Neonicotinoid Pesticides and Bees - The Food and Environment ...

More documents

Recommendations

Info

1. Executive Summary Mode of action and metabolism of neonicotinoids in bees Neonicotinoids have been shown to bind to the ligand gated ion channels at the α-bungarotoxin site on the nicotinic acetylcholine receptor (nAChR) and primarlily affect the post synaptic nAChRs. Once bound to the nAChR, neonicotinoids are not broken down by acetylcholinesterase like acetylcholine resulting in over-stimulation of the nervous system and a build up of acetylcholine in the synapse. The midgut in the honeybee is a major site of metabolism for ingested pesticides and interactions between chemicals at least in part may be influenced by effects on the detoxifying enzymes within the midgut, including microsomal oxidases, glutathione S transferases and esterases. Synergists of both Phase I and Phase II enzymes have been used to identify the metabolic pathways used in neonicotinoid detoxification and confirmed the role mixed function oxidases in the metabolism of many neonicotinoids. However P450s probably have a lesser role in the metabolism of imidacloprid which has an elimination half life of 5 hours. The main imidacloprid metabolites, urea derivative and 6-chloronicotinic acid, are found particularly in the mid gut and rectum and 4/5-hydroxy-imidacloprid and olefin are found mostly in the head, thorax and abdomen all of which are nAChR rich tissues and levels peaked 4 hours after ingestion.. Both of the latter metabolites have insecticidal properties (the olefin has toxicity similar to imidacloprid and both bind to the nAChR) and may be responsible for delayed onset of death. These profiles can be related to the two distinct phases to imidacloprid poisoning after acute exposure. There is a rapid onset of neurotoxicity in the form of hyper responsiveness, hyperactivity, and trembling; mortality is delayed until at least four hours post exposure. Acetamiprid is readily metabolised by mixed function oxidases, to seven main metabolites (none of which are insecticidal). Although metabolism is fast, the half life of acetamiprid approx 25 minutes but only 40% of the total radioactivity eliminated after 72 hours suggesting that the metabolites persist within the honeybee. The lower toxicity of acetamiprid is thought to be due to this rapid metabolism to relatively non-toxic metabolites. Acute toxicity of neonicotinoids In general, LD50 values are lower for oral exposure than for contact exposure, except for acetamiprid which is the reverse; this may be explained by low hydrophobicity and poor penetration through the cuticle of these compounds. The chloronicotinyl insecticides Neonicotinoid pesticides and bees Page 3 of 133 Report to Syngenta Ltd
(thiamethoxam, clothianidin, imidacloprid) are more toxic than the cyano substituted (thiacloprid, acetamiprid) The oral toxicity of imidacloprid, which has been extensively reported within the literature; is highly variable with 48 hour oral LD50 values ranging from 3.7 to as high as 400 ng/bee. Data across pesticides generally suggests that the toxicity to Apis mellifera reflects that in other bee species when it is expressed on a weight basis and is supported by data for the chloronicotinyl insecticides but there are far less robust data for the cyano substituted neonicotinoids. Synergism between neonicotinoids and other pesticides (update EFSA review) Pesticides widely used both in the agricultural and urban environment (pest control and home and garden uses) as well as by beekeepers to control pests, e.g. fluvalinate, amitraz, coumaphos to control varroa, are detectable in bees and hive matrices. Exposure of honeybees to any single pesticide application may occur over the short term or, unlike many organisms, over a longer period if residues are present in pollen and/or nectar stored within the colony or due to migration of lipophilic compounds into wax. These more persistent residues are likely to be available to the colony over a period of time depending on the active ingredient and the frequency of use, e.g. multiple applications. Bees may be exposed to mixtures of products applied to plants on which they forage. Recent data indicates the extent of mixing of formulations that occur on arable, vegetable orchards and soft fruit crops in the UK and includes tank mixing of EBI fungicides with neonicotinoid insecticides. In addition to the application of products as tank