Work ability in vibration-exposed workers.

BACKGROUND: Hand-arm vibration exposure may cause hand-arm vibration syndrome (HAVS) including sensorineural disturbances. AIMS: To investigate which factors had the strongest impact on work ability in vibration-exposed workers. METHODS: A cross-sectional study in which vibration-exposed workers referred to a department of occupational and environmental medicine were compared with a randomized sample of unexposed subjects from the general population of the city of Gothenburg. All participants underwent a structured interview, answered several questionnaires and had a physical examination including measurements of hand and finger muscle strength and vibrotactile and thermal perception thresholds. RESULTS: The vibration-exposed group (47 subjects) showed significantly reduced sensitivity to cold and warmth in digit 2 bilaterally (P < 0.01) and in digit 5 in the left hand (P < 0.05) and to warmth in digit 5 in the right hand (P < 0.01), compared with the 18 referents. Similarly, tactilometry showed significantly raised vibration perception thresholds among the workers (P < 0.05). A strong relationship was found for the following multiple regression model: estimated work ability = 11.4 - 0.1 × age - 2.3 × current stress level - 2.5 × current pain in hands/arms (multiple r = 0.68; P < 0.001). CONCLUSIONS: Vibration-exposed workers showed raised vibrotactile and thermal perception thresholds, compared with unexposed referents. Multiple regression analysis indicated that stress disorders and muscle pain in hands/arms must also be considered when evaluating work ability among subjects with HAVS.

Trace element pattern in patients with fibromyalgia.

An imbalance of the trace element status in human tissues and body fluids has been suggested as a contributing factor for the development of fibromyalgia (FM). The study comprised 38 females with defined fibromyalgia (FM) according to generally accepted criteria from the American College of Rheumatology (ACR). They were compared with 41 females matched for age and geographic location. The concentrations of about 30 trace element and ions were determined in whole blood, urine and drinking water of all participants by inductively coupled plasma mass spectrometry (ICP-MS) and inductively coupled plasma optical emission spectroscopy (ICP-OES). Significantly higher concentrations in whole blood of Cd, Co, Cu, Fe, Se, Sn and Zn (p< or =0.046) were observed in the FM-cases in comparison with the referents. A different pattern was noted in urine with increased urinary excretion of Ag (p=0.003) among the FM-patients. The urinary excretion of the other elements were of the same magnitude or slightly lower in FM-cases as compared to referents. As nearly all of the concentrations of the studied elements in blood and urine were within reported reference intervals in non-occupationally exposed populations, the clinical significance of the differences observed seems to be limited. The element concentrations of the studied elements in drinking water were within present national and international guideline values (EU, WHO) and the concentrations of potentially toxic metals such as e.g. Cd, Hg and Pb were low. In conclusion, the present investigation could not demonstrate abnormal levels of trace elements in blood or urine of FM-patients and, thus, does not support the hypothesis that trace element abnormalities play a significant role in the development of FM.

Concentrations of inorganic elements in 20 municipal waters in Sweden before and after treatment--links to human health.

The water chemistry of 20 municipal water treatment plants in southern Sweden, representing various bedrock situations, and water qualities, were investigated. Four water samples, raw and treated, were collected from each plant and analyzed by predominantly ICP-OES and ICP-MS at four occasions from June to December, 2001. The concentrations of Ca, Mg, K, Na, HCO(3) and a number of micronutrients, varied considerably in treated waters from the studied plants (ranges; Ca: 9.1-53.7 mg L(-1), Mg: 1.4-10.9 mg L(-1), K: 1.1-4.8 mg L(-1), Na; 5.4-75.6 mg L(-1), HCO(3): 27-217 mg L(-1)). The elimination of Fe and Mn from raw water was efficient in all treatments investigated, giving concentrations in treated waters below the detection limits at some plants. Softening filters gave waters with Ca-concentrations comparable to the softest waters in this study. Adjustment of pH by use of chemicals like lye, soda or lime, modified the consumer water composition significantly, besides raising the pH. It was estimated that drinking water contributed to approximately 2.2-13% of the daily Ca uptake, if the gastrointestinal uptake efficiency from food and water was estimated to be around 50%. The corresponding figures for Mg was 1.0-7% and for F 0-59%. None of the studied elements showed any significant time trends in raw or treated waters during the follow-up period. The concentrations of potentially toxic metals such as Al, Pb and U were low and did not indicate risks for adverse health effects (ranges; Al: 0.5-2.3 microg L(-1), Pb: 0-0.3 microg L(-1), U: 0.2.5 microg L(-1)).

