Part 4 - The Weapons
Thus far in this series on the restoration of Chena Slough, we've discussed the water, the weeds, and the war. In this part we will discuss the weapons being used. The Chena Slough is a local waterway located near North Pole, Alaska. It was recently found to be infested by an invasive species of aquatic vegetation, presumably an Elodea hybrid.
All eyes are (or should be) on the Chena Slough, "ground zero" of the first documented infestation of Elodea outside Eyak Lake.
Choosing Sides
There are several camps forming in what seemed to be a simple effort to restore vibrancy to a waterway that is losing its luster. On one side we have the State of Alaska's Department of Natural Resources (DNR), the US Forest Service, and rounding out the triumvirate is the Fairbanks Soil & Water Conservation District (FSWCD). On the other side we have landowners, recreational users of the waterways, and environmental groups. Caught in the middle is the Chena Slough.
It's unclear who is for or against the use of herbicides to eradicate Elodea. It's also unclear who will make the final decision, although the DNR has the responsibility to control invasive weeds in Alaska. The US Forest Service may play a role on federal lands. The FSWCD appears to play a supporting role as an outreach agency, working alongside state and federal agencies to solve a local problem. It's unclear who has a complete understanding.
Somewhere along the line, someone decided that Elodea can only be eradicated with the use of herbicides. Herbicides were applied to three lakes on the Kenai Peninsula in 2014 with the approval of state and federal agencies and the cooperation of the Homer Soil and Water Conservation District, with an important lesson learned (Morton, 2015):
- Eradicate from Kenai Peninsula;
- Understand the problem (no jurisdictional boundaries, no time to waste)
Irregardless of who decides, and who can block, the use of herbicides in our waters, we should first look critically at the herbicides proposed for use. A wide range of approved herbicides are available:
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| US Approved Aquatic Pesticides (adapted from US Army Corps of Engineers report) |
Fluridone
Fluridone is an aquatic herbicide that was registered with the Environmental Protection Agency (EPA) in 1986. Fluridone is sold under several brand names such as Avast, Sonar, and Whitecap. It comes in liquid and pellet forms.
The official chemical name of Fluridone is 1-methyl-3-phenyl-5-[3-(trifluoromethyl)phenyl]pyridin-4-one, and it looks like this:
Fluridone is a systemic herbicide, meaning it will kill the entire plant by interfering with its molecular functions. In this case, Fluridone interferes with carotene formation which leads to chlorophyll breakdown, killing the plant.
Sonar
Companies that sell Fluridone, such as Sepro, put out literature that says Fluridone is harmless to humans. Sepro bills their Sonar product as "An effective herbicide that poses negligible risk to human health and the environment (Sepro, n.d.)." In the Sepro Sonar "Risk Guide," the company discloses that the EPA has approved Sonar for use in water used for drinking as long as it does not exceed a certain parts per million, but that it may not be applied closer than 1/4 mile of the water intake in a reservoir used for drinking water.
Fluridone appears to have gone through rigorous testing on animals and there are established exposure limits which must not be exceeded. Fluridone, as an herbicide, has never been tested on people, because there is no requirement. Sepro calms fears in their risk guide:
Sonar inhibits a plant’s ability to make food. Specifically, Sonar inhibits carotenoid synthesis, a process specific only to plants. Carotenoids (yellow, orange and red pigments) are an important part of the plant’s photosynthetic (food making) system. These pigments protect the plant’s green pigments (called chlorophyll) from photo degradation or breakdown by sunlight. When carotenoid synthesis is inhibited, the chlorophyll is gradually destroyed by sunlight. As a plant’s chlorophyll decreases, so does its capacity to produce carbohydrates (its food source) through photosynthesis. Without the ability to produce carbohydrates, the plant dies.
With this description firmly established, Sepro makes an obvious conclusion for us:
Humans do not have carotenoid pigments. Therefore, the property of Sonar that makes it an effective herbicide at low doses does not affect the human body.
