The End of Doom

by Ronald Bailey

  Another point to keep in mind is that low-probability events do occur. Even if there is only a one in a million chance of something occurring to someone, with 7 billion people on the earth, it will occur 7,000 times somewhere. As the Internet reaches its tentacles further into human society, these odd occurrences have ever greater chances of being marveled at by wider and wider audiences.

  From a public policy perspective, one of the most common and problematic misperceived patterns is cancer clusters. Every year we are treated to reports of communities that purportedly suffer more than their share of cancer. We all know the script by heart: Ten people in a small town are diagnosed with cancer—say, leukemia—within five years. Victims, reporters, regulators, and trial lawyers frantically search for a corporation manufacturing some allegedly toxic chemical nearby on which to pin the blame. The victims’ suffering, it’s assumed, must be the result of corporate greed.

  This is exactly the script that played out on Long Island back in the 1990s. Under orders from Congress, the NCI conducted the most searching inquiry ever into an alleged cancer cluster and came up with exactly nothing. The NCI’s Deborah Winn told The New York Times the data “were very, very conclusive” that the synthetic chemicals studied “are not associated with breast cancer.”

  Interestingly, another study, reported just a month earlier, did find a very high correlation between a risk factor and a woman’s chances of getting breast cancer. That study confirmed that the longer a woman breast-fed, the lower her risk of getting breast cancer. Could it be that long-term breast-feeding was not fashionable among well-off suburban moms on Long Island two or three decades ago?

  Fate or bad luck are not acceptable to us pattern-searching humans. What we once blamed on the malevolence of witchcraft, we now blame on the malevolence of corporations. In a sense, we are still in hot pursuit of witches.

  We Are Now Living Long Enough to Get Cancer

  As our deepening knowledge of biology is revealing, many of the human body’s resources are aimed at keeping our cells’ natural tendency to become cancerous at bay long enough for us to reproduce successfully. The plain, unavoidable fact of life is that our bodies’ defenses against cancer break down as we age. It is true that high, prolonged exposures to some synthetic chemicals (or, in the case of cigarettes, natural chemicals) can cause cancer. But as the NCI epidemiologists found on Long Island, trace exposures to “environmental toxins” generally can’t be linked to cancer. Nevertheless, our built-in drive to identify patterns will guarantee that we will continue to seek someone to blame for our ills and that we will suffer through many more expensive, unnecessary, and self-defeating witch hunts for a long time to come.

  Even the US National Cancer Institute denies that there is a “cancer epidemic.” As the institute explains, the common misconception that we are experiencing a “cancer epidemic” stems largely from sensationalized media reports. “This only appears to be the case because the number of new cancer cases reported is rising as the population is both expanding and aging. Older people are more likely to develop cancer,” notes the institute. “So as more and more members of a 75-million-strong ‘baby-boomer’ cohort begin shifting en masse to older, more cancer-prone ages, the number of new cancer cases is expected to increase in the next several decades.”

  If you are male in the United States your lifetime risk of developing cancer is approximately 1 in 2, and your risk of dying of cancer is 1 in 4. If you are female your lifetime risk of contracting cancer is 1 in 3, and your risk of dying of malignancy is 1 in 5. Is an especially toxic environment responsible for these grim statistics? Actually, no. What these statistics signal is that you are likely to live a long time. If you live long enough you will get cancer.

  A look back in time is instructive. In 2012, the New England Journal of Medicine published a fascinating article comparing the annual death rates between 1900 and 2010. The annual death rate in 1900 from the top ten causes of death was 1,100 per 100,000 (the all-cause death rate was just over 1,700 per 100,000). Of those deaths, more than half were caused by infectious diseases. Pneumonia or influenza killed 202 per 100,000; tuberculosis 194 per 100,000; gastrointestinal infections 143 per 100,000; and diphtheria 40 per 100,000. What about cancer? Cancer accounted for just 64 deaths out of 100,000 in 1900.

