Hancock Watch HomeContents:ALSO CHECK OUT THESE IMPORTANT UPDATES:Updates Page including Timeline for Pesticide Pollution Events 1996-2009Aug 06: Hancock pollutes Geelong Drinking Water with Hexazinone for 31 months (and counting!)Environmental groups call for bans on aerial spraying of pesticidesPlantation 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 2Bluegum plantation insecticidesCHLORINATED PESTICIDESHistorical data on 2,4,5-T use in Victorian PlantationsThe Continuing Health Problems Associated with 2,4,5-THerbicides 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 and other plantation company's activities (in red): For more detailed information on these potentially impacted water supplies, please go to connecting links: http://hancockwatch.nfshost.com/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.
Glufosinate AmmoniumHealth and Environmental Impacts of Glufosinate Ammonium US EPA Federal Register Glufosinate Ammonium Pesticide Tolerance 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 inconclusive [15]. The evidence suggests hexazinone is either slightly or nonmutagenic. Carcinogenic effects: Rats, mice, and dogs have been tested for 1 to 2 years on diets containing up to 500 mg/kg. Hexazinone was not carcinogenic in rats, and was only carcinogenic in mice at dietary levels of over 300 mg/kg. At these levels in mice, liver adenomas were observed [15]. These studies suggest that hexazinone is unlikely to be carcinogenic to humans under normal circumstances. Organ toxicity: Target organs affected in lab animals by chronic hexazinone exposure include the liver. Fate in humans and animals: Hexazinone is fairly rapidly processed and excreted by animal systems. Rats typically excrete hexazinone almost completely within 3 to 6 days, the majority in urine [30]. Long-term exposure does not diminish this rapid processing and elimination; rats given prior exposure for 2 weeks excreted almost all of the product within 3 days [30]. Less than 1% of the parent hexazinone was detected in urine and feces. There does not appear to be any significant tissue accumulation [30]. Dairy cows given small amounts of hexazinone in their diets for 30 days had no detectable residues in milk, fat, liver, kidney, or lean muscle, but did have minute amounts of a hexazinone metabolite in their milk [30]. Lactating goats given small amounts of hexazinone for 5 days also had small amounts of the compound in their milk and livers [30].
Ecological Effects:Effects on birds: Hexazinone is slightly to practically nontoxic to birds. The acute oral LD50 of hexazinone in bobwhite quail is 2258 mg/kg [15]. The 5- to 8-day dietary LC50 in bobwhite quail and mallard ducklings is greater than 10,000 ppm [15].Effects on aquatic organisms: Hexazinone is slightly toxic to fish and other freshwater organisms. Some of the reported 96-hour LC50 values include: rainbow trout, 320 mg/L; bluegill, 370 mg/L; fathead minnow, 274 mg/L [6,15]. The 48-hour LC50 for hexazinone in the water flea, Daphnia magna, is 151 mg/L [15]. The bioconcentration factor in bluegill sunfish is only seven times the ambient water concentration, indicating very low bioaccumulation in fish [30]. Effects on other organisms: Hexazinone is nontoxic to honey bees. The herbicide is toxic to larch trees (Larix spp.), and should not be used for weed control in forested areas [6].
Environmental Fate:Breakdown in soil and groundwater: Hexazinone is of moderate to high persistence in the soil environment. Measured field half-lives range from less than 30 to 180 days, with a representative value of about 90 days [31]. Hexazinone is broken down by soil microbes, which release carbon dioxide in the process [15]. Sunlight may also break down the compound via photodegradation [31]. The rate of breakdown under natural field conditions will depend on many site-specific variables, including sunlight, rainfall, soil type, and rate of application. Hexazinone does not evaporate to any appreciable extent from soil [31]. Hexazinone is very poorly adsorbed to soil particles, very soluble in water, and slowly degraded, so it is likely to be mobile in most soils and has the potential to contaminant groundwater.Breakdown in water: Photodecomposition, biodegradation, and dilution are the prime mechanisms for loss of hexazinone activity in aquatic systems [15]. Breakdown in vegetation: Hexazinone is readily absorbed in the root zone and translocated throughout the plant. It is less mobile following uptake from the foliage. It is converted in non-susceptible plants to less phytotoxic compounds. In susceptible plants, it is more persistent and can result in disruption of photosynthesis and chloroplast damage [15].
Physical Properties:Appearance: Hexazinone is a colorless, odorless crystal at room temperature [6].Chemical Name: 3-cyclohexyl-6-(dimethylamino)-1-methyl-1,3,5-triazine-2,4(1H,3H)-dione [6] CAS Number: 51235-04-2 Molecular Weight: 252.32 Water Solubility: 33,000 mg/L @ 25 C [6] Solubility in Other Solvents: v.s. in acetone, hexane, and methanol [6] Melting Point: 115-117 C [6] Vapor Pressure: 0.03 Pa @ 25 C [6] Partition Coefficient: -4.40 (calculated) [16] Adsorption Coefficient: 54 [20] Exposure Guidelines:ADI: Not AvailableMCL: Not Available RfD: 0.033 mg/kg/day [26] PEL: Not Available HA: 0.20 mg/L (lifetime) [29] TLV: Not Available Basic Manufacturer:DuPont Agricultural ProductsWalker's Mill, Barley Mill Plaza P.O. Box 80038 Wilmington, DE 19880-0038 Phone: 800-441-7515 Emergency: 800-441-3637 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.
