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At least 19 recordsLinked to original sources
PubMed1993

Comparison of lead bioavailability in F344 rats fed lead acetate, lead oxide, lead sulfide, or lead ore concentrate from Skagway, Alaska.

An animal model using rats was developed to initiate investigations on the bioavailability of different sources of environmental lead. Lead must be absorbed and transported to target organs like brain, liver, kidney, and bone, before susceptible cells can be harmed. The bioavailability and therefore the toxicity of lead are dependent upon the route of exposure, dose, chemical structure, solubility, particle size, matrix incorporation, and other physiological and physicochemical factors. In the present study male F344 rats were fed < or = 38 microns size particles of lead sulfide, lead oxide, lead acetate, and a lead ore concentrate from Skagway, Alaska, mixed into the diet at doses of 0, 10, 30, and 100 ppm as lead for 30 d. No mortality or overt symptoms of lead toxicity were observed during the course of the study. Maximum blood lead concentrations attained in the 100 ppm groups were approximately 80 micrograms/dl in rats fed lead acetate and lead oxide, and were approximately 10 micrograms/dl in those fed lead sulfide and lead ore concentrate. Maximum bone lead levels in rats fed soluble lead oxide and lead acetate were much higher (approximately 200 micrograms/g) than those seen in rats fed the less soluble lead sulfide and lead ore (approximately 10 micrograms); kidney lead concentrations were also about 10-fold greater in rats fed the more soluble compared to the less soluble lead compounds. However, strong correlations between dose and tissue lead concentrations were observed in rats fed each of the four different lead compounds. Kidney lesions graded as minimal occurred in 7/10 rats fed 30 ppm and in 10/10 rats fed 100 ppm lead acetate, but not at lower doses or from other lead compounds. Similarly, urinary aminolevulinic acid excretion, a biomarker for lead toxicity, was increased in rats fed 100 ppm lead acetate or lead oxide, but was unaffected at lower doses or by the less soluble lead compounds. Although the histological and biochemical responses to lead toxicity were restricted to the more soluble lead compounds in this study, lead from Skagway lead ore concentrate and lead sulfide was also bioavailable, and accumulated in proportion to dose in vulnerable target organs such as bone and kidney. Longer-term studies with different mining materials are being conducted to determine if tissue lead continues to increase, and whether the levels attained are toxic. Data from such studies can be used to compare the toxicity and bioavailability of lead from different sources in the environment.

Administration, Oral↗
PubMed2001

Predictors of DMSA chelatable lead, tibial lead, and blood lead in 802 Korean lead workers.

OBJECTIVES: To examine the interrelations among chelatable lead (by dimercaptosuccinic acid, DMSA), tibial lead, and blood lead concentrations in 802 Korean workers with occupational exposure to lead and 135 employed controls with only environmental exposure to lead. METHODS: This was a cross sectional study wherein tibial lead, DMSA chelatable lead, and blood lead were measured. Linear regression was used to identify predictors of the three lead biomarkers, evaluating the influence of age, job duration, sex, education level, alcohol and tobacco use, creatinine clearance rate, and body mass index. RESULTS: DMSA chelatable lead concentrations ranged from 4.8 to 2102.9 microg and were positively associated with age, current smoking, and creatinine clearance rate. On average, women had 64 microg less DMSA chelatable lead than men. When blood lead and its square were added to a model with age, sex, current smoking, body mass index, and creatinine clearance rate, blood lead accounted for the largest proportion of the variance and sex became of borderline significance. Tibial lead concentrations ranged from -7 to 338 microg/g bone mineral and were positively associated with age, job duration, and body mass index. Women had, on average, 9.7 microg/g less tibial lead than men. Blood lead concentrations ranged from 4.3 to 85.7 microg/dl and were positively associated with age and tibial lead, whereas current smokers had higher blood lead concentrations and women had lower blood lead concentrations. CONCLUSIONS: The data suggest that age and sex are both predictors of DMSA chelatable lead, blood lead, and tibial lead concentrations and that tibial lead stores in older subjects are less bioavailable and may contribute less to blood lead concentrations than tibial lead stores in younger subjects. Although blood lead concentrations accounted for a large proportion of the variance in DMSA chelatable lead concentrations, suggesting that measurement of both in epidemiological studies may not be necessary, the efficacy of each measure in predicting health outcomes in epidemiological studies awaits further investigation.

