Archive for the ‘Uncategorized’ Category
Potential for Ice Buildup Could Cause Problems for Trees and Power Lines
RICHMOND (WRIC) – The potential for ice buildup could cause problems for trees and power lines.
An ice storm is something Central Virginia hasn’t seen in some time – not since January 2000.
There are a lot of trees that may not withstand that build up and local tree removers are getting ready.
Philip Tate and his fellow arborists have to get prepared.
The potential for ice buildup has his team worried about trees coming down this weekend.
“Come Friday evening we’re going to make sure our fuel tanks our full,” he says. “Our dump trucks empty.”
Tate has worked many kinds of storms over his seven years in the business, from snow storms to hurricanes.
But he says ice creates a unique problem that he hasn’t seen in quite some time.
“With an ice storm, we’re worried about the buildup,” he says. “Evergreens in particular can easily accumulate ice. That weight can bring down limbs fairly easily.”
In addition, older trees or leaning trees could be weighed down as well.
Leaves have fallen off which will certainly help, but ice can still create problems.
He recommends removing any dead wood and trim branches to thin out the trees.
Power lines are the other concern – especially if trees hit them.
Power companies say they’re prepared for the worst, just as Tate is.
“We do this day in and day out. It’s our duty to make this safe for everyone.”
Downed power lines and trees can be dangerous, and if you’re not sure how to deal with it, let those trained take care of it.
Stay with ABC 8 News on air and online throughout this and other winter storms that will affect our area this season.
Keep the ABC 8 News StormTracker weather team in your pocket—download the 8News StormTracker app on your Apple or Android device. Features include hour-by-hour forecasts, exclusive extended forecasts, live streaming radar, severe weather alerts and more.
Copyright 2013 by Young Broadcasting of Richmond
2013′s Notable Developments in Landscape Architecture
Charles A. BirnbaumDec 04, 2013
In surveying the year in landscape architecture, “aptness,” a word favored by the great Modernist landscape architect Dan Kiley seems, well, appropriate. For Kiley aptness meant reading a landscape and understanding what existed at a particular site before one intervenes. This raises issues of understanding a designed landscape’s evolution, balancing stewardship objectives, and communicating how we measure success.
With this in mind, let’s start with the people who help evaluate the built environment and shape debate – critics. In a 2011 column, I called for architecture criticism to transcend its fascination with objects and to understand and recognize the interconnectedness of landscapes and buildings, and the holistic planning innate to landscape architecture. Increasingly, this is happening. The Los Angeles Times‘ Christopher Hawthorne, the New York Times’ Michael Kimmelman, the Philadelphia Inquirer’s Inga Saffron, the San Francisco Chronicle’s John King and others regularly provide thoughtful, contextual writing that explains the larger narrative. Consider Saffron’s recent review of the Kimbell Art Museum’s recent addition by Renzo Piano in Fort Worth, TX. The new structure has been billed as having a “dialogue” with Louis Kahn’s original building. In assessing Piano’s design as a “wan companion to Kahn’s stirring museum,” Saffron notes:
[T]he dialogue Kahn intended was with the Texas landscape. In a letter to the Kimbell, the Dutch architect Wiel Arets (now dean at the prestigious Illinois Institute of Technology) complained that Piano’s pavilion is the equivalent of putting “an addition in front of the White House in Washington.” What makes it even worse, said William Whitaker, curator of Penn’s architectural archives, Piano removed a grove of century-old oaks, which “inspired Kahn’s whole design.”
Some other “dialogues” are also causing a stir. The Plaza at Harvard University in Cambridge, MA, a busy pedestrian crossroad, is home to the 1984 Tanner Fountain by landscape architect Peter Walker, the first institutional project in the “Landscape as Art” movement. The minimalist fountain is comprised of 159 granite boulders set within the existing asphalt pathways, lawn and adjacent trees. There’s much sotto voce, off-the-record chatter about a new project by Stoss Landscape Urbanism contiguous with Tanner and Harvard Yard, which occupies a portion of the space that once acted as the fountain’s proscenium.
Tanner Fountain, ca. 1980s. Photo courtesy The Cultural Landscape Foundation. Tanner Fountain, November 2013, showing new addition designed by Stoss Landscape Urbanism. Photo courtesy The Cultural Landscape Foundation.
The new project, which could serve as the connective tissue between these two iconic designs instead fills this interstitial space with an abundance of stuff and things — wooden and concrete sculptural benches, (which glow at night), moveable metal tables and chairs, and a paving and planting palette of diverse color, texture and scale. Throw in a few food trucks (Bon Me’s offerings are particularly tasty) and on a nice day it is teeming with students. Was this the only viable solution to the program? Is this a conversation or is one design “talking” over another? How do we measure aptness here? Another hot spot is Sunnyside Gardens, NY, a 1920s Progressive-Era development designed by architects Clarence S. Stein, Henry Wright, and Frederick L. Ackerman with landscape architect Marjorie Sewell Cautley. The site, significant for helping launch the influential planners’ careers, contains a contributing space, integral to the original plan, intended for a playground. Although there is a continuity of use, the playground is in a diminished state and there’s talk of inserting the Aluminaire House and some low-rise construction.
The house, an early 1930s pre-fabricated metal structure, is currently disassembled, in storage and looking for a home. Bold face names in the architecture community strongly support plopping the house into the historic designed open space, which would remove a continuity of use, and sever historic visual and spatial relationships. This suggests one form of design is more important than another.
