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We conducted a cross-sectional study in Sweden, Italy and Poland to assess environmental and occupational exposure to mercury from chloralkali (CA) plants and the potential association with biomarkers of early renal dysfunction. Questionnaire data and first-morning urine samples were collected from 757 eligible subjects. Urine samples were analysed for mercury corrected for creatinine (U-HgC), alpha-1-microglobulin (A1M), N-acetyl-beta-glucosaminidase (NAG) and albumin. Determinants of urinary mercury excretion were examined. Levels of kidney markers were compared in three U-HgC categories, and differences were tested taking age and other covariates into account. In the general population, the median U-HgC was higher in Italian (1.2 microg/gC) than in Polish (0.22 microg/gC) or Swedish (0.21 microg/gC) subjects, and no effect of living close to CA plants could be shown. Dental amalgam, chewing on amalgam, and fish consumption were positively associated with U-HgC. In subjects from the general population, no effects on the kidney markers could be detected, while in men, including workers occupationally exposed to mercury, U-HgC was positively associated with the kidney markers, especially with NAG, but to some extent also with A1M and albumin. Differences in urinary mercury and kidney markers in the general population between three studied countries could possibly be due to dietary factors, increased susceptibility to mercury at low selenium intake or co-exposure to other nephrotoxic metals.

The aim of this study was to investigate the impact of domestic wood burning on indoor levels of polycyclic aromatic hydrocarbons (PAHs). Indoor and outdoor concentrations of 27 PAHs were measured during wintertime in homes with (n= 13) or without (n 0) wood-burning appliances and at an ambient site in a Swedish residential area where wood burning for space heating is common. Twenty-four hour indoor levels of anthracene, benzo(ghi)fluoranthene, cyclopenta(cd)pyrene, benz(a)anthracene, chrysene/triphenylene, benzo(a)pyrene (BaP), indeno(1,2,3-cd)pyrene, benzo(ghi)perylene, and coronene were significantly (about 3- to 5-fold) higher in homes with, compared with homes without, wood-burning appliances. The outdoor levels of PAHs were generally higher than the indoor levelsfor all PAHs exceptforthe methylated phenanthrenes. The total PAH cancer potency (sum of BaP equivalents) was significantly higher (about 4 times) in the wood-burning homes compared with the reference homes, with BaP being the largest contributor, while phenanthrene made the largest contribution to the total PAH concentration in indoor and outdoor air. The median indoor BaP level in the wood-burning homes (0.52 ng/m3) was 5 times higher than the Swedish health-based guideline of 0.1 ng/m3, which was also exceeded outdoors on all days (median 0.37 ng/m3).

Particulate matter from wood smoke may cause health effects through generation of oxidative stress with resulting damage to DNA. We investigated oxidatively damaged DNA and related repair capacity in peripheral blood mononuclear cells (PBMC) and measured the urinary excretion of repair products after controlled short-term exposure of human volunteers to wood smoke. Thirteen healthy adults were exposed first to clean air and then to wood smoke in a chamber during 4h sessions, 1 week apart. Blood samples were taken 3h after exposure and on the following morning, and urine was collected after exposure, from bedtime until the next morning. We measured the levels of DNA strand breaks (SB), oxidized purines as formamidopyrimidine-DNA-glycosylase (FPG) sites and activity of oxoguanine glycosylase 1 (hOGG1) in PBMC by the comet assay, whereas mRNA levels of hOGG1, nucleoside diphosphate linked moiety X-type motif 1 (hNUDT1) and heme oxygenase 1 (hHO1) were determined by real-time RT-PCR. The excretion of 8-oxo-7,8-dihydro-oxoguanine (8-oxoGua) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine was measured by high performance liquid chromatography purification followed by gas chromatography with mass spectrometry. The morning following exposure to wood smoke the PBMC levels of SB were significantly decreased and the mRNA levels of hOGG1 significantly increased. FPG sites, hOGG1 activity, expression of hNUDT1 and hHO1, urinary excretion of 8-oxodG and 8-oxoGua did not change significantly. Our findings support that exposure to wood smoke causes systemic effects, although we could not demonstrate genotoxic effects, possibly explained by enhanced repair and timing of sampling.