Adult↗
PubMed1986

[Excretion of triethyl lead, diethyl lead and inorganic lead in the urine and feces of rabbits treated with diethyl lead dichloride].

One group of rabbits were injected intraperitoneally with diethyllead dichloride (7.7 mg Pb/kg) and another group of rabbits were likewise injected with an equivalent lead dose of lead acetate. These rabbits were followed up for changes in the lead amounts excreted daily in the urine and feces from 24 h through 7 d after the injection, respectively. In the group of rabbits injected with diethyllead dichloride (one of 3 rabbits died during the observation), an amount of lead equivalent to about 25% of the injected dose was excreted in the urine during the first 24 h after the injection. Also, an amount of lead equivalent to about 28% of the injected lead was excreted in the feces during the first 3 d, and the total lead excretion during the 7 d after the injection corresponded to about 60% of the injected dose of diethyllead. One day after dosing, the total lead in the urine was made up of about 92% diethyllead, about 7% inorganic lead and about 1% triethyllead. One day after dosing, the total lead in the feces consisted of about 63% inorganic lead, about 28% diethyllead and about 9% triethyllead. Three days after dosing, the total lead in feces comprised about 98% inorganic lead, about 1% diethyllead and about 1% triethyllead. In the group of 3 rabbits injected with lead acetate, the total lead amount excreted in both the urine and feces during the 7 d after the injection corresponded to only about 9% of the injected dose of lead acetate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Associations of blood lead, dimercaptosuccinic acid-chelatable lead, and tibia lead with neurobehavioral test scores in South Korean lead workers.

The authors performed a cross-sectional study to evaluate associations between blood lead, tibia lead, and dimercaptosuccinic acid (DMSA)-chelatable lead and measures of neurobehavioral and peripheral nervous system function among 803 lead-exposed workers and 135 unexposed controls in South Korea. The workers and controls were enrolled in the study between October 1997 and August 1999. Central nervous system function was assessed with a modified version of the World Health Organization Neurobehavioral Core Test Battery. Peripheral nervous system function was assessed by measuring pinch and grip strength and peripheral vibration thresholds. After adjustment for covariates, the signs of the beta coefficients for blood lead were negative for 16 of the 19 tests and blood lead was a significant predictor of worse performance on eight tests. On average, for the eight tests that were significantly associated with blood lead levels, an increase in blood lead of 5 microg/dl was equivalent to an increase of 1.05 years in age. In contrast, after adjustment for covariates, tibia lead level was not associated with neurobehavioral test scores. Associations with DMSA-chelatable lead were similar to those for blood lead. In these currently exposed workers, blood lead was a better predictor of neurobehavioral performance than was tibia or DMSA-chelatable lead, mainly in the domains of executive abilities, manual dexterity, and peripheral motor strength.

Adult↗
PubMed1994

Relationship between soil lead, dust lead, and blood lead concentrations in pets and their owners: evaluation of soil lead threshold values.

This paper reports the results of a study conducted in Granite City, Illinois during the months of August through October 1991. The study involved a subpopulation of 77 households having 106 dogs and cats which was a corollary to a major study conducted in humans by the Illinois Department of Public Health to evaluate lead exposure. A secondary lead smelter had been in operation in this town for almost 80 years and was shut down in 1982. Important soil contamination with lead was reported and this paper presents data regarding levels of soil and dust lead and associated blood lead concentrations in animals and their owners in a total of 77 households. Overall, blood lead concentrations (BLC) were low (0-13 micrograms/dl in the animal owners; 0-28 micrograms/dl in pets). There was no significant relationship between soil or dust lead and BLC in humans; however, the relationship was significant in animals. Odds ratios were computed to determine whether 500 or 1000 ppm lead in environmental samples was associated with increased risk of having a high BLC. We could not find any increased risk in humans, while the risk did increase in animals. It is concluded that animals are more at risk than their owners of having a high BLC when exposed to the same contaminated environment and can be used to monitor the bioavailability of lead.

