UPDATE 20/10/11: Today’s announcement is discussed here
Do mobile phones cause cancer? The debate has been raging for years, and we’ve covered it several times on this blog.
Today, the International Agency for Research into Cancer (IARC), which is part of the World Health Organisation – had their say. Over the last week, they convened a panel of 31 experts to look at the available evidence. Their verdict: “radiofrequency electromagnetic fields” – the sort given off by mobile phones – belong to “Group 2B”, which means that they “possibly” cause cancer in humans.
What does that mean?
It means that there is some evidence linking mobile phones to cancer, but it is too weak to make any strong conclusions. Specifically, IARC’s panel said that the evidence that mobile phones pose a health risk was “limited” for two types of brain tumours – glioma and acoustic neuroma – and “inadequate” when it comes to other types of cancer.
The Chairman of the group, Dr Jonathan Samet, said, “The conclusion means that there could be some risk, and therefore we need to keep a close watch for a link between cell phones and cancer risk.”
IARC classifies different things according to whether they are likely to cause cancer, from tobacco to viruses to certain jobs. They are the gold standard for this sort of thing. They have five possible categories of risk:
Group 1 is the highest, reserved for things like smoking, asbestos, alcohol and so on. It means that there’s extremely strong evidence that the thing in question causes cancer.
Group 2A includes things that are “probably carcinogenic to humans”. Here, the evidence is “limited” in humans, but “sufficient” from animal studies.
Group 2B – this is the one that mobile phones now fall under – means something is “possibly carcinogenic to humans”. It means there is “limited evidence” that something causes cancer in people, and even the evidence from animal studies is “less than sufficient”. Group 2B means that there is some evidence for a risk but it’s not that convincing. This group ends up being a bit of a catch-all category, and includes everything from carpentry to chloroform.
Group 3 means that something is “not classifiable as to its carcinogencity to humans”. This means that the evidence is “inadequate in humans or “inadequate or limited” in animals. Usually, there just haven’t been enough studies to say either way.
Group 4 means something probably doesn’t cause cancer in humans. So far, there is only one chemical – caprolactam – in this group. People jokingly take this to mean that everything causes cancer but it simply reflects the fact that IARC focuses its attention on things that could potentially pose a health risk.
Where does the evidence come from?
Even though this topic gets a lot of press attention, there have been a relatively small number of studies on mobile phones and cancer. Most of these are “case-control studies” – they compare people who already have cancer (cases) with healthy people (controls), and ask them about how they used their phones in the past. These studies include the InterPhone study, an international collaboration of scientists from 13 countries, and work by Lennart Hardell’s group at University Hospital, Orebro.
So far, only one Danish study has actually followed a group of healthy people (around 420,000 of them) to see if their use of mobile phones affected their future risk of cancer.
What does the evidence say?
A smaller number of publications, mostly from the Hardell group, have found associations between mobile phones and brain cancer risk. But the majority of papers, including those from InterPhone and the Danish study, have found that mobile phone use does not increase the risk of brain cancer, or any other type of cancer, for at least 10 years of use.
To give you an idea of the evidence to date, here are two images that represent the studies on mobile phones and glioma brain cancers up to 2009 (taken from this paper). The top one shows the effect of short-term use (less than 5 years), and the bottom one deals with long-term use (more than 5 years). Each dot shows the result from a single study. If it’s on the horizontal line, there is no effect. If it’s above or below the line, this suggests that phones might increase or reduce the risk of cancer respectively.
The bars above and below the dot are important – they represent the “confidence interval”, which indicates how reliable the result is. If the bars cross the horizontal line, this means the result is not statistically significant. It could have been down to chance, or bias. As you can see, only one study out of 14 found the mobile phones significantly affect the risk of cancer.
The dot that’s second from the right (labelled “pooled estimate”) represents the combined results from all the studies. Again, you can see that it’s pretty much sitting on the line, which suggests that mobile phones do not affect the risk of cancer.
Some studies have suggested that people have a higher risk of brain cancer specifically on the side of the head that they say they hold their phones to. However, many of these studies have also reported either no overall increased risk of cancer, or a lower risk of tumours on the other side of the head.
Scientists disagree as to whether this “side-of-head effect” is real. If phones were really increasing the risk of brain cancer on one side of the head, you would still expect to see this reflected in the overall result. Alternatively, the result could be due to bias, because people inaccurately remembered how they used their phones (see below). Nor is it clear if people actually hold their phones consistently to one side of their heads.
What are the weaknesses of these studies?
All the existing studies suffer from similar problems.
- Changing technology. Mobile phone technology has also changed considerably over the last decades and it is not clear if studies based on use of old models will apply to modern ones.
