Biomedical subjects

M J Emond

Publications and source records attributed to M J Emond.

At least 19 recordsLinked to original sources

PubMed2001

Loss of Werner syndrome protein function promotes aberrant mitotic recombination.

The chromosome 8p11-12 Werner syndrome (WRN ) locus encodes a RecQ helicase protein of unknown function that possesses both 3' --> 5' helicase and 3' --> 5' exonuclease activities. We show that WRN cell lines display a marked reduction in cell proliferation following mitotic recombination, and generate few viable gene conversion-type recombinants. These findings indicate that WRN plays a role in mitotic recombination, and that a loss of WRN function may promote genetic instability and disease via recombination-initiated mitotic arrest, cell death, or gene rearrangement.

Cell Death↗

PubMed2001

Ursodiol use is associated with lower prevalence of colonic neoplasia in patients with ulcerative colitis and primary sclerosing cholangitis.

BACKGROUND: Patients with ulcerative colitis and primary sclerosing cholangitis are at high risk for colonic dysplasia and cancer. This risk approaches 50% after 25 years of colitis. Ursodiol has been shown to protect against development of colorectal neoplasia in animal models. OBJECTIVE: To assess the relationship between ursodiol use and colonic dysplasia, the precursor to colon cancer, in patients with ulcerative colitis and primary sclerosing cholangitis. DESIGN: Cross-sectional study. SETTING: University medical center. PATIENTS: 59 patients with ulcerative colitis and primary sclerosing cholangitis who were undergoing colonoscopic surveillance for colonic dysplasia. MEASUREMENTS: Use of ursodiol was assessed in all patients. The presence or absence of colonic dysplasia was evaluated by colonoscopic surveillance. Other variables assessed were age at onset and duration of ulcerative colitis; duration of primary sclerosing cholangitis; Child-Pugh classification; and use of sulfasalazine, other 5-aminosalicylic acid preparations, prednisone, cyclosporine, azathioprine, and methotrexate. RESULTS: Ursodiol use was strongly associated with decreased prevalence of colonic dysplasia (odds ratio, 0.18 [95% CI, 0.05 to 0.61]; P = 0.005). The association between dysplasia and ursodiol use remained after adjustment for sex, age at onset of colitis, duration of colitis, duration of sclerosing cholangitis, severity of liver disease, and sulfasalazine use (adjusted odds ratio, 0.14 [CI, 0.03 to 0.64]; P = 0.01). Younger age at onset of colitis was associated with an increased risk for dysplasia. CONCLUSIONS: Ursodiol use appears to be associated with a lower frequency of colonic dysplasia in patients with ulcerative colitis and primary sclerosing cholangitis. A randomized trial investigating the chemoprotective effect of ursodiol in patients with ulcerative colitis may be warranted.

Adult↗

PubMed2001

Chromosomal changes in a dedifferentiated chondrosarcoma: a case report and review of the literature.

The chromosome abnormalities observed in a dedifferentiated chondrosarcoma are reported. A new molecular cytogenetic technique, spectral karyotyping, was used to identify and confirm structural rearrangements in this case. A review of the literature revealed that nine cases have been reported, in eight of which a complete description of the cytogenetic abnormalities was described. Structural aberrations were most frequently reported in chromosomes 1 and 9, and chromosomes 7 and 19 were most frequently observed to be involved in numerical aberrations (trisomy and tetrasomy). In chondrosarcomas, structural aberrations in chromosomes 1 and 9 and trisomy or tetrasomy of chromosome 7 are among the more frequently observed aberrations.

Arthroplasty, Replacement, Knee↗

PubMed2000

Genetic instability and hematologic disease risk in Werner syndrome patients and heterozygotes.

Werner syndrome (WRN) is an uncommon autosomal recessive disease in which progeroid features are associated with genetic instability and an elevated risk of neoplasia. We have used the glycophorin A (GPA) somatic cell mutation assay to analyze genetic instability in vivo in WRN patients and heterozygotes. GPA variant frequencies were determined for 11 WRN patients and for 10 heterozygous family members who collectively carry 10 different WRN mutations. Genetic instability as measured by GPA O/N allele loss variant frequency was significantly increased, and this increase was strongly age-dependent in WRN patients. GPA O/N allele loss variants were also significantly elevated in heterozygous family members, thus providing the first evidence for in vivo genetic instability in heterozygous carriers in an autosomal recessive genetic instability syndrome. Our results and comparable data on other human genetic instability syndromes allow an estimate of the level of genetic instability that increases the risk of human bone marrow dysfunction or neoplasia.