Metsulfuron Methyl(Also see: www.panna.org)EXTOXNET primary files maintained and archived at Oregon State University Revised 10/96
METSULFURON-METHYLTRADE OR OTHER NAMES: Product names include Ally, Allie, Gropper, and Escort.REGULATORY STATUS: Metsulfuron-methyl is classified by EPA in acute Toxicity Category III, and must bear the signal word "Caution" on commercial products (37). There are tolerances for residues of metsulfuron-methyl in or on raw commodities ranging from 0.05 ppm for sugar cane and milk, to 20.0 ppm for barley hay. INTRODUCTION: Metsulfuron-methyl is a residual sulfonylurea compound used as a selective pre- and postemergence herbicide for broadleaf weeds and some annual grasses. It is a systemic compound with foliar and soil activity, and it works rapidly after it is taken up by the plant. Its mode of action is by inhibiting cell division in the shoots and roots of the plant, and it is biologically active at low use rates. The most common uses of metsulfuron-methyl include wheat, barley, rye, and pastures. It can be used with other foliar herbicides, and is typically applied on cereals at 0.004 - 0.007 pounds active ingredient/acre, and on non-crop areas at 0.005-0.160 pounds active ingredient/acre. It is commercially available in the form of dry flowable formulations. Because it has residual activity in soils, it is necessary to allow ample time for the chemical to break down before planting certain crops (22 months for sunflowers, flax, corn, or safflower, and 10 months before planting sorghum). It should not be used on ryegrass or on pastures containing alfalfa or clovers (38).
TOXICOLOGICAL EFECTSAcute Toxicity: This chemical has very low toxicity in mammals. Based on laboratory tests, the oral dose of metsulfuron-methyl that causes mortality in half of the test animals (LD50) is > 5,000 mg/kg in rats. It has low dermal toxicity in tests with rabbits, with an LD50 > 2,000 mg/kg, and low inhalation toxicity in rats, with a median lethal concentration in air of greater than 5 mg/liter air. Moderate but reversible eye irritation has been seen in rabbits, and mild skin irritation has been observed in guinea pigs. No skin sensitization has been observed in guinea pigs (7).Signs and Symptoms of Poisoning: Systemic poisoning by sulfonylurea based compounds is unlikely, unless large quantities have been ingested. No accounts of poisoning by metsulfuron-methyl are currently available. (39). Chronic Toxicity: A 2-year feeding study in rats resulted in a No Observable Effects Level (NOEL) of 25.0 mg/kg/day (or 500 ppm in feed), based on decreased body weights seen at 250 mg/kg/day (5,000 ppm) which was the highest dose tested. EPA has based its reference dose (0.25 mg/kg/day) on this study (31). Reproductive Effects: Multigeneration studies in rats did not result in any reproductive effects at the highest doses tested of 250 mg/kg/day (31). Teratogenic Effects: Metsulfuron-methyl did not cause developmental abnormalities to offspring of rats and rabbits fed 1000 mg/kg/day and 700 mg/kg/day respectively during gestation. These doses represent the highest dose tested for each experiment (31). Mutagenic Effects: The weight of evidence presented by a battery of tests to measure mutagenicity and other adverse effects on DNA indicates that metsulfuron-methyl is neither mutagenic nor genotoxic (40). Carcinogenic Effects: Negative for rats and mice in laboratory tests, but studies may not have been at maximum tolerated dose (40). Organ Toxicity: Metsulfuron-methyl is a moderate eye irritant (40). Fate in Humans and Other Animals: The chemical is broken down quickly and eliminated from the body. In tests with radiolabeled metsulfuron-methyl in rats, the excretion half-lives ranged from 9 to 16 hours and 23 to 29 hours for rats administered low and high doses, respectively. It did not bioaccumulate in fish (40).
ECOLOGICAL EFFECTSEffects on Birds: Metsulfuron-methyl has very low avian toxicity. The oral LD50 value for mallard ducks is greater than 2510 mg/kg, and dietary LC50 values for mallard ducks and bobwhite quail are greater than 5620 ppm (40).Effects on Aquatic Organisms: The chemical has very low toxicity to aquatic organisms. 96-hour LC50 values are greater than 150 mg/l in rainbow trout and bluegill. Forty-eight hour toxicity tests with the freshwater invertebrate Daphnia magna resulted in a LC50 of greater than 150 mg/l (40). A 21-day life-cycle test with Daphnia magna also exhibited very low toxicity. The NOEL for survival and reproduction was >150 mg/l. Effects on Other Animals (Nontarget species): Metsulfuron-methyl has low acute toxicity to honey bees with a topical LD50 of greater than 25 ug/bee (40). The LC50 for earthworms is greater than 1,000 mg/kg soil.
