A physician offers sanity-based perspectives on EPA’s “Data Derangement Syndrome”
by Charles G. Battig, MD
Propaganda tactics employed by the Environmental Protection and its activist allies increasingly employ emotion as a primary media tool. Mothers and children pose on the US Capitol steps, waving signs that claim they are fighting for clean air and their children’s health. Images of these “lovable lobbyists” for EPA’s Clean Power Plan and other rules are intentionally heart-tugging.
It is maternal instinct versus scientific facts; emotions versus informed debate. If EPA issues dire warnings, that is all these moms need to hear. Indeed, it is hard to overcome such pleadings with cold facts alone.
The well-orchestrated “do something” demonstrations enable politicians and agencies to devise and implement new legislation and regulations. It is much like physicians who succumb to patients’ “do something” demands by prescribing antibiotics for common colds. It is a useless, if not dangerous practice.
The public’s general fear of anything labeled a chemical, or requiring some comfort with numbers, is a powerful psychological tool for alarmists. In-the-street TV interviews showing fearful reactions to di-hydrogen monoxide represent but one example. The scary-sounding chemical, of course, is H2O: ordinary water.
If the air is hazy, even from natural sources like pine trees, many people automatically assume it is injurious to their health, even if the “pollution” levels are perfectly safe. The dose makes the poison. It’s even worse for invisible toxins. The linear no-threshold mindset now governs virtually all government toxicology programs.
The attitude assumes there is no safe limit. Any and all substances in any amount may be injurious to health, until proven otherwise. Forgone possible health or economic benefits from the demonized substances are not considered. Economist Julian Simon coined the term “false bad news” to describe how activists, regulators and the media make innocuous substances sound harmful, when they target something and set-out to ban it.
These crusaders ignore impartial and even convincing scientific rebuttals, since they specialize in publicizing bad news and perpetuating their own prejudiced agendas. Hollywood celebrities and politicians have become pseudo-authoritative fonts of pseudo-scientific knowledge for the media-obsessed public. Actors should be the least believable, as they make a career by pretending to be what they are not and regurgitating words written for them by others. But somehow they become star experts. Many career politicians are little better.
EPA reports that the six major Clean Air Act pollutants have declined some 62% on average. Meanwhile, reported asthma incidence has risen from 8.9% in 2005 to 9.4% in 2010. How can that be? EPA blames air pollution. But more likely factors include increased public awareness and reporting; expanding the agency’s asthma definition to include all reactive airway diseases; and blunted development of natural immunity, as children exercise less and play less outdoors, in environments that may now be too clean to challenge and bolster developing immune systems.
EPA’s guiding principles seem to be “never let a hypothetical disease go to waste” and “look for data that prove the assumption” (but ignore all unsupportive data). A favorite new bogeyman is what EPA calls PM2.5 (particulate matter or soot 2.5 microns or smaller in diameter). Pollutants like this are appropriately categorized under the rubric of DDS: “Designer Disease Syndrome” or “Data Derangement Syndrome.”
PM2.5 is a most peculiar disease-causing agent, compared to traditional agents. Its pathophysiologic mechanism is undefined, even by EPA. It includes multiple substances whose only common characteristic is that they are really tiny: human hair is 16 to 48 times wider than 2.5 microns. However, they must pose a substantial health threat because EPA says they do – even though the particles have no unique chemical composition, arise from both natural and manmade activities, and vary in composition from one geographic location to another and over different periods of time.
EPA claims inhaling PM2.5 can cause death, including sudden death and long-term death (which the agency calls “premature deaths”). But what level is healthy or safe, and by whose and what criteria? Former EPA Administrator Lisa Jackson must have known, since she told Congress in 2011: “If we could reduce particulate matter to healthy levels, it would have the same impact as finding a cure for cancer in our country.”
Her claim has no scientific basis, and underscores EPA’s growing credibility problem. The agency claims PM2.5 particles cause death. However, epidemiological studies provide no direct evidence of definitive causation, or even validated explanations for the biological mechanisms allegedly causing death.
EPA claims “epidemiological studies … have found consistent, precise positive associations between short-term exposure to PM2.5 and cardiovascular mortality … at short lags (0-1 days).” Do we really face a zero to one-day timeframe? Is EPA predicting near-instant deaths? Even if so-called precise positive associations exist – and EPA has not shown that they actually do – how does this demonstrate cause-and-effect relationships?
Even EPA’s epidemiological tests on human subjects do not show such relationships. Volunteers were told PM2.5 is associated with health risks and death. However, EPA had conducted “297 controlled human exposures” to PM2.5, while encountering only “one clinically significant event” – and even that study participant experienced “no harm or injury.” Some tests even involved pollution levels close to what a person might encounter in “a typical urban center in America on a smoggy day,” also with no problems.
Valid, useful experimental designs must define what animal species, human test subjects and dose sizes are involved. Were all possible confounding factors identified and accounted for? Were these valid, random population samples – or biased selections? Were the computers programmed to find the sought-for correlations? We do not know. But we do know that weak statistical correlations are being presented as proof of cause-and-effect. We do know that EPA is a master at trolling data banks to find needle-in-the-haystack clinical correlations that can be used to predict “dire risks” and project “deep concerns” to mothers.
EPA has conducted controlled human exposure studies to air pollutants for more than thirty years, at the University of North Carolina. During that time, more than six-thousand volunteers were studied, without a single serious adverse event.
The Harvard Six Cities Study (Laden et al 2006) provides a key scientific basis for EPA claims regarding supposed PM toxicology. Yet examination of the data shows that the statistical “relative risk” (RR) for total mortality claims ranges from below one to barely above one and a fraction. That does not meet the minimum legal standard of a RR of at least 2 to identify a significant population risk.
Even worse, the Harvard study teams have walled-off their raw clinical data from independent investigators, by claiming patient confidentiality, thereby preventing verification of results by other experts. Independent reproducibility and verification of test results are the traditional (and essential) hallmarks of scientific research. Invoking patient confidentiality to block access to raw data casts doubt on the entire process, especially since providing adequate patient confidentiality is rather easy to do.
So is there a health problem to investigate, or not? How much more testing do we need to demonstrate an actual problem? It looks more like a disease concept in search of a susceptible victim.
Representative Lamar Smith (R-TX) has led the congressional effort to make governmental agencies provide open disclosure of data and analyses used to formulate policy. The Secret Science Reform Act of 2015 (H.R. 1030) is designed to ensure such ethical behavior. Public funds support most such research, which is used to justify costly rules. We have a right to expect that our funds are used in an open and ethical manner.
EPA claims PM2.5 mortality begins at just 35µg/m3. Then why are airport smokers and the Shanghai population not dropping dead on the spot? Airport smoker lounges have ambient levels of 600 to 10,000µg of PM2.5 per cubic meter. A single draw on a cigarette floods a smoker’s lungs with 10,000µg to 40,000µg. The Shanghai press reports PM outdoor levels of 600µg/m3 – and says average life expectancy there is 82.5 years – greater than in any major US city. Where are our overflowing emergency rooms and mortuaries?
EPA’s chosen path has been to fabricate a PM2.5 disease entity, endow it with a unique pathological profile, fund scientific reviewers who support its claims, and present as proof of serious health impacts the favorable published reviews it paid for – while ignoring contrary findings by other scientists. Post-modern medicine has fused with post-modern pseudo-science. This perverse combination does not justify expensive regulations that kill jobs and impair people’s health and welfare.
Charles G. Battig, MD is a physician in Charlottesville, VA: www.Climateis.com. This article is based on his presentation at the Heartland Institute’s 2015 International Conference on Climate Change.