Kathleen A. Cobb, BSN, RN, Anthony A. Scott, PhD, Victor F ...

10
40 AJN October 2008 Vol. 108, No. 10 http://www.nursingcenter.com When questioned by a nurse about possible sources of lead in her diet and environment, Ms. Lopez said that she ate pieces of Mexican clay pottery purchased from a local market, although she didn’t give a reason for her behavior. This pottery, pieces of which she was carrying in her pocket, was confirmed by city officials to contain high levels of lead. Her nurse and obstetri- cian counseled her to stop eating the pottery, inform- ing her of the risks of lead exposure for herself and her infant’s development. Ms. Lopez’s pregnancy pro- gressed to full term. At the time of delivery, her blood lead level had dropped to 45 micrograms per deciliter. W hen Maria Lopez (not her real name), a 28-year-old Mexican American woman in week 37 of her first preg- nancy, was given a blood lead test as part of a voluntary research pro- gram at her Texas clinic, results showed that her blood lead level was greater than 60 micrograms per deciliter. Although anemia had been identified earlier in her pregnancy, Ms. Lopez had experienced no other symptoms usually associated with lead poisoning, such as fatigue, dizziness, headache, nau- sea, or vomiting. Lead Hazards for Pregnant Women and Children: Part 1 By Lisa M. Cleveland, MN, RN, CPNP, IBCLC, Monica L. Minter, MS, Kathleen A. Cobb, BSN, RN, Anthony A. Scott, PhD, Victor F. German, MD, PhD Overview: Poor, urban, and immigrant populations are at far greater risk for lead exposure than are other groups in the United States. Children with even slightly elevated blood lead levels are at increased risk for significant neurobehavioral problems that can extend through adolescence. Research has shown that elevated blood lead levels in pregnant women, even those well below 10 micrograms per deciliter—the Centers for Disease Control and Prevention’s “level of concern”—can cause miscar- riage, premature birth, low birth weight, and subsequent developmental delays in their children. Despite these well-established dangers, routine prenatal lead screening and lead education is not a standard of care. Part 1 of this two-part article presents a short case example of a pregnant mother with lead poison- ing and describes the epidemiology of lead exposure in the United States, the main sources of lead exposure, and the effects of lead on the pregnant mother and the developing fetus and child. Prevention is crucial. Treatment options such as chelation must be used selectively and will not reverse damage once it’s occurred. Part 2 will describe recommendations for screening, education, nutrition, reducing environmental exposures, and treatment. Immigrants and the poor shoulder most of the burden of lead exposure in this country. Part 1 of a two-part article details how exposure happens, whom it affects, and the harm it can do. Continuing Education HOURS 2.5

Transcript of Kathleen A. Cobb, BSN, RN, Anthony A. Scott, PhD, Victor F ...

40 AJN t October 2008 t Vol. 108, No. 10 http://www.nursingcenter.com

When questioned by a nurse about possible sourcesof lead in her diet and environment, Ms. Lopez saidthat she ate pieces of Mexican clay pottery purchasedfrom a local market, although she didn’t give a reasonfor her behavior. This pottery, pieces of which she wascarrying in her pocket, was confirmed by city officialsto contain high levels of lead. Her nurse and obstetri-cian counseled her to stop eating the pottery, inform-ing her of the risks of lead exposure for herself andher infant’s development. Ms. Lopez’s pregnancy pro-gressed to full term. At the time of delivery, her bloodlead level had dropped to 45 micrograms per deciliter.

When Maria Lopez (not her real name),a 28-year-old Mexican Americanwoman in week 37 of her first preg-nancy, was given a blood lead test as part of a voluntary research pro-

gram at her Texas clinic, results showed that herblood lead level was greater than 60 microgramsper deciliter. Although anemia had been identifiedearlier in her pregnancy, Ms. Lopez had experiencedno other symptoms usually associated with leadpoisoning, such as fatigue, dizziness, headache, nau-sea, or vomiting.

Lead Hazards forPregnant Womenand Children: Part 1

By Lisa M. Cleveland, MN, RN, CPNP, IBCLC, Monica L. Minter, MS,Kathleen A. Cobb, BSN, RN, Anthony A. Scott, PhD, Victor F. German, MD, PhD

Overview: Poor, urban, and immigrant populations are at far greater risk for lead exposure than areother groups in the United States. Children with even slightly elevated blood lead levels are atincreased risk for significant neurobehavioral problems that can extend through adolescence. Researchhas shown that elevated blood lead levels in pregnant women, even those well below 10 microgramsper deciliter—the Centers for Disease Control and Prevention’s “level of concern”—can cause miscar-riage, premature birth, low birth weight, and subsequent developmental delays in their children.Despite these well-established dangers, routine prenatal lead screening and lead education is not astandard of care.

Part 1 of this two-part article presents a short case example of a pregnant mother with lead poison-ing and describes the epidemiology of lead exposure in the United States, the main sources of leadexposure, and the effects of lead on the pregnant mother and the developing fetus and child.

Prevention is crucial. Treatment options such as chelation must be used selectively and will notreverse damage once it’s occurred. Part 2 will describe recommendations for screening, education,nutrition, reducing environmental exposures, and treatment.

Immigrants and the poor shoulder most of the burden of lead exposure in this country. Part 1 of a two-part article details how exposure happens,whom it affects, and the harm it can do.