Adolescent↗

PubMed2000

Retinoblastoma expression in thyroid neoplasms.

Retinoblastoma (Rb) mutation in thyroid neoplasia has been identified in a few molecular studies; however, the utility of Rb immunohistochemistry in distinguishing benign and malignant thyroid lesions has not been documented in formalin-fixed, paraffin-embedded tissues. The present study investigated Rb immunohistochemistry in a series of 111 formalin-fixed, paraffin-embedded benign and malignant thyroid lesions. All of the major histologic subtypes were included to detect any heterogeneity in Rb-1 expression that might influence the diagnostic utility of this technique or further elucidate the pathogenesis of thyroid neoplasia among the categories. Altogether, 34 follicular adenomas, 9 follicular carcinomas, 7 Hürthle cell adenomas, 5 Hürthle cell carcinomas, 23 papillary carcinomas (8 of which were follicular variants), 4 insular carcinomas, 4 anaplastic carcinomas, 6 medullary carcinomas, and 19 nodular goiters were analyzed. Avidinbiotin immunohistochemistry was performed using the Dako Rb-1 clone. Pronase digestion was introduced into the epitope retrieval protocol to eliminate false-positive cytoplasmic stainig. Nuclear immunoreactivity was assessed as positive if 10% or more of thyroid epithelial nuclei stained positively, and conversely as negative. The majority of benign non-Hürthle thyroid lesions, whether hyperplastic or neoplastic, retained Rb nuclear immunopositivity in most cells (51 of 53 cases [96%]). Conversely, malignant thyroid neoplasms lacked Rb immunoreactivity in the majority (42 of 51 cases [82%]), including all papillary carcinomas (23 of 23) and almost all follicular carcinomas (8 of 9 [89%]). Virtually all Hürthle cell neoplasms were negative (11 of 12 [92%]), whether benign or malignant. In conclusion, Rb immunohistochemistry can aid in the distinction between benign and malignant thyroid lesions in conjunction with morphology. This seems to be most applicable to the often problematic differentiation between follicular adenoma and the follicular variant of papillary carcinoma (P < .0001; sensitivity and specificity, 100%) or minimally invasive follicular carcinoma (P = .0007; sensitivity, 89%; specificity, 100%).

Adenoma↗

PubMed1999

Pancolonic chromosomal instability precedes dysplasia and cancer in ulcerative colitis.

Patients with long-standing ulcerative colitis (UC) are at increased risk for colon cancer. These cancers are thought to arise from preexisting dysplasia in a field of abnormal cells that often exhibits aneuploidy and p53 abnormalities. Using dual color fluorescence in situ hybridization with centromere probes and locus-specific arm probes for chromosomes 8, 11, 17, and 18, we demonstrate that chromosomal instability (CIN) is present throughout the colon of UC patients with high-grade dysplasia or cancer. In rectal biopsies that were negative for dysplasia, abnormalities in chromosomal arms, especially losses, were most common, whereas centromere gains were most common in dysplasia and cancer. The frequency and type of abnormalities varied between the chromosomes examined; chromosome 8 was the least affected, and 17p loss was found to be an early and frequent event. Chromosomal arm instability showed 100% sensitivity and specificity for distinguishing control biopsies from histologically negative rectal biopsies from these UC patients, raising the possibility that a screen for CIN might detect the subset of UC patients who are at greatest risk for development of dysplasia and cancer. These results suggest that dysplasia and cancer in UC arise from a process of CIN that affects the entire colon; this may provide the mutator phenotype that predisposes to loss of tumor suppressor genes and evolution of cancer.

Centromere↗

PubMed1999

Relationship between iron concentration and hepatitis C virus RNA level in liver tissue.

