Growth chamber experiments were conducted to determine if certain genetic, environmental, and chemical factors or their interactions promote chloroacetamide herbicide injury to corn seedlings. Greater chloroacetamide injury occurred with ‘Pioneer 3320’ than with ‘Pioneer 3780’ hybrid corn, with 15 C than with 30 C soil temperature, with soil moisture at 105% field capacity (FC) than at 75% FC, with alachlor than with metolachlor, and with a herbicide rate of 2.2 kg/ha than with 1.1 kg/ha. Covering the plant containers with clear plastic until seedling emergence caused alachlor to be more phytotoxic to corn than metolachlor. Most factors evaluated increased the injury to corn in an additive manner.

Diclofop–methyl and haloxyfop–methyl (0.001 to 10 μM) caused 9 to 61% inhibition of 14C–acetate incorporation into lipids in corn leaf segments within 1 h of herbicide treatment, while neither herbicide affected this process in bean leaf segments. The herbicides did not affect 14C-malonate incorporation into lipids in corn leaf segments. Diclofop-methyl and haloxyfop-methyl reduced 14C-acetate incorporation into polar lipids and triglycerides in corn while incorporation into sterols was increased. In vitro activity of acetyl-coenzyme A carboxylase (EC 6.4.1.2) was inhibited from 26 to 94% within 5 min of exposure to the herbicides (1 to 10 μM). Diclofop acid inhibited this enzyme activity more than did haloxyfop acid. Differences in field activity between diclofop-methyl and haloxyfop-methyl are not related to differential sensitivity of acetyl–coenzyme A carboxylase to the two herbicides.

A field trial was conducted in 1988 and 1989 to confirm the efficacy of naphthalic anhydride (NA) for providing full-season protection of corn from imazethapyr applied at various times and rates. NA applied as a 1% by weight dust to corn seed caused 6% injury 2 weeks after treatment (WAT) in 1989; however, plants recovered within 6 WAT and grain yield was not affected. Imazethapyr applied to corn untreated with NA resulted in greater than 30% injury for all treatments in both years except PRE in 1988. NA reduced phytotoxicity from all imazethapyr applications in 1989 and from PPI, early POST, and 4- to 5-leaf stage (mid-POST) applications in 1988. Despite the safening effect, corn injury was still observed 6 WAT in NA-treated corn for all imazethapyr applications in both years except early POST in 1988. Higher yields were produced from NA-treated than untreated corn with imazethapyr applied PPI in both years, PRE in 1989, early POST in both years, and mid-POST in 1988. Safened corn treated PPI and early POST yielded the same as the safened corn in the control in both years. Imazethapyr applied at the 8- to 10-leaf stage caused total yield loss regardless of NA treatment. Drought conditions may have caused the lower corn injury and yield loss from imazethapyr observed in 1988 compared to 1989.