In-vivo measurements of lead concentrations in calcaneus (mainly trabecular bone) and tibia (mainly cortical bone) were performed by x-ray fluorescence (XRF) in 70 active and 30 retired lead smelter workers who had long-term exposure to lead. Comparison was made with 31 active and 10 retired truck assembly workers who had no known occupational exposure to lead. After physical examination, all participants provided blood and urine samples and answered a computerized questionnaire. Since 1950, blood lead has been determined repeatedly in lead workers at the smelter, which made it possible to calculate a time-integrated blood lead index for each worker. Lead concentrations in blood, urine, calcaneus, and tibia in active and retired lead workers were significantly higher than in the corresponding control groups (p < .001). The highest bone lead concentrations were found among retired lead workers (p < .001), which was the result of considerably higher lead exposure during 1940 to 1960. Lead concentrations in calcaneus in active lead workers were significantly higher than in tibia when expressed in ug of lead per gram of bone mineral, which suggests a quicker absorption over time in this mainly trabecular bone. The estimated biological half-times were 16 y in calcaneus (95% confidence interval [95% CI] = 11-29 y) and 27 y in tibia (95% CI = 16-98 y). A strong positive correlation was found between lead concentrations in calcaneus and tibia for all lead workers (r = 0.54; p < .001). A strong positive correlation was also found between the bone lead concentrations and the cumulative blood lead index. Blood lead, at the time of study, correlated well with bone lead concentrations in retired--but not in active--workers, reflecting the importance of the endogenous (skeletal) lead exposure. The findings in this study indicate that bone lead measurements by XRF can give a good index of long-term lead exposure. Tibia measurements offer a higher precision than calcaneus measurements. The method is of particular interest in epidemiologic studies of adverse health effects caused by long-term lead exposure.

OBJECTIVES: The purpose of this study was to monitor blood lead in a northern Swedish cohort of mothers and children during pregnancy and at birth. METHODS: Blood lead was analyzed during pregnancy and in the umbilical cords of 290 women living near a smelter and in 194 control subjects. RESULTS: During pregnancy, there were statistically significant overall increases in blood lead concentrations by 20% and 15% in the smelter and reference areas, respectively. Mean maternal blood lead concentrations at delivery were 0.15 mumol/L (3.11 micrograms/dL) in the smelter area and 0.13 mumol/L (2.69 micrograms/dL) in the control area. Umbilical cord blood lead levels were 80% to 87% of the maternal levels. Blood lead levels were influenced by place of residence, employment at the smelter, smoking, and wine consumption. Maternal serum calcium levels decreased during pregnancy and were significantly lower than those of the newborns. CONCLUSIONS: An increase in blood lead concentrations was found during pregnancy, despite increased blood volume and unchanged or decreasing environmental lead levels. The mobilization of lead from bone during pregnancy may explain the increase.

signs of renal impairment were found among Occupational exposure to lead may cause the workers. No correlations of clinical kidney damage. This study was carried out on a importance existed between concentrations of cohort of 70 active and 30 retired long'term-U-albumin,; f-Ii2-m, and U:.NAG activity -on exposed lead smelter workers. Their kidney the one hand and the concentrations of B-Pb, function was compared with 31 active and 10 cumulative blood lead index, U-Pb, and lead retired truck assembly workers who had no concentrations in the calcaneus and tibia on occupational exposure to lead. The lead the other, among lead workers and controls. workers had been regularly followed up with Despite many years of moderate to heavy measurements of lead concentration in blood exposure to lead, particularly for the retired since 1950. Previous exposure to lead was cal-lead workers, no signs of adverse effects on the culated as a time integrated blood lead index kidney such as early tubular or glomerular for each worker. Blood and urine samples were malfunction were found. Reversible changes in obtained from all subjects. The concentration kidney function during the 1950s and 1960s of lead in blood (B-Pb) and urine (U-Pb) was could not be excluded, however, due to a analysed. The urinary concentrations of greater exposure to lead during that time. several sensitive indicators of early tubular (U-p,-microglobulin (U-p2-m); U-N-acetyl-p-Inorganic lead is widely distributed. As well as glucosaminidase (U-NAG)) and glomerular exposure from the general environment, exposure to kidney damage (U-albumin) were determined. lead may occur in lead mines, lead smelting and The B-Pb and U-Pb values were significantly refining operations, storage battery factories, brass higher among active and retired lead workers foundries, and glass works. In the working environcompared with their corresponding control ment exposure may occur both through inhalation groups. The highest concentrations were found and through ingestion of contaminated food, drinks, among the active lead workers. The concentra-and snuff. tions of the parameters of kidney function The Ronnskar smelter in the northern part of investigated were of the same magnitude for Sweden has specialised in the processing of complex exposed workers and controls. No clinical and contaminated raw materials. In addition to the

Objectives The purpose of this study was to determine the mortality and cancer incidence of long-term lead smelter workers at a primary smelter. Methods A cohort of 3979 workers elnployed for at least 1 year during 1928-1979 and a subcohort of 1992 workers employed in lead-exposed departments (lead only workers) was formed. The expected mortality in 1955-1987 and cancer incidence in 1958-1987 were calculated relative to the county rates, specified for cause, gender, 5-year age groups, and calendar year. A cumulative blood-lead index was used for the doseresponse analyses. Results The lung cancer incidence of the total cohort [standardized incidence ratio (SIR) 2.8,95% confidence interval (95% CI) 2.1-3.81 and the group with the highest exposure (SIR 3.1, 95% CI 2.0-4.6) was high. Similar risk estimates were observed with a latency of 15 years. The workers hired before 1950 had higher lung cancer risk estimates (SIR 3.6, 95% CI 2.6-5.0) than the workers hired later (SIR 1.3, 95% CI 0.6-2.6, no latency period). The risk estimates for lung cancer were further elevated in the subcohort of lead-only workers (SIR 5.1,95% CI 2.0-10.5 in the highest exposed subgroup; latency period of 15 years). No excesses of other malignancies were noted. C O~C~U S~O~S The increased relative risks were probably mainly due to interactions between lead and other carcinogenic exposures, including arsenic. Further study is required concerning such possible interactions before a role in the induction of lung cancer can be ascribed to lead.

No abstract