Patients with chronic hepatitis C virus (HCV) infection frequently have increased hepatic iron stores. The role of hepatitis C in hepatic iron deposition is unknown. The authors examined whether there is a relation between hepatitis C virus level in liver tissue and hepatic iron concentration. Forty-two paired samples obtained from the liver explants of five patients who underwent transplantation for liver disease due to hepatitis C were studied. Hepatitis C virus levels were measured at multiple sites within each liver by a branched deoxyribonucleic assay. Measurements of hepatic iron concentration were made at adjacent sites by a colorimetric assay. Random effects modeling showed wide intrahepatic variation in hepatic HCV ribonucleic acid (RNA) concentration (variance = 1.2 x 10(4) [mEq/g]2) and hepatic iron concentration (variance = 1.3 x 10(6) [microg/g]2). There was, however, a trend toward an association between the mean HCV level and the mean hepatic iron concentration for each liver (r = 0.30, p = 0.05). In conclusion, HCV level and iron concentration varied within and between cirrhotic livers. Variability in intrahepatic iron concentration was not related to variability in intrahepatic HCV RNA concentration. More studies are needed to determine the cause of variability in hepatic iron and HCV RNA concentration within and between livers in patients with chronic hepatitis C.

Hepacivirus↗

PubMed1999

Quantitative study of the variability of hepatic iron concentrations.

BACKGROUND: The hepatic iron concentration (HIC) is widely used in clinical practice and in research; however, data on the variability of HIC among biopsy sites are limited. One aim of the present study was to determine the variability of HIC within both healthy and cirrhotic livers. METHODS: Using colorimetric methods, we determined HIC in multiple large (microtome) and small (biopsy-sized) paraffin-embedded samples in 11 resected livers with end-stage cirrhosis. HIC was also measured in multiple fresh samples taken within 5 mm of each other ("local" samples) and taken at sites 3-5 cm apart ("remote" samples) from six livers with end-stage cirrhosis and two healthy autopsy livers. RESULTS: The within-organ SD of HIC was 13-1553 microg/g (CV, 3.6-55%) for microtome samples and 60-2851 microg/g (CV, 15-73%) for biopsy-sized samples. High variability of HIC was associated with mild to moderate iron overload, because the HIC SD increased with increasing mean HIC (P <0.002). Livers with mean HIC >1000 microg/g exhibited significant biological variability in HIC between sites separated by 3-5 cm (remote sites; P <0.05). The SD was larger for biopsy-sized samples than for microtome samples (P = 0.02). CONCLUSION: Ideally, multiple hepatic sites would be sampled to obtain a representative mean HIC.

Biopsy↗

PubMed1998

I-PpoI and I-CreI homing site sequence degeneracy determined by random mutagenesis and sequential in vitro enrichment.

Plasmid libraries containing partially randomized cleavage sites for the eukaryotic homing endonucleases I-PpoI and I-CreI were constructed, and sites that could be cleaved by I-PpoI or I-CreI were selectively recovered by successive cycles of cleavage and gel separation followed by religation and growth in Escherichia coli. Twenty-one different I-PpoI-sensitive homing sites, including the native homing site, were isolated. These sites were identical at four nucleotide positions within the 15 bp homing site, had a restricted pattern of base substitutions at the remaining 11 positions and displayed a preference for purines flanking the top strand of the homing site sequence. Twenty-one different I-CreI-sensitive homing sites, including the native site, were isolated. Ten nucleotide positions were identical in homing site variants that were I-CreI-sensitive and required the addition of SDS for efficient cleavage product release. Four of these ten positions were identical in homing sites that did not require SDS for product release. There was a preference for pyrimidines flanking the top strand of the homing site sequence. Three of the 24 I-CreI homing site nucleotide positions apparently lacked informational content, i. e. were permissive of cleavage when occupied by any nucleotide. These results suggest that I-PpoI and I-CreI make a large number of DNA-protein contacts across their homing site sequences, and that different subsets of these contacts may be sufficient to maintain a high degree of sequence-specific homing site recognition and cleavage. The sequential enrichment protocol we used should be useful for defining the sequence degeneracy and informational content of other homing endonuclease target sites.

Base Sequence↗

PubMed1998

Endoscopic management of biliary strictures in liver transplant recipients: effect on patient and graft survival.