Continuing EducationHOURS2.5

[email protected] AJN t October 2008 t Vol. 108, No. 10 41

She gave birth to a seemingly healthy girl with one-and five-minute Apgar scores of 9 and a hematocritlevel of 48%, and both mother and child were dis-charged. But laboratory results from blood takenfrom the infant at two days of age showed that shehad a blood lead level of 70.8 micrograms perdeciliter. Physicians immediately readmitted theinfant, and she received an exchange transfusionand iv chelation therapy. Several days later, theinfant’s blood lead level had dropped to 27 micro-grams per deciliter, and she was discharged on oralchelation therapy. [Editor’s note: See Part 2 of thisarticle next month for a discussion of the appropri-ate use of chelation therapy.]

Had Ms. Lopez not participated in the researchstudy, her blood lead level and that of her infantwould most likely have gone undiagnosed. Overtime, both mother’s and infant’s blood lead levelshave continued to decrease, although neither has yetdropped below the 10 micrograms per deciliter thatthe Centers for Disease Control and Prevention

(CDC) has deemed a “level of concern.” The infantis now enrolled in a program to monitor her devel-opmental milestones for the first three years of life. Itis hoped that the early identification of lead exposurein this case will prevent long-term consequences.

LEAD EXPOSURE: WHO’S AT RISK?Healthy People 2010, national health objectives pro-moted by the Office of Disease Prevention andHealth Promotion at the U.S. Department of Healthand Human Services, has set the goal of completelyeliminating blood lead levels of 10 micrograms perdeciliter or higher in children by 2010.1 Greatprogress has been made in this effort. According tothe CDC, the percentage of children between the agesof one and five with blood lead levels of 10 micro-grams per deciliter or higher declined from nearly78% in the mid 1970s to below 5% by the mid1990s2; by 1999–2000, this figure had decreased evenfurther, to just over 2%.3 Adults showed similarlysteep declines in blood lead levels during this period.

This photograph, taken to highlight the plight of Russian children like Mica (foreground) who have been orphanedby HIV and AIDS, also reveals the dangers that old, poorly maintained buildings pose to children, who can easilyingest paint from walls and floors, putting themselves at risk for high blood lead levels. Children adopted from for-eign countries should be screened on their arrival to the United States.

Get

tyIm

ages

/Da

vid

Gilla

nder

s

42 AJN t October 2008 t Vol. 108, No. 10 http://www.nursingcenter.com

Usually credited for this improvement were wide-spread prevention policies instituted by the federalgovernment, especially those banning lead in gasolineand mandating aggressive lead screening in children.

As a result of this decrease, many U.S. health careproviders consider preventing lead exposure andscreening to be low priorities. But nearly one-halfmillion children—primarily those who are poor,belong to a minority population, or live in olderhouses and in poor urban areas—continue to be atrisk.1-3 These children are more likely to live in deteri-orating housing that contains lead-based paint orpaint residue in interior dust or exterior soil and toconsume foods low in iron and calcium, which hasbeen shown to increase lead absorption from the gut.1

Lead exposure can be especially detrimental dur-ing pregnancy, fetal development, and early child-hood. Lead is widely understood to be transmittedfrom mother to fetus through the placenta, and ananimal study by Goyer found that maternal andfetal blood lead levels were “nearly identical.”4, 5

Lead may also be stored in a person’s bones fordecades before being released into the bloodstreamor into soft tissues, thereby doing further damage tothat person’s internal organs, or before being passedto the developing fetus during pregnancy.6, 7

The following are just a few adverse effects oflead exposure for mother and child. • increased risk of hypertension in pregnant women8

• increased risk of miscarriage9

• decreased IQ scores in children ages five andyounger10

• impaired neurobehavioral development in chil-dren at age seven and a half years11

• deficits in academic and cognitive skills in chil-dren and adolescents12

Despite the documented risks of lead exposureto pregnant women, the developing fetus, and thedeveloping child—risks that may exist even whenblood lead levels are at or below 10 micrograms perdeciliter—routine prenatal lead screening and edu-cation is not a standard of care in the United States.

SOURCES OF LEAD EXPOSUREAccording to an American Academy of Pediatrics(AAP) policy statement on lead exposure in chil-dren, from 1976 to 1980 the median blood leadlevel in U.S. children between one and five years ofage was 15 micrograms per deciliter; by 1999, thisfigure had been reduced to 1.9 micrograms perdeciliter.13 However, as noted above, certain popu-lations, particularly immigrants and those who arepoor and live in old and deteriorating housing, con-tinue to have elevated blood lead levels.

The environment is still the most common sourceof exposure to lead, despite the removal or sharpreduction in recent years of some of lead’s most per-nicious reservoirs. When leaded fuel is burned, lead

particles from the exhaust are released into the air,where they can be inhaled or settle into the soil.During the 1970s the federal government graduallycurtailed the use of lead as an additive in gasoline;by 1986 it had imposed an outright ban on the saleof lead-containing gasoline for most uses. Duringthis period limits were also placed on smokestackemissions. The resulting reduction in airborne leadparticles has been drastic and airborne lead is nolonger considered a major public health concern,despite some local exceptions.13

Paint. The AAP states that the “source of mostlead poisoning in children now is dust and chipsfrom deteriorating lead paint on interior surfaces.”13

Prior to 1955, white house paint could contain upto 50% lead, a figure that was reduced to 0.06%by 1978.4 Despite this progress, old and decayinghomes are an ongoing danger: 70% of homes builtprior to 1960 contain lead paint4 and approximately25% of U.S. homes with one or more children underthe age of six contain exposed lead.13 Deteriorationor renovation projects can release the lead in paintinto the surrounding air, where it can be absorbedduring respiration. It can also settle into the soil, cre-ating a source of hand-to-mouth exposure. Childrenmay also eat paint chips.