Adolescent↗
PubMed1981

Clinical signs, radiology and tissue lead distribution of dogs administered a mixture of lead chloride, lead bromide and lead sulphate.

Eight-month-old dogs maintained on a high-fat-low-calcium diet were administered a mixture of lead chloride, lead bromide and lead sulphate for prolonged periods at 4 different dose levels. Dogs on high levels of leads showed marked weight loss and gastrointestinal symptoms followed by death. Two dogs on low lead levels developed neurological signs. Radiological investigations showed radiopaque particles in 27 per cent of abdominal radiographs and "lead lines' in the distal radius of 3 dogs. Highest tissue lead levels were found in bones followed by liver and kidney, brain and spinal cord.

Animals↗
PubMed1991

Sweat lead levels in persons with high blood lead levels: experimental elevation of blood lead by ingestion of lead chloride.

Blood lead levels were experimentally elevated in two subjects by ingestion of single oral doses of lead as lead chloride. Serial samples of blood, urine and sweat were collected subsequently. Sweat samples were collected in polythene armbags while subjects cycled on a bicycle ergometer in a hot chamber. In spite of increases in blood and urinary lead levels, no increases in sweat lead levels were recorded. Possible reasons for this observation are discussed.

Administration, Oral↗
PubMedDate not supplied

Clinical applications of L-line X-ray fluorescence to estimate bone lead values in lead-poisoned young children and in children, teenagers, and adults from lead-exposed and non-lead-exposed suburban communities in the United States.

In summary, LXRF estimates of Pb in tibial cortical bone have yielded highly relevant clinical data relating to the efficacy of chelation therapy with CaNa2EDTA in lead poisoned children; diagnostic approach(es) to childhood lead poisoning; and evaluations of exposure in children, teenagers, and adults in lead-exposed and non-lead-exposed suburban communities. It is anticipated that KXRF and LXRF estimates of Pb in bone will yield new information concerning the epidemiology of hypertension, osteoporosis, and the contribution of maternal Pb to the developing fetus. It would be premature to delineate the age-developmental time boundaries over which these two systems [KXRF, LXRF] can be viewed as operated optimally. Consequently, it is appropriate to view the two approaches as providing complementary information. All such information might, in fact, be required to obtain a complete exposure profile and a comprehensive framework for assessment of health risks.

Adolescent↗
PubMed1991

Sweat lead levels in persons with high blood lead levels: lead in sweat of lead workers in the tropics.

Samples of blood, sweat and urine were collected from eight control subjects and 19 lead workers in a battery manufacturing factory in the tropics. Sweat samples were collected while workers cycled on a bicycle ergometer at room temperature (27-31 degrees C). All samples were analysed by atomic absorption spectrophotometry. Workers with blood lead levels of 13-36 micrograms dl-1 had sweat levels of 72-256 micrograms l-1 and urinary levels of 28-288 micrograms/g creatinine, while controls had levels of 9-12.2 micrograms dl-1, 9-30 micrograms l-1 and 9-19.6 microgram/g creatinine, respectively. Estimations of sweat lead in lead workers can be masked by skin contamination.

Humans↗
PubMed2001

Interrelations of lead levels in bone, venous blood, and umbilical cord blood with exogenous lead exposure through maternal plasma lead in peripartum women.

