An Overview of Pesticides: Its Uses, Abuses, Effects and ...



An Overview of Pesticides: Its Uses, Abuses, Effects and Regulations.

Abstract:

Modern society is presented the world with a vast amount of new technology offering us more products, services and food to consume; warmth; travel; communication and other comforts of living. However, these advances are accompanied by a toxic burden that is becoming vastly more dangerous, complex and costly. For the first time in history every living thing in this world is in some form of danger by the threat of toxic agents that have already or threaten to contaminate our land, air, water and food supplies. (1).

Many of these chemicals come in the form of pesticides.

“The ideal pesticide would kill only the target pest, harm no other species, disappear or break down into something harmless after doing its job; not cause genetic resistance in target organisms; and be cheaper than doing nothing.” (2).

A pesticide is a “chemical substance or mixture of substances intended for preventing, destroying, repelling or mitigating any pests” (3) and “substances intended for use as a plant regulator or defoliant. (3) the current annual use of pesticides in the United States approaches about 500 million kilograms, of primarily synthetic organic chemicals, but also including 27 million kg of sulfur and copper sulfate fungicide. The breakdown of use in the U.S. was agricultural lands (68%); industrial and commercial sites (17%), home and gardens (8% ) and government lands (7%). (3) In addition, the United States is the largest market, with 34% of the world’s pesticide use. (3).

This paper will discuss the nature of pesticides, the benefits and liabilities of their use and misuse; how pesticides are regulated in the United States and how can that system be improved; and finally, what are the safest and most effective ways to combat pests that also preserves the public’s health and the environment’s integrity.

What are the benefits of pesticide use?

The demand for pesticides is enormous. Many believe that pesticides have great benefits.

“Plants that supply the world’s main source of food are susceptible to 80,000 to 100,000diseases caused by viruses, bacteria, mycoplasma-like organisms, rickettsias, fungi, algae and parasitic higher plants. They compete with 30,000 species of weeds the world over, which approximately 1,800 species cause serious economic losses. Some 3,000 species of nematodes attack crop plants, and more than 1,000 of these cause severe damage. An estimate of the total worldwide food losses from pests amount to about 45% of the total food production Pre- harvest losses from insects, plant pathogens and weeds amount to about 30%. And additional losses from microorganisms, insects and rodents range from 10 to 15 %.” (3)

With the use of pesticides, the yield increases 36%. In economic terms, this increases a return on investment of $12 billion to farmers annually. (3)

Other benefits include: (2)

• Pesticides save human lives by killing insects that transmit diseases such as malaria, bubonic plague, typhus and sleeping sickness;

• Pesticides increase food production and lower costs;

• increase profits for farmers;

• work faster and better than alternatives;

• some believe the health risks are less than the benefits;

• safer and more effective pesticides are being developed;

• many new pesticides are being used at very low rates per unit area compared to older products.

What are the drawbacks of pesticide use?

There are many who believe that pesticides are far more dangerous than disclosed and should be carefully used if at all. The drawbacks listed include: (2).

• genetic resistance – insects who breed rapidly can develop an immunity to pesticides through natural selection and come back stronger than before

• broad-spectrum pesticides kill natural predators and parasites that may have been maintaining the population of a pest species at a reasonable level.

• wiping out natural predators can also unleash new pests whose populations the predators had previously held in check, causing other unexpected effects.

• farmers can find themselves on a “pesticide treadmill” which is when the pest has developed genetic resistance, the manufacturers and salespersons recommend more frequent applications, larger doses or a switch to new and more expensive pesticide. This leads to falling profits.

• Also, when noting that such vast quantities of pesticides are used annually, it can only mean that misapplications, accidents and improper use of pesticides constitute real, and documented risks associated with pesticide use. (3) Pesticides are sprayed over large areas and whether they hit or miss their intended target, they also land in the air, surface water, ground water, bottom sediments, on other wildlife, humans and on inanimate objects. (2). Those who suffer the worst are the farm workers in developing countries. They do not have sufficient instructions for use; use the product by hand; do not wear protective clothing; and carry the pesticides home on their clothing so that members of their families are poisoned also. (4).

• Pesticides are pervasive. Not only do they attack their intended target, but they infest a lot of other things including humans. Pesticides enter the body through the skin; they can irritate the eyes, lungs and upper respiratory tract; they can damage the heart by either direct action on the myocardium or as a result of low tissue oxygenation.; they enter the gastrointestinal tract usually by accident through the mouth; they can be neurotoxicants and cause motor weakness and sensory deficits; or they can cause hematological effects such as anemia. (4.)

When did pesticides become an issue?

The first person to call attention to the dangers of toxic chemicals, particularly in pesticides, was Rachel Carson in her 1962 book “Silent Spring.” (5). This book was not well-received at first, and Ms. Carson was considered a zealot. She threatened the booming prosperity of the agriculture industry at large and chemical manufacturers in particular. However, the things she raised public concern were all true. Ms. Carson described the use of inorganic chemicals as pesticides used before World War II and the switch to “a seemingly endless stream of synthetic insecticides.” (5) The new pesticides were different than naturally occurring minerals and plant products – such as compounds of arsenic, copper, lead, manganese, zinc and other minerals, pyrethrum from the dried flowers of chrysanthemums, nicotine sulphate from some of the relatives of tobacco, and rotenone from leguminous plants of the East Indies.