- Assessment problems. There still are no clear ways of assessing someone’s actual exposure to mobile phone radiation. Instead, studies use questionnaires to work out whether and how people use mobile phones. These questionnaires rely on people accurately remembering their past mobile phone use years or decades ago. In some of the Hardell studies, a third of patients received help from relatives in completing the questionnaires (compared to just one in ten controls). In one case, the next-of-kin of deceased patients estimated how often their loved ones used their phones.
- Recall bias. It’s not clear if the replies to these questionnaires are accurate – a problem known as “recall bias”. Answers might be biased because people have heard about mobiles and brain cancer in the media, because brain cancer can distort memory, or simply because people misremember things that happened a long time ago.
The individual studies have drawn more specific criticisms.
The Danish study relied on subscriber records instead of questionnaires. However, there are concerns that subscribers aren’t always the ones who use the phones, and that this method excludes corporate users, who could use their phones heavily.
For example, the InterPhone study has been criticized for using unrealistic definition of “regular users” and having low response rates to its questionnaires. The authors have also disagreed as to how their results should be interpreted.
The Hardell group has been criticised for publishing the same data in multiple papers, inconsistently reporting data such as sample sizes, and having implausibly high response rates to its questionnaires.
The abstracts of their papers often highlight statistically significant links in very specific groups of people, while ignoring overall negative results. These types of analyses are difficult to interpret – if you split a sample far enough, you end up with small numbers of people in each group and greater odds of finding a positive result simply through chance.
Are there conflicts of interest?
The mobile phone industry has provided funding for the InterPhone study and the Danish study. In both cases, funds have been administered through independent, third-party organisations that are meant to act as “firewalls” to ensure the independence of the scientists. InterPhone, for example, received 19.2 million euros of funding. 5.5 million of this total came from industry sources, and was either administered through the International Union for Cancer Control, or collected via taxes and fees from government agencies.
Lennart Hardell has not received funding from industry sources but has appeared as an expert witness in litigation cases involving mobile phones.
Could mobile phones cause cancer?
This is an important question. Scientists are confident that tobacco, alcohol or asbestos can cause cancer because they can explain how these things affect the way our cells work. These explanations are called “biological mechanisms” – they play a vital role in establishing that something causes cancer.
So far no one has been able to provide a good biological mechanism for the link between mobile phones and cancer. The “how” question is an open one. The phones give off microwave radiation, but this has millions of times less energy than, say, an X-ray and is not powerful enough to damage our DNA. They mildly heat the body, but again, not enough to pose a health risk. Other suggestions have been put forward, but none are backed by consistent evidence.
Are brain cancer rates going up?
If mobile phones increase the risk of brain cancer, the rates of this disease should be skyrocketing since mobile phone use has risen dramatically over the last few decades.
But studies in the US, New Zealand, Denmark, Norway, Sweden and Finland have found no such trends. In the UK, the incidence of brain cancer has been flat for the past few decades. A recent English study concluded that “the increased use of mobile phones between 1985 and 2003 has not led to a noticeable change in the incidence of brain cancer in England between 1998 and 2007.”
Brain cancers can take many years to develop, so it is possible that trends would only start rising after more time.
What about base stations?
Base station exposures are much less likely to affect our health than phones themselves as their emissions are many times weaker and usually well below international guidelines.
Just last year, a British study (the largest of its kind) found “no association between risk of childhoodcancers and mobile phone base station exposures during pregnancy”.The authors say the results “should help to place any future reportsof cancer clusters near mobile phone base stations in a widerpublic health context.”
What should we make of the evidence?
It is understandable that people are concerned about mobile phones, especially because they are so widely used. But so far, the published studies do not show that mobile phones could increase the risk of cancer. This conclusion is backed up by the lack of a solid biological mechanism, and the fact that brain cancer rates are not going up significantly.
However, all of the studies so far have weaknesses, which make it impossible to entirely rule out a risk. Mobile phones are still a new technology and there is little evidence about effects of long-term use.
For this reason, the UK Government advises a precautionary stance. It suggests that if adults want to use a mobile phone, they can choose to minimise their exposure by keeping calls short. It also advises discouraging children under the age of 16 from making non-essential calls as well as also keeping their calls short.
And, as IARC’s working group said, there needs to be more research.
What studies are in the pipeline?
A large study called COSMOS, including researchers from the UK and four other countries, has been set up to look at the long-term effects of mobile phone use after 20-30 years. Like the Danish study, it will recruit healthy people, measure their mobile phone use and see if this affects their health in the long-term.
The MOBI-KIDS study, involving 13 countries, has been set up to look at health effects in children.
