Which of the Following Prints Was Intended as a Protest Again Pesticides?

PESTICIDES ARE USED widely in agriculture in the U.s.. When finer applied, pesticides can kill or control pests, including weeds, insects, fungi, bacteria, and rodents. Chemical pest control has contributed to dramatic increases in yields for most major fruit and vegetable crops. Its use has led to substantial improvements over the by xl years in the quantity and variety of the U.Due south. nutrition and thus in the health of the public (see, for example, Block et al., 1992).

On the negative side, many pesticides are harmful to the surround and are known or suspected to be toxic to humans. They tin can produce a wide range of adverse furnishings on human health that include acute neurologic toxicity, chronic neurodevelopmental impairment, cancer, reproductive dysfunction, and peradventure dysfunction of the immune and endocrine systems.

The diet is an important source of exposure to pesticides. The trace quantities of pesticides and their breakdown products that are present on or in foodstuffs are termed residues. Remainder levels reflect the corporeality of pesticide practical to a crop, the time that has elapsed since application, and the rate of pesticide dissipation and evaporation. Pesticide residues are widespread in the U.S. diet. They are consumed regularly by most Americans, including infants and children.

To protect the U.Southward. public against dietary pesticides and their potentially harmful effects, the U.Due south. Congress has enacted legislation to regulate residue exposures and to ensure that the food supply is prophylactic as well arable and nutritious. The two main components of the legislative framework—the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) and the Federal Food, Drug, and Corrective Deed (FFDCA)—have provided the foundation for a comprehensive regulatory system.

Concern has arisen in recent years that the current pesticide regulatory system, which is intended to minimize health hazard to the general population, may not adequately protect the wellness of infants and children. The traditional system assesses dietary pesticide take chances on the basis of the boilerplate exposure of the unabridged U.S. population. Still, it does non consider the range of exposures that exists within the population, nor does it specifically consider exposures of infants and children. The exposure of infants and children and their susceptibility to harm from ingesting pesticide residues may differ considerably from that of adults.

Business virtually this uncertainty led the U.S. Congress in 1988 to asking that the National University of Sciences (NAS) appoint a committee to written report scientific and policy issues concerning pesticides in the diets of infants and children through its National Research Council (NRC). The committee was specifically charged with examining.

• what is known most exposures to pesticide residues in the diets of infants and children;

• the adequacy of current take chances cess methods and policies; and

• toxicological issues of greatest business organization and in greatest demand of further research.

Pesticide Use

A pesticide is defined under FIFRA equally ''any substance or mixture of substances intended for preventing, destroying, repelling, or mitigating any insects, rodents, nematodes, fungi, or weeds, or any other forms of life declared to be pests, and any substance or mixture of substances intended for utilise as a plant regulator, defoliant, or desiccant."

Pesticides have been used by humankind for centuries. Their apply was recorded as early on equally the 8th century BC when the application of fungicides was documented in Homeric poems (Bricklayer, 1928; McCallan, 1967). From the until the present, numerous mixtures have been developed to control fungi, insects, weeds, and other pests.

In the 19th century, sulfur compounds were adult as fungicides, and arsenicals were used to control insects attacking fruits and vegetables. Those compounds were highly toxic and consequently were replaced by chlorinated organic pesticides such as DDT and benzenehexachloride (BHC), which were adult during the 1930s and became widely used in the 1950s and 1960s. Chlorinated hydrocarbon insecticides such as DDT, BHC, dieldrin, aldrin, and toxaphene were enthusiastically adopted by farmers who hoped to command previously uncontrolled insects with what were believed to exist relatively safe compounds with long ecology persistence. These chemicals were as well used widely in the command of malaria and other insectborne diseases. By 1955, more than than 90% of all pest control chemicals used in U.S. agriculture were constructed organic compounds, and in 1961 Ddt was registered for employ on 334 crops. Phenoxy herbicides such as two,iv-dichlorophenoxyacetic acrid (2,4-D), ii,iv,v-trichlorophenoxyacetic acrid (two,four,5-T), and ethylenebisdithiocarbamates (EBDCs) and dicarboximide fungicides also gained widespread use during that time.

