Evaluation of the HUD lead hazard control grant program: early overall findings.

This study evaluates the effectiveness of lead hazard control methods used in the Lead Hazard Control (LHC) grant program of U.S. Department of Housing and Urban Development. The LHC Program awards funds to local jurisdictions to address lead hazards in privately owned, low-income dwellings. Grantees in 14 cities, states, or counties collected environmental data in over 2600-treated dwellings making this the largest study of residential lead hazard control ever undertaken. Grantees employed a range of treatments, the most common being replacement of windows and repair of deteriorated lead-based paint. In this paper, dust lead loading levels and blood lead levels of children (6 months-6 years, if present) were observed at four periods of time (preintervention, immediate, and 6- and 12-months postintervention) in 1212 dwellings. Dust lead loading levels were also observed in a subset of these dwellings at 24- and 36-months postintervention. The geometric mean floor and window dust lead loadings declined at least 50 and 88% (P<0.0001), respectively, immediately postintervention. Three years later, floor dust lead loadings remained at or below the immediate postintervention levels. Window dust lead loadings had moderate increases, but remained substantially reduced from preintervention levels and below clearance standards. At 1 year after intervention, geometric mean age-adjusted blood lead levels had declined from 11.0 to 8.2 microg/dL, a 26% decline (P<0.0001). The LHC Program interventions produced blood lead declines similar to or greater than the percentage changes reported in earlier 1-year lead intervention studies.

The contribution of lead-contaminated house dust and residential soil to children's blood lead levels. A pooled analysis of 12 epidemiologic studies.

In 1992, the U.S. Congress passed the Residential Lead-Based Paint Hazard Reduction Act, which requires the promulgation of health-based dust lead and soil lead standards for residential dwellings to prevent undue lead exposure in children. Unfortunately, the levels of lead in house dust and soil that are associated with elevated blood lead levels among U.S. children remain poorly defined. This pooled analysis was done to estimate the contributions of lead-contaminated house dust and soil to children's blood lead levels. The results of this pooled analysis, the most comprehensive existing epidemiologic analysis of childhood lead exposure, confirm that lead-contaminated house dust is the major source of lead exposure for children. These analyses further demonstrate that a strong relationship between interior dust lead loading and children's blood lead levels persists at dust lead levels considerably below the U.S. Department of Housing and Urban Development's current postabatement standards and the Environmental Protection Agency's guidance levels. Finally, these analyses demonstrate that a child's age, race, mouthing behaviors, and study-site specific factors influence the predicted blood lead level at a given level of exposure. These data can be used to estimate the potential health impact of alternative health-based lead standards for residential sources of lead exposure.

Environmental exposures to lead and urban children's blood lead levels.

Lead-contaminated water, soil, and paint have been recognized as potential sources of children's lead exposure for decades, but their contributions to lead intake among urban children remain poorly defined. This analysis was undertaken to estimate the relationship of environmental lead exposures to lead intake among a random sample of urban children, adjusted for exposure to lead-contaminated house dust. Analyses of 183 urban children enrolled in a random sample, cross sectional study were conducted. Children's blood and multiple measures of household dust, water, soil, and paint were analyzed for lead, and interviews were conducted to ascertain risk factors for childhood lead exposure. Environmental sources of lead, including house-dust, soil lead, and water lead, were independently associated with children's blood lead levels. In contrast, paint lead levels did not have a significant effect on blood lead levels after adjusting for other environmental exposures. An increase in water lead concentration from background levels to 0.015 mg/L, the current EPA water lead standard, was associated with an increase of 13.7% in the percentage of children estimated to have a blood lead concentration exceeding 10 micrograms/dL; increasing soil lead concentration from background to 400 micrograms/g was estimated to produce an increase of 11.6% in the percentage of children estimated to have a blood lead level exceeding 10 micrograms/dL, and increasing dust lead loading from background to 200 micrograms/ft2 is estimated to produce an increase of 23.3% in the percentage of children estimated to have a blood lead level exceeding 10 micrograms/dL. These data support the promulgation of health-based standards for lead-contaminated dust and soil and the progressive lowering of standards for lead-contaminated water as the definition of undue lead exposure has been modified.

Mortality among plutonium and other radiation workers at a plutonium weapons facility.

Mortality among 5,413 white males who were employed for at least two years at a plutonium weapons facility was investigated to measure risks from exposures to low levels of plutonium and external radiation. When compared with US death rates, fewer deaths than expected were found for all causes of death, all cancers, and lung cancer. No bone cancer was observed. An excess of brain tumors was found for the cohort in general. Elevated rate ratios for all causes of death and all lymphopoietic neoplasms were found when employees with plutonium body burdens greater than or equal to 2 nCi were compared with those with body burdens less than 2 nCi, while accounting for age, calendar period, and induction time. Increased rate ratios were also found for esophageal, stomach, colon, and prostate cancers, and for lymphosarcomas and reticulum cell sarcomas. No elevated rate ratios were noted for bone and liver cancers. When employees with cumulative exposures greater than or equal to 1 rem were compared with those with exposures less than 1 rem, elevated rate ratios were found for myeloid leukemia, lymphosarcoma and reticulum cell sarcoma, liver neoplasms, and unspecified brain tumors. No overall dose-response relationships were found for plutonium or external radiation exposures. Standardized rate ratios increased, however, as plutonium body burden levels increased for all causes, all cancers, and digestive cancers at five years induction time. Standardized rate ratios also increased as external radiation exposure categories increased for all lymphopoietic cancers and unspecified brain tumors for a two-year induction period. With the exception of analyses of combined categories of death, and perhaps of lung cancer, confidence limits were wide, indicating limited precision. Nevertheless, these findings suggest that increased risks for several types of cancers cannot be ruled out at this time for individuals with plutonium body burdens of greater than or equal to 2 nCi. Plutonium-burdened individuals should continue to be studied in future years.