Fine Print
In the same risk guide that indicates Fluridone cannot harm a human because humans are not plants, is some fine print, shown here in normal font:
Throughout this document, we use the phrases “negligible risk” or “no significant risk.” We use these terms because it is beyond the capabilities of science to prove that a substance is absolutely safe, i.e., that the substance poses no risk whatsoever. Any substances, be it aspirin, table salt, caffeine, or household cleaning products, will cause adverse health effects at sufficiently high doses. Normal exposures to such substances in our daily lives, however, are well below those associated with adverse health effects. At some exposure, risks are so small that, for all practical purposes, no risk exists. We consider such risks to be negligible or insignificant.
How far to the Sun?
When Sepro came to North Pole to explain their plan for applying Fluridone to the Chena Slough, they used an analogy to demonstrate the magnitude of safety surrounding Fluridone:
Water treated with fluridone has no restrictions on drinking, swimming, fishing or eating those fish until levels surpass 150 parts per billion. One part per billion is equivalent to 1 second in 33 years, or 0.0027 pounds in 325,851 gallons of water.
And also in their risk guide, a similar analogy:
Studies in laboratory animals show that the lethal dose from a single oral exposure of Sonar is greater than 10,000 mg/kg... a 20-kg child would have to drink approximately 350,000 gallons.
And:
For reference, one (1) ppm can be considered equivalent to roughly one second in 12 days or one foot in 200 miles, and (0.1) ppm can be considered approximately equal to one second in 120 days or one foot in 2,000 miles.
And, our national debt, at $18 trillion, if stacked in $1 bills would reach the moon and back several times. People seem to have lost the awe of big numbers quite some time ago.
When looking at outright toxicity, an exposure limit is generally given to show how much of the reference product will cause harm. The study of pharmacodynamics and pharmacodynamics (PK-PD) uses different standards when determining dangers associated with drugs. PK-PD considers the organ systems, hormones, availability, and myriad other interactions of a drug to the human body.
What the Sonar salesman do not mention is was Fluridone is also a drug with very real effects on humans.
Fluridone, the drug
Fluridone, according to Heather Stewart, DNR’s invasive plant coordinator, is "one of the most benign chemicals that you can put in a water system. (Hollander, 2015)"
From the European Journal of Pharmacology, November, 2013: "Fluridone as a new anti-inflammatory drug."
According to the study on Fluridone as an anti-inflammatory drug, Fluridone contains a 4(1H)-pyridone and a trifluoromethyl-benzene moiety, which are also present in molecules with analgesic and anti-inflammatory properties. The mechanism of this "most benign" chemical is:
...in human monocytes, micromolar Fluridone inhibited cyclooxygenase-2 expression and the release of monocyte chemoattractant protein-1 and prostaglandin-E2, to a similar extent as Acetylsalicylic acid. Fluridone also inhibited the proliferation of aortic smooth muscle cells and reduced proliferation and cytokine release by human activated lymphocytes (Magnone, 2013).
As described by Sepro, Fluridone is harmelss to humans because humans do not use photosynthesis, yet the pharmacological investigations into Fluridone found a slight loophole in this line of thinking:
Interestingly, the mechanism of Fluridone's toxicity in plants relies on the inhibition of the enzyme phytoene desaturase, involved in the biosynthetic pathway of ß-carotene, the precursor of absciscic acid...
Absciscic acid, it turns out, it also manufactured by humans, and Fluridone interferes with this pathway. The study linked earlier from the European Journal of Pharmacology is not the only paper, there are others:
From "Chemical biology of abscisic acid (Kitahata and Asami, 2011)":
If ABA signal transduction pathway is common in humans and plants, ABA antagonists could lead to the development of new anti-inflammatory drugs. ... Interestingly, treatment with fluridone, a carotenoid biosynthesis inhibitor, reduced ABA levels...