Kickoff in the belatedly 1960s, the potential of the chlorinated hydrocarbons for bioaccumulation and long-term toxicity became widely recognized. Besides, pest resistance to chlorinated pesticides became increasingly evident and problematic throughout the 1960s, leading many farmers to substitute organophosphates and carbamates for Ddt and other chlorinated compounds. Public pressure level to end the utilize of chlorinated pesticides contributed to the cosmos of the Environmental Protection Agency (EPA) in 1970 and the ultimate administrative revocation in 1972 of the apply of DDT on all food sources in the United states of america. By the end of the 1980s, most food uses of chlorinated compounds were discontinued in this country, although heavy application continues in other nations.

Since the late 1960s, a decline has occurred in insecticide use on major commodities such every bit corn, soybeans, cotton, and wheat. This decrease was primarily the effect of pest management programs, which led to an approximately 50% reduction in pesticide application to cotton wool crops nationwide. Some other of import factor was the development and widespread adoption of synthetic pyrethroid compounds, which are practical in gram quantities rather than pounds per acre. During this menses, fungicide use on peanuts and wheat declined, just because of the continued awarding of fungicides to fruits and vegetables and the increasing acreage of those crops under cultivation, the overall volume of fungicides used has remained steady.

In contrast, the employ of herbicides has increased dramatically. In 1955 approximately three% of all acreage planted with corn and soybean crops were treated with a herbicide; by 1985 that figure had increased to more than 95%, primarily because of the evolution of effective herbicides that were applied earlier the crop was planted. Herbicides now account for approximately 66% of all agricultural pesticides, but for a lower percentage of dietary exposure than is attributed to fungicides and insecticides, which are practical straight to the nutrient closer to, or even after, its harvest. More than 90% of all herbicides are applied to just four crops: corn, soybeans, cotton fiber, and wheat.

Today, about pesticides are synthetically produced organic and inorganic chemicals or microbial agents. Some of these pesticides have been establish naturally and have been synthetically reproduced for commercial utilize. The diverseness and amounts of pesticides now used are far greater than at whatsoever previous time in human history. Approximately 600 pesticides are currently registered with the EPA (P. Fenner-Crisp, EPA, personal commun., 1993).

The most common food-use pesticides autumn into three classes: insecticides, herbicides, and fungicides. In 1991, an estimated 817 million pounds of active pesticide ingredients were used for agricultural application in the Usa. Of this total, herbicides accounted for 495 1000000 pounds; insecticides, 175 million pounds, fungicides, 75 million pounds; and other pesticides, 72 one thousand thousand pounds; (EPA, 1992). "Other" pesticides were defined as rodenticides, fumigants, and molluscicides but practise non include wood preservatives, disinfectants, and sulfur.

• Insecticides. Insecticides control insects that damage crops through a diversity of modes. Some work as nerve poisons, muscle poisons, desiccants, sterilants, or pheromones; others exert their effects by concrete means such as by clogging air passages. The classes of insecticides nigh commonly used today are chlorinated hydrocarbons, organophosphates, and carbamates, and of these, the organophosphates are the most widely used. Typically they are very acutely toxic, but they practise non persist in the environment. Well-known organophosphate pesticides include parathion, dichlorvos, malathion, chlorpyrifos, and azinphos-methyl. The toxicity to humans resulting from exposure to these compounds tin can differ markedly from chemical to chemical.

  The carbamate insecticides are also very widely used in the United States today. They too are highly toxic, e.k., aldicarb. Other insecticides such as synthetic pyrethroids, east.thou., permethrin, are valued because of their fast action and relatively low toxicity to mammals.

• Herbicides. Herbicides are used to control weeds, which compete with ingather plants for water, nutrients, infinite and sunlight. By reducing the weed population, the demand for farm labor is decreased and ingather quality is enhanced. Herbicides work through a diversity of modes of activeness. Some damage foliage cells and desiccate the constitute; others change nutrient uptake or photosynthesis. Some herbicides inhibit seed germination or bulb growth. Others are applied to foliage and kill on contact, thereby destroying leaf and stem tissues. Some of the most widely used herbicides are ii,4-D [(two,four-dichlorophenoxy) acetic acid], atrazine, simazine, dacthal, alachlor, metolachlor, and glyphosate.

