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Journal of the American College of Nutrition, Vol. 24, No. 1, 1-9 (2005)
Published by the American College of Nutrition

Determinants of the Blood Lead Level of US Women of Reproductive Age

Mi-Gyung Lee, PhD, Ock Kyoung Chun, PhD and Won O. Song, PhD, RD

Department of Food Science and Human Nutrition, Michigan State University, East Lansing, Michigan

Address reprint requests to: Won O. Song, PhD, MPH, RD, Professor and Associate Dean, Dept. of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824-1224. E-mail: Song{at}msu.edu


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Objectives: Blood lead concentration of an infant is largely affected by maternal blood lead recycling. This study aimed to identify sociodemographic, lifestyle, and nutritional determinants for blood lead levels (BLLs) of women of reproductive age in the United States.

Methods: Subjects (n = 4,394) were women (20–49 years old) included in the most recent complete National Health and Nutritional Survey (NHANES III). Certain sociodemographic, lifestyle and nutritional determinants for BLL were identified.

Results: The BLL of reproductive age women was 1.78 µg/dL geometric mean, The BLL was inversely associated with poverty income ratio and education level, hematocrit, intake of thiamine, and serum levels of folate, and positively associated with ethnicity (Black, Hispanic), living in urban areas or the Northeast region, age, alcohol consumption, cigarette smoking, serum protoporphyrin, and intake of pyridoxine, iron, and folate. Subjects in the lowest decile for serum ascorbic acid had significantly higher BLLs than those in the 2nd through 8th deciles.

Conclusion: Infants born to women who smoke, drink and maintain poor nutritional status for selected nutrients are at a greater risk of lead toxicity than those born to other women. Nutritional manipulation of thiamine, ascorbic acid and folate may impact BLL in women.

Key words: lead, children, women, nutrition, smoking, alcohol, vitamin

Abbreviations: NHANES III = Third National Health and Nutrition Examination Survey • BLL = blood lead level • PIR = poverty income ratio • ANCOVA = analyses of covariance • DRIs = dietary reference intakes • NCHS = National Center for Health Statistics • CI = confidence interval


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Lead toxicity is prevalent and a major concern of public health agencies in the U.S. and other countries. The World Health Organization has reported that blood lead levels (BLLs) in the range of 10–15 µg/dL cause adverse health effects [1]. The Centers for Disease Control and Prevention (CDC) also have established a critical value of 10 µg/dL for lead toxicity [2]. During the past decade, consistent efforts to abate environmental lead exposure in the U.S. have succeeded in reducing the mean BLL of 1–5 year-old children from 15.0 µg/dL (1976–80) to 3.6 µg/dL (1988–91) [3], 2.7 µg/dL (1991–94) and 2.0 µg/dL (NHANES 1999) [4]. The number and percent of children who are at risk however have not changed much. In 2001, 59.7% of children with BLLs ≥10.0 µg/dL had levels of 10–14 µg/dL; 21.3% had levels of 15–19 µg/dL; 9.2% had levels of 20–24 µg/dL; 8.6% had levels of 25–44 µg/dL; 1% had levels of 45–69 µg/dL; and 0.2% had levels ≥70 µg/dL [5].

One of the important sources of lead exposure for the fetus and infant is maternal blood. Lead in the maternal blood readily crosses the placenta and mammary glands. The level of lead in umbilical cord blood and breast milk is closely associated with that in maternal blood [68]. Breast milk lead level is also dependent on the maternal body burden of lead [8]. It was reported that 45%–70% of lead in the blood of reproductive age women originates from long-term tissue stores [9]. During pregnancy and lactation, the BLL increases by 15%–20% due to altered mineral metabolism [6,10,11]. Together, these data suggest that the blood and tissue levels of lead in reproductive age women determine the body burden of lead in their offspring. The FDA reports that reproductive age women in the U.S. are exposed to lead through food (43%), dust (31%), water (22%), and air (4%) [12]. Accordingly, efforts should be made to reduce the BLL of reproductive age women to minimize transfer of maternal blood lead into the fetus and nursing infant.

Several studies [1316] reported that BLLs of young children and their mothers are affected by sociodemographic and nutritional factors even after controlling for environmental exposure. A body of knowledge exists that certain vitamins and dietary components chelate with lead to reduce the body’s burden. BLLs have been reported in pregnant and lactating women [9,1719] and infants [20] in various regions. To our best knowledge, little is known on the cycling of blood lead through generations and means to reduce the body’s lead burden of child bearing age women.

