In vivo measurements of lead in fingerbone in active and retired lead smelters

 Object. The aim of this study was to determine the bone lead concentration in lead smelters and reference subjects, relate them to the lead concentration in blood (B-Pb) and urine (U-Pb), and to use the measured bone lead to calculate a biological half-life for lead in bone. Method and design. The lead concentration in the second phalanx of the left index finger (bone-Pb) was determined in vivo using an X-ray fluorescence technique. The study population comprised 89 smelters with a history of long-term exposure to lead (71 active and 18 retired) and 35 reference subjects (27 active and 8 retired) with no known occupational exposure to lead. Bone-Pb was related to the previous lead exposure, estimated as a time-integrated B-Pb (CBLI). Results. The retired smelters had the highest bone-Pb (median value 55 μg/g wet weight, as against 23 μg/g in active smelters) and 3 μg/g in the reference subjects. A strong positive correlation was observed between the bone-Pb and the CBLI among both active (r _s =0.73; P<0.001) and retired (r _s =0.71; P=0.001) smelters. The corresponding correlations between the bone-Pb and the period of employment were of the same magnitude. For retired workers, there were positive correlations between the bone-Pb and the B-Pb (r _s =0.58; P=0.011) and U-Pb (r _s =0.56; P=0.02). Multiple regression analyses showed that bone-Pb was best described by the CBLI, which explained 29% of the observed variance (multiple r ²) in bone-Pb in active workers and about 39% in retired workers. The estimated biological half-life of bone-Pb among active lead workers was 5.2 years (95% confidence interval 3.3–13.0 years). Conclusions. The high bone-Pb seen in retired workers can be explained by the long exposure periods, the higher exposure levels in earlier decades, and the slow excretion of lead accumulated in bone. The importance of the skeletal lead pool as an endogenous source of lead exposure in retired smelters was indicated by the associations between the B-Pb or U-Pb, on the one hand, and the bone-Pb, on the other. In active workers, the ongoing occupational exposure was dominant. The in vivo X-ray fluorescence technique is still mainly a research tool, and more work has to be done before it can be used more widely in clinical practice. However, over the next decade we can anticipate retrospective, prospective and cross-sectional epidemiological studies in which bone lead determinations reflecting the previous lead exposure in both occupationally and nonoccupationally lead exposed populations are related to various types of adverse health outcomes. Such studies will improve our knowledge of dose–response patterns and provide data that will have an impact on hygienic threshold limit values and prevention of lead-induced diseases. Received: 2 October 1995/Accepted: 8 March 1996     

Lead in finger bone, whole blood, plasma and urine in lead-smelter workers: extended exposure range

Objectives: To assess the historical exposure and to study the relationships between lead concentrations in whole blood (B-Pb), plasma (P-Pb), urine (U-Pb), finger bone (Bone-Pb) and duration of employment in workers at a secondary lead smelter and to compare the relationships between B-Pb and P-Pb with results from previous studies of populations with a wide range of lead exposure. Methods: In 39 lead workers (29 active, ten retired), recruited from those with the highest exposure at a German secondary lead smelter, levels of B-Pb, P-Pb and U-Pb were determined by inductively coupled plasma mass spectrometry (ICP-MS). Bone-Pb was determined by in vivo X-ray fluorescence (XRF). Results were compared with data from a previous study on 90 workers (71 active, 19 retired) with lower exposure, from a Swedish secondary lead smelter, as well as with previously collected data from 42 active Russian lead workers and 34 Ecuadorian lead-exposed subjects. Results: The median values in the active/retired German lead workers were: age 44/59 years, duration of employment 20/38 years, Bone-Pb 71/150 g/g, B-Pb 500/330 g/l, P-Pb 2.7/1.1 g/l, and U-Pb 25/13 mol/mol creatinine. Bone-Pb increased with duration of employment by 4.2 g/g per year and 1.6 g/g per year in German and Swedish workers, respectively. The median Bone-Pb was three times higher in both active and retired German workers than in Swedish smelter workers with essentially the same age distribution and duration of employment. The linear regression equation between B-Pb and log P-Pb in the combined group of Ecuadorian, German, Russian and Swedish lead-exposed subjects (n=176) was B-Pb=545×log[P-Pb] + 258 (r_s=0.94; P<0.001). Conclusions: The high Bone-Pb values recorded for the German smelters implied a historical lead exposure of considerable magnitude. The long-term high lead exposure also showed up in the B-Pb levels for both active and retired workers, leading to the implementation of necessary industrial safety measures in order to respond to biological threshold limits. The suggested equation describing the relationship between B-Pb and P-Pb in the combined group of subjects with a wide range of lead exposure can be useful in future cross-sectional and longitudinal studies of lead-exposed populations, relating, e.g., lead exposure to adverse health outcomes.     

