After reading this article you will learn about the toxicology of various herbicides.
On the basis of chemical nature, herbicides may be categorized as follows:
1. Di-nitro compounds e.g. di-nitro ortho cresol (DNOC), dinitrophenol etc.
2. Phenoxyacetic acids e.g. 2, 4-D, 2, 4, 5-T etc.
3. Bipyridinium compounds e.g. diquat, paraquat etc.
4. Heterocyclic compounds or triazenes e.g. atrazine, propazine, simizine etc.
5. Chloroaliphatic acids e.g. dalapon, sodium chloroacetate, sodium trichloroacetate etc.
6. Substituted ureas e.g. monouron, diuron, isoproturon etc.
7. Substituted dinitroaniline e.g. pendimethalin.
A. Di-Nitro Compounds:
The commonly employed di-nitro compounds are DNOC and dinitrophenol.
(a) Sources of Poisoning:
1. Ingestion of DNOC sprayed foliage by animals.
2. Licking of empty containers by curious animals.
(b) Mechanism of Toxicity:
Di-nitro compound act by interfering with electron transport chain of energy metabolism by uncoupling oxidative phosphorylation.
(c) Clinical Signs:
Peracute toxicosis. However, if animal survives-hyperpyrexia (due to excessive heat production), tachycardia, panting, dyspnea, incoordination, sweating, thirst, oliguria, weakness, cyanosis, collapse, terminal convulsions and death may be observed.
(d) Lesions:
Rapid onset of rigor mortis. The dinitrophenol imparts a yellowish green colour to tissues and urine. Degenerative changes of parenchymatous organs may be noted. Dark blood, gastroenteritis and hyperkeratosis of skin and hyperplasia of urinary bladder mucosa may also be recorded.
(e) Diagnosis:
1. History of exposure to di-nitro compounds.
2. Clinical diagnosis.
3. Post mortem lesions.
(f) Differential Diagnosis:
1. Heat stroke should be ruled out.
2. Nitrate/nitrite poisoning-chocolate colored blood and absence of hyperthermia.
3. CO poisoning-bright red blood, no pyrexia.
(g) Treatment:
No specific antidote is available.
1. Wash with soap and water if the source is through skin contact.
2. Keep the animal in cool and calm place.
3. Saline purgatives or gastric lavage.
4. Dextrose saline to check dehydration.
5. Tranquilizers and sedatives.
6. Other supportive therapies.
B. Phenoxyacetic Acid:
The 2, 4-D (2, 4-di-chloro-phenoxysaetic acid) and 2, 4, 5-T (2, 4, 5-trichlorophenoxyacetic acid) are relatively harmless to mammals. These agents are plant hormones which act as plant growth regulators selectively against dicotyledons. The use of these hormone weedicides to certain weeds increases nitrate content, thus they may be harmful indirectly by increasing the risk of nitrate poisoning.
(a) Mechanism of Toxicity:
The exact mechanism of toxicosis of phenoxyacetic acids are not precisely known. However, they are known to produce reproductive toxicity in cattle and hepatocarcinoma in laboratory animals.
(b) Clinical Symptoms:
Anorexia, weight loss, depression, un-thriftiness, and muscular weakness of hind limbs. Abortion, irregular estrus, anestrus and ovarian atrophy may be recorded in cattle. In laboratory animals, they are known to induce hypercholesterolemia and hepatocarcinoma.
(c) Treatment:
No specific antidote. Symptomatic and supportive therapies.
C. Bipyridinium Compounds:
The bipyridinium herbicides (paraquat and diquat) are broad spectrum desicant contact herbicides which are extensively used in agriculture.
(a) Mechanism of Toxicity:
The exact mechanism of toxicity of paraquat is not known; however, available literature suggests that it inhibits the DNA synthesis, phospholipid synthesis and excretion, release of platets and serotonin and release PGF2 alpha in the lungs.
(b) Clinical Symptoms:
Generally clinical signs are seen after 3 days of exposure to paraquat. Symptoms of toxicity observed are emesis, anorexia abdominal pain, dyspnea, jaundice and CNS depression. If survived for several days, animal may exhibit dehydration, pallor or cyanosis, tachycardia, uremia, rales, pulmonary edema and emphysema.
(c) Lesions:
Pulmonary congestion, edema and hemorrhage; lingual ulcers, congestion of liver, kidney and spleen with consistent histopathological lesions. Brain damage characterized by spongy degeneration of cerebral white matter may be noted.
(d) Diagnosis:
1. History.
2. Clinical signs.
3. Post mortem lesions.
(e) Differential Diagnosis:
1. Rule out pneumonia.
2. ANTU poisoning-more acute and fatal in nature.
3. In cattle, it should not be confused with bovine pulmonary edema.
(f) Treatment:
Symptomatic and supportive treatment.