The objectives of this study were 1) to estimate the BLL of reproductive age women in the U.S., 2) to identify demographic, lifestyle and nutritional determinants for the BLL of reproductive age women in the U.S., and 3) to estimate the odds ratios of modifiable (nutritional and lifestyle) factors for elevated BLLs of reproductive age women. The subjects were a nationally representative sample of women selected for the National Health and Nutrition Examination Survey (1988–94) (NHANES III).


    MATERIALS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects
The NHANES III was conducted to obtain nationally representative information on the health and nutritional status of the civilian, noninstitutionalized population of the U.S. between 1988–94 (phase I, 1988–91; phase II, 1991–94). The National Center for Health Statistics and Centers for Disease Control and Prevention (NCHS/CDC) conducted the survey through interviews, questionnaires and examinations.

Data from reproductive age women (20–49 years) who participated in NHANES III (phases I and II; 1988–94) were examined (n = 5,425). Those who were pregnant (n = 287) or lactating (n = 206), had unreliable dietary recall data (n = 16) or missing blood lead values (n = 515), or were examined at home (n = 7) were excluded. Of the remaining eligible women (n = 4,394), 3,716 had complete data for all variables investigated in this study.

Details of the survey procedures, handling of samples and analytical procedures are described elsewhere [21,22]. Briefly, blood samples in the survey were collected by venipuncture. The BLL was determined by graphite furnace atomic absorption spectrophotometry. The limit of detection for blood lead was 1 µg/dL. Values below the lower detection limit were replaced with a value equal to the detection limit divided by the square root of two (0.7 µg/dL). The survey obtained food consumption measurements for 1 d (24-h recall) along with dietary, nutritional and health status measurements. The information of dietary intakes included total energy intake, total fat, thiamine, pyridoxine, vitamin E, ascorbic acid, folate, calcium, phosphorus and iron. Hematocrit, RBC protoporphyrin and serum concentrations of ascorbic acid and folate were determined using conventional methods.

Description of Variables
Socioeconomic variables examined in the study are shown in Table 1. Participants were divided into the following race/ethnic categories: White (non-Hispanic); Black, (non-Hispanic); Mexican American; or Other. Rural-urban classification was based on the USDA rural-urban codes. "Urban" indicated central or fringe counties of metro areas with 1 million people or more and "Rural" encompassed all other areas. Regions were defined by the U.S. Bureau of the Census as Northeast, Midwest, South, and West. "Poverty income ratio" was the ratio of median family income over poverty threshold based on age of the family reference person and calendar year interviewed. "Education level" described the highest grade/year of regular school ever attended or grade/year finished. In this study, cigarette smoking indicated smoking habits at the time of interview. "Live birth" meant number of children born alive to mother. Breastfeeding history was judged by the response to the question regarding whether they breastfed more than one of their children. Bottled water was defined as the water which was commercially purchased in a bottle. "Year house built" included three categories: before 1946, 1946–73, and 1974 to present. Mobile homes were included in the third category.


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Table 1. Sociodemographic, Lifestyle, and Environmental Characteristics of the Study Subjects

 
Statistical Analyses
BLLs were log(10) transformed to decrease the skew, to achieve homogeneity of error variance and normality of error effects, and to obtain additivity of effect in the subsequent statistical analyses. Descriptive statistics and regression models incorporated the sampling weights of the complex multistage probability sample design of NHANES III. Data were analyzed using SAS (version 6.12) and WesVarPC (version 2.1).

First, the association of BLL (log10) with each independent, continuous variable (alcohol consumption [g/day]; smoking [number of cigarettes/day]; number of live births; and all variables for nutritional status) was determined by the polynomial regression model using SAS. The final regression model included sociodemographic variables (race/ethnicity, age, degree of urbanization, region, poverty income ratio [PIR]); survey phase; alcohol consumption; number of cigarettes smoked per day; breastfeeding history; year house was built; daily intake of total fat, thiamine, pyridoxine, folate, calcium and iron; serum concentration of ascorbic acid and folate; hematocrit; and RBC protoporphyrin. The polynomial regression model up to the second order included the terms of PIR; education level; alcohol consumption; number of cigarettes smoked per day; intake of thiamine, calcium and iron; serum folate; and hematocrit.