Evaluation of neuromotor function has been used in several epidemiological studies of workers with long-term exposure to mercury vapor (Hg 0). Some recent studies indicate adverse effects at relatively low exposure levels. In the present study, we used sensitive quantitative methods, developed specifically to detect subtle effects of exposure to toxins on motor function. After exclusion of individuals with neurological diseases or other conditions that may affect performance, 43 chloralkali workers with current low exposure to Hg 0, and 22 age-matched referents remained for further analysis. The median urinary mercury concentration in exposed workers was 5.9 microg/g (range 1.3-25) creatinine (microg/gC), while that in referents was 0.7 microg/gC (range 0.2-4.1). The mean exposure time was 15 years, and the median cumulative mercury index was 161 years x microg/gC in exposed workers. A eurythmokinesimeter (EKM) was used to quantify eye-hand coordination, and a diadochokinesimeter, to measure rapid alternating rotation of the forearms. In general, the differences in performance between the exposed workers and the referents were small. Age was associated with a decrease in speed, more tremor, and longer contact duration between the stylus and the metal targets in performance of rapid pointing movements. Smokers had significantly more tremor, and more contacts per event in the EKM test, than nonsmokers. Taking age, shift work, and smoking habits into account, no significant associations with current or cumulative mercury exposure were found for the majority of the outcome variables from the quantitative tests. In general, this study indicates no significant adverse effects of Hg 0 on neuromotor function at the exposure levels studied.

Personal exposure to PM(2.5) and PM(1), together with indoor and residential outdoor levels, was measured in the general adult population (30 subjects, 23-51 years of age) of Gothenburg, Sweden. Simultaneously, urban background concentrations of PM(2.5) were monitored with an EPA WINS impactor. The 24-h samples were gravimetrically analyzed for mass concentration and black smoke (BS) using a smokestain reflectometer. Median levels of PM(2.5) were 8.4 microg/m(3) (personal), 8.6 microg/m(3) (indoor), 6.4 microg/m(3) (residential outdoor), and 5.6 microg/m(3) (urban background). Personal exposure to PM(1) was 5.4 microg/m(3), while PM(1) indoor and outdoor levels were 6.2 and 5.2 microg/m(3), respectively. In non-smokers, personal exposure to PM(2.5) was significantly higher than were residential outdoor levels. BS absorption coefficients were fairly similar for all microenvironments (0.4-0.5 10(-5) m(-1)). Personal exposure to particulate matter (PM) and BS was well correlated with indoor levels, and there was an acceptable agreement between personal exposure and urban background concentrations for PM(2.5) and BS(2.5) (r(s)=0.61 and 0.65, respectively). PM(1) made up a considerable amount (70-80%) of PM(2.5) in all microenvironments. Levels of BS were higher outdoors than indoors and higher during the fall compared with spring. The correlations between particle mass and BS for both PM(2.5) vs. BS(2.5) and PM(1) versus BS(1) were weak for all microenvironments including personal exposure. The urban background station provided a good estimate of residential outdoor levels of PM(2.5) and BS(2.5) within the city (r(s)=0.90 and 0.77, respectively). Outdoor levels were considerably affected by long-range transported air pollution, which was not found for personal exposure or indoor levels. The within-individual (day-to-day) variability dominated for personal exposure to both PM(2.5) and BS(2.5) in non-smokers.

