environmental health hazards: how children are different from adults

Environmental HealthHazards: How Children AreDifferent from AdultsCynthia F. Bearer

Abstract

In policymaking on environmental health, it is often assumed that the entire popula-tion is exposed to and reacts to environmental contaminants in a similar manner.However, this assumption is misguided, especially where children are concerned. Thisarticle presents the scientific basis for the impacts of the environment on children,showing how children are different from adults in the ways in which they are exposedto environmental contamination and the ways in which they react to it when exposed.Specifically, the article examines the changing physical and biological environmentsof children. Children at different stages of development have unique physical riskfactors for certain types of exposure because of changing location, levels of mobility,oxygen consumption, eating patterns, and behavior. When children are exposed tocontaminants, their developing biological makeup—the way in which they absorb, dis-tribute, and metabolize chemicals—will also affect how their bodies deal with the for-eign substance. Each of these factors, along with the customs, laws, and regulationsthat affect the way in which children are exposed to the contaminants, has implica-tions for the well-being of children in the years to come.

As the human population increases, its demands on the earth alsoincrease. Today, the demand for food, potable water, clean air,energy, and manufactured goods; the need for solid and liquid

waste disposal; and the requirement for habitable land are all expanding.With this expansion, increasing amounts of pollutants are released intothe environment, and more and more people come into contact withpolluted environments.

Interaction with polluted environments can have an adverse impact onthe health of humans and other living creatures. This impact is felt firstamong the most vulnerable members of a population. Children, because oftheir unique physical, biological, and social characteristics, are among themost vulnerable members of our population.

We have become increasingly aware of the dangers posed by theaccumulation of pollutants in the environment and have looked to policy

11

The Future of Children CRITICAL ISSUES FOR CHILDREN AND YOUTHS Vol. 5 • No. 2 – Summer/Fall 1995

Cynthia F. Bearer, M.D.,Ph.D., is asssistant pro-fessor of pediatrics in theDepartment of Pediatricsat Case Western ReserveUniversity.

THE FUTURE OF CHILDREN – SUMMER/FALL 199512

in the form of legislation, regulation, and private, voluntary action for pro-tection. It may, however, be costly to identify and effectively deal with envi-ronmental hazards, particularly when there are benefits to be gained fromthe use of hazardous materials. Under these circumstances, effective poli-cymaking depends on honest and accurate assessment of the risks posedto all members of society, including children. For a variety of reasons, spe-cial consideration should be given to protecting children in formulatingenvironmental policies: children are less able than adults to protect them-selves, may be more vulnerable to particular toxins, and are not consid-ered responsible for pollution. Crafting environmental policies responsiveto the special needs of children requires a thorough consideration ofthese special needs and an understanding of how these needs may changeas children grow and develop.

This article presents the scientific basis for the impacts of the envi-ronment on children. It describes the differences between adults andchildren in physical, biological, and social environments, and highlightswhy children should not be treated as “little adults” in developing envi-ronmental policy.

Human EnvironmentsChildren exist within three broad types ofenvironments: physical, biological, andsocial (see Figure 1). Each affects theirwell-being, is at risk of degradation, and isamenable to policy intervention. Thephysical environment is anything thatcomes in contact with the body. Air, forexample, is in constant contact with ourlungs and skin, and is a large part of our

physical environment. To define the phys-ical environment precisely, it may be nec-essary to divide a large environment intosmaller units, called microenvironments.For example, in a room contaminatedwith radon, the radon will not be evenlydispersed; air near the floor has a higherradon concentration while air near theceiling has a lower radon concentration.Therefore, the environment of an infantplaying on the floor would be much dif-ferent from that of an adult standing inthe room. These microenvironments can

differ enormously between adults and chil-dren in many situations.

The biological environment consists ofthe internal physiological workings of thebody as it takes up, processes, and inter-acts with the substances it contacts. Thebody has specific chemical pathways usedto digest, process, and excrete substancesfound in air, food, and water. The multiplesteps by which a toxic hazard may result inadverse health effects help illustrate thecomplexity of the biological environment.The steps are (1) absorption (how thechemical gets into the body), (2) distribu-tion (once inside the body, how the chem-ical gets to each of the organs and in whatamount), (3) metabolism (how the bodyprocesses the chemical), and (4) the toxicaction (how the chemical interacts withthe biochemistry of the body). Each ofthese steps depends on the developmentalstage of the child because the child’s bio-logical environment changes over time.

The social environment includes theday-to-day circumstances of living in a fam-ily or other setting as well as the laws andregulations that affect day-to-day living.Children, because of their continued devel-opment and their different physical andbiological environments, are a uniquegroup of individuals in relation to toxichazards. If laws, regulations, policies, andbehavior do not reflect this fact, then chil-

Children are less able than adults to protectthemselves, may be more vulnerable toparticular toxins, and are not consideredresponsible for pollution.

13Environmental Health Hazards: How Children Are Different from Adults

dren may be unwittingly exposed to envi-ronmental hazards. In time, children maybecome bodies of evidence that environ-mental degradation can have severeimpacts on the health of societies.

This article concentrates largely on thephysical and biological environments ofchildren at various developmental stages.The social environment is discussed indetail in the article by Landrigan andCarlson in this journal issue.

