Pesticides are designed to control pests. They all are toxic to some level, otherwise they would not kill pests. They can also be toxic to non-target organisms such as plants, animals or humans. Exposure to a sufficient amount of almost any pesticide can affect a person—either through illness, eye exposure or skin sensitivity.

Since even fairly low risk pesticides can irritate the skin, eyes, nose or mouth, it is essential to understand pesticide toxicity in order to follow safe use practices and eliminate exposure.

How Pesticides Enter the Body

Before a pesticide can harm you, it must be taken into the body. Pesticides can enter the body orally (through the mouth and digestive system), dermally (through the skin), or by inhalation (through the nose and respiratory system).

Oral Exposure

Oral exposure may occur because of an accident, but is more likely to occur as the result of carelessness, such as blowing out a plugged nozzle; smoking or eating without washing your hands after using a pesticide; or eating food that has been recently sprayed with a pesticide. The seriousness of the exposure depends upon the oral toxicity of the material and the amount swallowed.

Dermal Exposure

Dermal or skin exposure accounts for about 90% of all pesticide exposure users receive from nonfumigant pesticides. It may occur any time a pesticide is mixed, applied, or handled, and it is often undetected. Dry materials-dusts, wettable powders, and granules as well as liquid pesticides can be absorbed through the skin. The seriousness of dermal exposure depends upon (1) the dermal toxicity of the pesticide, (2) rate of absorption through the skin, (3) the size of the skin area contaminated, (4) the length of time the material is in contact with the skin, and (5) the amount of pesticide on the skin.

Rates of absorption through the skin are different for different parts of the body (Figure 1). Using absorption through the forearm (1.0) as the standard, absorption is more than 11 times faster in the lower groin area. Absorption in the genital area is rapid enough to approximate the effect of injecting the pesticide directly into the bloodstream.

Absorption continues to take place on the affected skin area as long as the pesticide is in contact with the skin. The seriousness of the exposure is increased if the contaminated area is larger or if the material remains on the skin for a period of time.

Figure 1. Comparative rates of dermal absorption for different parts of the body.

Inhalation Exposure

Inhalation exposure results from breathing in pesticide vapors, dust, or spray particles. Like oral and dermal exposure, inhalation exposure is more serious with some pesticides than with others, particularly fumigant pesticides.

Inhalation exposure can occur from the applicator smoking, breathing smoke from burning containers, breathing fumes from pesticides while applying them without protective equipment, and inhaling fumes while mixing and pouring pesticides.

Toxicity

Toxicity refers to the ability of a poison to produce adverse effects. These adverse effects may range from slight symptoms such as headaches to severe symptoms like coma, convulsions, or death. Most toxic effects are reversible and do not cause permanent damage if prompt medical treatment is sought. However, some poisons cause irreversible (permanent) damage. Poisons work by altering normal body functions, consequently toxicity can occur in as many ways as there are body functions.

All new pesticides are tested to establish the type of toxicity and dose necessary to produce a measurable toxic reaction. In order to compare the results of toxicity tests done in different laboratories, there are strict testing procedures. Toxicity testing is expensive, intensive, and involves many phases. Humans, obviously, cannot be used as test animals, so toxicity testing is done with animals. Since different species of animals respond differently to chemicals, a new chemical is generally tested in mice, rats, rabbits, and dogs. The results of toxicity tests in these animals are used to assess the toxicity of new chemicals to humans.

Toxicity tests are based on two premises. The first premise is that information about toxicity in animals can be used to predict toxicity in humans. Years of experience have shown that toxicity data obtained from a single species may be inaccurate. The second premise is that by exposing animals to large doses of a chemical for short periods of time, we can assess human toxicity due to exposure to small doses for long periods of time.

Toxicity is usually divided into 2 types, acute or chronic, based on the number of exposures to a poison and the time it takes for toxic symptoms to develop. Acute toxicity is due to short-term exposure and happens within a relatively short period of time, whereas chronic exposure is due to repeated or long-term exposure and happens over a longer period (Table 1).

