risks. In a nutshell, the NTP voiced “some concern” for neural and behavioral effects and effects on the prostate gland in fetuses, infants and children at current exposures.
For the same age group, they said there is “minimal concern” about effects on the breast and on earlier puberty in girls. For adults, the concern about exposures adversely affecting pregnancy outcomes or the health of reproductive organs was “negligible.”
Among the long list of experts that responded to the NTP brief, the American Academy of Pediatrics said the report’s downplaying of the risks, particularly for infants and pregnant women, would falsely reassure the public. Sarah Janssen, science fellow for the Natural Resources Defense Council, responded to the brief more bluntly: “BPA should be considered a hazard to human development and reproduction with clear evidence of adverse effects.”
While the U.S. Food and Drug Administration maintains current levels of BPA are safe for humans, the Canadian government declared BPA toxic in April 2008, triggering a ban on the use of BPA in baby bottles.
But in October, a group of scientific advisers to the U.S. FDA rejected the assessment, stating that the agency had ignored crucial studies and employed flawed methods in its research. As the FDA risk assessment continues, some states are proposing legislation that would ban many plastics containing BPA.
Trouble with Phthalates
Phthalates represent another ubiquitous category of endocrine disruptors. Used to soften plastic, these chemicals pop up in PVC-containing plastic products, including:
• children’s toys
• personal care products (cosmetics, nail polish, hair spray, deodorant, shampoos, body washes, perfumes)
• air fresheners
• insect repellents
• detergents and other cleaning products
• lubricants
• vinyl products (shower curtains, raincoats, vinyl flooring)
• medical equipment (tubing, bags for intravenous fluids, vinyl gloves)
• the plastic in breast pumps
• the outer coating on many pills
• garden hoses
• pool liners
• modeling clay
• food packaging
With respect to pacifiers and baby bottle nipples, most companies have switched to latex- and silicone-based materials in their manufacturing.
Because phthalates aren’t tightly bound to plastics, they readily migrate into neighboring substances such as food, water, air, and saliva. Phthalates are thus present in our urine, blood, breast milk, saliva, amniotic fluid, and seminal fluid.
The biggest health concern is reproductive toxicity — particularly for males.
Numerous animal studies link phthalate exposure during fetal development with malformations of parts of the male reproductive system. Reports of ill effects in females aren’t as numerous, although higher levels of these chemicals have been associated with early breast development in girls and endometriosis in women.
Phthalates in indoor air have been associated with asthma and allergic conditions.
In 2005, the European Union banned three phthalate compounds from children’s toys and other children’s products.
California has passed a law limiting exposure to di(2-ethylhexyl) phthalate (commonly known as DEHP). And Minnesota, Maryland, Maine, and Oregon have proposed similar legislation. Washington state recently passed the Children’s Safe Products Act to protect kids from exposure to lead, cadmium and phthalates.
________________________________________
Keeping BPA Out of Food and Beverages
In addition to the potential health risks, there are many more reasons to reduce your use of plastic food containers, dishes, and cutlery. Plastics consume resources that are largely nonrenewable (crude oil and natural gas), their use contributes to needless waste, and their production and degradation create pollution. Here are a few BPA safety tips for food and drink.
• Can the cans. “Canned foods are likely to be the highest contributor to BPA in our diets, not plastics,” says Vandenberg. Also, she says parents should buy powdered rather than liquid infant formula, because the former has less exposure to the BPA lining the can.
• If you use plastic wrap, try to find one that doesn’t contain BPA. Vandenberg says the trouble is that companies are not required to tell you what’s in plastic wrap, adding, “Studies show that many stretch wraps contain BPA and other endocrine disruptors.”
• Warm and store food in ceramic or glass containers. The label “microwave safe” on a plastic food container only means that the plastic won’t melt. If the product contains BPA, it will leach into your food faster when warm.
• Make sure baby bottles, pacifiers and toys for infants and toddlers are BPA-free.
• Avoid bottled water, especially in plastic bottles. According to Food & Water Watch, bottled water is more expensive and no safer than tap water. In fact, it is often bottled tap water.
• Use metal or wooden utensils when you cook. Use wooden rather than plastic cutting boards, and clean thoroughly after use.
• Bring your own, BPA-free containers for leftovers and take-away foods.
• Recycle. Plastic containers and packaging are clogging our landfills and leaching endocrine disruptors into groundwater, plus marring the landscape and injuring wildlife.
________________________________________
How to Avoid Phthalates
Avoiding phthalates is challenging because manufacturers aren’t required to list them as product ingredients.
• Look for “phthalate-free” on the label of personal care products (especially nail polish). For information on product ingredients, check the Campaign for Safe Cosmetics website.
• Use fragrance-free detergents, cleansers and personal care products. Artificial fragrances commonly use diethyl phthalate (DEP).
• Avoid products made of vinyl plastic usually labelled as No. 3 (raincoats, shower curtains) and polyvinyl chloride (PVC pipe, other building materials, some lawn furniture, and some children’s and pets’ toys).
Note: In 2007, the Natural Resources Defense Council tested 14 common air fresheners. Although none of them listed phthalates as an ingredient, 12 of the 14 contained these chemicals, including those advertised as unscented or “all natural.” Read the NRDC's full report on phthalates and air fresheners.
You can find links to the reference materials for this article in the Plastics and Endocrine Disruptors Article Resources, below. Plus, follow FDA reviews and regulation updates.
From toys to water bottles, we're all surrounded by dangerous plastics. Here’s how to choose safe plastics.
By Linda B. White, M.D.
August/September 2009
You’ve been out — working, exercising, shopping. You open the car door and slip into the ovenlike interior. Throat dry, you reach for the water bottle that’s been sitting in the cup holder all day. It’s warm. But at least it’s water, right? Water, yes, albeit water potentially spiked with chemicals that migrated out of the plastic — chemicals that aren’t good for your health.
The latest scientific research has given us a lot of good reasons to think carefully about how we use plastics. The main concern with several types of plastic is that they contain endocrine disruptors — substances that, when taken into our bodies, alter normal hormonal function. Over the past several years, scientists and the media have struggled to find answers to mysteries such as precocious puberty, declining fertility rates in otherwise healthy adults, hyperactivity in kids, the fattening of America, and the persistent scourges of prostate cancer and breast cancer.
Although multiple factors play a role in all of these conditions, one recurrent theme is the brew of endocrine disruptors infiltrating our lives.
Effects of Endocrine Disruptors
Endocrine disruptors (which are now widespread in food, water, soil and even the air we breathe) include a long list of chemicals such as dioxins, cadmium, parabens, bisphenol A, phthalates, polychlorinated biphenyls (PCBs), agricultural chemicals, polybrominated flame retardants, and some of the active ingredients in sunscreens.
Many of these chemicals cause problems because they can mimic the action of natural estrogen.
These foreign estrogens (also known as xenoestrogens) can upset normal hormonal balance, stimulate the growth and development of reproductive tumors (breast, uterine, prostate), impair fertility, and disrupt pregnancy. Worse, many can cross the placenta to affect the fetus and get into breast milk.
Chemicals such as phthalates have an antiandrogenic effect, meaning they interfere with testosterone and other hormones responsible for male sex characteristics. Exposure to these agents during fetal life and early childhood can derail normal sexual development and heighten the risk for diseases that don’t become apparent until adulthood, such as cancer.
Problems with BPA
One of the most troubling endocrine disruptors is a common ingredient in plastic called bisphenol A (commonly called BPA). According to Laura N. Vandenberg, who holds a doctorate in cell, molecular and developmental biology and works at the Center for Developmental and Regenerative Biology at Tufts University, “BPA is one of the highest volume chemicals produced worldwide, with over 6 billion pounds produced each year.”
Used to produce polycarbonate plastics and epoxy resins, BPA is found in many drinking containers, the lining of most food and beverage cans (including soda cans), bottle caps, plastic cutlery, plastic food storage containers, toys, dental sealants, some dental composites, water pipes, eyeglass lenses, and more.
Polycarbonate is often blended with other plastics to create products such as mobile phone cases, car parts, electronic equipment, medical equipment, and household items. Because BPA is in printer ink, newspapers, and carbonless receipts, most recycled paper contains it, including paper towels and paper used to contain food.
The problem is that BPA migrates from the plastic into neighboring substances such as food, water, and saliva. Heat, contact with acidic (think vinegar or soda), and alkaline (think baking soda) substances, and repeated washing of polycarbonate plastics accelerate the process. BPA also leaches into groundwater from plastics piled in landfills.
Although most of our intake is dietary, BPA can also be inhaled, and can move across the skin into our blood by means of bath water.
Because it is so pervasive, we all have BPA on board.
One study by the Centers for Disease Control and Prevention found BPA in 95 percent of urine samples.
It’s also present in blood, amniotic fluid, fetal tissues, ovarian fluid, and breast milk.
Infants and small children take in more BPA than adults because — relative to their size — they breathe, drink and eat more, put everything within reach into their mouths, and don’t clear the chemical from their bodies as fast as adults.
Information on the potential dangers of BPA comes mostly from animal research. In lab rats and mice, even low doses during early development alter the reproductive hormone cycles in males and females. Specifically, females have earlier puberty, increased mammary (breast) development, prolonged estrous cycles (the equivalent of menstrual cycles), chromosomal abnormalities in their eggs, and other fertility problems.
Males have decreased testosterone levels, fewer and less motile sperm, more abnormal sperm, increased prostate size, and changes reflecting a heightened risk for prostate cancer. In some studies, both males and females tend to weigh more and have more body fat. Exposure during fetal development can alter brain structure and function, and lead to subsequent behavioral changes, such as increased aggressiveness, impaired motor activity, anxious behavior, and impaired learning.
Risk assessment reports before 2004 — particularly those funded by groups such as the American Plastics Council — dismissed the dangers to humans on the grounds that levels in humans fell short of the concentrations that caused ill effects in test-tube and animal studies.
However, Frederick vom Saal, who holds a doctorate in neurobiology and is a prominent researcher and professor at the University of Missouri, notes that of the 115 low-dose BPA studies published by the end of 2004, 94 found estrogen-like effects in animals. More pointedly, he says, “No industry funded studies have reported significant effects of low doses of BPA, although more than 90 percent of government funded studies have reported significant effects.”
