Harmful Effects of Pesticides on Human Physiology | Pharmacology

After reading this article you will learn about the harmful effects of pesticides on human physiology.

Introduction:

Living in the chemically polluted environment has caused a number of health problems. Acute toxicity syndromes are noticeable, attract attention and therefore, opportunities of suitable interventions to save victims are high.

In contrast, slow toxicity cases pass undetected because the symptoms are mostly unrelated or only indirectly related. For example, chronic toxicity due to chemical pesticides weakens defence system of body leading to infections of varied nature, even with opportunistic pathogens. In India, the use of insecticides, fungicides, herbicides and others is 80%, 10%, 7% and 3% respectively and about 1.0 million people suffer from pesticide toxicity of which about 20,000 die every year.

Human beings are exposed to a large number of chemicals, some of which may be agricultural chemicals like pesticides, herbicides, fungicides, rodenticides; food and feed additives and preservatives like antibiotics, drugs, hormones and chemicals.

Possible Harmful Effects:

Increased, indiscriminate and uncontrolled use of pesticides and other agricultural chemicals for increased crop production has polluted soil, air and water. Acharjyo (1996) quoted an assessment wherein 25% of the estimated 34,000 tonnes of pesticides annually used in India find their way to sea.

DDT for example, enters into food chain through meat food animals, fish, predators of crop eating pests (rats, frogs, reptiles, insects etc.), birds and other omnivorous or scavenging animals. A general sketch of translocation of these chemicals through plant and animal tissues to human beings is presented.

Acharjyo (1996) himself attended to fatal poisoning in free living elephants who had consumed paddy crop sprayed with insecticide. The harmful effects on human physiology are varied in nature depending upon chemical and degree of exposure.

These are:

1. Carcinogenic

2. Mutagenic

3. Teratogenic

4. Allergy

5. Acute Toxicity or Poisoning.

1. Carcinogenic Effect:

A substance that produces cancer is called Carcinogen and its cancer producing activity is called as Carcinogenic effect. The toxic dose of a Carcinogen is quite higher than the Carcinogenic dose. In food producing animals treated with or fed Carcinogenic compound, no residues are permitted in the edible tissue at the time of slaughter (e.g. di-ethyl-stilbestrtol).

The carcinogenic molecule interact with various intra-cellar components like protein, DNA, RNA, glycogen, phospholipids and glutathione and form a chemical receptor complex called adduct. The reaction is irreversible and therefore, the dissociation of the adduct to the free chemical and free receptor does not occur.

This leads to damage of the cellular component such as DNA which is permanent in nature. A cell has a natural capability to remove a carcinogen bound to DNA at the rate of approximately 1 x 10⁵ carcinogen molecule/cell/12 hours.

It has been observed that the radiolabeled 2-acetyl-amino-fluorine and azo dyes remained in hepatic DNA and glycogen for months. Therefore, the persistent covalently bound drug residue in food products would constitute a health hazard. For veterinary drugs the drug residue in meat, milk and eggs should not be more than 1 ppb or 1ppt.

2. Mutagenic Effect:

The chemical agents which damage the genetic component of a cell is called as mutagen and its activity is mutagenic effects. The mutagenic affect shown by a chemical substance is either by gene mutation or by chromosomal aberration.

A mutagen can cause three types of genetic injury of germinal or somatic cells:

1. Point mutation

2. Gene elimination

3. Chromosomal breakage.

The genetic mutagenesis is more important because it is hazardous to future generation while the somatic mutagenesis may lead to aging which is due to accumulation of damage DNA. The polycyclic hydrocarbon, natural or synthetic, have mutagenic and carcinogenic properties.

3. Teratogenic Effect:

The drug or chemical agents which produce a toxic effect on the embryo or fetus during gestation is called as teratogen. This lead to congenital malformation. The drug thalidomide is a well-known teratogen and causes phocomelia or ‘seal limb’ in children.

The feed containing methallibure an anterior pituitary inhibitor to control oestrus cycle in swine, results into congenital deformity in new born piglets. A number of compound derived from plant have teratogenic effect in animals.

4. Drug Allergy or Hypersensitivity:

Allergic reactions to drugs or chemicals are quite similar to the allergic responses to protein, carbohydrate and lipid and may include anaphylaxis, serum sickness, cutaneous reactions and delayed hypersensitive response. In humans, allergic or hypersensitive response to drugs appears to be more commonly associated with antibiotics, especially penicillin. However, its allergic response to animal is not well known.

5. Acute Toxicity:

A. Organophosphate:

According to a study in California, 75% of systemic poisoning with agricultural chemicals in human beings is due to phosphate esters.

For all organophosphate esters the approximate residual range is 0.003 ppm.

Symptoms in Animals:

The symptoms in animals after intoxication with organophosphate esters is due to inhibition of cholinesterases (these esterases hydrolyze acetylcholine, butyrylcholine, benzoyl choline, acetyl-B-methyl choline etc. depending on the species). This reflects stimulation of the autonomic and central nervous systems and subsequent accumulation of acetylcholine.

The prolongation and intensification of acetylcholine action results in two degree of response. The initial action in on smooth muscles, cardiac muscle and exocrine glands and is quite comparable to stimulation of the post ganglionic parasympathetic nerve.

This early signs of toxicity resembles with those of muscarine and hence this phase is also known as muscarinic action of acetylcholine and most common signs are intestinal cramp, tightness in the chest, blurred vision, headache, diarrhoea, decrease in blood pressure and salivation. This action can be counteracted by atropin.

The second phase results from stimulation of the peripheral motor system and all autonomic ganglia. This phase resembles with the classical action of nicotine, therefore, it is also known as nicotinic action of acetylcholine.

The complexity of toxic action during the second stage includes neuromuscular and ganglionic blockage. The ultimate effect is stimulation and/or paralysis of the somatic, autonomic and central nervous system. Sings of toxicity depends upon the toxicant, vehicle, route of administration dosage etc.

Gross Pathology in Animals:

This includes demyelination of peripheral nerves, Anterior horn cell degeneration, and fatty degeneration of spinal cord white matter. This results in a syndrome resembling “Jake leg” or “ginger jake” paralysis.

Prognosis:

It depends upon the exposure, type of compound and adequacy of treatment.

Treatment:

The onset of symptoms is rapid and maximum effects may develop within a few hours. It is thus important that medical case be attended to without delay. A general rule is that atropine should be administered until visible effects of atropinization are observed.

The muscarinic are only a part of the action produced by heavy exposure, therefore, patient be treated symptomatically with artificial respiration postural drainage, warmth etc. In addition to this PAM or DAM is recommended in doses of 20-50 mg/kg b. wt. I/M or slow i/v.