Next, multiple polynomial regression analyses were performed (using WesVarPC) to analyze the relationship between BLL and the independent predictors. All independent variables (including the second order term of each continuous variable) were simultaneously pooled into the model to eliminate possible confounding effects. For this analysis, Fay’s replication method was used with a backward elimination model with p ≥ 0.1 as an elimination criterion. Subcategories with small sample sizes (i.e. "other" ethnic group) were not included in the multiple polynomial regression model as recommended by the Analytic and Reporting Guidelines of National Center for Health Statistics (NCHS)/CDC [22].

Finally, a logistic regression analysis was performed to determine the extent of association between BLL, and modifiable (lifestyle and nutritional) factors in women. The odds ratios for each significant modifiable factor were calculated to predict the BLLs at the highest versus the lowest deciles. Statistical analyses were conducted utilizing WesvarPC, taking sample weights and the survey design into account. Alcohol consumption and cigarette smoking were treated as dichotomous variables. Thiamine intake and serum ascorbic acid concentration were treated as continuous variables. The effect of confounding variables was controlled for by a method similar to the multiple polynomial regression analysis.

The relationship between BLL and deciles of thiamine intake and serum ascorbic acid and folate concentration were analyzed using analyses of covariance (ANCOVA). Effects of all confounding variables (including second order terms of continuous variables) were controlled for.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Demographics
Characteristics of reproductive age women in the present study and their BLL are summarized in Tables 1 and 2. We observed that higher mean BLL was associated with Blacks and Mexican-Americans, lower PIR, less education, older age, urban dwelling, living in houses built before 1946, and residing in the Northeast region of the U.S. Alcohol consumption and smoking were also associated with higher BLLs. As shown in Table 2, the subjects’ average daily intake of calories, vitamin E, folate, and calcium were less than recommended levels. In contrast, their intake of ascorbic acid and phosphorus were higher than the Dietary Reference Intakes (DRIs) [23]. Average values of all clinical variables, such as hematocrit (%), protoporphyrin (µg/dL RBL), serum folate (ng/mL), serum ascorbic acid (mg/dL), serum vitamin E (µg/dL), were measured and were within normal limits.


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Table 2. Nutritional and Hematological Characteristics of the Study Subjects

 
The geometric mean BLL of the women was 1.78 µg/dL (Table 3). Approximately 30% and 6% had BLLs ≥2.5 µg/dL and ≥5 µg/dL, respectively and less than 1.0% of the women had a BLL ≥10 µg/dL.


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Table 3. The Distribution of Blood Lead Levels of US Women of Reproductive Age, NHANES III (1988–1994)

 
Association of Variables with Blood Lead Levels
Results of the multiple polynomial regression analysis revealed that BLLs were related to several different variables (Table 4). Our regression model explained 29% of the variance of the BLL of reproductive age women in the U.S. Variables that were positively associated with BLLs were survey phase, age, race (Black, Hispanic), urban, region (Northeast), alcohol consumption, cigarette smoking, intake of pyridoxine, iron (squared only) and folate, and erythrocyte protoporphyrin. Variables that were negatively associated with BLL were poverty income ratio, education level, thiamine intake, serum folate, and hematocrit (squared only). The fact that BLL was significantly associated with first and second orders of several variables (i.e., poverty income ratio, education level, cigarette smoking, thiamine intake, and serum folate) indicates curvilinear associations.


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Table 4. Determinants for Blood Lead Level (log µg/dL) by Multiple Polynomial Regression Analysis

 
The logistic regression model comparing subjects in the upper decile (>4.0 µg/dL) with the lowest decile of blood lead (<0.7 µg/dL) showed high odds ratios of four significant modifiable variables (alcohol consumption, cigarette smoking, thiamine intake, and serum ascorbic acid concentration) (Table 5). Covariates, such as breast feeding, year of house built, daily intake of total fat, thiamine, folate, calcium and iron, serum ascorbic acid, serum folate, hematocrit, and RBC folate, were controlled for in this model. Women who consumed alcohol were 5.6 times more likely than abstainers to be in the highest decile for BLL. Cigarette smokers had a 4.5 times higher odds ratio for high BLL than non-smokers. Women whose intake of thiamine was greater than 1 mg were 7.5 times less likely than those with intakes less than 1 mg/day to be in the highest decile group. A high serum ascorbic acid concentration was associated with 2.5 times lower odds of having BLLs in the highest decile.