ENVIRONMENTAL FATEBreakdown of Chemical in Soil and Groundwater: The breakdown of metsulfuron-methyl in soils is largely dependant on soil temperature, moisture content, and pH. The chemical will degrade faster under acidic conditions, and in soils with higher moisture content and higher temperature (41). The chemical has a higher mobility potential in alkaline soils than in acidic soils, as it is more soluble under alkaline conditions. Metsulfuron-methyl is stable to photolysis, but will break down in ultraviolet light. Half-life estimates for metsulfuron-methyl in soil are wide ranging from 14 - 180 days, with an overall average of reported values of 30 days (42). Reported half-life values (in days) for soil include: clay - 178 (41); sandy loam - 102 (41); clay loam - 70 (41), 14-28 (42), 14-105 (42); silty loam - 120-180 (43).Breakdown of Chemical in Surface Water: The dissipation time for metsulfuron-methyl was investigated in a mixed wood/boreal forest lake. The DT50 or length of time required for half of the material to dissipate in water was >84 days when high concentrations of metsulfuron-methyl were applied, and 29.1 days at concentrations that might be expected if the chemical is applied for forestry uses (43). The chemical is stable to hydrolysis at neutral and alkaline pHs, and has a half-life of 3 weeks at pH 5.0, 25 degrees C and >30 days at 15 degrees C (44). Breakdown of Chemical in Vegetation: Metsulfuron-methyl is rapidly taken up by plants at the roots and on foliage. The chemical is translocated throughout the plant, but is not persistent. It is broken down to non-herbicidal products in tolerant plants (40). Analytical Methods: Methods for the detection of metsulfuron-methyl exist for soil and water. Liquid chromatography/mass spectroscopy and bioassay methods are used for soils, and gas chromatography/electron capture detection is used for measuring trace levels of the chemical in water (45).
PHYSICAL PROPERTIES AND GUIDELINESPhysical Properties:Appearance: faint, sweet ester-like white to pale yellow solid Chemical Name: Methyl 2-[[[[(4-methoxy-6-methyl-1,3,5-triazin-2-yl)amino]carbonyl]amino]sulfonyl]benzoate (CA) Methyl 2-[3-(4-methoxy-6-methyl-1,3,5-triazin-2-yl)ureidosulphonyl]benzoate (IUPAC) CAS Number: 74223-64-6 Molecular Weight: 381.4 Water Solubility: Water @ 25 degrees C, pH 4.6 270 mg/l; Water @ 25 degrees C, pH 5.4 1,750 mg/l; Water @ 25 degrees C, pH 7.0 2,790 mg/l; Water @ 25 degrees C, pH 9.0 213,000 mg/l Solubility in Other Solvents: Acetone @ 20 degrees C 36,000 mg/l; n-Hexane @ 20 degrees C 0.79 mg/l; Methanol @ 20 degrees C 7,300 mg/l; Methylene chloride @ 20 degrees C 121,000 mg/l; Melting Point: 158 degrees C Vapor Pressure: 2.5 X 10 to the minus 12 mm Hg @ 25 degrees C Partition Coefficient: Not Available Adsorption Coefficient: Not Available Exposure Guidelines:ADI: Not AvailableMCL: Not Available RFD: 0.25 mg/kg/day PEL: Not Available HA: Not Available TLV: Not Available SimazineOther useful links about problems with Simazine: FSC Board Committee Decision Regarding Simazine Use in Victorian Plantations 3/11/03 Simazine (US EPA) In 1998 organic farmers near Bendoc in East Gippsland found traces of simazine on their property and linked it to plantations established to Harris-Daishowa. In the ruling of the case the magistrate found that the council failed; i) to undertake further sampling to determine the extent of the use of Simazine . . . and the long term impact of simazine on the proposed plantation site and organic farm, ii) to consider whether the prior use and proposed use of Simazine has and will continue to jeopardise the capacity of the organic farm to obtain organic certification from the Biodynamic Farming Association or the National Association of Sustainable Agriculture Australia, iii) to consider whether the proposed use of Simazine and Roundup on the proposed plantation site is simply incompatible with the agricultural practices of the adjacent organic farm, iv) to adequately consider the potential consequences of the use of Simazine and Roundup at the proposed maximum application rates upon the organic farm and nearby watercourses; or v) to specify any requirements for monitoring the effects of the use of Simazine and Roundup and any other effects of the establishment of the timber plantation upon the organic farm and nearby watercourses. 'Prior to this application, there had been no planning permit conditions relating to the use of herbicides for plantation development. In fact, no individual nor any authority has raised the issue of herbicide use in plantations with Council even though the use there of it clearly indicated in each proposal'. E X T O X N E T EXTOXNET primary files maintained and archived at Oregon State University Revised June 1996
SimazineTrade and Other Names: Trade names include Aquazine, Caliber, Cekusan, Cekusima, Framed, Gesatop, Primatol S, Princep, Simadex, Simanex, Sim-Trol, Tanzine and Totazine. This compound may also be found in formulations with other herbicides such as amitrole, paraquat dichloride, metolachlor, and atrazine.Regulatory Status: Simazine is a General Use Pesticide (GUP). It is in EPA toxicity class IV - practically nontoxic. Products containing simazine bear the Signal Word CAUTION. In November 1994, the U.S. EPA began a Special Review of simazine which could result in use restrictions or even cancellation if data warrant such action. Chemical Class: Triazine Introduction: Simazine is a selective triazine herbicide. It is used to control broad-leaved weeds and annual grasses in field, berry fruit, nuts, vegetable and ornamental crops, turfgrass, orchards, and vineyards. At higher rates, it is used for nonselective weed control in industrial areas. Before 1992, simazine was used to control submerged weeds and algae in large aquariums, farm ponds, fish hatcheries, swimming pools, ornamental ponds, and cooling towers. Simazine is available in wettable powder, water dispersible granule, liquid, and granular formulations. It may be soil-applied. Formulation: Simazine is available in wettable powder, water dispersible granule, liquid and granular formulations. It may be soil-applied.
