Insecticide

Systemic insecticides become incorporated and distributed systemically throughout the whole plant. When insects feed on the plant, they ingest the insecticide. Systemic insecticides produced by transgenic plants are called plant-incorporated protectants (PIPs). For instance, a gene that codes for a specific Bacillus thuringiensis biocidal protein was introduced into corn (maize) and other species. The plant manufactures the protein, which kills the insect when consumed.[4]

Contact insecticides are toxic to insects upon direct contact. These can be inorganic insecticides, which are metals and include the commonly used sulfur, and the less commonly used arsenates, copper and fluorine compounds. Contact insecticides can also be organic insecticides, i.e. organic chemical compounds, synthetically produced, and comprising the largest numbers of pesticides used today. Or they can be natural compounds like pyrethrum, neem oil, etc. Contact insecticides usually have no residual activity.

Efficacy can be related to the quality of pesticide application, with small droplets, such as aerosols often improving performance.[5]

The best known organochloride, DDT, was created by Swiss scientist Paul Müller. For this discovery, he was awarded the 1948 Nobel Prize for Physiology or Medicine.[6] DDT was introduced in 1944. It functions by opening sodium channels in the insect's nerve cells.[7] The contemporaneous rise of the chemical industry facilitated large-scale production of chlorinated hydrocarbons including various cyclodiene and hexachlorocyclohexane compounds.

Organophosphates are another large class of contact insecticides. These also target the insect's nervous system. Organophosphates interfere with the enzymes acetylcholinesterase and other cholinesterases, disrupting nerve impulses and killing or disabling the insect. Organophosphate insecticides and chemical warfare nerve agents (such as sarin, tabun, soman, and VX) have the same mechanism of action. Organophosphates have a cumulative toxic effect to wildlife, so multiple exposures to the chemicals amplifies the toxicity.[8] In the US, organophosphate use declined with the rise of substitutes.[9]

Carbamate insecticides have similar mechanisms to organophosphates, but have a much shorter duration of action and are somewhat less toxic.

Pyrethroid pesticides mimic the insecticidal activity of the natural compound pyrethrin, the biopesticide found in Pyrethrum (Now Chrysanthemum and Tanacetum) species. These compounds are nonpersistent sodium channel modulators and are less toxic than organophosphates and carbamates. Compounds in this group are often applied against household pests.[10]

Neonicotinoids are synthetic analogues of the natural insecticide nicotine (with much lower acute mammalian toxicity and greater field persistence). These chemicals are acetylcholine receptor agonists. They are broad-spectrum systemic insecticides, with rapid action (minutes-hours). They are applied as sprays, drenches, seed and soil treatments. Treated insects exhibit leg tremors, rapid wing motion, stylet withdrawal (aphids), disoriented movement, paralysis and death.[11] Imidacloprid may be the most common. It has recently come under scrutiny for allegedly pernicious effects on honeybees[12] and its potential to increase the susceptibility of rice to planthopper attacks.[13]

Phenylpyrazole insecticides, such as fipronil are a class of synthetic insecticides that operate by interfering with GABA receptors.[14]

Butenolide pesticides are a novel group of chemicals, similar to neonicotinoids in their mode of action, that have so far only one representative: flupyradifurone. They are acetylcholine receptor agonists, like neonicotinoids, but with a different pharmacophore.[15] They are broad-spectrum systemic insecticides, applied as sprays, drenches, seed and soil treatments. Although the classic risk assessment considered this insecticide group (and flupyradifurone specifically) safe for bees, novel research[16] has raised concern on their lethal and sublethal effects, alone or in combination with other chemicals or environmental factors.[17][18]

Diamides are synthetic ryanoid analogues with the same mode of action as ryanodine, a naturally occurring insecticide extracted from Ryania speciosa (Salicaceae). They bind to calcium channels in cardiac and skeletal muscle, blocking nerve transmission. The first insecticide from this class to be registered was Rynaxypyr, generic name chlorantraniliprole.[19]

Transgenic crops that act as insecticides began in 1996 with a genetically modified potato that produced Cry proteins, derived from the bacterium Bacillus thuringiensis, which is toxic to beetle larvae such as the Colorado potato beetle.[24]

The technique has been expanded to include the use of RNAi insecticides which fatally silence crucial insect genes. (RNAi likely originally evolved as a defense against viruses.)[24] This was first demonstrated by Baum et al. 2007, who incorporated a V-APTase as a protectant into transgenic Zea mays and demonstrated effectiveness against Diabrotica virgifera virgifera. This suggests oral delivery against Coleoptera as a whole will probably be effective. Similar studies have followed Baum's technique to protect with dsRNAs targeting detox, especially insect P450s. Bolognesi et al. 2012 is one of these following studies, however they found dsRNA to be processed into siRNAs by the plants (in this case Solanum tuberosum) themselves, and siRNAs to be less effectively taken up by insect cells. Bolognesi therefore produced additional transgenic S. tuberosum plants which instead produced longer dsRNAs in the chloroplasts, which naturally accumulate dsRNAs but do not have the machinery to convert them to siRNAs.[25] Midgut cells in many larvae take up the molecules and help spread the signal. The technology can target only insects that have the silenced sequence, as was demonstrated when a particular RNAi affected only one of four fruit fly species. The technique is expected to replace many other insecticides, which are losing effectiveness due to the spread of insecticide resistance.[24]

