Feeding practices and blood lead levels in infants in Nagpur, India

In a hospital-based cross-sectional study of 200 infants age 4-9 months in an Indian city (Nagpur), the authors determined the prevalence of elevated blood lead level (EBLL) and mean blood lead levels with respect to feeding patterns, i.e., breastfed or fed with formula or dairy milk. The blood lead levels in this study population ranged from 0.048 microg/dl to 42.944 microg/dl; the mean blood lead level was 10.148 microg/dl (+/- 9.128); EBLL prevalence was 38.2%. EBLL risk factors included removal of house paint in the past year, odds ratio (OR), 5.6 (95% confidence interval [CI], 1.6-19.65); use of surma (eye cosmetic), OR 4.27 (95% CI, 1.39-13.08); maternal use of sindur (vermillion), OR 2.118 (95% CI, 1.07-4.44). Feeding method (breastfed or not) did not appear to have an effect on blood lead level. In non-breastfed infants, boiling of water was significantly associated with EBLL, OR 1.97 (95% CI, 1.01-3.84).     

Correlation between maternal and cord blood lead levels

Whole blood lead levels were estimated by atomic absorption analysis in 226 blood samples from 113 mothers of 23 different nationalities. Samples were collected before delivery, and from cord blood from their respective neonates. The concentrations of blood lead were within the expected range of occupationally unexposed populations. Mean maternal blood lead levels were 0.72 0.10 mumol/l (14.9 2.14 mug/dl), range 0.32-1.34 mumol/l (6.6-27.8 mug/dl) and mean cord blood levels were 0.64 0.12 mumol/l (range 0.29-1.46 mumol/l). Sixteen percent of the mothers and nearly 10% cord blood samples were found to have blood lead level greater than 0.97 mumol/l (20 mug/dl). Very high levels, in excess of 1.21 mumol/l (25 mug/dl), were detected in 3.5% of mothers as compared to 2.6% of cord blood samples. Out of 113 infants, 65 (58%) were males with a mean cord blood lead level of 0.63 mumol/l and 48 (42%) were females with a mean level of 0.66 muol/l. The lowest maternal blood lead levels 0.68 mumol/l were observed in ages 20 to 25 years old, and lowest cord blood levels 0.58 mumol/l were seen in maternal age of less than 20 years old. On the other hand, the highest maternal and cord blood lead levels (0.82 and 0.75 mumol/l, respectively) were observed in maternal ages of greater than 35 years old. The results show a direct correlation of blood lead level between mothers and umbilical cord as seen in the linear regression distribution curve.     

Effects of prenatal exposure to mercury on cognitive and psychomotor function in one-year-old infants: epidemiologic cohort study in Poland

PURPOSE: The aim of the study is to assess the cognitive and psychomotor status of 1-year-old infants whose mothers were exposed to low, but varying, amounts of mercury during pregnancy. METHODS: Mercury levels in cord and maternal blood at delivery were used to assess prenatal environmental exposure to mercury. Bayley Scales of Infant Development were used to assess neurobehavioral health outcomes. The cohort consisted of 233 infants who were born at 33 to 42 weeks of gestation between January 2001 and March 2003 to mothers attending ambulatory prenatal clinics in the first and second trimesters of pregnancy. Enrollment included only nonsmoking women with singleton pregnancies between the ages of 18 and 35 years who were free from chronic diseases. RESULTS: The geometric mean (GM) for maternal blood mercury level for the group of infants with normal neurocognitive performance was lower (GM = 0.52 mug/L; 95% confidence interval [CI], 0.46-0.58) than that observed in the group with delayed performance (GM = 0.75 mug/L; 95% CI, 0.59-0.94), and this difference was significant (p = 0.010). The GM of cord blood mercury level in the normal group also was lower (GM = 0.85 mug/L; 95% CI, 0.78-0.93) than that observed in the group with delayed performance (GM = 1.05 mug/L; 95% CI, 0.87-1.27), and this difference was of borderline significance (p = 0.070). The relative risk (RR) for delayed performance increased more than threefold (RR = 3.58; 95% CI, 1.40-9.14) if cord blood mercury level was greater than 0.80 mug/L. Risk for delayed performance in the group of infants with greater maternal mercury levels (>0.50 mug/L) also was significantly greater (RR = 2.82; 95% CI, 1.17-6.79) compared with children whose mothers had mercury levels less than 0.50 mug/L. CONCLUSIONS: The results may be of public health importance because delayed psychomotor or mental performance in infants is assumed to be an indicator of later neurocognitive development in children, which may persist into adult life.     