Harmonious Marriages of Landscape and Building
Among the praiseworthy new developments is the mausoleum complex at Lakewood Cemetery in Minneapolis, MN. Here, Adolph Strauch and C.W. Folsom laid out the Picturesque-style cemetery in the 1870s, and Arthur Nichols of Morell and Nichols designed a 1948 addition.
The new project is by Halvorson Design Partnership and HGA Architects. Halvorson has long been involved with Lakewood – they developed the cemetery’s master plan a decade ago; helped develop the RFP (Request For Proposals) for the mausoleum complex and interviewed all of the architecture firms that applied. Moreover, Lakewood’s very hands-on owners insisted Halvorson be the landscape architect for the project. The resulting Modernist addition is sublime. Important, existing sight lines are maintained and reinforced, structures are subordinate while also contributing to the overall composition, and the environment created is reverential and contemplative.
Another winning proposition is HM White’s three-acre project at New York’s Brooklyn Botanical Garden (BBG), which includes a new 10,000-square-foot visitor center by Weiss/Manfredi. The project, which officially opened in 2012, continues to receive awards and accolades. White’s involvement, like Halvorson, is broader; the firm was retained by BBG in 2006 to develop the site’s master plan, which carefully integrated the visitor center into the broader site narrative.
Elsewhere in Brooklyn, a new 26-acre, $74 million project opens this month at Frederick Law Olmsted, Sr. and Calvert Vaux’s masterwork, Prospect Park. Tod Williams Billie Tsien Architects collaborated with Prospect Park Alliance Vice President and landscape architect Christian Zimmerman on the effort, which includes a 34,000-square-foot multi-use facility.
The result honors the original Olmsted and Vaux design intent, restores formerly compromised visual and spatial relationships to the lake and its associated landscape, while still addressing 21st century recreational and environmental demands.
Credits and Designations
For Modernist designs, 2013 was a banner year for sites added to the National Register of Historic Places and/or designated National Historic Landmarks (NHL) with the Portland Open Space Sequence, OR (designed by Lawrence Halprin); Gas Works Park in Seattle, WA (Richard Haag); Peavey Plaza, Minneapolis, MN (M. Paul Friedberg) and Allegheny Commons, Pittsburgh (Simonds & Simonds) all listed on the National Register.
Portland Open Space Sequence, designed by Lawrence Halprin, is one of the Modernist landscapes added to the National Register of Historic Places in 2013. Photo courtesy The Cultural Landscape Foundation. The Camden Amphitheater, designed by Fletcher Steele, became a National Historic Landmark in 2013. Photo courtesy The Cultural Landscape Foundation.
In addition, Fletcher Steele joined Frederick Law Olmsted, Sr. and Dan Kiley as landscape architects who designed more than one work deemed an NHL. His Camden Library Amphitheater in Maine, arguably the nation’s first Modernist landscape, became an NHL following a similar, 2007 designation for his work at Naumkeag, the Choate family summer home in Stockbridge, MA. Naumkeag is managed by the Trustees for Reservations, which is amidst an ambitious and thus far very successful $3.3 million effort to return the site to its original design intent, including Steele’s iconic Blue Steps, restored this past summer.
The Blue Staircase at Naumkeag, designed by Fletcher Steele, following a recent restoration. Photo courtesy The Cultural Landscape Foundation.
What Next for New York?
Will the impending departure of Michael Bloomberg as New York City’s Mayor affect the design trajectory that led to a bevy of nationally and internationally significant projects? While other cities ponder their own High Lines, Phase Two of the original, from the design team led by James Corner Field Operations, is open and plans for Phase Three have been unveiled.
Other notable big vision projects completed in Gotham this year include the second phase of Brooklyn Bridge Park by Michael Van Valkenburgh Associates and the initial phases of Governors Island Park by West8. The bar has been set high for the next administration.
View of the new Governors Island Park looking across Hammock Grove, with play structures in the foreground and the Statue of Liberty beyond. Photo by Timothy Schenck, courtesy of The Trust for Governors Island. In Memoriam
Finally, we mourn the passing of James van Sweden, who with the late Wolfgang Oehme created the New American Garden. His voluptuous designs wed texture, color and light with the same élan and genius that Helen Frankenthaler did with her stained Color Field paintings. His clients became lifelong friends, collaborators and willing co-conspirators, as well as evangelists for Jim’s brilliance and for landscape architecture. His great sweeps of grasses at places as stodgy sounding as the Federal Reserve Board seemed perfectly appropriate – wonderful design conversations worthy of Kiley’s “aptness” designation.
‘Major ice storm’ threatens power supply in South, Midwest; temperatures dip
Millions of Americans are living in regions of the country under a severe cold spell. From whirling snow to icy rain, the freeze is even threatening a billion dollar crop industry in California. NBC’s Miguel Almaguer reports.
By Henry Austin, NBC News contributor
An arctic blast which threatens 32 million people could knock out power by coating parts of the South and Midwest with ice and send temperatures sinking by as much as 50 degrees Thursday, forecasters warned.
“A major ice storm is possible from northeast Texas into west Tennessee where ice accretions of 1/2 inch or more are possible,” said Kevin Roth, lead meteorologist with The Weather Channel. He added that ice would weigh down power lines and tree limbs, potentially causing power outages as they fall.
In some parts of the country wind chills are 30 below zero. And as temperatures continue to nosedive, there will be heavy ice accumulation near Dallas. The Weather Channel’s Mike Seidel reports.
Roth said the region faced a “good 12 to 14 hours of freezing rain and ice” as a winter storm and “surging arctic air mass meet in the southern Plains.”