“What sets these new synthetic insecticides apart is their enormous biological potency. They have the immense power not merely to poison but to enter into the most vital processes of the body and change them in sinister and often deadly ways… They destroy the very enzymes whose function is to protect the body from harm, they block the oxidation processes from which the body receives its energy, they prevent the normal functioning of various organs, and they may initiate in certain cells the slow and irreversible change that leads to malignancy." (5.)

“Rachel Carson demonstrated that it was not just acute incidents that we had to fear. The accumulation of small doses of chemicals over long periods of time constituted another source of danger. ..Carson made Americans question the ultimate fate of these chemicals. When the smell was gone, where the chemicals themselves gone?” (6)

The vast majority of pesticides fall into one of two large groups of chemicals. (5). One represented by DDT, is known as the “chlorinated hydrocarbons.” the other group is the organic phosphorus insecticides and is represented by the reasonably familiar malathion and parathion. They both have one thing in common – they are built of carbon atoms, which are the building blocks of the living world and are classed as “organic.” Their basic element carbon, is one whose atoms have an almost infinite capacity for uniting with each other in chains and in various configurations and to be linked with atoms of other substances.

The chemicals used as pesticides are very dangerous to all living things. Though many have been tested, there are vast amounts on the market today that are not adequately tested either on their solo effects, cumulative effects or on their synergistic effects when interacting with other chemicals.

There has been a well-publicized number of toxic incidents involving chemical contamination: PCBs from the General Electric plant on the Upper Hudson River; kepone contamination in the James River in Virginia; chemical contamination in drinking water in the lower Mississippi River; hazardous wastes at Love Canal in New York. (1) More than just isolated instances, similar but less dramatic problems regularly cropped up all over the nation, as communities discovered toxic chemicals in their drinking water, workers became aware of contaminants in the workplace and consumer groups called attention to chemical pesticides in foods. (1). Congress responded by passing new laws in the 1970’s and 80’s. (1)

Currently the United States Government has implemented regulations on the manufacture, sale, use and labeling of pesticides in order to begin to deal with the health and safety issues. This paper will take a look at how effective those regulations are and show areas where they can be improved.

DDT: An example of one of the first pesticides used in massive amounts. (Now banned for its toxic properties).

A general view of the group of pesticides composed of chlorinated hydrocarbons can best be described by the now-banned pesticide DDT (short for dicholor-diphenyl-trichloro-ethane). DDT was first made by a German chemist in 1874 but its use as an insecticide was not discovered until 1939 when Paul Muller of Switzerland won the Nobel Prize for it. (2). It was first used to combat lice on the battlefields during wartime. It was sprayed from the air and people thought that because nobody experienced immediate bad effects, that DDT was safe. That was before scientists realized that unlike most other chlorinated hydrocarbons, DDT in powder form was not readily absorbed through the skin. DDT made it to the American market in 1946. and was considered “remarkably safe.” (7). It became widely used for agricultural purposes and sales went from $10 million in 1944 to $110 million by 1051. It was used on farms and on suburban gardens everywhere in America. However, things came to light by the 1960’s that changed the world’s view of DDTs safety.

As aforementioned, Rachel Carson sounded the DDT alarm in Silent Spring. (5) (7) Subsequent laboratory testing on animals showed the following: that even though DDT seemed safe in powder form, once it was used as a liquid and dissolved in oil, it became lethally toxic. DDT then becomes absorbed through the lungs and the digestive tract. It is stored in organs rich in fatty substances (because DDT is fat soluble,) and settles in the liver, kidneys and intestines. DDT can be ingested from food, breathed in from the air that was recently sprayed, or inside the animal or plant that an organism uses as food. The amount of concentration, therefore, increases up the food chain. The bigger the animal the higher the concentration of DDT and the greater the total amount of exposure. DDT concentration adds up cumulatively as the numbers of exposures increase, so do the levels of DDT in the body increase and eventually surpass the body’s ability to tolerate the substance and the living organism – be it pest, plant or person, dies. Another factor of chlorinated hydrocarbons is that the chemicals can be passed from mother to neonate or mother to infant. “In just six months of breast feeding, a baby in the United States and Europe gets the maximum recommended lifetime dose of dioxin, which rides through the food web like PCBs and DDT. The same breast feeding baby gets five times the allowable daily level of PCBs set by international health standards for a 150-pound adult.” (7)

Since it was proved scientifically by the early 1970’s that DDT caused cancer in laboratory animals, in 1972 the United States Environmental Protection Agency Administrator William Ruckelshaus made a decision to restrict most of its uses. (7.)

