Articles Exposure of the U.S. Population to Lead, 1991-1994 James L. Pirkle,7 Rachel B. Kaufmann,1 Debra J. Brody,2 Tamy Hickman,2 Elaine W. Gunter,1 and Daniel C. Paschal' 'National Center for Environmental Health and 2National Center for Health Statistics, Centers for Disease Control and Prevention, Atlanta, GA 30341 USA Blood lead measurements were obtained on 13,642 persons aged 1 year and older who partici- pated in Phase 2 of the Third National Health and Nutrtion mination Survey (NHANES III) from 1991 through 1994. NHANES III is a national representative survey of the civilian, noninstitutionaized U.S. population. The overall mean blood lead level for the U.S. population aged 1 year and older was 2.3 pg/dl, with 2.2% of the population having levels 10 p/dl, the level of health concern for children. Among U.S. children aged 1-5 years, the mean blood lead level was 2.7 pg/dl, and 890,000 of these children (4.4%) had elevated blood lead levels. Sociodemographic factors associated with higher blood lead levels in children were non-Hispanic black race/ethnicity, low income, and residence in older housing. The prvlence of elevated blood lead levels was 21.9% among non-Hispanic black children living in homes built before 1946 and 16.4% among children in low-income families who lived in homes built before 1946. Blood lead levels continue to decline in the U.S. population, but 890,000 children still have ele- vated levels. Public health efforts have been successfil in removing lead from population-wide sources such as gasoline and lead-soldered food and drink cans, but new elforts must address the difficult problem of leaded paint, especially in older houses, as well as lead in dust and soil. Lead poisoning prevention programs should target high-risk persons, such as children who live in old homes, children of minority groups, and children living in families with low income. Key work& air pollution, food contamination, gasoline lead, lead, leaded paint, lead poisoning, water pollu- tion. Environ Health Perspect 106:745-750 (1998). [Online 19 October 1998] http://eepnetl.niehs.nih.gov/docs/1998/106p745-750pirkklabstract.html Human exposure to lead remains a serious public health problem. Lead adversely affects the nervous, hematopoietic, endocrine, renal, and reproductive systems of the body (1,4. Of particular concern are the effects of relatively low levels of lead exposure on cognitive devel- opment of children (1,2). Since the 1970s, federal regulations and abatement efforts have mainly focused on reducing the amount of lead in gasoline, paint, and soldered cans (1,3). In addition, federal programs have supported screening for lead poisoning in children by state and local health departments and physi- cians and lead abatement in housing (1). Currently, lead exposure usually results from lead in deteriorating household paint, lead at the workplace, lead used in hobbies, lead in some "folk" medicines and cosmetics, and lead in crystal or ceramic containers that leaches into water or food (1). Since the late 1970s, the extent of lead exposure in the U.S. population has been assessed by the National Health and Nutrition Examination Surveys (NHANES) (3-8). These national surveys have measured blood lead levels (BPb) of tens of thousands of children and adults and assessed the extent of lead exposure in the civilian population by age, sex, race/ethnicity, income, and degree of urbanization. The surveys have demon- strated an overall decline in BPbs since the 1970s, but they also have shown that a large number of children continue to have elevat- ed blood lead levels (?10 pg/dl) (3). We report here on the most recent blood lead data for the U.S. population from Phase 2 of the third NHANES (NHANES III), which sampled the U.S. population from 1991 to 1994. The BPbs are presented by sociodemographic characteristics for persons aged 1 year and older. Methods Survey design. NHANES III was a strati- fied, multistage probability cluster sample of households whose target population was civilian, noninstitutionalized persons resid- ing in the United States. The 6-year survey consisted of two nationally representative samples: one in Phase 1, from October 1988 to September 1991, and a second in Phase 2, from October 1991 to September 1994. In NHANES III, non-Hispanic blacks, Mexican Americans, children aged 2 months-5 years, and persons aged 60 years and older were oversampled to increase the reliability of estimates for these groups (91. A detailed description of the sample design has been published (10). The survey included a household interview and a stan- dardized physical examination conducted in a mobile examination