Common bean and azuki bean are poor competitors with weeds and demonstrate sensitivity to herbicides used for weed control in soybean. S-metolachlor, flufenacet, and acetochlor are categorized as Group 15 herbicides and provide control of multiple annual grass and select small-seeded broadleaf weeds. By way of field trials near Exeter and Ridgetown, Ontario, in 2019, 2020, and 2021, four dry bean market classes (azuki, kidney, small red, and white bean) were evaluated for their tolerance to 1× established label rates and 2× rates of S-metolachlor (1,600 and 3,200 g ai ha−1), flufenacet (750 and 1,500 g ai ha−1) and acetochlor (1,700 and 3,400 g ai ha−1) applied preplant incorporated (PPI). Injury was evaluated by assessing visible injury symptoms, density, shoot biomass, height, seed moisture content, and seed yield. Azuki bean was more sensitive to the Group 15 herbicides than other dry bean market classes; the Group 15 herbicides caused a 12% reduction in azuki bean growth at 2 wk after emergence; growth reduction was ≤2% in the other bean classes. Flufenacet (2× rate) was the most injurious treatment, causing a 27% reduction in azuki bean yield. This study concludes that kidney, small red, and white bean have a sufficient margin of crop safety to flufenacet, acetochlor, and S-metolachlor applied PPI. Azuki bean was sensitive to flufenacet; additional research is needed to investigate azuki bean tolerance to acetochlor and S-metolachlor applied PPI.

During 2016 and 2017, four field experiments were conducted at Huron Research Station near Exeter, ON, to evaluate the sensitivity of dry bean grown under a strip-tillage cropping system, to potential herbicides for the control of glyphosate-resistant (GR) horseweed. At 8 wk after emergence (WAE), saflufenacil, metribuzin, saflufenacil+metribuzin, 2,4-D ester, flumetsulam, cloransulam-methyl, and chlorimuron-ethyl caused 13% to 32%, 8% to 52%, 32% to 53%, 5% to 7%, 13% to 21%, 16% to 29%, and 23% to 43% visible injury in dry beans, respectively. Saflufenacil decreased aboveground biomass 65% in kidney bean and 80% in white bean. Metribuzin decreased biomass 82% in kidney bean and 50% in white bean. Saflufenacil+metribuzin decreased biomass 88% in kidney bean, 68% in small red bean, and 80% in white bean. Chlorimuron-ethyl decreased biomass 40% in white bean. There was no decrease in dry bean biomass with the other herbicides evaluated. Metribuzin and saflufenacil+metribuzin reduced kidney bean seed yield 72% and 76%, respectively. Saflufenacil+metribuzin, flumetsulam, cloransulam-methyl, and chlorimuron-ethyl reduced small red bean seed yield 39%, 27%, 30%, and 54%, respectively. Saflufenacil, metribuzin, saflufenacil+metribuzin, flumetsulam, cloransulam-methyl, and chlorimuron-ethyl reduced seed yield of white bean 52%, 32%, 62%, 33%, 42%, and 62%, respectively. There was no decrease in dry bean yield with the other herbicides evaluated. Among herbicides evaluated, 2,4-D ester caused the least crop injury with no effect in dry bean seed yield.

There is little information on the sensitivity of dry beans to flumioxazin. Tolerance of eight cultivars of dry beans representing four market classes (black, cranberry, kidney, and white beans) to preplant incorporated (PPI) and preemergence (PRE) applications of flumioxazin at the rate of 52.5, 70, and 140 g ai/ha were studied in three field experiments in Ontario in 2002 and 2003. There were no differences (P < 0.05) between two cultivars within a market class in their responses to flumioxazin. However, the four market classes differed in their responses to flumioxazin. Black and white beans were more sensitive to the PRE application of flumioxazin than cranberry and kidney beans. Flumioxazin applied PRE at 140 g/ha caused as much as 34% visual injury and reduced plant height by 23 to 28%, shoot dry weight by 35 to 39%, and yield by 20 to 30% in black and white bean market classes. Flumioxazin-applied PPI did not injure any market class. On the basis of this research, there is an acceptable margin of crop safety in these black and white bean cultivars only when flumioxazin is applied PPI. The two cranberry and kidney bean cultivars were tolerant to all rates of flumioxazin applied both PPI and PRE.

Three field trials were established from 2001 to 2003 in Ontario to determine the effect of foramsulfuron POST (35 and 70 g ai/ha), isoxaflutole PRE (105 and 210 g ai/ha), and isoxaflutole plus atrazine PRE (105 + 1063 and 210 + 2126 g ai/ha) applied in the previous years to field corn on cranberry, black, kidney, and white (navy) bean. Foramsulfuron residues did not cause visible injury, or reductions in shoot dry weight or yield of dry bean 1 yr after application in corn. In contrast, visual injury across the four market classes varied from 4 to 37% 1 yr after application of isoxaflutole, and from 30 to 54% 1 yr after application of isoxaflutole plus atrazine. Isoxaflutole residues reduced shoot dry weight and yield as much as 81 and 44% in cranberry, 52 and 39% in black, 53 and 19% in kidney, and 42 and 19% in white bean, respectively. Isoxaflutole plus atrazine residues reduced shoot dry weight and yield as much as 87 and 64% in cranberry, 75 and 61% in black, 71 and 46% in kidney, and 65 and 33% in white navy bean, respectively. Injury was not detected regardless of market classes 2 yr after application of isoxaflutole alone or in tank mix with atrazine. Based on these results, it is recommended that none of the market classes of dry bean tested in this study should be grown 1 year after an application of isoxaflutole or isoxaflutole plus atrazine. A recropping interval of 2 years is currently recommended following applications of isoxaflutole or isoxaflutole plus atrazine for these market classes of dry bean.

The effects of inclusion of different levels of raw kidney bean (Phaseolus vulgaris) of high lectin content (27 g/kg meal) in a high-quality (lactalbumin) control diet were tested in nutritional trials on the growth and metabolism of obese Zucker (fafa) rats and their lean littermates in comparison with pair-fed controls. All diets contained 100 g total protein/kg and either 50 g lipids/kg (low fat) or 150 g lipids/kg (moderate fat). The growth of both obese and lean rats on bean diets was retarded by the daily bean intake in a dose-dependent manner. However, most of this was because bean-fed rats contained less body fat than the controls after 10 d. Thus, after feeding low-fat diets containing up to 130 g kidney bean/kg (lectin intake ≤ 0·2 g/kg body weight (BW) per d) in both 10 d and 70 d trials, the bodies of obese rats contained less fat but not protein than their pair-fed controls. Moreover, by increasing the lipid content of the diet to 150 g/kg, the level of bean inclusion could be increased to 280 g/kg (lectin intake ≥ 0·4 g/kg BW per d) without loss of body protein and skeletal muscle. Although these rats contained more body fat than those which were fed on low-fat diets, their weight reduction could be accounted for exclusively by reduced lipid content. In contrast, significant body protein loss occurred when the same diet of high lectin content was fed to lean littermates. Plasma insulin levels were significantly depressed in the obese Zucker rats on bean diets but the pancreas was not significantly enlarged nor its insulin content changed in 10 d trials. However, significant pancreatic growth occurred on long-term (70 d) bean feeding compared with pair-fed controls. The results suggest that, in addition to animal nutrition, it may also be possible to use the bean lectin as a dietary adjunct or therapeutic agent to stimulate gut function and ameliorate obesity if a safe and effective dose-range can be established for human subjects.