From "Occurrence, function and potential medicinal applications of the phytohormone abscisic acid in animals and humans (Li et al., 2011)":
Abscisic acid (ABA) is an important phytohormone...in animals and has potential medicinal applications for several human diseases was conversely inhibited by the inhibitor of plant ABA synthesis Fluridone.
From "Phenotypic screening of the ToxCast chemical library to classify toxic and therapeutic mechanisms (Kleinstreuer et al., 2014)":
Addressing the safety aspects of drugs and environmental chemicals has historically been undertaken through animal testing. However, the quantity of chemicals in need of assessment and the challenges of species extrapolation require the development of alternative approaches. ... [several chemicals have been found to have] analgesic activity (the antioxidant propyl gallate and the herbicide fluridone).
From: "Toward a Medicine-Oriented Use of the Human Hormone/Nutritional Supplement Abscisic Acid (De Flora et al., 2014)":
This property suggested the possible development of new anti-inflammatory drugs. Indeed, we
recently reported that Fluridone, a known herbicide devoid of adverse effects in different animals,
exerts broad-spectrum anti-inflammatory effects, both in vitro and in vivo...
And lastly, a patent: "Fluridone as an anti-inflammatory agent, US Patent # US 7786042 B2 (Zocchi et al. 2010)":
The invention relates to a novel use of fluridone—compound known per se and used as an aquatic erbicide—in the medical field, in particular as an active compound for preparing a medicament having anti-inflammatory activity. Pharmaceutical compositions comprising fluridone as an active compound and pharmaceutically acceptable carriers and/or diluents are also disclosed. Finally, there is disclosed the pro-inflammatory activity of abscisic acid (ABA), a plant hormone which is also found in mammal serum and against which fluridone acts an inhibitor.
A literature search does not reveal past instances where an approved herbicide was later patented as a drug. Using certain weed killers for human disease, however, is a possibility (Smith, 2008). Should this patent be approved by the FDA as a drug, the future of Fluridone may be in jeopardy.
Short Term Effects
What seems to be a jumble of confusing words to the layman, is a treasure trove of information to those involved in drug discoveries. Drinking "one second in 12 days" worth of Fluridone may not seem to cause much toxic reaction, but when discussing drugs with hormonal interactions, "one second in 33 years" may be enough to make thousands of doses of a drug.
And indeed it is! Drug researchers from the anti-oxidant paper above discovered that an effective dose of Fluridone would be "1.25mg/kg/day [for] blood concentrations of Fluridone between 4 and 50 mmol/L"
According to the EPA, 1.25mg/kg is well below any toxic threshold they have tested by a large margin (EPA, 2015). 125mg/kg negatively affected rabbits. While a diluted dose of Fluridone, applied correctly, may not deliver 1.25mg/kg to a human who took a sip, it does show that Fluridone can have a systemic effect in humans in very small concentrations.
Long Term Effects
Additionally, the EPA has not conducted any tests involving the cumulative damage that may be caused by Furidone exposure (EPA, 2015). The risk guide for Sonar indicates that Fluridone is "short-lived" in water, yet the Alaska DNR tells us:
Fluridone is removed from treated water by photo degradation by sunlight, adsorption to sediments, and absorption by plants. In partially treated water bodies, dilution reduces the level of the pesticide more rapidly following application. In field studies, fluridone (various formulations) decreased logarithmically with time after treatment and approached zero detectable presence between 64 and 69 days after treatment (Langeland and Warner 1986). In other studies, fluridone levels decreased rapidly to a value below detection limits after 60 days in various parts of the water column, with a half-life of 7-21 days or less (Kamarianos et al.1989, Osborne et al.1989, Muir et al.1980, McCowen et al. 1979). Fluridone persistence in hydrosoils (sediments) can be over one year half-life (Muir et al.1980). [Emphasis added]
Muir et al. found Fluridone is only degraded by 50% at one year when it accumulates in sediment. The Chena Slough and most Alaskan bodies of water are noted for their high sedimentation. With a one year half-life, Fluridone could be with us for decades in the soil.
