This monograph is one in a series of selfinstructional publications designed to 

increase the primary care provider’s 

knowledge of hazardous substances in the 

environment and to aid in the evaluation 

of potentially exposed patients. This 

course is also available on the ATSDR 

Web site, www.atsdr.cdc.gov/HEC/CSEM/. 

See page 3 for more information about 

continuing medical education credits, 

continuing nursing education units, 

continuing education units, and continuing health education specialist credits. 

Case Studies in 

Environmental Medicine 

Course: SS3098 

Date: July 2002

Expiration Date: July 30, 2008 

PEDIATRIC 

ENVIRONMENTAL HEALTH 

Environmental Alert 

Childhood is a time of rapid growth and development, accompanied by 

changes in organ system functioning, metabolic capabilities, physical 

size, and behavior that can dramatically modify potential illness caused 

by a toxicant. 

Pediatricians and other child health care providers need to develop the 

expertise necessary to take an environmental history, deliver 

anticipatory guidance, and conduct appropriate risk-based laboratory 

tests for environmental illnesses. 

Pediatric Environmental Health Specialty Units are available for 

consultation and referral. Pediatricians and other child heatlh care 

providers should be aware of this resource. 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Agency for Toxic Substances and Disease Registry 

Division of Toxicology and Environmental Medicine 
Pediatric Environmental Health 

Table of Contents 

2 

Guest Contributors: Robert Amler, 

MD, MS (ATSDR); Sherlita Amler, MD, 

MS (ATSDR); Sophie J. Balk, MD 

(Albert Einstein College of Medicine, 

Children’s Hospital at Montefiore); 

Robert K. McLellan, MD, MPH 

(American College of Occupational 

and Environmental Medicine) 

Guest Editor: Jonathan Borak, MD 

(American College of Occupational 

and Environmental Medicine) 

ATSDR/DHEP Authors: Kimberly 

Gehle, MD, MPH; Kristina Larson, 

MHEd, CHES; Cherryll Ranger, RN, 

BSN 

ATSDR/DHEP Case Studies Team: 

Diane Dennis-Flagler, MPH; Sharon 

Hall, RN, PhD (CDC/PHPPO); Kimberly 

Gehle, MD, MPH; Kristina Larson, 

MHEd; Ralph O’Connor Jr, PhD; Felicia 

Pharagood-Wade, MD, FACEP 

Edited By: Pamela S. Wigington 

Disclaimer 

The state of knowledge regarding 

the treatment of patients potentially 

exposed to hazardous substances 

in the environment is constantly 

evolving and is often uncertain. In 

this monograph, ATSDR has made 

diligent effort to ensure the accuracy 

and currency of the information 

presented, but makes no claim that 

the document comprehensively 

addresses all possible situations 

related pediatrics and environmental health. This monograph is 

intended as a resource for pediatricians and other child health care 

providers in assessing the 

condition and managing the 

treatment of patients potentially 

exposed to hazardous substances. 

It is not, however, a substitute for 

the professional judgment of a 

health care provider. The document 

must be interpreted in light of 

specific information regarding the 

patient and in conjunction with other 

sources of authority. 

Use of trade names and commercial sources is for identification only 

and does not imply endorsement 

by the Agency for Toxic Substances 

and Disease Registry or the U.S. 

Department of Health and Human 

Services. 

Case Study .......................................................................................... 5
 

Direct Biologic Indicators ..................................................................... 7
 

Diagnosis ............................................................................................. 7
 

Case Study (Continued) ..................................................................... 8
 

Case Study (Continued) ..................................................................... 9
 

The Exposure-Disease Model ............................................................ 10
 

The Child as Susceptible Host: A Developmental Approach
 

to Pediatric Environmental Medicine ............................................. 12
 

Sources of Exposure .......................................................................... 22
 

Principles of Environmental Medical Evaluation ................................... 24
 

Pediatric Environmental Health Interventions ....................................... 30
 

References ........................................................................................ 33
 

Answers to Pretest and Challenge Questions ...................................... 38
 

Evaluation Questionnaire and Posttest, Course Number SS3098 ........ 43
 

Answer Sheet, Course Number SS3098 ............................................ 49
 

Appendices 

Appendix A: Figure and Tables .......................................................... 51
 

Appendix B: Important Issues Regarding Mercury .............................. 69
 

Appendix C: Summary of Questions for an Environmental History ....... 72
 

Appendix D: Environmental Health Concerns: Resources and
 

Sources of Information ................................................................. 74
 

Appendix E: Lead Screening .............................................................. 82
 

Appendix F: Additional Information for Performing a Comprehensive
 

Pediatric Environmental Medical Evaluation .................................. 83
 

Information on the Pediatric Environmental Health 

Specialty Units can be found in Appendix D. 

Each content expert for this case study indicated no conflict of interest 

to disclose with the case study subject matter. 

Final responsibility for the contents and views expressed in this monograph resides with ATSDR. 

ATSDR Publication No.: ATSDR-HE-CS-2002-0002 
Pediatric Environmental Health

Case Studies in Environmental Medicine 

(CSEM): Pediatric Environmental Health 

Goals and Objectives 

The goals of this CSEM are to increase the knowledge of health care 

providers, especially pediatricians, of the special susceptibilities of children 

to hazardous substances in the environment and to aid in their evaluation of 

potentially exposed patients. 

After completion of this educational activity, the reader should be able to 

describe how and why children differ from adults in their susceptibility to 

environmental hazards, apply the knowledge of environmental medicine in 

the evaluation of well and sick children, identify parental occupation and 

hobbies as a part of the environmental history, and identify additional 

sources of environmental health information. 

Accreditation 

Continuing Medical Education (CME) 

The Centers for Disease Control and Prevention (CDC) is accredited by 

the Accreditation Council for Continuing Medical Education (ACCME) to 

provide continuing medical education for physicians. CDC designates this 

educational activity for a maximum of 2.0 hours in category 1 credit toward 

the American Medical Association (AMA) Physician’s Recognition Award. 

Each physician should claim only those hours of credit that he/she actually 

spent in the educational activity. 

Continuing Nursing Education (CNE) 

This activity for 2.3 contact hours is provided by CDC, which is accredited 

as a provider of continuing education in nursing by the American Nurses 

Credentialing Center’s Commission on Accreditation. 

Continuing Education Units (CEU) 

CDC has been approved as an Authorized Provider of continuing 

education and training programs by the International Association for 

Continuing Education and Training and awards 0.2 continuing education 

units (CEUs). 

Continuing Health Education Specialist (CHES) 

CDC is a designated provider of continuing education contact hours 

(CECH) in health education by the National Commission for Health 

Education Credentialing, Inc. This program is a designated event for the 

CHES to receive 2.0 category 1 contact hours in health education. 

Instructions 

See page 4 

3 
 

 

Pediatric Environmental Health 

The questionnaire and posttest must be completed and returned electronically,
 

by fax, or by mail for eligibility to receive continuing education credit.
 

Instructions for Completing CSEM Online 

1.	 Read this CSEM, Pediatric Environmental Health; all answers are in the text. 

2.	 Link to the MMWR/ATSDR Continuing Education General Information page (www.cdc.gov/atsdr/index.html). 

3.	 Once you access this page, select the Continuing Education Opportunities link. 

4.	 Once you access the MMWR/ATSDR site online system, select the electronic file and/or register and test for a 

particular ATSDR course. 

a. Under the heading “Register and Take Exam,” click on the test type desired. 

b. If you have registered in this system before, please use the same login and password. This will ensure an 

accurate transcript. 

c. If you have not previously registered in this system, please provide the registration information requested. 

This allows accurate tracking for credit purposes. Please review the CDC Privacy Notice (www.cdc.gov/ 

privacy.htm). 

d. Once you have logged in/registered, select the test and take the posttest. 

5.	 Answer the questions presented. To receive continuing education credit, you must answer all of the questions. 

Some questions have more than one answer. Questions with more than one answer will instruct you to “indicate 

all that are true.” 

6.	 Complete the course evaluation and posttest no later than July 30, 2008. 

7.	 You will be able to immediately print your continuing education certificate from your personal transcript. 

Instructions for Completing CSEM on Paper 

1.	 Read this CSEM, Pediatric Environmental Health; all answers are in the text. 

2.	 Complete the evaluation questionnaire and posttest, including your name, mailing address, phone number, and 

e-mail address, if available. 

3.	 Circle your answers to the questions. To receive your continuing education credit, you must answer all of the 

questions. 

4.	 Sign and date the posttest. 

5.	 Return the evaluation questionnaire and posttest, no later than July 1, 2008, to CDC by mail or fax: 

Mail	 or Fax 

Continuing Education Coordinator 770-488-4178
 

Division of Toxicology and ATTN: Continuing Education Coordinator
 

Environmental Medicine, ATSDR
 

4770 Buford Hwy, NE (Mail Stop F-32)
 

Atlanta, GA 30341-3717
 

6.	 You will receive an award certificate within 90 days of submitting your credit forms. No fees are charged for 

participating in this continuing education activity. 

4 
Pediatric Environmental Health 

Case Study

A mother brings her 21⁄2-year-old son to you for consultation. She explains 

that her family moved to your community about 7 months ago when her 

husband changed jobs. Over the past month and a half, the boy has 

developed progressive anorexia and weight loss. He has also suffered from 

an increasingly severe and itchy rash. Although normally very active and 

pleasant, he has become ill-tempered and, for the past couple of days, he 

refuses to walk around, preferring to lie in bed or be carried. He rubs his 

knees and cries periodically throughout the day. Neither the parents nor the 

child’s grandmother, who lives with them, has been ill. 

The boy’s medical history has been unremarkable. His birth was at full-term 

by a normal spontaneous vaginal delivery without complications. His height 

and weight have been consistently in the 25th percentile for his age. He is on 

a regular toddler diet, and all developmental milestones have been 

appropriately met. His immunizations are up-to-date. He is not taking any 

medications. He had been taking a multivitamin with iron at the correct 

dosage as prescribed by his doctor. The mother denies any other family use 

of dietary supplements or herbal medicines. The family history is negative for 

blood transfusions and use of illicit drugs, human immunodeficiency virus 

(HIV) infection, and metabolic or genetic diseases. A review of systems and 

a brief assessment of how the family functions are noncontributory. No one 

in the family has been traveling in a foreign country. 

Physical examination reveals an irritable, pale child with photophobia. 

His height is 351⁄2 inches (90.17 centimeters [cm]) and his weight is 

27.7 pounds (12.6 kilograms), both of which are in the 25th percentile for 

his age. (His mother remembers that he weighed 30 pounds the last time he 

was checked by his pediatrician, just before they relocated.) The child’s 

head circumference is 15.2 inches (38.6 cm), also in the 25th percentile. His 

temperature is 98.3°F (36.8°C), blood pressure is 125/75 mmHg 

(90th percentile for his age is 105/69), heart rate is 96 breaths/min, and 

respiratory rate is 30 breaths/min. His skin and mucous membranes are dry. 

His trunk and face have an erythematous papulovesicular rash with signs of 

excoriation, but no petechia. His neck is supple without enlarged nodes, 

masses, or thyromegaly. No other adenopathy is noted. Head, eyes, ears, 

nose, and throat (HEENT) are within normal limits. Lungs are clear to 

auscultation. Heart rate is regular without murmurs. His abdomen is soft and 

is not distended or tender to palpation. No hepatosplenomegaly is noted. His 

joints have full range of motion and no signs of inflammation. His hands and 

feet are pink, sweaty, and scaling. Neurologic examination reveals a tongue 

tremor, diffuse muscle weakness, and unsteady gait, but no focal 

abnormalities. 

During the day, the child stays at home with his mother or grandmother. The 

mother works part-time as a bookkeeper-clerk in a local dry cleaning 

A 21⁄2-year-old boy has 

progressive anorexia, weight 

loss, and a severe, itchy rash 

The Figure and 

Tables for this case 

study can be found in 

Appendix A (begins 

on p. 51). 

5 
Pediatric Environmental Health 

Pretest 

(a) What additional information 

should you gather by 

interview? 

(b) What would you include in 

this patient’s problem list? 

(c)	 What is the differential 

diagnosis for this patient? 

(d) What baseline laboratory 

tests would you order to 

support your differential 

diagnosis at this point? 

(e) What laboratory test would 

you order to confirm your 

diagnosis? 

facility. The father works as a production manager in a mercury 

thermometer factory. The mother states that both parents are concerned 

about environmental contaminants, specifically those that might be 

associated with their workplaces, and whether or not these contaminants 

can put their family at risk. The parents have heard neighbors’ and coworkers’ comments about ailments associated with mercury exposures. The 

parents also mention recent reports of a group of teenagers in the 

community taking elemental mercury over the past several months from the 

local junior high school chemistry lab and the resulting ongoing investigation 

by the environmental division of the state health department. One of the 

teenagers who reportedly took mercury from the lab helped with odd jobs 

around the parents’ house, including indoor house-cleaning. The mother 

expresses the family’s concern and asks for your help. 

On further questioning, you learn that the family lives in a converted loft 

apartment in a building that was once part of a jewelry factory complex. No 

additional remodeling or interior painting has occurred since the conversion 

2 years ago. Drinking water is supplied by the city. Each apartment has its 

own natural gas heating system. The bedrooms and living room are 

carpeted. The family does not have a garden, but the child often plays at a 

park and playground within walking distance. The family has no pets. The 

parents have no more information regarding the teenager, although they have 

been trying to contact her since the report came out this past week 

regarding the ongoing investigation conducted by the environmental division 

of the state heath department. 

The child is hospitalized for further evaluation and workup. Baseline 

laboratory tests include 

white blood cell count with differential; 

blood smear; 

electrolytes, with blood urea nitrogen and creatinine; 

urinary mercury and blood lead levels; 

erythrocyte sedimentation rate, antinuclear antibody, antistreptolysin-O 

titer; 

urine analysis with specific gravity; 

radiograph of the chest, knees, and bilateral hips; 

computed tomography scan of the brain (to rule out degenerative 

changes or space-occupying lesion); and 

a spinal tap (after risk for herniation has been excluded). 

Of these laboratory tests, only the urine mercury is elevated. 

6 
Pediatric Environmental Health 

Direct Biologic Indicators
 A 24-hour urine collection is obtained from the child and tested. It reveals a 

total mercury level of 321 micrograms per gram (μg/g) creatinine. Urine 

specimens are collected from the parents and grandmother and tested. The 

test results are expressed as urine mercury per gram creatinine, and are as 

follows: father, 18 μg/g creatinine; mother, 12 μg/g creatinine; and 

grandmother, 37 μg/g creatinine. 

The World Health Organization’s upper limit of normal for adults is 

50 μg/g creatinine (World Health Organization 1991). The upper limit of 

normal for unexposed adults is 20 micrograms per liter (μg/L); most 

unexposed individuals have levels <5 μg/L (ATSDR 1999). However, the 

respective levels for children have not yet been established. More than 

likely, however, the upper limits are lower than those for adults. Urine 

mercury levels might be reported in different units of measure (e.g., 

micrograms per gram creatinine and micrograms per liter). A number of 

issues must be considered when interpreting results in children. These issues 

are discussed in more detail in Appendix B (p. 69). 

Some pediatric experts would regard a urinary mercury level >50 μg/g 

creatinine as in the toxic range and blood mercury >7–10 μg/dL as elevated. 

More information on acceptable urine and blood mercury levels in children 

can be found in Paulson (2001). However, the diagnosis of mercury 

poisoning should never be based solely on the results of a blood or urine 

test—environmental history and physical findings must support the diagnosis. 

Urine or blood measurements in both adults and children who have chronic 

mercury exposure might not correlate with signs and symptoms of mercury 

toxicity. This might be due to several factors, including the storage of 

mercury in a relatively unexchangeable tissue compartment (i.e., renal 

cortex) or clearance from past exposure after irreversible signs and 

symptoms are manifested. 

Further information on elemental mercury direct biologic indicators and 

treatment is in Appendix B (p. 69). 

Diagnosis 

Chronic elemental mercury exposure in children can cause a severe form of 

poisoning called acrodynia (i.e., painful extremities; also called pink disease) 

weeks or months after exposure. This condition is rare. Acrodynia is 

characterized by pruritus; paresthesia; generalized pain; pink rash; and 

peeling hands, nose, and feet (Table 1; p. 54). Other cases of acrodynia in 

7 
Pediatric Environmental Health 

the literature are discussed in Environmental Health Perspectives (2000) 

and Paulson (2001). 

The most common manifestations of long-term exposure to mercury vapor 

are effects on the central and peripheral nervous systems. Early nonspecific 

signs of exposure include insomnia, forgetfulness, loss of appetite, and mild 

tremor, and symptoms might be misdiagnosed as psychiatric illness. 

Continued exposure leads to progressive tremor, erethism (which is 

characterized by red palms, emotional lability, and memory impairment), 

distal paresthesia, motor and sensory conduction delay, and limb weakness. 

Other accompanying signs include salivation, excessive sweating, and 

hemoconcentration. Mercury can also accumulate in kidney tissues, with 

resulting renal toxicity (including proteinuria or nephrotic syndrome), alone 

or in addition to other signs of mercury exposure. Differences between adult 

and childhood manifestations of mercury poisoning are discussed in Weiss 

(2000). 

Case Study (Continued) 

In the hospital, you make a working diagnosis of mercury poisoning and 

consult with a pediatric environmental medicine specialist. You determine 

that this is a case of acrodynia. The child is treated. In this case of 

acrodynia, succimer (2,3-dimercaptosuccinic acid [DMSA]) is administered 

orally in three daily dosages. DMSA is dispensed in 100-milligram (mg) 

capsules that can easily be opened, allowing the drug to be mixed with a 

food product (e.g., applesauce) if necessary. This treatment is continued for 

several days; urine mercury excretion peaks shortly after introducing the 

chelation treatment. Clinical reassessment and urine mercury excretion are 

measured on day 7 of treatment. Urine mercury levels are still elevated and 

treatment is resumed at a lower dosage for 5 more days, during which the 

child’s mood and rash begin to improve. He is completely asymptomatic the 

next week, and has no elevation in urine mercury excretion. 

Appendix B (p. 69) includes further information regarding the treatment of 

elemental mercury poisoning. 

NOTE: Chelation has been used to reduce body burden of elemental 

mercury; however, whether it reduces toxic effects or speeds 

recovery in mercury-poisoned children remains unclear (Etzel 

2001). Chelation should only be used for symptomatic patients with 

known mercury exposure, and only after consideration of the risk 

and benefits by a specialist experienced in the use of chelators and 

in consultation with the patient or family. 

8 
Pediatric Environmental Health 

Challenge 

(1) What is the likely explanation for this apparent pattern of mercury 

exposure? 

(2) What agencies might help you assess the nature and extent of this 

problem, and what procedures can help confirm the source of the 

mercury exposure? 

(3) You call local public health officials to discuss the case. You are 

asked your thoughts about the case. They ask whether you suspect 

that others have been exposed. What is your answer? 

(4) How do you explain the finding of high urine mercury levels in the 

child, but normal levels in other household members? 

Case Study (Continued) 

An investigation reveals that the mercury thermometer factory employees 

(including the child’s father) change their clothing after working with 

mercury, but that most do not change their shoes. You also find out that the 

teenagers who took the elemental mercury from the local high school 

chemistry lab were questioned and evaluated. The elemental mercury was 

retrieved and environmental testing of possible points of exposure was 

completed. One of the teenagers who had been doing odd jobs at the 

patient’s home admitted spilling mercury in the child’s room on the carpet. 

She tried to clean up what she could see with a paper towel, then flushed it 

down the toilet. In addition to mercury contamination in the patient’s home, 

more than a dozen other homes, several cars, shops, schools, and 

recreational areas in the community have also been contaminated. A 

surveillance program finds that urine mercury levels in the thermometer 

factory workers, their spouses, and adults not associated with the 

thermometer factory do not exceed levels of public health concern, but that 

elevated levels were found in a few young children whose homes and family 

cars were contaminated. These children have been followed up with 

pediatric environmental medicine expert consultation. In addition, the state 

division of environmental protection has been addressing the environmental 

contamination issues. 

The environment is remediated before the child returns to his home (the 

carpet is replaced [Goldman et al. 2001] and follow-up testing of elemental 

mercury levels in the home within acceptable limits). The father changes his 

work clothes and shoes before coming home from work. The state division 

of environmental protection is also addressing any possible source of 

mercury from when the building in which the family lives was used for 

commercial activities (as a jewelry factory complex) and whether mercury 

might be continuing to undergo subsequent volatilization. Whether the 

elevated urinary mercury level and acrodynia in this child is due to the 

9 
Pediatric Environmental Health 

take-home exposures, the jewelry factory complex, or the spill in his room, 

all possible exposure pathways have been mitigated. 

Challenge 

(5) The wife of another thermometer factory worker is breastfeeding 

her newborn infant. She is concerned that her breast milk might be 

exposing the infant to mercury. How would you advise her? 

(6) A neighbor’s teenage son plans to work this summer as an errand 

boy and custodian at the thermometer factory. His father hears 

about your patient’s recent mercury exposure and calls to ask for 

your advice. Are there any special dangers to an adolescent 

working on the production floor of the factory? How would you 

advise him? 

This case study addresses a situation where a high index of suspicion for an 

environmental cause of disease is warranted. However, different types of 

office visits—a well child coming in for routine care, a child coming in for an 

illness that might be related to an environmental exposure, or a child with a 

known or suspected exposure (with or without symptoms)—would call for 

different evaluative approaches. In any of these scenarios, however, a 

pediatrician or other child health care provider can integrate environmental 

health issues into practice. This integration will be explored later in the text. 