Lead in vertebral bone biopsies from active and retired lead workers

Samples of vertebral bone were obtained by skeletal biopsy and lead concentrations were determined by atomic absorption spectroscopy. The median level of lead in bone in 27 active lead workers was 29 micrograms/g wet weight (range 2-155), corresponding to 370 micrograms/g calcium (range 30-1,120). In 9 retired workers, the corresponding levels were 19 micrograms/g (5-76) and 250 micrograms/g calcium (60-700); in 14 reference subjects without occupational exposure, 1.3 micrograms/g (1-4) and 13 micrograms/g calcium (8-40). The bone lead content rose with time of exposure. Comparison of levels in vertebra with those in fingerbone, as measured by in vivo x-ray fluorescence in the same subjects, strongly suggested the presence of lead pools with different kinetics. The accumulation pattern, as well as the relation between levels in vertebra and fingerbone, suggests a much shorter half-time of lead in the mainly trabecular vertebral bone as compared to the mainly cortical fingerbone. Further, there was an association between vertebral and blood lead levels in the retired workers, which shows a considerable endogenous lead exposure from the skeletal pool.     

Kidney effects in long term exposed lead smelter workers.

Occupational exposure to lead may cause kidney damage. This study was carried out on a cohort of 70 active and 30 retired long term exposed lead smelter workers. Their kidney function was compared with 31 active and 10 retired truck assembly workers who had no occupational exposure to lead. The lead workers had been regularly followed up with measurements of lead concentration in blood since 1950. Previous exposure to lead was calculated as a time integrated blood lead index for each worker. Blood and urine samples were obtained from all subjects. The concentration of lead in blood (B-Pb) and urine (U-Pb) was analysed. The urinary concentrations of several sensitive indicators of early tubular (U-beta 2-microglobulin (U-beta 2-m); U-N-acetyl-beta-glucosaminidase (U-NAG)) and glomerular kidney damage (U-albumin) were determined. The B-Pb and U-Pb values were significantly higher among active and retired lead workers compared with their corresponding control groups. The highest concentrations were found among the active lead workers. The concentrations of the parameters of kidney function investigated were of the same magnitude for exposed workers and controls. No clinical signs of renal impairment were found among the workers. No correlations of clinical importance existed between concentrations of U-albumin, U-beta 2-m, and U-NAG activity on the one hand and the concentrations of B-Pb, cumulative blood lead index, U-Pb, and lead concentrations in the calcaneus and tibia on the other, among lead workers and controls. Despite many years of moderate to heavy exposure to lead, particularly for the retired lead workers, no signs of adverse effects on the kidney such as early tubular or glomerular malfunction were found. Reversible changes in kidney function during the 1950s and 1960s could not be excluded, however, due to a greater exposure to lead during that time.     

Kidney effects in long term exposed lead smelter workers.