Umbilical cord blood lead levels in California

During the fall of 1984, we conducted a survey of umbilical cord blood lead levels of 723 live births that occurred at 5 hospitals located in 5 cities in California. Historical ambient air lead levels were used as a qualitative surrogate of air and dust exposure. The area-specific cord blood means (all means approximately 5 micrograms/dl), medians, deciles, and distributions did not vary among locations. The California distributions included means that were lower than the 6.6 micrograms/dl reported in Needleman et al.'s Boston study in 1979. Indeed, the entire California distribution was shifted to the left of the Boston study distribution, even though 3% of the California cord lead levels exceeded 10 micrograms/dl--the level above which Needleman et al. have documented psychoneurological effects in children during the first few years of life. Fourteen percent of premature babies had cord blood lead levels above 10 micrograms/dl. The association between prematurity (i.e., less than 260 d gestation) and elevated (greater than 5 micrograms/dl) cord blood lead was observed in all hospitals and yielded a relative risk of 2.9 (95% CI: .9, 9.2) and a population attributable risk of 47%. Further research is needed to confirm this association and to explore the roles of endogenous and exogenous sources of lead exposure to the mothers who give birth to premature infants.     

Levels of lead in breast milk and their relation to maternal blood and bone lead levels at one month postpartum

Despite the many well-recognized benefits of breast-feeding for both mothers and infants, detectable levels of lead in breast milk have been documented in population studies of women with no current environmental or occupational exposures. Mobilization of maternal bone lead stores has been suggested as a potential endogenous source of lead in breast milk. We measured lead in breast milk to quantify the relation between maternal blood and bone lead levels and breast-feeding status (exclusive vs. partial) among 310 lactating women in Mexico City, Mexico, at 1 month postpartum. Umbilical cord and maternal blood samples were collected at delivery. Maternal breast milk, blood, and bone lead levels were obtained at 1 month postpartum. Levels of lead in breast milk ranged from 0.21 to 8.02 microg/L (ppb), with a geometric mean (GM) of 1.1 microg/L; blood lead ranged from 1.8 to 29.9 microg/dL (GM = 8.4 microg/dL); bone lead ranged from < 1 to 67.2 microg/g bone mineral (patella) and from < 1 to 76.6 microg/g bone mineral (tibia) at 1 month postpartum. Breast milk lead was significantly correlated with umbilical cord lead [Spearman correlation coefficient (rS) = 0.36, p < 0.0001] and maternal blood lead (rS= 0.38, p < 0.0001) at delivery and with maternal blood lead (rS = 0.42, p < 0.0001) and patella lead (rS= 0.15, p < 0.01) at 1 month postpartum. Mother's age, years living in Mexico City, and use of lead-glazed ceramics, all predictive of cumulative lead exposure, were not significant predictors of breast milk lead levels. Adjusting for parity, daily dietary calcium intake (milligrams), infant weight change (grams), and breast-feeding status (exclusive or partial lactation), the estimated effect of an interquartile range (IQR) increase in blood lead (5.0 microg/dL) was associated with a 33% increase in breast milk lead [95% confidence interval (CI), 24 to 43%], whereas an IQR increase in patella lead (20 microg/g) was associated with a 14% increase in breast milk lead (95% CI, 5 to 25%). An IQR increase in tibia lead (12.0 microg/g) was associated with a 5% increase in breast milk lead (95% CI, -3% to 14%). Our results indicate that even among a population of women with relatively high lifetime exposure to lead, levels of lead in breast milk are low, influenced both by current lead exposure and by redistribution of bone lead accumulated from past environmental exposures.     