Toxicological Effects:Acute toxicity: Simazine is slightly to practically nontoxic. The reported oral LD50 for technical simazine in rats and mice is >5000 mg/kg [6,15]; its dermal LD50 is 3100 mg/kg in rats and > 10,000 mg/kg in rabbits [6,15]. The 4-hour inhalation LC50 in rats is greater than 2 mg/L (6). The formulated products, in most cases, are less toxic via all routes [15]. Simazine is nonirritating to the skin and eyes of rabbits except at high doses [3]. Patch tests on humans have shown that simazine is not a skin irritant, fatiguing agent, or sensitizer [3]. However, rashes and dermatitis from occupational exposure to simazine have occurred [3]. The triazine herbicides disturb energy metabolism (thiamin and riboflavin functions). Symptoms include difficulty in walking, tremor, convulsions, paralysis, cyanosis, slowed respiration, miosis (pinpoint pupils), gut pain, diarrhea, and impaired adrenal function [3]. No cases of poisoning in humans have been reported from ingestion of simazine [3]. Rats given an oral dose of 5000 mg/kg exhibited drowsiness and irregular breathing. In another study, a single oral dose of 4200 mg/kg produced anorexia, weight loss, and some deaths in rats within 4 to 10 days [26]. For unknown reasons, sheep and cattle are especially susceptible to poisoning by simazine. Doses of 500 mg/kg were fatal in sheep with death delayed for 5 to 16 days. Symptoms exhibited by poisoned sheep included lower food intake, higher water intake, incoordination, tremors, and weakness, especially in the hindquarters [3].Chronic toxicity: Some 90-day feeding studies showed reduced body weight at 67 to 100 mg/kg/day [10]. This same effect and kidney toxicity were seen in rats at doses of 150 mg/kg/day [10]. In 2-year chronic oral feeding studies in which rats were given daily dosages of 5 mg/kg/day of simazine in the diet, no gross or microscopic signs of toxicity were seen [3]. When rats were given repeated doses of 15 mg/kg/day, some liver cells degenerated during the first 3 days, but the condition did not progress. Instead, the liver adapted and the compound was metabolized [3]. Other effects observed in test animals include tremors, damage to the testes, kidneys, liver, and thyroid, disturbances in sperm production, and gene mutations [10]. Reproductive effects: No adverse effects on reproductive capacity or development were observed in a three-generation study of rats fed 5 mg/kg/day simazine [10]. High rates of fetotoxicity and decreased birth weight were noted in the fetuses of pregnant rabbits fed 75 mg/kg/day [26]. Reproductive effects are not likely in humans under normal circumstances. Teratogenic effects: No dose-related teratogenic effects were observed when rabbits were given daily doses of 5, 75, or 200 mg/kg for days 7 through 19 of pregnancy [26]. Chronic inhalation of a cumulative dose of 0.3 mg/L for 8 days in pregnant rats resulted in no treatment-related developmental abnormalities [10]. Simazine does not appear to be teratogenic. Mutagenic effects: Simazine has shown negative results in a variety of mutagenicity tests on bacterial cultures [10]. Tests on human lung cell cultures have produced both positive and negative results [10]. When injected into adult male fruitflies, simazine increased the frequency of sex-linked lethal mutations, but failed to do so when fed to larvae. Other tests for mutagenicity in fruitflies were negative [3]. It is likely that simazine is either nonmutagenic or weakly mutagenic. Carcinogenic effects: Simazine was not tumorigenic in mice at the maximum tolerated dose of 215 mg/kg/day over an 18-month period [10]. In other studies, doses as low as 5 mg/kg/day produced excess tumors (thyroid and mammary) in female rats [3,10]. Because of inconsistencies in the data, it is not possible to determine simazine's carcinogenic status. Organ toxicity: Damage to the testes, kidneys, liver, and thyroid has been observed in test animals [3,10]. Fate in humans and animals: Studies in rats, goats, and sheep reveal that 60 to 70% of the ingested dose may be absorbed into the system [10], with approximately 5 to 10% distributed systemically to tissues. The remainder is eliminated via urine within 24 hours [6]. Distribution led to detectable levels in red blood cells (highest), liver, kidney, fat, bone, and plasma [10]. When a cow was fed 5 ppm for 3 days, no simazine was found in the cow's milk during the next 3 days. It has been reported that simazine residues were present in the urine of sheep for up to 12 days after administration of a single oral dose. The maximum concentration in the urine occurred from 2 to 6 days after administration [16].
