Blog 37
The spraying of the herbicide on hundreds of hectares of northern Ontario is sanctioned by the provincial government, but it's paid for by forest companies looking to plant more trees to cut down in the years ahead. Eacom Timber Corporation plans to spray 780 hectares in the north shore forest near Massey this year.
Governments say glyphosate is safe, but some say 'poison' is being sprayed on northern forests
Hundreds of hectares of Crown land in northern Ontario sprayed every summer
All this poison is going to affect the water in the rivers.
"I had bear hunters up here at the time and these helicopters flew over top of them and were spraying on them," remembers the owner of East Bull Lake Wilderness Resort north of Massey.
"I felt it was my responsibility to find out exactly what it was they were spraying and they said 'Oh, it's just Roundup. There's no problem with Roundup."
In the decade since Vautour has learned that many people have a problem with Roundup and its active herbicide glyphosate.
The makers of Roundup have been sued successfully by Americans who claim it gave them cancer and several U.S. states have banned the herbicide.
Nova Scotia and Quebec have also stopped spraying it from helicopters on clear cuts so newly planted trees can grow.
Vautour, now 75, has prostate cancer and doctors are worried it might be spreading to his thyroid.
He wonders if it's related to the spraying, but he doesn't know.
"Nobody can tell me that. But why are all these things happening?" Vautour says.
Glyphosateis a poison and is cancerigen.
Question
Who decided to poison the atmosphere the water and who is paying for this poison to be sprayed on the land of Ontario?
Who can decide that this poison should stop being sprayed?
This chemical enter into the rivers and lakes and oceans!!!
What kind of people are those that think this is ok?
When he first heard about the spraying all those years ago, one of the first people Vautour told was his friend Raymond Owl, an elder from Sagamok First Nation.
Both men have heard stories about trees and blueberries suddenly dying in the bush and have noticed a disturbing absence of animal life in areas that have been sprayed with glyphosate.
The 76-year-old Owl has been lobbying both governments through the Traditional Ecological Knowledge Elders group.
After not getting anywhere with federal and provincial bureaucrats, Owl says his group is planning to file a lawsuit against Canada for violating the Robinson-Huron Treaty of 1850.
He says the government did not consult First Nations living along the North Shore of Lake Huron before it began spraying this chemical on their forests.
"It's still our land. We never sold it. We just gave you a right to live here. That's all you got. But you don't have authority what you do to our land," says Owl.
"First Nations doesn't want any chemical at all. If it kills one little bug, one blade of grass, that's too much."
The spraying of the herbicide on hundreds of hectares of northern Ontario is sanctioned by the provincial government, but it's paid for by forest companies looking to plant more trees to cut down in the years ahead.
Eacom Timber Corporation plans to spray 780 hectares in the north shore forest near Massey this year.
But director of public affairs Christine Leduc points out that is less than 0.1 per cent of the total forest.
She says in response to some of the concerns from the public, Eacom is looking to move away from aerial herbicide spraying and clean up some clear cuts using crews on the ground instead.
"Ultimately the decision to use those methods lies with the province, but for our part, where there's opportunities and reasonable alternatives we are committed to reducing our use of aerial spraying," Leduc says.
So Cristine Leduc is one of the responsible people for poisoning the air land and water. The premier of Ontario is another one responsible for the crime against the environment and the peoples.
Statement from the Ministry:
The Ministry of Natural Resources and Forestry did not make anyone available for an interview, but did provide the following statement:
"Herbicide use is very limited in Ontario and they are only used when absolutely necessary – it usually amounts to less than 0.2 per cent of Ontario's forested area in any given year.
Glyphosate is used on Crown forests, only when necessary. Under the Crown Forest Sustainability Act, people operating in the forest are required to ensure management practices provide for healthy, diverse and productive Crown forests and their associated ecological processes and biological diversity. Conifer is renewed to ensure the long-term sustainability of the forest, to provide economic benefits to Ontarians, and to provide important wildlife habitat (including marten, moose, deer, and caribou).
Forest managers control vegetation to meet forest stand objectives. They make decisions on which control methods to use, including herbicides, based on site conditions and the competing species to be controlled.
The Ministry of Natural Resources and Forestry is also responsible for poisoning the air land and water. They should be fired not paid from tax dollars.
In April, 2017 Health Canada's Pest Management Regulatory Agency completed a re-evaluation of glyphosate, finding it does not present unacceptable risks to human health or the environment when used as directed. The re-evaluation reaffirmed current use of glyphosate in forestry including its safety for people entering sprayed areas, such as hunters.