Occupational exposure to lead may cause kidney damage. This study was carried out on a cohort of 70 active and 30 retired long term exposed lead smelter workers. Their kidney function was compared with 31 active and 10 retired truck assembly workers who had no occupational exposure to lead. The lead workers had been regularly followed up with measurements of lead concentration in blood since 1950. Previous exposure to lead was calculated as a time integrated blood lead index for each worker. Blood and urine samples were obtained from all subjects. The concentration of lead in blood (B-Pb) and urine (U-Pb) was analysed. The urinary concentrations of several sensitive indicators of early tubular (U-beta 2-microglobulin (U-beta 2-m); U-N-acetyl-beta-glucosaminidase (U-NAG)) and glomerular kidney damage (U-albumin) were determined. The B-Pb and U-Pb values were significantly higher among active and retired lead workers compared with their corresponding control groups. The highest concentrations were found among the active lead workers. The concentrations of the parameters of kidney function investigated were of the same magnitude for exposed workers and controls. No clinical signs of renal impairment were found among the workers. No correlations of clinical importance existed between concentrations of U-albumin, U-beta 2-m, and U-NAG activity on the one hand and the concentrations of B-Pb, cumulative blood lead index, U-Pb, and lead concentrations in the calcaneus and tibia on the other, among lead workers and controls. Despite many years of moderate to heavy exposure to lead, particularly for the retired lead workers, no signs of adverse effects on the kidney such as early tubular or glomerular malfunction were found. Reversible changes in kidney function during the 1950s and 1960s could not be excluded, however, due to a greater exposure to lead during that time.     

Measurement by ICP-MS of lead in plasma and whole blood of lead workers and controls.

OBJECTIVES: To test a simple procedure for preparing samples for measurement of lead in blood plasma (P-Pb) and whole blood (B-Pb) by inductively coupled plasma mass spectrometry (ICP-MS), to measure P-Pb and B-Pb in lead workers and controls, and to evaluate any differences in the relation between B-Pb and P-Pb between people. METHODS: P-Pb and B-Pb were measured by ICP-MS in 43 male lead smelter workers and seven controls without occupational exposure to lead. For analysis, plasma and whole blood were diluted 1 in 4 and 1 in 9, respectively, with a diluted ammonia solution containing Triton-X 100 and EDTA. The samples were handled under routine laboratory conditions, without clean room facilities. RESULTS: P-Pb was measured with good precision (CV = 5%) even at concentrations present in the controls. Freeze storage of the samples had no effect on the results. The detection limit was 0.015 microgram/l. The P-Pb was 0.15 (range 0.1-0.3) microgram/l in controls and 1.2 (0.3-3.6) micrograms/l in lead workers, although the corresponding B-Pbs were 40 (24-59) micrograms/l and 281 (60-530) micrograms/l (1 microgram Pb/I = 4.8 nmol/l). B-Pb was closely associated with P-Pb (r = 0.90). The association was evidently non-linear; the ratio B-Pb/P-Pb decreased with increasing P-Pb. CONCLUSIONS: By means of ICP-MS and a simple dilution procedure, P-Pb may be measured accurately and with good precision down to concentrations present in controls. Contamination of blood at sampling and analysis is no major problem. With increasing P-Pb, the percentage of lead in plasma increases. In studies of lead toxicity, P-Pb should be considered as a complement to current indicators of lead exposure and risk.     

High lead exposure and auditory sensory-neural function in Andean children.

We investigated blood lead (B-Pb) and mercury (B-Hg) levels and auditory sensory-neural function in 62 Andean school children living in a Pb-contaminated area of Ecuador and 14 children in a neighboring gold mining area with no known Pb exposure. The median B-Pb level for 62 children in the Pb-exposed group was 52.6 micrograms/dl (range 9.9-110.0 micrograms/dl) compared with 6.4 micrograms/dl (range 3.9-12.0 micrograms/dl) for the children in the non-Pb exposed group; the differences were statistically significant (p < 0.001). Auditory thresholds for the Pb-exposed group were normal at the pure tone frequencies of 0.25-8 kHz over the entire range of B-Pb levels, Auditory brain stem response tests in seven children with high B-Pb levels showed normal absolute peak and interpeak latencies. The median B-Hg levels were 0.16 micrograms/dl (range 0.04-0.58 micrograms/dl) for children in the Pb-exposed group and 0.22 micrograms/dl (range 0.1-0.44 micrograms/dl) for children in the non-Pb exposed gold mining area, and showed no significant relationship to auditory function.     

Chelated lead in relation to lead in bone and ALAD genotype.

