Health care workers may be occupationally exposed to known and suspected teratogens including viruses, anesthetic gases, sterilants, mercury, and x-radiation. To assess the risk of congenital defects among offspring of health care workers, we analyzed parental occupational histories for 4,915 case babies with congenital defects, registered during the years 1968-1980 by the Metropolitan Atlanta Congenital Defects Program (MACDP) registry, and for 3,027 control babies born without defects during the same period. Offspring of mothers employed in a nursing occupation during the periconceptional period had a modest excess risk of having at least one congenital defect (relative risk [RR] = 1.42; 95% confidence interval [CI] 1.06-1.88); the offspring were at statistically significant increased risk of having anencephaly or spina bifida (RR = 2.00; 95% CI 1.01-4.30), coarctation of the aorta (RR = 2.06; 95% CI 1.10-3.82), genital system defects (RR = 1.61; 95% CI 1.03-2.53), and urinary system defects (RR = 3.43; 95% CI 1.41-8.34). These associations were not confounded by maternal age, education, or alcohol consumption. Offspring of mothers employed in administrative or clerical jobs in the health care industry also had a modest excess risk of defects (RR = 1.35; 95% CI 0.96-1.90), including a statistically significant excess risk of limb defects. We also found associations between neural tube defects and potential exposure to anesthetic gases and to x-radiation, but each association was based on only three case babies of potentially exposed parents. We found no associations between defects and paternal health care employment, except for a few individual defects, and these were based on small numbers of exposed subjects. Only one of five previous studies reviewed found an increased risk of congenital defects among offspring of nurses, but three of the four negative studies had substantially smaller sample sizes than the present study. Detection bias may be a possible explanation for the apparent excess risk of certain defects among offspring of nurses.
To investigate the risk of lead poisoning among household members exposed to 'backyard' battery repair shops (BBRS) in Kingston, Jamaica, environmental and blood lead (PbB) were measured at 24 households (112 individuals) with a BBRS worker or located at a BBRS premises and at 18 neighbourhood control households (74 individuals). Elevated PbB (greater than or equal to 25 micrograms per decilitre [micrograms/dl]) was common among subjects of all ages living at BBRS premises, especially among children less than age 12, 43% of whom had PbB greater than 70 micrograms/dl. Potentially hazardous soil and house dust lead levels were also common at BBRS premises, where 84% of yards had soil lead levels above 500 parts per million (geometric mean 3388 parts per million [ppm] at BBRS premises households with a BBRS worker). Geometric mean blood and environmental lead levels were significantly lower at control households, where less than 10% of subjects in all age groups had elevated PbB (maximum 33 micrograms/dl). Sharing a premises with a BBRS was a stronger determinant of household blood lead and environmental contamination than was the presence of a BBRS worker in a household. Blood lead levels were associated with soil and house dust lead levels in all age groups. We conclude that small battery repair shops, which have also been described in other developing countries, create a high lead poisoning risk for nearby residents.
Objectives. To evaluate trends in blood lead levels among children in Chicago from 1968 through 1988, and to determine the impact of the changes in the Centers for Disease Control and Prevention (CDC) blood lead level of concern. Methods. We reviewed a systematic sample of blood lead screening records of the Chicago Department of Health Laboratory for high-risk children aged 6 months to 5 years. Median blood lead levels for each quarter of the years 1974 through 1988 were determined and regressed against mean air lead levels recorded at air-monitoring stations in Chicago during the same period. Results. Median blood lead levels declined from 30 µg/dL in 1968 to 12 µg/dL in 1988, and were strongly associated with declining average air lead levels (r = .8, P < .001) from 1974 through 1988. A regression model using log-transformed data predicted a decline of 0.56 µg/dL in the median blood lead level with each 0.1 µg/m3 decline in the mean air lead level when the air lead level was near 1.0 µg/m3; the predicted slope was steeper at lower air lead levels. Despite the nearly 20-fold reduction in air lead levels, the median blood lead level of 12 µg/dL in 1988 indicates substantial continuing lead exposure. The CDC blood lead level of concern was lowered twice from 1968 to 1988, but due to the decline in blood lead levels, fewer than 30% of the children were above the level of concern throughout most of the study. Conclusion. Although substantial lead exposure persists in Chicago, reductions in airborne lead emissions seem to have contributed to a long-term decline in the median blood lead level of high-risk Chicago children.
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