CGA-43089 [α-(cyanomethoximino)-benzacetonitrile], CGA-92194 {α-[(1,3-dioxolan-2-yl-methyl)imino] benzeneacetonitrile}, and MON-4606 [5-thiazolecarboxylic acid, benzyl ester, 2-chloro-4-(trifluoromethyl)], applied as seed treatments at 1.25 g/kg seed, prevented yield losses in grain sorghum [Sorghum bicolor (L.) Moench.] in the field due to metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide], alachlor [2-chloro-2′, 6′-diethyl-N-(methoxymethyl)acetanilide] or acetochlor [2-chloro-N-(ethoxymethyl)-6′-ethyl-o-acetotoluidide] applied at 1.7, 2.2 and 1.7 kg/ha, respectively. CGA-92194, applied at 0.8 g/kg seed, prevented yield reduction from metolachlor applied at 4.5 kg/ha. MON-4606 was more effective in protecting grain sorghum when applied as a seed treatment than when applied in the furrow with a clay or sand granule as carrier.

Field and greenhouse experiments were conducted during 1984 through 1986 to examine the efficacy of the seed protectants CGA-92194 {α-[(1,3-dioxolan-2-yl-methyl)imino]benzacetonitrile} and flurazole [2-chloro-4-(trifluoromethyl)-5-thiazolecarboxylic acid] for protecting grain sorghum [Sorghum bicolor (L.) Moench.] from alachlor [2-chloro-N-(2,6-diethylphenyl)-N-(methoxymethyl) acetamide], metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide], and propachlor [2-chloro-N-(1-methylethyl)-N-phenylacetamide] injury. In the field, CGA-92194 and flurazole protected sorghum from injury, stand reduction, and yield loss due to alachlor and metolachlor. In general, sorghum was protected with either antidote, and protected response to alachlor or metolachlor was similar to sorghum subjected to propachlor. Greenhouse experiments were conducted to examine the response of bronze and yellow pericarp color to seed protectants, six sorghum hybrids to these antidotes, and the effects of cool soil temperature on the early seedling vigor of sorghum protected with the antidotes. The response of sorghum with yellow and bronze pericarp color was similar when compared across antidotes. However, there were differences among the sorghum hybrids when compared across protectants. The potential of CGA-92194 and flurazole to protect against alachlor injury was reduced when sorghum was grown in cool soil.

The persistence of alachlor [2-chloro-2′,6′-diethyl-N-(methoxymethyl) acetanilide], metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide], and propachlor (2-chloro-N-isopropylacetanilide) in soil was examined under laboratory and field conditions using sorghum (Sorghum vulgare Pers. ‘NB280S′) or annual ryegrass (Lolium multiflorum Lam.) as bioassay species. In laboratory studies, degradation rate of alachlor and propachlor was greater at 50 and 80% than at 20% field capacity at 20 C. Degradation of metolachlor was greater at 80 than at 20% field capacity. Degradation rate of alachlor and metolachlor at 50% field capacity was greater at higher temperatures. Propachlor degradation rate varied with temperature. Under irrigated, cropped field conditions, the order of persistence was metolachlor > alachlor > > propachlor.

The effects of chloracetamides on protein synthesis were studied both in vivo and in vitro. Four chloracetamide herbicides, alachlor [2-chloro-2′,6′-diethyl-N-(methoxymethyl)acetanilide], metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide], CDAA (N–N-diallyl-2-chloroacetamide), and propachlor (2-chloro-N-isopropylacetanilide) were tested for inhibition of [3H]-leucine incorporation into protein. Incorporation of 3H-leucine into trichloroacetic acid (TCA)-insoluble protein was inhibited in oat (Avena sativa L. ‘Victory’) seedlings grown in sand culture and treated 12 h at 1 × 10−4M with these chloracetamides. The herbicides were also tested in a cell-free protein synthesizing system containing polyribosomes purified from oat root cytoplasm. These herbicides had no effect on the rates of polypeptide elongation nor on the synthesis of specific polypeptides when herbicides (1 × 10−4M) were added directly to the system. Polypeptide formation was inhibited 89% when 1 × 10−4M cycloheximide was added during translation. Cytoplasmic polyribosomes were isolated from oat roots treated 12 h with 1 × 10−4M herbicide. Translation rates and products were not altered when these polyribosomes were added to the in vitro system. Protein synthesis is inhibited when tested in an in vivo system; however, the inhibition does not occur during the translation of mRNA into protein.

