In this article we will discuss about the classification of organic pesticides.
About 75% of the animal species in the world are insects. Some are beneficial predators and pollinators but many are pests acting as competitors for food. Others are vectors of infections and parasitic diseases. Not surprisingly, man has tried always to control such pests.
In the past, preparations containing sulphur, arsenic compounds, extract of tobacco and chrysanthemum and strychnine were used, but only the synthetic pesticides (insecticides) produced by the application of modern chemistry have been really successful.
Agricultural yield has increased dramatically over the last 50 years and insecticides have played a major role in this. Unfortunately, many of the compounds used may be harmful to the environment when used carelessly. Most of the insecticides come into three classes i.e., organochlorines; organophosphates, and carbamates.
Organochlorines are also known as chlorinated hydrocarbons. These were used extensively in the mid-1940s to 1960s for agricultural pest control and for malarial control programmes. Their properties of low volatility, chemical stability and environmental persistence led to their bioaccumulation or biomagnification in the food chain of fishes, birds and mammals owing to their lipophilicity and slow metabolic degradation.
It was then demonstrated that these compounds possess strong estrogenic and enzyme inducing properties which interfere with the reproductive system, although the presenting symptoms are varied and non-specific.
In avian species of a high trophic level like pelicans, seagulls, eagles and vultures, the adverse effects of the dichlorodiphenyl derivatives are related to induction of steroid- metabolizing enzymes and the inability of the reproductive organs to mobilize enough calcium in the production of the eggshell. This eggshell- thinning leads to cracks allowing bacteria to infiltrate with resultant death of the fetus even if there is not complete breakage of the egg in the nest.
Recently the hormone-like activity of DDD (Dichlorodiphenyl Dichloroethane) has raised concern in connection with the steady decline of sperm counts in man over the past 30 years.
Organochlorine insecticides have largely been replaced by organophosphate (OP) compounds. The OP compounds are essentially polar, hydrophilic (water soluble) and are derivatives of the mineral acid i.e., phosphoric acid, having generally one — rarely two — atoms of phosphorus. Its one or more hydrogen atoms are replaced by alkyl groups. In some cases oxygen atoms are replaced with sulphur atoms.
The sulphur derivative of phosphoric acid may not themselves be active as pesticides, and are activated only by the enzymatic transformation taking place within the organisms. These reactions usually involve the replacement of one or more of the sulphur atoms by oxygen in the phosphoric acid portion of the molecule. They are very toxic even in small quantities, exhibiting anticholinesterase activities. OPIs inhibit cholinesterase at the neuromuscular junction.
Needless to mention that the OP compounds are structurally similar to acetylcholine, a potent neurotransmitter. At the enzyme site, they compete with acetylcholine and bind with cholinesterase, thus inhibiting its normal function.
OP insecticides, in general, are less persistent than the organochlorines, a property due to which they are preferred to the organochlorines. But this property also brings their repeated application during the crop period.
R1 and R2 = alkyl groups
X = diversified form of structure containing OH
The first OPI to be introduced was TEPP, which was developed in Germany during World War II (1939-45) as a substitute for nicotine. The OPs are esters, amides, or other simple derivatives of phosphoric and thiophosphoric acids. Most OPIs are esters of alcohol with a phosphorus acid or anhydrides of a phosphorus acid with some other acids.
The most commonly used OPIs are listed in Table 3.8. The OPIs act as stomach and contact poisons as fumigants and as systemic insecticides for nearly every type of insect control.
Shown in Table 3.8.
Malathion is also known as Carbophos, Mercaptothion and Maldison.
It is a non-systemic wide-spectrum organophosphate insecticide. It is of low persistence in soil, with reported field half-lives of 1-25 days. Its life in air is of about 1-5 days. It is moderately bound to soils and soluble in water. Technical Malathion is a clear, amber liquid at room temperature. Its melting point is 285°C and adsorption coefficient is 1,800. It is an indirect inhibitor of cholinesterase.
It is widely used as home garden insecticide. It is suited for the control of sucking and chewing insects on fruits and vegetables. It is also used to control mosquitoes, flies, household insects, animal ectoparasites viz., head and body lice.
Malathion is slightly toxic via the oral route, with reported oral (96 hours) LD50 value of 100 mg/kg on the rat.
Symptoms of the acute exposure are:
b. Tingling sensation
h. Blurred vision
i. Abdominal cramps
j. Respiratory depression
k. Slow heartbeat
Higher doses may cause convulsions or fatality.
Rats fed dietary doses of 5 – 25 mg/kg/day over 2 years showed no symptoms apart from depressed cholinesterase activity.