Michael Evans January 30, 2012
It seems to me that it matters little what is true or untrue. It is always the case that the big companies have more money than the “honest” research people, so they will nearly always win. This was the case for decades with cigarettes, so I for one will advise my family to use this item in a way that will lessen the possibility of exposure, should it be decided in the future that it does cause problems, as then it may be too late!
Roger White December 6, 2011
It is hard to know what is a real concern or scare mongering these days. Anything in excess is bad for you, that is the rule I usually go by.
Henry Honda June 30, 2011
I notice that what is not mentioned is the fact that Cancer Research UK used to be proud of their new university research centre in Cambridge – partially funded by a leading MOBILE OPERATOR to the tune of £5 million plus.Nowadays that fact is barely mentioned.
When the above news broke, a CR UK representative appeared on TV and made a better job of protecting the interests of the mobile operators than the Mobile Operators Association (Their ‘union’).
joke June 25, 2011
“red-herring” to people who don’t study physics, but is far short of saying there is damage.
Ed Yong June 20, 2011
OR stands for “odds ratio”
In this case, it refers to the odds of developing brain cancer if you’re a mobile phone user, compared to the odds of developing brain cancer if you’re not a mobile phone user. If mobile phones do not cause cancer, those odds are the same and the odds ratio will be 1.
Amigo kit June 20, 2011
Science teaching us that concepts could change, the causes of a certain disease change with medical research, years ago science said cell phones maybe could induce cancer, then thy said it could be wrong, today again cell phones are bad for health, i don’t understand too much about medicine but i think you should be offer proves of what you are saying.
Dr. Goulu June 15, 2011
Just a small question about the figure : what is this “OR” scale, why is it log and why does “1” mean no correlation ?
I ask because I copied it on my own article on the subject and a reader raised that point… Thanks!
Ricky June 9, 2011
Some people insist to not respect the review of WHO. If WHO give his review to the world thats because are studies in this problem are serious and well done studies. There are people with a opossite review because they win something with the use of this phones.
Ed Darrell June 7, 2011
Paul Lewis, my recollection is that Prof. Goldsmith and others concluded that there was no detectable long-term injury done to anyone working in the embassy as a result of the alleged microwaving, and consequently, no damages paid to victims.
Assuming no risk might be a “red-herring” to people who don’t study physics, but is far short of saying there is damage. Do you have any evidence Goldsmith or anyone else found injury?
Paul Lewis June 7, 2011
seems like there are a lot of closed minds on here. Open them up
Following the long term low level microwaving of the American Embassy by the Soviet Union, during the Cold War, which lead to many leukaemias and cancers,
miscarriages and illnesses of the embassy staff, Professor John Goldsmith was called in to diagnose the problem and write a report on such. Professor Goldsmith is possibly the world’s leading professor in microwave radiation. He holds 11 professorships, represented Europe for the World Health Organisation and is an International Consultant for Microwave Communication Systems.
Regarding heat, he says:
‘To use the lack of significant heating effect as evidence of lack of risk is a Red
Mario June 6, 2011
It is the pneumatic pulsing effect on the HUMAN CELLS which as I understand it, communicate on similar electro-chemical frequencies of between 1.8 – 2.4 Ghz
Which in my opinion is more of a concern !
Roz June 5, 2011
I would like to add that my husband was a BT Engineer and he at times had to use is mobile phone for over an hour at a time whilst sorting out problems. This was in the late 80’s and the older type phone. He noticed that the side of his face where he held the phone became hotter and over a period of time the sight in the eye on that side was also affected, this was confirmed by having an eye test and he visited his doctor. My husband was concerned enough to tell his manager that he would NOT use a mobile phone in this wayand they did not insist that he should! After a time his sight returned to normal. I think that there could well be a risk and I would suggest not useing mobiles for any length of time and I would not be supprised that in the not too distant future, there will be evidence confirming the connection to cancers.
Bryan Harrison June 4, 2011
About 4 years ago now I took part in a study at the Imperial college hospital in London regarding Tetra / airways radio. Tetra is supposed to be about 4 times more powerful that mobile telephones and the study formed a series of test carried out over the course of a day. The results should have been given out about two years ago however still have not been released. The report that was released can be found at http://www.police-health.org.uk/docs/PilotReportvFinal.pdf
But the conclusion doesn’t fill me with confidence,
We have now solved the technical problems related to reducing the interference level
between the Airwave radio and EEG machine. Having started with an interference level of
~3μV, by adding ferrite sleeves and pi-filters to a redesigned shielded headbox, and using
coaxial screened recording leads, interference has now been reduced to ~50nV; a reduction of
>80% (~16dB). Having solved these technical problems, recruitment of Police personnel
started in December 2005. We have received a good response from the Police and the study
commences with participants at the end of January 2006.