  By 2010, the top ten causes of death killed just over half as many Americans, at the rate of about 600 per 100,000 (the all-cause death rate was just shy of 800 per 100,000). In the list of contemporary leading causes of death, infectious diseases hardly figure at all in the New England Journal of Medicine statistics. In fact, the infectious diseases listed are pneumonia and influenza, which kill 16 per 100,000 annually now. Cancer? In 2010, the disease caused 186 out of 100,000 deaths annually, triple the number in 1900. That initially sounds terrible until one considers the fact that only 47 percent of Americans lived past age sixty in 1900. Today, 88 percent of Americans live past age sixty.

  The median age at which cancer is diagnosed is sixty-five, and 53 percent of all cancers are diagnosed in people over age sixty-five. Seventy percent are diagnosed in people over age fifty-five. In 1929, the first year for which the US Centers of Disease Control has national data, average life expectancy in the United States was fifty-seven years. Roughly speaking, this suggests that in the first decades of the twentieth century Americans were not living long enough for them to have developed around 75 percent of today’s cases of cancer. That’s why cancer was then comparatively rarer. And that’s not taking into account the lower incidence rates that would likely have existed due to higher levels of physical activity and lower rates of obesity, cigarette smoking, and alcohol consumption that prevailed among Americans in the early part of the twentieth century. For example, the lung cancer death rate for men was just shy of 5 per 100,000 in 1930; by 1990, the rate had risen to 76 per 100,000.

  Hormone Havoc: Half the Men Our Fathers Were?

  While some environmental groups remain loyal to the old belief that exposures to trace amounts of synthetic chemicals are causing a cancer epidemic, others are now pushing the notion that these chemicals are generating hormone havoc. In Silent Spring, Carson does vaguely speculate that pesticide residues might increase endogenous estrogens, and she also worries about the exposures to synthetic estrogens in cosmetics, drugs, foods, and workplaces. She mentions in passing medical reports that suggest there is reduced sperm production among crop dusters. Nearly thirty years later, a group of Carson disciples meeting in 1991 at the Wingspread Center in Wisconsin under the auspices of the World Wildlife Fund developed their guru’s suspicions about the effects of synthetic chemicals on sex hormones into the endocrine disruptor conjecture. The idea is that some synthetic chemicals harmfully produce the effects of estrogen, testosterone, and other hormones on human bodies and in wildlife.

  I suspect the endocrine disrupting chemical (EDC) controversy will play out much the same way as the cancer controversy has. Basically it will turn out that some synthetic compounds in high doses will have deleterious effects on those exposed, but background exposures will have no detectable effects on the larger population.

  As it happens, proponents of the idea that endocrine disruption is a major public health problem have issued a couple of consensus statements recently. For example, one such was issued in 2013 by a group working under the auspices of the United Nations Environment Programme. The State of the Science of Endocrine Disrupting Chemicals report begins by confidently asserting that many endocrine-related disorders are on the rise, including low semen quality and deformed penises, early breast development in girls, attention deficit and hyperactivity disorder in children, obesity and type 2 diabetes, and testicular, prostate, breast, and thyroid cancer. The “consensus” on all of these damaging effects was derived by combing selectively through the epidemiological literature. Interestingly, if you read through the data cited by the consensus architects, it becomes clear that the confident assertions in the State of the Science consensus are based on a
lot of vigorous hand-waving and embarrassingly weak data.

  For example, it bears noting that the State of the Science report itself admits that current research does not support the claim that synthetic endocrine disrupting chemicals are responsible for the trends that it identifies. The State of the Science report observes that “evidence linking estrogenic environmental chemicals with [breast cancer] is not available.” In addition, the State of the Science report acknowledges that “there is very little epidemiological evidence to link EDC [endocrine disrupting chemical] exposure with adverse pregnancy outcomes, early onset of breast development, obesity or diabetes.” Furthermore, the State of the Science report concedes, “There is almost no information about associations between EDC exposure and endometrial or ovarian cancer,” and “no studies exist that explore the potential link between fetal exposure to EDCs and the risk of testicular cancer occurring 20–40 years later.” Additionally, the State of the Science report notes that “high accidental exposures to PCBs [polychlorinated biphenyls] during fetal development or to dioxins in childhood increase the risk of reduced semen quality in adulthood.” If PCBs do lower sperm quality, it’s a problem of the past rather than the future, since the production of PCBs was banned in the United States in 1979. Let’s look beyond the feeble findings of the State of the Science report and see what other research has to say about the asserted trends.

