Risk analysis needed before spraying permethrin

Contributed by one of Dontsprayme’s consulting scientists, in response to spraying activity this summer

I am concerned about the recent decision to spray in an area of Chester County for West Nile carrying mosquitoes, considering what is currently known about permethrin, the availability of less toxic alternatives and methods for mosquito control, and the demonstrated resistance of mosquito populations to this pesticide. Even if there are some West Nile positive mosquitoes in the vicinity, has a risk analysis been done to see that the perceived benefits of spraying outweigh the long term risk to human health?

While permethrin was studied at length in 1994 by the US Army and found to be relatively safe, this early study should be taken in context: more American soldiers have died from insect-borne illness than of enemy fire. For troops deploying to tropical areas, and who have already willingly put their lives on the line for our country, permethrin is the lesser of two evils. Since the 1994 study, there has been a great deal of research into the toxicity of permethrin, and the picture grows more and more grim with the passing years. Work that supports the use of permethrin, such as the EPA’s cumulative risk assessment (2011)[1], is very thorough at the surface, but consider limited endpoints: specifically, those derived from the a priori known ways in which pyrethrins and pyrethroids disrupt neural function.

As complete as the EPA study seems to be, its flaw is in its failure to consider other endpoints besides neural function. A recent review article[2] identified 29 studies in which permethrin-induced toxicity was identified in various species (and cited a number of other studies where human toxicity was shown). It also goes into far more detail than the Army study about the mechanisms of toxicity in the various bodily systems.

From the article:

Although it was believed that PER showed low mammalian toxicity, an increasing number of studies have shown that PER can also cause a variety of toxicities in animals and humans, such as neurotoxicity (Carloni et al., 2012, 2013; Falcioni et al., 2010; Gabbianelli et al., 2009b; Nasuti et al., 2014, 2008, 2007b), immunotoxicity (Gabbianelli et al., 2009a; Jin et al., 2010; Olgun and Misra, 2006), cardiotoxicity (Vadhana et al., 2010, 2011a, 2011b, 2013), hepatotoxicity (Gabbianelli et al., 2004, 2013), reproductive (Issam et al., 2011), genotoxic (Turkez and Aydin, 2012, 2013; Turkez and Togar, 2011; Turkez et al., 2012), and haematotoxic (Nasuti et al., 2003) effects, digestive system toxicity (Mahmoud et al., 2012; Sellami et al., 2014b, 2015), anti-androgenic activity (Christen et al., 2014; Xu et al., 2008), fetotoxicity (Erkmen, 2015), and cytotoxicity (Hu et al., 2010) in vertebrates and invertebrates.

Additionally (Vadhana et al., 2013):

Early life environmental exposure to PER could play a critical role in the onset of age-related diseases (Carloni et al., 2012, 2013; Fedeli et al., 2013; Gabbianelli et al., 2013; Vadhana et al., 2011b). Previous findings demonstrate that early life pesticide exposure to low doses of the PER insecticide has long-term consequences leading to toxic effects such as cardiac hypotrophy, increased Ca2 ©≠ level and increased Nrf2 gene expression….

In fact, there is evidence that effects of this nature are transgenerational and that there are epigenetic changes that ensue due to exposure. What’s clear is that the pesticide research community has NOT signed off on the harmlessness of such pesticides to humans despite the EPA guidelines or material safety data sheets. 

In addition its toxicity, it’s also fairly clear that mosquitoes evolve resistance to permethrin and other pesticides relatively rapidly. From Ramkumar et al (2015), after exposure to permethrin, within 10 generations, the 50% lethal dose concentration (LC50) of permethrin increased 17-fold. 

Ramkumar, G., & Shivakumar, M. S. (2015). Laboratory development of permethrin resistance and cross-resistance pattern of Culex quinquefasciatus to other insecticides. Parasitology Research, 114(7), 2553–2560.

Research on West Nile carrying mosquitoes indicates that when field collected mosquitos were tested for pesticide resistance, in one case there was a 299-fold increase in dosage to reach the LC50.

Kasai, S., Shono, T., Komagata, O., Tsuda, Y., Kobayashi, M., Motoki, M., … Tomita, T. (2007). Insecticide resistance in potential vector mosquitoes for West Nile virus in Japan. Journal of Medical Entomology, 44(5), 822–829.

An alternative to using such pesticides is a larvicide, BT, which has been studied extensively. This appears to be safe at the moment (except for mega-doses, or deviant genetic strains), and is a champ at killing mosquito larvae. 

Ibrahim, M. A., Griko, N., Junker, M., & Bulla, L. A. (2010). Bacillus thuringiensis. Bioengineered Bugs, 1(1), 31–50.