Although temperatures neared 80 degrees on Wednesday in the Dallas-Fort Worth area, the mercury was expected to dip into the 30s on Thursday. In Lubbock, Texas, the high Tuesday was 77. The low Saturday morning could be below 10.
A winter storm alert will be in effect for the Dallas-Fort Worth area from 6 p.m. Thursday until 6 p.m. Friday, with sleet and freezing rain expected, NBCDFW.com reported.
“The arctic air continues to ooze southward Friday possibly changing rain to ice in northwest Mississippi and central Tennessee,” Roth added.
Temperatures could dip to minus 20 or worse in the northern midsection of the country, forecasters said.
Colorado homeless shelters opened extra beds as temperatures in Denver were expected to drop just below zero through Friday but remain below 20 through the middle of next week. The storm dumped several inches of snow in Denver, and parts of Colorado’s mountains could get up to 3 feet by the end of the day.
Some Rocky Mountain ski resorts surpassed 100 inches of snow for the season on Wednesday.
Snowfall totals could also approach 3 feet in northeastern Minnesota, where the weather has contributed to hundreds of traffic collisions around the state.
Chicago could plunge from the mid-50s on Wednesday to the low teens by Friday night. Roth said that ice was most likely in southern Missouri and southern Illinois.
He added: “A major ice storm is possible in the lower Ohio Valley and western Kentucky with ice accretions of 1/2 inch or greater. Snow accumulations of 4 to 8 inches are possible from southern Missouri to north Ohio through Friday night.”
In North Dakota, the bitter cold predicted ranged from minus 9 degrees in Missoula to minus 27 in Butte and Shelby.
In Montana, the cold spot will be the northern city of Havre, with low temperatures expected to dip as low as minus 30 between Thursday and Saturday. The city isn’t expected to get warmer than minus 6 degrees during that period.
National Weather Service meteorologist Dave Bernhardt told The Associated Press last extended cold period in Montana he could recall was in the winter of 1996.
While the Northeast has escaped the worst of the weather so far, Roth predicted that “the wintry stuff will come Sunday or Monday.”
The Associated Press contributed to this report.
This story was originally published on Thu Dec 5, 2013 6:08 AM EST
Bring back the 40-hour work week
Wednesday, Mar 14, 2012 08:00 AM EDT
150 years of research proves that long hours at work kill profits, productivity and employees
This article originally appeared on AlterNet.
If you’re lucky enough to have a job right now, you’re probably doing everything possible to hold onto it. If the boss asks you to work 50 hours, you work 55. If she asks for 60, you give up weeknights and Saturdays, and work 65.
Odds are that you’ve been doing this for months, if not years, probably at the expense of your family life, your exercise routine, your diet, your stress levels and your sanity. You’re burned out, tired, achy and utterly forgotten by your spouse, kids and dog. But you push on anyway, because everybody knows that working crazy hours is what it takes to prove that you’re “passionate” and “productive” and “a team player” — the kind of person who might just have a chance to survive the next round of layoffs.
This is what work looks like now. It’s been this way for so long that most American workers don’t realize that for most of the 20th century, the broad consensus among American business leaders was that working people more than 40 hours a week was stupid, wasteful, dangerous and expensive — and the most telling sign of dangerously incompetent management to boot.
It’s a heresy now (good luck convincing your boss of what I’m about to say), but every hour you work over 40 hours a week is making you less effective and productive over both the short and the long haul. And it may sound weird, but it’s true: the single easiest, fastest thing your company can do to boost its output and profits — starting right now, today — is to get everybody off the 55-hour-a-week treadmill, and back onto a 40-hour footing.
Yes, this flies in the face of everything modern management thinks it knows about work. So we need to understand more. How did we get to the 40-hour week in the first place? How did we lose it? And are there compelling bottom-line business reasons that we should bring it back?
The Making of the 40-Hour Week
The most essential thing to know about the 40-hour work-week is that, while it was the unions that pushed it, business leaders ultimately went along with it because their own data convinced them this was a solid, hard-nosed business decision.
Group’s goal: Chase ivy out of town
P. Kevin Morley
Suzette Lyon, master naturalist Laura Greenleaf, master gardener Robin Ruth and master naturalist Kitty Hardt cut away invasive English ivy on trees at Forest Hill Park in South Richmond.
BY REX SPRINGSTON
Richmond Times-Dispatch | Updated 11 hours ago
Laura Greenleaf took a break from the hard work of sawing through a garden-hose-size ivy vine that clung to an elm in Richmond’s Forest Hill Park.
She looked straight up the ivy-engulfed trunk and said: “I hope you appreciate this, tree.”
The elm, apparently in a weakened state, had no immediate response. But Greenleaf and three other Richmond women were undeterred as they sawed, snipped and pulled up the fast-growing vines in the South Side park in mid-November.
The women are part of a loose anti-ivy league of local volunteers who spread the word about ivy’s evils and fight a never-ending battle to remove it from their yards and, with permission, from parks.
“I probably pulled 100 ivy seedlings out of my yard this summer,” said Suzette Lyon, who worked in the park with Greenleaf. “It’s like an epidemic.”
Often called English ivy or common ivy, the well-known vine is frequently associated with attractive gardens and august halls of academe. Indeed, many people love ivy’s shiny, evergreen leaves.
But the non-native vine has a nasty habit of escaping its garden confines, covering forest floors so completely that it crowds out native flowers and shrubs that birds, butterflies and other animals need.
Conservationists call these one-species expanses “ivy deserts.”
Lyon and a fellow ivy fighter, Robin Ruth, created the website IvyOutOfRichmond.org. Its tone blends despair with humor.