MNRF relies on Health Canada's pesticide registration and the Ministry of Environment, Conservation and Park's classification to ensure that pesticides used in Ontario's forests are safe."
So another one responsible is Health Canada's Pest Management Regulatory Agency. They all should be fired and jailed.
To help ban the spraying in Ontario, contact your MLA,
sign a petition & spread awareness. ONTARIO Petition - LINK http://chng.it/PWByCXLDCC
It is interesting to note, however, that Bayer, the company that owns the Roundup brand, announced in 2021 that it would cease selling Roundup in the residential lawn and garden market in 2023. It cited the risks to farmworkers and consumers from exposure to this toxic pesticide as the primary reason for the decision.
This announcement came just two years after the company was ordered to pay more than $80 million in damages to a man who claimed in a Roundup lawsuit that the product caused his non-Hodgkin lymphoma.
The broad-spectrum herbicide glyphosate (common trade name “Roundup”) was first sold to farmers in 1974. Since the late 1970s, the volume of glyphosate-based herbicides (GBHs) applied has increased approximately 100-fold.
All these chemicals end up in rivers and lakes. This should STOP!!!
With respect to glyphosate-based herbicides, we are certain of the following:
GBH Use, exposure, presence
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1.
GBHs are currently the most heavily applied herbicides in the world.
Trends in the volume and intensity of GBH uses have been rising sharply since the mid-1990s, in step with global adoption of genetically engineered, glyphosate-tolerant crops [10, 52, 53]. Use of GBHs is likely to continue increasing if Roundup Ready glyphosate-tolerant maize, soybeans, cotton, canola, alfalfa and sugar beet are approved for planting in regions not now dominated by such cultivars.
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2.
GBHs contaminate drinking water via rainwater, surface runoff and leaching into groundwater, thereby adding drinking water, bathing, and washing water as possible routine exposure pathways [48, 54, 55].
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3.
The half-life of glyphosate in water and soil is longer than previously recognized. In field studies, the half-life of glyphosate in soil ranged between a few days to several months, or even a year, depending on soil composition [56]. Studies have shown that soil sorption and degradation of glyphosate exhibit great variation depending on soil physical, chemical, and biological properties. The risk of long-term, incremental buildup of glyphosate contamination in soil, surface water, and groundwater is therefore driven by highly site-specific factors, and as a result, is difficult to predict and costly to monitor.
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4.
Residues of glyphosate and its principle metabolite AMPA are present in nearly all soybeans harvested from fields planted with Roundup Ready soybeans [13, 16]. The intensity of glyphosate use has trended upward on most GE Roundup Ready crops. In addition, applications are now being made later in the crop cycle on GE crops. In addition, wheat, barley and other grain, and some vegetable crops are sprayed very late in the crop season to accelerate crop death, drying, and harvest operations. For these reasons, average residue levels on and in some harvested grains, oilseeds, and certain other crops are substantially higher than they were a decade ago and, as a result, human dietary exposures are rising.
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5.
The emergence and spread of glyphosate-resistant weeds requires farmers to spray additional herbicides, including older herbicides posing documented environmental and public health risks and/or newer, more costly herbicides to avoid crop yield losses and slow the spread of these weeds [37]. This is particularly problematic in grain and row-crop fields planted for several years with Roundup Ready GE crops. In the U.S., contending with resistant weeds has already increased total herbicide use per acre by approximately 70 % in soybeans, and 50 % in the case of cotton compared to herbicide rates on these crops in the mid-1990s when GE varieties were first introduced [10].
Section II
We estimate with confidence that:
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1.
Glyphosate provokes oxidative damage in rat liver and kidneys by disrupting mitochondrial metabolism [57–59] at exposure levels currently considered safe and acceptable by regulatory agencies [4, 25, 26]. Therefore, the ADI governing exposures to GBHs is overestimated. Adverse effects impacting other endpoints are less certain, but still worrisome and indicative of the need for more in-depth research (see following sections).
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2.
Residues from GBHs may pose higher risks to the kidneys and liver. Metabolic studies in a variety of laboratory and farm animal species show that levels of glyphosate and AMPA in kidney and liver tissues are 10- to 100-fold (or more) higher than the levels found in fat, muscle (meat) and most other tissuesFootnote 3. Increases in the frequency of serious, chronic kidney disease have been observed among male agricultural workers in some regions in which there is a combination of heavy GBH use and ‘hard’ water [60, 61]. These possible adverse effects of GBH exposure on kidney and liver warrant a focused, international research effort.
