US EPA claims 25 parts per billion of imidacloprid in nectar has no ill effects on bees

Imidacloprid, one of the most commonly used insecticides, is highly toxic to bees and other beneficial insects. The regulatory challenge to determine safe levels of residual pesticides can benefit from information about the time-dependent toxicity of this chemical. Using published toxicity data for imidacloprid for several insect species, we construct time-to-lethal-effect toxicity plots and fit temporal power-law scaling curves to the data. The level of toxic exposure that results in 50% mortality after time t is found to scale as t1.7 for ants, from t1.6 to t5 for honeybees, and from t1.46 to t2.9 for termites. We present a simple toxicological model that can explain t2 scaling. Extrapolating the toxicity scaling for honeybees to the lifespan of winter bees suggests that imidacloprid in honey at 0.25 microgram/kg (ppb) would be lethal to a large proportion of bees nearing the end of their life. EPA's threshold level of 25 ppb is 2 orders of magnitude higher than our Low-Observed-Adverse-Effect-level (LOAEL) of 0.25 ppb, suggesting that the risk of imidacloprid to bees is seriously underestimated by EPA.
Source:
G. Rondeau, F. Sánchez-Bayo, H.A. Tennekes, A. Decourtye, R. Ramirez-Romero, N. Desneux (2014)
Delayed and time-cumulative toxicity of imidacloprid in bees, ants and termites.
Sci. Rep. 4, 5566; DOI:10.1038/srep05566
(www.nature.com/scientificreports)

With hundreds of studies conducted and their demonstrated safe use on farmland across the country, we know more about the safe use of neonics to honey bees than any other pesticide. New studies continue to confirm their safety to bees and other pollinators when used appropriately. We will review the EPA document, but at first glance it appears to overestimate the potential for harmful exposures in certain crops, such as citrus and cotton, while ignoring the important benefits these products provide and management practices to protect bees. We hope the final risk assessment is based on the best available science, as well as a proper understanding of modern pest management practices.
Source:
https://www.bayercropscience.us/news/press-releases/2016/01062016-state…

After years of frustration with the EPA Office of Pesticide Programs (EPA-OPP) for conducting hazard assessments of pesticides that are almost totally reliant on industry-sponsored toxicity testing data, I hired a contractor to review the published scientific hazard data using the GreenScreen® for Safer Chemicals (GreenScreen) method. I chose the GreenScreen method because of its widespread acceptance by governments, industry, and non-governmental organizations alike. The three neonicotinoid pesticides (neonics) assessed were thiamethoxam, imidacloprid, and clothianidin. In contrast to EPA-OPP's hazard assessment, which relied exclusively on industry-sponsored data for its hazard determinations, GreenScreen assessments include both industry-sponsored data and non-industry scientific studies from the published literature. Beyond the established very high risks that neonics pose to aquatic and terrestrial invertebrates like bees - even EPA-OPP finally admitted harm to bees last week, years after the scientific community (Goulson et al 2015; Task Force on Systemic Pesticides2015 report; NRDC fact sheet 2015) - the GreenScreen assessments also identified potential hazards for a number of human health endpoints. GreenScreen identified the following human health endpoints of concern: cancer, reproductive harm, developmental harm, and potential adverse endocrine disruption effects. With these high hazard scores for human health endpoints, all three neonics are classified as a Benchmark 1 chemical, which GreenScreen considers to be a chemical of high concern to be avoided.
Source: Jennifer Sass, NRDC, 11 January 2016
http://switchboard.nrdc.org/blogs/jsass/greenscreens_show_neonic_pesti…

Manufacturers incorporate imidacloprid into exterior products like polystyrene insulation, vinyl siding, adhesives, sealants, and pressure-treated wood decking. Imidacloprid migrates from exterior building materials into water and soil. Bees also use sawdust to help build their hives. Beekeepers use treated wood for stands and treated insulation for nucs. But EPA's bee research on neonicotinoids like imidacloprid has ignored the potential contribution of these materials. Instead, the agency has approved an ever-expanding list of building products in which it may be used.
Building products can contain a lot of imidacloprid. At minimum, treated solid wood must retain 11 parts per million (ppm) imidacloprid to be effective. Lanxess suggests the use of up to 300 ppm in wood surface treatments. Composite woods like particleboard, OSB, and plywood can contain over 150 ppm imidacloprid. Expanded polystyrene insulation commonly contains 200 ppm (0.02% by weight) imidacloprid. Adhesives and sealants can contain up to 1,200 ppm (0.12%). And plastics like PVC siding can contain 10,000 ppm (1% by weight) - a concentration 400,000 times higher than what EPA determined is toxic to bees in nectar.