Developmental StagesA child’s vulnerability to environmentalexposures is closely related to his or herdevelopmental stage. Changes in growth,hormonal levels, and biochemical makeupcontinually occur. Developmental stagesare periods in a child’s life characterizedby the achievement of certain intellectualand physical milestones. For organization-al purposes, this article recognizes fivestages: the newborn (from birth to 2months of age), the infant/toddler (2months to 2 years of age), the preschool

child (2 to 6 years of age), the school-agechild (6 to 12 years), and the adolescent(12 to 18 years). The fetus is considered asa single separate stage, although there aremultiple critical stages of developmentfor the fetus.1

The Physical EnvironmentExposure to an environmental agent is thefirst step in a sequence of environmentallyrelated health effects. Exposure may occurat any point as people move through sev-eral environments during the course of aday. Adult environments include home,work, and errands outside home andwork. Infants and children spend time athome, school, day care, and play. Becausethe environments of children are typicallydifferent from those of adults and mayvary according to the age of the child, chil-dren’s exposure to environmental agentsmay be different from exposures of adultsand may vary with the developmental stageof the child. In addition, different patternsof exposure to a toxin may yield different

Figure 1

A Child’s Environments

CHILD

Biological

Social

Physical

14 THE FUTURE OF CHILDREN – SUMMER/FALL 1995

health effects. For example, nitrates inwell water may cause the hemoglobin inblood to become methemoglobin. If toomany nitrates are ingested, this chemicalchange can cause insufficient oxygen toreach the body tissues.2 However, if thenitrates are ingested at a rate that is slowenough for the enzymes in the blood toconvert the methemoglobin back tohemoglobin, no health effect will occur.3

Exposure Before BirthExposures that have profound healtheffects on an individual may occur beforebirth. Even exposures that occur to womenbefore the conception of a child may havean effect on that child (see Table 1). Forexample, women who conceived after eat-ing cooking oil contaminated with poly-chlorinated biphenyls (PCBs) gave birth toinfants with a pattern of abnormal physicalcharacteristics called yusho.4,5 In anothercase, a woman inadequately treated forlead poisoning in childhood gave birth toan infant with congenital lead poisoning.6,7

An individual can also be affected byexposures that had direct effects on theovum and sperm prior to conception. Theovum, formed within the fetus of thefuture mother, is affected by the exposuresboth of the grandmother and the futuremother. Studies have measured chemicalsforeign to the human body in the fluidthat bathes the ova prior to ovulation,showing the potential for exposure.8Sperm, in contrast, are created only a fewhours to a few days prior to conception.Thus, harmful effects to the sperm aremost likely the result of the father’s expo-

sure in the period immediately beforeconception.

In most instances, exposures after con-ception are dependent on exposures tothe mother. Infants may experience theresult of exposure to many of the toxinsmothers come into contact with duringthe pregnancy. For example, maternalsmoking during pregnancy is associatedwith reductions in forced expiratory flowrates for the child.9

Exposure from Birth toAdolescenceExposures for newborns, infants and tod-dlers, preschool children, school-agedchildren, and adolescents depend on theirphysical location, breathing zones, oxygenconsumption, food consumption, types offoods consumed, and normal behavioraldevelopment (see Table 2)—all of whichchange as the child develops.

Physical Location

That the physical location of childrenchanges with development has large impli-cations for a child’s exposure. Prematureand sick newborn infants are exposed tonoise, light, compressed gases, intravenoussolutions, and benzyl alcohol, amongother things, during their stay in neonatalintensive care.10 Most newborns, however,are usually near their mothers, so expo-sures will be similar to those experiencedby the mothers. Moreover, a newborn fre-quently spends prolonged periods of timein a single environment, such as a crib.Infants and toddlers, on the other hand,are frequently placed on the floor, carpet,

Table 1

Periconceptual Exposures of Possible Importance

Grandmother Exposures to ova developing in mother while a fetus

Father Preconception exposures to sperm

Father-mediated exposures to pregnant mother

Mother Preconception exposures to ova

Exposures during pregnancy


or grass. They therefore have more expo-sure to chemicals associated with these sur-faces, such as formaldehyde and volatileorganic chemicals from synthetic carpets11

and pesticide residues from flea bombs.12

Children who are not yet able to walkor crawl may also experience sustainedexposure to noxious agents because theycannot remove themselves from hazardousenvironments. The infant who is badly sun-burned because of his or her inability toescape from the sun is a good example.13

Many preschool children spend part oftheir day in a day-care facility, which can belocated anywhere from church buildingsto private homes. In addition, preschoolchildren may spend a significant period oftime in outdoor environments such asplaygrounds and backyards.

School-aged children spend a signifi-cant period of time at school, a very differ-ent physical environment from a house oran apartment. Schools are sometimes builton relatively undesirable land. School sitesmay be near highways (resulting in expo-sure to auto emissions and lead), underpower lines (resulting in exposure to elec-tromagnetic fields14), or on old industrialsites (resulting in exposure to benzeneand arsenic).

