Study Links Widely Used Pesticides to Antibiotic Resistance
Glyphosate, 2,4-D, and dicamba found to affect bacteria in ways that could promote resistance to common antibiotics.
This has not been a good week for glyphosate,
the active ingredient in Roundup and
other herbicides. On Friday, the World Health Organization (WHO) announced that
it had classified glyphosate, the United States’ most
widely-used pesticide, as “probably carcinogenic
to humans.”
Now, the chemical has another strike against it. A study published
today by theAmerican Society of Microbiology’s journal mBio has linked glyphosate and two other widely-used herbicides–2,4-D ( ~50% of Agent Orange) and dicamba–
This study found that exposure to these herbicides in their commercial
forms changed the way bacteria responded to a number of antibiotics,
including ampicillin,ciproflox
Dicamba, 2,4-D, and glyphosate have been in use for decades, so why have
their antibacterial-resistance effects not been documented before? As
the study’s lead author, Jack
Heinemann, professor of genetics at the University of Canterbury in
New Zealand, explains, when pesticides are tested for adverse effects,
“it’s the lethal toxicity that people focus on.” In other words, how
much of the chemical will kill an organism.
“What makes our study different, is that it is looking at a sub-lethal
effect,” says Heinemann. “The effect we see requires that the bacteria
stay alive.”
Previous studies done by other researchers have found that substances
chemically similar to dicamba and 2,4-D can cause antibiotic resistance,
Heinemann explains. So he and his colleagues decided to investigate
whether these herbicides would produce similar
effects. They added glyphosate to the study because it is chemically
unlike the other two. But, to their surprise, it also produced some
antibiotic resistance.
Heinemann explains that because these herbicides are not “supertoxic” to the bacteria the study tested–E.
coli and Salmonella–they
are not killed outright at levels typically used to kill weeds.
Instead, the bacteria stay alive while activating proteins known asefflux
pumps in order to rid themselves of toxins. And this defense
mechanism can make the bacteria develop resistance to the threat from
which it is defending itself.
Scientists know that overuse
of antibiotics in humans can decrease their effectiveness. In the same way, says Heinemann, “exposure to these pesticides make the pathogens stronger.”
Although this study only looked at two laboratory strains of human
pathogens, the antibiotics examined represent what he calls “broad
classes” of drugs we’ve come to depend on to fight infections and the
herbicides are three of the most-used
worldwide.
Heinemann also notes that the different pesticides produced a variety of
responses. While all three produced an antibacterial-resistant response
to some of the antibiotics, some of the combinations his team tested
produced no response and some increasedthe
antibiotic’s effect.
Although the study is likely to be seen as controversial by some,
University of Massachusetts Dartmouth assistant professor of biology,
Dr. Mark Silby says it “followed established protocols” and the existing
scientific literature supports its findings.
“This is a very carefully-designed study,” says Dr. Michael Hansen, a
senior staff scientist at Consumers Union. “It’s incredibly important
work showing the complexity of an effect that hadn’t been thought about
before.” The mechanisms by which the bacteria
respond to toxics–in this case herbicides–are already well-known,
Hansen explains. What’s new and important is looking at non-lethal
levels of exposure in combination with the antibiotics.
The weed-killers used in the study were purchased
at a local store and were used at levels specified in use
directions, which means the scientists were testing chemicals actually
in use worldwide rather than a special laboratory sample of the active
compound.
How could any of this affect people?
“These herbicides are now used at such a scale that we can almost use
the term ubiquitous,” says Heinemann. For one, glyphosate is used on about
94 percent of the soybeans and 89 percent of the corn grown
in the U.S, while 2,4-D is the third-most
widely used herbicide in the U.S., while dicamba ranks fifth
in use worldwide.
The levels at which the researchers saw effects were higher than the
residues allowed on food, but below what is often used in rural
settings, says Heinemann.
The results of Heinemann’s study suggest there is probably a small
chance that exposure through food would produce these effects, but they
could be a concern in areas where the pesticides are being applied, says
Hansen. Thus, the people most likely to be affected
are farmers, farmworkers, and other people who live in agricultural
communities.
Also to consider is the approval earlier this year of a
new pesticide that combines glyphosate and 2,4-D and soybean
and cotton seeds genetically
engineered to resist dicamba, all of which are expected to increase use of these pesticides.
Pesticide-induced antibiotic resistance could also affect honeybees since many commercial hives are now being treated
with antibiotics. It’s possible, Heinemann says, that “comingling
of antibiotics and herbicides could be compromising the effectiveness of
those antibiotics,” and thus honeybee health.
Meanwhile, Monsanto says
it disagrees with WHO’s announcement on glyphosate. “All labeled uses
of glyphosate are safe for human health and supported by one of the most
extensive worldwide human health databases ever compiled on an
agricultural product,” the company says in a statement
on its website.
Neither Monsanto nor other pesticide manufacturers have had the opportunity to respond to the new mBio study. But the Council for Biotechnology Information said
on its website “GMO Answers” last month, that glyphosate had once
been considered for use as an antibiotic but that “levels needed to kill
microbes are relatively high, and resistance can develop readily.” In
other words, the phenomenon Heinemann and colleagues
observed is not entirely unexpected.
“A jigsaw puzzle is a good metaphor,” for how these effects fit together, says the scientist.
The next steps in this research will be to test additional bacteria and
pure samples of the pesticides. But for now, it’s clear that “further
work is needed,” says Hansen. “This is something we need to look at as
we expand the use of these herbicides.”