Lead has not been banned as an additive inindustrial paint that may be used on bridges or inother industrial projects,14 many of which are locatednear poor urban areas. In addition, some countriesstill allow the use of leaded fuel; immigrants fromthese countries may have been exposed to high lev-els of ambient lead that has been stored in theirbones for decades.14

Water. Although more than 90% of U.S. watersystems meet Environmental Protection Agency (EPA)standards for tap water quality,15 drinking water stillaccounts for approximately 10% to 20% of leadexposure in children.16 Homes built before 1986may have lead in pipes, fittings, and solder; this leadcan leach out of pipes and into drinking water.1 Incertain cities, elevated lead levels have also beenfound in school drinking water. A study by Bryantrevealed that between 2000 and 2001, more than57% of public school buildings in Philadelphia hadwater lead levels exceeding the EPA’s recommendedaction level.17 Sathyanarayana and colleaguesreported that in 2004, elevated lead levels were alsofound in the Seattle public school district, when22% of the water sampled was found to have leadlevels above the EPA’s recommended limits; however,the authors concluded that any increase in overallstudent blood lead levels would fall far short of theCDC’s stated level of concern of 10 micrograms perdeciliter.18

Occupational exposure. According to the CDC,in 2003–2004 “94% of adults with identified lead-exposure sources were exposed via occupational

[email protected] AJN t October 2008 t Vol. 108, No. 10 43

sources.”3 The construction, manufacturing, andmining industries had the highest number of adultswith elevated blood lead levels. Adult occupationalexposures have been tracked since 1994 throughthe CDC’s Adult Blood Lead Epidemiology andSurveillance program (ABLES); during this time asteady decline has been observed in occupation-related blood lead levels. In 2004 the number ofpeople known to have occupation-related bloodlead levels greater than or equal to 25 microgramsper deciliter was 7.5 per 100,000, a figure that isexpected to continue to diminish.3

Hobbies and other pursuits. Exposure can alsooccur through such activities as making stained glass,casting and ceramics, hunting, target shooting,remodeling and renovation, auto repair, or liquordistillation.3, 14, 19

Pica, home remedies, candy, and contaminatedfood. Of the adults found by ABLES in 2003–2004to have blood lead levels of 25 micrograms perdeciliter or greater, 3% had been exposed to leadthrough pica or by ingesting lead-contaminatedfoods or home remedies.3

Pica is described by the Diagnostic and StatisticalManual of Mental Disorders, fourth edition, textrevision, as a disorder usually characterized by “theeating of one or more nonnutritive substances on apersistent basis for a period of at least one month.”20

Commonly ingested substances include soil, clay,ice, starch, baking powder, chalk, and paint. Al-though its prevalence is not known, pica is mostcommon among young children and pregnantwomen. It has frequently been associated with men-tal retardation but is also common (and considerednormal) in cultures in which “the eating of dirt andother nonnutritive substances is believed to be ofvalue.”20 On occasion, pica is found to result fromnutritional deficiencies, particularly of iron or zinc.

Pica in pregnancy occurs most often in womenin low socioeconomic groups, in rural areas, amongblack women, in women who practiced pica as chil-dren, and in those whose family members engage inpica.21-23 Smulian and colleagues interviewed 125pregnant women in rural Georgia and found that14% reported pica behavior.22 A study of pregnant,low-income, Mexican-born women found that picabehavior was reported by 44% of those inter-viewed at a clinic in Mexico and by 31% of thoseinterviewed at a clinic in southern California.24 It islikely that pica is underreported by women becauseof embarrassment and shame.

Herbal medicine. In many cultures, herbal med-icines are used for the prevention or treatment ofsuch ailments as arthritis, infertility, and menstrualcramps. The Food and Drug Administration classi-fies herbal medicines as “dietary supplements” anddoesn’t require approval before they are marketed.

Ayurveda is a traditional health care system origi-

nally practiced in South Asian countries. From 2000to 2003 the CDC received 12 reports of adults withlead poisoning associated with the use of Ayurvedicmedicines.25 And in 2004 a study published in JAMAreported that 13 of 70 Ayurvedic products producedin South Asia and sold in Boston-area stores con-tained “potentially harmful” levels of lead.26 Azarconand greta, used for the treatment of stomach ail-ments among some Mexican Americans, are brightlycolored industrial powders that may contain from70% to more than 90% lead.27, 28

Patients with high blood lead levels who havebeen using these substances may continue to believe

in their efficacy, not consider them to be “homeremedies,” or fear potential legal consequences ofadmitting their use. For these and other reasons theyoften fail to report using them when initially asked.29

Contaminated food and candy. Several brands ofcandies imported from Mexico have been identifiedas having high levels of lead. In April the CaliforniaDepartment of Public Health warned against eatingChaca Chaca Chacatrozo, a candy produced inMexico, because it had been found to containunsafe levels of lead.30 Lead-contaminated candyproduced in Mexico and transported across theborder is available particularly in California, NewMexico, Arizona, and Texas.31 For example, in2004 reporters at the Orange County Register inSouthern California purchased samples of 74brands of Mexican candies and found lead in thecandy or wrapper of 32% of them.32

Storage of foods and liquids in certain types ofcontainers may present another risk factor for leadexposure. High levels of lead can be found in pot-tery containing lead glaze as well as in leaded crys-tal. When the glaze used on these products is notfired properly, lead may be leached out of thesecontainers by the foods stored in them. Liquids thatare acidic or hot may increase the rate at which leadleaches out.1, 33

Toys. Recalls of Chinese-made toys have occurredwith alarming frequency in recent years. An August2007 Mattel recall of 1.5 million toys included

Pregnancy, lactation,

menopause, chronic disease, or

calcium deficiency increase

the risk of lead toxicity.

