The neonicotinoids represent a relatively new group of insecticides. They were introduced in the
early 1990s to counter widespread resistance in insect pests and increasing health and safety
objections to the organophosphorous insecticides. Although of lower acute toxicity to vertebrates
than the latter, the neonicotinoids’ longer persistence, high water solubility, runoff and leaching
potential as well as their very high toxicity to pollinators are placing them under increasing public
and political scrutiny, especially now that they have become the most widely used pesticides in the
world. Their toxicity to pollinators has brought them the most attention so far and has dominated the
recent concerns of regulatory institutions worldwide.
The intent of this report is to review the risk that neonicotinoids pose to birds. Birds have borne more
than their fair share of impacts from pesticides – from the early issues of eggshell thinning with DDT
to the extensive mortality caused by the organophosphorous and carbamate insecticides that
followed. Some researchers have suggested that birds may already be affected by neonicotinoids
and that, at least in Europe, bird population declines can be blamed on these popular insecticides.
The main products reviewed here are acetamiprid, imidacloprid, thiacloprid, clothianidin and
thiamethoxam. Minor compounds include dinotefuran, nitenpyram and nithiazine. For the sake of
comparison, this report will discuss, where appropriate, a number of older insecticides that the
neonicotinoids have replaced. This includes the organophosphorous insecticides diazinon,
chlorpyrifos, malathion, terbufos and methamidophos, the carbamate insecticides carbofuran,
methomyl, the pyrethroids tefluthrin and deltamethrin as well as the seed treatment insecticide
The report will emphasize US regulatory history although it will make reference to Canadian and EU
regulatory reviews where relevant. For ease of consultation, summary points made here are detailed
in the body of the report under the same section heading:
1. The history of neonicotinoid registrations highlights many of the critical failings of our current
pesticide registration system. Regulatory agencies in both the US and Canada (and to some
extent in Europe as well) exhibited a conflicted approach to the neonicotinoid class of
compounds – on the one hand expressing serious concerns about the persistence, mobility and
toxicity of the products – on the other hand, granting registrations in an ever-widening range of
crops and non-agricultural use sites.
There is evidence the neonicotinoids got a very ‘soft ride’ through registration. Based on the
existing record, registration decisions concerning the neonicotinoid insecticides were
overwhelmingly positive despite a consistent record of cautionary warnings from the scientists
involved in the assessment process. Increased concerns in the scientific and popular literature
over imidacloprid, clothianidin and other neonicotinoid insecticides did not deter pesticide
manufacturers, who appeared to be in a race to register as many uses as possible. It looks as if
the USEPA and other regulatory agencies consistently approved registrations despite their own
scientists’ repeated and ever-growing concerns. It is relevant to ask why we conduct scientific
evaluations of products if those evaluations have little or no bearing on the registration decisions
that are made, and when staff scientists warning of ‘major risk concerns’ appear to be ignored.
Even though several early reviews of the first neonicotinoid, imidacloprid, correctly identified
Neonicotinoid Insecticides and Birds
issues of bird and mammal toxicity, persistence, runoff/leaching and aquatic toxicity, regulators
failed to apply some of the lessons learned in the 1990s with imidacloprid to more recently
developed compounds such as clothianidin and thiamethoxam. They also failed (and continue to
fail) to consider the impact of combined neonicotinoid residues in the environment. Regulators
have tended to place inordinate faith in precautionary labelling to mitigate very serious terrestrial
and aquatic risks.
2. The acute toxicity of neonicotinoids to birds is lower than the acute toxicity of many of the
insecticides they have replaced, notably the organophosphorous and carbamate insecticides.
However, EPA and other regulatory agencies worldwide have underestimated the toxicity of
these compounds to birds. This undervaluation is partly because the risk assessment methods
fail to account sufficiently for interspecies variation in toxicity.
Depending on the specific insecticide, we have found that EPA underestimates toxicity by 1.5 -
10 fold if the intent of the exercise is to protect most potentially exposed bird species, and not
merely mallards and bobwhites, the two test species.
In addition, there is some evidence that the neonicotinoid insecticides will debilitate birds at a
much reduced fraction of a lethal dose compared to other pesticides and this debilitation will be
longer-lasting. Small non-lethal doses are likely to cause partial paralysis and other sub-lethal
effects in birds. These effects slip under the radar screen in regulatory assessments based
entirely on lethal levels.
3. The chronic/reproductive toxicity of neonicotinoids to birds is high. This was recognised very
early on in the regulatory reviews of the various active ingredients. Yet high reproductive toxicity
in birds is typically ignored in the pesticide review process – whether for neonicotinoids or for
other pesticides. Many pesticides fail the current reproduction screen, and many uncertainties
exist surrounding the extrapolation of laboratory data to actual field conditions. These problems
are not new but regulatory agencies have failed to address the situation. Because the
neonicotinoids are systemic and persistent in soils, and because several are used as seed
treatment chemicals, they are available to birds in a chronic fashion, making their potential to
affect reproduction an even greater concern.
