Environmental Risks Facing Children and Recommendations for Response

This article was presented at the symposium on "Preventing Child Exposures to Environmental Hazards: Research and Policy Issues" held March 18-19, 1993 in Washington DC. Received for publication (date).

Address correspondence to Dr. Lynn R. Goldman, Assistant Administrator, Office of Prevention, Pesticides and Toxic Substances, U.S. Environmental Protection Agency, 401 M Street SW, TS788, Washington, DC 20460. Telephone (202) 260-2897. Fax (202) 260-1847.

Introduction

Children may be more susceptible to environmental exposures than adults and, because of their developing systems, uniquely vulnerable to their effects.

There is a growing urgency for researchers in the private and public sectors to move to fill gaps in the data and for decision makers to incorporate available information into pollution control and prevention strategies. Damage caused to children can be devastating and permanent, and the latency period for certain effects can be decades.

Because of this potential, the health care community and those responsible for children need to be alert to possible environmental factors in identifying and responding to health problems confronting children. All too often, the immediate focus is on symptoms and their treatment, rather than causes, and environmental sources of effects are the last considered, if ever.

There are particular environmental exposures, pesticides, and air pollutants for which the combination of increased susceptibility and increased opportunity for exposure combine to increase the hazards and risks for children. One of the most effective strategies immediately available is to prevent pollution and so preclude potentially toxic exposures.

A Changing Environment

With the synthetic organic chemical revolution in the post-World War II period came an enormous influx of new chemical substances together with frequently unchecked releases of pollutants into the air, water, and land. Some of those pollutants, such as DDT, are particularly persistent and pervasive, as Rachel Carson eloquently warned in Silent Spring.

Past pollution practices, combined with dependence on fossil fuels, served to create an environment in which the air and waterways all too often became living laboratories for toxic damage. Love Canal symbolized what could go wrong when it was found that an elementary school had been built directly over a hazardous waste disposal site.

Environmental legislation of the 1970s and 1980s responded to the public outcry against the pattern of environmental destruction in America, creating a network of laws and regulations to control it. Congress enacted hallmark statutes, including the Clean Air and Water Acts; Toxic Substances Control Act; Resource Conservation and Recovery Act; Comprehensive Environmental Response, Compensation, and Liability Act (Superfund law); and Safe Drinking Water Act. States adopted implementing laws and programs, in numerous cases going beyond the federal mandate.

The resulting legislative and regulatory framework delivered substantial benefits to public health and environmental protection. But what is becoming clear is that their predominant emphasis on command-and-control strategies has limits. From the point of view of protecting public health and the environment, pollution prevention is essential. Preventing pollution and consequent exposure to potential environmental risk is all the more necessary to protect children from harm's way.

This is particularly important in the case of pesticides. The sheer volume of pesticide use necessitates a pollution prevention approach. In 1993, for instance, an estimated 4.23 billion pounds of pesticides were used in the United States; this total is based on the amount of active ingredients only (1). The figure includes conventional pesticides used in agriculture, wood preservatives, disinfectants, and water treatment, such as swimming pool chemicals.

NAS Report Examines Diet, Pesticides

One of the primary routes of exposure to potential environmental risk for children is diet, underscoring the importance of scrutinizing pesticides under the two federal statutes governing their use in food--the Federal Insecticide, Fungicide, and Rodenticide Act and the Federal Food, Drug, and Cosmetic Act.

Concern about the link between pesticide residues in food and children's health prompted Congress in 1988 to ask the National Academy of Sciences (NAS) to examine the issue. NAS established a committee through its National Research Council to do so. The committee examined scientific and policy issues confronted by government agencies, particularly the U.S. Environmental Protection Agency, in regulating pesticide residues in foods eaten by children and infants.

The resulting NAS report, Pesticides in the Diets of Infants and Children, issued in 1993, includes two major findings of particular importance to the protection of children from pesticide exposures (2). The first is that the federal government is not doing enough to protect children from exposures to pesticides. The second is that risk assessments for pesticides and toxic chemicals do not differentiate between risk to children and risk to adults, but should do so.

Children are not simply little adults, the NAS report emphasized. Children are different from adults in terms of sensitivity because they are growing and their internal organs are developing and maturing. Children are also different in terms of exposures because they have distinctly different behavioral and eating patterns.

Doing a better job of assessing risks for children requires more information about both susceptibility and exposures. Too many critical gaps in existing data persist. Although developing the needed information is a complex matter, scientists in government, academia, and elsewhere have succeeded in filling some of the gaps, and research currently underway needs continued support. At the same time, however, incorporating existing information into the assessment of children's risks must become a priority.

