Guest post by S. Stanley Young and Warren Kindzierski
We were asked by Heritage Foundation to write two papers on the alleged link between climate change, predicted changes in air quality, and public health effects. Both papers are available on their website. One paper is a discussion of a climate change-fine particulate matter (PM2.5)-public health link (or lack thereof). The second paper is a discussion of how ozone fits (or rather how it fails to fit) into a climate change-ozone-asthma link. A summary of both papers is provided, and an open question is posed to WUWT readers below.
First and foremost... for both PM2.5 and ozone, ALL of the studies we refer to in our two papers are not founded on proven biological plausibility of these factors causing diseases or deaths. They are founded on an assumption of what may be a cause of disease or death -- for example, PM2.5 or ozone.
PM2.5
Our first paper examined the two key public health endpoints that the U.S. Environmental Protection Agency (EPA) claims result from PM2.5 exposure -- nonfatal heart attacks and premature deaths. For both endpoints, we show that health effect studies -- observational epidemiology studies -- cited by the EPA to support their claims do not take proper accounting of hidden biases, nor do they apply rigorous tests for reproducibility of these studies.
The most glaring biases to us, but hidden to most readers, are use of questionable (poor) research practices, multiple hypotheses testing, and irreproducibility (falseness) of the research claims. Our paper also points to numerous null association studies in scholarly literature showing that PM2.5 does not cause nonfatal heart attacks and premature death.
It is up to the interpretation of the scientific method to answer the PM2.5-nonfatal heart attack/premature death claims: If the methods are flawed, so is the evidence. Studies engaging in poor research practices should be treated as untrustworthy until proven otherwise. Studies that perform many statistical comparisons tend to produce more errors of false-positive associations in the absence of statistical corrections. Finally, PM2.5-heart attack/premature death association studies failed our statistical reproducibility tests using p-value plots.
Herein lies the problem with PM2.5-health effect studies relied upon by the EPA: They are non-randomized designs with no effective researcher controls. They allow infinite researcher flexibilities in designing, analyzing, interpretating, and reporting of their results. Their data sets are not available to others for independent reproducibility testing. These types of designs and lack of controls cannot address biases and confounding. Spurious risk statistics that resemble genuine effects can (and do) easily occur in these studies when, in fact, they are nothing more than artifacts of hidden biases and confounding.
With no reproducible causal effects and given persistent, hidden biases and confounding in PM2.5 health research, any purported link between PM2.5 and public health is entirely unsupported and should not be taken seriously.
Ozone
Our second paper shows that the EPA's own data for emissions of ozone precursors and ozone levels recorded at air monitoring stations in the U.S. over the past several decades show very different trends (declines) to what climate change models are predicting in the future. For example:
Thus, any potential impacts theorized from climate change models on air quality and asthma should be treated with skepticism.
The ozone-asthma link
The EPA considers respiratory effects, including asthma, as the key health effect for ozone exposure. They use results from controlled human exposure studies (i.e., chamber studies) and animal toxicology studies to claim that ozone can cause lung function effects. They use results from observational epidemiology studies to claim that ozone levels in outdoor air are associated with asthma attacks. They use results from observational studies and animal toxicological studies to claim that ozone causes onset of asthma. Sounds complicated, but not really.
First off - chamber studies. We present numerous compelling arguments demonstrating that no adverse effects or differences in effects can be shown to exist between non-asthmatics AND asthmatics exposed to ozone in controlled chamber studies. These include confounding from awareness bias and measurement variability, and lack of external validity.
Secondly - observational epidemiology studies. Our findings can be succinctly summarized as follows... same methods as PM2.5, same flaws, no proof.
Thirdly - laboratory animal studies. The EPA has hypothesized several mechanisms for how ozone exposure may cause an asthma attack or onset of asthma. Of course, laboratory animals are not humans and suffer from numerous problems. The most important being that they do not spontaneously develop asthma, nor can they be tested in traditional ways that people are diagnosed for asthma or asthma symptoms.
Only by imaginative use of smoke and mirrors, perhaps with the aid of AI, could one conclude that evidence cited by the EPA from chamber, epidemiology, and animal studies support casual effects of asthma or asthma symptoms from ozone exposure.
Our question for WUWT readers
We pose an open question for WUWT readers which is part and parcel of the problems we encountered in our assessment of an alleged climate change-air quality-public health link.
The Reference Manual on Scientific Evidence is a document created for U.S. federal judges to help them understand and interpret difficult issues involving scientific testimony. The third edition of the Reference Manual, a 1000+ page document, was published in 2011 as a collaboration with the Federal Judicial Centre and the National Research Council (NRC) of the U.S. National Academies of Sciences, Engineering, and Medicine (NASEM).
NASEM is primarily comprised of established academics. Authors contributing to the 2011 Reference Manual included many such academics. Of 16 chapters in the 2011 Reference Manual, 14 had established academics as primary author or as co-authors. Of 30 authors or co-authors contributing overall, 22 were academics.
Junk science -- spurious (false) or fraudulent scientific data, research, or analysis -- has proliferated in peer-reviewed literature over the past several decades simultaneously as these 'established' academics built their careers. False or fraudulent evidence from junk science has been used to advance special interests and hidden government regulatory agendas on many topics important to society - climate change, environmental pollution, health impact, etc. As government funds much academic research, they should not be viewed as independent.
The U.S. Supreme Court recently overruled itself on a longstanding, controversial doctrine that gave regulatory agencies, e.g., the EPA, an unfair advantage in court - the so-called "Chevron doctrine." This decision now places the obligation on U.S. Congress to legislate more explicitly and on the courts to interpret the law without defaulting to agency judgment, which in the case of the EPA is suspect -- as we have established above.
Given this outcome, it is essential in our view that the Reference Manual be properly updated for judges (and lawyers), so they better understand junk science and how it has proliferated in academic research, government policy making, and the setting of regulations.
[Our question] How can updating the Reference Manual to address junk science best be accomplished given such a massive input from entrenched academics in the past?
Little has changed regarding the credibility of peer-reviewed literature since John Ioannidis published his 2005 paper Why Most Published Research Findings Are False, and NASEM published their two reports on irreproducibility of scientific results (one in 2016 and one in 2019), and the National Association of Scholars published their science irreproducibility report in 2018.
The last thing that should be allowed in updating the Reference Manual is for the makeup of authors to be overweight with established academics to figure out how to deal with the 800-pound junk science gorilla they helped create and/or allowed to flourish on their watch.