• Fungicides. Fungicides control plant molds and other diseases. They include compounds of metals and sulfur as well as numerous synthetics. Some fungicides act past inhibiting the metabolic processes of fungal organisms and can be used on plants that have already been invaded and damaged past the organism. Other fungicides protect plants from fungal infections and retard fungal growth before damage to plants can occur. Fungicides frequently provide direct benefit to humans by retarding or eliminating fungal infections that can produce toxicants such every bit aflatoxins. Fungicides that have been used heavily over the years include benomyl, captan, and the EBDC family unit of fungicides such as mancozeb.

In addition to their agronomical applications, pesticides are too used for many nonagricultural purposes, eastward.g., in homes and public buildings to kill termites and other pests; on lawns and ornamental plantings to kill weeds, insects, and fungi; and on ponds, lakes, and rivers to control insects and weeds. Therefore, humans are exposed to pesticides from a variety of sources other than the nutrition, for example, through the skin or by inhalation. Some of these exposures are particularly important when because total exposures of infants and children.

Pesticide Control Legislation

The societal response to the dual nature of pesticides—to their combination of benefits and toxicity—has been to develop a comprehensive regulatory system that seeks to brand possible the benign use of pesticides while minimizing their hazards to public health and the environment. This regulatory system originated with the enactment of FIFRA in 1947. The legislation regulating pesticides in the Us now consists of FIFRA, its comprehensive amendments of 1972, 1975, 1978, 1980, and 1988, and certain provisions of the FFDCA, which was enacted in 1954 and later amended.

FIFRA is intended by Congress to be a "balancing" or chance-do good statute. It states that a pesticide when used for its intended purpose must not cause "unreasonable adverse effects on the environs." This balancing process must take into account "the economical, social, and environmental costs as well every bit the potential benefits of the use of whatsoever pesticide" [7 USC 136(a) (1978)]. Wilkinson (1990, p. xi) has commented: ''While utilise of the term 'unreasonable hazard' implies that some risks will be tolerated nether FIFRA, it is conspicuously expected that the anticipated benefits will outweigh the potential risks when the pesticide is used co-ordinate to commonly recognized, good agricultural practices."

Under FIFRA, pesticide use is controlled through a registration process. This process is administered by EPA. A given pesticide may have several different uses, and each use is required to have its own registration. EPA registration of a pesticide use and blessing of a label detailing the legally binding instructions for that employ are required before a pesticide tin be legally sold.

For a pesticide to be registered, manufacturers must submit to EPA the data needed to back up the product'due south registration, including substantiation of its usefulness and disclosure of its chemical and toxic properties, its probable distribution in the surround, and its possible effects on wildlife and plants.

Pesticides that are to exist registered for use on food crops must be granted a tolerance by EPA. These tolerances establish the main mechanism by which EPA limits levels of pesticides residues in foods. A tolerance concentration is defined nether FFDCA every bit the maximum quantity of a pesticide residuum allowable on a raw agricultural commodity (RAC) (FFDCA, Section 408) and in processed nutrient when the pesticide has full-bodied during processing (FFDCA, Section 409). A tolerance must be defined for whatsoever pesticide used on food crops. Tolerance concentrations on RACs are based on the result of field trials conducted by pesticide manufacturers and are designed to reflect the highest remainder concentrations likely under normal agricultural do. Thus, tolerances are based on good agricultural practice rather than on considerations of human being health.

The determination of what might be a safe level of residue exposure is made by considering the results of toxicological studies of the pesticide's effects on animals and, when data are available, on humans. Both astute and chronic effects, including cancer, are considered, although currently, acute furnishings are treated separately. These information are used to establish human being exposure guidelines (i.due east., reference dose, RfD) against which one tin can compare the expected exposure. Exposure is a function of the corporeality and kind of foods consumed and the amount and identity of residues in the foods (i.e., Theoretical Maximum Residue Contributions, TMRCs). If the TMRCs exceed the RfD, then predictable residues are calculated and compared with the proposed tolerance. The percentage of crop acreage treated is as well considered. If the anticipated residues exceed the RfD, then the proposed tolerance is rejected, and the manufacturer may recommend a new level.

Tolerances are the single almost of import tool past which the U.Southward. Government regulates pesticide residues in food. More than than 8,500 nutrient tolerances for all pesticides are currently listed in the Lawmaking of Federal Regulations (CFR). Approximately 8,350 of these tolerances are for residues on raw commodities (promulgated under section 408) and about 150 are for residues known to concentrate in processed foods (promulgated under Section 409). Table i-1 shows the number of tolerances established for insecticides, herbicides, and fungicides in the mid-1980s for purposes of comparison.

