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Contents:ALSO CHECK OUT THESE IMPORTANT UPDATES:Aug 06: Hancock pollutes Geelong Drinking Water with Hexazinone for 31 months (and counting!)Environmental groups call for bans on aerial spraying of pesticidesFSC Review of Chemical Policy by Pesticide Action NetworkPlantation Forestry Pesticides Australian Drinking Water GuidelinesModes of Actions of HerbicidesPlantation pesticide misuse in Tasmania makes national news SEP04Plantation pesticide misuse in Tasmania makes national news JUL04UPDATES 1UPDATES 2Bluegum plantation insecticidesCHLORINATED PESTICIDESHistorical data on 2,4,5-T use in Victorian PlantationsThe Continuing Health Problems Associated with 2,4,5-TForest Stewardship CouncilHerbicides and Plantation Forestry - IntroductionHerbicides can create an environment that is barren and hostile to many native insects, birds and animals by knocking out understory species / food plants. A decrease in the number of birds in some regions has been attributed to the widespread use of herbicides such as Roundup. In September 1999 Hancock Victorian Plantations announced that they would be dropping granular Velmac G herbicide over several radiata pine plantations in Gippsland and the Strzelecki Ranges.Hancock also have a massive weed problem to deal with, with many plantations infested with blackberries and other weeds. This will probably mean more herbicides treated on plantation areas. " . . . Managers of crown land which border roadsides were also criticised. South Gippsland farmer Marilyn Lewis was horrified after a trip to Tarra Bulga National Park from Mirboo North recently. 'For nearly the whole of the unsealed road there was weeds on both sides of the road. I felt I was travelling down hedgerows of weeds,' she said. She said Hancocks Victorian Plantations, which controlled most of the land along the route, had failed to clean up. 'I'm a farmer and I have to keep my roadsides clean so I'd like to know what a multinational like Hancocks has for an excuse," she said. A Hancocks spokesman said it took its responsibility seriously for roadside weeds bordering its plantations. But with some 160,000 hectares and some 2500km of roads to look after, it was a huge task, the spokesman said. It worked with catchment management authorities and community groups to do as much weed control as possible . . . " From The Weekly Times January 24, 2001. Velmac G is made by a Queensland based company (but whose primary place of business is in Delacombe Victoria) called Macspred Pty Ltd, a manufacturer, wholesaler and retailer of herbicides as well as being a distributor for major chemical companies. Macspred has an annual revenue of $10 million and also export to New Zealand. Current forest herbicides sold by Macspred include Velmac G for control of annual and perennial grasses, broadleaf weeds and woody weeds (ie native vegetation) in Pinus Radiata plantations, Macspred Eucmix GR for the control of certain annual and perennial weeds in E. globulus, E. regnans and E. nitens plantations, Forest Mix made by Macspred for use in radiata pine plantations, Forest Mix - special blend and the infamous Atrazine which has been linked to cancers in the United States was also on Macspred's shopping list. Macspred also recommended the liquid herbicides Oust made by Du Pont for the control of perennial and annual weeds and Cut-Out, another Du Pont herbicide used to control woody weeds. Herbicides applied as liquid and sold by Macspred include Atrazine, Brush-Off, Cut-Out, Fusilade, Garlon, Grazon DS, Lontrel, Oust, Roundup, Roundup Bioactive, Roundup CT, Roundup CT Xtra, Tordon TCM, Trounce, Simazine, Velpar DF and Visor. The active constituents of the granular herbicides are : Velmac G (200g/kg Hexazinone), Simazine 500 (500g/l Simazine), Eucmix GR (44g/kg Terbacil - 2g/kg, Sulfometuron Methyl), Forest Mix (50g/kg Hexazinone, 150g/kg Atrazine). Oust's active constituent was (750g/kg Sulfometuron Methyl) and Cut-Out (63.2g/kg Metsulfuron Methyl, 760.5g/kg Glyphosate). Further research on the active constituents revealed that little work had been done on the environmental dangers of these herbicides in Australia.