Rats fed high doses of 240 mg/kg/day during pregnancy showed an increased rate of newborn mortality. Low doses caused no reproductive effects in rats. It is not likely that Malathion may cause reproductive effects in human under normal circumstances.
Current evidences reveal that Malathion is not teratogenic.
Available evidences reveal that Malathion is not mutagenic.
Available evidences reveal that Malathion is not carcinogenic, but the data are not conclusive.
Malathion affects CNS, immune system, adrenal glands and circulatory system.
Malathion is moderately toxic to birds. The observed acute oral LD50 values for different avian species are:
a. In pheasants – 167 mg/kg
b. In chickens – 525 mg/kg
c. In mallards – 1,485 mg/kg
Malathion has a wide range of toxicity (highly to slightly toxic) in fishes:
a. In walleye (96 hours) LC50 – 0.06 mg/l
b. In brown trout (96 hours) LC50 – 0.1 mg/l
c. In cutthroat trout (96 hours) LC50 – 0.28 mg/l
d. In fathead minnows (96 hours) LC50 – 8.6 mg/l
Malathion is highly toxic to honey-bees.
Dazzel, Spectracide, Nucidol and Basudin.
Diazinon is a non-systemic organophosphate insecticide. It is a colourless to dark brown liquid. It has a flashpoint of 180°F (82°C). Its adsorption coefficient is 1,000. It has a low persistence in soil. The half-life in soil is 2 – 4 weeks and in animals about 12 hours. Metabolism and excretion rates for diazinon in human is also about 12 hours.
It is used to control cockroaches, ants, silver fishes and fleas in residential and non-food buildings. It also used in home gardens and farms to control a wide variety of sucking and leaf-eating insects. It is used on rice, fruits trees, sugarcane, corn, tobacco, potatoes and horticultural plants. Diazinon has veterinary uses against fleas and ticks.
Toxic effects of diazinon are due to the inhibition of acetylcholinesterase, an enzyme needed for proper nervous system function. The LD50 (96 hours) is 300 – 400 mg/kg for technical grade diazinon in rats.
The inhalation LC50 (24 hours) in rats is 3.5 mg/l. In rabbits, the dermal LD50 (96 hours) is 3,600 mg/kg.
The symptoms associated with diazinon poisoning in humans include:
c. Tightness in the chest
d. Blurred vision
j. Abdominal cramps
k. Slurred speech
Death has occurred from both dermal and oral exposures at very high levels.
Chronic effects have been observed at doses ranging from 10 mg/kg/day to 1,000 mg/kg/day for rats. Inhibition of RBC cholinesterase occurred at lower doses in the rats.
Actually, diazinon itself is not a potent cholinesterase inhibitor. However, in animals, it is converted to diazoxon, a metabolite that is a strong enzyme inhibitor.
One study has revealed that injection of diazinon into chicken eggs resulted in skeletal and spinal deformities in the chicks. However, the data on teratogenic effects due to chronic exposure are inconclusive.
(C) Mutagenic Effects:
Some tests have suggested that diazinon is mutagenic.
(D) Carcinogenic Effects:
It is not considered carcinogenic.
(E) Ecological Effects:
i. Effects on Birds:
Birds are significantly more susceptible to diazinon than other wild lives. LD50 values for birds range from 2.75 – 40.8 mg/kg.
ii. Effects on Fishes:
Diazinon is highly toxic to fishes as it may be justified by its LC50 value (96 hours) in rainbow trout, which is 2.6 – 3.2 mg/l. However, diazinon does not bioconcentrate significantly in fishes.
iii. Effects on Non-Target Species:
Diazinon is highly toxic to bees.
Carbamates were developed into commercial pesticides in the 1950s. Although members of this family of chemicals are effective as herbicides and fungicides, they are most commonly used as insecticides. Some carbamates are also used as nematicides.
There are approximately 25 carbamate compounds currently in use as pesticides or pharmaceutical agents. Perhaps the most widely applied carbamate insecticide is carbaryl, which is especially utilized for lawns and gardens.
Pesticidal carbamates are analogs of carbamic acid (NH2COOH), in which the carbonyl hydrogen and the amino hydrogen(s) are substituted with an alkyl, phenyl or other aromatic structures as shown below:
In simple words, carbamates are derivatives of carbamic acid. These are colourless compounds which are crystallic at normal temperature. Most pesticidal carbamates are lipophilic, a characteristic imparted to them by non-polar substitution groups.
Actually, carbamates are not broad-spectrum insecticides and they show erratic patterns of selectivity to insects. They are widely used for the control of ectoparasites in both large and small animals. Because of extreme toxicity they are recommended only for limited use.
