What are Herbicides?
Herbicides are synthetic chemicals that are used to kill unwanted plants in a geographical area. They are also termed weed killers or weedicides as they are used for mitigating the emergence of so-called weeds (undesired plants which are not intentionally sown in an area). They are used in modern agriculture setups, landscaping purposes, homestead farms, industries, schools, hospitals and even roadsides.
Herbicides; a major concern
Herbicides have made their way into agricultural systems since World War II. Over the years, they have become a major concern and an emerging issue in the world due to their surging consumption and ravaged impact on biodiversity and life forms. Now, they are the largest produced pesticide type in the world despite the fact that they are capable of deteriorating human health.
The chemical era for the development of herbicides started with the synthesis of 2,4-dichloro phenoxy acetic acid or 2,4-D during the year 1946. Later, the accelerating demand for these chemicals persuaded the industries to put money and mind into introducing new herbicide formulations. Now herbicides come in different variations or chemical families depending on their target and purpose.
Herbicides can be classified according to,
- Mode of application
- Mechanism of transport
- Soil degradation
- Time of application
- Chemical groups
- Type of formulation
- Specificity and
- Mechanism of action
HERBICIDES AND CLASSIFICATION
Mode of application
Herbicides are generally applied in the soil or on the foliage of the weeds; accordingly, they are called soil-applied herbicides and foliage-applied herbicides. Soil-applied herbicides are usually applied during pre-planting period or before the emergence of weed seeds (pre-emergence). E.g., Fluchloralin. While the other is applied during post emergence periods of weeds. E.g., Glyphosate, Paraquat
Mechanism of transport
Based on whether the action of herbicides direct or distributive, they can be considered contact herbicides and systemic herbicides respectively. The former destroys only those plant parts in contact. Most foliage applied herbicides are contacted in action. Eg. Paraquat. While the latter, when applied, are translocated to untreated parts through xylem and phloem tissues. They are generally applied to soil. E.g., Glyphosate.
Herbicides can remain active in treated soils after application for days to years. Their water solubility, vapor pressure and biodegradation susceptibility accounts for their “persistence” in the soil. Higher the persistence, higher will be the exposure risk. According to this, herbicides are classified as,
i) Short-persistent herbicides: Herbicides whose residual effect (effects caused by the herbicides that remain in the soil after they are applied to plants) stays up to a week are called short-persistent herbicides. E.g., Paraquat, Diquat, Amitrole.
ii) Medium persistent herbicides: The residual effect of these herbicides remains in the soil for up to 2 to 6 weeks.
iii) Very long persistent herbicides: If the residual effect of the herbicides remains for a few months to years, they are called very long persistent herbicides. E.g., Prometon, Fenuron.
Time of application
Depending on their action, herbicides can be applied at different stages of weed growth. Some herbicides are applied before the weed emerges. They are called pre-emergence herbicides. E.g., Atrazine, Pendimethalin, Butachlor. While those which are applied after weed emergence are called post emergence herbicides. E.g., Glyphosate, Paraquat, 2,4-D Na Salt.
The functional groups present in the active ingredients of herbicides determine the activity, selectivity, persistence and mode of action of that particular herbicide. Understanding chemical groups in a herbicide is very important to learn about its mode of action in plants and toxicity in organisms. According to the chemical groups present in them, herbicides can be classified as follow.
