Herbicides play a pivotal weed management role in modern commercial agriculture. However, their use sometimes leads to crop injury. Identifying the cause of the injury can be complicated because herbicide injury symptoms overlap nutrient deficiencies, pathogen infection and general abiotic stressors. This publication is a guide to the accurate identification of herbicide injuries. This is a crucial first step to preventing future problems.
Identifying herbicide injury requires that you understand the factors influencing crop tolerance to herbicides. Key considerations include:
- Field history: Herbicides can persist in the soil for over a year. These soil-stored herbicides can impact crops in subsequent seasons. Herbicide labels provide replanting interval restrictions ranging from a few days to 24 months.
- Soil amendments: Herbicide residues can be introduced in grass clippings, hay, manure or mulch used as soil amendments. Group 4 plant growth regulators, particularly, can carry over in these materials.
- Crop age and architecture: In perennial crops like blueberries, younger plants may be more sensitive to herbicides due to underdeveloped bark or smaller plant size. Likewise, new growth and basal shoot growth on plants of any age are often more sensitive to herbicide damage.
- Plant health and vigor: Healthy and vigorous plants tolerate herbicides better than stressed plants.
- Soil characteristics: Soil texture, organic matter content, pH, moisture, mulches and gravel affect herbicide performance for weed control and crop tolerance to herbicide injury. The herbicide rate that will produce injury varies with soil type. Soils with high clay and organic matter content retain herbicides more than other soils.
- Environmental conditions: Air and soil temperature, humidity, rainfall and wind influence crop tolerance, affecting pesticide volatilization, drift and efficacy.
- Equipment calibration and selection: Proper calibration and selection of spray nozzles prevent excess herbicide applications and reduce crop damage.
- Equipment contamination: Equipment must be thoroughly cleaned between herbicide applications to avoid crop injury.
Diagnosing herbicide injury
Diagnosing herbicide injury is a challenge because of similarities to other types of crop stress. Considerations for accurate identification include:
- Patterns: Observe distinct patterns in the field, such as tank contamination gradients or uniform damage from herbicide carryover.
- Affected and unaffected areas: Compare symptoms in nearby areas to distinguish between disease, drought, hail or other damage types. Symptoms expressed by weeds may indicate the herbicide’s mode of action.
- Information-gathering: Record crop age, soil type, cropping history and management practices. Note weather conditions preceding the injury.
- Rate dependence: Herbicide injury symptoms vary with application rates, ranging from transient chlorosis at low rates to tissue necrosis at higher rates. Following exposure to contact herbicides, the exposed tissue wilts and dies. In the case of systemic herbicides, necrosis is expressed as wilting on non-exposed plant parts.
Understanding herbicide symptoms involves recognizing their distinct properties and classification by mode of action. The Weed Science Society of America categorizes herbicides by numbered Groups based on the biochemical processes leading to plant death. Here, we focus on herbicides commonly used in blueberries, organized by their mode-of-action group. For more information, see the Herbicide Resistance Action Committee. Experimental images in this guide demonstrate herbicide effects on container-grown blueberry plants.
Injury symptoms
Group 2 herbicides. Acetolactase synthase inhibitors (ALS)
Example active ingredients: halosulfuron (Sandea) and rimsulfuron (Matrix)
Mode of action: Herbicides in Group 2 inhibit the synthesis of specific amino acids, the building blocks of proteins. Without proteins, plants do not grow well and eventually die. Group 2 herbicides are active in broadleaf, grass and sedge species. These herbicides affect the plant when applied to the foliage or the soil. They have both pre- and postemergence activity and are systemic in the plant.
Diagnostic keywords: leaf chlorosis, leaf malformation, stunting, reddish to purple leaves
Symptoms: Injury symptoms of Group 2 herbicides appear one or two weeks after exposure. Plant stunting is the first noticeable response. Leaves become chlorotic and yellowish, and in time develop purple coloration (Figure 1). Leaf veins become yellowish or purple, and the death of terminal growth can be present, as seen in Figure 2.
