Blood collection for screening children for exposure to lead.
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Biomedical subjects
Publications and source records attributed to H T Delves.
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We measured the levels of cobalt and chromium in the serum in three groups of patients after uncemented porous-coated arthroplasty. Group 1 consisted of 14 consecutive patients undergoing revision for aseptic loosening. Group 2 comprised 14 matched patients in whom the arthroplasty was stable and group 3 was 14 similarly matched patients with arthritis awaiting hip replacement. Specimens were analysed using atomic absorption spectrophotometry. Aseptic loosening of a component resulted in a significant elevation of serum cobalt (p < 0.05), but not of serum chromium. The relative risk of a component being loose, if the patient had a serum cobalt greater than 9.0 nmol/l, was 2.8.
Microbial generation of toxic gases from antimony, arsenic, or phosphorus in compounds used as fire retardants in cot mattresses has been proposed as a cause of sudden infant death. To test this hypothesis, 23 polyvinyl chloride mattress samples from cot death cases were incubated on malt agar plates until good microbial growth was obtained. Silver nitrate and mercuric chloride test papers were then inserted and the colour reactions recorded. The predominant organism, recovered from all mattresses tested, was not, as claimed in earlier work, the fungus Scopulariopsis brevicaulis, but a mix of common environmental Bacillus spp. Test paper colour changes occurred whenever bacterial growth was present, but these reactions also occurred in control tests in which no mattress material was present on the plates. Chemical and instrumental analyses of exposed test papers showed that the colour reactions were not due to deposits of antimony, arsenic, or phosphorus. Our findings do not support the hypothesis that toxic gases derived from antimony, arsenic, or phosphorus are a cause of sudden infant death. More sulphur was found in test papers exposed in plates containing bacterial growth than in those without such growth. This result suggests that the test paper reactions were due to the generation of sulphur-containing compounds during bacterial growth on the agar medium.
OBJECTIVE: The concentrations of metals in fluids surrounding the first-trimester fetus were measured. STUDY DESIGN: Atomic absorption spectrometry was used to measure concentrations of metals in matched samples of amniotic and extraembryonic coelomic fluids in 17 women between 9 and 12 weeks of pregnancy. RESULTS: Concentrations of calcium, magnesium, iron, copper, and manganese (but not zinc, cadmium, or lead) were significantly higher in coelomic than in amniotic fluid. There was no significant difference between levels of iron, manganese, and lead in controls and amniotic fluid or between concentrations of manganese, cadmium, and lead in controls and coelomic fluid. There was no relationship between the concentrations of each metal in amniotic and coelomic fluid. CONCLUSION: The extraembryonic coelom is an important site of concentration of metals in early pregnancy. This might represent a store of metals essential for normal embryonic and fetal development or constitute a defense mechanism against environmental conditions adverse to the fetus.
Following the incident of acidic pollution of water by aluminium sulfate centred around Camelford in July 1988, we have carried out a retrospective analysis of the mobilization of toxic metals to residents of the area. An advanced nuclear technique was used to measure trace levels of elements within hair, thus, avoiding surface contamination. In contrast to controls, lead, but no other toxic metals, was consistently found within sections of hair that dated to mid-1988 from four residents; they must, therefore, have consumed this metal around the time of the incident. The source of this lead was probably local water pipe residue, and this was found on analysis to have a matrix specific to such soft-water areas that, prior to the incident, had slowly accumulated certain toxic metals such as cadmium and uranium and particularly lead. Lead is mobilized from such residues by acidic water and could, therefore, have heavily contaminated mains water after the incident. However, analyses of residents' plasma and whole blood, and of urine following a lead-chelation test, showed no evidence of either long-term increased body burdens of toxic metals or depletion of essential elements. In addition, we found no evidence of continued poor water quality in the area. In conclusion, during a short period following the pollution, some residents who consumed mains water would have been acutely exposed to lead and other toxic metals. Prediction of the scale of metal exposure to individuals was not possible owing to heterogeneity of the water distribution network, but long-term effects to residents from lead are not anticipated.(ABSTRACT TRUNCATED AT 250 WORDS)
Aluminium was measured in samples of plasma and samples of feed obtained from 74 infants with normal renal function established on various feeds (breast, whey-based, fortified whey-based, preterm, soy, and casein hydrolysate). All infants were bolus fed, and blood samples were collected midway between feeds. Aluminium was measured using electrothermal atomization and atomic absorption spectrometry. Mean aluminium concentrations in milks were as follows: breast, 9.2 micrograms/L [95% confidence interval (CI), 5.6-12.7]; whey-based, 165 micrograms/L (95% CI, 151-180); fortified, 161 micrograms/L (95% CI, 143-180); preterm, 300 micrograms/L (95% CI, 272-328); soy, 534 micrograms/L (95% CI, 470-598); casein hydrolysate, 773 micrograms/L (95% CI, 632-914). Mean plasma aluminium concentrations in infants receiving different milks were as follows: breast, 8.6 micrograms/L (95% CI, 5.6-10.6); whey-based, 9.2 micrograms/L (95% CI, 7.4-11.0); fortified, 10.3 micrograms/L (95% CI, 8.3-12.3); preterm, 9.7 micrograms/L (95% CI, 5.3-17.1); soy, 12.5 micrograms/L (95% CI, 5.0-20.0); casein hydrolysate, 15.2 micrograms/L (95% CI, 10.7-19.8). Mean plasma aluminium concentration was significantly different in infants fed casein hydrolysate formulae than in those fed breast milk (difference, 6.7 micrograms/L; 95% CI, 2.8-10.5; p = 0.028). We conclude that infants may be at risk from aluminium toxicity when consuming formula containing > 300 micrograms/L--in particular, casein hydrolysate formulae. We speculate that the aluminium compounds found in breast milk are more bioavailable than those found in other milks and that some constituents of infant formula affect aluminium absorption from the gut lumen.