Towns Downstream of Hancock's plantations possibly sourcing drinking water from Hancock's herbicide treated plantations.This list doesn't include all towns and villages - just the main ones. It also doesn't list towns that source their drinking water from ground water which may or may not be polluted with chemicals such as Atrazine. The list was compiled from maps showing plantation areas and the creeks coming from those plantations. Hancock Watch has listed the town, with the name of the source of water supply. Some places get their water from a number of reservoirs or creeks. We've only listed the creeks that have a plantation on them. Industrial Plantations mean herbicides, fertilisers, insecticides, fungicides, shorter rotations and massive hydrological changes to water systems. This often means extra chemical treatment is required by water authorities. Please note that this list does not contain towns downstream of Australian Paper Plantations, Weyerhauser or the recent bluegum explosion out west. This list just refers to Hancock Victorian Plantations. Update November2006
Water supplies most likely to be impacted by Hancock activities (in red): For more detailed information on these potentially impacted water supplies, please go to connecting links: http://www.hancock.forests.org.au/directory/regional.html
ATRAZINE (also www.panna.org)Other interesting Atrazine Links; Assessing exposure to atrazine & its metabolites using biomonitoring Ban on herbicide unlikely (Oct 26 07) Mindfully: The Story of Syngenta and Tyrone Hayes at UC Berkeley: The Price of Research October 2003 Please note that Hancock does not use Atrazine on its plantations in Victoria - although Australian Paper Plantations who Hancock took over in 2001 were using Atrazine. Click here for information regarding Atrazine disasters in South Australia and Tasmania. (Friends of the Earth was one of the local groups very active in getting a moratorium placed on Atrazine use in plantations in Tasmania in the mid 1990's). National Registration Authority Review on Atrazine 2002 (including information from the Forest Herbicide Research Management Group) NRA Summary of Atrazine Review Pesticide and Chemical News Organic Federation of Australia Organic Update June 2005 www.ofa.org.au Atrazine Causes Brain Cell Damage A new study conducted by researchers at the University of Medicine and Dentistry of New Jersey has found the minute amounts of atrazine damage the critical areas of the nervous system that are involved with understanding, intelligence, movement and most importantly over all body function. The Authors stated "Collectively, these studies demonstrate that ATR [atrazine] can produce neurotoxicity in dopaminergic systems that are critical to the mediation of movement as well as cognition and executive function." This is yet another of the long list of studies that confirm why Australia should follow Europe's example and ban this toxic residual chemical. E X T O X N E T EXTOXNET primary files maintained and archived at Oregon State University Revised June 1996
AtrazineTrade and Other Names: Trade names include Aatrex, Aktikon, Alazine, Atred, Atranex, Atrataf, Atratol, Azinotox, Crisazina, Farmco Atrazine, G-30027, Gesaprim, Giffex 4L, Malermais, Primatol, Simazat, and Zeapos.Regulatory Status: Atrazine has been classified as a Restricted Use Pesticide (RUP) due to its potential for groundwater contamination [2]. RUPs may be purchased and used only by certified applicators. Atrazine is toxicity class III - slightly toxic. In November, 1994, the EPA initiated a Special Review which could result in use restrictions or cancellation of atrazine if health data warrant such action. Products containing atrazine must the Signal Word CAUTION. Chemical Class: triazine Introduction: Atrazine is a selective triazine herbicide used to control broadleaf and grassy weeds in corn, sorghum, sugarcane, pineapple, christmas trees, and other crops, and in conifer reforestation plantings. It is also used as a nonselective herbicide on non-cropped industrial lands and on fallow lands. Over 64 million acres of cropland were treated with atrazine in the U.S. in 1990. It is available as dry flowable, flowable liquid, liquid, water dispersible granular, and wettable powder formulations. Formulation: It is available as dry flowable, flowable liquid, liquid, water dispersible granular, and wettable powder formulations.
Toxicological Effects:Acute toxicity: Atrazine is slightly to moderately toxic to humans and other animals. It can be absorbed orally, dermally, and by inhalation. Symptoms of poisoning include abdominal pain, diarrhea and vomiting, eye irritation, irritation of mucous membranes, and skin reactions [3]. At very high doses, rats show excitation followed by depression, slowed breathing, incoordination, muscle spasms, and hypothermia [3]. After consuming a large oral dose, rats exhibit muscular weakness, hypoactivity, breathing difficulty, prostration, convulsions, and death [16]. Atrazine is a mild skin irritant. Rashes associated with exposure have been reported. The oral LD50 for atrazine is 3090 mg/kg in rats, 1750 mg/kg in mice, 750 mg/kg in rabbits, and 1000 mg/kg in hamsters. The dermal LD50 in rabbits is 7500 mg/kg and greater than 3000 mg/kg in rats [15,16]. The 1-hour inhalation LC50 is greater than 0.7 mg/L in rats. The 4-hour inhalation LC50 is 5.2 mg/L in rats [3,6].Chronic toxicity: Some 40% of rats receiving oral doses of 20 mg/kg/day for 6 months died with signs of respiratory distress and paralysis of the limbs. Structural and chemical changes in the brain, heart, liver, lungs, kidney, ovaries, and endocrine organs were observed [3,16]. Rats fed 5 or 25 mg/kg/day of atrazine for 6 months exhibited growth retardation. In a 2-year study with dogs, 7.5 mg/kg/day caused decreased food intake and increased heart and liver weights. At 75 mg/kg/day, there were decreases in food intake and body weight gain, increased adrenal weight, lowered blood cell counts, and occasional tremors or stiffness in the rear limbs [3]. Reproductive effects: Dietary doses of atrazine given to rats on days 3, 6 and 9 of gestation up to about 50 mg/kg/day caused no adverse reproductive effects [3]. Teratogenic effects: Atrazine does not appear to be teratogenic. In mice, atrazine did not cause abnormalities in fetuses whose dams were given doses of 46.4 mg/kg/day during days 6 through 14 of gestation [3]. Mutagenic effects: The weight of evidence from more than 50 studies indicates that atrazine is not mutagenic [3]. Carcinogenic effects: Atrazine did not cause tumors when mice were given oral doses of 21.5 mg/kg/day from age 1 to 4 weeks, followed by dietary doses of 82 mg/kg for an additional 17 months. However, mammary tumors were observed in rats after lifetime administration of high doses of atrazine [3]. Thus, available data regarding atrazine's carcinogenic potential are inconclusive. Organ toxicity: Lethal doses of atrazine in test animals have caused congestion and/or hemorrhaging to the lungs, kidneys, liver, spleen, brain, and heart [3]. Long-term consumption of high levels of atrazine has caused tremors, changes in organ weights, and damage to the liver and heart [3]. Fate in humans and animals: Atrazine is readily absorbed through the gastrointestinal tract. When a single dose of 0.53 mg atrazine was administered to rats by gavage, 20% of the dose was excreted in the feces within 72 hours. The other 80% was absorbed across the lining of the gastrointestinal tract into the bloodstream. After 72 hours, 65% was eliminated in the urine and 15% was retained in body tissues, mainly in the liver, kidneys, and lungs [3].
