POLLINATORS POLLINATION AND FOOD PRODUCTION

THE ASSESSMENT REPORT ON POLLINATORS, POLLINATION AND FOOD PRODUCTION
BOX 2.3.5
Assessing the possible contribution of neonicotinoids to pollinator declines: What do we still need to know?
FIGURE 2.3.7 Relative abundance of data on specific memory, behavioural, morphological, physiological and molecular
effect endpoints (excluding mortality) in honey bee individuals and colonies (as reported in EFSA, 2015)
INDIVIDUAL HONEYBEE ENDPOINTS
locomotor-activity
PER olfactory-learning wing-block
foraging-activity
confirm...
individual-interaction
confirm...
abdomen-arching confirm...
confirm...
confirm... confirm...
water-consumption
sucrose-responsiveness
food-consumption
HONEYBEE COLONY ENDPOINTS
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2. DRIVERS OF CHANGE OF POLLINATORS,
POLLINATION NETWORKS AND POLLINATION
2. Exposure. To quantify field-realistic exposure levels
we need to estimate both the potential total exposure to
residues (parent and relevant metabolites), e.g., via pollen
and nectar, and understand the relative consumption of
these versus consumption of uncontaminated sources,
because contaminated food will often form only part of the
total available food resources within the landscape (Lundin
et al., 2015). It is important to know what the impact is of the
chemicals as applied in the field or in residential or amenity use
at the colony or population level. What are the residue levels in
different compartments of the plant, after real field applications
and in subsequent crops grown on the treated fields, how do
these translate into levels in pollen and nectar, and what are
the consequences for the exposure of adult bees and larvae
of different bee species, e.g. species that feed their larvae raw
pollen versus processed brood food?
3. Interactions & Synergisms. What are the consequences
of the sublethal effects of neonicotinoids with additional
additive or synergistic stressors? A key area of challenge
is the need to study the effects of realistic combinations
and scales of stressors, some of which are not readily
manipulated, e.g. pesticides and disease within the honey bee
colony (Goulson et al., 2015; Lundin et al., 2015). Modelling
(Bryden et al., 2013; Becher et al., 2014) may provide an
opportunity to study both the potential interactions of such
sublethal effects with each other and the effects of other
factors, e.g. landscape, climate, as drivers of pollinator decline
(Kielmanowicz et al., 2015).
with concentration addition) were rare (7%) and 95% of
these could be predicted based on their mode of action,
e.g. ergosterol biosynthesis inhibitor (EBI) fungicides and
pyrethroids (Cedergreen, 2014). For the remainder the
effects were at worst additive with many combinations
showing no significantly increased toxicity or even
antagonistic effects. This limited evidence of synergistic
interactions, other than those through deliberately applied
insecticide synergists (such as piperonyl butoxide or
mixtures of insecticides (Andersch et al., 2010), is also
evident in honey bees, and the vast majority of the literature
relates to synergistic interactions resulting from EBI fungicide
exposure (Thompson, 2012; Glavan and Bozic, 2013).
The first evidence of unintended synergistic interactions
in honey bees with increases in toxicity (decrease in LD 50
)
of up to 1,000-fold was that between EBI fungicides and
pyrethroids (Colin and Belzunces, 1992; Pilling, 1992; Pilling
et al., 1995; Johnson et al., 2006) and was identified as
due to the inhibition of the P450s, responsible for pyrethroid
metabolism. More limited evidence has identified the