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Table 5. Lifestyle and Nutrition Determinants Associated with High Probability of Reproductive Age Women Having Blood Lead Level in the Top Decile (>4.0 µg/dL) versus the Lowest Decile (<0.7 µg/dL)

 
The average BLL of subjects with the lowest decile of thiamine intake was significantly higher than that of all other deciles (except the 2nd and 5th) (p < 0.05) (Fig. 1). Similarly, the mean BLL of subjects with the lowest decile for serum ascorbic acid was significantly higher than that of those with levels in the 2nd through 8th deciles (p < 0.05) (Fig. 2). As shown in Fig. 3, those who had serum folate levels that ranked in the lowest decile had significantly higher BLLs than those with serum folate levels in the upper deciles (7th through 10th).



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Fig. 1. Blood lead levels (mean and 95% CI) by deciles of intake of thiamine. Means were adjusted for sociodemographic, lifestyle, environmental, and nutritional variables. Significantly different from mean of the lowest decile at *p < 0.05 or **p < 0.01.

 


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Fig. 2. Blood lead levels (mean and 95% CI) by deciles of serum ascorbic acid. Means were adjusted for sociodemographic, lifestyle, environmental, and nutritional variables. Significantly different from mean of the lowest decile at *p < 0.05 or **p < 0.01.

 


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Fig. 3. Blood lead levels (mean and 95% CI) by deciles of serum folate. Means were adjusted for sociodemographic, lifestyle, environmental, and nutritional variables. Significantly different from mean of the lowest decile at *p < 0.05 or **p < 0.01.

 

    DISCUSSION
 
In an effort to identify secondary interventions for lowering BLLs of children, we analyzed the relationship between certain sociodemographic and modifiable (lifestyle and nutritional) determinants and the BLL of reproductive age women in the U.S. To our knowledge, this paper shows for the first time that BLLs are associated with thiamine or pyridoxine intake and serum folate in US women.

The geometric mean BLL of reproductive age women in the U.S. was 1.78 µg/dL, and was higher in phase I than in phase II. The decrease in geometric mean BLL from phase I to II may have been due to reduced environmental exposure to lead, as use of lead in paint and gasoline was phased-out during the 1980’s. Although the mean blood level of lead was below the level of concern for pregnant women and young children (10 µg/dL), four out of every thousand women had BLLs above this level. Recent studies on the blood lead levels in the NHANES III survey reported that at blood lead levels below the CDC level of concern (10 µg/dL), delayed puberty and sexual maturation were observed in U.S. girls [24,25], and that blood lead levels, even those below 10 µg/dL, were inversely associated with children’s IQ scores at 3–5 y and associated declines in IQ were greater at these levels than at higher levels [26].

All sociodemographic variables examined in this study were significant determinants for BLL. Reproductive age women who were Black or Hispanic, between 40–49 years of age, were poor or had little education, or lived in urban areas or the Northeast region of the U.S. were most likely to have the highest BLLs. The direction and magnitude of these associations were consistent with a previous study conducted in men and women (20–49 years of age) who participated in phase I of NHANES III [27].

Lifestyle variables such as alcohol consumption and cigarette smoking were positively associated with BLL, even after the differences in sociodemographic variables were controlled for. Other researchers have reported similar findings [2831]. Those who drank alcohol or smoked cigarettes were 5.6 or 4.5 times more likely to be in the highest decile than the lowest decile of BLL, respectively. Similar odds ratios for these variables have been found in women who live in southern Germany [29]. As hypothesized by Hense and colleagues [29], the effect of alcohol may be due to increased gastrointestinal lead absorption or lead contamination of foil capsules on wine bottles. Others have shown that smokers can inhale 1–5 g of lead by smoking 20 cigarettes [32]. Altogether, these studies support the public health efforts against alcohol and cigarette smoking in US women and children.

In agreement with results of others, we found that living in houses built before 1946 (when interior paints were as much as 50% lead by dry weight) was positively associated with BLL [33,34].

Researched on the underreporting of energy intake and its effect on the intake of other nutrients were carried out with the NHANES survey based on 1 d of intake estimated with use of 24-h recalls [35]. About 28% of the women were classified as under-reporters and underreporting of energy intake was highest in women and persons who were older, overweight, or trying to lose weight [35]. Therefore the fact that the daily intake of calories was much less than the DRI might be partly attributed to the underreporting.