Unfortunately my technical ability on electronics are not great enough to gain a full understanding of the consequences!
Bryon June 3, 2011
Facts versus fears: DDT
Extract from the American Council on Science and Health publication “Facts Versus Fears” – Edition 3, June 1998. © American Council on Science and Health – all rights reserved.
DDT (dichlorodiphenyltrichloroethane) was first synthesized in 1877,1 but it was not until 1940 that a Swiss chemist discovered that it could be sprayed on walls and would cause any insect to die within the next six months, without any apparent toxicity to humans.2 DDT’s effectiveness, persistence, and low cost (only 17 cents per pound) resulted in its being used in antimalarial efforts worldwide. It was introduced into widespread use during World War II and became the single most important pesticide responsible for maintaining human health through the next two decades. The scientist who discovered the insecticidal properties of DDT, Dr. Paul Müller, was awarded the 1948 Nobel Prize in Physiology and Medicine.3
In 1962 Rachel Carson’s lyrical yet scientifically flawed book Silent Spring was released. The book argued eloquently but erroneously that pesticides, and especially DDT, were poisoning both wildlife and the environment and also endangering human health. The emotional public reaction to Silent Spring launched the modern environmental movement.4 DDT became the prime target of the growing anti-chemical and anti-pesticide movements during the 1960s. Reasoned scientific discussion and sound data on the favorable human health effects of DDT were brushed aside by environmental alarmists who discounted DDT’s enormous benefits to world health with two allegations: (1) DDT was a carcinogen, and (2) it endangered the environment, particularly for certain birds.
In 1969 a study found a higher incidence of leukemia and liver tumors in mice fed DDT than in unexposed mice.5 Soon, too, environmentalists were blaming the decline in populations of such wild bird species as the osprey and peregrine falcon on the contamination by DDT of their environment. A number of states moved to ban DDT, and in 1970 the U.S. Department of Agriculture announced a plan to phase out all but essential uses.6
Numerous scientists protested that the laboratory-animal studies flew in the face of epidemiology, given that DDT had been used widely during the preceding 25 years with no increase in liver cancer in any of the populations among whom it had been sprayed. And when the World Health Organization (WHO) investigated the 1969 mice study, scientists discovered that both cases and controls had developed a surprising number of tumors. Further investigation revealed that the foods fed to both mice groups were moldy and contained aflatoxin, a carcinogen.7 When the tests were repeated using noncontaminated foods, neither group developed tumors. In 1970 the National Academy of Sciences declared, “In little more than two decades, DDT has prevented 500 million human deaths due to malaria, that would otherwise have been inevitable.”8
Additionally, the evidence regarding the effect of DDT on eggshell thinning among wild birds is contradictory at best. The environmentalist literature claims that the birds threatened directly by the insecticide were laying eggs with thin shells. These shells, say the environmentalists, would eventually become so fragile that the eggs would break, causing a decline in bird populations, particularly among raptors (birds of prey).
In 1968 two researchers, Drs. Joseph J. Hickey and Daniel W. Anderson, reported that high concentrations of DDT were found in the eggs of wild raptor populations. The two concluded that increased eggshell fragility in peregrine falcons, bald eagles, and ospreys was due to DDT exposure.9 Dr. Joel Bitman and associates at the U.S. Department of Agriculture likewise determined that Japanese quail fed DDT produced eggs with thinner shells and lower calcium content.10
In actuality, however, declines in bird populations either had occurred before DDT was present or had occured years after DDT’s use. A comparison of the annual Audubon Christmas Bird Counts between 1941 (pre-DDT) and 1960 (after DDT’s use had waned) reveals that at least 26 different kinds of birds became more numerous during those decades, the period of greatest DDT usage. The Audubon counts document an overall increase in birds seen per observer from 1941 to 1960, and statistical analyses of the Audubon data confirm the perceived increases. For example, only 197 bald eagles were documented in 194111; the number had increased to 891 in 1960.12
At Hawk Mountain, Pennsylvania, teams of ornithologists made daily counts of migrating raptors for over 40 years. The counts—published annually by the Hawk Mountain Sanctuary Association—reveal great increases in most kinds of hawks during the DDT years. The osprey counts increased as follows: in 1946, 191; in 1956, 288; in 1967, 457; and in 1972, 630.13 In 1942 Dr. Joseph Hickey—who in 1968 would blame DDT for bird population decline—reported that 70 per-cent of the eastern osprey population had been killed by pole traps around fish hatcheries.14 That same year, before DDT came into use, Hickey noted a decline in the population of peregrine falcons.15