In addition to mercury, children might be exposed to a variety of 

environmental toxicants encountered in indoor and outdoor environments of 

the home, child care setting, school, or workplace (including take-home 

exposures). Children might also be exposed to out-of-home pollutants, 

including those found in hazardous waste sites. About 15,000 uncontrolled 

hazardous waste sites exist throughout the United States, with 1,508 sites 

proposed or listed on the National Priorities List (NPL). ATSDR has used 

geographic information systems to estimate the number of children living 

near NPL sites. On the basis of data from 1,255 sites, 1,127,563 children 

<6 years of age live within 1 mile of the sites (about 11% of the potentially 

affected population), although it is important to realize that proximity alone 

does not mean that exposure will occur. 

The Exposure-Disease Model
 To better conceptualize “exposure” and the steps necessary to effect disease, 

the exposure-disease model (Figure 1; p. 53) is often used. 

No matter how toxic, no chemical can harm a person (a child or an adult) 

unless exposure occurs. After a sufficient level of exposure (dose) to the 

chemical, with subsequent biologic uptake and target organ contact, biologic 

change can occur, which might lead to disease (Figure 1; p. 53). This 

10 
Pediatric Environmental Health 

process is the same for everyone, although some toxicants might be more 

hazardous to a child than to an adult or vice-versa. Special consideration of 

a child’s exposure and consumption patterns combined with critical periods 

of target organ development is necessary to assess a child’s risk from a 

particular toxicant exposure. This is discussed further in the Age-Dependent 

Toxicokinetic Changes section. 

Application of the preceding case study to the exposure-disease model 

follows: 

Environmental contamination (potential exposure): Elemental mercury, 

whether spilled or tracked on the carpet from contaminated work boots 

(or both), volatized at room temperature in the child’s room or 

aerosolized by vacuuming the carpet. Vapors accumulate near the floor 

where children play and breathe. 

Biologic uptake (exposure): In this case, exposure occurs primarily 

though the respiratory system via inhalation. The respiratory rate is 

considerably higher in a child than in an adult. In the case study, the 

21⁄2-year-old child’s respiratory rate is 30 breaths/minute. In adults, it is 

about 16 breaths/minute. Indicators of exposure in this case include 

increased urinary mercury. 

Target organ contact: Target organs might include the skin, central 

nervous system (CNS), peripheral nervous system (PNS), renal 

system, and respiratory system. 

Biologic change: In this case study, biologic changes include CNS 

changes (e.g., irritability), dermal changes (e.g., erythema of palms, 

soles, and face; with the characteristic edema and desquamation of the 

skin of the hands and feet), ocular changes (e.g., photophobia), and 

PNS changes (e.g., limb weakness and tongue tremor). 

Clinical disease: acrodynia. 

NOTE: This condition is rare (see discussion under Diagnosis section). 

Not all children exposed to mercury vapors will have acrodynia. 

The exposure-disease model (Figure 1; p. 53) depicts the relationship 

between an environmental contaminant and an adverse health effect. The 

model predicts that the harm caused by a contaminant depends on its 

toxicity, route of exposure, and host factors. (For chemical properties, 

personal risk, biologic fate, and other information about mercury poisoning, 

see Case Studies in Environmental Medicine: Mercury Toxicity [ATSDR 

1992].) 

11 
Pediatric Environmental Health 

The Child as Susceptible

Host: ADevelopmental

Approach to Pediatric

Environmental Medicine 

Childhood is a time of rapid growth and development, accompanied by 

changes in organ system functioning, metabolic capabilities, physical size, 

and behavior that can dramatically modify the potential effects and illness 

caused by exposure to a toxicant. 

Research has not yet satisfactorily answered how host characteristics can 

affect the harm caused by a toxic substance. The federal government has 

begun to mobilize the scientific community to focus on the possible unique 

vulnerabilities of children. Although for some selected agents, children are 

no more susceptible (and are sometimes less susceptible) than adults to an 

adverse outcome, theory and empirical observations point to common 

overall themes of increased susceptibility to environmental hazards 

throughout childhood. 

Differing Susceptibilities of Children 

Factors That Affect Exposure and Are Unique to Children 

and Infants 

Caregivers have a direct impact on the safety and health of children. 

Caregivers are entrusted to not only protect children from danger, but to 

consult child health care providers appropriately. A child relies on adults for 

protection from environmental tobacco smoke (ETS), excessive exposure 

to sunlight, pesticides in the home, take-home occupational exposure, and 

other environmental exposures including noise. Children’s own behaviors, 

physical characteristics, and diet peculiar to each developmental phase 

(Table 2; p. 55) can put them at greater risk for exposure to environmental 

hazards. 

Opportunities for exposure change as a child grows from total dependence 

on his or her parents or other caregivers to adolescent independence. 

Economic circumstances, environmental regulations, and legislation can 

restrict or reinforce pediatric exposures. 

Multiple factors that enhance a child’s opportunity for exposure (Tables 2 

and 3; pages 55 and 61, respectively) include the following: 

Children breathe more air, drink more water, and eat more food per 

kilogram of body weight than adults do. 

An infant’s respiratory rate is more than twice an adult’s rate. 

12 
•

Pediatric Environmental Health 

In the first 6 months of life, children drink seven times as much water 

per kilogram of weight than an adult does. 

From 1 to 5 years old, children consume three to four times more food 

per kilogram of weight than an adult does. 

Restricted food choices in the dietary patterns of infants and toddlers 

lead to greater exposures to contaminants unique to certain foods that 

often dominate their diets. For example, because children consume 

about 15 times more apples and apple products per unit of body 

weight than adults do, risk assessments based on a typical adult diet 

might underestimate a child’s risk of exposure to pesticide residues on 

apples. 

Deficiencies of dietary iron and calcium can increase lead absorption. 

Some toxicants more readily penetrate children’s skin, especially in the 

newborn period when the skin is highly permeable (e.g., dermal 

exposure to lindane and hexachlorophene, with subsequent 

development of neurotoxicity). 

Other factors influencing both exposure to and absorption of environmental 

agents include a child’s 

home, play, or day care environment; 

physical stature; 

mobility; 

metabolic rate; and 

increased surface area to body mass ratio (in young children). 

For example, in a home contaminated with mercury (e.g., caused by spillage 

or from mercury carried home on work shoes), a toddler’s high respiratory 

rate, proximity to surfaces likely to be contaminated, and playful rolling 

around on the floor will increase his or her chance for mercury exposure. 

Other possible contaminants that settle near the floor are pesticides, 

formaldehyde (from new synthetic carpet), and radon. 

Age-Dependent Toxicokinetic Changes 

As children age, changes in their physiology and body composition affect 

the absorption, distribution, storage, metabolism, and excretion of chemicals 

(Behrman et al. 1996). Organ-system function changes with development. 

As muscle and bone mass increase, internal organs become a smaller part 

of the total body.As the size and function of organs change, so does the 

dose necessary to alter those target tissues. The kinetics and toxicity of a 

chemical cannot simply be predicted from data derived entirely from adults 

or even from children of different ages. For example, methemoglobinemia 

from nitrate exposure might occur in newborns more readily than in other 

age groups because during the first 4 months of life, newborns have low 

13 
Pediatric Environmental Health 

concentrations of reduced nicotinamide adenine dinucleotide (NADH) 

methemoglobin reductase (i.e., erythrocyte cytochrome b5 reductase). This 

enzyme reduces methemoglobin, rendering the enzyme nonfunctional for its 

oxygen-transporting function. 

No simple generalization can be made about age-dependent changes in the 

metabolism of xenobiotics (i.e., foreign organic chemicals). First, efficient 

metabolism of a substance does not necessarily decrease its toxicity. In 

some cases, metabolic by-products are more toxic than their parent 

compound. Methyl parathion, an organophosphate pesticide for use on 

outdoor crops, but with a history of misuse indoors, is metabolized to more 

toxic by-products once exposure has occurred. It is the toxic by-products 

that cause organ damage. 

Second, enzymatic pathways do not mature at equal rates: some mature 

rapidly, others slowly. For example, caffeine has a half-life of about 

4 days in the neonate, compared to about 4 hours in the adult. Infants 

achieve adult rates of metabolizing caffeine by 7 to 9 months of age. 

Metabolism of some substances, such as theophylline (which is metabolized 

by the P450 cytochrome system), begins slowly at birth, exceeds that of 

adults in early childhood, and then falls gradually to adult rates by late 

adolescence. Further, different enzymatic pathways might be used in the 

metabolism of a particular chemical at different ages. For all of these 

reasons, studies of the variation in toxicokinetics with age must be 

compound-specific. 

Under some circumstances, the immaturity of certain metabolic pathways in 

children might result in a lower susceptibility to certain toxicants (e.g., 

acetaminophen). In the adult, high levels of acetaminophen can cause fatal 

hepatotoxicity. However, infants delivered by mothers with high levels of 

acetaminophen will also have elevated acetaminophen levels in their blood, 

but will not sustain liver damage. It is thought that the fetus’ inability to 

metabolize the acetaminophen protects the fetus from end-organ damage. 

Therefore, the biotransformation of xenobiotics is developmentally regulated 

and can either protect or harm the individual. 

Organ Susceptibilities 

The rapid development of a child’s organ systems during embryonic, fetal, 

and early newborn periods makes him or her more vulnerable when 

exposed to environmental toxicants. These critical periods of vulnerabilities 

vary according to each organ system. CNS development occurs over a 

protracted period of time. Neuronal cell division is thought to be complete 

by 6 months of gestational age. However, CNS development continues to 

involve timed sequences of cell migration, differentiation, and myelination 

until adolescence. Disruption of these processes or their coordination before 

completion can result in irreparable damage. Different toxicants affect 

14 
Pediatric Environmental Health 

different aspects of these sequences of events (e.g., cell proliferation is 

affected by irradiation, cell migration by ethanol, and cell differentiation by 

hypothyroidism) (Rice and Barone 2000), each resulting in functional 

impairments. Notably, the myelination of the brain and alveolarization of the 

lungs continue to develop throughout adolescence. Also during adolescence, 

the reproductive organs undergo hyperplasia, as well as maturation of 

structure and function. 

Because children are at the beginning of their lives, more opportunity exists 

for both exposure to and expression of harmful effects from exposure to 

toxicants—especially those diseases with a protracted latency period 

(cancer). For example, the 1986 Chernobyl radiation exposure in Belarus, 

Ukraine, and Russia resulted in substantial increases in reported cases of 

thyroid cancer. Alterations in immunologic and thyroid parameters were 

observed in the exposed children monitored in one study for health status 

and level of internal contamination (DeVita et al. 2000). The Ukraine Health 

Ministry announced in 1997 that 10 times as many people (i.e., 50) are 

being diagnosed with thyroid cancer each year, compared to 5 per year 

before the accident. The ministry also stated that the death rate among those 

who stayed in the contaminated area was 18.3% higher than the national 

average. 

Variations in Susceptibility With 

Developmental Stages 

Much of the information in this section as well as in Table 2 (p. 55) is 

adapted from the work of Cynthia Bearer, MD, PhD (Bearer 1995a, 

1995b). 

Developmental milestones mark phases of changing susceptibility (“windows 

of vulnerability”) that can profoundly affect the consequences of chemical 

exposures. This section highlights critical aspects of each stage to form the 

basis of anticipatory guidance and clinical evaluation (Table 2; p. 55). Not 

only are children different from adults with regard to susceptibilities, they are 

different among themselves according to age. Various exposure scenarios, 

and issues important to each developmental stage, will be presented by 

route. Environmental exposures occur predominantly through three major 

routes: ingestion (oral), inhalation (respiratory), and dermal (skin). Specific 

examples of exposures through these major routes are included for 

newborns and toddlers. 

Preconception 

Because oogonia fully develop during fetal life, oocytes rest dormant, 

vulnerable to environmental insults until the time of ovulation. Ova forming 

within the fetus of the future mother are affected by exposure from both her 

grandmother and her mother. 

Anticipatory guidance is 

the education provided to 

parents or caretakers 

during a routine prenatal or 

pediatric visit to prevent or 

reduce the risk that their 

fetuses or children will 

develop a particular health 

problem (CDC 1997). 

15 
Pediatric Environmental Health 

Although injury to stem-cell spermatogonia can occur at any time and lead 

to infertility, male reproductive biology presents repeated, narrow windows 

of vulnerability in parallel with the continual postpubertal production of 

semen and regeneration of spermatozoa. Paternal exposures might also lead 

to adverse reproductive outcomes by transmission of toxicants in seminal 

fluid. (See ATSDR’s Case Studies in Environmental Medicine: 

Reproductive and Developmental Hazards [ATSDR 1993].) 

Parental exposures before conception can result in an array of adverse 

reproductive effects ranging from infertility to spontaneous abortion, as well 

as genetic damage that can lead to a viable, though defective, fetus. For 

example, a woman who has experienced a prepregnancy exposure to lead 

and who was inadequately treated for lead poisoning in childhood might 

give birth to an infant with congenital lead poisoning (Shannon and Graef 

1992). The most logical explanation for this would be storage of the lead in 

bone with mobilization during pregnancy (Silbergeld 1991). 

Environmental tobacco smoke and alcohol are known, preventable human 

growth retardants. Anticipatory guidance by the primary health care 

provider to prospective parents can help prevent adverse fetal outcomes by 

encouraging prospective parents to protect their health and that of their 

unborn infant. Preconception counseling is imperative in proactively 

addressing issues that can significantly impact the health of the unborn child. 

The Fetus 

The fetus cannot escape the transplacental transport of toxicants 

encountered by the mother; that is a fact of fetal life. Both historic and 

gestational maternal exposures can affect the fetus. During gestation, the 

placenta, which establishes its circulation by around day 17 after 

fertilization, acts as the most important route of exposure. The placenta is a 

semipermeable membrane that permits easy transport of low-molecularweight (i.e., carbon monoxide) and fat-soluble (i.e., polycyclic aromatic 

hydrocarbons and ethanol) compounds, as well as certain other compounds 

such as lead. Some water-soluble and high-molecular-weight compounds 

might also cross the placenta, albeit more slowly. The placenta has limited 

detoxification ability that helps mitigate only very low concentrations of 

toxicants. 

Contaminants in a pregnant woman’s current and past diet can harm the 

fetus. Physiologic changes during pregnancy mobilize stored toxicants, such 

as lead from bone or polychlorinated biphenyls (PCBs) from fat cells, 

resulting in fetal exposure. Maternal alcohol ingestion can lead to fetal 

alcohol syndrome, and maternal smoking during pregnancy has been 

associated with lower mean birth weight, increased risk of infant mortality, 

and decrements in lung function noted later in the life of the exposed child. 

16 
Pediatric Environmental Health 

Anticipatory guidance by the child health care provider can help stop the 

parental consumption of tobacco and alcohol. 

Fetal exposures can also occur independently of the placenta. These 

exposures include heat, noise, and ionizing radiation (Paulson 2001). A 

mother’s exposure to ionizing radiation can increase the likelihood of the 

occurrence of childhood leukemia and neurologic delays. Although the 

mechanism is uncertain, some parental exposures during gestation, including 

anesthetic gases and some solvents, might be associated with adverse 

reproductive outcomes (ATSDR 1993). 

During critical periods of organogenesis (i.e., the 6-week period that follows 

the establishment of the placental circulation), exposures can cause profound 

systemic damage that is out of proportion with the usual dose response. The 

fetal brain is particularly vulnerable because it lacks a blood-brain barrier or 

detoxification capabilities. In utero exposure to lead during this stage causes 

more damage to the nervous system than does exposure at any other stage 

of development. In the fetal brain, neurons originate in a central location 

(germinal matrix) and later migrate to predetermined sites. Exposure to 

ethanol during this stage might interrupt migration and lead to brain 

malformation, as is sometimes seen in fetal alcohol syndrome. High levels of 

methylmercury exposure from maternal consumption of contaminated fish 

from Minimata Bay, Japan, caused cerebral palsy and severe mental 

retardation in children born in Minimata. Some studies suggest that lower 

concentrations of maternal dietary methylmercury also can lead to 

neurodevelopmental delays and mild retardation. The fetus is at an increased 

risk of acute toxicity from carbon monoxide; levels that are harmless to 

healthy children can create permanent deficits of cognitive and motor 

functions in a fetus. 

Rapidly dividing fetal cells might have increased sensitivity to carcinogens. 

Epidemiologic evidence, however, is contradictory on the relationship 

between age of exposure and cancer risk. As previously noted, it appears 

that during childhood, sensitivity to carcinogens increases in some organs 

and decreases in others. The only two generally accepted carcinogenic in 

utero exposures proven to result in cancer later in life in the exposed 

offspring include diethylstilbestrol (DES) (via placenta) and ionizing radiation 

(acting directly on the fetus) (Anderson et al. 2000; DeBaun and Gurney 

2001; Lemasters et al. 2000). 

Newborns (Birth to 2 Months), Infants (2 Months to 1 Year of Age), 

and Toddlers (1 to 2 Years of Age) 

The growth rate during the first few months of life is faster that than during 

the rest of life. Tissues with rapidly dividing cells might be especially 

vulnerable to carcinogens; those vulnerable include tissues in the 

hematopoietic cells, lungs, and epithelium. Children’s growth velocity 

17 
Pediatric Environmental Health 

smoothly decreases around 9 months, to about half the initial rate. Although 

resistance increases, toddlers exhibit similar vulnerabilities in absorption, 

detoxification, and organ development as do newborns and infants. 

Exposure by Ingestion 

The small intestine of a newborn responds to nutritional needs by increasing 

the absorption of specific nutrients. For example, calcium transport in 

newborns and infants is about five times the rate in adults. If lead exposure 

occurs, the lead will compete with the calcium for transport at this high rate. 

Breastfeeding 

Breastfeeding is considered the optimal form of infant nutrition in most 

circumstances. Research indicates that human milk and breastfeeding of 

infants provide advantages with regard to general health, growth, and 

development, while significantly decreasing the child’s risk for a large number 

of acute and chronic diseases. The many benefits to the infant provided by 

breastfeeding greatly outweigh the risk from possible contaminants in breast 

milk. For more information regarding contaminants in breast milk, a good 

resource is the AAP Handbook of Pediatric Environmental Health (Etzel 

and Balk 1999) chapter on human milk (Schreiber 2001). 

When breastfed, a baby remains vulnerable to both current and historic 

maternal exposures. Lactation mobilizes previously sequestered fat-soluble 

toxicants such as dioxins, other chlorinated pesticides, PCBs, and bone lead, 

which then contaminate breast milk. Maternal toxicokinetics, the solubility 

and binding properties of a toxicant, and the characteristics of breast milk 

determine the milk-maternal plasma (M/P) ratio. The higher the ratio, the 

more complete the transfer of the substance into the breast milk. Neutral, 

basic, low-molecular-weight, highly lipophilic substances transfer most 

readily into breast milk. M/P ratios have been published for a variety of 

xenobiotics (Schreiber 2001). The M/P ratio for lipophilic substances 

such as PCBs range from 4 to 10; the ratio for organic and inorganic 

mercury is 0.9. 

Formula Feeding 

On a daily basis, a newborn infant consumes a much larger amount of water 

(equivalent to 10%–15% of his or her body weight) compared to an adult 

(2%–4% of body weight). Formula-fed infants consume significant amounts 

of water; average daily consumption might be 180 mL/kg/day (6 fluid 

ounces/kg/day), which is the equivalent for an average adult male of 

thirty-five 360-mL (12 fluid ounces) cans of soft drink per day (Paulson 

2001 and Table 3 [p. 61]). Contaminants such as heavy metals and nitrates 

are not eliminated by boiling water, and are concentrated when water is 

boiled away. Water from municipal water systems is usually low in lead 

content, but the water can acquire lead from soldered pipe joints and brass 

fixtures inside the home. The first-draw water (i.e., water that has stood in 

18 
Pediatric Environmental Health 

pipes) should be discarded. Boiling before formula preparation need not 

exceed 1 minute. Water in municipal systems might also contain 

contaminants such as microbes and trace amounts of organic chemicals. 

Many families use private well water and consider it safe, perhaps safer than 

municipal water. However, private well water is largely unregulated and 

unmonitored and presents the potential for exposure to a spectrum of 

contaminants at high concentrations. 

Nitrates are a well-recognized problem in private well water. Factors 

leading to increased risk of methemoglobinemia from nitrate exposure in 

infants younger than 6 months of age include the following: 

Gastric pH of infants is higher for the first 1–2 months of life and does 

not drop to adult levels until 3 years of age (Marino 1991), leading to 

excess bacterial colonization, which increases the conversion of nitrates 

to nitrites. 

NADH-dependent methemoglobin reductase activity in infants is 60% 

of that in adults. The relative lack of methemoglobin reductase enzyme 

necessary to convert methemoglobin back to functioning hemoglobin 

leads to methemoglobinemia. At about 6 months of age, infants begin to 

have adult levels of NADH-cytochrome b5 reductase, which converts 

methemoglobin back to hemoglobin (Avery 1999). Other causes of 

methemoglobinemia include genetic deficiency in methemoglobinreducing enzymes; genetic abnormalities in the hemoglobin making the 

protein more susceptible to oxidation; GI infections and inflammation 

and the ensuing overproduction of nitric oxide; and exposure to oxidant 

drugs and chemicals, including nitrites. 

Pica 

The avid oral exploratory behavior of infants and toddlers makes ingestion 

an important exposure route to consider. Children who eat nonfood items 

are exhibiting pica behavior. Soil pica is the recurrent ingestion of unusually 

high amounts of soil (i.e., on the order of 1,000–5,000 mg per day). 

Groups at risk of soil-pica behavior include children age 6 years and 

individuals who are developmentally delayed (ATSDR 2001a). ATSDR 

uses 5,000 mg soil per day as an estimate of soil intake for children with 

soil-pica behavior. Accessible environments might be contaminated with 

lead paint, chips, or dust particles; pesticides; take-home contaminants 

(e.g., mercury); lawn chemicals; or floor-cleaning products. 