“With cancer as the ultimate measure of our fears, it was widely assumed that setting levels based on cancer risk would protect humans as well as fish and wildlife from all other hazards as well. So over the past two decades, pesticide manufacturers and federal regulators looked mainly for cancer and obvious hazards such as lethal toxicity and gross birth defects in screening chemicals for safety... This preoccupation with cancer has blinded us to evidence signaling other dangers. It has thwarted investigation of other risks that may prove equally important not only to the health of individuals but also to the well-being of society.” (7)

In fact, within twelve years of the 1939 use of DDT as an insecticide, it was documented at Syracuse University that DDT which was used to kill insects seemed to have the effect of estrogen when it was given to young roosters: it feminized them. The males treated with DDT had severely underdeveloped testes and failed to grow the ample combs and wattles that roosters display. Like DES (diethylstilbestrol), which is another now-banned synthetic chemical which was used in place of the hormone estrogen for pregnant women which ultimately was shown to cause birth defects.) DDT also has been shown to mimic hormones. (7) Chemically, DDT does bear a resemblance to DES even though neither one resembles real hormones at all.

Organophosphates are another example of a toxic pesticide.

The origin of these organic esters of phosphoric acid was first used by a German chemist, Gerhard Schrader in the late 1930’s as an insecticide. Concurrently, a similar substance was being used as deadly nerve gasses to be used in war and were considered government secrets. (5). The organic phosphorus insecticides act on the living organism by destroying enzymes that perform necessary functions in the body. Their target is the same whether the organism is a pest or a mammal. What happens is that normally, an impulse passes from nerve to nerve with the aid of a chemical transmitter called “acetylcholine” which performs its function and then disappears. If any acetylcholine remains in the body it would cause uncoordinated movements, tremors, muscular spasms, convulsions and death. The body naturally takes this contingency into account by producing a protective enzyme called “cholinesterase” to destroy the transmitting chemical once it is no longer needed. When an organic phosphorous insecticide is introduced, the cholinesterase is destroyed and the transmitting chemical, acetylcholine, builds up. Repeated exposures increase levels until an organism becomes acutely poisoned, sometimes from the introduction of the tiniest amount. Parathion is one of the most widely used organic phosphates. (5).

One of the biggest dangers of the organic phosphate insecticides is when they are used in combinations. their toxicity seems to be stepped up or “potentiated” through combined action. (5). This synergism happens when one compound destroys the liver enzyme responsible for detoxifying the other. The two do not need to be given simultaneously, either. “The full scope of the dangerous interaction of chemicals is as yet little known, but disturbing findings now come regularly from scientific laboratories. Among those is the discovery that the toxicity of an organic phosphate can be increased by a second agent that is not necessarily an insecticide.” (5)

Another factor found in many organophosphates (and also in fewer chlorinated hydrocarbons) is the chemicals called “systemic insecticides.” These are chemicals with the property that are used to convert plants and animals into becoming poisonous. This is done with the purpose of killing any insect that comes into contact with them, such as from sucking their juices or blood. (5). The ability to permeate all the tissues of a plant or animal and make them toxic is the calling card of a systemic insecticide. Systemic insecticides also extend these effects to their offspring if soaked or coated with carbon. In addition, many herbicides, used to kill weeds, are toxic to animals. (5).

What are some of the tests to determine toxicity of a pesticide?

Depending on the chemical involved, the EPA mandates various testing measures to be undertaken by anyone interested in registering their product as a pesticide. This is done at the registrant’s expense. It can cost millions of dollars to put a product on the market. Sometimes studies are conducted by the government.

The broadest test which is also a quick way to determine the most dangerous pesticides in terms of instant destruction is the “acute toxicity test.”(8) “The degree of hazard presented by a pesticide depends on many complex factors. Although no single way of expressing potential hazard is completely reliable, a rapid and convenient indicator of hazard as represented by a compound’s inherent toxicity is the acute oral toxicity test. This is the single dose needed to cause death. The usual method is to express toxicity by means of an LD50 (mean lethal dosage value.)” (8). The LD50 is a bio-assay based statistical estimate of the dosage in mg chemical/kg of body weight of the animal exposed that would be fatal to 50% of the population of the tested species. This is merely a benchmark figure and by no means gives information on a lethal dosage for each member of a species. Also, this does not represent the vulnerability of a species in the field, only in a laboratory setting and only with regard to the precise chemical administered. (Does not take into account any synergistic effects.) (8)

The following factors must be taken into account:

• Amount of pesticides applied per unit area or per unit time.

• The degree of contamination of different environmental components such as air, water, vegetation as influenced by such factors as the carrier (inert ingredient) in the pesticide formula, the evenness of application, wind, temperature, vegetative composition, and other variables.

• The various species present in the habitat when the pesticide is applied.

• Routes by which the animal contacts the pesticide (oral, dermal, inhalation) as well as the amount and duration of contact with different components of the environment.

• Persistence of the pesticide (chemical breakdown rates)

• Formation of biologically active metabolites and their distribution.

• Degree of accumulation of the pesticide or its active metabolites in the animal.

This method of testing is not always the best one, nor is it the easiest to compare from chemical to chemical. It does not always measure the potential hazard most sensitively. This is because many pesticides do no harm with one application be it big or small. Some pesticides are more dangerous when cumulatively applied in small doses. In addition, not all dangerous pesticides kill but rather produce more subtle, yet damaging effects on animals, such as impairing them from fleeing danger or confusing their reproductive systems. (8).