Alachlor at 3.4 and 6.7 kg ha-1, metolachlor at 2.8 and 5.6 kg ha-1, and propachlor at 4.5 and 9.0 kg ha-1 were applied to grain sorghum in field experiments conducted in 1981 and 1982. ‘Dekalb E-59’ and ‘Pioneer 8311’ grain sorghum were tested with and without the seed protectants cyometrinil and flurazole in both experiments. ‘Funk's G-1350’ was tested with and without cyometrinil and CGA-92194 in one experiment. Alachlor and metolachlor caused serious injury (stunting and, in some instances, reductions in stand and yield) to grain sorghum without the seed protectants. Less severe injury to grain sorghum occurred with alachlor and metolachlor at high rates even in the presence of the seed protectants. The three seed protectants were equally effective in preventing crop injury. Only minor injury to grain sorghum, with or without the seed protectants, occurred with propachlor at both rates. Overall, early-season weed control was 81 to 100%; however, propachlor at the rates tested was noticeably weaker than alachlor and metolachlor against some annual grasses.

Four experiments were conducted in 1985 and 1986 at three locations to assess weed control efficacy and phytotoxicity of several preemergence herbicides applied between beds (row middles) of polyethylene-mulched cauliflower grown on raised beds. Efficacy of most herbicide treatments varied among the four experiments; however, 4.5 kg ai/ha diethatyl and tank mixes of oxyfluorfen with cinmethylin consistently controlled weeds best. Plant stand, yield, and cauliflower curd size were not affected by treatment for any of the varieties used at any of the locations.

Field studies were conducted from 1984 to 1986 to assess cabbage injury and yield response to several acetanilide herbicides. When incorporated, metolachlor significantly injured cabbage and reduced yields while post-transplant applications caused foliar flecking but did not reduce yields. Crop injury from pretransplant applications of 4.4 kg ai/ha was significant for all herbicides in both 1985 and 1986. Although total yields in 1985 and 1986 were comparable, maturity was delayed in 1986. With few exceptions, the acetanilides did not differ in either injury or yield-reducing potential. However, compared to trifluralin, metolachlor reduced yields in both years and at both rates.

Metolachlor has been evaluated both as a herbicide for use in cultivated oats (Avena sativa L.) and for its potential as an alternative herbicide for the control of herbicide-resistant rigid ryegrass. Eight herbicide-resistant and two susceptible biotypes of rigid ryegrass were tested for their susceptibility to metolachlor. Response to metolachlor was determined both in soil and an agar germination medium. The LD50 for metolachlor in agar for a susceptible biotype (VLR1) was 0.13 μM. Five biotypes, SLR5 (6.9 fold), SLR31 (5.2 fold), SLR10 (2.5 fold), NLR12 (2.1 fold) and VLR69 (1.9 fold), were cross-resistant to metolachlor when compared with VLR1. Relative response of the biotypes was similar in both soil and agar, validating the use of an agar germination test to determine the susceptibility of rigid ryegrass biotypes to metolachlor. Biotypes cross-resistant to metolachlor also were cross-resistant to alachlor (SLR5 6.7 fold, SLR31 5.9 fold, SLR10 2.4 fold, and VLR69 1.6 fold with the LD50 for VLR1 being 0.49 μM) and propachlor (SLR57.2 fold, SLR31 7.2 fold, SLR10 3.0 fold and VLR69 2.5 fold with the LD50 for VLR1 being 0.47 μM) indicating that cross-resistance extends to other members of the chloroacetamide group. Cross-resistance to chloroacetamides was observed in biotypes that previously had been reported as cross-resistant to other herbicides. In contrast, biotypes with limited herbicide histories were generally not cross-resistant to metolachlor. These results indicate that there is a high probability of chloroacetamide cross-resistance in populations of herbicide-resistant rigid ryegrass.