Our regression model explained 29% of the variance of the BLL of reproductive age women in the U.S. In the multivariate regression analysis for the association of blood lead levels among a general population in Germany [29], the total percentage of variation explained by age, haematocrit, place of residence, BMI, cigarettes smoked, and alcohol consumption was 12% for men and 24% for women. On the other hand, in another study on the association of blood lead levels among 172 urban children, the percent of variation explained by environmental lead exposures, demographic characteristics and children’s behaviors was 44% for black children and 32% for white children [36]. Therefore, the percent of variation explained in the multivariate regression analysis depends on the subjects characteristics and variables included.

Although results of the multiple polynomial regression analysis suggested that ascorbic acid intake or serum ascorbic acid concentration was not related to BLL, further analyses indicated that subjects with very low serum ascorbic acid concentrations were more likely to have high BLLs than those with intermediate serum ascorbic acid levels. Houston and Johnson [37] also found that BLLs of NHANES III participants (aged 6–90) were inversely associated with serum (but not dietary) concentrations of ascorbic acid. Conversely, Dawson and colleagues [38] found that ingestion of ascorbic acid supplements (1000 mg/day) was associated with reductions in BLLs of men smokers. Altogether, these results suggest that further research into the relationship between dietary and serum levels of ascorbic acid, and their involvement in regulation of BLL in humans should be performed.

We found that intake of thiamine had a strong, inverse, and curvilinear association with BLL (Fig. 1). Those in the lowest decile of thiamine intake had the highest BLL. In addition, the odds of having a high BLL were greater for those with lower thiamine intake. Thiamine has been reported to inhibit the lead uptake in Chinese hamster peritoneal cells, and to reduce lead toxicity [39]. Flora and colleagues [40] identified thiamine and pyridoxine as inhibitors of lead intoxication. Thiamine enhanced the efficacy of chelating agents in mobilizing tissue lead and induced its excretion in lead-exposed animals [41]. The thiol group of thiamine may complex with lead by conformational transformation in vivo resulting into thiazole open-ring conformation [42,43]. Furthermore, rats injected subcutaneously with lead acetate increased lead excretion in feces via bile when thiamine was given [44]. In addition to the therapeutic effects against lead toxicity in animals [3941], results from a cross-sectional human study showed that the BLL of men occupationally exposed to lead was negatively correlated with the daily dietary intake of fiber, iron and thiamine [45]. Our observational study results, along with animal studies, support the preventive effect of thiamine intake.

The present study analyzed the diet datasets of NHANES III collected by a 24-h dietary recall between 1998–1994. We acknowledge one weakness in the study is the reliability of the dietary measures. The nutrient intakes were based on a single day’s intake, done by recall rather than direct measurement. In addition, there was no information on the subjects’ dietary patterns after the baseline measurement.

Our findings of a positive relationship between folate intake and BLL and an inverse relationship between serum folate and BLL are somewhat puzzling. This suggests that folate in blood may enhance lead excretion, while dietary folate in the GI system may facilitate lead absorption. Tandon and colleagues [46] reported that the supplementation of folic acid through gastric gavage enhanced the urinary excretion of lead, mobilized tissue lead and restored lead induced biological alteration in lead intoxicated rats. We have to notice that, however, the folate intake of subjects in our study was only 58% of DRI, which might induce a different metabolism in vivo.

In our study, we found a positive association between blood lead and intake of iron (when curvilinear data were square transformed) or pyridoxine. In contrast, smaller studies involving urban preschool children (n = 299), pregnant women (n = 831), and middle-aged and older men (n = 747), have shown negative associations between blood lead and dietary iron intake [15,28,47]. The results on pyridoxine also show discordance with a study by Fischer and colleagues [39] which demonstrated that the B vitamins, pyridoxine and thiamine had a protective effect against lead uptake and toxicity in mammalian cells. Tandon and colleagues [48] reported that lead intoxication could be prevented by the application of vitamin B complex and different parameters of lead poisoning were aggravated by vitamin B deficiency. The authors also treated lead poisoned rats with vitamin B, alone and in combination with CaNa2-EDTA, and found that pyridoxine as well as folic acid might be factors responsible for the favorable effects [46]. However, there is no human research, and the metabolic interactions between pyridoxine and BLLs cannot be explained with the existing body of knowledge.

As expected, we found a strong positive association between erythrocyte protoporphyrin and BLL. It is well recognized that elevated erythrocyte protoporphyrin is a marker for lead exposure. Our finding of a weak inverse association between hematocrit and BLL also was somewhat expected given that lead inhibits heme synthesis and shortens the life span of erythrocytes [49]. Low hematocrits have been found in children and adults who have been exposed to lead [50,51].

