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Imidacloprid, the largest selling insecticide in the world, has received particular attention from scientists, policymakers and industries due to its potential toxicity to bees and aquatic organisms. The decline of aquatic macro-invertebrates due to imidacloprid concentrations in the Dutch surface waters was hypothesised in a recent paper by Van Dijk, Van Staalduinen and Van der Sluijs (PLOS ONE, May 2013). Although we do not disagree with imidacloprid's inherent toxicity to aquatic organisms, we have fundamental concerns regarding the way the data were analysed and interpreted. Here, we demonstrate that the underlying toxicity of imidacloprid in the field situation cannot be understood except in the context of other co-occurring pesticides. Although we agree with Van Dijk and co-workers that effects of imidacloprid can emerge between 13 and 67 ng/L we use a different line of evidence. We present an alternative approach to link imidacloprid concentrations and biological data. We analysed the national set of chemical monitoring data of the year 2009 to estimate the relative contribution of imidacloprid compared to other pesticides in relation to environmental quality target and chronic ecotoxicity threshold exceedances. Moreover, we assessed the relative impact of imidacloprid on the pesticide-induced potential affected fractions of the aquatic communities. We conclude that by choosing to test a starting hypothesis using insufficient data on chemistry and biology that are difficult to link, and by ignoring potential collinear effects of other pesticides present in Dutch surface waters Van Dijk and co-workers do not provide direct evidence that reduced taxon richness and abundance of macroinvertebrates can be attributed to the presence of imidacloprid only. Using a different line of evidence we expect ecological effects of imidacloprid at some of the exposure profiles measured in 2009 in the surface waters of the Netherlands.

Single dose of imidacloprid (IMI-20 mg/kg bodyweight) was orally administered in female rats. Its disposition along with two metabolites 6-chloro nicotinic acid (6-CNA) and 6-hydroxy nicotinic acid (6-HNA) was monitored in organs (brain, liver, kidney, and ovary) and bodily fluids (blood, urine) at 6, 12, 24 and 48 h and faeces at 24 and 48 h. Maximum concentration (Cmax) of IMI and metabolites in each organ and bodily fluid occurred after 12 h. Area under curve (AUC) of IMI ranged from 35 to 358 μg/ml/h; 6-CNA: 27.12–1006.42 μg/ml/h and 6-HNA: 14.98–302.74 μg/ml/h in different organs and bodily fluids. Clearance rate of IMI was maximum in ovary followed by kidney, liver, brain, faeces, blood and urine. Percent inhibition of acetyl-cholinesterase (AChE) was comparable in brain and Red Blood Cells (RBC) at 6–48 h which suggests the RBC-AChE as valid biomarker for assessing IMI exposure. It is evident that IMI was absorbed, metabolized, and excreted showing increased level of serum enzymes like Glutamic oxaloacetic transaminase (GOT), Glutamic pyruvic transaminase (GPT) and biochemical constituents like billirubin and Blood Urea Nitrogen (BUN) at 48 h. These data suggest that IMI is widely distributed, metabolized and induced toxicology effects at 20 mg/kg bodyweight to female rats.

Changes in food uptake by detritivorous macroinvertebrates could disrupt the ecosystem service of leaf litter breakdown, necessitating the study of shredding under anthropogenic influences. The impact of the neonicotinoid insecticide imidacloprid on the feeding rate of individual Gammarus pulex was measured at a daily resolution both during and after a 4-d exposure period. The authors found that imidacloprid inhibits feeding of G. pulex during exposure at concentrations ≥30 µg/L and that there was no recovery in feeding on transfer into clean media for 3 d. Exposure to imidacloprid at concentrations ≥0.81 µg/L and ≤9.0 µg/L resulted in increased feeding after exposure even though there was no significant effect on feeding during the exposure itself. Comparison with the literature shows that concentrations found to influence feeding lie within the range of estimated and measured environmental concentrations. Additionally, effects on feeding rate were observed at concentrations 2 orders of magnitude lower than those causing mortality. The lethal concentration for 50% of test organisms after 4 d of exposure (270 µg/L, literature data) and the effect concentration for a reduction in feeding by 50% (5.34 µg/L) were used for this comparison. The present study discusses the potential that effects on feeding may evoke effects at the population level or disturb leaf litter breakdown in the environment.

