The pesticides in question are called Neonicotinoids, since they are derived from nicotine (used as a pesticide since the 1700′s). “Neonics” are systemic insecticides, or insecticides that are taken up by a plant’s tissues and circulate within the plant. This makes these pesticides a highly effective and relatively safe insect control method, since only insects that eat the plant will be affected. It also is sometimes the only way to kill insects inside a plant; an insect boring into a tree, for example, can’t be sprayed directly.
Neonicotinoid pesticides can also be applied as a root drench or a seed treatment, so there is no pesticide sprayed into the air, or landing where it should not go. Farmers love neonicotinoids, since they not only reduce “off-target” effects, they last a really long time–usually one application can last for months, and sometimes over a year. That saves a lot of money.
Carl Zimmer’s excellent New York Times summary of the research on bees and pesticides is a must read: Bees’ decline linked to pesticides.
“In Thursday’s issue of the journal Science, two teams of researchers published studies suggesting that low levels of a common pesticide can have significant effects on bee colonies. One experiment, conducted by French researchers, indicates that the chemicals fog honeybee brains, making it harder for them to find their way home. The other study, by scientists in Britain, suggests that they keep bumblebees from supplying their hives with enough food to produce new queens….The authors of both studies contend that their results raise serious questions about the use of the pesticides, known as neonicotinoids.”
Carl (I shook his hand once, so I can call him Carl, right?) does a great job of showing how the scientific community is still resolving how all this research adds up. In a post on his blog providing supplimental information to the NYTimes story above, Carl discusses the difficulty of making sense of all this information:
I found this story to be especially challenging to sum up in a single nut graph. To begin with, these experiments came after many years of previous experiments and surveys, which often provide conflicting pictures of what’s going on with insecticides and bees. The experiments themselves were not–could not–be perfect replicas of reality, and so I needed to talk to other scientists about how narrow that margin was. As they should, the scientists probed deep, pointing out flaws and ambiguity–in many cases even as they praised the research.
At the same time, these two papers did not appear in a vacuum. Other scientists have recently published studies (or have papers in review at other journals) that offer clues of their own to other factors that may be at work. And, biology being the godawful mess that it is, it seems that these factors work together, rather than in isolation.
If Carl Zimmer–an exceptional science journalist with access to the actual scientists that are doing the research–is having trouble trying to create a coherent picture of the information about these pesticides, I KNOW that the rest of us regular schmoes are struggling too.
Here is the important thing to remember as you process this new bee research: CCD, or colony collapse disorder in honeybees, does not have a single cause. It’s likely that many different factors work together to create CCD. It is a complex set of specific symptoms, and it’s been known since around 1900 by many other names. Additionally, not all observed bee declines (and deaths) are CCD. It’s hard out there for a bee.
There is clearly a pesticide problem with bees–even if we can’t fully quantify it right now. The Xerces Society white paper, A Review of Research into the Effects of Neonicotinoid Insecticides on Bees, with Recommendations for Action, had this to say about CCD:
“There is no direct link demonstrated between neonicotinoids and the honeybee bee syndrome known as Colony Collapse Disorder. However, recent research suggests that nenonicotinoids may make honey bees more susceptible to parasites and pathogens….which has been implicated as one causitive factor for CCD.”
The Xerces paper is probably the best review of the recent research that you are going to find. Not only is it written by Xerces scientists, who are folks what really know their bees, it also was reviewed by several other bee researchers I have a great deal of respect for.
Xerces thoroughly documents what we know about these pesticides and bees–and, unfortunately, we don’t know nearly enough. Most of the published research focuses on honey bees, rather than the native bee species in the US. (Honey bees are an introduced species in North America). That means we don’t have much data to work with to figure out how different bee species will be affected.
Personally, I found the most disturbing piece of the Xerces report to be their discovery of how many of these neonicotinoid insecticides are available over the counter to homeowners. Calculating pesticide application rates is one of the toughest parts of farming (or pesticide applicator exams), and Xerces does the math to uncover some startling facts:
- “Products approved for homeowners to use in gardens, lawns, and on ornamental trees have manufacturer-recommended application rates up to 120 times higher than rates approved for agricultural crops.
- Many neonicotinoid pesticides that are sold to homeowners for use on lawns and gardens do not have any mention of the risks of these products to bees, and the label guidance for products used in agriculture is not always clear or consistent.
- Neonicotinoids can persist in soil for months or years after a single application. Measurable amounts of residues were found in woody plants up to six years after application.”
That is really scary.
Xerces raises some very important questions about what this means for our native bees that are already struggling with habitat loss and a spill-over of parasites and pathogens from introduced bee species. Butterflies, beetles, and flies also drink nectar and feed on pollen–pretty much any of our pollinators, including hummingbirds, could be affected if they feed on trees and plants treated with these insecticides.
I hope that new labeling is introduced so consumers know that these products have the potential to kill bees and other pollinators. Unfortunately, because these pesticides are so very useful in agriculture, there are no easy answers. The things that make these compounds so very well suited for so many purposes–their ability to remain stable for a long time and spread through plant tissues–are also why they pose dangers for pollinating insects.
- The Xerces White Paper on Bees and Neonicotinoid pesticides
- Carl Zimmer’s NYT article on Bees and Neonicotinoid pesticides
- Xerces guide to promoting native bees; tons of free information to download!
- Take a short training course on creating bee-friendly habitat!
I discovered that bed bug evolution–specifically resistance to pesticides–was also the subject of the National Evolutionary Synthesis Center‘s podcast this month. A FASCINATING interview with one of the grand old men of evolutionary genetics, James Crow. He worked on DDT resistance back in the late 40s and 50s.
