Can We Work Less and Save the Planet, Too?
By Todd Miller
In 2008, performance artist Pilvi Takala took her seat as a new employee at the company Deloitte, a global consulting firm, and began to stare into space. When asked by other employees what she was doing, she said, "brain work" or that she was working "on her thesis." One day she rode the elevator up and down the entire workday. When asked where she was going, she said nowhere.
This image of utter inactivity, writes Jenny Odell in her book How to Do Nothing: Resisting the Attention Economy, is what completely "galled" Takala's coworkers.
In capitalist American culture, productivity is sacrosanct. If somebody says they had a productive day, the implicit assumption is that they had a good day. Descriptions like "non-contributing member of society" and "loiterer" clearly stigmatize those who aren't considered productive.
For Odell, this stigma on unproductivity is a real problem. What we really need is to loiter more, do less — in fact, she seems to say, life on this planet might depend on it.
For years, my work as a journalist has centered on the climate crisis, the displacement of people, and the proliferation of segregating, militarized borders around the world. I've seen the ways that the hyperproductivity that drives capitalism helped create these problems.
According to the Carbon Dioxide Information Analysis Center, human industry has pumped more than 400 billion metric tons of carbon dioxide — the approximate equivalent of 1.2 million Empire State Buildings — into the atmosphere since 1751, half of that since the late 1980s. The use of solid and liquid fossil fuels, like oil or coal, produced three-quarters of these emissions. That Western modern civilization was going to uplift the masses was rarely questioned, even as factories continued to pump out plastic commodities on the backs of the global poor.
Now the catastrophic results of elite injustice, corporate lies and collective thoughtlessness are coming in: the hottest years on record, encroaching seas, destructive floods, devastating wildfires, powerful hurricanes, crop-wilting droughts — and 1 million animal and plant species on the verge of extinction, according to a UN report. All of this is displacing people by the millions across the globe.
I remember seeing the production quotas in the workers' stations in maquiladoras across northern Mexico. Between 2001 and 2004, I visited dozens of such factories as part of the work I did for the binational organization BorderLinks, a nonprofit that arranges educational delegations for universities and churches. Workers, often in windowless rooms with a chemical stench, make suitcases, bank pens, dentures, cotton swabs and electrical components for rockets and fighter jets. People are "optimized" for productivity in a global economy in which progress is measured by constant growth, more stuff and more box stores.
I've seen the paychecks. The approximately $8 a day earned by a line worker is hardly a living wage when the combined cost of a gallon of milk and carton of eggs is more than a half-day's work. And every minute counts: If a worker is a minute late in many maquilas, they lose their on-time bonus (their paycheck is docked). If a worker is pregnant, they're fired. Workers often live in homes first built with discarded wood pallets and cardboard as insulation, structures that are extremely vulnerable to ever worse and more frequent 21st-century storms. And the inequality is as ferocious as the weather. According to Oxfam, a top fashion CEO has to work just four days to earn what a Bangladeshi garment worker will earn their whole life.
While there are other outcomes of Western progress and economic productivity, inequality — especially along racial and gender lines — and emissions lead the charge. At the end of 2018, 26 people owned about the same amount of wealth as the 3.8 billion poorest people on planet Earth, according to Oxfam; and emissions reached, yet again, an all-time high.
Increasingly militarized political borders reinforce the discrepancies between the haves and the have-nots, the environmentally protected and the environmentally exposed, and those who are White and those who are Black and Brown. When the Berlin wall fell in 1989, there were 15 border walls. Now there are 70, most constructed since 2001, almost always situated on the boundaries of inequality, between the Global North and the Global South.
This isn't the only world that's possible. But Odell suggests that imagining something else will require first reexamining — and dismantling — the cultural ethos of productivity that creeps into our lives every day.
By doing nothing, people like Takala are "refusing or subverting an unspoken custom," Odell writes, revealing "its often-fragile contours. For a moment, the custom is shown to be not the horizon of possibility, but rather a tiny island in a sea of unexamined alternatives."
It's such a simple idea, but it's entirely radical. The strip malls and big box stores and endless cars coming and going; the constant consumption and ever accelerating emissions; our nervous systems attached to constantly buzzing smartphones; and the cyberscapes that displace landscapes in our imaginations — none of this is inevitable. Our current model of productivity and capitalism — and profit and segregation — isn't the only way.
It is possible to create something else, but mental space is needed to dream up new possibilities. Doing nothing creates that space, and shifts attention to other ways of living, loving and working alongside others.
One radical alternative is imagined in a recent study, "The Ecological Limitations of Work": a less than 10-hour work week. Study author Philipp Frey argues for a dramatically reduced work week for environmental reasons. Work — or "the economic activity that causes GHG emissions" — is at an unsustainable level, requiring a dramatic reduction.
This idea raises all kinds of questions. Is there a way to both work less and redistribute wealth more evenly? And what is work, even — is it merely that which contributes to a bloated and catastrophic world economy? Perhaps our very salvation, and slowing down, is in the words of the Lebanese poet Khalil Gibran, who wrote, "What is it to work with love? It is to weave the cloth with threads drawn from your heart, even as if your beloved were to wear that cloth."
And what about borders? Near the end of the book, Odell describes the 1872 painting "American Progress" by John Gast. The painting depicts Manifest Destiny, the idea that White people moving west were a civilizing force. In the painting, a blond woman in white robes strides westward, trampling "hundreds of species and thousands of years' worth of knowledge," Odell writes. This westward expansion was the origin of U.S. territorial borders.
So Odell imagines the opposite of Manifest Destiny. She calls it "Manifest Dismantling."
Manifest Dismantling would purposefully undo the damage of Manifest Destiny by reckoning with productivity's assault on the living world. Tearing down a dam, for Odell, would be an example of a creative act of Manifest Dismantling because it would facilitate the return of an ecological landscape.
The same could be said about the 70 border walls, or the nearly 700 miles of walls and barriers along the U.S.–Mexico border. Dismantling these would allow people to move without fear. The saguaros and mesquite in the Sonoran Desert would grow back, and pronghorns, jaguars, and gray wolves could travel freely across borders. But it would also open space for a new vision to emerge, of a more equitable way to relate with each other and the living planet.
Reposted with permission from our media associate YES! Magazine.
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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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Growing Contribution<img lazy-loadable="true" src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yMzM3NDY5Ny9vcmlnaW4ucG5nIiwiZXhwaXJlc19hdCI6MTY0NjM4MTgyM30.IuQTKQs1stvYYKD6vaVTrqAyoBsUG0BhDvlhxsyKwPA/img.png?width=980" id="02a05" class="rm-shortcode" data-rm-shortcode-id="2841f82b1785df5d5ed7bf64d3bb882b" data-rm-shortcode-name="rebelmouse-image" />
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