The skeletal system. Lead can remain up to 30 years in bone, which bears 70% of

a child’s body burden and 95% ofan adult’s. When bone metabo-lism increases, during pregnancyand lactation, fracture healing,and chelation therapy, forexample, stored lead leaves thebone and reenters the circula-tion. This can expose a fetus to

lead the mother was exposed towhen she herself was a child.1, 2

Lead can also be toxic to osteoblastsand inhibit new bone vascularization,

which can result in osteopenia, osteoporo-sis, and impaired fracture healing.3

Figure 1.The Effects of Lead on Body Systems

44 AJN t October 2008 t Vol. 108, No. 10 http://www.nursingcenter.com

Fisher-Price products such as Elmo, Big Bird, andDora the Explorer.34 Concern over lead paint usedon toys has prompted several states to take action.In recent years, Maryland joined California andIllinois in regulating the level of lead allowed in toysmarketed in the state.35 Children’s jewelry has alsobeen identified as a potential source of lead expo-sure. In 2003 a four-year-old boy swallowed asmall metal medallion purchased from a toy vend-ing machine in Oregon.36 He subsequently devel-oped severe symptoms of lead poisoning, includingvomiting and edema. Once the medallion was dis-covered in his stomach, it was removed and hissymptoms began to subside. The U.S. ConsumerProduct Safety Commission (CPSC) requested avoluntary recall of almost 1.5 million similar neck-laces; in 2004 the CPSC sought recalls of more than150 million pieces of toy jewelry sold in vendingmachines and chain stores.37 In 2005, responding toseveral cases “in which children developed highblood lead levels after swallowing or repeatedlysucking on jewelry items,” the CPSC put into effecta new enforcement policy providing clear guidanceto manufacturers, importers, and retailers as to howtoys will be tested for lead and what limits will bedeemed acceptable.38

To avoid the confusion of multiple laws at thestate level, in July Congress took quick action, pass-ing a bill banning lead and six types of phthalatesin all toys for children 12 years of age and youngerand requiring that all U.S. toys be tested for danger-ous chemicals, including lead and phthalates, beforethey’re sold. The bill will also double the funding forthe CPSC.

LEAD IN THE BODY Absorption and storage. Lead usually enters thebody through ingestion or through the inhalationof dust containing lead particles or fuel exhaust.Absorption of lead through the skin is far less effi-cient and is a concern only in relatively rare situa-tions. Inhaled inorganic lead, when in sufficientlyminute particles, can be completely absorbed throughthe respiratory tract. Although limited studies havebeen conducted on lead absorption in humans, ani-mal studies and the few human studies that existsuggest that ingested lead is absorbed through thegastrointestinal system and at higher rates by chil-dren than by adults. Children absorb 40% to 50%of ingested lead and adults absorb closer to 10%(although absorption rates as high as 70% havebeen seen when adults have no food in their stom-ach at the time of ingestion).39

Lead that enters the bloodstream is eventuallyexcreted through renal or biliary clearance andleaves the body in urine and stool. Lead that is notimmediately excreted may be retained in the blood,

The peripheral nervous system.Lead causes peripheral neu-ropathy through Schwanncell destruction, followed bysegmental demyelinationand axonal degeneration of motor neurons. This canpresent as bilateral wrist

drop, seen more often inadults than in children.2

The renal system. The classicsigns of lead damage to

the cells of the proximaltubules of the kidney areaminoaciduria, glycos-uria, and hyperphos-phaturia. It’s believedthat this damage isreversible, although

chronic lead exposuremay bring about irre-

versible nephropathy.1, 2, 4

The reproductive system. Lead readily crosses theplacenta through simple diffusion. Therefore,neonatal blood lead levels are typically as highas the mother’s. Lead poisoning in utero hasbeen linked to premature birth, fetal malforma-tion and death, and neurobehavioral deficits.2, 5

The central nervous system. Lead not only easily crosses theblood–brain barrier, it can damage it; theresulting increased intracranial fluid cancreate intracranial pressure and causeacute encephalopathy. Chronic leadexposure also damages neurotrans-

mitters, producing an increase inrandom synaptic signals known

as “synaptic noise,” which isespecially problematic in

children. In normal braindevelopment, somesynapses are kept while oth-ers are destroyed; by interfer-ing with the feedback betweenneurotransmitters and their receptors,lead can disrupt brain development.1, 2

AJN t October 2008 t Vol. 108, No. 10 45

The gastrointestinal system. Ingestion is theprimary avenue for lead exposure inchildren. Symptoms can include nau-sea, vomiting, and abdominal pain.It’s hypothesized that lead increasesthe activity of the sodium–calciumexchange pump and interferes withsodium–potassium adenosinetriphosphatase (ATPase) activity,which then leads to increased con-tractility of smooth muscle.1—ChristineMoffa, MS, RN, clinical editor

REFERENCES1. Ibrahim D, et al. Heavy metal poisoning: clinical presentations and

pathophysiology. Clin Lab Med 2006;26(1):67-97. 2. Gracia RC, Snodgrass WR. Lead toxicity and chelation therapy.

Am J Health Syst Pharm 2007;64(1):45-53.3. Woolf AD, et al. Update on the clinical management of childhood

lead poisoning. Pediatr Clin North Am 2007;54(2):271-94.4. Lockitch G. Perspectives on lead toxicity. Clin Biochem

1993;26(5):371-81.5. Shannon M. Severe lead poisoning in pregnancy. Ambul Pediatr

2003;3(1):37-9.

