WE THOUGHT IT WOULD BE IMPORTANT FOR YOU TO REVIEW THE HEALTH CONCERNS FOR FLURIDONE EXPRESSED BY THE MINNESOTA DEPARTMENT OF HEALTH.
PLEASE CLICK BELOW:
WE THOUGHT IT WOULD BE IMPORTANT FOR YOU TO REVIEW THE HEALTH CONCERNS FOR FLURIDONE EXPRESSED BY THE MINNESOTA DEPARTMENT OF HEALTH.
PLEASE CLICK BELOW:
BY CALIFORNIANS FOR PESTICIDE REFORM
Pesticides and human health:
Pesticides can cause short-term adverse health effects, called acute effects, as well as chronic adverse effects that can occur months or years after exposure. Examples of acute health effects include stinging eyes, rashes, blisters, blindness, nausea, dizziness, diarrhea and death. Examples of known chronic effects are cancers, birth defects, reproductive harm, neurological and developmental toxicity, immunotoxicity, and disruption of the endocrine system.
Some people are more vulnerable than others to pesticide impacts. For example, infants and young children are known to be more susceptible than adults to the toxic effects of pesticides. Farm workers and pesticide applicators are also more vulnerable because they receive greater exposures.
For more information about the effects of specific chemicals or pesticide products, see Pesticide Action Network’s Pesticide Database. For a survey of scientific studies linking pesticides to specific diseases, see Beyond Pesticides’ Pesticide-induced diseases database.
Acute (Immediate) Health Effects
Immediate health effects from pesticide exposure includes irritation of the nose, throat, and skin causing burning, stinging and itching as well as rashes and blisters. Nausea, dizziness and diarrhea are also common. People with asthma may have very severe reactions to some pesticides, particularly pyrethrin/pyrethroid, organophosphate and carbamate pesticides.
In many cases, symptoms of pesticide poisoning mimic symptoms of colds or the flu. Since pesticide-related illnesses appear similar or identical to other illnesses, pesticide poisonings are often misdiagnosed and under-reported. Immediate symptoms may not be severe enough to prompt an individual to seek medical attention, or a doctor might not even think to ask about pesticide exposure. Still, seek medical attention immediately if you think you may have been poisoned by pesticides.
Chronic (Long-term) Health Effects
Chronic health effects include cancer and other tumors; brain and nervous system damage; birth defects; infertility and other reproductive problems; and damage to the liver, kidneys, lungs and other body organs. Chronic effects may not appear for weeks, months or even years after exposure, making it difficult to link health impacts to pesticides.
Pesticides have been implicated in human studies of leukemia, lymphoma and cancers of the brain, breasts, prostate, testis and ovaries. Reproductive harm from pesticides includes birth defects, still birth, spontaneous abortion, sterility and infertility.
Endocrine disruptors are chemicals that — often at extremely low doses — interfere with important bodily functions by mimicking or blocking hormones (the chemical messengers that circulate in blood and regulate many body processes including metabolism, brain development, the sleep cycle and stress response). Some pesticides act as endocrine disruptors and have been shown to cause serious harm to animals, including cancer, sterility and developmental problems. Similar impacts have been associated with human exposure to these chemicals.
Children are More Vulnerable to Pesticide Exposure
Children are not simply “little adults.” Children are more vulnerable to pesticides exposure because their organs, nervous systems and immune systems are still developing; their higher rates of cell division and lower body weight also increase children’s susceptibility to pesticide exposure and risks. Their immature organs and other developing biological systems are particularly vulnerable to toxic contaminants. Exposure during certain early development periods can cause permanent damage.
In addition to being more vulnerable to pesticide toxicity, children’s behavior and physiology make them more likely to receive greater pesticide exposure than adults. Most pesticide exposure occurs through the skin and children have more skin surface for their size than adults. Children have a higher respiratory rate and so inhale airborne pesticides at a faster rate than adults. Children also consume proportionately more food and water — and pesticide residues — than adults. With their increased contact with floors, lawns and playgrounds, children’s behavior also increases their exposure to pesticides.
