Hazardous health effects of pesticides

By Dr. Mohamed Isa Abdul Majid
The Sun, February 22, 1997

THOUGH BENEFICIAL TO THE agricultural sector and in vector borne disease control, pesticedes can couse both illnesses and death in humans. These problems arise from various circum-stances, either direct of indirect human contact with pesticides.

The group of people most susceptible to direct contact with such chemicals are workers constantly exposed to or work with pesticides such as those in the agricultural or pesticide manufacturing sector. Workers who mix, load and apply pesticides are exposed to the concentrated forms of pesticides and the primary route of exposure is the skin. If these workers are not equipped with protective clothing during the application of the chemicals, absorption of pestocides through the skin would be significant.

Once in contact with the skin, pesticides can either be absorbed into the body or localised to the skin only. The common local effect seen are skin problems such as determatitis. Absorption into the body can lead to various health problems eye irritation to upper respiratory tract problems to systemic poisoning, which can lead to death.

Indirect contact with pesticides comes from the ingestion of pesticide comes from the ingestion of pesticide residues in food which would lead to an increased level of pesticide in the body is normally associated with long - term exposure to pesticides and thus may or may not be associated witj illness.

The human body is a vasity complex biochemical organism, finely tuned and adaptable. It contain many diferent regulatory systems to make sure that things work properly in response to external conditions.

This type of regulation, known as homeostasis, occurs for all bodily processes. and usually withoutany awareness or thought on our part. When external circumstances (like extreme heat or cold) or internal condition (disease or poisoning) cannot be adjusment by normal mechanisms, the signs of discomfort and disease appear.

The types of physical effects seen or felt (signs and symptoms) depend on the types of stress to which the body has been exposed. Because there are so many complex inter-relationships between the systems within the body, a single change in any system may result in numerous efects in other systems.

In addition types of response to disease are limited, thus signs and symtoms of disease are often quite similar for different diseases. For example, headaches, fever, nauses,vomiting and diarrhoea are very common non-specific symptoms of deasease, produced by many different conditions. Due to the generality of most physiological responses to disease, many other methods have been developed to help diagnose the actual causes of diasease.

A body's homeostasis can be upset by physical chemical and/or biological body's racction to prologed stress depends on the nature of the agent as well as the degree and duration of stress. When the stress is too strong or too long and homeostassis cannot be maintained or restored, diasease occurs. Poisoning by chemical agents is nothing more than chemically-induced diasease and the symtoms of chemical poisoning often are the same as symtoms caused by biological agents such as bacteriaa or viruses.

To better understand how disease is caused by exposure to toxic chemicals, we must first understand how pesticides work within the body.

Pesticides work by changing the speed of different body funtions, increasing them (eg increasing the heart rate or sweating) or decreasing them (sometimes to the point of stopping them entirely, like breathing)

For instance, people poisoned by malathion, an insecticide, may experience increased sweating. This results in a series of event in the body as a responseto the chemical. First is the biochemical inactivation of an enzyme. This (1) biochemical change leads to a (2) cellular change (in this case an increase in nerve activitay). The cellular change is then responsible for (3) physiological changes, which are the symtons of poisoning seen or felt in particular organ systems (in this case the sweat glands). The basicprogression of effects from biochemical to cellular to physiological ossurs in most cases of poisoning.

Depending on the speccific biochemical mechanisma of action, a poison may have very widespread effects throughout the body, or may cause a very limited change in physiological functioning in a particular region or organ. Malathion causes a very simple inactivation of an enzyme which is involve in communication between nerves. The enzyme which parathion, another type of pesticide, inactivates is, however, widespread in the body and thus a variety of effects on many body systems are seen besides sweating.

Toxicity is a general term used to indicate adverse effects produced by pesticides. These adverse edverse effects cam range from slight symtoms such as headache and nausea to severe ones such as coma, convulsions and even death.

Toxicity is normal divided into four types, based on the amount of exposure to a pesticide and the time it takes for toxic symptoms to develop. The acute toxicity and chronic toxicity. The former is due to short-term exposure and happens within a relatively short period of times whereas the latter is due to long-term exposure and happens over a longer period.