Lead-glazed ceramic ware and blood lead levels of children in the city of Oaxaca, Mexico

Although Mexico substantially reduced use of leaded gasoline during the 1990s, lead-glazed pottery remains a significant source of population exposure. Most previous studies of lead in nonoccupationally exposed groups in Mexico have been conducted in the Mexico City metropolitan area. Oaxaca, a poor southern state of Mexico, has a centuries-old tradition of use of low temperature lead-glazed ceramic ware manufactured mainly by small family businesses. We measured blood lead levels in 220 8-10-y-old children (i.e., not from pottery-making families) who were students in the innercity of Oaxaca and in the mothers of all children. The geometric mean blood lead level of the children was 10.5 microg/dl (+7.0/-4.3 microg/dl standard deviation; range = 1.3-35.5 microg/dl). The corresponding mean value for the mothers was 13.4 (+9.0/-5.4 microg/dl standard deviation; range = 2.8-45.3 microg/dl). We used cutoffs that were greater than or equal to 10 microg/dl, 20 microg/dl, and 30 microg/dl, and we determined that 54.9%, 10.3%, and 3.0% of the children were at or above the respective criteria. We accounted for 25.2% of the variance in blood lead levels of the children, using maternal responses to a questionnaire that assessed possible lead sources in a linear multiple-regression model. The most important factors related to lead levels were family use of lead-glazed pottery, use of animal fat in cooking, and family income. The addition of maternal blood lead level to the model increased accounted variance in blood lead to 48.0%. In logistic-regression modeling of children's blood lead levels, we used a cutoff of greater than or equal to 10 microg/dl, and we found that use of lead-glazed pottery was the most important of all questionnaire items that were predictive of blood lead levels (odds ratio = 2.98). In Oaxaca, as is the case elsewhere in Mexico, lead-glazed ceramic ware remains a significant risk factor for elevated blood lead levels in children.     

Screening housing to prevent lead toxicity in children

OBJECTIVE: Screening children to identify those with blood lead levels > or = 10 microg/dl fails to protect children from lead-associated cognitive deficits and behavioral problems. To broaden our efforts at primary prevention, screening criteria are needed to identify lead-contaminated housing before children are unduly exposed. The purpose of this study was to identify and validate housing characteristics associated with children having elevated blood lead levels (> or = 10 microg/dl). METHODS: Two existing studies were used to examine housing characteristics linked with undue lead exposure: a cross-sectional study of 205 children aged 12 to 31 months, and a random sample from a longitudinal study of 276 children followed from 6 to 24 months of age. Logistic regression analysis was conducted to examine the association of children's blood lead levels > or = 10 microg/dl. RESULTS: The mean age of the 481 children was 17.8 months; 99 (20.6%) had a blood lead concentration of 10 microg/dl or higher. The following characteristics were associated with blood lead concentration > or = 10 microg/dl: floor lead loading > 15 microg/ft2 (odds ratio [OR]=2.2; 95% confidence interval [CI] 1.3, 3.8); rental housing (OR=3.2; 95% CI 1.3, 7.6); poor housing condition (OR=2.1; CI 1.2, 3.6); African American race (OR=3.3; CI 1.9, 6.1); paint chip ingestion (OR=5.8; CI 1.3, 26.5); and soil ingestion (OR=2.2; CI 1.1, 4.2). Housing characteristics including rental status, lead-contaminated floor dust, and housing condition had a range of sensitivity from 47% to 92%; specificity from 28% to 76%; a positive predictive value from 25% to 34%; and a negative predictive value of 85% to 93%. CONCLUSIONS: Housing characteristics and floor dust lead levels can be used to screen housing to identify lead hazards prior to occupancy, before purchasing a home, or after renovation to prevent children's exposure to lead hazards.     