Fine particles (PM2.5) were sampled indoors and outdoors at 40 sampling sites; in ten classrooms in five schools, at ten preschools and 20 non-smoking homes, in three communities in Stockholm, Sweden, during nine 2-week periods. Each sampling site was sampled twice, once during winter and once during spring. The samples were analysed for elemental concentrations using X-ray fluorescence (XRF) spectroscopy. In all locations significantly higher outdoor concentrations were found for elements that are related to long-range transported air masses (S, Ni, Br and Pb), while only Ti was higher indoors in all locations. Similar differences for S, Br and Pb were found in both seasons for homes and schools. In preschools different seasonal patterns were seen for the long-range transported elements S, Br and Pb and the crustal elements Ti, Mn and Fe. The indoor/outdoor ratios for S and Pb suggest an outdoor PM2.5 particle net infiltration of about 0.6 in these buildings. The community located 25 km from the city centre had significantly lower outdoor concentrations of elements of crustal or traffic origin compared with the two central communities, but had similar levels of long-range transported elements. Significant correlations were found between PM2.5 and most elements outdoors (rs = 0.45-0.90). Copper levels were found to correlate well (rs = 0.64-0.91) to the traffic marker NO2 during both winter and spring in all locations. Copper may be a suitable elemental marker for traffic-related aerosols in health studies in areas without other significant outdoor Cu sources.

The aim of this study was to quantify personal exposure and indoor levels of the suspected or known carcinogenic compounds 1,3-butadiene, benzene, formaldehyde and acetaldehyde in a small Swedish town where wood burning for space heating is common. Subjects (wood burners, n = 14), living in homes with daily use of wood-burning appliances were compared with referents (n = 10) living in the same residential area. Personal exposure and stationary measurements indoors and at an ambient site were performed with diffusive samplers for 24 h. In addition, 7 day measurements of 1,3-butadiene and benzene were performed inside and outside the homes. Wood burners had significantly higher median personal exposure to 1,3-butadiene (0.18 microg m(-3)) compared with referents (0.12 microg m(-3)), which was also reflected in the indoor levels. Significantly higher indoor levels of benzene were found in the wood-burning homes (3.0 microg m(-3)) compared with the reference homes (1.5 microg m(-3)). With regard to aldehydes, median levels obtained from personal and indoor measurements were similar although the four most extreme acetaldehyde levels were all found in wood burners. High correlations were found between personal and indoor levels for all substances (r(s) > 0.8). In a linear regression model, type of wood-burning appliance, burning time and number of wood replenishments were significant factors for indoor levels of 1,3-butadiene. Domestic wood burning seems to increase personal exposure to 1,3-butadiene as well as indoor levels of 1,3-butadiene and benzene and possibly also acetaldehyde. The cancer risk from these compounds at exposure to wood smoke is, however, estimated to be low in developed countries.

Measurement of tremor has been used in several occupational studies of workers with long-term exposure to mercury vapor (Hg(0)). Recent studies indicate an adverse effect even at relatively low exposure levels. In the present study, we used sensitive quantitative methods to assess tremor in chloralkali workers with current low exposure to Hg(0). Neurological examinations and recordings of tremor using both an accelerometer and a laser-based system were conducted in 43 mercury-exposed workers and 22 age-matched referents. The median urinary mercury concentration in exposed workers was 5.9 (1.3-25) microg/g creatinine (microg/gC), while it was 0.7 (0.2-4.1) microg/gC in referents. The mean exposure time was 15 years, and the median cumulative mercury index was 161 years x microg/gC in exposed workers. There were no differences between the exposed workers and the referents in the clinical evaluation of tremor. In the quantitative tremor tests, no associations were found with current or cumulative mercury exposure for the majority of tremor measures. There were indications that exposure to Hg(0) was associated with a lowering of tremor frequency in the non-dominant hand, and a possible interaction with smoking. The differences were small, however, and overall, this study indicates no significant adverse effects on tremor at these exposure levels.

Experimental studies are used to evaluate effects of human exposure to diesel exhaust and concentrated ambient particles. This article describes a system for studying exposure of humans to wood smoke. Wood smoke was generated using a wood stove placed outside an exposure chamber that can hold at least 10 subjects. A partial flow of the generated wood smoke from the stove was mixed with filtered indoor air. Personal and stationary measurements were performed of PM2.5 and PM1 mass concentrations and various volatile organic compounds (VOCs): 1,3-butadiene, benzene, and aldehydes. In addition, particulate matter (PM) mass, number concentrations, and size distributions of particles (0.007-6.7 microm), as well as nitrous oxides, CO2, and CO, were measured online. Filters were analyzed for trace elements and black smoke. Polycyclic aromatic compounds, toluene, and xylenes were determined in stationary samples. Results of the first experiment showed no differences between personal and stationary measurements for particles or VOCs. Consequently, stationary measurements can be used to predict personal exposure. All PM mass (about 250 microg/m3) was in the PM1 fraction. Subjective symptoms were generally weak, while clear objective signs were found, for example, in biomarkers of inflammation. With careful control of the combustion process, relatively constant mass and number concentrations were obtained over each exposure session. By varying the combustion and dilution of the wood smoke, different exposure scenarios can be achieved and thus, knowledge about which of the properties of particles and gaseous compounds are crucial for the effects.