This article will examine how children may be more vulnerable to potential toxic effects of chemicals because of the developmental nature of their systems, behavior patterns, and environmental conditions. It will also draw on a series of examples to illustrate risk issues involving children. These include: sensitivity, exposure patterns, multiple sources of exposure to the same chemicals, and multiple exposures to chemicals that can act in the same way and can affect the same child.

Sensitivity and Pesticides

The first case illustrates the importance of considering sensitivity in determining environmental risks to children. Sensitivity, in an environmental context, is the capacity to be harmed. It varies among different populations, ethnic groups, genetic backgrounds, as well as by age and childhood experience and development. Age-related differences have a significant effect on metabolism (or how humans handle toxic substances), physiology (or how the body works), developmental stages, behavior, and diet.

In 1981, vinclozolin was registered for use as a fungicide on fruits and vegetables, having satisfied registration criteria under FIFRA. Federal regulations allow registration only if there are "no unreasonable adverse health effects" when compared with benefits gained. If that test is met, the risks involved are not considered unreasonable.

However, in 1988, the manufacturer of vinclozolin had important new findings from hormonal studies of rats and reported them to EPA, as mandated by law when new significant findings of an adverse effect from a pesticide are found. The company determined that in utero, or during fetal development, vinclozolin was acting as an antiandrogen. This term means that maternal exposure was associated with feminization of the male fetus. During in utero development, male fetuses were developing feminine sexual characteristics.

The Health Effects Research Laboratory in EPA's Office of Research and Development, which had been working on hormonal effects of pesticides, took a closer look at vinclozolin and determined that effects were found at doses six times lower than those reported when the pesticide was originally registered. Feminization of male fetuses, sterility later in life in the male animals, and other developmental variations were all confirmed (3,4).

As a result, no new uses have been allowed for vinclozolin, and as vinclozolin goes through the re-registration process under the 1988 FIFRA amendments, all uses currently allowed will be reassessed.

The potential implications of the effects of vinclozolin for children are inconclusive, but the data underscore the need for a cautionary regulatory approach and continued vigilance in regulating pesticide residues in food. Growing children are sensitive to imbalances in hormone levels, and the question of potential adverse health effects from exposure to pesticide residues in food needs to be the subject of continued research.

Sensitivity and Wildlife

Evidence of abnormal sexual development possibly due to environmental contaminants also comes from case studies involving wildlife, raising the issue of potential implications for childbearing and children's postnatal development. Much more research needs to be done in this area.

In the highly evolved chain of ecological connections, air, water, land, vegetation, and animals are linked in a complex web of interactions. For example, pollutants move among air, water, and land and are taken up by plants, which, in turn, are consumed by animals and humans. What goes into the air from near and far becomes deposited in rivers and lakes, for example, contaminating fish and fowl to varying degrees.

In recent years, scientists have begun observing marked effects on the reproductive systems of wildlife in areas that have been subjected to significant environmental contamination, provoking questions about potential implications for human beings' ability to have healthy children. Many of the instances have involved a group of widely used chemicals called organochlorines.

Perhaps the most noted case involves alligators living in Lake Apopka in central Florida (5). A number of endocrine-related effects were observed, including low hatching rates, males with abnormal reproductive tracts, and females with ovaries bearing abnormal eggs. These effects were purported to be due to a large quantity of DDE, a potent metabolite of the insecticide DDT, which had been spilled there. DDE's effects apparently led to an imbalance between androgens and estrogens in the developing alligators, which in turn caused abnormal sexual development.

Both DDT/DDE and vinclozolin are endocrine disrupters, substances that mimic or block the action of natural hormones. DDT is an estrogen, and vinclozolin is an antiandrogen. Estrogens are the group of human hormones responsible for many of the more feminine parts of sexual development throughout life, and androgens, mainly testosterone, are responsible for development of many male sexual characteristics. Both males and females naturally have levels of estrogens and androgens; it is the proper balance between the two that results in appropriate sexual development.

Endocrine disrupters may be persistent in the environment, such as DDT/DDE. Environmental estrogens mimic or block estrogen, may be persistent, and may bioaccumulate. Possible side effects of environmental estrogens include pregnancy, abnormal sexual development, potential cancer risks, i.e., breast and prostate; and other diseases such as endometriosis. Many endocrine disrupters like DDT/DDE bioaccumulate or concentrate in the food chain. In humans, effects on lactation have been demonstrated. Dr. Walter J. Rogan studied breast milk DDT levels for approximately 800 women in North Carolina (6). The intent was to look for health effects in children exposed to DDT in breast-feeding. Researchers found no evidence of increased illnesses among the children. However, they discovered that women with the highest levels of DDT in their milk breast-fed less than 40 percent as long as women with the lowest levels of DDT. Impaired lactation would have profound effects when breast milk is the only safe alternative for feeding infants.