TABLE one-one

Food Tolerances Established Under Sections 408 and 409 of the Federal Food, Drug, and Cosmetic Human action.

Approach to the Report

Infants and children are unique. They are undergoing growth and development. Their metabolic rates are rapid. Their diets and their patterns of dietary exposure to pesticide residues are quite different from those of adults.

To determine whether the current regulatory system in the U.s.a. adequately protects infants and children against dietary residues of pesticides, the committee considered two main issues—susceptibility and exposure:

• Susceptibility: Are infants and children more or less susceptible (sensitive) than adults to the toxic effects of pesticides? Is there a uniform and predictable departure in susceptibility, or must each pesticide (and each toxic response) be considered separately? Does susceptibility increase during periods of rapid growth and development? Does high metabolic activity atomic number 82 to more rapid excretion of xenobiotic compounds and thus to reduced susceptibility? Is the ability to repair damaged tissues and organs greater in childhood, thus leading to apparently lower sensitivity? In what style does the potentially long life span of infants and children affect their susceptibility to diseases with long latent periods?

• Exposure: What foods do infants and children consume? How much of these foods do they eat? How much variation in nutrition is there amongst children in the United States? How much, and what residues are institute in or on the food eaten by infants and children? What are the nonfood sources of pesticide exposure? How important are they? What data are available on exposure? Are there adequate, oftentimes collected nutrient consumption information categorized by age, sex, and race that can serve as a basis for computations of intakes by potentially more than sensitive subgroups in the population? What are the proper measures of exposure?

The commission examined current procedures for toxicity testing of pesticides to learn whether these approaches provide sufficient information on toxicity in the young. Specific questions posed by the committee included: How are toxic effects identified? If they are determined by experiments in laboratory animals, what problems exist in transferring the results to humans? To infants and children? What data on toxicity is needed? For example, is data on mechanisms of action needed to establish risks to children? Are brute studies on weanlings and older animals adequate to guess toxicity in infants and children at relatively earlier stages of development? Are in that location toxicities unique to some species of laboratory animals? To humans? How can exposures of animals to toxicants late in life predict responses in humans exposed early in life?

The committee reviewed approaches to pesticide chance assessment to assess whether these approaches adequately consider the effects of exposure in young age groups. Specific problems included: How is exposure to pesticide residues associated with response? If special consideration needs to be given to babyhood exposures that upshot in risk, how tin laboratory data from lifetime animal studies be used to develop meaningful estimates? Does take chances accrue faster during the early on years of life? When exposure to a pesticide leads to more one toxic responses, how can, or should, the total toxicity be described or evaluated?

Two final bug that the committee considered were:

• How tin the lifetime risks associated with exposures to pesticides and other chemicals during infancy and childhood be assessed?

• How tin can methods for assessing and controlling these risks be improved?

In this report, the committee considers the development of children from the last trimester of gestation (26 weeks) through boyhood—approximately eighteen years of age. Xx-six weeks of gestation is considered the start of infancy because this age coincides closely with the earliest point at which an baby tin survive outside the uterus. All major organ systems can function independently at that point, and the lungs have adult to the degree that reasonable exchanges of oxygen and carbon dioxide tin take identify.

Capacity 2, 3, and iv of the report consider the susceptibility of infants and children to pesticides. Affiliate ii examines current bear witness on the bear on of children's exposures to pesticides and other toxicants in lite of the special demands imposed by their rapid evolution, their special nutritional requirements, and their rapid metabolism. Affiliate 3 explores electric current data on perinatal and pediatric toxicity. In Chapter iv, the committee reviews EPA's current and proposed toxicity testing requirements for pesticide registration and tolerance setting.