In 2007, the University of North Carolina’s Chapel Hill Bisphenol A Expert Panel, which included Vandenberg and 38 other experts, published a report stating that human exposure levels are well within the range that has proven harmful to rats and mice.
Furthermore, these adverse effects in lab animal studies mirror health conditions that have been on the rise in humans over the past 50 years: infertility, breast and prostate cancer, type-2 diabetes, obesity, attention deficit disorder, cardiovascular diseases, autism, and abnormal development of the penis. More research is needed to confirm these correlations.
Despite the Panel’s report, the U.S. National Toxicology Program’s (NTP) Center for the Evaluation of Risks to Human Reproduction issued a brief in April 2008 that fell short of sounding the alarm. In June 2008, the NTP Board of Scientific Counselors further downgraded some of the potential risks. In a nutshell, the NTP voiced “some concern” for neural and behavioral effects and effects on the prostate gland in fetuses, infants and children at current exposures.
For the same age group, they said there is “minimal concern” about effects on the breast and on earlier puberty in girls. For adults, the concern about exposures adversely affecting pregnancy outcomes or the health of reproductive organs was “negligible.”
Among the long list of experts that responded to the NTP brief, the American Academy of Pediatrics said the report’s downplaying of the risks, particularly for infants and pregnant women, would falsely reassure the public. Sarah Janssen, science fellow for the Natural Resources Defense Council, responded to the brief more bluntly: “BPA should be considered a hazard to human development and reproduction with clear evidence of adverse effects.”
While the U.S. Food and Drug Administration maintains current levels of BPA are safe for humans, the Canadian government declared BPA toxic in April 2008, triggering a ban on the use of BPA in baby bottles.
But in October, a group of scientific advisers to the U.S. FDA rejected the assessment, stating that the agency had ignored crucial studies and employed flawed methods in its research. As the FDA risk assessment continues, some states are proposing legislation that would ban many plastics containing BPA.
Trouble with Phthalates
Phthalates represent another ubiquitous category of endocrine disruptors. Used to soften plastic, these chemicals pop up in PVC-containing plastic products, including:
• children’s toys
• personal care products (cosmetics, nail polish, hair spray, deodorant, shampoos, body washes, perfumes)
• air fresheners
• insect repellents
• detergents and other cleaning products
• lubricants
• vinyl products (shower curtains, raincoats, vinyl flooring)
• medical equipment (tubing, bags for intravenous fluids, vinyl gloves)
• the plastic in breast pumps
• the outer coating on many pills
• garden hoses
• pool liners
• modeling clay
• food packaging
With respect to pacifiers and baby bottle nipples, most companies have switched to latex- and silicone-based materials in their manufacturing.
Because phthalates aren’t tightly bound to plastics, they readily migrate into neighboring substances such as food, water, air, and saliva. Phthalates are thus present in our urine, blood, breast milk, saliva, amniotic fluid, and seminal fluid.
The biggest health concern is reproductive toxicity — particularly for males.
Numerous animal studies link phthalate exposure during fetal development with malformations of parts of the male reproductive system. Reports of ill effects in females aren’t as numerous, although higher levels of these chemicals have been associated with early breast development in girls and endometriosis in women.
Phthalates in indoor air have been associated with asthma and allergic conditions.
In 2005, the European Union banned three phthalate compounds from children’s toys and other children’s products.
California has passed a law limiting exposure to di(2-ethylhexyl) phthalate (commonly known as DEHP). And Minnesota, Maryland, Maine, and Oregon have proposed similar legislation. Washington state recently passed the Children’s Safe Products Act to protect kids from exposure to lead, cadmium and phthalates.
________________________________________
Keeping BPA Out of Food and Beverages
In addition to the potential health risks, there are many more reasons to reduce your use of plastic food containers, dishes, and cutlery. Plastics consume resources that are largely nonrenewable (crude oil and natural gas), their use contributes to needless waste, and their production and degradation create pollution. Here are a few BPA safety tips for food and drink.
• Can the cans. “Canned foods are likely to be the highest contributor to BPA in our diets, not plastics,” says Vandenberg. Also, she says parents should buy powdered rather than liquid infant formula, because the former has less exposure to the BPA lining the can.
• If you use plastic wrap, try to find one that doesn’t contain BPA. Vandenberg says the trouble is that companies are not required to tell you what’s in plastic wrap, adding, “Studies show that many stretch wraps contain BPA and other endocrine disruptors.”
• Warm and store food in ceramic or glass containers. The label “microwave safe” on a plastic food container only means that the plastic won’t melt. If the product contains BPA, it will leach into your food faster when warm.
• Make sure baby bottles, pacifiers and toys for infants and toddlers are BPA-free.
• Avoid bottled water, especially in plastic bottles. According to Food & Water Watch, bottled water is more expensive and no safer than tap water. In fact, it is often bottled tap water.
• Use metal or wooden utensils when you cook. Use wooden rather than plastic cutting boards, and clean thoroughly after use.
• Bring your own, BPA-free containers for leftovers and take-away foods.
• Recycle. Plastic containers and packaging are clogging our landfills and leaching endocrine disruptors into groundwater, plus marring the landscape and injuring wildlife.
________________________________________
How to Avoid Phthalates
Avoiding phthalates is challenging because manufacturers aren’t required to list them as product ingredients.
• Look for “phthalate-free” on the label of personal care products (especially nail polish). For information on product ingredients, check the Campaign for Safe Cosmetics website.
• Use fragrance-free detergents, cleansers and personal care products. Artificial fragrances commonly use diethyl phthalate (DEP).
• Avoid products made of vinyl plastic usually labelled as No. 3 (raincoats, shower curtains) and polyvinyl chloride (PVC pipe, other building materials, some lawn furniture, and some children’s and pets’ toys).
Note: In 2007, the Natural Resources Defense Council tested 14 common air fresheners. Although none of them listed phthalates as an ingredient, 12 of the 14 contained these chemicals, including those advertised as unscented or “all natural.” Read the NRDC's full report on phthalates and air fresheners.
You can find links to the reference materials for this article in the Plastics and Endocrine Disruptors Article Resources, below. Plus, follow FDA reviews and regulation updates.
Cell phones and brain tumors: a review including the long-term epidemiologic data
Surgical Neurology
Volume 72, Issue 3, September 2009, Pages 205–214
Cell phones and brain tumors: a review including the long-term epidemiologic data ☆
Vini G. Khurana, PhD, FRACSa, b, , , Charles Teo, MBBS, FRACSc, Michael Kundi, PhDd, Lennart Hardell, MD, PhDe, Michael Carlberg, MSce
Abstract
Background
The debate regarding the health effects of low-intensity electromagnetic radiation from sources such as power lines, base stations, and cell phones has recently been reignited. In the present review, the authors attempt to address the following question: is there epidemiologic evidence for an association between long-term cell phone usage and the risk of developing a brain tumor? Included with this meta-analysis of the long-term epidemiologic data are a brief overview of cell phone technology and discussion of laboratory data, biological mechanisms, and brain tumor incidence.
Methods
In order to be included in the present meta-analysis, studies were required to have met all of the following criteria: (i) publication in a peer-reviewed journal; (ii) inclusion of participants using cell phones for ≥10 years (ie, minimum 10-year “latency”); and (iii) incorporation of a “laterality” analysis of long-term users (ie, analysis of the side of the brain tumor relative to the side of the head preferred for cell phone usage). This is a meta-analysis incorporating all 11 long-term epidemiologic studies in this field.
Results
The results indicate that using a cell phone for ≥10 years approximately doubles the risk of being diagnosed with a brain tumor on the same (“ipsilateral”) side of the head as that preferred for cell phone use. The data achieve statistical significance for glioma and acoustic neuroma but not for meningioma.
Conclusion
The authors conclude that there is adequate epidemiologic evidence to suggest a link between prolonged cell phone usage and the development of an ipsilateral brain tumor.
Abbreviations
CBTRUS, Central Brain Tumor Registry of the United States; CDMA, code division multiple access; CI, confidence interval; CNS, central nervous system; EMF, electromagnetic field; EMR, electromagnetic radiation; FCC, Federal Communications Commission; GSM, global system for mobile communication; IARC, International Agency for Research on Cancer; MRI, magnetic resonance imaging; NHL, non-Hodgkin lymphoma; OR, odds ratio; SAR, specific absorption rate; TDMA, time division multiple access; WHO, World Health Organization
Keywords
Acoustic neuroma; Brain tumor; Cell phone; Electromagnetic radiation; Glioma; Incidence; Mechanism; Meningioma; Radiofrequency fields
☆
There is no author conflict of interest, and no funding was requested or received for this review. The conclusions expressed in this article do not necessarily reflect those of the authors' affiliated institutions and employers.
Corresponding author. Department of Neurosurgery, The Canberra Hospital, Garran ACT 2605, Australia. Tel.: +61 2 6244 3937; fax: +61 2 6244 2718.
Copyright © 2009 Published by Elsevier Inc.
Volume 72, Issue 3, September 2009, Pages 205–214
Cell phones and brain tumors: a review including the long-term epidemiologic data ☆
Vini G. Khurana, PhD, FRACSa, b, , , Charles Teo, MBBS, FRACSc, Michael Kundi, PhDd, Lennart Hardell, MD, PhDe, Michael Carlberg, MSce
Abstract
Background
The debate regarding the health effects of low-intensity electromagnetic radiation from sources such as power lines, base stations, and cell phones has recently been reignited. In the present review, the authors attempt to address the following question: is there epidemiologic evidence for an association between long-term cell phone usage and the risk of developing a brain tumor? Included with this meta-analysis of the long-term epidemiologic data are a brief overview of cell phone technology and discussion of laboratory data, biological mechanisms, and brain tumor incidence.