  Penis Problems and the Sperm Apocalypse?

  Alarm about allegedly falling sperm counts due to exposure to synthetic estrogens was first raised in a 1992 article by Scandinavian researchers, who reported there had been a decline of nearly 50 percent in fifty years. Ever ready to fan the flames of panic, the publicists at Greenpeace quickly initiated a clever campaign of advertisements declaring, “You’re not half the man your father was.”

  Although the originators of the 1992 finding of falling semen quality and increasing penile anomalies continue to produce epidemiology to bolster those claims, many other researchers report contrary trends. For example, a 2013 comprehensive review of thirty-five sperm quality studies published after the purported decline was first announced in 1992 finds no such overall trend. The researchers report that eight studies involving a total of 18,109 men suggest a decline in semen quality; twenty-one studies encompassing 112,386 men show either no change or an increase in semen quality; and six studies involving 26,007 men show ambiguous or conflicting results. According to the researchers, the upshot is that “allegations for a worldwide decline in semen parameter values have not withstood scientific scrutiny.”

  What about the epidemic of deformed penises that endocrine disruptors are supposedly engendering? One of the more common birth defects in males is hypospadias, in which the urethral opening occurs elsewhere along the penis rather than at the tip. A 2012 comprehensive review of data on trends for this birth defect reported that “generalized statements that hypospadias is increasing are unsupported” and that “firm conclusions cannot be made regarding the association of endocrine-disrupting exposures with hypospadias.” Another systematic review of studies looking for genetic and environmental influences on hypospadias found that “[w]hile genes involved in the aetiology of hypospadias have received a considerable amount of attention, research on environmental factors has been even more extensive. Despite the large number of studies, however, clear evidence for causal environmental factors is still lacking.”

  A similar 2009 report, “Rising Hypospadias Rates: Disproving a Myth,” concluded, “A review of the epidemiologic data on this issue amassed to date clearly demonstrates that the bulk of evidence refutes claims for an increase in hypospadias rates.”

  Testicular cancer does appear to be increasing in many developed nations. Proponents of the endocrine disruption thesis have conducted epidemiological studies that weakly suggest that they do correlate with greater risk for testicular cancer. On the other hand, lots of other physiological phenomena also correlate with higher testicular cancer rates. A 2012 study reports that one of the stronger correlations uncovered by several studies is that the risk of testicular cancer increases with adult height. The researchers in that study find that men over six feet tall have a higher risk of testicular cancer, and they suggest that “the trend of increasing adult height and the increasing TC [testicular cancer] incidence are biologically interconnected with improved nutrition in early life.” They note that while testicular cancer rates in Europe increased throughout the twentieth century, they stalled for the generation that suffered nutritional deprivation as a result of World War II. Interestingly, being overweight reduces the chances of testicular cancer, so one might think that as the obesity rate rises, the testicular cancer rate should fall.

  The State of the Science consensus report notes, “The prevalence of obesity and type 2 diabetes has dramatically increased worldwide over the last 40 years.” As noted above, the consensus report, however, admits there is very little epidemiological evidence linking endocrine disrupting chemicals to increasing obesity rates, but that does not stop researchers from trying to do so. A typical study, “Association of Endocrine Disruptors and Obesity: Perspectives from Epidemiologic Studies,” published in 2010, found a correlation between excess weight and endocrine disrupting chemicals. However, that study begins by acknowledging that “changes in diet and physical activity are undoubtedly key causal factors related to the increase in obesity.” Well, yes.