Ecological Effects:Effects on birds: Atrazine is practically nontoxic to birds. The LD50 is greater than 2000 mg/kg in mallard ducks. At dietary doses of 5000 ppm, no effect was observed in bobwhite quail and ring-necked pheasants [15,16].Effects on aquatic organisms: Atrazine is slightly toxic to fish and other aquatic life. Atrazine has a low level of bioaccumulation in fish. In whitefish, atrazine accumulates in the brain, gall bladder, liver, and gut [16]. Effects on other organisms: Atrazine is not toxic to bees [16].
Environmental Fate:Breakdown in soil and groundwater: Atrazine is highly persistent in soil. Chemical hydrolysis, followed by degradation by soil microorganisms, accounts for most of the breakdown of atrazine. Hydrolysis is rapid in acidic or basic environments, but is slower at neutral pHs. Addition of organic material increases the rate of hydrolysis. Atrazine can persist for longer than 1 year under dry or cold conditions [21]. Atrazine is moderately to highly mobile in soils with low clay or organic matter content. Because it does not adsorb strongly to soil particles and has a lengthy half-life (60 to >100 days), it has a high potential for groundwater contamination despite its moderate solubility in water [20]. Atrazine is the second most common pesticide found in private wells and in community wells [16]. Trace amounts have been found in drinking water samples and in groundwater samples in a number of states [23,21]. A 5-year survey of drinking water wells detected atrazine in an estimated 1.7% of community water systems and 0.7% of rural domestic wells nationwide. Levels detected in rural domestic wells sometimes exceeded the MCL [23]. The recently completed National Survey of Pesticides in Drinking Water found atrazine in nearly 1% of all of the wells tested [23].Breakdown in water: Atrazine is moderately soluble in water. Chemical hydrolysis, followed by biodegradation, may be the most important route of disappearance from aquatic environments. Hydrolysis is rapid under acidic or basic conditions, but is slower at neutral pHs. Atrazine is not expected to strongly adsorb to sediments. Bioconcentration and volatilization of atrazine are not environmentally important [21]. Atrazine has been detected in each of 146 water samples collected at 8 locations from the Mississippi, Ohio and Missouri Rivers and their tributaries. For several weeks, 27% of these samples contained atrazine concentrations above the EPA's maximum contaminant level (MCL) [24]. Breakdown in vegetation: Atrazine is absorbed by plants mainly through the roots, but also through the foliage. Once absorbed, it is translocated upward and accumulates in the growing tips and the new leaves of the plant. In susceptible plant species, atrazine inhibits photosynthesis. In tolerant plants, it is metabolized [6]. Most crops can be planted 1 year after application of atrazine. Atrazine increases the uptake of arsenic by treated plants [16].
Physical Properties:Appearance: Atrazine is a white, crystalline solid [6].Chemical Name: 2-chloro-4-ethylamine-6-isopropylamino-S-triazine [6] CAS Number: 1912-24-9 Molecular Weight: 215.69 Water Solubility: 28 mg/L @ 20 C [6] Solubility in Other Solvents: chloroform v.s.; diethyl ether v.s.; dimethyl sulfoxide v.s. [6] Melting Point: 176 C [6] Vapor Pressure: 0.04 mPa @ 20 C [6] Partition Coefficient: 2.3404 [6] Adsorption Coefficient: 100 [20] Exposure Guidelines:ADI: Not AvailableMCL: 0.003 mg/L [25] RfD: 0.035 mg/kg/day [26] PEL: Not Available HA: Not Available TLV: 5 mg/m3 (8-hour) [16] Basic Manufacturer:Ciba-Geigy Corp.P.O. Box 18300 Greensboro, NC 27419-8300 Phone: 800-334-9481 Emergency: 800-888-8372 References: References for the information in this PIP can be found in Reference List Number 8 DISCLAIMER: The information in this profile does not in any way replace or supersede the information on the pesticide product labeling or other regulatory requirements. Please refer to the pesticide product labeling.