“Left unchecked, English ivy could be the vine that ate Richmond. … Practice deVINE intervention now,” the site advises.
Scientists have long sounded the alarm over invasive species, typically plants and animals that made their way to new lands and spread so quickly that they overpowered native species. Some famous examples in the U.S. include kudzu (“the vine that ate the South”) and pushy birds called European starlings.
Colonial settlers brought English ivy to North America as an ornamental plant. Like so many cases involving the transport of trouble-making plants and animals, it seemed like a good idea at the time.
Today, many experts consider invasive species the No. 2 threat to natural areas, behind the outright destruction of habitats.
Its opponents say ivy may be the most widespread invasive plant in the city of Richmond, where it has had a lot of time to infest old parks and neighborhoods.
“It’s the most irritating to me, because it comes out of people’s yards,” said naturalist Kitty Hardt. “They’re still planting it, and the nurseries are still selling it.”
Jeff Miller, executive director of the Virginia Nursery & Landscape Association, said via email that a lot of places troubled by ivy stem from plantings that were abandoned.
“English ivy makes an excellent ground cover if used in the appropriate location” and maintained, Miller said. Homeowners should get advice from a certified horticulturist on the best ground cover for them, he added.
Ivy “is not as popular as it once was, because growers, landscape designers/contractors and garden centers are more cognizant of improper siting of ivy and recommend alternative choices,” he said.
Other states are also dealing with ivy. In Oregon, for example, it’s illegal to sell it.
“English ivy was the ground cover of choice for many, many years,” said Linda McMahan, a horticulturist at Oregon State University. “Now there are a lot of people all over the country trying to get rid of it.”
Efforts in the Virginia General Assembly to limit the use of ivy have failed.
Tom Smith, director of Virginia’s Natural Heritage Program, which protects important natural areas, has fought ivy at his Henrico County home near the Huguenot Bridge.
Smith knocked back a big patch by cutting it with a weed trimmer, then treating the scarred vines with an herbicide.
But hard-to-reach ivy remains, so once or twice a year Smith continues to pull and cut the vines.
“I would say once you get it on your property, it’s the gift that will keep on giving until no one lives there and it will have its way,” Smith said. “I think English ivy is definitely a plant that is here to stay. We are not getting rid of it.”
As a plant pathologist, Smith admires ivy’s ability to persist. “You’ve got to love a successful plant, even if it’s one you hate.”
Ivy can quickly spread along the ground, and tiny roots that exude a glue-like substance enable it to climb trees and buildings. When it gets off the ground, it produces purplish berries. Birds eat the berries and spread ivy seeds in their droppings.
That means ivy spreads in three ways — through its crawling vines, its seeds and from new plants that people put in their gardens.
There is debate over whether ivy can kill trees, because some trees persist with thick coats of ivy from vines as thick as your fist.
Some experts say those trees are weakened and susceptible to disease. Also, those extra ivy leaves can catch the wind like sails, increasing the chance of the tree blowing down in a storm.
Rick Myers, a plant expert with the Natural Heritage Program, compared planting ivy to smoking a cigar — you can legally do it, but what if your actions affect someone nearby?
“I know there’s no (Virginia) law saying you can’t plant ivy that will spread into your neighbor’s yard, but it’s still a valid ethical question: Should you do that?”
There are many people who remove ivy and other invasive plants locally, but there is no official count.
As the four Forest Hill Park ivy fighters prepared to leave, numerous trees remained covered in vines.
Talking to trees again, Greenleaf assured the victims, “We’re coming back.”
Going to work in the world of gardening
Every year, more people find a garden-related career, some as landscapers, others as arborists and many in nurseries, helping to grow plants for market. In the third of a four-part series on gardening and professional horticulture, Steve Whysall looks at some of the young people who are working in the field.
Jeff Case: Passion for trees
Jeff Case, graduate of the arborists technician level 1 program at Kwantlen School of Horticulture, is now working full time with the tree crew for North Vancouver’s parks department.
Originally from Ottawa, Case, 37, came to Vancouver four years ago after working with the Canadian Forest Service in Ontario on reforestation projects, as well as working with a research scientist on various tree studies.
He already had a forest technician diploma and a degree in forestry before enrolling at Kwantlen to get some technical skills suitable for a career in urban arboriculture.
While he is still working with trees, the switch to working arborist has been a career change for Case, and one that has given him much more individual responsibility, as well as a far more active working day.
“There is a difference in terms of practical application in dealing with trees in an urban environment compared to traditional forestry.
“The Kwantlen courses focused a lot more on practical techniques of arboriculture and taught me basic skills, such as how to use rigging, proper cutting techniques, operate chippers and stump grinders properly, and so on.”
For two years, he was one of the key arborists with Davey Tree in Burnaby, where he was classified as a “ground arborist,” primarily responsible for site cleanup, operating the chipper and working with a certified arborist, whether felling a tree or pruning or hedging.
He is an expert at deep root fertilization, a technique that pumps organic nutrients into the ground around a tree that is failing to thrive or declining because of being planted in impoverished soil.
Case has quickly progressed into the role of a climbing arborist.
“I have a real passion for trees, particularly trees in the urban environment,” Case says.
“And I particularly enjoy educating people about the benefits of trees and the right way to look after them.”
He says even during his years working in forestry, he always had an interest in the “dynamics and synergies” of tress in an urban environment and he also found he was happiest working with his hands doing practical arboriculture work.
“It is important to do cuts properly in order to maximize the benefit to the tree. Any time you do cut a tree, it negatively impacts it, but there is a way of making cuts to minimize that.