Illustr

atio

nsby

Jay

LeVa

sseu

r/A

pplie

dA

rt

The hematologic system. After lead enters the circulationthrough the respiratory or digestive system, itbinds to red blood cells and inhibits vari-ous enzymes, causing anemia. This canoccur either through the destabiliza-tion of the cell membrane, leadingto early cell death, or through theinhibition of the biosynthesis ofheme, the oxygen-carrying compo-nent of hemoglobin, or both. Oneof the inhibited enzymes, pyrimi-dine 5’-nucleotidase, is needed forthe removal of degraded RNA fromthe cell. Clumping of the red bloodcells results, producing the basophilicstippling seen microscopically.1

46 AJN t October 2008 t Vol. 108, No. 10 http://www.nursingcenter.com

soft tissues, and mineralizing tissues (bones andteeth). Lead retention in vital organs can lead to renaldisease, hypertension, peripheral neuropathy, gout,encephalopathy, and death. Summarizing the avail-able literature, the Agency for Toxic Substances andDisease Registry of the Department of Health and Human Services reports that 95% of lead in

adults and approximately 73% of lead in children isstored in bone.1 While the blood lead level is themost widely accepted measure of lead exposure, it isonly a reflection of recent or continued lead expo-sure and does not adequately reflect past exposureor accumulated bone lead levels. Although lead inthe blood has a half life of 28 to 36 days,1 leadcan be stored in the bones for several decades; dur-ing periods of physiologic stress or immobilization,where an increase in bone turnover occurs, lead canleave the bones and reenter the blood and soft tis-sues. Therefore, pregnancy, lactation, menopause,chronic disease, or calcium deficiency may increasethe risk of lead toxicity.1

Symptoms of lead toxicity may be subtle andcan go unnoticed until blood lead levels reach 40micrograms per deciliter or higher.14 (See Signs andSymptoms of Toxicity Associated with OngoingLead Exposure, at left.) At low blood lead levels,neurobehavioral impairment may occur, includingreduced academic ability, irritability, and other non-specific symptoms. As lead builds up in the body andlevels approach 40 micrograms per deciliter, moreobvious symptoms may appear, such as headache,abdominal pain, anemia, and vomiting.1 Blood leadlevels of 70 to 80 micrograms per deciliter have beenassociated with encephalopathy, the signs of whichinclude ataxia, convulsions, and coma. Even withoutsymptoms, lead levels this high are associated with ahigh incidence of permanent neurologic damage.1

LEAD IN PREGNANCY Elevated blood lead levels during pregnancy areassociated with an increased risk of preterm births40

and can increase the risk of spontaneous abortion.9, 41

The first pregnancy carries the greatest risk of leadtoxicity.42 Blood lead levels may actually increase inwomen during pregnancy as a result of increasedmobilization of lead from bones into the blood.6

Gulson found that blood lead levels increase approx-imately 20% throughout pregnancy, even in womenwith low blood lead levels,6 and Rabinowitz and col-leagues found an association between even slightlyelevated blood lead levels of less than 10 microgramsper deciliter and pregnancy-induced hypertension.8

Women with low calcium intake may be at increasedrisk for increased blood lead levels as well.43

The developing fetus. Lead freely crosses the pla-centa, and there is a strong correlation betweenmaternal and umbilical cord blood lead levels.44, 45 Infact, the fetal blood lead level may be even greaterthan the maternal lead level: an observational studyand literature review by Shannon and colleaguesfound that at the time of delivery, infants’ blood leadlevels were, on average, 19% higher than those oftheir mothers.46

Because of the incomplete blood–brain barrier,the effect of lead on the fetus’s central nervous sys-

Lowest Exposure: Impaired Abilities (patient may appear asymptomatic)• decreased learning and memory • lowered IQ • decreased verbal ability • impaired speech and hearing functions • early signs of hyperactivity or attention deficit hyperactivity

disorder

Low Exposure • myalgia or paresthesia • mild fatigue • irritability • lethargy • occasional abdominal discomfort

Moderate Exposure • arthralgia • general fatigue • difficulty concentrating• muscular exhaustibility • tremor • headache • diffuse abdominal pain • vomiting • weight loss • constipation

High Exposure • paresis or paralysis • encephalopathy—may abruptly lead to seizures, changes in

consciousness, coma, and death • lead line (blue-black) on gingival tissue • colic (intermittent, severe abdominal cramps)

Adapted from the Agency for Toxic Substances and Disease Registry (ATSDR). Case studies inenvironmental medicine (CSEM). Lead toxicity. 2007. http://www.atsdr.cdc.gov/csem/lead/docs/lead.pdf.

Signs and Symptoms of ToxicityAssociated with Ongoing LeadExposure

[email protected] AJN t October 2008 t Vol. 108, No. 10 47

tem is greater during gestation and in the first 36months of life than it is later in life.1 The effects oflead exposure on the fetus during gestation may bemanifested after birth by low performance on cog-nitive tests.47 Lead is destructive to the developingcentral nervous system and interferes with synapticmechanisms for neurotransmitter release.5 In ani-mal studies, lead-related losses in developmentalareas such as visual–motor integration and increasederrors in tasks of perseverance have pointed to thehippocampus as the area of injury regarding neu-robehavioral effects.5, 48, 49

Although these findings raise concerns for thedeveloping fetus, it is still unclear if lead is a terato-gen. In a 1984 study analyzing umbilical cord bloodobtained from more than 5,000 births, Needlemanand colleagues reviewed cord blood lead levels andfound an associated dose-dependent increase in theincidence of minor birth defects when maternal leadlevels were elevated.50 However, no one type of defector syndrome was identified, and the authors con-cluded that lead may interact with other environ-mental teratogens to increase the likelihood of fetalanomalies.