There have also been concerns about the potential for effects on sexual development and cancer risks that might be hormonally related, such as breast cancer in women and prostate and testicular cancer in men (7).

EPA has developed testing protocols for evaluating hormonal effects of pesticides. The revised protocols call for using extended dosing periods, testing for development milestones in the animals, and looking for developmental end points after birth or postnatally. EPA's Scientific Advisory Panel, which is made up of outside experts, endorsed the changes, clearing the way for them to be added to the Agency's testing requirements. The new protocols will add a further layer of protection in discerning potential environmental risks to human health, but troubling questions about effects on reproductive systems remain.

Dietary Exposure to Toxicants

On the issue of exposures, children's diets differ significantly from those of adults, the NAS report confirmed (8). They eat more fruit in proportion to their body size; they also have less varied diets. As every parent knows, as children go through the first few years of life, they develop preferences for certain foods and often only will eat those particular foods for months at a time.

But NAS found that knowledge about what children eat is much more limited than it should be. Not only are existing data inadequate, current information is based on surveys conducted in the late 1970s. Dietary habits have changed substantially since then. Much higher consumption of fresh fruits and vegetables is a key example.

In looking at the diets of infants and children, NAS was critical of the current system for evaluating dietary intake for children because it groups all children between the ages of one and six. Data are available for children up to age one. However, the distinctions that exist between the diet of a one-year-old child and that of a five-year-old child are not taken into account. In assessing exposure and potential risk, NAS recommended being much more precise about what children eat during the first few years of life by addressing each year of life between one and six separately.

Work is underway with the U.S. Department of Agriculture to accomplish that objective. For example, USDA is revising the national food consumption survey, called the Continuing Survey of Food Intake, to characterize more accurately consumption patterns for foods children eat most frequently.

In addition to using the USDA data, EPA is planning to use data collected in the National Health and Nutrition Examination Survey to get a better idea of the food children eat. This survey also gathers information about young children, including those from various income and ethnic groups.

The foods children most commonly eat are identified in the NAS report (Table 1). In addition to foods that might be expected, such as milk and apples, there are some interesting and unexpected items, like coconut oil, which is in a number of processed foods, including sweet cereals and candy bars that children often love.

Exposure and Bananas

A specific example of the need to protect children from dietary exposure to risk involves the use of the pesticide aldicarb on bananas, one of the foods that children frequently prefer. A toddler can easily eat an entire banana. Some can eat several in a sitting, and children typically eat more of them than adults per pound of body weight.

Aldicarb is an insecticide that has been used for a number of years on fruits, nuts, potatoes, and various other vegetables. It is a systemic pesticide, which means it is taken up by the roots of the plant and ends up in the plant itself, and so cannot be removed by simply washing or peeling fruits and vegetables.

Aldicarb is a carbamate pesticide. It acts by inhibiting cholinesterase, the enzyme necessary for the proper transmission of nerve impulses, and can be very toxic to humans, causing a number of effects, including diarrhea, vomiting, and changes in the function of the central nervous system.

The manufacturer of aldicarb notified EPA in 1991 of some unexpected aldicarb residues on bananas. Generally, the residues were below the legal limit or tolerance. "Tolerances," the NAS report noted, "constitute the single, most important mechanism by which EPA limits levels of pesticide residues in foods. A tolerance is defined as the legal limit of a pesticide residue allowed in or on a raw agricultural commodity and, in appropriate cases, on processed foods. A tolerance must be established for any pesticide used on any food crop (9). Tolerances are set on the basis of composite samples. Under this approach, bunches of bananas were blended and then analyzed.

The level detected from this test method using this test method was found to be below the legal limit. However, when bananas were analyzed one at a time, some of these bananas were found to be very "hot." They had levels of aldicarb that were up to 10 times greater than the legal limit. When the legal limit was originally established, it was considered safe. This conclusion was based, in part, on the assumption that any exposure to aldicarb would be spread over a day. More recently, it has become apparent that a whole day's exposure could occur in a single serving. With chemicals like aldicarb that can produce acute effects, the original legal limits may no longer be considered safe for certain age groups, such as young children.