Recent research has raised the possibility that fetal lead exposure is not estimated adequately by measuring lead content in maternal whole blood lead because of the variable partitioning of lead in whole blood between plasma and red blood cells. Lead in maternal plasma may derive in large part from maternal bone lead stores. In this study we aimed to estimate the contribution of maternal whole blood lead, maternal bone lead levels, and environmental lead to umbilical cord blood lead levels (as a measure of fetal lead exposure). In the model, we assumed that lead from all of these sources reaches the fetus through the maternal plasma lead pathway. In 1994-1995, we recruited 615 pregnant women for a study of lead exposure and reproductive outcomes in Mexico City. We gathered maternal and umbilical cord blood samples within 12 hr of each infant's delivery and measured maternal lead levels in cortical bone and trabecular bone by a K-X-ray fluorescence (K-XRF) instrument within 1 month after delivery. We administered a questionnaire to assess use of lead-glazed ceramics (LGC) to cook food and we obtained data on regional air lead levels during the 2 months before delivery. We used structural equation models (SEMs) to estimate plasma lead as the unmeasured (latent) variable and to quantify the interrelations of plasma lead, the other lead biomarkers, and environmental lead exposure. In the SEM analysis, a model that allowed plasma lead to vary freely from whole blood lead explained the variance of cord blood lead (as reflected by a total model R(2); R(2) = 0.79) better than did a model without plasma lead (r(2) = 0.67). Cortical bone lead, trabecular bone lead, use of LGC, and mean air lead level contributed significantly to plasma lead. The exchange of lead between plasma and red blood cells was mostly in the direction of plasma to cells. According to the final model, an increase in trabecular bone lead and cortical bone lead was associated with increases in cord blood lead of 0.65 and 0.25 microg/dL, respectively. An increase of 0.1 microg/m(3) in air lead was associated with an increase in the mean level of fetal cord blood lead by 0.67 microg/dL. With one additional day of LCG use per week in the peripartum period, the mean fetal blood lead level increased by 0.27 microg/dL. Our analyses suggested that maternal plasma lead varies independently from maternal whole blood lead and that the greatest influences on maternal plasma lead are maternal bone lead stores, air lead exposures, and recent cooking with LGC. The contributions from endogenous (bone) and exogenous (environmental) sources were relatively equal. Measurement of plasma and bone lead may be important in accurately assessing fetal lead exposure and its major sources, particularly if exogenous exposures decline.

Air Pollutants↗
PubMed2000

Associations of blood lead, dimercaptosuccinic acid-chelatable lead, and tibia lead with polymorphisms in the vitamin D receptor and [delta]-aminolevulinic acid dehydratase genes.

A cross-sectional study was performed to evaluate the influence of polymorphisms in the [delta]-aminolevulinic acid dehydratase (ALAD) and vitamin D receptor (VDR) genes on blood lead, tibia lead, and dimercaptosuccinic acid (DMSA)-chelatable lead levels in 798 lead workers and 135 controls without occupational lead exposure in the Republic of Korea. Tibia lead was assessed with a 30-min measurement by (109)Cd-induced K-shell X-ray fluorescence, and DMSA-chelatable lead was estimated as 4-hr urinary lead excretion after oral administration of 10 mg/kg DMSA. The primary goals of the analysis were to examine blood lead, tibia lead, and DMSA-chelatable lead levels by ALAD and VDR genotypes, controlling for covariates; and to evaluate whether ALAD and VDR genotype modified relations among the different lead biomarkers. There was a wide range of blood lead (4-86 microg/dL), tibia lead (-7-338 microg Pb/g bone mineral), and DMSA-chelatable lead (4.8-2,103 microg) levels among lead workers. Among lead workers, 9.9% (n = 79) were heterozygous for the ALAD(2) allele and there were no homozygotes. For VDR, 10.7% (n = 85) had the Bb genotype, and 0.5% (n = 4) had the BB genotype. Although the ALAD and VDR genes are located on different chromosomes, lead workers homozygous for the ALAD(1) allele were much less likely to have the VDR bb genotype (crude odds ratio = 0.29, 95% exact confidence interval = 0.06-0.91). In adjusted analyses, subjects with the ALAD(2) allele had higher blood lead levels (on average, 2.9 microg/dL, p = 0.07) but no difference in tibia lead levels compared with subjects without the allele. In adjusted analyses, lead workers with the VDR B allele had significantly (p < 0.05) higher blood lead levels (on average, 4.2 microg/dL), chelatable lead levels (on average, 37.3 microg), and tibia lead levels (on average, 6.4 microg/g) than did workers with the VDR bb genotype. The current data confirm past observations that the ALAD gene modifies the toxicokinetics of lead and also provides new evidence that the VDR gene does so as well.