A second test, the sub-chronic test is given with a continuous feeding regime lasting for 90 days. The factors which are evaluated include signs of toxicity, change in body weight, diet consumption, mortality, organ weight, clinical chemistry measurements, gross necropsy and histopathology. In addition to providing information on target organs affected and possible test substance accumulation, the results estimate the doses to be used in longer toxicity tests.(9.)

A third test, used for the more slow action pesticides, is called the chronic test. Adverse effects resulting from long-term exposure to a pesticide are best evaluated using this method. Mostly this test is used to detect cancer and are performed in the rat and mouse. The test lasts for the animal’s life. Chronic feeding studies, also done on dogs, are designed to evaluate other effects besides tumor growth. (9)

In this category of testing the EPA also includes tests which are designed to evaluate the effects of a pesticide on reproduction. (9) In general, the EPA mandates three dose levels for this category of testing. This must include the highest dose used in the study is the maximum tolerated dose (MTD). MTD is what produces some toxicological effect in the test animal. Also a lower dose level must be included, one which produces no evidence of toxicity This is the “no observed effect level” (NOEL)

There can be problems when the MTD overloads the metabolic pathway which can happen at doses far below toxic levels. It is important to carefully pre-test to determine what the maximum dose should be before overloading occurs. (9.)

As far as the reproduction studies, it has been discovered that the most vulnerable time for an animal is when they are in the early stages of prenatal birth. In humans it is considered to occur during the first trimester of pregnancy. (9).

This phenomenon was studied by Theo Colburn in her book, “Our Stolen Future” when she discusses the discovery that some pregnant mothers who took thalidomide had babies which were deformed and yet others who took the same drug while pregnant did not.

“It wasn’t that some mothers had taken a great deal of thalidomide and others had taken very little. Researchers found that the difference between devastating defects and an unscathed outcome appeared to depend on the timing of drug use, not on the dose. ….The principle that “timing is all” would be demonstrated again and again as scientists explored the power of chemicals to disrupt the environment. A small dose of a drug or hormone that might have no effect at one point in a baby’s development, for example, might be devastating just a few weeks earlier.” (7)

The final toxicology requirements needed for a pesticide to be included in the federal registration program include a battery of mutagenicity studies and a rodent metabolism and dermal penetration study. The latter is under the category of “special testing.”

Mutagenicity testing is done to see how the pesticide will affect genetic components in the nucleus of a mammalian cell. (9) These tests can detect gene mutations, structural chromosome aberrations and other genetic effects such as DNA damage. They can also screen for potential carcinogens since the initial step in cancer is believed to be a mutation of sorts. The special testing of dermal absorption is used evaluate the toxic effects of oral or inhalation of a substance because these are significant routes of exposure on humans. (9).

Even though there are grey areas between the different tests used, particularly between acute and chronic toxicity tests, it is sometimes possible to draw certain sharp distinctions between the two. (10)

The following is a comparison between the acute and chronic tests of the organophosphates and the halogenated hydrocarbons.

Organophosphates:

1. The acute toxicity of organophosphates derives from the anticholinesterase property of these chemicals. (See infra page 5. ) That is when the enzyme acetylcholine accumulates at neural connections. This causes poisoning in humans with the following symptoms: pinpoint pupils, blurred vision, the SLUD response (salivation, lacrimation, urination and diarrhea). More severe poisoning includes convulsions, paralysis, depressed respiration and cardiovascular functions and coma. (10)(5).

2. The chronic toxicity is divided into four areas: carcinogenicity; delayed neurotoxicity, experimental myopathy and (in humans) psychological disorders. It was found that there was only limited carcinogenicity which occurred only at extremely high doses. As for the other three categories, this was considered by scientists to be the grey areas. The three effects can be induced with one or a few exposures over a short period of time and could be classified as acute toxicity. However, they are grouped under the chronic toxic test because exposure periods are often unknown, as are latency periods. The effects of delayed neurotoxicity stems from degeneration of the myelin sheath on nerve cells. The symptoms include sensory disturbances, ataxia, weakness, muscle twitching and flaccid paralysis in extreme cases. It was found that 47% of all organophosphates can cause this response. Experimental myopathy was characterized by a breakdown of muscle fiber, usually in the diaphragm. Related symptoms include muscle soreness, changes in electromyography (EMG) and increase in muscle enzymes. As for the psychiatric evaluation, long term exposure to organophosphates can cause acute psychosis or severe depression to greenhouse workers or scientists working with such pesticides. (10.)

Halogenated Hydrocarbons

1. The acute toxicity of some of these pesticides is very low to moderate and depends upon the salt being used as an additive. At a lethal dose, which is very high, animals appear to die from ventricular fiibrillation. At sublethal doses it seems to affect neuromuscular involvement including stiffness of the extremities, paralysis, ataxia and coma. The central nervous system seems to be the target organ in acute toxicity tests. (3).

2. Chronic toxicity tests revealed there was inadequate evidence of carcinogenicity to humans and animals. Most symptoms related to chronic low doses include neurotoxic symptoms such as trembling, ataxia and paralysis. Death was due to neurotoxic effects. (3)

Finally, an important area of testing involves toxicological interactions involving pesticides. This is called synergism or potentiation. Without exception all pesticides are chemical formulations of chemical mixtures and so this is probably the most important area of testing today. (3.) There have been reports where a chemcial used at an environmentally realistic level (for example, 10 parts per million (ppm)), caused a dramatic synergistic reaction in the toxicity of another chemical. Some of the effects include marked increases of tumors as well as a shorter latency period for symptoms to occur. (10).

