© 2000 CRC Press LLC chapter nine Ureas 9.1Class overview and general description Background Substituted urea compounds (compounds in which different functional groups are substituted for one or more of the hydrogens in the urea molecule) are widely used as herbicidal agents, and to a lesser degree as insecticides (1,2). The general structure of the substituted urea molecule is shown in Figure 9.1. The compound’s identity, structure, and activity are defined by the substituents and their arrangement on the molecule (1,2). The substituted urea herbicides include the phenylurea her- bicides (Figure 9.1A) and the sulfonylurea herbicides (Figure 9.1B), which are the two major groups of substituted urea herbicides (2). The benzoylphenylureas (Figure 9.1C) are the major class of ureas used for insect control (1). Examples of these three types of substituted urea compounds are listed in Table 9.1. Ureas usage Phenyl- and sulfonylureas The phenylurea compounds include some of the most commercially important herbicides: fenuron and diuron (2). There are at least 20 different compounds within this subgroup. They are principally used for the control of annual and perennial grasses and are applied pre-emergence, i.e., before target plants have emerged (2,4). The sulfonylurea compound group is a relatively new class of herbicides first introduced in 1982, and has fewer members than the phenylurea class (2). Sulfonyl ureas are also used for control of broadleaf weed species in addition to annual and perennial grasses (2,4). They may be applied pre- or post-emergence (4). The sulfonyl urea herbicides are nearly 100 times more toxic to target plants than the older compounds (2). In addition, they are applied at relatively low application rates and have a low toxicity to humans and other animals. Thus, this class of compound is expected to see continuing research and development activity in the coming years (3). Benzoylphenylureas Benzoylphenylurea compounds are very useful in controlling a wide variety of insect pests, both within and outside of Integrated Pest Management systems (1). The potential for their use as insecticidal agents was first recognized in the early © 2000 CRC Press LLC 1970s by researchers in the Netherlands (1). A number of benzoylphenylurea com- pounds have been developed for this use, and have a number of advantages over broad-spectrum organochlorine or organophosphate insecticides (1). Chief among these are their specificity for larval and juvenile stages, very low toxicity to verte- brates, and consistent performance in the field (1). Benzoylphenyl compounds are generally expected to show low environmental persistence and relatively low or temporary impacts on most non-target invertebrate species, especially beneficial species (e.g., pollinators) (1,5,6). A notable exception to this rule are aquatic inver- tebrates, which may be severely affected by exposure (5,6). Mechanism of action and toxicology: phenylureas Mechanism of action Phenylurea herbicides are generally well-absorbed through the roots (but not foliage) and moved through xylem to the leaves where they disrupt photosynthesis (2,4). One exception is siduron, which does not affect photosynthesis but rather root growth (2). Disruption of photosynthesis occurs by binding of the herbicide to a critical site in the Photosystem II region of the chloroplasts, shutting down CO 2 fixation and energy production (4). Indirect production of reactive lipid peroxides contributes to a loss of membrane integrity and organelle function within the cell (4). Outward signs of these processes include yellowing or blanching of the leaves (foliar chlorosis) and browning (necrosis) due to changes in the chlorophyll and cell death (4). Acute toxicity Phenylureas exhibit a range of acute oral toxicities, ranging from moderately to practically nontoxic; reported acute oral rodent LD 50 values range from a low of 644 mg/kg (in the case of tebuthiuron) to greater than 5000 mg/kg (in the case of fluometuron) (4,7–13). Via the dermal