Adolescents may not only have a newschool environment, but also select forthemselves other physical environmentsin which they misjudge or ignore therisks.15 Attendance at concerts with dam-aging sound levels is a relatively benignexample of a situation in which adoles-cents willingly put themselves at risk.Many adolescents also have part-time jobsthat place them in physical environmentswhich may be hazardous because of occu-pational exposures.16

Breathing Zones

Breathing zones, the places in space whereindividuals breathe, are also closely relatedto development. The breathing zone foran adult is typically four to six feet abovethe floor. However, for a child, it will becloser to the floor. It is within these lowerbreathing zones that heavier chemicalssuch as mercury and large breathable par-ticulates settle out17 and radon accumu-lates.18 The presence of mercury in a

child’s breathing zone which came fromlatex house paint accounted for a Michiganchild’s case of acrodynia, a form of toxicityfrom mercury exposure.19 (See the articleby Goldman in this journal issue.)

Oxygen ConsumptionBecause children are physically smallerthan adults, their metabolic rate is higherthan that of adults and they consumemore oxygen relative to their size than doadults. As a result, a child’s exposure to anair pollutant may be greater than anadult’s. For example, if radon is present, asix-month-old child with an average oxy-gen consumption rate will, over a givenperiod of time, receive twice the exposureto radon as will an adult with an averageoxygen consumption rate.20

Quantity and Quality of FoodConsumedSimilar to their need for proportionatelymore oxygen than adults, children’s high-er metabolic rates mean that they need to

consume more calories per pound ofbody weight than adults. Quite simply, theamount of food that children consumeper pound of body weight is higher thanthat of adults.21 The reason for this differ-ence is that children not only maintainhomeostasis, as adults do, but also grow.

Consider the amount of water that aninfant who receives formula reconstitutedin boiled tap water drinks every day. Theaverage infant consumes six ounces of for-mula per kilogram of body weight. For theaverage male adult, this is equivalent todrinking 35 cans of soda pop a day. If thewater contains a contaminant, then infantswill receive more of it relative to their sizethan will an adult. Because of this differ-ence, lead in tap water is of particular con-cern for formula-fed infants. High bloodlead levels (greater than 10 mcg/dl) have

The average infant consumes six ounces offormula per kilogram of body weight. For theaverage male adult, this is the equivalent todrinking 35 cans of soda pop a day.


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been found in infants with heavy expo-sure to tap water from reconstituted for-mula.6 Adults consuming the same tapwater would suffer no adverse healtheffects because they would ingest muchless lead relative to their body weight.

In addition, the types of food childrenconsume differ from those consumed byadults.22 The diet of many newborns is lim-ited to breast milk, which may containenvironmental pollutants including lead,PCBs, and dioxins.23–25 The diet of chil-dren also contains more milk products,fruits, and vegetables than the typical adultdiet, and as a result, children may beexposed to more dangerous levels of pesti-cides and other chemical residues thanadults.26

Normal Behavioral DevelopmentThe normal behavioral development of achild will also influence environmentalexposures. Infants and young children maynot be able to remove themselves fromnoxious environments. Normal childrenpass through a developmental stage of

intense oral exploratory behavior fromabout age six months to two years, whenmost objects grasped will be placed in themouth. This behavior is one commoncause of lead poisoning in environmentswith high levels of lead dust, such as hous-es painted with lead-based paint.27 It alsoplaces the child at risk in environmentsthat have not taken the oral orientation ofyoung children into account. For exam-ple, some wood used in playground equip-ment is treated with arsenic and creosote.In the course of normal play, children willfrequently place their mouths on play-ground equipment, inadvertently expos-ing themselves to these toxic chemicals.28

The ability to walk often places chil-dren in play situations that have the poten-tial for dangerous exposures, such as nearempty lots, mud puddles, and used con-tainers holding oil or other liquid sub-

stances. As children become adolescents,they gain more and more freedom fromthe parental supervision that might other-wise protect them from some exposures.Their physical strength and stamina arewell developed, but they are still acquiringabstract thinking.29 They do not considercause and effect, particularly delayedeffects, in the same way that adults do.Because of this lack of perception, theyoften place themselves in situations withgreater risk than an adult would willinglyface. An example is the higher incidenceof farm injuries among adolescents thanamong adults.30

The Biological EnvironmentThe biological environment—the internalphysiological workings of the body as ittakes up, processes, and interacts with thechemicals it contacts—is another impor-tant part of a child’s overall environment.The body has specific chemical pathwaysused to digest, process, and excrete sub-stances found in air, food, and water,which vary at different stages of develop-ment. A chemical that comes into contactwith the biological systems of a child’sbody can produce adverse health effects orbe processed into nonharmful substances.

AbsorptionAbsorption is the way a chemical entersthe body. Absorption generally occurs inone of four ways: through the placenta,the skin, the respiratory tract, or the diges-tive tract. Each of these portals of entry isdependent on the developmental stage ofthe child.

Through the Placenta

During the fetal stage, the placenta is amajor pathway of absorption.31 Severalclasses of compounds readily cross the pla-centa, including compounds with low mo-lecular weight, those that are fat-soluble,and other specific compounds such as cal-cium and lead. Carbon monoxide, a poi-sonous compound of low molecularweight, crosses the placenta readily. Whencarbon monoxide enters the blood, itbinds to hemoglobin, creating carboxyhe-moglobin. This bond prevents hemoglo-bin from binding to oxygen and delivering

The diet of children also contains moremilk products, fruits, and vegetables thanthe typical adult diet.


it to the cells. Because carbon monoxidehas a higher affinity for fetal hemoglobinthan it does for adult hemoglobin, theconcentration of carboxyhemoglobin ishigher in the fetus than in the mother.32

Therefore, the infant may have reducedoxygen delivered to tissues, with subse-quent organ damage.