center. Blood lead results from Phase 1 have previously been published (3,4), and selected findings from Phase 2 have been reported (5). Laboratory methods. During the physi- cal examination, a 1-ml sample of EDTA- anticoagulated whole blood was obtained by venipuncture from participants aged 1 year and older. Blood specimens were frozen and shipped on dry ice for analysis to the NHANES Laboratory, Division of Environmental Health Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia. Blood specimens remained frozen at -20?C until analyzed. Lead was measured by graphite furnace atomic absorption spectrophotometry (GFAAS) using the method of Miller et al. (11,12). The GFAAS method included deu- terium background correction and had a limit of detection of 1.0 pg/dl. The lead result is the mean of duplicate measurements. The blood lead measurements were calibrated by using standards prepared from lead nitrate Standard Reference Material 928 obtained from the National Institute of Standards and Technology, Gaithersburg, Maryland. Demographic and socioeconomic covari- ates. Race/ethnicity was categorized as non- Hispanic black, non-Hispanic white, Mexican American, and other. Because of small sample size, persons not defined by the three largest U.S. race/ethnicity groups were induded only in the estimates for the overall population. Income was categorized using the poverty- income ratio (PIR), defined as the ratio of total family income to the poverty threshold for the year of the interview. Low income was defined as a PIR <1.300, middle income as a PIR 1.301-3.500, and high income as a PIR ?3.501. These categories were selected in part to be consistent with major government food assistance programs that use a PIR of 1.3 to determine eligibility (13). Urban status was based on the U.S. Department of Agriculture codes that classify counties by total population and proximity to major metropolitan areas (14). The two categories were metropolitan areas with pop- ulation ?1 million and metropolitan and nonmetropolitan areas with a population <1 million. These urban status categories did not separate residence in central city areas from noncentral city areas. Year of housing construction was obtained from self-report Address correspondence J.L. Pirkle, Centers for Disease Control and Prevention, 4770 Buford Highway NE, MS-F20, Atlanta, GA 30341 USA. All of the NHANES III blood lead measurements, Phase 1 and Phase 2, were performed by Philip E. Stroud, a chemist in the NHANES Central Laboratory. Received 15 April 1988; accepted 15 July 1998. Environmental Health Perspectives . Volume 106, Number 1 1, November 1998 745 Articles * Pirkle et al. using three categories: before 1946, 1946- 1973, and after 1973. Statistical analysis. Statistical analyses were performed using SAS software (15) and SUDAAN (16), a software package that incorporates the sample weights and adjusts the analyses for the complex sample design of the survey. Survey sample weights were used in all analyses to produce esti- mates that were representative of the non- institutionalized, civilian U.S. population. Geometric mean blood lead levels were calculated by taking the antilog of the mean of log10 of the BPb levels. Multivariate lin- ear regression analyses were performed to determine the relationship between BPb lev- els and sociodemographic variables. Separate models were run for five age categories: 1-5 years, 6-11 years, 12-19 years, 20-49 years, and 50 years and older. Loglo of the BPbs was used as the dependent variable. Independent variables included age, sex, race/ethnicity, PIR, urban status, and age of housing categories. Both backward and for- ward stepwise regression were used to be sure the final model was independent of the stepwise regression approach. Results Blood lead levels of children. The geometric mean BPb for children ages 1-5 years was 2.7 pg/dl, and 4.4% of these children (890,000 in the U.S. population) had elevat- ed BPbs (i.e, ?10 pg/dl). Children aged 1-2 years had a geometric mean BPb of 3.1 pg/dl and 5.9% had elevated BPbs. For children aged 3-5 years, BPbs were slightly lower, with a geometric mean of 2.5 pg/dl, and 3.5% of these children had elevated BPbs. Table 1 shows BPbs for children by selected demographic characteristics. Males and females had similar geometric mean Table 1. Blood lead levels of children aged 1-5 years by selected demographic characteristics: United States, Third National Health and Nutrition Examination Survey, Phase 2, 1991-1994 Geometric % Children with mean blood blood lead levels Population group Sample size lead level (pg/dl) Cl ?10 pg/dl Cl All 2,392 2.7 2.5-3.0 4.4 2.9-6.6 Sex Female 1,181 2.7 2.4-2.9 3.3 2.1-5.0 Male 1,211 2.8 2.5-3.1 5.5 3.5-8.7 Race/ethnicity Black, non-Hispanic 783 4.3 3.7-5.0 11.2 6.7-18.7 Mexican American 827 3.1 2.7-3.5 4.0 2.2-7.2 White, non-Hispanic 631 2.3 2.1-2.5 2.3 1.0-5.0 Year housing built Pre-1946 368 3.8 3.1-4.5 8.6 5.2-14.2 1946-1973 889 2.8 2.1-3.0 4.6 2.9-7.5 After 1973 744 2.0 1.9-2.2 1.6 0.6-4.4 Income Low 1,249 3.8 3.3-4.2 8.0 5.4-11.7 Middle 740 2.3 2.1-2.5 1.9 1.1-3.2 High 261 1.9 1.7-2.1 1.0 0.3-3.4 Urban status Population ?1 million 1,323 2.8 2.4-3.2 5.4 3.)