Other observers also documented that the great peregrine decline in the eastern United States occurred long before any DDT was present in the environment.16,17 In Canada peregrines were observed to be “reproducing normally” in the 1960s even though their tissues contained 30 times more DDT than did the tissues of the midwestern peregrines allegedly being extirpated by the chemical.18 And in Great Britain, in 1969, a three-year government study noted that the decline of peregrine falcons in Britain had ended in 1966 even though DDT levels were as abundant as ever. The British study concluded that “There is no close correlation between the decline in population of predatory birds, particularly the peregrine falcon and the sparrow hawk, and the use of DDT.”19
In addition, later research refuted the original studies that had pointed to DDT as a cause for eggshell thinning. After reassessing their findings using more modern methodology, Drs. Hickey and Anderson admitted that the egg extracts they had studied contained little or no DDT and said they were now pursuing PCBs, chemicals used as capacitor insulators, as the culprit.20
When carefully reviewed, Dr. Bitman’s study revealed that the quail in the study were fed a diet with a calcium content of only 0.56 percent (a normal quail diet consists of 2.7 percent calcium). Calcium deficiency is a known cause of thin eggshells.21–23 After much criticism, Bitman repeated the test, this time with sufficient calcium levels. The birds produced eggs without thinned shells.24
After many years of carefully controlled feeding experiments, Dr. M. L. Scott and associates of the Department of Poultry Science at Cornell University “found no tremors, no mortality, no thinning of eggshells and no interference with reproduction caused by levels of DDT which were as high as those reported to be present in most of the wild birds where ‘catastrophic’ decreases in shell quality and reproduction have been claimed.”23 In fact, thinning eggshells can have many causes, including season of the year, nutrition (in particular insufficient calcium, phosphorus, vitamin D, and manganese), temperature rise, type of soil, and breeding conditions (e.g., sunlight and crowding).25
In the years preceding the DDT ban, the National Academy of Sciences,26,27 the American Medical Association, the U.S. Surgeon General,28 the World Health Organization,29 and the Food and Agriculture Organizations of the United Nations30 had been among those who spoke out in support of the continued use of DDT as a disease fighter and crop protectant.
In 1971 authority over pesticides was transferred from the Department of Agriculture to the newly formed Environmental Protection Agency (EPA). In April 1972, after seven months of testimony, Judge Edmund Sweeney stated that “DDT is not a carcinogenic hazard to man. . . . The uses of DDT under the regulations involved here do not have a deleterious effect on freshwater fish, estuarine organisms, wild birds, or other wildlife. . . . The evidence in this proceeding supports the conclusion that there is a present need for the essential uses of DDT.”31
Two months later EPA head William Ruckelshaus—who had never attended a single day’s session in the seven months of EPA hearings, and who admittedly had not even read the transcript of the hearings— overturned Judge Sweeney’s decision. Ruckelshaus declared that DDT was a “potential human carcinogen” and banned it for virtually all uses.32
The ban on DDT was considered the first major victory for the environmentalist movement in the U.S. The effect of the ban in other nations was less salutary, however. In Ceylon (now Sri Lanka) DDT spraying had reduced malaria cases from 2.8 million in 1948 to 17 in 1963. After spraying was stopped in 1964, malaria cases began to rise again and reached 2.5 million in 1969.33 The same pattern was repeated in many other tropical— and usually impoverished—regions of the world. In Zanzibar the prevalence of malaria among the populace dropped from 70 percent in 1958 to 5 percent in 1964. By 1984 it was back up to between 50 and 60 percent. The chief malaria expert for the U.S. Agency for International Development said that malaria would have been 98 percent eradicated had DDT continued to be used.34
In addition, from 1960 to 1974 WHO screened about 2,000 compounds for use as antimalarial insecticides. Only 30 were judged promising enough to warrant field trials. WHO found that none of those compounds had the persistence of DDT or was as safe as DDT. (Insecticides such as malathion and carbaryl, which are much more toxic than DDT, were used instead.) And—a very important factor for malaria control in less developed countries—all of the substitutes were considerably more expensive than DDT.35
[Insertion: See the human toll of not using DDT here. Ends.]