“It is exciting, as well as challenging work with a variety of challenges that you need to overcome each day.”
Case plans to continue his education at Kwantlen and will take the next two levels in the arborist program, which will focus on consultation and assessment work as well as advance skills as a climbing arborist.
“I know that in discussions with a client it is often necessary to say what would work best for the tree because we are always looking to satisfy the client while at the same time protect the esthetic integrity of the tree.”
Medical mystery jump-starts investigation of the link between Parkinson’s disease and crop-protectin g chemicals
The Pesticide Connection
Medical mystery jump-starts investigation of the link between Parkinson’s disease and crop-protecting chemicals
PEERING INTO PARKINSON’S
Greenamyre examines microscope images of rat nerve cells treated with the pesticide rotenone.
Credit: Pittsburgh Institute For Neurodegenerative Diseases
The rats in a room at the University of Pittsburgh regularly get hit with doses of pesticide. But the researchers in J. Timothy Greenamyre’s lab don’t expose the rodents because of an infestation problem. They give the neurotoxin to the animals to learn more about Parkinson’s disease.
After receiving a low daily dose of the pesticide rotenone for a week or two, rats in Greenamyre’s lab begin to lose mobility in ways similar to Parkinson’s patients. The rodents move at a glacial pace, they have trouble keeping their balance, and their limbs become impossibly stiff. Even the animals’ brains develop classic signs of the nervous system disorder: Nerve cells in a region called the substantia nigra accumulate clumps of the protein α-synuclein and die.
It’s not unusual to use animal models such as these to probe the molecular causes of Parkinson’s, which affects 7 million to 10 million people worldwide, and to test treatments. But their use also raises a question: If a chemical gives lab rats Parkinson’s symptoms, might it do the same to humans exposed in the real world?
A number of population studies have reported that people living in rural areas and people who work with pesticides have a higher incidence of Parkinson’s disease. In the past five years, some investigations have even associated the use of specific pesticides, such as rotenone, with a higher risk of having the disorder. And most recently, researchers have been investigating whether specific people might be vulnerable to pesticides because of their genes: People are at greater risk if they have mutated versions of enzymes or protein pumps that protect cells against damaging substances.
To download a pdf of this article, visit http://cenm.ag/pesticides.
On the basis of these results, many in academia say the link between pesticides and Parkinson’s is clear. But others, including pesticide industry representatives, argue that these studies are fraught with bias, and other research has not shown a Parkinson’s-pesticide tie-in.
One thing these two camps agree upon, though, is that the story of how scientists connected pesticides to Parkinson’s is a medical mystery worthy of the big screen.
THE CASE OF THE FROZEN ADDICTS
In the summer of 1982, a 42-year-old man named George Carillo was transported from a nearby prison to Santa Clara Valley Medical Center, in San Jose, Calif. Unable to speak and rigid from head to toe, Carillo perplexed many of the center’s doctors. At a loss, they gave him an initial diagnosis of catatonic schizophrenia.
After spending some time with Carillo, the facility’s head neurologist, J. William Langston, came to a different conclusion. He felt that the paralyzed man’s symptoms more closely aligned with advanced Parkinson’s disease. The trouble with this diagnosis was that Parkinson’s doesn’t take hold of a person overnight—which seemed to be the case with Carillo. Complicating matters was the disturbing discovery that Carillo’s girlfriend, 30-year-old Juanita Lopez, was “frozen” too. Surely this wasn’t coincidence, but then again, Parkinson’s isn’t contagious either.
When Langston—who is now the chief executive officer of the Parkinson’s Institute & Clinical Center, in Sunnyvale, Calif.—gave the immobile pair a popular therapeutic for Parkinson’s patients called levodopa, they sprang back to life almost immediately. Both patients were once again able to walk and move normally.
Around the same time, four similarly afflicted patients popped up at medical centers in the nearby San Francisco area. What all of them had in common, Langston would come to learn, was that they were heroin addicts. And they had all recently shot up with a designer, heroin-like concoction. The drug underworld was about to electrify Parkinson’s research and raise some difficult questions about pesticides.
Around 1980, chemistry-savvy criminals, looking for ways to get around illegal-substance laws, began synthesizing modified versions of illegal and controlled compounds such as LSD and morphine that gave users similar highs. One drug a few of the criminal chemists made was 1-methyl-4-phenyl-propionoxypiperidine (MPPP), a derivative of the painkiller Demerol with five times the potency.
But some of these crooked chemists did sloppy work. To speed up the MPPP synthesis, they increased the reaction temperature, unwittingly generating a dangerous by-product, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
Together with Ian Irwin, the director of the Drug Assay Laboratory at Stanford University Hospital, Langston identified MPTP in drug samples recovered from his patients. In a paper the scientists published in the Feb. 25, 1983, issue of Science, they hypothesized that MPTP had caused the addicts’ Parkinson’s-like behaviors (DOI: 10.1126/science.6823561).
About five months after Irwin and Langston’s Science paper came out, researchers at the National Institute of Mental Health confirmed MPTP’s toxicity. Upon repeatedly injecting monkeys with low doses of MPTP, the scientists observed the animals slow down and go rigid (Proc. Natl. Acad. Sci. USA1983,80, 4546). And just as it had helped Carillo and the others, the drug levodopa gave the monkeys back their ability to move freely.
The compound that seemingly crippled at least six people had simultaneously helped generate an animal model of Parkinson’s disease. It also sparked a movement in the research community to look for other substances that might be causing Parkinson’s in the wider population.