route, they are generally slightly toxic, with AB C Figure 9.1 Generic structures for phenylurea (A), sulfonylurea (B), and benzoylphenyl- urea (C) compounds. © 2000 CRC Press LLC reported dermal LD 50 values above 5000 mg/kg in rabbits (4,7–12). Tebuthiuron again stands out, with a reported dermal LD 50 of greater than 200 mg/kg in rabbits, indicating moderate toxicity via this route (4). Via the inhalation route, the phenyl- ureas are generally slightly toxic, with reported 4-hour inhalation LC 50 values of greater than 2 mg/L in rats (4,7–13). Most of them do not cause skin sensitization in guinea pigs or skin irritation in rabbits, but most do cause slight to mild eye irritation in rabbits (4,7–12). Linuron has shown the capacity to cause skin sensitization in guinea pigs, and tebuthiuron caused slight skin irritation in rabbits (4). The symptoms that accompany acute exposure to phenylurea compounds vary widely. For instance, acute exposure of rats to tebuthiuron by ingestion caused a loss of appetite, a lack of energy, and muscle incoordination (13), while similar exposure of rats to fluometuron caused muscle weakness, watery eyes, extreme exhaustion, and collapse (11). Fluometuron also has caused cholinesterase depression in guinea pigs exposed to 0.6 mg/L over a 2-hour period (11). Signs of diuron exposure in rats Table 9.1 Examples of Substituted Urea Compounds Phenylureas Benzthiazuron Chlorbromuron Chlorotoluron Chloroxuron Daimuron Difenoxuron Dimefuron Diuron* Ethidimuron Fenuron Flufenoxuron Fluometuron* Forchlorfenuron Isouron Linuron* Monuron Neburon Siduron Tebuthiuron* Sulfonylureas Bensulfuron Chlorimuron Chlorsulfuron Primisulfuron-methyl* Sulfometuron-methyl* Triasulfuron Benzoylphenylureas Chlorfluazuron Diflubenzuron* Penfluron Trilumuron Note: * indicates that a profile of this compound is included in this chapter. © 2000 CRC Press LLC included depression of central nervous system activity (10). Whether these differ- ences are due to variation in reporting the symptoms or due to differences in the way the compounds act in the organisms is currently unknown (14). Chronic toxicity Phenylurea compounds may cause skin sensitization with repeated or prolonged exposure over extended periods of time (4,8). Anemia, effects on red blood cell levels, or other changes in blood parameters have been seen in different test animals at various dose levels. These range from 2.75 mg/kg/day in rats over a 2-year test period (linuron) to greater than 50 mg/kg/day for the same time (tebuthiuron) (4,10–17). Reproductive effects For most members of the class, reproductive effects have not been consistently observed. No reproductive effects were seen in any of three studies of tebuthiuron at doses up to 180 mg/kg/day during gestation of pregnant rats (4). No reproductive effects were seen on rats given linuron at 12.5 mg/kg/day in a three-generation study, nor in rats given fluometuron at doses of 50 mg/kg/day during gestation, although some maternal toxicity was seen in the latter case (4,8). Another study of fluometuron using rabbits showed increases in fetal resorptions at doses of 50 mg/kg/day and higher on days 6 to 19 of gestation (17). Some maternal toxicity was also seen at the higher dose levels in this study (17). Teratogenic effects Some members of the phenylurea class have shown the capacity to cause devel- opmental effects in animal tests. Diuron has caused irregularities in skeletal forma- tion in rats at doses above 125 mg/kg/day over days 6 to 15 of gestation, and has also caused developmental effects in offspring of rabbits given 2000 mg/kg/day during gestation (4,8). Flurometuron also caused some secondary effects in rats and rabbits receiving 100 mg/kg/day during gestation (4,8). Both linuron and tebuthiuron have not shown adverse effects on fetal develop- ment at relevant doses. Linuron was negative for teratogenicity at doses (adminis- tered during gestation) of 25 mg/kg/day in rabbits or approximately 6 mg/kg/day in rats (4,14). Tebuthiuron did not show any