INFANCY THROUGH ADOLESCENCELactation. Elevated maternal blood lead levels don’tdisappear after birth; in fact, they may increase. Astudy by Téllez-Rojo and colleagues found that bloodlead levels that rise during late pregnancy continueto do so during lactation.51 Women who continuedbreastfeeding exclusively showed a mean increase inblood lead levels of 19%, compared with womenwho discontinued nursing. Such differences matter. Asmall study by Counter and colleagues noted thatlead levels found in human milk were comparableto those found in maternal serum.52 And in a studyof healthy infants and their mothers, Sanín and col-leagues found that high maternal bone lead levelsnegatively affected weight gain in nursing infants atone month of age.53

This doesn’t necessarily mean that mothersshould stop breastfeeding if they have elevatedblood lead levels. Manton found that an infant’srisk of developing lead toxicity from breast milk isless likely than originally thought: while themother’s blood lead level increased during lacta-tion, the infant’s blood lead level decreased.42

Another consideration is that lead may also be pres-ent in commercial infant formula. In a study of thedaily lead intake and excretion in 15 infants inAustralia, Gulson and colleagues noted that leadconcentration in formula ranged from 0.07 to 11.4micrograms per deciliter and in breast milk from0.09 to 3.1 micrograms per deciliter.54 Such datasuggest that recommending formula use over breast-feeding may not significantly reduce an infant’s riskof lead exposure.

Early childhood. Lead exposure in early child-hood is a major risk factor for poor neurobehav-ioral outcomes. In an examination of data on nearly5,000 children between the ages of six and 16 fromthe Third National Health and Nutrition Exam-ination Survey, which took place between 1988 and1994, Lanphear and colleagues found that cogni-tive deficits can occur even when blood lead levelsare lower than 5 micrograms per deciliter. Despitea geometric mean blood lead concentration of only1.9 micrograms per deciliter in this population ofchildren, for every 1-microgram per deciliter in-

crease in blood lead level, there was an associateddecrease in short-term memory, nonverbal reason-ing, reading, and arithmetic.12 Canfield and col-leagues estimated a 4.6-point decrease in IQ foreach 10-microgram per deciliter increase in lifetimeblood lead concentration in children ages three andfive; even more alarmingly, the greatest decrease inIQ occurred in those children whose blood lead lev-els remained below 10 micrograms per deciliter.10

Chiodo and colleagues, conducting a systematicanalysis of the effects of blood lead levels on 246inner-city black children who were seven and a halfyears of age, identified negative effects on attention,intelligence, fine-motor skills, social engagement, andnumerous other neurobehavioral measures at bloodlead levels as low as 3 micrograms per deciliter.11

Mendelsohn and colleagues found that childrenbetween 12 and 36 months of age with a mean leadlevel between 10 and 24.9 micrograms per deciliterhad more difficulty with “emotional regulation” thandid children with blood lead levels less than 10 micro-grams per deciliter, and were more impulsive, hyper-active, and easily frustrated.55

Adolescence. Abnormalities have also beenobserved in adolescents who were exposed to lead.A prospective longitudinal study by Dietrich andcolleagues of inner-city adolescents reported thatboth “prenatal and postnatal exposure to [lead] wereassociated with reported antisocial acts and may playa measurable role in the epigenesis of behavioralproblems independent of the other social and bio-

Lead freely crosses the placenta,

and there is a strong correlation

between maternal and umbilical

cord blood lead levels.

48 AJN t October 2008 t Vol. 108, No. 10 http://www.nursingcenter.com

medical cofactors.”56 Needleman and colleaguesfound that children ages 12 to 18 who had been“arrested and adjudicated . . . as delinquents” werefour times more likely to have bone lead levels greaterthan 25 micrograms per deciliter than were thosewho had not.57 In fact, the consequences may extendinto adulthood: a recent prospective study by Wrightand colleagues found an association between prena-tal and early childhood exposure to lead and violentcrimes committed as adults by those who had beenexposed.58 t

Lisa M. Cleveland is a clinical nursing instructor at theUniversity of Texas Health Science Center at San Antonio,where Kathleen A. Cobb is a research nurse, Anthony A.Scott is a clinical professor of pediatrics, and Victor F.German is a professor as well as the division chief in thecommunity pediatrics division and the interim division chiefin the pediatric pulmonary division. Monica L. Minter wasformerly the project coordinator for the Project LIFE grantfrom the U.S. Department of Housing and Urban Develop-ment (HUD) that funded the writing of this article. ProjectLIFE consisted of voluntary lead screening offered to preg-nant women and children at several clinics in San Antonioand a presentation designed to educate health care providersin the community on lead poisoning. This manuscript wasdeveloped from that presentation. HUD reviewed andapproved the contents of this article. Contact author: Lisa M.Cleveland, [email protected]. The authors of this articlehave no other significant ties, financial or otherwise, to anycompany that might have an interest in the publication ofthis educational activity.

REFERENCES1. U.S. Department of Health and Human Services. Environ-

mental health. In: Healthy People 2010. Understanding and improving health. 2nd ed. Washington, DC; 2000.http://www.healthypeople.gov/Document/pdf/Volume1/08Environmental.pdf.

2. Centers for Disease Control and Prevention. Blood leadlevels—United States, 1999–2002. MMWR Morb MortalWkly Rep 2005;54(20):513-6.

3. Centers for Disease Control and Prevention. Adult blood leadepidemiology and surveillance—United States, 2003–2004.MMWR Morb Mortal Wkly Rep 2006;55(32):876-9.

4. Gardella C. Lead exposure in pregnancy: a review of the lit-erature and argument for routine prenatal screening. ObstetGynecol Surv 2001;56(4):231-8.

5. Goyer RA. Results of lead research: prenatal exposure andneurological consequences. Environ Health Perspect 1996;104(10):1050-4.

6. Gulson BL, et al. Pregnancy increases mobilization of leadfrom maternal skeleton. J Lab Clin Med 1997;130(1):51-62.

7. Hernandez-Avila M, et al. Effect of maternal bone lead onlength and head circumference of newborns and 1-month-old infants. Arch Environ Health 2002;57(5):482-8.

