Cancer incidence in Swedish oil refinery workers exposed to benzene.

BACKGROUND: Oil refinery workers are exposed to benzene, which is a well-known cause of leukaemia, but results on leukaemia in oil refinery workers have been mixed, and the data on workers' exposure is limited. Oil refinery workers are also exposed to asbestos and several studies have shown increased risk of mesothelioma. AIM: The objective was to investigate cancer incidence, especially leukaemia, at low to moderate exposure to benzene in an update of a previous study of employees at three Swedish oil refineries. METHODS: Cancer incidence was followed up in 2264 men (1548 refinery operators) employed at three oil refineries in Sweden for at least one year. Job types and employment times were collected from complete company files. A retrospective assessment of the benzene exposure was performed by occupational hygienists in collaboration with the refineries using historic measurements as well as detailed information on changes in the industrial hygiene and technological developments. Cases of cancer were retrieved by a linkage with the Swedish Cancer Register through 35-47 years of follow-up and standardized incidence ratios (SIR) with 95% confidence intervals (CI) were calculated. RESULTS: In total, 258 tumors had occurred versus 240 expected (SIR 1.07; 95% CI 0.95-1.21). There were 10 cases of leukaemia, all in refinery operators (SIR 2.4; 95% CI 1.18-4.51). There were three cases of pleural mesothelioma, two of which in refinery operators. The mean estimated cumulative benzene exposure for the cases of leukaemia was 7.9 ppm-years (median 4.9, range 0.1-31.1). DISCUSSION: The study suggests that low to moderate average cumulative benzene exposure increases the risk of leukaemia. Limitations include the modest number of cases and potential misclassification of exposure. CONCLUSION: The present study indicated an increased risk of leukaemia in male oil refinery workers with low to moderate exposure to benzene.

Low personal exposure to benzene and 1,3-butadiene in the Swedish petroleum refinery industry.

PURPOSE: Petroleum refinery workers are exposed to the carcinogens benzene and 1,3-butadiene. Declining exposures have been reported internationally but information on current exposure in the Swedish refinery industry is limited. The aim was to examine refinery workers' personal exposure to benzene and 1,3-butadiene and increase awareness of exposure conditions by collaboration with involved refineries. METHODS: Altogether 505 repeated personal exposure measurements were performed among workers at two refineries. Full-shift measurements were conducted in different exposure groups using Perkin Elmer diffusive samplers filled with Carbopack X. Mean levels were calculated using mixed-effects models. A large fraction of measurements below the limit of detection (LOD) required imputation of computer-generated data. RESULTS: Mean benzene exposure among process technicians was 15.3 µg/m3 (95% CI 10.4-22.5 µg/m3) and 13.7 µg/m3 (95% CI 8.3-22.7 µg/m3) for Refinery 1 and 2, respectively. Process technicians working outdoors had higher exposure than maintenance workers (20.7 versus 5.9 µg/m3, p < 0.01). Working in the harbour and tank park (Refinery 1), compared with the process area, was associated with higher exposure. The 1,3-butadiene exposure was low, 5.4 and 1.8 µg/m3, respectively. The total variation was generally attributed to within-worker variability. CONCLUSIONS: Low benzene and 1,3-butadiene levels were found among refinery workers. Mean benzene exposure was about 1% of the Swedish occupational limit (1500 µg/m3) and for 1,3-butadiene, exposure was even lower. A large fraction of values below the LOD can be managed by carefully modelled, computer-generated data.

Increased blood cadmium levels were not associated with increased fracture risk but with increased total mortality in women: the Malmö Diet and Cancer Study.