Fat-soluble, or lipophilic, compounds,such as polycyclic aromatic hydrocarbons(found in cigarette smoke) and ethanol(found in alcoholic beverages), readilygain access to the fetal circulation andthereby may cause toxic effects in thefetus. Also, mechanisms in the placentaactively transport specific nutrients andtoxins to the fetus. Lead, for example, isfound in equal concentrations in themother and the fetus.33

Through the Skin

The skin undergoes enormous changeswith development which affect its absorp-tive properties. Pathways of absorptionthrough the skin are particularly impor-tant for fat-soluble compounds. Becausethe skin is mainly composed of fatty chem-icals, fat-soluble chemicals generally crossit more readily than other chemicals.

The outside skin layer of a fetus lacksthe rough exterior dead skin layer called

keratin34 and thus is without one of themajor barriers of the skin.35 The acquisi-tion of keratin occurs over the initial threeto five days following birth. Therefore, theskin of a newborn is a particularly absorp-tive surface, and absorption of chemicalsthrough the skin has caused many cases ofillness in newborns. For example, hypothy-roidism has resulted from iodine in beta-dine scrub solutions used for sterilizationof the skin prior to birth or other skin pen-etrating procedures, such as obtainingblood or starting intravenous fluids.36

Neurotoxicity has occurred from hexa-chlorophene solutions which were used tobathe infants following birth,37 and hyper-bilirubinemia has resulted from a pheno-lic disinfectant used to clean equipmentbetween use for different patients.38

An additional factor in the absorptionof these chemicals through the skin is thelarger surface-to-volume ratio of newbornscompared with older children and adults.This means that for the same amount ofskin covered with a chemical, the youngerchild may receive up to three times thedose received by an adult.

Through the Respiratory Tract

During prenatal life, the fetus makesbreathing motions. Although the net flowof fluid is from the lungs out of the tra-

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chea into the amniotic fluid, some chemi-cals in amniotic fluid may come in contactwith the lining of the respiratory tract.Studies on this pathway of exposure to for-eign chemicals are limited.

The surface absorptive properties ofthe lung do not change during develop-ment; the lungs continuously absorb air-borne chemicals in the same manner.However, from birth to adolescence, thelung continues to develop more alveoli,the terminal air sacs through whichhumans breathe.39 The increase in thenumber of alveoli increases the size of theabsorptive area in the lungs. Thus, someairborne chemicals may gain greateraccess to the body through the lungs as thechild ages.

Through the Gastrointestinal TractThe gastrointestinal (digestive) tract, at allstages of development, provides manyopportunities for exposure to environ-mental toxins. The fetus actively swallowsamniotic fluid.40 Chemicals, including cer-tain pesticides as well as chemicals from

tobacco smoke, can be present in amniot-ic fluid, but it is not known if the fetusabsorbs those chemicals by swallowing thefluid. Following birth, stomach acid secre-tion is relatively low, but it will achieveadult levels by several months of age.41 Asthe infant grows, the difference in aciditywill markedly affect absorption of chemi-cals from the stomach.42

The small intestine in the newborn canrespond to increased nutritional needs byincreasing absorption of a particularlyneeded nutrient. For example, becausechildren’s bones are still growing, theyrequire more calcium than adults. Thus,children absorb more calcium than adultsdo from the same food sources. However,this enhanced absorption can create prob-lems. Lead, because it is absorbed in placeof calcium when it is present, is absorbedto a greater extent in children than in

adults. An adult will absorb 10% of ingest-ed lead, whereas a one- to two-year-oldchild will absorb 50% of ingested lead.43

DistributionThe distribution of chemicals, the processby which chemicals get to body organs,varies with the developmental stage of thechild. For example, many drugs becomemore diluted in newborns than they do inadults, spreading out so that more of thebody has contact with them at lower lev-els.44 In animal models, it has been shownthat lead is retained to a larger degree inthe infant animal brain than in theadult.45 Lead also accumulates morerapidly in children’s bones than in adultbones, doubling between infancy and thelate teen years.46

MetabolismMetabolism is the way the body processeschemicals using a series of steps, or path-ways, to alter chemicals for use as fuel orfor waste. It may result in activation ordeactivation of the chemical by the body.The metabolism of chemicals depends onthe child’s developmental stage, and theend result may either protect or harm thechild, depending on the chemical inquestion.

The activity in each step of a metabolicpathway is determined by developmentalstage and the genetic background of eachindividual. Therefore, some people aremore susceptible to adverse effects fromcertain exposures. There are also large dif-ferences in the ways enzymes work inmetabolic pathways between developmen-tal stages.47 The same enzyme may workmore or less depending on the age of theindividual.48

In some instances, the lack of certainpathways can be a protective factor. In theadult, high levels of acetaminophen maycause fatal liver poisoning, because adultmetabolism breaks down the drug intosubcomponents that are harmful to theliver. However, infants are not as easily hurtby acetaminophen. Infants born to moth-ers with high acetaminophen levels willalso have high acetaminophen levels in theblood, but they will not have liver damage.


An adult will absorb 10% of ingested lead,whereas a one- to two-year-old child willabsorb 50% of ingested lead.