8. Rabinowitz M, et al. Pregnancy hypertension, blood pressureduring labor, and blood lead levels. Hypertension 1987;10(4):447-51.

9. Hertz-Picciotto I. The evidence that lead increases the riskfor spontaneous abortion. Am J Ind Med 2000;38(3):300-9.

10. Canfield RL, et al. Intellectual impairment in children withblood lead concentrations below 10 microg per deciliter. N Engl J Med 2003;348(16):1517-26.

11. Chiodo LM, et al. Neurodevelopmental effects of postnatallead exposure at very low levels. Neurotoxicol Teratol2004;26(3):359-71.

12. Lanphear BP, et al. Cognitive deficits associated with bloodlead concentrations <10 microg/dL in US children and ado-lescents. Public Health Rep 2000;115(6):521-9.

13. American Academy of Pediatrics Committee on Environ-mental Health. Lead exposure in children: prevention,detection, and management. Pediatrics 2005;116(4):1036-46.

14. Hackley B, Katz-Jacobson A. Lead poisoning in pregnancy:a case study with implications for midwives. J MidwiferyWomens Health 2003;48(1):30-8.

15. U.S. Environmental Protection Agency. Ground water anddrinking water. Frequently asked questions. How can I getmy water tested? 2007. http://www.epa.gov/safewater/faq/faq.html#test.

16. Centers for Disease Control and Prevention. Lead anddrinking water from private wells. Atlanta; 2003 Summer.http://www.cdc.gov/ncidod/dpd/healthywater/factsheets/pdf/lead.pdf.

17. Bryant SD. Lead-contaminated drinking waters in the publicschools of Philadelphia. J Toxicol Clin Toxicol 2004;42(3):287-94.

18. Sathyanarayana S, et al. Predicting children’s blood leadlevels from exposure to school drinking water in Seattle,Washington, USA. Ambul Pediatr 2006;6(5):288-92.

19. Minnesota Department of Health. Environmental HealthDivision. Blood lead screening guidelines for pregnantwomen in Minnesota. St. Paul, MN; 2007 Dec. http://www.health.state.mn.us/divs/eh/lead/reports/pregnancy/pregnancy1page.pdf.

20. American Psychiatric Association. Pica. In: Diagnostic andstatistical manual of mental disorders. 4th, text revision ed.Washington, DC: The Association; 2000. p. 103 (5).

21. Horner RD, et al. Pica practices of pregnant women. J AmDiet Assoc 1991;91(1):34-8.

22. Smulian JC, et al. Pica in a rural obstetric population. SouthMed J 1995;88(12):1236-40.

23. Sule S, Madugu HN. Pica in pregnant women in Zaria,Nigeria. Niger J Med 2001;10(1):25-7.

24. Simpson E, et al. Pica during pregnancy in low-incomewomen born in Mexico. West J Med 2000;173(1):20-4; discussion 25.

25. Centers for Disease Control and Prevention. Lead poisoningassociated with ayurvedic medications—five states,2000–2003. MMWR Morb Mortal Wkly Rep 2004;53(26):582-4.

26. Saper RB, et al. Heavy metal content of ayurvedic herbalmedicine products. JAMA 2004;292(23):2868-73.

27. Centers for Disease Control and Prevention. Lead poisoningfrom Mexican folk remedies—California. MMWR MorbMortal Wkly Rep 1983;32(42):554-5.

28. Weizsaecker K. Lead toxicity during pregnancy. Prim CareUpdate Ob Gyns 2003;10(6):304-9.

29. Centers for Disease Control and Prevention. Lead poisoningassociated with use of traditional ethnic remedies—California, 1991–1992. MMWR Morb Mortal Wkly Rep1993;42(27):521-4.

30. California Department of Public Health. CaliforniaDepartment of Public Health warns consumers not to eatChaca Chaca Chacatrozo candy imported from Mexico[press release]. 2008 Apr 17. http://www.cdph.ca.gov/HealthInfo/news/Pages/NR2008-17ChacaChacaCandy.aspx.

31. Medlin J. Sweet candy, bitter poison. Environ HealthPerspect 2004;112(14):A803.

32. McKim JB, et al. Toxic treats, part one: Hidden threat.Orange County Register 2004 Apr 25. http://www.ocregister.com/investigations/2004/lead/part1.shtml.

33. Centers for Disease Control and Prevention. Childhood leadpoisoning from commercially manufactured French ceramicdinnerware—New York City, 2003. MMWR Morb MortalWkly Rep 2004;53(26):584-6.

34. Associated Press. Mattel issues new massive China toyrecall. About 9 million items recalled; danger from magnetsand lead paint. MSNBC 2007 Aug 14. http://www.msnbc.msn.com/id/20254745/.

35. Conner C. State law targets lead in toys. WMAR-TV 2008Jun 30. http://tinyurl.com/59atuv.

[email protected] AJN t October 2008 t Vol. 108, No. 10 49

36. Centers for Disease Control and Prevention. Brief report:lead poisoning from ingestion of a toy necklace—Oregon,2003. MMWR Morb Mortal Wkly Rep 2004;53(23):509-11.

37. U.S. Consumer Product Safety Commission. Office ofCompliance. Interim enforcement policy for children’s metaljewelry containing lead. Washington, DC; 2005 Feb 3.http://www.cpsc.gov/BUSINFO/pbjewelgd.pdf.

38. U.S. Consumer Product Safety Commission. Office ofInformation and Public Affairs. CPSC announces new policyaddressing lead in children’s metal jewelry [press release].News from CPSC 2005 Feb 3. http://www.cpsc.gov/CPSCPUB/PREREL/prhtml05/05097.html.

