Cover Story

Pesticides and PCBs:
Does the evidence show that they threaten children's health?

By Philip J. Landrigan, MD, MSc

Most pediatricians are ill-prepared to address the growing concern of parents about children's exposures to environmental toxins such as pesticides and polychlorinated biphenyls (PCBs). This environmental health expert reviews the evidence about the potentially harmful effects of these chemicals and explains what makes children particularly vulnerable.

Concern about children's exposures to pesticides, polychlorinated biphenyls (PCBs), and other environmental toxins has increased in recent years.¹ With growing frequency, parents are asking pediatricians whether chemicals in the environment pose a danger to their children now or in the future and whether even low levels of exposure can be harmful. They want to know if chemicals can damage their child's immune system, nervous system, or reproductive organs. And they ask about cancer. Couples who are expecting a baby are concerned, too, wondering about the risks of prenatal, and even preconception, exposure.

Such concerns are hardly surprising. The newspapers are full of stories about pesticide spraying, hazardous waste dumps, contaminated ground water, and polluted air. Parents are besieged by a welter of information about the potential health risks of chemicals to children. Pediatricians have, for the most part, been unprepared to address these issues, because the topics are so new and little attention has traditionally been focused on environmental health in medical school curricula or postgraduate programs.²

Children are, in fact, vulnerable to environmental toxins. In this article, I will try to unravel some of the complexities that surround the health effects of two major classes of environmental chemicals: pesticides and PCBs. I refer readers who would like more detailed information to the Handbook of Pediatric Environmental Health, released in November 1999 by the American Academy of Pediatrics (AAP).³ This landmark guide, intended by the academy to be a counterpart to its handbook on infectious diseases ("The Red Book"), is an authoritative source of information. Like the Red Book, the "Green Book" will be updated periodically.

What makes kids so vulnerable to toxins?

Several factors explain why children are particularly vulnerable to pesticides, PCBs, and other environmental toxins (Table 1).⁴ First, children have proportionately heavier exposures than adults to any toxins present in water, food, or air. That's because, pound for pound of body weight, kids drink more water, eat more food, and breathe more air. For example, children ages 1 through 5 years eat three to four times more food per pound than the average adult American. The air intake of a resting infant is twice that of an adult per pound of body weight. These patterns of increased consumption reflect the rapid metabolism of children.

TABLE 1
Factors that put children at increased risk for toxicity

Two other characteristics further magnify children's exposures to environmental toxins: (1) their hand-to-mouth behavior, which increases their ingestion of any toxic chemicals in dust or soil, and (2) their likelihood of playing close to the ground, which increases their exposure to toxins in dust, soil, and carpets, as well as to toxins that form low-lying layers in the air, such as certain pesticides.

In addition to being more heavily exposed to chemicals than adults, infants and children are biologically more vulnerable, for three reasons.⁴ First, their metabolic pathways are immature, so their ability to detoxify and excrete certain toxins is different than that of adults. In some instances, children's bodies are actually better able to deal with environmental chemicals because they are unable to transfer them to toxic metabolites. More commonly, however, children's bodies are less able to handle toxic chemicals, and thus are more vulnerable to their effects.

Second, children mature rapidly, and their developmental processes are easily disrupted. Many organ systems in young children—the nervous system, the reproductive organs, the immune system—grow very quickly in the first months and years of life. During this period, structures are developed and vital connections are established. Indeed, the nervous system continues to develop all through childhood, as evidenced by the fact that children continue to acquire new skills as they get older—crawling, walking, talking, reading, writing. The nervous system has difficulty repairing any structural damage caused by environmental toxins. Thus, if cells in the developing brain are destroyed by chemicals, or if the formation of vital connections between nerve cells is blocked, there is a high risk that the resulting neurobehavioral dysfunction will be permanent and irreversible. The consequences can be lifelong loss of intelligence and alteration of normal behavior.⁵

Third, because children have more future years of life than adults, they have more time to develop chronic diseases that may be triggered by early environmental exposures. Many such diseases require decades to develop. Examples include mesothelioma caused by exposure to asbestos, leukemia caused by benzene, breast cancer that may be caused by dichlorodiphenyltrichloroethane (DDT),⁶ and possibly some chronic neurologic diseases, such as Parkinson's disease, that may be caused by exposure to neurotoxins.⁷ Many of these diseases are now thought to be the result of multistage processes within the body's cells that continue for many years before manifesting as illness. Consequently, certain carcinogenic and toxic exposures sustained early in life appear more likely to lead to disease than the same exposures encountered later in life.⁴

What are pesticides?

