What is a Vector Index?

As of 2016, Chester County is using the Vector Index method of using mosquito data to predict the West Nile Virus threat to humans. Here is a summary from “2013 West Nile Virus in the United States: Guidelines for Surveillance, Prevention, and Control” at the CDC site, p. 18 (boldface added):

The Vector Index (VI) is an estimate of the abundance of infected mosquitoes in an area and incorporates information describing the vector species that are present in the area, relative abundance of those species, and the WNV infection rate in each species into a single index (Gujaral et al. 2007, Bolling et al. 2009, Jones et al. 2011). The VI is calculated by multiplying the average number of mosquitoes collected per trap night by the proportion infected with WNV, and is expressed as the average number of infected mosquitoes collected per trap night in the area during the sampling period. In areas where more than one WNV vector mosquito species is present, a VI is calculated for each of the important vector species and the individual VIs are summed to represent a combined estimate of the infected vector abundance. By summing the VI for the key vector species, the combined VI accommodates the fact that WNV transmission may involve one or more vectors in an area. Increases in VI reflect increases in risk of human disease (Bolling et al. 2009, Jones et al. 2011, Kwan et al. 2012, Colborn et al. 2013 in press) and have demonstrated significantly better predictive ability than estimates of vector abundance or infection rate alone, clearly demonstrating the value of combining information for vector abundance and WNV infection rates to generate a more meaningful risk index (Bolling et al. 2009). As with other surveillance indicators, the accuracy of the Vector Index is dependent upon the number of trap nights used to estimate abundance and the number of specimens tested for virus to estimate infection rate. Instructions for calculating the Vector Index in a system with multiple vector species present are in Appendix 2.

For the actual VI formula and a detailed example, see pp. 64-66 of the above Guidelines.

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.