Fluridone Resistance
Fluridone has been used heavily in parts of the U.S. for decades to combat invasive aquatic species. If Alaska decides to take this route, there is no guarantee that our Elodia alaskana will not become resistant to its effects as other plants have, noted here:
Fluridone has been heavily used in the USA for aquatic plant management, and as a result, biotypes of hydrilla have developed that are resistant (Richardson, 2008). The development of fluridone resistance has significantly impacted hydrilla management, and further research is underway to find alternative products (Puri et al., 2009).
Puri et al. (2009) also discovered that when hydrilla became resistant to Fluridone, it also became reistant to most other herbicides.
The Wisconsin DNR uses Fluridone in their Elodea management plan, but cautions (Wisconsin DNR, 2012):
Plants have been shown to develop resistance to repeated fluridone use, so it is recommended to rotate herbicides with different modes of action when using fluridone as a control [for Elodea].
Contact Time
All available documentation shows that to be effective, Fluridone must stay in constant contact with Elodea for 45-90 days to kill it. This contact must be at a minimum concentration of approximately 40ppm. In a flowing water system like the Chena Slough, this would require a constant drip system, according to Sepro (n.d.). Should water levels change considerably, the concentration will be quickly diluted, negating all treatment done up until that point. The Chena Slough is frozen from mid-October through Mid-May, leaving only about a 150 day window for treatment. The water levels in the lower 2 miles of the Chena Slough are determined by the level of water in the Chena River. 2014 had many floods, it would not be possible to accurately dose Fluridone with wildly changing water levels.
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| Chena River Level Near Chena Slough, 2014 Open Water Season (USGS) |
In the summer of 2014, the water level in the Chena Slough near Persinger Bridge fluctuated continually. These were not minor fluctuations, but changes in water level of 2-10 feet in depth. There have been no historically stable periods of water height in this section of Chena slough since records have been kept. Keeping a constant percentage of Fluridone in the lower 2 miles of the Chena Slough will be impossible.
Diquat
Diquat was used in 2014 in Daniels Lake on the Kenai Peninsula according to the Peninsula Clarion (Boettger, 2015). The theory, as explained in the article:
In the five partially-infested areas of Daniels Lake, a second herbicide, diquat, was applied in June. Morton said diquat was “a contact killer” of aquatic plants. “It kills anything it comes in contact with that’s green,” Morton said. “Fluridone literally takes weeks to have an impact. Diquat, it takes 72 hours.” However, parts of a plant untouched by diquat, such the roots, remain alive. Morton said that the more rapid but less thorough Diquat was used to quickly stop the five elodea masses in Daniels Lake from spreading while the Fluridone worked to eradicate it completely. “We killed everything on the surface (using Diquat),” Morton said. “That means that everything that’s regrowing, from the roots up, is growing up into a fluridone-laced water system.”
As a case study to kill Elodea, they did everything right in Daniels Lake. Using a "scorched earth" methodology, they left no stone unturned.
Looking very much like Mad Max, this effort is probably going to prove very effective where chemicals are welcome.
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| Applying Diquat to Daniels Lake (From FWS report) |
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| Mad Max Flame Thrower |
Chemical Makeup of Diquat
Diquat is a contact herbicide that dries and kills foliage. Available as Aquacide, Dextrone, and Weedol (among others), it is easily purchased by anyone. Diquat is non-selective, killing any plant it touches. It acts quickly, killing in hours, but it only kills where it touches the plant. Diquat is often used by large farming operations to defoliate crops, such as tomatoes, to make harvesting easier. Diquat persists for many years in soils.
Diquat is "moderately toxic" and is fatal if swallowed, inhaled, or absorbed through the skin. Diquat looks like this, in chemical notation:
Diquat's recognized chemical name is: 6,7-Dihydrodipyrido[1,2-a:2',1'-c]pyrazinediium dibromide.
