Department of Anesthesiology. Charles R. Drew University of Medicine and Science. Los Angeles, California and. Department of Developmental Neurobiology.
Blood Lead Levels in Children in South Central Los Angeles STEPHEN I. ROTHENBERG Department of Anesthesiology Charles R. Drew University of Medicine and Science Los Angeles, California and Department of Developmental Neurobiology National Institute of Perinatology Mexico City
EREDDiEA. WILLIAMS, JR. SANDRA DELRAHIM FUAD KHAN MICHAEL KRAFT MINHUI LU MARIO MANALO MARGARITA SANCHEZ DANIEL j . WOOTEN Department of Anesthesiology Charles R. Drew LJniversity of Medicine and Science Los Angeles, California
ABSTRACT. We retrospectively reviewed 3 679 pedialric records from King/Drew Medical Center, south central Los Angeles, between 1991 and 1994. Blood lead levels of children were followed to age 18 y. Patients were not referred specifically for lead poisoning. The sample was primarily Latino. Geometric mean blood lead peaked at 6.7 |ig/dl (0.32 |imol/l) between 2 and 3 y of age. There was a downward secular trend and a seasonal trend. Males had higher lead levels than females. Children who lived in several zipcode areas, in which the lowest family incomes were reported, had higher lead levels. More Latino children had higher lead levels than African American children. Latino children (i.e., 20.2%) who were 1-5 y of age had blood lead levels that were > 10 fig/dl. Young Latino children in this zone of Los Angeies may be at increased risk for lead exposure.
THROUGHOUT THE UNITED STATES national blood lead levels have fallen precipitously during the past 20 y in the nonindustrially exposed population. Preliminary Third National Health and Nutrition Examination Survey (NHANES-III> data (1988-1991) indicated that the mean blood lead level in the United States was 78% less, compared with a similar study conducted in 1976.' This decrease can be attributed to extraordinary efforts aimed at environmental lead control during that period. Permissible levels of lead in gasoline have been reduced periodically, more automobiles use unleaded gasoline, and we are approaching the point of eliminating leaded gasoline for private automobiles nationwide. Lead in solder for articles in contact witb food or drink (e.g., solder for copper water pipes or soldered tinned foods) has been reduced or eliminated. Import controls, product testing, and professional and public education have served to reduce tbe contamination of foodstuffs from lead-glazed pottery. Lead in paint September/October 1996 [VoL 51 (No. 5)]
for new domestic use bas been eliminated. Statewide childhood screening programs, sucb as the California Childhood Lead Poisoning Prevention Program, bave also contributed to tbe decrease by the timely identification of children with high blood lead levels. Nevertheless, tbe same data confirm tbat blood lead levels are not uniform across tbe country. The blood lead levels of poor, inner-city urban dwellers (i.e., primarily children of minority groups) are still significantly higher tban tbe national average.^ Recent studies of the effects of low-level perinatal and childhood lead demonstrated that even blood lead levels below the most recent surveillance limit of 10 |ig/dl set by tbe Centers for Disease Control (CDC) can result in damage to young children.^ The NHANES-lll data confirm that 8.9% of children (i.e., 1-5 y of age) nationwide bave blood lead levels tbat exceed the lowest CDC surveillance limit. It bas been sbown that 21.6% of African American and 10.1% of Mexican383
American children (i.e., 1-2 y of age) have lead levels that exceed 10 Mg/dl. Statewide reporting of elevated lead levels in California is limited to statistics solely for children who have blood lead levels that exceed certain state limits. Although these reports can be used to identify areas of the state that have an especially high incidence of lead intoxication in children, they reveal little of the prevalence rates of lead exposure over the entire exposure range. We initiated tbe present retrospective study to assess childhood lead exposure in children screened at the King-Drew Medical Center in south central Los Angeles. The catchment area includes some of the poorest areas of the city, and the residents belong mainly to minority ethnic groups.
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Statistical analyses: first blood sample. We tabulated
descriptive statistics and performed simple univariate or bivariate tests of lead levels against other variables. We 3B4
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btood Fig. 1. Frequency distribution of blood lead levels. Dotted line represents the theoretical log-normal distribution, based on calculated geometric mean and standard deviation of actual data.
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Sample. The sample comprised all children {N = 3 679) between 1 mo and 1B y of age who had been seen at any King/Drew clinic or service during the period from 1991 to 1994, inclusive, and for whom blood lead levels had been determined. Testing, which was done from November 1, 1991, to the end of the study period, was part of the California Child Health and Disability Prevention screening program for all children between the ages of 1 and 60 mo. These data, therefore, are representative of children who were not specifically seen for treatment of lead exposure. The results of tbe first blood lead analysis for eacb patient were grouped. Subsequent blood lead analyses for the same patients were treated individually. We retrospectively screened all case records of all children seen at the King/Drew Medical Center during the study period. Blood lead analyses. Lead analysis was completed by atomic absorption spectrometry (AAS), with graphite furnace or anodic stripping voltammetry. The data did not distinguish between finger-stick and venous samples. Laboratories that performed blood lead analyses were licensed by the State of California as clinical laboratories, with competence for measuring blood lead. One laboratory analyzed 98.3% of all samples, and the remaining samples were analyzed among three other laboratories. Variables. Blood lead was reported to the nearest whole |ag/dl. Subject ethnic group was by self- or parent identification. We used a Spanish surname if there was no ethnic identification in the record. Zipcodes were verified by cross-cbecking with given street addresses; in cases of conflict, the zipcode that corresponded to the street address was used. Sex, age at time of blood sample, and date the blood was drawn were obtained from tbe hospital record. For some samples, we found incomplete data (e.g., sex, ethnic group, zipcode address, dates). Incomplete data prevented statistical analysis of additional variables (e.g., age of mother, socioeconomic status).