Group 3 herbicides. Inhibitors of microtubule assembly (DNA)
Example active ingredients: pronamide (Kerb), pendimethalin (Sattelite Hydrocap)
Mode of action: Herbicides in Group 3 are preemergence herbicides. They target emerging weed seedlings. Group 3 herbicides are applied from fall to early spring when plants are dormant or in early bud break. They arrest cell division by targeting microtubule synthesis. Microtubules are protein filaments attached to chromosomes in the cell nucleus, separating the chromosomes during cell division.
Diagnostic keywords: leaf stunting, leaf distortion, browned fruit skin, browned roots
Symptoms: New shoots display smaller, malformed leaves. Fruit circumference may display rough brown skin. Root growth may cease, and roots may turn dark brown in color. See Figures 3 and 4.
Group 4 herbicides. Auxin mimics
Example active ingredients: 2,4-D, quinclorac (Quinstar 4L), clopyralid (Stinger)
Mode of action: Herbicides in Group 4 are systemic postemergence herbicides largely targeting broadleaf and perennial weeds. These plant growth regulators are applied from spring to fall while plants are actively growing. They work in a similar fashion to certain plant hormones, disrupting the balance of plant growth, causing plants to grow in an uncontrolled manner or causing other abnormalities. These herbicides have both foliar and soil activity and can persist in the soil or in soil amendments. Injury to new growth is often the first symptom.
Diagnostic keywords: leaf cupping, stem twisting, chlorosis, wilting, stacked growth
Symptoms: New shoots display twisting (Figure 5). Leaves fail to expand, resulting in cupping (Figures 6 and 7).
Groups 5, 6 and 7 herbicides. Photosystem inhibitors (PSII)
Example active ingredients: 5 — simazine (Princep) diuron (Karmex), 6 — bentazon (Basagran)
Mode of action: Herbicides in groups 5 and 6 inhibit electron flow from photosystem I during photosynthesis. The plant cannot dissipate absorbed light energy. Ultimately, this leads to the buildup of toxic compounds that damage chloroplasts and result in cell membrane rupture. Herbicides in groups 5 and 7 exhibit foliar and soil activity. They can be applied to soil, after which plants take them up through their roots. Groups 5 and 7 herbicides then move with water through the xylem. Herbicides in Group 6 are contact herbicides with negligible movement within the plant and no soil activity.
Diagnostic keywords: interveinal chlorosis, leaf margin necrosis, leaf bronzing
Symptoms: Damage typically first appears on older leaves. Leaf margins become necrotic, and leaf veins become yellow (that is, chlorotic). See Figures 8–13.
Group 9 herbicide. EPSP synthase inhibitors (EPSP)
Example active ingredients: glyphosate (there are various labels)
Mode of action: Glyphosate is the only herbicide in Group 9. It inhibits a key enzyme (EPSP) in the biochemical pathway synthesizing the essential amino acids tryptophan, tyrosine and phenylalanine. This is a postemergence foliar-active herbicide that is highly mobile within the plant. Symptoms in blueberry occur one or two weeks after exposure. Symptoms are first observed as yellowing of the newest leaves. Occasionally, a whitish color is noted. Leaves may also assume a reddish color. New growth may exhibit shortened internodes and narrower leaves.
Diagnostic keywords: interveinal chlorosis, leaf margin necrosis, leaf bronzing
Symptoms: Typically, damage first appears on younger leaves. The leaf margins turn necrotic, and leaf veins yellow. See Figures 14–16.
Group 10 herbicide. Glutamine synthetase inhibitor (GS)
Example active ingredients: glufosinate (there are various labels)
Mode of action: Glufosinate is the only herbicide in Group 10. It inhibits the enzyme responsible for nitrogen assimilation. When this enzyme is inhibited, ammonia and other toxic compounds accumulate in plant cells. Cells are destroyed, and photosynthesis is inhibited. Glufosinate is a fast-acting herbicide with postemergence foliar activity. Its effect is typically limited to the tissue treated, although it can move with water through the xylem. Symptoms in blueberry will occur within one week of exposure.
Diagnostic keywords: chlorosis, wilting of leaf margins, rapid tissue necrosis
Symptoms: Damage can be observed within days of application. Chlorosis is the first visible symptom. The leaf margins may become necrotic within two weeks. See Figures 17–19.