Spider venom peptide fractions are another class of potential transgenic traits which could expand the mode of action repertoire and help to answer the resistance question.[26]

Many plants exude substances to repel insects. Premier examples are substances activated by the enzyme myrosinase. This enzyme converts glucosinolates to various compounds that are toxic to herbivorous insects. One product of this enzyme is allyl isothiocyanate, the pungent ingredient in horseradish sauces.

Biosynthesis of antifeedants by the action of myrosinase.

The myrosinase is released only upon crushing the flesh of horseradish. Since allyl isothiocyanate is harmful to the plant as well as the insect, it is stored in the harmless form of the glucosinolate, separate from the myrosinase enzyme.[27]

Bacillus thuringiensis is a bacterial disease that affects Lepidopterans and some other insects. Toxins produced by strains of this bacterium are used as a larvicide against caterpillars, beetles, and mosquitoes. Toxins from Saccharopolyspora spinosa are isolated from fermentations and sold as Spinosad. Because these toxins have little effect on other organisms, they are considered more environmentally friendly than synthetic pesticides. The toxin from B. thuringiensis (Bt toxin) has been incorporated directly into plants through the use of genetic engineering.

Other biological insecticides include products based on entomopathogenic fungi (e.g., Beauveria bassiana, Metarhizium anisopliae), nematodes (e.g., Steinernema feltiae) and viruses (e.g., Cydia pomonella granulovirus).

A major emphasis of organic chemistry is the development of chemical tools to enhance agricultural productivity. Insecticides represent a major area of emphasis. Many of the major insecticides are inspired by biological analogues. Many others are not found in nature.

Some insecticides kill or harm other creatures in addition to those they are intended to kill. For example, birds may be poisoned when they eat food that was recently sprayed with insecticides or when they mistake an insecticide granule on the ground for food and eat it.[8] Sprayed insecticide may drift from the area to which it is applied and into wildlife areas, especially when it is sprayed aerially.[8]

The development of DDT was motivated by desire to replace more dangerous or less effective alternatives. DDT was introduced to replace lead and arsenic-based compounds, which were in widespread use in the early 1940s.[28]

DDT was brought to public attention by Rachel Carson's book Silent Spring. One side-effect of DDT is to reduce the thickness of shells on the eggs of predatory birds. The shells sometimes become too thin to be viable, reducing bird populations. This occurs with DDT and related compounds due to the process of bioaccumulation, wherein the chemical, due to its stability and fat solubility, accumulates in organisms' fatty tissues. Also, DDT may biomagnify, which causes progressively higher concentrations in the body fat of animals farther up the food chain. The near-worldwide ban on agricultural use of DDT and related chemicals has allowed some of these birds, such as the peregrine falcon, to recover in recent years. A number of organochlorine pesticides have been banned from most uses worldwide. Globally they are controlled via the Stockholm Convention on persistent organic pollutants. These include: aldrin, chlordane, DDT, dieldrin, endrin, heptachlor, mirex and toxaphene.

Solid bait and liquid insecticides, especially if improperly applied in a location, get moved by water flow. Often, this happens through nonpoint sources where runoff carries insecticides in to larger bodies of water. As snow melts and rainfall moves over and through the ground, the water picks applied insecticides and deposits them in to larger bodies of water, rivers, wetlands, underground sources of previously potable water, and percolates in to watersheds.[29] This runoff and percolation of insecticides can effect the quality of water sources, harming the natural ecology and thus, indirectly effect human populations through biomagnification and bioaccumulation.

Insecticides can kill bees and may be a cause of pollinator decline, the loss of bees that pollinate plants, and colony collapse disorder (CCD),[30] in which worker bees from a beehive or Western honey bee colony abruptly disappear. Loss of pollinators means a reduction in crop yields.[30] Sublethal doses of insecticides (i.e. imidacloprid and other neonicotinoids) affect bee foraging behavior.[31] However, research into the causes of CCD was inconclusive as of June 2007.[32]

Besides the effects of direct consumption of insecticides, populations of insectivorous birds decline due to the collapse of their prey populations. Spraying of especially wheat and corn in Europe is believed to have caused an 80 per cent decline in flying insects, which in turn has reduced local bird populations by one to two thirds.[33]