Table 1. Types of Toxicity

Acute Toxicity

The acute toxicity of a chemical refers to its ability to do systemic damage as a result of a one-time exposure to relatively large amounts of chemical. A pesticide with a high acute toxicity may be deadly when a very small amount is absorbed. The signal words on the label (Table 2) are based on the acute toxicity of the pesticide. Acute toxicity may be measured as acute oral (through the mouth), acute dermal (through the skin), and acute inhalation (through the lungs).

Table 2. Acute Toxicity Measures and Warnings

Acute Toxicity Measure

The commonly used term to describe acute toxicity is LD50. LD means Lethal Dose (deadly amount) and the subscript 50 means that the dose was acutely lethal for 50 percent of the animals to whom the chemical was administered under controlled laboratory conditions. The test animals are given specific amounts of the chemical in either one oral dose or by a single injection, and are then observed for 14 days.

Since LD50 values are measured from zero up, the lower the LD50 the more acutely toxic the pesticide. Therefore, a pesticide with an oral LD50 of 500 would be much less toxic than a pesticide with an LD50 of 5. LD50values are expressed as milligrams per kilogram (mg/kg), which means milligrams of chemical per kilogram of body weight of the animal. Milligram (mg) and kilogram (kg) are metric units of weight similar to ounce and ton. Milligrams per kilogram is the same as parts per million. For example, if the oral LD50 of the insecticide is 4, it would require a dose of 4 parts of the insecticide for every million parts of body weight to be lethal to at least half of the test animals.

To determine the ounces of actual pesticide that would be lethal to one of every two 187-pound men or other warm blooded animals, multiply the factor .003 times the LD50 value for the pesticide. For example, the oral LD50value formalathion is 1,200 mg/kg; thus, if a group of men each weighing 187 pounds ate 3.6 ounces (1,200 x 0.003) of technical malathion per man, we might expect half of them to die. The dermal LD50 value of malathion is approximately 4,000 mg/kg, or 12 ounces, for a 187-pound man. Since toxicities depend on body weight, it would take only one-third of this amount to be lethal to a 60-pound child and about five times as much to kill a 900 pound animal.

For standards of comparison, the oral LD50 value of table salt is 3,320 mg/kg, while for aspirin it is 1,200 mg/kg or 3.6 ounces per 187-pound man, the equivalent of malathion.

LD50 values are generally expressed on the basis of active ingredient. If a commercial material is only 50 percent active ingredient, it would take 2 parts of the material to make 1 part of the active ingredient. In some cases, chemicals mixed with the active ingredient for formulating a pesticide may cause the toxicity to differ from that of the active ingredient alone.

Acute inhalation toxicity is measured by LC50. LC means lethal concentration. Concentration is used instead of dose because the amount of pesticide inhaled from the air is being measured. LC50 values are measured in milligrams per liter. Liters are metric units of volume similar to a quart. The lower LC50 value, the more poisonous the pesticide.

Chronic Toxicity

Chronic Toxicity refers to harmful effects produced by long-term, low-level exposure to chemicals. Less is known about the chronic toxicity of pesticides than is known about their acute toxicity, not because it is of less importance, but because chronic toxicity is much more complex and subtle in how it presents itself. Increased emphasis is being given to the chronic toxicity of pesticides by the U.S. Environmental Protection Agency (EPA). In the past, more emphasis was placed on acute toxicity rather than chronic. While situations resulting in acute exposure (a single large exposure) do occur, they are nearly always the result of an accident or careless handling. On the other hand, persons may be routinely exposed to small amounts of pesticides while mixing, loading, and applying pesticides or by working in fields after pesticides have been applied.