Concentrations of inorganic elements in bottled waters on the Swedish market.

This study presents the concentrations of about 50 metals and ions in 33 different brands of bottled waters on the Swedish market. Ten of the brands showed calcium (Ca) concentrations

Lung cancer risks among lead smelter workers also exposed to arsenic.

Recent publications indicate an increased incidence of lung cancer in non-ferrous smelter workers exposed to lead. The present study provides further data on selected subgroups in one such cohort. The cohort was based on 3979 smelter workers employed for at least 1 year between 1928 and 1979, and also exposed to lead and included in the Blood Lead Register that was started at the smelter in 1950. Two subcohorts were formed from the original cohort. One consists of 710 workers employed at the lead departments (Lead subcohort 1), and the other of 383 workers employed at the lead departments (Lead subcohort 2), but never at other works where an excess lung cancer risk was previously identified. Standardized Cancer Incidence Rates (SIR) 1958-1987 were calculated relative to county rates. In the subcohorts, arsenic exposure in lung cancer cases was assessed in detail based on occupational hygiene information from the company. Lung cancer incidence was raised in both subcohorts (Lead subcohort 1: SIR 2.4; 95% CI 1.2-4.5; Lead subcohort 2: SIR 3.6; 95% CI 1.2-8.3). Total cancer incidence in the cohorts was not increased. A detailed study of arsenic exposure in the 10 lung cancer cases in these two subcohorts revealed that all but one of these cases had a significant exposure also to arsenic. An elevated incidence of lung cancer was observed in smelter workers exposed to lead. However, considerable arsenic exposure also occurred in a majority of the lung cancer cases in the investigated subcohorts. In this multifactorial exposure situation it has not been possible to separate the carcinogenic effects of lead and arsenic, but a possible interaction between these metals may be involved in explaining the carcinogenic risks.

Kidney cadmium as compared to other markers of cadmium exposure in workers at a secondary metal smelter.

BACKGROUND: The aim of the study was to evaluate whether cadmium concentrations in kidney (K-Cd), blood (B-Cd) or urine (U-Cd) could reveal previous occupational cadmium exposure at a metal smelter. METHODS: The study included 90 smelters and 35 controls (B-Cd and U-Cd determination). In a subgroup (N = 33), K-Cd was also determined. RESULTS: B-Cd (median 4.6; range 0.5-53 nmol/L), U-Cd (0. 29; 0.04-1.9 micromol/mol creatinine) and K-Cd (14; 3-61 microg/g wet weight) were similar to reported concentrations in the general Swedish population. In the subgroup, significant associations (P<0. 001) were obtained between B-Cd and K-Cd (r = 0.70), U-Cd and K-Cd (r = 0.60) and between U-Cd and B-Cd (r = 0.62). Multiple regression analyses revealed smoking as the major predictor of K-Cd, B-Cd, and U-Cd. B-Cd and U-Cd were both associated with the duration of employment at the smelter. CONCLUSIONS: There was no statistically significant evidence of previous occupational exposure at the smelter from measurement of K-Cd.

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.

Environmental health in the Baltic region--toxic metals.