The standard tests carried out by manufacturers place reproductive effects at dosing levels
ranging from 2 to 13 mg/kg/day depending on the product. This level of exposure is easily
achieved with seed treatment chemicals. However, very recent toxicological information from
Japan suggests that testicular function in male birds as well as embryonic development in the
offspring of exposed males is affected at levels much lower than indicated from these standard
4. Of particular concern to birds are those compounds that are used as seed treatments, primarily
imidacloprid, clothianidin, thiamethoxam and acetamiprid. Regardless of the exact label
directions and requirements, seed-treatment chemicals are widely available to birds. Seeds are
never fully covered with soil, making them easy to find by foraging birds. Spills are commonplace
with current machinery. And many species have the ability to scrape and dig for planted seed.
Seed treatments, by definition, will result in a high exposure situation for birds (as well as for
small mammal species not discussed in this report). Both the EPA in the US and Pest
Neonicotinoid Insecticides and Birds
Management Regulatory Agency (PMRA) in Canada have failed at times to consider this high
exposure potential in their assessments.
5. The amount of insecticide adhering to the average corn (maize) seed can result in acute
intoxications in birds with all three registered products – imidacloprid, clothianidin and
thiamethoxam. With imidacloprid, a single seed may prove lethal for an average-sized bird (e.g.
blue jay-sized) likely to be picking up whole corn seed from seeded fields. A few seeds only are
required in the case of clothianidin or thiamethoxam. Indeed, we believe that imidacloprid is too
acutely toxic to be used as a seed treatment insecticide on any seed type based on our
assessment of its use in cereals and oilseeds. Acute intoxications in wheat or canola are less
likely with clothianidin or thiamethoxam because these neonicotinoids are less acutely toxic to
birds. The birds would need to ingest a greater number of the treated seeds to receive a lethal
However, based on chronic/reproduction endpoints, all seed treatments are predicted to cause
effects given the very small number of seeds (as low as 1/10 of a seed per day during egg laying
season) needing to be ingested to push birds into a ‘critical range’ where reproductive effects are
expected. The main uncertainty here is how long the seeds will be available to birds and how
long dosing is necessary before the type of effects seen in the laboratory will be seen in the wild.
There are huge uncertainties – for instance what types of effects might be seen in altricial
species (those in which the newly-hatched young are born relatively helpless, such as most
passerines, or perching birds) and how this differs from effects seen in precocial species (in
which the newly hatched young are relatively mature, such as ducks and geese, grouse and
Based on our current understanding and risk assessment procedures in place, the
neonicotinoids as a group have a high potential to affect avian reproduction. This is due in large
part to the very high exposure potential that seed treatment chemicals represent and the
persistent nature of the neonicotinoids.
A publication currently in press advances the hypothesis that the neonicotinoids are a
contributory factor to many wildlife diseases through immune suppression. The authors make
this claim on the basis of geographic and temporal associations. The sheer scale and
seriousness of the issue demands that this hypothesis be investigated more fully.
Despite industry claims, the neonicotinoids are not repellant to birds. Any demonstrated
avoidance can be explained by hesitation before a new food source or post-ingestion intoxication
and illness. Neither is sufficient to spare birds from either acute or chronic effects. There are
parallels with the cholinesterase-inhibiting insecticides where repellency was similarly thought to
reduce in-field risks. For example, the organophosphorous insecticide diazinon is extremely well
avoided in the laboratory. Yet, thousands of geese and other species have grazed their way to
an early death on diazinon-treated turf.
6. The link between impacts on the insect food of birds and declines of bird species is difficult to
establish unequivocally, save for the evidence linking the grey partridge to pesticide use in the
UK. A review of the existing literature suggests that it is difficult to predict the relative importance
of food supply during the breeding season (i.e. when an insect food base is critical) compared to
other risks such as habitat loss, food supply during migration and during winter, predation or
Neonicotinoid Insecticides and Birds
even direct losses from poisoning or disturbances such as mowing or tillage. Each species
responds to a different set of stressors and it is likely that many of the declines have multiple
Nevertheless, it would be foolhardy to argue that dramatic losses of insect biomass from
ecosystems is not going to have potential consequences on the integrity of those ecosystems
and on the species that depend to varying degrees on the spring-summer flush of insect food.
The impacts on terrestrial food chains from neonicotinoid (and other systemic) insecticides may
be much longer-lived and pernicious than those we have seen with non-systemic products.
Generally speaking, an over-efficient removal of insects in crop fields is seldom seen as a matter
of serious concern by regulators – especially in North America. The indirect impacts of pesticides
are not considered in registration reviews – whether in the US or anywhere else in the world.