teratogenic capacity at 56 mg/kg/day in rats over three generations, at 180 mg/kg/day in rats during gestation, nor at 25 mg/kg/day in rabbits (4,8). Mutagenic effects The vast majority of mutagenicity assays and tests for genotoxicity performed using diuron, fluometuron, linuron, and tebuthiuron have not shown them to have the potential to cause these effects (4,17,18). They have included the Ames mutage- nicity assay, tests for chromosomal aberration with Chinese hamster ovary cell cul- tures and mouse micronuclei, and tests for DNA repair inhibition in rat liver cell lines (4,17,18). Carcinogenic effects Some members of the class have been linked to increased tumor production in animal systems. Fluometuron has shown mixed results, causing increased liver tumors and leukemia at doses of 87 mg/kg/day in mice over 2 years, but not in rats © 2000 CRC Press LLC at any dose tested (4,17). Diuron has not caused cancer in rats at low levels of exposure (10), nor has tebuthiuron at the highest doses tested in rats and mice (4). Linuron has shown the capacity to produce increased tumors of the liver in mice at 180 mg/kg/day, and of the testes in rats at doses of 72.5 mg/kg/day (4,10,14). Organ toxicity Animal studies have shown the blood-forming system, liver, pancreas, spleen, and kidneys to be potentially affected by exposure to phenylurea compounds. Fate in humans and animals Some members of the phenylurea class (e.g., linuron and tebuthiuron) are fairly readily absorbed through the gastrointestinal tract, whereas others are rather poorly absorbed (4,7,17). Those that are not readily absorbed are excreted via feces unchanged (4,17). Those which may be absorbed and distributed systemically typi- cally undergo rapid transformation and elimination via urine, typically within a few days (4,8). Overall, most class members possess a low potential for bioaccumulation in food animals or humans. Ecological effects Effects on birds Phenylurea compounds are typically slightly to practically nontoxic to birds, with reported acute oral LD 50 values above 2000 mg/kg for bobwhite quail in most cases (4,8). The reported acute oral LD 50 for diuron is 1730 mg/kg in bobwhite quail (4). The reported subchronic dietary LC 50 values in pheasants, mallards, and Japanese quail are above 5000 ppm for most members of this chemical class (4,8). Effects on aquatic organisms Phenylurea compounds are slightly to moderately toxic to freshwater fish, and in most cases only slightly toxic to freshwater invertebrates. Reported 48- and/or 96-hour LC 50 values for most members of the class range from 4 to greater than 40 mg/L in such species as rainbow trout, bluegill sunfish, carp, and catfish (4,8). Diuron is more toxic to aquatic invertebrates than most members of this class, with a reported 48-hour LC 50 of 1 to 2.5 mg/L in Daphnia (4,8). Effects on other organisms (non-target species) Phenylurea compounds are generally nontoxic to bees (4,8). Some of them (e.g., tebuthiruon) may be less selective, and may impact non-target plant species (4). Environmental fate Breakdown in soil and groundwater All of the phenylureas will remain active in the soil from a few months up to a year in some cases and are broken down by the action of soil microorganisms (2). The measured field half-lives for many members of the class range from 25 to over 360 days (19). They are generally poorly bound to most soils, with reported K oc values of 80 to 500, indicating a moderate to high potential for migration (19). Phenylurea compounds show little tendency to evaporate from soil, and soil pH does not appear to significantly affect their adsorption (20). Many phenylurea compounds have been detected in groundwater (20). © 2000 CRC Press LLC Breakdown in water Phenylureas are generally stable and long-lived in aqueous systems, and will not easily undergo hydrolysis except with extreme acidic or basic conditions (3,4,20). One example is fluometuron, which has been reported to have a half-life in aqueous systems of over 100 weeks, and is