Systemic Effects
Despite Diquat's widespread sue in the US, it has been studied for its toxic effects since it was developed in 1958. According to Gallagher (1995), Diquat causes systemic damage at the genetic level:
We examined the effects of diquat (0.1 mmol/kg, ip) and ciprofibrate (0.025% w/w, diet), chemicals which induce oxidative stress via different biochemical mechanisms, on the steady-state messenger RNA (mRNA) levels of six cytochrome P450 enzymes, seven glutathione S-transferase (GST) isoenzymes, UDP-glucuronosyl transferase 1-06 (UGT1*06), gamma-glutamylcysteine synthetase (gamma GCS), NADP(H):quinone oxidoreductase (quinone reductase), Cu/Zn superoxide dismutase (SOD), catalase, and 18S ribosomal RNA...These effects may involve the pretranslational loss of hepatic mRNAs, possibly due to accelerated production of reactive oxygen species.
Others found that a condition known as Parkinsonism may result from exposure and "elicit chronic parkinsonism in humans" (Ellenhorn et al., 1997).
Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. Parkinsonism shares symptoms found in Parkinson's disease, from which it is named. (Wikipedia)
Diquat and Fish
According to Cornell University, "Diquat dibromide is slightly toxic to fish. Its toxicity to fish, and food organisms on which fish survive, has been reported in many studies." And gives cautions when applying to water (Cornell, n.d.):
Some species of fish may be harmed, but not actually killed, by sublethal levels of diquat dibromide. Oxygen can become depleted in diquat-treated water by decaying aquatic plants. This decreases the amount of oxygen available for fish survival. Research indicates that yellow perch suffer significant respiratory stress when herbicide concentrations in the water are similar to those normally present during aquatic vegetation control programs. Strip application of the herbicide over water is recommended to prevent large scale fish kills.
Persistence
Diquat is an indiscriminate, temporary killer of aquatic plants such as Elodea and all native species. It persists for many years in the water and in the soil, though it is taken up by plants and made inert by the soil. Cornell University toxological database informs:
Since diquat is purposely applied to water to control the growth of aquatic weeds, its ability to last as an effective residue has been studied carefully. These studies suggest that diquat is not persistent in water. When diquat is applied to open water, it disappears rapidly because it binds to suspended particles in the water. These particles are then taken up by plants. Diquat dibromide's half-life, or the period of time that it usually takes for half of the amount of the material to be broken down by natural processes, is less than 48 hours in water. As affected plants decompose, the adsorbed diquat rapidly disappears from open waters. Disappearance may be due to degradation by microbes or sunlight, or due to adsorption to bottom sediments. Twenty-two days after a weed infested artificial lake was treated, only 1% of the applied diquat remained in the water and 19% was adsorbed to sediments. Adsorbed diquat was subject to microbial degradation. Diquat has been found in the bottom soil of pools and ponds four years after application. Diquat will photodegrade in surface layers of water in 1 to 3 or more weeks when it is not adsorbed to suspended particles.
The EPA requires a 14-day interval between treatment of water with diquat dibromide and use of treated waters for domestic, livestock, or irrigation purposes. Swimming, fishing and watering of domestic animals should not be allowed for at least 14 days after application of the herbicide to water. The herbicide cannot be used for any purpose in commercial fish processing areas.
As with Fluridone, Diquat shows the propensity to persist for years in the sediments as found in Alaska lakes and sloughs.
Conclusion
Fluridone and Diquat are being used in Alaska to treat Elodea. There effectiveness in Alaska has not been time-tested and public support will be required if continued applications are to proceed. As an Elodea management tool, these herbicides will need to be repeatedly used around the state and Elodea may become resistant. These chemicals are not without proven hazards, though they have enjoyed widespread usage in the lower 48 states for many decades with little concern for human safety.
Should Alaskans decide they wish to keep Fluridone and Diquat in the arsenal for Elodea control, it is at our own risk. Contracts for the sales of these herbicides will be lucrative for suppliers. Alaska has already spent $600,000 to treat three lakes, with a quote for $600,000 more to treat Chena Slough and Chena Lakes. As more and more lakes become infected, the price tag becomes an issue. Will the State permit continued reliance on chemicals or will other means be needed?
