Via @longreads on Twitter, a summation of what we know about the relationship between cell phones and brain cancer from Dr. Siddhartha Mukherjee of Columbia University.
The crudest method to capture a carcinogen’s imprint in a real human population is a large-scale population survey. If a cancer-causing agent increases the incidence of a particular cancer in a population, say tobacco smoking and lung cancer, then the overall incidence of that cancer will rise. That statement sounds simple enough â€” to find a carcinogen’s shadow, follow the trend in cancer incidence â€” but there are some fundamental factors that make the task complicated.
The most important of these is life expectancy, which is growing almost everywhere. The average life expectancy of Americans has increased â€” from 49 in 1900 to 78 in 2011. Several cancers are strongly, often exponentially, age-dependent. An aging population will seem more cancer-afflicted, even if the real cancer incidence has not changed.
But what if we make an â€œage adjustmentâ€ for the population and shrink or expand the cancer incidence to match the changes in age structure? To ask whether cellphones increase the risk of brain cancer, then, we might begin by turning to this question: Has the age-adjusted incidence of brain cancer increased in the recent past?
The quick answer is no. Brain cancer is rare: only about 7 cases are diagnosed per 100,000 men and women in America per year, and a striking increase, following the introduction of a potent carcinogen, should be evident. From 1990 to 2002 â€” the 12-year period during which cellphone users grew to 135 million from 4 million â€” the age-adjusted incidence rate for overall brain cancer remained nearly flat. If anything, it decreased slightly, from 7 cases for every 100,000 persons to 6.5 cases (the reasons for the decrease are unknown).
In 2010, a larger study updated these results, examining trends between 1992 and 2006. Once again, there was no increase in overall incidence in brain cancer. But if you subdivided the population into groups, an unusual pattern emerged: in females ages 20 to 29 (but not in males) the age-adjusted risk of cancer in the front of the brain grew slightly, from 2.5 cases per 100,000 to 2.6. These cancers appear in the frontal lobe â€” a knuckle-shaped area immediately behind the forehead and the eye.
It is difficult to imagine that cellphones caused these frontal-lobe tumors: how, or why, would a phone’s toxicity have skipped over the area nearest to it and caused a tumor in a distant site? Most epidemiologists and biologists do not find such a tissue-skipping mechanism plausible and most doubt that there is any causal link between frontal tumors and phones.
But thus far, this extraordinarily wide-cast net has yet to find solid proof of risk for cellphone radiation: not a single trial or test that has attributed carcinogenic potential has been free of problems. Populationwide studies have failed to demonstrate an increased incidence; retrospective trials have been contradictory and riddled with biases; animal studies negative; human physiological experiments inconclusive; cellular studies inconsistent and weak. What is clearly needed, experts agree, is a single, definitive, unbiased study â€” â€œone trial,â€ to borrow Paget’s terminology.
Logistically speaking, the simplest such human trial is a case-control study that compares cancer patients with healthy patients, using phone-log data that companies have thus far been reluctant to provide. The simplest animal study involves subjecting rats and mice to long-term exposure to cellphone radiation. The National Toxicology Program has begun such a study. Cellphone radiation will be turned on and off for 10-minute stretches for 20 hours each day. This experiment â€” the closest we will get to making mice use actual cellphones â€” is likely to be published in 2014.
Might the cellphone industry have already performed such experiments and conspired to keep real data on brain cancers from us â€” just as the tobacco industry conspired to obfuscate real data on tobacco and carcinogenesis in the 1950s? It’s possible, but there are important differences in comparing these trials with the tobacco studies. With smoking, despite active attempts by the industry to stifle data, the epidemiological trials were incontrovertibly positive, human physiological data markedly suggestive and animal studies (including Roffo’s painted-rabbit experiment) striking.