Solid Foods 

Because a typical toddler’s diet is relatively rich in fruit, grains, and 

vegetables, the risk is higher for a toddler’s exposure to food-borne 

pesticide residues than it is for adults, who routinely consume fewer of 

these foods. Some regulations now acknowledge children’s different 

exposures and susceptibilities in an attempt to lessen children’s exposures 

to toxic chemicals. For example, the Food Quality Protection Act of 1996 

19 
Pediatric Environmental Health 

states that pesticide tolerances need to be set to protect the health of infants 

and children. 

Exposure by Dermal Absorption 

The ratio of the newborn’s skin surface area to body weight is 

approximately three times greater than that of an adult (Table 3; p. 61). 

Therefore, covering a similar percentage of the body with a substance that 

can be dermally absorbed will lead to a larger dose on a weight basis in a 

child than in an adult. Other factors affecting dose include the surface area 

exposed and the vehicle (which may promote contact/residence time). In 

addition, characteristics of the skin of a newborn (birth to 2 months) 

enhance the absorption of xenobiotics. The thick keratin layer, which 

protects an adult’s skin when in contact with a toxicant, does not form 

during the fetal stage. This keratin layer begins to develop in the first 

3–5 days after birth; it remains more susceptible to absorption throughout 

the newborn period and is independent of gestational age. As a result, the 

newborn skin readily absorbs chemicals. Hexachlorophene-containing 

compounds were routinely used in the 1950s for the skin care of newborns 

as a prophylaxis against Staphylococcus aureus infection. By 1971, the use 

of hexachlorophene preparation as a skin cleanser for newborns was 

restricted because studies showed that it disrupted the cell walls and 

precipitated cellular protein, causing vacuolization in the CNS. Other 

examples include Betadine scrubs, which have caused hypothyroidism in 

infants, and dermal absorption of aniline dyes, which were used in a laundry 

service’s advertisement printed on diapers and resulted in methemoglobinemia (Graubarth et al. 1945; Howarth 1951; Chai and Bearer 1999). 

Exposure by Inhalation: Respiration 

The younger the child, the higher the respiratory rate and the higher the 

weight-adjusted dose of an air pollutant (Table 3; p. 61). A baby’s exposure 

to indoor and outdoor air pollution closely mirrors that of its parents or 

caregivers; however, the vulnerability of the infant’s respiratory system 

increases the risk that early exposures to combustion air pollutants (e.g., 

ETS) will slow the rate of pulmonary growth. Acute clinical effects in infants 

exposed to ETS can include laryngitis, tracheitis, pneumonia, increased 

morbidity from respiratory syncytial virus (RSV) infection, and chronic 

middle ear effusions (Cook and Strachan 1999; Gitterman and Bearer 

2001). Respiratory exposures to air contaminants (e.g., ETS, dust mites, 

and cockroach antigens) during the first year of life have a greater influence 

on the incidence and severity of asthma than do exposures later in life (Etzel 

2001). 

As infants and toddlers begin to explore the world away from the arms of 

parents or caregivers, they are often in the microenvironments of the floor 

and ground. Some toxic gases, including mercury vapor, are heavier than air 

and layer close to the floor in these microenvironments. A child’s high 

20 
Pediatric Environmental Health 

respiratory rate in breathing zones close to the floor results in higher inhaled 

doses of toxicants than an adult would receive in the same room. Mercury 

vapors can cause severe respiratory complications and other health effects. 

Young Child (2 Years to 6 Years of Age) 

Special circumstances increase susceptibility in this age range. With the 

newly acquired ability to run, climb, ride tricycles, and perform other mobile 

activities, the young child’s environment expands and so does the risk of 

exposure. Exploratory behaviors also continue, making this age group’s 

susceptibilities very different than those of their younger peers. 

If a young child’s diet is deficient in iron or calcium, as is possible with 

children in this age group, the small intestine will be able to avidly absorb 

lead. Pica is also a consideration for this age group. Children <6 years are 

at high risk for soil pica (ATSDR 2001a). 

School-Aged Children (6 Years to 12 Years of Age) 

School-aged children spend increasingly greater amounts of time outdoors 

and in school and after-school environments—each of which has its own 

hazards. Outdoor air pollution includes widespread air pollutants such as 

ozone, particulates, and oxides of nitrogen and sulfur, which result primarily 

from fossil fuel combustion. Although these pollutants concentrate in urban 

and industrial areas, they are wind-borne and distribute widely. Woodburning and industry in rural towns can create local pockets of intense 

exposure. Toxic air and soil pollutants might result from local sources such 

as hazardous waste sites, leaking underground storage tanks, or local 

industry. Children exposed to high doses of lead released into the air from a 

lead smelter in Idaho showed reduced neurobehavioral and peripheral nerve 

function when tested 15 to 20 years later (ATSDR 1997, 2001b). 

History of school and after-school environments should be included when 

assessing exposure to indoor and outdoor air pollutants and contaminated 

drinking water and soil. During play or normal activity, children might ingest 

or inhale dirt or dust contaminated with arsenic, mercury, or other 

environmental toxicants. 

Adolescents (12 Years to 18 Years of Age) 

Adolescent behavior leads to new categories of potential exposures. Risktaking behaviors of adolescents might result in exploring off-limit industrial 

waste sites or abandoned buildings or experimenting with psychoactive 

substances (e.g., glue sniffing). Adolescents might take jobs or enter 

vocational schools where they are exposed to workplace hazards. For 

more information about labor issues and adolescents, see Goldman et al. 

(2001). Adolescents sustain more occupational injuries and suffer more 

illnesses than their elder co-workers. Hobbies and school activities, such as 

arts and crafts or chemistry, are also more likely to involve exposure to 

21 
Pediatric Environmental Health 

hazards than are the activities of younger children. Few schools include basic 

training in industrial hygiene as a foundation for safety at work, at school, or 

while enjoying hobbies. For example, there have been reports of teenagers 

taking elemental mercury from an old industrial facility and playing with and 

spilling the elemental mercury in homes and cars (Nadakavukaren 2000). 

During the adolescent period, the metabolism rate of some xenobiotics 

dependent on the cytochrome P450 (CYP enzyme) system decreases as a 

result of changes in cytochrome P450 expression (Nebert and Gonzalez 

1987) (e.g., theophylline, which has a subsequent increase in blood) 

(Gitterman and Bearer 2001). Studies indicate that the metabolic rate of 

some xenobiotics is reduced in response to the increased secretion of growth 

hormone and/or steroids that occur during the adolescent years (steroids 

compete with theophylline metabolism) (Gitterman and Bearer 2001). The 

implications of these changes for environmental contaminants is an area of 

intense research. Pubertal changes lead to new tissues with the special 

vulnerabilities associated with rapidly growing, dividing, and differentiating 

cells. Profound scientific and public interest in endocrine disruptors reflects 

concerns about the impact of persistent synthetic organic chemicals on the 

developing reproductive system. Studies have shown that by the end of 

puberty, the metabolism of some xenobiotics have achieved adult levels. 

Sources of Exposure 

Exposure to environmental toxicants can occur through contact with 

contaminated soil, food, water, or air. Examples throughout the Variations in 

Susceptibility With Developmental Stages section reflect the special 

exposure susceptibilities by age group. Table 4 (p. 62) summarizes common 

sources of contamination for different environmental media, by route; 

however, it is not exhaustive. Although many potential sources of exposure to 

environmental toxicants exist, this section will focus on take-home sources of 

exposure because these sources are an often overlooked, yet important, 

source of exposure. 

Take-Home Contamination 

The transmission of potentially toxic quantities of industrial chemicals from 

occupational settings to homes and residences is referred to as take-home 

contamination. Sometimes thought of as paraoccupational exposure, takehome contamination has been more vividly called “fouling one’s own nest.” 

Unlike the types of environmental contamination that might impact many 

individuals and large geographic areas (e.g., air pollution, spills of industrial 

chemicals, and accumulations of toxic wastes), take-home contamination 

most often affects the immediate exposed families of the involved workers. 

22 
Pediatric Environmental Health 

Take-home contamination can occur even when appropriate precautions 

seem to be in place. For example, it is not enough that contaminated 

workers change clothing and shoes before returning home. Because some 

exposure risks are associated with laundering contaminated work clothes, 

such clothing should not be brought home to be cleaned. Instead, these 

clothes should be professionally laundered, preferably as part of the 

employer’s occupational safety program. The hazards of seemingly casual 

exposure should also be recognized. In addition to laundering clothing at 

work, showering at work might also be necessary in some work settings to 

ensure that contaminants are removed from hair and skin. 

Industrial Chemicals 

The most direct form of take-home contamination results when industrial 

chemicals are carried from the workplace to the home on clothing, tools, 

shoes, skin, and hair (Chisolm 1978). The nature of the chemical and 

individual variables (e.g., age and activities) determine which family 

members are most at risk for developing adverse health effects from 

exposure. Small children are often most susceptible. For example, 

numerous reports document lead contamination among the children of lead 

workers (Watson et al. 1978; Etzel and Balk 1999). In such cases, 

preschool children might have blood lead levels equal to or greater than 

those found in the parent or parents who work with or around lead. 

Similarly, take-home contamination by mercury-exposed workers involved 

in thermometer manufacturing has led to the greatest blood levels of 

mercury documented in young children (Schreiber 2001) and in elevated 

mercury levels in children whose parents worked in a mercury thermometer 

plant (Hudson 1987). 

A less obvious form of take-home exposure results from industrial chemicals 

in breast milk. Because human milk contains high levels of fat (about 4%), 

lipophilic compounds are preferentially taken up into breast milk (Schreiber 

2001). For some industrial chemicals, breast milk concentrations are 

threefold to tenfold greater than corresponding maternal blood levels. Very 

few instances of harm have occurred in a nursing baby because of the baby 

ingesting chemicals found in his or her mother’s milk. The many benefits to 

the infant provided by breastfeeding greatly outweigh the risk from possible 

contaminants in breast milk. Good resources discussing breast milk 

contaminants and breastfeeding are the AAP Handbook of Pediatric 

Environmental Health (Etzel and Balk 1999) chapter on human milk and 

Schreiber (2001). 

Fibrous Materials 

Workplace asbestos has been linked to asbestosis and mesothelioma in 

family members of asbestos workers (Anderson et al. 1979; Etzel and Balk 

1999). Among spouses of asbestos workers (who may have laundered 

contaminated clothing) and children at home, radiographic abnormalities 

23 
Pediatric Environmental Health 

consistent with asbestos exposure were almost seven times more frequent 

than expected. Asbestos take-home contamination can also be persistent. It 

has been found in the homes of former asbestos workers 20 years after the 

workers stopped working at the plant. 

Organic Compounds 

Chloracne has occurred in the children of workers exposed to 

trichlorophenol, dioxins, and other polycyclic halogenated compounds 

(Jensen 1972; Yoshimura 1974; Mocarelli et al. 1991). Contact with the 

parent’s or caregiver’s contaminated work clothing was the likely cause of 

this chloracne. Gynecomastia and breast discomfort occurred in children of 

workers employed in the manufacture of synthetic estrogens (Budzynska et 

al. 1967). Children of agricultural workers might have increased exposure to 

pesticides. In another example, a toddler suffered status epilepticus-type 

seizures after chewing plastic pellets that had adhered to her mother’s work 

boots (Woody et al. 1986). The pellets contained an explosive compound 

used in munitions and rockets that were manufactured at the mother’s 

workplace. 

Principles of Environmental 

Medical Evaluation 

Pediatricians and other child health care providers should continue to expand 

their skills in taking an environmental history, delivering anticipatory guidance, 

and conducting appropriate risk-based laboratory tests for environmental 

illnesses (in consultation with pediatric environmental specialists as 

necessary). Table 5 (p. 64) is a basic environmental database form that can 

be used in an office setting to keep a baseline environmental record handy in 

the patient’s chart and update it as necessary. Portions of this tool could be 

self-administered in the waiting room, as is done with medical history 

questionnaires. The practitioner can review the form with the patient as 

necessary. Appendix C (p. 72), taken from the work of Sophie Balk, MD 

(Balk 1996), provides a summary of environmental health questions for an 

environmental history.Appendix C also includes a table describing when to 

introduce specific environmental health questions appropriate to age. Other 

pediatric environmental health history tools are also available (e.g., Goldman 

et al. 1999). 

To determine whether an environmental factor plays a role in a child’s illness, 

a high index of suspicion should be maintained. Most investigations that 

require the help of a specialist in environmental medicine begin in the primary 

care provider’s office. Further probing can be done when a clinical 

presentation warrants. (See ATSDR’s Case Studies in Environmental 

Medicine: Taking an Exposure History [ATSDR 2001c].) 

24 
Pediatric Environmental Health 

Clinicians rarely see a child with a disease pathognomonic for environmental 

exposure, such as fetal alcohol syndrome or acrodynia (a manifestation of 

chronic mercury poisoning). Instead, a child generally will have a complex of 

signs and symptoms for which there is an extensive differential diagnosis and 

the possibility of multiple causes. Some common conditions might be caused 

by one of several environmental contaminants; for example 

seizures can occur as the result of lead poisoning or carbon monoxide 

intoxication; 

learning disabilities can have multiple contributing environmental factors, 

such as intrauterine alcohol exposure and lead intoxication; or 

eczema and other preexisting diseases can be aggravated by 

environmental factors (e.g., if an adolescent begins working with 

solvents in an auto mechanics class at a trade school). 

Preconception and Prenatal Counseling 

Preconception and prenatal counseling present opportunities to prevent 

exposures that might have devastating and lifelong effects. The March of 

Dimes and the U.S. Surgeon General recommend that preconception 

counseling be done by all primary care physicians. When providing 

preconception and prenatal counseling, a primary health care provider 

should include a screening environmental exposure history to assess basic 

environmental information about the home, occupations, and hazardous 

hobbies of both parents and of other adults living in the home (Table 5; 

p. 64). 

Child health care providers should 

Provide parents with an environmental hazards checklist to be used to 

prepare the home for the arrival of their baby (Table 6; p. 67). 

Discuss the hazards associated with remodeling (e.g., lead poisoning) 

and furnishing a nursery (e.g., what items are considered safe). 

Warn parents about the intake of certain potentially contaminated 

foods, such as fish that might be contaminated with mercury. Health 

care providers can use local public health advisories or those provided 

by the U.S. Food and Drug Administration, ATSDR, or the U.S. 

Environmental Protection Agency (EPA). 

Counsel parents and caregivers about the use of prescribed and overthe-counter medications (e.g., Tylenol, aspirin, and cough suppressants 

that contain alcohol), nutritional supplements, alternative remedies, and 

other “natural” treatments. 

Review and discuss at length the hazards of alcohol and controlled 

substance use and abuse while pregnant. It is important to emphasize 

that environmental tobacco smoke, marijuana smoke, and cocaine 

smoke can adversely affect fetal health (Etzel and Balk 1999) 

25 
Pediatric Environmental Health 

(Appendix D, p. 74, provides resources for further information) and 

that these are all preventable causes of potential adverse fetal health 

effects. 

Visiting the Doctor’s Office 

Pediatricians or child health care providers can integrate environmental 

health issues into their practices in three basic scenarios. 

For the Well Child 

For the well child, a developmentally appropriate environmental 

checklist should be used to identify the child’s potential exposure risks. 

Age-appropriate, environmental, anticipatory guidance should be provided 

(Table 2; p. 55), and risk-based screening tests for lead poisoning should be 

performed (Centers for Disease Control and Prevention 1997 and 

Appendix E [p. 82]). This is another opportunity to provide parents and 

caregivers with educational materials on how to prevent exposure to 

hazardous substances and what to do if exposure occurs. The reality of a 

general pediatrician or primary health care provider’s practice is that there is 

little time to do an extensive environmental exposure history. At a minimum, 

the following questions taken from the AAP Handbook of Pediatric 

Environmental Health (Etzel and Balk 1999) should be integrated into the 

well-child visit: 

1. Where does the child live or spend time? 

2. Does anyone in the home smoke? 

3. Do you use well water? Tap water? 

4. Is the child protected from excessive exposure to the sun? 

5. What do parents/teenagers do for a living? 

Appendix C (p. 72) and Table 5 (p. 64) include information about taking an 

environmental history; Appendix D (p. 74) includes additional information 

and resources for environmental health concerns. Responses to the 

questions in Appendix C and Table 5 can guide the child health care 

provider in providing anticipatory guidance about preventing or stopping 

harmful environmental exposures. Additional questions can be added as 

necessary when trying to determine if specific community environmental 

health risks might be a problem for the child. 

For the Sick Child 

For the sick child whose illness might be environmentally related, the 

physician should consider an environmental agent as potentially related to a 

child’s current illness, particularly when the illness in question does not 

follow a usual pattern, or when more than one family member or schoolmate 

is affected. 

26 
Pediatric Environmental Health 

For the Child With a History of Known or Suspected 

Specific Exposure 

For the child with a history of a known or suspected specific exposure 

(with or without symptoms), concerned parents might visit a child’s health 

care provider with worries that their child might become sick in the future as 

a result of a suspected exposure. The parents might inquire about signs and 

symptoms associated with such exposures. This inquiry will help raise 

suspicion for a possible environmental etiology and thus guide the history 

and subsequent differential diagnosis. 

Evaluating the Exposed or Sick Child 

Because most environmental or occupational illnesses manifest as common 

medical problems or have nonspecific symptoms, an environmental etiology 

might be missed. Therefore, it is important to take an exposure history, 

especially if an illness has been unresponsive to therapy or has an atypical 

presentation. In a practical sense, an extensive environmental exposure 

history is beyond the scope of a primary child health care provider’s 

practice. However, asking a few screening questions that would alert the 

provider to a possible environmental cause would then allow the general 

provider to contact experts in pediatric environmental medicine for further 

guidance in the diagnosis, treatment, and management of such cases. 

Following is the evaluation process in its entirety, with emphasis on what is 

generally feasible within the clinical generalist’s practice and what would 

probably be referred to a pediatric environmental specialist. 

Identify Specific Health Concerns 

Questions that might help in discerning whether an illness is related to the 

environment (in addition to the screening exposure history questions taken at 

the well child visit) follow. [Questions taken from the AAP Handbook of 

Pediatric Environmental Health (Etzel and Balk 1999).] 

1.	 Do symptoms subside or worsen in a particular location (e.g., home, 

child care, school, or room)? 

2.	 Do symptoms subside or worsen on weekdays or weekends? At a 

particular time of day? 

3.	 Do symptoms worsen during hobby activities, such as working with arts 

and crafts? 

4.	 Are other children that your child spends time with experiencing 

symptoms similar to your child’s? 

Establish a Problem List 

Using the traditional tools of interviewing, physical examination, and 

problem-specific laboratory tests, the child health care provider should 

attempt to objectify complaints and establish a problem list and a differential 

diagnosis. The evaluation might identify a specific organ disorder such as 

27 
Pediatric Environmental Health 

eczematous changes in the skin, asthma, or hepatitis, or broad abnormalities 

such as developmental delays. In other situations, the initial problem list 

might only include signs, symptoms, and laboratory test results. The child 

health care provider who has experience with environmental toxicants might 

be quick to suspect a disease or a syndrome that has been associated with 

hazardous environmental exposures, such as asthma or acute lead toxicity. 

However, the problem list should still be used to keep the differential 

diagnosis broad in the beginning. Any and all specific exposures identified 

by the child’s parents or caregiver(s) or suspected by the child health care 

provider should also be listed. Clinicians should be trained to seek 

sophisticated environmental etiologies when dealing with possible hazardous 

environmental exposures. In most cases, these etiologies will involve 

consultation and/or referral to a pediatric environmental medicine specialist. 

Appendix D (p. 74) includes information on the Pediatric Environmental 

Health Specialty Units. 

Identify Key Exposures and Routes of Exposure 

Every clinical evaluation of a sick child should include an exposure history 

that is developmentally appropriate and relevant to the problem list (Table 5 

[p. 64], Appendices C [p. 72] and D [p. 74], and ATSDR’s Case Studies 

in Environmental Medicine: Taking an Exposure History [ATSDR 

2001c]). If certain responses to a few screening questions point to a 

possible environmental etiology, a more detailed environmental history 

should be taken. In some cases, consultation with a specialist in pediatric 

environmental medicine might be indicated. The child health care provider 

should also be alert to clusters of cases that come into the office that would 

prompt further investigations. Augment the basic environmental history that 

might already be part of the patient’s chart with problem-specific questions. 

Even if a parent is focused on a specific exposure, collect information about 

all possible sources of exposure to environmental hazards. For example, 

when assessing a 4-year-old child with asthma, focus questions on sources 

of allergens at home, at preschool, or at the child care center, as well as 

exposure to outdoor or indoor irritating pollutants (e.g., cat hair, mold, ETS, 

home pesticides, cockroaches, and periodic high ozone levels). Health care 

providers must specifically identify chemicals and the routes by which a 

child might be exposed. 

No matter how toxic, no chemical will harm anyone unless exposure 

(biologic uptake) with subsequent target organ contact occurs, thus causing 

biologic changes that can lead to disease (Figure 1; p. 53). 

When parental occupations might result in take-home exposures, the child 

health care provider should request copies of the material safety data sheets 

(MSDSs) from the parent’s employer about hazardous substances at work 

(see shaded box on p. 29). MSDSs can also be obtained from other 

28 
Pediatric Environmental Health 

sources. To obtain more reliable information on substance-specific health 

effects, see Appendix D (p. 74). 

An MSDS describes harmful routes of exposure for specific hazardous 

substances. The particular route of exposure often determines whether an 

environmental contaminant will cause harm. For example, a child might bite 

and break a thermometer and swallow its liquid contents. Fortunately, 

elemental mercury is relatively nontoxic when ingested because it is not well 

absorbed by the intestinal route. However, because of its high absorption 

rate by the respiratory route, elemental mercury is highly toxic when it 

volatilizes and is inhaled. 

