Recognition of Weed-Killer Injury to Trees

Signs of Injury

“Sensitivity should not be confused with pronounced distortion after sufficient exposure, since some plants eventually respond and may even exhibit dying or damaged tissue at sustained 2,4-D levels lower than those which appreciably affect tomatoes or roses.” (Sherwood, et al, 1970).

The more common expressions of herbicide injury include parallel leaf venation on normally netveined leaves, cupped leaves, chlorosis, nastic growth, and wavy or curled leaf margins. Grape and redbud are known to be good indicator species and exhibit these common signs of herbicide injury. Other signs are not so obvious.

Purple stem coloration may indicate herbicidal root inhibition. Whether absorbed through the leaves or the roots, 2,4-D and other phenoxys can restrict root development. Sugars produced in the leaves then build up in the stem, causing a purple coloration. This herbicide-induced sign has been observed on pin oak, hard maple, ash, and walnut wood generally less than four years old.

Tough, leathery, or weather-beaten leaves also indicate phenoxy injury (Sherwood, et al, 1970). Hard maple exhibits a pebbled leaf; pin oak retains its normal shape but becomes quite leathery. Sherwood also cites enlarged bud size and more obvious lenticels on stems as signs of 2,4-D injury.

Loss of apical growth is typial of phenoxy herbicide injury. This sign has been observed on hard maple, boxelder, hackberry, redbud, walnut, ash, cherry, poplar, willow, and birch. Affected trees suffer a gradual crown dieback, leading to eventual tree mortality. This may be related to winter injury, in that chemical exposure reduces winter hardiness. With winter-weakened buds, trees tend to leaf out later to coincide with peak herbicide conditions the following spring, increasing the likelihood of repeated herbicide drift injury (Hibbs, 1976). Concomitant with the loss of apical growth is restricted lateral leaf development (Phipps, 1963). Sherwood, et al, (1970) reported fewer normal leaves, flowers, and fruits produced by plants exposed to 2,4-D drift. The resultant “thin crown” characteristic typifies hackberry response to phenoxy herbicides.

Leaf scorch can indicate chemical injury, particularly in instances of gross exposure. Ash, cherry, and cottonwood have exhibited scorched leaves without expressing more common signs of herbicide injury.

Weed-killers also cause stem lesions and bark abnormalities. Otta (1974) reported bark abnormalities of Siberian elm at 2,4-D exposure levels of 25 ppm, with injury persisting one year after treatment. Walnut, poplar, and Russian olive will show 2 mm to 5 mm stem splits on wood less than 3 years old. Black lesions of this size occur on the mid-vein of walnut leaves exposed to 2,4-D. Hard maple and cottonwood injected with phenoxy herbicides develop abnormal callous tissue at the point of injury.

Though evergreens are somewhat resistant to phenoxy herbicide injury, instances of such injury have been suspected. Fir occasionally exhibits curled leader growth, “burned” needle tips, and needle cast. Spruce will show a loss of terminal growth and needle cast. Pine is most susceptible during the May to June period of active growth, and will exhibit nastic growth of the candles if exposed to phenoxy herbicides.

Discussion

Signs of chemical injury should not be confused with other plant deficiencies related to site conditions, nutrient availability, or the presence of insects and diseases. Careful examination is necessary prior to attributing injury to any one causal agent. It is also possible that a primary causal agent has been disguised by invasion of secondary pathogens. Pimentel (1976) found corn leaf aphids, European corn borers, and southern corn leaf blight more abundant on corn exposed to 2,4-D than they were on unexposed corn.

Expression of herbicide injury need not be restricted to the exact time of exposure, nor even to the same year of exposure. Data from Otta and Sherwood indicate recurring signs of 2,4-D injury for 6 months to 2 years following exposure. Klepper (1974) found that phenoxy herbicides interfere with plant nitrite reduction. This supports the conclusion that signs of injury can occur after the herbicide has dissipated. If the injured plant is unable to reduce nitrite, then the effects of repeated exposures become cumulative, eventually leading to plant toxicity.

Chemical injury symptoms are most evident in June, subsequent to the time of maximum weed-killer usage. Trees situated near agriculturally active lands, railroad rights-of-way, roadside ditches, or fence rows receiving shrub control materials are particularly subject to chemical injury. Foliage browning and abnormal plant growth in these areas can indicate the likelihood of plant injury on adjacent lands. Noticeable chemical odors followed by plant maladies can also be indicative of herbicide pollution.

When attempting to assess the cause of injury to plants, rapid and simplistic diagnoses should be avoided. All possibilities must be considered. With chemical injury, two or more signs are frequently present. Knowledge of these signs coupled with inspection of known sensitive plants (grape, boxelder or redbud) can confirm the presence of weed-killer injury.