Methods
In order to be included in the present meta-analysis, studies were required to have met all of the following criteria: (i) publication in a peer-reviewed journal; (ii) inclusion of participants using cell phones for ≥10 years (ie, minimum 10-year “latency”); and (iii) incorporation of a “laterality” analysis of long-term users (ie, analysis of the side of the brain tumor relative to the side of the head preferred for cell phone usage). This is a meta-analysis incorporating all 11 long-term epidemiologic studies in this field.
Results
The results indicate that using a cell phone for ≥10 years approximately doubles the risk of being diagnosed with a brain tumor on the same (“ipsilateral”) side of the head as that preferred for cell phone use. The data achieve statistical significance for glioma and acoustic neuroma but not for meningioma.
Conclusion
The authors conclude that there is adequate epidemiologic evidence to suggest a link between prolonged cell phone usage and the development of an ipsilateral brain tumor.
Abbreviations
CBTRUS, Central Brain Tumor Registry of the United States; CDMA, code division multiple access; CI, confidence interval; CNS, central nervous system; EMF, electromagnetic field; EMR, electromagnetic radiation; FCC, Federal Communications Commission; GSM, global system for mobile communication; IARC, International Agency for Research on Cancer; MRI, magnetic resonance imaging; NHL, non-Hodgkin lymphoma; OR, odds ratio; SAR, specific absorption rate; TDMA, time division multiple access; WHO, World Health Organization
Keywords
Acoustic neuroma; Brain tumor; Cell phone; Electromagnetic radiation; Glioma; Incidence; Mechanism; Meningioma; Radiofrequency fields
☆
There is no author conflict of interest, and no funding was requested or received for this review. The conclusions expressed in this article do not necessarily reflect those of the authors' affiliated institutions and employers.
Corresponding author. Department of Neurosurgery, The Canberra Hospital, Garran ACT 2605, Australia. Tel.: +61 2 6244 3937; fax: +61 2 6244 2718.
Copyright © 2009 Published by Elsevier Inc.
Cell Phones and Cancer Risk NIH-NCI
Cell Phones and Cancer Risk. NCI
Why is there concern that cell phones may cause cancer or other health problems?
What is radiofrequency energy and how does it affect the body?
How is radiofrequency energy exposure measured in epidemiologic studies?
What has research shown about the possible cancer-causing effects of radiofrequency energy?
Why are the findings from different studies of cell phone use and cancer risk inconsistent?
What do expert organizations conclude?
What studies are under way that will help further our understanding of the health effects of cell phone use?
Do children have a higher risk of developing cancer due to cell phone use than adults?
What can cell phone users do to reduce their exposure to radiofrequency energy?
Where can I find more information about radiofrequency energy from my cell phone?
What are other sources of radiofrequency energy?
How common is brain cancer? Has the incidence of brain cancer changed over time?
Why is there concern that cell phones may cause cancer or other health problems?
There are three main reasons why people are concerned that cell phones (also known as “wireless” or “mobile” telephones) might have the potential to cause certain types of cancer or other health problems:
Cell phones emit radiofrequency energy (radio waves), a form of non-ionizing radiation. Tissues nearest to where the phone is held can absorb this energy.
The number of cell phone users has increased rapidly. As of 2010, there were more than 303 million subscribers to cell phone service in the United States, according to the Cellular Telecommunications and Internet Association.
This is a nearly threefold increase from the 110 million users in 2000. Globally, the number of cell phone subscriptions is estimated by the International Telecommunications Union to be 5 billion.
Over time, the number of cell phone calls per day, the length of each call, and the amount of time people use cell phones have increased. Cell phone technology has also undergone substantial changes.
What is radiofrequency energy and how does it affect the body?
Radiofrequency energy is a form of electromagnetic radiation. Electromagnetic radiation can be categorized into two types: ionizing (e.g., x-rays, radon, and cosmic rays) and non-ionizing (e.g., radiofrequency and extremely low-frequency or power frequency).
Exposure to ionizing radiation, such as from radiation therapy, is known to increase the risk of cancer. However, although many studies have examined the potential health effects of non-ionizing radiation from radar, microwave ovens, and other sources, there is currently no consistent evidence that non-ionizing radiation increases cancer risk (1).
The only known biological effect of radiofrequency energy is heating. The ability of microwave ovens to heat food is one example of this effect of radiofrequency energy. Radiofrequency exposure from cell phone use does cause heating; however, it is not sufficient to measurably increase body temperature.
A recent study showed that when people used a cell phone for 50 minutes, brain tissues on the same side of the head as the phone’s antenna metabolized more glucose than did tissues on the opposite side of the brain (2). The researchers noted that the results are preliminary, and possible health outcomes from this increase in glucose metabolism are still unknown.
How is radiofrequency energy exposure measured in epidemiologic studies?
Levels of radiofrequency exposure are indirectly estimated using information from interviews or questionnaires. These measures include the following:
How “regularly” study participants use cell phones (the minimum number of calls per week or month)
The age and the year when study participants first used a cell phone and the age and the year of last use (allows calculation of the duration of use and time since the start of use)
The average number of cell phone calls per day, week, or month (frequency)
The average length of a typical cell phone call
The total hours of lifetime use, calculated from the length of typical call times, the frequency of use, and the duration of use
What has research shown about the possible cancer-causing effects of radiofrequency energy?
Although there have been some concerns that radiofrequency energy from cell phones held closely to the head may affect the brain and other tissues, to date there is no evidence from studies of cells, animals, or humans that radiofrequency energy can cause cancer.
It is generally accepted that damage to DNA is necessary for cancer to develop. However, radiofrequency energy, unlike ionizing radiation, does not cause DNA damage in cells, and it has not been found to cause cancer in animals or to enhance the cancer-causing effects of known chemical carcinogens in animals (3–5).
Researchers have carried out several types of epidemiologic studies to investigate the possibility of a relationship between cell phone use and the risk of malignant (cancerous) brain tumors, such as gliomas, as well as benign (noncancerous) tumors, such as acoustic neuromas (tumors in the cells of the nerve responsible for hearing), most meningiomas (tumors in the meninges, membranes that cover and protect the brain and spinal cord), and parotid gland tumors (tumors in the salivary glands) (6).
In one type of study, called a case-control study, cell phone use is compared between people with these types of tumors and people without them. In another type of study, called a cohort study, a large group of people is followed over time and the rate of these tumors in people who did and didn’t use cell phones is compared.
Cancer incidence data can also be analyzed over time to see if the rates of cancer changed in large populations during the time that cell phone use increased dramatically. The results of these studies have generally not provided clear evidence of a relationship between cell phone use and cancer, but there have been some statistically significant findings in certain subgroups of people.
Findings from specific research studies are summarized below:
The Interphone Study, conducted by a consortium of researchers from 13 countries, is the largest health-related case-control study of use of cell phones and head and neck tumors.
Most published analyses from this study have shown no statistically significant increases in brain or central nervous system cancers related to higher amounts of cell phone use. One recent analysis showed a statistically significant, albeit modest, increase in the risk of glioma among the small proportion of study participants who spent the most total time on cell phone calls. However, the researchers considered this finding inconclusive because they felt that the amount of use reported by some respondents was unlikely and because the participants who reported lower levels of use appeared to have a slightly reduced risk of brain cancer compared with people who did not use cell phones regularly (7–9).
Another recent study from the group found no relationship between brain tumor locations and regions of the brain that were exposed to the highest level of radiofrequency energy from cell phones (10).
A cohort study in Denmark linked billing information from more than 358,000 cell phone subscribers with brain tumor incidence data from the Danish Cancer Registry. The analyses found no association between cell phone use and the incidence of glioma, meningioma, or acoustic neuroma, even among people who had been cell phone subscribers for 13 or more years (11–13).
The prospective Million Women Study in the United Kingdom found that self-reported cell phone use was not associated with an increased risk of glioma, meningioma, or non-central nervous system tumors.
The researchers did find that the use of cell phones for more than 5 years was associated with an increased risk of acoustic neuroma, and that the risk of acoustic neuroma increased with increasing duration of cell phone use (14). However, the incidence of these tumors among men and women in the United Kingdom did not increase during 1998 to 2008, even though cell phone use increased dramatically over that decade (14).
An early case-control study in the United States was unable to demonstrate a relationship between cell phone use and glioma or meningioma (15).
Some case-control studies in Sweden found statistically significant trends of increasing brain cancer risk for the total amount of cell phone use and the years of use among people who began using cell phones before age 20 (16). However, another large, case-control study in Sweden did not find an increased risk of brain cancer among people between the ages of 20 and 69 (17).
In addition, the international CEFALO study, which compared children who were diagnosed with brain cancer between ages 7 and 19 with similar children who were not, found no relationship between their cell phone use and risk for brain cancer (18).
NCI's Surveillance, Epidemiology, and End Results (SEER) Program, which tracks cancer incidence in the United States over time, found no increase in the incidence of brain or other central nervous system cancers between 1987 and 2007, despite the dramatic increase in cell phone use in this country during that time (19, 20). Similarly, incidence data from Denmark, Finland, Norway, and Sweden for the period 1974–2008 revealed no increase in age-adjusted incidence of brain tumors (21, 22).
A 2012 study by NCI researchers, which compared observed glioma incidence rates in SEER with projected rates based on risks observed in the Interphone study (8), found that the projected rates were consistent with observed U.S. rates. The researchers also compared the SEER rates with projected rates based on a Swedish study published in 2011 (16).
They determined that the projected rates were at least 40 percent higher than, and incompatible with, the actual U.S. rates.
Studies of workers exposed to radiofrequency energy have shown no evidence of increased risk of brain tumors among U.S. Navy electronics technicians, aviation technicians, or fire control technicians, those working in an electromagnetic pulse test program, plastic-ware workers, cellular phone manufacturing workers, or Navy personnel with a high probability of exposure to radar (6).
Why are the findings from different studies of cell phone use and cancer risk inconsistent?
A limited number of studies have shown some evidence of statistical association of cell phone use and brain tumor risks, but most studies have found no association. Reasons for these discrepancies include the following:
Recall bias, which may happen when a study collects data about prior habits and exposures using questionnaires administered after disease has been diagnosed in some of the study participants.