Source: Healthy Building News, January 21, 2016

United States Environmental Protection Agency
Office of Pesticide Programs
Environmental Fate and Effects Division
Environmental Risk Branch V
1200 Pennsylvania Ave.
Mail Code 7507P
Washington, D.C. 20460

Attention: Milbourn.cathy@epa.gov

2nd February 2016

To whom it may concern,
We would like to offer some comments on the regulatory endpoints that are proposed in the first Preliminary Pollinator Assessment to Support the Registration Review of Imidacloprid (January 4th, 2016).
Below is a figure from our paper (Rondeau et al. 2014), with the toxicity endpoints and the colony-level feeding exposure endpoint shown along with our summary of time dependent toxicity data for imidacloprid.
Indeed, the EPA has chosen the 10-day LOAEC and 48-h LD50 to be safely on the low side of most of the reported results in the literature. However, we feel that the colony level exposure of 25µg/L as determined from the Tier 2 study results should be viewed with much caution. The recommendation of <25µLa.i./L is shown as the red vertical line on the plot. Nectar consumed at 25µLa.i./L with typical daily consumption of 20µL/day yields a daily dose of 0.5ng a.i. per individual. A single day’s exposure, 0.5ng/bee, exceeds by a factor of 2 EPA’s accepted LOAEC of 0.24ng/bee. It is very hard to imagine that the cumulative dose to individual bees at this level of contamination would not give rise to neuro-toxic symptoms.
Curiously, the 25µLa.i./L exposure rate corresponds on our graph to the LT50 time of about 20 days, roughly the age when nurse workers enter the field foraging force. With the colony getting much of its nourishment from the contaminated nectar, there may be little need for a robust work force aged much more than that. Clearly the colony is providing services that transcend the health of individual bees. In fact, it can be expected that there may be colony-wide paradoxical effects. The colony response to a shorter lifespan of individual bees could very well be acceleration of brood production. If colony health was measured by the amount of capped brood, such a seemingly positive effect would be interpreted incorrectly.
In our study we found that the results from many diverse toxicity studies for imidacloprid on insects could be understood in terms of a simple power law scaling,
LT50 ∞ D tP
Where D is the dose rate, t is time and P is the power law exponent. We discovered that much of the honeybee toxicity experiments can be unified with such a scaling law where the time exponent is approximately 2.
Although there is an abundance of toxicity data for imidacloprid and honeybees, there is still missing a good study that can determine the time when such t2 scaling is likely to come to an end. Absent such a study, the prudent policy is to assume that the scaling we present continues indefinitely until individual bees die. If you use bees as proxies for solitary pollinators and other beneficial insects, then you are left without the benefit of robust colony services to maintain health in the presence of pesticide residue. Instead the best estimate we would have would be individual toxicity scaling, with a maximum time based upon natural insect lifetimes or reproductive cycles. This will vary dramatically from species to species, and could approach good fractions of a year for insects on an annual cycle. Unfortunately, the regulatory process is not as simple as assigning a threshold guideline concentration for which to stay below, since the organism life span becomes part of the equation.
The EPA’s continued adherence to the concept of threshold toxicity levels should be questioned with pesticides like imidacloprid that are designed to bind strongly to synaptic receptors and which act to directly stimulate the post synaptic junction. Relatively few molecules of the pesticide can have long lasting effects, as we demonstrated with a model in our paper. This is in contrast to acetylcholine esterase inhibitors, where the action of a just few molecules does almost nothing, since there would still be many acetylcholine esterase sites to clear the junction of neurotransmitter. Hence, for this latter class of chemicals (organophosphates), there is a natural threshold built into the toxic effect, namely the point where concentration of pesticide is sufficient to inhibit a large fraction of the acetylcholine esterase sites.
EPA’s history of successful regulation of the organophosphate insecticide can be seen as a vindication of the threshold theory for the acetylcholine esterase inhibitors. The neonicotinoids present the EPA with a major change in mode of action. Hence a fundamental change in the regulatory framework that backs away from the threshold concept and looks more deeply at the accumulation and persistence of toxic effects is required (Sánchez-Bayo & Tennekes 2015).
Sincerely yours

Gary Rondeau, Applied Scientific Instrumentation, Oregon, USA
Francisco Sánchez-Bayo, The University of Sydney, NSW, Australia
Henk A. Tennekes, Experimental Toxicology Services (ETS) Nederland BV, Zutphen, The Netherlands
Axel Decourtye, ITSAP-Institut de l’Abeille, Avignon, France
Ricardo Ramírez-Romero, Universidad de Guadalajara, Jalisco, Mexico
Nicolas Desneux, French National Institute for Agricultural Research (INRA), Sophia-Antipolis, France

References cited
Rondeau, G. et al. Delayed and time-cumulative toxicity of imidacloprid in bees, ants and termite. Sci. Rep. 4, 5566, doi:10.1038/srep05566 (2014).
Sánchez-Bayo, F. & Tennekes, H. A. in Toxicity and Hazard of Agrochemicals (ed Marcelo L. Larramendy) Ch. 1, 1-37 (InTech Open Science, 2015).