Effect of breast milk lead on infant blood lead levels at 1 month of age

Nursing infants may be exposed to lead from breast milk, but relatively few data exist with which to evaluate and quantify this relationship. This route of exposure constitutes a potential infant hazard from mothers with current ongoing exposure to lead as well as from mothers who have been exposed previously due to the redistribution of cumulative maternal bone lead stores. We studied the relationship between maternal breast milk lead and infant blood lead levels among 255 mother-infant pairs exclusively or partially breast-feeding through 1 month of age in Mexico City. A rigorous, well-validated technique was used to collect, prepare, and analyze the samples of breast milk to minimize the potential for environmental contamination and maximize the percent recovery of lead. Umbilical cord and maternal blood lead were measured at delivery; 1 month after delivery (+/- 5 days) maternal blood, bone, and breast milk and infant blood lead levels were obtained. Levels of lead at 1 month postpartum were, for breast milk, 0.3-8.0 microg/L (mean +/- SD, 1.5 +/- 1.2); maternal blood lead, 2.9-29.9 microg/dL (mean +/- SD, 9.4 +/- 4.5); and infant blood lead, 1.0-23.1 microg/dL (mean +/- SD, 5.5 +/- 3.0). Infant blood lead at 1 month postpartum was significantly correlated with umbilical cord (Spearman correlation coefficient rS = 0.40, p < 0.0001) and maternal (rS= 0.42, p < 0.0001) blood lead at delivery and with maternal blood (rS= 0.67, p < 0.0001), patella rS = 0.19, p = 0.004), and breast milk (rS = 0.32, p < 0.0001) lead at 1 month postpartum. Adjusting for cord blood lead, infant weight change, and reported breast-feeding status, a difference of approximately 2 microg/L (ppb; from the midpoint of the lowest quartile to the midpoint of the highest quartile) breast milk lead was associated with a 0.82 microg/dL increase in blood lead for breast-feeding infants at 1 month of age. Breast milk lead accounted for 12% of the variance of infant blood lead levels, whereas maternal blood lead accounted for 30%. Although these levels of lead in breast milk were low, they clearly have a strong influence on infant blood lead levels over and above the influence of maternal blood lead. Additional information on the lead content of dietary alternatives and interactions with other nutritional factors should be considered. However, because human milk is the best and most complete nutritional source for young infants, breast-feeding should be encouraged because the absolute values of the effects are small within this range of lead concentrations.     

Living in a sea of lead--changes in blood- and hand-lead of infants living near a smelter

Thirteen infants born into the lead contaminated environment of Port Pirie, South Australia, were followed approximately monthly from birth until they were about 36 months. Blood-lead levels of infants at birth were similar to their mothers but fell rapidly during the first 35 days of life. Thereafter, infants born with blood-lead levels at about 2-4 microg/dl began a slow linear increase until 14-18 months where a plateau occurred of 10.8-17.2 microg/dl. The blood-lead levels were well correlated with hand-lead loadings of infant (r(2)=0.72, P<0.01, log transformed data) and mother (r(2)=0.62, P<0.01, log transformed data) unless the birth lead level was exceptionally high. The principle factor determining exposure was the impact of smelter emissions on the house. Blood-lead increase was caused by the relatively more rapid increase in dose of lead compared with the increasing body mass, which was related directly to the maturation of motor development. Hand-lead of mothers were closely related to both infants' blood- and hand-lead levels until the point of blood-lead plateau then substantially fell as infants began to walk unaided. The estimated slope factor using the ICRP model was 0.75-0.94 microg/dl per microg/day with a maximum daily dose of 3-5 microg/kg/day, assuming 45% absorption. Ingestion appears to be the most likely route for at least 95% of the dose.     

Occupational determinants of bone and blood lead levels in middle aged and elderly men from the general community: the Normative Aging Study

BACKGROUND: Few studies of the general population have investigated risk factors for elevated levels of lead in bone in relation to occupation. METHODS: Six hundred and fifty six community-exposed men had their bone and blood lead levels measured (by K-X-ray fluorescence). Based on their occupational histories, participants were categorized into those who worked in white-collar (WC) occupations (59%) or blue-collar (BC) occupations (41%). No subjects had worked in a primary lead industry (e.g., smelting). RESULTS: In multivariate regression models that adjusted for age, race, education, smoking, alcohol ingestion and retirement status, BC subjects had tibia and patella lead concentrations that were 5.5 (95% CI: 3.2-7.8) and 6.5 (95% CI: 3.1-9.8) microg/g higher than WC subjects, respectively. Interaction terms pairing race with occupational status indicated that in non-white BC subjects, tibia and patella lead levels were higher still by 11.3 (95% CI: -2 to 24.5) and 20.5 (95% CI: 1.2-39.8) microg/g, respectively. Blood lead levels were low for these mostly retired men (mean [SD]: 6.1 [3.9] microg/g) and in multivariate regression models, occupational status was not a significant predictor of blood lead levels; however, an interaction between race and occupational status was also suggested, with non-white BC subjects having blood lead levels that were predicted to be higher by 4.5 (95% CI: 0.3-8.7) microg/dl. CONCLUSIONS: Bone lead levels are higher in the men who worked in BC occupations even if they have not worked in primary lead-exposed occupations. This effect is markedly stronger in non-white BC workers and suggests an interaction between occupational exposures and race/ethnicity with respect to cumulative exposure to lead. A similar interaction was suggested by models of blood lead levels.     