It is possible that study participants who have brain tumors may remember their cell phone use differently than individuals without brain tumors. Many epidemiologic studies of cell phone use and brain cancer risk lack verifiable data about the total amount of cell phone use over time.
In addition, people who develop a brain tumor may have a tendency to recall using their cell phone mostly on the same side of their head where the tumor was found, regardless of whether they actually used their phone on that side of their head a lot or only a little.
Inaccurate reporting, which may happen when people say that something has happened more or less often than it actually did. People may not remember how much they used cell phones in a given time period.
Morbidity and mortality among study participants who have brain cancer. Gliomas are particularly difficult to study, for example, because of their high death rate and the short survival of people who develop these tumors.
Patients who survive initial treatment are often impaired, which may affect their responses to questions. Furthermore, for people who have died, next-of-kin are often less familiar with the cell phone use patterns of their deceased family member and may not accurately describe their patterns of use to an interviewer.
Participation bias, which can happen when people who are diagnosed with brain tumors are more likely than healthy people (known as controls) to enroll in a research study. Also, controls who did not or rarely used cell phones were less likely to participate in the Interphone study than controls who used cell phones regularly.
For example, the Interphone study reported participation rates of 78 percent for meningioma patients (range 56–92 percent for the individual studies), 64 percent for the glioma patients (range 36–92 percent), and 53 percent for control subjects (range 42–74 percent) (9). One series of Swedish studies reported participation rates of 85 percent in people with brain cancer and 84 percent in control subjects (17).
Changing technology and methods of use. Older studies evaluated radiofrequency energy exposure from analog cell phones. However, most cell phones today use digital technology, which operates at a different frequency and a lower power level than analog phones. Digital cell phones have been in use for more than a decade in the United States, and cellular technology continues to change (6).
Texting, for example, has become a popular way of using a cell phone to communicate that does not require bringing the phone close to the head. Furthermore, the use of hands-free technology, such as wired and wireless headsets, is increasing and may decrease radiofrequency energy exposure to the head and brain.
What do expert organizations conclude?
The International Agency for Research on CancerExit Disclaimer (IARC), a component of the World Health Organization, has recently classified radiofrequency fields as “possibly carcinogenic to humans,” based on limited evidence from human studies, limited evidence from studies of radiofrequency energy and cancer in rodents, and weak mechanistic evidence (from studies of genotoxicity, effects on immune system function, gene and protein expression, cell signaling, oxidative stress, and apoptosis, along with studies of the possible effects of radiofrequency energy on the blood-brain barrier).
The American Cancer SocietyExit Disclaimer (ACS) states that the IARC classification means that there could be some risk associated with cancer, but the evidence is not strong enough to be considered causal and needs to be investigated further. Individuals who are concerned about radiofrequency exposure can limit their exposure, including using an ear piece and limiting cell phone use, particularly among children.
The National Institute of Environmental Health Sciences (NIEHS) states that the weight of the current scientific evidence has not conclusively linked cell phone use with any adverse health problems, but more research is needed.
The U.S. Food and Drug Administration (FDA), which is responsible for regulating the safety of machines and devices that emit radiation (including cell phones), notes that studies reporting biological changes associated with radiofrequency energy have failed to be replicated and that the majority of human epidemiologic studies have failed to show a relationship between exposure to radiofrequency energy from cell phones and health problems.
The U.S. Centers for Disease Control and Prevention (CDC) states that, although some studies have raised concerns about the possible risks of cell phone use, scientific research as a whole does not support a statistically significant association between cell phone use and health effects.
The Federal Communications Commission (FCC) concludes that there is no scientific evidence that proves that wireless phone use can lead to cancer or to other health problems, including headaches, dizziness, or memory loss.
What studies are under way that will help further our understanding of the health effects of cell phone use?
A large prospective cohort study of cell phone use and its possible long-term health effects was launched in Europe in March 2010. This study, known as COSMOSExit Disclaimer, has enrolled approximately 290,000 cell phone users aged 18 years or older to date and will follow them for 20 to 30 years.
Participants in COSMOS will complete a questionnaire about their health, lifestyle, and current and past cell phone use. This information will be supplemented with information from health records and cell phone records.
The challenge of this ambitious study is to continue following the participants for a range of health effects over many decades. Researchers will need to determine whether participants who leave are somehow different from those who remain throughout the follow-up period.
Another study already under way is a case-control study called Mobi-KidsExit Disclaimer, which will include 2000 young people (aged 10-24 years) with newly diagnosed brain tumors and 4000 healthy young people. The goal of the study is to learn more about risk factors for childhood brain tumors. Results are expected in 2016.
Although recall bias is minimized in studies that link participants to their cell phone records, such studies face other problems. For example, it is impossible to know who is using the listed cell phone or whether that individual also places calls using other cell phones. To a lesser extent, it is not clear whether multiple users of a single phone will be represented on a single phone company account.
The NIEHS, which is part of the National Institutes of Health, is carrying out a study of risks related to exposure to radiofrequency energy (the type used in cell phones) in highly specialized labs that can specify and control sources of radiation and measure their effects on rodents.
Do children have a higher risk of developing cancer due to cell phone use than adults?
In theory, children have the potential to be at greater risk than adults for developing brain cancer from cell phones. Their nervous systems are still developing and therefore more vulnerable to factors that may cause cancer.
Their heads are smaller than those of adults and therefore have a greater proportional exposure to the field of radiofrequency radiation that is emitted by cell phones. And children have the potential of accumulating more years of cell phone exposure than adults do.
So far, the data from studies in children with cancer do not support this theory. The first published analysis came from a large case-control study called CEFALO, which was conducted in Denmark, Sweden, Norway, and Switzerland. The study included children who were diagnosed with brain tumors between 2004 and 2008, when their ages ranged from 7 to 19. Researchers did not find an association between cell phone use and brain tumor risk in this group of children.
However, they noted that their results did not rule out the possibility of a slight increase in brain cancer risk among children who use cell phones, and that data gathered through prospective studies and objective measurements, rather than participant surveys and recollections, will be key in clarifying whether there is an increased risk (19).
Researchers from the Centre for Research in Environmental Epidemiology in Spain are conducting another international study—Mobi-KidsExit Disclaimer—to evaluate the risk associated with new communications technologies (including cell phones) and other environmental factors in young people newly diagnosed with brain tumors at ages 10 to 24 years.
What can cell phone users do to reduce their exposure to radiofrequency energy?
The FDA and FCC have suggested some steps that concerned cell phone users can take to reduce their exposure to radiofrequency energy (1, 23):
Reserve the use of cell phones for shorter conversations or for times when a landline phone is not available.
Use a hands-free device, which places more distance between the phone and the head of the user.
Hands-free kits reduce the amount of radiofrequency energy exposure to the head because the antenna, which is the source of energy, is not placed against the head.
Where can I find more information about radiofrequency energy from my cell phone?
The FCC provides information about the specific absorption rate (SAR) of cell phones produced and marketed within the last 1 to 2 years. The SAR corresponds with the relative amount of radiofrequency energy absorbed by the head of a cell phone user (24). Consumers can access this information using the phone’s FCC ID number, which is usually located on the case of the phone, and the FCC’s ID search form.
What are other sources of radiofrequency energy?
The most common exposures to radiofrequency energy are from telecommunications devices and equipment (1). In the United States, cell phones currently operate in a frequency range of about 1,800 to 2,200 megahertz (MHz) (6). In this range, the electromagnetic radiation produced is in the form of non-ionizing radiofrequency energy.
Cordless phones (phones that have a base unit connected to the telephone wiring in a house) often operate at radio frequencies similar to those of cell phones; however, since cordless phones have a limited range and require a nearby base, their signals are generally much less powerful than those of cell phones.
Among other radiofrequency energy sources, AM/FM radios and VHF/UHF televisions operate at lower radio frequencies than cell phones, whereas sources such as radar, satellite stations, magnetic resonance imaging (MRI) devices, industrial equipment, and microwave ovens operate at somewhat higher radio frequencies (1).
How common is brain cancer? Has the incidence of brain cancer changed over time?
Brain cancer incidence and mortality (death) rates have changed little in the past decade. In the United States, 23,130 new diagnoses and 14,080 deaths from brain cancer are estimated for 2013.
The 5-year relative survival for brain cancers diagnosed from 2003 through 2009 was 35 percent (25). This is the percentage of people diagnosed with brain cancer who will still be alive 5 years after diagnosis compared with the survival of a person of the same age and sex who does not have cancer.
The risk of developing brain cancer increases with age. From 2006 through 2010, there were fewer than 5 brain cancer cases for every 100,000 people in the United States under age 65, compared with approximately 19 cases for every 100,000 people in the United States who were ages 65 or older (25).
Selected References
U.S. Food and Drug Administration (2009). Radiation-Emitting Products: Reducing Exposure: Hands-free Kits and Other Accessories. Silver Spring, MD. Retrieved June 18, 2012.
Volkow ND, Tomasi D, Wang GJ, et al. Effects of cell phone radiofrequency signal exposure on brain glucose metabolism. JAMA 2011; 305(8):808–813. [PubMed Abstract]
Hirose H, Suhara T, Kaji N, et al. Mobile phone base station radiation does not affect neoplastic transformation in BALB/3T3 cells. Bioelectromagnetics 2008; 29(1):55–64. [PubMed Abstract]
Oberto G, Rolfo K, Yu P, et al. Carcinogenicity study of 217 Hz pulsed 900 MHz electromagnetic fields in Pim1 transgenic mice. Radiation Research 2007; 168(3):316–326. [PubMed Abstract]
Zook BC, Simmens SJ. The effects of pulsed 860 MHz radiofrequency radiation on the promotion of neurogenic tumors in rats. Radiation Research 2006; 165(5):608–615. [PubMed Abstract]
Ahlbom A, Green A, Kheifets L, et al. Epidemiology of health effects of radiofrequency exposure. Environmental Health Perspectives 2004; 112(17):1741–1754. [PubMed Abstract]
Cardis E, Richardson L, Deltour I, et al. The INTERPHONE study: design, epidemiological methods, and description of the study population. European Journal of Epidemiology 2007; 22(9):647–664. [PubMed Abstract]
International Agency for Research on Cancer (2008). INTERPHONE Study: latest results update—8 October 2008Exit Disclaimer. Lyon, France. Retrieved June 18, 2012.