Health Effects of Certain Classes of Pesticides
Organophosphates & Carbamates: These pesticides are like nerve gas: they attack the brain and nervous system, interfering with nerve signal transmission. Symptoms include headaches, nausea, dizziness, vomiting, chest pain, diarrhea, muscle pain and confusion. In severe poisoning incidents, symptoms can include convulsions, difficulty breathing, involuntary urination, coma and death. Acute poisoning of the nervous system by these pesticides affects hundreds of thousands of people around the world each year.
Fumigants: Fumigants like methyl bromide and metam sodium can severely injure any tissue they touch. Effects from even minor exposures can include burning and itching of the eyes and skin, respiratory tract irritation as well as coughing and nose bleeds. Fumigants can severely injure the lungs.
Organochlorines: Many banned pesticides (including DDT) are organochlorines, although several organochlorine pesticides are still in use in California, including lindane and parathion. Organochlorines are central nervous system stimulants that can cause tremors, hyperexcitability and seizures. Although these pesticides are generally less acutely (immediately) toxic than organophosphates or carbamates, since they persist in the environment and tend to accumulate in tissue as they pass up the food chain, they are extremely hazardous. Organochlorine pesticide residues and breakdown products are found in human breast milk worldwide, and also in soil and plant and animal tissue from the middle of the Pacific Ocean to the Arctic Circle.
Pyrethroids: These organic compounds, similar to the natural pyrethrins produced by chrysanthemum flowers, are promoted by their manufacturers as harmless to humans, and are in increasingly wide use. In fact, pyrethroids are a synthetic copy of a natural poison. While pyrethroids are among the least toxic pesticides to humans, they are an excitatory nerve poison and known carcinogen. They are also highly toxic to insects, fish and birds, even in very small doses. While natural pyrethrum breaks down in as little as twelve hours, the synthetic forms have been engineered to be more stable, and persist in the environment for weeks.
Overview of Herbicide Poisoning
By P. K. Gupta, PhD, Post Doc (USA), PGDCA, MSc VM & AH BVSc, FNA VSc, FASc, AW, FST, FAEB, FACVT (USA), Gold Medalist, Editor-in-Chief, Toxicology International
Herbicides are used routinely to control noxious plants. Most of these chemicals, particularly the more recently developed synthetic organic herbicides, are quite selective for specific plants and have low toxicity for mammals; other, less-selective compounds (eg, sodium arsenite, arsenic trioxide, sodium chlorate, ammonium sulfamate, borax, and many others) were formerly used on a large scale and are more toxic to animals.
Vegetation treated with herbicides at proper rates normally will not be hazardous to animals, including people. Particularly after the herbicides have dried on the vegetation, only small amounts can be dislodged. When herbicide applications have been excessive, damage to lawns, crops, or other foliage is often evident.
The residue potential for most of these agents is low. However, runoff from agricultural applications and entrance into drinking water cannot be excluded. The possibility of residues should be explored if significant exposure of food-producing animals occurs. The time recommended before treated vegetation is grazed or used as animal feed is available for a number of products.
Most health problems in animals result from exposure to excessive quantities of herbicides because of improper or careless use or disposal of containers. When herbicides are used properly, poisoning problems in veterinary practice are rare. With few exceptions, it is only when animals gain direct access to the product that acute poisoning occurs. Acute signs usually will not lead to a diagnosis, although acute GI signs are frequent. All common differential diagnoses should be excluded in animals showing signs of a sudden onset of disease or sudden death. The case history is critical. Sickness after feeding, spraying of pastures or crops adjacent to pastures, a change in housing, or direct exposure may lead to a tentative diagnosis of herbicide poisoning. Generally, the nature of exposure is hard to identify because of storage of herbicides in mis- or unlabeled containers. Unidentified spillage of liquid from containers or powder from torn or damaged bags near a feed source, or visual confusion with a dietary ingredient or supplement, may cause the exposure. Once a putative chemical source has been identified, an animal poison control center should be contacted for information on treatments, laboratory tests, and likely outcome.
