Disbanded Air Pollution Panel Finds EPA Standards Don’t Protect Public Health
By Gretchen Goldman
The Independent Particulate Matter Review Panel has released their consensus recommendations to the EPA administrator on the National Ambient Air Quality Standards for Particulate Matter. The group of 20 independent experts, that were disbanded by Administrator Wheeler last October and reconvened last week, hosted by the Union of Concerned Scientists, has now made clear that the current particulate pollution standards don't protect public health and welfare.
The Clean Air Scientific Advisory Committee (CASAC) — the remaining seven-person committee that is providing science advice to the EPA on the particulate matter standards — meets this week to discuss their recommendations on whether the current standards are adequate. The letter from the Independent Panel will be the elephant in the room.
The Elephant in the CASAC Meeting
CASAC has already acknowledged that they don't have the expertise to conduct the review but you know who does? The Independent Panel. The Panel has more than double the experts of CASAC, and importantly, it has multiple experts in each of the necessary scientific disciplines critical to ensure a comprehensive, robust review of the science supporting the standards.
As a result, we should watch whether or not CASAC aligns with the panel in their recommendations on the standards. If CASAC doesn't decide this week to make a similar recommendation as the Independent Panel, they'll have to explain why they disagreed with a larger, more experienced, and more diverse set of experts on the topic. In any event, the administrator will have access to both CASAC and the Independent Panel's recommendations when he ultimately makes the decision of where to set particulate pollution standards. The panel's recommendations should hold the administrator's feet to the fire.
The Fine Particulate Matter Standards Don’t Protect Public Health
The standards of greatest interest are the primary PM2.5 standards. These are the standards for particulate matter less than 2.5 micrometers (fine particulate matter) that are designed to protect public health. The panel supported the preliminary conclusions of a Draft EPA Policy Assessment that the current standards aren't requisite to protect public health.
The letter cited new and consistent epidemiological findings, supported by human and animal studies and other studies with natural experiments, as providing "clear and compelling scientific evidence" for tighter standards. Since the last particulate matter review, several new large-scale epidemiological studies provide powerful evidence that particulate matter is causing adverse health outcomes (such as early death, heart attacks, and respiratory stress) at locations and during time periods with concentrations at or below the level of the current standards.
They write, "New and compelling evidence that health effects are occurring in areas that already meet or are well below the current standards." Notably, this evidence cuts across different locations with different study populations, different study designs, and different statistical approaches.
Given the weight of the evidence from new studies across scientific disciplines and consistent with the decision-making process that EPA and its science advisers have used for many years, the panel recommends a particulate matter standard between 8 µg/m3 and 10 µg/m3 for the annual PM2.5 standard (compared to the current standard of 12 µg/m3) and between 25 µg/m3 and 30 µg/m3 for the 24-hour standard (compared to the current standard of 35 µg/m3) to protect public health. These ranges are tighter than those recommended in EPA's Draft Policy Assessment.
Keeping the Current Fine Particulate Matter Standards Ignores the Science
The Independent Panel rejected a potential argument for maintaining the current primary PM2.5 standards. The Draft Policy Assessment offered up an alternative rationale that might be used if the agency were to reject the draft assessment's recommendation to strengthen the standards and maintain the current standards. This alternative rationale explains that such a move would require the administrator to be arbitrarily selective in choosing which new studies to accept and which to toss and to disregard new epidemiologic evidence showing effects at lower levels.
The panel roundly rejected this justification, noting that, "Arguments offered in the draft Policy Assessment for retaining the current standards are not scientifically justified and are specious." This is important because if the administrator fails to strengthen the standards, he'll have to explain (both in court and in the court of public opinion) why he feels such a decision is science-based, as required under the Clean Air Act. And one proposed argument he could use has just been debunked by this expert Panel.
Otherwise, the EPA’s Draft Policy Assessment Is Scientifically Sound
While the Independent Panel critiqued some details of the EPA's Draft Policy Assessment, the panel agreed that the draft science and policy assessments were cohesive and robust and the panel commended the "good faith effort" involved in the policy assessment. Specifically, the panel affirmed the use of EPA's causality framework used in the Integrated Science Assessment they reviewed last year and the Policy Assessment's new use of a hybrid modeling technique that allows for better assessment of risk from particulate matter exposure across the country especially in rural areas.