In 1984, a research team at the University of California, San Francisco, proved that a metabolite of MPTP called 1-methyl-4-phenylpyridinium (MPP+) was the actual neurotoxic culprit that crippled the addicts (Biochem. Biophys. Res. Commun. 1984,120, 574). Once inside their brains, MPTP got converted by a monoamine oxidase enzyme into MPP+, a nerve cell killer.
Researchers also discovered that MPP+ had been going by another name: cyperquat. During the 1970s, at least one firm, Gulf Oil Chemical Co., was developing cyperquat as an herbicide to protect crops against the weed nutsedge. Although cyperquat isn’t used today, its structurally similar cousin, paraquat, is one of the 25 most commonly used pesticides in the U.S., according to a 2007 survey conducted by the Environmental Protection Agency.
The MPTP saga had put scientists everywhere on high alert to the possibility that pesticides played some role in Parkinson’s.
MOLECULAR DETECTIVE WORK
What motivated Pittsburgh’s Greenamyre to test rotenone in rats in the first place wasn’t the fact that it was a pesticide. Nor was it because of any structural similarity to MPP+. Rotenone, a naturally occurring pesticide derived from the roots of tropical plants, is a much larger molecule than MPP+, with five carbon-based rings in its flavonoid backbone rather than just a biphenyl set of two.
Greenamyre tested rotenone because, like MPP+, it inhibits complex I, a group of proteins in the membrane of mitochondria, cells’ power-generating organelles. When complex I gets blocked, cells can’t produce the chemical energy they need to survive. “We thought it was a good way to test the idea that complex I inhibition would lead to the selective neurodegeneration seen in Parkinson’s,” Greenamyre recalls.
In Parkinson’s disease as well as in the condition afflicting the California addicts, nerve cells in the brain’s substantia nigra that produce the neurotransmitter dopamine die. This stops the flow of dopamine molecules to neurons in another area called the striatum, causing a short circuit in the brain’s ability to tell a person’s limbs to move.
When Greenamyre and his group—then at Emory University—administered rotenone to their rats in the late 1990s, they saw the selective neurodegeneration in the substantia nigra they’d guessed at (Nat. Neurosci. 2000, DOI: 10.1038/81834). What’s most interesting about this nerve cell die-off, Greenamyre says, is that even though rotenone is injected into the rats’ bloodstream and blocks complex I in cells all over the body, the neurons in the substantia nigra are the only ones to show signs of damage. “People don’t yet understand the selectivity of it, but clearly the dopamine neurons in that region are most vulnerable,” he adds.
MPP+ also blocks complex I and kills neurons in the substantia nigra, but it’s even more selective because of the way it enters cells. Rotenone, a lipophilic compound, gets inside cells by squeezing through their membranes. MPP+, on the other hand, gets taken up only by dopamine-producing nerve cells. Protein pumps that stud the surface of these neurons transport MPP+ inside, trying to usher back in excess dopamine that’s released when a nerve fires, but getting a lethal compound instead.
But Greenamyre’s rotenone-exposed rats are helping his team and others do more than just learn about the mechanisms behind Parkinson’s disease. “They’re providing proof of concept that exposure to certain classes of chemicals—pesticides being one—can cause selective nerve cell damage,” he says.
Once used for household gardening, rotenone is now applied outdoors only as a piscicide—a chemical that can clear pest fish from a lake or pond. Recognizing rotenone’s toxicity, the U.S. voluntarily restricted its use to fish in 2007.
The same can’t be said about MPP+’s cousin, paraquat. In 2007, about 3 million lb of the chemical was applied to land in the U.S. as a broad-spectrum herbicide. Although the mechanism of how the compound gets into the brain’s nerve cells is still under dispute, a handful of research groups have shown that it does damage to neurons in the substantia nigra—although not nearly as much damage as MPP+.
One reason paraquat causes less damage might be that the compound doesn’t directly bind to complex I, Greenamyre says. Instead, it undergoes a process called redox cycling in cells, in which it forms harmful reactive oxygen species. “Because of the oxidative damage that ensues, complex I ends up getting damaged,” Greenamyre explains, “so paraquat indirectly inhibits complex I,” at least at high, millimolar concentrations.
However, other teams have failed to elicit any nerve cell damage in paraquat-treated mice. Phil Botham, European head of product safety at Syngenta Crop Protection, says he and a team of scientists have gone to great lengths to test a variety of paraquat doses in mice and have observed no neuronal loss in the rodents’ substantia nigra (Neurotoxicol. 2013, DOI: 10.1016/j.neuro.2013.03.005). Syngenta manufactures paraquat.
“After a great deal of animal research, we’ve concluded that paraquat isn’t an adequate model for inducing Parkinson’s syndrome or Parkinson’s disease,” says Tim Pastoor, principal scientist at Syngenta.
Critics also say that the extreme amount of pesticides that get injected into animals in the lab to produce Parkinson’s behaviors is a far cry from how people would be exposed in everyday life. Therefore, researchers have turned to epidemiological studies to get at whether pesticides are triggering the disease outside the lab.
One of the first surveys to implicate pesticides as a causative agent in Parkinson’s disease was carried out in Canada in the mid-1980s. After hearing of the MPTP hullabaloo, neurologist Ali H. Rajput of the University of Saskatchewan and his team surveyed approximately 20 early-onset Parkinson’s patients—those diagnosed under the age of 40—living in the province. Rajput’s team found that early in life, the patients spent 92% of their time in a rural environment, where they could have been exposed to a “wide range of pesticides” and where they could have drank a lot of potentially contaminated well water (Can. J. Neurol. Sci.1986,13, 312.)