-9.8 Population <1 million 1,069 2.7 2.3-3.0 3.3 1.5-7.0 Cl, 95% confidence interval. BPbs. A greater percentage of males had elevated BPbs, but the difference was not statistically significant. Blood lead levels were highest in non-Hispanic black chil- dren, followed by Mexican-American chil- dren, with non-Hispanic white children having the lowest levels. Children living in homes built before 1946 had higher BPbs, as did children liv- ing in lower income families. Children liv- ing in metropolitan areas with a population ?1 million had similar geometric mean BPbs to children living in metropolitan and nonmetropolitan areas with a popula- tion <1 million. However, children living in the more populated metropolitan areas were more likely to have elevated BPbs, though this difference did not achieve sta- tistical significance. Table 2 presents the geometric mean BPbs and percentage of elevated BPbs for children stratified by selected demographic characteristics and age of housing. The prevalence of elevated BPbs was highest (21.9%) among non-Hispanic black chil- dren living in homes built before 1946. The prevalence of elevated BPbs among children living in older homes whose fami- lies had low incomes was also high (16.4%). Geometric mean BPbs were con- sistently higher in persons living in older homes and in non-Hispanic black, low income, and large urban population groups. In general, the trends in percentage of children with elevated BPbs that were observed by race/ethnicity and income per- sisted when these categories were stratified by age of housing. Results of multiple regression analysis of children's BPbs are shown in the first column of Table 3. Final regression models showed that BPbs of children aged 1-5 years were significantly associated with age, non-Hispanic black race/ethnicity (com- pared to non-Hispanic whites), low income Table 2. Percentage of children aged 1-5 years with blood lead levels ?10 pg/dl, by year housing was built and selected demographic characteristics: United States, Third National Health and Nutrition Examination Survey, Phase 2, 1991-1994 Year housing built Before 1946 1946-1973 After 1973 Population group Geometric mean % Cl Geometric mean % Cl Geometric mean % Cl Race/ethnicity Black, non-Hispanic 5.8 21.9 9.4-51.1 4.5 13.7 9.1-20.6 3.3 3.4 1.4-7.9 Mexican American 3.9 13.0 5.7-29.8 3.0 2.3 1.1-5.1 2.6 1.6 0.5-5.2 White, non-Hispanic 3.3 5.6 2.2-14.4 2.4 1.4 0.3-6.0 1.8 1.5 0.3-7.0 Income Low 5.5 16.4 9.9-27.2 3.6 7.3 4.6-11.4 3.0 4.3 2.1-9.1 Middle 2.9 4.1 13-12.8 2.4 2.0 1.0-4.1 1.9 0.4 0.1-1.3 High 3.1 0.9 0.1-6.5 1.9 2.7 0.6-11.3 1.6 -a _@ Urban status Population ?1 million 4.1 11.5 6.-20.2 2.9 5.8 3.2-10.4 2.1 0.8 0.3-2.1 Population <1 million 3.5 5.8 2.0-16.8 2.7 3.1 0.9-10.1 2.0 2.5 0.7-9.6 Cl, 95% confidence interval. &Sample size too small for valid estimate. Volume 106, Number 1 1, November 1998 * Environmental Health Perspectives 746 Articles * Exposure of U.S. population to lead (compared to high income), and residence in homes built before 1946 or from 1946 to 1973 (compared to homes built after 1973). As in the stratified analysis, sex and urban status were not significantly associat- ed with BPbs in children. Season of the year was not a significant predictor of BPbs in children. Blood lead levels of persons aged ?1 year. The geometric mean BPb for persons aged ?1 year was 2.3 pg/dl, and 2.2% of these persons had elevated BPbs. Table 4 presents BPbs for this age range by selected demographic characteristics. Geometric mean BPbs follow a U-shape, with BPbs higher among the very young and the very old. The prevalence of elevated BPbs had a similar U-shaped distribution. Males had higher mean levels than females and a greater prevalence of elevated BPbs, especial- ly among those aged 12 and older (Fig. 1). The BPb trend with race/ethnicity followed the same pattern as for children, with high- est levels seen in non-Hispanic blacks. Blood lead levels were also found to be higher among persons living in older homes and persons living in lower income households. Persons living in urban residences in more populated metropolitan areas had slightly higher