And what of the charges leveled against DDT? A 1978 National Cancer Institute report concluded—after two years of testing on several different strains of cancer-prone mice and rats—that DDT was not carcino-genic.36 As for the DDT-caused eggshell thinning, it is unclear whether it did, in fact, occur and, if it did, whether the thinning was caused by DDT, by mercury, by PCBs, or by the effects of human encroachment.16,37 And as recently as 1998 researchers reported that thrush eggshells in Great Britain had been thinning at a steady rate 47 years before DDT hit the market; the researchers placed the blame on the early consequences of industrialization.38
Regardless of whether DDT, exclusive of other chemicals, presented a threat to bird populations, it remains in the news. DDT has a long half-life, and residues sometimes persist for years in certain environments. Also, DDT is an organochlorine. Some organochlorines have been shown to have weak estrogenic activity, but the amounts of naturally occurring estrogens in the environment dwarf the amounts of synthetic estrogens.39 A recent article in the journal Environmental Health Perspectives suggested that the ratio of natural to synthetic estrogens may be as much as 40,000,000 to 1.40
In addition, Dr. Robert Golden of Environmental Risk Studies in Washington, DC, reviewed the research of numerous scientists and concluded that DDT and DDE (a breakdown product of DDT) have no significant estrogenic activity.41
The 1996 book Our Stolen Future speculated on a link between DDT and breast cancer, noting that DDE has been found in some breast tumors.42 Recently, charges have been made associating DDT and DDE with breast cancer—specifically, the finding that women with breast cancer had higher levels of DDE in their blood than did women without breast cancer.43 However, elevated blood DDE could quite plausibly be a result of the mobilization of fat from storage depots in the body due to weight loss associated with breast cancer. Breast cancer thus may be a risk factor for elevated DDE, rather than DDE’s being a risk factor for breast cancer.44
In a 1994 study published in the Journal of the National Cancer Institute, researchers concluded that their data did not support an association between DDT and breast cancer.45 The researchers did note that breast cancer rates are higher than the national average in many places in the northeastern United States; but the data also indicated that the higher levels could be accounted for by nonenvironmental factors among women living in these regions—factors such as higher socioeconomic status and deferral or avoidance of pregnancy, both of which increase the risks of breast cancer by up to twofold.45,46
In October 1997 the New England Journal of Medicine published a large, well-designed study that found no evidence that exposure to DDT and DDE increases the risk of breast cancer.47 In the accompanying editorial Dr. Steven Safe, a toxicologist at Texas A&M University, stated, “weakly estrogenic organochlorine compounds such as PCBs, DDT, and DDE are not a cause of breast cancer.”48 Dr. Sheila Zahm, deputy chief of the occupational epidemiology branch at the National Cancer Institute, agrees that the body of evidence that DDT can cause breast cancer “is not very compelling.”49
Whelan E. Toxic Terror. 2nd ed. Buffalo, NY: Prometheus Books; 1993:100.
Desowitz R. The Malaria Capers: More Tales of Parasites and People, Research and Reality. New York: W.W. Norton; 1991:62–63.
Edwards JG. Pesticides in Medicine & Politics. Prepared address to Doctors for Disaster Preparedness. San Diego, CA. June 14, 1997.
Tarjan R, Kemeny T. Multigeneration studies on DDT in mice. Food Cosmet and Toxicol. 1969; 7:14–222.
Edwards JG. Testimony and affidavit: California Department of Food and Agriculture. Los Angeles, CA. March 1978.
National Academy of Sciences. The Life Sciences. Washington, DC: National Academy of Sciences Press; 1970.
Hickey JJ, Anderson DW. Chlorinated hydrocarbons and eggshell changes in raptorial and fish-eating birds. Science. 1968; 162:271–273.
Bitman J, Cecil HC, Harris SJ, Gries GF. DDT induces a decrease in eggshell calcium. Nature. 1969; 224:44–46.
The 42nd Annual Christmas Bird Census. Audubon Magazine. 1942; 44:1–75.
The 61st Annual Christmas Bird Census. Audubon Field Notes. 1961; 15(2): 84–300.
Taylor JW. Summaries of Hawk Mountain migration of raptors, 1934 to 1970. Hawk Mtn Assn Newsletter. 1970; 42.
Hickey JJ. Guide to Bird Watching. Madison, WI: University of Wisconsin Press; 1943.
Hickey JJ. Only 170 pairs of peregrines in eastern U.S. in 1940, before DDT. Auk. 1942; 59:176.
Beebe FL. The Myth of the Vanishing Peregrine. North Surrey, BC, Canada: Canadian Raptor Society Press; 1971.
Rice JN. Peregrine Falcon Populations. Madison, WI: University of Wisconsin Press; 1969:155–164.
Enderson JH, Berger DD. Chlorinated hydrocarbons in peregrines from northern Canada. Condor. 1968; 70:149–153.
Wilson Report. Review of organochlorine pesticides in Britain. Report by Advisory Committee on Toxic Chemicals. Department of Education and Science; 1969.
Anderson DW, Hickey JJ, Risebrough RW, Hughes DF, Christensen RE. Significance of chlorinated hydrocarbon residues to breeding pelicans and cormorants. The Canadian Field-Naturalist. 1969; 83:91–112.
Greely F. Effects of calcium deficiency. J Wildlife Management. 1960; 70:149–153.
Romanoff AL, Romanoff AJ. The Avian Egg. New York: Wiley & Sons; 1949:154.
