Insecticides are universally used, not just by farmers, but by household gardener’s as a way to prevent, mitigate or repel pests.
Due to outbreaks of infectious disease in honey bees and amphibians, the use of systematic insecticides has significantly increased over the last 20 years.
And is now thought to be the preferred choice; because of their toxicity and mechanistic action.
One type, in particular, seen to show a usage increase is – neonicotinoids - a class of agrochemicals derived from nicotine (a substance found in cigarettes).
It is thought this derivative form is solely based on the chemical similarity of the two.
First introduced within the 1990’s, neonicotinoids were principally used for their systematic nature.
While most insecticides are placed on the surfaces of yielding crops, neonicotinoids are taken up by the roots and translocated to separate areas.
This, therefore, makes the plant toxic to certain insect species.
It is this mechanism of action that has now simultaneously been linked to the adverse impacts on several other invertebrate and vertebrate species.
A Critical Evaluation of the Use of Neonicotinoid Insecticides on Human Health
Insecticides are universally used, not just by farmers, but by household gardener’s as a way to prevent, mitigate or repel pests. Due to outbreaks of infectious disease in honey bees and amphibians, the use of systematic insecticides has significantly increased over the last 20 years (Mason et al., 2012). And is now thought to be the preferred choice; because of their toxicity and mechanistic action. One type, in particular, seen to show a usage increase is – neonicotinoids - a class of agrochemicals derived from nicotine (a substance found in cigarettes). It is thought this derivative form is solely based on the chemical similarity of the two (Calderon-Segura et al., 2012). First introduced within the 1990’s, neonicotinoids were principally used for their systematic nature. While most insecticides are placed on the surfaces of yielding crops, neonicotinoids are taken up by the roots and translocated to separate areas. This, therefore, makes the plant toxic to certain insect species (Pisa et al., 2014). It is this mechanism of action that has now simultaneously been linked to the adverse impacts on several other invertebrate and vertebrate species (Sluijs et al., 2014).
There are currently, five authorised neonicotinoid insecticides available for use in the UK, including (1) acetamiprid, (2) clothianidin, (3) imidacloprid, (4) thiacloprid, and (5) thiamethoxam (Kimura-Kuroda et al, 2012); these are continually divided into separate categories, known as N-nitroguanidines and N-cyano-aminides (Kanne et al., 2005). Two of these insecticides, in particular, acetamiprid (ACE) and imidacloprid (IMI), are known for their cytotoxic and genotoxic effects on the human genome (Stocker et al., 2004) and are currently the basis of clinical investigations among the mammalian population. Both ACE and IMI are thus, seen to have the highest adverse effects on the complete family of neonicotinoids (Stocker et al., 2004).
ACE is an odourless neonicotinoid insecticide, composed of a synthetic organic compound. In insects, ACE targets the nervous system, causing paralysis and extermination, by binding to the nicotine acetylcholine receptors (nAChRs) in the neuronal pathways (Imamura et al., 2010). The Environmental Protection Agency (EPA) has established that ACE is of low risk to both the environment and to human health. Risk to health can only be attributed to an adverse effect if directly contacted through consumption. ACE is, however, also a recognised irritant to human skin, which should always be handled with care in large quantities (Environmental Protection Agency, 2002). Overall, it should be noted, that ACE has been classified as an unlikely carcinogen to human health (Environmental Protection Agency, 2002).
IMI, on the other hand, is a neonicotinoid in the chloronicotinyl nitroguanidine chemical family (Horowitz et al., 1998). Similar to ACE, it is widely recognised as a neurotoxin. Acting on the central nervous system (CNS), IMI blocks the nicotinergic neuronal pathway, preventing the release of the neurotransmitter acetylcholine; causing paralysis in insects (Horowitz et al., 1998). Again, IMI has a low toxicity to animals and humans and has been classified as an unlikely carcinogen by EPA. IMI is, however, weakly mutagenic and must be tested for under the Endocrine Disruptor Screening Program (EDSP) (Environmental Protection Agency U.S., 2009). There is currently no published studies involving humans being chronically exposed to IMI, which has questioned as to whether IMI is toxic at all to human health. Adverse effects to IMI are completely dependent on length and level of exposure, as well as previous health records; both ACE and IMI are therefore selectively more toxic to insects than any other mammal species (Horowitz et al., 1998).