Group 14 herbicides. Protoporphyrinogen oxidase inhibitors (PPO)
Example active ingredients: carfentrazone (Aim), flumioxazin (Chateau)
Mode of action: Group 14 herbicides block an enzyme in the chlorophyll and heme pathways leading to the accumulation of photosynthetic precursor molecules. When exposed to light, these precursor molecules promote the formation of free radicals that oxidize lipids and membranes. Cells rupture and plants die. Herbicides in this group can be postemergence, having only foliar activity, or pre- and postemergence, having both foliar and soil activity.
Diagnostic keywords: foliage browning, foliage wilting, necrosis
Symptoms: Damage typically appears within one day of treatment. Leaf margins become necrotic, and leaf veins become yellow (chlorotic). See Figures 20–22.
Group 22 herbicides. Photosystem I electron diverters (PSI)
Example active ingredients: paraquat (Gramoxone), diquat (Reglone)
Mode of action: Group 22 herbicides divert electrons from Photosystem I during photosynthesis and create reactive oxygen species. These reactive oxygen species are toxic and readily destroy cell membranes and organelles. These fast-acting herbicides produce visible symptoms within hours of application. They exhibit contact postemergence activity and are absorbed by plant leaves. They have minimal movement within the plant. Although they bind to soil clay particles, they do not move into the roots.
Diagnostic keywords: water-soaking, brown spotting, wilting, necrosis
Symptoms: Damage typically appears within hours of treatment. Damaged spots become necrotic. Symptoms are similar to damage resulting from Group 14 herbicides. See Figures 23–26.
Group 12 and 27 herbicides. Pigment synthesis inhibitors
Example active ingredients: mesotrione (Callisto), norflurazon (Solicam)
Mode of action: Group 12 and 27 herbicides block the synthesis of carotenoids. These pigments protect chlorophyll from light damage. Without carotenoids, chlorophyll damage exceeds the plant’s ability to repair itself, and all pigments are depleted. Plant tissue eventually dies. Group 12 and 27 herbicides control grass and broadleaf plant species and are absorbed by leaves and roots. Herbicides in these groups are systemic and have pre- and postemergence activity.
Diagnostic keywords: whitened leaves, bleached leaves, deformed leaves, vein discoloration, stunted growth
Symptoms: Damage typically appears on new growth. Bleaching is noticed within days of application. White leaves eventually become necrotic. See Figure 27.
Group 29 herbicides. Cellulose biosynthesis inhibitors (CBI)
Example active ingredients: dichlobenil (Casoron), indaziflam (Alion), isoxaben (Trellis)
Mode of action: Group 29 herbicides are preemergence herbicides. They inhibit cellulose formation, an essential component of cell walls. Growth is stunted. Although these are soil-applied herbicides, they can be absorbed through foliage and damage exposed tissue.
Diagnostic keywords: wrinkled foliage, distorted growth, bronzed leaves, leaf necrosis
Symptoms: Injury to foliage appears within days of treatment. Symptoms include malformed tissue, reddening of leaves, and necrosis. Localized damage is observed in foliar applications. Soil uptake will reduce root growth, stunt shoot growth, and pucker leaves. See Figures 28–33.
Group O herbicides. Unknown
Example of active ingredients: capric + caprylic acid (Suppress)
Mode of action: The mode of action of Group O herbicides is not well understood. They are known to damage cell membranes and lead to plant desiccation. These herbicides are absorbed by foliage and lack soil activity. They are classified as contact postemergence herbicides.
Diagnostic keywords: water-soaking, wilting, necrosis
Symptoms: Initial symptoms appear within minutes of treatment on hot, sunny days. The first observable symptoms are water-soaked leaves. Wilting follows. Necrosis is observed within 24 hours. See Figures 35 and 36.
Acknowledgment
This work was supported by the Oregon Blueberry Commission and Fall Creek Nursery.
Use pesticides safely!
- Wear protective clothing and safety devices as recommended on the label. Bathe or shower after each use.
- Read the pesticide label—even if you’ve used the pesticide before. Follow closely the instructions on the label (and any other directions you have).
- Be cautious when you apply pesticides. Know your legal responsibility as a pesticide applicator. You may be liable for injury or damage resulting from pesticide use.