USDA checked aldicarb levels in bananas used for baby food. Those levels were very low, probably because the baby foods were made by blending large numbers of bananas. The problem was high levels of aldicarb in individual bananas that, at random, some children could end up eating. Some of these bananas were not only well above the legal limit but had levels potentially high enough to make a child acutely ill.

The dietary risk assessment found that, for the hottest bananas, the allowable daily limit of aldicarb would be exceeded by an adult eating more than an eighth of a banana and by a child eating more than one bite of a banana. But even for bananas at the legal limit, just one-third of a banana would be an excess for a toddler and one-seventh of a banana would be above the allowable daily intake for an infant.

In 1991, EPA and the manufacturer reached an agreement to stop the sale of aldicarb for use on bananas. The registration for bananas has since been canceled and the tolerance revoked. The company also has voluntarily withdrawn its use on white potatoes for the time being because of reasons similar to those in the case of bananas. Sampling single potatoes revealed a few with residues at or above levels of concern. The agency also compelled the company to reduce the amount of aldicarb used on citrus fruits. The pesticide is currently undergoing special review. The situation involving aldicarb residues in bananas is a good example of the need to monitor children's exposures to pesticides in food and respond accordingly.

A cautionary approach holds true for food imported from abroad. There has been concern for some time about potential risk from pesticides banned or not registered for use in the United States but sometimes detected in imported food. The U.S. Food and Drug Administration, which oversees the safety of imported food, generally has found a 2 to 3% higher violation rate for imported foods compared to domestic foods, usually due to residues of pesticides without tolerances rather than for pesticide residues above prescribed tolerance levels (10).

The food supply in the United States is considered the safest in the world, and adults as well as children should eat a diet high in fruits and vegetables. But efforts to ensure its safety with still higher certainty are key, particularly in view of children's patterns of food consumption and their vulnerability to toxicity.

Variety of Exposure Routes

There are multiple sources and avenues of exposure to pesticides and other toxic substances for children (11). Food and water are obvious sources. There can be direct inhalation and contact with agents inside and outside the home. Some exposures are occupationally related, like parents carrying home chemical residues on their clothing or the transfer to breast milk of chemicals contacted at work. Another type involves the bioaccumulation or body burden of chemicals in excess of their concentration in the general environment, such as pollutants in food, water, and air and in the home. Still other exposures can come from discharges to the air and water, certain waste sites, and, on occasion, industrial accidents.

The task of trying to account for all exposures is complex and difficult. Pesticides, for example, can be ingested during food consumption, inhaled when present in the air, and absorbed through skin contact (Table 2). They are commonly found in food and drinking water, in the air, on lawns and gardens, in households, and, for adults, in the workplace.

Infants, for example, individually can face a higher level of exposure than adults to the same level of toxic contaminants in drinking water (12). This would include pesticides. Although infants typically weigh only one-tenth as much as adults, they drink about one-third as much water each day. In addition, water constitutes a higher percentage of their body weight. They also have a higher daily rate of water replacement. These factors combine to increase the exposure of infants to toxic contaminants in water, compared with that of adults, underscoring the need for preventive action to protect them.

An EPA study completed in 1990, entitled The Non-Occupational Pesticide Exposure Study, found that 85 percent of the total daily exposure to airborne pesticides comes from breathing air inside the home (13). Because of this finding, EPA developed a new residential exposure research strategy.

However, it is now apparent that pesticide residues in and around the home are a significant source of exposure to infants and toddlers and that developing additional information about how these exposures occur will be increasingly necessary.

Some of the ways in which children can be exposed involve hand-to-mouth behavior, like sucking on thumbs and fingers. Other behaviors include object-to-mouth, elbow-to-lawn, hand-to-surface, and elbow-to-floor. There are many permutations of these. As a result, residues that persist on such things as carpets, floors, furniture, grass, soil, and playground equipment may be sources of exposure for children.

In communities with contaminated air, improving overall air quality for disease prevention is vitally important. In terms of protecting children's health, specifically, pediatric asthma is a major concern. Poor air quality conditions exacerbate asthma for children and possibly lead to an increased incidence of attacks, a number of studies have shown (14,15).

But indoor air environments cannot be ignored. There are a number of important sources of pollutants in indoor environments, including tobacco smoke, stove and fireplace fumes, household cleaners, paints and glues, and synthetic fabrics, as well as pesticides.