Scott ML, Zimmermann JR, Marinsky S, Mullenhoff PA. Effects of PCBs, DDT, and mercury compounds upon egg production, hatchability and shell quality in chickens and Japanese quail. Poultry Science. 1975; 54:350–368.
Cecil HC, Bitman J, Harris SJ. No effects on eggshells, if adequate calcium is in DDT diet. Poultry Science. 1971; 50:656–659.
The Avian Egg:152–156, 266.
Handler P. The federal government and the scientific community. Science. 1971; 171(967):144–151.
Steinfeld JL. Surgeon General testimony before EPA. September 9, 1971.
The place of DDT in operations against malaria & other vector-borne disease. Official Records, WHO, Geneva: No. 190, April 1971:176–182.
Special Report of United Nations Food and Agriculture Organization. The New York Times. November 29, 1969.
Sweeney EM. EPA Hearing Examiner’s recommendations and findings concerning DDT hearings. 25 April 1972 (40 CFR 164.32).
Ackerly RL. DDT: a re-evaluation, part II. Chemical Times and Trends. October 1981:55.
Gerberg EJ, Wilcox III H. Environmental Assessment of Malaria and Control Projects–Sri Lanka. Agency for International Development. 1977; 20:32–33.
Bast J, Hill P, Rue R. Eco-Sanity: A Common Sense Guide to Environmentalism. Lanham, MD: The Heartland Institute; 1994:100–101.
Service MW. Some problems in the control of malaria. In: Ecological Effects of Pesticides (Perring, FH and Mellanby K, eds). New York: Academic Press; 1977:156.
Efron E. The Apocalyptics. New York: Touchstone/Simon & Schuster; 1985:268.
Jukes TH. Insecticides in health, agriculture and the environment. Die Naturwissensch. 1974; 61:6–16.
Milius S. Birds’ eggs started to thin long before DDT. Science News. 1988; 153(17):261.
Jukes TH. Chasing a receding zero: impact of the zero threshold concept on actions of regulatory officials. J Amer Coll Toxicol. 1983; 2(3):147–160.
Safe S. Environmental and dietary estrogens and human health: is there a problem? Environ Health Perspect. 1995; 103:346–351.
Golden, R. Proceedings of the International Environmental Conference, Washington, DC, 1995.
Colborn T, Dumanoski D, Myers JP. Our Stolen Future. New York: Dutton. 1996:184.
National Cancer Institute. DDT and Breast Cancer. NCI CancerFax. National Cancer Institute Office of Cancer Communications; August 1996:1.
Ottoboni MA. Personal communication with Dr. N. Snyderman, 1993.
Krieger N, Wolff MS, Haitt RA, et al. Breast cancer and serum organochlorines: a prospective study among white, black, and Asian women. JNCI. April 20, 1994.
Sturgeon SR, Schairer C, Gail M, McAdams M, Brinton LA, Hoover RN. Geographic variation in mortality from breast cancer among white women in the United States. JNCI. December 20, 1995.
Hunter DJ, Hankinson SE, Laden F, Colditz G, Manson JE, Willett WC, Speizer FE, Wolff MS. Plasma organochlorines levels and the risk of breast cancer. N Engl J Med. 1997; 337:1253–1258.
Safe S. Xenoestrogens and breast cancer. N Engl J Med. 1997; 337:1303–1304.
Kolata G. Study discounts DDT role in breast cancer. The New York Times. October 10, 1997:A26
John Cupis June 3, 2011
In Sept. 2007 my late wife Jackie finally lost the battle against Ovarian Cancer. Neither of us used mobile phones and we live in a “dead area” miles away from any transmitter. I would like to suggest that there is far more danger from the intense radiation of transmitter masts and indeed, from 136,000 volt power transmission lines. These last mentioned have a two metre diameter plasma field around the cables and some radiation must go way beyond that. Living under transmission lines and within a few yards of a mobile transmission mast must surely be far more in need of investigation. Breast cancer is increasing because of drinking Polish milk. In Poland the cows are pumped full of oestrogen to boost their milk yield. You can’t get English milk because our dairy farmers are being driven out of business by the cheap stuff from Poland.
Mahesh June 3, 2011
@Gwalachmai The central question is this:
Where is the physical/chemical explanation about how microwave radiation of a few microwatts can harm human tissue and cause cancer?
In spite of the implausibility of low power 50/60 Hz electromagnetic radiation causing cancer, millions of dollars were spent on epidemiological studies. Are we headed here in a similar direction- based on anecdotes and such?