This study aimed to investigate if high levels of blood cadmium at baseline were associated with increased fracture risk during follow-up in middle-aged women. No increased fracture risk was observed during follow-up, but women with higher levels of cadmium had an increased overall mortality. INTRODUCTION: Exposure to high levels of cadmium has been associated with an increased fracture risk. The aim was to investigate a perceived association between low levels of blood cadmium (B-Cd) at baseline and risk of first incident fracture. METHODS: From the population-based Malmö Diet and Cancer Study Cardiovascular cohort, 2920 middle-aged women with available background questionnaire and B-Cd measurements were included. Women were divided into quartiles (Q) according to their cadmium levels (Cd-Q1 <0.18 µg/L, Cd-Q2 0.18-0.28 µg/L, Cd-Q3 0.28-0.51 µg/L, and Cd-Q4 >0.51 µg/L). National registries were analysed for prospective risk of fractures or death. Associations between B-Cd and fracture risk were assessed by survival analysis (Cox regression analysis). RESULTS: In total, 998 first incident fractures occurred in women during a follow-up lasting 20.2 years (median) (12.5-21.2 years) (25th-75th percentile). Women in Cd-Q4 were more often current smokers than in Cd-Q1 78.4 vs. 3.3% (p < 0.001) and the number of cigarettes smoked per day correlated with B-Cd (r = 0.49; p < 0.001). The risk of fracture was not associated with baseline B-Cd in adjusted models. The hazard ratio (HR) Cd-Q4 vs. Cd-Q1 was 1.06 (95% confidence interval (CI) 0.89-1.27). In the multivariate Cox regression, independent variables for increased fracture risk were history of gastric ulcer and increasing age, whereas increasing body mass index (BMI) lowered fracture risk. Overall mortality was significantly higher for women with high B-Cd, HR 2.06 (95% CI 1.57-2.69). CONCLUSIONS: Higher blood levels of cadmium did not increase fracture risk in middle-aged women but reduced overall survival.

Personal exposure to benzene and 1,3-butadiene during petroleum refinery turnarounds and work in the oil harbour.

PURPOSE: Petroleum refinery workers' exposure to the carcinogens benzene and 1,3-butadiene has decreased during normal operations. However, certain occupational groups or events at the refineries still involve a risk of higher exposures. The aim of this study was to examine the personal exposure to benzene and 1,3-butadiene at refinery turnarounds and during work in the oil harbour. METHODS: Personal exposure measurements of benzene and 1,3-butadiene were taken during work shifts, with a priori assumed higher benzene exposure, using PerkinElmer diffusive samplers filled with Carbopack X. Mean exposure levels were calculated, and repeated exposure measurements, when available, were assessed using mixed effect models. Group and individual compliance with the Swedish occupational exposure limit (OEL) was tested for the different exposure groups. RESULTS: Mean benzene exposure levels for refinery workers during the three measured turnarounds were 150, 610 and 960 µg/m3, and mean exposures for oil harbour workers and sewage tanker drivers were 310 and 360 µg/m3, respectively. Higher exposures were associated with handling benzene-rich products. Most occupational groups did not comply with the Swedish OEL for benzene nor did the individuals within the groups. The exposure to 1,3-butadiene was very low, between <1 and 3 % of the Swedish OEL. CONCLUSIONS: Work within the petroleum refinery industry, with potential exposure to open product streams containing higher fractions of benzene, pose a risk of personal benzene exposures exceeding the OEL. Refinery workers performing these work tasks frequently, such as contractors, sewage tanker drivers and oil harbour workers, need to be identified and protected.

8-isoprostane in exhaled breath condensate after experimental exposure to wood smoke in humans.

Wood smoke, a well-known indoor and outdoor air pollutant, may cause adverse health effects through oxidative stress. In this study 8-isoprostane, a biomarker of oxidative stress, was measured in exhaled breath condensate (EBC) and urine before and after experimental exposure to wood smoke. The results were compared with measurements of other biomarkers of oxidative stress and inflammation. Thirteen subjects were exposed first to clean air and then, after 1 week, to wood smoke in an exposure chamber during 4-hour sessions. Exhaled breath condensate, exhaled nitric oxide, blood and urine were sampled before and at various intervals after exposure to wood smoke and clean air. Exhaled breath condensate was examined for 8-isoprostane and malondialdehyde (MDA), while exhaled air was examined for nitric oxide, serum for Clara cell protein (CC16) and urine for 8-isoprostane. 8-isoprostane in EBC did not increase after wood smoke exposure and its net change immediately after exposure was inversely correlated with net changes in MDA (r(s)= -0.57, p= 0.041) and serum CC16 (S-CC16) (r(p)= -0.64, p= 0.020) immediately after the exposure. No correlation was found between 8-isoprostane in urine and 8-isoprostane in EBC. In this study controlled wood smoke exposure in healthy subjects did not increase 8-isoprostane in EBC.

Experimental exposure to wood smoke: effects on airway inflammation and oxidative stress.