This diverges from what the seven-member CASAC has said and done around the EPA's assessment of the science and policy. In December, they concluded that the agency's draft science assessment was not a scientific document (it is) and CASAC Chair Dr. Tony Cox has been critical of the agency's causality framework that has been developed with dozens of experts over more than a decade. This view is not shared by the scientific community, and now, not shared by the Independent Panel either.
Other Particulate Pollution Standards Also May Need Revamping
The Independent Panel decided other particulate standards were also inadequate. On PM10, particulate matter less than 10 micrometers, the panel recommended revising this standard downward given that the PM2.5 component would also be tightened and noted several research and monitoring areas that need further work. On the secondary standards, i.e. the standards designed to protect welfare effects, such as visibility, the panel concluded that the standards should be tightened in order to be more protective.
The Panel Condemns the EPA’s Broken Process
The Independent Panel's deliberations, demands for further research, and unanswered questions highlight how broken the EPA process is. In a normal review cycle, the panel would have had the opportunity to talk with agency scientists directly. The EPA staff would then have considered their comments and revised the Integrated Science Assessment in response to the committee and panel's suggestions. But because the administrator disbanded the panel and abbreviated the process, there was no opportunity for such dialogue and refinement of the agency's science assessment before policy decisions were discussed. But alas, the panel had to make do with what was available to them and CASAC does too.
Fortunately for CASAC, an Independent Panel has already done their job, and they are free (and encouraged) to run with it, especially given the long list of ways that EPA Administrator Wheeler has damaged the ambient air pollution review process.
Listen and watch this week as CASAC discusses the same questions that the Independent Panel did last week. If CASAC comes to different conclusions than the larger, more experienced, and more diverse Independent Panel, we should ask why.
You can raise these questions yourself and demand that the administrator follow the panel's recommendations, by providing written or oral public comments at a future CASAC meeting and commenting on the docket for the particulate matter rule-making. I'll be providing public comments this afternoon urging CASAC to follow the advice of the Independent Panel and commenting on the EPA's problematic process and drawing attention to that elephant in the room.
Gretchen Goldman is the research director at the Center for Science and Democracy.
Reposted with permission from our media associate Union of Concerned Scientists.
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By Jacob L. Steenwyk and Antonis Rokas
From the mythical minotaur to the mule, creatures created from merging two or more distinct organisms – hybrids – have played defining roles in human history and culture. However, not all hybrids are as fantastic as the minotaur or as dependable as the mule; in fact, some of them cause human diseases.
When Looking Through a Microscope Isn’t Close Enough.<p>For the last few years, <a href="http://www.rokaslab.org/" target="_blank">our team at Vanderbilt University</a>, <a href="https://www.researchgate.net/lab/Gustavo-Goldman-Lab" target="_blank">Gustavo Goldman's team at São Paulo University in Brazil</a> and many other collaborators around the world have been collecting samples of fungi from patients infected with different species of <em>Aspergillus</em> molds. One of the species we are particularly interested in is <a href="https://doi.org/10.1006/rwgn.2001.0082" target="_blank"><em>Aspergillus nidulans</em>, a relatively common and generally harmless fungus</a>. Clinical laboratories typically identify the species of <em>Aspergillus</em> causing the infection by examining cultures of the fungi under the microscope. The problem with this approach is that very closely related species of <em>Aspergillus</em> tend to look very similar in their broad morphology or physical appearance when viewing them through a microscope.</p><p>Interested in examining the varying abilities of different <em>A. nidulans</em> strains to cause disease, we decided to analyze their total genetic content, or genomes. What we saw came as a total surprise. We had not collected <em>A. nidulans</em> but <em>Aspergillus latus</em>, a close relative of <em>A. nidulans</em> and, as we were to soon find out, <a href="https://doi.org/10.1016/j.cub.2020.04.071" target="_blank">a hybrid species that evolved through the fusion of the genomes</a> of two other <em>Aspergillus</em> species: <em>Aspergillus spinulosporus</em> and an unknown close relative of <em>Aspergillus quadrilineatus</em>. Thus, we realized not only that these patients harbored infections from an entirely different species than we thought they were, but also that this species was the first ever <em>Aspergillus</em> hybrid known to cause human infections.</p>