Lifetime low-level exposure to environmental lead and children's emotional and behavioral development at ages 11-13 years. The Port Pirie Cohort Study

The Port Pirie Cohort Study is the first study to monitor prospectively the association between lifetime blood lead exposure and the prevalence of emotional and behavioral problems experienced by children. Lead exposure data along with ratings on the Child Behavior Checklist were obtained for 322 11-13-year-old children from the lead smelting community of Port Pirie, Australia. Mean total behavior problem score (95% confidence interval (CI)) for boys whose lifetime average blood lead concentration was above 15 microg/dl was 28.7 (24.6-32.8) compared with 21.1 (17.5-24.8) in boys with lower exposure levels. The corresponding mean scores (95% CI) for girls were 29.7 (25.3-34.2) and 18.0 (14.7-21.3). After controlling for a number of confounding variables, including the quality of the child's HOME environment (assessed by Home Observation for Measurement of the Environment), maternal psychopathology, and the child's IQ, regression modeling predicted that for a hypothetical increase in lifetime blood lead exposure from 10 to 30 microg/dl, the externalizing behavior problem score would increase by 3.5 in boys (95% CI 1.6-5.4), and by 1.8 (95% CI -0.1 to 11.1) in girls. Internalizing behavior problem scores were predicted to rise by 2.1 (95% CI 0.0-4.2) in girls but by only 0.8 (95% CI -0.9 to 2.4) in boys.     

Weight gain and maturity in fetuses exposed to low levels of lead

The relationship between prenatal low-level lead exposure and fetal growth was evaluated in a sample of 4354 pregnancies in which the mean umbilical cord blood lead level was 7.0 micrograms/dl (SD = 3.3; 10th percentile, 3.4 micrograms/dl, 90th percentile, 10.9 micrograms/dl). Higher cord blood lead levels were significantly associated with gestations of slightly longer duration. Comparing infants with cord blood lead levels greater than or equal to 15 micrograms/dl to those with levels less than 5 micrograms/dl, adjusted risk ratios of 1.5 to 2.5 were observed for low birth weight (less than 2500 g) and for fetal growth indices that express birth weight as a function of length of gestation (e.g., small-for-gestational age, intrauterine growth retardation). The 95% confidence intervals of these risk ratios included 1, however, precluding rejection of the null hypothesis of no association. We conclude that the risk of adverse fetal growth is not increased at cord blood lead levels less than 15 micrograms/dl but that modest increases in risk may be associated with levels greater than or equal to 15 micrograms/dl.     

Relation between blood lead levels and childhood anemia in India

Lead pollution is a substantial problem in developing countries such as India. The US Centers for Disease Control and Prevention has defined an elevated blood lead level in children as > or = 10 microg/dl, on the basis of neurologic toxicity. The US Environmental Protection Agency suggests a threshold lead level of 20-40 microg/dl for risk of childhood anemia, but there is little information relating lead levels <40 microg/dl to anemia. Therefore, the authors examined the association between lead levels as low as 10 mug/dl and anemia in Indian children under 3 years of age. Anemia was divided into categories of mild (hemoglobin level 10-10.9 g/dl), moderate (hemoglobin level 8-9.9 g/dl), and severe (hemoglobin level <8 g/dl). Lead levels <10 mug/dl were detected in 568 children (53%), whereas 413 (38%) had lead levels > or = 10-19.9 microg/dl and 97 (9%) had levels > or = 20 microg/dl. After adjustment for child's age, duration of breastfeeding, standard of living, parent's education, father's occupation, maternal anemia, and number of children in the immediate family, children with lead levels > or = 10 microg/dl were 1.3 (95% confidence interval: 1.0, 1.7) times as likely to have moderate anemia as children with lead levels <10 microg/dl. Similarly, the odds ratio for severe anemia was 1.7 (95% confidence interval: 1.1, 2.6). Health agencies in India should note the association of elevated blood lead levels with anemia and make further efforts to curb lead pollution and childhood anemia.     