BACKGROUND: Particulate air pollution affects cardiovascular and pulmonary disease and mortality. A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress. OBJECTIVES: To examine whether short-term exposure to wood smoke in healthy subjects affects markers of pulmonary inflammation and oxidative stress. METHODS: 13 subjects were exposed first to clean air and then to wood smoke in a chamber during 4-hour sessions, 1 week apart. The mass concentrations of fine particles at wood smoke exposure were 240-280 mug/m(3), and number concentrations were 95 000-180 000/cm(3), about half of the particles being ultrafine (<100 nm). Blood and breath samples were taken before and at various intervals after exposure to wood smoke and clean air and examined for exhaled nitric oxide and Clara cell protein in serum and urine, and malondialdehyde in exhaled breath condensate. RESULTS: Exposure to wood smoke increased alveolar nitric oxide 3 hours post-exposure while malondialdehyde levels in breath condensate were higher both immediately after and 20 hours after exposure. Serum Clara cell protein was increased 20 hours after exposure. CONCLUSIONS: Wood smoke at levels that can be found in smoky indoor environments caused an inflammatory response and signs of increased oxidative stress in the respiratory tract, especially in the lower airways.

Self-reported symptoms and their effects on cognitive functioning in workers with past exposure to solvent-based glues: an 18-year follow-up.

OBJECTIVES: To examine to what extent exposure to organic solvents during the working life affects general well-being in the long term, and to explore the relationship between self-reported symptoms and cognitive functioning in previously solvent-exposed floor layers. METHODS: The study included 41 solvent-exposed floor layers and 40 unexposed referents participating in a longitudinal follow-up study 18 years after the baseline assessment. Symptom prevalence and level of spare time activities were studied using the same methods as in the initial study. These include a general health examination, the Q16 symptom questionnaire, and a questionnaire for spare time activities. Relationships between symptoms and cognitive functioning were analysed based on recently published data on cognitive functioning of the participants at follow-up. RESULTS: At follow-up neuropsychiatric symptoms such as need to check things, depressive mood, and abnormal fatigue, were more prevalent among floor layers, particularly the most exposed individuals, than among referents. In addition, the most highly exposed floor layers reported more concentration difficulties and irritability. Fatigue and depressive mood increased over the follow-up time in the most exposed floor layers but not in the referents. Memory difficulties, although more frequent among floor layers than among referents, had decreased in floor layers while increased in referents. Floor layers also reported some negative effects on intimate relations and activity level. Neuropsychiatric symptoms were related to poorer performance chiefly in memory tasks and tests of complex attention and perceptual speed, more seldom in visuospatial tasks. CONCLUSIONS: Findings of exposure-related, long-lasting, partly deteriorating neuropsychiatric complaints indicate that general well-being later in life has been affected in floor layers with past heavy solvent exposure. We also found frequent associations between symptom prevalence and the cognitive functioning. Together with previous findings of dose-related cognitive decrements, the present results strengthen the evidence that long-term heavy occupational solvent exposure may negatively interact with the normal ageing process.

Influence of solvent exposure and aging on cognitive functioning: an 18 year follow up of formerly exposed floor layers and their controls.

OBJECTIVES: To extend our knowledge of how exposure to neurotoxic substances during working life affects cognitive functioning in the long term. Does long term occupational exposure to organic solvents lead to aggravated cognitive impairment later in life? METHODS: A follow up was conducted of floor layers exposed to solvents and their unexposed referents (carpenters) 18 years after the baseline assessment. The pattern of cognitive changes in the two groups was compared, with the same 10 neuropsychological tests from the test battery for investigating functional disorders (TUFF) that were used at baseline. The study included 41 floor layers and 40 carpenters. A medical examination focused on health at the present and during the past 18 years. An extensive exposure assessment made in the initial study included questionnaires, interviews, and measurements. Additional exposure during the follow up period was minor, as explored in interviews at follow up. RESULTS: The entire group of floor layers did not deteriorate significantly more over time than did the carpenters. However, among the oldest subjects (>60 years), only floor layers showed decline in visual memory. Moreover, the most highly exposed floor layers deteriorated significantly more than their referents in visual memory and perceptual speed, and they tended to display larger decrements in motor speed. Significant dose effect relations were found; higher cumulative exposure was associated with decrements in visual episodic memory, perceptual speed and attention, and visuospatial skill. CONCLUSIONS: The hypothesis that floor layers would deteriorate more in cognitive performance than their unexposed referents over a period of 18 years was partly supported by the results of this study. The results are consistent with the view that the negative effects of exposure to solvents may interact with the normal aging process, primarily at heavy exposure.