Pesticides are a diverse group of chemical compounds (Table 2), and they are among the classes of toxic chemicals most commonly encountered by children. Pesticides include insecticides, fungicides, herbicides, and rodenticides. In homes and apartments, pesticides kill termites, roaches, and rodents. In gardens and lawns, as well as along highways and under power line right-of-ways, chemical herbicides limit the growth of unwanted plants. By controlling agricultural pests, pesticides contribute to dramatic increases in crop yields and in the quantity and variety of the diet. Indeed, agriculture is the major setting for pesticide use in the United States. By controlling insect vectors, pesticides help limit the spread of disease.

TABLE 2
Pesticides commonly found in the US

But pesticides also cause injury to human health, as well as damage to the environment. The health effects include acute and persistent injury to the nervous system, lung damage, injury to the reproductive organs, dysfunction of the immune and endocrine systems, birth defects, and cancer.⁸

Approximately 600 pesticide active ingredients, found in insecticides, herbicides, rodenticides, and fungicides, are registered with the United States Environmental Protection Agency (EPA). These compounds are mixed with one another and blended with inert ingredients to produce more than 20,000 commercial pesticide products. The EPA estimates that each year domestic users in the US spend $8.5 billion for 1.1 billion pounds of pesticide active ingredients.⁹

The principal classes of insecticides in use in the US are the organophosphates, carbamates, and pyrethroids. Unlike earlier generations of pesticides, such as DDT, these compounds are short-lived in the environment and do not accumulate in human and animal tissues.¹⁰ However, the organophosphates and carbamates are toxic to the nervous system,¹¹ and some of the pyrethroids are believed to be toxic to the reproductive system and disruptive to endocrine function.¹²

How are children exposed to pesticides?

Children may be exposed to pesticides in schools, day-care centers, parks, and gardens. Farm children can be exposed in the fields as well as at home, when pesticides are transported into the house. Pesticides from agricultural runoff can contaminate drinking water supplies. Diet is also an important source of exposure.

The largest source of children's exposure is the use of pesticides in the home and on lawns and gardens. Approximately 90% of American households use pesticides. Homeowners accounted for the purchase of an estimated 74 million pounds of the pesticides used in the US in 1995, representing a nearly $2 billion industry.⁹ These multiple exposures may be additive in their effect on children's health.⁴

Pesticides are used especially heavily in urban environments where constant control of insects and rodents is required. Because urban pest control occurs in apartments and other confined spaces, great potential exists for intimate exposure of children.¹³

Chlorpyrifos (Dursban, Lorsban), an organophosphate insecticide, has been the pesticide used most heavily in cities over the past decade. It is applied around baseboards and injected into cracks and crevices to control termites and cockroaches, and it may be sprayed in rooms to control fleas. Occasionally, it is applied with a fogger. A nationwide survey conducted by the EPA found that chlorpyrifos is one of the pesticides most widely detected in American homes. For example, chlorpyrifos residues were found in air samples in 83% to 97% of homes in Jacksonville, FL, and in 30% to 40% of homes in Massachusetts.¹⁴

Organochlorine pesticides, such as chlordane, DDT, dieldrin, and lindane, have also been widely detected in residential air and on indoor surfaces in homes in US cities.¹⁵ Many of these pesticides have been banned for decades, and hence they are found more often in older homes. Chlordane was used in an estimated 24 million US homes, usually as a termiticide, and it has been detected in the home environment as long as 35 years after use.

