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From Wikipedia. Imidacloprid. https://en.wikipedia.org/wiki/Imidacloprid#Neonicotinoids_banned_by_the_European_Union
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Regulation
Neonicotinoids banned by the European Union
In February 2018, the European Food Safety Authority published a new report indicating that neonicotinoids pose a serious danger to both honey bees and wild bees.[51] In April 2018, the member states of the European Union decided to ban the three main neonicotinoids (clothianidin, imidacloprid and thiamethoxam) for all outdoor uses.[52]
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Bees and other insects
To members of the species Apis mellifera, the western honey bee, imidacloprid is one of the most toxic chemicals ever created as an insecticide. The acute oral LD50 of imidacloprid ranges from 5 to 70 nanograms per bee.[24] Honeybee colonies vary in their ability to metabolize toxins, which explains this wide range. Imidacloprid is more toxic to bees than the organophosphate dimethoate (oral LD50 152 ng/bee) or the pyrethroid cypermethrin (oral LD50 160 ng/bee).[24] The toxicity of imidacloprid to bees differs from most insecticides in that it is more toxic orally than by contact. The contact acute LD50 is 0.024 µg active ingredient per bee.[25]
Imidacloprid was first widely used in the United States in 1996 as it replaced three broad classes of insecticides. In 2006, U.S. commercial migratory beekeepers reported sharp declines in their honey bee colonies. Such declines had happened in the past; however unlike as was the case in previous losses, adult bees were abandoning their hives. Scientists named this phenomenon colony collapse disorder (CCD). Reports show that beekeepers in most states have been affected by CCD.[26] Although no single factor has been identified as causing CCD, the United States Department of Agriculture (USDA) in their progress report on CCD stated that CCD may be “a syndrome caused by many different factors, working in combination or synergistically.”[27] Several studies have found that sub-lethal levels of imidacloprid increase honey bee susceptibility to the pathogen Nosema.[28][29][30]
Dave Goulson (2012) of the University of Stirling showed that trivial effects of imidacloprid in lab and greenhouse experiments can translate into large effects in the field. The research found that bees consuming the pesticide suffered an 85% loss in the number of queens their hives produced, and a doubling of the number of bees who failed to return from food foraging trips.[31][32]
Lu et al. (2012) reported they were able to replicate CCD with sub-lethal doses of imidacloprid. The imidacloprid-treated hives were nearly empty, consistent with CCD, and the authors exclude Varroa or Nosema as contributing causes.[33]
In May 2012, researchers at the University of San Diego released a study showing that honey bees treated with a small dose of imidacloprid, comparable to what they would receive in nectar and formerly considered a safe amount, became “picky eaters,” refusing nectars of lower sweetness and preferring to feed only on sweeter nectar. It was also found that bees exposed to imidacloprid performed the “waggle dance,” the movements that bees use to inform hive mates of the location of foraging plants, at a lower rate.[34]
Researchers from the Canadian Forest Service showed that imidacloprid used on trees at realistic field concentrations decreases leaf litter breakdown owing to adverse sublethal effects on non-target terrestrial invertebrates. The study did not find significant indication that the invertebrates, which normally decompose leaf litter, preferred uncontaminated leaves, and concluded that the invertebrates could not detect the imidacloprid.[35]
A 2012 in situ study provided strong evidence that exposure to sublethal levels of imidacloprid in high fructose corn syrup (HFCS) used to feed honey bees when forage is not available causes bees to exhibit symptoms consistent to CCD 23 weeks post imidacloprid dosing. The researchers suggested that “the observed delayed mortality in honey bees caused by imidacloprid in HFCS is a novel and plausible mechanism for CCD, and should be validated in future studies”.[36][37]
Sublethal doses (<10 ppb) to aphids have been found to lead to altered behavior, such as wandering and eventual starvation. Very low concentrations also reduced nymph viability.[38] In bumblebees exposure to 10 ppb imidacloprid reduces natural foraging behaviour, increases worker mortality and leads to reduced brood development.[39] A 2013 study showed that bumblebee colonies exposed to 10 ppb of imidacloprid started failing after three weeks when the death rate increased and the birth rate decreased. The researchers attributed this to exposed colonies performing essential tasks, such as foraging, thermoregulation and brood care, less well than unexposed colonies.[40] This suggests that sublethal imidacloprid causes colony failure through reduced colony function.
