Soils did not remain enhanced for EPTC degradation when EPTC was applied in a biennial rotation with cyanazine, cycloate, or alachlor as indicated by laboratory analysis and early-season weed control in the year of EPTC use. Control of late-season weeds was less when EPTC was rotated with alachlor than with a first-time use of EPTC. EPTC degradation remained enhanced in an EPTC-butylate rotation. The reversion rate of soil from an enhanced condition to normality was gradual and varied with location, year, and number of prior EPTC applications. At Clay Center and Scottsbluff, soils reverted to a nonenhanced EPTC degradation rate 18 months after initial EPTC application. At Scottsbluff, soil was not enhanced for EPTC degradation 18 months after the second of two annual EPTC applications. Soil from Clay Center was partially enhanced for EPTC degradation 18 months after the second of two annual EPTC applications but was not enhanced after 30 months.

Field and laboratory studies were conducted to examine the influence of continuous use and rotation of extenders on EPTC persistence in soils from Clay Center and Scottsbluff, NE. Rotation of EPTC + dietholate and EPTC + fonofos in soils with three prior annual treatments of each combination did not improve weed control compared to continuous use. SC-0058 was generally effective in slowing EPTC biodegradation in soils previously treated with EPTC, EPTC + dietholate, EPTC + fonofos, or EPTC + SC-0058. Dietholate was effective in slowing EPTC biodegradation in soil previously treated with EPTC or EPTC + SC-0058. SC-0058 appeared to have an inhibitory influence on the initial development of soil-enhanced EPTC biodegradation. Any enhanced biodegradation of dietholate or SC-0058 that may occur after repeated use was not a factor in enhanced EPTC degradation in EPTC + extender history soils.

Field and laboratory studies were conducted to examine the influence of previous pesticide use, number of prior EPTC (S-ethyl dipropyl carbamothioate) and butylate [S-ethyl bis(2-methylpropyl)carbamothioate] applications, and pretreatment of soil with EPTC and butylate metabolites on EPTC and butylate degradation. EPTC degradation was enhanced in Clay Center and Scottsbluff soils following three annual EPTC, butylate, or vernolate (S-propyl dipropylcarbamothioate) applications, but was not affected in soils following three annual atrazine [6-chloro-N-ethyl-N′-(1-methylethyl)-1,3,5-triazine-2,4-diamine], cyanazine {2-[[4-chloro-6-(ethylamino)-1,3,5-triazin-2-yl] amino]-2-methylpropanenitrile}, metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide], alachlor [2-chloro-N-(2,6-diethylphenyl)-N-(methoxymethyl)acetamide], or cycloate (S-ethyl cyclohexylethylcarbamothioate) applications. EPTC degradation rate was not affected in a Scottsbluff soil following three annual carbofuran (2,3-dihydro-2,2-dimethyl-7-benzofuranyl methylcarbamate) applications, but was partially enhanced in a Clay Center soil. Self- and cross-enhanced degradation of EPTC and butylate did not change regardless of the number of prior annual applications of each herbicide. The degradation rates of EPTC and butylate were not affected by soil pretreated with butylate sulfone, but the degradation rates-were fully enhanced by pretreatment with the respective sulfoxides of each herbicide. In cross-enhancement testing, EPTC and butylate degradation was partially enhanced in Clay Center soil pretreated with the sulfoxides of each.

Five classes of herbicides (carbamothioates, chloroacetamides, substituted pyridazinones, cyclohexanediones, and aryloxyphenoxypropionic acids) have been reported to inhibit lipid biosynthesis in higher plants. Carbamothioates impair the synthesis of surface lipids (waxes, cutin, suberin). These effects have been attributed to the ability of this herbicide class to inhibit one or more acyl-CoA elongases. Though as yet poorly characterized, these enzymes are associated with the endoplasmic reticulum and catalyze the condensation of malonyl-CoA with fatty acid acyl-CoA substrates to form very long-chain fatty acids used in the synthesis of surface lipids. There is contradictory evidence regarding the effects of chloroacetamide herbicides on de novo fatty acid biosynthesis. Selected substituted pyridazinones decrease the degree of unsaturation of plastidic galactolipids. This effect is attributed to the ability of selected members of this herbicide class to inhibit fatty acid desaturases which are thought to be located in the chloroplast envelope. Aryloxyphenoxypropionic acid and cyclohexanedione herbicides inhibit de novo fatty acid biosynthesis in grasses. The target site for these herbicide classes is the enzyme acetyl-CoA carboxylase which is found in the stroma of plastids. In most cases, selectivity between grasses and dicots is expressed at this site. Aryloxyphenoxypropionic acids and cyclohexanediones are reversible, linear, noncompetitive inhibitors of acetyl-CoA carboxylase from grasses. Both classes are also mutually exclusive inhibitors of grass acetyl-CoA carboxylase which suggests that they bind at a common domain on the enzyme.