Self-reliance and sustainability in the 21st century.
MOTHER EARTH NEWS’s sister magazine Utne Reader has just published an excellent report on new evidence that the systemic neonicotinoid pesticides widely used to grow corn are one of the reasons so many honeybees and other pollinators are dying. One study has shown that the suspected residues of neonicotinoid pesticides in high fructose corn syrup (fed to bees by commercial beekeepers) can cause honeybee hives to die out.
We should all write to the Environmental Protection Agency (EPA) and demand that they cancel all registrations for neonicotinoid pesticides immediately. Leaked EPA memos on one neonicotinoid called clothianidin show that even this government agency doubts the validity of studies showing the pesticide is safe.
Utne’s report doesn’t tackle the huge question raised by this discovery of pesticide residues in corn syrup — What about the effects on humans who eat huge amounts of food containing corn syrup and many other corn products? Persistent, systemic pesticides simply have no place in food production. The reasons to grow your own food just keep growing.
Here are abstracts from several recent neonicotinoid toxicity studies.
1) “In Situ Replication of Honey Bee Colony Collapse Disorder” abstract:
The concern of persistent loss of honey bee (Apis mellifera L.) colonies worldwide since 2006, a phenomenon referred to as colony collapse disorder (CCD), has led us to investigate the role of imidacloprid, one of the neonicotinoid insecticides, in the emergence of CCD. CCD is commonly characterized by the sudden disappearance of honey bees (specifically worker bees) from hives containing adequate food and various stages of brood in abandoned colonies that are not occupied by honey bees from other colonies.
This in situ study was designed to replicate CCD based on a plausible mechanistic hypothesis in which the occurrence of CCD since 2006 was resulted from the presence of imidacloprid, one of the neonicotinoid insecticides, in high-fructose corn syrup (HFCS), fed to honey bees as an alternative to sucrose-based food. We used a replicated split-plot design consisting of 4 independent apiary sites. Each apiary consisted of 4 different imidacloprid-treated hives and a control hive. The dosages used in this study were determined to reflect imidacloprid residue levels reported in the environment previously. All hives had no diseases of symptoms of parasitism during the 13-week dosing regime, and were alive 12 weeks afterward. However, 15 of 16 imidaclopridtreated hives (94%) were dead across 4 apiaries 23 weeks post imidacloprid dosing. Dead hives were remarkably empty except for stores of food and some pollen left, a resemblance of CCD. Data from this in situ study provide convincing evidence that exposure to sub-lethal levels of imidacloprid in HFCS causes honey bees to exhibit symptoms consistent to CCD 23 weeks post imidacloprid dosing. The survival of the control hives managed alongside with the pesticide-treated hives unequivocally augments this conclusion. 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.
2) “A Common Pesticide Decreases Foraging Success and Survival in Honey Bees” abstract:
Nonlethal exposure of honey bees to thiamethoxam (neonicotinoid systemic pesticide) causes high mortality due to homing failure at levels that could put a colony at risk of collapse. Simulated exposure events on free-ranging foragers labeled with an RFID tag suggest that homing is impaired by thiamethoxam intoxication. These experiments offer new insights into the consequences of common neonicotinoid pesticides used worldwide.
3) “Neonicotinoid Pesticide Reduces Bumble Bee Colony Growth and Queen Production” abstract:
Growing evidence for declines in bee populations has caused great concern due to the valuable ecosystem services they provide. Neonicotinoid insecticides have been implicated in these declines as they occur at trace levels in the nectar and pollen of crop plants. We exposed colonies of the bumble bee Bombus terrestris in the lab to field-realistic levels of the neonicotinoid imidacloprid, then allowed them to develop naturally under field conditions. Treated colonies had a significantly reduced growth rate and suffered an 85 percent reduction in production of new queens compared to control colonies. Given the scale of use of neonicotinoids, we suggest that they may be having a considerable negative impact on wild bumble bee populations across the developed world.
4) “Translocation of Neonicotinoid Insecticides from Coated Seeds to Seedling Guttation Drops: A Novel Way of Intoxication for Bees” abstract:
The death of honey bees, Apis mellifera L., and the consequent colony collapse disorder causes major losses in agriculture and plant pollination worldwide. The phenomenon showed increasing rates in the past years, although its causes are still awaiting a clear answer. Although neonicotinoid systemic insecticides used for seed coating of agricultural crops were suspected as possible reason, studies so far have not shown the existence of unquestionable sources capable of delivering directly intoxicating doses in the fields. Guttation is a natural plant phenomenon causing the excretion of xylem fluid at leaf margins. Here, we show that leaf guttation drops of all the corn plants germinated from neonicotinoid-coated seeds contained amounts of insecticide constantly higher than 10 mg/1, with maxima up to 100 mg/1 for thiamethoxam and clothianidin, and up to 200 mg/1 for imidacloprid. The concentration of neonicotinoids in guttation drops can be near those of active ingredients commonly applied in field sprays for pest control, or even higher. When bees consume guttation drops, collected from plants grown from neonicotinoid-coated seeds, they encounter death within few minutes.
5) “Nicotine-Like Effects of the Neonicotinoid Insecticides Acetamiprid and Imidacloprid on Cerebellar Neurons from Neonatal Rats” abstract:
Background: Acetamiprid (ACE) and imidacloprid (IMI) belong to a new, widely used class of pesticide, the neonicotinoids. With similar chemical structures to nicotine, neonicotinoids also share agonist activity at nicotinic acetylcholine receptors (nAChRs). Although their toxicities against insects are well established, their precise effects on mammalian nAChRs remain to be elucidated. Because of the importance of nAChRs for mammalian brain function, especially brain development, detailed investigation of the neonicotinoids is needed to protect the health of human children. We aimed to determine the effects of neonicotinoids on the nAChRs of developing mammalian neurons and compare their effects with nicotine, a neurotoxin of brain development.
Methodology/Principal Findings: Primary cultures of cerebellar neurons from neonatal rats allow for examinations of the developmental neurotoxicity of chemicals because the various stages of neurodevelopment—including proliferation, migration, differentiation, and morphological and functional maturation—can be observed in vitro. Using these cultures, an excitatory Ca2+-influx assay was employed as an indicator of neural physiological activity. Significant excitatory Ca2+ influxes were evoked by ACE, IMI, and nicotine at concentrations greater than 1 µM in small neurons in cerebellar cultures that expressed the mRNA of the α3, α4, and α7 nAChR subunits. The firing patterns, proportion of excited neurons, and peak excitatory Ca2+ influxes induced by ACE and IMI showed differences from those induced by nicotine. However, ACE and IMI had greater effects on mammalian neurons than those previously reported in binding assay studies. Furthermore, the effects of the neonicotinoids were significantly inhibited by the nAChR antagonists mecamylamine, α-bungarotoxin, and dihydro-β-erythroidine.
Conclusions/Significance: This study is the first to show that ACE, IMI, and nicotine exert similar excitatory effects on mammalian nAChRs at concentrations greater than 1 µM. Therefore, the neonicotinoids may adversely affect human health, especially the developing brain.
Photo by Fotolia/Sergey Lavrentev
Cheryl Long is the editor in chief of MOTHER EARTH NEWS magazine, and a leading advocate for more sustainable lifestyles. She leads a team of editors which produces high quality content that has resulted in MOTHER EARTH NEWS being rated as one North America’s favorite magazines. Long lives on an 8-acre homestead near Topeka, Kan., powered in part by solar panels, where she manages a large organic garden and a small flock of heritage chickens. Prior to taking the helm at MOTHER EARTH NEWS, she was an editor at Organic Gardening magazine for 10 years. Connect with her on Google+.