Chapters 5, vi, and seven assess the dietary exposure of infants and children to pesticides. The committee began this examination by reviewing in Chapter 5 the food consumption patterns of this age group and exploring the ways that the patterns differ from those of adults—not only in the types and amounts of nutrient and water consumed, but also in the proportion of the diet comprising sure foods. So in Chapter 6 the committee reviews the information available on pesticide residues in food and gives particular attention to sampling of the foods consumed virtually past infants and children. In Affiliate vii, the committee ties together the information on dietary patterns and residue levels from the 2 preceding capacity and provides examples for estimating the dietary pesticide exposures of infants and children. This linking of the data on dietary patterns of infants and children with data on pesticide residue levels was achieved past applying a computer-based technology that enabled the committee to examine and quantify the total range of dietary pesticide exposures. This methodologic innovation obviates the need to study the average exposure of the hypothetical "normal" child and focuses instead on the full distribution of exposures.

In Chapter 8, the commission focuses on gamble assessment. Using the data developed in Chapters 5, half dozen and 7 on exposure levels, the committee presents a new method that tin be used by government regulatory agencies to assess the health risks to infants and children resulting from exposures to pesticide residues in the diet. Like the exposure assessment method adult in Affiliate 7, the hazard assessment method permits test of the full range of risks across the unabridged pediatric population.

This study embodies three unique features:

• It is the first assessment of dietary exposures to pesticides that has focused specifically on infants and children. It makes the instance that children are unlike from the residue of the population, both in their vulnerability to toxicants also every bit in their patterns of dietary exposure to pesticide residues. Children therefore deserve specific attention in the risk cess and regulatory processes.

• It considers the total distribution of dietary exposures to pesticides among infants and children. It does not focus only on average exposure, nor does information technology just use summary statistics to examine the pesticide exposures of a hypothetical "average" child. Instead, through the use of newly applied statistical techniques, the committee was able to examine and quantify the unabridged range of exposures against the pediatric population of the Usa. In this manner, the committee was able to develop improved estimates of the numbers of children with high levels of dietary exposure to pesticides. This approach should be of considerable value to the government regulatory agencies, specially EPA, as they continue their efforts to use risk assessment methodologies to safeguard the health of the U.S. population.

• Information technology proposes new cancer hazard assessment methods that take into account temporal patterns of exposure to pesticide residues in the nutrition of infants and children, as well as tissue growth and changes in cell kinetics with age. Because of their greater consumption of certain foods relative to body weight, children may be at greater risk than adults from pesticides with carcinogenic potential. Infants and children are subject to rapid tissue growth and development, which volition accept an impact on cancer take a chance.

This report indicates how such variations in exposure with age can be accommodated in the Moolgavkar-Venzon-Knudson model of carcinogenesis (Moolgavkar et al., 1988), along with data on tissue growth and changes in cell kinetics. The methods proposed hither tin can exist adapted and extended, based on the availability of appropriate data on dietary exposure to pesticides and on tissue growth and cell kinetics, to arrive at improved estimates of lifetime cancer risks that may be posed by dietary exposure to pesticides.

References

• Block, G., B. Patterson, and A. Subar. 1992. Fruit, vegetables, and cancer prevention: A review of the epidemiological evidence. Nutr. Cancer 18:i–29. [PubMed: 1408943]

• EPA (U.S. Environmental Protection Agency). 1992. Pesticide Industry Sales and Usage. 1990 and 1991 Market Estimates. Office of Pesticide Programs. Washington, D.C.: U.S. Environmental Protection Bureau.

• Mason, A.F. 1928. Spraying, Dusting, and Fumigating of Plants. New York: Macmillan.

• McCallan, Southward.E.A. 1967. History of fungicides. In Fungicides: An Advanced Treatise, Vol. 1, D.C. Torgeson, editor. , ed. New York: Academic.

• Moolgavkar, S.H., A. Dewanji, and D.J. Venzon. 1988. A stochastic 2-stage model for cancer hazard assessment. I. The take a chance function and the probability of tumor. Take chances Anal. 8:383–392. [PubMed: 3201016]

• NRC (National Enquiry Council). 1987. Regulating Pesticides in Food: The Delaney Paradox. Washington, D.C.: National Academy Printing. 288 pp. [PubMed: 25032281]

• Wilkinson, C.F. 1990. Introduction and overview. Pp. v–33 in Advances in Mod Environmental Toxicology: The Effects of Pesticides on Human Health, Vol. Eighteen, S.R. Baker, editor; and C.F. Wilkinson, editor. , eds. Princeton, N.J.: Princeton Scientific. 438 pp.

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Source: https://www.ncbi.nlm.nih.gov/books/NBK236265/

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