The INTERPHONE Study Group. Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study. International Journal of Epidemiology 2010; 39(3):675–694. [PubMed Abstract]
Larjavaara S, Schüz J, Swerdlow A, et al. Location of gliomas in relation to mobile telephone use: a case-case and case-specular analysis. American Journal of Epidemiology 2011; 174(1):2–11. [PubMed Abstract]
Johansen C, Boice J Jr, McLaughlin J, Olsen J. Cellular telephones and cancer: a nationwide cohort study in Denmark. Journal of the National Cancer Institute 2001; 93(3):203–207. [PubMed Abstract]
Schüz J, Jacobsen R, Olsen JH, et al. Cellular telephone use and cancer risk: update of a nationwide Danish cohort. Journal of the National Cancer Institute 2006; 98(23):1707–1713. [PubMed Abstract]
Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk of brain tumours: update of Danish cohort study. British Medical Journal 2011; 343:d6387. [PubMed Abstract]
Benson VS, Pirie K, Schüz J, et al. Mobile phone use and risk of brain neoplasms and other cancers: Prospective study. International Journal of Epidemiology 2013; First published online: May 8, 2013. doi:10.1093/ije/dyt072Exit Disclaimer
Muscat JE, Malkin MG, Thompson S, et al. Handheld cellular telephone use and risk of brain cancer. JAMA 2000; 284(23):3001–3007. [PubMed Abstract]
Hardell L, Carlberg M, Hansson Mild K. Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects. International Journal of Oncology 2011; 38(5):1465–1474. [PubMed Abstract]
Lönn S, Ahlbom A, Hall P, Feychting M. Long-term mobile phone use and brain tumor risk. American Journal of Epidemiology 2005; 161(6):526–535. [PubMed Abstract]
Aydin D, Feychting M, Schüz J, et al. Mobile phone use and brain tumors in children and adolescents: a multicenter case-control study. Journal of the National Cancer Institute 2011; 103(16):1264–1276. [PubMed Abstract]
Inskip PD, Hoover RN, Devesa SS. Brain cancer incidence trends in relation to cellular telephone use in the United States. Neuro-Oncology 2010; 12(11):1147–1151. [PubMed Abstract]
Little MP, Rajaraman P, Curtis RE, et al. Mobile phone use and glioma risk: comparison of epidemiological study results with incidence trends in the United States. British Medical Journal 2012; 344:e1147. [PubMed Abstract]
Deltour I, Johansen C, Auvinen A, et al. Time trends in brain tumor incidence rates in Denmark, Finland, Norway, and Sweden, 1974–2003. Journal of the National Cancer Institute 2009; 101(24):1721–1724. [PubMed Abstract]
Deltour I, Auvinen A, Feychting M, et al. Mobile phone use and incidence of glioma in the Nordic countries 1979–2008: consistency check. Epidemiology 2012; 23(2):301–307. [PubMed Abstract]
U.S. Federal Communications Commission (2010). Wireless. Washington, D.C. Retrieved June 18, 2012.
U.S. Federal Communications Commission. (n.d.). FCC Encyclopedia: Specific Absorption Rate (SAR) for Cellular Telephones. Retrieved June 18, 2012.
Howlader N, Noone AM, Krapcho M, et al. (eds.). (2013) SEER Cancer Statistics Review, 1975-2010. Bethesda, MD: National Cancer Institute. Retrieved June 24, 2013.
Related Resources
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Reviewed: June 24, 2013
Why is there concern that cell phones may cause cancer or other health problems?
What is radiofrequency energy and how does it affect the body?
How is radiofrequency energy exposure measured in epidemiologic studies?
What has research shown about the possible cancer-causing effects of radiofrequency energy?
Why are the findings from different studies of cell phone use and cancer risk inconsistent?
What do expert organizations conclude?
What studies are under way that will help further our understanding of the health effects of cell phone use?
Do children have a higher risk of developing cancer due to cell phone use than adults?
What can cell phone users do to reduce their exposure to radiofrequency energy?
Where can I find more information about radiofrequency energy from my cell phone?
What are other sources of radiofrequency energy?
How common is brain cancer? Has the incidence of brain cancer changed over time?
Why is there concern that cell phones may cause cancer or other health problems?
There are three main reasons why people are concerned that cell phones (also known as “wireless” or “mobile” telephones) might have the potential to cause certain types of cancer or other health problems:
Cell phones emit radiofrequency energy (radio waves), a form of non-ionizing radiation. Tissues nearest to where the phone is held can absorb this energy.
The number of cell phone users has increased rapidly. As of 2010, there were more than 303 million subscribers to cell phone service in the United States, according to the Cellular Telecommunications and Internet Association.
This is a nearly threefold increase from the 110 million users in 2000. Globally, the number of cell phone subscriptions is estimated by the International Telecommunications Union to be 5 billion.
Over time, the number of cell phone calls per day, the length of each call, and the amount of time people use cell phones have increased. Cell phone technology has also undergone substantial changes.
What is radiofrequency energy and how does it affect the body?
Radiofrequency energy is a form of electromagnetic radiation. Electromagnetic radiation can be categorized into two types: ionizing (e.g., x-rays, radon, and cosmic rays) and non-ionizing (e.g., radiofrequency and extremely low-frequency or power frequency).
Exposure to ionizing radiation, such as from radiation therapy, is known to increase the risk of cancer. However, although many studies have examined the potential health effects of non-ionizing radiation from radar, microwave ovens, and other sources, there is currently no consistent evidence that non-ionizing radiation increases cancer risk (1).
The only known biological effect of radiofrequency energy is heating. The ability of microwave ovens to heat food is one example of this effect of radiofrequency energy. Radiofrequency exposure from cell phone use does cause heating; however, it is not sufficient to measurably increase body temperature.
A recent study showed that when people used a cell phone for 50 minutes, brain tissues on the same side of the head as the phone’s antenna metabolized more glucose than did tissues on the opposite side of the brain (2). The researchers noted that the results are preliminary, and possible health outcomes from this increase in glucose metabolism are still unknown.
How is radiofrequency energy exposure measured in epidemiologic studies?
Levels of radiofrequency exposure are indirectly estimated using information from interviews or questionnaires. These measures include the following:
How “regularly” study participants use cell phones (the minimum number of calls per week or month)
The age and the year when study participants first used a cell phone and the age and the year of last use (allows calculation of the duration of use and time since the start of use)
The average number of cell phone calls per day, week, or month (frequency)
The average length of a typical cell phone call
The total hours of lifetime use, calculated from the length of typical call times, the frequency of use, and the duration of use
What has research shown about the possible cancer-causing effects of radiofrequency energy?
Although there have been some concerns that radiofrequency energy from cell phones held closely to the head may affect the brain and other tissues, to date there is no evidence from studies of cells, animals, or humans that radiofrequency energy can cause cancer.
It is generally accepted that damage to DNA is necessary for cancer to develop. However, radiofrequency energy, unlike ionizing radiation, does not cause DNA damage in cells, and it has not been found to cause cancer in animals or to enhance the cancer-causing effects of known chemical carcinogens in animals (3–5).
Researchers have carried out several types of epidemiologic studies to investigate the possibility of a relationship between cell phone use and the risk of malignant (cancerous) brain tumors, such as gliomas, as well as benign (noncancerous) tumors, such as acoustic neuromas (tumors in the cells of the nerve responsible for hearing), most meningiomas (tumors in the meninges, membranes that cover and protect the brain and spinal cord), and parotid gland tumors (tumors in the salivary glands) (6).
In one type of study, called a case-control study, cell phone use is compared between people with these types of tumors and people without them. In another type of study, called a cohort study, a large group of people is followed over time and the rate of these tumors in people who did and didn’t use cell phones is compared.
Cancer incidence data can also be analyzed over time to see if the rates of cancer changed in large populations during the time that cell phone use increased dramatically. The results of these studies have generally not provided clear evidence of a relationship between cell phone use and cancer, but there have been some statistically significant findings in certain subgroups of people.
Findings from specific research studies are summarized below:
The Interphone Study, conducted by a consortium of researchers from 13 countries, is the largest health-related case-control study of use of cell phones and head and neck tumors.
Most published analyses from this study have shown no statistically significant increases in brain or central nervous system cancers related to higher amounts of cell phone use. One recent analysis showed a statistically significant, albeit modest, increase in the risk of glioma among the small proportion of study participants who spent the most total time on cell phone calls. However, the researchers considered this finding inconclusive because they felt that the amount of use reported by some respondents was unlikely and because the participants who reported lower levels of use appeared to have a slightly reduced risk of brain cancer compared with people who did not use cell phones regularly (7–9).
Another recent study from the group found no relationship between brain tumor locations and regions of the brain that were exposed to the highest level of radiofrequency energy from cell phones (10).
A cohort study in Denmark linked billing information from more than 358,000 cell phone subscribers with brain tumor incidence data from the Danish Cancer Registry. The analyses found no association between cell phone use and the incidence of glioma, meningioma, or acoustic neuroma, even among people who had been cell phone subscribers for 13 or more years (11–13).
The prospective Million Women Study in the United Kingdom found that self-reported cell phone use was not associated with an increased risk of glioma, meningioma, or non-central nervous system tumors.
The researchers did find that the use of cell phones for more than 5 years was associated with an increased risk of acoustic neuroma, and that the risk of acoustic neuroma increased with increasing duration of cell phone use (14). However, the incidence of these tumors among men and women in the United Kingdom did not increase during 1998 to 2008, even though cell phone use increased dramatically over that decade (14).
An early case-control study in the United States was unable to demonstrate a relationship between cell phone use and glioma or meningioma (15).
Some case-control studies in Sweden found statistically significant trends of increasing brain cancer risk for the total amount of cell phone use and the years of use among people who began using cell phones before age 20 (16). However, another large, case-control study in Sweden did not find an increased risk of brain cancer among people between the ages of 20 and 69 (17).
