The impact of lead in soil and dust on blood lead concentrations in young children (i.e., 1-5 y of age, N = 202) and the risk of health effects were investigated in an urban and a mining area of Sweden. Blood, soil, and indoor dust, as well as information on lead-exposure factors, were collected. The blood lead concentrations (total range = 9-77 microg/l) the authors measured indicated a low risk for lead-induced health effects. Lead in soil (i.e., < 10-5,000 microg/g) and in dust (i.e., < 1-316 microg/g) had little effect on blood lead concentrations, given the present conditions and present concentration range--especially in the mining area. Urban children had significantly higher blood lead concentrations than children in the mining area, despite higher concentrations of lead in soil in the mining area. In the urban children, blood lead concentrations were influenced by parental smoking and lead in dust at day-care centers.

Air Pollutants↗

PubMedDate not supplied

Cadmium in kidney cortex, liver, and pancreas from Swedish autopsies. Estimation of biological half time in kidney cortex, considering calorie intake and smoking habits.

Cadmium and zinc have been analyzed in tissues from 292 persons autopsied in Stockholm. In kidney cortex, liver, and pancreas the individual cadmium levels are distributed in a lognormal way. In kidney cortex there is a continuous accumulation of cadmium with age up to 50 years, followed by a decrease. Smokers show a higher cadmium accumulation. For nonsmokers, the biological half time of cadmium in kidney cortex is estimated at 30 years, with an average concentration at age 50 of 11 mug/g wet weight. When smokers are included, the average cadmium concentration at age 50 is 22 mug/g wet weight. Based on the more pronounced cadmium accumulation among smokers than nonsmokers, the respiratory absorption rate of cadmium from tobacco smoke is estimated to be approximately 50%.

Adolescent↗

PubMedDate not supplied

Wine--an important source of lead exposure.

Blood lead levels in 32 male chronic alcoholic patients were measured and related to drinking habits. An external reference group and a group with previous high alcohol consumption served as controls. Blood lead concentrations were significantly higher (P less than 0.05) in the group with current high alcohol consumption (mean +/- S.D.) (90 +/- 48 micrograms/l, n = 17) than in the external reference group (57 +/- 27 micrograms Pb/l, n = 35). The blood lead concentrations in the latter group were similar to those in the group with previous high alcohol consumption (55 +/- 20 micrograms Pb/l, n = 15). Patients with excessive consumption of wine only (average intake 2.61 wine/day, range 1.3-4.5 l/day) had particularly elevated blood lead concentrations (149 +/- 31 micrograms Pb/l, n = 5), whereas blood lead levels were close to the control value in patients with excessive consumption of spirits only (68 +/- 28 micrograms Pb/l, n = 7). Furthermore, within the external reference group blood lead levels were higher in those who regularly drank more than 0.51 of wine on several occasions each week (96 +/- 22 micrograms Pb/l, n = 6) than in those who consumed less wine (48 +/- 20 micrograms Pb/l, n = 29). In a recent study of table wines sold in Sweden the average lead concentration in 84 samples was found to be 73 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Clinical feasibility trials of barbiturate therapy after cardiac arrest.

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Brain Damage, Chronic↗

PubMedDate not supplied

Comparison between diagnostic results obtained by transthoracic needle biopsy and by sputum cytology.

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Adult↗

PubMedDate not supplied

Urinary and fecal elimination of nickel in relation to air-borne nickel in a battery factory.

Nickel in urine and in air from the breathing zone of 18 male workers in a battery factory was determined weekly during 11 consecutive weeks. The study started immediately following three weeks of Christmas vacation. The nickel levels in air varied but did not increase with time. The average urinary excretion of nickel showed an increase during the first weeks, after which a steady state seemed to have been reached. There was a considerable individual variation in both exposure levels and urine nickel levels. However, a correlation between the averages of nickel in air and urine could be demonstrated on a group basis. In a second study, during one week, measurements of nickel in air and feces were made on 15 of the workers. A significant correlation was found between nickel in air and fecal nickel. Smoking habits did not seem to influence neither urinary nor fecal nickel concentrations.

Adult↗