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month of year Fig. 2. Seasonal trend of natural log blood lead over study period. Mid-points represent mean lead, and error bars are 9S% confidence intervals. Lead levels were lowest in late winter and early spring and were highest in late summer.
characterized variables that showed obvious nonlinear relationships with lead (e.g., age, season of sampling) with nonlinear regression, using minimum parameter models. A multiple regression analysis was also performed, and we determined the joint contribution OT the significant variables to blood lead levels. The number of subjects in each of the univariate or bivariate tests differed because the data were sometimes incomplete. Incomplete data about one or more of the control variables were found for 11 cases. The multiple regression tests were performed using only subjects for whom there were complete data. Multiple blood samples. We used ANOVA for repeated measures and post-hoc Tukey contrasts to determine if there were significant changes in blood lead Archives of Environmental Health
when children were tested more than once. All statistical tests were conducted by Statgraphics Plus (Manugistics [Rockville, Maryland]); 5PSS (SPSS [Chicago, Illinois]); and SAS (SAS Institute [Cary, North Carolina]). Results
The first analysis of blood lead included 3 679 subjects. The ethnic distribution was 73.3% Latino, 24.7% African American, and the remaining 2.0% was "other" or "unknown." The distribution of the first blood lead measurement for the entire sample of subjects is shown in Figure 1. We noted the log-normal distribution frequently encountered in population lead studies. To reduce outlier effects, we performed all subsequent analyses with natural logarithm (In) -transformed lead data. There was a significant difference in blood lead level with respect to gender. Males had, on average, a 1 |ig/d! higher blood lead level than females (F [1, 3669] = 25.44 Ip < .001 ]). We found a small, but highly significant, linear secular trend in blood lead levels between January 1991 and December 1994 (r = -0.135, df = 3 679 [p < .0001]). The downward trend totaled approximately 1 |ig/dl over the study period. There was a significant seasonal effect on blood lead levels: the lowest blood lead levels occurred during late winter and early spring, and the highest levels occurred in summer (Fig. 2). The maximum difference between early spring and mid-summer lead levels was 1.3 |xg/d!. The seasonal effect was fitted empirically by a nonlinear regression, using a Fourier model. The correlation coefficient of the model, adjusted for degrees of freedom, was r = .788. One-way ANOVA showed a highly significant age effect (Fll8,3660] =25.76 [p < .001]). EaHy childhood lead levels increased with age of child, and they reached a maximum in the third year of life (geometric mean \GM] = 6.7 |ig/dl) (Fig. 3). A double exponential model was fitted empirically by nonlinear regression with an adjusted r^ 0.890. These variables, or their models in the cases of seasonal trend and age, were entered into a multiple regression, with lead level stratified by zipcode (Table 1). Multiple regression showed that all the variables discussed earlier were significant and were independent predictors of blood lead level. The variables in the model accounted for 13.5% of the variation in lead levels (adjusted r= 0.368). The number of cases for whom there was more than one blood sample totaled 1 479. We stratified these patients into groups by lead level (i.e., < 10 [i&'dl, 10-20 ng/dl, and > 20 ng/dl). Approximately 50% of the patients returned for retesting in 50 wk, 8 wk, and 4 wk, respectively, for each lead group. Separate repeated-measures ANOVAs, with two timeadjacent blood lead tests as the within-subject factor and with a three-level between-subject factor of blood lead range (i.e., < 10 ^g/dl, 10-20 |ag/dl, and > 20 fig/dl), were performed for all cases with two, three, and four or more repeated lead tests. Post-hoc analysis September/October 1996 [Vol. 51 (No. 5)]
showed that all three ranges of blood lead levels changed significantly (p < .05) from the first test to the second (Fig. 4). The levels of the low-lead group increased significantly, from a GM of 4.9 Hg/dl to 5.3 jig/dl; the levels of the mid-level and high-lead groups decreased from 13.2 |ig/dl to 11.0 |ig/dl and from 28.2 |ig/dl to 21.2 fxg/dl, respectively. Blood lead in the highlead group decreased significantly (p < .05) from the second to third test (i.e., 28.2 ^g/dl to 20.9 |ig/dl). There were no significant changes in any group from the third to the fourth test.
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year of llta Fig. 3. Blood lead plotled by year of life. Mid-points represent mean natural log lead, and error bars are 95% confidence intervals. Tlie data entered for each year of life are the mean and confidence interval calculated from all subjects who contributed a blood sample from d 1 after the prior birthday until the birthday indexed on tbe x axis.
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