In the cold winter of 2012-13, 29% of honeybee colonies in the UK died, with only Belgium suffering a higher rate of losses (34%) of the 17 countries surveyed. By contrast, only 5% of colonies in Italy were lost. Summer losses of colonies were also high in the UK, at 9.7%, with only France (14%) exceeding this. The Epilobee study surveyed 31,800 colonies and is the first pan-European assessment of the rate of colony deaths. It provides a valuable baseline for future research but does not indicate the relative effects of factors such as disease, habitat loss and pesticide use in honeybee decline. Neither does it examine why some countries are worse affected.

Austin Bradford Hill's landmark 1965 paper contains several important lessons for the current conduct of epidemiology. Unfortunately, it is almost exclusively cited as the source of the "Bradford-Hill criteria" for inferring causation when association is observed, despite Hill's explicit statement that cause-effect decisions cannot be based on a set of rules. Overlooked are Hill's important lessons about how to make decisions based on epidemiologic evidence. He advised epidemiologists to avoid over-emphasizing statistical significance testing, given the observation that systematic error is often greater than random error. His compelling and intuitive examples point out the need to consider costs and benefits when making decisions about health-promoting interventions. These lessons, which offer ways to dramatically increase the contribution of health science to decision making, are as needed today as they were when Hill presented them.

Pesticide contamination and agricultural intensification threaten 24 percent of Europe’s bumblebees, according to research conducted by the International Union for Conservation of Nature (IUCN) and funded by the European Commission. The study is part an ongoing project called European Red List of pollinators, with contribution from experts of the “Status and Trends of European Pollinators” (STEP) project, which assesses the conservation status of all bees —approximately 2000 species— occurring throughout Europe. The study concludes that almost half of the 68 species in the European Union (EU) are in decline, including those at risk of extinction. Of these, a total of 16 species are listed as at risk according to the IUCN’s Red List of Threatened Species, which represents the world most trusted authority on the conservation status of species. In comparison, only 13 percent of bumblebee populations are increasing. “We are very concerned with these findings. Such a high proportion of threatened bumblebees can have serious implications for our food production,” says Ana Nieto, European Biodiversity Officer of IUCN and coordinator of the study. “Protecting bumblebee species and habitats, restoring degraded ecosystems and promoting biodiversity-friendly agricultural practices will be essential to reverse the negative trends in European bumblebee populations.”

The study from the British Trust for Ornithology (BTO) has chronicled the fortunes of our seabirds and found that last summer a single pair in Larne Lough laid at least one egg, but no young are known to have fledged. It comes after the species suffered a "near-terminal decline" in the 1980s, according to the first annual Northern Ireland Seabird Report 2013, which charts the changing fortunes of the seabirds making their homes on our coastal habitats. BTO spokesman Shane Wolsey said roseate terns (Sterna dougallii) used to breed in good numbers in some coastal colonies here but stopped breeding on Mew Island in the Copelands in the early 1960s, and left Green Island in Carlingford Lough in the early 1990s. "It's been a long time coming. Roseate terns have just declined over donkey's years. The last ones have been breeding for some time in Larne Lough," he said. "We have one pair in Larne Lough. You only need something to happen to one of those birds and that is the end of that."

During the neurodevelopmental period, the brain is potentially more susceptible to environmental exposure to pollutants. The aim was to determine if neonatal exposure to permethrin (PERM) pesticide, at a low dosage that does not produce signs of obvious abnormalities, could represent a risk for the onset of diseases later in the life.

You hear a lot these days about genetically modified organisms, with many people arguing that they’ll be a necessity in the not-so-distant future, as climate change stresses agriculture, and as a growing, and increasingly affluent, population consumes more food, and more inefficient animal-based foods. Others argue that we’ll need GMOs to reduce global warming emissions, harm to biodiversity from pesticides, pollution from fertilizers (such as coastal “dead zones”), and overuse of scarce resources like fresh water by industrial agriculture. You might have seen one such argument a few months ago from David Rotman, the editor of MIT Technology Review, in his feature called “Why We Will Need Genetically Modified Foods.” But all these arguments rest on certain assumptions, and these assumptions are flawed, at best. Rotman, for example, argued that we’ll need GMOs because simpler, less controversial options such as breeding are simply too slow. He thinks breeding doesn’t give growers access to enough genetic diversity to allow adaptation to climate challenges and to sufficiently increase yields. Many breeders and molecular biologists disagree.