Illegal pesticides are of great concern in cities—so-called street pesticides.¹⁶ For example, a very highly concentrated and illegal preparation of the carbamate insecticide aldicarb is available in inner-city communities under the name Tres Pasitos ("three little steps," the distance a rodent is said to be able to walk after ingesting this agent). A recent case report described a 2-year-old girl in New York City who had an acute toxic episode after eating Tres Pasitos. Another roach killer bought on urban street corners is Tiza China (Chinese chalk), which reportedly contains boric acid. Finally, a 1996 episode involved methyl parathion. Eleven hundred homes in Chicago and Cleveland and on the Gulf Coast were illegally sprayed with this highly toxic pesticide, whose use is supposed to be restricted.¹⁷

How can pesticides injure children?

The effects of pesticide poisoning on children can be acute and obvious, or chronic, cumulative, and subtle. The Consumer Product Safety Commission collects data on acute pesticide poisonings in the US, based on a statistical sample of emergency rooms in 6,000 selected hospitals.¹¹ From 1990 to 1992, an estimated 20,000 emergency room visits were the result of pesticide exposure. The incidence was disproportionately high among children, who accounted for 61%, or more than 12,000, of these cases.¹¹ Organophosphates were the class of compounds most frequently involved.

Acute high-dose exposure to organophosphate pesticides inhibits the enzyme acetylcholinesterase in the nervous system, leading to a spectrum of cholinergic symptoms, including lacrimation, abdominal cramps, vomiting, diarrhea, miosis, and profuse sweating. The more severe cases progress to respiratory arrest and death. Studies in animals indicate that young animals are more susceptible than adults to this acute neurotoxic syndrome, probably because the young are less able to detoxify and excrete organophosphates.

Concern about the chronic effects of pesticides focuses on two particular areas: subclinical neurotoxicity and disruption of endocrine function.

Subclinical injury. The notion of the possible "subclinical toxicity" of pesticides has gained increasing attention in recent years. This term denotes the idea that relatively low-dose exposure to certain chemicals, pesticides among them, may harm various organ systems without producing acute symptoms or being evident in a standard clinical examination. The concept arose from studies of children exposed to relatively low levels of lead who were found to have suffered loss of intelligence and altered behavior even in the absence of clinically detectable symptoms.¹⁸ The underlying premise is that there exists a continuum of toxicity in which clinically apparent effects have asymptomatic, subclinical counterparts. It is important to note that these subclinical changes represent truly harmful outcomes and are not merely homeostatic or physiological "adjustments" to the presence of pesticides.¹⁹

Recent findings on the developmental toxicity of chlorpyrifos in animals illustrate the potential of pesticides to produce subclinical neurotoxicity in infants and children. The mechanism of chlorpyrifos-induced neurotoxicity appears to involve injury to the adenylyl cyclase cascade, a system in brain cells that mediates cholinergic as well as adrenergic signals.²⁰ Even at low doses of exposure, insufficient to compromise survival or growth, chlorpyrifos was found to "produce cellular deficits in the developing brain that could contribute to behavioral abnormalities."²¹

Because these animal data are so recent, studies of the developmental toxicity of chlorpyrifos in human infants have not yet been conducted. However, the animal data raise the concern that chlorpyrifos may not be the only organophosphate pesticide that could be a developmental toxicant in humans. The potential for such toxicity may be substantial in urban communities, where chlorpyrifos is heavily applied in closed apartments.¹³

On the basis of these findings, the EPA recently issued a ruling that bans the use of chlorpyrifos in schools, parks, and day-care settings and that prohibits and phases out nearly all residential use. Preventing developmental disability in children was the major reason for this ruling.

Endocrine disruption. The potential of pesticides to disrupt endocrine function has been recognized for nearly four decades, ever since the 1962 publication of Rachel Carson's Silent Spring. Carson's work showed that eagles and ospreys who had been heavily exposed to DDT had suffered disrupted estrogen cycles. As a result, these two predatory species at the top of the food chain were producing thin-shelled, nonviable eggs. Carson's work, along with the desire to prevent the bald eagle from becoming extinct, prompted the EPA to ban DDT in the early 1970s.