The reason for this lack of damage is thatthe metabolic pathways of the fetus havenot yet developed enough to break downthe drug into harmful subparts.49

Target Organ SusceptibilityChildren are also different from adultsbecause their organs are undergoinggrowth and maturation, a process that maybe adversely affected by exposure to harm-ful chemicals. Responses of children’sbodies to harmful exposures may differfrom responses of adults’ bodies to theseexposures in both the nature and theseverity of the effect. Examples of suchoutcomes are poor fetal growth, poorgrowth in childhood, diminished intelli-gence quotient (IQ), precocious puberty,small head size, and diminished lungcapacity.

The body experiences three types ofgrowth: multiplicative, where cells divide;auxelic, where existing cells become larg-er; and accretionary, where ground sub-stance and nonliving structural compo-nents accumulate.50 Multiplicative growthis complete around six months after con-ception for tissues that do not undergocontinual turnover throughout life, suchas skin cells. After that point, all growth isaccretionary or auxelic.

Cells undergo two further processes tobecome the adult organism: differentia-tion and migration. Differentiation occurswhen cells take on their individual taskswithin the body and lose the ability todivide. The trigger for differentiation maybe hormones, so when chemicals mimichormones they can alter the differentia-tion of some tissues. Because the organsystems in children, including the repro-ductive system, are continuing to differ-entiate, a chemical that mimics a hor-mone can have drastic effects on thedevelopment of those organ systems.Chlorinated insecticides are an exampleof this mechanism. Studies have showneffects on the adult rat reproductive sys-tem from neonatal exposure to chlorde-cone,51 including abnormal growth of thevagina and sterility.52

Cell migration is necessary for certaincells to reach their destination for func-

tion. Neurons, for example, originate in astructure near the center of the brain,then migrate out to a predestined locationin one of the many layers of the brain.53

Chemicals such as the ethanol in alcoholicbeverages may have a profound effect onthis process, as shown in children withfetal alcohol syndrome. Prenatal exposureto ethanol may result in interruption inthis process severe enough to cause obvi-ous malformations of the brain.54,55

Some organs continue to develop forseveral years. The brain and the lungsboth have prolonged periods of postnatal

development which are not complete untiladolescence.39,56 This protracted period ofgrowth and development increases the vul-nerability of these organs. For example,brain tumors are frequently treated byradiation therapy in adults, with uncom-fortable but reversible side effects. However,in infants, radiation therapy needs to beminimized when possible because of pro-found and permanent effects on the devel-oping central nervous system.57

Another example of the unique vulner-ability of children is the toxic effects oflead on the brain and nervous system. Thecurrent blood lead concentration of con-cern for children is 10 mcg/dl,58 based onstudies59 which found that children withblood lead concentrations above that levelmay have measurable decreases in intelli-gence quotient. Because of differences indevelopmental stage, the occupationallimit for exposure to lead for adults is sixtimes higher than the limit for children.60

The Social EnvironmentFor every developmental stage, there areunique combinations of developmentalcharacteristics, physical environment, andbiological environment that place childrenat special risk of harm. To protect childrenfrom the harms caused by exposure to

Responses of children’s bodies to harmfulexposures may differ from responses of adults’bodies to these exposures in both the natureand the severity of the effect.

environmental toxins, it is necessary also toconsider the customs, laws, and regulationsthat help define children’s environments.

In many ways, regulatory policies havenot taken the characteristics of childreninto account. For example, for infants whoare formula-fed, the amount of water con-sumed is enormous, and yet our watersafety policies do not always take theincreased consumption and special vul-

nerabilities of newborns into accountwhen they are determined. Standards forradon testing and reentry times listed onthe label of home pesticides should allowadequate protection for infants who spendso much of their time on the floor, butsuch considerations may not be reflectedin recommended practice. Similarly, pesti-cide regulations should be made with thespecial diet of children in mind. Adequatelaws to prevent exposure to environmentaltobacco smoke for children attending day-care facilities could prevent the exposureof many children to environmental tobac-co smoke.61

For the school-aged child, regulationof the school environment is of particularconcern. The drinking water at the tap inschools should be judged safe for a child’sconsumption. Arts and crafts suppliesshould be designed and purchased keep-ing in mind a child’s unique way of han-dling these materials. For adolescents whoare beginning to work, child labor lawsshould be adequate not only to protectthem from occupational risks, but also toensure that their ability to learn in schoolis not adversely affected.

These are only a few examples of thepotential effects of laws and regulations onthe environments of children. These socialenvironment effects are discussed morethoroughly in the article by Landrigan and

Carlson in this journal issue.

ConclusionThere are many reasons children cannotbe considered little adults in the area ofenvironmental health. Important differ-ences exist between children and adults inexposures, absorption pathways, tissue dis-tribution, ability to transform and elimi-nate chemicals, and body response to envi-ronmental chemicals and radiation. Eachof these differences is dependent on thedevelopmental stage of the child, and allchildren are not the same during eachstage (see Table 2). When considering thehealth impacts of a particular exposure onthe population and potential policies toalleviate those impacts, each of these dif-ferences must be heeded.

What can be done to alleviate theharm—both potential and actual—doneto children by environmental pollution?Health care providers, policymakers,teachers, community leaders, parents, andchildren all have roles to play in prevent-ing children’s exposure to harmful agentsin their environment and in addressingthe consequences for children who areexposed.