GlyphosateRoundup kills amphibians 2005 study Monsanto's Roundup Linked to Pregnancy & Reproductive Problems & Endocrine Disruption More at: http://www.organicconsumers.org/monsanto/pregnancy060305.cfm June 3, 2005 Conclusion Our studies show that glyphosate acts as a disruptor of mammalian cytochrome P450 aromatase activity from concentrations 100 times lower than the recommended use in agriculture; this is noticeable on human placental cells after only 18 hr, and it can also affect aromatase gene expression. It also partially disrupts the ubiquitous reductase activity but at higher concentrations. Its effects are allowed and amplified by at least 0.02% of the adjuvants present in Roundup, known to facilitate cell penetration, and this should be carefully taken into account in pesticide evaluation. The dilution of glyphosate in Roundup formulation may multiply its endocrine effect. Roundup may be thus considered as a potential endocrine disruptor. Moreover, at higher doses still below the classical agricultural dilutions, its toxicity on placental cells could induce some reproduction problems. Chemical Mixtures The Need for Testing Chemical Mixtures Organic Update has commented several times on the need to test chemical mixtures rather than the current approach of only testing a single active ingredient of pesticides and herbicides. The two recently published studies, below, add to this need. Roundup Twice as Toxic as Glyphosate An editorial in the latest issue of the peer reviewed scientific Journal Environmental Health Perspectives has commented on the important issue of testing the whole product due to a study that shows that both glyphosate and Roundup severely damage placental cells. The journal editorial stated "Roundup was nearly twice as toxic as the single chemical alone. Further, the viability of cells exposed to glyphosate was considerably reduced when even minute dilutions of Roundup were added." "The study showed that the effect of Roundup on cell viability increased with time and was obtained with concentrations of the formulation 10 times lower than those recommended for agricultural use. Roundup also disrupted aromatase activity at concentrations 100 times lower than those used in agriculture." The editorial stated "Virtually all previous testing of Roundup for long-term health damage has been done on glyphosate rather than on the full herbicide formulation, of which glyphosate makes up only around 40%." This study highlights the urgent need for product testing rather than only testing a single ingredient. Predicting the Effects of Low Dose Mixtures. A study published in Environmental Health Perspectives has found that mixtures of minute amounts of chemicals can cause health and reproductive problems at doses where individually they have no effect. The paper was published by researchers from Brunel University, UK, The School of Pharmacy, London, UK, University of Bremen, Germany; Vrije Universiteit, The Netherlands and University of Venice, Italy. Most importantly the researchers have established a predictive model to determine effect of these mixtures. The Researchers stated "These findings demonstrate that estrogenic chemicals have the capacity to act together in an additive manner and that their combined effects can be accurately predicted by concentration addition." "These findings highlight the potential for existing environmental risk assessment procedures to underestimate the hazard posed by mixtures of chemicals that act via a similar mode of action, thereby leading to erroneous conclusions of absence of risk." See: http://www.mindfully.org/Pesticide/Monsanto-Roundup-Glyphosate.htm (Also see: www.panna.org - Glyphosate) The Trouble with IBT Roundup (Glyphosate) Information Package Prepared by Karen Talberth, Lois Yoshishige and Margie Juris February 1985, Northwest Coalition for Alternatives to Pesticides Eugene, Oregon, 97440. The main problem citizens are having with Round-up (and glyphosate in general) center around a lack of information and questions as to the validity of the research that has been done. All but a handful of studies done for the registration of glyphosate with the EPA are not available to the public, and many of the chronic toxicity tests were done at the Industrial Bio-Tech Laboratories, Inc. A major scandal in 1975 revealed that conditions at IBT resulted in many invalid tests. Out of 26 studies done by IBT for glyphosate's registration, 17 were found to be invalid by the EPA and two were found to be only partially valid. Out of these 19 studies, 10 have been replaced, two replacement studies are under review at the EPA, five replacement studies are to be "processed via registration standards", and two do not require replacement. Meanwhile, in response to demands that pesticides having invalid IBT studies as the major grounds for their registration (such as glyphosate) be removed from the market until valid studies are provided, the EPA responds that registration is not cancelled "merely for the lack of data." They are consequently kept on the market without adequate, legally required information on their toxicity or risks. Another interesting facet of the IBT scandal involves a man named Paul Wright. Dr Wright was a main character in the IBT scandal, and is an employee of Monsanto. In fact, Dr Wright was a toxicologist at Monsanto before he started work at IBT in March 1971. At IBT, Wright oversaw the study done on TCC, another chemical manufactured by Monsanto. This study was so fraudulent that the prosecuting attorneys in the lawsuit against IBT used it as part of the bases for their case. According to Dr Donovan E Gordon, IBT's pathologist, "postmortem data were removed from the (TCC) report, because they incriminated the TCC compound." Dr Wright allegedly had a part in this cover-up. He returned to Monsanto in early October 1972, which places him at IBT during the course of at least three studies done for Round-Up: Mutagenicity Mice completed 1/24/72 Subchronic Rabbit filed 6/30/72 Reproduction Rat started 7/8/81 Out of the 19 tests done on chronic toxicity for the registration of glyphosate, 11 were done by IBT. Only one test as done for carcinogenicity (also called oncogenicity - tests for tumors); this test was done by IBT. The EPA does have a regulation stating that tests for carcinogenicity must be done on at least two species, but they often waive this requirement. As of April 30, 1984, the replacement study for this test had been received at the EPA, and is under review. A breakdown of chronic toxicity tests follows:
+This test was ruled valid by the EPA References 1. Environmental Protection Agency, Office of Pesticides and Toxic Substances. Information obtained under a Freedom of Information Request, April 30, 1984. 2. Shearer, Ruth W. 1984. "Health Effects of Glyphosate." Unpublished Paper. 3. Schneider, Keith. 1983. "Faking It: The Case Against Industrial Bio-Test Labotatories." The Amicus Journal (Spring): 16-14 (Used in Roundup). Glyphosate is a broad-spectrum, nonselective systemic herbicide used for control of annual and perennial plants including grasses, sedges, broad-leaved weeds and woody plants. US based multi-national Monsanto markets many of the glyphosate products made in Australia. When formulated as Roundup, it has been shown to affect enzymes found in mammals such as rats where it decreased the activity of two detoxification enzymes in the liver and intestine. Acute effects from accidental exposure to Roundup include burning eyes, blurred vision, blisters, rapid heartbeat, chest pains, nausea and Swedish oncologists have recently released a study linking Roundup to non-Hodgkin's lymphoma, a form of cancer. Roundup 360 has been found to be more toxic to adult frogs and tadpoles than technical grade glyphosate and in 1996 the NRA states that the 'acquatic toxicity of currently registered glyphosate formulations is undesirably high and is mainly due to surfacants in the formulations'. The US EPA has called glyphosate extremely persistent under typical conditions and half lives of 3 days to 22.8 years have been reported. In 1997 Monsanto negotiated an agreement with the New York State Attorney General to alter its Roundup adds to delete claims that the herbicide is 'biodegradable' and 'environmentally friendly'. Reference: Eco News WA November 1999 - article by Karen Thomas Environment Centre of WA. Roundup Inhibits Steroidogenesis by Disrupting Steroidogenic Acute Regulatory (StAR) Protein Expression Lance P. Walsh, Chad McCormick, Clyde Martin, and Douglas M. Stocco -
Department of Cell Biology and Biochemistry, Texas Tech University
Health AbstractRecent reports demonstrate that many currently used pesticides have the capacity to disrupt reproductive function in animals. Although this reproductive dysfunction is typically characterized by alterations in serum steroid hormone levels, disruptions in spermatogenesis, and loss of fertility, the mechanisms involved in pesticide-induced infertility remain unclear.Because testicular Leydig cells play a crucial role in male reproductive function by producing testosterone, we used the mouse MA-10 Leydig tumor cell line to study the molecular events involved in pesticide-induced alterations in steroid hormone biosynthesis. We previously showed that the organochlorine insecticide lindane and the organophosphate insecticide Dimethoate directly inhibit steroidogenesis in Leydig cells by disrupting expression of the steroidogenic acute regulatory (StAR) protein. StAR protein mediates the rate-limiting and acutely regulated step in steroidogenesis, the transfer of cholesterol from the outer to the inner mitochondrial membrane where the cytochrome P450 side chain cleavage (P450scc) enzyme initiates the synthesis of all steroid hormones. In the present study, we screened eight currently used pesticide formulations for their ability to inhibit steroidogenesis, concentrating on their effects on StAR expression in MA-10 cells. In addition, we determined the effects of these compounds on the levels and activities of the P450scc enzyme (which converts cholesterol to pregnenolone) and the 3ß-hydroxysteroid dehydrogenase (3ß-HSD) enzyme (which converts pregnenolone to progesterone). Of the pesticides screened, only the pesticide Roundup inhibited dibutyryl [(Bu)2]cAMP-stimulated progesterone production in MA-10 cells without causing cellular toxicity. Roundup inhibited steroidogenesis by disrupting StAR protein expression, further demonstrating the susceptibility of StAR to environmental pollutants. Key words: chemical mixtures, cytochrome P450 side chain cleavage, environmental endocrine disruptor, 3ß-hydroxysteroid dehydrogenase, Leydig cells, Roundup, steroid hormones, steroidogenesis, steroidogenic acute regulatory protein. Environ Health Perspect 108:769-776 (2000). [Online 12 July 2000] http://ehpnet1.niehs.nih.gov/docs/2000/108p769-776walsh/abstract.html EXTOXNET primary files maintained and archived at Oregon State University Revised June 1996
GlyphosateWhile Monsanto maintains that Roundup is safe, many others disagree, including the New York State Attorney General. Based on its investigation, the Attorney-General’s office filed a lawsuit arguing that the company‘s advertising inaccurately portrayed Monsanto’s glyph sate-containing produce as safe and not causing any harmful effects to people or the environment. As part of an out-of-court settlement, Monsanto agreed to discontinue use of terms such as "biodegradable" and "environmentally friendly" in all advertising of glyph sate-containing products in New York State and paid US$50,000 toward the State’s costs of pursuing the case.http://www.voteyeson27.com/monsanto.htm Trade and Other Names: Trade names for products containing glyphosate include Gallup, Landmaster, Pondmaster, Ranger, Roundup, Rodeo, and Touchdown. It may be used in formulations with other herbicides. Regulatory Status: Glyphosate acid and its salts are moderately toxic compounds in EPA toxicity class II. Labels for products containing these compounds must bear the Signal Word WARNING. Glyphosate is a General Use Pesticide (GUP). Chemical Class: Not Available Introduction: Glyphosate is a broad-spectrum, nonselective systemic herbicide used for control of annual and perennial plants including grasses, sedges, broad-leaved weeds, and woody plants. It can be used on non-cropland as well as on a great variety of crops. Glyphosate itself is an acid, but it is commonly used in salt form, most commonly the isopropylamine salt. It may also be available in acidic or trimethylsulfonium salt forms. It is generally distributed as water-soluble concentrates and powders. The information presented here refers to the technical grade of the acid form of glyphosate, unless otherwise noted. Formulation: Glyphosate itself is an acid, but it is commonly used in salt form, most commonly the isopropylamine salt. It may also be available in acidic or trimethylsulfonium salt forms. It is generally distributed as water-soluble concentrates and powders.
