Trump Vows to Kill 50 Years of Federal Health and Safety Protections
By Elliott Negin
President Trump wants to set the regulatory clock back to 1960, and last week he acted it out for the cameras.
Wielding a pair of golden scissors at a White House photo op, he cut red tape strung around two stacks of paper. One was a small pile of some 20,000 pages representing the amount of regulations in 1960; the other a mound of more than 185,000 pages representing those of today.
"We're getting back below the 1960 level," Trump declared, "and we'll be there fairly quickly."
There's only one problem. That mountain of paper Trump used as a prop symbolizes hard-won measures that protect us.
To refresh the president's memory, back in the 1960s, smog in major U.S. cities was so thick it blocked the sun. Rivers ran brown with raw sewage and toxic chemicals. Cleveland's Cuyahoga River and at least two other urban waterways were so polluted they caught on fire. Lead-laced paint and gasoline poisoned children, damaging their brains and nervous systems. Cars without seatbelts, air bags or safety glass were unsafe at any speed. And hazardous working conditions killed an average of 14,000 workers annually, nearly three times the number today.
In response, Congress enacted the Clean Air Act, Clean Water Act, Safe Drinking Water Act and other landmark pieces of legislation to protect public health and safety. Some of those laws also created the Consumer Product Safety Commission, U.S. Environmental Protection Agency (EPA), National Highway Traffic Safety Commission, Occupational Safety and Health Administration, and other federal agencies to write and enforce safeguards.
None of those laws, or the regulations they spawned, existed in 1960.
Trump Grew Up on Dirty Air
Trump should remember quite well what it was like in the 1960s. After all, he lived in New York, at the time one of the dirtiest cities in the country. Garbage incinerators routinely rained ash on city streets, while coal- and oil-fired power plants spewed a noxious mix of sulfur dioxide, nitrogen oxide and toxic metals. John V. Lindsay, the city's mayor from 1966 to 1973, famously quipped, "I never trust air I can't see," but it was no laughing matter. On Thanksgiving weekend the year Lindsay took office, the smog was so bad it killed some 200 people.
The waterways coursing around the city's boroughs, especially the Hudson River, were just as filthy. In 1965, then-New York Gov. Nelson Rockefeller accurately called the Hudson "one great septic tank." Indeed, 170 million gallons of raw sewage fouled the river daily while factories along its banks treated it as a waste pit. A General Motors plant in Sleepy Hollow, 27 miles north of New York City, poured its paint sludge directly into the river. Even worse, General Electric manufacturing plants in Fort Edwards and Hudson Falls dumped about 1.3 million pounds of polychlorinated biphenyls (PCBs), a probable human carcinogen, into the river over a 30-year period ending in 1977. Since 1984, a 200-mile stretch of the river from Hudson Falls to Manhattan's southern tip has been on the EPA's Superfund program list of the country's most hazardous waste sites.
Protections Prevent Disease and Save Lives
Fast forward to today. By and large, the environmental laws Congress began passing in the 1970s have been remarkably successful.
Thanks to the Clean Water Act, for example, tens of billions of pounds of sewage, chemicals and trash have been kept out of U.S. waterways since it was enacted 45 years ago. In New York City, harbor water quality has improved so much that humpback whales have returned for the first time in a century.
Thanks to the Clean Air Act, nationwide emissions of six common pollutants—carbon monoxide, lead, nitrogen dioxide, ozone, particulate matter (soot) and sulfur dioxide—plunged 70 percent on average between 1970 and 2015.
New Yorkers are breathing easier, too. On Earth Day last April, the city's health department released a report announcing that air pollution in the Big Apple is at the lowest level ever recorded. Between 2008 and 2015, nitrogen dioxide and particulate matter declined 23 percent and 18 percent, respectively, while sulfur dioxide levels plummeted 84 percent after the city and state tightened heating oil rules.
That's all good news for public health. In 2010 alone, according to an EPA study, Clean Air Act programs that reduced levels of fine particulate matter and ground-level ozone prevented an estimated 160,000 premature deaths, 130,000 heart attacks, and 1.7 million asthma attacks across the country.
These accomplishments, however, do not mean it's time to eliminate or weaken environmental safeguards. There is still much left to do. Consider that in just one year—2015—polluters dumped more than 190 million tons of toxic chemicals into waterways nationwide; at least 5,000 community drinking water systems violated federal lead regulations; and some 116 million Americans lived in counties with harmful levels of ozone or particulate matter pollution, which have been linked to lung cancer, asthma, cardiovascular damage, reproductive problems and premature death.
If You Can't Kill 'Em, Just Don't Enforce 'Em
Fortunately, it will be very difficult for the Trump administration to roll back 50 years' worth of congressionally mandated rules protecting the public from industrial poisons, harmful drugs, adulterated food and defective products. Trump's regulation czar conceded the point immediately after the December 14 White House photo op.
"I think returning to 1960s levels would likely require legislation. It's hard for me to know what that looks like," said Neomi Rao, director of the Office of Information and Regulatory Affairs at the Office of Management and Budget. "Deregulation also takes time. If we're doing something consistent with the law, it takes time to reduce rules."
In the meantime, the Trump administration is resorting to the next best—or worst—thing, depending on your perspective: It has cut back dramatically on enforcing environmental laws.
A recent New York Times investigative report compared the number of enforcement actions filed in the first nine months of the Trump EPA with what the two previous administrations did over the same time period. Under Scott Pruitt, the EPA initiated about 1,900 cases, about a third fewer than under Lisa Jackson, President Obama's first EPA administrator, and about a quarter fewer than under Christine Todd Whitman, who directed the agency under President George W. Bush and was not known for aggressive enforcement.
The Times also found that the Trump EPA is reluctant to seek civil penalties. In its first nine months, the agency tagged polluters for about $50.4 million for violations. Adjusted for inflation, that amounts to roughly 70 percent of what the Bush EPA levied and only about 39 percent of what the Obama EPA sought over the same time frame.
To make matters worse, Pruitt is threatening to cut off funding for the Justice Department's Environment and Natural Resources Division, which files lawsuits on behalf of the EPA's Superfund program to force polluters to cover the cost of cleaning up contaminated sites. In recent years, the EPA has reimbursed the division more than $20 million annually.
In an apparent attempt to blunt criticism, Trump acknowledged at last week's photo op that purging a half century of protections could have an adverse impact, and he assured Americans that he would not let that happen.
"We know that some of the rules contained in these pages have been beneficial to our nation, and we're going to keep them," he said. "We want to protect our workers, our safety, our health, and we want to protect our water, we want to protect our air, and our country's natural beauty."
Somehow, I'm not convinced. Given the president's penchant for lying, his administration's abysmal track record, and now his avowed intention to kill nearly 90 percent of federal regulations, the smoke Trump is blowing is as thick as 1960s New York smog.
Elliott Negin is a senior writer at the 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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