What Do Suburban Lawns and the Vietnam War Have in Common?

Answer: The herbicide 2,4-D.

You may be familiar with this herbicide as an active ingredient in “Weed ‘n Feed®”, “Weed B Gon MAX®”, Turf Builder® With Weed Control”, etc..

During the Vietnam War, it was an active ingredient in Agent Orange.

On lawns it’s used to kill the dandelions, but NOT the grass. (Find out how it does this below).

In the Vietnam War the U.S. military used it to defoliate the trees (so that they could more easily spot the Viet Cong). It was also used to kill crops that would potentially provide the North Vietnamese troops with a food source. (see comment below)

You’re likely familiar with the term “Agent Orange” because of the controversy regarding the tragic health problems it caused to U. S. soldiers. (For current info re. this issue see here).

The serious health issues to both Americans and Vietnamese caused by Agent Orange are due to contaminants called dioxins produced during its chemical synthesis. (For more info on this see 2,4-D and dioxins and also here.)

But since this post is about how such herbicides work on the plants, let’s leave dioxin issues aside (for now).

Herbicides Such as 2,4-D are Auxins

Auxin in perhaps the most well-known plant hormone. (I’ve previously discussed auxin in this blog here.)

The herbicide 2,4-D is a synthetic auxin first produced in the 1940’s. It is one of many so-called phenoxy herbicides. These herbicides all are both structural and functional analogs of the natural auxin indole-3-acetic acid (IAA). That is, these synthetic auxins not only are structurally similar to IAA, but they are also biologically active as auxins in plants.

Although they both look and act like auxins, plants can not metabolize these phenoxy herbicides as they can with IAA, the natural auxin.

This turns out to be the key to why phenoxy herbicides such as 2,4 D are able to kill some plants.

How Does 2,4-D Kill Dandelions…?

Auxin-based herbicides are referred to as “selective” herbicides because they kill so-called “broadleaf” plants (a.k.a., dicots) but not grasses, for example. (Hence, that’s why they’re such popular herbicides with both growers of lawns as well as of wheatfields.)

But how exactly does spraying 2,4-D on susceptible plants kill them?

This turns out to be very poorly understood, and it’s also the subject of much misinformation. For example, I’ve heard people say that such herbicides “grow the plant to death” and read that 2,4-D “…simply confuses the plant to death”. Huh?

At the present time nobody really knows precisely how the auxin-like herbicides kill susceptible plants. As with most effects of plant hormones, it probably has a lot to do with the plant species in question.

However, recent findings have provided important clues. And these clues support the idea that plant death may occur as a result of a combination of factors.

Here’s a summary of the story:

First off, one of the well-know effects of excess amounts of auxin on dicots is to cause them to overproduce the plant hormone ethylene. For example, in 1969, Mary Hallaway and Daphne J. Osborne first showed that ethylene is a factor in defoliation caused by 2,4-D.

Because plants can’t break down 2,4-D, it’s action persists. This action includes the excess production of ethylene, which may result in a number of plant responses, including epinasty and senescence.

Another effect of excess ethylene production in response to 2,4-D is to stimulate the production of yet another plant hormone, abscisic acid (ABA). The effects of ABA on the plant may contribute to eventual plant death. (For an illustration of the complex effects of auxin-based herbicides on plants, see Figure 1 in the reference listed below.)

…and why doesn’t 2,4, D Kill the Grass? (and You?)

Perhaps the simplest explanation for both questions has to do with sensitivity to the plant hormone auxin.

In general, grasses are much less sensitive to synthetic auxin herbicides than are dicots. That is, a much higher threshold level of auxin-based herbicide is required to elicit physiological responses in grasses versus the so-called “broadleaf” plants. So, at the doses used to kill dandelions, for example, grasses are largely unaffected. (Higher doses of 2,4-D may kill the grass, too, however.) Grasses may be more resistant to such herbicides because of differences in leaf morphology, translocation of the herbicide inside the plant, and the ability to metabolize (breakdown) synthetic auxins.

Aside from the toxic contaminant dioxin, 2,4-D has no physiological effects on animals at hormonal levels, that is, at the concentrations that affect plants. (Indeed, there is no reputable evidence that any of the five main plant hormones affects animals.)

Reference

Grossmann, K. (2007) “Auxin Herbicide Action: Lifting the Veil Step by Step”, Plant Signaling & Behavior 2:421-423. (PDF)

Bottom Line: The herbicide 2,4-D mimics the plant hormone auxin and sets off a complex series of events – involving two other plant hormones – that eventually lead to the death of susceptible plants. At hormonal levels, auxins affect plants but not people.

Next-Time: More on Herbicides (Is Roundup® Losing Its Punch?)

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