geometric mean BPbs than those from less populated areas; the difference was of borderline statistical significance. Figure 1 shows geometric mean BPbs stratified by age group and sex. The overall difference between males and females noted in Table 4 is seen in this figure to be more pronounced in persons aged 12 and older. Figure 2 shows geometric mean BPbs strati- fied by age group and race/ethnicity. In gen- eral, non-Hispanic blacks had the highest levels, with differences most pronounced in the age groups 1-2 years, 3-5 years, 50-59 years, 60-69 years and ?70 years. Except for persons 60 years and older and those 20-29 years, Mexican Americans had BPbs inter- mediate between non-Hispanic blacks and non-Hispanic whites. Table 5 shows BPbs for persons aged ?1 year by age group, sex, and race/ethnici- ty. In these three characteristic stratifica- tions, trends are similar to those seen when age group, sex, and race/ethnicity were examined separately (Table 4). The highest geometric mean BPbs were found in non- Hispanic black males (5.4 pg/dl for ages 1-2 years, 5.9 pg/dl for ages 50-69 years, and 6.6 pg/dl for ages ?70 years). Table 6 provides a similar stratification by age, sex, and age of housing. In every age and sex subgroup, except ?70 years, BPbs are higher in persons living in older homes. The U-shaped association of BPbs with age is found in each of the subgroups defined by sex and age of housing. Results of multiple regression analysis for age groups 6-11 years, 12-19 years, 20-49 years, and >50 years are presented in Table 3. The multiple regression results for age, Table 3. Regression coefficients (standard errors) from linear regression analysis of log0o blood lead by age group: United States, 1991-1994 Covariates Intercept Age Race Non-Hispanic black Mexican American Non-Hispanic whitea Sex Male Femalea Income Low Middle Higha Year housing built Before 1946 1946-1973 After 19738 Urban status Population ?1 million Population <1 milliona Season of year Spring Summer Fall Winters 1-5 0.359 (0.034)* -0.046 (0.008)* 0.190(0.032)* NS 0 NS 0 6-11 0.268 (0.052)* -0.021 (0.006)* 0.180 (0.024)* NS 0 Age (years) 12-19 0.015 (0.022) NS NS NS 0 20-49 -0.174 (0.031)* 0.010 (0.001)* >50 0.140 (0.054)* 0.003 (0.001)* 0.077 (0.017)* 0.118 (0.030)* 0.071 (0.018)* NS 0 0 NS 0.188 (0.024)* 0.247 (0.012)* 0.172 (0.015)* 0 0 0 0 0.201 (0.025)* 0.166 (0.034)* 0.199 (0.024)* NS NS NS 0 0 0 0.258 (0.040)* 0.095 (0.021)* 0 NS 0 NS NS NS 0 0.241 (0.038)* 0.096 (0.030)* 0 NS 0 NS NS NS 0 0.070 (0.031)* NS 0 NS 0 NS NS NS 0 0.068 (0.012)* NS 0 0.057 (0.018)* NS 0 NS 0 NS NS NS 0 0.094 (0.025)* 0.060 (0.019)* 0 NS NS 0 NS 0 NS NS 0.061 (0.023)** 0 NS, not statistically significant (p>0.05). &Reference category for variables in group. *p< 0.01; **0.011 .. ` -. ... ..-`.1. .. .,.'.:f:,... .:...",::. .-- 1,,,, --1, ,' . ..... ....:.:.?. :, ?'...,.:,. :. ..--- . ... ..... ...:!?..:. -...,.... ..:.,?:.:..,. ..,.;.... .::::,.,., . ?.f.?:-...:. .- ..":?:Z?:'??,. .....:..,. .... ... .. --":.,?..'. . .''.?;,f ,??;.??,??..;?': ... 111 ...I.. --- --- .... ...-.?.'.'. .. ....... .1.... ...5;., .. ; .. ::,:.1....... ......... .... :?.. ...... 1 .1 .... 1 .. ... 1 .. 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':-.:: .. - '--?ful;?,?,::,..:...? --- : t- .,... .1 1: H : .;: ? ? :5 z:,; . : i:. :: ? ?.:,'?: ... :: multiple efforts to reduce exposure to lead. f? x:??:::: ?.?:r;, '..5. .. . :.. :- :- ?::.:.. :'-:ff': : ,.::: ..... .. ... 5. . 1.... :-:: : .. ..,:::':5: . .:.. :: ...?': ..,.: ?. .. ... ...1..... .: ..... ' ?:.:.:..f .... ..-..' : .... ....---.'.... .' ::-, ....... .- .... ... .- . . ....:::.:. .. .:;: J:L. :.5--- . ::.":5::"15 "' '--- :.. :--'-, -. '?,:: ,;::':, ---.:?;?. ' -.: : .- . 'U .,:::. .. .,: :55 ?. ?. :..i??;;?,.'??.????i?f; ' :."?:.,? ;?::?: ?.,: -; .:: : :? ::,: ::f '?. .: .::?.??,;:'???::-'?-.1... 1 ,:;::z...:? :?: ?:f ::??n f?. .::'.???;:: .z.?z?: 'U: ,:,z::?, .. 111---1.1 ....... :h: ?,:::?: "' ---.:. ??!Ja????i????????: 1? ...?.... 1... ....... ,..I.Ii1.. .... --- .?,5? ?: ? ?? ??,, ??',????,???,?. ??:.,, ': ?The reductions in the amount of lead in .???l:lzl:,:,?. :: --?ff?z:5;uz:?,' ? ? 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U: ::: :::: - ?. 5. . .. .. .:.1 ::,...::: : - f?.: ... ?: .,?:,n '. ...-:: ?-: .z.:- .1 .5,::: ? .1 .... .......... ---5 ;:: : :: ? :: .... ':? z?5 ..... - --- .... .. :5:. :: .:?:?:z:;::?,:::, ------ :?.. f :?.; :... 1.1..11 .???.?'. .. .: ::?.. ?::: ?.,.:...:5.?:,.:.,:::: ... ---1.1 ??:. .11 "U W; --- ?,? f; U fz: z: .: J:.: :5t? f: - M.- .9 drink cans, and plumbing systems greatly ---z------------------------ .,:z??,?:? ::M: :? :::"z :. :; :: : 1 ?: g r: ', --- "' .. 