Research the Properties of Toxicants 

After identifying the relevant environmental contaminants, their properties 

need to be researched. If the primary child health care provider is not 

familiar with the contaminant or if the case is complex, consultation with a 

pediatric environmental specialist, poison control center, and/or toxicologist 

is indicated (Appendix D; p. 74). Physical and chemical properties of a 

contaminant help to determine the likelihood of exposure and absorption 

and how a chemical will be metabolized and excreted if exposure or 

absorption occur. 

For example, knowing that metallic (elemental) mercury volatilizes at room 

temperature helps predict the occurrence of respiratory exposure if a rug is 

contaminated with mercury. Air monitoring can contribute to an 

understanding of the extent of exposure. Because mercury vapor layers 

close to the floor, this situation leads to greater concern for exposure of 

young children. 

Details about a substance’s metabolism and excretion (toxicokinetic) 

characteristics help to predict the type of biologic monitoring that would be 

useful in measuring exposure. With information about the half-life of a 

substance, the clinician can better interpret the results of biologic testing for 

exposure. Finally, information about animal and human toxicities helps focus 

laboratory testing on organs known to be affected. 

Characterize Exposure 

Dose response refers to the extent of a biologic effect in relation to the 

received dose of an agent. Although variations exist, generally, the higher the 

dose, the greater the effect. One exception, as discussed previously, is that 

low doses at critical periods of organ development might have a greater 

effect than higher doses at other times. An environmental medical evaluation 

must characterize the extent of exposure with the goal of estimating as 

closely as possible the absorbed dose (Figure 1; p. 53). This is usually done 

in consultation with or referral to a pediatric environmental medicine 

specialist. Exposure intensity, duration, and frequency all contribute to dose 

An MSDS provides information 

about the hazardous ingredients 

of a product, its physical and 

chemical properties, relevant 

occupational standards, basic 

toxicologic and industrial 

hygiene data, and information 

about how to contact the 

manufacturer for additional 

details. Although they are a 

good beginning, MSDSs 

might be incomplete, 

inaccurate, or unhelpful— 

particularly with respect to 

chronic exposures and their 

potential effect on children. 

A health care provider only 

needs the name of a product to 

obtain its MSDS through the 

manufacturer or obtain reliable 

substance-specific medical 

information through the local 

poison control center or 

one of several Internet sites 

(Appendix D [p. 74]). 

The Occupational Safety and 

Health Administration (OSHA) 

requires employers to maintain 

MSDSs on all chemical 

products used in their facilities. 

OSHA regulations require 

employers, if asked, to provide 

relevant MSDSs to their 

employees, their 

representatives, and their health 

care providers. The Superfund 

Reauthorization Act also 

requires businesses to provide 

MSDSs to concerned 

community members when the 

products in question might be 

released into the community. 

29 
Pediatric Environmental Health 

considerations. The exposure assessment relies on three tools: the exposure 

history; the environmental monitoring performed on environmental samples; 

and the biologic monitoring performed on samples of blood, urine, or other 

body fluids or tissues from the exposed person. 

Further Considerations 

Even though more detailed information regarding environmental history, 

environmental monitoring, biologic monitoring, risk communication, and risk 

assessment goes beyond what a primary health care provider will 

realistically know and do in the midst of a busy practice setting, this 

information is provided in Appendix F (p. 83) to help with understanding the 

role of others and communication with others (e.g., staff at the state or local 

health department, poison control center, ATSDR, Association of 

Occupational and Environmental Clinics’ Pediatric Environmental Health 

Specialty Units [PEHSUs; p. 79], and experts at other organizations). 

Appendix F also provides a better understanding of what is involved in 

doing a comprehensive pediatric environmental medical evaluation. 

Pediatric Environmental 

Health Interventions 

The Six Interventions for Clinical Management 

of an Environmental Medical Problem 

1. Cessation or Minimization of Offending Exposures 

Orchestrating the elimination or reduction of ongoing exposure of a child to 

an environmental contaminant deemed hazardous or potentially hazardous is 

one important role for the child health care provider. By hospitalizing a child 

poisoned by a heavy metal, the physician might initiate hazard reduction by 

removing the child from the offending environment. Before returning the child 

to his or her home, however, the environmental hazard must be eliminated or 

mitigated. Whenever possible, the offending agent should be entirely 

removed from the child’s environment. If the agent serves an important 

function and it is possible to substitute a less toxic alternative, substitution 

should be made. For example, homeowners might replace lead paint with a 

nonlead alternative. However, because a toxicant becomes hazardous only 

to the extent exposure occurs, other measures can often accomplish the goal 

of hazard reduction more quickly and inexpensively. For example, measures 

could include (a) blocking pathways of exposure by encapsulating friable 

asbestos insulative lagging on pipes to reduce indoor air asbestos 

contamination or (b) putting household chemicals out of reach. Polluted tap 

water and poor indoor air quality can sometimes be managed through 

treatment technologies. Other measures for reducing hazards might include 

30 
Pediatric Environmental Health 

careful home and personal hygiene, including weekly wet-wiping of leaddust–contaminated windowsills and, for those children living in homes with 

lead paint, enforced handwashing before meals and at bedtime. 

In many cases, specially trained workers and anticipatory guidance from 

child health care providers can provide appropriate direction to a family to 

make an environment safer for a child. Parents of children with asthma can 

be given information from the American Lung Association on reducing 

environmental asthma triggers. Preprinted information for a variety of other 

hazards such as medicines, pesticides, or other household chemicals can 

supplement age-appropriate anticipatory guidance. Appendix D (p. 74) lists 

books and organizations that provide detailed information for families about 

reducing a child’s exposure to environmental hazards. 

Improper attempts by untrained persons to mitigate environmental 

contaminants can lead to dramatic exposures. For example, an untrained 

individual who attempts to remove lead paint might acutely poison himself or 

herself and others (such as children). When in doubt, medical providers 

should collaborate with public health agencies and remediation specialists. In 

some cases of typically acute exposures, the exposure cessation involves 

medical as well as environmental interventions. For example, the first 

responder’s treatment of a person who has been exposed to a hazardous 

pesticide begins with removing the individual from the contaminated 

environment, removing the individual’s tainted clothing, and grossly 

decontaminating the individual’s body (e.g., by giving the individual a 

shower). More refined decontamination then continues in the medical 

setting. Other medical interventions designed to stop the absorption of 

certain toxicants include the use of activated charcoal, gastric lavage, 

emetics, and cathartics for acute ingestion. However, it is important to 

remember that these measures are not recommended for all toxicants and 

might be contraindicated for some. Therefore, you must check with an 

up-to-date resource, such as the local poison control center, for current 

substance-specific treatment recommendations. 

2. Standard Supportive Medical Therapy 

Standard supportive medical protocols and pharmaceuticals are used to 

treat the majority of environmental illnesses. In most situations, the 

environmental contribution to an illness will not be immediately apparent. 

Respiratory failure, asthma, contact dermatitis, cancer, and other medical 

conditions call for standard therapies, pending determination of an 

environmental cause or trigger. Even then, medical treatment only rarely 

involves the use of medical therapies specific to a particular chemical agent. 

The Medical Management Guidelines for Acute Chemical Exposures 

(ATSDR 2001d) reviews the appropriate medical management of many of 

the most common acute chemical exposures. For many acute known 

exposures, when or if the child is very ill, or for unknown exposures, when 

31 
Pediatric Environmental Health 

the child’s signs and symptoms do not follow a usual pattern, consultation 

with hospital emergency room physicians, pediatric intensive care specialists, 

medical toxicologists, and/or environmental medicine specialists should be 

considered (e.g., PEHSUs [p. 79]). 

3. Substance-Specific Medical Interventions 

Although only relatively few substances have specific medical therapies, 

these therapies can enhance the elimination of an agent, block its absorption, 

reverse its effect, or otherwise render it less harmful. After identifying the 

offending agent, the child health care provider should consult texts, 

electronic databases, agencies, or experts to ascertain whether specific 

therapies exist for the exposure. Telephone hotlines through regional poison 

control centers, ATSDR, and PEHSUs, provide 24-hour support for clinical 

decision-making in cases of acute exposure (Appendix D; p. 74). 

4. When to Refer 

The primary health care provider’s privileged position of trust with patients 

provides an early opportunity for more effective communication with parents 

and coordination of medical care in the event of an exposure. The pediatric 

generalist, however, will rarely have the specialized knowledge necessary for 

the management of less common environmental problems. The practitioner 

should work with specialized professionals to develop and support an 

appropriate therapeutic plan. Indications for referral to an environmental 

medicine specialist or government or private organization for assistance 

include the following: 

uncertainty about the extent and nature of relevant exposures, 

uncertainty about an environmental relationship to a specific health 

problem, 

uncertainty in risk characterization, 

the need for assistance with accurate and understandable risk
 

communication information,
 

presentation of similar problems from similar environments for several 

patients, 

the need for specialized diagnostic or therapeutic interventions, 

the need for expensive environmental mitigation management, 

consideration of a novel environmental diagnosis, and 

a hazardous exposure with public health implications. 

5. Family Education and Risk Communication: Talking With Parents 

Communication is essential in forming the necessary therapeutic alliance 

among the health care worker, the patient, and the patient’s family. A 

32 
Pediatric Environmental Health 

communication tool designed by Bernzweig et al. (1994) can enhance 

clinician-patient interaction. 

6. Public Health Reporting 

Many states require reporting of specific environmental illnesses such as 

lead or pesticide poisoning. Beyond these requirements, however, every 

case of environmental illness that the child health care provider identifies 

presents the opportunity for preventing further harm not only to the actual 

patient, but also to others. If one household member was exposed, 

presumably others in the household or community might also be exposed 

unless the physician initiates an appropriate environmental investigation with 

the help of those with special expertise. The physician has an obligation to 

take steps to prevent these additional exposures. In cases where public 

health reporting is not an issue (e.g., urging parents to eliminate exposure to 

ETS or remove animals from the home), anticipatory guidance could be 

important. In complex situations, the physician should report environmental 

exposures and illnesses to the appropriate public health authorities. 

References 

*References cited in text. 

*Agency for Toxic Substances and Disease Registry. 2001a. Summary 

report for the ATSDR soil-pica workshop, June 2000, Atlanta, Georgia. 

Atlanta: US Department of Health and Human Services. 

*Agency for Toxic Substances and Disease Registry. 2001b. Case studies 

in environmental medicine: lead toxicity. Atlanta: US Department of Health 

and Human Services. 

*Agency for Toxic Substances and Disease Registry. 2001c. Case studies 

in environmental medicine: taking an exposure history. Atlanta: US 

Department of Health and Human Services. 

*Agency for Toxic Substances and Disease Registry. 2001d. Medical 

management guidelines for acute chemical exposures. Atlanta: US 

Department of Health and Human Services. (Managing hazardous 

substances incidents; Vol. 3). 

*Agency for Toxic Substances and Disease Registry. 2000. ATSDR gives 

special emphasis to children’s health. Atlanta: US Department of Health and 

Human Services. Available from URL: www.atsdr.cdc.gov/child/ 

ochchildhlth.html#dhac. 

*Agency for Toxic Substance and Disease Registry. 1999. Toxicological 

profile for mercury. Atlanta: US Department of Health and Human Services. 

33 
Pediatric Environmental Health 

Agency for Toxic Substances and Disease Registry. 1998. Agency profile and annual report. Atlanta: US 

Department of Health and Human Services. 

*Agency for Toxic Substance and Disease Registry. 1997. A cohort study of current and previous residents of the 

Silver Valley: assessment of lead exposure and health outcomes. Atlanta: US Department of Health and Human 

Services. 

*Agency for Toxic Substance and Disease Registry. 1993. Case studies in environmental medicine: reproductive 

and developmental hazards. Atlanta: US Department of Health and Human Services. 

*Agency for Toxic Substances and Disease Registry. 1992. Case studies in environmental medicine: mercury 

toxicity. Atlanta: US Department of Health and Human Services. 

*American Academy of Pediatrics Committee on Infectious Diseases and Environmental Health. 1999. Thimerosal 

in vaccines: an interim report to clinicians. Pediatrics 104:570–4. 

American Academy of Pediatrics. 1997. Workgroup on Breastfeeding. Breastfeeding and use of human milk 

[RE9729]. Pediatrics 100(6):1035–9. 

*Anderson HA, Lilis R, Daum SM, Selikoff IJ. 1979. Asbestosis among household contacts of asbestos factory 

workers. Ann N YAcad Sci 330:387–99. 

*Anderson LM, Diwan BA, Fear NT, Roman E. 2000. Critical windows of exposure for children’s health: cancer in 

human epidemiological studies and neoplasms in experimental animal models. Environ Health Perspect 108 (suppl 

3):573–94. 

Aronow R, Cubbage C, Weiner R, Johnson B, Hesse J, Bedford J. 1990. Mercury exposure from interior latex 

paint—Michigan. MMWR 39(8):125–6. 

*Avery AA. 1999. Infantile methemoglobinemia: reexamining the role of drinking water nitrates. Environ Health 

Perspect 107:583–6. 

Baker EL, Folland DS, Taylor TA, Frank M, Peterson W, Lovejoy G, et al. 1997. Lead poisoning in children of 

lead workers: home contamination with industrial dust. N Engl J Med 296(5):260–1. 

*Balk SJ, Walton-Brown S, Pope A. 1999. Environmental history-taking. In: Training manual on pediatric 

environmental health: putting it into practice. Washington (DC): Children’s Environmental Health Network. 

p. 82–95. 

*Balk SJ. 1996. The environmental history: asking the right questions. Contemp Pediatr 13:19–36. 

*Bearer CF. 1995a. How are children different from adults? Environ Health Perspect 103(suppl 6):7–12. 

*Bearer CF. 1995b. Environmental health hazards: how children are different from adults. Future Child 5(2):11–26. 

*Behrman RE, Kliegman RM, Arvin AM, Nelson WE, editors. 1996. Nelson textbook of pediatrics. 15th ed. 

Philadelphia: W.B. Saunders. 

34 
Pediatric Environmental Health 

*Bernzweig J, Pantell R, Lewis CC. 1994. Talking with children. In: Parker S, Zuckerman B, editors. Behavioral 

and developmental pediatrics: a handbook for primary care. New York: Little, Brown and Company. p. 6–9. 

Borak J, Callan M, Abbott W. 1991. Hazardous materials exposure—emergency response and patient care. 

Englewood Cliffs (NJ): Brady. 

Brooks SM, Gochfeld M, Herzstein J, Schenker M, Jackson RM, editors. 1995. Environmental medicine— 

principles and practice. Boston: Mosby. 

*Budzynska A, Wasikowa R, Zajac J. 1967. Hyperestrogenism in children of employees of the Polfa 

pharmaceutical laboratories in Jelenia Gora. Pol Med J 6(5):1249–56. 

*Centers for Disease Control and Prevention. 1997. Screening young children for lead poisoning: guidance for state 

and local public health officials. Atlanta: US Department of Health and Human Services. 

*Centers for Disease Control and Prevention. 2001. Mercury and vaccines (thimerosal). Atlanta: US Department of 

Health and Human Services. Available from URL: www.cdc.gov/nip/vacsafe/concerns/thimerosal/. 

*Chai S, Bearer CF. 1999. A developmental approach to pediatric environmental health. In: Training manual on 

pediatric environmental health: putting it into practice. Washington (DC): Children’s Environmental Health Network. 

p. 57–75. 

Chazotte C. 1995. The March of Dimes substance abuse curriculum by obstetricians and gynecologists. Rosen R,
 

editor. White Plains (NY): March of Dimes Birth Defects Foundation.
 

*Chisolm JJ. 1978. Fouling one’s own nest. Pediatrics 62(4):614–7.
 

*Cook DG, Strachan DP. 1999. Health effects of passive smoking: summary of effects of parental smoking on the
 

respiratory health of children and implications for research. Thorax 54:357–66.
 

*DeBaun MR, Gurney JG. 2001. Environmental exposure and cancer in children: a conceptual framework for the
 

pediatrician. Ped Clin N Am 48(5):1215–1222.
 

*DeVita R, Olivieri A, Spinelli A, Grollino MG, Padovani L, Tarroni G, et al. 2000. Health status and internal
 

radiocontamination assessment in children exposed to the fallout of the Chernobyl accident. Arch Environ Health
 

55(3):181–6.
 

*Environmental Health Perspectives. 2000. Child health. Environ Health Perspect 108 (suppl 3).
 

*Etzel RA. 2001. Indoor air pollutants in homes and schools. Ped Clin N Am 48(5):1153–66.
 

*Etzel RA, Balk SJ, editors. 1999. Handbook of pediatric environmental health. Elk Grove (IL): American
 

Academy of Pediatrics.
 

Fisher J, Mahle D, Bankston L, Greene R, Gearhart J. 1997. Lactational transfer of volatile chemicals in breast milk. 

Am Ind Hyg Assoc J 58(6):425–31. 

35 
Pediatric Environmental Health 

*Food Quality Protection Act of 1996. Public Law 104-170. 3 Aug.
 

*Fullilove MT. 2001. Links between the social and physical environments. Ped Clin N Am 48(5):1253–66.
 

*Gitterman BA, Bearer CF. 2001. A developmental approach to pediatric environmental health. Ped Clin N Am
 

48(5):1071–84.
 

*Goldman RH, Shannon M, Woolf A. 1999. Pediatric environmental health history [CD-ROM]. Boston: Pediatric
 

Environmental Health Center, Children’s Hospital.
 

*Goldman LR, Shannon MW, Committee on Environmental Health. 2001. Technical report: mercury in the
 

environment: implications for pediatricians (RE109907). Pediatrics 108:197–205.
 

*Graubarth J, Bloom CJ, Coleman FC, Solomon HN. 1945. Dye poisoning in the nursery: a review of seventeen
 

cases. JAMA 128:1155–7.
 

*Hill AB. 1965. Environment and disease. Proc Roy Soc Med:295–300.
 

*Howarth BE. 1951. Epidemic of aniline methaemoglobinaemia in nursery babies. Lancet 1:934–5.
 

*Hudson PJ, Vogt RL, Brondum J, Witherell L, Myers G, Paschal DC. 1987. Elemental mercury exposure among
 

children of thermometer plant workers. Pediatrics 79:935–8.
 

Hurwitz S. 1993. Clinical pediatric dermatology: a textbook of skin disorders of childhood and adolescence.
 

Philadelphia: W.B. Saunders Company.
 

*Jensen NE. 1972. Chloracne: 3 cases. Proc R Soc Med 65:687–8.
 

Kacew S, Lambert GH, editors. 1997. Environmental toxicology and pharmacology of human development.
 

Washington (DC): Taylor & Francis.
 

*Klaassen C, editor. 1996. Casarett and Doull’s toxicology: the basic science of poisons. New York: McGraw-Hill.
 

5th ed.
 

Knishkowy B, Baker EL. 1986. Transmission of occupational disease to family contacts. Am J Ind Med 9(6):
 

543–50.
 

*Lemasters GK, Perreault SD, Hales BF, Hatch M, Hirshfield AN, Hughes CL, et al. 2000. Workshop to Identify
 

Critical Windows of Exposure for Children’s Health: Reproductive Health in Children and Adolescents Work Group
 

summary. Environ Health Perspect 108 (suppl 3):505–9.
 

*Marino LR. 1991. Development of gastric secretory function. In: Polin RA, Fox WW, editors. Fetal and neonatal
 

physiology. Philadelphia: WB Saunders. p. 1041.
 

Mayer JL, Balk SJ. 1988. A pediatrician’s guide to environmental toxins. Contemp Pediatr Part 1: 5(7):22–40;
 

part 2:5(8):63–76.
 

36 
Pediatric Environmental Health 

McDiarmid MA, Weaver V. 1993. Fouling one’s own nest revisited. Am J Ind Med 24(1):1–9.
 

McLellan RK. 1991. Assessing residential environmental hazards. Occup Environ Med 5:(8)77–80.
 

*Mocarelli P, Needham LL, Marocchi A, Patterson DG Jr, Brambilla P, Gerthoux PM, et al. 1991. Serum
 

concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin and test results from selected residents of Seveso, Italy. 

J Toxicol Environ Health 32:357–66. 

*Nadakavukaren A. 2000. Our global environment: a health perspective. Prospect Heights (IL): Waveland Press. 

National Institute for Occupational Safety and Health. 1995. Report to Congress on worker’s home contamination 

study conducted under the Workers’ Family Protection Act (29 USC 671A). Cincinnati (OH): US Department of 

Health and Human Services. Publication No. 95-123. 

National Research Council. 1993. Pesticides in the diets of infants and children. Washington (DC): National 

Academy Press. 

*Nebert DW, Gonzalez FJ. 1987. P450 genes: structure, evolution, and regulation. Annu Rev Biochem 56:945–93.
 

Paul M, editor. 1993. Occupational and environmental reproductive hazards: a guide for clinicians. Baltimore:
 

Williams & Wilkins.
 

*Paulson JA, editor. 2001. Children’s environmental health. Ped Clin N Am 48(5).
 

*Rice D, Barone S Jr. 2000. Critical periods of vulnerability for the developing nervous system: evidence from
 

humans and animal models. Environ Health Perspect 108 (suppl 3):511–33.
 

*Schreiber JS. 2001. Parents worried about breast milk contaminants: what is best for baby? Ped Clin N Am
 

48(5):1113–1128.
 

*Selevan S, Kimmel CA, Mendola P. 2000. Identifying critical windows of exposure for children’s health. Environ
 

Health Perspect 108 (suppl 3):451–5.
 

*Shannon MW, Graef JW. 1992. Lead intoxication in infancy. Pediatrics 89:87–90.
 