Education about the unique vulnera-bility of children to environmental pollu-tion is one powerful tool for change.Teaching parents and children how toavoid harmful exposures and thereforeprevent environmental illnesses is animportant piece of prevention, which canoccur at many levels and in different set-tings. However, education can and shouldgo beyond parents and children. Clinicianscan be especially helpful when serving aseducators, investigators, and advocates forchildren. Most environmentally causeddiseases have been diagnosed by alert,environmentally aware clinicians, andpublication of case studies has allowed fur-ther education of other clinicians aboutenvironmentally mediated diseases.Increased awareness of the effects of envi-ronmental hazards on children can influ-ence both exposure and treatment forchildren.

Community leaders and policymakerscan use information presented by par-ents, clinicians, scientists, and other advo-


Health care providers, policymakers,teachers, community leaders, parents, andchildren all have roles to play in preventingchildren’s exposure to harmful agents intheir environment.


cates for children and the environment to take the unique vulnerability of childreninto account when establishing regulatory policy. To bring about change, policymak-ers must understand the basis for this unique vulnerability—that children are not lit-tle adults.

1. The fetus represents a unique period of time in life when many critical chemical reactionsare occurring, the disruption of which can have far-reaching consequences. In addition, theenvironment of the fetus is unique.

2. Luykens, J.N. The legacy of well-water methemoglobinemia. Journal of the American MedicalAssociation (1987) 257:2793–95.

3. This is an example of a threshold effect, where the health effects will not occur until thetoxin reaches a particular level in the body.

4. Tilson, H.A., Jacobson, J.L., and Rogan, W.J. Polychlorinated biphenyls and the developingnervous system: Cross-species comparisons. Neurotoxicology and Teratology (1990)12:239–48.

5. The reason for the linkage of PCBs with birth defects is not completely clear. The most like-ly explanation is that, when the women were exposed to high levels of the PCBs, their bod-ies stored them in their fat tissues, where they slowly were released into the bloodstream.When these women became pregnant, the PCBs in the bloodstream crossed the placentaand affected the fetus. Taylor, P.R., Lawrence, C.E., Hwang, H.L., and Paulson, A.S.Polychlorinated biphenyls: Influence on birthweight and gestation. American Journal ofPublic Health (1984) 74:1153–54; Yu, M-L., Chen-Chin, H., Gladen, B.C., and Rogan, W.J. Inutero PCB/PCDF exposure: Relation of developmental delay to dysmorphology and dose.Neurotoxicology and Teratology (1991) 13:195–202.

6. Shannon, M.W., and Graef, J.W. Lead intoxication in infancy. Pediatrics (1992) 89:87–90.

7. Storage in the woman’s bones of lead that became mobilized during pregnancy is the mostlogical explanation for this result, although definitive proof is awaiting further technologi-cal advances. Silbergeld, E.K. Lead in bone: Implications for toxicology during pregnancyand lactation. Environmental Health Perspectives (1991) 91:63–70.

8. Trapp, M., Baukloh, V., Bohnet, H.G., and Heeschen, W. Pollutants in human follicularfluid. Fertility and Sterility (1984) 42:146–48.

9. Hanrahan, J.P., Tager, I.B., Segal, M.R., et al. The effect of maternal smoking during preg-nancy on early infant lung function. American Review of Respiratory Disease (1992)145:1129–35.

10. Brown, A.K., and Glass, L. Environmental hazards in the newborn nursery. Pediatric Annuals(1979) 8:698–700.

11. Bernstein, R.S., Stayner, L.T., Elliot, L.J., et al. Inhalation exposure to formaldehyde: Anoverview of its toxicology, epidemiology, monitoring, and control. American IndustrialHygiene Association Journal (1984) 261:1183–87.

12. Fenske, R.A., Black, K.G., Elkner, K.P., et al. Potential exposure and health risks of infantsfollowing indoor residential pesticide applications. American Journal of Public Health (1990)80:689–93.

13. In addition, because the risk of skin cancer is most closely related to the amount of sundamage the skin sustains during the first 18 years of life, an infant’s caregiver determinespart of an infant’s personal risk for this disease later in life. Jackson, R.J. Testimony to theU.S. House of Representatives, Select Committee on Children, Youth and Families, 1990.

14. The evidence that exposure to electromagnetic fields is hazardous to children is inconclu-sive. Several studies have found an association between children’s cancer and exposure toelectromagnetic fields, but a causal relationship between exposure and disease has notbeen established. For further information, see Savitz D. Overview of epidemiologic researchon electric and magnetic fields and cancer. American Industrial Hygiene Association Journal(April 1993) 54,4:197-204; Hendee, W.R., and Boteler, J.C. The question of health effectsfrom exposure to electromagnetic fields. Health Physics (February 1994) 66,2:127–36.

15. Perry, C.L., and Silvis, G.L. Smoking prevention: Behavioral prescriptions for the pediatri-cian. Pediatrics (1987) 79:790–99.


16. Pollack, S.H., Landrigan, P.H., and Mallino, D.L. Child labor in 1990: Prevalence andhealth hazards. Annual Review of Public Health (1990) 11:359–75.

17. Leaderer, B.P. Assessing exposures to environmental tobacco smoke. Risk Analysis (1990)10:19–26.

18. Blot, W.J., Xu, Z.Y., Boice, J.D., Jr., et al. Indoor radon and lung cancer in China. Journal ofthe National Cancer Institute (1990) 82:1025–30.