Several Different Fungal Hybrids Cause Human Disease.<p>Hybrid fungi that can cause infections in humans are well known to occur in several different lineages of single-celled fungi known as yeasts. Notable examples include multiple different species of <a href="https://doi.org/10.1002/yea.3242" target="_blank">yeast hybrids</a> that cause the human diseases <a href="https://rarediseases.info.nih.gov/diseases/6218/cryptococcosis" target="_blank">cryptococcosis</a> and <a href="https://www.cdc.gov/fungal/diseases/candidiasis/index.html" target="_blank">candidiasis</a>. Although pathogenic yeast hybrids are well known, our discovery that the <em>A. latus</em> pathogen is a hybrid is a first for molds that cause disease in humans.</p>
(Left) Candida yeasts live on parts of the human body. Imbalance of microbes on the body can allow these yeasts, some of which are hybrids, to grow and cause infection. (Right) Cryptococcus yeasts, including ones that are hybrids, can cause life-threatening infections in primarily immunocompromised people. Centers for Disease Control and Prevention<p><a href="https://doi.org/10.1371/journal.ppat.1008315" target="_blank">Why certain <em>Aspergillus</em> species are so deadly</a> while others are harmless remains unknown. This may in part be because <a href="https://doi.org/10.1016/j.fbr.2007.02.007" target="_blank">combinations of traits, rather than individual traits</a>, underlie organisms' ability to cause disease. So why then are hybrids frequently associated with human disease? Hybrids inherit genetic material from both parents, which may result in new combinations of traits. This may make them more similar to one parent in some of their characteristics, reflect both parents in others or may differ from both in the rest. It is precisely this mix and match of traits that hybrids have inherited from their parental species that <a href="https://www.nytimes.com/2010/09/14/science/14creatures.html" target="_blank">facilitates their evolutionary success</a>, including their ability to cause disease.</p>
The Evolutionary Origin of an Aspergillus Hybrid.<p>Multiple evolutionary paths can lead to the emergence of hybrids. One path is through mating, just as the horse and donkey mate to create a mule. Another path is through the merging or fusion of genetic material from cells of different species.</p><p>It is this second path that appears to have been taken by our fungus. <em>A. latus</em> appears to have two of almost everything compared to its parental species: twice the genome size, twice the total number of genes and so on. But unlike other hybrids, which are often sterile like the mule, we found that <em>A. latus</em> is capable of reproducing both asexually and sexually.</p><p>But how distinct were the parents of <em>A. latus</em>? By comparing the parts contributed by each parent in the <em>A. latus</em> genome, we estimate that its parents are approximately 93% genetically similar, which is about as related as we humans are with lemurs. In other words, <em>A. latus</em>, an agent of infectious disease, is the fungal equivalent of a human-lemur hybrid.</p>
How A. Latus Differs From its Parents.<p>Elucidating the identity of closely related fungal pathogens and how they differ from each other in infection-relevant characteristics is a key step toward reducing the burden of fungal disease. For example, we found that <em>A. latus</em> was three times more resistant than <em>A. nidulans</em>, the species it was originally identified as using microscopy-based methods, to one of the most common antifungal drugs, <a href="https://www.drugbank.ca/drugs/DB00520" target="_blank">caspofungin</a>. This result provides a clear example of the potential importance of accurate identification of the <em>Aspergillus</em> pathogen causing an infection.</p><p>We also examined how <em>A. latus</em> and <em>A. nidulans</em> interact with cells from our immune system. We found that immune cells were less efficient at combating <em>A. latus</em> compared to <em>A. nidulans</em>, suggesting the hybrid fungus may be trickier for our immune systems to identify and destroy.</p><p>In the midst of the COVID-19 pandemic, our quest to understand <em>Aspergillus</em> pathogens is becoming more urgent. Growing evidence suggests that <a href="https://doi.org/10.1111/myc.13096" target="_blank">a fraction of COVID-19 patients are also infected with <em>Aspergillus</em>.</a> More worrying is that these <a href="https://doi.org/10.3201/eid2607.201603" target="_blank">secondary <em>Aspergillus</em> infections</a> can worsen the clinical outcomes for those infected with the novel coronavirus. That being said, we stress that little is known about <em>Aspergillus</em> infections in COVID-19 patients due to a lack of systematic testing, and none of the infections identified so far appear to have been caused by hybrids.</p><p>So, when it comes to hybrids, some are fantastic (the minotaur), some are helpful (the mule) and some are dangerous (<em>Aspergillus latus</em>). Understanding more about the biology of <em>Aspergillus latus</em> may help in our understanding of how microbial pathogens arise and how to best prevent and combat their infections.</p>
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