One way that synergistic responses can be predicted is to use a “scale up” analogy from an animal test to estimate the effects on a human being. These methods, which were initiated in the 1960’s and 1970’s. (10) “The physical and chemical processes interact such that the pharmocokinetics of any given chemical between one species and another may be predictable depending on the amount of background information available.” (10). In the past the application was limited by the complexity of the mathematics involved because of the great number of parameters in the situation. Computers have solved this problem. (10). By using Advanced Continuous Simulation Language, (ACSL) physiologically based pharmacokinetic modeling may be carried out on personal computers with reasonably short turn-around times (6 to 8 minutes for execution time) and in a “user-friendly manner.” (10).

How are Pesticides regulated in the United States?

The regulating act which governs use of pesticides is FIFRA (Federal Insecticide, Fungicide and Rodenticide Act (7 U.S.C. 136 et. seq.) (14) The standards, laid out in Section 3 of FIFRA, require that a pesticide be able to accomplish its intended purpose without causing “unreasonable adverse effects on the environment.” (7 U.S.C. 136a(c)(5)) – without causing “any unreasonable risk to man or the environment, taking into account the economic, social and environmental costs and benefits of the use of the pesticide.” (FIFRA Section 2(bb) (14). If a chemical is found by the EPA to be too dangerous to meet the standards for registration, the EPA can cancel this registration under FIFRA section 6. (14)

In other words the EPA requires that all commercial pesticides be approved for general or restricted use. (2). Pesticide companies have to first evaluate the biologically active ingredients in their products. Then the EPA sets a tolerance level specifying the amount of toxic pesticide residue that can legally remain on the crop when the consumer gets it. [1] Pesticide makers are also required to evaluate the effects of the active ingredients of the pesticide on wildlife. However, the EPA has stopped requiring manufacturers to conduct field tests on birds and fish for newly developed pesticides. (2).

FIFRA requires the pesticide manufacturer to identify the “active” ingredient used in the product and give by percentage, (by weight) of each “active” ingredient. However, the contents of the “inactive” ingredients do not have to be disclosed, only the “total percentage by weight of all inert ingredients.” (40 C.F.R. 156.10(g)(1). (14) According to FIFRA, an “inactive” ingredient is one that is “not active.” That means the “inert” ingredients are substances formulated into the pesticide product for some reason other than their direct effect on the target pest. “Inert” ingredients may serve as carriers for the active ingredients, help dissolve them, preserve them or make them easier to apply. (11)

However, these “inert” ingredients can be toxic. In fact a chemical may be an “active” ingredient on one pesticide product and an “inactive” ingredient in another one, depending only on the manufacturer’s designation of the pests to be controlled by each product. (52 Fed. Reg. 13305, 13307, 1987).(14)

“Unfortunately, many people conclude that the term “inert” refers in some way to the toxicity of those ingredients, and are under the impression that “inert” ingredients have no adverse effects on human health or the environment. This is not the case. The chemicals used as “inerts” include some that are quite hazardous. A consumer would never know however, under current labeling requirements.” (11)

What the New York State Attorney General’s Office concluded in their report , “The Secret Ingredients In Pesticides: Reducing the Risk,” published in 2000 by its Environmental Protection Bureau, was that, “Pesticide products contain a variety of ingredients that either are known to be toxic or have not been adequately tested for toxicity, and the public is denied knowledge of their presence.” (11.)

In fact, many “inert” ingredients allowed to be secretly used in pesticides, are highly regulated under other laws. (11)

Congress has passed, and EPA implements, laws that regulate pollutants in our 1 air[2], and water[3], as well as laws that identify chemicals found at Superfund cites[4], which must be reported to state and local emergency planning and response committeees[5], or which must be reported to EPA’s Toxic Chemical Release Inventory.[6] More than 20 “inerts” are on EPA’s list of priority pollutants found at Superfund sites, and 14 are considered “extremely hazardous substances” which must be reported to emergency planning and response committees. Furthermore, 127 chemicals used as “inert’ ingredients are classified by the Occupational Safety and Health Administration as occupationally hazardous chemicals[7]. (11)

Another problem regarding these “inert” ingredients is how difficult it is for a consumer to gain access to these ingredients because they are protected as “trade secrets”. A consumer who wants to know what is in the pesticide product must first file a FOIA (Freedom of Information Request) under the Freedom of Information Act, 5 U.S.C. 552.

According to the EPA, requests for disclosure of “inert” information can take

“as little as six weeks” but may take as much as several years. (NYS AG p. 15) That certainly does not help the consumer who wants to know whether it is safe to use it today. (11).

Over the years, the public has put pressure on the EPA to revamp its policy on disclosing inactive ingredients.

In 1987 the EPA announced an “Inerts Strategy” which was designed to eliminate the most toxic “inert” ingredients and increase the toxicity testing required for “inerts.” The classification of these chemicals was layered into five categories:

List 1: Inerts of Toxilogical Concern

List 2: Potentially Toxic Interts, High Priority for Testing

List 3: Inerts of Unknown Toxicity

List 4A: Minimal Risk Inerts

List 4B: Inerts that will not adversely affect public health or the environment given current use patterns.

