This article is a continuation of a piece by Dr Rosemary Mason and Palle Uhd Jepsen. Please read the first part of this feature by clicking first part of this feature
In 1991,
Bayer CropScience introduced a new type of pesticide into the US; a
group known as neonicotinoids. They differed from conventional spray
pesticides in that they could be used as seed dressings or soil
treatments.
When used as a seed dressing the insecticide will migrate from the stem to the leaf tips, and eventually into flowers and pollen. Any insect that feeds on the crop dies, but bees or butterflies that collect pollen or nectar from the crop are also poisoned.
They act by causing virtually irreversible blockage of post-synaptic nicotinergic acetylcholine receptors in the central nervous systems of insects. Tennekes has found that the damage is cumulative, and with every exposure more receptors are blocked.
In fact he says that there may not be a safe level of exposure [1,2]. Subsequently, several independent scientists have shown that disruption of foraging and hive activity can occur with doses of imidacloprid as low as 6 ppb and fipronil 2 ppb.
In July 1994 beekeepers in France noticed something new [3]. Over the course of a few days, just after the sunflowers had bloomed, a substantial number of their hives would collapse, as the worker bees flew off and never returned, leaving the queen and some immature workers to die.
Normally, scavengers such as beetles and mites would move in and take over a dead hive, but here the scavengers would leave the affected hive boxes alone for weeks. Something unusual must have been repelling them.
The French beekeepers soon believed they knew the reason; that a brand-new insecticide called GAUCHO had just been authorised and was being applied to sunflowers for the first time.
In 2003, in a 108-page
document, the Comité Scientifique and Technique in France reviewed all
the independent scientific evidence on systemic pesticides. Their
findings were that “the treatment of sunflowers is a significant risk to
bees in several stages of life” [4].
In 2004, in France,
tunnel tests were done by scientists from Montpellier, Orléans and
Avignon Universities. They demonstrated that sub-lethal doses of 6 ppb
imidacloprid or 2 ppb fipronil were enough to disrupt feeding [5]. These
were precisely the effects that Bayer itself had advertised for its use
in termite control. In addition, the bees also exhibited signs of
intoxication.
In 2006, disappearances and deaths amongst
managed bee colonies in the US had reached such epidemic proportions
that the term ‘Colony Collapse Disorder’ (CCD) came into use. In fact
high bee losses had begun in 1995, when Varroa mites were first
identified in the hives by beekeepers [6].
Although treatment for the
mites was instituted, colony losses continued to escalate. Initially the
declines were termed ‘Fall-Dwindle Disease’ [7], but by 2006, when many
commercial colonies collapsed, it became known as CCD.
In 2008 Yang et al. performed field tests that confirmed the French scientists’ findings of disruption of foraging [8]. These showed that treatment with sublethal doses of imidacloprid (as low as 50 ppb) delayed the return visit of a bee, and the time delay was dose-dependent.
They found
that the higher the dose to which they were exposed, the more
likelihood that the bees would show abnormalities in revisiting the
site, or even to go missing.
In 2009 and 2011, there was
laboratory evidence from Bee Researchers in France that the
administration of tiny amounts of a systemic neonicotinoid,
imidacloprid, to Colony Collapse Disorder (CCD) bees was associated with
a weakening of bee immunity, such that they became more susceptible to
bee diseases.
Alaux et al. (2009) from INRA, Avignon, France demonstrated that the interaction between the microsporidia Nosema and a neonicotinoid (imidacloprid) significantly weakened honey bees [9].
Vidau et al. (2011) showed that exposure to sublethal doses of fipronil
and thiacloprid highly increased the mortality of honeybees previously
infected by Nosema ceranae [10].
In 2009, Pettis and Van
Engelsdorp from the USDA had produced identical results to Alaux; this
was despite the fact that subsequently the levels of neonicotinoid in
the bees were below the limit of detection using the researchers’ own
equipment.
However, this work remains unpublished. In April 2011, Bayer CropScience brought Pettis over to Westminster, to take part in a debate on Bee Health and Pesticides at a meeting of the All-Party Parliamentary Group on Science and Technology in Agriculture.
By this
time, Pettis was playing down his findings. Nevertheless, in a film by
Mark Daniels at Apimondia, the World Bee Congress in 2009, Van
Engelsdorp had said: “we are not finding a consistent virus or a
consistent pathogen; that implies that something else is happening
underneath it, something is breaking down their immune system” [11].
We decided to look more closely at the patterns of recent deaths/epidemics in the UK, Europe and the US, involving a variety of other wildlife, the pathogens involved and the timescale in relation to use of neonicotinoid-coated seeds and sprays on a wide variety of crops, gardens, greenhouses and amenity grasslands.
We also discovered work
published in 2002 by Kiesecker (when at Penn State University) showing
similar immune system weakening in frogs in areas of pesticide run-off
[12]. This suggested that immune suppression can involve vertebrates as
well as invertebrates.
Continues... Amphibians, Bats And Bumblebees