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3.
There are profound gaps in estimates of worldwide human GBH exposure. Glyphosate and AMPA are not monitored in the human population in the United States, despite the 100-fold increase in use of GBHs over recent decades. In circumstances where there is substantial uncertainty in a pesticide’s dietary risk, the EPA is presumptively required by the U.S. Food Quality Protection Act (FQPA) of 1996 to impose an added safety factor of up to 10-fold in the setting of glyphosate’s cRfD. Such uncertainty can arise from gaps in the scope and quality of a pesticide’s toxicology dataset, or uncertainty in exposure assessments. Considering the uncertainties regarding both GBH safety and exposure, the EPA should impose a 10-fold safety factor on glyphosate, which would reduce the EPA chronic Population Adjusted Dose (cPAD) to 0.175 mg/kg bw/day. [Note: the U.S. EPA adopted the new term cPAD to designate a chronic Reference Dose for a pesticide that had been lowered by the Agency as a result of the application of an added, FQPA-mandated safety factor. Virtually all FQPA safety factors have reduced chronic Reference Doses by 3-fold or 10-fold].
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Nevertheless, imposing a 10-fold decrease in glyphosate’s chronic Reference Dose, as seemingly called for in current U.S. law, should only be viewed as an interim step in the reassessment of glyphosate toxicity and risk, and re-adjustment of glyphosate uses and tolerances in food. Considerable work on glyphosate and GBH toxicity, mechanisms of action, and exposure levels must be completed before the U.S. EPA can credibly conclude that GBH uses and exposures are consistent with the FQPA’s basic safety standard, namely that there is a “reasonable certainty of no harm” from ongoing, chronic exposures to GBHs across the American population.
Section III
Current models and data from the biological sciences predict that:
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1.
Glyphosate and GBHs disrupt endocrine-signaling systems in vitro, including multiple steroid hormones, which play vital roles in the biology of vertebrates [21, 22, 24, 62]. Rat maternal exposure to a sublethal dose of a GBH resulted in male offspring reproductive development impairment [21]. As an endocrine-disrupting chemical (EDC), GBH/glyphosate can alter the functioning of hormonal systems and gene expression patterns at various dosage levels. Such effects will sometimes occur at low, and likely environmentally-relevant exposures. Contemporary endocrine science has demonstrated that dose–response relationships will sometimes deviate from a linear increase in the frequency and severity of impacts expected as dose levels rise [19, 63].
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2.
The timing, nature, and severity of endocrine system impacts will vary depending on the levels and timing of GBH exposures, the tissues exposed, the age and health status of exposed organisms, and other biotic or abiotic stressors impacting the developmental stage and/or physiology of the exposed organism. Exposures can trigger a cascade of biological effects that may culminate many years later in chronic degenerative diseases or other health problems. Exposures leading to serious complications later in life might occur over just a few days to a month in short-lived animals, and over a few days to several months in humans.
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3.
The study used by the EPA to establish the current glyphosate cRfD used gavage as a system of delivery, as recommended by OECD guidelines for prenatal developmental toxicity studies, which in all likelihood underestimates both exposure and toxicity [64]. This conclusion is derived from two considerations: (i) gavage bypasses sublingual exposure, and thus overestimates the portion of the chemical subjected to first pass metabolism in the liver, and (ii) gavage stresses the experimental subjects inducing endocrine effects that can lead to artefacts including, crucially, a reduction in the difference between control and experimental groups.
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4.
The incidence of non-Hodgkin’s Lymphoma (NHL) has nearly doubled in the U.S. between 1975 and 2006 [65]. GBHs are implicated in heightened risk of developing NHL among human populations exposed to glyphosate occupationally, or by virtue of residence in an area routinely treated with herbicides [66]. A causal link between GBH exposures and NHL may exist, but has not been rigorously studied in human populations.
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5.
Uncertainty persists over the doses required to cause most of the above endocrine-system-mediated effects. Some published data indicate that doses well within the range of current human exposure may be sufficient [22, 25], whereas other studies demonstrating distinct, adverse impacts have explored high doses and exposures that are unlikely to reflect any real world levels of ingestion. Additional in vivo studies are needed at environmentally relevant doses to distinguish the combination of factors likely to give rise to endocrine-system-driven morbidity and mortality. Nevertheless, the epidemiological data described above provides evidence of heightened cancer risk in human populations at levels of exposure actually experienced in human populations.