Mahesh June 3, 2011
@Gwalachmai You don’t seem to get the point of my comment, which I urge you to read to the end. Your “correction” of the logic in my comment is exactly what I am trying to say. I understand you are a super-rationalist, but to deflate your sense of scientific superiority, what you mention is exactly what I say in my comment. My grandfather’s long dead and dust, without a soul to rest in peace, even without your smug condolences. Anyway I was 3 when that happened, and your condolences don’t matter to me, thanks.
Gwalachmai June 3, 2011
@Mahesh: My grandmother was a teacher, and suffered from breast cancer. My mother was also a teacher, and also suffered from breast cancer. Does this prove a link between teaching and cancer? Of course not. I’m sorry to hear about your grandfather and his coworker, but a few anecdotes do not make a statistic, never mind prove a correlation, never mind prove causation.
Laura June 2, 2011
I wonder if some people are more susceptible. When I had an old style mobile about 8 years ago I noticed almost immediately I used the phone that my head would heat and I would feel kind of uncomfortable. It’s hard to describe, but I know that feeling instantly now. My iphone also causes this, but it’s less swift and also less strong. My friends have never mentioned this, so maybe I’m extra sensitive for some reason. Touch wood, I’ve not had any diagnosis of brain cancer, but I have always used my speaker phone as much as possible because of this heat and odd discomfort, because I was very suspicious.
protonsforbreakfast June 2, 2011
This post doesn’t have a named author, but I just wanted to say ‘Thank you’ for a really well written article on a tricky topic.
I am a scientist at the National Physical Laboratory and I talk extensively to the public about mobile phone safety. I found the WHO categorisation technically correct, but really unhelpful. That use of a mobile phone is lumped in the same category as ‘drinking coffee’ really does no one any service.
There is a potential risk of harm from use of any device that emits microwaves. By law the power of microwave emissions from mobile phones is limited and happily it is in the manufacturers interests to keep emissions low because this prolongs battery life. The safety level is set (by ICNIRP) by looking to find a level at which there is borderline evidence of harm. The allowed dose is 10% of this level for workers in the industry, and 2% of that level for the general public. And there is not a single incident where any harm has definitely been associated with use a mobile phone. (neglecting accidents caused by inattention).
To Brian, first my sympathy: and best wishes. As you know, it is impossible to rule out the possibility that use of a mobile phone gave rise to your brain tumor. But there has no been increase in the incidence of brain tumours despite the exponential rise in mobile phone use. The heating effect on you ear is unlikely to have been caused by microwave emissions – typically it amounts 0.01 C – and is more likely to have been caused by the warmth of the phone.
To Marilyn, I express my sympathy. My mother in law was diagnosed with this disease a couple of years ago now, but she never used a mobile phone. If the phone was in your pocket but you were not using it, then it would typically be emitting no microwaves, except for a short burst every 10 or 15 minutes or so, lasting just a second or so. The power of the emission would have been less than 1 watt – less power than is emitted from a small hand held torch. The mobile phone radiation is absorbed in roughly the outer 2 to 3 cm of your skin and would not penetrate significantly to your stomach.
If you are interested my blog on the WHO press release can found here
and a general article looking at Brain tumour statistics with links to sources can be found here
Michael de Podesta
marilyn June 2, 2011
I am required to wear a uniform for work which has breast pockets. 11years ago, when my father was terminally ill, I acquired a mobile phone, which I stored in my right-hand breast pocket. I continued to keep a phone in this pocket, 8-9hours a day, 5 days week, 52 weeks year. In 2009 I was diagnosed with Non hodgkins lymphoma which appeared firstly as a cancerous stomach ulcer in close proximity to where my mobile phone was usually placed in my pocket. I cant help believing there is a link.
Brian Pearce June 2, 2011
I was issued with a Ericsson mobile about some 20 years ago, which after a few minutes use it heated my ear and head by a large ammount.I have now been diagnoised with a brain tumour which I have been treated for using radiotherapy and appears to have been sucessful. My opinion is that mobile phones could be the cause of my Tumour
Yewtree June 2, 2011
I do consistently hold all phones to the left side of my head – it feels really weird holding them to the right side and I would re-arrange whatever else I was holding to accommodate it being on the left side.
mousomer June 2, 2011
1. What is the current “background” risk for these kinds of cancer? An increase of even 100% of an extremely rare type of cancer is not significant.
2. Low frequency radiation cannot directly cause mutations, but it can influence the folding of complex proteins. And if you succeed in affecting the ribosome while it’s work on the DNA (or the polymerase while it is duplicating DNA), you might get in trouble. There are enough complicated ways in which low frequency radiation can affect the body. The question must be, therefor, not “can it?” (sure it CAN) but “does it?”.
Irene Gibson June 2, 2011
From experience with similar situations, I would concur with Dilip Das’ comment……and am doing just THAT.