Adolescent↗
PubMed2004

The influence of exterior dust and soil lead on interior dust lead levels in housing that had undergone lead-based paint hazard control.

To aid in understanding the contribution of exterior dust/soil lead to postintervention interior dust lead, a subset of housing from the HUD Lead-Based Paint Hazard Control Grant Program Evaluation was selected for study. Housing from 12 state and local governments was included. Exterior entry and street dust samples were obtained by a vacuum method, and soil samples were building perimeter core composites. Interior dust wipe lead data (microg/ft(2)) and paint lead data (mg/cm(2)) were also available for each of the dwelling units and included in the modeling. Results from 541 dwelling units revealed a wide range of exterior dust and soil lead levels, within and between grantees. Minimum and maximum geometric mean lead levels, by grantee, were 126 and 14400 microg/ft(2) for exterior entry dust; 325 and 4610 microg/ft(2) for street dust; and, for soil concentration, 383 and 2640 ppm. Geometric mean exterior entry dust lead concentration (1641 ppm) was almost four times as high as street dust lead concentration (431 ppm), suggesting that lead dust near housing was often a source of street dust lead. Geometric mean exterior entry dust lead loading was more than four times as high as window trough dust lead loading and more than an order of magnitude higher than interior entry dust lead loading. Statistical modeling revealed pathways from exterior entry dust lead loading to loadings on interior entryway floors, other interior floors, and windowsills. Paint lead was found to influence exterior entry dust lead. Results of this study show that housing where soil lead hazard control activities had been performed had lower postintervention exterior entry, interior entry floor, windowsills, and other floor dust loading levels. Soil was not present for almost half the buildings. Statistical analysis revealed that exterior strategy influenced soil lead concentration, and soil lead concentration influenced street dust lead loading. This study represents one of the few where an impact of soil treatments on dust lead levels within the housing has been documented and may represent the first where an impact on exterior entry dust lead has been found. The inclusion of measures to mitigate the role of exterior sources in lead hazard control programs needs consideration.

Dust↗
PubMed1995

Contribution of tissue lead to blood lead in adult female subjects based on stable lead isotope methods.

Public health and medical recommendations on prevention of lead toxicity rely on use of blood lead concentrations to assess lead exposure and predict onset of adverse health effects. Blood lead levels have generally been thought to reflect recent environmental lead exposures. However, tissue lead stores are accumulated over a long time period (i.e., years). These tissue stores, primarily from bone, can be remobilized as part of both normal physiologic and pathologic processes. Although chemical analyses do not differentiate lead isotopes, mass spectrometric determinations can differentiate the quantities of stable lead isotopes present in particular samples (e.g., lead 207, lead 206, lead 204, and lead 208). Selected geographic locations may have distinct isotopic profiles. For example, on mainland Australia the 206Pb/204Pb ratios reported in both environmental lead sources and blood samples are typically less than 17.0. By contrast, stable lead isotope profiles in blood samples of adult women immigrating from Eastern Europe and the former Soviet Union usually have 206Pb/204Pb ratios greater than 17.5 and as high as 18.5 on entry into Australia. Longitudinal monitoring of blood samples to determine stable lead isotope profiles by mass spectrometry and chemical analyses of blood samples for total lead content were conducted over a 300-day period. These data show that between 45% and 70% of lead in blood comes from long-term tissue lead stores. Recognition that the predominant source of lead in blood was tissue stores rather than the contemporaneous environment should greatly modify recommendations on use of blood lead to monitor occupational or environmental interventions. In addition, internal biokinetics of lead, documented through presence of tissue lead in blood, underlie the long-term health risks of lead exposure. Transfer of lead to the fetus from maternal tissue stores represents a special area of concern.