*Silbergeld EK. 1991. Lead in bone: implication for toxicology during pregnancy and lactation. Environ Health
 

Perspect 91:63–70.
 

*Silvaggio T, Mattison DR. 1993. Comparative approach to toxicokinetics. In: Paul M, editor. Occupational and
 

environmental reproductive hazards: a guide for clinicians. Baltimore:Williams and Wilkins. p. 25–36.
 

*Snodgrass WR. 1992. Physiological and biochemical differences between children and adults as determinants of
 

toxic response to environmental pollutants. In: Guzelian PS, Henry CJ, Olin SS, editors. Similarities and differences
 

between children and adults: implications for risk assessment. Washington (DC):ILSI Press. p. 35–42.
 

*US Environmental Protection Agency and the Agency for Toxic Substances and Disease Registry. 2001. Should I
 

eat the fish I catch? Washington (DC): US Environmental Protection Agency.
 

37 
Pediatric Environmental Health 

*US Environmental Protection Agency. 1997a. Exposure factors handbook. Washington (DC):US Environmental 

Protection Agency. p. 3–7. Vol 1: general factors. Report No.: EPA/600/P-95/002Fa. 

*US Environmental Protection Agency. 1997b. Exposure factors handbook. Washington (DC):US Environmental 

Protection Agency. Vol 2: food ingestion factors. Report No.: EPA/600/P-95/002Fb. 

*US Environmental Protection Agency. 1997c. Exposure factors handbook. Washington (DC):US Environmental 

Protection Agency. p. 4–16. Vol 1: general factors. Report No.: EPA/600/P-95/002Fa. 

*Watson WN, Witherell LE, Giguere GC. 1978. Increased lead absorption in children of workers in a lead storage 

battery plant. J Occup Med 20:759. 

Weiss B. 2000. Vulnerability of children and the developing brain to neurotoxic hazards. Environ Health Perspect 

108 (suppl 3):375–81. 

Wolff MS. 1983. Occupationally derived chemicals in breast milk. Am J Ind Med 4(1–2):259–81. 

*Woody RC, Kearns GL, Brewster MA, Turley CP, Sharp GB, Lake RS. 1986. The neurotoxicity of 

cyclotrimethylenetrinitramine (RDX) in a child: a clinical and pharmacokinetic evaluation. J Toxicol Clin Toxicol 

24(4):305–19. 

World Health Organization. 1991. Environmental health criteria 118: inorganic mercury. Geneva: World Health 

Organization. 

*Yoshimura T. 1974. Epidemiological study on Yusho babies born to mothers who had consumed oil contaminated 

by PCB. Fukuoka Acta Medica 65:74–80. 

Answers to Pretest and Challenge Questions
 Pretest 

(a) Relevant information should be obtained about the child’s home environment and neighborhood. For example, it 

is important to find out the following information: 

type and age of the child’s home, 

whether the home was recently remodeled, 

history of previous industrial use of the property, 

water source and heating system used in the home, 

any use of household chemicals (e.g., pesticides), 

occupations of adults in the home (e.g., the mother or father could bring hazardous materials home from work 

on clothes or shoes), 

hobbies of household members, 

herbal medicine consumption by anyone in the home, and 

38 
Pediatric Environmental Health 

whether any rituals that use mercury are conducted. (Some ethnic traditions encourage sprinkling of mercury 

around the house for religious reasons. Mercury or azogue is sold at shops or botanicas.) 

Questions should also be asked about child care arrangements (e.g., type, condition, and age of the facility; location; 

habits of the caregiver [e.g., smoker or nonsmoker]; commonly used play areas; outdoor activities; and other 

potential sources of hazardous exposures to chemicals) (Tables 4 and 5 and Appendix C; pages 62, 64, and 72, 

respectively). In most cases, the interview alone will be sufficient to gather the information needed to assess the 

potential for hazardous exposures at home. Data collected by interview can then focus biologic testing to consider an 

environmental etiology of the presenting problem. 

The interview and the results of clinical laboratory assessments will direct where focused evaluation of the child’s 

environment is needed. If an environmental cause of a syndrome is strongly suspected, but no obvious source is 

identified by interview or clinical examination, a house call by an environmental assessment specialist might be 

indicated to determine the potential for hazardous environmental exposures. 

(b) The patient’s problem list is as follows: anorexia and weight loss; irritability and photophobia; weakness; pruritic 

rash on trunk and face; peeling, erythematous rash on hands and feet; and mild hypertension. 

(c) The differential diagnoses for a 21⁄2-year-old child who has new, but insidious, onset of behavioral change with 

irritability; photophobia; anorexia; and an excoriated papulovesicular rash on his trunk and face, with sweaty, pink 

and scaling skin on his hands and feet, include the following: 

heavy metal intoxication (e.g., lead or mercury), 

collagen vascular disease (e.g., juvenile rheumatoid arthritis [JRA]), 

brain tumor, 

acute rheumatic fever, 

meningitis, 

Fifth disease (erythema infectiosum), 

Kawasaki syndrome, 

nutritional deficiency, 

leukemia, 

immune deficiency disorder, 

metabolic disturbances, 

CNS degenerative disorders, 

pheochromocytoma, and 

psychosocial disturbances. 

Because of the relatively long history (11⁄2 months) of symptoms, the likelihood seems small for most infectious 

diseases. The history of normal growth, diet, and past use of multivitamins with iron makes the likelihood of a 

primary nutritional deficiency remote. CNS degenerative conditions do not show up with rash; then again, the rash 

on the trunk and face could be unrelated to the child’s refusal to walk. Metabolic disturbances cannot yet be ruled 

out, but they do not include photophobia. Psychosocial disturbances could be a consequence rather than a causal 

39 
Pediatric Environmental Health 

factor. Leukemia, collagen vascular diseases (e.g., JRA), acute rheumatic 

fever, vasculitis (e.g., Kawasaki syndrome), and intoxications also cannot NOTE: This is not a 

yet be ruled out. comprehensive listing of all 

differential diagnoses a health From an environmental/medical point of view, possible sources of care provider would or could intoxication include exposure to heavy metals such as lead and mercury. The consider for this case scenario. distinctive dermatitis of hands and feet, along with CNS symptoms, suggest The list should be used as a acrodynia, a form of childhood poisoning usually due to chronic elemental or working guide only. inorganic mercury intoxication. Acrodynia develops after the mercury 

volatilizes or oxidizes, or both. In acrodynia, also known as “pink disease,” 

the hands and feet are described as puffy, pink, paresthetic, perspiring, and 

painful. 

(d) Without prompting or experience with a recent evaluation of a case of pediatric mercury poisoning, a 

pediatrician or family physician is not likely to include environmental exposure as a primary or even secondary 

consideration when elaborating a differential diagnoses on the basis of the clinical picture presented. More than 

likely, the baseline tests ordered would include 

white blood cell count with differential; 

blood smear; 

electrolytes, with blood urea nitrogen and creatinine; 

erythrocyte sedimentation rate, antinuclear antibody, antistreptolysin-O titer; 

urine analysis with specific gravity; 

radiograph of chest, knees, and bilateral hips; 

a computed tomography scan of the brain to rule out degenerative changes or a space-occupying lesion; and 

a spinal tap (after risk for herniation has been excluded). 

For those health care providers alert to environmental etiologies, screening for heavy metals (e.g., blood lead and 

urine mercury) in spot urine would be ordered. 

(e) Urine tests provide the best estimates of the current body burden of chronic mercury poisoning. Elemental and 

inorganic mercury are mainly excreted in the urine. Laboratory confirmation of exposure to elemental and inorganic 

mercury can best be obtained by measuring the level of total mercury in a 24-hour urine collected in an acid-washed 

container. A first morning void can provide reasonable accuracy if the sample is adjusted for concentration of urine 

by using urine creatinine or specific gravity. Blood mercury levels reflect mainly recent elemental and inorganic 

mercury exposure (i.e., within 5 to 7 days) and correlate poorly with clinical effects. Appendix B (p. 69) has more 

information about lab testing and elemental mercury. 

Also, for many acute known exposures, when or if the child is very ill, or for unknown exposures, when the child’s 

signs and symptoms do not follow a usual pattern, consultation with hospital emergency room physicians, pediatric 

intensive care specialists, medical toxicologists, and/or environmental medicine specialists should be considered 

(e.g., PEHSUs; p. 79). 

40 
Pediatric Environmental Health 

Challenge 

(1) The child and grandmother have evidence of exposure to elemental and/or inorganic mercury at the following 

levels: 321 and 37 μg/g creatinine, respectively. The father and the mother have lower levels of exposure 

(18 and 12 μg/g creatinine, respectively). This pattern of mercury exposure suggests that the child’s and 

grandmother’s exposures are occurring at home, where both spend more time than either parent. 

Three possible explanations should be considered. First, the father, who is almost certainly exposed to mercury in 

his work, might be bringing mercury home on his shoes or clothing, which has subsequently contaminated the rugs 

and volatilized at room temperature. Second, mercury might have been spilled recently in the family’s home (a) by 

the teenager who cleans the home and who was involved with taking mercury from the chemistry lab, (b) by a 

broken thermometer or other mercury-containing instrument, or (c) as a result of a family hobby (e.g., cosmetic 

products or metallurgy); this mercury might have volatilized after exposure to room temperature. Third, mercury 

might have been spilled at some earlier time, when the building in which the family lives was used for commercial 

activities, and might be continuing to undergo subsequent volatilization. In any case, a 21⁄2-year-old boy spends 

considerably more time playing closer to the floor than an adult does; thus, the boy will be exposed to the volatilized 

mercury. 

About 30% of interior latex paints manufactured before 1990 contain mercury compounds that might volatilize at 

room temperatures. Although paint manufacturers voluntarily removed mercury from latex paints in August 1990, 

many people keep partially used cans of old paint for repainting. Therefore, pre-1990 paints might continue to be a 

source of mercury exposure. In this case, however, paint is an unlikely contributor to the mercury contamination 

because significant mercury exposures occur shortly after the application of mercury-containing paint (Aronow et al. 

1990), and this home was not painted recently. 

(2) Levels of ambient mercury should be measured in the home. Such testing and related assistance can usually be 

obtained through local or state public health officials. In some communities, poison control center professionals can 

facilitate appropriate testing of the home environment. Other sources of clinical toxicologic information and technical 

assistance include ATSDR and EPA (Appendix D; p. 74). 

Information should also be gathered about possible take-home contamination from the father’s workplace. The child 

health care provider and/or pediatric environmental medicine specialist might interview the father and also talk to a 

safety officer at the thermometer factory. MSDSs, listing hazardous agents used in the factory, should be requested 

by the child’s father or the child health care provider. Because elemental mercury used in the manufacture of 

thermometers adheres easily to work clothing, work practices at the factory should be reviewed. The physician 

should ask whether factory workers wear appropriate protective clothing and whether contaminated shoes and 

clothing are left at the factory. In some cases, contaminated shoes and clothing might either be worn home or 

brought home for laundering, which allows take-home contamination. State and federal OSHA offices can provide 

information and assistance to reduce such workplace health concerns. The National Institute for Occupational 

Safety and Health (NIOSH) is another resource for workplace health information (Appendix D; p. 74). 

Before discharging the child from the hospital, the health care provider must ensure no possible mercury exposure 

exists at home (i.e., remediation has taken place). Because of the high risk for increased mercury absorption after 

chelation, this is especially important if the child received chelation therapy.As part of discharge planning, health 

care providers should share usable information and materials or provide informational resources to parents and 

caregivers on how to properly store and discard medications, batteries, tools (e.g., thermometers), disinfectants, 

and cooking and garden products, among others. Parents and caregivers can conduct their own environmental 

surveillance in the home. A checklist of possible contaminants and steps to take to prevent accidents that result in 

41 
Pediatric Environmental Health 

exposure is available for health care providers to distribute to parents and caregivers as part of anticipatory 

guidance practices (Table 6; p. 67). Health care providers should also encourage parents and caregivers to keep the 

local poison control center number close to all telephones in the home (Appendix D; p. 74). 

(3) Mercury exposure might have affected others in the same apartment building or community. If exposures 

resulted from take-home contamination, the homes of other workers also might be contaminated. If exposure 

resulted from a spill of the mercury taken by teenagers from their school chemistry lab, others might also be at risk. 

If the exposure resulted from old contamination of the loft building, other residents of that building are at risk. Public 

health officials should conduct evaluations to determine if other groups have actually been exposed. In addition, the 

industrial hygiene practices at the thermometer factory should be reviewed to ensure that they are adequate. 

(4)Young children are at particular risk from take-home as well as “in-home” contamination. A young child usually 

spends more time in the contaminated home compared to the parents and school-aged siblings. Also, mercury vapor 

is much heavier than air and tends to collect near the floor, where infants crawl, toddlers walk, and young children 

play, thus risking greater exposure to higher mercury air levels than are encountered by most adults. 

(5) Mercury can be found in breast milk, but levels of concern regarding infant toxicity have mainly been associated 

with maternal exposure to organic mercury compounds (e.g., methylmercury), not elemental mercury vapor. If levels 

of mercury in the mother’s urine are normal, breastfeeding will probably pose no exposure hazard to the infant. If 

the mother’s urine mercury levels are high, however, mercury levels in breast milk should be measured to ensure that 

they pose no risk to the infant. Breast milk mercury levels >4 μg/L exceed the safe intake level for an infant. Because 

breastfeeding is the optimal infant nutrition, the child health care provider should evaluate each case individually, after 

a careful physical examination of the child (although with low-level exposures, overt symptoms are unlikely), to 

determine whether the risks of breastfeeding outweigh the benefits. For more information about breastfeeding issues, 

see the AAP Handbook of Pediatric Environmental Health (Etzel and Balk 1999) chapter on human milk. 

(6) This teenage boy might be at increased risk of toxic mercury exposures for a number of reasons. 

First, his proposed cleaning activities might involve extended contact with mercury-contaminated waste 

materials. 

Second, part-time and temporary workers might not have an adequate opportunity to learn the proper use of 

personal protective equipment or might not fully understand or be aware of which hazardous substances to 

which they could be exposed at work and the health risks involved with such exposures. 

Third, the typical sense of invulnerability in adolescents might reduce the boy’s vigilance in the use of protective 

equipment and other measures to minimize exposure. Fourth, the higher physical activity level of many 

teenagers might result in increased respiratory rate and volume and, therefore, greater inhalation exposures. 

Fifth, an adolescent might be fascinated with mercury as a toy or object to show off to his friends and he might 

be tempted to take some home. 

As a result of increased risk of toxic mercury exposure, this teenager might exhibit neurologic effects similar to those 

seen in adults. In addition, he shares a similar risk of being the source of mercury take-home exposure to family 

members, who could include young children, by taking it home on his clothing, shoes, hair, and body. 

42 
Pediatric Environmental Health 

Case Studies in Environmental Medicine: 

Pediatric Environmental Health 

Evaluation Questionnaire and Posttest, Course Number SS3098 

Course Goal: To increase the primary care provider’s knowledge of hazardous substances in the environment and 

to aid in the evaluation of potentially exposed patients. 

Objectives 

Describe how and why children differ from adults in their susceptibility to environmental hazards. 

Apply the knowledge of environmental medicine in the evaluation of well and sick children. 

Identify parental occupation and hobbies as a part of the environmental history. 

Identify additional sources of environmental health information. 

Tell Us About Yourself 

Please carefully read the questions. Provide answers on the answer sheet (page 49). Your credit will be 

awarded based on the type of credit you select. 

1.	 What type of continuing education credit do you wish to receive? 

**Nurses should request CNE, not CEU. See note on page 48. 

A. CME (for physicians) 

B. CME (for non-attending) 

C. CNE (continuing nursing education) 

D. CEU (continuing education units) 

E. [Not used] 

F. [Not used] 

G. [Not used] 

H. None of the above 

I. CHES (certified health education specialist) 

2. Are you a... 

A. Nurse 

B. Pharmacist 

C. Physician 

D. Veterinarian 

E. None of the above 

3. What is your highest level of education? 

A. High school or equivalent 

B. Associate, 2-year degree 

C. Bachelor’s degree 

D. Master’s degree 

E. Doctorate 

F. Other 

43 
Pediatric Environmental Health 

4. Each year, approximately how many children do you see as patients? 

A. None 

B. 1–5 

C. 6–10 

D. 11–15 

E. More than 15 

5. Which of the following best describes your current occupation? 

A. Environmental Health Professional 

B. Epidemiologist 

C. Health Educator 

D. Laboratorian 

E. Physician Assistant 

F. Industrial Hygienist 

G. Sanitarian 

H. Toxicologist 

I. Other patient care provider 

J. Student 

K. None of the above 

6. Which of the following best describes your current work setting? 

A. Academic (public and private) 

B. Private health care organization 

C. Public health organization 

D. Environmental health organization 

E. Non-profit organization 

F. Other work setting 

7. Which of the following best describes the organization in which you work? 

A. Federal government 

B. State government 

C. County government 

D. Local government 

E. Non-governmental agency 

F. Other type of organization 

Tell Us About the Course 

8. How did you obtain this course? 

A. Downloaded or printed from Web site 

B. Shared materials with colleague(s) 

C. By mail from ATSDR 

D. Not applicable 

44 
Pediatric Environmental Health 

9. How did you first learn about this course? 

A. State publication (or other state-sponsored communication) 

B. MMWR 

C. ATSDR Internet site or homepage 

D. PHTN source (PHTN Web site, e-mail announcement) 

E. Colleague 

F. Other 

10. What was the most important factor in your decision to obtain this course? 

A. Content 

B. Continuing education credit 

C. Supervisor recommended 

D. Previous participation in ATSDR training 

E. Previous participation in CDC and PHTN training 

F. Ability to take the course at my convenience 

G. Other 

11. How much time did you spend completing the course, evaluation, and posttest? 

A. 1 to 1.5 hours 

B. More than 1.5 hours but less than 2 hours 

C. 2 to 2.5 hours 

D. More than 2.5 hours but less than 3 hours 

E. 3 hours or more 

12. Please rate your level of knowledge before completing this course. 

A. Great deal of knowledge about the content 

B. Fair amount of knowledge about the content 

C. Limited knowledge about the content 

D. No prior knowledge about the content 

E. No opinion 

13. Please estimate your knowledge gain after completing this course. 

A. Gained a great deal of knowledge about the content 

B. Gained a fair amount of knowledge about the content 

C. Gained a limited amount of knowledge about the content 

D. Did not gain any knowledge about the content 

E. No opinion 

45 
Pediatric Environmental Health 

Please use the scale below to rate your level of agreement with the following statements 

(questions 14–23) about this course. 

A. Agree 

B. No opinion 

C. Disagree 

D. Not applicable 

14. The objectives are relevant to the goal. 

15. The tables and figures are an effective learning resource. 

16.	 The content in this course was appropriate for my training needs. 

17. Participation in this course enhanced my professional effectiveness. 

18. I will recommend this course to my colleagues. 

19.	 Overall, this course enhanced my ability to understand the content. 

20.	 I am confident I can describe how and why children differ from adults in their susceptibility to 

environmental hazards. 

21.	 I am confident I can apply the knowledge of environmental medicine in the evaluation of well and 

sick children. 

22.	 I am confident I can identify parental occupation and hobbies as a part of the environmental history. 

23.	 I am confident I can identify and identify additional sources of environmental health information. 

46 
Pediatric Environmental Health 

Posttest 

If you wish to receive continuing education credit for this program, you must complete this posttest. Each question 

below contains five suggested answers, of which one or more is correct. Circle all correct answers on the 

answer sheet. 

24. The acrodynia (pink disease) syndrome includes all of the following except: 

A. hypertension 

B. tachycardia 

C. hypotonia 

D. dry mouth 

E. desquamation of the skin of hands and feet. 

25. Circumstances where a primary health care provider might refer to an environmental medicine 

specialist or government or private organization for assistance include 

A. uncertainty about the extent and nature of relevant exposures 

B. uncertainty in risk characterization 

C. consideration of a novel environmental diagnosis 

D. the need for specialized diagnostic or therapeutic intervention 

E. well-child visit. 

26. Likely sources of mercury poisoning in this case study include all of the following except: 

A. take-home contamination from the father’s workplace 

B. spillage of elemental mercury in the child’s carpeted bedroom 

C. take-home contamination from the mother’s workplace 

D. mercury spilled in the building long before conversion to apartments 

E. accidental ingestion of mercury from a broken thermometer. 

27. Environmental toxicants other than mercury stored in fat and cleared from the body by breast 

milk include 

A. lead 

B. dioxin 

C. polybrominated biphenyls 

D. environmental tobacco smoke 

E. polychlorinated biphenyls. 

28. What are the special susceptibilities of newborn infants that place this age group at increased risk 

of exposure? 

A. restricted diets 

B. low respiratory rate compared to adults 

C. thin keratin layer of their skin 

D. sleeping patterns 

E. larger skin surface-to-volume ratio. 

47 
Pediatric Environmental Health 

29. Which of the following statements are true? 

A. Efficient metabolism of the toxicants will always decrease their toxicity. 

B. Metabolic by-products can be less or more toxic than the parent compound. 

C. The toxicity of all compounds decreases with increasing age. 

D. The study of the variation in toxicokinetics with age must be compound specific. 

E. The placenta permits easy transport of high-molecular-weight and water-soluble compounds. 

30. When taking an exposure history, it is essential to include which of the following? 

A. Type of heating system in the home where the children live. 

B. Location and year the house was built. 

C. Parental occupation(s) and hobbies. 

D. History of renovations and interior decoration and/or acquisition of new furniture in the last 3 years. 

E. Environmental tobacco smoke. 

31. The adolescent period leads to new categories of potential exposures because of 

A. cell proliferation of the reproductive system 

B. tutoring time needed by some youths 

C. risk-taking behavior, disregard for warnings 

D. accelerated growth 

E. increased respiratory rate. 

32. Which of the following are not part of the clinical management interventions in an environmental 

medical problem? 