1. Emesis or gastric lavage to check further absorption.
2. Tranquilizers and sedatives.
3. Vitamins A, C and E may have some beneficial effect.
4. NSAIDs may block synthesis of prostaglandins.
Oxygen therapy is contraindicated because it will act as a ready source for the formation of more and more super-oxides (O2-).
Heterocyclic Compounds (Triazenes):
The heterocyclic compounds include atrazine, simazine, propazine, prometone and aminonitriazole. This group of herbicides has very low mammalian toxicity potential.
The mechanism by which these agents produce toxicity is not well understood.
(a) Clinical Symptoms:
Weakness, ataxia and posterior paralysis appear after three weeks of ingestion of the compound. Comparatively, prometone is more toxic than propazine. Aminotriazole poisoning is characterized by stimulation of GI and bronchial smooth muscles and causes pulmonary edema and severe gastric and intestinal hemorrhages.
(b) Treatment:
No specific treatment is available. Provide symptomatic/supportive treatment.
E. Chloroaliphatic Acids:
The most commonly used chloroaliphatic acids are dalapon, sodium chloroacetate and sodium trichloroacetate. These agents are relatively harmless compounds.
F. Substituted Ureas:
This group of herbicides include monouron, diuron and isoproturon. Substituted ureas have low toxicity potential. Poisoning with these compounds is rare.
(a) Clinical Signs:
Signs such as anorexia, laboured breathing, abnormal gait, excitability are followed by depression and prostration.
(b) Treatment:
No specific treatment. Supportive treatment may be given.
G. Substituted Di-nitro-aniline Compound:
Pendimethalin-a substituted di-nitro-aniline compound is a broad spectrum weedicide having very low mammalian toxicity.
(a) Clinical Symptoms:
CNS depression, swelling of the face, incoordination, hypothermia, conjuctival hemorrhages, dyspnea and death at very high dose have been recorded in laboratory animals.
(b) Treatment:
Symptomatic treatment may be provided.
Rodenticides:
Rodenticides are agents which destroy the rodent pests. Some of the commonly used rodenticides are alpha-naphthyl thiourea (ANTU), warfarin, zinc phosphide, red squill etc.
A. Alpha-naphthyl thiourea (ANTU):
(a) Source of Poisoning: Accidental ingestion of baits intended for target rodents.
(b) Mechanism of Toxicity: ANTU interferes with effective uptake of O2 from pulmonary alveoli by producing extensive edema of the lungs due to increased capillary permeability and seepage of fluid into the airways. This leads to formation of froth which further blocks the air passage and virtually the animal drowns in its own body fluids.
ANTU induces vomiting in dog if the stomach is empty as it is highly irritant to gastric mucosa. However, ANTU will fatally poison if the stomach is full.
(c) Clinical Symptoms:
Signs of ANTU poisoning include vomiting, dyspnea, cyanosis, rales, tachycardia, anorexia, incoordination, prostration, cough, snort, asphyxiation, coma, clonic convulsions and death.
(d) Lesions:
Cyanosis, dark colored arterial blood, heavy and edematous lungs, presence of blood-tinged fluid and froth in the bronchi, hydrothorax, hyperemic tracheal, bronchial and GI mucosae, liver and kidneys may be noted.
(e) Diagnosis:
1. History of employing ANTU as baits:
2. Clinical signs.
3. Post mortem lesions.
(f) Treatment:
1. Emetics or gastric lavage.
2. Sedatives like barbiturates.
3. Oxygen under positive pressure.
4. Competitive ANTU antagonist, 1-ethyl-l-phenyl thiourea may reverse ANTU toxicosis in rats.
5. Alpha adrenoceptor antagonists to dilate pulmonary vessels.
6. Osmotic diuretics (50% glucose or mannitol).
B. Warfarins:
Warfarins and its analogs are anticoagulant rodenticides. Commonly used warfarin rodenticides are warfarin, pindone, chlorphacinone, naphthyllindandione etc.
(a) Sources of Poisoning:
Ingestion of residues of the rodenticides or baits intended for rats and mice. Pigs, dogs and cats, if they ingest dead rats or mice which are killed by these groups of agents.
(b) Mechanism of Toxicity:
Warfarins interfere with normal function of Vitamin K and cause coagulation defect characterised by decreased blood concentrations of coaugulation proteins-factor II (prothrombin), factor VII (proconvertin, auto-prothrombin I), factor IX (Christmas factor, – auto-prothrombin II) and factor X (Stuart factor, auto-prothrombin III). The decreased coagulation factors cause massive internal bleeding and the onset time is 2-5 days and death of animals is due to tissue hypoxia.
(c) Clinical Symptoms:
Massive haemorrhages, blood discharge from body orifices, haematoms under skin and at joints, purpura, dyspnea, weakness, shock and death.