Chronic disease caused by herbicides is even more difficult to diagnose. It may include a history of herbicide use in proximity to the animals or animal feed or water source, or a gradual change in the animals’ performance or behavior over a period of weeks, months, or even years. Occasionally, it involves manufacture or storage of herbicides nearby. Samples of possible sources (ie, contaminated feed and water) for residue analysis, as well as tissues from exposed animals taken at necropsy, are essential. Months or even years may be required to successfully identify a problem of chronic exposure.
To recognize whether an animal has been exposed to herbicides or accidental poisoning, standardized analytical procedures for diagnostic investigation of biologic materials have become established and are subsumed under the term “biomonitoring.” Accurate biomonitoring is an important tool to evaluate human or animal exposure to such herbicides by measuring the levels of these chemicals, their metabolites, or altered biologic structures or functions in biologic materials such as urine, blood or blood components, exhaled air, hair or nails, and tissues. The use of urine is advantageous because of ready availability. As such, urine has been used for biomonitoring of several herbicides, including 2,4-D, 2,4,5-T, MCPA (2-methyl-4-chlorophenoxyacetic acid), atrazine, diuron, alachlor, metolachlor, paraquat, diquat, imazapyr, imazapic, imazethapyr, imazamox, imazaquin, and imazamethabenz-methyl herbicides, with the objective to assess exposure and health risk to exposed animals.
If poisoning is suspected, the first step in management is to halt further exposure. Animals should be separated from any possible source before attempting to stabilize and support them. If there are life-threatening signs, efforts to stabilize animals by general mitigation methods should be started. Specific antidotal treatments, when available, may help to confirm the diagnosis. As time permits, a more detailed history and investigation should be completed. The owner should be made aware of the need for full disclosure of facts to successfully determine the source of poisoning, eg, unapproved use or failure to properly store a chemical.
Toxicity and Management of Poisoning
There are >200 active ingredients used as herbicides; however, some of them are believed to be obsolete or no longer in use. Of these, several have been evaluated for their toxic potential and are discussed below. More specific information is available on the label and from the manufacturer, cooperative extension service, or poison control center. Selected information on herbicides, such as the acute oral toxic dose (LD50) in rats, the amount an animal can be exposed to without being affected (no adverse effect level), the likelihood of problems caused by dermal contact in rabbits (dermal LD50, eye and skin irritation), deleterious effects on avian species, and toxicity to fish in water, is included for some commonly used herbicides (see Table: Herbicide Poisoning). Comparative toxic doses (TD) and lethal doses (LD) of selected herbicides in domesticated species, such as monkeys, cattle, sheep, pigs, cats, dogs, and chickens, is also summarized (see Table: Oral Toxic Doses (TD) and Lethal Doses (LD) of Herbicides in Domestic Species). The information is only a guideline, because the toxicity of herbicides may be altered by the presence of other ingredients (eg, impurities, surfactants, stabilizers, emulsifiers) present in the compound. With a few exceptions, most of the newly developed chemicals have a low order of toxicity to mammals. However, some herbicides, such as atrazine, buturon, butiphos, chloridazon, chlorpropham, cynazine, 2,4-D and 2,4,5-T alone or in combination, dichlorprop, dinoseb, dinoterb, linuron, mecoprop, monolinuron, MCPA (2-methyl-4-chlorophenoxyacetic acid), prometryn, propachlor, nitrofen, silvex, TCDD (a common contaminant during manufacturing process of some herbicides such as 2,4-D and 2,4,5-T), and tridiphane, are known to have adverse effects on development of embryos and reproduction abnormalities in experimental animals. A list of such chemicals is summarized in Herbicides with Potential to Cause Developmental Toxicity in Experimental Animals.