A. Family education and risk communication. 

B. Substance-specific interventions. 

C. Diet rich in proteins. 

D. Cessation or minimization of offending exposure(s). 

E. Public health reporting of parental environmental tobacco smoke. 

33. Components of the Exposure-Disease Model necessary to arrive at clinical disease include which of 

the following? 

A. biologic plausibility 

B. biologic uptake 

C. target organ contact 

D. biologic change 

E. all of the above. 

Note to Nurses 

CDC is accredited by the American Nurses Credentialing Center’s (ANCC) Commission on Accreditation. 

ANCC credit is accepted by most State Boards of Nursing. 

California nurses should write in “ANCC - Self-Study” for this course when applying for relicensure. A provider 

number is not needed. 

Iowa nurses must be granted special approval from the Iowa Board of Nursing. Call 515-281-4823 or e-mail 

marmago@bon.state.ia.us to obtain the necessary application. 

48 
Pediatric Environmental Health 

Case Studies in Environmental Medicine: 

Pediatric Environmental Health
 Answer Sheet, Course Number SS3098 

Instructions for submitting hard-copy answer sheet: Circle your 

answers. To receive your certificate, you must answer all questions. 

Mail or fax your completed answer sheet to Remember, you can access the 

case studies online at 

Fax: 770-488-4178, ATTN: Continuing Education Coordinator www.atsdr.cdc.gov/HEC/CSEM/ 

and complete the evaluation Mail: Continuing Education Coordinator questionnaire and posttest Agency for Toxic Substances and Disease Registry online at www2.cdc.gov/ 

Division of Toxicology and Environmental Medicine atsdrce.
 

4770 Buford Hwy, NE (Mail Stop F-32)
 

Atlanta, GA 30341-3717 Online access allows you to
 

receive your certificate as soon 

Be sure to fill in your name and address on the back of this as you complete the posttest.

form. 

1. A B C D E F G H 17. A B C D 

2. A B C D E 18. A B C D 

3. A B C D E F 19. A B C D 

4. A B C D E 20. A B C D 

5. A B C D E F G H I J K 21. A B C D 

6. A B C D E F 22. A B C D 

7. A B C D E F 23. A B C D 

8. A B C D 24. A B C D E 

9. A B C D E F 25. A B C D E 

10. A B C D E F G 26. A B C D E 

11. A B C D E 27. A B C D E 

12. A B C D E 28. A B C D E 

13. A B C D E 29. A B C D E 

14 A B C D 30. A B C D E 

15. A B C D 31. A B C D E 

16. A B C D 32. A B C D E 

33. A B C D E 

49 
Pediatric Environmental Health 

Name: E-mail (not required): 

Address: 

Zip code: 

Check here to be placed on the list to 

pilot test new case studies 

fold here first 

Continuing Education Coordinator 

Agency for Toxic Substances and Disease Registry 

Division of Toxicology and Environmental Medicine 

4770 Buford Hwy, NE (Mail Stop F-32) 

Atlanta, GA 30341-3717 

fold here second 

Place
 

Stamp
 

Here
 

Access the case studies online at www.atsdr.cdc.gov/ 

HEC/CSEM/ and complete the evaluation questionnaire 

and posttest online at www2.cdc.gov/atsdrce. 

Online access allows you to receive your certificate as 

soon as you complete the posttest. 

50 tape or staple here 
Pediatric Environmental Health 

Appendices 

Appendix A: Figure and Tables 

Figure 1. Exposure-Disease Model 

Table 1. Clinical Characteristics of Acrodynia 

Table 2. Special Susceptibilities and Anticipatory Guidance About Opportunities for Hazardous Exposure 

by Developmental Stage 

Table 3. Differences in Children and Adults 

Table 4. Sources of Common Environmental Hazards 

Table 5. Basic Environmental Database 

Table 6. Environmental Hazards Checklist for Home Assessment 

Appendix B: Important Issues Regarding Mercury 

Direct Biologic Indicators and Treatment—Elemental Mercury 

Treatment Considerations 

Treatment 

Different Forms of Mercury and Differing Health Effects 

Dental Amalgams 

Thimerosal 

Fish Consumption 

Appendix C: Summary of Questions for an Environmental History 

When To Introduce Environmental Questions 

Appendix D: Environmental Health Concerns: Resources and Sources of Information 

General Resources 

General Resources for Parents and Caregivers 

General Resources for Clinicians 

Consultation Sources 

Government Agencies 

Association of Occupational and Environmental Clinics 

Pediatric Environmental Health Specialty Units 

National Institute for Occupational Safety and Health’s Education and Research Center Grants 

American Association of Poison Control Centers 

State and Local Health Departments 

Appendix E: Lead Screening 

Appendix F: Additional Information for Performing a Comprehensive Pediatric Environmental 

Medical Evaluation 

Exposure History 

Environmental Monitoring 

Biologic Monitoring 

Final Steps 

51 
Pediatric Environmental Health 

52 
Pediatric Environmental Health 

Appendix A: Figure and Tables
 

Figure 1. Exposure-Disease Model 

*

Contamination of environmental medium: air, water, soil, or food. Assessment tools: 

exposure history and environmental monitoring. 

†

Primary routes of exposure: respiratory, oral, and dermal. Secondary routes of 

exposure: breast milk, transplacental, nonplacental/intrauterine, and parenteral. 

Assessment tools: exposure history and biologic monitoring. 

‡

Assessment tools: biologic monitoring. 

§

Assessment tools: history, physical, biologic monitoring (to include advanced diagnostic 

testing of target organ), and specialty referral (if necessary). 

53 
Pediatric Environmental Health 

Table 1. Clinical Characteristics of Acrodynia 

System	 Characteristic 

Central nervous	 Irritability 

Extreme photophobia (patient burrows head or covers eyes to block out light) 

Cardiovascular	 Hypertension 

Tachycardia 

Gastrointestinal	 Stomatitis with anorexia 

Colitis with diarrhea or constipation 

Salivation 

Renal	 Proteinuria 

Nephrotic syndrome progressing to renal failure in extreme cases 

Dermal	 Erythema of the palms, soles, and face 

Edema and desquamation of the skin of hands and feet 

Pruritus 

Muscular/Skeletal	 Hypotonia 

Various	 Gingivitis 

Diaphoresis 

Paresthesia 

Generalized pain 

54 
Pediatric Environmental Health 

Table 2. Special Susceptibilities and Anticipatory Guidance About Opportunities for Hazardous Exposure by 

Developmental Stage 

Developmental Developmental 

Stage Characteristics Vulnerabilities Anticipatory Guidance 

Preconception — Male and female parental Dietary advisories (mercury 

reproductive systems and PCBs) 

Occupational, environmental, 

and vocational exposures 

Pharmaceuticals 

Substance abuse 

Fetal Rapid cell division Dividing cells sensitive to Dietary advisories (mercury 

Organogenesis transplacental carcinogens and PCBs) 

Mother’s internal environment Developing reproductive Occupational, environmental, 

system can lead to and avocational exposures 

transgenerational effects Take-home occupational 

Critical periods of organ exposures 

development Pharmaceuticals and herbal 

Immature blood-brain and alternative remedies 

barrier Substance abuse 

Placenta as semipermeable Topical insect repellents 

membrane Baseline household 

environmental survey 

Maternal exposures during 

preparation of nursery and 

other remodeling (lead and 

volatile organic 

compounds) 

Continued on page 56 

The information in this table is adapted from Bearer (1995b). 

Anticipatory guidance is the education provided to parents or caretakers 

during a routine prenatal or pediatric visit to prevent or reduce the risk 

that their fetuses or children will develop a particular health problem 

(CDC 1997). 

55 
Pediatric Environmental Health 

Table 2. Special Susceptibilities and Anticipatory Guidance About Opportunities for Hazardous Exposure by 

Developmental Stage (Continued from page 55) 

Developmental Developmental 

Stage Characteristics Vulnerabilities Anticipatory Guidance 

Newborn (birth Nonambulatory Brain development Consider day care and home,

 to 2 months) Restricted environment - Immature blood-brain indoor, and outdoor 

High calorie and water intake barrier environments 

High air intake - Synapse formation Ingestion 

Highly permeable skin Lungs - Breast milk 

Alkaline gastric secretions - alveolar development - Infant formula (tap or well­

(low gastric acidity) - lung fluid cleared by water contaminants) 

pulmonary lymphatic Respiratory 

system - Indoor air contaminants, 

High respiratory rate especially those layering 

Skin very permeable with near the floor (e.g., 

large surface-to-volume mercury, pesticides, 

ratio allergens, radon, asbestos, 

Gastrointestinal tract: highly and take-home 

permeable, increased pH occupational agents). 

Immature detoxification - Outdoor air pollutants, 

capacity of liver, kidney, especially ozone and 

and digestive system particulates 

Skin 

- Contaminants used or 

deposited on floor, 

especially household 

products, pesticides, and 

take-home occupational 

agents 

Continued on page 57 

The information in this table is adapted from Bearer (1995b). 

Anticipatory guidance is the education provided to parents or caretakers 

during a routine prenatal or pediatric visit to prevent or reduce the risk 

that their fetuses or children will develop a particular health problem 

(CDC 1997). 

56 
Pediatric Environmental Health 

Table 2. Special Susceptibilities and Anticipatory Guidance About Opportunities for Hazardous Exposure by 

Developmental Stage (Continued from page 56) 

Developmental Developmental 

Stage Characteristics Vulnerabilities Anticipatory Guidance 

Infant/Toddler Crawling and early walking Brain development Consider day care and home,

 (2 months Oral exploration - Immature blood-brain indoor, and outdoor

 to 2 years) Limited diet barrier environments 

High intake of fruits and - Synapse formation Ingestion 

vegetables Lungs: alveolar - Pesticides on fruit and 

development vegetables 

High respiratory rate - Tap water contaminants 

Skin very permeable with - Contaminants on floor and 

large surface-to-volume within easy reach, 

ratio especially medicines, 

Small intestine avidly household products, 

absorbs lead if diet pesticides, lead, and takedeficient in iron home occupational agents 

and calcium - Pica 

Immature detoxification Respiratory 

- capacity of liver, - Indoor air contaminants, 

kidney, and especially those layering 

digestive system near the floor (e.g., mercury, 

pesticides, allergens, radon, 

asbestos, and take-home 

occupational agents) 

- Outdoor air pollutants, 

especially ozone and 

particulates 

Skin 

- Contaminants on floor and 

within reach, especially 

household products, 

pesticides, and take-home 

occupational agents 

- Topical insect repellents 

Continued on page 58 

The information in this table is adapted from Bearer (1995b). 

Anticipatory guidance is the education provided to parents or caretakers 

during a routine prenatal or pediatric visit to prevent or reduce the risk 

that their fetuses or children will develop a particular health problem 

(CDC 1997). 

57 
Pediatric Environmental Health 

Table 2. Special Susceptibilities and Anticipatory Guidance About Opportunities for Hazardous Exposure by 

Developmental Stage (Continued from page 57) 

Developmental Developmental 

Stage Characteristics Vulnerabilities Anticipatory Guidance 

Young child Expanded environment, still Brain developing Consider home, day care,

 (2 to 6 years includes significant time Lungs: alveolar preschool, and playmates’

 of age) on floor development and indoor and outdoor 

Increased independence increasing volume environments 

High intake of fruits and Small intestine avidly Ingestion 

vegetables absorbs lead if diet - Pesticides on fruit and 

deficient in iron or vegetables 

calcium - Tap water contaminants 

Immature detoxification - Contaminants on floor and 

capacity of liver, kidney, within easy reach, especially 

and gastrointestinal medicines, household 

system products, pesticides, lead, 

and take-home 

occupational agents 

- Pica 

Respiratory 

- Indoor air contaminants, 

especially those layering 

near the floor (e.g., mercury, 

pesticides, allergens, radon, 

asbestos, and take-home 

occupational agents) 

- Outdoor air pollutants, 

especially ozone and 

particulates 

Skin 

- Contaminants on floor and 

within reach, especially 

household products, 

pesticides, and take-home 

occupational agents 

- Topical insect repellents 

Continued on page 59 

The information in this table is adapted from Bearer (1995b). 

Anticipatory guidance is the education provided to parents or caretakers 

during a routine prenatal or pediatric visit to prevent or reduce the risk 

that their fetuses or children will develop a particular health problem 

(CDC 1997). 

58 
Pediatric Environmental Health 

Table 2. Special Susceptibilities and Anticipatory Guidance About Opportunities for Hazardous Exposure by 

Developmental Stage (Continued from page 58) 

Developmental Developmental 

Stage Characteristics Vulnerabilities Anticipatory Guidance 

School-aged child	 Increased number of Brain developing Consider home, school,

 (6 to 12 years)	 environments and less Lungs: increasing volume friends, and afterschool 

supervised play: programs’ indoor and 

school, playground, outdoor environments 

friends’ houses Ingestion 

- Tap water 

- Food 

Respiratory 

- Indoor and outdoor air 

quality 

- Hazards associated with 

hobbies and school crafts 

- Take-home occupational 

hazards 

Skin 

- Hazards associated with 

hobbies and school crafts 

- Take-home occupational 

hazards 

- Topical insect repellents 

Continued on page 60 

The information in this table is adapted from Bearer (1995b). 

Anticipatory guidance is the education provided to parents or caretakers 

during a routine prenatal or pediatric visit to prevent or reduce the risk 

that their fetuses or children will develop a particular health problem 

(CDC 1997). 

59 
Pediatric Environmental Health 

Table 2. Special Susceptibilities and Anticipatory Guidance About Opportunities for Hazardous Exposure by 

Developmental Stage (Continued from page 59) 

Developmental Developmental 

Stage Characteristics Vulnerabilities Anticipatory Guidance 

Adolescent Puberty Brain and lungs Consider home, school,

 (12 to 18 years) Accelerated growth continue to develop friends, occupational, 

Experimentation with controlled Muscles and bones and trade school 

substances grow rapidly environments 

Independence and exposure Gonad maturation Ingestion 

to multiple environments Breast development - Tap water 

Possible employment, work Ova and sperm - Food 

in family business, or maturation - Occupational hazards 

training in hazardous ingested because of poor 

trades poor hygiene 

- Substance abuse 

Respiratory 

- Indoor and outdoor air 

quality 

- Occupational and trade 

school hazards 

- Take-home occupational 

exposures 

- Hazards associated with 

hobbies and school crafts 

- Substance abuse 

Skin 

- Occupational and trade 

school hazards 

- Take-home occupational 

exposures 

- Hazards associated with 

hobbies and school crafts 

- Topical insect repellents 

The information in this table is adapted from Bearer (1995b). 

Anticipatory guidance is the education provided to parents or caretakers 

during a routine prenatal or pediatric visit to prevent or reduce the risk 

that their fetuses or children will develop a particular health problem 

(CDC 1997). 

60 
Table 3. Differences in Children and Adults 

Pediatric Environmental Health 

Infants Children Teens Adults Reference 

Surface area: body mass ratio (m2/kg)* Newborn Young child Older child Adult Silvaggio and Mattison 

0.067 0.047 0.033 0.025 (1993) 

Respiratory ventilation rates Infant – – Adult Silvaggio and Mattison 

Respiratory volume (mL/kg/breath)† 10 – – 2 (1993) 

Alveolar surface area (m2)

‡ 3 – – 10 

Respiration rate (breaths/min)§ 40 – – 75 

Respiratory minute ventilation – – – –

 rate¶ 133 – 2 

Drinking water (tap) <1 year 1–10 years 11–19 years 20–64 years Snodgrass (1992) 

Mean intake (mL/kg/day)** 43.5 35.5 18.2 19.9 

Fruit consumption (g/kg/day)†† <1 year 3–5 years 12–19 years 40–69 years U.S. Environmental 

Citrus fruits 1.9 2.6 1.1 0.9 Protection Agency 

Other fruits (including apples) 12.9 5.8 1.1 1.3 (1997a) 

Apples 5.0 3.0 0.4 0.4 

Soil ingestion (mg/day)‡‡ – 5,000§§ – Adult U.S. Environmental 

Pica child – 2.5 years – – Protection Agency 

Outdoor – 50 – 20¶¶ (1997b) 

Indoor – 60 – 0.4 

Differences in gastrointestinal 0–2 years 2–6 years – Adult U.S. Environmental 

absorption of lead 42%–53% 30%–40% – 7%–15% Protection Agency 

6–7 years (1997c) 

18%–24% 

Adapted from Selevan et al. (2000). 

*

Square meters per kilogram. 

†

Milliliters per kilogram per breath. 

‡

Per square meter.
 §

Breaths per minute.
 ¶

Milliliters per kilogram body weight per square meter lung surface area per minute.
 **Milliliters per kilogram per day.
 ††Grams per kilogram per day. 

‡‡Milligrams per day. 

§§ATSDR (2001a). 

¶¶Gardening for adults. 

61 
Pediatric Environmental Health 

Table 4. Sources of Common Environmental Hazards 

Hazards Outdoor Furnishings Occupant 

and Routes Air and Building and Mechanical Activities/ 

of Exposure* Soil Structure Finishings Systems Source Tap Water Food 

Asbestos Hazardous waste Sprayed-on Ceiling and Gaskets Selected Asbestos —

 (R, D, O) sites fireproofing floor tiles Pipe and consumer cement 

Abrasion of Roofing Textured wall furnace products water pipes 

brake linings and siding and ceiling insulation Take-home 

Building Thermal finishing occupational 

demolition insulation exposures 

Biologic Local flora Wet insulation Carpet Humidifiers Communicable Contamination Contamination

 (R, O) Molds Wet carpet Fleecy Condensate occupational at source, at source, 

Animal Wet wallboard furnishings pans in air infections distribution transportation, 

droppings Bedding conditioners Respiratory system, tap, processing, 

Insects (All worse and droplet storage storage, 

Microorganisms when damp) refrigerators Body fluids containers preparation 

Composting Moist, dirty 

ductwork 

Combustion Combustion House fires House fires Malfunctioning Tobacco — —

 products engines and poorly smoking

 (R) Incinerators vented Environmental 

Forest fires heating and tobacco smoke 

Residential cooking 

and industrial devices 

furnaces 

Lead Hazardous waste Lead plumbing Lead paint — Hobbies Water service Imported

 (O, R) Industrial effluent fixtures and Folk remedies mains, canned food 

Exterior paint solder Remodeling plumbing Pottery glazes 

Demolition and Consumer before 1978 

sandblasting products 

Lead pipes Take-home 

occupational 

exposures 

Mercury Hazardous waste Old household Thermometers, Take-home — — —

 (R) Industrial emissions paints before thermostats, occupational 

Food source (fish) mercury ban and medical agents 

Industrial or instruments Folk remedies 

marine paints Hobbies 

Pesticides Spray drift from Treated Carpets Contaminated Consumer Ground and Residues from

 (O, D) foundation building Wall coverings ductwork products, surface water agricultural 

exterminations materials Shower curtains Biocides in including contami­ applications 

Lawn and Paints humidifiers aerosols, nation from Bioconcenagricultural residue and air shampoos, agricultural trated 

Hazardous waste conditioners pet collars, and lawn persistent 

hanging strips, chemicals organorepellents chlorines 

Take-home in fish, meat, 

occupational and cow’s and 

exposures breast milk 

Continued on page 63 

62 
Pediatric Environmental Health 

Table 4. Sources of Common Indoor Environmental Hazards (Continued from page 62) 

Hazards Outdoor Furnishings Occupant 

and Routes Air and Building and Mechanical Activities/ 

of Exposure Soil Structure Finishings Systems Source Tap Water Food 

Polychlorinated — — — — — — Bioconcenor brominated trated in food

 biphenyls chain, 

including 

breast milk 

Occupational 

exposures 

leading to 

breast milk 

contamination 

Radon Soil Stone — — — Well —

 (R) Well water Brick 

Natural gas Cement block 

Respirable Wind-blown soil Demolition Fleecy Poorly Tobacco smoke — —

 particulates Industrial of wall and furnishings, ventilated and Remodeling

 (R) emissions internal including malfunctioning Hobbies 

Fossil fuel structures shag carpets, heating and Cleaning 

combustion upholstered cooling 

Forest and furniture devices 

brush fires Humidifiers 

Volcanic eruptions Degrading 

fiberglass 

ductwork 

Volatile Underground Composition Spackling Fugitive fossil Use and Hazardous Breast milk

 organic storage tanks board compound fuel emissions storage of waste contaminated

 compounds Hazardous Urea Paints and Office machines consumer Leaking as the result

 (R, O, D) waste formaldehyde other surface Lubricants products underground of occupant 

Industrial insulation coatings Duct sealants Cosmetics storage activites 

emissions Adhesives Cabinetry and cleaners Hobbies tanks 

Tap water Caulks Furniture Tobacco smoke 

pollution Additives to Carpets Human 

Inadequately fiberglass Plastics metabolism 

aired dry cleaning insulation 

Plastics 

*R: respiratory; D: dermal; O: oral. Routes of exposure are listed for each contaminant in the usual order of importance. 

63 
 

 

Pediatric Environmental Health 

Table 5. Basic Environmental Database 

Name: Date Completed:
 

Address of this home:
 

Date moved in:
 

Parents and other adults in the home:
 

Current jobs of occupants (including how long in job): 

1.	 Do you think you or a family member have a health problem caused by your home environment? 

_____ Yes _____ No 

2.	 Building type: 

_____ Single-family, detached _____ Single-family, condo 

_____ Mobile home _____ Multifamily 

3.	 Features: Single story _____ Multistory _____ Attached garage 

4.	 Lowest level of home: 

_____ On-grade level _____ Below-grade basement _____ Crawl space 

_____ Dirt floor _____ Finished floor (material: ) 

5.	 Ownership: _____ Self _____ Other family member _____ Tenant 

6.	 Year built:________ 

Location: 

_____ Industrial or agricultural pollution sources nearby (<1 mile) _____ Municipal landfills 

_____ Commercial orchards, fields _____ Livestock _____ Underground tanks 

_____ Hazardous waste site _____ Industry or business 

7.	 Does anyone living in the household smoke tobacco products? Yes No 

If yes, how many smokers at home? 