Most toxic effects are reversible and do not cause permanent damage but complete recovery may take a long time. However, some pesticides may cause irreversible or permanent damage.

Pesticides can effects just one particular organ system or they may produce generalised toxicity by effecting a number of systems. Usually, the type of toxicity is subdivided intio categories based on the major organ systems affected. Some of these are listed in Table 1.

Because the body only has a certain number of responses to chemical and biological stressors, it is a complicated process sorting out the signs and symtoms and determining the actual cause of human disease or illness. In many cases, it is imposible to determine whether an illness was caused by chemical exposure or by a biological agent (eg a flu virus).

A history of exposure to a chemical is one important clue in helping to establish the cause of illness. However, such history does not constitute conclusive evidence that the chemical was the cause. To establish this cause/effect relationship, it is important that the chemical be detected in the body (such as in the blood stream) at level known to cause illness. If the chemical produces a specific and easily detected biochemical effect (like the inhibition of the enzyme acetyl-cholinesterase), the resulting biochemical change in the body may be used as conclusive evidence. People handling chemicals frequently in the course of their jobs who become ill and need medical attention should tell their physician about their previous exposure to chemicals.

If absorption of pesticide is an established fact the possibility that the absorbed dosage will be sufficient to couse death depends on the inherent toxicity of the compound.

Various ways of measuring toxicity have been developed to measure this property which include the mean lethal dose or LD50. The term LD50 describes acute oral dermal toxicity needed to kill at least 50% of the total test animals. Usually, information derived from the test studies would provide classificataion of pesticide according to the degree of toxicity with the more toxic pesticides having the smallest LD50. However, it must said that the value from LD50 should be interpreted cautiously since there is a wide difference in response between different species of organic life.

The dosage of the pesticide determines, to a large extent, the outcome of poisoning caused by them. If a large dosage has been absorbed, the poisoning that arises would be serious for not only compounds of relatively high toxicity but also to compounds of low toxicity. The control of dosage is the basis of safety in the use of pesticides. It is important to note taht a sufficiently large dose of an ordinarily harmless material is fatal. On the other hand, a sufficiently small dosage of the most toxic pesticide is without effect.

The toxic manifestations of a pesticide may vary depending not only on the dose but also on the duration of the exposure. For many pesticides, the toxic effects observed from a single exposure may be quite different from that of repeated exposure. Many symtoms of repeated exposures are slow to develop and in some instances may mimic symtoms of other chronic disease, making it difficult to differentiate betweeb a poisoning or a disease.

The final determinant on the outcome of pesticide poisoning is the route of exposure into the boy. Pesticide exposure occurs through ingestion, inhalation or absorption through the skin. Certain chemicals, for instance malathion, are equally toxic by all three routes of exposure while the majority are not equally toxic by all three routes of exposure, irrespective of the duration and the dosage of exposure.

The dermal route represents the most common way for exposure and toxic effects would normally be seen if significant amounts of the pesticide have been absorbed into the body. On the whole, the number of pesticides known to beabsorbed to a great extent through the skin is quite small. The efects seen in most number of cases are usually confined to the skin with symtoms such as irritation and skin sensitisation.

How to use chemical pesticides

LIKE ANY CHEMICAL PESTICIDES must be used with care. Follow these tips for safe use of such chemicals:

• Always read the label on each container before using and follow directions.
• Store pesticides out of reach of children and keep in labelled original containers.
• Avoid smoking while spraying or dusting. Many of these chemicals are flammable.
• Wear protective clothing and masks. Keep your sleeves rolled down and your collar up. Wash immediately with soap and water if you spill pesticide material on your skin.
• Wash your hands thoroughly after spraying or dusting and before eating or smoking. Change your clothes too.
• If you feel sick while using a pesticide or shortly after, see your physician immediately.

The writer is a pharmacist and head of the Toxicology Laboratory at the National Poison Centre, Universiti Sains Malaysia, Penang.