THE BELOW LISTED PRESENTATION IS BY DR. KEN WAGNER, THE CONSULTANT USED BY WLPOA
THIS ARTICLE IS FROM THE NEW ENGLAND CHAPTER OF NALMS BLOG
Ice Out and Its Meaning for Lakes
May 9, 2017
The annual date of ice out for some lakes is fodder for prognostication and even wagers, but for aquatic plants and animals, that date has deeper ecological significance. Light and temperature are key cues in the aquatic environment, and ice cover keeps lakes cold and dark in late winter. As the air temperature warms, the ice melts, usually leaving open water around the edge and then falling apart over deeper water over a short time period. If that date is earlier, algae and rooted plants can get a head start on spring growth. If that date is later, growth is delayed. Temperature also affects when hibernating aquatic animals, like turtles and frogs, become active. Fish are active even under the ice, as any ice fisherman will tell you, but are more aggressive after ice-out and turn to spawning activities based on temperature cues.
While lakes may not actively manage time, it is a lot like it is for people; if you get up early, you can get a lot more done in a day, and you may not be able to finish your to-do list if you sleep in. As the water warms and light penetrates further without ice, lots of biological processes increase in lakes. Bacteria decompose organic bottom sediments, using oxygen and releasing various substances into the water column. Algae take up nutrients and use sunlight to photosynthesize and make more biomass. Zooplankton eat algae and reproduce more frequently, but small fish also eat zooplankton and limit that trophic level by early summer in most lakes. Fish spawn and make small fish that eat those zooplankton. In the meantime, rooted plants are growing, either from seeds, various winter buds, or root stocks, anywhere that light penetrates to a hospitable bottom substrate. Benthic invertebrates, often dependent on those plants, grow, reproduce and are eaten by fish or each other. A lake waking up from what seems like a winter sleep is indeed a busy place!
With variation in ice out date from year to year, and weather variation once the ice does go out, the sequence and intensity of cues will vary considerably from year to year, making every year unique to some extent. General patterns of plant growth, algae succession, fish spawning and other biological processes are known, but small changes can make quite a difference. A cold snap or windy period in May can retard stratification or cause a downturn in fish spawning that is not recoverable in that year. A very mild winter like we had going into 2016 can let perennial plants like invasive species of watermilfoil get a very early start (some plants may not even have died back to roots and stems) that outcompetes native species and makes it hard for harvesting programs to keep up. Weather plays a big role, and is influenced by climate change.
Climate change is a popular topic and the subject of spirited debates, but the data clearly show that lakes have been experiencing earlier ice-out dates over the last century (see graph). We seem to be losing a day of ice about every decade, such that based on the period of record going back about 150 years ice-out is now occurring two weeks earlier on average. Just keep in mind that aquatic organisms do not live in the “average”, and lakes have experienced both very late and very early ice out dates in just the last few years.
Ice out dates for various lakes.
FOR YEARS WE HAVE ALL HEARD ABOUT MILFOIL AND HOW IT WILL TAKE OVER THE LAKE. WELL, MILFOIL HAS BEEN CONTROLLED BY THE HERBIVORE PROGRAM AND THIS PROGRAM CONTINUES TO WORK.
WHAT IS NOW A PROBLEM IS A NEW INVASIVE WEED, CURLY LEAF POND WEED. THIS WEED PROBABLY CAME INTO OUR LAKE WHEN THE TYLER LAKE DAM WAS REPLACED. THIS INVASIVE WEED WAS FIRST FOUND IN OUR LAKE BY PAUL LORD, THE SCIENTIST WHO LED THE HERBIVORE PROGRAM FOUND SOME IN THE NORTH COVE.