In addition, the international CEFALO study, which compared children who were diagnosed with brain cancer between ages 7 and 19 with similar children who were not, found no relationship between their cell phone use and risk for brain cancer (18).
NCI's Surveillance, Epidemiology, and End Results (SEER) Program, which tracks cancer incidence in the United States over time, found no increase in the incidence of brain or other central nervous system cancers between 1987 and 2007, despite the dramatic increase in cell phone use in this country during that time (19, 20). Similarly, incidence data from Denmark, Finland, Norway, and Sweden for the period 1974–2008 revealed no increase in age-adjusted incidence of brain tumors (21, 22).
A 2012 study by NCI researchers, which compared observed glioma incidence rates in SEER with projected rates based on risks observed in the Interphone study (8), found that the projected rates were consistent with observed U.S. rates. The researchers also compared the SEER rates with projected rates based on a Swedish study published in 2011 (16).
They determined that the projected rates were at least 40 percent higher than, and incompatible with, the actual U.S. rates.
Studies of workers exposed to radiofrequency energy have shown no evidence of increased risk of brain tumors among U.S. Navy electronics technicians, aviation technicians, or fire control technicians, those working in an electromagnetic pulse test program, plastic-ware workers, cellular phone manufacturing workers, or Navy personnel with a high probability of exposure to radar (6).
Why are the findings from different studies of cell phone use and cancer risk inconsistent?
A limited number of studies have shown some evidence of statistical association of cell phone use and brain tumor risks, but most studies have found no association. Reasons for these discrepancies include the following:
Recall bias, which may happen when a study collects data about prior habits and exposures using questionnaires administered after disease has been diagnosed in some of the study participants.
It is possible that study participants who have brain tumors may remember their cell phone use differently than individuals without brain tumors. Many epidemiologic studies of cell phone use and brain cancer risk lack verifiable data about the total amount of cell phone use over time.
In addition, people who develop a brain tumor may have a tendency to recall using their cell phone mostly on the same side of their head where the tumor was found, regardless of whether they actually used their phone on that side of their head a lot or only a little.
Inaccurate reporting, which may happen when people say that something has happened more or less often than it actually did. People may not remember how much they used cell phones in a given time period.
Morbidity and mortality among study participants who have brain cancer. Gliomas are particularly difficult to study, for example, because of their high death rate and the short survival of people who develop these tumors.
Patients who survive initial treatment are often impaired, which may affect their responses to questions. Furthermore, for people who have died, next-of-kin are often less familiar with the cell phone use patterns of their deceased family member and may not accurately describe their patterns of use to an interviewer.
Participation bias, which can happen when people who are diagnosed with brain tumors are more likely than healthy people (known as controls) to enroll in a research study. Also, controls who did not or rarely used cell phones were less likely to participate in the Interphone study than controls who used cell phones regularly.
For example, the Interphone study reported participation rates of 78 percent for meningioma patients (range 56–92 percent for the individual studies), 64 percent for the glioma patients (range 36–92 percent), and 53 percent for control subjects (range 42–74 percent) (9). One series of Swedish studies reported participation rates of 85 percent in people with brain cancer and 84 percent in control subjects (17).
Changing technology and methods of use. Older studies evaluated radiofrequency energy exposure from analog cell phones. However, most cell phones today use digital technology, which operates at a different frequency and a lower power level than analog phones. Digital cell phones have been in use for more than a decade in the United States, and cellular technology continues to change (6).
Texting, for example, has become a popular way of using a cell phone to communicate that does not require bringing the phone close to the head. Furthermore, the use of hands-free technology, such as wired and wireless headsets, is increasing and may decrease radiofrequency energy exposure to the head and brain.
What do expert organizations conclude?
The International Agency for Research on CancerExit Disclaimer (IARC), a component of the World Health Organization, has recently classified radiofrequency fields as “possibly carcinogenic to humans,” based on limited evidence from human studies, limited evidence from studies of radiofrequency energy and cancer in rodents, and weak mechanistic evidence (from studies of genotoxicity, effects on immune system function, gene and protein expression, cell signaling, oxidative stress, and apoptosis, along with studies of the possible effects of radiofrequency energy on the blood-brain barrier).
The American Cancer SocietyExit Disclaimer (ACS) states that the IARC classification means that there could be some risk associated with cancer, but the evidence is not strong enough to be considered causal and needs to be investigated further. Individuals who are concerned about radiofrequency exposure can limit their exposure, including using an ear piece and limiting cell phone use, particularly among children.
The National Institute of Environmental Health Sciences (NIEHS) states that the weight of the current scientific evidence has not conclusively linked cell phone use with any adverse health problems, but more research is needed.
The U.S. Food and Drug Administration (FDA), which is responsible for regulating the safety of machines and devices that emit radiation (including cell phones), notes that studies reporting biological changes associated with radiofrequency energy have failed to be replicated and that the majority of human epidemiologic studies have failed to show a relationship between exposure to radiofrequency energy from cell phones and health problems.
The U.S. Centers for Disease Control and Prevention (CDC) states that, although some studies have raised concerns about the possible risks of cell phone use, scientific research as a whole does not support a statistically significant association between cell phone use and health effects.
The Federal Communications Commission (FCC) concludes that there is no scientific evidence that proves that wireless phone use can lead to cancer or to other health problems, including headaches, dizziness, or memory loss.
What studies are under way that will help further our understanding of the health effects of cell phone use?
A large prospective cohort study of cell phone use and its possible long-term health effects was launched in Europe in March 2010. This study, known as COSMOSExit Disclaimer, has enrolled approximately 290,000 cell phone users aged 18 years or older to date and will follow them for 20 to 30 years.
Participants in COSMOS will complete a questionnaire about their health, lifestyle, and current and past cell phone use. This information will be supplemented with information from health records and cell phone records.
The challenge of this ambitious study is to continue following the participants for a range of health effects over many decades. Researchers will need to determine whether participants who leave are somehow different from those who remain throughout the follow-up period.
Another study already under way is a case-control study called Mobi-KidsExit Disclaimer, which will include 2000 young people (aged 10-24 years) with newly diagnosed brain tumors and 4000 healthy young people. The goal of the study is to learn more about risk factors for childhood brain tumors. Results are expected in 2016.
Although recall bias is minimized in studies that link participants to their cell phone records, such studies face other problems. For example, it is impossible to know who is using the listed cell phone or whether that individual also places calls using other cell phones. To a lesser extent, it is not clear whether multiple users of a single phone will be represented on a single phone company account.
The NIEHS, which is part of the National Institutes of Health, is carrying out a study of risks related to exposure to radiofrequency energy (the type used in cell phones) in highly specialized labs that can specify and control sources of radiation and measure their effects on rodents.
Do children have a higher risk of developing cancer due to cell phone use than adults?
In theory, children have the potential to be at greater risk than adults for developing brain cancer from cell phones. Their nervous systems are still developing and therefore more vulnerable to factors that may cause cancer.
Their heads are smaller than those of adults and therefore have a greater proportional exposure to the field of radiofrequency radiation that is emitted by cell phones. And children have the potential of accumulating more years of cell phone exposure than adults do.
So far, the data from studies in children with cancer do not support this theory. The first published analysis came from a large case-control study called CEFALO, which was conducted in Denmark, Sweden, Norway, and Switzerland. The study included children who were diagnosed with brain tumors between 2004 and 2008, when their ages ranged from 7 to 19. Researchers did not find an association between cell phone use and brain tumor risk in this group of children.
However, they noted that their results did not rule out the possibility of a slight increase in brain cancer risk among children who use cell phones, and that data gathered through prospective studies and objective measurements, rather than participant surveys and recollections, will be key in clarifying whether there is an increased risk (19).
Researchers from the Centre for Research in Environmental Epidemiology in Spain are conducting another international study—Mobi-KidsExit Disclaimer—to evaluate the risk associated with new communications technologies (including cell phones) and other environmental factors in young people newly diagnosed with brain tumors at ages 10 to 24 years.
What can cell phone users do to reduce their exposure to radiofrequency energy?
The FDA and FCC have suggested some steps that concerned cell phone users can take to reduce their exposure to radiofrequency energy (1, 23):
Reserve the use of cell phones for shorter conversations or for times when a landline phone is not available.
Use a hands-free device, which places more distance between the phone and the head of the user.
Hands-free kits reduce the amount of radiofrequency energy exposure to the head because the antenna, which is the source of energy, is not placed against the head.
Where can I find more information about radiofrequency energy from my cell phone?
The FCC provides information about the specific absorption rate (SAR) of cell phones produced and marketed within the last 1 to 2 years. The SAR corresponds with the relative amount of radiofrequency energy absorbed by the head of a cell phone user (24). Consumers can access this information using the phone’s FCC ID number, which is usually located on the case of the phone, and the FCC’s ID search form.
What are other sources of radiofrequency energy?
The most common exposures to radiofrequency energy are from telecommunications devices and equipment (1). In the United States, cell phones currently operate in a frequency range of about 1,800 to 2,200 megahertz (MHz) (6). In this range, the electromagnetic radiation produced is in the form of non-ionizing radiofrequency energy.
Cordless phones (phones that have a base unit connected to the telephone wiring in a house) often operate at radio frequencies similar to those of cell phones; however, since cordless phones have a limited range and require a nearby base, their signals are generally much less powerful than those of cell phones.
Among other radiofrequency energy sources, AM/FM radios and VHF/UHF televisions operate at lower radio frequencies than cell phones, whereas sources such as radar, satellite stations, magnetic resonance imaging (MRI) devices, industrial equipment, and microwave ovens operate at somewhat higher radio frequencies (1).
How common is brain cancer? Has the incidence of brain cancer changed over time?
Brain cancer incidence and mortality (death) rates have changed little in the past decade. In the United States, 23,130 new diagnoses and 14,080 deaths from brain cancer are estimated for 2013.
The 5-year relative survival for brain cancers diagnosed from 2003 through 2009 was 35 percent (25). This is the percentage of people diagnosed with brain cancer who will still be alive 5 years after diagnosis compared with the survival of a person of the same age and sex who does not have cancer.