Toxicological Effects:Acute toxicity: Glyphosate is practically nontoxic by ingestion, with a reported acute oral LD50 of 5600 mg/kg in the rat. The toxicities of the technical acid (glyphosate) and the formulated product (Roundup) are nearly the same [58,96]. The oral LD50 for the trimethylsulfonium salt is reported to be approximately 750 mg/kg in rats, which indicates moderate toxicity [58]. Formulations may show moderate toxicity as well (LD50 values between 1000 mg/kg and 5000 mg/kg) [58]. Oral LD50 values for glyphosate are greater than 10,000 mg/kg in mice, rabbits, and goats [8,96]. It is practically nontoxic by skin exposure, with reported dermal LD50 values of greater than 5000 mg/kg for the acid and isopropylamine salt. The trimethylsulfonium salt has a reported dermal LD50 of greater than 2000 mg/kg. It is reportedly not irritating to the skin of rabbits, and does not induce skin sensitization in guinea pigs [58]. It does cause eye irritation in rabbits [58]. Some formulations may cause much more extreme irritation of the skin or eyes [58]. In a number of human volunteers, patch tests produced no visible skin changes or sensitization [58]. The reported 4-hour rat inhalation LC50 values for the technical acid and salts were 5 to 12 mg/L [58], indicating moderate toxicity via this route. Some formulations may show high acute inhalation toxicity [58]. While it does contain a phosphatyl functional group, it is not structually similar to organophosphate pesticides which contain organophosphate esters, and it does not significantly inhibit cholinesterase activity [1,58].Chronic toxicity: Studies of glyphosate lasting up to 2 years, have been conducted with rats, dogs, mice, and rabbits, and with few exceptions no effects were observed [96]. For example, in a chronic feeding study with rats, no toxic effects were observed in rats given doses as high as 400 mg/kg/day [58]. Also, no toxic effects were observed in a chronic feeding study with dogs fed up to 500 mg/kg/day, the highest dose tested [58,97]. Reproductive effects: Laboratory studies show that glyphosate produces reproductive changes in test animals very rarely and then only at very high doses (over 150 mg/kg/day) [58,96]. It is unlikely that the compound would produce reproductive effects in humans. Teratogenic effects: In a teratology study with rabbits, no developmental toxicity was observed in the fetuses at the highest dose tested (350 mg/kg/day) [97]. Rats given doses up to 175 mg/kg/day on days 6 to 19 of pregnancy had offspring with no teratogenic effects, but other toxic effects were observed in both the mothers and the fetuses. No toxic effects to the fetuses occurred at 50 mg/kg/day [97]. Glyphosate does not appear to be teratogenic. Mutagenic effects: Glyphosate mutagenicity and genotoxicity assays have been negative [58]. These included the Ames test, other bacterial assays, and the Chinese Hamster Ovary (CHO) cell culture, rat bone marrow cell culture, and mouse dominant lethal assays [58]. It appears that glyphosate is not mutagenic. Carcinogenic effects: Rats given oral doses of up to 400 mg/kg/day did not show any signs of cancer, nor did dogs given oral doses of up to 500 mg/kg/day or mice fed glyphosate at doses of up to 4500 mg/kg/day [58]. It appears that glyphosate is not carcinogenic [97]. Organ toxicity: Some microscopic liver and kidney changes, but no observable differences in function or toxic effects, have been seen after lifetime administration of glyphosate to test animals [97]. Fate in humans and animals: Glyphosate is poorly absorbed from the digestive tract and is largely excreted unchanged by mammals. At 10 days after treatment, there were only minute amounts in the tissues of rats fed glyphosate for 3 weeks [98]. Cows, chickens, and pigs fed small amounts of glyphosate had undetectable levels (less than 0.05 ppm) in muscle tissue and fat. Levels in milk and eggs were also undetectable (less than 0.025 ppm). Glyphosate has no significant potential to accumulate in animal tissue [99].
Ecological Effects:Effects on birds: Glyphosate is slightly toxic to wild birds. The dietary LC50 in both mallards and bobwhite quail is greater than 4500 ppm [1].Effects on aquatic organisms: Technical glyphosate acid is practically nontoxic to fish and may be slightly toxic to aquatic invertebrates. The 96-hour LC50 is 120 mg/L in bluegill sunfish, 168 mg/L in harlequin, and 86 mg/L in rainbow trout [58]. The reported 96-hour LC50 values for other aquatic species include greater than 10 mg/L in Atlantic oysters, 934 mg/L in fiddler crab, and 281 mg/L in shrimp [58]. The 48-hour LC50 for glyphosate in Daphnia (water flea), an important food source for freshwater fish, is 780 mg/L [58]. Some formulations may be more toxic to fish and aquatic species due to differences in toxicity between the salts and the parent acid or to surfactants used in the formulation [58,96]. There is a very low potential for the compound to build up in the tissues of aquatic invertebrates or other aquatic organisms [96]. Effects on other organisms: Glyphosate is nontoxic to honeybees [1,58]. Its oral and dermal LD50 is greater than 0.1 mg/ bee [98]. The reported contact LC50 values for earthworms in soil are greater than 5000 ppm for both the glyphosate trimethylsulfonium salt and Roundup [58].