Mechanism of Toxic Action of Carbamates:
The primary way that insecticidal carbamates work on both target and non-target species is through the inhibition of the enzyme acetylcholinesterase. Acetylcholine (ACh) is a substance that transmits nerve impulse from a nerve cell to a specific receptor such as another nerve cell or a muscle cell. Acetylcholine, in essence, acts as a chemical switch. When it is present (produced by the nerve cell) it turns the nerve impulse on. When it is absent, the nerve impulse is discontinued.
The transmission ends when the enzyme acetylcholinesterase breaks down the ACh into choline and acetic acid. Without the action of this enzyme, ACh builds up at the junction of the nerve cell and the receptor site, and the nerve impulse continues. Carbamate insecticides block (or inhibit) the ability of this enzyme, acetylcholinesterase, to break down the ACh and end the nerve impulse.
Carbamate inhibition of acetylcholinesterase is a reversible process. Estimate of the recovery time in humans range from immediate up to 4 days, depending on the dose, the specific pesticide, and the method of exposure. The breakdown of carbamate compounds within an organism is a complex process and is dependent on the specific pesticide structure.
In nutshell, the mode of action of carbamates, like OPIs, is the inhibition of acetylcholinesterase. In fact, carbamates are potent reversible inhibitors of cholinesterase. In addition, all the carbamates inhibit aliesterase of insects, but they kill insects and mammals entirely by cholinesterase inhibition.
Absorption and Excretion of Carbamates:
Carbamates are well-absorbed through skin, lungs and the gastrointestinal tract and widely distributed in tissues. They are rapidly metabolised and are excreted in urine, mainly as sulphate or glucuronide conjugates within 24 hours. A small amount is also eliminated via feces and milk. Unlike the OPIs, most of the carbamates produce low dermal toxicity.
Symptoms of Carbamate Toxicity:
In general, carbamates produce toxicity similar to that of organophosphates, but poisoning is less severe and the effects do not last long.
Symptoms of acute poisoning are typically cholinergic with salivation, lacrimation, miosis, convulsions and death.
Chronic toxicity produces signs of neuromuscular type characterized by incoordination, ataxia, recumbency and prostrating but there is no demyelination or damage to nerves. Carbaryl has been reported to be teratogenic in dogs.
Synthetic pyrethroids are currently the most widely used pesticides. Historically they were extracted from Chrysanthemum cinerariaefolium flowers which contain the insecticidal esters (pyrethrins). Being very potent insecticides with low mammalian toxicity (due to their rapid biotransformation), they have gained a strong market share. Based on the characteristics of poisoning, pyrethroids are distinguished into two classes, as shown in Table 3.10.
Members of both the classes of Table 3.10 are rapidly decomposed on exposure to metabolizing systems such as soil microbes. Hence, they are not much important from environmental pollution and related health hazard view point.
With natural pyrethrum, allergic sensitisation occurs but rarely any other toxic effect. Inappropriate use and careless handling of pesticides has resulted in some cases of human intoxication. Most prominent symptoms are burning, itching, tingling sensation of the skin, paresthesia upon dermal contact and after ingestion, epigastric pain, nausea, vomiting, headache, vertigo, blurred vision, muscular fasciculations, convulsions and seizures.
The Type I esters affect the sodium channels in nerve membranes with prolongation of sodium influx causing repetitive neuronal discharge and prolonged after potential but no severe membrane depolarisation. The Type II α- cyanoesters lead to greater and more prolonged sodium influx with persistent membrane depolarisation and eventually nerve blockade.
Whereas the first group exerts its main effects on synaptic transmission causing hyperexcitability and tremor, the second group shows its first effects on the sensory nervous system. Other actions include inhibition of Na+/Mg2+ ATPase (adenosine triphosphatase) and alteration of calcium and chloride ion homeostasis.
Toxicokinetics of Pyrethroids:
Pyrethrins are lipophilic and are readily absorbed by oral, dermal or inhalation routes. Because of their rapid metabolism, the distribution of pyrethroids is relatively unimportant. Plasma and live esterase enzymes rapidly hydrolyse the ester linkage. The hydrolysed insecticide is less toxic. Metabolism also occurs readily in GIT, so oral toxicity is low. Metabolites of pyrethroids are conjugated with glysine, glucuronic acid and sulphate and are eliminated in urine.
These are insecticides as well as acaricides. These kill mite eggs and are also used as weedicides. Example Dinitrocresol. It is highly toxic to mammals.