Recent reports on concentrations of lead, cadmium, methylmercury, arsenic and nickel in some biological media in populations in the Baltic region are reviewed. In particular, children in parts of Poland, the Czech Republic, and Germany have uptakes of lead sufficient to cause adverse effects on the central nervous system and kidneys. Cadmium exposure is also high in Poland. Slight cadmium-induced effects on the kidneys have been reported from Germany and Sweden. Methylmercury uptake is dependent upon the intake of fish, in particular from contaminated lakes and rivers in Sweden and Finland, as well as the eastern coast of the Baltic Sea. There are some indications of immunotoxic effects associated with the intake of such fish. However, fish also contain other immunomodulating agents. Exposure to arsenic seems to be low everywhere in the Baltic region. There is high nickel exposure in northern Russia.

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.

In vivo XRF as a means to evaluate the risk of kidney effects in lead and cadmium exposed smelter workers.

The effect on kidney function was studied in 22 smelter workers with concomitant exposure to lead and cadmium. One active and five retired workers showed early signs of kidney dysfunction. They all had a long-term and high lead exposure, while their kidney cadmium concentrations measured in vivo by XRF techniques were low to moderate. Thus, the exposure to lead has been a greater risk, although an interaction between lead and cadmium could not be excluded.

Lead concentrations in tibial and calcaneal bone in relation to the history of occupational lead exposure.

OBJECTIVES: This study tested a simple model of the relationship between the lead concentration in bone (bone-Pb), exposure time, and lead in plasma (P-Pb) and whole blood (B-Pb) to make it possible to use bone-Pb as a retrospective exposure index. METHODS: Seventy-seven active lead workers and 24 referents were studied. The bone-Pb in tibia (T-Pb) and calcaneus (C-Pb) was measured by in vivo X-ray fluorescence. P-Pb was calculated from B-Pb by use of the nonlinear relationship between these variables. Cumulative B-Pb (cumB-Pb) and P-Pb (cumP-Pb) were calculated to the time of the bone-Pb measurements. In addition, cumP-Pb was adjusted by applying varying rate constants for the transfer of lead from bone to plasma. RESULTS: There were close linear associations between the lead concentrations in tibia (proportion of variance explained, R2 = 0.78) and calcaneus (R2 = 0.80), on one hand and the cumB-Pb on the other. The best fit of bone-Pb to the adjusted cumP-Pb (0.79 for T-Pb; 0.82 for C-Pb) was obtained for the terminal phase half-times of 13 and 12 years, respectively. CONCLUSIONS: The combined data on bone-Pb and exposure time make it possible to estimate previous mean P-Pb and B-Pb. Such estimates will be valuable in studies of toxic effects on long-term exposed lead workers when data on the intensity of previous exposure are lacking. The use of P-Pb in modeling bone-Pb kinetics is physiologically relevant, but the use of adjusted cumP-Pb, as compared with cumB-Pb, did not significantly change the variance in the relation to bone-Pb.

Lead concentrations in human plasma, urine and whole blood.

OBJECTIVES: Blood-lead levels (B-Pb), and to some extent urinary lead (U-Pb), are the most employed measures of lead exposure and risk. However, the small fraction of lead present in plasma (usually below 1% of that in blood) is probably more relevant to lead exposure and toxicity. Nevertheless, the lead content of plasma lead (P-Pb) has only seldom been used, mainly due to analytical limitations, which have now been overcome. We examined P-Pb in occupationally exposed subjects, as well as its relationship with B-Pb and U-Pb. METHODS: Blood samples were obtained from 145 male workers, 110 of whom were employed in lead work. After a simple dilution of plasma, P-Pb was determined by inductively coupled plasma mass spectrometry. The detection limit was 0.04 microg/l, and the imprecision was 5%. RESULTS: The lead concentration ranges were 0.20-37 microg/l for P-Pb, 0.9-176 microg/l (density adjusted) for U-Pb, and 9-930 microg/l for B-Pb. A close exponential relation was obtained between B-Pb and P-Pb. When B-Pb was plotted versus log P-Pb, a straight line (log P-Pb = 0.00225 x B-Pb - 0.58; r = 0.97) was obtained. Both the relation between U-Pb and P-Pb and that between U-Pb and B-Pb showed a large scattering (r = 0.78 in both cases). The relation to B-Pb appeared to be exponential, while that to P-Pb appeared to be linear. CONCLUSIONS: The low detection limit and good precision of P-Pb determinations make it possible to use P-Pb in assessments of lead exposure and risk. Furthermore, in relative terms, P-Pb is a more sensitive measure than B-Pb, especially at high lead levels. This development is of importance for studies of exposure, possibly also for studies of risks.