In this study, we did not find a relationship between BLL and dietary fat, calcium or phosphorus. In contrast, Lucas and colleagues [14] found that total fat intake enhanced the absorption of lead in preschool children. The lack of an inverse effect of calcium intake on BLL also is inconsistent with findings of previous smaller-scale studies [7,18,28,47]. Our observation can partly be explained by the lower calcium intake by our study population (718.6 ± 12.3 mg/day) than those in other studies. Although the effect of vitamin D on blood lead was not measured in our study, others have shown that calcium has no effect on blood lead if vitamin D is controlled for [47].

This cross-sectional study may be limited to detecting delayed response to repeated exposure.


    CONCLUSION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
We conclude that one of the important efforts to reduce blood lead toxicity in children is to reduce the body burden of lead in reproductive age women. This may be accomplished by modifying lifestyle and nutritional factors in addition to controlling primary exposure. Determinants of BLLs of reproductive age women in the U.S. include sociodemographic and modifiable lifestyle and nutritional factors such as cigarette smoking, alcohol consumption and vitamin status. Longitudinal studies should be performed to further investigate the inverse associations between BLL and thiamine, ascorbic acid and folate; and the positive associations with iron and pyridoxine intake. To our knowledge, the promising approach of employing vitamins, such as thiamine and ascorbic acid for the prevention or therapy of lead toxicity has not yet been introduced into human medicine. Our studies suggest that there may be some scope in this strategy. It is also hoped that results of these studies will identify intervention measures to reduce lead exposure and toxicity to women and children.


    ACKNOWLEDGMENTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
This study was supported by the Korea Science and Engineering Foundation and the Food and Nutrition Database Research Center, Department of Food Science and Human Nutrition at Michigan State University. We would like to thank Dr. Laurie Deyo for her assistance in preparing this manuscript.