Heterogeneity in sources of exposure variability among groups of workers exposed to inorganic mercury.

Many exposure assessment strategies rely on the occupational group as the unit of analysis in which workers are classified on the basis of job title, location, or on other characteristics related to the workplace or the job. Although statistical methods that combine exposure data collected on workers from different occupational groups are more efficient, the underlying assumption that the degree of variation over time and among workers is the same for all groups has yet to be fully investigated. Given the utility of different modeling approaches when assessing exposures, we investigated assumptions of homogeneity of variance within and between workers using both random- and mixed-effects models. In our study of four groups of workers exposed to inorganic mercury (Hg) at a chloralkali plant, there was no evidence of significant heterogeneity in the levels of variation over time or between workers for air Hg levels. For the biological monitoring data, however, our findings indicate that groups did not share common levels of variability and that it was not appropriate to pool the data and obtain single estimates of the within- and between-worker variance components. Classification of job group as a random or fixed effect had no effect on the results and yielded the same conclusions when the models were compared. To illustrate effects related to the proper specification of a model, the likelihood of exceeding certain levels (which is a function of the parameters of the underlying distribution of the natural log-transformed exposures) was evaluated using the results obtained from the different models. Although the probability that workers' mean exposures exceeded occupational exposure limits for air, urine and blood Hg was generally low (<10%) for all groups except maintenance workers, the estimated values sometimes varied depending upon the particular model that was applied. Given the growing use of random- and mixed-effects models that combine data across occupational groups, additional studies are warranted to evaluate whether it is reasonable to assume common variances and covariances among measurements collected on workers from different groups.

Mortality from cardiovascular diseases and exposure to inorganic mercury.

OBJECTIVE: To study the mortality from cardiovascular and other chronic non-neoplastic diseases after long term exposure to inorganic mercury. Limited information is available on the effect of chronic exposure to mercury on the cardiovascular system. METHODS: The mortality was studied among 6784 male and 265 female workers from four mercury mines and mills in Spain, Slovenia, Italy, and the Ukraine. Workers were employed between 1900 and 1990; the follow up period lasted from the 1950s to the 1990s. The mortality of the workers was compared with national reference rates. RESULTS: Among men, there was a slight increase in overall mortality (standardised mortality ratio (SMR) 1.08, 95% confidence interval (95% CI) 1.04 to 1.12). An increased mortality was found from hypertension (SMR 1.46, 95% CI 1.08 to 1.93), heart diseases other than ischaemic (SMR 1.36, 95% CI 1.20 to 1.53), pneumoconiosis (SMR 27.1, 95% CI 23.1 to 31.6), and nephritis and nephrosis (SMR 1.55, 95% CI 1.13 to 2.06). The increase in mortality from cardiovascular diseases was not consistent among countries. Mortality from hypertension and other heart diseases increased with estimated cumulative exposure to mercury; mortality from ischaemic heart disease and cerebrovascular diseases increased with duration of employment, but not with estimated exposure to mercury. Results among women were hampered by few deaths. CONCLUSION: Despite limited quantitative data on exposure, possible confounding, and likely misclassification of disease, the study suggests a possible association between employment in mercury mining and refining and risk in some groups of cardiovascular diseases.

A small dose of ethanol increases the exhalation of mercury in low-level-exposed humans.

Inorganic mercury is mainly eliminated by urinary and fecal excretion, but it is also eliminated by exhalation and sweat. There are only a few reports on exhalation of mercury in humans. In volunteers with short-term mercury exposure, an increased exhalation of mercury was found after alcohol intake. The aim of this study was to determine mercury in end-exhaled air and the influence of ethanol on mercury exhalation in subjects with long-term mercury exposure from diet, amalgam fillings, or the work environment. Fourteen subjects, with different grades of mercury exposure, were given 0.2 g ethanol/kg body weight. Measurements of mercury in end-exhaled air were performed before and after alcohol intake. Mercury in end-exhaled air could be detected in all subjects. In 10 individuals without amalgam fillings the mercury concentration was 3 to 12 pg/L. A marked increase, in general about fivefold, in mercury concentrations in end-exhaled air was seen in all subjects 30 min after intake of alcohol, regardless of the level of mercury exposure. Higher ethanol doses resulted in higher mercury levels in end-exhaled air and longer time periods before a return to background levels. An increase was seen even after an ethanol dose of only 0.1 g ethanol/kg body weight (about 0.08 L wine). The decrease in exhaled mercury at higher alcohol doses followed approximately zero-order kinetics and probably reflects the elimination of ethanol in tissues. In conclusion, low levels of mercury can be detected in end-exhaled air also in individuals without amalgam fillings. About a fivefold increase was seen 30 min after alcohol intake, and the relative increase seemed to be independent of the body burden of mercury. Exhalation of mercury represents only a small percentage of the total elimination of mercury.