In the past, both ACE and IMI have been disregarded due to their impacts on environmental ecosystems and populations. For example, the increase in neonicotinoids was found to be linked with honey bee colony collapse disorder (CCD) and a population decrease of both birds and insects (co-dependent of one another) (Gill et al., 2012). It should however, be noted that the existent use for these was focused on rats and fruit flies (Yamamoto et al., 1999), before there now known common use on aphids (Pesticide Action Network, 2013). Previous animal studies have indicated a low toxicity to neonicotinoids, due to the resistance of their nicotinic receptors against chemical substances. When compared to insects, however, this toxicity was increased, as protection from the blood brain barrier and central nervous system is limited (open-circulatory present) (Wu et al., 2001); thus providing easy access to chemical and physical influences.
Despite the pre-misconception of neonicotinoids having a limited effect on human health, it could be argued that this class of insecticides is now thought to even play a role in the neurotoxicity of the central nervous system (CNS). Thus, the fundamental effector to adverse health effects is the human exposure to these neonicotinoids. While it may be limited, human exposure is thought to be mainly due to food and water intake. As neonicotinoids are widely used in the UK, this treatment is given to crops, during growth and before consumption; consequently increasing the attributable risk by more than 30 % (Eriksson, 1997). It is therefore thought most human exposure is self-inflicted by personal agricultural routines at home or by acquiring the produce grown in pesticide-based conditions (Mohamed et al., 2009). Neonicotinoids are, however, also found in treatment creams for animals, and used to prevent or kill infestations. The residue of these neonicotinoid creams is thought to remain for up to 3-4 weeks post-usage; thus, increasing the likelihood of human contact during activities such as petting or playing (Mohamed et al., 2009).
Frequently asked questions
What is the main topic of the text?
The text critically evaluates the use of neonicotinoid insecticides and their potential impact on human health.
What are neonicotinoids and where do they come from?
Neonicotinoids are a class of agrochemicals derived from nicotine, similar in chemical structure.
How do neonicotinoids work?
Neonicotinoids are systemic insecticides, meaning they are absorbed by the plant and transported to all parts, making the plant toxic to certain insects. They target the nervous system of insects, causing paralysis and death.
Which neonicotinoids are authorized for use in the UK?
The five authorized neonicotinoid insecticides for use in the UK are acetamiprid, clothianidin, imidacloprid, thiacloprid, and thiamethoxam.
Which neonicotinoids are specifically mentioned as having cytotoxic and genotoxic effects?
Acetamiprid (ACE) and imidacloprid (IMI) are mentioned as having cytotoxic and genotoxic effects on the human genome.
What is the effect of acetamiprid (ACE) on insects?
ACE targets the nervous system of insects, causing paralysis and extermination by binding to nicotinic acetylcholine receptors (nAChRs).
What are the reported risks of ACE to humans?
The EPA considers ACE to be of low risk to human health unless directly consumed. It is a recognized irritant to human skin and is classified as an unlikely carcinogen.
How does imidacloprid (IMI) affect insects?
IMI acts on the central nervous system (CNS), blocking the nicotinic neuronal pathway and preventing the release of acetylcholine, causing paralysis in insects.
What is the potential risk of IMI to humans?
IMI has low toxicity to animals and humans and is classified as an unlikely carcinogen by the EPA. It is weakly mutagenic and must be tested for under the Endocrine Disruptor Screening Program (EDSP). Adverse effects are dependent on length and level of exposure.
What environmental impacts have been linked to neonicotinoids?
Neonicotinoid use has been linked to honey bee colony collapse disorder (CCD) and a population decrease of birds and insects.
How are humans exposed to neonicotinoids?
Human exposure is thought to be mainly due to food and water intake, due to the widespread use of neonicotinoids on crops. Exposure can also occur from residue from treatment creams for animals.
What is the proposed mechanism behind the adverse effects of neonicotinoids on humans?
The chemical similarity of neonicotinoids to nicotine allows them to share agonist activity at nicotinic acetylcholine receptors (nAChRs), disrupting signaling pathways in the central nervous system (CNS) and potentially causing developmental neurotoxicity (DNT).
- Quote paper
- Jess White (Author), 2015, A Critical Evaluation of the Use of Neonicotinoid Insecticides on Human Health, Munich, GRIN Verlag, https://www.grin.com/document/304171