In order to assess whether lead in bone is available for chelation by 2,3 meso-dimercaptosuccinic acid (DMSA), 21 workers (10 active and 11 retired) from a secondary lead smeltery were studied. A morning urine sample was obtained from all participants, followed by ingestion of 10 mg per kg body weight of the chelating agent DMSA. All urine produced during the following 24 h was collected in consecutive 6- and 18-h portions. Concentrations of lead in blood (B-Pb) and urine were determined by flameless atomic absorption spectrometry (AAS), in plasma (P-Pb) by inductively coupled plasma mass spectrometry (ICP-MS), and in finger bone (Bone-Pb) by K X-ray fluorescence technique (XRF). DMSA-chelatable lead excreted in the 24-h portion correlated well with the excretion in the 6-h portion (U-Pb6h; rs=0.95; P<0.001). U-Pb6h showed a non-linear relationship to B-Pb (rs=0.84; P<0.001) and linear relationships to P-Pb (rs=0. 91; P<0.001) and lead in morning urine (rs=0.95; P<0.001). In active workers, but not in retired ones, P-Pb and U-Pb6h showed some relationship to Bone-Pb. In alternative multiple regression models B-Pb or P-Pb were both significant predictors of U-Pb6h, while Bone-Pb did not significantly improve the models. It can, thus, be concluded that DMSA-chelatable lead mainly reflects lead concentrations in blood, soft tissues, and possibly also trabecular bone. It is not a good index of total body burden and long-term exposure. For such estimations cortical Bone-Pb is more valid, as it contains the major fraction of long-term accumulated lead in the body. Further, the mobilization test did not give better information than measurements of lead levels in blood, plasma, or urine without chelation.     

Yearly measurements of blood lead in Swedish children since 1978: the declining trend continues in the petrol-lead-free period 1995-2007

Background

We have measured blood lead concentrations (B-Pb) in Swedish children, yearly since 1978. As reported previously, a substantial decrease of B-Pb was found for the period 1978-1994 (2440 children measured), as an effect of gradual reduction of lead in petrol. In another report focusing on the petrol-lead-free period 1995-2001, we noted that B-Pb seemed to stabilize at an average level close to 20 μg/L.

Objective

We here analyze data from the extended petrol-lead-free period 1995-2007.

Methods

B-Pb was measured in 1268 children, aged 7-11 years, from the municipalities of Landskrona and Trelleborg in southern Sweden, yielding 1407 measurements on B-Pb (since 139 children were measured in two different calendar years).

Results

We observed statistically significant decreases of the average concentrations during the recent years. The average B-Pb reduction rate was close to 5%/yr in the petrol-lead-free period 1995-2007; a similar reduction rate was estimated for the period with gradual reduction of lead in petrol, 1978-1994. The most recent geometric mean of B-Pb was 13.1 (range, 6.9-29.1) μg/L in Trelleborg (sample year 2005) and 13.2 (5.7-58.5) μg/L in Landskrona (2007). A declining B-Pb time trend was observed during the recent years among children who lived in near smelter, urban, and rural residential areas, respectively. B-Pb was influenced by the variables sex (boys had higher B-Pb), parents’ smoking habits (children with one or both parents smoking had higher B-Pb), and potentially lead-exposing hobbies (for example, shooting air guns).

Conclusion

Children's B-Pb levels can continue to decline markedly more than a decade after lead in petrol has been phased out in a country.     

Environmental Notes

Samples of vertebral bone were obtained by skeletal biopsy and lead concentrations were determined by atomic absorption spectroscopy. The median level of lead in bone in 27 active lead workers was 29 μg/g wet weight (range 2–155), corresponding to 370 μg/g calcium (range 30–1, 120). In 9 retired workers, the corresponding levels were 19 μg/g (5–76) and 250 μg/g calcium (60–700); in 14 reference subjects without occupational exposure, 1.3 μg/g (1–4) and 13 μg/g calcium (8–40). The bone lead content rose with time of exposure. Comparison of levels in vertebra with those in fingerbone, as measured by in vivo x-ray fluorescence in the same subjects, strongly suggested the presence of lead pools with different kinetics. The accumulation pattern, as well as the relation between levels in vertebra and fingerbone, suggests a much shorter half-time of lead in the mainly trabecular vertebral bone as compared to the mainly cortical fingerbone. Further, there was an association between vertebral and blood lead levels in the retired workers, which shows a considerable endogenous lead exposure from the skeletal pool.     