A neurobehavioural study of long-term occupational inorganic lead exposure.

A group of 38 male workers at a secondary smelter (period of employment 2-35 years; median 10 years) was divided into two subgroups depending on bone-lead concentration, arranged as 19 matched pairs according to age, education and job level. The median concentrations for finger-bone lead (Bone-Pb) were 16 vs. 32 micrograms/g; for current blood-lead (B-Pb), 1.6 vs. 1.8 mumol/1; for retrospective peak blood-lead (Peak-Pb), 2.7 vs. 3.0 mumol/1; and for a retrospective cumulative blood lead index (CBLI), 143 vs. 233 mumol/l x months. Nineteen unexposed male workers from a nearby mechanical plant served as controls, using the same matching algorithm. The triplets were examined with a standardised neuropsychological test battery, and four questionnaires for self-rating of symptoms and activity/stress level related to work environment. No sign of behavioural deterioration was observed in the exposed groups, either in objective cognitive tests or in subjective symptom/mood self-rating scales. Despite the limited sample size, the statistical power was sufficient to conclude that a concealed lead-associated effect was unlikely. Covariations between behavioural measures and lead exposure indices were generally low and non-significant, as a whole not exceeding a random level. No confounding or effect-modifying factor was detected that could explain the results as a type II error. To conclude, a current B-Pb of 1.8 mumol/l was not associated with adverse behavioural effects, and a long-term lead exposure around 2.0 mumol/l for 13 years (mean values) was not associated with permanent brain dysfunction.

Lead in fingerbone: a tool for retrospective exposure assessment.

Exposure to inorganic lead may cause many adverse health effects. When absorbed, lead is accumulated in large part in bone. In this study, we investigated the relationship between lead concentration in fingerbone, exposure time, and lead in blood. We also sought to design a model that made it possible to use fingerbone lead as an indicator of earlier exposure. The study comprised 137 active workers from a secondary lead smeltery. Workers had undergone regular determinations of blood lead (i.e., up to 6 times/y) for up to 24 y. In addition, during the period 1979-1992, workers underwent up to four fingerbone lead assessments via noninvasive x-ray fluorescence. We calculated cumulative blood lead, adjusted for time-related reduction of bone lead according to a transfer of lead from bone to blood, for each worker. We obtained the best fit of bone lead to cumulative adjusted blood lead when we assumed a 14-y half-time for the transfer coefficient. This half-time was similar to the terminal half-time for lead in bone in retired smelters, whom we studied earlier by longitudinal in vivo measurements. We described models for the accumulation of bone lead on blood lead and exposure time. The combined data on bone lead and exposure time may be used to estimate a mean blood lead during previous exposure. Such estimates will be valuable in epidemiological studies aimed at evaluating the toxic effects of long-term lead exposure in lead workers for whom data on previous blood lead levels are lacking.

Delta-aminolevulinic acid dehydratase polymorphism: influence on lead levels and kidney function in humans.

