Impact Of Neonicotinoids On The Environment And Wildlife And Human Health
This feature is a continuation of an article by Dr Rosemary Mason and Palle Uhd Jepsen. Read on or go to beginning of the feature.
The health of the global environment is declining rapidly.
The general use of insecticides, herbicides and fungicides has caused widespread deterioration of the environment for pollinators over the last 60 years; this includes loss of wild plants on which they depend to complete their life cycles, loss of nesting places for bumble bees, loss of habitat and use of herbicides and insecticides in wild places for control of tree diseases.
The systemic neonicotinoids were introduced into the US in 1991 and into the UK in 1994. The percentage of UK cropland treated with neonicotinoids has gone from 0.65% in 1994, to 24.4% in 2008. But the biggest increases have occurred in the last 10 years, from 1 million acres in 2000, to 2.5 million acres in 2008 [62].
However, by 1994 in the US, it was evident that something more sinister was happening to the environment; in Europe and the UK the crises started later; between 2001 and 2005.
The use of neonicotinoid pesticides is associated with AIDS in Wildlife
Most ecologists had considered these infections as
‘novel’ but caused by very virulent pathogens.
However, Vredenburg (2010) and colleagues, in their excellent study of pathogen spread through three lake basins during large-scale amphibian population extinctions (2004-6) in California’s Sierra Nevada, provided us with the probable key to the problem [20].
They stated that epidemiological theory suggests that “pathogens will not cause host extinctions because the pathogen should fade out when the host population is driven below some threshold density”.
Although until recently there had
been doubts about the importance of disease in driving global amphibian
declines, these ecologists said that this theory had now been overcome
by “weight of evidence”.
Four papers from different parts of the world were quoted in which precisely the same “exception to the rule” (i.e. total extinction of the host species) had occurred.
In 1998, 2006, 2007
and 2008 infections in amphibians had led to rapid declines and in some
cases extinction. This suggested to us that the problem lay not with the
virulence of the pathogen, but with the state of immunity of the host
species. This has been confirmed by the registration document.
In addition the document went on to say: The
fate and disposition of clothianidin in the environment suggest a
compound that is a systemic insecticide that is persistent and mobile,
stable to hydrolysis, and has potential to leach into ground water, as
well as run-off to surface waters.
This part was confirmed in
2008 when the California Department of Chemical Regulation gave notice
of: Decision to initiate re-evaluation of chemicals in the
Nitroguanidine insecticide class of neonicotinoids, following studies by
their own scientists.
“Where imidacloprid was applied to the soil, no significant decline in residue levels was observed in any of the studies, even in studies where residues were tested at 540 days after treatment.” On page 3 of the California Notice 2009-02: “DPR plans to work closely with the USEPA’s OPP throughout the re-evaluation process.
The USEPA’s registration review docket for
imidacloprid opened in December 17, 2008….In order to better ensure a
“level playing field” for the neonicotinoid class as a whole, and to
best take advantage of new research as it becomes available, US EPA has
scheduled the docket openings for the remaining neonicotinoids
(acetamiprid, clothianidin, dinotefuran, thiacloprid and thiamethoxam)
for fiscal year 2012.”
This explains the reply we received from Mrs Gesalman, EPA
Communications Directorate on behalf of Thomas Moriarty, Office of
Pesticides Programs on 21st March 2011: “In the interest of developing
the best science to guide our pesticide regulatory decisions, EPA plans
to bring a proposed pollinator field study protocol for review before
the independent Federal Insecticide, Fungicide, and Rodenticide Act
Scientific Advisory Panel (FIFRA SAP) in 2012.
We are waiting to develop the draft protocol until the Society of Environmental Toxicology and Chemistry (SETAC) publishes its findings from a January 2011 International Workshop on Risk Assessment for Insect Pollinators.” (The Executive Summary from this appeared in September 2011.
Our analysis of
this document appears on pdf Final. The truth about Neonicotinoid
Insecticides, which is the ‘sister’ document to this one).
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Amphibians,
particularly tadpoles, are considered to be an environmental indicator
because of their unique sensitivity to pollutants.
The WWF Living Planet Report 2010 has shown that biodiversity is declining faster in freshwater, than in any other biome, including coral reefs and tropical forests [23].
In 2011, the study in Nature said that amphibian population declines far exceed those of other vertebrate groups [22]. In 2011 Mendelson, who graduated in 1989, wrote: “I am a taxonomist and I have seen my career vacillate between the thrill of discovering new species and the chill of tracking extinction events – including species that I described” [25].
The neonicotinoid insecticides are toxic to all taxa, not just invertebrates
Evidence from basic neuroscience research demonstrates that that the neonicotinoids have effects on mammalian neurons as well as on invertebrate ones, and that the effects on the nicotinic acetylcholine receptors (nAChRs) are more significant in vertebrates than was initially suggested by the pesticide companies.
Two recent independent studies were done in rats. The first shows that imidacloprid has acute oxidant and inflammatory effects on the mammalian central nervous system (CNS) and liver [63].
The second was a study to determine to what extent the neonicotinoids imidacloprid and acetamiprid affected the nicotinic acetylcholine receptors of rat cerebellar neurons and to compare their effects with nicotine by using in vitro excitatory Ca-influx assay.
Although nicotine excited rather higher proportions of neurons and a higher peak of Ca-influx compared with the two neonicotinoids, both had higher binding to the neurons and were significantly inhibited with nAChR antagonists [64].
All of the authors suggested that the neonicotinoids might have adverse effects on human health, and especially on the developmental brain. [64]. This paper accords with evidence of the effects of clothianidin on the rat immune system noted in the US EPA registration document.
Continues....
Neonicotinoids And Human Health