mixes, the increasing use of seed treatments raises the possible scenario of nectar, pollen or guttation water containing active ingredients also being contaminated with sprays applied during the flowering period, e.g. oilseed rape. Although many reports of residues in pollen being returned to the hive by foragers are published the majority of these are based on individual pesticide residues rather than assessments of the total pesticide residue levels and the data are often not reported in sufficient detail to determine the residue levels of the individual components within multiple detections. Data reported for residues of chemicals applied by beekeepers in honeybee colonies have primarily been directed at single varroacides with some limited data after antibiotic dosing. Those that are available show that very high levels of varroacides may be present within colonies and are regularly detected in live bees The risk from most mixtures can be assessed using the additive approaches of concentration addition (or dose addition) and independent action (IA). In identifying the relevance of synergy in determining the toxicity of mixtures it is important to understand the route of metabolism of pesticides in honeybees and the effects of age, season etc on this. The role of oxidative Neonicotinoid pesticides and bees Page 4 of 133 Report to Syngenta Ltd
Page 1 and 2: Neonicotinoid Pesticides and Bees R
Page 3: Contents 1. Executive Summary .....
Page 7 and 8: why some immune competence effects
Page 9 and 10: metabolite 6-chloronicotinic acid a
Page 11 and 12: Nectar collected by foragers from p
Page 13 and 14: 2. Introduction This literature rev
Page 15 and 16: 4. Results 2.1 Mode of Action and M
Page 17 and 18: and O-demethlase activity which is
Page 19 and 20: toxicity similar to imidacloprid an
Page 21 and 22: Table 1: Oral and contact 48 LD50 v
Page 23 and 24: Table 1. It is particularly true fo
Page 25 and 26: Incidentally, (Suchail et al., 2001
Page 27 and 28: Table 5:Summary of toxicity of neon
Page 29 and 30: Table 8: Showing published acute to
Page 31 and 32: Insecticide Concentration Range Bee
Page 37 and 38: 2.3 Multiple exposure to pesticides
Page 39 and 40: Insecticide Clothianidin Imidaclopr
Page 41 and 42: 2.4 Interactions between neonicotin
Page 43 and 44: 2.5 Exposure of bees to pesticides
Page 45 and 46: contaminated pollen and nectar brou
Page 47 and 48: none reported effects at or below t
Page 49 and 50: Figure 4. Comparison of reported ef
Page 51 and 52: Table 11 Overview of laboratory stu
Page 53 and 54: Compound tested Species Imidaclopri
Page 55 and 56:
Compound tested Species 5hydroxymid
Page 57 and 58:
Compound tested Species (Gaucho) Ap
Page 59 and 60:
Compound tested Species Imidaclopri
Page 61 and 62:
Compound tested Species ligustica t
Page 63 and 64:
Compound tested Species Thiamethoxa
Page 65 and 66:
Compound tested Species Fipronil (9
Page 67 and 68:
Compound tested Species Fipronil Ap
Page 69 and 70:
Table 16 Overview of semi-field, do
Page 71 and 72:
Page 73 and 74:
Page 75 and 76:
Page 77 and 78:
Page 79 and 80:
Page 81 and 82:
Page 83 and 84:
Compound tested Species Thiamethoxa
Page 85 and 86:
Compound tested Species (analytical
Page 87 and 88:
Table 20 Overview of studies of the
Page 89 and 90:
Compound tested species/subspecies
Page 91 and 92:
Page 93 and 94:
Page 95 and 96:
Page 97 and 98:
Page 99 and 100:
Clothianidin (99.75% TG) Bombus imp
Page 101 and 102:
Bombus terrestris oral/adults Thiam
Page 103 and 104:
5. References References in bold ar
Page 105 and 106:
Bernadou A, Damares F, Couret-Fauve
Page 107 and 108:
Colin M, Bonmatin J, Moineau I, Gai
Page 109 and 110:
EFSA (2012b) Public consultation on
Page 111 and 112:
Gauthier, M. (2010). State of the A
Page 113 and 114:
Iwasa, T., N. Motoyama, et al. (200
Page 115 and 116:
Liu, M. Y. and J. E. Casida (1993).
Page 117 and 118:
Nakajima C, Sakogawa T, Okayama A,
Page 119 and 120:
Megachile rotundata (Hymentoptera:
Page 121 and 122:
Tomizawa, M. and I. Yamamoto (1993)
Page 123 and 124:
Wu JY, Anelli CM, and Sheppard WS,
Page 125 and 126:
14. Apis mellifera.mp. [mp=ab, bc,
Page 127 and 128:
SYSTEM:OS - DIALOG OneSearch File 1
Page 129 and 130:
S21 486 S11 AND S19 S22 500316 ROUT
Page 131 and 132:
COBOMBUS OR CERATINA OR ZADONTOMERU
Page 133:
DEFRA hereby excludes all liability
show all

Neonicotinoid Pesticides and Bees - The Food and Environment ...

Create successful ePaper yourself

Delete template?

Save as template?