WHAT WE ARE DOING TO CONTROL THIS WEED IS NOT WORKING. THE HERBIVORE PROGRAM ONLY WORKS ON MILFOIL, NOT CURLY LEAF POND WEED. CURLY LEAF PONDWEED IS CONTROLLED BY EARLY SEASON HARVESTING, HERBICIDES, AND GRASS CARP.. WE DID NOT START HARVESTING THIS YEAR EARLY ENOUGH (FOR A VARIETY OF EXCUSES) SO THAT NOW WHEN WE HARVEST IT THE TURIONS BY WHICH IT REPRODUCES ARE SPREAD ALL OVER THE LAKE. HERBICIDES ARE A “NO…NO” IN OUR COMMUNITY PLUS HERBICIDES ARE ONLY EFFECTIVE WHEN USED EARLY IN THE SEASON. AND, WE ARE STILL IN THE APPLICATION PROCESS TO STOCK GRASS CARP IN THE LAKE. THE GOOD NEWS IS THAT THIS WEED WILL DIE DOWN IN JULY AND FALL TO THE LAKE’S BOTTOM. THE BAD NEWS IS THIS DECOMPOSING BIOMASS WILL REDUCE OXYGEN LEVELS IN THE WATER AND WILL ALSO SPREAD THE TURIONS TO BECOME NEW PLANTS.
YES, IT APPEARS THE “RUSSIANS ARE COMING” AND TAKING OVER OUR LAKE. THE TRUTH IS THAT THIS INVASIVE IS SPREADING FASTER THAN WE WOULD LIKE, BUT WE NEED TO REMAIN CALM AND REALIZE THAT THIS IS PROBABLY A BAD YEAR FOR US AND NOT OVER EXAGGERATE THE PROBLEM. BECAUSE OF THE HEAT AND WATER TEMPERATURE, THESE WEEDS HAVE GROWN FASTER THIS YEAR. WE NEED A DELIBERATE PLAN FOR NEXT YEAR BY HARVESTING MUCH EARLIER BEFORE THE CURLY LEAF POND WEED REACHES THE SURFACE. THE ASSOCIATION IS NOW OVER REACTING BY RENTING ANOTHER HARVESTING MACHINE AT GREAT EXPENSE ONLY TO FURTHER SPREAD THE TURIONS.
CHEMICALS ARE NOT NECESSARY. THEY ARE COSTLY AND NOT EFFECTIVE.
DEEP DRAWDOWNS ARE NOT NECESSARY. THIS APPROACH IS NOT EFFECTIVE WITH CURLY LEAF PONDWEED.
WE ALSO NEED ALL MEMBERS TO QUIT USING FERTILIZERS AND PESTICIDES IN THEIR YARDS. WE ARE SPENDING OVER A HUNDRED THOUSAND DOLLARS TO CONTROL THE WEEDS IN OUR LAKE. WHY SHOULD MEMBERS BE FEEDING THESE WEEDS AND HURTING OUR CONTROL EFFORTS.
Medical researchers are now uncovering clues that appear to link some cases of ALS to people’s proximity to lakes and coastal waters
For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.”
Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease.
In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters.
About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role.
Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS.
No known cause
As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H.
Three years and many doctors’ appointments later, Gilmore received the news in June that the progressive weakening in his limbs was caused by ALS.
Neither Hampton nor Rochester is considered a hot spot for ALS. Gilmore is one of roughly 5,600 people in the United States diagnosed each year with the disease. The average patient lives two to five years from the time of diagnosis.
There is no cure, and for the majority of patients, no known cause. For 90 to 95 percent of people with ALS, there’s no known genetic mutation. Researchers assume that some unknown interaction between genes and the environment is responsible.
In recent years, some of this research has focused on blue-green algae, also known as cyanobacteria.
“There’s a growing awareness of the importance of gene/environment interactions with neurodegenerative diseases. There is more interest in examining environmental exposures, including exposures to cyanobacteria, as possible risk factors for sporadic ALS,” said Paul Alan Cox, director of the nonprofit Institute of Ethnomedicine in Wyoming, which focuses on treatments for ALS and other neurodegenerative diseases.
Cyanobacteria—some of the oldest organisms on the planet—can occur wherever there is moisture. Blooms are fed largely by nutrients in agricultural and urban runoff.