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Glyphosate is a chelating agent with potential to sequester essential micronutrient metals such as zinc, cobalt and manganese [67, 68]. This property of GBHs can alter the availability of these micronutrients for crops, people, wildlife, pets, and livestock. These micronutrient metals are enzymatic cofactors, so their loss has the potential to contribute to a number of deleterious effects, especially on kidney and liver function [69].
Section IV
Existing data suggest, but do not empirically confirm, a wide range of adverse outcomes:
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1.
Multiple studies on GBHs have reported effects indicative of endocrine disruption [21–24]. Based on knowledge from studies of other endocrine disruptors, the developing fetus, infants, and children are most at risk. Effects following GBH exposure may not be immediately apparent, because some adverse conditions caused by early-life exposure only manifest in later stages of development and/or in adulthood. These include both acute diseases and chronic health problems. In addition, proving links between chronic disease and exposures to GBHs is made more difficult by the fact that people are routinely exposed to complex mixtures of glyphosate and other toxic chemicals.
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The action of glyphosate as an antibiotic may alter the gastrointestinal microbiome in vertebrates [33, 70–72], which could favor the proliferation of pathogenic microbes in humans, farm animals, pets and other exposed vertebrates.
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3.
Increased incidence of severe birth defects in Argentina and Paraguay in areas where GE Roundup Ready crops are widely grown may be linked to the ability of GBHs to increase retinoic acid activity during fetal development [23]Footnote 4. Glyphosate-contaminated soybean feeds used in the pork industry have also been associated with elevated rates of gastrointestinal-health problems and birth defects in young pigs [32]. Related impacts have been observed in poultry [33].
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4.
Some developmental studies in rats undertaken at relatively high levels of exposure suggest possible GBH-induced neurotoxicity through multiple mechanisms [73]. Replication of these studies using doses relevant to human exposures should be a high priority. Further work on GBH-induced neurotoxicity should be conducted to test whether glyphosate can act as a disruptor of neurotransmitter function given its similarity in structure to glycine and glutamateFootnote 5.
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5.
GBHs may interfere with normal sexual development and reproduction in vertebrates. Experiments with zebrafish with dosing of GBH in the upper range of environmentally-relevant contamination levels, show morphological damage to ovaries [74].
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A recent report demonstrates that environmentally relevant concentrations of commercially available GBHs alter the susceptibility of bacteria to six classes of antibiotics (for example, either raise or lower the minimum concentration needed to inhibit growth) [75]. Furthermore, GBHs can also induce multiple antibiotic-resistance phenotypes in potential human pathogens (E. coli and Salmonella enterica serovar typhimurium). Such phenotypes could both undermine antibiotic therapy and significantly increase the possibility of mutations conferring more permanent resistance traits. Since GBHs and antibiotics are widely used on farms, farm animals may be exposed to both, with a concomitant decrease in antibiotic effectiveness and increase in the diversity of newly resistant bacterial phenotypes that might find their way into the human population. Risk assessors have not previously considered the finding that herbicides might have sublethal adverse effects on bacteria, but this should be considered in future risk assessments.
Section V
Uncertainties in current assessments persist because:
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1.
A steadily growing portion of global GBH use is applied in conjunction with multiple other herbicides, insecticides, and fungicides. Herbicide and other pesticide active ingredient safety levels are calculated for each active ingredient separately, despite the fact that tank mixes including two to five, or even more active ingredients account for a significant portion of the volume of pesticides applied. Regulators do not require further testing of such mixtures, nor do they conduct any additional risk assessments designed to quantify possible additive or synergistic impacts among all herbicides applied, let alone the combination of all herbicides, insecticides, fungicides, and other pesticides applied on any given field.
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2.
The full list of chemicals in most commercial GBHs is protected as “confidential business information,” despite the universally accepted relevance of such information to scientists hoping to conduct an accurate risk assessment of these herbicide formulations. The distinction in regulatory review and decision processes between ‘active’ and ‘inert’ ingredients has no toxicological justification, given increasing evidence that several so-called ‘inert’ adjuvants are toxic in their own right [42]. Moreover, in the case of GBHs, the adjuvants and surfactants, which include ethoxylated tallowamines, alkylpolyglycosides or petroleum distillates in most commonly used commercial formulations, alters both the environmental fate and residue levels of glyphosate and AMPA in harvested foodstuffs and animal feeds. They do so by enhancing the adhesion of glyphosate to plant surfaces, as well as facilitating the translocation of applied glyphosate from the surface of weed leaves into sub-surface plant tissues, where it exerts its herbicidal function and where rainfall can no longer dissipate the glyphosate.