Chronic Toxicity Measures

There is not a standard measure like the LD50 for chronic toxicity. How chronic toxicity of chemicals is studied depends upon the adverse effect being studied. The major chronic adverse effects include:

Carcinogenesis (oncogenesis)

These terms mean the production of tumors. The terms tumor, cancer, neoplasm are all used to mean an uncontrolled progressive growth of cells. In medical terminology, a cancer is considered a malignant (potentially lethal) neoplasm. Carcinogenic or oncogenic substances are substances that can cause the production of tumors. Examples are asbestos and cigarette smoke.

Teratogenesis

Teratogenesis is the production of birth defects. A teratogen is anything that is capable of producing changes in the structure or function of the offspring when the embryo or fetus is exposed before birth. An example of a chemical teratogenis is the drug thalidomide that caused birth defects in children when their mothers used it during their pregnancy. Measles virus infection during pregnancy also has teratogenic effects.

Mutagenesis

Mutagenesis is the production of changes in genetic structure. A mutagen is a substance that causes a genetic change. Many mutagenic substances are oncogenic meaning they also produce tumors. Many oncogenic substances are also mutagens.

Reproductive toxicity

Some chemicals have effects on the fertility or reproductive rates of animals.

Chronic Toxicity Testing

Chronic toxicity testing is both lengthy and expensive. EPA and regulatory agencies in other countries require an extensive battery of tests to identify and evaluate the chronic effects of pesticides. These studies, which may last up to two years, utilize several species of animals to evaluate toxicity from multiple or continuous long-term exposure.

Label Identification of Acute and Chronic Toxicity

To alert pesticide users to the acute toxicity of a pesticide, a signal word must appear on the label. Four different categories are used (Table 2). Signal words are used to tell the user whether the chemical is highly toxic, moderately toxic, slightly toxic, or relatively non-toxic. If the pesticide meets all of Category IV toxicity levels, that pesticide is not required to have a signal word on the label. These label warnings are based for the most part on the chemical's acute toxicity. For example, the acute oral and acute dermal toxicity of a pesticide may be in the slightly toxic category. But if the acute inhalation toxicity is in the highly toxic category, the pesticide label will have the signal words for a highly toxic pesticide. The degree of eye or skin irrigation caused by the pesticide also influences the signal word.

There is no comparable set of signal words like those used for acute toxicity to alert pesticide users to chronic toxicity problems with pesticides. Instead a statement identifying the specific chronic toxicity problems will be used on the label. Such a statement might read “This product contains (name of chemical) which has been determined to cause tumors or birth defects in laboratory animals.” Associated with chronic toxicity warning statements will be label directions to wear certain kinds of protective clothing when handling or working with the pesticide to minimize or eliminate exposure to the pesticide.

It is important to read the label to look for signal words identifying the product's acute toxicity and for statements identifying any chronic toxicity problem. A pesticide may be low in acute toxicity (signal word caution), but it may have a label statement identifying potential chronic toxicity.

Safety Factors

In feeding studies, the pesticide being investigated is incorporated into the daily diet and fed to animals from a very young to a very old age. These as well as the reproductive effects studies are designed to arrive at a No-Observable-Effect-Level (NOEL); that is, a level in the total diet that causes no effect in treated animals when compared to untreated animals maintained under identical conditions. This NOEL is expressed on a mg/kg of body weight/day basis. An Acceptable Daily Intake (ADI) is usually established at 1/100 of the NOEL, in order to add an additional margin of safety. The ADL is the amount of chemical that can be consumed daily for a lifetime without ill effects.

Extensive residue trials are conducted to determine levels of the pesticide that will remain in or on growing crops after treatment with the pesticide. These trials lead to the establishment of a tolerance for residues of the chemical on food commodities. A tolerance is the maximum allowable amount of the pesticide permitted in or on a specific food commodity at harvest. Use directions for a pesticide are written to assure that residues in food commodities are below the tolerance. The tolerance is set low enough to ensure that even if someone ate only food items with residues of a given pesticide at the tolerance limit, there would still be a safety factor of at least 100 when compared to a level causing no observable effects in laboratory animals. This is, of course, a worst-case situation since all crops on which the pesticide is registered for use would not be treated with the chemical, and in most cases residue levels would be well below the tolerance due to preharvest intervals being longer than the minimum period stated on the label. Further reduction of residues may occur in storage, or due to washing, trimming, and processing.