Received October 23, 2003. Accepted March 26, 2004.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. World Health Organization:Inorganic lead (Environmental Health Criteria, 165),1995 .
  2. Public Health Service:"Preventing Lead Poisoning in Young Children, a Statement by the Centers for Disease Control." Atlanta: Centers for Disease Control,1991 .
  3. Pirkle JL, Brody DJ, Gunter EW, Kramer RA, Paschal DC, Flegal KM, Matte TD: The decline in blood lead levels in the United States. The National Health and Nutrition Examination Surveys (NHANES).JAMA272 :284 –291,1994 .[Abstract]
  4. Center for Disease Control (CDC), Morbidity and Mortality Weekly Report (MMWR):Blood lead levels in young children—United States and selected states, 1996–1999 . December 22,49(50); 1133 –1137,2000 .
  5. Meyer PA, Pivetz T, Dignam TA, Homa DM, Schoonover J, Brody D:Surveillance for elevated blood lead levels among children—United States, 1997–2001 . September 12,52(SS10); 1 –21,2003 .
  6. Lagerkvist BJ, Edesrydh S, Englyst V, Nordberg GF, Soderberg H-A, Wiklund D-E: Increased blood lead and decreased calcium levels during pregnancy: a prospective study of Swedish women living near a smelter.Am J Public Health86 :1247 –1252,1996 .[Abstract/Free Full Text]
  7. Mahaffey KR: Biokinetics of lead during pregnancy.Fundam Appl Toxicol16 :15 –16,1991 .[Medline]
  8. Ong CN, Phoon WO, Law HY, Tye CY, Lim HH: Concentrations of lead in maternal blood, cord blood, and breast milk.Arch Dis Child60 :756 –759,1985 .[Abstract]
  9. Gulson BL, Mahaffey KR, Mizon KJ, Korsch MJ, Cameron MA, Vimpani G: Contribution of tissue lead to blood lead in adult female subjects based on stable lead isotope methods.J Lab Clin Med125 :703 –712,1995 .[Medline]
  10. Silbergeld EK: Lead in bone: implications for toxicology during pregnancy and lactation.Environ Health Perspec91 :63 –70,1991 .[Medline]
  11. Watson L, Silbergeld EK: The effects of lead on pregnancy and lactation in rats.Toxicologist14 :78 ,1994 .
  12. Bolger PM, Carrington CD, Capar SG, Adams MA: Reductions in dietary lead exposure in the United States.Chem Speciation Bioavailab3 :31 –37,1991 .
  13. Mahaffey KR, Gartside PS, Glueck CJ: Blood lead levels and dietary calcium intake in 1- to 11-year-old children: the second National Health and Nutrition Examination Survey, 1976 to 1980.Pediatrics78 :257 –262,1986 .[Abstract/Free Full Text]
  14. Lucas SR, Sexton M, Langenberg P: Relationship between blood lead and nutritional factors in preschool children: a cross-sectional study.Pediatrics97 :74 –78,1996 .[Abstract/Free Full Text]
  15. Hammad TA, Sexton M, Langenberg P: Relationship between blood lead and dietary iron intake in preschool children. A cross-sectional study.Ann Epidemiol6 :30 –33,1996 .[Medline]
  16. Ivanova L, Pentieva K, Tsachev K: The lead level in the blood of pregnant women from the city of Sofia.Akush Ginekol (in Bulgarian)36 :7 –9,1997 .
  17. Graziano JH, Popovac D, Factor-Litvak P, Shrout P, Kline J, Murphy MJ, Zhao YH, Mehmeti A, Ahmedi X, Rajovic B: Determinants of elevated blood lead during pregnancy in a population surrounding a lead smelter in Kosovo, Yugoslavia.Environ Health Perspect89 :95 –100,1990 .[Medline]
  18. Farias P, Borja-Aburto VH, Rios C, Hertz-Picciotto I, Rojas-Lopez M, Chavez-Ayala R: Blood lead levels in pregnant women of high and low socioeconomic status in Mexico City.Environ Health Perspect104 :1070 –1074,1996 .[Medline]
  19. Hernandez-Avila M, Gonzalez-Cossio T, Palazuelos E, Romieu I, Aro A, Fishbein E, Peterson KE, Hu H: Dietary and environmental determinants of blood and bone lead levels in lactating postpartum women living in Mexico City.Environ Health Perspect104 :1076 –1082,1996 .[Medline]
  20. Recknor JC, Reigart JR, Darden PM, Goyer RA, Olden K, Richardson MC: Prenatal care and infant lead exposure.J Pediatr130 :123 –127,1997 .[Medline]
  21. National Center for Health Statistics:"NHANES III reference manuals and reports," CD-ROM,1996 .
  22. National Center for Health Statistics:"Third National Health and Nutrition Examination Survey, 1988–1994, NHANES III Laboratory Data File," CD-ROM,1996 .
  23. Committee on Dietary Reference Intakes:"Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids," Washington, DC: National Academy Press,2002 .
  24. Selevan SG, Rice DC, Hogan KA, Euling SY, Pfahles-Hutchens A, Bethel J: Blood lead concentration and delayed puberty in girls.N Eng J Med348 :1527 –36,2003 .[Abstract/Free Full Text]
  25. Wu T, Buck GM, Mendola P:Blood lead levels and sexual maturation in U.S. girls: The Third National Health and Nutrition Examination Survey, 1988–94 . Environ Health Perspect online February 4,2003 .