Effects of lead on the endocrine system in lead smelter workers.

In this study of the effects of lead on the endocrine system, 77 secondary lead-smelter workers (i.e., 62 active and 15 retired) were compared with 26 referents. Lead concentrations were determined in plasma with inductively coupled plasma mass spectrometry (i.e., index of recent exposure), in blood with atomic absorption spectrophotometry, and in fingerbone with K x-ray fluorescence technique (i.e., index of long-term exposure). In addition, pituitary hormones were determined in serum by fluoroimmunoassay, and thyroid hormones and testosterone in serum were determined with radioimmunoassay. Nine lead workers and 11 referents were challenged with gonadotrophin-releasing hormone and thyrotrophin-releasing hormone, followed by measurements of stimulated pituitary hormone levels in serum. Median levels of lead in plasma were 0.14 microg/dl (range = 0.04-3.7 microg/dl) in active lead workers, 0.08 microg/dl (range = 0.05-0.4 microg/dl) in retired lead workers, and 0.03 microg/dl (range = 0.02-0.04 microg/dl) in referents (1 microg/dl = 48.3 nmol/l). Corresponding blood lead concentrations were 33.2 microg/dl (range = 8.3-93.2 microg/dl), 18.6 microg/dl (range = 10.4-49.7 microg/dl), and 4.1 microg/dl (range 0.8-6.2 microg/dl), respectively. Respective bone lead levels were 21 microg/gm (range = -13 to 99 microg/gm), 55 microg/gm (range = 3-88 microg/gm), and 2 microg/gm (range = -21 to 14 microg/gm). Concentrations of basal serum hormone (i.e., free thyroid hormones, thyrotrophin, sex hormone binding globulin, and testosterone) were similar in the 3 groups. There were no significant associations between the hormones mentioned herein and blood plasma, blood lead, and bone lead levels. In the challenge test, stimulated follicle-stimulating hormone levels were significantly lower in lead workers (p = .014) than in referents, indicating an effect of lead at the pituitary level. Also, there was a tendency toward lower basal stimulated follicle-stimulating hormone concentrations in lead workers (p = .08). This effect, however, was not associated with blood plasma level, blood lead level, or bone lead level. In conclusion, a moderate exposure to lead was associated with only minor changes in the male endocrine function, particularly affecting the hypothalamic-pituitary axis. Given that sperm parameters were not studied, the authors could not draw conclusions about fertility consequences.     

Lead exposure of welders and bystanders in a ship repair yard

Blood samples were collected from 126 long-term ship repair workers and 42 retirees. Lead concentrations were determined by electrothermal atomic absorption spectrophotometry. Three groups with different degrees of lead exposure were identified: (1)59 welders, burners, and combination men (median blood lead, 39 μg/100 ml); (2) 67 painters, laborers, shipfitters, riggers, and other ship repair workers (median blood lead, 26 μg/100 ml); and (3) 42 retired welders, painters, and shipfitters (median blood lead, 23 μg/100 ml). Thirty active ship repair workers, including 28 welders and burners, had blood lead concentrations above the OSHA “action level” of 40 μg/100 ml. Increased levels in several men without direct exposures to lead were apparently caused by “bystander's exposure.” In the retirees, blood lead levels decreased with increasing length of retirement. Thus, after eight or more years, the average level was below 20 μg/100 ml.     

In vivo measurements of lead in bone at four anatomical sites: long term occupational and consequent endogenous exposure.