(d) Lesions:
Massive internal haemorrhages, blood is found in GIT, thorax, joints and pericardium, hepatic necrosis and jaundice may be seen.
(e) Diagnosis:
1. History;
2. Clinical signs;
3. Post-mortem lesions.
(f) Treatment:
1. Sedatives or tranquilizers;
2. Artificial respiration;
3. Provide clotting factors by blood transfusion at the rate of 20 ml/ kg body weight.
4. Injection Vitamin K, 5 mg/kg, slow IV dogs and cats. Repeat for two days by IM route. In large animals, a dose of 0.5- 1.0 mg/kg by slow IV injection and oral Vitamin K should be administered daily for 4-6 days.
C. Zinc Phosphide:
Zinc phosphide (Zn3P2) is commonly used rodenticide for destroying the rats, mice, ground squirrels and dogs.
(a) Sources of Poisoning:
1. Baits intended for target rodents may be eaten by other animals or birds.
2. Malicious poisoning.
(b) Mechanism of Toxicity:
Zinc phosphide is directly irritant to gut. This action causes vomition, a life saving reflex in animals that can vomit. Produces severe gastroenteritis.
Acute Zn3P2 toxicosis is neither due to zinc nor phosphorus. The Zn3P2 liberates phoshine (PH3) in the stomach and upper intestine. Any factor which stimulates the gastric HCl concentration, increases Zn3P2 toxicity. Absorbed phoshine is responsible for development of toxicosis. However, chronic toxicity is possibly due to both Zn3P2 and phoshine.
(c) Clinical Symptoms:
Anorexia, lethargy, increase in rate and depth of respiration, sterterous respiration, abdominal pain, bloat (in ruminants) ataxia, weakness, prostration, dyspnea, gasping, struggling, convulsions, coma and death in 4-48 hours.
(d) Lesions:
Pulmonary congestion and edema, pleural effusion, subpleural haemorrhages, congestion of liver and kidneys and gastroenteritis. Acetylene odour in stomach may be detected.
(e) Diagnosis:
1. History.
2. Clinical signs.
3. Post-mortem lesions.
(f) Treatment:
No specific treatment, however, following supportive therapies may be given.
1. Gastric lavage with 5 per cent sodium bicarbonate.
2. Injection Calcium borogluconate.
3. Treatment for shock.
4. Anticonvulsants.
D. Fluoroacetate:
Fluoroacetate as such is non-toxic but becomes highly toxic after its conversion in the body to fluorocitrate (lethal synthesis).
(a) Mechanism of Toxicity:
Due to structural similarities, fluoroacetate competes with acetate. In place of acetate, fluoroacetate condenses with CoA and oxalocetate to form fluorocitrate. Fluorocitrate competes with citrate for the active site of Kreb’s cycle enzyme aconitase (the target receptor of fluoroacetate poisoning). This results in inhibition of aconitase leading to slowing of Kreb’s cycle and decreasing cellular respiration. The brain and heart functions are most severely affected.
(b) Clinical Signs:
CNS excitation, restlessness, vomitting, diarrhoea, urination, hyperirritability, hypermobility, frenzied running, barking, frothing at mouth, clonic-tonic convulsions, terminal coma, gasping and death within 2-12 hours have been observed in dogs and guinea pigs.
In horse, cattle, sheep and goats, colic, unrest, trembling staggering, cardiac arrythmias, tachycardia, terminal ventricular fibrillation and death. Both CNS and cardiac signs are observed in swine, cats and hasmters.
(c) Diagonsis:
1. History of accidental ingestion of fluoroacetate bait.
2. Clinical signs.
(d) Treatment:
No specific treatment.
1. Barbiturates to control the convulsions.
2. Glycerol monoacetate 0.1-0.5 mg/kg, IM.
3. Treatment for cardiac arrythmias may be tried.
E. Red Squill:
Red squill is obtained from the plant-Urginea martima sea onion. Red squill contains a cardiac glycoside-scilliroside. This compound is comparatively one of the safest rodenticides as it is non-toxic to poultry, causes emesis in animals that are capable of vomiting and very unpalatable to domestic animals. Red squill is more toxic to female rats than males.
(a) Clinical Signs:
Small doses of red squill cause convulsions and higher doses may produce cardiac arrest before exhibiting convulsions. In livestock, CNS stimulation symptoms such as hyperesthesia, incoordination and flank convulsions may be noted.
(b) Lesions:
Gastritis and enteritis-sometimes haemorrhagic. Pronounced congestion of mesenteric vessels; swelling and congestion of kidneys, liver, lungs and myocardium may be noticed. Histopathological examinations of these organs may reveal degenerative changes.
(c) Diagonsis:
1. History;
2. Clinical signs.
(d) Treatment:
Symptomatic and supportive therapies.