Variability in airborne and biological measures of exposure to mercury in the chloralkali industry: implications for epidemiologic studies.

Exposure assessment is a critical component of epidemiologic studies, and more sophisticated approaches require that variation in exposure be considered. We examined the intra- and interindividual sources of variation in exposure to mercury vapor as measured in air, blood, and urine among four groups of workers during 1990-1997 at a Swedish chloralkali plant. Consistent with the underlying kinetics of mercury in the body, the variability of biological measures was dampened considerably relative to the variation in airborne levels. Owing to the effects of intraindividual variation, estimating workers' exposures from a few measurements can attenuate measures of effect. To examine such effects on studies relating long-term exposure to a continuous health outcome, we evaluated the utility of each exposure measure by comparing the necessary sample sizes required for accurate estimation of a slope coefficient obtained from a regression analysis. No single measure outperformed the others for all groups of workers. However, when workers were evaluated together, creatinine-corrected urinary mercury better discriminated workers' exposures than airborne or blood mercury levels. Thus, pilot studies should be conducted to examine variability in both air and biomonitoring data because quantitative information about the relative magnitude of the intra- and interindividual sources of variation feeds directly into our efforts to design an optimal sampling strategy when evaluating health risks associated with occupational or environmental contaminants.

Cadmium, mercury, and lead in kidney cortex of the general Swedish population: a study of biopsies from living kidney donors.

Cadmium, mercury, and lead concentrations were determined in deep-frozen kidney cortex biopsies taken from 36 living, healthy Swedish kidney donors (18 males and 18 females), who were 30-71 (mean 53) years of age. Information about occupation, smoking, the presence of dental amalgam, and fish consumption could be obtained for 27 of the donors. The samples (median dry weight 0.74 mg) were analyzed using inductively coupled plasma mass spectrometry, and the results were transformed to wet-weight concentrations. The median kidney Cd was 17 micrograms/g (95% confidence interval, 14-23 micrograms/g), which was similar in males and females. In 10 active smokers, the median kidney Cd was 24 micrograms/g, and in 12 who never smoked, it was 17 micrograms/g. The median kidney Hg was 0.29 micrograms/g, with higher levels in females (median 0.54 micrograms/g) than in males (median 0.16 micrograms/g). Subjects with amalgam fillings had higher kidney Hg (median 0.47 micrograms/g, n = 20) than those without dental amalgam (median 0.15 micrograms;g/g, n = 6), but kidney Hg was below the detection limit in some samples. Nearly half of the samples had kidney Pb below the detection limit. The median kidney Pb was estimated as 0. 14 micrograms/g. This is the first study of heavy metals in kidney cortex of living, healthy subjects, and the results are relatively similar to those of a few previous autopsy studies, indicating that results from autopsy cases are not seriously biased in relation to kidney metal concentrations in the general population. Cd concentrations in those who never smoked were relatively high, indicating considerable Cd intake from the diet in Sweden. The effect of dental amalgam on kidney Hg was as expected, although the reason for the difference in Hg levels between males and females is unclear.

Tissue levels of mercury determined in a deceased worker after occupational exposure.

OBJECTIVES: To examine mercury (Hg) and selenium (Se) levels in autopsy samples from a thermometer worker who had been exposed over a long period to, and monitored for, mercury vapor. CASE REPORT: Hg and Se levels were determined using radiochemical neutron activation analysis in a worker who had commited suicide 4 weeks after the end of 14 years of exposure and in an unexposed age-matched referent. Histochemical staining of cerebellum was performed according to the method of Danscher and Schroder. RESULTS: The Hg concentrations (wet weight) were 25 microg/g in the kidney cortex, 1.2 microg/g in the liver, 0.72 microg/g in the lung, 0.025 microg/g in the testis, and 0.014-0.018 microg/g in the cerebellum (gray matter, dentate nucleus, and white matter). The Se level in the kidney cortex was high, 4.6 microg/g, whereas the concentration detected in the other tissue samples was normal. Light microscopy of the cerebellum was normal, and no histochemical staining for mercury was observed. Autopsy samples from the referent showed low Hg and Se levels consistent with other reports. CONCLUSIONS: The observed kidney-Hg, which was 50-100 times higher than that occurring in the general population, is in agreement with previous sparse data from ongoing occupational exposure. The high Se level detected in the kidney indicates coaccumulation with mercury. The low Hg concentration found in the cerebellum was unexpected, since some reports have shown much higher brain-Hg long after the cessation of exposure.