11 .. ?.1 :1 :5 1.1---. !.n11 '?:::: ::: f1.:?:::? .. .::...I.,,., 1. .. .5? 1? ? z? 1 .1 : :? ? ------ ..I..A:?? ?z...?... f? ?1 -%:: 1? 111-h . . .:,..:.. d?? l.:.z:?;: ?:" ... . :. .?,?,..5,:, :1 ?;-? :f,z?. ' .?:r:' ::. . ::?,?.::.:.::-.:' 1: ?. . ::: .5 1? .? ?:.. '..:.: ' .. ... :? ? - : .. ,:. . . ...:5 contributed to decreased lead exposure for . ----. .... .: f ?j" --- .1. ,:..j; --------- --- ... ;ki?,'....f....:5C? : ......1 .. -1?: .'.I.I. .f ?:. -1. z:.' . 1. :: ?--- .11.:11. .. .'?z:. 11.1 ..I... ;.1112t::: --- :::. : T :hgz.?? :. .. '!.!,,? . ?i?z.::1' ??11 ..::? ?'I ... ---1 ..: ? ? iffl: . ,?:?: .U :. the overall population (1,3,18-22). From .1::: W: ?:? -z: :,: 1? :.- .1.....::? .. .11 -..... .. ':. ---.?11 .:,. :?? : .: ...I. :::: ,,,? : ?,:.: .- f 1... .... :f, .- :- ..z --- ... .. ---. 1..' .. ? : 1976 to 1990, the amount of lead in gasoline ? -11 ::: "-::;? r:?:: ..... 1. 111:111---. ---U ,?::: :..::: ::?:. ;f;: 1.?:: ?.; : :. .?.f ,:, :z ?.J ?:: .? decreased by 99.8% (18). In 1980, 47% of .?,? . .:.:.. :- 11 --- les :5??:: .:: . .... :' .:- 1... ', ,:.f.:.. ... ... .X .. . .. ..,::;: . ..'S .j., . .. . .. -- ?' ale ... ', .. : '-;M -- ---::;: --- .: .' ?:.x?: .z:%. f: :P': .:,.,?? 5,: f. ?l.i ------ 11,11 .. food and soft-drink cans were lead soldered. .....I ?:::" i?,?? . ?.:, ??? :- f::::; f:.. 'z: ....11 5;:,?? .?:.1. .= . -? ?? ------:fi?. ...I. 'I :??f :f ::1:: :?i :f?z: . z :..? 111. :,?:i? .. :. 1?. ... :. --- .1.5 :?.1 ... . :::...: .:: .1 . BY 199 1, lead-soldered food and soft-drink 1-2 3-5 6-11 12-19 20-29 30-39 40-49 50-59 6"9 k70 cans were no longer manufactured in the Age (years) United States (20,21). In addition, treatment 'eometric mean blood lead levels by age category and sex: United States, 1991-1994. of water to make it less corrosive to pipes, 1 regulations to protect workers from lead exposure, and chfidhood lead poisoning pre- '..... . .. ? - : :: :. :: ?1 .:: 549 5 -- :: . ... ... :.: X - ::. :.. - .. -- ::.X:::: ,:. ,:. - . ..::,:f?,X.;:?%.:... .... , .:.,:..- :..... .... :. .... . .:f: ?. 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', :....:z :5 :?:.. :,:.: ? -:'. ::-.: z 1'1;? ::; ,??: ' Tf '`:.: ,!..,?::: .::??:f:f ?:f .........1:: f;?:f? p???',. ,??.,-.?i??.???.;" - ',-.?i,?lead exposure. Continuing decreases in air .1:1? ..:??::":zz?"f:??,?.'. ::? : , 5 z ?-,.ll?l????,?l?? f :.' .?:?-,????,????,??? 1. .; .. --- A? 2, .? .. - -....: .::?:?????.:.::,,?:? . ...??:. 1?V.1M',?E''1,:.. .:5.?? ? :?:z::;:: 1'.?1...... .. .. --- ,.: --- 1. ,?.::??:, :?. ?'?-- :'.. ,:.? ...... --- 1.-1.:, ,;: ' ' : ' ' ?: '..:,:::?::?:.::?:..: . ?:::; ::5; : ::, . .-:-.!::,:.: :- - ?' : ? ": ::...5 ' ? ? ?: ; -.:.., .'.:. --- ' .: .; - ?' . f- ,5, :f ??5%,... .:: :11:':'. :- - ,.. .. .......;-.. ---.. . ..I. . .".:f,!,:,;,,., r :.? ' : '- - :'...?.: :' :?: " -1, ? ?::. ...... ..1?1. ,??n: .:?. , . :: . ::?.::f ': :: :,:::: H;1.:. - -- --..-- .' ..?...; :- - ,,: ??-.? ?:; ?; ? -II! ." .' '. .. .- --- ' ., . '.,:f?.::: ?.1? ...,?..? 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'.:' :???;?,?:: ? d 5. 11 .. 15 ?? ?; i? ?i i 1 1 1.:: :m : ; ? ow Z ;:: !: 5 :::?:?:: ::? ; : ? : ? ? ? ? : : j? y : l?,? ? ;: !: ;, :1 MR,;:::? ? i!',!?.?-5??i-? li'-!i,?? ,: ?? ? ? ? ??',.?i ??-,!;f? ?::!, %?,:::?,I?j?,?l ??-?? 9?': ? ? ?? P ? W,% .. ........ .;;;:?.?i??:? '....1... 1. .. .a..;:ulz ...... ;;??????:: ? ?; ' M7 :: f? = ??:,: .... ... ::??f ` ? .? :;:?:?.::? : ?;:u : ? ::...a: J. Em: w?. ' --- z Ui 1. --- : '-- ...1 ::,:??;.?:;z?!?:??;.,:.u:.:?::?? ','?'f'u'?f,:,: ??::."". .. ?l.l:::? ation that lives in pre~1950 housing have ?;:?.. .:: :::?:? ,?:f?llzf:?:?i?;;:: : ?' 5....--- 5 ?z1?1 ::;! :?:5: ::f: : 1- ..:;: :.?l: :: :: :, : ', ": 1: ?: z, ; ?1 55C 1 ?_ - :-'?::?'?:... ... -1-111 .... .1.?; :?, .11 .1.11.1---. ::? ?'.:?:: ng?.?:????????:;i.????????????-???? .1:: ? :%. .1 : ?? ? ? :?:z ?:...: .?;: ?..r.:?-- ....... :: - - 1- ---1 -..; .?;: ?::.". 111.1 ...1.. .. 11 ..... 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' - z-. :: :....:. . ... :: . ..: --- ::: ' : - .. .. ,?: g:' 45,-,z. 5; X . :: .:- ::.--- ...... 1. :-.-,;;:".:.:- .If.;.:-?-::.,:: ---? ??-',-',- ... i? ? ?,',?'? ? ?,.'.? h .' ? - ? .-.: ?5??.:: ..... ..... ?::f,: .1:-?.?:"?:?:: ?.;:..:..:.::?:?::.:.; ??:?:?,??.f?... ., 1 .....%. ::%: f5???i; :: ,z:: f .? W: - ,.: likely contributed to the continuing dedine :::. ?: : :??: ????.?:.?:?.:???,,?????;??., ::.,'?:5;z?.,.:? :.:.5 :.::5:"5::, 5... :.. 111. . 1:111.... . .. .' .: .:?.:::z?.." 1 : :? 1 ?,, 5 : in??,? 5;i.:???n:?????n?z!;:: .: ::::i 111.11 ....1... "...I.."'?l"...::?: ?.'5 : 11 1. .. 