A positive development that came from this plan was the EPA ruled that the identity of the “inerts” on List 1 had to be named on the package. As a result of this law, the registrants removed them from their products. However, the going is very slow. Even though 68 inerts have been designated potentially toxic, the EPA has no specific procedures or timetables for insuring that they are reviewed. (NYS AG, p. 12) Also, the EPA does not even know how many chemicals are being used by registrants in their products because the inerts were not accurately coded into the EPA data base. “There were about 600 registrations for which the chemical name was not available.” (11)

The EPA does have the power to mandate a listing of such inert ingredients on product labels. This is being done with food, pharmaceuticals, and cosmetics under other laws[8].

In fact, the federal courts have already spoken on the issue of confidentiality for pesticide “inert” ingredients in the context of the Freedom of Information Act and ruled decisively in favor of public disclosure. The case was Northwest Coalition for Alternatives to Pesticides v. Browner, Slip Opinion, D.D.C. October 11, 1996. In this case, a judge from the United States District Court of the District of Columbia ruled that the EPA, in refusing to disclose information about inert ingredients to the consumer, improperly relied on unsubstantiated claims by the manufacturers that the identity of the ingredients was a “trade secret” or “confidential business information.” The Court also ruled that the EPA and manufacturers failed to show any competitive harm that would ensue if the contents were disclosed to the public. The most important holding of that case however, was that with limited exceptions, the EPA must now provide information about the identity of “inert” ingredients in pesticide products in response to FOIA requests. More needs to be done because that case did not mandate that the ingredients be listed on the product. “The process of getting information from EPA in this fashion can still be extraordinarily slow and difficult.” (11.)

Would it not be much better overall, to simply have the ingredients listed right on the label?. It is not practical for consumers who want to use it on their pest problem to have to wait. People have a right to full disclosure.

Overall, FIFRA has made inroads into safety issues with pesticide controls. Since its inception, the EPA under FIFRA has acted to suspend, cancel or restrict the use of more than 60 pesticides, including DDT, aldrin, dieldrin, hephtaclor, chlordane and EDB. A 1988 amendment to FIFRA requires manufacturer to assume the responsibility for disposing of the remaining stocks of these now-banned toxic chemicals. (1) In fact, most chlorinated hydrocarbon insecticides, several carbamates and organophosphates and the systemic herbicides 2,4, 5-T and Silvex. However, banned or unregistered pesticides may be manufactured in the United States and exported to other countries. (2)

In addition, Special Review, the process EPA uses to determine whether the use of a pesticide poses an unreasonable effect on man or the environment and weather the chemical should stay registered or not is frequently used to limit the most dangerous of pesticides. (1). If a pesticide exceeds the risk criteria set forth in CFR (Code of Federal Regulation) part 154, then a Special Review is initiated and information on the risks and benefits of the pesticide product uses are gathered and evaluated. If they are determined to pose an unreasonable risk, the registration can be cancelled or modified. The EPA may also issue a suspension order of any pesticide found to be an “imminent hazard” under Section 6 (c). (14) What this does is ensures that the now discovered to be imminently hazardous product will be immediately taken off the shelves. Every suspension order must be accompanied by a concurrent cancellation notice as per FIFRA Section 6( c)(1). (14)

There is also judicial review of any order issue. Following a public hearing in the Court of Appeals under FIFRA Section 16 (b). Review can be obtained by “any person who will be adversely affected by such order and who had been a party to the proceedings.” Obviously a serious problem built into this statute is the fact that a citizen group who disagrees with a finding by the EPA that a pesticide should be either granted or denied registration have no recourse whatsoever under this statute, as it states that only the parties involved have the right of review. FIRFA reserves exclusive authority over pesticide labels to EPA. The states or local governments cannot change label content or design. (11)(14) One problem with this appeals process is that it can keep a dangerous chemical on the market for up to 10 years. (2).

Generally, the U.S Supreme Court has ruled that FIFRA should give States wide latitude to regulate the sale and use of pesticides. See, e.g., Wisconsin Public Intervenor v. Mortier, 501 U.S. 5997 (1991). However, the one area that courts uniformly hold that FIFRA pre-empts state law claims is for inadequate labeling or failure to warn. See e.g., MacDonald v. Monsanto Co., 27 F.3d 1021 (5th Cir. 1994). What that means is once the Federal government has given a pesticide label its imprimatur, an injured citizen has no recourse under FIFRA for a tort claim involving a failure to warn. That is another big drawback to this statute. (11)

Outside of the United States, other countries are imposing regulations to control the use of pesticides too. Membership in the European Economic Community (EC) has had a far reaching impact upon environmental regulation in the United Kingdom, for example. (12). In the field of environmental use of pesticides, the UK Pesticides Safety Precaution Scheme governing the licensing and use of pesticides had to be put on mandatory basis because the existing informal procedures were in breach of the free trade provisions of the Treaty of Rome. It seems that in pesticide regulation, pressure works to modify and improve health and safety concerns both on the manufacturers as well as on the lawmakers. (12)

Since Pesticides are here to stay, what are the best ways to apply them safely?