Ecological Effects:Effects on birds: Simazine is practically nontoxic to birds [6,16]. The reported LD50 values in mallard and Japanese quail are >4600 mg/kg and 1785 mg/kg, respectively [6]. The acute dietary LD50 values in hens and pigeons are both greater than 5000 ppm [2]. The 8-day dietary LC50 in bobwhite quail is >5260 ppm and in mallard ducks is >10,000 ppm [6,15].Effects on aquatic organisms: Simazine is slightly to practically nontoxic to aquatic species [6,15]. The 96-hour LC50 for simazine is >100 mg/L [46] in rainbow trout, 100 mg/L (wettable powder) in bluegill sunfish, 0.100 mg/L in fathead minnows [46], as well as carp [2]. It may be more toxic to Daphia and stoneflies [46]. A 96-hour LC50 of >3.7 mg/L is reported in oysters [15]. Effects on other organisms: While many mammals may be insensitive to simazine [16], sheep and cattle are especially sensitive [3]. Simazine is nontoxic to bees [6,16]. A soil LC50 in earthworms of >1000 mg/kg has been reported [16].
Environmental Fate:Breakdown in soil and groundwater: Simazine is moderately persistent with an average field half-life of 60 days [20]. Soil half-lives of 28-149 days have been reported [20]. Residual activity may remain for a year after application (2 to 4 kg/ha) in high pH soils. Simazine is moderately to poorly bound to soils [20]. It does, however, adsorb to clays and mucks. Its low water solubility, however, makes it less mobile, limiting its leaching potential [15]. Simazine has little, if any, lateral movement in soil, but can be washed along with soil particles in runoff. Simazine is subject to decomposition by ultraviolet radiation, but this effect is small under normal field conditions. Loss from volatilization is also insignificant. In soils, microbial activity probably accounts for decomposition of a significant amount of simazine in high pH soils. In lower pH soils, hydrolysis will occur [15]. Simazine residues have been detected in groundwater in at least 16 states. The range was from 0.00002 mg/L to 0.0034 mg/L [23].Breakdown in water: The average half-life of simazine in ponds where it has been applied is 30 days, with the actual half-life dependent on the level of algae present, the degree of weed infestation, and other factors [15]. Simazine may undergo hydrolysis at lower pH. It does not readily undergo hydrolysis in water at pH = 7 [15]. Breakdown in vegetation: Plants absorb simazine mainly through the roots, with little or no foliar penetration. From the roots, it is translocated upward to the stems, leaves, and growing shoots of the plant [6,15]. It acts to inhibit photosynthesis [6,15]. Resistant plants readily metabolize simazine. Plants that are sensitive to simazine accumulate it unchanged [6]. It is possible that livestock or wildlife grazing on these plants could be poisoned.
Physical Properties:Appearance: Simazine is a white or colorless crystalline solid [6].Chemical Name: 6-chloro-N2,N4-diethyl-1,3,5-triazine-2,4-diamine [6] CAS Number: 122-34-9 Molecular Weight: 201.70 Water Solubility: 5 mg/L @ 20 C [6] Solubility in Other Solvents: s. in methanol, chloroform, and diethyl ether [6]; s.s. in pentane [6] Melting Point: 225-227 C [6] Vapor Pressure: 0.000810 mPa @ 20 C [6] Partition Coefficient: 1.9600 [6] Adsorption Coefficient: 130 [20] Exposure Guidelines:ADI: Not AvailableMCL: 0.004 mg/L [25] RfD: 0.005 mg/kg/day [26] PEL: Not Available HA: Not Available TLV: Not Available Basic Manufacturer:Ciba-Geigy CorporationP.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.