Inconsistent effects of iron-folic acid and/or zinc supplementation on the cognitive development of infants

Despite concerns over the neurocognitive effects of micronutrient deficiencies in infancy, few studies have examined the effects of micronutrient supplementation on specific cognitive indicators. This study investigated, in 2002, the effects of iron-folic acid and/or zinc supplementation on the results of Fagan Test of Infant Intelligence (FTII) and the A-not-B Task of executive functioning among 367 Nepali infants living in Sarlahi district. Infants were enrolled in a cluster-randomized, placebo-controlled clinical trial of daily supplementation with 5 mg of zinc, 6.25 mg of iron with 25 microg of folic acid, or zinc-iron-folic acid, or placebo. These were tested on both the tasks using five indicators of information processing: preference for novelty (FTII), fixation duration (FTII), accelerated performance (> or = 85% correct; A-not-B), deteriorated performance (< 75% correct and > 1 error on repeat-following-correct trails; A-not-B), and the A-not-B error (A-not-B). At 39 and 52 weeks, 247 and 333 infants respectively attempted the cognitive tests; 213 made an attempt to solve both the tests. The likelihood of females completing the A-not-B Task was lower compared to males when cluster randomization was controlled [odds ratio = 0.67; 95% confidence interval 0.46-0.97; p < 0.05]. All of the five cognitive outcomes were modelled in linear and logistic regression. The results were not consistent across either the testing sessions or the information-processing indicators. Neither the combined nor the individual micronutrient supplements improved the performance on the FTII or the A-not-B Task (p > 0.05). These findings suggest that broader interventions (both in terms of scope and duration) are needed for infants who face many biological and social stressors.     

High frequency of maternal vitamin B12 deficiency as an important cause of infantile vitamin B12 deficiency in Sanliurfa province of Turkey

Summary Background Vitamin B₁₂ deficiency in infancy may cause failure to thrive, severe neurological disorders and megaloblastic pancytopenia. It is well known that infants born with deficient vitamin B₁₂ storage have increased the risk of vitamin B₁₂ deficiency. Vitamin B₁₂ deficiency is more prevalent in infancy in Sanliurfa province (at the southeast region of Turkey). Aim of the study The aim of this study was to determine the frequencies of vitamin B₁₂, folic acid and iron deficiencies in pregnants and their babies at birth and to what extend the mothers’ deficiency becomes effective on babies’ deficiencies. Methods The study groups were constituted by 180 pregnant women and their single and term babies. Venous blood samples of pregnants were obtained 1–3 h before delivery and babies’ cord bloods were collected at birth. Vitamin B₁₂ and folic acid levels were measured with electro chemiluminiscence method; serum iron and iron binding capacities were measured by colorimetric method and complete blood counts were performed by automatic blood counter. Results Mean vitamin B₁₂ levels in maternal and cord blood serum were 130 ± 61.7 pg/ml and 207 ± 141 pg/ml; mean folic acid levels were 8.91 ± 6.46 ng/ml and 17.8 ± 11.8 ng/ml; mean serum iron levels were 56.9 ± 37.5 μg/dl and 147 ± 43.2 μg/dl; and mean transferrin saturations were 11.8 ± 8% and 65.6 ± 24%, respectively. There were vitamin B₁₂ deficiency (<160 pg/ml) in 72% of the mothers and 41% of the babies, and severe deficiency (<120 pg/ml) in 48% of the mothers and 23% of the babies. Folic acid deficiency was found in 12% of the mothers, but was not found in the babies. There were iron deficiency in 62% of the mothers and 1% of the babies. There were statistically significant correlation between maternal and cord blood serum vitamin B₁₂ levels (r = 0.395, P < 0.001) and folic acid levels (r = 0.227, P = 0.017), while there were no correlation between maternal and cord blood iron levels and transferrin saturations. Conclusion The study results showed that vitamin B₁₂ deficiency is prevalent in pregnants in this region and that 41% of infants have born with deficient vitamin B₁₂ storages. Therefore, prophylactic use of vitamin B₁₂ by pregnant women in Sanliurfa and other poor communities could have considerable benefits to prevent vitamin B₁₂ deficiency and its complications in infants.     