  26. Canfield RL, Henderson CR, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP: Intellectual impairment in children with blood lead concentrations below 10 µg per deciliter.N Eng J Med348 :1517 –1526,2003 .[Abstract/Free Full Text]
  27. 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 III, 1988 to 1991).JAMA272 :277 –283,1994 .[Abstract]
  28. Baghurst PA, McMichael AJ, Vimpani GV, Robertson EF, Clark PD, Wigg NR: Determinants of blood lead concentrations of pregnant women living in Port Pirie and surrounding areas.Med J146 :69 –73,1987 .
  29. Hense HW, Filipiak B, Novak L, Stoeppler M: Nonoccupational determinants of blood lead concentrations in a general population.Int J Epidemiol21 :753 –762,1992 .[Abstract/Free Full Text]
  30. Muldoon SB, Cauley JA, Kuller LH, Scott J, Rohay J: Lifestyle and sociodemographic factors as determinants of blood lead levels in elderly women.Am J Epidemiol139 :599 –608,1994 .[Abstract/Free Full Text]
  31. Symanski E, Hertz-Picciotto I: Blood lead levels in relation to menopause, smoking, and pregnancy history.Am J Epidemiol141 :1047 –1058,1995 .[Abstract/Free Full Text]
  32. World Health Organization:Lead (Environmental Health Criteria, 3) ,1977 .
  33. Alder RJ, Dillon JA, Loomer S, Poon HC, Robertson JM: An analysis of blood lead data in clinical records by external data on lead pipes and age of household.J Expo Anal Environ Epidemiol3 :299 –314,1993 .[Medline]
  34. Nordin JD, Rolnick SJ, Griffin JM: Prevalence of excess lead absorption and associated risk factors in children enrolled in a midwestern health maintenance organization.Pediatrics93 :172 –177,1994 .[Abstract/Free Full Text]
  35. Briefel RR, Sempos CT, McDowell MA, Chien S, Alaimo K: Dietary methods research in the third national health and nutrition examination survey: underreporting of energy intake.Am J Clin Nutr65 :1203S –1209S,1997 .[Abstract/Free Full Text]
  36. Lanphear BP, Weitzman M, Eberly S: Racial differences in urban children’s environmental exposures to lead.Am J Public Health86 :1460 –1463,1996 .[Abstract/Free Full Text]
  37. Houston DK, Johnson MA: Does vitamin C intake protect against lead toxicity?Nutr Rev58 :73 –75,2000 .[Medline]
  38. Dawson EB, Evans DR, Harris WA, Teter MC, McGanity WJ: The effect of ascorbic acid supplementation on the BLOOD LEAD LEVELs of smokers.J Am Coll Nutr18 :166 –170,1999 .[Abstract/Free Full Text]
  39. Fischer AB, Hess C, Neubauer T, Eikmann T: Testing of chelating agents and vitamins against lead toxicity using mammalian cell cultures.Analyst123 :55 –58,1998 .[Medline]
  40. Flora SJ, Singh S, Tandon SK: Prevention of lead intoxication by vitamin B complex.Z Gesamte Hyg30 :409 –411,1984 .[Medline]
  41. Tandon SK, Singh S: Role of vitamins in treatment of lead intoxication.J Trace Elem Exp Med13 :305 –315,2000 .
  42. Olkowski AA, Gooneratne SR, Christensen DA: The effects of thiamine and EDTA in bilary and urinary lead excretion in sheep.Toxicol Lett59 :153 –159,1991 .[Medline]
  43. Barton JC: Retention of radiolead by human erythrocytes in vitro.Toxicol Appl Pharmacol99 :314 –322,1989 .[Medline]
  44. Ito Y, Niiya Y, Otani M, Sarai S, Shima S: Effect of food intake on blood lead concentration in worker occupationally exposed to lead.Toxicol Lett37 :105 –114,1987 .[Medline]
  45. Ito Y, Niiya Y, Otani M, Shima S: Effect of thiamine on the excretion of subcutaneously injected lead in rats.Toxicol Lett37 :221 –228,1987 .[Medline]
  46. Tandon SK, Flora SJ, Singh S: Chelation in metal intoxication XXIV: Influence of various components of vitamin B complex on the therapeutic efficacy of disodium calcium versenate in lead intoxication.Pharmacol Toxicol60 :62 –65,1987 .[Medline]
  47. Cheng Y, Willett WC, Schwartz J, Sparrow D, Weiss S, Hu H: Relation of nutrition to bone lead and BLOOD LEAD LEVELs in middle-aged to elderly men. The Normative Aging Study.Am J Epidemiol147 :1162 –1174,1998 .[Abstract/Free Full Text]
  48. Tandon SK, Flora SJ, Singh S: Influence of vitamin B-complex deficiency on lead intoxication in young rats.Ind J Med Res80 :444 –448,1984 .[Medline]
  49. Goyer RA: Toxic effects of metals. In Amdur MO, Doull J, Klaassen CD (eds):"Casarett and Doull’s Toxicology: The Basic Science of Poisons," 14th ed. New York: Pergamon Press, pp623 –680,1990 .
  50. Schwartz J, Landrigan PJ, Baker Jr EL, Orenstein WR, von Lindern IH: Lead-induced anemia: dose-response relationships and evidence for a threshold.Am J Public Health80 :165 –168,1990 .[Abstract/Free Full Text]
  51. Horiguchi S, Matsumura S, Fukumoto K, Karai I, Endo G, Teramoto K, Shinagawa K, Kiyota I, Wakitani F, Takise S: Erythrocyte deformability in workers exposed to lead.Osaka City Med J37 :149 –155,1991 .[Medline]
  52. Chernecky CC, Berger BJ:"Laboratory Tests and Diagnostic Procedures," 2nd ed. Toronto: WB Saunders Co.,1997 .



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