Particulate air pollution is known to increase cardiovascular morbidity and mortality. Proposed mechanisms underlying this increase include effects on inflammation, coagulation factors, and oxidative stress, which could increase the risk of coronary events and atherosclerosis. The aim of this study was to examine whether short-term exposure to wood smoke affects markers of inflammation, blood hemostasis, and lipid peroxidation in healthy humans. Thirteen subjects were exposed to wood smoke and clean air in a chamber during two 4-h sessions, 1 wk apart. The mass concentrations of fine particles at wood smoke exposure were 240-280 mug/m3, and number concentrations were 95,000-180,000/cm3. About half of the particles were ultrafine (< 100 nm). Blood and urine samples were taken before and after the experiment. Exposure to wood smoke increased the levels of serum amyloid A, a cardiovascular risk factor, as well as factor VIII in plasma and the factor VIII/von Willebrand factor ratio, indicating a slight effect on the balance of coagulation factors. Moreover, there was an increased urinary excretion of free 8-iso-prostaglandin2alpha, a major F2-isoprostane, though this was based on nine subjects only, indicating a temporary increase in free radical-mediated lipid peroxidation. Thus, wood-smoke particles at levels that can be found in smoky indoor environments seem to affect inflammation, coagulation, and possibly lipid peroxidation. These factors may be involved in the mechanisms whereby particulate air pollution affects cardiovascular morbidity and mortality. The exposure setup could be used to establish which particle characteristics are critical for the effects.

As part of the European Mercury Emissions from Chlor Alkali Plants (EMECAP) project, we tested the hypothesis that contamination of ambient air with mercury around chlor alkali plants using mercury cells would increase the internal dose of mercury in people living close to the plants. Mercury in urine (U-Hg) was determined in 225 individuals living near a Swedish or an Italian chlor alkali plant, and in 256 age- and sex-matched individuals from two reference areas. Other factors possibly affecting mercury exposure were examined. Emissions and concentrations of total gaseous mercury (TGM) around the plants were measured and modeled. No increase in U-Hg could be demonstrated in the populations living close to the plants. This was the case also when the comparison was restricted to subjects with no dental amalgam and low fish consumption. The emissions of mercury to air doubled the background level, but contributed only about 2 ng/m(3) to long-term averages in the residential areas. The median U-Hg levels in subjects with dental amalgam were 1.2 microg/g creatinine (micro/gC) in Italy and 0.6 microg/gC in Sweden. In individuals without dental amalgam, the medians were 0.9 microg/gC and 0.2 microg/gC, respectively. The number of amalgam fillings, as well as chewing, fish consumption, and female sex were associated with higher U-Hg. The difference between the countries is probably due to higher fish consumption in Italy, demethylated methyl mercury (MeHg) being partly excreted in urine. Post hoc power calculations showed that if the background mercury exposure is low it may be possible to demonstrate an increase in U-Hg of as little as about 10 ng/m(3) as a contribution to ambient mercury from a point source.

