Stop concocting unscientific excuses for ignoring brain injuries from football

NFL football is a game of inches, a “bruising ballet” and powered by iconic statistics.

Fans recognize the number 55 as the most touchdown passes in a year (Peyton Manning), 197 as the most receiving touchdowns in a career (Jerry Rice), and so on.

But for scientists, lawyers and players and their families concerned about life or death after football, a new statistic looms over the others: 110/111. This fraction represents the number of deceased NFL players found to have a pattern of brain lesions known as CTE (chronic traumatic encephalopathy), out of the nearly-identical number of all NFL players tested for the disease to date.

110/111 is a curious kind of number — both potentially misleading and yet highly informative. Using these case reports to estimate how widespread CTE and its hallmark symptoms of mental decline and mood disturbances will be over the next several decades is tricky because the sample is not representative; the 111 whose families sought autopsies for their next-of-kin tend to include those players who suspected they might have CTE because of symptoms they suffered during retirement.

Unfortunately, advocates on both sides are desperately misusing the 110/111 statistic. A few claim we will eventually learn that a “shockingly high percentage” of all NFL players will develop CTE, but this may over-rely on the skewed nature of the first 111 autopsies.

More misleading, and more abhorrent, however, are the arguments made by many physicians and lawyers to the effect that 110/111 means nothing.

For the past several years, I worked with colleagues at Harvard Law School to craft recommendations for how government agencies, particularly the U.S. Occupational Safety and Health Administration (OSHA), could help to reduce the risk of CTE (our work was published earlier this year in the Arizona Law Review). But in the course of that work, I repeatedly encountered experts outside the risk and public health disciplines who would not accept mainstream risk-based observations as to why the 110/111 series of case reports — along with other human and animal studies — are ominous about the odds that a player will develop CTE.

Critics lacking public health training are routinely making four illogical claims to “manufacture doubt” about this emerging issue.

First, I was buffeted with repeated claims that “some players never developed CTE despite long careers.” I hope it’s obvious that this is a completely useless fact. A risk factor never has to result in disease or injury among everyone for it to cause grave harm in a few or in many victims; that’s the very definition of “risk” (as opposed to certainty).

Imagine the claim that “smoking can’t cause lung cancer because I heard of someone who smoked for 60 years and died in a car crash” and the derision that would, or at least should, dismiss that fallacy. Similarly, our draft OSHA study was criticized because we didn’t mention the mirror-image observation — that it may be possible to develop CTE without ever having experienced repeated head trauma. Again, change this utterance to “smoking can’t cause lung cancer because radon can,” and one should shudder at the illogic.

Besides, it’s not even clear that a single human being has ever developed CTE without some history of head trauma: the Mayo Clinic examined 264 specimens from a brain bank, and found CTE in 21 of the 66 persons who had been contact-sport athletes, but not in even a single one of 198 matched control subjects without contact-sport experiences.

Other skeptics, using two similar spasms of illogic, actually argue that although CTE is associated with devastating symptoms, the brain lesions themselves may be “tiny abnormalities [that] might not have any specific clinical significance.” Again, anecdotes about a specific person with CTE lesions and no symptoms, or the opposite fact that many people can have similar symptoms without CTE lesions, are just noise, not signals of anything relevant.

And it turns out, we can learn much about the true risk of CTE among football players by starting with, though not accepting at face value, the series of 110 case reports. We can readily estimate the lowest possible risk, simply by exploring the unrealistic best-case scenario that not a single additional CTE case will ever be found among the rest of the players who were in the League at the same time as the 110 were.

Using individual player data from the NFL on the number of his team’s snaps each player was on the field for, and on the length of his career in the League, I estimated that there was a total of about 12,000 player-careers worth of on-field activity (about 26,000 different players suited up during this time period, but many of them played only occasionally and in a very few games). So 110 cases out of 12,000 players yields a best-case risk of 0.0092, or just under a 1 percent risk.

A 1-in-100 chance (at the bare minimum) of a grave disease caused by environment or occupation is a huge risk that any law or regulation would deem unacceptable. The Supreme Court instructed OSHA in 1980 that occupational disease risks above one chance per thousand must be worthy of regulation, and Congress has instructed the EPA in various laws to regulate cancer and other risks exceeding one chance per million.

What, then, could OSHA do to reduce this significant risk of disease, in football and in other occupations (logging, commercial driving, the military) where repeated head trauma is commonplace? OSHA could propose regulatory limits for the cumulative head-trauma forces workers could undergo, just as it has regulated various chemicals based on case series of as few as seven workers afflicted with cancer or sterility, and having a common exposure.

In the 2014 court decision in Secretary of Labor v. SeaWorld, the D.C. Circuit ruled that OSHA indeed can reduce risks in entertainment industries just as it does in manufacturing, over the lone dissent from new Supreme Court appointee and self-described “textualist” Brett Kavanaugh, who wrote that Congress “must have silently intended” to exempt entertainment when it established OSHA, even though Congress never wrote anything of the sort.

But regulation is sometimes clumsy, especially when remedies are largely untested and need to adapt to changing circumstances and evolving science. At the other extreme, agency partnerships with industries and other forms of self-regulation have a generally poor track record of accomplishing much more than freezing in place the status quo.

One promising middle ground between the dictatorial and the useless is a concept we pioneered at OSHA in the late 1990s: “enforceable partnerships” wherein government, industry, and labor cooperate to develop a detailed but flexible code of practice for anticipating and controlling health and safety risks, and where industry agrees that government can enforce the code of practice as if it was a private contract.

If football can evolve to remain thrilling and inspirational without being a grave gamble for those who work at it, as I hope it will, all the stakeholders (especially the physicians) need to stop playing defense by concocting unscientific excuses for inaction, and start drawing up plays that will better preserve the game and its workers’ health.

Adam M. Finkel is a pioneer in improving methods for the quantitative risk assessment of occupational and environmental health hazards. He is a clinical professor of environmental health at the University of Michigan School of Public Health, and was both the chief scientist and a high-ranking enforcement official at OSHA during the Clinton and George W. Bush administrations.

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