Herbal remedies from the Indian subcontinent have been found to have high concentrations of heavy metals and unsupervised treatment may result in toxicity. We report the case of an Indian patient with hepatitis who was found to have lead poisoning where the source was traced to ethnic remedies he had been taking for diabetes.
Atomic absorption spectrometry with electrothermal atomization was used for the determination of aluminium in brain, liver, spleen, kidney cortex, skeletal muscle and bone of the rat following digestion by nitric acid and in serum following simple dilution and in situ oxygen ashing. The method of standard additions in the presence of a chemical modifier, ammonium dihydrogen-phosphate, was essential for bone tissues. The detection limits ranged from 3 to 58 ng per gram of wet mass of tissue and were 4-19 times lower than the observed physiological levels of aluminium. The between-day precision for serum was 8.9% at a mean concentration of 6.8 micrograms I-1 and 2.4% at a mean concentration of 125.3 micrograms I-1. Additionally, repeated analyses of National Institute of Standards and Technology Standard Reference Material 1577b Bovine Liver gave a relative standard deviation of 12.2% (mean concentration = 0.8 microgram g-1). Of the tissues studied, bone had at least ten times higher levels of aluminium than others (0.959 +/- 0.322 micrograms g-1). The aluminium concentration in cerebellum (0.073 +/- 0.043 micrograms g-1) was approximately twice that in the cerebral hemisphere (0.034 +/- 0.009 micrograms g-1).
Fast protein liquid chromatography and SDS-PAGE have been used to isolate and purify Helicobacter pylori urease. A nickel component of the urease was detected in the purified proteins by atomic absorption spectroscopy. The nickel was present only in the 61 kDa polypeptide and in the ratio of between five and six atoms to one molecule of urease, suggesting a hexameric structure. These results are discussed in relation to other bacterial ureases and urease activity at low pH.
Recent research has shown that some adult flamingos Phoenicopterus roseus collected from the Camargue Biosphere Reserve had tissue metal concentrations considerably higher than the average for this species. As the range of these birds is large, the origin of the contamination was unknown. Blood and feather samples from nestling flamingos were therefore analysed for trace metals to determine the presence and origin of local contamination. A comparison of elemental concentration in the feathers of nestling and adult flamingos revealed higher concentrations of Cd, Cu, Pb and Se in adults, and higher concentrations of Zn in juveniles. This was attributed to increased exposure to atmospheric pollutants of adults, and either differences in Zn requirements and metabolism between adults and juveniles, or a local contamination of the juveniles' food supply by Zn. Concentrations of Zn in serum were also very elevated compared with human standards. Cd, Cu, Zn and Se concentrations were analysed in outer (O) and inner (I) barbs (i.e. barbs that are, respectively, exposed or not exposed to external deposits) of greater coverts of nestling flamingos. A comparison of elemental concentrations in these two feather components indicates a local atmospheric contamination by Cd, Cu and Pb.
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A comprehensive study of a group of 2-year-old urban children (n = 97), designed to provide quantitative information simultaneously for lead intakes via all identified pathways, has been carried out in Birmingham (U.K.). Results showed that for children whose blood levels and exposure to environmental lead were within the normal range for the U.K., blood lead concentration was significantly related to a combination of house dust lead loading and an overall rate of touching objects, to water lead concentration and to the parents' smoking habits. On the basis of assumptions used by the Royal Commission on Environmental Pollution (RCEP), the estimated average total uptake of lead was 36 micrograms day-1; of this, 97% was from ingestion from dust, food and water and only 3% from inhalation.