Measurements of bone lead concentrations in the tibia, wrist, sternum, and calcaneus were performed in vivo by x ray fluorescence on active and retired lead workers from two acid battery factories, office personnel in the two factories under study, and control subjects. Altogether 171 persons were included. Lead concentrations in the tibia and ulna (representative of cortical bone) appeared to behave similarly with respect to time but the ulnar measurement was much less precise. In an analogous fashion, lead in the calcaneus and sternum (representative of trabecular bone) behaved in the same way, but sternal measurement was less precise. Groups occupationally exposed to lead were well separated from the office workers and the controls on the basis of calculated skeletal lead burdens, whereas the differences in blood lead concentrations were not as great, suggesting that the use of concentrations of lead in blood might seriously underestimate lead body burden. The exposures encountered in the study were modest, however. The mean blood lead value among active lead workers was 1.45 mumol l-1 and the mean tibial lead concentration 21.1 micrograms (g bone mineral)-1. The kinetics of lead in the tibia appeared to be noticeably different from that in the calcaneus. Tibial lead concentration increased consistently both as a function of intensity of exposure and of duration of exposure. Calcaneal lead concentration, by contrast, was strongly dependent on the intensity rather than duration of exposure. This indicated that the biological half life of lead in calcaneus was less than the seven to eight year periods into which the duration of exposure was split. Findings for retired workers clearly showed that endogenous exposure to lead arising from skeletal burdens accumulated over a working lifetime can easily produce the dominant contribution to systemic lead concentrations once occupational exposure has ceased.     

Extensive lead exposure in children living in an area with production of lead-glazed tiles in the Ecuadorian Andes

We have determined the concentrations of lead (Pb), cadmium (Cd), and mercury (Hg) in the blood of children living in two Andean villages in Ecuador with many family-owned cottage-type industries using Pb from discarded car batteries and occasionally, utility batteries containing Cd and Hg for the production of glazed tiles. The battery metals are ground together with water to a suspension, which is applied manually onto the tiles and then fused at about 1,200° C in sawdust-fired kilns. Children aged 4–15 years were recruited from the schools with the assistance of the school-teachers. Children from homes with and without tile-glazing activities were to be included. Blood metal concentrations were determined by inductively coupled plasma mass spectrometry (ICP-MS). The children had extremely high blood lead concentrations (B-Pb), which ranged between 100 and 1,100 μg/l (median 510 μg/l, n = 82). Children from families engaged in tile-glazing production had significantly higher B-Pb (median 600 μg/l) than those living in homes with no such activity (median 210 μg/l), although the B-Pb of the latter were nonetheless clearly elevated. B-Cd and B-Hg were low (medians 0.25 μg Cd/l and 1.6 μg Hg/l, respectively), indicating that the exposure from utility batteries containing Cd and Hg was low. The blood hemoglobin concentrations decreased significantly with rising B-Pb, indicating an effect on the heme synthesis. This was supported by a marked increase in the blood concentration of protoporphyrins with increasing B-Pb. It can be concluded that children from families with cottage industries producing glazed tiles are at risk for severe health effects due to high lead exposure. Received: 20 November 1996 / Accepted: 30 April 1997     

In vivo measurements of lead in bone at four anatomical sites: long term occupational and consequent endogenous exposure.

Measurements of bone lead concentrations in the tibia, wrist, sternum, and calcaneus were performed in vivo by x ray fluorescence on active and retired lead workers from two acid battery factories, office personnel in the two factories under study, and control subjects. Altogether 171 persons were included. Lead concentrations in the tibia and ulna (representative of cortical bone) appeared to behave similarly with respect to time but the ulnar measurement was much less precise. In an analogous fashion, lead in the calcaneus and sternum (representative of trabecular bone) behaved in the same way, but sternal measurement was less precise. Groups occupationally exposed to lead were well separated from the office workers and the controls on the basis of calculated skeletal lead burdens, whereas the differences in blood lead concentrations were not as great, suggesting that the use of concentrations of lead in blood might seriously underestimate lead body burden. The exposures encountered in the study were modest, however. The mean blood lead value among active lead workers was 1.45 mumol l-1 and the mean tibial lead concentration 21.1 micrograms (g bone mineral)-1. The kinetics of lead in the tibia appeared to be noticeably different from that in the calcaneus. Tibial lead concentration increased consistently both as a function of intensity of exposure and of duration of exposure. Calcaneal lead concentration, by contrast, was strongly dependent on the intensity rather than duration of exposure. This indicated that the biological half life of lead in calcaneus was less than the seven to eight year periods into which the duration of exposure was split. Findings for retired workers clearly showed that endogenous exposure to lead arising from skeletal burdens accumulated over a working lifetime can easily produce the dominant contribution to systemic lead concentrations once occupational exposure has ceased.     