stable over the pH range of 1 to 13 (11). The primary means of breakdown in aquatic systems is via microbial systems, although they may also undergo photolysis (2,8). Conditions that limit the availability of oxygen for microbial aerobic breakdown of the phenylureas will increase their lon- gevity in the water environment. Breakdown in vegetation Phenylureas are readily absorbed from roots and translocated to foliage through xylem; they are not readily absorbed through the foliage (4). In tolerant plants, they are rapidly metabolized by loss of methyl groups (N-demethylation) and addition of hydroxyl groups in their place (hydroxylation), thus forming compounds that do not adversely affect the plant like the unmetabolized herbicide (4). Plants incapable of detoxifying the phenylureas, or which process them only slowly, will suffer the adverse effects the herbicides cause (4). Mechanism of action and toxicology: sulfonylureas Mechanism of action Sulfonylurea herbicides are also well-absorbed and translocated through the roots, as well as through the foliage (4). Some members of the class (e.g., sulfometu- ron-methyl) may show lesser translocation (4). These compounds inhibit a key enzyme in the biosynthesis of necessary branched-chain amino acids (e.g., leucine, isoleucine, and valine), and thereby limit the plant’s ability to construct the proteins necessary to build more cells (4). Deprived of the ability to manufacture necessary proteins, growth (meristematic) regions suffer inhibited growth and survival. Acute toxicity Sulfonylurea compounds are, in general, practically nontoxic via the oral route, with reported rodent LD 50 values of greater than 5000 mg/kg for most of the com- pounds (4,7,8). Via the dermal route, they are generally slightly toxic, with reported dermal LD 50 values of greater than 2000 mg/kg in rabbits (8,15). They are, in general, slightly toxic via the inhalation route in rodents, with reported 4-hour inhalation LC 50 values of greater than 5 mg/L (4,8,15). They generally test negative for skin sensitization in guinea pigs, although sulfometuron can cause slight skin irritation in rabbits, and both primisulfuron and sulfometuron can cause slight to mild eye irritation in rabbits (4,15). Chronic toxicity Much like the phenylureas, sulfonylurea compounds have caused decreased body weight gain, increased liver weights, and anemia-like conditions in test animals, but at generally higher dose levels. These effects were caused by primisulfuron- methyl in dogs at doses levels of 125 mg/kg/day over 1 year, and by sulfometuron- methyl at 25 mg/kg/day in the same animals for the same length of time (15,21). In rats, these effects occurred at much higher dose levels, 180 and 375 mg/kg/day, © 2000 CRC Press LLC respectively, over 90 days (15,21). Studies of primisulfuron in rats and mice over 18 months showed disorders of the teeth and bones (4). Reproductive effects No reproductive effects due to sulfometuron-methyl were seen in rats or rabbits at 300 mg/kg/day in separate studies (4), but 300 mg/kg/day did cause decreased fecundity (litter size) in rats in another study (4). Primisulfuron-methyl has caused effects on the testes of males rats exposed to 250 mg/kg/day over two generations (15). These effects were also observed in other chronic studies in rats. It is not clear what the overall trend for this chemical class might be. Teratogenic effects Sulfometuron was not observed to cause teratogenic effects in rats or rabbits at doses of 300 mg/kg/day (21), but primisulfuron-methyl did cause delayed skeletal development and/or lack of bone formation in offspring of rats given doses of 100 mg/kg/day in two separate studies (15). Mutagenic effects Various mutagenicity and genotoxicity assays have not shown either primisul- furon-methyl or sulfometuron-methyl to be mutagenic (4,15,21). Carcinogenic effects Carcinogenicity assays for sulfometuron-methyl have not shown carcinogenic activity in rats at any dose tested or mice at doses up to 120 mg/kg/day (4). Primisulfuron-methyl