“Like pyrethrums, DDT kills insects by acting on the sodium pores in their nerve cells — and it just so happens that many of the same mutations that protect an insect against DDT also happen to protect it from pyrethrums. When DDT was first introduced, such mutations were probably extremely rare. However, with the widespread use of DDT in the 1950s and 60s, such mutations became much more common among bed bugs through the process of natural selection. Though DDT is rarely used today because of its environmental effects, these mutations have stuck around and are still present in modern bed bug populations. Because of the action of natural selection in the past (favoring resistance to DDT), many bed bug populations today are primed with the right sort of genetic variation to evolve resistance to pyrethrums rapidly.”
Since I mentioned bedbugs recently, I thought I would also cover this paper:
Kyong Sup Yoon, Deok Ho Kwon, Joseph P. Strycharz, Craig S. Hollingsworth, Si Hyeock Lee, J. Marshall Clark (2008). Biochemical and Molecular Analysis of Deltamethrin Resistance in the Common Bed Bug (Hemiptera: Cimicidae) Journal of Medical Entomology, 45 (6), 1092-1101 DOI: 10.1603/0022-2585(2008)45[1092:BAMAOD]2.0.CO;2
One of the biggest issues in bed bug control right now is the development of resistance to insecticides. In fact, the New York City population of bedbugs used in this study was 264-fold more resistant to 1% deltapermethrin compared with a population collected in Florida!
To put it another way: the Florida bed bugs were killed in 19 minutes; the New York bedbugs took 5,048 minutes, or over 3.5 days, to die. Uh Oh.
The research paper itself is a rather technical evaluation of just how and where, in terms of molecular biology, the mutation that makes the bed bugs resistant occurs. Interestingly, it’s kdr resistance once again! (kdr stands for “Knock-Down Resistance.”)
I’ve mentioned kdr mutations several times here at the Bug Blog in discussions about DDT. Basically, most insecticides act as a nerve poison for insects. Insecticides block ion flow (alternate animation) across a nerve membrane by attacking sodium channels. If the nerve can’t depolarize, the cell (and animal) is effectively paralyzed.
Kdr mutations are usually point mutations — a tiny change in one amino acid in a giant string of DNA. It makes just enough of a change to make the bugs resistant.
Kdr mutations are also problematic because they often make a bug resistant to more than one insecticide. This means that an already difficult to control insect just got a lot harder to kill, since your tools (insecticides) wear out faster.
The conclusion of the paper:
“This evidence suggests that the two mutations are likely the major resistance-causing mutations in the deltamethrin-resistant NY-BB through a knockdown-type nerve insensitivity mechanism.”
“Because DDT has been used indiscriminately to control many insect pest species including bed bug, the widespread and frequent use of DDT is likely to have predisposed bed bug populations to pyrethroid resistance through the neuronal insensitivity mechanism.“
So, what does this new information tell us?
- DDT will be utterly useless against bed bugs, so people should stop asking for it.
- We’re going to need a lot more research on ways to kill bedbugs other than just poisoning them with the usual pesticide suspects.
- In cities where there are active bed bug populations, insecticide choice for resistance management will be very important in urban entomology.
- Bedbugs are not going to go away, and you should probably be getting a little paranoid.
If, you know, you weren’t already paranoid when you read stuff like this. What a nightmare.
I saw this beautiful ad–full size here–and while the art work is lovely, I’m really puzzled. Are they advertising a product to kill moths in your closets and on clothes?
The ad agency is from Bucharest, Romania, so I’m not sure if this is meant to run in the US or not. The Raid website does not list any products for clothes moths. (SC Johnson is the parent company for Raid, BTW.)
I have to mention that spraying as shown in this illustration, however lovely, is a terrible idea. I’d suggest using clothes moth pheromone traps, and then laundering/freezing the clothes when an infestation is detected.
There are some additional versions of the ad:
Is it bad that I think these would make awesome tattoos?
Hanna at This Garden is Illegal recently reviewed a product called the Mosquito 86:
“As was pitched by the representative of the company, the Mosquito 86 is “a new, innovative way to eliminate mosquitoes in a manner that has previously only been offered through professional mosquito and pest sprayers that use commercial sized foggers or truck-mounted systems.”
I.E. It is commercial grade pesticide.”
First, I want to know why I’m not getting cool free stuff to review! *pouts*
Second, I have to say that this product sounds suspiciously like a portable version of this mosquito mister. It uses a low mist of permethrin. I don’t have a problem with the pesticide itself (it’s safe in low amounts), but this method seems to have some of the same problems as the misters. Primarily, Non-target impacts. It kills everything around, not just mosquitoes.
So bees, butterflies, parasitic and predatory insects, etc. would be killed along with whatever mosquitoes were in the area. If the spray/fog is applied just in the yard, when mosquitoes are present, I can live with that.
I suspect, though, that it will be used prophylactically, and that will lead not only to non-target effects, but increased potential for insecticide resistance. And not just resistance in mosquitoes, but all the pest insects exposed.
It is really a pain to not be able to frolic outdoors without dealing with mosquitoes.
But personally, I’d either stick with DEET, take steps to prevent mosquitoes, or invest in one of these devices for large area control. At least you are only killing the animal you mean to kill.
I’d rather be in my screened-in porch, or wearing my non-stylish mosquito repellent clothing, than have a barren landscape.
- ACMA statement on mosquito misters
- Mosquito prevention
- Mosquito repellent clothing: does it work?
- What’s the best way to repel mosquitoes?
Also, don’t miss Hanna’s awesome tomato tasting posts!