  A far more plausible explanation for the rise in obesity can be found in a 2013 study that tracked the changes in the number of calories Americans consumed daily between 1971 and 2010. The researchers found that in 1971, Americans ate an average of 1,955 calories daily. That average rose to 2,269 per day by 2003 and has recently dropped a bit, to 2,195 calories daily. While Americans are eating more, they are also exercising less. A 2011 study reported, “Over the last 50 years in the U.S. we estimate that daily occupation-related energy expenditure has decreased by more than 100 calories, and this reduction in energy expenditure accounts for a significant portion of the increase in mean U.S. body weights for women and men.” It is well established that being overweight escalates considerably the risk of type 2 diabetes. A 2012 workshop organized by the US National Institute of Environmental Health Sciences reviewed seventy-five studies relating exposures to synthetic endocrine disruptors to type 2 diabetes and concluded, “In no case was the body of data considered sufficient to establish causality.” It’s hard not to conclude that in comparison to eating more calories and increasingly sedentary lifestyles, the effects of endocrine disrupting chemicals on rising obesity and the prevalence of type 2 diabetes, if such effects exist, would be negligible.

  The State of the Science report also asserts that there is a “trend towards earlier onset of breast development in young girls.” Again, some epidemiologists have sought to identify synthetic endocrine disruptors as the possible villains behind this trend. However, considerable research persuasively suggests that earlier breast development and puberty onset in girls is linked to increases in body fat. In other words, rising obesity rates strongly correlate with earlier onset of puberty in girls. There does appear to be an epidemic of diagnoses of attention deficit hyperactivity disorder (ADHD), but many researchers question the claim that actual cases are increasing. A 2014 comprehensive review in the International Journal of Epidemiology analyzed 135 studies dealing with trends in ADHD and reports, “In the past three decades, there has been no evidence to suggest an increase in the number of children in the community who meet criteria for ADHD when standardized diagnostic procedures are followed.”

  A devastating article, “Endocrine Disruption: Fact or Urban Legend,” by a team of European and American toxicologists, published in the journal Toxicology Letters in December 2013, reviews hundreds of studies on the effects of alleged endocrine disrupting chemicals. Their review of the science finds no effects on sperm counts, no effects on the rate of penile deformations, no effects on any cancer, no effects on diabetes, no effects on breast development, and
… simply no effects whatsoever from exposures to chemicals, natural and synthetic, that emit a weak hormonal signal in very sensitive lab tests. Among many other things, the researchers point out that voluntary human exposures to powerful hormone modifying substances such as the estrogens in birth control pills have resulted in practically no significant health effects on either those who take them or their progeny. The effective potency of contraceptive pills is more than a million times greater than the potencies of the weak endocrine disrupting chemicals on which environmental activists focus. Taking this and much other evidence into account, the researchers assert that “the hypothesis that the negligible exposure of humans to chemicals of negligible hormonal potency could have an effect on human fertility is absurd, defying a scientific basis as well as common sense.” They conclude that the man-made environmental disruptor hypothesis “has now been evaluated experimentally and epidemiologically for nearly 20 years and no convincing evidence has been found of an actual decline in human fertility, and even less of a causal relation with synthetic hormonally active substances.”

  The Problem of Epidemiology

  Epidemiologists are hard at work sincerely trying to uncover relationships between all sorts of exposures and health outcomes. Many of the assertions made about the possible effects of endocrine disrupting chemicals in the State of the Science report are based on the results of observational studies by epidemiologists. The number of observational studies has increased from 80,000 in the 1990s to more than 260,000 in the first decade of the twenty-first century. Most observational studies are case-control studies in which epidemiologists identify a population that suffers from a disease or other condition and then attempt to match them with a similar population free of the disease or condition. They then look for differences in lifestyle, diet, or the environment that might account for the disease. This should work in theory, but the problems with controlling for biases in the data and for confounding factors are well known to epidemiologists. Confounding factors are variables that have been overlooked by researchers. Confounders can easily generate spurious associations.