The pesticides employed to kill weeds (unwanted plants) are called herbicides or weedicides. In other words, herbicides are the chemicals employed to control the weed plants. In early 20th century various inorganic salts viz., copper salts, sodium salts, organic compounds, etc. were used to control weeds, but they were costly and practically ineffective. Most of the herbicides at present are organic compounds characterized by high physiological activity and effectiveness at relatively low rates of use.
Principal categories of herbicides or weedicides are:
(a) Selective contact herbicides
(b) Non-selective contact herbicides
(c) Residual herbicides
(d) Translocated herbicides.
Selective contact herbicides (weed-killers) are those which are employed for destroying weeds without injuring crops. Example 2,4-D.
Non-selective herbicides (weed-killers) e.g. Simazine, Reglone, Glyphosate, etc. are used for cleaning up roads, canals, railway tracks, irrigation canals etc. from all types of unwanted vegetation.
Residual herbicides are applied to the soil at the time of sowing where they remain active for several weeks and check the growth of weeds in competition with the germinating crop.
Translocated herbicides are sprayed on leaves and are capable of moving to all parts of the plants through the internal translocation mechanism.
Actually, the herbicides kill the plants primarily by contact with plant tissue (contact herbicides), or move within the plant tissue from the site of application to the sites of action (systemic herbicides).
(i) Phenoxy Herbicides:
Phenoxy herbicides are used against a wide variety of broad-leaved weeds to protect crops such as maize, sorghum, cereal grains, fruit trees and some vegetables. Phenoxy compounds have varying degrees of selectivity for certain types of broad leaved weeds and crops. These compounds have very little effect on grasses.
Among various derivatives of phenoxyacetic acids, 2,4-D salts and esters and 2,4,5-T are widely used as selective herbicides.
These herbicides act as growth regulators, hence also termed as hormone weed-killers. 2,4,5-T is also used as military defoliant. 2,4-D has low soil persistence. The half-life in soil is less than 7 days. Contact must be avoided since these produce neuromuscular disorders, paralysis etc. Actually the phenoxy herbicide compounds affect the peripheral nervous system in mammals.
The phenoxy herbicides such as 2,4-D are taken up by the roots or absorbed through the leaves and then distributed throughout the plant. They accumulate in the active growth regions at the tips of the stems and roots where they disrupt normal cell growth.
The phenoxy herbicides act like plant growth hormones (auxins). They stimulate the growth of old cells and the rapid expansion of new cells. This rapid growth in cell size, without normal cell division, effectively crushes the plant’s water and nutrient transport system, the phloem, in the active growing regions.
(ii) Triazine Derivatives:
The compounds of class of triazine herbicides possess a six-numbered ring, with 3N atoms replacing alternatively. These are systemic as well as contact herbicides. Some chlorine substituted derivatives are simazine, atrazine and propazine. The derivatives happen to penetrate into plants mainly through their roots and, therefore, are used as soil herbicides. Such derivatives inhibit the growth of plants and their leaves become chlorotic which indicates the retardation of photosynthesis.
Recent researches revealed that triazines inhibit the photolysis of water and the Hill reaction of photosynthesis. These derivatives have longer persistence in the soil and have moderate toxicity to humans and other mammals. Atrazine and simazine are valuable selective weed-killers, especially for broad-leaved grasses; however, atrazine is the best- known example of triazine herbicides.
I. (Simazine) 2-chloro-4, 6-di (ethyl amino) 1,3,5-Triazine
II. (Atrazine) 2-chloro-4-ethyl amino-6- (isopropylamino) 3,5 Triazine
III. (Propazine) 2-chloro-4, 6-di(isopro- pylamino) 1,3,5 Triazine
This group of herbicides are widely used for ground clearance prior to sowing. It includes two important compounds, diquat and paraquat, which are no selective contact herbicides and kill the weeds even in small doses. These generally kill dicotyledonous weeds and show mammalian toxicity.
Diuron is used as a pre-emergence herbicide. It has a low acute and chronic toxicity. The LD50 (96 hours) for male rat is around 3,400 mg/kg.
Toxicity of Herbicides:
The recently developed organic synthetic weed killers have selective toxicity for specific plants and are safe for mammals. But other less selective ones cause fatal poisoning.
These are described below:
1. Arsenicals (e.g., Sod. Arsenide, Arsenic Trioxide, Mono Sodium Mono Arsenate (MSMA) and Di Sodium Mono Arsenate (DSMA):
These are highly toxic to livestock in recommended doses. These are used as cotton defoliants and have high environmental persistence. Symptoms are profuse watery diarrhea, colic, dehydration, depression and weak pulse.