From that modest start, epidemiological studies of the association between pesticides and Parkinson’s took off. During the 1990s, risk factors fluctuated from study to study. Many investigations found that people who worked with pesticides regularly were about two times more likely to have Parkinson’s. Others showed no association.
To calculate pesticide exposure for residents of California’s Central Valley over a 25-year period, Ritz and coworkers pulled data from the state’s Pesticides Use Reporting program. As shown for the town of Shafter in 1988, the researchers first located all fields being sprayed with a particular pesticide and determined the compound’s application rate. Then, the team drew a 500-meter-radius radius circle around a person’s residence (bottom). If a sprayed field fell within the circle, the resident—either a Parkinson’s patient or a control subject—was counted as being exposed. This procedure was carried out for each year of the study period.
Credit: Courtesy of Beate Ritz
A lot of these early investigations weren’t very sophisticated, says Beate Ritz, an epidemiologist at the University of California, Los Angeles. Patients would report from memory whether they’d worked with pesticides, so “there was a lot of recall bias,” Ritz says. Plus, she adds, the studies sometimes probed only a yes or no relationship: “Have you ever worked with a pesticide?”
Nowadays, “more and more studies are being done where the exposure information is much higher quality,” says Freya Kamel, an epidemiologist at the National Institute of Environmental Health Sciences, in Research Triangle Park, N.C.
Kamel recently worked with a team including Caroline M. Tanner, the director of clinical research at the Parkinson’s Institute, to poll more than 100 registered pesticide users—mostly farmers—in Iowa and North Carolina. The so-called FAME (Farming & Movement Evaluation) study reported that people who worked with paraquat or rotenone during their lifetimes were two to three times more likely to have Parkinson’s than those never exposed (Environ. Health Perspect. 2011, DOI: 10.1289/ehp.1002839).
Ritz, on the other hand, wants to know whether living and working near farm fields correlates with a higher incidence of Parkinson’s, just as inhaling secondhand smoke affects a nonsmoker’s health.
To probe the issue, in 2011 she surveyed some 700 subjects living in California’s Central Valley, one of the most farmed regions in the world. To participate in her study, Ritz says, “you didn’t have to be a farmer—you could’ve been a firefighter in a firehouse next to a crop field.”
On the basis of subjects’ residential and work addresses, Ritz and her group used California’s Pesticide Use Reporting (PUR) program to estimate individuals’ pesticide exposure over a 25-year period. PUR mandates that farmers report their pesticide use monthly.
By itself, ambient paraquat exposure increased the risk of having Parkinson’s only a small amount, according to Ritz’s results. But people exposed to a combination of paraquat and the fungicides maneb and ziram at their workplaces were three times more likely to have Parkinson’s than people not exposed (Eur. J. Epidemiol. 2011, DOI: 10.1007/s10654-011-9574-5). Ritz believes pesticides may work in concert to lower a person’s molecular defenses.
“Many pesticides are designed to be neurotoxic to pests. Why should we be surprised that they’re neurotoxic to humans?” she asks.
Syngenta disputes the link between paraquat and Parkinson’s. The company has done its own epidemiological work, surveying the death certificates of people who worked in one of its paraquat manufacturing plants, in Widnes, England, between 1961 and 1995. The number of deaths due to Parkinson’s was no higher than that caused by Parkinson’s in the general population, Syngenta found (BMJ Open 2011, DOI: 10.1136/bmjopen-2011-000283).
“From an industry standpoint, it’s somewhat defensible to say, ‘Hey, how do you know it’s really that specific compound?’ when there are thousands of them out there,” says Gary W. Miller, a neurotoxicologist at Emory. “It’s tricky when you do a population study that shows there’s an increased incidence. It’s not like people were exposed only to one chemical.”
One of the main reasons controversy rages in the field is simply because of the nature of epidemiology. “It’s a science of observation,” says Serge Przedborski, a neuroscientist at Columbia University. “Epidemiology cannot give you a link. It can only say, ‘When I see A, I see B.’ ”
Nonetheless, the fact that cigarette smoking causes cancer is pretty much accepted today, says Samuel M. Goldman of the Parkinson’s Institute. It took 40 years of epidemiological and biological work to get there, but connections like that do get made.
Still, “the vast majority of us are not getting Parkinson’s, and the vast majority of people who work with pesticides don’t get Parkinson’s,” Goldman says. “So there’s obviously something else at play.”
That “something,” today’s scientists believe, is genetic susceptibility. Along with Tanner and Kamel, Goldman explored this gene-environment interaction recently by surveying a group of male farmers. The researchers genotyped the participants’ DNA to determine which subjects had mutations in a gene coding for glutathione S-transferase T1. This type of enzyme is responsible for cleansing cells of foreign substances such as pesticides and protecting against oxidative stress.
Men who were exposed to paraquat and who had nonfunctional glutathione S-transferase were 11 times more likely to have Parkinson’s disease than nonexposed men who had functional enzymes (Mov. Disord. 2012, DOI: 10.1002/mds.25216).
Another recent study examined the association of pesticides, Parkinson’s, and mutations to a protein pump called P-glycoprotein. This macromolecule sits on cells lining blood vessels in the brain, defending a person’s gray matter by pushing out molecular intruders.
Agricultural workers in France who were exposed to organochlorine insecticides and who had gene mutations affecting P-glycoprotein’s performance were three to seven times more likely to have Parkinson’s than those who weren’t exposed (Arch. Neurol. 2010, DOI: 10.1001/archneurol.2010.101).
