Toxicity of HERBICIDES

HERBICIDES

            On the basis of chemical nature, herbicides may be categorized as follows:

1.      Dinitro compounds e.g. dinitro 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.

Dinitro Compounds

            The commonly employed dinitro compounds are DNOC and dinitrophenol.

            Sources of poisoning Ingestion of DNOC sprayed foliage by animals; Licking of empty containers by curious animals.

            Mechanism of toxicity Dinitro compound act by interfering with electron transport chain of energy metabolism by uncoupling oxidative phosphorylation.

            Clinical signs Peracute toxicosis. However, if animal survives-hypepyrexia (due to excessive heat production), tachycardia, panting, dyspnea, incoordination, sweating, thirst, oliguria, weakness, cyanosis, collapse, terminal convulsions and death may be observed.

            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.

            Diagnosis History of exposure to dinitro compounds; Clinical diagnosis; Post mortem lesions.

            Differential diagnosis Heat stroke should be ruled out; Nitrate/nitrite poisoning - chocolate colored blood and absence of hyperthermia; CO poisoning - bright red blood, no pyrexia.

            Treatment No specific antidote is available. Wash with soap and water if the source is through skin contact. Keep the animal in cool and calm place. Saline purgatives or gastric lavage. Dextrose saline.to check dehydration. Tranqriilizers and sedatives. Other supportive therapies.

Phenoxyacetic acid

            The 2, 4-D (2, 4-dichlorophenoxysaetic acid) and 2, 4, 5-T (2, 4, 5 - trichlorophenoxyacetic acid) are relatively harmless to mammals. These agents are plant hormones which acts 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.

            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.

            Clinical symptoms Anorexia, weight loss, depression, unthriftiness, 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 hypocholesterolemia and hepatocarcinoma.

            Treatment No specific antidote. Symptomatic and supportive therapies.

Bipyridinium Compounds

            The bipyridinium herbicides (paraquat and diquat) are broad spectrum desicant contact herbicides which are extensively used in agriculture.

            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 platlets and serotonin and release PGF₂ alpha in the lungs.

            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.

            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.

            Diagnosis History, C1inical signs, post mortem lesions.

            Differential diagnosis Rule out pneumonia. ANTU poisoning - more acute and fatal in nature. In cattle, it should not be confused with bovine pulmonary edema.

            Treatment Symptomatic and supportive treatment. Emesis or gastric lavage to check further absorption. Tranquilizers and sedatives. Vitamins A, C and E may have some beneficial effect. NSAIDs may block synthesis of prostaglandins. Oxygen therapy is contraindicated because it will act as a ready source for the formation of more superoxides (0₂^-).

Heterocyclic compounds (Triazenes)

            The heterocyclic compounds include atrazine, 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.

            Clinical symptoms Weakness, ataxia and posterior paralysis appear after three weaks of ingestion of the compound. Comparatively, prometone is more toxic than propazine. Aminotriazole is characterized by stimulation of GI and bronchial smooth muscles and causes pulmonary edema and severe gastric and intestinal hemorrhages.

            Treatment No specific treatment is available. Provide symptomatic/supportive treatment.

Chloroaliphatic acids

            The most commonly used chloroaliphatic acids are dalapon, sodium chloroacetate and sodium trichloroacetate. These agents are relatively harmless compounds.

Substituted ureas

            This group of herbicides include monouron, diuron and isoproturon.

            Substituted ureas have low toxicity potential. Poisoning with these compounds is rare.

            Clinical signs Signs such as anorexia, laboured breathing, abnormal gait, excitability are followed by depression and prostration.

            Treatment No specific treatment. Supportive treatment may be given.

Substituted dinitroaniline compound

            Pendimethalin - a substituted dinitroaniline compound is a broad spectrum weedicide having very low mammalian toxicity.

            Clinical symptoms CNS depression, swelling of the face, incoordination, hypothermia, conjunctival hemorrhages, dyspnea and death at very high dose have been recorded in laboratory animals.

            Treatment Symptomatic treatment may be provided.