Effects of Lead on the Endocrine System in Lead Smelter Workers

In this study of the effects of lead on the endocrine system, 77 secondary lead-smelter workers (i.e., 62 active and 15 retired) were compared with 26 referents. Lead concentrations were determined in plasma with inductively coupled plasma mass spectrometry (i.e., index of recent exposure), in blood with atomic absorption spectrophotometry and in fingerbone with K x-ray fluorescence technique (i.e., index of long-term exposure). In addition, pituitary hormones were determined in serum by fluoroimmunoassay and thyroid hormones and testosterone in serum were determined with radioimmunoassay. Nine lead workers and 11 referents were challenged with gonadotrophin-releasing hormone and thyrotrophin-releasing hormone, followed by measurements of stimulated pituitary hormone levels in serum. Median levels of lead in plasma were 0.14 μg/dl (range = 0.04–3.7 μg/dl) in active lead workers, 0.08 μg/dl (range = 0.05–0.4 μg/dl) in retired lead workers and 0.03 μg/dl (range = 0.02–0.04 μg/dl) in referents (1 μg/dl = 48.3 nmol/l). Corresponding blood lead concentrations were 33.2 μg/dl (range = 8.3–93.2 μg/dl), 18.6 μg/dl (range = 10.4–49.7 μg/dl) and 4.1 μg/dl (range 0.8–6.2 μg/dl), respectively. Respective bone lead levels were 21 μg/gm (range = -13 to 99 μg/gm), 55 μg/gm (range = 3–88 μg/gm) and 2 μg/gm (range = -21 to 14 μg/gm). Concentrations of basal serum hormone (i.e., free thyroid hormones, thyrotrophin, sex hormone binding globulin and testosterone) were similar in the 3 groups. There were no significant associations between the hormones mentioned herein and blood plasma, blood lead and bone lead levels. In the challenge test, stimulated follicle-stimulating hormone levels were significantly lower in lead workers (p = .014) than in referents, indicating an effect of lead at the pituitary level. Also, there was a tendency toward lower basal stimulated follicle-stimulating hormone concentrations in lead workers (p = .08). This effect, however, was not associated with blood plasma level, blood lead level, or bone lead level. In conclusion, a moderate exposure to lead was associated with only minor changes in the male endocrine function, particularly affecting the hypothalamic-pituitary axis. Given that sperm parameters were not studied, the authors could not draw conclusions about fertility consequences.     

Variation in blood concentrations of cadmium and lead in the elderly

This study aims at characterizing blood concentrations of cadmium (B-Cd) and lead (B-Pb) in a group of 176 men and 248 women, 49-92 years of age (mean 68 years), selected from the Swedish Twin Registry. Metal concentrations were determined using graphite furnace atomic absorption spectrophotometry. B-Cd ranged from 0.05 to 6.8 microg Cd/L (median 0.36 microg Cd/L) and B-Pb from 5.6 to 150 microg Pb/L (median 27 microg Pb/L). As expected, smokers had higher B-Cd than nonsmokers (median 1.3 versus 0.32 microg Cd/L), while B-Pb was not significantly related to smoking habits. Among nonsmokers, women had higher B-Cd than men (median 0.35 versus 0.25 microg Cd/L). In men, but not women, B-Cd increased with age and consequently the gender-related difference in B-Cd was most obvious in the youngest age group. On the other hand, women had lower B-Pb than men (median 24 versus 30 microg Pb/L). In both men and women, B-Pb decreased between 50 and 70 years of age, perhaps reflecting decreased energy intake. In women, the highest B-Pb in the 50-55 years age group is probably related to an increased release of Pb from the skeleton during postmenopausal bone demineralization. After about 70 years, B-Pb tended to increase, which probably is a cohort effect due to much higher Pb exposure 10-30 years ago when leaded gasoline was used.     

