K.L. Heong, International Rice Research Institute, Los Baños, Philippines
Two weeks ago I attended a medical symposium in Kitasato University, Tokyo, Japan and was shocked to learn of the lesser known chronic effects of insecticides on human health, particularly brain damages. As most of us seldom read medical research papers or attend medical conferences, I thought of sharing some of the new information in the medical front. Dr J. Kimura-Kuroda of the Brain Development Department of the Tokyo Metropolitan Institute of Medical Science presented her findings. They concluded that their study is the first to show that neonicotonoid insecticides, acetamiprid (ACE) and imidacloprid (IMI), with chemical structures similar to nicotine exert similar excitatory effects on mammalian nAChRs and thus can have adverse effects on human health, especially the developing brain. Their paper was published in PLoS One in February 2012. Earlier scientists have demonstrated that neonicotinoids cause brain damage in bees causing memory loss and their inability to return to their hives, one of the factors of colony collapse disorder (CCD). The EU suspended 3 neonics, imidacloprid, thiamethoxan and clothianidin to protect bees and pollination services in Europe. The EU ban can trigger increased use of neonics in Asia and we need to be concerned about similar threats to Asian agriculture. Neonics act on the nAChR channels which are involved both in physiological functions (including cognition, reward, motor activity and analgesia) and in pathological conditions such as Alzheimer’s disease, Parkinson’s disease, some forms of epilepsy, depression, autism and schizophrenia (Gotti et al 2006).
The nervous systems of both insects and humans are rather similar and even more similar at the chemical level in facilitating neurotransmission. Insecticides are chemicals designed to interfere with this process thus insects inflicted with insecticides suffer death or paralysis. At sub lethal doses, these chemicals often interfere in the insects’ biology, like reducing egg laying and recently researchers showed that they cause brain damages thus affecting their behavior.
Organophosphate (OPs) and neonicotinoid (neonics) insecticides are both neurotoxins that have different mechanisms in disrupting neurotransmission in both insect and mammalian nervous systems. The nerve target of OPs is the acetylcholinesterase (AChE) and the neonics, the nicotinic acetylcholine receptor (nAChR) (Fig 3 and 4 c and d). A cohort study done by Dr Maryse Bouchard and her team in Harvard found direct links between OP exposure and neurobehavioral deficits in the children born, like ADHD (attention deficit/hyperactive disorder). The main source of OP exposure of the children was from consumption of fruits and vegetables with residues. Children are generally more vulnerable to toxicity by neurotoxins because of their developing brain and the larger dose per body weight. Prenatal exposures to OPs were also found to be associated with poorer intellectual development (IQ) in 7-year-old children (Bouchard et al 2011).
OP and methylcarbamate (MC) insecticides not only target the AChE but also many other hydrolases in the nerve tissues. There is now concerns about OP-induced delayed neuropathy (OPIDN) and behavioral effects associated with disruptions of the cannabinoid system (Casida and Durkin 2013). This involves axonopathy and peripheral paralysis (Fig 4 (a)). The cannabinoid system is involved with appetite, pain, synaptic pasicity, mood and psychoactive effects of cannabis and can be affected by Ops and MCs (Fig 4 b).
Between 1997 and 2010 there has been a marked shift from OPs and MCs to neonics and non neuroactive insecticides. There is now increasing concerns on problems arising from the use of neonics, like the development of insecticide resistance, toxicity to bees, pollinators, aquatic as well as bird fauna and more importantly the health effects discussed above. To safely protect crops from losses due to insect pests in a sustainable manner, there is now need to place more emphasis onto discovering novel, effective and safe management methods that are not neuro-toxic (Casida and Durkin 2013).
Bouchard, MF, Bellinger, DC, Wright, RO, Weisskopf, MG 2010. Attention deficit hyperactivity disorder and urinary metabolites of organophosphate pesticides. Pediatrics 125, 1270 – 1277. (pdf)
Bouchard, M.F., Chevrier, J., Harley, K.G., ogut, K., Vedar, M., Calderon, N., Trujillo, C, Johnson, C., Bradman, A., Barr, D.B. and Eskenazi, B. 2011. Prenatal exposure to organophosphate pesticides and IQ in 7-year-old children. Environmental Health Perspectives, 119, 1185 – 1189. (pdf)
Casida, J.E. and Durkin, K.A. 2013. Neuroactive insecticides: Targets, selectivity, resistance and secondary effects. Annu. Rev. Entomol., 58, 99 – 117. (pdf)
Gotti, C., Zoli, M. and Clementi, F. 2006. Brain nicotinic acetylcholine receptors: native subtypes and their relevance. Trends in Pharmacological Sciences, 27, 482 – 491. (pdf)
Kimura-Koroda, J., Komuta, Y., Kurodda, Y., Hayashi, M. & Kawano, H. 2012. Nicotine-like effects of the neonicotinoid insecticides acetamiprid and imidacloprid on cerebellar neurons from neonatal rats. (pdf )