39. Agency for Toxic Substances and Disease Registry (ATSDR).Toxicological profile for lead. Atlanta; 2007 Aug. http://www.atsdr.cdc.gov/toxprofiles/tp13.pdf.

40. McMichael AJ, et al. The Port Pirie cohort study: maternalblood lead and pregnancy outcome. J Epidemiol Com-munity Health 1986;40(1):18-25.

41. Borja-Aburto VH, et al. Blood lead levels measuredprospectively and risk of spontaneous abortion. Am JEpidemiol 1999;150(6):590-7.

42. Manton WI, et al. Acquisition and retention of lead byyoung children. Environ Res 2000;82(1):60-80.

43. Sowers M, et al. Blood lead concentrations and pregnancyoutcomes. Arch Environ Health 2002;57(5):489-95.

44. Goyer RA. Transplacental transport of lead. Environ HealthPerspect 1990;89:101-5.

45. Korpela H, et al. Lead and cadmium concentrations in maternaland umbilical cord blood, amniotic fluid, placenta, and amnioticmembranes. Am J Obstet Gynecol 1986;155(5):1086-9.

46. Shannon M. Severe lead poisoning in pregnancy. AmbulPediatr 2003;3(1):37-9.

47. Bellinger D, et al. Longitudinal analyses of prenatal andpostnatal lead exposure and early cognitive development. N Engl J Med 1987;316(17):1037-43.

48. Gilbert ME, Mack CM. Chronic lead exposure acceleratesdecay of long-term potentiation in rat dentate gyrus in vivo.Brain Res 1998;789(1):139-49.

49. Nihei MK, et al. N-methyl-D-aspartate receptor subunitchanges are associated with lead-induced deficits of long-term potentiation and spatial learning. Neuroscience2000;99(2):233-42.

50. Needleman HL, et al. The relationship between prenatalexposure to lead and congenital anomalies. JAMA 1984;251(22):2956-9.

51. Téllez-Rojo MM, et al. Impact of breastfeeding on themobilization of lead from bone. Am J Epidemiol 2002;155(5):420-8.

52. Counter SA, et al. Current pediatric and maternal lead levelsin blood and breast milk in Andean inhabitants of a lead-glazing enclave. J Occup Environ Med 2004;46(9):967-73.

53. Sanin LH, et al. Effect of maternal lead burden on infantweight and weight gain at one month of age among breast-fed infants. Pediatrics 2001;107(5):1016-23.

54. Gulson BL, et al. Longitudinal study of daily intake andexcretion of lead in newly born infants. Environ Res2001;85(3):232-45.

55. Mendelsohn AL, et al. Low-level lead exposure and behav-ior in early childhood. Pediatrics 1998;101(3):E10.

56. Dietrich KN, et al. Early exposure to lead and juveniledelinquency. Neurotoxicol Teratol 2001;23(6):511-8.

57. Needleman HL, et al. Bone lead levels in adjudicated delin-quents. A case control study. Neurotoxicol Teratol 2002;24(6):711-7.

58. Wright JP, et al. Association of prenatal and childhoodblood lead concentrations with criminal arrests in earlyadulthood. PLoS Med 2008;5(5):e101.

GENERAL PURPOSE: To present registered professionalnurses with a case example of a pregnant mother withlead poisoning as well as a description of the epidemiol-ogy of lead exposure in the United States, the mainsources of lead exposure, and the effects of lead onpregnant women and on children before and after birth.

LEARNING OBJECTIVES: After reading this article and takingthe test on the next page, you will be able to• review the classification, incidence, and risk factors for

lead exposure and toxicity.• outline the etiology and pathogenesis of lead poison-

ing.• describe the various manifestations of lead exposure

and toxicity.

TEST INSTRUCTIONSTo take the test online, go to our secure Web site at www.nursingcenter.com/CE/ajn.To use the form provided in this issue, • record your answers in the test answer section of the

CE enrollment form between pages 48 and 49. Eachquestion has only one correct answer. You may makecopies of the form.

• complete the registration information and course evalua-tion. Mail the completed enrollment form and registrationfee of $24.95 to Lippincott Williams and Wilkins CEGroup, 2710 Yorktowne Blvd., Brick, NJ 08723, byOctober 31, 2010. You will receive your certificate in fourto six weeks. For faster service, include a fax number andwe will fax your certificate within two business days ofreceiving your enrollment form. You will receive your CEcertificate of earned contact hours and an answer key toreview your results. There is no minimum passing grade.

DISCOUNTS and CUSTOMER SERVICE• Send two or more tests in any nursing journal published

by Lippincott Williams and Wilkins (LWW) together, anddeduct $0.95 from the price of each test.

• We also offer CE accounts for hospitals and otherhealth care facilities online at www.nursingcenter.com. Call (800) 787-8985 for details.

PROVIDER ACCREDITATIONLWW, publisher of AJN, will award 2.5 contact hours

for this continuing nursing education activity.LWW is accredited as a provider of continuing nursing

education by the American Nurses CredentialingCenter’s Commission on Accreditation.

LWW is also an approved provider of continuingnursing education by the American Association ofCritical-Care Nurses #00012278 (CERP category A),District of Columbia, Florida #FBN2454, and Iowa #75.LWW home study activities are classified for Texas nurs-ing continuing education requirements as Type 1. Thisactivity is also provider approved by the CaliforniaBoard of Registered Nursing, provider number CEP11749, for 2.5 contact hours.

Your certificate is valid in all states. TEST CODE: AJN1008

Continuing Education2.5HOURS

EARN CE CREDIT ONLINEGo to www.nursingcenter.com/CE/ajn and receive

a certificate within minutes.