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Piperonyl Butoxide: The Trojan Horse of Pesticides

by Bill Chameides | July 11th, 2011
posted by Erica Rowell (Editor)

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More than 80,000 chemicals are produced, used, and present in the United States. This is one of their stories.

When it comes to pesticides, it’s not just the pesticides you should be concerned about.

Our subject today is a common ingredient in insecticides: piperonyl butoxide, affectionately known as PBO. Interestingly, it comes from some of the same stuff we used to make root beer out of. Also interestingly, it does not actually kill bugs.

The Chemical Marketplace
A series that looks at chemicals in everyday consumer products
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     Dioxin and eggs »
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     Fluoride and water »
     Formaldehyde and no-iron shirts
     Insect repellents »
     Nanoparticles and food »
     PAH and seal coats: A no-brainer »
     PBDE and fire retardants »
     PFOA and popcorn »
     Pesticides and PBO
     Propoxur and bedbugs »
     Rotenone, a pesticide »
     Spray foams, sealants, diisocyanates »
     TDCPP and the air »
     Triclosan and toothpaste »
     Trihalomethanes (THM) and
showering »

PBO [pdf] is a colorless, sometimes yellowish, oily combustible liquid, first synthesized in the late 1940s. It’s typically derived from sassafras oil (also called safrole), formerly a key ingredient in root beer. (Safrole was banned for food and drug use in 1960 when it was linked to cancer in animals. Today root beer is generally made with artificial sassafras or sassafras extracts that do not contain the oil.)

PBO’s primary commercial use is as an additive to insecticides such as prytheroids — insecticides that dominate the home market and are used to kill everything from cockroaches to bedbugs and are even used as a bug repellent in impregnated clothing. Suffice it to say, these prytheroids are not without their own risks to the health of folks who come into contact with them. But it could turn out the PBO may be far more dangerous than the prytheroids and it isn’t even an insecticide.

If PBO Doesn’t Kill Bugs, Why Is It Used in Insecticides?

PBO acts as a synergist, meaning it makes the killing ingredients in insecticides more effective. Think of a battlefield with attacks and counterattacks and you begin to get the picture. With insecticides on one side and bugs on the other, the insecticide charges with the goal of decimating its opposition. But the insects have their own natural defenses — they can produce enzymes that block the insecticide’s toxicity, thus sending the attacking brigade into retreat. PBOs are the insecticide’s reinforcements, a veritable counter-defense against the insects’ defense. How? By blocking the bugs’ ability to form those enzymes. In short, with PBOs the poor little buggers are rendered defenseless.

Our yellow, oily liquid born of sassafras must be doing a really great job of disarming insects because it’s now used in a panoply of insecticides. As of 2006, it was registered as an active ingredient in more than 1,500 products [pdf] for use in a variety of settings (from agricultural and commercial to industrial to residential) for public health reasons (e.g., mosquito abatement).

If PBO Doesn’t Kill Bugs, No Prob for Us, Right? Maybe Not.

Because PBO is added to a host of home insecticides, it’s almost certain that people are exposed to the stuff. Is that a problem? A study published in February in the journal Pediatrics by Megan Horton of Columbia University and colleagues suggests it very well could be, at least for prenatals.

Horton and her colleagues measured PBO (and the insecticide permethrin) in personal air samples collected in low-income homes in New York City. They followed a cohort of pregnant mothers and their newborns through their first 36 months. At the end of this period, they tested the children for cognitive and psychomotor development.

The authors found a significant association between PBO concentrations and delayed cognitive development at 36 months similar to problems posed by other prenatal neurotoxicants such as lead. (Little or no association was found for permethrin.*) Given that PBO is thought to have low systemic toxicity for people, the authors speculated that the developmental effects were caused by inhibiting enzyme activity in the prenatal and neo-natal children thereby limiting their bodies’ natural ability to breakdown other toxic compounds they were exposed to. Irony of ironies, if true, it means that PBOs are doing in children exactly what they’re doing in bugs.

However, that’s just speculation and it runs counter to a 2006 assessment by the Environmental Protection Agency which implied this wasn’t a concern: “enzyme inhibition in mammals [based on small mammal studies] is transient and occurs at high doses.” That same EPA assessment also noted
, however, that “the kinetics of PBO inhibition and/or stimulation of … enzymes in humans … [had] not been established.”

Of the entire Horton study, the National Pest Management Association notes that it is preliminary [pdf] — an appropriate characterization I think. The trade group recommends that concerned consumers should consult with “a qualified and licensed pest professional to discuss these concerns as well as the proactive and preventative measures they can take to minimize risks, including risks posed by pests.”

Yeah, I guess that’s one thing you could do. You might also look for products without PBO, products that may be increasingly easier to find. Over the last couple of years a number of PBO pesticide formulations have already been voluntarily canceled (though not necessarily because of PBO).

PBO or not, you can rest assured that the human-bug battle will continue as we keep developing new pesticides to zap bugs that continue to evolve new defense mechanisms. But, as is the case in most battles, you’d better beware of friendly fire — you could be among the casualties of the pesticide barrage.


End Note

* Horton et al note that a lack of association for permethrins may in part reflect the difficulty in measuring them. They are not volatile and so are difficult to track in personal air samples and they breakdown quickly in our bodies often to nonspecific metabolites and so are difficult to track there as well.

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