Delta-aminolevulinic acid dehydratase (ALAD) polymorphism has been reported to modify lead pharmacokinetics (i.e., individuals who express the ALAD2 allele [ALAD2 subjects] have higher blood lead levels than homozygotes for the ALAD1 allele [ALAD1 subjects]). In our study of 89 lead-exposed workers (7 ALAD2 homozygotes or heterozygotes) and 34 unexposed workers (10 ALAD2 heterozygotes), concentrations of urinary calcium and creatinine were lower in ALAD2 subjects than in ALAD1 subjects (respective medians: calcium--78 mg/l versus 185 mg/l, p = .003; creatinine--11.2 mmol/l versus 14.9 mmol/l, p = .008). No association was found between ALAD genotype and blood lead levels or bone lead levels. However, expression of the ALAD2 allele occurred less frequently among lead-exposed workers than in unexposed controls. The results indicated the presence of ALAD allele-specific differences in kidney function, as well as a possible genetic healthy-worker selection.

Cumulative lead exposure in relation to mortality and lung cancer morbidity in a cohort of primary smelter workers.

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 employed 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 dose-response analyses. RESULTS: The lung cancer incidence of the total cohort [standardized incidence ratio (SIR) 2.8, 95% confidence interval (95% CI) 2.1-3.8] 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. CONCLUSIONS: 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.

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 micrograms/g wet weight, as against 23 micrograms/g in active smelters) and 3 micrograms/g in the reference subjects. A strong positive correlation was observed between the bone-Pb and the CBLI among both active (rs = 0.73; P < 0.001) and retired (rs = 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 (rs = 0.58; P = 0.011) and U-Pb. (rs = 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 r2) 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.

Evaluation of selected publications on reference values for lead in blood.

As a part of the global Tracy project, whose aim is to define metal concentrations in tissues and body fluids of reference populations, more than 1000 papers published from 1980 to 1994 were scrutinized that presented tentative reference values for lead in blood in occupationally unexposed adult populations. Ten studies exemplifying criteria for proper sampling, analysis and data treatment are presented and discussed. Levels of lead in blood are influenced by numerous factors. Accordingly, a wide variation in blood lead concentrations was observed. As an example, in a global study in 1983 of nonsmoking female schoolteachers, the geometric mean value for lead in blood varied from 52 micrograms. l-1 in Tokyo, Japan, up to 193 micrograms. l-1 in Mexico City. The Tracy survey demonstrates the importance of factors such as age, gender, ethnicity, food, drinking and smoking habits, hobbies, season and year of sampling, residential area, and geographic location. Lead in blood was shown to be both time and area specific. Thus it was not possible to establish a general reference value for lead in blood.

Lead in tissues of deceased lead smelter workers.

Smelter workers are exposed to a number of metals and other substances in dust, fumes and gases. The concentrations of lead in liver, lung, kidney, brain, hair and nails were determined in 32 deceased, long-term exposed male lead smelter workers, and compared with those of 10 male controls. The lead levels in liver, lung, kidney and brain were analyzed by atomic absorption spectrophotometry. X-ray fluorescence was used for the determinations in hair and nails. Lead in blood had been determined repeatedly in the lead workers since 1950, which made it possible to calculate a time-integrated blood lead index for each worker. The highest lead levels in soft tissues were found in liver, followed in order of concentration by kidney, lung and brain, among both exposed workers and controls. These organ lead concentrations were all significantly higher among the workers as compared with the control group (p < or = 0.02). The largest difference between workers and controls was found in brain tissue (ratio between median values = 5.6). The lead levels in hair and nails were of the same magnitude in the two groups. The workers showed positive correlations between lead concentrations in liver and kidney (Spearman's rho = rs = 0.59; p < 0.001), liver and hair (rs = 0.51; p = 0.003), liver and nails (rs = 0.52; p = 0.002) and hair and nails (rs = 0.52; p = 0.002). Lead concentrations in kidney correlated well with lead levels in hair (rs = 0.57; p = 0.001) and nails (rs = 0.51; p = 0.003), respectively. The positive correlation between the lead concentrations in liver and kidney indicates that these organs belong to the same soft tissue lead pool in the body. In retired lead workers, positive correlations were observed between the lead concentrations in liver and the cumulative blood lead index (CBLI) (rs = 0.50; p = 0.016), as well as between lead levels in kidney and CBLI (rs = 0.51; p = 0.014).