has shown inconsistent results in carcinogenicity assays; doses of 180 mg/kg/day produced increased liver tumors in mice over 18 months in one study, but not in another (4,15). Organ toxicity Animal studies have shown the liver, kidneys, spleen, and blood-forming system to be potentially affected by exposure to sulfonylurea compounds. Fate in humans and animals Primisulfuron is not readily absorbed via the intestines, and is generally elimi- nated unchanged via the feces (15). Sulfometuron is readily absorbed through the intestine, but rapidly metabolized and eliminated within 28 to 40 hours, depending on the dose (22). Neither compound is expected to bioaccumulate in animal systems. Ecological effects Effects on birds Sulfonylurea compounds are practically nontoxic to wildfowl, with reported subchronic dietary LC 50 values greater than 2000 ppm in bobwhite quail and mallard ducks (4). Effects on aquatic organisms Sulfonylurea compounds are only slightly toxic to freshwater fish, with reported 96-hour LC 50 values of greater than 10 mg/L in rainbow trout and bluegill sunfish (15,23). They are practically nontoxic to Daphnia, with 96-hour LC 50 values reportedly greater than 100 mg/L (15,23). Sulfometuron has been implicated in some instances © 2000 CRC Press LLC of mass fish kills, but it is not clear what its actual role might have been in those cases (24). Effects on other organisms (non-target species) Sulfonylurea compounds are not considered toxic to bees (4). Environmental fate Breakdown in soil and groundwater Sulfonylurea compounds are of low to moderate persistence in the soil environ- ment, with reported field half-lives of 4 to 60 days (19,25). They are readily broken down by soil microbes, and more rapidly under well-oxygenated (aerobic) conditions (4,15,24). Degradation by sunlight may play a greater role in the breakdown of sulfo- meturon-methyl than primisulfuron-methyl (15,24). Ground cover, pH, and soil type have all been shown to influence the rate of disappearance of sulfometuron-methyl in several field studies (24,26,27). Since photodegradation is of lesser importance for primisulfuron, ground cover may not show very much effect on its loss from soils. The sulfonylurea compounds are poorly bound to most soils, and may be mobile (19,25), depending on pH and water solubility (4). At pH 7, solubility ranges from 70 mg/L for primisulfuron to 27.9 mg/L for chlorsulfuron. If the water has a pH of 5, the solubility of sulfometuron-methyl decreases to 8 mg/L. The half-lives of most of the sulfonylurea compounds in soil are 1 or 2 months (4,8). Though the sulfony- lurea compounds are potentially mobile within the soil, field studies show that neither primisulfuron-methyl nor sulfometuron-methyl were significantly mobile beyond a depth of 3 inches (8,20,26,27). Breakdown in surface water Sulfometuron is relatively short-lived in the water environment, with reported field half-lives of several days to 1 or 2 months; primisulfuron may be more persistent (15,24). Both compounds undergo aerobic breakdown, and anaerobic conditions may lengthen their residence time in water (15,24). Breakdown in vegetation Primisulfuron-methyl is readily absorbed by both the roots and foliage of plants, and quickly translocated to all parts of the plant (4). In resistant plants, it is rapidly metabolized, mainly by hydroxylation of the phenyl and pyrimidinyl ring structures, and subsequent linkage to glucose and elimination (4). The metabolism of sulfometu- ron-methyl is not well-understood (4). Mechanism of action and toxicology: benzoylphenylureas Mechanism of action Benzoylphenylurea compounds inhibit the ability of insects to synthesize an integral component of their exoskeleton cuticles, chitin (1,6). These protein and chitin shells are secreted by insect epidermal cells at regulated intervals within the insect lifespan, with most chitin production occurring during early and juvenile stages of development (6). Depending on the insect species and dose rates, benzoylphenylurea