A 68 year old man with a creatinine clearance rate of only 15 ml/min took twice the recommended dose of tripotassium dicitrato bismuthate (TDB) as DeNol liquid; 10 ml qds; a total of 864 mg bismuth daily for two months. Whole blood bismuth concentrations rose to 880 micrograms/l and he developed global cerebral dysfunction with hallucinations, ataxia, and an abnormal EEG. Renal clearance of bismuth rose from 0.24 to 2.4 ml/min when the heavy metal chelator 2-3 dimercapto-1 propane sulphonic acid (DMPS) was given by mouth. Bismuth was measured by a novel method involving inductively coupled plasma source mass spectrometry. Fifty days after stopping TDB, whole blood bismuth concentrations fell to 46 micrograms/l and the patient's EEG returned to normal. His mental function also recovered completely. The case serves as a timely reminder that TDB should not be administered to patients with renal disorders, as stated in the data sheet.
The aetiology of Perthes' disease of the hip, avascular necrosis of the head of the femur, is unknown. Children with the disease have a generalised abnormality of growth. A similar disproportionate growth is found in chicks given a diet deficient in manganese. In Liverpool, which has the highest incidence of Perthes' disease reported anywhere in the world, children with the disease were shown to have lower blood manganese levels than controls. This is evidence that manganese deficiency around the time of birth may be a cause of Perthes' disease, but the results require confirmation.
The Department of the Environment (DOE) undertook an extensive programme to monitor blood lead concentrations annually over the period 1984 to 1987 in the context of the reduction in the maximum permissible lead content of petrol from 0.4 to 0.15 g/l from 1st January 1986. Blood samples (all venous) were analysed for lead by atomic absorption spectrophotometry (AAS); considerable efforts were made to ensure the validity of the analytical results. In 1986, emissions from petrol driven vehicles effectively fell by 60% and air lead concentrations fell by just over 50%. Against the background of a long-term downward trend in blood lead concentrations of 4-5% per year, there were average falls in blood lead in 1986, compared with 1985, of around 1 microgram/100 ml (9-10%) for adults in both 'exposed' and 'control' groups; about 2 micrograms/100 ml (18%) in traffic police; and about 1.5 micrograms/100 ml (16%) in children. Levels fell in 1986 in all age groups, in all social classes, and in all categories of smoking and drinking habits, age of dwelling and length of residence. Exposure to lead from a number of sources was being reduced simultaneously; blood lead concentrations probably fell in both 1985 and in 1986 for reasons additional to the reduction in the lead content of petrol. For children, petrol lead appeared to have been made a slightly larger contribution to the body burden than for adults.
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Blood cadmium concentrations were determined for 6919 men aged 40-59 randomly selected from general practice registers in 24 British towns. The mean and median blood cadmium were 1.9 and 1.4 micrograms/1 respectively and the distribution was highly skewed. The mean levels in non-smokers was 1.0 micrograms/l and current smokers showed a marked gradient with the daily amount smoked, with a mean of 3.9 micrograms/l in men smoking 40 or more cigarettes per day. Whereas 95% of men who never smoked had blood cadmium less than 2.0 micrograms/l, 80% of men smoking 20 or more cigarettes a day exceeded this figure. 1% of the men had blood cadmium concentrations greater than or equal to 7 micrograms/l virtually all of whom currently smoked cigarettes. Blood cadmium levels in ex-smokers were much lower than in current smokers even for those who had stopped within the past year. However, the mean levels in ex-smokers remained higher than the 'never smoked' for several years after stopping. There was little evidence that age, social class, or alcohol consumption were associated with blood cadmium levels after allowance for cigarette smoking. There is substantial geographic variation in mean blood cadmium for middle-aged men which could not be completely accounted for by smoking differences. Towns in the south and east of England all had mean levels under 2.0 micrograms/l whereas the majority of towns in other parts of Britain had mean levels greater than 2.0 micrograms/l. Possible reasons for this geographic pattern (e.g. geochemistry, industrial exposure, dietary differences) need further exploration.
The Department of the Environment (DOE) has undertaken an extensive programme to monitor blood lead concentrations annually over the period 1984 to 1987 in the context of the reduction in the maximum permissible lead content of petrol from 0.4 to 0.15 g/l from 1 January 1986. The 2500 participants in the study include adults living in heavily trafficked urban areas and in occupational groups particularly exposed to petrol lead; children aged 6-7 years attending schools in heavily trafficked urban areas; and control groups of adults and children in rural areas. Blood samples (all venous) are being analysed for lead by atomic absorption spectrophotometry (AAS); considerable efforts are being made to ensure the validity of the analytical results during the period of the study. Average blood lead concentrations in 1984 and 1985 in both adults and children were generally low and were in line with levels expected on the basis of earlier surveys; only a very small proportion of individuals had raised levels. Detailed statistical analyses have confirmed that blood lead concentrations are related to a range of personal, social and environmental factors including age, sex and smoking and drinking habits. Blood lead levels in the exposed groups of adults and children were on average just under 1 microgram/100 ml lower in 1985 than in 1984, while overall changes in the police and control groups were smaller; there was, however, considerable variability in the changes in the individual surveys, particularly those of children. Levels fell in all social classes and in both categories of age of dwelling, but changes tended to be less marked in those who were older (particularly for men), smoked more, drank more or had lived for more than 15 years at their current address.