Is there a child in your family exposed to smoke at day care or in cars? Yes No 

8.	 Have there been renovations, interior decorating, or new furniture in the home in the last 3 years? 

Yes _____ No_____ 

If yes, please describe: 

64 

Continued on page 65 
 

 

 

 

 

Pediatric Environmental Health 

Table 5. Basic Environmental Database (Continued from page 64) 

9. How do you heat your home? 

a. Primary energy source: 

_____ Oil _____ Natural gas _____ Propane Coal 

_____ Wood _____ Electric heat pump _____ Solar 

b. Distribution of heat: 

_____ Forced air _____ Steam _____ Hot water Radiant 

c. Do you use another heat source? Yes No 

d. Secondary energy source(s): 

_____ Oil Natural gas _____ Propane Coal 

_____ Wood Electric Heat pump Solar 

_____ Kerosene 

e. Location of secondary heat source: __________ 

f. If this heat source burns fuel, is it vented outdoors? Yes No 

g. If you use a wood stove or fireplace, how often do you use it? 

_____ Rarely Every week of winter Every day of winter 

10. Do you have any of the following equipment or appliances? 

Air filter (Describe ) 

Humidifier (Describe ) 

Air conditioner (Describe ) 

Gas appliances: Kitchen stove Hot water heater Dryer 

11. Do you or a family member have a hobby or home business that might involve 

_____ biologic agents _____ chemicals _____ dusts _____ fibers _____ fumes 

_____ radiation _____ loud noise _____ vibration _____ metals _____ paints 

_____ extreme heat or cold 

For those that apply, please list and/or describe the hobby: 

12. Is any part of your home damp or have you had a major leak or flood in your house? 

Yes No
 

If yes, please describe
 

13. Have any pesticides or herbicides been used in or around your home within the last year (including on pets)? 

Yes No
 

If yes, please describe
 

Continued on page 66 

65 
 

 

 

 

 

 

 

 

 

Pediatric Environmental Health 

Table 5. Basic Environmental Database (Continued from page 65) 

14. Have you ever tested your home for radon? Yes No 

If yes, in which season of the year did you test your home?

 Spring Summer Fall Winter 

In which part of your home did you conduct the test? 

What was the length of test? 

What levels of radon, if any, were found? 

Have any radon reduction measures been taken? Yes No 

If yes, please describe 

If radon reduction measures have been taken, have the levels been rechecked? 

Yes No 

If yes, were the radon levels reduced? 

Yes No 

15. Where do you get your water supply?

 Bottled Municipal

If you get your water from a well, was the well 

When was the well last tested for contaminants? 

Private well

 dug or 

or spring 

 drilled? 

What were the results? 

16. Do you use a water treatment device in your well (e.g., filter or softener)? 

Yes No
 

If yes, please describe
 

17. Do you have a septic system or do you use municipal sewers? 

If you use a septic system, when was the tank last pumped? 

18. Does any member of the household work at a job that might result in bringing chemicals home on his or her

 clothes or shoes? Yes No 

If yes, please describe 

19. Have industrial chemicals been brought home from the workplace for domestic use? 

Yes No
 

If yes, please describe
 

66 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Pediatric Environmental Health 

Table 6. Environmental Hazards Checklist for Home Assessment* 

Family Name 

Address 

Housing 

Type of Housing? Ownership? 

How old? Rental 

Condition? Owner-occupied

 Public housing 

Renovation/repairs occurring? 

Existing rodents/insects? 

Existence of molds/fungi? 

What source of drinking water?

Yes

Yes

Yes

 Describe: 

 No 

 No 

 No 

Describe: 

Describe: 

Describe: 

Heating Source 

Uses gas stoves/ovens for heating? 

Adequate ventilation? 

Uses fireplaces/woodburning stoves? 

Wood smell indoors? 

Yes

Yes

Yes

Yes

 No 

No 

 No 

No

What is burned? 

Evidence of smoke/soot? 

Uses kerosene heaters? 

Yes

Yes

 No 

No 

Environmental Tobacco Smoke 

Household members smoke? Yes No 

Regular visitors smoke? Yes

Smoking allowed in car? Yes

IndoorAir Pollution—Formaldehyde and Asbestos 

No 

No 

Sources of formaldehyde? Yes

 (particle board, urea in foam insulation, other) 

Potential asbestos hazards? Yes

 No 

 No 

Describe:

Describe:

 (friable pipe/boiler insulation, old vinyl linoleum, wall board repair, home renovation or repairs) 

Continued on page 68 

67 
 

 

 

 

 

 

 

 

 

 

Pediatric Environmental Health 

Table 6. Environmental Hazards Checklist for Home Assessment (Continued from page 67) 

Air Pollution—Toxic Organic Hydrocarbons 

Uses cleaners/polishers/air fresheners/disinfectants Yes No 

Uses glues/solvents/varnishes/building materials? Yes No 

Where are these materials stored? 

Pest/Mold/Fungi Control 

Home garden Yes No 

Use of pesticides outdoors Yes No 

Evidence of rodents/insects Yes No 

Use of pesticides indoors? Yes No 

Use of pesticides on children? Yes No What type? 

Use of pesticides on pets? Yes No What type? 

Is re-entry after pesticide use according to instructions? Yes No 

Evidence of molds/fungi? Yes No 

*Adapted from Balk et al. (1999). 

68 
Pediatric Environmental Health 

Appendix B: Important Issues Regarding 

Mercury 

Direct Biologic Indicators and Treatment—Elemental Mercury 

Urine mercury levels might be reported in different units of measure (e.g., micrograms per gram creatinine and 

micrograms per liter) that are not equivalent. This should be considered when interpreting results in children because 

creatinine levels in children differ by age due to developmental changes. In addition, fluid intake in children differs 

from fluid intake in adults, which can also affect the volume when converting values into different units. Other factors, 

such as chronic illness in both children and adults, might need to be considered when interpreting laboratory results. 

The method used by the laboratory to report values should be known. For example, the National Center for 

Environmental Health (NCEH) laboratory reports values in micrograms per gram creatinine, which is adjusted per 

sample by direct urine creatinine measurement. NCEH considers direct creatinine adjustment of urine mercury 

values imperative for proper interpretation. Age-specific reference ranges for urine volume and urine creatinine 

excretion are published if a conversion between the two units of measure is necessary (Behrman et al. 1996). 

However, interpretation should be done in consultation with a specialist who has experience managing cases of 

childhood mercury poisoning. 

Treatment Considerations 

For children exposed to mercury, no current standard medical guideline exists for treatment on the basis of mercury 

urine levels and clinical signs and symptoms. For this reason, the interpretation of laboratory values for urine mercury 

and choice of treatment regimen, if necessary, should be determined in consultation with a specialist in pediatric 

environmental medicine who has experience managing patients with mercury poisoning. In situations where a 

24-hour urine mercury specimen is not easily attainable for a young child, such as in an outpatient clinic setting, a 

spot mercury level can be obtained for screening purposes. It is important to remember, however, that for this type 

of sample, the units of measure used in the reporting of laboratory results and the methods of adjustment for the 

concentration of the urine (e.g., using specific gravity versus amount of creatinine present) are not standardized 

across laboratories and, therefore, this should be considered when interpreting reported laboratory values. 

Treatment 

Removal from exposure is the first step, followed by an assessment of the child’s clinical condition to ensure that the 

patient is stable. Chelation has been used to reduce body burden of elemental mercury, although whether it reduces 

toxic effects or speeds recovery in mercury-poisoned children remains unclear (Fullilove 2001). Chelation should 

only be used for symptomatic patients with known mercury exposure, and only after consideration of the risk and 

benefits by a specialist experienced in the use of chelators and in consultation with the patient or family. Mercury 

poisoning should be treated in consultation with experts in the field of environmental toxicology and pediatricians 

who have experience in management of children with this exposure. 

Succimer, which has been used as an oral chelating agent in the treatment of lead poisoning, also increases urinary 

mercury excretion. However, its efficacy and long-term benefits are uncertain, thus classifying this treatment mode as 

experimental. Adverse side effects from succimer include abdominal distress, transient rash, increased liver function, 

and neutropenia. Other agents available for treatment, but not yet approved in the United States, might be more 

efficacious at removing mercury (e.g., 2,3-dimercaptopropan-1-sulfonate). Ethylenediamine tetra-acetate and 

69 
Pediatric Environmental Health 

penicillamine are not very effective for mercury. When treating a patient with similar symptoms, consult with a 

pediatric toxicologist at your local poison control center or at a Pediatric Environmental Health Specialty Unit 

(Appendix D, page 74). 

Different Forms of Mercury and Differing Health Effects 

Mercury occurs naturally in the environment and exists in several forms, which can be organized under three 

headings: metallic mercury (i.e., elemental mercury—Hg0

, quicksilver), inorganic mercury (i.e., Hg+1 [mercurous 

salts] or Hg+2 [mercuric salts]), and organic mercury (i.e., methyl-, ethyl-, and phenylmercury). Because mercury’s 

absorption and metabolism depend on its chemical and physical form, it is important to determine the form of 

mercury to which an individual is exposed. Different forms of mercury can have differing health effects (e.g., 

absorption and metabolism of different forms of mercury vary and, therefore, have different effects on the nervous 

system). When metallic mercury vapors are inhaled, they readily enter the bloodstream and cross the blood-brain 

barrier. Inhaling or ingesting large amounts of methylmercury also results in some of the mercury crossing the bloodbrain barrier and affecting the nervous system. Inorganic mercury salts, such as mercuric chloride, do not cross the 

blood-brain barrier like methylmercury or metallic mercury vapor do. Mercury affects other systems in addition to 

the nervous system (ATSDR 1999, 1992). 

Dental Amalgams 

The ATSDR Toxicological Profile for Mercury (ATSDR 1999) states that 

One way in which people are routinely exposed to extremely small amounts of mercury is through the 

gradual (but extremely slow) wearing-away process of dental amalgam fillings, which contain 

approximately 50% mercury. The amount of mercury to which a person might be exposed from dental 

amalgams would depend on the number of amalgams present as well as other factors. The Centers for 

Disease Control and Prevention (CDC) has determined that dental amalgam fillings do not pose a health 

risk, although they do account for some mercury exposure in those having such fillings. People who 

frequently grind their teeth or often chew gum can add to the small amount of mercury normally released 

from those fillings over time.... The practice of having all your dental amalgam fillings replaced with 

nonmercury filling materials just to remove the possibility of mercury exposure is not recommended by 

ATSDR. In fact, the removal of the mercury amalgam fillings would actually expose the patient to a 

greater amount of mercury, at least for a while. There are other sources of mercury that may increase your 

overall exposure, such as the amount of fish consumed per week or an exposure to mercury from a 

nearby hazardous waste site or incinerator. 

Thimerosal 

Since the 1930s, some, but not all, of the vaccines routinely recommended for children have contained small 

amounts of thimerosal, a mercury-containing preservative. In July 1999, the U.S. government asked vaccine 

manufacturers to eliminate or reduce, as expeditiously as possible, the mercury content of their vaccines to avoid any 

possibility of infants who receive vaccines being exposed to more mercury than is recommended by federal 

guidelines. For additional information, see Mercury and Vaccines (Thimerosal) (CDC 2001), Thimerosal in 

Vaccines: An Interim Report to Clinicians (American Academy of Pediatrics 1999), and Goldman et al. (2001). 

70 
Pediatric Environmental Health 

Fish Consumption 

For those populations that rely on local fish for a major portion of their diet, a complete exposure history should 

include questions exploring subsistence fishing as a possible source of mercury exposure. Bioaccumulation occurs 

when mercury in lake and stream sediments is converted by bacteria into organic mercury compounds that 

accumulate in the food chain. Physicians living in active fishing areas with fish advisories related to mercury should 

ask women and children if their consumption of fish is in accordance with state-issued fish advisories. In general, 

freshwater fish have higher levels of contaminants than saltwater fish, but not always. Increased methylmercury 

content has been found in the larger ocean fish (e.g., tuna, swordfish, and shark) because of naturally occurring and 

manmade sources of mercury pollution. In the 1950s, when pregnant women in Minimata Bay, Japan, ingested fish 

with high levels of methylmercury, the result was at least 30 cases of infantile cerebral palsy (Klaassen 1996). As 

listed in the Handbook of Pediatric Environmental Health (Etzel and Balk 1999), to reduce hazards from fish 

consumption, individuals can be counseled to eat nonpredator fish rather than predator fish (e.g., shark, swordfish, 

and tuna); to eat small rather than large game fish; and to eat fewer fatty fish (e.g., carp, catfish, and lake trout), 

which accumulate higher levels of chemical toxicants. Emphasize to women of childbearing age, pregnant women, 

nursing mothers, and parents of young children the need to follow fish advisory guidelines. Fish advisories can be 

obtained from state health, environmental, and conservation departments (ATSDR 1999, 1992; EPA and ATSDR 

2001). 

71 
Pediatric Environmental Health 

Appendix C: Summary of Questions for an 

Environmental History 

Issue: The child’s home, school, or day-care center might expose him or her to potential toxicants. 

Do you live in an apartment, house, or mobile home? 

On what level of your dwelling is the child’s room located? 

What are the age and condition of your home? 

How is your home heated? 

Do you have a fireplace or a wood stove? 

Do you use pesticides inside or outside your home (including use on children and pets)? 

What are the hobbies of your child and other family members? 

Is your home (day-care center, etc.) near a polluted body of water, industrial plant, commercial business, 

or dump site? 

Issue: Family members’ jobs might involve exposure to contaminants. 

What is your occupation? 

What is your spouse’s occupation? 

Do other members of the family have jobs? 

If so, what are they? 

For teenagers:
 

Do you work?
 

What kind of job do you have and what hours do you work?
 

Issue: The child might be exposed to tobacco smoke. 

Do you smoke tobacco products?
 

If yes, do you smoke in your home?
 

Does your spouse, other family member, or babysitter smoke? 

If you take your child to a babysitter, does he or she smoke at home? 

Do visitors smoke in your home? 

Does anyone smoke in your car? 

Continued on page 73 

72 
Pediatric Environmental Health 

Continued from page 72 

Issue: The child might eat food contaminated with environmental toxicants. 

For breastfeeding mothers:
 

Have you tested your water supply for lead?
 

If not and you make the baby’s formula with tap water, what procedure do you follow?
 

Do you ever use hot tap water or water from instant hot taps or refrigerator taps to make the formula?
 

Do you wash fruits and vegetables before giving them to your child?
 

What do you wash them with?
 

What kind of produce do you usually buy? Organic? Local? In season?
 

Does the child live with an adult whose job or hobby involves exposure to lead? 

Issue: The child might be at high risk for lead poisoning. 

Is there a brother, sister, housemate, or playmate being followed or treated for lead poisoning (i.e., blood lead 

15 μg/dL)? 

Does the child live with an adult whose job or hobby involves exposure to lead? 

Does the child live near an active lead smelter, battery recycling plant, or other industry likely to release lead? 

Do you use home remedies or pottery from another country? 

Adapted from Balk (1996). 

When To Introduce Environmental Questions 

Topics The Right Time 

Home renovation, smoking, breast and bottle issues Prenatal period 

Environmental tobacco smoke When child is 2 months old 

Poison exposures, including household pesticides and lead poisoning When child is 6 months old 

Arts-and-crafts exposures Preschool period 

Occupational exposures, exposures from hobbies When patient is a teenager 

Lawn and garden products, lawn services, scheduled chemical applications Spring and summer 

Wood stoves and fireplaces, gas stoves Fall and winter 

73 
Pediatric Environmental Health 

Appendix D: Environmental Health 

Concerns: Resources and Sources 

of Information 

General Resources 

General Resources for Parents and Caregivers 

General Resources for Clinicians 

Consultation Sources 

Government Agencies 

Association of Occupational and Environmental Clinics 

Pediatric Environmental Health Specialty Units 

National Institute for Occupational Safety and Health’s Education and Research Center Grants 

American Association of Poison Control Centers 

State and Local Health Departments 

74 
Pediatric Environmental Health 

General Resources 

General Resources for Parents and Caregivers 

Agency for Toxic Substances and Disease Registry. 2002. Child health web page. Atlanta: US Department of 

Health and Human Services. Available from: URL: www.atsdr.cdc.gov/child/ochchildhlth.html. 

Children’s Environmental Health Network. 2000. The household detective primer: how to protect your children 

from toxins in the home. Princeton (NJ): Children’s Environmental Health Network. Available from: URL: 

www.cehn.org. 

Needleman HL, Landrigan PJ. 1994. Raising children toxic free: how to keep your child safe from lead, asbestos, 

pesticides, and other environmental hazards. New York: Farrar, Straus and Giroux. 

Schoemaker JM, Vitale CY. 1991. Healthy homes, healthy kids—protecting your children from everyday 

environmental hazards. Washington (DC): Island Press. 

Upton AC, Graber E. 1993. Staying healthy in a risky environment: the New York University Medical Center 

family guide. New York: Simon & Schuster. 

General Resources for Clinicians 

Children’s Environmental Health Network. 1997. Resource guide on children’s environmental health. Washington 

(DC): Children’s Environmental Health Network. 

Goldman R, Shannon M, Woolf A. 1999. Pediatric environmental health history [on CD-ROM]. Boston: Pediatric 

Environmental Health Unit Cambridge Hospital and Children’s Hospital. 

Textbooks 

Behrman RE, Kliegman RM, Arvin AM, Nelson WE, editors. Nelson textbook of pediatrics, 15th edition. 

Philadelphia: W.B. Saunders Company; 1996. 

Burgess WA. Recognition of health hazards in industries: a review of materials and processes, 2nd edition. New 

York: John Wiley & Sons, Inc.; 1995. Contains work-site analyses that facilitate recognition of health 

problems in design and operation of industrial processes. In addition to identifying health issues, provides 

information on control measures. 

Encyclopedia of occupational health and safety, 3rd edition. International Labor Office/Boyd Printing; 1991. 

Extensive information on all aspects of occupational health and safety, including occupational diseases, 

hazards, prevention, institutions. Two-volume set of more than 3,600 pages. 4th edition, with a CD-ROM 

version, 1997. 

Harris RL. Patty’s Industrial Hygiene and Toxicology, 5th edition. New York: John Wiley & Sons Inc.; 2000. 

Guide to principles and practice of industrial hygiene, hazard evaluation and control, toxic exposures, and 

similar topics. 

Hathaway GJ, Proctor NH, Hughes JP, Fischman ML. Proctor and Hughes’ chemical hazards in the workplace, 

4th edition. New York: John Wiley & Sons; 1996. This is the classic text on more than 500 chemicals that may 

result in workplace exposure. Provides definitive information on effects of exposure and on treatment 

approaches. 

75 
Pediatric Environmental Health 

LaDou J, editor. Occupational and environmental medicine, 2nd edition. Stamford (CT): Appleton & Lange; 1997. 

Manuele FA. On the practice of safety, 2nd edition. New York: John Wiley & Sons; 1997. Discussion of basic 

principles and aspects of safety as an evolving discipline. 

Rogers B. Occupational health nursing—concepts and practice. Philadelphia: W.B. Saunders Co.; 1994. Primary 

reference for occupational health nursing principles and practice. Provides clinical nursing guidelines for 

common occupational health problems. 

Rom WM, editor. Environmental and occupational medicine, 3rd edition. Philadelphia: Lippincott-Raven, 1998. 

Another helpful reference that considers environmental as well as occupational health problems. 

Rosenstock L, Cullen MR, editors. Textbook of clinical occupational and environmental medicine. Philadelphia: 

Saunders, 1994. Useful reference for both environmental and occupational medicine concerns. 

Vincoll J. Basic guide to accident investigation and loss control. New York: John Wiley & Sons; 1994. Provides 

information on safety principles and techniques, including preparation of safety system applications. 

Wald P, Stave G. Physical and biological hazards in the workplace, 2nd edition. New York: John Wiley & Sons; 

2001. Focuses on physical and biological hazard in the workplace and serves as a companion to Proctor and 

Hughes’ Chemical Hazards in the Workplace. Available on CD-ROM. 

Zenz C, Dickerson OB, Horvath EP, editors. Occupational medicine, 3rd edition. St. Louis (MO): Mosby, 1994. 

Information on occupational medicine principles and practice as well as on specific hazards and agents; 

1,336 pages. 

Web and Other Sources 

Abelsohn A, Sanborn M. Environmental health in family medicine. Available at URL: www.ijc.org/boards/hptf/ 

modules/content.html. Set of six full-text modules (lead, outdoor air quality, indoor air quality, pesticides, 

clusters of disease [water quality], and persistent organic pollutants). The modules are based on clinical 

cases that can be used for self-learning, or for teaching residents or practicing physicians. Also available on 

CD-ROM. 

National Library of Medicine’s Medline. Available via NLM’s Health Information Web site at URL: 

www.nlm.nih.gov/hinfo.html. Medline is the National Library of Medicine’s premier bibliographic database 

covering the fields of medicine, nursing, dentistry, veterinary medicine, the health care system, and the 

preclinical sciences. 

TOMES Plus. Available from Micromedix, Inc. 6200 South Syracuse Way, Suite 300, Englewood, CO 80111­

4740 (USA and Canada phone: 1-800-525-9083 or 303-486-6400; International Department phone: +1 303 

486-6444); Web page: www.micromedex.com/products/tomesplus. The TOMES System provides rapid, easy 

access to medical and hazard information needed for managing chemicals safely in the workplace, 

evaluating exposures, quick response to emergency situations, and regulatory compliance. The system 

includes MEDITEXT, medical managements; HAZARDTEXT, hazard managements with initial response 

information; and INFOTEXT, Documents with regulatory listings and other general information. 