More recent evidence of the capacity of organochlorine pesticides to produce endocrine and reproductive toxicity in animals comes from studies of alligators in Lake Apopka in Florida, a body of water heavily contaminated with DDT and other organochlorines. Male alligators in Lake Apopka have been found to have significantly smaller penises than alligators from nearby uncontaminated lakes.²²

Recent concern about the endocrine toxicity of pesticides in humans has focused especially on the pyrethroids, a class of insecticides widely used as substitutes for chlorpyrifos and other organophosphate and carbamate pesticides. Pyrethroids have been used in pediatric practice to control body lice and scabies instead of more toxic agents such as lindane, and their acute toxicity is generally low. However, hormonal activity has been reported for certain pyrethroids in laboratory systems, suggesting that their capacity to affect hormonal and reproductive development in children should be investigated further.¹² The pyrethroid sumithrin (Anvil) has been used recently in New York City and elsewhere on the East Coast in the spraying of mosquitoes to prevent the spread of West Nile Virus.

In fetal life, even low-dose exposure to endocrine-disrupting pesticides can have devastating effects, because hormones play critical roles in shaping the early development of the immune, nervous, and reproductive systems.²³ The developmental effects of exposure to endocrine disrupters vary depending on age at exposure and sex.

The Food Quality Protection Act of 1996 now requires that pesticides be tested for potential endocrine toxicity. Although much remains to be learned about the full range of this toxicity and its molecular mechanisms, the EPA has designed a new screening protocol for testing pesticides for endocrine-disrupting potential and will be making recommendations for safety standards based on these tests. The endocrine toxicity of pesticides and other environmental chemicals promises to be a very exciting area of research in the next decade.

What are polychlorinated biphenyls?

PCBs are a family of synthetic organic compounds with a common two-ring structure and one to 10 substituted chlorine atoms (Figure 1). Commercial PCB products, which were used as insulating fluids and dielectrics in the manufacture of electrical capacitors and transformers, consisted of mixtures of isomers of varying degrees of chlorination. They were dispersed widely in the environment, and production of PCBs was halted in the US in the 1970s because of concern about their extreme persistence. Indeed, low-level exposure to these chemicals via the food chain remains widespread even 25 years later.

Once ingested, PCBs concentrate in lipid-rich tissues, including brain and breast milk, and they readily cross the placenta from mother to fetus. The principal source of human exposure is consumption of fish and shellfish from contaminated waterways. Contamination occurs through a process known as bioaccumulation. In this process, plankton pick up insoluble PCBs from sediments. They are then eaten by little fish, who in turn are eaten by larger, predatory species. The PCBs become increasingly concentrated as they move up the food chain.

In New York, PCBs are present in high concentrations in Hudson River sediments and in fish from Hudson Falls, NY (the site of a former General Electric capacitor manufacturing facility) all the way to the southern tip of Manhattan, a distance of more than 200 miles. To reduce the risk of fetal PCB toxicity, the New York State Department of Health advises pregnant women not to consume fish from the Hudson and adjoining waters. Recent surveys of river anglers indicate, however, that families in New York City, including women and children, continue to eat local fish and shellfish and therefore run the risk of PCB exposure. These studies found that poor people and people of color are the most likely to consume locally caught fish and that the highest levels of PCBs are found in those who consume the most fish. Similar patterns of exposure to PCBs have been noted in the Great Lakes and areas of New England, where PCB contamination is also widespread (Figure 2).²⁴

Are PCBs developmental toxicants?

A growing body of evidence indicates that PCBs can have neurodevelopmental effects in young children at levels of exposure that are widely prevalent in the general population.^24,25 Concern about the neurodevelopmental effects of PCBs stemmed initially from studies of children exposed to high levels of PCBs in two poisoning incidents in Asia. In the Yu-cheng (oil disease) incident in Taiwan, cooking oil was contaminated by PCBs and related polychlorinated compounds, including furons. Children exposed prenatally exhibited a variety of conditions, including low birth weight, abnormal skin pigmentation, delayed developmental milestones, and lower IQs than unexposed siblings. The difference in mean, full-scale IQ ranged from nine to 19 points during six years of annual testing. Exposed boys, but not girls, showed deficits in spatial reasoning compared with control subjects.²⁵ A similar episode occurred in Japan.