The risk of developing brain cancer increases with age. From 2006 through 2010, there were fewer than 5 brain cancer cases for every 100,000 people in the United States under age 65, compared with approximately 19 cases for every 100,000 people in the United States who were ages 65 or older (25).
Selected References
U.S. Food and Drug Administration (2009). Radiation-Emitting Products: Reducing Exposure: Hands-free Kits and Other Accessories. Silver Spring, MD. Retrieved June 18, 2012.
Volkow ND, Tomasi D, Wang GJ, et al. Effects of cell phone radiofrequency signal exposure on brain glucose metabolism. JAMA 2011; 305(8):808–813. [PubMed Abstract]
Hirose H, Suhara T, Kaji N, et al. Mobile phone base station radiation does not affect neoplastic transformation in BALB/3T3 cells. Bioelectromagnetics 2008; 29(1):55–64. [PubMed Abstract]
Oberto G, Rolfo K, Yu P, et al. Carcinogenicity study of 217 Hz pulsed 900 MHz electromagnetic fields in Pim1 transgenic mice. Radiation Research 2007; 168(3):316–326. [PubMed Abstract]
Zook BC, Simmens SJ. The effects of pulsed 860 MHz radiofrequency radiation on the promotion of neurogenic tumors in rats. Radiation Research 2006; 165(5):608–615. [PubMed Abstract]
Ahlbom A, Green A, Kheifets L, et al. Epidemiology of health effects of radiofrequency exposure. Environmental Health Perspectives 2004; 112(17):1741–1754. [PubMed Abstract]
Cardis E, Richardson L, Deltour I, et al. The INTERPHONE study: design, epidemiological methods, and description of the study population. European Journal of Epidemiology 2007; 22(9):647–664. [PubMed Abstract]
International Agency for Research on Cancer (2008). INTERPHONE Study: latest results update—8 October 2008Exit Disclaimer. Lyon, France. Retrieved June 18, 2012.
The INTERPHONE Study Group. Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study. International Journal of Epidemiology 2010; 39(3):675–694. [PubMed Abstract]
Larjavaara S, Schüz J, Swerdlow A, et al. Location of gliomas in relation to mobile telephone use: a case-case and case-specular analysis. American Journal of Epidemiology 2011; 174(1):2–11. [PubMed Abstract]
Johansen C, Boice J Jr, McLaughlin J, Olsen J. Cellular telephones and cancer: a nationwide cohort study in Denmark. Journal of the National Cancer Institute 2001; 93(3):203–207. [PubMed Abstract]
Schüz J, Jacobsen R, Olsen JH, et al. Cellular telephone use and cancer risk: update of a nationwide Danish cohort. Journal of the National Cancer Institute 2006; 98(23):1707–1713. [PubMed Abstract]
Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk of brain tumours: update of Danish cohort study. British Medical Journal 2011; 343:d6387. [PubMed Abstract]
Benson VS, Pirie K, Schüz J, et al. Mobile phone use and risk of brain neoplasms and other cancers: Prospective study. International Journal of Epidemiology 2013; First published online: May 8, 2013. doi:10.1093/ije/dyt072Exit Disclaimer
Muscat JE, Malkin MG, Thompson S, et al. Handheld cellular telephone use and risk of brain cancer. JAMA 2000; 284(23):3001–3007. [PubMed Abstract]
Hardell L, Carlberg M, Hansson Mild K. Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects. International Journal of Oncology 2011; 38(5):1465–1474. [PubMed Abstract]
Lönn S, Ahlbom A, Hall P, Feychting M. Long-term mobile phone use and brain tumor risk. American Journal of Epidemiology 2005; 161(6):526–535. [PubMed Abstract]
Aydin D, Feychting M, Schüz J, et al. Mobile phone use and brain tumors in children and adolescents: a multicenter case-control study. Journal of the National Cancer Institute 2011; 103(16):1264–1276. [PubMed Abstract]
Inskip PD, Hoover RN, Devesa SS. Brain cancer incidence trends in relation to cellular telephone use in the United States. Neuro-Oncology 2010; 12(11):1147–1151. [PubMed Abstract]
Little MP, Rajaraman P, Curtis RE, et al. Mobile phone use and glioma risk: comparison of epidemiological study results with incidence trends in the United States. British Medical Journal 2012; 344:e1147. [PubMed Abstract]
Deltour I, Johansen C, Auvinen A, et al. Time trends in brain tumor incidence rates in Denmark, Finland, Norway, and Sweden, 1974–2003. Journal of the National Cancer Institute 2009; 101(24):1721–1724. [PubMed Abstract]
Deltour I, Auvinen A, Feychting M, et al. Mobile phone use and incidence of glioma in the Nordic countries 1979–2008: consistency check. Epidemiology 2012; 23(2):301–307. [PubMed Abstract]
U.S. Federal Communications Commission (2010). Wireless. Washington, D.C. Retrieved June 18, 2012.
U.S. Federal Communications Commission. (n.d.). FCC Encyclopedia: Specific Absorption Rate (SAR) for Cellular Telephones. Retrieved June 18, 2012.
Howlader N, Noone AM, Krapcho M, et al. (eds.). (2013) SEER Cancer Statistics Review, 1975-2010. Bethesda, MD: National Cancer Institute. Retrieved June 24, 2013.
Related Resources
Magnetic Field Exposure and Cancer
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Magnetic Field Exposure and Cancer NIH-NCI
Magnetic Field Exposure and Cancer NCI
What are electric and magnetic fields?
Why are ELF-EMFs studied in relation to cancer?
What is the evidence for an association between magnetic field exposure and cancer in children?
What is the evidence that magnetic field exposure is linked to cancer in adults?
Where can people find additional information on EMFs?
What are electric and magnetic fields?
Electric and magnetic fields are invisible areas of energy that are produced by electricity, which is the movement of electrons, or current, through a wire.
An electric field is produced by voltage, which is the pressure used to push the electrons through the wire, much like water being pushed through a pipe. As the voltage increases, the electric field increases in strength.
A magnetic field results from the flow of current through wires or electrical devices and increases in strength as the current increases. The strength of a magnetic field decreases rapidly with increased distance from its source.
Electric fields are produced whether or not a device is turned on, but magnetic fields are produced only when current is flowing, which usually requires a device to be turned on. Power lines produce magnetic fields continuously because current is always flowing through them.
Electric and magnetic fields together are referred to as electromagnetic fields, or EMFs. There are both natural and human-made sources of EMFs. The earth’s magnetic field, which causes a compass to point North, is an example of a naturally occurring EMF. Power lines, wiring, and electrical appliances, such as electric shavers, hair dryers, computers, televisions, and electric blankets produce what are called extremely low frequency (ELF) EMFs.
ELF-EMFs have frequencies of up to 300 cycles per second, or Hertz (Hz); for example, the frequency of alternating current in power lines is 50 or 60 Hz. Cell phones produce radiofrequency EMFs above the ELF range. For more information about cell phones, see the NCI Fact Sheet Cell Phones and Cancer Risk.
Electric fields are easily shielded or weakened by walls and other objects, whereas magnetic fields can pass through buildings, living things, and most other materials. Consequently, magnetic fields are the component of ELF-EMFs that are usually studied in relation to their possible health effects.
Why are ELF-EMFs studied in relation to cancer?
Any possible health effects of ELF-EMFs would be of concern because power lines and electrical appliances are present everywhere in modern life, and people are constantly encountering these fields, both in their homes and in certain workplaces. Also, the presence of ELF-EMFs in homes means that children are exposed.
Even if ELF-EMFs were to increase an individual’s risk of disease only slightly, widespread exposure to ELF-EMFs could translate to meaningful increased risks at the population level.
Several early epidemiologic studies raised the possibility of an association between certain cancers, especially childhood cancers, and ELF-EMFs. Most subsequent studies have not shown such an association, but scientists have continued to investigate the possibility that one exists.
No mechanism by which ELF-EMFs could cause cancer has been identified. Unlike high-energy (ionizing) radiation, ELF-EMFs are low energy and non-ionizing and cannot damage DNA or cells directly. Some scientists have speculated that ELF-EMFs could cause cancer through other mechanisms, such as by reducing levels of the hormone melatonin. (There is some evidence that melatonin may suppress the development of certain tumors.)
However, studies of animals exposed to ELF-EMFs have not provided any indications that ELF-EMF exposure is associated with cancer (1, 2).
What is the evidence for an association between magnetic field exposure and cancer in children?
Numerous epidemiologic studies and comprehensive reviews of the scientific literature have evaluated possible associations between exposure to ELF magnetic fields and risk of cancer in children (1, 3, 4). Most of the research has focused on leukemia and brain tumors, the two most common cancers in children. Studies have examined associations of these cancers with living near power lines, with magnetic fields in the home, and with exposure of parents to high levels of magnetic fields in the workplace.
Exposure from power lines
Although a study in 1979 pointed to a possible association between living near electric power lines and childhood leukemia (5), more recent studies have had mixed findings. Currently, researchers conclude that there is little evidence that exposure to ELF-EMFs from power lines causes leukemia, brain tumors, or any other cancers in children (1, 6–10).
Exposure in homes
Many studies have also looked for possible associations between magnetic fields measured in homes and residences and the risk of childhood cancers, especially leukemia. Individual studies have had varying results, but most have not found an association or have found it only for those children who lived in homes with very high levels of magnetic fields, which are present in few residences (11–14).
To develop the most accurate estimates of the risks of leukemia in children from magnetic fields in the home, researchers have analyzed the combined data from many studies.
In one such analysis that combined data from nine studies done in several countries, leukemia risk was increased only in those children with the highest exposure (a category that included less than 1 percent of the children); these children had a twofold excess risk of childhood leukemia (15). In another analysis that combined data from 15 individual studies, a similar increase in risk was seen in children with the highest exposure level (16).
A more recent analysis of seven studies published after 2000 found a similar trend, but the increase was not statistically significant (17).
Overall, these analyses suggest that if there is any increase in leukemia risk from magnetic fields, it is restricted to children with the very highest exposure levels. But it is possible that this increase is not real, because if magnetic fields caused childhood leukemia, certain patterns would have been found, such as increasing risk with increasing levels of magnetic field exposure. Such patterns were not seen.