Biological monitoring of lead exposure in high risk groups in Berat, Albania

STUDY OBJECTIVE: To determine blood lead concentrations in children living in an area with a battery plant in Berat, Albania. Another aim was to determine blood lead concentrations in mothers and cord blood levels in neonates from Berat and compare them with values found in Tirana. DESIGN: Cross sectional survey with a 10% random sample of children, and a 10% sample of mothers and newborn. SETTING: Hospitals, schools, and kinder-gartens in Berat and Tirana, Albania PARTICIPANTS: 129 preschool children, 373 school children, 151 mothers and their newborn. MAIN RESULTS: The mean observed blood lead concentrations in 84 preschool children living less than 2 km from the battery plant was 43.4 micrograms/dl (SD 23.0) and significantly higher than in 45 preschool children (mean 15.0 micrograms/dl, SD 3.5) living more than 2 km from the plant. Mean lead concentrations in 145 school children living close to the plant were 26.6 micrograms/dl (SD 14.4) compared with 16.0 micrograms/dl in 228 school children living at a greater distance. In 67% of the preschool children and 41% of the school children lead levels exceeded the WHO borderline level of 20 micrograms/dl, and 98% of preschool children, and 82% of school children had values greater than 10 micrograms/dl. Mean lead concentrations in cord blood of 151 newborn was 8.9 micrograms/dl (median 8.8, range 4.9-20.0 micrograms/dl), and 10.6 micrograms/dl in blood of their mothers (median 10.0, range 5.0-25.4 micrograms/dl). Mean lead concentrations in Tirana were 8.9 (newborn), and 7.0 micrograms/dl (mothers). CONCLUSIONS: Blood lead concentrations in children from Berat are comparatively high and abatement measures are needed.

 

     

Body burdens of mercury, lead, selenium and copper among Baltimore newborns

Umbilical cord blood or serum concentrations of mercury, lead, selenium and copper were measured with inductively coupled plasma mass spectrometry in a population of 300 infants born in Baltimore, Maryland. Geometric mean values were 1.37 μg/L (95% confidence interval: 1.27, 1.48) for mercury; 0.66 μg/dL (95% CI: 0.61, 0.71) for lead; and 38.62 μg/dL (95% CI: 36.73, 40.61) for copper. Mean selenium was 70.10 μg/L (95% CI: 68.69, 70.52). Mercury, selenium and copper levels were within exposure ranges reported among similar populations, whereas the distribution of lead levels was lower than prior reports; only one infant had a cord blood lead above 10 μg/dL. Levels of selenium were significantly correlated with concentrations of lead (Spearman's ρ=0.20) and copper (Spearman's ρ=0.51). Multivariable analyses identified a number of factors associated with one of more of these exposures. These included: increase in maternal age (increased lead); Asian mothers (increased mercury and lead, decreased selenium and copper); higher umbilical cord serum n−3 fatty acids (increased mercury, selenium and copper), mothers using Medicaid (increased lead); increasing gestational age (increased copper); increasing birthweight (increased selenium); older neighborhood housing stock (increased lead and selenium); and maternal smoking (increased lead). This work provides additional information about contemporary prenatal element exposures and can help identify groups at risk of atypical exposures.     

Relationships of lead in breast milk to lead in blood, urine, and diet of the infant and mother.