In his book, Dutch toxicologist Henk Tennekes (2010) makes the case that the contamination of
surface water by neonicotinoids is so widespread in the Netherlands (and possibly elsewhere in
Europe), that loss of insect biomass on a continental scale is behind many of the widespread
declines that are being seen, be they of marsh birds, heath or meadow birds or even coastal
species. This suggests that we should be looking at possible links between neonicotinoid
insecticides and birds, not on a farm scale, but in the context of whole watersheds and regions.
Impacts from the neonicotinoids may very well be further afield than the arable area on which
they are used, and many of those impacts may be mediated through the aquatic environment.
Because aquatic impacts are considered during product registration reviews, it is reasonable to
ask whether the potential impact of neonicotinoids to aquatic life has been assessed correctly.
7. Unfortunately, North American regulators have greatly underestimated the toxicity of imidacloprid
and other neonicotinoids to aquatic invertebrates. Reference doses are set using outdated
methodology which has more to do with a game of chance than with a rigorous scientific
process. A complete disregard for the peer-reviewed literature is a constant factor throughout the
history of neonicotinoid assessments.
For imidacloprid, we believe that a scientifically defensible reference level (a water concentration
at which undesirable effects are likely to be seen in reasonably sensitive species) for acute
invertebrate effects (following short term exposure) is approximately 0.2 ug/l. European
regulators acknowledge that acute effects are likely at levels exceeding 0.5 ug/l. In contrast, the
EPA’s regulatory and non-regulatory reference levels are set at 35 ug/l.
Similarly, a reasonable reference level for effects following chronic exposure is at least an order
of magnitude lower, or between 0.01 and 0.03 ug/l rather than the 0.5 ug/l used in the U.S..
EPA’s approach to the assessment of aquatic risk is scientifically unsound and places aquatic
environments at risk. In addition, there is evidence that risk managers at EPA have ignored
aquatic risk ratios that exceeded the usual level of concern, notwithstanding the fact that those
risk ratios were grossly underestimated in the first place.
Based on the relative sensitivity of aquatic insects tested with several of the neonicotinoid
insecticides, we suggest that these reference levels should also apply to the other neonicotinoid
insecticides, notably acetamiprid, thiacloprid, clothianidin and thiamethoxam. In fact, because of
their similarity in mode of action, the above reference levels should apply to the sum of all
residues for all parent neonicotinoid compounds as well as some of the degradates.
Neonicotinoid Insecticides and Birds
Neonicotinoid insecticides may be totally unprecedented in the history of pesticide registration in
that measured groundwater contamination levels have been high enough to cause aquatic
Data on surface water contamination from surveys to date, notably from California and from the
Canadian Prairies, indicate that concentrations of several of the neonicotinoid insecticides are
high enough to be causing impacts in aquatic food chains. Data from other jurisdictions (e.g. the
Netherlands) show even higher levels of contamination.
It is clear that neonicotinoids have often replaced other insecticides of higher short-term toxicity
to aquatic life – especially fish. However, the mode of action of neonicotinoids, which entails a
cumulative irreversible action and delayed effects in invertebrates, as well as their persistence in
the environment, makes them particularly worrisome. It is clear that we are witnessing
contamination of the aquatic environment at levels that will affect aquatic food chains. This has
a potential to affect consumers of those aquatic resources, be they birds, fish or amphibians.
In conclusion, policymakers and the public should be very concerned about the impact of
neonicotinoid insecticides on birds and on the broader environment. Specifically, we should be
regulatory procedures are scientifically deficient and prone to the vagaries of chance
risk managers appear to place minimal weight on concerns raised by environmental
scientists who carry out the scientific evaluations of the products
despite all the red flags, regulators are adding to the list of permissible uses
neonicotinoids – the most heavily used insecticides in the world – are systemic products
that are extremely persistent and very much prone to runoff and groundwater infiltration
some neonicotinoids are capable of causing lethal intoxications and all are predicted to
cause reproductive dysfunction in birds
where we have looked, we have found broad-scale aquatic contamination at levels
expected to cause impacts on aquatic food chains.
any future re-evaluation of these products appears to focus solely on pollinator toxicity.
The seriousness of pollinator losses should not be underestimated, but there is much
more at stake.
A moratorium on any further use expansion is currently being discussed in the EU and Member
States. Some countries have moved forward on limited cancellations. The North American
regulatory system needs to act rather than continue to ignore evidence of widespread environmental
damage. There is evidence that US regulators waited far too long to impose needed restrictions on
the toxic insecticides responsible for millions of bird deaths per year (Mineau 2004) and that this is
one of the more plausible reasons for the decline of grassland/farmland birds in North America
(Mineau and Whiteside, 2013). The neonicotinoids have largely replaced that older generation of
chemicals. We are urging regulators to take seriously the red flags raised by this persistent,
cumulative, irreversibly-acting new class of pesticides.