Great Lakes Flooding: The Warning Signs That Homes Must Be Moved
Every fall, I take my environmental studies class camping at Sleeping Bear Dunes National Lakeshore on Lake Michigan. Some years the beach extends more than three meters to the water. This year, in many spots, there was no beach at all.
The story is the same throughout the Great Lakes. During my summer research trip to Lake Ontario and the St. Lawrence River, I lost track of the number of submerged docks and buildings; swimming near the shore of Lake Huron was a bad idea because of the high risk of electrocution from inundated boathouses that still had the juice flowing.
Water levels in the Great Lakes have always fluctuated. But climate change is throwing past patterns out of whack. Almost every Great Lake reached record levels in 2019. And the latest studies predict that levels might reach even higher in 2020.
But instead of engineered solutions, we should be concentrating on getting out of the way.
Lake Michigan's high water levels consumed beaches at Sleeping Bear Dunes National Lakeshore in 2019. Daniel Macfarlane / Author provided
My research looks at the ways that Canada and the U.S., along with the bilateral International Joint Commission, have tried to understand and control water in the Great-Lakes St. Lawrence River Basin for well more than a century.
Both countries have made large diversions in and out of the Great Lakes, such as the Chicago Sanitary and Ship Canal, as well as numerous smaller diversions and canals.
In the 1950s, dams along the St. Lawrence transformed this gigantic river into a hydropower pool and navigation channel and, controversially, to help regulate water levels in Lake Ontario. Control works in the St. Marys River partially regulate Lake Superior. Niagara Falls is treated like a tap to generate both hydropower and beauty. Then there is the 100-plus years of perpetually dredging channels and harbours for navigation.
Cumulatively, these anthropogenic interventions have likely changed water levels on the lakes by less than one meter.
Meanwhile, communities have steadily encroached on the water. We turned seasonal sandbars into subdivisions. Metropolises like Toronto and Chicago extended their footprints hundreds of meters into the lake.
And it's not only large dams, diversions and cities that have impacts. Thousands of small individual actions add up, such as the breakwalls, retaining walls and the rip-rap (graded stone or crushed rock) property owners erect to protect boathouses, cottages and other structures.
Collectively, we might be the proverbial fool who built our house on sand — often literally.
These engineered interventions have myriad ecological impacts and unintended consequences, such as invasive species and impaired water quality. They've also instilled a societal hubris that we can — and should — control water on a large scale in the Great Lakes-St. Lawrence system.
High water levels inundate a waterfront home on the St. Lawrence River in May 2017.
However, natural forces — rain, snow, ice cover, temperature, evaporation — are the biggest determinant of water levels in the Great Lakes.
As long as humans have kept records, Great Lakes water levels have oscillated. Depending on which of the Great Lakes one considers, the maximum range of water level fluctuations has been about one to two meters in the past 150 years. For example, very high water occurred in the early 1950s, early 1970s, mid-1980s and mid-1990s.
Now, pushed by a changing climate, the swings in levels that used to take several decades are occurring in half a decade. Instead of a gradual rise and fall, the lakes are going from extreme to extreme.
For example, Lakes Michigan and Huron hit record lows in 2013, and docks on Georgian Bay didn't reach the water. To compensate, the U.S. Army Corps of Engineers proposed putting riffles, basically water speed bumps, on the bottom of Lake Huron's outflow at the St. Clair River.
Now Lake Huron is close to record high levels and docks are under water. If those St. Clair riffles had been installed, the water levels on Lakes Huron and Michigan would be even higher today. This is the type of short-sighted thinking we need to avoid.
Water needs breathing space. We need to move out of the way, rather than try to move water out of our way.
Humans have removed, impaired or destroyed many of the lakes' natural buffers, which accommodate fluctuating water. We've eradicated shoreline wetlands and beaches and covered them with concrete.
If a property along the Great Lakes is getting wet now, it will almost certainly be wetter in the future. While there is some scientific uncertainty about exactly what climate change will do to water levels, the extreme highs and lows will get worse. Volatility is the new normal.
Like climate change, when it comes to addressing Great Lakes levels, the biggest hurdles aren't scientific — they are political, economic and social.
Any new infrastructure along Great Lakes shorelines must be flexible, adaptable and resilient.
But we must also realize that the answer isn't more infrastructure. Infrastructure is too often the cause of our environmental issues.
We need to remove structures entirely and avoid building anything near the water's edge. This will have the added benefit of making more of the Great Lakes accessible to everyone. Since governments zoned vulnerable areas for construction, government funding should be provided.
We should use the opportunity to restore natural shorelines and wetlands. These provide many benefits for both water quality and water quantity. In terms of the latter, they can serve as water retention areas, while wetland plants provide erosion control.
This is all going to be very hard for many people to hear — there will be major resistance. But not moving is going to cost more in the long run. We think we can control water levels, but we need to think differently.
Reposting with permission from our media associate The Conversation.
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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>
This Saturday, June 6, marks National Trails Day, an annual celebration of the remarkable recreational, scenic and hiking trails that crisscross parks nationwide. The event, which started in 1993, honors the National Trail System and calls for volunteers to help with trail maintenance in parks across the country.
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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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