Of greater concern today are studies suggesting that low levels of exposure, still very common in the American population, may have detectable health effects in humans. Rogan and colleagues examined a general population cohort of children in North Carolina to study the effects of PCB exposure on growth and neurodevelopment.²⁶ They found an association between transplacental PCB exposure and lower scores at 18 and 24 months on the Bayley Scales of Infant Development. The mean effect on the Psychomotor Development Index (PDI) at 24 months was an eight-point reduction in the highest exposure group. Preliminary data in this group of children also show associations between antenatal exposure to PCB and early onset of puberty.²⁵

Jacobson has followed a cohort of children in Michigan that was selected to overrepresent children with above-average exposure to PCBs via maternal consumption of contaminated Lake Michigan fish.²⁴ They found an adverse effect at age 4 years on the verbal and memory scale scores of the McCarthy Scales of Children's Abilities. This effect appeared dose-dependent across a range of cord serum PCB levels. A follow-up of the Michigan cohort at age 11 found that among 178 children, full-scale IQ was inversely associated with prenatal, but not postnatal, PCB exposure.

Studies of the neurodevelopmental toxicity of PCBs in animals are generally consistent with the human data. They also show that prenatal exposure is more dangerous than exposure via breast milk after birth, and they document damage to similar functional domains. For example, learning and visual recognition memory in rats were effected by prenatal, but not postnatal, PCB exposure.

How do we protect children?

For fetuses, infants, and children alike, subclinical developmental neurotoxicity is the major threat posed by exposure to pesticides and PCBs. Evidence of that toxicity has become too great to ignore. The combination of young children's disproportionately heavy exposures to pesticides and PCBs, coupled with their developmental vulnerabilities, places them at increased risk for neurologic, endocrine, and other developmental disabilities.⁴ Because these injuries cannot be reversed medically, prevention of exposure must be emphasized.²⁶

Pediatricians can undertake a series of actions to reduce the exposure of children to pesticides:

• Counsel parents to minimize the use of pesticides in their homes and on their lawns and gardens. A rich literature on nonchemical alternatives to pesticides exists. Publications such as Organic Gardening offer many suggestions, and a nonchemical approach to pest control termed Integrated Pest Management (IPM) has been used extensively with considerable success.

• Urge parents to feed their children a balanced diet that includes a wide variety of fruits and vegetables. Also advise families to wash all fruits and vegetables, buy organic products, and serve fresh produce in season. In addition, while fruits and vegetables are certainly much healthier for children than sweets or fatty foods, encouraging families to rotate the diet to include different foods will further reduce pesticide exposure.

• Take action in local communities to encourage the reduction of pesticide use in schools and hospitals. Advocate that routine chemical pest control be replaced with IPM.

• Participate locally and nationally in the environmental health activities of the AAP. In this way, pediatricians have been very effective in advocating for stricter testing of pesticides prior to marketing and for limiting the use of the most dangerous pesticides, such as chlorpyrifos.

• Encourage families not to eat fish, crabs, and shellfish from waters known to be contaminated with PCBs and other persistent chlorinated organic compounds. This is the single most effective action for reducing children's exposures to PCBs. It is especially important that pregnant women and young women contemplating pregnancy not consume fish from such waters, given that PCBs from contaminated fish are well known to accumulate in fatty tissues, where they can persist for many years before crossing the placenta and reaching the fetal brain.

Education is the key to preventing both the short- and long-term effects of chemical exposure. By informing families about the risks of toxicity and ways to prevent exposures, pediatricians can help make a child's environment a healthier place, whether that environment is the great outdoors, the family home, or a mother's womb.