In January 2013, the European Food Safety Authority stated that neonicotinoids pose an unacceptably high risk to bees, and that the industry-sponsored science upon which regulatory agencies’ claims of safety have relied might be flawed, concluding that, “A high acute risk to honey bees was identified from exposure via dust drift for the seed treatment uses in maize, oilseed rape and cereals. A high acute risk was also identified from exposure via residues in nectar and/or pollen.”[41] An author of a Science study prompting the EFSA review suggested that industry science pertaining to neonicotinoids may have been deliberately deceptive, and the UK Parliament has asked the manufacturer Bayer Crop Science to explain discrepancies in evidence they have submitted to an investigation.[42]
Birds
In bobwhite quail (Colinus virginianus), imidacloprid was determined to be moderately toxic with an acute oral LD50 of 152 mg a.i./kg. It was slightly toxic in a 5-day dietary study with an acute oral LC50 of 1,420 mg a.i./kg diet, a NOAEC of < 69 mg a.i./kg diet, and a LOAEC = 69 mg a.i./kg diet. Exposed birds exhibited ataxia, wing drop, opisthotonos, immobility, hyperactivity, fluid-filled crops and intestines, and discolored livers. In a reproductive toxicity study with bobwhite quail, the NOAEC = 120 mg a.i./kg diet and the LOAEC = 240 mg a.i./kg diet. Eggshell thinning and decreased adult weight were observed at 240 mg a.i./kg diet.[11][13]
Imidacloprid is highly toxic to four bird species: Japanese quail, house sparrow, canary, and pigeon. The acute oral LD50 for Japanese quail (Coturnix coturnix) is 31 mg a.i./kg bw with a NOAEL = 3.1 mg a.i./kg. The acute oral LD50 for house sparrow (Passer domesticus) is 41 mg a.i./kg bw with a NOAEL = 3 mg a.i./kg and a NOAEL = 6 mg a.i./kg. The LD50s for pigeon (Columba livia) and canary (Serinus canaria) are 25–50 mg a.i./kg. Mallard ducks are more resistant to the effects of imidacloprid with a 5-day dietary LC50 of > 4,797 ppm. The NOAEC for body weight and feed consumption is 69 mg a.i./kg diet. Reproductive studies with mallard ducks showed eggshell thinning at 240 mg a.i./kg diet.[11][13] According to the European Food Safety Authority, imidacloprid poses a potential high acute risk for herbivorous and insectivorous birds and granivorous mammals. Chronic risk has not been well established.[13][16] The hypothesis that imidacloprid has a negative impact on insectivorous bird populations is supported by a study of bird population trends in the Netherlands, where correlation has been identified between surface-water concentrations of imidacloprid and population decline. At imidacloprid concentrations of more than 20 nanograms per litre, bird populations tended to decline by 3.5 per cent on average annually.[43] Additional analyses in this study revealed that spatial pattern of bird population decline appeared only after the introduction of imidacloprid to the Netherlands, in the mid-1990s, and that this correlation is not linked to any other land usage factor.
Aquatic life
Imidacloprid is highly toxic on an acute basis to aquatic invertebrates, with EC50 values = 0.037 – 0.115 ppm. It is also highly toxic to aquatic invertebrates on a chronic basis (effects on growth and movement): NOAEC/LOAEC = 1.8/3.6 ppm in daphnids; NOAEC = 0.001 in Chironomus midge, and NOAEC/LOAEC = 0.00006/0.0013 ppm in mysid shrimp. Its toxicity to fish is relatively low; however, the EPA has requested review of secondary effects on fish with food chains that include sensitive aquatic invertebrates.[8]