EPA programs that evaluate the risks of toxic substances need to pay more attention to the question of whether and how products in homes and the workplace lead to indoor air pollution problems. They also need to take a more preventive strategy. This means preventing chemicals in these products from being present in indoor environments in the first place and so precluding exposure to children and others.

Health Effects and Lead

The medical community played an important role in uncovering the link between children's exposure to lead and the effects of their health (16). In decades past, paint containing lead was widely used in the interior of American homes. As homes began to deteriorate and suffered from the lack of upkeep, children frequently ingested the paint chips; this was particularly true in lower economic areas. Children experienced various symptoms, ranging from constipation and retardation to encephalopathy, with coma, convulsions, and even death. Still the link with lead was unclear.

In the 1980s, however, studies tracking children from birth resulted in credence being given to the idea that exposure to lead caused a lowering of intelligence and behavioral disorders. Further, the effects were detected at much lower levels than expected and lasted longer than expected; these exposures were at levels once thought to be safe.

Fortunately, lead levels are coming down, due to government action to reduce lead exposure not only from house paint, but also from gasoline, drinking water, and other household products. There is still much to be done, however, particularly to protect children living in lower income areas.

Role of Clinicians

Identifying children's exposures to the multitude of potential hazards is difficult. Following are cases that illustrate not only the problems involved but also the crucial role clinicians can play in helping to identify environmental sources of toxicity and responding to them.

The first case involves a three-year-old child in Oregon who was diagnosed with chronic diazinon poisoning (17). The child was suspected of having cerebral palsy. He was floppy, which means he was not developing according to normal milestones.

Fortunately, the clinician in the case was astute. As part of the history taken from the parent, he discovered that the home had been sprayed with the insecticide diazinon several months prior to the examination. The clinician recommended that diazinon residues be evaluated in the home, and residues were found. He also sent a urine sample for testing to get an alkyl phosphate level. Not only was this elevated in the child, it was comparable to the level found in farm workers who work with this pesticide. Happily, one month after leaving the home environment, the child's signs resolved. The child no longer exhibited symptoms of developmental delay.

The unusual feature in this case is that the clinician took the time to take the history which revealed this exposure, and, second, understood what was needed to do the laboratory work, to identify diazinon in the home, and to find metabolites in the child's urine. Under other circumstances, this child might have gone on to have chronic neurological damage from the exposure and no one would have known why.

The second example concerns chronic mercury toxicity of a child, as reported in Morbidity and Mortality Weekly Reports in 1991 (18,19). The case involves a four-year-old child from Michigan with sweating, itching, headaches, difficulty walking, gingivitis, hypertension, and red discoloration of the palms and the soles of the feet. The physician involved suspected mercury poisoning. Older and more experienced, the doctor remembered the days when mercury compounds were used for teething powders. He also knew the significance of a particular array of symptoms that are characteristic of acrodynia, which is pathognomonic, that is, indicative of mercury exposure.

What the physician learned from the patient's history was that much of the inside of the home had recently been painted with latex paint, and the family had closed the windows and used air conditioning. Since that was the only change in the environment, he investigated further and found not only elevated urinary mercury levels in the child's urine but also mercury vapors in the house. He learned that mercury had been used as a fungicide in the paint.

Since then, the mercury compound involved has been banned for use in house paints, but this case raises the question of whether there have been a number of instances of exposure for children in the past that went unrecognized.

Multiple Exposures

Children may have multiple chemical exposures, which are difficult to identify and evaluate. Suppose, for example, that a child's home is treated with one pesticide. Others are used to treat the child's school for pests. Still other pesticides are in the food the child eats. All may have the same mechanism of action.

Several classes of pesticides contain specific chemicals that are likely to act by the same method of action. Examples include the organophosphates and carbamates which both inhibit cholinesterase.

It is not known how to combine the effects from these exposures and so estimate potential risk. Not known, for example, is whether these exposures are simply additive, if these pesticides sometimes inhibit each other, or if they sometimes are synergistic, multiplying each other's potential effects on children.

One of the first priorities must be to develop a plan to evaluate the issue of multiple exposures to pesticides that act by the same mechanism. This was recommended by the NAS. Such information could lead logically to developing procedures to take multiple exposures into account in the regulatory process. The methodology to accomplish this has not yet been fully developed. Work on this issue needs to be accelerated.

There are still many unknowns about the effects of pesticides on people and on infants and children in particular. Filling the information gaps on effects and exposures, primarily nondietary exposures, is essential, but achieving that goal will take time, focused effort, and unwavering support for research dedicated to this end.