111.11. .?:f? .. .1 .. : 5::'''?. '51: :? ...' :: ' ?: '.1''I??!!,?:???il? ,ilii 'n :?', ', 1",?? ?? M' ?lli?l?l???????zl?, '.??t '.???j . : ,?: : ?.. ..... ------ '.::??,,: ??il!'?,, 5, '...' 5` ? ?:. 5 '? X?z'.5---. --- : ' j- ' 51--- ' f?t;:,' ', ?: :: : ?: : ?? ? t: ?5 :?:: .... 111'--- 1-1 :?:? - '- .1' ,: ?5 ??!:il?-z?: :: : ?: 5::: : ? ? 11 : z ?' ?: ?: ? :??: ??; f??; ..?!? :::? :: ? ?.:. 1??:, .1.11,11 ::.. - a'?.-:; ?::E, 1 ---11 ,??,n?;; :???:???;???. ,?, .` .: . .z-X::.. ? ?:5.??5; f? -::?i 1 . . z 1111;1?? "1:1??' ? 111'n' :::::n. ::::,:: ? 5::::? :?:,,? ? z : 1.?!:.?????;???-????_.?? ?:'.:, .. -1-,:..... .. g...;;f .f?????t:z .... i:.:.:- ?:f?zn!;?z,:: .Ill.:f ..: ez :C f:,;?:- ;-?.::.? .z - --Ay . ;;: ?l ?5?!?i!?,???,: 1.. :- ?:?,.1z:;? ?:, .:.,: :5:.... 1... 59:' ?;: :. ? U: f ?: f5 z".,?? ... ....z:. - .' :: : ? ;:; u?_ f' ?' ---' ---1:?:5,?: :. ?: :? '. .. :.,. ::. : .: - ' , --- :? , - A. z?.?:?????!b?;??????:?. ?:?7 .. ............. .'.?????iii ---: .j. ??:?r?',i :::... in BPbs since NHANES III, Phase 1 (23, 9A 11 :,::: f ?: ?x:? .... ... ::.;,mt-:f?: ... ... . .... .:f .j.x:f:; :..: n..'. ''?.. ? ?: '--------- . ------ 1.-.? .. ...... . :,X.r: ... .. Z: -1.. . .. .. ?. .1? .... . ..: .. .?..:.: ?1-11 .z. .. ?.... ........1...? .1 ?:, . . ?. .... 1;?'..:;,.,:. f.. X- .1. ..?... .:: =1':.. ..I;:, e .... ... W. .:%7:?.C. - 1--- .. ......:--T,;....::..'..-?. 1: .:: :. 1 ......... .... .:: --- .. 5,5.. ..? .. .: : . ? 1 --..- .. 1_. ..... 1. :::. --- .. .1.:? h:?:.j:m5:: ---11-1 ... . ... ---- --- .. ?l???:.,?? :?" ::', :f". 1.5 :.? ?:: . . . .11' :'', ?:,? ::? .??f? .1. ;?':.??.::.?:5 z:?????? ::,::1? :5 ' ? ?; hj?: .- : ', 2-1 :? ;??;??????,?i",j? .1 . :?:?.;:f:E;,??fXz5 !::? ' :?? --- , ?:: ::::: : :M z ? ?f ;:: ? ? f? ,:,:: ? 1: ??. ?, ,: : ? :: t.. ?::::? --- The data reported here indicate that some i? :?: :: :? :J :o w. :.. :::5:,????zi-e?'!'..f??.::. 'k: 1?:.::,?.:. -z. :?? ;?::: ?? ?:? ?f .1.1..W--- .?:?l, ---n .. :? :::R::? : ?l: : :: .?: -,?? ? ?: ', ?f :.:?:?: :5,? .:::: : : :!.':?'5'_k : .,::,!"5?,, ?1m?---'.. ..... .C..::.: -?151. ? ?:'--- 11,1 11---.... 1-.;, ,Pi ffl-5.: ?'.. -?::.il???lli!I?5,.???,,?.,?:?,?? :??l?,f??:?,nz??l ;:1 115 9M i PP%1U:'1 :?:?:? f '--- ,u5?,?"gz?!;:?'' :.?......... w?? ? ?!!?-11?l, -; ; ... ... :?::: '--. ..n;:f ?::f'? :: :::,? : :,z:.-A 151?1:?n. ..?. -- ?.? ':: .. %'z::? ":: ?:5 z: :, :. : ::: :: ::: ? : w: 5:; ;.1 .. TI. ? ? ?',?t'?iJ. : .: - .:: : ', :; . .. -1 ? ::: 5 :: % . - --- ?? 5; z., ` . :,:::.. .:. - - . fl .f:,:::".?:'..population groups continue to be dispropor- ---1. .... ....: -:.!:? ,j:;...::-- .,.,...... :-.', .;"..1. :--- ......... ...,-. ------ -.z,;. 5..' . ... ....:f. .f?: .f. .. :?:. ., 1.::.. :,.,?,.,?.: :... ... :: . M .: .. .. ..-:f- :: . --- .. --- . ... .. . .. -::, ',. .Z%... 1..". .:. .. :::: :: .?: ?. ?i ?g'?.... .::::. :,:: --- ,,??.... :... :?::,? ::%; C. ...-1 ::,:::?ii?,?illf..?,5 :z::,.?5?z? :: :.. ... : '. :.i?i?f??;??;?i????. ij 5?.i .?,:??:P.. 1 1?:::; ,?:-?: 5 ??,,?i?!,,'i?????:?I??.i? ????i?,.::;,: .... tionately at high risk for elevated lead expo- noted in the late 1970s and early Phase 1 (1988-1991) to 2.7 in Phase 2 deteriorated to the point of being a health 17). The most likely explanation for (1991-1994). Over the same time interval, hazard (27. Hazard control costs are highly f significant seasonal variation in the the percentage of children ages 1-5 years with variable, depending on the extent of the Volume 106, Number 1 1, November 1998 * Environmental Health Perspectives 748 Articles * Exposure of U.S. population to lead Table 5. Geometric means and 95% confidence intervals (CI) of blood lead levels (pg/dl) for persons 1 year of age and older by age category, sex, and race/eth- nicity: United States, 1991-1994 Non-Hispanic white Non-Hispanic black Mexican American Geometric Geometric Geometric Age (years) Sample size mean Cl Sample size mean Cl Sample size mean Cl Males 1-2 163 2.8 2.5-3.2 148 5.4 4.6-6.3 172 3.6 3.1-4.1 3-5 153 2.1 1.7-2.4 246 4.3 3.6-5.0 248 3.1 2.6-3.5 6-11 162 1.7 1.5-1.9 291 3.2 2.7-3.5 201 2.2 1.8-2.7 12-19 149 1.7 1.4-1.9 315 2.5 2.1-2.8 246 2.4 2.2-2.5 20-49 526 2.7 2.4-2.9 663 3.3 3.0-3.6 732 3.3 3.1-3.5 50-69 399 3.4 3.1-3.6 245 5.9 5.2-6.7 249 4.3 3.9-4.8 >70 423 4.4 4.2-4.6 112 6.6 5.5-7.8 105 4.0 3.3-4.7 Females 1-2 139 2.6 2.0-3.2 145 4.2 3.4-5.0 158 3.0 2.4-3.5 3-5 176 2.1 1.9-2.3 244 3.9 3.2-4.6 249 2.9 2.4-3.3 6-11 148 1.7 1.4-2.0 294 2.8 2.4-3.1 178 2.2 1.9-2.5 12-19 192 1.2 1.0-1.3 360 1.5 1.3-1.7 260 1.4 1.2-1.5 20-49 801 1.5 1.4-1.6 1,001 1.8 1.7-2.0 770 1.7 1.6-1.8 50-69 483 2.5 2.3-2.7 278 3.3 2.7-3.8 255 2.4 2.1-2.7 ?70 639 2.9 2.7-3.1 116 3.3 2.8-3.8 100 2.7 2.4-3.0 Table 6. Geometric means and 95% confidence intervals (CI) of blood lead levels (pg/dl) for persons 1 year of age and older by age category, sex, and year hous- ing built: United States, 1991-1994 House built before 1946 House built 1946-1973 House built after 1973 Geometric Geometric Geometric Age (years) Sample size mean Cl Sample size mean Cl Sample size mean Cl Males 1-2 93 4.1 3.3-4.8 184 3.6 3.0-4.3 389 2.6 2.2-3.1 3-5 113 3.8 2.9-4.8 260 2.5 2.1-2.8 197 1.7 1.5-1.9 6-11 112 2.6 2.2-3.0 262 2.0 1.7-2.2 207 1.4 1.3-1.6 12-19 126 2.1 1.6-2.5 293 1.9 1.5-2.3 221 1.6 1.4-1.8 20-49 327 3.2 2.8-3.5 749 2.8 2.4-3.1 645 2.5 2.2-2.7 50-69 188 4.1 3.6-4.6 478 3.7 3.3-4.1 190 3.3 3.0-3.6 >70 213 4.7 4.3-5.0 319 4.3 3.9-4.7 82 4.9 4.4-5.5 Females 1-2 60 5.2 4.2-6.1 177 2.9 2.5-3.4 152 2.2 1.9-2.4 3-5 102 2.9 2.3-3.5 268 2.6 2.3-2.9 232 2.0 1.7-2.2 6-11 112 2.6 2.1-3.2 232 1.9 1.5-2.2 196 1.4 1.2-1.7 12-19 147 1.5 1.1-1.9 338 1.3 1.1-1.4 261 1.1 0.9-1.2 20-49 430 1.7 1.5-1.8 1,026 1.6 1.5-1.7 853 1.5 1.3-1.6 50-69 242 2.9 2.5-3.3 557 2.5 2.4-2.7 197 2.5 1.9-3.0 ?70 286 2.9 2.6-3.2 389 2.8 2.6-3.0 139 2.9 2.5-3.2 intervention, existing market conditions (such as degree of competition among con- tractors and licensing laws), type of hous- ing, and associated housing rehabilitation work. However, median costs range from several hundred dollars for spot repairs to around $10,000 for complete abatement of paint with window replacement (28,29). Because of the high cost of abatement, the scarcity of adequately trained lead- abatement professionals, and the absence (until 1995) of federal guidelines for imple- menting less costly methods of leaded paint hazard containment, residential lead-paint- abatement efforts have focused on homes in which there is a resident child with an ele- vated BPb (i.e., secondary prevention), rather than on homes that have the poten- tial to expose a child to lead (i.e., primary prevention). Similarly, publicly funded lead poisoning prevention programs have focused on screening children to identify those who already have elevated BPbs so that they may receive interventions, rather than on preventing future lead exposure among children without elevated levels. However, at least some of the adverse health effects that occur even at relatively low lev- els of lead may be irreversible (306. As the number of children with elevated BPbs has decreased, lead poisoning prevention pro- grams may now be able to redirect some of their resources to primary prevention, thus protecting many young children from need- less health damage. Still, secondary preven- tion efforts through screening will remain vitally important to ensure that children with elevated BPbs receive prompt and effective interventions to reduce further lead exposure and minimize health conse- quences. As this analysis demonstrates, the risk for lead exposure is not spread evenly throughout the pediatric population. Rather, lead hazards can be localized within neighborhoods, largely due to such factors as housing conditions, industrial emissions, or dust and soil contamination; more rarely, lead hazards occur sporadically as a result of such factors as parental activities and use of leaded ceramics, cosmetics, or folk medicines (1). In accordance with these findings, the Centers for Disease Control and Prevention recently advised health departments to evaluate the distrib- ution of risk for lead poisoning in their communities and devise locally appropriate screening recommendations (25). Universal blood lead screening is recommended only in high-risk areas; in generally low-risk areas, screening should be targeted to those individual children at high risk. Physicians are advised to follow the recommendations of their state and local health departments to determine which of their pediatric patients should be screened. REFERENCES AND NOTES 1. CDC. Preventing Lead Poisoning in Young Children: A Statement by the Centers for Disease Control. Atlanta, GA:Centers for Disease Control, 1991. 2. ATSDR. Toxicological Profile for Lead. Publ no PB93- 182475. Atlanta, GA:Agency for Toxic Substances and Disease Registry, 1993. 3. Pirkle JL, Brody DJ, Gunter EW, Kramer RA, Paschal DC, Flegal KM, Matte TD. The decline in blood lead Environmental Health Perspectives * Volume 106, Number 1 1, November 1998 749 Articles * Pirkle et al. levels in the United States: the National Health and Nutrition Examination Surveys (NHANES). JAMA 272:284-291 (1994). 4. Brody DJ, Pirkle JL, Kramer RA, Flegal KM, Matte TD, Gunter EW, Paschal DC. Blood lead levels in the U.S. population: Phase 1 of the Third National Health and Nutrition Examination Survey (NHANES IlIl, 1988 to 1991). JAMA 272:277-283 (1994). 