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3.
The vast majority of GBH-toxicology studies used for regulatory assessments lack a sufficient range of dose levels to adequately assess adverse impacts that might be initiated by low, environmentally-relevant exposuresFootnote 6. Most toxicology studies examine only a high dose between the LD50 (the dose required to kill 50 % of treated animals) and the maximum tolerated dose (a dose that has high toxicity but does not kill), and then typically two lower doses (allowing for the identification of the Lowest Observed Adverse Effect Level [LOAEL] and the No Observed Adverse Effect Level [NOAEL]). Environmentally relevant doses are rarely examined [63]. A further complication arises specifically for endocrine disrupting chemicals: there are theoretical and empirical findings concluding that one cannot assume any no-impact exposure threshold for endocrine processes that are already underway because of endogenous hormones [76].
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4.
Residues of GBHs in plants are often present in conjunction with: (a) residues of systemic seed treatments, especially neonicotinoid insecticides (for example, clothianidin and thiamethoxam) and their adjuvants (such as organosilicone surfactants), (b) residues of systemic insecticides and fungicides applied during the season, and (c) Bt endotoxins in the case of GE, insect-protected Bt cultivars. Such mixtures and combinations are never tested, and thus it is unknown how GBHs might interact with these other agents.
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Large-scale and sophisticated biomonitoring studies of the levels of glyphosate, its metabolites, and other components of GBH mixtures in people have not been conducted anywhere in the world. Biomonitoring studies should include measurement of glyphosate residues, metabolites, and adjuvants in blood and urine to obtain meaningful insights into internal contamination levels and the pharmacokinetics of GBHs within vertebratesFootnote 7.
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6.
Adequate surveys of GBH contamination in food products have not as yet been conducted on a large scale, even in the U.S. The first and only in-depth USDA testing of glyphosate and AMPA residues in food targeted soybeans, and occurred once in 2011 [13]. Of the three hundred samples tested, 90.3 % contained glyphosate at a mean level of 1.9 ppm, while 95.7 % contained AMPA at 2.3 ppm. In contrast, the next highest residue reported by USDA in soybeans was malathion, present at 0.026 ppm in just 3.7 % of samples. Thus, the mean levels of glyphosate and AMPA in soybeans were 73-fold and 83-fold higher than malathion, respectively. Residues in animal products, sugar beet, pre-harvest treated wheat, corn silage, and alfalfa hay and sprouts are unknown, but likely much higher, given the series of recent requests by Monsanto to increase tolerance levels in a range of foods and animal feeds [12].
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7.
There is no thorough, up-to-date government survey of glyphosate and AMPA residues in U.S. grown Roundup Ready GE soybeans, nor manufactured foods that contain soy-based ingredients. However, changes in the rate of GBH applications on many other crops, and/or the timing of applications, have clearly increased residue levels in some circumstances. In particular, GBH uses late in the growing season as a pre-harvest desiccant have become more common. Such applications speed up the drying of crops in the field, so that harvest operations can be completed before bad weather sets in. Such harvest-aid uses are popular, especially in wet years, on wheat, canola, and other grain farms in some humid, temperate climates, such as in the UK and northern-tier states in the US. While pre-harvest uses have only modestly increased the total volume of GBHs applied, they have significantly increased the frequency and levels of residues in harvested grains, and have required GBH registrants to seek significant increases in tolerance levels. These residues are also contributing to dietary exposures via a number of grain-based products, as clearly evident in data from the U.K. Food Standard Agency’s residue testing program [14].
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8.
Glyphosate residues are generally uncontrolled for in the standard rations fed to animals in laboratory studies. GBH residues can often be found in common laboratory animal chows used in feeding studies, thus potentially confounding the results of GBH toxicity tests [77]. Out of 262 pesticide residues analyzed in 13 commonly used rodent laboratory diets, glyphosate was the most frequently found pesticide, with concentrations reaching 370 ppb [78]. Therefore, GBH residues should be accounted for in animal chows used in controls for GBH studies.
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9.
The limited data currently available on glyphosate pharmacokinetics in vertebrates are insufficient to predict transport and fate of glyphosate in different mammalian tissues, organs and fluids in the body, and to determine whether or where bioaccumulation occurs, although animal metabolism studies point strongly to the kidney and the liver.
Links
https://www.facebook.com/StoptheSprayOntario/
https://ehjournal.biomedcentral.com/articles/10.1186/s12940-016-0117-0#Tab1