THE PROMISE OF PESTICIDES
While epidemiologists, neurologists, and industrial scientists continue to debate the pesticide-Parkinson’s connection, Pittsburgh’s Greenamyre is thankful for what pesticides offer in the lab. By studying rotenone-treated mice, he says, his group has uncovered certain aspects of human Parkinson’s not previously known. For instance, they uncovered a mechanism by which Parkinson’s patients accumulate iron in the nerve cells of their substantia nigra (Neurobiol. Dis. 2009, DOI: 10.1016/j.nbd.2009.02.009). Excess iron has the ability to generate harmful reactive oxygen species in cells, so the route by which it accumulates is a potential target for treatments.
As far as a link between pesticides and Parkinson’s goes, “I’m highly doubtful that there is any pesticide in the world that is completely safe to all humans exposed to it,” he says. But the neurologist doesn’t think the chemicals should be blindly banned. “We wouldn’t have a modern society and be able to feed the world without them,” he says. What we do need, he argues, is a better understanding of the ones that are most problematic.
Scientists Discover Another Cause of Bee Deaths, and it’s Really Bad News
So what is with all the dying bees? Scientists have been trying to discover this for years. Meanwhile, bees keep dropping like… well, you know.
Is it mites? Pesticides? Cell phone towers? What is really at the root? Turns out the real issue really scary, because it is more complex and pervasive than thought.
Scientists had struggled to find the trigger for so-called Colony Collapse Disorder (CCD) that has wiped out an estimated 10 million beehives, worth $2 billion, over the past six years. Suspects have included pesticides, disease-bearing parasites and poor nutrition. But in a first-of-its-kind study published today in the journal PLOS ONE, scientists at the University of Maryland and the US Department of Agriculture have identified a witch’s brew of pesticides and fungicides contaminating pollen that bees collect to feed their hives. The findings break new ground on why large numbers of bees are dying though they do not identify the specific cause of CCD, where an entire beehive dies at once.
The researchers behind that study in PLOS ONE – Jeffery S. Pettis, Elinor M. Lichtenberg, Michael Andree, Jennie Stitzinger, Robyn Rose, Dennis vanEngelsdorp — collected pollen from hives on the east coast, including cranberry and watermelon crops, and fed it to healthy bees. Those bees had a serious decline in their ability to resist a parasite that causes Colony Collapse Disorder. The pollen they were fed had an average of nine different pesticides and fungicides, though one sample of pollen contained a deadly brew of 21 different chemicals. Further, the researchers discovered that bees that ate pollen with fungicides were three times more likely to be infected by the parasite.
The discovery means that fungicides, thought harmless to bees, is actually a significant part of Colony Collapse Disorder. And that likely means farmers need a whole new set of regulations about how to use fungicides. While neonicotinoids have been linked to mass bee deaths — the same type of chemical at the heart of the massive bumble bee die off in Oregon – this study opens up an entirely new finding that it is more than one group of pesticides, but a combination of many chemicals, which makes the problem far more complex.
And it is not just the types of chemicals used that need to be considered, but also spraying practices. The bees sampled by the authors foraged not from crops, but almost exclusively from weeds and wildflowers, which means bees are more widely exposed to pesticides than thought.
The authors write, “More attention must be paid to how honey bees are exposed to pesticides outside of the field in which they are placed. We detected 35 different pesticides in the sampled pollen, and found high fungicide loads. The insecticides esfenvalerate and phosmet were at a concentration higher than their median lethal dose in at least one pollen sample. While fungicides are typically seen as fairly safe for honey bees, we found an increased probability of Nosema infection in bees that consumed pollen with a higher fungicide load. Our results highlight a need for research on sub-lethal effects of fungicides and other chemicals that bees placed in an agricultural setting are exposed to.”
While the overarching issue is simple — chemicals used on crops kill bees — the details of the problem are increasingly more complex, including what can be sprayed, where, how, and when to minimize the negative effects on bees and other pollinators while still assisting in crop production. Right now, scientists are still working on discovering the degree to which bees are affected and by what. It will still likely be a long time before solutions are uncovered and put into place. When economics come into play, an outright halt in spraying anything at all anywhere is simply impossible.
Quartz notes, “Bee populations are so low in the US that it now takes 60% of the country’s surviving colonies just to pollinate one California crop, almonds. And that’s not just a west coast problem—California supplies 80% of the world’s almonds, a market worth $4 billion.”
Eddie (2067 Posts)
Eddie L. is the founder and owner of WorldTruth.TV. This website is dedicated to educating and informing people with articles on powerful and concealed information from around the world. I have spent the last 30+ years researching Bible, History, Secret Societies, Symbolism
Toys ‘R’ Us messes with Mother Nature: trees vs. toys [+video]
Hey kids: Forget boring nature. Get a new plastic toy instead!
That’s the basic message behind this new Toys “R” Us ad touting a surprise outing in which they took a busload of kids and let them each pick out any toy they wanted in a Toys “R” Us store.
Giving a free toy to kids in need is great. What’s not so great is the way Toys “R” Us chose to frame this special outing, both to the kids and to viewers of this “make all their wishes come true” promo.
The kids are told they’re going on a field trip to the forest, and get on a green bus with “Meet the Trees Foundation” painted on the side, along with a faux ranger, who tells them, “We’re not going to waste any time. Let’s play ‘Name that leaf.’ “
The camera pans to yawning kids, and we’re all invited to ridicule this totally lame field trip, until the actor rips off his fake ranger uniform and announces, “You know what I like more than trees? I like toys. We’re going to Toys “R” Us, kids!”
The kids erupt into screaming, jumping, joyful chaos.