Adult↗
PubMed2003

The effect of lead-based paint hazard remediation on blood lead levels of lead poisoned children in New York City.

Despite the widespread use of lead paint hazard control for children with lead poisoning, few controlled studies that estimate the effect of such control on children's blood lead levels have been published. This retrospective follow-up study examined the effects of lead hazard remediation and its timing on the blood lead levels of lead-poisoned children. From the New York City child blood lead registry, 221 children were selected who had an initial blood lead level of 20-44 micro g/dL between 1 July 1994 and 31 December 1996; were 6 months to 6 years of age; had a report of a follow-up blood lead test between 10 and 14 months after the initial test; had a lead-based paint hazard identified in the primary dwelling unit prior to the 10- to 14-month follow-up blood lead test; had resided or spent time at only one address with an identified lead-based paint hazard; and were not chelated. The decline in geometric mean blood lead levels from baseline to 10-14 months later was compared for children whose homes were remediated and whose homes were not remediated during the follow-up period. Regardless of remediation, geometric mean blood lead levels declined significantly from 24.3 micro g/dL at the initial diagnosis to 12.3 micro g/dL at the 10- to 14-month follow-up blood lead test (P<0.01). Among the 146 children whose homes were remediated the geometric mean blood lead levels declined 53% compared to 41% among the 75 children whose homes were not remediated by the follow-up blood lead test, a remediation effect of approximately 20% (P<0.01). After adjusting for potential confounders, the remediation effect was 11%, although it was no longer significant. Race was the only factor that appeared to confound the relationship: Black children had higher follow-up blood lead levels even after controlling for other factors, including the natural logarithm of the initial blood lead level. The effect of remediation appeared to be stronger for younger (10 to <36 months old) than for older (36 to 72 months old) children (P=0.06). While children in homes with earlier remediation (within less than 3 months) appeared to have greater declines in blood lead levels at the follow-up test than children in homes with later remediation (after 3 or more months), this trend was not significant when controlling for confounding factors. The findings of this study suggest that early identification of lead-poisoned children and timely investigation and abatement of hazards contribute to reducing blood lead levels. However, the apparent effect is modest and further research is needed to systematically test and improve the effectiveness of lead hazard controls.

Air Pollution, Indoor↗
PubMed1983

The monoclonal antibody directed to difucosylated type 2 chain (Fuc alpha 1 leads to 2Gal beta 1 leads to 4[Fuc alpha 1 leads to 3]GlcNAc; Y Determinant).

One of the monoclonal (AH-6) antibodies prepared by hybridoma technique against human gastric cancer cell line MKN74 was found to react with a series of glycolipids having the Y determinant (Fuc alpha 1 leads to 2Gal beta 1 leads to 4[Fuc alpha 1 leads to 3]GlcNAc). The structure of one such glycolipid isolated from human colonic cancer and from dog intestine was identified as lactodifucohexaosyl-ceramide (Fuc alpha 1 leads to 2Gal beta 1 leads to 4[Fuc alpha 1 leads to 3]GlcNAc beta 1 leads to 3Gal beta 1 leads to 4Glc beta 1 leads to 1-ceramide; IV3,III3Fuc2nLc4Cer). The hapten glycolipid did not react with monoclonal antibodies directed to Lea, Leb, and X-hapten structures, and the AH-6 antibody did not react with the X-hapten ceramide pentasaccharide (Gal beta 1 leads to 4[Fuc alpha 1 leads to 3]GlcNAc beta 1 leads to 3Gal beta 1 leads to 4Glc beta 1 leads to 1-ceramide), H1 glycolipid (Fuc alpha 1 leads to 2Gal beta 1 leads to 4GlcNAc beta 1 leads to 3Gal beta 1 leads to 4Glc beta 1 leads to 1-ceramide), nor with glycolipids having the Leb (Fuc alpha 1 leads to 2Gal beta 1 leads to 3[Fuc alpha 1 leads 4]GlcNAc beta 1 leads to R) determinant. The antibody reacted with blood group O erythrocytes, but not with A erythrocytes. Immunostaining of thin layer chromatography with the monoclonal antibody AH-6 indicated that a series of glycolipids with the Y determinant is present in tumors and in O erythrocytes.