Cancer occurrence among European mercury miners.

OBJECTIVES: To study the carcinogenicity of inorganic mercury in humans. METHODS: We studied the mortality from cancer among 6784 male and 265 female workers of four mercury mines and mills in Spain, Slovenia, Italy and the Ukraine. Workers were employed between the beginning of the century and 1990; the follow-up period lasted from the 1950s to the 1990s. We compared the mortality of the workers with national reference rates. RESULTS: Among men, there was no overall excess cancer mortality; an increase was observed in mortality from lung cancer (standardized mortality ratio [SMR] 1.19, 95 percent confidence interval [CI] 1.03-1.38) and liver cancer (SMR 1.64, CI 1.18-2.22). The increase in lung cancer risk was restricted to workers from Slovenia and the Ukraine: no relationship was found with duration of employment or estimated mercu ry exposure. The increase in liver cancer risk was present both among miners and millers and was stronger in workers from Italy and Slovenia: there was a trend with estimated cumulative exposure but not with duration of employment, and the excess was not present in a parallel analysis of cancer incidence among workers from Slovenia. No increase was observed for other types of cancer, including brain and kidney tumours. Among female workers (Ukraine only), three deaths occurred from ovarian cancer, likely representing an excess. CONCLUSIONS: Exposure to inorganic mercury in mines and mills does not seem strongly associated with cancer risk, with the possible exception of liver cancer; the increase in lung cancer may be explained by co-exposure to crystalline silica and radon.

Urinary excretion of mercury, copper and zinc in subjects exposed to mercury vapour.

The excretion of mercury, copper and zinc in urine, and mercury in whole blood and plasma, was determined in 40 chloralkali workers exposed to mercury vapour and 40 age-matched referents. The Hg concentrations in whole blood, plasma and urine were higher in the exposed group (35 nmol l-1, 30 nmol l-1, and 11.5 nmol mmol-1 creatinine, respectively) in comparison with the reference group (15 nmol l-1, 6.3 nmol l-1, and 1.8 nmol mmol-1 creatinine, respectively). The urinary copper excretion was similar in the two groups, while U-Zn excretion was significantly higher (P = 0.04) in the exposed group, median 0.83 mumol mmol-1 creatinine versus 0.76 munmol mmol-1 creatinine in the reference group. In a subgroup of exposed workers with current U-Hg above 11.5 nmol l-1 mmol-1 creatinine (20 micrograms g-1 creatinine) the median U-Zn was 1.1 mumol mmol-1 creatinine. In both groups smokers had high U-Zn levels than non smokers. When both U-Hg and smoking were taken into account in a linear regression model, there was a significant association between U-Hg and U-Zn in the combined group of exposed and referents (P = 0.002). This study indicates that mercury exposure in humans, as in animals, causes increased urinary excretion of zinc. The mechanisms may be induced synthesis of metallothionein in the kidneys, displacement of Zn from preexisting metallothionein by Hg, or a decreased reabsorption of zinc in the kidneys owing to a slight tubular dysfunction.

Exposure to mercury vapor and impact on health in the dental profession in Sweden.