Environmental Fate:Breakdown in soil and groundwater: Glyphosate is moderately persistent in soil, with an estimated average half-life of 47 days [58,11]. Reported field half-lives range from 1 to 174 days [11]. It is strongly adsorbed to most soils, even those with lower organic and clay content [11,58]. Thus, even though it is highly soluble in water, field and laboratory studies show it does not leach appreciably, and has low potential for runoff (except as adsorbed to colloidal matter) [3,11]. One estimate indicated that less than 2% of the applied chemical is lost to runoff [99]. Microbes are primarily responsible for the breakdown of the product, and volatilization or photodegradation losses will be negligible [58].Breakdown in water: In water, glyphosate is strongly adsorbed to suspended organic and mineral matter and is broken down primarily by microorganisms [6]. Its half-life in pond water ranges from 12 days to 10 weeks [97]. Breakdown in vegetation: Glyphosate may be translocated throughout the plant, including to the roots. It is extensively metabolized by some plants, while remaining intact in others [1].
Physical Properties:Appearance: Glyphosate is a colorless crystal at room temperature [1].Chemical Name: N-(phosphonomethyl) glycine [1] CAS Number: 1071-83-6 Molecular Weight: 169.08 Water Solubility: 12,000 mg/L @ 25 C [1] Solubility in Other Solvents: i.s. in common organics (e.g., acetone, ethanol, and xylene) [1] Melting Point: 200 C [1] Vapor Pressure: negligible [1] Partition Coefficient: -3.2218 - -2.7696 [58] Adsorption Coefficient: 24,000 (estimated) [11] Exposure Guidelines:ADI: 0.3 mg/kg/day [12]MCL: Not Available RfD: 0.1 mg/kg/day [13] PEL: Not Available HA: 0.7 mg/L (lifetime) [98] TLV: Not Available Basic Manufacturer:Monsanto Company800 N. Lindbergh Blvd. St. Louis, MO 63167 Phone: 314-694-6640 Emergency: 314-694-4000 References: References for the information in this PIP can be found in Reference List Number 10 DISCLAIMER: The information in this profile does not in any way replace or supersede the information on the pesticide product labeling or other regulatory requirements. Please refer to the pesticide product labeling.
Hexazinone(Also see: www.panna.org) Environmental Fate of Hexazinone Hexazinone found in South Australian Groundwater http://www.uaptimberland.com/NWLinks/Hexazinone-forestry.pdf http://www.srs.fs.usda.gov/pubs/rpc/1999-12/rpc_99dec_13.pdf. http://www.cdpr.ca.gov/docs/empm/pubs/ehapreps/forsherb.htm http://lomaprieta.sierraclub.org/lp0109_Trees.html http://www.cnps.org/forestry/special_topics/herbicides/LongDamonAppeal.htm http://www.environmentcommissioner.act.gov.au/actforestsweedtreatmentoptionspdf.pdf. http://certifiedforests.org.au/documents/nz/nz5.6.html http://www.wccc.com.au/Minutes/WCCC%20Minutes%20Mar%2001.htm http://www.ncasi.org/forestry/ForestryNews/2000/fn-12-01.pdf. http://www.fs.fed.us/r5/ecoplan/appeals/2001/fy01_0010_0011.htm http://www.ngwa.org/publication/gwmr/summergwmrab.html In March 1994 Victorian Plantation Corporation (now Hancock Victorian Plantations) accidently sprayed 800 square kilometres of land near Ballarat with the herbicide Hexazinone. see UPDATES 1 FOREST SERVICE SUSPENDS AERIAL USE OF HEXAZINONE PENDING REVIEWMARE ISLAND, VALLEJO, June 16, 1999–Acting Pacific Southwest Regional Forester Brad Powell has declared a temporary moratorium on aerial application of the herbicide hexazinone on the national forests (NF's) in California. Internal and external concerns over several aspects of misapplication of the herbicide into a creek on the Stanislaus NF in mid-March led to the suspension. "If we cannot apply this herbicide safely from the air, then we will not do it," Powell said. "To decide whether this moratorium should be made permanent, I am appointing a review team made up of USDA Forest Service (FS) experts in hydrology, pesticides, contracting and aquatic invertebrates, along with senior FS officials from inside and outside this region, plus a representative of the state's Department of Pesticide Regulation. I am asking them to assess all aspects of this situation by the end of June. After that, I will make a long-term decision on aerial application of hexazinone in this region. I will also take whatever actions are appropriate in light of the March misapplication." The suspension does not affect ground spraying of hexazinone or any other herbicide approved in the Pacific Southwest Region's 1988 Final Environmental Impact Statement on Vegetation Management for Reforestation. Nor does it affect aerial application of the other approved herbicides. A preliminary review has already been conducted of the March 17 incident, in which a contractor inadvertently applied hexazinone directly into Rose Creek and some tributaries. The project was in the area burned by the 1992 Ruby wildfire, and designed to ensure survival of tree seedlings by reducing competing brush and grass. The form of hexazinone used is commercially known as Pronone 10G.