Another way that people can be exposed to magnetic fields in the home is from household electrical appliances. Although magnetic fields near many electrical appliances are higher than those near power lines, appliances contribute less to a person’s total exposure to magnetic fields because most appliances are used only for short periods of time.
Again, studies have not found consistent evidence for an association between the use of household electrical appliances and risk of childhood leukemia (18).
Parental exposure and risk in children
Several studies have examined possible associations between maternal or paternal exposure to high levels of magnetic fields before conception and/or during pregnancy and the risk of cancer in their future children. The results to date have been inconsistent (19, 20). Studies are ongoing to evaluate this question.
Exposure and cancer survival
A few studies have investigated whether magnetic field exposure is associated with prognosis or survival of children with leukemia. Several small retrospective studies of this question have yielded inconsistent results (21–23).
An analysis that combined prospective data for more than 3000 children with acute lymphoid leukemia from eight countries showed that ELF magnetic field exposure was not associated with their survival or risk of relapse (24).
What is the evidence that magnetic field exposure is linked to cancer in adults?
Although some studies have reported associations between ELF-EMF exposure and cancer in adults, other studies have not found evidence for such associations.
The majority of epidemiologic studies have shown no relationship between breast cancer in women and exposure to ELF-EMFs in the home (25–28), although several individual studies have shown hints of an association (29, 30).
Several studies conducted in the 1980s and early 1990s reported that people who worked in some electrical occupations (such as power station operators and phone line workers) had higher-than-expected rates of some types of cancer, particularly leukemia, brain tumors, and male breast cancer (1).
Some occupational studies showed very small increases in the risks of leukemia and brain cancer, but these results were based on participants’ job titles and not on actual measurements of their exposures. More recent studies, including some that considered the participant’s job title as well as measurements of their exposures, have not shown consistent findings of an increasing risk of leukemia, brain tumors, or female breast cancer with increasing exposure to magnetic fields at work (29, 31–35).
Where can people find additional information on EMFs?
The National Institute of Environmental Health Sciences (NIEHS) website has information about EMFs and cancer.
Selected References
World Health Organization, International Agency for Research on Cancer. Non-ionizing radiation, Part 1: Static and extremely low-frequency (ELF) electric and magnetic fieldsExit Disclaimer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans 2002; 80:1-395.
Lagroye I, Percherancier Y, Juutilainen J, De Gannes FP, Veyret B. ELF magnetic fields: Animal studies, mechanisms of action. Progress in Biophysics and Molecular Biology 2011; 107(3):369-373. [PubMed Abstract]
Ahlbom IC, Cardis E, Green A, et al. Review of the epidemiologic literature on EMF and Health. Environmental Health Perspectives 2001; 109 Suppl 6:911-933. [PubMed Abstract]
Schüz J. Exposure to extremely low-frequency magnetic fields and the risk of childhood cancer: Update of the epidemiological evidence. Progress in Biophysics and Molecular Biology 2011; 107(3):339-342. [PubMed Abstract]
Wertheimer N, Leeper E. Electrical wiring configurations and childhood cancer. American Journal of Epidemiology 1979; 109(3):273-284. [PubMed Abstract]
Kleinerman RA, Kaune WT, Hatch EE, et al. Are children living near high-voltage power lines at increased risk of acute lymphoblastic leukemia? American Journal of Epidemiology 2000; 151(5):512-515. [PubMed Abstract]
Kroll ME, Swanson J, Vincent TJ, Draper GJ. Childhood cancer and magnetic fields from high-voltage power lines in England and Wales: A case–control study. British Journal of Cancer 2010; 103(7):1122-1127. [PubMed Abstract]
Wünsch-Filho V, Pelissari DM, Barbieri FE, et al. Exposure to magnetic fields and childhood acute lymphocytic leukemia in São Paulo, Brazil. Cancer Epidemiology 2011; 35(6):534-539. [PubMed Abstract]
Sermage-Faure C, Demoury C, Rudant J, et al. Childhood leukaemia close to high-voltage power lines--the Geocap study, 2002-2007. British Journal of Cancer 2013; 108(9):1899-1906. [PubMed Abstract]
Kabuto M, Nitta H, Yamamoto S, et al. Childhood leukemia and magnetic fields in Japan: A case–control study of childhood leukemia and residential power-frequency magnetic fields in Japan. International Journal of Cancer 2006; 119(3):643-650. [PubMed Abstract]
Linet MS, Hatch EE, Kleinerman RA, et al. Residential exposure to magnetic fields and acute lymphoblastic leukemia in children. New England Journal of Medicine 1997; 337(1):1-7. [PubMed Abstract]
Kheifets L, Ahlbom A, Crespi CM, et al. A pooled analysis of extremely low-frequency magnetic fields and childhood brain tumors. American Journal of Epidemiology 2010; 172(7):752-761. [PubMed Abstract]
Mezei G, Gadallah M, Kheifets L. Residential magnetic field exposure and childhood brain cancer: A meta-analysis. Epidemiology 2008; 19(3):424-430. [PubMed Abstract]
Does M, Scélo G, Metayer C, et al. Exposure to electrical contact currents and the risk of childhood leukemia. Radiation Research 2011; 175(3):390-396. [PubMed Abstract]
Ahlbom A, Day N, Feychting M, et al. A pooled analysis of magnetic fields and childhood leukaemia. British Journal of Cancer 2000; 83(5):692-698. [PubMed Abstract]
Greenland S, Sheppard AR, Kaune WT, Poole C, Kelsh MA. A pooled analysis of magnetic fields, wire codes, and childhood leukemia. Childhood Leukemia-EMF Study Group. Epidemiology 2000; 11(6):624-634. [PubMed Abstract]
Kheifets L, Ahlbom A, Crespi CM, et al. Pooled analysis of recent studies on magnetic fields and childhood leukaemia. British Journal of Cancer 2010; 103(7):1128-1135. [PubMed Abstract]
Hatch EE, Linet MS, Kleinerman RA, et al. Association between childhood acute lymphoblastic leukemia and use of electrical appliances during pregnancy and childhood. Epidemiology 1998; 9(3):234-245. [PubMed Abstract]
Infante-Rivard C, Deadman JE. Maternal occupational exposure to extremely low frequency magnetic fields during pregnancy and childhood leukemia. Epidemiology 2003; 14(4):437-441. [PubMed Abstract]
Hug K, Grize L, Seidler A, Kaatsch P, Schüz J. Parental occupational exposure to extremely low frequency magnetic fields and childhood cancer: A German case–control study. American Journal of Epidemiology 2010; 171(1):27-35. [PubMed Abstract]
Svendsen AL, Weihkopf T, Kaatsch P, Schüz J. Exposure to magnetic fields and survival after diagnosis of childhood leukemia: A German cohort study. Cancer Epidemiology, Biomarkers & Prevention 2007; 16(6):1167-1171. [PubMed Abstract]
Foliart DE, Pollock BH, Mezei G, et al. Magnetic field exposure and long-term survival among children with leukaemia. British Journal of Cancer 2006; 94(1):161-164. [PubMed Abstract]
Foliart DE, Mezei G, Iriye R, et al. Magnetic field exposure and prognostic factors in childhood leukemia. Bioelectromagnetics 2007; 28(1):69-71. [PubMed Abstract]
Schüz J, Grell K, Kinsey S, et al. Extremely low-frequency magnetic fields and survival from childhood acute lymphoblastic leukemia: An international follow-up study. Blood Cancer Journal 2012; 2:e98. [PubMed Abstract]
Schoenfeld ER, O'Leary ES, Henderson K, et al. Electromagnetic fields and breast cancer on Long Island: A case–control study. American Journal of Epidemiology 2003; 158(1):47-58. [PubMed Abstract]
London SJ, Pogoda JM, Hwang KL, et al. Residential magnetic field exposure and breast cancer risk: A nested case–control study from a multiethnic cohort in Los Angeles County, California. American Journal of Epidemiology 2003; 158(10):969-980. [PubMed Abstract]
Davis S, Mirick DK, Stevens RG. Residential magnetic fields and the risk of breast cancer. American Journal of Epidemiology 2002; 155(5):446-454. [PubMed Abstract]
Kabat GC, O'Leary ES, Schoenfeld ER, et al. Electric blanket use and breast cancer on Long Island. Epidemiology 2003; 14(5):514-520. [PubMed Abstract]
Kliukiene J, Tynes T, Andersen A. Residential and occupational exposures to 50-Hz magnetic fields and breast cancer in women: A population-based study. American Journal of Epidemiology 2004; 159(9):852-861. [PubMed Abstract]
Zhu K, Hunter S, Payne-Wilks K, Roland CL, Forbes DS. Use of electric bedding devices and risk of breast cancer in African-American women. American Journal of Epidemiology 2003; 158(8):798-806. [PubMed Abstract]
Tynes T, Haldorsen T. Residential and occupational exposure to 50 Hz magnetic fields and hematological cancers in Norway. Cancer Causes & Control 2003; 14(8):715-720. [PubMed Abstract]
Labrèche F, Goldberg MS, Valois MF, et al. Occupational exposures to extremely low frequency magnetic fields and postmenopausal breast cancer. American Journal of Industrial Medicine 2003; 44(6):643-652. [PubMed Abstract]
Willett EV, McKinney PA, Fear NT, Cartwright RA, Roman E. Occupational exposure to electromagnetic fields and acute leukaemia: Analysis of a case-control study. Occupational and Environmental Medicine 2003; 60(8):577-583. [PubMed Abstract]
Coble JB, Dosemeci M, Stewart PA, et al. Occupational exposure to magnetic fields and the risk of brain tumors. Neuro-Oncology 2009; 11(3):242-249. [PubMed Abstract]
Li W, Ray RM, Thomas DB, et al. Occupational exposure to magnetic fields and breast cancer among women textile workers in Shanghai, China. American Journal of Epidemiology 2013; 178(7):1038-1045. [PubMed Abstract]
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Reviewed: November 3, 2014
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