BACKGROUND: Biliary strictures in liver transplant recipients cause significant morbidity and can lead to reduced patient and graft survival. METHODS: Of 251 liver transplant recipients, 22 patients with biliary strictures were categorized into two groups: donor hepatic duct (n = 12) or anastomotic (n = 10). Strictures were dilated and stented. Endoscopic therapy was considered successful if a patient did not require repeat stenting or dilation for 1 year. RESULTS: Patient and graft survival did not differ significantly in the 22 patients compared with patients without strictures (relative risk of death and graft survival 1.8 and 1.3). Donor hepatic duct strictures required significantly longer therapy than anastomotic strictures (median days 185 versus 67, p = 0.02). Twenty-two months after the first endoscopic treatment, 73% of the donor hepatic duct stricture group were stent free compared with 90% of the anastomotic group (p = 0.02). The former group had significantly more (p < 0.05) hepatic artery thrombosis (58.3% versus 10%), cholangitis (58.3% versus 30%), choledocholithiasis (91% versus 10%), and endoscopic interventions. No patient undergoing endoscopic treatment required retransplantation or biliary reconstruction during a median follow-up of 35.7 months. CONCLUSION: Endoscopic therapy of biliary strictures after liver transplantation is effective and is not accompanied by reduced patient or graft survival.

Adult↗

PubMed1998

End-stage liver disease without hemochromatosis associated with elevated hepatic iron index.

BACKGROUND/AIMS: The utility of standard diagnostic tests for hereditary hemochromatosis in end-stage liver disease is unknown. A homozygous mutation (Cys 282 Tyr) has been identified in most patients with hereditary hemochromatosis. We examined whether serum iron studies and hepatic iron measurement distinguish end-stage liver disease patients with Cys 282 Tyr-associated hereditary hemochromatosis. METHODS: Serum iron, total iron binding capacity, and ferritin were measured in 106 cirrhotic patients prior to liver transplantation. Hepatic iron concentration and hepatic iron index were measured from explant liver tissue. Genotyping was performed on explant liver tissue in patients with an elevated hepatic iron index (>1.9). RESULTS: Thirty-three of 106 (31%) patients had elevated serum iron studies suggestive of hereditary hemochromatosis. Only four of 33 (12%) had a mean hepatic iron index >1.9, and none of the four patients was homozygous for Cys 282 Tyr. All four had liver disease due to hepatitis C and/or alcohol. CONCLUSIONS: (i) Serum transferrin saturation and hepatic iron index lack specificity for hereditary hemochromatosis in end-stage liver disease. (ii) Genotyping for Cys 282 Tyr may provide the best method to identify hereditary hemochromatosis in the setting of end-stage liver disease.

Female↗

PubMed1998

Donor-recipient sharing of HLA class II alleles predicts earlier recurrence and accelerated progression of hepatitis C following liver transplantation.

Both direct viral cytopathic effects and host immune responses appear to be important in the pathogenesis of hepatitis C virus (HCV) infection. Liver transplantation provides a means to explore the role of the immune system in the development of HCV-related liver damage through comparing the natural history of HCV in patients with different degrees of donor-recipient human leukocyte antigen (HLA) matching. We evaluated 36 patients with recurrent hepatitis C viremia following liver transplantation to determine whether hepatocellular injury or progression to bridging fibrosis occur more rapidly when donor and recipients share HLA alleles. HLA typing for the HLA-A and HLA-B loci was performed by serological techniques and PCR-based oligotyping was used to type alleles of the DRB1, DRB3, DQA1, and DQB1 loci. A median of eight liver biopsies, obtained during a median follow-up of 36 months, were reviewed per patient. Donor-recipient sharing of alleles of HLA-DQB1 or DRB1 was associated with more rapid development of recurrent hepatitis by univariate analysis (chi2=5.7, P=0.02 and chi2=5.54, P=0.02 respectively). However, only sharing of HLA-DRB1 alleles was identified as an independent predictor of reduced time to recurrent histologic injury by multivariate analysis (chi2 =5.74, P=0.02). Furthermore, sharing of HLA-DRB3 and histologic evidence of rejection were associated with more rapid progression to bridging fibrosis both by univariate methods (chi2=4.12, P=0.04 and chi2=4.66, P=0.03 respectively), and by multivariate analysis (chi2=13.01, P=0.001). These findings suggest that HLA class II-restricted immune responses may contribute to the pathogenesis of HCV-related liver injury in liver transplant recipients.

