For Many Reporters Covering Climate, Population Remains the Elephant in the Room
By Wudan Yan
In June, New York Times journalist Andy Newman wrote an article titled, "If seeing the world helps ruin it, should we stay home?" In it, he raised the question of whether or not travel by plane, boat, or car—all of which contribute to climate change, rising sea levels, and melting glaciers—might pose a moral challenge to the responsibility that each of us has to not exacerbate the already catastrophic consequences of climate change. The premise of Newman's piece rests on his assertion that traveling "somewhere far away… is the biggest single action a private citizen can take to worsen climate change."
But that's not true. In 2017, Seth Wynes of Lund University in Sweden and Kimberly Nicholas of the University of British Columbia estimated the carbon emissions that various individual lifestyle choices would have. The foremost way to reduce climate change, their report said, would be to have one fewer child (which would otherwise annually contribute an additional 58.6 tons of carbon dioxide, on average in developed countries, according to the researchers' estimates). The runner-ups were living car free (2.4 tons of carbon dioxide per year), and not taking one transatlantic flight (1.6 tons of carbon dioxide per year).
Newman told me that, although he fact-checked his article meticulously, neither he nor his editors caught the error on which he established the premise of his story. (In emailed comments, Newman wrote that not having a child "wasn't in the story simply because it did not occur to me while I was writing the story," though he questioned whether one should consider having a child "a single action." "It's the millions of activities that occur in the life of that human you've created that generate the CO2," he wrote. "To me it doesn't seem fair to compare taking a flight—a self-contained event that occupies only a few hours—with an entire lifetime of carbon emission.")
On the heels of Newman's piece, The Guardian published an interactive story focused exclusively on how much carbon dioxide is emitted per flight. A month on from Newman's story, Quartz published a story titled, "If you care about your impact on the planet you should stop flying." For that story, Quartz replicated a graph from the Wynes and Nicholas study, but failed to include the impact that not having another child would have. When I asked the reporter, Natasha Frost, why Quartz decided to omit part of the data, she said the graphing software couldn't fit the data properly on the graph.
If any article is only talking about flying less, or eating less meat, "it's borderline dangerous and misleading," Erica Gies, an independent journalist who has written about population and her personal decision not to have children, says. "Or the writer is ill-informed, doesn't want to look at the reality, or open themselves up to the personal attack that is writing about it."
If not having another child saves more than 20 times more carbon per year, why aren't more journalists talking about human population in proportion to the climate impact that it can have?
Environmentalists believe that overpopulation is how we arrived at our current climate crisis. To explain the impact humans have on the environment, they use the formula I = PAT: the human impact on the environment (I) is the product of population (P), affluence (A), and technology (T). "Changing population is the one factor—the one that's most movable — that will have the most impact," activist and documentary filmmaker Terry Spahr says.
Environmental activist Bill McKibben, who, in 1999, wrote Maybe One about his decision to have just one kid due to the climate crisis, believes population is not discussed as much because population growth is not immediate and birth rates in America are already at an all-time low. "If indeed we have a decade to make transformative change, there are other things"—such as taking on the giant institutions of the fossil fuel industry—"that are more crucial," McKibben told me.
The issue of population was more widely discussed in the 1970s, after biologist Paul Ehrlich wrote The Population Bomb, a warning that the world population was spiraling out of control. Population growth then led India to implement a program to forcibly sterilize men, and China to introduce its one-child policy.
Around the same time, mainstream environmental organizations in the U.S. such as the Sierra Club, World Wildlife Foundation, and Audubon Society, all embraced policies and platforms that would limit population growth. (The Sierra Club, for instance, believed that the population of the U.S. should be stabilized by limiting immigration.) But they eventually got rid of it. "It got twisted by people," says Spahr. That is, "if you believed in population policies, you were racist, or colonialist, imperialistic, or a believer in euthanasia and all kinds of crazy things." As a result, says Spahr, population control "lost its presence as a real, viable and important part of the conversation."
That backlash can intimidate writers keen to discuss how population and reproductive choice are tied into climate impact. Ash Sanders, who recently published an essay in BuzzFeed about why she chose not to have children, was initially nervous to pitch the story for those very reasons.
Gies wrote her first piece about population control for Forbes in 2011. For a long time, she says, it felt like no one else was willing to write about it.
"I got a lot of shame," she says. "People told me: if you're so concerned, you should kill yourself. And having a child in most cultures is an automatic good, so people hear you criticizing them and their choices when you talk about your own choices." But at the same time, Gies says, she received heartfelt messages from people who felt similarly, supported, and seen.
Although journalists are reaching a consensus on the gravity of the climate crisis, there is no such consensus on how to link the issue of population with climate change—or whether the link should be made at all. Talking about not having children, Frost says via email, raises "complicated ethical questions about the difference between actions where if everyone took them, the world would likely be a better place (like not eating meat), and ones where everyone doing them would make the world worse (like not having children, if you think the human race is a valuable thing to protect)."
David Roberts, an environmental journalist with Vox wrote in a 2017 article that he refused to talk about overpopulation because it was morally and politically fraught. In that article, he explains that discussing things such as empowering women would be an indirect way to get at population. (I.e., if you educate women on family planning and give them opportunities for income, they will opt to have fewer children.)
Gies, meanwhile, says population needs to be discussed directly. "That's the problem: we haven't been talking about it directly," she says.
Spahr says he's seen the conversation about population and climate change become more public over the last five years. Prince Harry recently announced that he and his partner, Meghan, will only be having two children because of climate change (although having two children will merely hit the replacement rate and not actually reduce climate impact). In February, Alexandria Ocasio-Cortez asked whether or not it's ethical to have children given the climate crisis.
Given the urgency of crisis, says Sanders, "we need to attack climate change from so many different structural and cultural angles. I don't think population is the silver bullet, but I think it's the one tool we have that we're not talking about enough. I think there are ways to have this conversation ethically that will lead to freedom and choice."
The #planet cannot accommodate the "alarming rate" of human #overpopulation and our unsustainable use of natural resources. Experts agree that human population growth must end quickly for the planet and all of its inhabitants to survive.https://t.co/ntfUk9eH72— InDefenseOfAnimals (@IDAUSA) October 11, 2018
Wudan Yan is an independent journalist in Seattle, Washington. Her work has appeared in California Sunday Magazine, Discover, Harper's, High Country News, The New Yorker, The New York Times and The Washington Post, among others.
Editor's Note: This article has been updated for clarity.
This story originally appeared in Columbia Journalism Review. It is republished here as part of EcoWatch's partnership with Covering Climate Now, a global collaboration of more than 250 news outlets to strengthen coverage of the climate story.
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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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