The following remedies have been suggested:

• In the United States, make it a law that all ingredients should be listed on the product label and expedite Freedom of Information requests on ingredients protected by “trade secrets.”

• Enforce testing mandates on all chemicals and increase EPA review of all registered products. Make it a priority.

• Broaden testing to incorporate more synergistic effects of both interactive pesticides and pesticides with non-pesticide chemicals.

• Using Advanced Continuous Simulation Language, (ACSL) physiologically based pharmacokinetic modeling may be carried out on personal computers to estimate and predict the synergistic effects of a combination of chemicals. This would help to prevent pesticide problems before they happen and would save the costs involved in producing and marketing an unsafe product, which would be taken off the market eventually.

• Educate the public on the importance of proper use, taking reasonable precautions, keeping children and pets safe from accidental harm, and wearing protective clothing.

• Utilize vegetation management by selective spraying – minimizing the amount of chemical applied to a landscape. This theory woks with the inherent stability of nature. If one is interested in getting rid of trees to allow shrubs to grow, the method would be to selectively spray the tall plants and preserve the lower vegetation. This may be completed by using only one treatment, with a possible follow-up for extremely resistant species. (5).

• Use natural predators to crowd out the unwanted pest. (5 )

• Use cultivation and rotation: this involves preparing the soil to include weed and pest control through manipulations of fertilizers, controlling temperatures, aeration and water content. The pest control components may harm the pest directly, or they may promote plant growth that minimizes the effects of the pests. (4)

• Plan the timing of planting and harvesting: Plants are susceptible to pests only during certain growth phases of the plants or the pests. Many pests are present for only a certain number of days per year. Modifying planting dates and harvesting dates can avoid such pestilence. (4)

• Vary the plant density: this can deter some pests. (4)

• Use nutrients creatively: Fertilizers can create uniform density in a crop, which discourages pests; some organic manure has antibiotic effects from the microorganisms in it. (4)

• Use biological control of pests. This plan relies on using living natural enemies such as parasites, predators and pathogens to reduce a pest population to levels lower than would otherwise occur. This works particularly well on non-indigenous pests – those introduced from a foreign country. When a non-native pest is introduced into a new environment, often there are no natural enemies to control that pest. This approach searches the area of origin of the pest and identifies natural enemies and introduces them into the environment as part of the ecosystem. That way the pest suppression will be permanent. (13)

• Holistic program: Control of pests requires the use of many approaches rather than relying on a single method. The holistic program considers all causes of plant stress such as pathogens, weeds, insects and other arthropods, water and nutrient excesses and deficiencies, soil ph, salinity. This requires an enormous amount of knowledge and understanding of all the interactions involved. (13)

• Integrated Pest Management: is a new approach to crop protection that works best on a large community scale. Based on ecological principles, it integrates multidisciplinary methods that are practical, effective and economical and which protect both the environment and public health. (4). This method has been endorsed by the United States Congress, Office of Technology Assessment. (13)

Integrated Pest Management:

Of all the proposed remedies, Integrated Pest Management seems to be the most comprehensive and calculated mathematically. IPM is based on the idea that below a certain pest population or economic threshold, the cost of pest control will be greater than the value of the losses from the pests. On farms, this decision is made based on three factors: the nature of the pest attack; the damage it causes; the range of protection available and information on hand available to farmers; and what farmers want. To determine the economic feasibility, information is needed to guide the farmer’s decision:

h = the level of pest attack;

d= damage in yield per hectacre;

k = mortality coefficient involved with the pesticide used;

p = the price of the crop;

c= the cost of applying the control.

The loss in revenue associated with the attack becomes p(dh). The reduction in loss associated with applying the control is equal to pdhk. It is profitable to apply control where pdhk is greater than c. Overall, the economic threshold is(h*) is h* = c/pdk. (4).

Conclusion

Though much has been already done to safeguard the public against the chemical dangers of pesticides, but more needs to be done. The effects are not only immediate and toxic, but can be chronic over long-term low dose exposure and cause not only cancer but other mutations, neurological problems, hormonal disruptions and even psychological disorders. Just as an holistic approach to the use of pesticides is the safest and most effective way to keep down pests while preserving the environment and insuring public safety, so will an all out effort by lawmakers, scientists, mathematicians, and the public in order to persuade manufacturers that pesticide use must be done as carefully and prudently as possible.

Literature Cited:

(1) Schoenbaum, Thomas J. and Ronald H. Rosenberg. Environmental Policy Law: Problems, Cases, and Readings. 3rd Ed. Westbury, N.Y.: The Foundation Press, Inc., 1996.

(2) Miller, G. Tyler, Jr. Living In The Environment. 11th Ed.. Pacific Grove: Brooks/Cole Pub. Co., 2000.

(3) Young, Alivin L. “Minimizing the Risk Associated with Pesticide Use: An Overview.” Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(4) Rola, Agnes C. and Pingali, Prbhu L. Pesticides, Rice Productivity, and Farmers’ Health: An Economic Assessment. Washington, D.C.: World Resources Institute, 1993.

(5) Carson, Rachel. Silent Spring. 25th Edition. Boston: Houghton Mifflin Co., 1962.