Adult↗

PubMed1998

Increased prevalence of gastroesophageal reflux in patients with idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal interstitial lung disease (ILD) of unknown etiology. Introduction of acid into the respiratory tree can produce pulmonary fibrosis. Gastroesophageal reflux (GER) has previously been associated with several other respiratory conditions, including pneumonia, bronchitis, and asthma. To investigate prospectively the possible association of GER and IPF, 17 consecutive patients with biopsy-proven IPF and eight control patients with ILD other than IPF underwent dual-channel, ambulatory esophageal pH monitoring. Sixteen of 17 patients with IPF had abnormal distal and/or proximal esophageal acid exposure compared with four of eight control patients (p = 0.02). In the patients with IPF, mean percent distal total (13.6 versus 3.34, p = 0.006), distal upright (12.4 versus 5.1, p = 0.04), distal supine (14.7 versus 0.88, p = 0.02), and proximal supine (7.48 versus 0.24, p = 0.04) esophageal acid exposure times were significantly greater than those in control patients. Only four patients with IPF (25%) with increased acid exposure had typical reflux symptoms such as heartburn or regurgitation. Patients with IPF have a high prevalence of increased esophageal acid exposure, usually without typical GER symptoms. GER in these patients tends to occur at night and extend into the proximal esophagus. Acid reflux may be a contributing factor in the pathogenesis of IPF.

Adult↗

PubMed1998

Detection of optic disc changes with Glaucoma-Scope probability maps.

PURPOSE: To test whether a statistical method using a probability map could detect true changes in optic disc topography. METHODS: The average of three Glaucoma-Scope images (Ophthalmic Imaging Systems were used for analysis at each of two sessions. A Glaucoma-Scope probability map was constructed for each eye using statistical methods. The proportion of topographic locations with p values less than 0.05 on a modified two-sample t test (p-proportion) and the difference in the mean position of the disc (MPD) from two imaging sessions were calculated. Two pairs of stereoscopic disc photographs for 43 eyes with longitudinal follow-up were evaluated for change by four experienced glaucoma specialists masked to patient clinical information. Clinical change was considered to have occurred when the assessments of at least three of the four specialists were agreed on. The cutoff values for p-proportion and change in MPD that provided 95% specificity were calculated using a separate sample of 69 subjects who had serial images taken at two separate sessions on the same day, and thus showed no clinical change in the optic disc. RESULTS: The cutoff values of 95% specificity for the p-proportion and the change in MPD were 18% and 25.1 microns, respectively. Of 43 eyes with longitudinal follow-up, 14 showed definite clinical change. Sensitivity of the p-proportion and change in MPD for detecting this change was 100% and 85.7%, respectively. For all 43 patients with longitudinal follow-up, the percent change in intraocular pressure (IOP) correlated strongly with both the p-proportion and the change in MPD. CONCLUSION: Using data obtained with the Glaucoma-Scope, a statistical method based on probability mapping can be used to detect true changes in disc topography. The p-proportion was more sensitive than change in MPD in detecting clinical change in the study eyes. This statistical methodology may also be applicable for interpretation of data obtained with other optic disc analyzers.

Adult↗

PubMed1997

p16INK4a promoter is hypermethylated at a high frequency in esophageal adenocarcinomas.

Loss of heterozygosity (LOH) of 9p21, which contains the p16INK4a tumor suppressor gene locus, is one of the most frequent genetic abnormalities in human neoplasia, including esophageal adenocarcinomas. Only a minority of Barrett's adenocarcinomas with 9p21 LOH have a somatic mutation in the remaining p16 allele, and none have been found to have homozygous deletions. To determine whether p16 promoter hypermethylation may be an alternative mechanism for p16 inactivation in esophageal adenocarcinomas, we examined the methylation status of the p16 promoter in flow-sorted aneuploid cell populations from 21 patients with premalignant Barrett's epithelium or esophageal adenocarcinoma. Using bisulfite modification, primer-extension preamplification, and methylation-specific PCR, we demonstrate that the methylation assay can be performed on 2 ng of DNA (approximately 275 cells). Eight of 21 patients (38%) had p16 promoter hypermethylation and 9p21 LOH, including 3 patients who had only premalignant Barrett's epithelium. Our data suggest that promoter hypermethylation with LOH is a common mechanism for inactivation of p16 in the pathogenesis of esophageal adenocarcinomas.

Adenocarcinoma↗

PubMed1997

Renal disease in hepatitis C-positive liver transplant recipients.