|Sl. No||Chemical class||Group||Chemical class|
|Anilide||Flufenacet, Metamifop, Propanil|
|Chloroacetanilide||Butachlor, Metolachlor, Pretilachlor|
|2||Aromatic acid||Benzoic acid||Bispyribac|
|Pyrimidinyl thiobenzoate||Pyrithiobac, Bispyribac-sodium|
|Picolinic acid||Aminopyralid, clopyralid, picloram|
|Quinolinecarboxylic acid||Quinclorac, quinmerac|
|8||Dinitroaniline||Fluchloralin, Pendimethalin, |
|9||Diphenyl ether||Diphenyl ether||Fomesafen|
|12||Organophosphorus||Glufosinate ammonium, |
|15||Phenoxy||Chlorophenoxy acid||2,4 D, MCPA|
|Aryloxyphenoxy propionic||Clodinafop, Cyhalofo p butyl, |
Fenoxaprop ethyl, Fluazifop,
Haloxyfop P, Metamifop,
|16||Phosphonoglycine||Glufosinate ammonium, glyphosate|
|18||Pyridine carboxylic acid||Flroxypyr-meptyl||Pyridine carboxylic acid|
|20||Triazine(chloro/methoxy/methylthio)||Triazine||Ametryn, Atrazine, indaziflam|
|21||Triazinone||Metribuzin, hexazinone, metamitron|
|23||Triazolopyrimidine||Diclosulam, Florasulam, Flumetsulam, |
|Sulfonylurea||Ethoxysulfuron, Metsulfuronmethyl, |
|26||Unclassified||Cinmethylin, Fluthiacet, |
Mode of action
This is based on how herbicides produce its effect on target sites of weed plants. I.e. specific biochemical interactions between molecular sites in plants and active ingredient. Once come in contact with the weed plant parts, the active ingredients in the formulations are absorbed by the parts. Then they move to their specific sites of action and interfere with the metabolic machinery of weeds and disrupts the biochemical pathways causing irreversible damages. This leads to the death of the plant. Herbicides that are plant-specific and kill only certain plant species leaving others unharmed are called selective herbicides. E.g., Atrazine. Herbicides, which are non-specific and destroy plants, in general, are called non-selective herbicides. E.g., Paraquat. The major mode of action and associated target sites are tabulated below.
|Mode of action||Site of action||Chemical family||Herbicides|
|Auxin growth regulators||Auxin mimics||Benzoates, Phenoxy-carboxylates |
Pyridyloxy-carboxylates, Quinoline-carboxylates, Pyridine-carboxylates
|2,4-D, MCPA, Florpyrauxifen, Fluroxypyr, Picloram Halauxifen|
|Amino Acid Inhibitors||EPSP synthase inhibitor (5-enolpyruvyl-shikimate-3-phosphate)||Glycine||Glyphosate|
Sulfonylureas, Triazolopyrimidine – Type 1, Triazolopyrimidine – Type 2
|Imazamox, Imazethapyr, Bispyribac-sodium, |
Chlorimuron-ethyl, Ethoxysulfuron Flucetosulfuron,
Metsulfuron-methyl, Orthosulfamuron, Sulfosulfuron Florasulam, Penoxsulam
|Pigment inhibitors||Phytoene desaturase (PDS) Inhibitor||N-Phenyl heterocycles,|
|Lipid biosynthesis inhibitors||ACCase inhibitors (Acetyl Co A carboxylase)||Aryloxyphenoxy-propionates (FOPs) Cyclohexanediones (DIMs) |
|Clodinafop-propargyl, Cyhalofop-butyl Diclofop-methyl, Fenoxaprop-ethyl |
Fluazifop-butyl, Haloxyfop-methyl Metamifop,
Quizalofop-ethyl, Clethodim, Pinoxaden
|Cell membrane disruptors||Photosystem 1 electron diverter||Pyridiniums||Paraquat|
|Diphenyl ethers, |
|Fomesafen, Oxyfluorfen, Flumioxazin Oxadiargyl, Oxadiazon, |
|Nitrogen metabolism inhibition||Glutamine synthetase inhibitor||Phosphinic acids||Glufosinate-ammonium|
|Photosynthesis inhibition||Inhibition of Photosynthesis at PSll – Serine 264 Binders||Phenlcarbamates, |
|Ametryne, Atrazine, Metamitron Metribuzin, Propanil, Diuron Methabenzthiazuron|
|Inhibition of Photosynthesis at PSll – Histidine 215 Binders||Benzothiadiazinone, |
|Cell division Inhibition||Microtubule inhibitors||Dinitroanilines, |
|Fluchloralin, Pendimethalin, Trifluralin|
|Thiobencarb ,Tri-allate, Alachlor Butachlor, |
Pretilachlor, Metolachlor Anilofos