Some cyanobacteria produce toxic compounds that can sicken people. In August, hundreds of thousands of people in Toledo, Ohio, were left without tap water for days when toxins from an algal bloom in Lake Erie were found in the water supply.
While the cyanobacteria toxin that prompted the Toledo water crisis can cause diarrhea, intestinal pain and liver problems, other toxins produced by the blue-green algae can harm the nervous systems of humans and wildlife.
Scientists have long suspected that a cyanobacteria toxin could play a role in some forms of ALS. After World War II, U.S. military doctors in Guam found that many indigenous Chamorro suffered from a rapidly progressing neurological disease with symptoms similar to both ALS and dementia. Years later, scientists found the neurotoxin BMAA in the brains of Chamorro people who died from the disease. Cyanobacteria that grow on the roots and seeds of cycad trees produce the toxin.
Cox, a researcher in Guam in the 1990s, hypothesized that BMAA worked its way up the food chain from the cycad seeds to bats to the Chamorro who hunted them. But Cox and his colleagues also found BMAA in the brains of Canadian Alzheimer’s patients who had never dined on Guam’s fruit bats. In patients who had died from other causes, they found no traces of it. The source of the BMAA in the Canadians remains unknown.
Some researchers have suggested that fish and shellfish from waters contaminated with cyanobacteria blooms may be one way that people ingest BMAA. In southern France, researchers suspect ALS cases may be linked to consumption of mussels and oysters. Lobsters, collected off the Florida coast near blooms, also have been found with high levels of BMAA.
Scientists around the world are investigating how the neurotoxin gets into the body and whether it contributes to disease.
“We don’t really know what exposure routes are most important,” Cox said.
New England’s ALS hot spots
In New Hampshire, Dartmouth neurologist Elijah Stommel noticed that several ALS patients came from the small town of Enfield in the central part of the state. When he mapped their addresses, he saw that nine of them lived near Lake Mascoma.
Around the lake, the incidence of sporadic ALS—cases for which genetics are not a likely cause—is approximately 10 to 25 times the expected rate for a town of that size.
“We had no idea why there appeared to be a cluster around the lake,” Stommel said.
Based on the link between ALS and the neurotoxin in other parts of the world, Stommel and his colleagues hypothesize that the lake’s cyanobacteria blooms could be a factor.
Across northern New England, the researchers have continued to identify ALS hot spots—a large one in Vermont near Lake Champlain and a smattering of smaller ones among coastal communities in New Hampshire and Maine.
Earlier this year, the researchers reported that poorer lake water quality increased the odds of living in a hot spot. Most strikingly, they discovered that living within 18 miles of a lake with high levels of dissolved nitrogen—a pollutant from fertilizer and sewage that feeds algae and cyanobacteria blooms—raised the odds of belonging to an ALS hot spot by 167 percent.
The findings, they wrote, “support the hypothesis that sporadic ALS can be triggered by environmental lake quality and lake conditions that promote harmful algal blooms and increases in cyanobacteria.”
How people in New England communities could be ingesting the neurotoxin remains largely a mystery. While fish in the lakes do contain it, not everyone in the Dartmouth studies eats fish.
“We’ve sent questionnaires to patients and there’s really no common thread in terms of diet or activities,” Stommel said. “The one common thing that everybody does is breathe.”
In other words, it’s possible that a boat, jet ski or even the wind could stir up tiny particles of cyanobacteria in the air, where people then breathe it in.
Testing the air for a neurotoxin
Last August, at Lake Attitash, Jim Haney, a University of New Hampshire biologist, waded knee-deep into swirling green water. Cyanobacteria were blooming at the small lake in the northeastern corner of Massachusetts. Haney had rigged up three vacuum-like devices with pipes, plastic funnels and paper to suck up and filter air near the lake’s surface.
He took the filter papers back to his laboratory and measured the cyanobacteria cells, BMAA and other toxins stuck to them.
“We want to know what level lake residents may be exposed to through airborne particles,” said Haney, who is sampling the air at Massachusetts and New Hampshire lakes in collaboration with the Dartmouth team.