Sulfometuron MethylAlso see: www.panna.org EXTOXNET primary files maintained and archived at Oregon State University Revised June 1996
Sulfometuron-methylTrade and Other Names: Trade names for products containing sulfomturon-methyl include Oust Weed Killer and DPX 5648.Regulatory Status: Sulfometuron-methyl is a General Use Pesticide (GUP). It is EPA toxicity class III - slightly toxic. Products containing this compound require the Signal Word CAUTION on their labels. Chemical Class: sulfonylurea Introduction: Sulfometuron-methyl is a broad-spectrum sulfonylurea herbicide. It is used for the control of annual and perennial grasses and broad leaved weeds in non-crop land. It also has forestry applications where it is used to control woody tree species. It is applied either post-emergent or pre-emergent. It works by blocking cell division in the active growing regions of stem and root tips (meristematic tissue). Formulation: Not Available
Toxicological Effects:Acute toxicity: Sulfometuron-methyl's acute oral toxicity is very low. The LD50 of sulfometuron methyl in rats is greater than 5000 mg/kg [4,8]. One study showed an LD50 greater than 17,000 mg/kg [8]. The acute dermal toxicity of the compound is also low. The LD50 values for exposure through the skin ranges from over 2000 mg/kg in female rabbits to over 8000 mg/kg in male rabbits [21]. The technical compound is not a skin irritant or a skin sensitizer [21]. It has mild eye irritant properties in rabbits [3]. The acute inhalation LC50 is above 5.3 mg/L in rats, indicating its slightly toxic nature by this route [4].Chronic toxicity: Several toxic effects have been seen with chronic exposure to sulfometuron-methyl in test animals. At doses of 25 mg/kg/day, dogs experienced reduced red-blood cell counts and increased liver weight [4,21]. In this study, dogs were fed the compound in their food for a year. In two other studies conducted over 90 days, rats had increased white-blood cell counts (leukocytes) and anemia only at the highest dose tested (375 mg/kg/day) [4,21]. In a 2-year feeding study, no effects were noted below 7.5 mg/kg/day in rats [21]. Reproductive effects: In a 90-day reproductive effects study in rats, no reproductive effects were observed at doses of 300 mg/kg/day [21]. Another study in rats showed decreased fecundity and body weight at 300 mg/kg/day [4]. Studies of rabbits showed no fetotoxic effects at 300 mg/kg/day, the highest dose tested [21]. Reproductive effects due to sulfometuron-methyl are not likely. Teratogenic effects: No tetatogenic effects were observed in studies of rats and rabbits at doses of 300 mg/kg/day [21]. It is unlikely that sulfometuron-methyl is teratogenic. Mutagenic effects: The compound was not mutagenic in a variety of assays conducted on Salmonella cells and Chinese hamster ovary cells [21]. It is unlikely that the compound poses a mutagenic risk. Carcinogenic effects: No carcinogenic effects have been detected in either rats or mice exposed to sulfometuron-methyl [4,21]. Organ toxicity: As was noted above, increased liver weight may result from chronic exposure. Damage to blood forming agents may also occur [4,21]. Fate in humans and animals: Sulfometuron-methyl is readily absorbed through the gastrointestinal tract and is rapidly broken down and removed from the organism. Half-lives of the compound in rats ranged from 28 to 40 hours, depending on the dose (16 mg/kg and 3000 mg/kg, respectively). The compound did not accumulate in rats [22].
Ecological Effects:Effects on birds: Sulfometuron-methyl is practically nontoxic to birds. The acute oral LD50 in mallards is greater than 5000 mg/kg [4,8]. An 8-day dietary study with mallard ducks and bobwhite quail also showed an LC50 greater than 5000 ppm for both species [4].Effects on aquatic organisms: The compound is slightly toxic to freshwater fish. Its LC50 in rainbow trout and in bluegill sunfish is greater than 12.5 mg/L [23]. While the compound may not present a significant threat to adult aquatic organisms, the embryo hatch stage of fathead minnow may be at particular risk from the presence of the compound [23]. Fish kills have been associated with sulfometuron-methyl, but other causes have not been ruled out [24]. Sulfometuron-methyl is practically nontoxic to the water flea, Daphnia magna. Its LC50 in the water flea is greater than 125 mg/L for the technical material and greater than 1000 mg/L for dispersible granules [23]. No bioaccumulation has been detected [21]. Effects on other organisms: No data are currently available.
Environmental Fate:Breakdown in soil and groundwater: Sulfometuron-methyl is of low to moderate persistence in the soil environment. It is broken down in soil by the action of microorganisms, by the chemical action of water (hydrolysis), and through the action of sunlight (photodegradation) [4,24]. Reported field half-lives of sulfometuron-methyl range from 20 to 28 days [19]. In several field dissipation studies, half of the initial applied amount of the compound remained for 1 to 3 weeks, depending on soil type, vegetation cover, and pH [24,26,27]. Under anaerobic soil conditions, the compound persists slightly longer, though the half-life is still rather short (up to 8 weeks) [24]. Sulfometuron-methyl does not bind strongly to soil [19] and is slightly soluble in water [19], but is rapidly degraded and does not appear to pose a threat to groundwater. Field study data indicated a majority of the parent compound stays within the top 3 inches of soil [23].Breakdown in water: In well aerated acidic water, the compound is broken down quickly. Reported field half-lives for sulfometuron-methyl in water vary from 1 to 3 days [23] to 2 months or more [24]. Photolysis is generally less important than hydrolysis in its breakdown [24]. Under non-oxygenated (anaerobic) conditions in water sediments, the compound had a half-life of several months [24]. Breakdown in vegetation: Because sulfometuron-methyl is toxic to a number of plants and is non-selective, the use of the compound on non-croplands, including rights of way and along ditch banks, may endanger both terrestrial and aquatic plant species [4,24].
