ALEC-Affiliated Legislators Launch Premature Attacks on Carbon Pollution Limits
By Aliya Haq
For many of us, this winter makes June feel far away, but you’d think summer is right around the corner judging by the frenzied activity of the American Legislative Exchange Council (ALEC). The Environmental Protection Agency (EPA) is scheduled to propose limits on carbon pollution from power plants this coming June, but ALEC and other polluter groups are not waiting to see EPA's draft standard before they declare opposition.
EPA's upcoming standards will be the first time that carbon limits have ever been set for existing power plants – the largest source of U.S. carbon pollution. The final standard will be issued next year, giving state governments until June of 2016 to design a plan to achieve the needed pollution reductions. But ALEC, a secretive cabal of corporations and conservative state lawmakers, is already pushing two pro-polluter resolutions opposing EPA action. Several of ALEC's corporate members are linked to the coal industry, including Peabody Coal, American Electric Power, and the American Coalition for Clean Coal Electricity.
Most state legislatures are only a few weeks into their 2014 sessions, yet ALEC legislators have already introduced a dozen anti-EPA bills and resolutions across the country, including in Arizona, Florida, Georgia, Illinois, Ohio, Kansas, Missouri, Tennessee, Virginia and West Virginia. These attacks on carbon limits use weak ALEC arguments that don't stand up to scrutiny:
- ALEC claims that EPA standards will hurt the economy, but an analysis from the Natural Resources Defense Council shows that we can significantly cut carbon pollution while adding 200,000 jobs nationally and lowering average monthly home electric bills.
- ALEC asserts that power plants will not singlehandedly solve the global climate problem, failing to recognize that addressing power plant emissions, a significant portion of global carbon pollution, is an essential step forward. We must deliver on our promise to the international community that we will cut emissions 17 percent below 2005 levels by 2020 in order to persuade other countries to follow our lead.
- ALEC implies that coal is already clean, citing recent declines in carbon pollution. Of course, the actual reason for this decline is less coal use due to low natural gas prices, energy efficiency increases and more renewable energy like wind and solar. Additionally, the Department of Energy forecasts that carbon pollution will increase again in the absence of policy action.
In a misguided effort to protect coal companies, ALEC-affiliated legislators in Missouri, Florida, Kansas, and West Virginia are also pushing legislation that would create serious obstacles for Governors and state agencies. These self-defeating bills would take away a Governor’s flexibility in meeting the EPA standard, forcing the state into more expensive and difficult compliance pathways than necessary. Thankfully, sensible state legislators are already defeating these kinds of bills—in Virginia, the shoddy, restrictive parts of SB 615 were replaced with benign language to study the effects of implementing carbon pollution standards.
Although ALEC resolutions will not change state law, they provide vehicles for polluters to lobby local officials and for politicians to grandstand on behalf of their coal industry campaign contributors. ALEC and its industry supporters are hoping these resolutions will discourage Governors and impede EPA action.
Many public interest groups, including the Natural Resources Defense Council, the Center for Media and Democracy, the Union of Concerned Scientists, Greenpeace and the Energy & Policy Institute among many others are working to expose ALEC’s secretive activity and curb polluter influence in state politics. The National Caucus of Environmental Legislators is also educating their network of state lawmakers to counteract ALEC’s presence in statehouses.
We expect ALEC’s attacks on the EPA to fail, especially since most legislators know their constituents want them to stand up to polluters and to protect their families from climate change.
This piece was originally published on NRDC’s Switchboard blog.
Visit EcoWatch’s CLIMATE CHANGE page for more related news on this topic.
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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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