In Part 5, some ideas for Chena Slough and the rest of the state.
References:
Boettger, B (2015). Group declares partial victory over
elodia. Retrieved
from http://peninsulaclarion.com/news/2015-06-13/a-partial-victory-over-elodea
Cornell, (n.d.). Diquat. Retrieved from
http://pmep.cce.cornell.edu/profiles/extoxnet/dienochlor-glyphosate/diquat-ext.html
and
http://pmep.cce.cornell.edu/profiles/herb-growthreg/fatty-alcohol-monuron/fluridone/herb-prof-fluridone.html
De Flora, A.,
Bruzzone, S., Guida, L., Sturla, L., Magnone, M., Fresia, C., ... & Zocchi,
E. (2014). Toward a Medicine-Oriented Use of the Human Hormone/Nutritional
Supplement Abscisic Acid. Messenger, 3(1-2), 86-97.
Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger.
Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd
ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1637
EPA (2015). Report of the Food Quality Protection
Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision
(TRED) for Fluridone. Retrieved from
http://www.epa.gov/pesticides/reregistration/REDs/fluridone_tred.pdf
Gallagher, E. P., Buetler, T. M., Stapleton, P. L., Wang, C.
H., Stahl, D. L., & Eaton, D. L. (1995). The effects of diquat and
ciprofibrate on mRNA expression and catalytic activities of hepatic xenobiotic
metabolizing and antioxidant enzymes in rat liver. Toxicology and applied
pharmacology, 134(1), 81-91.
Hollander, Z. (2015). Weed killer proposed for invasive plant
choking West Anchorage lakes. Retrieved from
http://www.adn.com/article/20150606/weed-killer-proposed-invasive-plant-choking-west-anchorage-lakes
Kitahata, N.,
& Asami, T. (2011). Chemical biology of abscisic acid. Journal of plant
research, 124(4), 549-557.
Kleinstreuer, N. C.,
Yang, J., Berg, E. L., Knudsen, T. B., Richard, A. M., Martin, M. T., ... &
Houck, K. A. (2014). Phenotypic screening of the ToxCast chemical library to
classify toxic and therapeutic mechanisms. Nature biotechnology, 32(6),
583-591.
Li, H. H., Hao,
R. L., Wu, S. S., Guo, P. C., Chen, C. J., Pan, L. P., & Ni, H. (2011). Occurrence,
function and potential medicinal applications of the phytohormone abscisic acid
in animals and humans. Biochemical pharmacology, 82(7), 701-712.
Magnone, M., Scarfì,
S., Sturla, L., Guida, L., Cuzzocrea, S., Di Paola, R., ... & Zocchi, E.
(2013). Fluridone as a new anti-inflammatory drug. European journal of
pharmacology, 720(1), 7-15. retrieved from
http://www.ncbi.nlm.nih.gov/pubmed/24211328
Morton, J. (2015). Elodea on the Kenai Peninsula and what
we’re doing about it. Kenai National Wildlife Refuge presentation. Retrieved
from http://www.fws.gov/uploadedFiles/Morton_JM_2014-10_Elodea_CNPM.pdf
Puri, A., Haller, W.
T., & Netherland, M. D. (2009). Cross-resistance in fluridone-resistant
hydrilla to other bleaching herbicides. Weed science, 57(5),
482-488.
Sepro (n.d.). Risk Guide for Sonar. Retrieved from
http://www.sepro.com/documents/Risk_Guide.pdf
Smith, K. (2008). Can weedkillers whack human parasites?
Retrieved from http://www.nature.com/news/2008/080109/full/news.2008.424.htm
Wisconsin DNR (2012).
Fluridone Chemical Fact Sheet. Retrieved from
http://dnr.wi.gov/lakes/plants/factsheets/FluridoneFactsheet.pdf
I want you to be my neighbor to ensure that I am informed on the issues of my neighborhood. :)
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