Physical Properties:Appearance: Sulfometuron-methyl is an off white or colorless solid compound. The compound is odorless [7].Chemical Name: 2-(4,6-dimethylpyrimidin-2-ylcarbamoylsulfamoyl)benzoic acid [7] CAS Number: 74222-97-2 Molecular Weight: 364.40 Water Solubility: 70 mg/L @ 25 C [7] Solubility in Other Solvents: s. in acetone, acetonitrile, and ethanol; s.s. in xylene; all @ 25 C [7] Melting Point: 203-205 C [7] Vapor Pressure: 8 mPa @ 25 C [7] Partition Coefficient: -0.5086 @ pH 7 [7] Adsorption Coefficient: 78 [19] Exposure Guidelines:ADI: Not AvailableMCL: Not Available RfD: Not Available PEL: Not Available HA: Not Available TLV: 5 mg/m3 (8-hour) [8] Basic Manufacturer:DuPont Agricultural ProductsWalker's Mill, Barley Mill Plaza P.O. Box 80038 Wilmington, DE 19880-0038 Phone: 800-441-7515 Emergency: 800-441-3637 References: References for the information in this PIP can be found in Reference List Number 9 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.
Terbacil (also see www.panna.org Terbacil)Also see: www.panna.org E X T O X N E T EXTOXNET primary files maintained and archived at Oregon State University Revised June 1996
TerbacilTrade and Other Names: Trade names include Compound 732, DuPont Herbicide 732, Geonter, and Sinbar. This compound may also be found in mixed formulations with other herbicides.Regulatory Status: Terbacil is registered by the U.S. Environmental Protection Agency (EPA) as a General Use Pesticide (GUP). The Signal Word CAUTION is required on containers of formulated terbacil. Terbacil is in EPA class IV - practically nontoxic. Chemical Class: substituted uracil Introduction: Terbacil is a selective herbicide used for control of both annual grasses, broad-leaved weeds, and some perennial weeds in sugarcane, apples, alfalfa, peaches, pecans, and mints. It is sprayed on soil surfaces preferably just before, or during, the period of active weed growth. Terbacil works in plants by inhibiting photosynthesis. It is a member of the substituted uracil chemical family. Terbacil is available in wettable powder formulations. Technical terbacil is 95% pure active material. Formulation: Terbacil is available in wettable powder formulations. Technical terbacil is 95% pure active material.
Toxicological Effects:Acute toxicity: Terbacil has low acute toxicity [128]. Clinical signs of poisoning in rats include weight loss, pallor, prostration, and rapid breathing. In dogs, a single dose of 5 mg/kg caused repeated vomiting [128]. Terbacil may irritate the skin, eyes, and mucous membranes of the nose and throat. It is not a skin sensitizer [129]. The oral LD50 of terbacil is 5000 to 7500 mg/kg in rats [1,22]. The dermal LD50 is greater than 5000 mg/kg (the maximum feasible dose) in rabbits [1]. These rabbits did not show clinical signs of toxicity, nor any obvious gross changes caused by disease. No skin irritation and only mild eye irritation was seen in rabbits at this dose [23]. Similarly, there was no skin irritation or sensitization in terbacil-treated guinea pigs [23]. Dogs given 5000 mg/kg of terbacil exhibited vomiting and a lack of eye pupil responsiveness [128].Chronic toxicity: No evidence of toxicity was seen in 2-year studies of rats fed doses as high as 12.5 mg/kg/day, or in dogs fed doses as high as 6.25 mg/kg/day of terbacil. At 125 to 500 mg/kg/day, there was a lower rate of weight gain, liver enlargement, and other liver changes in rats. The highest dose produced a slight increase in liver weight in dogs [23]. Reproductive effects: There were no adverse effects on lactation, fertility, birth rate, pup survival, or any other aspect of reproduction in rats fed 2.5 and 12.5 mg/kg/day of terbacil for three generations [23]. However, the average number of live rat fetuses per litter and the average final maternal body weight were significantly lowered in another study in the 103 and 391 mg/kg/day dosage groups [130]. Based on these data, adverse effects on reproduction in humans are not likely at expected exposure levels. Teratogenic effects: When doses of 30, 200, or 600 mg/kg/day were administered by gavage to pregnant rabbits on days 7 to 19 of gestation, adverse effects on the fetuses appeared only at the highest dose tested. This dose also produced maternal toxicity and increased maternal mortality. No adverse effects on the mothers or the pups were observed at lower doses. In another study, pregnant rats were fed doses of 23, 103, or 391 mg/kg/day on days 6 to 15 of gestation. Abnormalities occurred in the renal pelvis, and ureter dilation was found in pups from all the treatment groups [129]. Evidence of teratogenicity is inconclusive. Mutagenic effects: Terbacil was not mutagenic in several screening tests [129]. Carcinogenic effects: No evidence of carcinogenicity was found in rats fed 2.5, 12.5, 125, or 500 mg/kg/day of terbacil for 2 years, nor in dogs fed as much as 12.5 mg/kg/day for 2 years [23]. When mice were fed dietary doses of 2.5, 62.5, or 250 mg/kg for 2 years, no increased incidence of cancer was found [130]. Terbacil does not appear to be carcinogenic. Organ toxicity: Liver changes have been seen in laboratory rats exposed to high doses of terbacil [23]. Fate in humans and animals: In general, the uracil herbicides, the chemical class in which terbacil is included, are rapidly excreted in urine by mammals. This may account for their reportedly low toxicity [131]. When given in the feed of lactating cows at 5 and 30 ppm, terbacil was excreted in the milk at levels up to 0.03 and 0.08 ppm, respectively. No herbicide was detected in the cows' urine and feces [131].