Possible adverse effects of mercury exposure in dentistry have been discussed in several studies. The objective of the present study was to carry out detailed measurements of mercury exposure in the dental profession in Sweden, and to search for adverse health effects from such exposure. We examined 22 dentists and 22 dental nurses, working in teams, at six Swedish dental clinics. Measurements of air mercury, performed with personal, active air samplers, showed a median air Hg of 1.8 micrograms/m3 for the dentists, and 2.1 micrograms/m3 for the dental nurses. Spot measurements with a direct reading instrument displayed temporarily elevated air Hg, especially during the preparation and application of amalgam. The average concentration of mercury in whole blood (B-Hg) was 18 nmol/L, in plasma (P-Hg) 5.1 nmol/L, and in urine (U-Hg) 3.0 nmol/mmol creatinine. Possible effects on the central nervous system (CNS) were registered with three questionnaires: Q16, Eysenck Personality Inventory (EPI), and the Profile of Mood Scales (POMS). In the Q16, the number of symptoms was statistically significantly higher in the dentistry group compared with an age- and gender-matched control group (n = 44). The urinary excretion of albumin and urinary activity of the tubular enzyme N-acetyl-beta-glucose-aminidase (NAG) did not differ between the two groups. The results confirm that exposure to mercury in the dental profession in Sweden is low. The air Hg levels were mainly influenced by the method of amalgam preparation and inserting, and by the method of air evacuation during drilling and polishing.

Blood lead in Uruguayan children and possible sources of exposure.

Blood samples and questionnaire background data were collected from 96 children (age 2-14 years) living in urban, suburban, or rural areas with varying traffic intensity and industrial lead pollution in Uruguay. Spot samples of tap water were collected from the homes of 44 children, and samples of top soil were taken from seven areas. Samples of air-borne dust were collected in central and suburban Montevideo. Blood lead concentrations (B-Pb) in children ranged between 47 and 191 (mean 96) micrograms/L and exceeded in 36% of the children 100 micrograms/L, the intervention level adopted by the United States Centers for Disease Control. Lead in tap water ranged from 0.2 to 230 (mean 15) micrograms/L and exceeded in 39% of the samples the maximum level recommended by WHO, 10 micrograms/L. Lead pipes were used in parts of the water supply systems. Lead in air varied between different locations from 0.15 to 1.7 micrograms/m3, highest in the very center of Montevideo. The median soil lead ranged from 6 to 2100 micrograms/g and was highest in industrially polluted areas. At multiple regression analysis, B-Pb was significantly associated only with age (P = 0.032) and traffic intensity at school (P = 0.045). No significant impact on B-Pb of lead in water or soil could be established.

Polychlorinated dibenzo-p-dioxin and dibenzofuran levels and patterns in polyvinylchloride and chloralkali industry workers.

The production of chlorine and vinyl chloride (VCM) is associated with the formation of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). The objective of the present study was to determine whether the levels and congener patterns of PCDDs and PCDFs in the blood of workers involved in the production of such substances could be related to their occupational environment. PCDD and PCDF levels in blood plasma from VCM and chloralkali workers and in referents were determined by means of high-resolution gas chromatography/high resolution mass spectrometry (HRGC/HRMS) techniques and the results were evaluated through principal component analysis (PCA). The overall levels of PCDDs and PCDFs were low, but the relative congener distribution detected in the workers differed from that found in the referents. 1,2,3,4,6,7,8-HpCDF, 1,2,3,4,7,8- and 1,2,3,6,7,8-HxCDFs are congeners related to work in VCM and chloralkali industries. Exposure to PCDDs and PCDFs in these industrial environments changes the congener-distribution pattern in the blood of workers as compared with referents. A combination of isomer-specific analysis of PCDDs and PCDFs in blood plasma and PCA is suitable for the differentiation between nonoccupational and occupational exposure and provides a means of assessing workers' exposure situation in different occupational settings.

Dose-dependent elimination kinetics for mercury in urine: observations in subjects with brief but high-level exposure.

OBJECTIVES: To study the elimination kinetics for mercury in urine (U-Hg) after brief but high-level exposure. METHODS: U-Hg was examined in 11 workers after 2-10 days of exposure to inorganic Hg and after symptoms and signs of Hg intoxication had appeared. Initial U-Hg excretion varied between 60 and 2360 micrograms/g creatinine. The subjects were followed up for 1-11 months. In each subject, one- and two-compartment models were fitted to the U-Hg values, assuming an exponential decrease, by weighted non-linear least-squares regression (weight = 1/U-Hg). RESULTS: The data indicated two elimination phases in subjects with initial U-Hg above 600 micrograms/g. In the two-compartment models, there was a fast phase with a half-time of 2-16 days, and a slow phase with a half-time of more than a month. The fast phase contributed 70-90% to the sum of the Y intercepts. CONCLUSIONS: The kinetics of U-Hg excretion after cessation of exposure seems to be dose-dependent and, at least in certain cases, to have two phases. The explanation for the fast phase may be that the capacity of certain binding sites in the kidney was exceeded.