inhibition of chitin synthesis results in the inability of fertilized eggs to hatch prop- erly, the ability of hatched larvae to secrete chitin, or the ability of juvenile stages to © 2000 CRC Press LLC molt properly and advance to the next life stage (6). There are several schools of thought as to how the benzoylphenylureas may act to inhibit chitin synthesis and exoskeleton formation (6). It is thought by some researchers that the most plausible mechanism is that benzoylphenylureas inhibit chitin synthetase, the enzyme respon- sible for stringing together the N-acetylglucosamine (amino-substituted glucose sugar molecules) building blocks into the polymer to form chitin (6). Relatively less is known about the toxicology and environmental fate of the members of this class other than diflubenzuron (1). Insofar as the structure of a chemical compound determines its activity in biological and environmental systems, diflubenzuron can be considered representative of the toxicological and environmen- tal properties of other members of the benzoylphenylurea chemical class. Typically, the generic chemical structure may yield reliable predictive information about mem- bers of a general chemical class, but until actual data are gathered and analyzed for a specific compound, such predictions must be considered tentative in nature. 9.2Individual profiles 9.2.1 Diflubenzuron Trade or other names Diflubenzuron is sold under the trade name Dimilin. Other trade names include DU112307, ENT-29054, Micromite, and OMS-1804. Regulatory status Some formulations of diflubenzuron may be classified as Restricted Use Pesti- cides (RUPs) in the U.S. RUPs may be purchased and used only by certified appli- cators. Diflubenzuron is classified as toxicity class III — slightly toxic. Products containing it bear the Signal Word CAUTION. Introduction Diflubenzuron is a benzoylphenylurea used on forest and field crops to selec- tively control insects and parasites. Principal target insect species are the gypsy moth, forest tent caterpiller, several evergreen-eating moths, and the boll weevil. It is also used as a larvae control chemical in mushroom operations and animal houses. Diflubenzuron is a stomach and contact poison. It acts by inhibiting the production of chitin, a compound that makes the outer covering of the insect hard and thus interferes with the formation of the insect’s cuticle or shell. It is available as a suspension concentrate, wettable powder, or granules. Figure 9.2 Diflubenzuron. © 2000 CRC Press LLC Toxicological effects Acute toxicity No overt signs of toxicity were observed in any of the acute studies conducted (16). The oral LD 50 in rats and mice is greater than 4640 mg/kg, and the dermal LD 50 is greater than 10,000 mg/kg in rats and greater than 4000 mg/kg in rabbits. It is nonirritating to skin and slightly irritating to eyes (8). Chronic toxicity Rats given moderate amounts of the compound for 2 years had enlarged spleens, while mice in a similar study had liver and spleen enlargement at slightly lower levels of exposure. In a study with cats fed over a wide range of doses for 21 days, all of the females had dose-related blood chemistry changes at low doses, and the males exhibited changes at dose levels that were slightly higher (9). The changes were reversible. The chemistry changes were associated with the formation of met- hemoglobin, a form of hemoglobin that is unable to carry oxygen. Reproductive effects Day-old ducks and turkeys fed moderate amounts of the pesticide in their diets for 90 days had decreased testosterone levels after 42 days, but this did not occur in chickens and pheasants in the same study. Combs and wattles, which reflect hormone activity, showed some abnormalities. Some were underdeveloped and others more developed compared to controls. A short-term decrease in testosterone levels was shown in the sexually immature rats, but no clear-cut change was shown in young bull calves (16). A three-generation study on rats at low doses showed no effect on mating