Animals↗
PubMedDate not supplied

Lip lead as an alternative measure for lead exposure assessment of lead battery assembly workers.

This study investigated lead exposures of lead battery assembly workers in Taiwan. A special attempt was made to evaluate the use of lip lead as an alternative index for occupational lead exposure. Ninety-six of 113 workers from a lead battery plant were recruited as study subjects. Air lead; lead loadings on workers' sleeves, gloves, hands, cheeks, and lips; and blood lead were determined for exposure assessment. A questionnaire also was administered to collect information on work history, suspected exogenous lead sources, and personal behavior and activities. Geometric means of total air lead at different subareas ranged from 0.070 (2.5 geometric standard deviation [GSD]) to 0.159 (1.8 GSD) mg/m3. Geometric means of respirable air lead level for different subgroups of workers varied from 0.009 (2.0 GSD) to 0.032 (1.9 GSD) mg/m3, whereas those of the blood lead level ranged from 22.4 (1.3 GSD) to 44.5 (1.3 GSD) microg/dL. The heaviest lead loadings were found for plate-processing workers (e.g., 66.4 [1.5 GSD] on gloves, 0.80 [3.7 GSD] on cheeks, and 0.79 [3.2 GSD] microg/cm2) on bare-hands after washing. Blood lead level was significantly correlated with lead levels in air, lead loadings on lips, and bare hands after washing (r=0.24-0.30). Results of multiple regression analysis showed that only lip lead had a significant effect on the blood lead, whereas respirable air lead and personal behavior had only mild effects in this model. It was concluded that lip lead level may be used as an alternative index of lead exposure to facilitate the estimation of lead uptake through ingestion.

Cheek↗
PubMed1997

Log-additive versus log-linear analysis of lead-contaminated house dust and children's blood-lead levels. Implications for residential dust-lead standards.

The Environmental Protection Agency has been mandated to develop a health-based standard for lead in residential dwellings in the United States. Prior estimates of the relationship between residential dust-lead levels and children's blood-lead concentrations have usually been obtained by using a log-linear regression of blood-lead concentration on levels of lead-contaminated house dust. It remains unknown, however, whether the log-linear model or a frequently cited alternative, the log-additive model, is the preferable regression method for analyzing these data. Secondary analysis of the Lead-in-Dust Study data was undertaken to compare log-additive with log-linear regression analysis for the purpose of developing a health-based dust lead standard. Specifically, we were interested in comparing the log-additive and log-linear analyses in their ability to characterize adequately the relationship of dust-lead loading on various surfaces with blood-lead concentrations among urban children and to develop a predictive model to estimate the risk that a child will develop an elevated blood-lead level on the basis of a known level of dust lead. We used two dust sampling methods, the Baltimore Repair and Maintenance (BRM) vacuum method and the wipe method, to compare the log-linear and log-additive models. The log-linear model was consistently superior to the log-additive model in its ability to explain the variability in the observed blood-lead concentrations of the studied children, for both the wipe sampler and the BRM sampler. In addition, the log-additive model often predicted only a limited increase in the probability of blood-lead concentrations exceeding 10 micrograms/dl as a result of doubling the dust-lead loading exposure, whereas the log-linear model consistently demonstrated a significant increase in the probability of blood-lead concentrations exceeding 10 micrograms/dl. BRM lead loading explained additional variability in blood lead above and beyond that explained by wipe loading for both carpeted and uncarpeted floors. In contrast, wipe-lead loading explained significant additional variability after adjustment for BRM loading for both uncarpeted floors and interior window sills. Although BRM loading better predicted children's blood-lead concentrations than did wipe loading, these differences were not statistically significant. We conclude that the log-linear model explained a greater percentage of the variability in blood-lead concentrations than did the log-additive model, indicating that the log-linear model should be the default model of choice for developing a dust-lead standard.

Air Pollution, Indoor↗