Honeybees

We used LC/MS-MS to analyze samples of honey bees, pollen stored in the hive and several potential exposure routes associated with plantings of neonicotinoid treated maize. Our results demonstrate that bees are exposed to these compounds and several other agricultural pesticides in several ways throughout the foraging period. During spring, extremely high levels of clothianidin and thiamethoxam were found in planter exhaust material produced during the planting of treated maize seed. We also found neonicotinoids in the soil of each field we sampled, including unplanted fields. Plants visited by foraging bees (dandelions) growing near these fields were found to contain neonicotinoids as well. This indicates deposition of neonicotinoids on the flowers, uptake by the root system, or both. Dead bees collected near hive entrances during the spring sampling period were found to contain clothianidin as well, although whether exposure was oral (consuming pollen) or by contact (soil/planter dust) is unclear. We also detected the insecticide clothianidin in pollen collected by bees and stored in the hive. When maize plants in our field reached anthesis, maize pollen from treated seed was found to contain clothianidin and other pesticides; and honey bees in our study readily collected maize pollen. These findings clarify some of the mechanisms by which honey bees may be exposed to agricultural pesticides throughout the growing season. These results have implications for a wide range of largescale annual cropping systems that utilize neonicotinoid seed treatments.

Dans le texte proposé, deux éminents toxicologues, doublés d'excellents mathématiciens, Henk A. TENNEKES hollandais, et Francisco SANCHEZ-BAYO australien, ont mis en commun leur compétence pour démontrer que les "Tests Standards", aujourd'hui en usage dans le domaine des travaux préalables à l'homologation des substances chimiques -en particulier des pesticides-, ne sont pas en mesure de définir des "niveaux sûrs d'exposition", tant pour les êtres humains que pour la biodiversité. Cette incapacité relève tant des points de vue "conceptuel que statistique". S'appuyant sur les travaux, anciens certes, de Haber d'une part, et de Druckrey (pharmacologue) et Küpfmüller (mathématicien) d'autre part, mais pourtant toujours d'une évidente actualité, ils démontrent d'un côté les failles des Tests Standards, de l'autre ils démontrent qu'un test, fondé sur une base conceptuelle et une pratique différentes, le test "Time-To-Event" ou TTE, "Temps-pour-un-Evènement", permet au contraire de prévoir les effets probables, au cours du temps, des substances sur les espèces non-cibles. Ainsi s'effondre le postulat (idéologique car jamais démontré) de l'innocuité des "faibles doses". Sous certaines conditions, résultant de l'interaction entre la substance et les récepteurs de l'organisme, plus le temps d'exposition s'allonge plus la dose totale reçue diminue pour produire un même effet. La substance est ainsi plus toxique à faible dose qu’à forte dose, le temps jouant ainsi un rôle majeur dans l’expression de la toxicité. Ce démenti scientifique formel infligé au postulat "d'un seuil d'innocuité" des faibles doses ouvrira-t-il les yeux des différentes Agences gouvernementales ? Si l’on souhaite assurer la sécurité des humains et l’avenir de la biodiversité il y a urgence !
Christian Pacteau

Imidacloprid is the first highly effective insecticide whose mode of action has been found to derive from almost complete and virtually irreversible blockage of postsynaptic nicotinic acetylcholine receptors (nAChRs) in the central nervous system of insects. Imidacloprid mimics the action of acetylcholine, but unlike acetylcholine, imidacloprid is not deactivated by acetylcholinesterase and thus persistently activates nAChRs. Chronic exposure of insects to imidacloprid therefore leads to cumulative and virtually irreversible blockage of nAChRs in their central nervous system, which play roles in many cognitive processes. A honey bee during a foraging flight must learn and recall many complex visual patterns. These cognitive functions may be perturbed when nAChRs, necessary for the formation of longterm memory and involved in acquisition and retrieval processes, are persistently blocked. At sub-lethal doses imidacloprid can alter honey bee foraging and learning. Imidacloprid has been detected at levels of 5.7 μg kg-1 in pollen from French hives and foraging honey bees reduced their visits to a syrup feeder when it was contaminated with 3 μg kg-1 of imidacloprid. Foraging as well as hive worker bees and brood are likely to be continuously exposed to imidacloprid when contaminated food is collected and stored inside the hive. This may in the course of time be detrimental to the bee colony and ultimately cause colony collapse.

The traditional approach to toxicity testing is to consider dose (concentration)-effect relationships at arbitrarily fixed exposure durations which are supposed to reflect ‘acute’ or ‘chronic’ time scales. This approach measures the proportion of all exposed individuals responding by the end of different exposure times. Toxicological databases established in this way are collections of endpoint values obtained at fixed times of exposure. As such these values cannot be linked to make predictions for the wide range of exposures encountered by humans or in the environment. Thus, current toxicological risk assessment can be compromised by this approach to toxicity testing, as will be demonstrated in this paper, leading to serious underestimates of actual risk. This includes neonicotinoid insecticides and certain metallic compounds, which may require entirely new approaches. In order to overcome this handicap, an increasing number of researchers are using a variant of the traditional toxicity testing protocol which includes time to event (TTE) methods. This TTE approach measures the times to respond for all individuals, and provides information on the acquired doses as well as the exposure times needed for a toxic compound to produce any level of effect on the organisms tested. Consequently, extrapolations and predictions of toxic effects for any combination of concentration and time are now made possible.

New Zealand agriculture and horticulture is dependent solely upon bees to carry out pollination. We have no other insects capable of doing the job. Yet these vital workers are under extraordinary threat, not only from insecticides but also from disease, habitat loss and the varroa mite. Currently, this mite poses the most immediate danger. Since its arrival in 2000 it has exterminated feral bees whose role in pollinating clover was taken for granted by farmers. Clover is an important source of natural nitrogen, the prime fertiliser of pasture. We can’t afford, therefore, to compromise the health of bees that are managed in hives or we risk losing everything – the export basis of our economy, along with the security of the food which keeps us alive. But by using insecticides whose active ingredient is a systemic neonicotinoid chemical, it’s likely we are. The National Beekeepers Association points out that all the conditions which are implicated in bee die-off overseas exist here, namely: the threat of increased pests and diseases, the long term effects of the varroa mite, the sub-lethal and synergistic effects of agricultural chemicals and the loss of habitat.