performance. It does not appear that diflubenzuron has a significant effect on repro- duction (16,28). Teratogenic effects Diflubenzuron does not appear to be teratogenic. Newborn rats and rabbits did not develop any birth defects after their mothers were exposed to low levels of diflubenzuron (1 to 4 mg/kg/day) on days 6 to 18 of gestation (16,28). Mutagenic effects Extensive testing on mammalian bacterial cells shows that diflubenzuron is not mutagenic (16,28). Carcinogenic effects Rats fed diets containing low to moderate amounts of diflubenzuron daily for 2 years had no increase in the number of new or abnormal tissue growths or lesions. Mice fed low doses for 80 weeks showed no significant tumor development. Other studies on both species at higher levels were also negative for malignant tumors (16). Diflubenzuron does not appear to be carcinogenic. Organ toxicity Animal studies have shown the liver and spleen to be target organs. [...]... Chemical name: 3-( 3,4-dichlorophenyl )-1 -methoxy-1-methylurea (7) CAS #: 33 0-5 5-2 Molecular weight: 2 49. 11 (7) Solubility in water: 81 mg/L @ 25°C, slightly soluble (7) Solubility in solvents: s.s in aliphatic hydrocarbons; m.s in ethanol; s in acetone (7) Melting point: 93 94 °C (7) Vapor pressure: 2 mPa @ 24°C (7) Partition coefficient (octanol/water ): 1010 (4) Adsorption coefficient: 400 ( 19) © 2000 CRC... Tebuthiuron is an off-white to buff-colored crystalline solid with a pungent odor (7) © 2000 CRC Press LLC Chemical name: 1-( 5-tert-butyl-1,3,4-thiadiazol-2-yl )-1 ,3-dimethylurea (7) CAS #: 3401 4-1 8-1 Molecular weight: 228.31 (7) Water solubility: 2500 mg/L at 25°C (7) Solubility in other solvents: i.s in benzene and hexane (7); s.s in chloroform, methanol, acetone, and acetonitrile (7) Melting point: 161.5 @... guidelines ADI: Not available HA: Not available RfD: Not available PEL: Not available Basic manufacturer Ciba-Geigy Corp P.O Box 18300 Greensboro, NC 2741 9- 8 300 Telephone: 80 0-3 3 4 -9 481 Emergency: 80 0-8 8 8-8 372 9. 2.6 Sulfometuron-methyl Trade or other names Trade names for products containing sulfometuron-methyl include Oust Weed Killer and DPX 5648 © 2000 CRC Press LLC Figure 9. 7 Sulfometuron-methyl Regulatory... compound on non-croplands, including rights-of-way and along ditch banks, may endanger both terrestrial and aquatic plant species (4,24) Physical properties 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 #: 7422 2 -9 7-2 Molecular weight: 364.4 (7) Solubility in water: 70 mg/L @... pressure: 0.41 mPa @ 50°C (7) Partition coefficient (octanol/water ): Not available Adsorption coefficient: 480 ( 19) Exposure guidelines ADI: Not available HA: 0.01 mg/L (lifetime) (32) RfD: 0.002 mg/kg/day (31) TLV: 10 mg/m3 (8-hour) (31) Basic manufacturer DuPont Agricultural Products Walker’s Mill, Barley Mill Plaza P.O Box 80038 Wilmington, DE 198 8 0-0 038 Telephone: 80 0-4 4 1-7 515 Emergency: 80 0-4 4 1-3 637 9. 2.3... (7) Vapor pressure: 0.27 mPa @ 25°C (7) Partition coefficient (octanol/water ): 61 @ 25°C and pH 7 (7) Adsorption coefficient: 80 ( 19) Exposure guidelines ADI: Not available HA: 0.5 mg/L (36) RfD: 0.07 mg/kg/day (31) PEL: Not available Basic manufacturer DowElanco 93 30 Zionsville Road Indianapolis, IN 4626 8-1 054 Telephone: 31 7-3 3 7-7 344 Emergency: 80 0-2 5 8-3 033 References (1) Retnakaran, A and Wright, J E.,... (7) Vapor pressure: . Press LLC RfD: 0.00025 mg/kg/day (31) PEL: Not available Basic manufacturer Ciba-Geigy Corporation P.O. Box 18300 Greensboro, NC 2741 9- 8 300 Telephone:80 0-3 3 4 -9 481 Emergency:80 0-8 8 8-8 372 9. 2.4 Linuron Trade. 198 8 0-0 038 Telephone:80 0-4 4 1-7 515 Emergency:80 0-4 4 1-3 637 9. 2.3 Fluometuron Trade or other names Trade names include C-20 59, Ciba-20 59, Cotoran, Cotorex, Cottonex, Flo-Met, Higalcoton, Lanex, and Pakhtaran. Regulatory. plants and weeds to this chemical. Physical properties Fluometuron is a white to tan powder or crystalline material with an amine-like odor (7). Chemical name: 1,1-dimethyl- 3-( a,a,a-trifluoro-m-tolyl)