Clinicians can play an important role in accomplishing this goal through special awareness of the potential effects of pesticide poisoning. Although environmental toxicity typically is not the first item on a doctor's mind in making a diagnosis, increased alertness to environmental toxicity can be a direct route to identifying causes of disease. Parents can contribute as well by identifying possible environmental links and advising the physician involved in treating the child's health problem about them.

One of the major strategies immediately available for protecting children from exposures to environmental risk is pollution prevention. It is time for parents and schools to take a careful look at how pesticides and other toxic chemicals are used around children. Pesticides should not be used on a "preventive" basis but rather to treat specific pest problems. It is important to use Integrated Pest Management (IPM) techniques to avoid the use of pesticides. Around the home this means keeping pests out in the first instance and denying them access to food and shelter. If a pesticide is needed, use the safest product available and follow label instructions carefully. Be sure that any pest control contractors are licensed. And stay out of the house during treatment, ventilating it well before reoccupying it. Likewise, it is important to reduce the risks of agricultural pesticides. EPA is working with farmers to reduce unnecessary use, encourage IPM practices, and help the transition to safer alternatives. We are working to strengthen regulation of pesticides to protect children. What these changes will mean is fewer pesticide residues in drinking water and on food.

REFERENCES

1. U.S. Environmental Protection Agency. Quantities of Pesticides Used in the United States, Information Sheet, Washington, DC, (1994).

2. National Academy of Sciences--National Research Council, Pesticides in the Diets of Infants and Children, Washington, DC:National Academy Press, 1993.

3. Kelce WR, Monosson E, Gamcsik MP, Laws SC, Gray LE, Jr. Environmental hormone disruptors: evidence that vinclozolin developmental toxicity is mediated by antiandrogenic metabolites. Toxicol Appl Pharmacol 126:276-285 (1994).

4. Gray LE, Jr, Ostby JS, Kelce WR. Developmental effects of an environmental antiandrogen: the fungicide vinclozolin alters sex differentiation of the male rat. Toxciol Appl Pharmacol 129:46-52 (1994).

5. Hileman B. Environmental estrogens linked to reproductive abnormalities, cancer. Chemical & Engineering News, January 31, 1994.

6. Rogan WJ, Gladen BC, McKinney JD, Carreras N, Hardy P, Thullen J, Tingelsad J, Tully M. Polychlorinated biphenyls (PCBs) and dichlorodiphenyl dichloroethene (DDE) in human milk: effects on growth, morbidity, and duration of lactation. Amer J Pub Health 77(10):1294-1297.

7. McLachlan JA. Functional toxicology: a new approach to detect biologically active xenobiotics. Environ Health Perspect 101(5):386-87.

8. See note no. 2, NAS report, p. 23.

9. See note no. 2, NAS report, p. 1.

10. U.S. Food and Drug Administration. Pesticide program -- residue monitoring 1993. Journal of the AOAC International 77(5):161A-85A.

11. Rogan WJ. The sources and routes of childhood chemical exposures. J Pediat 97(5):861-865 (1980).

12. David DL, Miller Poore L, Levin R. Chemical contamination of food and water. In: Textbook of Clinical Occupational and Environmental Medicine (Rosenstock L, Cullen MR, eds). Philadelphia:W.B. Saunders Company, 1994;47-53.

13. Immerman FW, Schaum JL. Nonoccupational Pesticides Exposure Study. U.S. Environmental Protection Agency, Office of Research and Development, Document No.:600/S3-90/003, April 1990.

14. Morgan WJ, Martinez FD. Risk factors for developing wheezing and asthma in childhood. The Pediatric Clinics of North America 39(6):1185-1203 (December 1992).

15. Bloomberg GR, Strunk RC. Crisis in asthma care. The Pediatric Clinics of North America 39(6):1225-1241 (December 1992).

16. Rogan WJ. Environmental Poisoning of Children -- Lessons from the Past. National Institute of Environmental Health Sciences, unpublished paper.

17. Wagner SL, Orwick DL. Chronic organophosphate exposure associated with transient hypertonia in an infant. Pediatrics 94(1):94-97 (1994).

18. Acute and chronic poisoning from residential exposures to elemental mercury -- Michigan, 1989-1990. Morbidity and Mortality Weekly Reports 40(23):393-95 (June 1991).

19. Blondell JM, Knott SM. Risk analysis for phenylmercuric acetate in indoor latex house paint. In: Pesticides in Urban Environments: Fate and Significance (Racke K,Leslie A, eds). American Chemical Society:Washington, DC, 1993.

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Last Update: September 14, 1998