Ecological Effects:Effects on birds: Terbacil is slightly toxic to birds [131]. The 8-day dietary LC50 for terbacil is more than 56,000 ppm in Peking ducklings, and greater than 31,450 ppm in pheasant chicks [58]. The LD50 for terbacil in quail is greater than 2250 mg/kg [129].Effects on aquatic organisms: Terbacil is slightly to practically nontoxic to aquatic organisms. The 48-hour LC50 of terbacil is 86 mg/L in sunfish [1]. The LC50 for terbacil is 102.9 mg/L in bluegill sunfish and 46.2 mg/L in rainbow trout. Terbacil is slightly toxic to freshwater invertebrates, with an LC50 of 65 mg/L in Daphnia, a small freshwater crustacean. The LC50 for terbacil is greater than 4.9 mg/L in marine oysters and 49 mg/L in shrimp [129]. Terbacil does not bioaccumulate in bluegill sunfish [130]. Estuarine and marine organisms may be exposed to terbacil due to its use as a sugarcane herbicide [128]. A study on grass shrimp with an 84.7% formulated terbacil product was sufficient to characterize the herbicide as slightly toxic to marine invertebrates. The 48-hour LC50 of terbacil is 1000 mg/L in fiddler crabs [1]. Effects on other organisms: Terbacil is nontoxic to bees [1].
Environmental Fate:Breakdown in soil and groundwater: Terbacil is highly persistent in soils [11]. Soil half-lives of 50 to 180 days have been reported [1,11]. Data from field dissipation studies showed that terbacil persistence in soil varied with application rate, rainfall, soil type, and mobility, as well as available oxygen [129]. In most soil types, terbacil has a relatively low tendency to be adsorbed. It also is highly soluble in water. Thus, terbacil is likely to be highly mobile in soil and potentially pollute groundwater [11,131]. Because of this, it should not be used on sandy or gravelly soils that have less than 1% organic matter, particularly if the water table is near the soil surface [128] and when deep tillage is used [132]. Leaching may be slower in soils that are finer textured and/or have higher organic matter content [128]. Terbacil was not detected in a national groundwater survey conducted by EPA [8]. In moist soils, terbacil is subject to microbial degradation. However, data suggest that recommended rates of terbacil use may result in its persistence for more than one growing season [8].Breakdown in water: Contamination of surface waters near terbacil-treated areas, and subsequent exposure of humans and non-target organisms, is possible due to terbacil's mobility in soil and its high water solubility [132]. Terbacil is stable in water and does not readily undergo hydrolysis or photodegradation [129]. Breakdown in vegetation: At normal application rates, terbacil has residual phytotoxicity to affected species in treated soils for 1 to 2 years [128]. Terbacil residues were phytotoxic to oats planted 3 years after a previous application of the herbicide. For example, in alfalfa, 12% of terbacil plus its metabolites were still found 6 to 8 months after application [8]. Terbacil is most readily absorbed through the root system of plants to which it is applied. Less is absorbed through the leaves and stems of plants. Studies of sugarcane plants indicate that terbacil is moved, or "translocated," upward into the leaves after absorption by the roots [58].
Physical Properties:Appearance: Terbacil is a white, crystalline, odorless solid which is noncorrosive and nonflammable [1].Chemical Name: 3-tert-butyl-5-chloro-6-methyluracil [1] CAS Number: 5902-51-2 Molecular Weight: 216.70 Water Solubility: 710 mg/L @ 25 C [1] Solubility in Other Solvents: s.s. in mineral oils and aliphatic hydrocarbons; v.s. in methyl isobutyl ketone, butyl acetate, xylene, cyclohexanone, dimethylformamide, and strong aqueous alkalis [1] Melting Point: 175-177 C [1] Vapor Pressure: 0.0625 mPa @ 30 C [1] Partition Coefficient: 1.8921 [58] Adsorption Coefficient: 55 [11] Exposure Guidelines:ADI: Not AvailableMCL: Not Available RfD: 0.013 mg/kg/day [13] PEL: Not Available HA: 0.09 mg/L (lifetime) [130] TLV: Not Available Basic Manufacturer:DuPont Agricultural ProductsWalker's Mill, Barley Mill Plaza P.O. Box 8003 Wilmington, DE 19880-0038 Phone: 800-441-7515 Emergency: 800-441-3637 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. |