5. Centers for Disease Control and Prevention. Update: Blood lead levels- United States, 1991-1994. MMWR Morbid Mortal Wkly Rep 46:141-146 (1997). 6. Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG. Chronological trend in blood lead levels between 1976 and 1980. N EngI J Med 308(23): 1373-1377 (1983). 7. Carter-Pokras 0, Pirkle JL, Chavez G, Gunter E. Blood lead levels of 4-11 year old Mexican American, Puerto Rican, and Cuban children. Public Health Rep 105:388-393 (1990). 8. Mahaffey KR, Annest JL, Roberts J, Murphy RS. National estimates of blood lead levels: United States 1976-1980. N EngI J Med 307:573-579 (1982). 9. CDC. Plan and Operation of the Third National Health and Nutrition Examination Survey, 1988-94. Vital and Health Statistics Series 1, No 32. PHS 94-1308. Atlanta, GA:Centers for Disease Control and Prevention, 1994. 10. Ezzati TM, Massey JT, Waksburg J, Chu A, Maurer KR. Sample Design: Third National Health and Nutrition Examination Survey. Vital and Health Statistics Series 2, No 113. PHS 92-1387. Atlanta, GA:Centers for Disease Control and Prevention, 1992. 11. Miller DT, Paschal DC, Gunter EW, Stroud PE, D'Angelo J. Determination of lead in blood using electrothermal atomisation atomic absorption spec- trometry with L'vov platform and matrix modifier. Analyst 112:1701-1704 (1987). 12. Gunter.EW, Lewis BL, Koncikowski SM. Laboratory methods used for the Third National Health and Nutrition Examination Survey (NHANES III), 1988-1994. Hyattsville, MD:Centers for Disease Control and Prevention, 1996. 13. USDA Food and Nutrition Service Financial Management and Program Information Division. Annual Historical Review of FNS Programs: Fiscal Year 1987. Washington, DC:U.S. Department of Agriculture, 1987. 14. Butler MA, Beale CL. Rural-Urban Continuum Codes for Metro and Nonmetro Counties, 1993. Staff report no. 9425. Washington, DC:U.S. Department of Agriculture, Economic Research Service, Agriculture and Rural Economy Division, 1994. 15. SAS Institute Inc. SAS Language: Reference, Version 6. 1st ed. Cary, NC:SAS Institute Inc, 1990. 16. Shah BV, Barnwell BG, Bieler GS. SUDAAN User's Manual, Release 7.0. Research Triangle Park, NC:Research Triangle Institute, 1996. 17. U.S. EPA. Seasonal Rhythms of Blood-lead Levels: Boston, 1979-1983. EPA 747-R-94003. Washington DC:U.S. Environmental Protection Agency, 1995. 18. U.S. EPA. Quarterly Summary of Lead Phasedown Reporting Data. Washington DC:Office of Mobile Sources, Office of Air and Radiation, U.S. Environmental Protection Agency, 1991. 19. U.S. EPA. Air Quality Criteria for Lead. EPA/600/8- 83/028aF. Research Triangle Park, NC:U.S. Environmental Protection Agency, 1986. 20. Can Manufacturers Institute. Food and Soft Drink Can Shipments. Washington, DC:Can Manufacturers Institute, 1992. 21. Bolger PM, Carrington CD, Capar SG, Adams MA. Reductions in dietary lead exposure in the United States. Chem Speciation Bioavailability 3:31-36 (1991). 22. Adams MA. FDA total diet study: dietary intakes of lead and other chemicals. Chem Speciation Bioavailability 3:37-41 (1991). 23. U.S. EPA. National Air Quality and Emissions Trends Report, 1995. EPA 454/R-96-005. Research Triangle Park, NC:U.S. Environmental Protection Agency, 1996. 24. American Housing Survey for the United States in 1993. Current Housing Reports, H150/93. Washington, DC:U.S. Department of Commerce, 1993. 25. CDC. Screening Young Children for Lead Poisoning: Guidance for State and Local Public Health Officials. Atlanta, GA:Centers for Disease Control and Prevention, 1997. 26. Office of Pollution Prevention and Toxics. Report on the National Survey of Lead-based Paint in Housing: Base Report. EPA/747-R95-003. Washington, DC:US Environmental Protection Agency, Office of Pollution Prevention and Toxics, 1995. 27. Lead-based Paint Hazard Reduction and Financing Task Force. Putting the Pieces Together: Controlling Lead Hazards in the Nation's Housing. Washington, DC:US Department of Housing and Urban Development, 1995. 28. Requirements Notification, Evaluation, and Reduction of Lead-based Paint Hazards in Federally Owned Residential Property and Housing Receiving Federal Assistance; Proposed Rule. Part 11. Office of the Secretary-Office of Lead-based Paint Abatement and Poisoning Prevention, Department of Housing and Urban Development. 24 CFR Parts 35, 36 and 37. Fed Reg 61(111):29169-29232 (1996). 29. Jacobs DE. U.S. Department of Housing and Urban Development Office of Lead Hazard Control, personal communication, 1997. 30. Silbergeld EK. Mechanisms of lead neurotoxicity, or looking beyond the lamppost. FASEB J 6:3201-3206 (1992). 750 Volume 106, Number 1 1, November 1998 * Environmental Health Perspectives