(6) Bormann, F. Herbert, Diana Balmori, Diana and Gordon T. Geballe. Redesigning the American Lawn: A Search for Environmental Harmony. New Haven: Yale University Press, 1993.

(7) Colborn, Theo, Dianne Dumanoski and John Peterson Myers. Our Stolen Future. New York: Penguin Books, 1997.

(8) Hudson, Rick H., Richard K. Tucker, M.A. Haegele. Handbook of Toxicity of Pesticides to Wildlife. United States Department of the Interior Fish and Wildlife Service, Resource Pub.153. Washington, D.C., 1984.

(9) Cardona, Raymond A. “Current Toxicology Requirements for Registration.” Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(10) Yang, Raymond S.H. “Acute Versus Chronic Toxicity and Toxicological Interactions involving Pesticides” Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(11) “The Secret Ingredients In Pesticides: Reducing the Risk,” Eliot Spitzer, Attorney General of New York State: published by its Environmental Protection Bureau, May 2000.

(12) Howarth, William and Rodgers, Christopher P. Agriculture Conservation and Land Use: Law and Policy Issues for Rural Areas. Cardiff: University of Wales Press, 1993.

(13) U.S. Congress, Office of Technology Assessment. A New Technological Era for American Agriculture. OTA-F-474. Washington, D.C.: U.S. Government Printing Office, August, 1992.

(14) (Statutory Material):

(A) Environmental Protection Agency Website: 1/labeling/Irm/abstract.htm. EPA Office of Pesticide Programs. “Label Review Manual Chapters 1-16.” Last visited Nov. 12, 2000.

(B) Environmental Protection Agency Website: 1/labeling/Irm/abstract.htm. EPA Office of Pesticide Programs. “Laws Affecting EPA’s Pesticide Program.” Last visited Nov. 12, 2000.

(C) Environmental Protection Agency Website: . EPA Office of Pesticide Programs. “Consumer Products Treated With Pesticides.” Last visited Nov. 12, 2000.

(D) Environmental Protection Agency Website: . EPA Office of Pesticide Programs. “Using Insect Repellants Safely.” Last visited Nov. 12, 2000.

(E) Environmental Protection Agency Website: 1/aceto/index.htm. EPA Office of Pesticide Programs. “Acetochlor: Welcome to the OPP Acetochlor Page.” Last visited Nov. 12, 2000.

(F) Environmental Protection Agency Website: . EPA Office of Pesticide Programs. “The Triazine Pesticides: Atrazine, Cyanazine, Simazine, and Propazine.” Last visited Nov. 12, 2000.

(G) Environmental Protection Agency Website: . EPA Office of Pesticide Programs.”Questions and Answers on the Chlorine Gas Registration Eligibility Decision (RED.)” Last visited Nov. 12, 2000.

General References:

(15) Gordon, Rue E., Ed. 1998 Conservation Directory. 43rd Edition. Vienna, Va.: Natinal Wildlife Federation, 1998.

(16) Stevens, J.T. and D.D. Sumner. “Simulation Modeling in Toxicology.” in Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(17) Hollingworth, Robert M. “Vulnerability of Pests: Study and Exploitation for Safer Chemcial Control.” Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(18) Madden, L.V. “Pests as Part of the Ecosystem.” Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(19) Seiber, James N. “Principles Governing Environmental Mobility and Fate.” Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(20) Dorough, H. Wyman. “Mammalian Metabolism.”Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(21) Hock, W.K. “Pesticide Use: The Need for Proper Protection, Application, and Disposal.” Ragsdale, Nancy N. and Ronald J. Kuhr, Eds. Pesticides: Minimizing the Risks. Washington, D.C.: American Chemical Society Symposium, 1987.

(22) Steering Committee on Identification of Toxic and Potentially Toxic Chemicas for Consideration by the National Toxicology Program. Toxicity Testing: Strategies to Determine Needs and Priorities. Washington, D.C.: National Academy Press, 1984.

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[1] According to the National Academy of Sciences “tolerance levels are not based primarily on health considerations.” (Miller p. 569.)

[2] Federal Clean Air Act, 42 U.S.C. 7401 et. seq.

[3] Federal Clean Water Act, 33 U.S.C. 121 et. seq.

[4] 42 U.S.C. § 9604(i) Superfund Amendments and Reauthorization Act, Sect. 110.

[5] 42 U.S.C. §11002(a) Superfund Amendments and Reauthorization Act, Sect. 302A.

[6] 42 U.S.C. §11023(a) Superfund Amendments and Reauthorization Act, Sect. 313.

[7] Northwest Coalition for Alternatives to Pesticides, “Worst Kept Secrets” Toxic Ingredients in Pesticides” p. 3, 1998.

[8] See, Food, Drug and Cosmetic Act, 21 U.S.C. 352 (e)(1) Sec. 502 (e) and 21 CFR 201.10 (non-prescription drugs); Food, Drug and Cosmetic Act, 21 U.S.C. 343 Sec. 403(i), and 21 CFR 101 et seq. (foods); and Food, Drug and Cosmetic Act, 21 U.S.C. 362 Sec. 602, and 21 CFR 701 et.seq. (cosmetics.)

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