We have obtained stable lead isotope and lead concentration data from a longitudinal study of mobilization of lead from the maternal skeleton during pregnancy and lactation and in which the newly born infants were monitored for 6 months postpartum to evaluate the effects of the local environment on lead body burden of the infant. Samples of maternal and infant blood, urine, and diet and especially breast milk were measured for 21 mothers and 24 infants. Blood lead concentrations were less than 5 microg/dl in all except one subject. The mean lead concentration in breast milk +/- standard deviation was 0.73 +/- 0.70 microg/kg. In seven subjects for whom serial breast milk sampling was possible, the lead concentration varied by factors of from 2 to 4, and for three subjects there was an increase at or after 90 days postpartum. For the first 60-90 days postpartum, the contribution from breast milk to blood lead in the infants varied from 36 to 80%. Multiple linear regression analyses indicated statistically significant relationships for some of the variables of isotope ratios and lead concentrations between breast milk, blood, urine, and diet for infants and mothers. For example, the analyses revealed that both a mother's breast milk 207Pb/206Pb and 206Pb/204Pb ratios and lead concentration provide information to predict her infant's blood 207Pb/206Pb and 206Pb/204Pb ratios. The major sources of lead in breast milk are from the maternal bone and diet. An evaluation of breast milk lead concentrations published over the last 15 years indicates that studies in which the ratio of lead concentrations in breast milk to lead concentrations in whole maternal blood (Multiple>100) were greater than 15 should be viewed with caution because of potential contamination during sampling and/or laboratory analyses. Selected studies also appear to show a linear relationship between breast milk and maternal whole blood, with the percentage of lead in breast milk compared with whole blood of <3% in subjects with blood lead levels ranging from 2 to 34 microgram/dl. The levels of lead in breast milk are thus similar to those in plasma. Breast-fed infants are only at risk if the mother is exposed to high concentrations of contaminants either from endogenous sources such as the skeleton or exogenous sources.     

Lead, mercury, and organochlorine compound levels in cord blood in Québec, Canada

We conducted this study to evaluate blood levels of lead, mercury, and organochlorine compounds in newborns in the Province of Quebec. During 1993 to 1995, we carried out a survey in 10 hospitals located in southern Quebec. During that time, umbilical cord blood samples were obtained from 1109 newborns, and we analyzed each for lead, mercury, 14 polychlorinated biphenyl congeners, and 11 chlorinated pesticides. We used the geometric mean and 95% confidence interval (CI) to describe the results. Mean concentrations of lead and mercury in cord blood were 0.076 micromol/l (95% CI = 0.074, 0.079) and 4.82 nmol/l (95% CI = 4.56, 5.08), respectively. The mean concentrations of total polychlorinated biphenyls (Aroclor 1260) and dichlorodiphenyl dichloroethylene were 0.514 microg/I (95% CI = .493, 0.536) and 0.412 microg/l (95% CI = 0.390, 0.435), respectively. We observed a statistically significant relationship between maternal age and cord blood concentrations of (a) lead, (b) mercury, (c) polychlorinated biphenyls, and (d) dichlorodiphenyl dichloroethylene. In addition, maternal smoking during pregnancy was associated with cord blood lead levels. The cord blood concentrations of lead, mercury, polychlorinated biphenyls, and dichlorodiphenyl dichloroethylene we measured in our study were the lowest levels recently reported in industrialized countries. The results of this study underline the role of public health authorities in the evaluation of biological levels of environmental contaminants among children for the assessment of risk of adverse health effects.     

Delta-aminolevulinate dehydratase polymorphism and blood lead levels in Chinese children

This study investigated the relationship between the delta-aminolevulinate dehydratase (ALAD) isozymes and the blood lead levels of Chinese children. The purpose of this study was to determine the precise ALAD genotyping in Chinese children and identify the contribution of the ALAD genotype to the body lead burden. Blood samples were obtained from 109 boys and 120 girls. These children were 6-10 years old and from a single primary school. Both the school and their homes were within a community in which a large smelter was located. An environmental questionnaire was obtained for each subject, and blood lead levels and ALAD isozyme phenotype were analyzed in a double-blinded fashion. The blood lead levels of 229 children ranged from 4.5 to 26.4 microg/dl; the mean was 10.3 microg/dl and the standard deviation was 3.3 microg/dl. The gene distribution of the ALAD isozyme phenotypes in these environmentally exposed children was ALAD 1-1 (92%), ALAD 1-2, (8%), and ALAD 2-2 (0%). The mean blood level of the environmentally exposed children, who were homozygous for the ALAD1 allele, was 9.7 microg/dl; the mean for those who were heterozygous for the ALAD2 allele was 11.7 microg/dl. Using the t test, the means of the groups were different at the level of t=2.2058, P<0.05. Step-wise regression and multiple analyses of covariance were employed to control the confounders to measuring the independent contribution of the ALAD genotype on blood lead levels. After controlling the confounders, the contribution of the ALAD genotype to the blood lead level was greater and still statistically significant (F=7.3201, P<0.01). These results indicate that individuals carrying the ALAD2 allele are more likely to have sustained increases in blood lead levels when exposed to a lead-contaminated environment.