Personal exposures and indoor, residential outdoor, and urban background levels of PM(2.5) and PM(1) were measured simultaneously in Göteborg, Sweden. A total of 270 24 hour samples from 30 subjects were analyzed for elemental concentrations using X-ray fluorescence (XRF) spectroscopy. Personal exposures to PM(2.5) were significantly higher for Cl, Ca, Ti, and Fe compared with the other locations. For most elements, residential outdoor levels were significantly higher than urban background levels. Correlations between personal exposure and stationary measurements were moderate to high for Zn, Br, and Pb (r(s)= 0.47-0.81), while Ca and Cu showed low correlations. The penetration indoors from outdoors was 0.7, as calculated from S and Pb ratios. For the pairs of parallel PM(1) and PM(2.5) measurements, only Ca and Fe levels were significantly lower for PM(1) at all sites. Significant correlations were found between urban background mass concentrations and personal exposure levels for elements attributed to combustion processes (S, V, and Pb) and resuspended dust (Ti, Fe, and Zn), indicating that both sources could be relevant to health effects related to urban background mass. Air mass origin strongly affected the measured urban background concentrations of some elements (S, Cl, V, Ni, Br, and Pb). These findings were also seen for personal exposure (S, Cl, V, and Pb) and indoor levels (S, Cl, V, Ni, and Pb). No differences were seen for crustal elements. Air mass origin should be taken into account in the description and interpretation of time series studies of air pollution and health.

In the study reported here semipermeable membrane devices (SPMDs) were used to sample 28 PAHs and 19 PCBs in the gas phase in 15 single-family houses located in an area where domestic wood burning is widespread. Eight of the households used wood burning appliances whereas the others used other systems for residential heating. Most of the studied compounds were found in the houses: the PAHs at levels that were similar to or slightly higher than published SPMD-sampled levels for background or urban sites in Sweden, and the PCBs at levels that were somewhat lower than those recently found in both indoor and outdoor urban locations. A principal component analysis revealed that wood-burning heating systems may contribute to PAHs in indoor air. The sources may be emissions indoors or penetration from outdoors. The convenience of SPMD technology facilitates its use for semi-quantitative screening and monitoring of various persistent organic compounds indoors in dwellings and working environments.

Formaldehyde is a ubiquitous environmental pollutant and is probably carcinogenic to humans. Exposure to formaldehyde was investigated in the general population with personal as well as stationary measurements. The results from two campaigns in two Swedish cities are presented, including measurements of personal exposure among a total of 65 randomly selected subjects together with simultaneous measurements of individual indoor and outdoor concentrations. Diffusive GMD samplers were placed in the breathing zone, in the participants' bedrooms, and outside their homes for 24 h in campaign A and six days in campaign B. Repeated measurements were also conducted in order to study the variability between and within individuals. Median personal exposure to formaldehyde was 22 microg/m(3) (campaign A) and 23 microg/m(3) (campaign B), which is within the guideline value range of 12-60 microg/m(3) proposed in Sweden. Bedroom concentrations were generally slightly higher than personal exposure, while outdoor concentrations (measured only in campaign B) were low. In campaign B, the stationary measurements were used to model personal exposure. Bedroom concentrations were found to explain 90% of the variation of the measured personal exposure and predicted personal exposure nearly as well as an extended model that also included the outdoor contribution. Subjects living in single-family houses had significantly higher exposure to formaldehyde compared with subjects living in apartments. The 24-h and 6-day sampling periods yield a relatively low within-individual variability for formaldehyde measurements with GMD samplers.

Human exposure to methylmercury occurs mainly via consumption of fish. The aim of the study was to investigate the influence of freshwater fish consumption on mercury levels in hair, blood, urine, and end-exhaled air. Twenty subjects without dental amalgam fillings were recruited from sport-fishing societies. They ranged in age from 61 to 87 yr. Six individuals ate freshwater fish at least once a week and were categorized as high consumers. Eight individuals were classified as medium consumers and ate freshwater fish at least once a month but less than once a week. Six individuals were categorized as low consumers and had not eaten freshwater fish in the past 3 mo. Among the high consumers, median concentrations of mercury were 8.6 microg/L in blood, 2.4 microg/g in hair, 10 pg/L in end-exhaled air, and 1.1 microg/g creatinine in urine. The relationship between freshwater fish consumption and mercury was significant in all biological media. The high-consumption group had much higher mercury levels in blood (9-fold), hair (7-fold), alveolar air (3-fold), and urine (15-fold) than the low-consumption group. The latter finding may be explained by demethylation of methylmercury in the body. The ratio between mercury concentration in blood and hair was 1:270. This implies that the typical blood-hair ratio of 1:250, specified by the World Health Organization (WHO) in 1990, is valid also for exposure to low amounts of methylmercury.

