Americans spend literally billions of dollars annually keeping their lawns “healthy”—green, weed-free, and bug-free. But there’s an increasing body of evidence linking the lawn care products that fill the shelves at home improvement stores to serious health issues. Multiple studies have linked fungicide exposure to a significant increase in Parkinson’s disease among agricultural workers, and there is evidence that even low- level exposure to some common lawn chemicals may put preadolescent girls at risk for developing breast cancer later in life.
Epidemiological studies, however, are not proof. And proof is what biology professor Kate Susman and psychology professor Janet Gray are after. For several years now, Susman and Gray and their student researchers have been investigating the effects of ordinary lawn chemicals on the nervous system and behavior of a model organism called C. elegans, a transparent nematode about one millimeter long.
The first phase of the study involved a fungicide with an active ingredient called Mancozeb. Introduced for agricultural use in the United States in 1948, Mancozeb was for most of those years classified as nontoxic, and was widely available for residential as well as commercial use. More recently, Mancozeb has come under scrutiny from environmental groups and researchers. After a lengthy review, the U.S. Environmental Protection Agency recently reregistered Mancozeb, albeit with some labeling requirements for safe handling, but the State of California has labeled the compound a known carcinogen, and halfway through the first phase of Susman and Gray’s study, it was banned from sale in New York State.
“In our study last summer, our student researcher, Eunice Chou ’14, found that the dopamine neurons in the nematodes that had been exposed to the chemical seemed to go through neurodegeneration,” Susman says, “and dopamine is the neuron that gets damaged in Parkinson’s disease. Next fall, she is going to continue with phase two of that project and look at the mechanism by which these cells are damaged.”
How do you go about looking at the mechanism? “Essentially, we have to genetically dissect the pathway,” Susman says. “Right now, we suspect that the chemical gets into the cell via a transporter, which is sort of like a little turnstile. So, one thing we can do is purchase a mutant strain of C. elegans where the transporter is defective, and we can test that idea. And if that pans out, we go on to the next step—what happens once the chemical enters the cell?—and use the same kind of genetic process of elimination.”
A third phase of the study is looking at so-called “green” chemicals to assess their effects on C. elegans. “These are the ones that say, ‘safe for organic gardening’ on the label, so if you’re in the store, and you see that on the label, you assume that it will be safe for you and your kids and your pets and your water supply, right?”
Susman explains that previous pesticides, including many still in use by agribusiness, block an essential enzyme in the neuromuscular junction. “This nerve-muscle system is very precise and evolutionarily common. It’s found in mammals, amphibians, reptiles, fish, and insects—pretty much all animals,” Susman says. Basically, the way the nerve-muscle system works is that when the nerve is stimulated, a neurotransmitter activates the muscle, and then the enzyme breaks down the neurotransmitter, which helps shut off the muscle. “Without this enzyme, we would have seizures, or we would be paralyzed,” she says.
This is exactly what happens to the targeted insects. They die of paralysis. Unfortunately, non-targeted insects are also affected—honeybees, for example, which play a crucial role in our agricultural system. And this enzyme blocker turns out to be toxic to fish, amphibians, and mammals as well.
“So, the chemical companies shifted their focus to the receptor molecules in the neuromuscular junction. We all have these receptors, but they’re slightly different from insects to fish to amphibians to mammals,” Susman says. “So, if the drug can target an area of the receptor molecule that’s found in insects but not in people or mammals or fish, then it would be a better, safer drug. The problem is that we all do have a version of this receptor, and how selective is this drug? And you still have the problem of the bees because they’re going to respond to this new insecticide the same way that other insects respond.”
Susman and her student researchers are looking at one of these new pesticides—Bug-B-Gon, a Scotts product that purports to kill over 100 different types of lawn insects. “This is supposed to be much less harmful to honeybees and people and pets than the previous pesticides,” Susman says. Two students in her lab, Casey Rice ’13 and J.R. Ko ’14, began preliminary investigations on Bug-B-Gon during the academic year, and Tushar Agarwal ’14 is continuing the research this summer as an Undergraduate Research Summer Institute (URSI) Fellow.
“J.R. and Casey looked at low-dose exposure and moderate-dose exposure, and they found some effects in terms of development and locomotion,” Agarwal says. “So, what I am doing this summer is looking at high-dose exposure, and my first finding was that the chemical appears to affect egg laying.” Using a wild-type nematode, Agarwal found that the nematodes grown in the pesticide produced significantly fewer eggs than the nematodes grown under normal conditions. He is now working on replicating that finding using a larger number of subjects.
“I’m also looking at locomotion,” Agarwal says. “So, the normal nematodes move forward, and if they encounter something predatory, they do a quick reverse and then turn and go in a different direction. But the exposed nematodes curl up and stay in that position for a while and then turn, so there’s obviously something wrong.” Agarwal is looking at the nematodes’ motor neurons using a confocal microscope to ascertain whether the neurons are deformed or different from those in the normal nematodes.
Agarwal and Susman are aiming for publication in the fall. “But there’s still a lot of work to do,” Agarwal says. “I need a lot more data, so I have to increase the sample size. I can’t just go to the scientific community with one Petri dish and say, ‘Look what I found.’”
If the research pans out, the implications are huge. “The neuromuscular receptor in C. elegans is different from the neuromuscular receptor in insects,” Susman says. “If this chemical affects the nematode receptor, chances are it’s more general than they thought, and at certain levels, and over time, it’s going to be affecting mammals, fish, and everything else.”
—Julia Van Develder
Photos (c) Vassar College-Buck Lewis