So the question is: if permethrin has already been shown to be dangerous to animals and humans AND it’s been shown to have diminishing effects on mosquitoes, and there are alternative measures that work, why is there such a strong push to spray? One must remember that where spraying of this nature is used by the WHO, it is used as the lesser of two evils in regions where the risk of mosquito-borne illness and subsequent death or disability is high enough to justify its use. Are there enough cases of West Nile in our area that spraying is justified? Has there been enough sampling of mosquito populations? What is the correlation between the ratio of mosquitoes with West Nile and the number of diagnosed cases? Are larvicide or other control measures being optimally used?

As a scientist who teaches the physical sciences and who does health-related research, I’m struggling to understand how the data can possibly support a decision to spray.

[1] US Environmental Protection Agency; Office of Pesticide Programs. (2011). “Pyrethrins/Pyrethroid Cumulative Risk Assessment.” Retrieved from US Environmental Protection Agency.

[2] Xu Wang et al., “Permethrin-induced oxidative stress and toxicity and metabolism. A review,” Environmental Research, Volume 149, August 2016, Pages 86-104.

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What we can learn from anti-zika spraying

by Nathaniel Smith, Politics: A View from West Chester, 8/9/16

Zika virus is transmitted by mosquitoes and people.

So, health authorities have been working on the twin challenges of eradicating mosquitoes and educating people.

Transmission of Zika virus from mosquitoes to people (and vice versa) in the continental US has occurred only in one small tropical enclave: a square mile (or now it seems even less) of Miami. Pennsylvanians might worry about catching zika from travelers returning from the Rio Olympics but not from mosquitoes this summer so far north. (1)

However, we should be worrying about the effects of being sprayed with pesticides, of which there is really no safe level for the environment and human exposure.

As someone involved in the current campaign to cut down on both mosquitoes and pesticide spraying in West Chester, I think we can learn a lot from zika, even if it is not currently being transmitted by mosquitoes anywhere near us.

Many insects, like the viruses that attack the human body, reproduce quickly and can develop resistance to whatever we throw against them. As doctors turn from one antibiotic to another to find one that still kills a given virus, so health officials experiment to see what still kills different mosquito species.

The Aedes aegypti mosquito, the chief transmitter of zika, is particularly problematic for traditional mosquito elimination programs and the standard anti-mosquito pesticide permethrin, a pesticide usually applied from ground-based equipment such as trucks. (2)

Aedes aegypti has been acquiring immunity in Thailand (3) to permethrin and even to DDT (which was banned in the US in 1972 after severe impacts such as almost driving our national bird into extinction); and similarly in Mexico (4) and, more recently, in Puerto Rico (5) and now Florida. (6)

As time goes on, scientists have to look farther up the pesticide chain—with further likely risks—to find more effective pesticides. This is not good news….

aerial spraying

read more and see end notes at Politics: A View from West Chester, 8/9/16

Zika Surge in Miami Neighborhood Prompts Travel Warning

By PAM BELLUCK, New York Times, AUG. 1, 2016,

This excerpt details why we find reliance on pesticides to solve mosquito problems not only undesirable but potentially unreliable:

…Dr. Thomas R. Frieden, the director of the C.D.C., said that the Aedes aegypti mosquito, which transmits the Zika virus, has proved to be a wily adversary in Wynwood, a crowded, urban neighborhood in north Miami where all the cases were found. The mosquito may be resistant to the insecticides being used or may be able to hide in standing water.

“Aggressive mosquito control measures don’t seem to be working as well as we would like,” he said in a press briefing on Monday.

The authorities had expected additional cases of Zika infection linked to the neighborhood, he said. But officials were particularly concerned by indications over the weekend that “moderately high” numbers of Aedes aegypti mosquitoes and their larvae were still being found in a one-square-mile section in Wynwood, an area of warehouses, art galleries, restaurants, bars, apartments and condominiums….

read the full article at New York Times

Pyrethroids and insect resistance

excerpt from “Pyrethroids: Not as safe as you think” at Melissa Kaplan’s Herp Care Collection, last updated January 1, 2014:

…Some insects have developed ways to detoxify the naturally occurring pyrethrums encountered when feeding on the nectar of feverfew and chrysanthemums, a not uncommon adaptive response. Unfortunately, while insects and plants have had millions of years to work out these survival pathways, we humans haven’t.

An increasing number of insects have developed high levels of resistance to pyrethroids, such as cockroaches, head lice, and tobacco budworm, pear psylla, fall army-worm, German cockroach, spotted tentiform leafminer, diamondback moth, house fly, stable fly, head lice, and tobacco budworm. Many of these species are resistant to more than one pyrethroid. Because insects reproduce – and adapt – far more quickly than do vertebrates, they are far better able to evolve defenses against the toxins we throw at them, resulting in an ever expanding range of poisons developed and thrown into our environment.

Pyrethroids, like all toxins, are indiscriminate: they affect all the organisms who come into contact with them in the air, on plants, on the ground, in the soil, and in the water. While your local grower – or you – may be applying it to deal with a specific pest, the products affect everything around it. And, since particulates are easily airborne, they travel, often great distances, from the actual point of application….