Yearly measurements of blood lead in Swedish children since 1978: an update focusing on the petrol lead free period 1995-2001

Methods: In the south of Sweden, each year from 1995 to 2001, B-Pb was measured in 329 boys and 345 girls, aged 7–11 years.

Results: The geometric mean (GM) of B-Pb was 21 (range 6–80) µg/l. There was no consistent change of B-Pb from 1995 to 2001. Children living near a lead smelter had raised B-Pb (GM 24 µg/l, range 11–80). Passive smoking, but not age and sex, influenced B-Pb significantly.

Conclusions: B-Pb in Swedish children, no longer exposed to petrol lead, seems to have stabilised at an average level close to 20 µg/l (provided there is no nearby industrial lead emission).

     

Clinical and neurobehavioural study of the acute and chronic neurotoxicity of styrene

A cross sectional field study of workers exposed to styrene was performed to evaluate possible acute and chronic neurotoxic effects. A total of 36 workers of four companies handling polyester resin materials for one to 16 years (median: 7 years) and two control groups were each examined on a Monday. The control group 1 (formed to compare acute effects) consisted of 20 men from two companies with no exposure to neurotoxic chemicals. To compare chronic effects, a second control group was formed by "one to one matching" with respect to age, socioeconomic status, and pre-exposure intelligence level. Ambient air monitoring using active sampling (short time) and passive samplers (long time) showed styrene in air concentrations as follows: range 3-251 ppm (median: 18 ppm) and concentrations 140-600 ppm during lamination of the inside of boats. For biological monitoring the results were as follows (postshift samples: range/median): styrene in blood: 5-482 micrograms/dl (39 micrograms/dl), mandelic acid urine: 0.01-3.64 g/l (0.21 g/l), and phenylglyoxylic acid urine: 0.01-0.87 g/l (0.19 g/l). The clinical examination found no signs or symptoms of peripheral neuropathy or encephalopathy. The principal work related health complaints were acute, reversible irritation of the eyes that occurred after exposure to styrene concentrations of 200 ppm or more. The neurobehavioural tests showed no significant differences in acute effects (p greater than 0.05) between the two groups or between preshift and postshift testing. Nor were there any significant differences in the relevant neurobehavioural variables between the styrene workers and the controls. It is concluded that occupational exposure to styrene concentrations in air up to 100 ppm causes no adverse acute or chronic effects on the central nervous system.     

Relation of cumulative exposure to inorganic lead and neuropsychological test performance.

OBJECTIVES--To determine if measures reflecting chronic occupational lead exposure are associated with performance on neuropsychological tests. METHOD--467 Canadian male lead smelter workers (mean (SD) age 43.4 (11.00) years, education 9.8 (3.18) years, years of employment 17.7 (7.43), and current blood lead concentration (B-Pb) 27.5 (8.4) micrograms dl-1) were given a neuropsychological screening battery. Time weighted average (TWA) and time integrated blood levels (IBL) were developed from B-Pb records obtained through regular medical monitoring (mean (range) TWA 40.1 (4.0-66.4) micrograms dl-1, mean IBL 765.2 (0.6-1625.7) micrograms-y dl-1). 14 neuropsychological variables were included in three multivariate analyses of covariance, with each exposure variable as the grouping variable (high, medium, and low) and age, education, score on a measure of depressive symptoms, and self reported alcohol use as the covariates. Groups did not differ in history of neurological conditions. RESULTS--Neither the B-Pb, TWA, nor IBL was significant by multivariate analyses of covariance (MANCOVA). When years of employment, a suppressor variable, was included as a covariate, IBL exposure groups differed significantly on digit symbol, logical memory, Purdue dominant hand, and trails A and B. CONCLUSIONS--A dose-effect relation was found between cumulative exposure (IBL) and neuropsychological performance at a time when current B-Pb concentrations were low and showed no association with performance.