76 
Pediatric Environmental Health 

Specific information, such as reports by the Hazard Evaluation and Technical Assistance Branch of the National 

Institute for Occupational Safety and Health, is available through the National Technical Information Service (NTIS) 

database at www.ntis.gov. 

Professional Journals 

Professional journals provide information on research, clinical practice, prevention techniques, new hazards, and 

similar topics. A few examples include the following: 

American Industrial Hygiene Journal, published by the American Industrial Hygiene Association. 

American Journal of Industrial Medicine, published by John Wiley & Sons, Inc. 

Annals of Occupational Hygiene, published by Elsevier Science Publishers. 

Archives of Environmental Health, published by Heldref Publications. 

Environmental Epidemiology and Toxicology, published by Stockton Press. 

Environmental Health Perspectives, published by the National Institute of Environmental Health Sciences. 

International Archives of Occupational and Environmental Health, published by Springer-Verlag. 

Journal of Occupational and Environmental Medicine, published by Williams & Wilkins. 

Journal of Toxicology—Clinical Toxicology, published by Marcel Dekker. 

Occupational and Environmental Medicine (formerly British Journal of Industrial Medicine), published by 

BMJ Publishing Group. 

Scandinavian Journal of Work, Environment and Health, published by the Finnish Institute of Occupational 

Health. 

Professional Organizations 

Web sites for a few professional organizations include the following: 

American Academy of Pediatrics: www.aap.org. 

American Association of Occupational Health Nurses: www.aaohn.org. 

American College of Medical Toxicology (ACMT): www.acmt.net. 

American College of Occupational and Environmental Medicine: www.acoem.org. 

American College of Preventive Medicine: www.acpm.org. 

American Industrial Hygiene Association: www.aiha.org. 

American Society of Safety Engineers: www.asse.org. 

Children’s Environmental Health Network: www.cehn.org. 

Physicians for Social Responsibility: www.psr.org. 

Government Agencies 

Essentially every national agency with health and safety information or activities has an Internet Web site. These sites 

can be found by direct search using the agency’s name or initials. A few examples include 

Agency for Toxic Substances and Disease Registry: www.atsdr.cdc.gov. 

Centers for Disease Control and Prevention: www.cdc.gov. 

National Institute of Environmental Health Sciences: www.niehs.nih.gov. 

National Institute for Occupational Safety and Health: www.cdc.gov/niosh. 

77 
Pediatric Environmental Health 

U.S. Department of Agriculture: www.usda.gov. 

U.S. Department of Housing and Urban Development: www.hud.gov. 

U.S. Environmental Protection Agency: www.epa.gov. 

U.S. Food and Drug Administration: www.fda.gov. 

U.S. Occupational Safety and Health Administration (OSHA): www.osha.gov. 

Consultation Sources 

Government Agencies 

Agency for Toxic Substances and Disease Registry: emergency response line 404-498-0120;
 

1-888-42-ATSDR (1-888-422-8737).
 

Centers for Disease Control and Prevention Hotlines:
 

National AIDS Hotline 1-800-342-2437.
 

National HIV/AIDS Hotline (Spanish) 1-800-344-7432.
 

National Immunization Hotline (English) 1-800-232-2522.
 

National Immunization Hotline (Spanish) 1-800-232-0233.
 

National STD Hotline 1-800-227-8922.
 

SafeUSA Federal Safety 1-888-252-7751.
 

Traveler’s Health 1-877-394-8747.
 

National Institute of Environmental Health Sciences: 919-541-3345. 

National Institute for Occupational Safety and Health: 1-800-35-NIOSH (1-800-356-4674). 

U.S. Environmental Protection Agency (National Response Center for environmental emergencies):
 

1-800-424-8802.
 

U.S. Food and Drug Administration: 1-888-INFO-FDA (1-888-463-6332). 

U.S. Occupational Safety and Health Administration (OSHA): 1-800-321-OSHA (1-800-321-6742) 

TTY 1-877-889-5627. 

Association of Occupational and Environmental Clinics 

The Association of Occupational and Environmental Clinics (AOEC) is a network of more than 60 clinics and more 

than 250 individuals committed to improving the practice of occupational and environmental medicine through 

information sharing and collaborative research. 

The primary goal of AOEC is to facilitate the prevention and treatment of occupational and environmental illnesses 

and injuries through collaborative reporting and investigation of health problems. AOEC members develop 

curriculum materials in occupational and environmental health and provide Education Activities (EA) programs for 

primary care practitioners and others. 

For more information and a listing of AOEC clinics in your area, contact the AOEC office: 

1010 Vermont Avenue, NW #513 

Washington, DC 20005 

Telephone: 202-347-4976 

Fax: 202-347-4950 

Web site: www.aoec.org. 

78 
Pediatric Environmental Health 

Pediatric Environmental Health Specialty Units 

The Pediatric Environmental Health Specialty Units (PEHSUs) are a resource for pediatricians, other health care 

providers, parents, teachers, the general public, and U.S. Environmental Protection Agency (EPA) and ATSDR 

staff members nationwide. PEHSUs provide medical education and training, consultation, and clinical specialty 

referrals. Health care providers can use this resource when responding to suspected clinical presentations, known 

exposures, and in community settings. 

Ten PESHUs are now in operation across the United States; contact information for each unit is listed below. 

Check AOEC’s Web site (www.aoec.org/pesu.htm) for the most up-to-date information on the units. 

Massachusetts: 

Pediatric Environmental Health Center, Children Hospital, Boston 

Telephone: 1-888-Child14 

Web site: www.childrenshospital.org (In the “find” box, enter the key word “environmental”) 

Washington State: 

Pediatric Environmental Health Specialty Unit, Harborview Medical Center, Seattle 

Telephone: 1-887-KID-CHEM (toll-free west of the Mississippi River) or 206-526-2121 

Web site: www.depts.washington.edu/oemp/grants/PEHSU.html 

New York: 

Mt. Sinai Pediatric Environmental Health Unit/Mt. Sinai-Irving J. Selikoff Center for Occupational and 

Environmental Medicine, New York 

Telephone: 212-241-6173 

Web site: www.mssm.edu/cpm/peds_environ.shtml 

Illinois: 

Great Lakes Center for Children’s Environmental Health, Cook County Hospital, Chicago 

Telephone: 1-800-672-3113 (toll-free) or 312-633-5310 

Web site: www.uic.edu/sph/glakes/kids 

Georgia: 

The Southeast Pediatric Environmental Health Specialty Unit at Emory University, Atlanta 

Telephone: 1-877-337-3478 (1-877-33PEHSU) 

Web site: www.sph.emory.edu/PEHSU 

California: 

University of California-San Francisco (UCSF)/University of California-Irvine (UCI) Pediatric 

Environmental Health Specialty Unit 

Telephone: 1-415-206-4320 (for both sites)
 

Web site: www.ucsf.edu/ucpehsu
 

Texas: 

Southwest Center for Pediatric Environmental Health, University of Texas Health Center at Tyler, 

Tyler, Texas 

Telephone: 1-888-901-5665 (toll-free)
 

Web site: research.uthct.edu/swcpeh/
 

79 
Pediatric Environmental Health 

Washington, District of Columbia: 

Mid-Atlantic Center for Children’s Health and the Environment (MACCHE), George Washington 

University, Washington, District of Columbia 

Telephone: 1-866-MACCHE1 (1-866-622-2431)
 

Web site: www.health-e-kids.org
 

Colorado: 

Rocky Mountain Regional Pediatric Environmental Health Specialty Unit, National Jewish Medical and 

Research Center, Denver 

Telephone: 1-877-800-5554 (toll-free) 

Web site: rmrpehsu.org 

Iowa: 

Midwest Regional Pediatric Environmental Health Center, University of Iowa, Iowa City, Iowa 

Telephone: 1-866-697-7342 

Web site: www.uihealthcare.com/depts/pediatricenvironmentalhealth/index.html 

National Institute for Occupational Safety and Health’s Education and Research Center Grants 

The National Institute for Occupational Safety and Health (NIOSH) has established centers throughout the 

United States for learning about occupational safety and health. The Education and Research Centers (ERCs) are in 

33 universities in 14 states. The ERCs conduct training courses on occupational and environmental medicine topics 

(continuing medical education credits available). 

Telephone: 1-800-35-NIOSH (1-800-356-4674)
 

Web site: www.cdc.gov/NIOSH/centers.html.
 

American Association of Poison Control Centers 

Poison control centers were established in 1953 to help physicians and other clinicians deal with poisonings of adults 

and children in the United States. In 1983, the American Association of Poison Control Centers was established as 

the professional organization for poison control centers. The regional poison control centers can act as valuable 

resources in providing information about the toxicity and health effects of hazardous exposures involved in 

poisonings. 

The local poison control center can specify the ingredients of common household products when labels do not 

provide adequate information. 

Each certified poison control center is required to publicize its location and methods of contact. Typically, the 

contact telephone number can be found on the inside front cover of telephone books, where other emergency 

numbers are usually located. 

The main emergency number across the country is 1-800-222-1222, although some states have other contact 

numbers as well as a number for the hearing impaired. For more information, contact the American Association of 

Poison Control Centers: 

American Association of Poison Control Centers 

3201 New Mexico Avenue, Suite 310 For poisoning emergencies, call Washington, DC 20016 1-800-222-1222. AAPCC does not Telephone: (202) 362-7217 manage poison exposure cases. E-mail: aapcc@poison.org 

Web site: www.aapcc.org. 

80 
Pediatric Environmental Health 

State and Local Health Departments 

Both state and local health departments frequently have departments and staff with environmental health expertise. 

In some instances, a separate government agency addresses environmental concerns. In addition to providing 

assistance in evaluating individual patients, these organizations establish mandatory reporting requirements for 

selected environmental exposures or diseases related to environmental exposures. If necessary, department 

members can also help in obtaining assistance from federal agencies, such as the Agency for Toxic Substances and 

Disease Registry (ATSDR), Centers for Disease Control and Prevention (CDC), National Institute for 

Occupational Safety and Health (NIOSH), and Occupational Safety and Health Administration (OSHA). State 

health departments or the federal ATSDR both maintain inventory lists of chemicals at hazardous waste sites. 

EPA and state health departments maintain the Toxic Release Inventory (TRI), which lists the amount of hazardous 

chemicals released by industry into the atmosphere at levels above the allowable threshold amount. These 

organizations can also help elucidate the history of former industrial or agricultural properties converted to 

residential use. 

81 
Pediatric Environmental Health 

Appendix E: Lead Screening 

The 1997 revised Centers for Disease Control and Prevention (CDC) guidelines are based on blood lead and 

housing age data (CDC 1997). 

Universal screening is still the policy for communities with inadequate data on the prevalence of elevated blood 

lead level (BLL) and in communities with >27% of the housing built before 1950. 

Targeted screening is recommended in communities where <12% of children have BLLs 10 micrograms per 

deciliter (μg/dL) or where 27% of houses were built before 1950. This recommendation is based on an analysis 

suggesting that the benefits of universal screening outweigh the cost only when the prevalence of elevated BLLs is in 

the range of 11% to 14% or higher. 

Other candidates to be considered for target screening include children 

1 to 2 years of age living in housing built before 1950 in an area not designated for universal screening 

(especially if the housing is not well maintained) 

of ethnic or racial minority groups who might be exposed to lead-containing folk remedies 

who have emigrated (or been adopted) from countries where lead poisoning is prevalent 

with iron deficiency 

exposed to contaminated dust or soil 

with developmental delay whose oral behaviors place them at significant risk for lead exposure 

who are victims of abuse or neglect 

whose parents are exposed to lead (vocationally, avocationally, or during home renovation) 

of low-income families who receive government assistance (Supplemental Feeding Program for Women, 

Infants, and children; Supplemental Security Income; welfare; Medicaid [note that blood lead screening for 

children on Medicaid is required by Federal law]; or subsidized child care). 

According to CDC, children who receive government assistance and who live in areas where targeted screening is 

recommended do not require screening if they are at low risk based on the screening questionnaire (CDC 1997, 

section 5.2.3, p. 62) and if <12% of the children in that community have BLLs 10 μg/dL. 

In addition to screening of children on the basis of risk questionnaires, screening for lead exposure should be 

considered in the differential diagnosis of children with unexplained illness such as severe anemia, seizures, lethargy, 

and abdominal pain. 

82 
Pediatric Environmental Health 

Appendix F: Additional Information for 

Performing a Comprehensive Pediatric 

Environmental Medical Evaluation 

Even though more detailed information regarding environmental history, environmental monitoring, biologic 

monitoring, risk communication, and risk assessment goes beyond what a primary health care provider will 

realistically know and do in the midst of a busy practice setting, this information is provided to help with 

understanding the role of others and communication with others (e.g., staff at the state or local health department, at 

the poison control center, at ATSDR, at the Association of Occupational and Environmental Clinics’ Pediatric 

Environmental Health Specialty Units [PEHSUs], and experts at other organizations). It also gives a better 

understanding of what is involved in doing a comprehensive pediatric environmental medical evaluation. 

Exposure History 

The exposure history provides rough-estimate information about dose; the information rarely reflects the accurate 

quantitative value. Although the beliefs and concerns of the person providing the history can sometimes skew 

estimates of exposure, the interview usually successfully frames the boundaries of likely exposures. Reference to the 

scientific literature or the experience of specialists, such as industrial hygienists, might also provide reasonable 

estimates of dose based on monitoring done in similar situations. For example, knowing that a child lives in a house 

built in 1940 and that throughout the first 3 years of his life his father actively scraped, sanded, and repainted interior 

wood trim vividly points to potentially substantial lead exposure of the child. Similarly, if a father brings a pound of 

mercury home from work as a toy for his children, and it is known that this mercury spilled on a shag rug, an 

industrial hygienist can roughly predict the mercury air concentrations. This exposure information points the child 

health care provider directly to the appropriate biologic tests to measure the absorbed dose. 

Environmental Monitoring 

Environmental monitoring sharpens exposure estimates when the history is vague, when biologic tests of absorbed 

dose are not available, and when the effectiveness of environmental mitigation activities is being assessed. 

Monitoring allows a measurement of a contaminant’s concentration in a medium (e.g., air, soil, water, or food). 

Some tests might serve as indicators of exposure to other agents of concern. For example, water might be tested for 

coliforms as an index of exposure to other pathogenic fecal contaminants. Alternatively, monitoring might focus 

directly on the substances of concern, such as lead concentration in paint. As with any laboratory test, the physician, 

with the help of those with special expertise (e.g., environmental medicine doctors and toxicologists), should be able 

to interpret measures of environmental contaminants with knowledge of the potential for misleading results. When 

doing environmental monitoring, consider the following basic considerations: 

Laboratory certification to perform the test. (NOTE: Both EPA and OSHA certify laboratories for specific 

contaminants. Contact the environmental division of your health department for further information.) 

Qualifications of the person performing the sampling. (Incorrect field techniques can invalidate the results.) 

Appropriateness of the test. (The child health care provider needs to have some idea of the chemical for which 

the test is being done [e.g., using a test to check for carbamate pesticide on a wipe sample in a house is 

meaningless if the pesticide used was a pyrethrin].) 

83 
Pediatric Environmental Health 

Inclusion of typical and worst-case exposure scenarios in the sampling. (A first-flush sample of tap water from 

lead pipes will contain higher amounts of lead than a sample taken after the tap has run for 60 seconds. Air 

monitoring done 1 month after a fuel oil spill in a basement will not accurately reflect the potential for exposure 

during the first few days after the spill.) 

Relevance of location of sample to the exposure area. (An elevated radon level in a crawl space might have little 

health significance as long as the radon level in the living area is low.) 

Level of concentration: average or peak. (Peak exposures to mold spores are more significant as a sensitizer 

than cumulative, average exposures.) 

Using the monitoring results plus certain estimates (e.g., how much air children of a specific age breathe in a minute 

or how much soil they might ingest in a day), risk assessors in government agencies, including state health 

departments, can assist the child health care provider calculate dose estimates. 

Biologic Monitoring 

Biologic monitoring gets closest to the ultimate question of internal dose estimation: Has this patient absorbed 

sufficient amounts of a toxicant to cause harm? Knowledge of the metabolism, distribution, and excretion of a 

toxicant dictates the appropriate time and biologic fluid or tissue sample to obtain for testing. Most commonly, blood 

components and urine are tested. Biologic testing might do the following: 

Directly measure a toxicant such as blood lead or urine mercury. 

Measure a metabolite of a toxicant, such as urine hippuric acid, as an indicator of toluene absorption. 

Measure an effect of the interaction of a toxicant with the host’s biochemistry, such as carboxyhemoglobin as a 

measure of carbon monoxide exposure. 

Indirectly measure the absorption of a toxicant by assessing the toxicity of a body fluid, such as testing 

carcinogen absorption in the urine. This is done with the Ames test, which detects compounds that are 

mutagenic. The test uses a strain of Salmonella that is auxotrophic for histidine (i.e., it cannot grow on a 

minimal media without added histidine). 

Measure effects on target organs, such as elevated liver enzymes in a child exposed to a hepatotoxin. [NOTE: To 

avoid incorrect conclusions, the physician must interpret biologic tests with attention to the toxicokinetics of the 

specific contaminant of concern, particularly the half-life and distribution of the toxicant into different body 

partitions, such as bone, fat, and blood. For example, a plasma acetylcholinesterase level reflects 

organophosphate exposures within the last few days, whereas a red blood cell acetylcholinesterase level might 

indicate exposures dating back several months.] 

• Characterize the significance of exposure. 

In the final phase of the evaluation, the clinician decides whether the identified environmental exposures are related to 

the presenting illness or are likely to cause a future health problem. 

84 
•

Pediatric Environmental Health 

Final Steps 

After a careful physical examination of the child, a conclusion is reached by answering several questions. 

For the well, but exposed child and/or worried parent: 

Have the identified environmental exposures been associated with health effects in people? If so, how 

convincingly?
 

How does the dose compare with known dose-response relationships?
 

What are existing exposure standards? Note that occupational standards should not be considered protective 

of children. Whenever possible, environmental standards should be used as benchmarks. 

If standards do not exist, is there any available published information on human exposures? 

If no relevant human data exist, but animal data suggest a risk, consultation with a toxicologist or pediatric 

environmental medicine specialist should be obtained. 

What factors might increase or decrease the patient’s susceptibility? 

What other community or home exposures might contribute to an adverse health effect? 

For the sick child: 

How specifically can the medical problem be defined? 

Have any environmental factors been associated with the problem in others? If so, how convincingly? 

Could the identified hazards cause this problem? 

Has the dose been sufficient to result in an illness? 

Does the temporal relationship of exposure make sense? 

How does an environmental contribution to the problem compare in overall likelihood to other etiologies under 

consideration? 

Rarely will a child health care provider have sufficient data or time, or the expertise, to conclude an environmental 

medical assessment with certainty. Rather, the data will usually permit only an estimate ( 0.5 or 50% chance) of the 

likelihood (risk) of a future illness or the probability of a causal connection to an existing disease. 

NOTE: Hill (1965) defined five criteria that should be fulfilled to establish a causal relationship. These five criteria 

have been generally adopted as a test of causation. The criteria are 

1. consistency of the association (i.e., different studies resulted in the same association); 

2. strength of the association (i.e., size of the relative risk found increased if dose response can be established); 

3.	 specificity of the association (i.e., measurability of the degree to which one particular exposure produces a 

specific disease); 

4.	 temporal relationship of the association (i.e., exposure to the factor must have preceded development of the 

disease); and 

5. coherence of the association (i.e., biologic plausibility). 

Risk estimates can range from negligible (a lifetime excess cancer risk of 1 in 106

) to levels of public health concern. 

In most forensic settings, the expression “more probable than not” ( 0.5 or 50% chance) describes the 

appropriate standard for decision-making. In most public policy decision-making, environmental agencies aim to 

85 
Pediatric Environmental Health 

reduce risks to negligible levels. Doses relevant to risk assessments are expressed in milligrams/kilograms/day based 

on age/weight and physiologic differences. 

In the exam room, no single probability threshold exists for 

recommending intervention. The more certain the hazard is as 

associated with an exposure, the stronger the indication for 

action. The clinician must consider the probability of adverse 

effects, as well as what interventions are available and their 

benefits. 

On the basis of personal, social, and economic considerations, 

the risks that families consider acceptable vary. EPA has told the 

public that radon causes lung cancer, yet only a small percentage 

of people have measured and remediated radon problems in their 

homes. The clinician’s responsibility is to blend knowledge of the 

medical significance of environmental exposure with an 

understanding of the other factors that families consider when 

deciding to take action. 

For example: If a child has acrodynia 

clearly linked to chronic mercury 

contamination at home, removal of the 

child from the home pending remediation 

of the hazard is mandatory. On the other 

hand, the negligible risks of future illness 

from undisturbed, nonfriable asbestos 

insulative pipe covering (i.e., lagging to 

prevent heat loss) in a basement, 

compared to the high costs and difficulty 

of safe removal, point to the wisdom of 

encapsulating and/or leaving the asbestos 

alone. 

86 
Pediatric Environmental Health 

87 
Pediatric Environmental Health 

DEPARTMENT OF HEALTH

 AND HUMAN SERVICES 

Agency for Toxic Substances 

and Disease Registry 

Division of Toxicology and 

Environmental Medicine (MS E-33) 

Atlanta, GA 30341-3717 

Official Business 

Penalty for Private Use $300 

Return Service Requested 

FIRST-CLASS MAIL
 

POSTAGE & FEES
 

PAID
 

PHS/CDC
 

Permit No. G-284
 

88