2. Amides (e.g., Bensulide, Propanil, Alachlor, Propachlor, Diphenamid):
These are toxic at very high doses. Prominent symptoms are anorexia, weight loss and muscular weakness, fibrosis. Oral intake causes gastritis, renal impairment, CNS excitement and death.
3. Methyl Uracil Compounds (e.g., Bromocif, Terbacit):
These cause mild toxicities at high doses. Symptoms include bloating, incoordination, depression and anorexia.
4. Phenyl or Substituted Urea Compounds (e.g., Diuron, Monuron, Fenuron, Linuron):
Chances of toxicity are rare under normal use – These induce hepatic microsomal enzymes and alter metabolism of other xenobiotics. Symptoms include general depression, muscular weakness and anorexia.
Poisoning from triazines is not common. Large dose ingested accidentally can cause toxic effects or death. Symptoms are muscular weakness, anorexia and posterior paralysis.
Pesticides (biocides) employed to protect agricultural crops, edible and commercial products against fungal diseases/infections are called fungicides. These are also applied on seed, grains, plants, soil or wood for preventing fungal growth. Some fungicides are applied before the onset of fungal infection and some are applied after infection of fungal pathogens.
Based upon the mode of action against pathogens, fungicides are grouped into two:
I. Protective fungicides
II. Eradicative (curative) fungicides.
Protective fungicides are applied before fungal infection in the crop takes place. Most of them have a specific mode of action and disturb different processes of the cells. Some common protective fungicides are alkyl mercury, phenyl mercury, organothiocarbamates such as Thiram, Ziram, Zineb, Karathana, Dineb, Captan etc.
Eradicative or curative fungicides penetrate and move within the tissues of that plants. Example – benzo-imidizoles (benomyl carbendazin).
With respect to the distribution relative to plants, the fungicides are further divided into two types:
I. Contact fungicides
II. Systemic fungicides.
Contact fungicides act on the pathogens by direct contact with them. In other words, they do not penetrate into plants but remain on pathogen surface.
Systemic fungicides are assimilated by the plants, prevent infection and exterminate the pathogens.
Dithiocarbamates form the major group of fungicides, largely employed by the farmers. Of the other fungicides, hexachlorobenzene is of great concern and interest.
In general, fungicides may be considered broadly under two heads:
I. Agricultural fungicides
II. Industrial fungicides.
Agricultural fungicides are used in the control of plant diseases in 3 ways:
I. Protection against infection
II. Eradication of active or latent infections, and
III. Destruction of loci of infection in the vicinity of crops.
Agricultural fungicides are also used for the disinfection of seeds, tubers and fruits. Some mercury and copper compounds are used as industrial fungicides.
All the fungicides have a low toxicity to other phytons, aves and mammals. However, in long term, some fungicides or their products containing metals are known to accumulate in food chains. The main hazard to livestock occurs from their use as seed dressings.
These fungicides are classified into three main groups:
The best example of this group is phenyl mercuric chloride acetate. Toxicity is due to mercury which causes CNS stimulation in cats and dogs producing symptoms of blindness, convulsions and hypersensitivity. Posterior weakness, tremors, incoordination and death due to destruction of central neurons. Lesions include degenerative changes in central neurons and nephrosis.
In cattle and poultry, organomercurials cause CNS depression producing symptoms of depression anorexia, incoordination, tremors, recumbency, dyspnea, hypersalivation and mucosal hemorrhage. Lesions include congestion and hemorrhage in brain, enlargement of kidney and lymph nodes, hemorrhagic enteritis and hepatic necrosis.
Neurotoxicity by organomercurials is due to inhibition of sulfhydryl and disulphide groups of enzymes and due to reduction of glutathione.
Treatment is done with mercury chelators such as dimercaptosuccinic acid, mercapto dextran, glultathione or pinicillamine orally which form a complex with mercury in the gut and prevent its absorption. Vitamin E also protects from toxicity.
These include such compounds as Pentachlorophenate, DNP, DNOC. Toxicity mostly occurs by ingestion but it may also occur by vapours — either by inhalation or through skin. They accumulate in body fats. Mechanism of toxicity is by uncoupling of oxidative phosphorylation, resulting in increased demand for O2 and heat generation. Treatment is symptomatic, mainly O2 is supplied and body temperature is lowered.
Symptoms of Thiaram toxicity in poultry are weakness of legs, diarrhea, weight loss, decreased production and abnormal eggs. In sheep, symptoms are anorexia, dyspnea, lethargy, weight loss and death from cardiac failure. Sulphur causes violent purgation and colic in horse and cattle.