Stommel said,“it’s very compelling to look at the filter paper and see it just coated with cyanobacteria.”
At this point, Haney and graduate students are trying to understand under what conditions the toxins might be coming out of the lake and whether the airborne particles are an important route of exposure.
Preliminary findings suggest that BMAA and other cyanobacteria cells are being aerolized. “There is potentially a large quantity of cyanobacteria that could be inhaled,” Haney said. He noted, however, that the measurements were taken about eight inches above the water’s surface, making it likely that concentrations would be much lower farther away.
While the toxins are likely to be most abundant in the air around lakes, they exist all over the planet, even in deserts.
In 2009, BMAA was even detected in the sands of Qatar. Crusts containing cyanobacteria may lie dormant in the soil for most of the year, but get kicked up during spring rainstorms. Cox and colleagues hypothesized that breathing in toxins from dust might be a trigger for a doubling of ALS incidence in military personnel after Operation Desert Storm.
Near Haney’s workstation at Lake Attitash, a child splashed in the shallow water off a dock. Haney scooped up a cupful of water. He peered at the tiny green particles in the cup that reflect the sunlight, making the mixture resemble a murky pea soup.
“We’ve developed this view of nature as idyllic, which is wonderful, but not everything in nature is benign,” he said. “Rattlesnakes are natural and you wouldn’t get too close to one of those.”
“Proximity does not equal causality”
The hypothesis that exposure to BMAA may trigger the disease in some people remains controversial.
Researchers have evidence that people living close to lakes with blooms may be at increased risk for ALS. They’ve even found BMAA in the diseased brain tissue of people who have died of neurodegenerative diseases. Nevertheless, “proximity does not equal causality,” said Deborah Mash, a neuroscientist at the University of Miami in Florida.
The big, unanswered question is whether the toxin can actually cause the disease. So far, there’s little evidence to show how it could induce the type of brain changes seen in people with ALS.
Tests of human cells have found that BMAA kills the motor neurons—nerve cells that control muscles—implicated in ALS. Primates fed high levels of BMAA in the 1980s showed signs of neurological and muscular weakness. But the toxin did not kill their motor neurons.
“What is lacking at this point is a clear animal model that demonstrates that BMAA exposure results in ALS-like neuropathy,” Cox said.
So what is a possible mechanism for how the toxin may lead to the disease? The body may mistake BMAA for the amino acid L-serine, a naturally occurring component of proteins. When the toxin is mistakenly inserted into proteins, they become “misfolded,” meaning they no longer function properly and can damage cells.
Cox and colleagues soon will test two drugs in FDA-approved clinical trials. They’re about to enter second-phase testing with L-serine. The idea, explained Sandra Banack, a researcher at the Institute for Ethnomedicine, is that large doses of L-serine may be able to “outcompete” low levels of BMAA in the body, preventing it from becoming incorporated into proteins.
For ALS patients like Gilmore, the research can’t come soon enough. “If they can figure out a cause, then hopefully they can find a cure,” Gilmore said.
This article originally ran at Environmental Health News, a news source published by Environmental Health Sciences, a nonprofit media company.
SEPTEMBER, 14, 2015
Last week, the Association was caught discharging swimming pool water into our lake. This appears to be in direct violation of CT DEEP regulations.
According to our understanding of the appropriate CT DEEP regulations, we must have a permit to discharge swimming pool water. Before the water is discharged a permit must be in place and there must be appropriate record keeping of tested chlorine content of water released. If the swimming pool water is released into the lake it must have zero Chlorine content and this fact must be recorded.
Chlorine is quite harmful to our lake environment. Chlorine can impact fish, invertebrates, plants, and other life forms. With all the discussion about not using chemicals at Woodridge Lake it is unconscionable that Association Management did not think of this before discharging the swimming pool water and that they took the CT DEEP regulations so lightly.
Lets work together to make sure this does not happen again!