19. Centers for Disease Control. Mercury exposure from interior latex paint—Michigan.Morbidity and Mortality Weekly Report (1990) 39:125–26.

20. World Health Organization. Environmental Health Criteria 59. Principles for evaluating healthrisks from chemicals during infancy and early childhood: The need for a special approach. Geneva:World Health Organization, 1986.

21. Biller, J.A., and Yeager, A.M., ed. The Harriet Lane Handbook. 9th ed. Chicago: Year BookMedical Publishers, 1981, p. 202.

22. U.S. Department of Agriculture. Nationwide food consumption survey: Continuing survey of foodintakes by individuals, women 19–50 years and their children 1–5 years. Washington, DC: HumanNutrition Information Service, CSFII, 1985.

23. Hayward, D.G., Ward, C., Lance, L.L., et al. PCDD and PCDF in breast milk as correlatedwith fish consumption in California. Chemosphere (1989) 18:455.

24. Ong, C.N., Phoon, W.O., Law, H.Y., et al. Concentrations of lead in maternal blood, cordblood, and breast milk. Archives of Disease in Childhood (1985) 60:756–59.

25. Rogan, W.J., Gladen, B.C., McKinney, J.D., et al. Polychlorinated biphenyls (PCBs) anddichlorodiphenyl dichlorethene (DDE) in human milk: Effects of maternal factors and pre-vious lactation. American Journal of Public Health (1986) 76:172–77.

26. Zeise, L., Painter, P., Berteau, P.E., et al. Alar in fruit: Limited regulatory action in the faceof uncertain risks. In The analysis, communication, and perception of risk. B.J. Garrick and W.C.Gekler, eds. New York: Plenum Press, 1991, pp. 275–84.

27. Chao, J., and Kikano, G.E. Lead poisoning in children. American Family Physician (1993)47:113–20.

28. Kosnett, M., ed. Case studies in environmental medicine: Arsenic toxicity. U.S. Department ofHealth and Human Services, Agency for Toxic Substances and Disease Registry, 1990.

29. Campbell, S.F., ed. Piaget sampler: An introduction to Jean Piaget through his own words. NewYork: Wiley, c1976.

30. Karlson, T., and Noren, J. Farm tractor fatalities: The failure of voluntary safety standards.American Journal of Public Health (1979) 69:146–49.

31. Newman, C.G.H. The thalidomide syndrome: Risks of exposure and spectrum of malforma-tions. Clinics in Perinatology (1986) 13:555–73.

32. Visnjevac, V., and Mikov, M. Smoking and carboxyhaemoglobin concentrations in mothersand their newborn infants. Human Toxicology (1986) 5:175–77.

33. Goyer, R.A. Transplacental transport of lead. Environmental Health Perspectives (1990)89:101–105.

34. Cartlidge, P.H.T., and Rutter, N. Skin barrier function. In Fetal and neonatal physiology. R.A.Polin and W.W. Fox, eds. Vol. 1. Philadelphia, PA: W.B. Saunders, 1991, p. 577.

35. Although chemicals have been described in amniotic fluid, the absorption of these com-pounds through the skin has not been studied. Van Vunakis, H., Longone, J.J., andMilunsky, A. Nicotine and cotinine in the amniotic fluid of smokers in the second trimesterof pregnancy. American Journal of Obstetrics and Gynecology (1974) 120:64–66.

36. Clemens, P.C., and Neumann, R.S. The Wolff-Chaikoff effect. Hypothyroidism due toiodine application. Archives of Dermatology (1989) 125:705.

37. Shuman, R.M., Leech, R.W., and Alvord, E.K. Neurotoxicity of hexachlorophene in thehuman. I.A. Clinicopathologic study of 248 children. Pediatrics (1974) 54:689.


38. Wysowski, D.K., Flynt, J.W., Jr., Goldfield, M., et al. Epidemic neonatal hyperbilirubinemiaand use of a phenolic disinfectant detergent. Pediatrics (1978) 61:165.

39. Hodson, W.A. Normal and abnormal structural development of the lung. In Fetal and neona-tal physiology. R.A. Polin and W.W. Fox, eds. Vol. 1. Philadelphia, PA: W.B. Saunders, 1991,pp. 774–75.

40. Miller, A.J. Deglutition. Physiological Reviews (1982) 62:129.

41. Marino, L.R. Development of gastric secretory function. In Fetal and neonatal physiology. R.A.Polin and W.W. Fox, eds. Vol. 2. New York: W.B. Saunders, 1991, p. 1041.

42. Chemtob, S. Basic pharmacologic principles. In Fetal and neonatal physiology. R.A. Polin andW.W. Fox, eds. Philadelphia, PA: W.B. Saunders, 1991, p. 109.

43. Rout, U.K., and Holmes, R.S. Postnatal development of mouse alcohol dehydrogenases:Agarose isoelectric focusing analyses of the liver, kidney, stomach and ocular isozymes.Biology of the Neonate (1991) 59:93–97.

44. Nagourney, B.A., and Aranda, J.V. Physiologic differences of clinical significance. In Fetaland neonatal physiology. R.A. Polin and W.W. Fox, eds. Philadelphia, PA: W.B. Saunders,1991, pp. 169–170.