Glomerular abnormalities are frequent in patients undergoing liver transplantation; however, renal dysfunction following transplantation is mainly attributed to cyclosporine toxicity. Membranoproliferative glomerulonephritis (MPGN) is seen in patients infected with hepatitis C virus (HCV), the virus responsible for 30% of the end-stage liver disease leading to liver transplantation. To determine the incidence of renal abnormalities in liver transplant recipients and the association with HCV, we undertook a longitudinal study in HCV-positive (n=91) and HCV-negative (n=106) liver transplant recipients. Mean creatinine clearance before transplantation was 94 ml/min/1.73 m2 in HCV+ patients and 88 ml/min/1.73 m2 in HCV- patients. By 3 months after transplantation, the mean creatinine clearance decreased by approximately one third in both groups. A greater proportion of HCV+ patients excreted >2 g protein/day after transplantation (P=0.05) and had renal biopsies showing MPGN than did HCV- recipients (4/10 HCV+ patients vs. 0/7 HCV- patients; P=0.1). In the HCV+ group, proteinuria was not associated with recurrent HCV hepatitis, DQ matching, posttransplant diabetes, or hypertension. Treatment of HCV-related MPGN with interferon-alpha2b appeared to stabilize proteinuria and renal function but did not reverse renal dysfunction nor cause liver allograft rejection. After transplantation, HCV+ patients had similar renal function over 3 years after transplantation, compared with HCV- patients, but they had an increased risk of proteinuria and occurrence of MPGN that was only partially responsive to interferon.

Adult↗

PubMed1997

Hepatitis G virus co-infection does not alter the course of recurrent hepatitis C virus infection in liver transplantation recipients.

Although hepatitis G virus infection (HGV) is usually asymptomatic, it has been associated with mild hepatic injury. Whether hepatitis G co-infection alters the natural history of other viral hepatitis infections remains to be determined. In the present study, we investigated whether hepatitis G impacts on the time to recurrent hepatitis or on the time to progression to fibrosis in hepatitis C-infected patients who undergo liver transplantation. Forty-five liver transplantation recipients with persistent hepatitis C viremia by polymerase chain reaction (PCR) were evaluated. Stored sera obtained before and after liver transplantation was tested for HGV RNA by reverse transcriptase (RT)-PCR using primers to the 5' region of the HGV genome. A median of eight serial liver biopsy specimens were reviewed per patient. The prevalence of HGV co-infection was 21% before transplantation and 22% following transplantation. During a median follow-up of 29 months, 78% (35/45) of patients with hepatitis C viremia developed histological features of recurrent hepatitis. Fifty-one percent (23/45) progressed to fibrous portal expansion and 16% (7/45) developed bridging fibrosis. Comparisons of patients with and without hepatitis G co-infection following transplantation showed no significant difference in time to recurrent hepatitis, fibrous portal expansion, bridging fibrosis, or of allograft or patient survival. In conclusion, hepatitis G co-infection does not seem to impact on the time to recurrent hepatitis C or progression of hepatitis C-related histological injury after liver transplantation.

Flaviviridae↗

PubMed1997

Measurement error and its impact on the estimated relationship between dust lead and children's blood lead: Members of the Rochester Lead-in-Dust Study Group.

OBJECTIVE: Lead-contaminated house dust is a major contributor to lead intake among urban children, but the reliabilities of various dust lead measurement methods and their impact on the estimated correlations between dust lead and children's blood lead levels are unknown. METHODS: Repeated field measurements of lead-contaminated dust from children's homes were taken from 16 housing units using five dust lead measurement methods. Estimates of measurement error were used to obtain reliability ratios for the dust lead measurements, which were then used to correct estimated correlations between lead-contaminated dust and children's blood lead. RESULTS: Reliability varied over methods and surface types (from 0.0 to 0.8), but wipe loading and the BRM vacuum loading methods generally had greater reliability. Technician effects, inadvertent field exposure to lead, contamination of collection equipment, and laboratory instrument error were found to contribute little to total measurement error. Corrected correlations between blood lead and wipe loading measurements were 7 to 104% higher than uncorrected correlations. The multiple R2 and partial R2 for a wipe composite measurement in a multivariate regression model increased from 0.43 to 0.64 and from 0.053 to 0.26, respectively, after correction for measurement error bias. CONCLUSIONS: Variation in lead deposition within small areas and variations in collection inherent to the devices are major contributors to measurement error. Measurement error causes dramatic underestimation of correlation between lead-contaminated house dust and children's blood lead.

Air Pollution, Indoor↗