Hair mercury levels were determined in 143 individuals from households of members in angling societies in an area of Sweden with many lakes that have freshwater fish with relatively high mercury levels. Thus, the individuals had a potentially high intake of methyl mercury. The mean mercury concentration of pike and perch was approximately 0.7 microg/g. One-third of the subjects consumed these freshwater fish at least once a week. As could be expected, there was a clear increase in hair Hg with reported freshwater fish consumption (P < 0.001). The median mercury level in hair was 0.9 microg Hg/g for the whole group, and for those who reported consumption of freshwater fish at least once a week it was 1.8 microg/g. The highest hair mercury level was 18.5 microg/g, in a man who consumed pike and perch several times per week. Men had higher hair Hg than women, also when stratified for fish consumption. This was verified in 32 couples, of which the man and woman consumed the same fish and reported the same consumption. The median hair mercury level in these 32 couples was 1.3 microg/g for men and 0.8 microg/g for women (P = 0.002). About half of the subjects had hair mercury exceeding 1 microg/g, corresponding to the reference dose (RfD) of 0.1 microg of mercury per kilogram body weight set by the US Environmental Protection Agency. Although the RfD applies to all populations, the most at-risk group at these levels is pregnant women. There were only 2 women (of 12) of fertile age with hair mercury above 1 microg/g. In Sweden pregnant women are advised not to eat perch and pike at all during pregnancy. Since fish is rich in many important nutrients, it is unsatisfactory that fish consumption must be restricted, and thus there is a need to reduce mercury levels in fish.

The authors used tests of attention and memory, which are sensitive to the influence of aging, to explore possible adverse effects on cognitive functioning following past heavy exposure to solvent-based glues, with special reference to dose-effect relationships and interactions with the aging process. The study included 41 floor layers and 40 carpenters (referents) who participated in a longitudinal follow-up assessment. The authors assessed cognitive functioning with the following tests: trail-making, color words, and word recall. Higher cumulative exposure was associated with poorer test performance that was related to concept shifting, episodic memory, and speed of congruent and incongruent color naming. The magnitude of the decrements in memory tasks was equivalent to about 20 yr of age-related decline. Dose-effect relationships were seen mainly for contact adhesives, and there was partial evidence for an interaction between exposure and aging.

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.

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.

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.

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.

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.

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.

The objective of this study was to determine the concentrations of mercury in organs of occupationally exposed workers using in vivo x-ray fluorescence analysis. Twenty mercury exposed workers and twelve occupationally unexposed referents participated in the study. Their mercury levels in kidney, liver and thyroid were measured using a technique based on excitation with partly plane polarized photons. The mercury levels in blood and urine were determined using atomic absorption spectrophotometry. The detection limit for mercury in the kidney was exceeded in nine of the exposed workers, but in none of the referents. The mean kidney mercury concentration (including estimates below the detection limits) was 24 micrograms g-1 in the exposed workers, and 1 microgram g-1 in the referents. The association between mercury in the kidney and in urine was statistically significant, but it was unclear whether the relation was linear. The measurements on liver (n = 10) and thyroid (n = 8) in the exposed workers showed mercury levels below the detection limit. The study shows that it is now possible to measure the mercury concentrations in kidneys of occupationally exposed persons, using in vivo x-ray fluorescence. The estimated concentrations are in reasonable agreement with the limited human autopsy data, and the results of animal studies.