45. Momcilovic, B., and Kostial, K. Kinetics of lead retention and distribution in suckling andadult rats. Environmental Research (1974) 8:214–20.

46. Barry, P.S.I. A comparison of concentrations of lead in human tissues. British Journal ofIndustrial Medicine (1975) 32:119–39.

47. Warholm, M., Guthenberg, C., Mannevik, B., et al. Glutathione S-transferases in humanfetal liver. Acta Chemica Scandinavica (1981) B35:225–27.

48. For example, theophylline, a drug commonly prescribed for all age groups by physicians, ismetabolized by several different chemical pathways. During the newborn period, thesepathways operate at low levels, so theophylline remains in the body unchanged for a longperiod of time. However, the pathways become increasingly present over the next severalmonths, breaking theophylline down so it is not in the body as long in the same chemicalform. To keep the same level in the body, the prescribing physician has to increase the pre-scribed dose. In adolescence, the metabolic breakdown of theophylline slows again, possiblybecause steroid hormones are competing for the same pathways. (Levi, P.E. Toxic action. InA textbook of modern toxicology. E. Hodgson and P.E. Levi, eds. New York: Elsevier, 1987, p. 152.)To accommodate this change, the dose of the drug must be reduced to avoid overdosingthe patient.

49. Riggs, B.S., Bronstein, A.C., Kulig, K., et al. Acute acetaminophen overdose during preg-nancy. Obstetrics and Gynecology (1989) 74:247–53.

50. Sinclair, D. Human growth after birth. 5th ed. Oxford: Oxford University Press, 1989, p. 3.

51. Gellert, R.J. Kepone, mirex dieldrin, and aldrin: Estrogenic activity and the induction ofpersistent vaginal estrus and anovulation in rats following neonatal treatment. EnvironmentalResearch (1978) 16:131–38.

52. Tissues undergoing multiplicative growth (by cells dividing) and the final stages of growthand change (differentiation) are particularly susceptible to cancer. (Levi, P.E. Toxic action.In A textbook of modern toxicology. E. Hodgson and P.E. Levi, eds. New York: Elsevier, 1987,p. 152.) This increased susceptibility is due to the shortened time period for DNA repairand the multiple changes that are occurring within the DNA as the cell grows. The epidem-ic of scrotal cancer among the chimney sweeps of Victorian England shows how exposureto chemicals can interfere with these stages of development. (Nethercott, J.R. Occupationalskin disorders. In Occupational medicine. J. LaDou, ed. San Mateo, CA: Appleton & Lange,1990, p. 218.) Chimney sweeps were usually adolescent boys with developing secondary sex-ual characteristics who would climb naked inside chimneys to clean them, exposing theirentire bodies to soot. Occupational exposure to cancer-causing chemicals such as soot wascommon for many occupations at the time, but scrotal tumors were uncommon in groupsother than young male chimney sweeps. Thus, it is likely that the scrotum at this stage ofdevelopment had increased susceptibility to the chemicals in soot.


53. Miller, M.W. Effects of prenatal exposure to ethanol on cell proliferation and neuronalmigration. In Development of the central nervous system: Effects of alcohol and opiates. M.W. Miller,ed. New York: Wiley-Liss, 1992, p. 58.

54. Clarren, S.K., Alvord, E.C., Jr., Sumi, S.M., et al. Brain malformations related to prenatalexposure to ethanol. Journal of Pediatrics (1978) 92:64–67.

55. In the brain, two other processes deserve mention: the making of synapses (synaptogenesis)and dendritic trimming. Nerve cells communicate through cellular structures called synap-ses, which are the basis for the circuitry of the brain. Up to two years of age, the brainmakes synapses rapidly. After age two, while specific synapses are formed as learning occurs,formation is much slower. In fact, after age two, the brain begins actively to remove synaps-es, so that a two-year-old’s brain contains more synapses than it will at any other age. Thisprocess, called dendritic trimming, occurs so that the resulting network of neurons will bemore specific.

56. Hoar, R.M., and Monie, I.W. Comparative development of specific organ systems. InDevelopmental toxicology. C.A. Kimmel and J. Buelke-Sam, eds. New York: Raven Press, 1981,pp. 13–33.

57. Duffner, P.K., Horowitz, M.E., Krischer, J.P., et al. Postoperative chemotherapy and delayedradiation in children less than three years of age with malignant brain tumors. New EnglandJournal of Medicine (1993) 328:1725–31.

58. Centers for Disease Control. Preventing lead poisoning in young children: A statement by theCenters for Disease Control. Atlanta: Centers for Disease Control, 1991.

59. Needleman, H.L., and Bellinger, D. Low-level lead exposure and the IQ of children: Ameta-analysis of modern studies. Journal of American Medical Association (1990) 263:673–78.

60. At that level, adults do not have brain problems but may have impaired kidney function,decreased fertility, and problems with the peripheral nerves. Royce, S.E., ed. Case studies inenvironmental medicine: Lead toxicity. U.S. Department of Health and Human Services,Agency for Substances and Disease Registry, Washington, DC, 1990, p. 5.

61. Samet, J.M., Lewit, E.M., and Warner, K.E. Involuntary smoking and children’s health. TheFuture of Children (Winter 1994) 4,3:94–114.

environmental health hazards: how children are different from adults

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