REFERENCES

1. Needleman HL, Landrigan PJ: Raising Children Toxic Free: How to Keep Your Child Safe From Lead, Asbestos, Pesticides and Other Environmental Hazards. New York, Farrar, Straus and Giroux, 1994

2. Levy BS: The teaching of occupational health in United States medical schools: 5-year follow-up of an initial survey. Am J Public Health 1985;75:79

3. Committee on Environmental Health, American Academy of Pediatrics: Handbook of Pediatric Environmental Health. Elk Grove, IL, American Academy of Pediatrics, 1999

4. National Research Council: Pesticides in the Diets of Infants and Children. Washington, National Academy Press, 1993

5. Weiss B, Landrigan P: The developing brain and the environment: An introduction. Environmental Health Perspectives 2000;108(Supplement):373

6. Schecter A, Toniolo P, Dai LC, et al: Blood levels of DDT and breast cancer among women living in the North of Vietnam. Arch Environ Contam Toxicol 1997;33:453

7. Tanner CM, Ottman R, Goldman SM, et al: Parkinson's disease in twins: An etiologic study. JAMA 1999;281:341

8. Hayes WJ, Laws ER: Handbook of Pesticide Toxicology. San Diego, Academic Press, 1991

9. Schierow LJ: Pesticide Policy Issues. Washington, The Library of Congress, 1996

10. Schuman SH, Simpson W: A clinical historical overview of pesticide health issues. Occup Med-State of the Art Rev 1997;12:203

11. Blondell J: Epidemiology of pesticide poisonings in the United States, with special reference to occupational cases. Occup Med—State of the Art Rev 1997;12:209

12. Garey J, Wolff MS: Estrogenic and anti-progestagenic activities of pyrethroid insecticides. Biochem Biophys Res Comm 1998; 251:855

13. Landrigan PJ, Claudio L, Markowitz SB, et al: Pesticides and inner-city children: Exposures, risks, and prevention. Environ Health Perspec 1999;107(Suppl 3):431

14. Whitmore RW, Immerman FW, Camann DE, et al: Nonoccupational exposures to pesticides for residents of two US cities. Arch Environ Contam Toxicol 1994;26:47

15. Wargo J: Our Children's Toxic Legacy. New Haven, CT, Yale University Press, 1996

16. Poisonings associated with illegal use of aldicarbs as a rodenticide-New York City, 1994-1997. MMWR 1997;46:961

17. Methyl parathion comes inside. Environ Health Perspect 1997;105:690

18. Needleman HL, Gunnoe C, Leviton A, et al: Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Engl J Med 1979;300:689

19. Landrigan PJ: The toxicity of lead at low dose. (Editorial) Brit J Industr Med 1989;46:593

20. Song X, Seidler FJ, Saleh JL, et al: Cellular mechanisms for developmental toxicity of chlorpyrifos: Targeting the adenylyl cyclase signaling cascade. Toxicol Appl Pharmacol 1997;145:158

21. Campbell CG, Seidler FJ, Slotkin TA: Chlorpyrifos interferes with cell development in rat brain regions. Brain Res Bull 1997;43:179

22. Guillette LJ Jr, Gross TS, Masson GR, et al: Developmental abnormalities of the gonad and abnormal sex hormone concentrations in juvenile alligators from contaminated and control lakes in Florida. Environ Health Perspect 1994;102:680

23. Soto, AM, Cheng, KL, Sommerschein C: The pesticides endosulfan toxaphene and dieldrim have estrogenic effects on human estrogen sensitive cells. Environ Health Perspect 1994;102:380

24. Jacobsen JL, Jacobson SW: Intellectual impairment in children exposed to polychlorinated biphenyls in utero. New Engl J Med 1996;335:783

25. Longnecker MP, Rogan WJ, Lucier G: The human health effects of DDT (dichlorodiphenyltrichloroethane) and PCBs (polychlorinated biphenyls) and an overview of organochlorines in public health. Annu Rev Public Health 1997;18:211

26. Bearer C: How are children different from adults? Environ Health Perspect 1995;103(suppl 6):7

THE AUTHOR is Professor of Pediatrics and Director of the Center for Children's Health and the Environment, Mount Sinai School of Medicine, New York, NY.

 

Philip Landrigan. Pesticides and PCBs: Does the evidence show they threaten children's health. Contemporary Pediatrics 2001;2:110.