Objectives: To describe people with high mercury (Hg) uptake from their amalgam fillings, and to estimate the possible fraction of the occupationally unexposed Swedish population with high excretion of urinary Hg., Methods: Three case reports are presented. The distribution of excretion of urinary Hg in the general population was examined in pooled data from several sources., Results: The three cases excreted 23-60 micrograms of Hg/day (25-54 micrograms/g creatinine), indicating daily uptake of Hg as high as 100 micrograms. Blood Hg was 12-23 micrograms/l, which is five to 10 times the average in the general population. No other sources of exposure were found, and removal of the amalgam fillings resulted in normal Hg concentrations. Chewing gum and bruxism were the probable reasons for the increased Hg uptake. Extrapolations from data on urinary Hg in the general population indicate that the number of people with urinary excretion of > or = 50 micrograms/g creatinine could in fact be larger than the number of workers with equivalent exposure from occupational sources., Conclusion: Although the average daily Hg uptake from dental amalgam fillings is low, there is a considerable variation between people; certain people have a high mercury uptake from their amalgam fillings.

The aim of the present cohort study was to investigate whether exposure to paper dust causes increased risk for respiratory symptoms or asthma. The cohort included all workers at a soft paper mill who had worked there for more than 1 year 1960-1986 (n = 1,697). Randomly selected inhabitants of the mill town (n = 781) were used as unexposed referents. Both groups were investigated using a postal questionnaire. From the paper mill cohort, workers with high cumulative exposure (n = 313), with medium cumulative exposure (n = 321), and with low cumulative exposure (n = 338) to paper dust were selected. In the 1960s and 1970s, the dust levels were between 5 and 10 mg/m3. After adjustment for smoking and gender, paper dust exposure resulted in elevated prevalence ratios for chronic cough, chronic phlegm, wheeze, and breathlessness. The prevalence ratios ranged from 1.3 to 2.5. No significantly increased risk of asthma was found among the exposed, incidence rate ratio 1.4 (95% confidence interval 0.93-1.8). Among the exposed, there was an insignificantly increasing incidence rate ratio, 1.0, 1.4, 2.1, with increasing cumulative exposure. In conclusion, an increased risk for respiratory symptoms was observed among workers exposed to paper dust, but the study does not permit any definite conclusions regarding asthma and paper dust exposure.

Mercury (Hg) and protein levels in cerebrospinal fluid (CSF), and mercury in plasma (P), erythrocytes (Ery), and urine (U), were determined in 10 workers exposed to mercury vapor for 2-28 (median 13) years and in 16 occupationally unexposed referents. CSF-Hg was analyzed using radiochemical neutron activation analysis and P-Hg, Ery-Hg, and U-Hg were analyzed using cold-vapor atomic absorption spectrometry. P-Hg and U-Hg were significantly higher, but Ery-Hg was similar in the exposed workers (37 nmole/liter, 16 nmole/mmole creatinine, and 56 nmole/liter, respectively) compared with the referents (7.1 nmole/liter, 1.9 nmole/mmole creatinine, and 52 nmole/liter, respectively). CSF-Hg was correlated to P-Hg, and in workers with current high exposure (P-Hg > 50 nmole/liter), the CSF-Hg was significantly higher than in the reference group (1.08 versus 0.35 nmole/liter; P = 0.002). In two individuals, studied after ceased occupational exposure, a decrease of CSF-Hg was seen. There were no indications of changes in the CSF protein pattern in the exposed workers.

The elimination of mercury (Hg) in blood was investigated in 14 chloralkali workers exposed to metallic Hg vapour for 1-24 (median 10) years. Blood and urine samples were collected on several (median eight) occasions during a period of 17-26 days. The initial Hg concentrations were about 80 nmol/l in whole blood (B-Hg) and 17 nmol/mmol creatinine in urine (U-Hg). The decrease in Hg in whole blood, plasma (P) and erythrocytes (Ery) was best characterised by a two compartment model. In a model with a common half life for all subjects, the best fit for B-Hg was obtained with half lives of 3.8 days for a fast phase and 45 days for a slow phase. The half life of the fast phase was shorter for P-Hg than for Ery-Hg, whereas the opposite was the case for the slow phase. The half lives of the slow phases in whole blood and plasma were longer, and the relative fractions of the slow phases were higher (about 50%) after long term exposure than those (about 20%) reported after brief exposure. Slower elimination indicates higher accumulation of Hg in organs with long half lives, and possibly the presence of at least one additional, even slower compartment. The U-Hg fluctuated substantially during the sampling period, and average concentrations decreased only slightly.