Dose Response

Ironically, the extensive amount of data developed about a pesticide is often used against it by conveniently ignoring the dose response. For example, some acute studies, which are designed to include dosage levels high enough to produce deaths, are cited as proof of the chemical's dangers. Chronic effects seen at very high doses in lifetime feeding studies are misinterpreted and considered as proof that no exposure to the chemical should be allowed. Major improvements in analytical chemistry permit detection of chemicals at levels of parts per billion (ppb) or even parts per trillion (ppt). People are constantly hearing that they are being exposed to toxic chemicals in their foods and beverages and that exposure levels are so many parts per billion or parts per trillion, with no comprehension of the real meaning of these numbers. Most stories on pesticides reported by the media completely neglect the issue of dose-response, the key principle of toxicology. The concentration of a chemical in any substance is meaningless unless it is related to the toxicity of the chemical and the potential for exposure and absorption. Chemicals of low toxicity such as table salt or ethyl alcohol can be fatal if consumed in large amounts. Conversely a highly toxic material may pose no hazard when exposure is minimal.

Monitoring for Residues

Monitoring foods for pesticide residues is carried out by the Food and Drug Administration. Crops containing residues over the official tolerance established by the EPA must be destroyed. The threat of crop destruction with resultant financial loss is a strong incentive for farmers to observe use instructions on pesticide labels and thus ensures that residues will be below established tolerances. Crops grown for export are often checked for residues by foreign residue laboratories to assure that the local tolerance limits are not exceeded. Lastly, market basket surveys (analyses of food items from grocery stores) have confirmed the low exposure of the general public to pesticides in foods.

Hazard

Hazard is a function of the toxicity of a pesticide and the potential for exposure to it. We do not have control of the toxicity of a pesticide since toxicity is a given characteristic of a particular pesticide; however, we can have control over our exposure to pesticides. This is done by following several safety practices including the use of protective clothing and equipment.

All pesticides are hazardous if misused, no matter what their toxicity. All pesticides can be handled safely by using safety practices that minimize or eliminate your exposure to them.

Federal laws regulating pesticides have placed the burden of proving safety of pesticide usage on the manufacturer. Hazard evaluation studies are generally done by scientific laboratories maintained by the manufacturer or through outside contract laboratories. Few products are subjected to such extensive and vigorous testing as pesticides, prior to being marketed. Many promising pesticide products are not marketed because they to not pass the extensive toxicology testing. Older pesticide products that were registered before the current toxicology testing standards were established are being reevaluated under current standards. Precautions and other safety information found on the product's label are based on information from these tests. By reading and following the directions on the label, the user can minimize or eliminate hazards due to use of the pesticide to him or herself and others.

Toxicity Tables

Complete information is not available on the toxicity of all pesticides. The following tables give the acute oral and, when available, the acute dermal toxicity for some common insecticides, fungicides and nematicides, and herbicides. These tables do not identify any chronic toxicity effects. Pesticide chemicals with identified chronic toxicities will have label statements identifying the specific chronic effect and practices to use when using the pesticide.

Some of the preceding material was adapted from Pesticide Toxicities, Leaflet 21062, Division of Agricultural Sciences, University of California; The Dose Makes the Poison by Alice Ottoboni, PhD, Vincente Books; and the Farm Chemical Handbook, Meister Publishing Company.

Table 3a. Insecticides

Table 3b. Rodenticides

Table 3c. Herbicides

Table 3d. Fungicides and Nematicides

Brad Kard

Professor Structural and Urban Entomology

Kevin Shelton
Extension Pesticide Coordinator

Charles Luper
Extension Associate