Forest Service Puts Severe Limitations on Aerial Use of HexazinoneMARE ISLAND, VALLEJO, Dec. 6, 1999--Pacific Southwest Regional Forester Brad Powell has placed severe limits on the aerial application of the herbicide hexazinone on the national forests (NF's) in California. In his decision, Powell outlined a number of specific practices that must be implemented prior to such future use."These new restrictions are designed to ensure that future aerial application of hexazinone will occur only when it is determined to be essential, and when we can strictly adhere to the label requirement that it not be applied directly to surface water," Powell said. "While I am allowing aerial use of hexazinone to continue, I want to avoid any situations in which we inadvertently fail to follow the label directions." Specifically, Powell set 14 restrictions and practices that must be incorporated into any future use. These include establishing that terrain and other factors would make other herbicides, application methods or brush removal techniques ineffective, and ensuring that buffers around streams and other surface water can be reliably established. The new restrictions also tighten contracting and monitoring procedures, and strengthen measures to ensure compliance with all requirements. Given these new restrictions, Powell said he is lifting his June 16 suspension of the aerial application of hexazinone. That suspension stemmed from a March 17 incident on the Stanislaus NF, in which a contractor inadvertently applied hexazinone directly into Rose Creek and some tributaries. The project was in the area burned by the 1992 Ruby wildfire, and designed to ensure survival of tree seedlings by reducing competing brush and grass. The form of hexazinone used at Rose Creek is commercially known as Pronone 10G. Today's decision follows the recommendations of a review team established by Powell after the March 17 misapplication. Ground spraying of hexazinone or other approved herbicides, and aerial application of other approved herbicides, can continue as needed under previously-established guidelines. E X T O X N E T EXTOXNET primary files maintained and archived at Oregon State University Revised June 1996
HexazinoneTrade and Other Names: Trade names for products containing hexazinone are DPX 3674, Pronone, and Velpar. It may be used in combination with other herbicides such as bromacil and diuron.Regulatory Status: Hexazinone is a slightly toxic compound in EPA toxicity class I. Labels for products containing hexazinone bear the Signal Word DANGER - POISON due its ability to cause serious and irreversible eye irritation. It is a General Use Pesticide (GUP). Chemical Class: triazine Introduction: Hexazinone is a triazine herbicide used against many annual, biennial, and perennial weeds, as well as some woody plants. It is mostly used on non-crop areas; however, it is used selectively for the control of weeds among sugar cane, pineapples, and lucerne. Hexazinone is a systemic herbicide that works by inhibiting photosynthesis in the target plants. Rainfall or irrigation water is needed before it becomes activated. It is available in soluble concentrate, water-soluble powder, or granular formulations. Formulation: It is available in soluble concentrate, water-soluble powder, or granular formulations.
Toxicological Effects:Acute toxicity: Hexazinone is slightly toxic via the oral route, with a reported LD50 of 1690 mg/kg in rats, and 860 mg/kg in male guinea pigs [6,15]. Via the dermal route, it is practically nontoxic, with a reported dermal LD50 in rabbits of greater than 5278 mg/kg [6,15]. Hexazinone does not cause significant skin irritation or sensitization in guinea pigs or rabbits, but it does cause severe eye irritation in rabbits [15]. Hexazinone's inhalation toxicity is very low, its 1-hour inhalation LC50 is greater than 7.48 mg/L in rats [15]. Effects due to acute exposure may include irritatation the eyes, nose and throat, as well as nausea and vomiting [29].Chronic toxicity: Over a 2-week period, male rats receiving dietary doses of 300 mg/kg/day showed no evidence of cumulative toxicity [15]. Male rats receiving doses of 50 mg/kg/day over 90 days showed no effects, but higher doses caused decreased body weights. Body weight gain was seen in dogs at doses of about 35 mg/kg/day and higher over 1 year [15]. Very high doses for 8 weeks did not affect hamsters and caused only increased liver weights in mice [29]. Reproductive effects: Female rats, fed moderate to high doses (up to 150 mg/kg) over two generations, showed no effects on reproduction or milk production, but only reduced offspring weight [15,29]. Available evidence suggests that hexazinone is unlikely to cause reproductive effects in humans. Teratogenic effects: Pregnant female rats receiving doses up to 100 mg/kg/day during gestation, and rabbits receiving up to 125 mg/kg/day, evidenced no fetal abnormalities [15]. Teratogenic effects were observed in rats only at maternal doses greater than 400 mg/kg/day during gestation [15]. It is unlikely that hexazinone would pose a teratogenic effects in humans under normal conditions. Mutagenic effects: Hexazinone showed no mutagenic activity in the Ames assay and tests using Chinese hamster ovary cell cultures [15]. In living animal tests, no changes in chromosomal structure occurred. In other laboratory analyses of its capacity to induce genetic disruption, results were inco |