The decrease in mercury (Hg) levels in whole blood (B), plasma (P), erythrocytes (Ery), and urine (U) was investigated in nine men after 3 d of intense (greater than 100 micrograms/m3) exposure to metallic Hg vapor. In a model in which common half-times for all subjects were used, the best fit for B-Hg was obtained with half-times of 3.1 d for a fast phase and 18 d for a slow phase. P-Hg seemed to decay more rapidly than Ery-Hg. Peak U-Hg (morning, creatinine-corrected samples) was not observed until 2-3 wk after exposure. Thereafter, the median half-time was 40 d (assuming individual one-compartment models). In a model for which common half-times were used, the point estimates were 59 d for a one-compartment model and 28 and 141 d for a two-compartment model. The fractions of the fast phases (i.e., two-compartment models with common half-times) were 80% for B-Hg and 84% for U-Hg.

For 26 chloralkali workers exposed to inorganic mercury and 26 age-matched, occupationally unexposed referents, the frequency and size distribution of micronuclei were determined in peripheral lymphocytes stimulated with either phytohemagglutinin or pokeweed mitogen. For the exposed workers the mean concentrations of mercury in urine, plasma, and erythrocytes were 16 nmol/mmol of creatinine, 48 nmol/l, and 78 nmol/l, respectively, and their mean exposure time was 10 years. Neither the frequency nor the size of micronuclei was significantly different in the two groups; nor were there any correlations to current mercury levels. However, in the exposed group, and with phytohemagglutinin as the mitogen, a statistically significant correlation between previous exposure to mercury (cumulative exposure or number of blood mercury peaks) and the frequency of micronuclei was found. This association was also present when the effects of age and smoking were allowed for, and it may indicate an accumulation of cytogenetic effects in T-lymphocytes.

A slowly developing, mainly sensory, polyneuropathy was found in a 60-year-old man exposed to n-hexane (10-100 mg/m3) for 30 years in a mountain fuel stockpile. The nerve damage was verified by electromyography and sural nerve biopsy, and it is proposed that also a low-grade, but prolonged, exposure to n-hexane may cause polyneuropathy.

In an earlier case-referent study from a soft-paper mill with levels of paper dust exceeding 5 mg/m3, an increased mortality was found (OR = 3.8, p less than 0.05) from asthma and chronic obstructive pulmonary disease (COPD) among the employed. Furthermore, other studies on paper mill workers have also indicated an increased mortality from lung cancer. The main objectives of the present case-referent study were to investigate the mortality from asthma. COPD, and lung cancer in two other Swedish paper mills. In these mills, the levels of paper dust have been below 3 mg/m3. The subjects for the study were all men who died between 1961 and 1985 from asthma and COPD (n = 31), respiratory cancer (n = 27), and stomach cancer (n = 33) selected in three parishes surrounding two paper mills. As referents we randomly selected about six times as many men who had died from nonmalignant nonrespiratory diseases in these parishes (n = 550). On the basis of information found in the personnel records in the mills, the men were classified into different occupational categories or as unexposed. No increased risk of asthma or COPD was found among the workers exposed to paper dust. However, it was found that there was significantly increased mortality (OR = 5.7, p less than 0.05) for asthma and COPD among workers in a previous log sorting department. The study also showed a significantly increased risk of lung cancer (OR = 2.1, p less than 0.05) among maintenance workers. There was no increased risk of stomach cancer in the study.(ABSTRACT TRUNCATED AT 250 WORDS)

In a mercury mobilization test, 0.3 g of the complexing agent sodium 2,3-dimercaptopropane-1-sulfonate (DMPS) was given orally to 10 workers with moderate occupational exposure to elemental mercury vapour, to 8 dentists with slight exposure, to 18 matched controls, and to 5 referents without amalgam fillings. In the workers, DMPS caused an increase in 24-h urinary mercury excretion by a factor of 10; in the dentists, 5.9; in the controls, 5.3; and in the amalgam-free referents, 3.8. Of the mercury excreted during 24 h, 59% appeared during the first 6 h. Close, albeit non-linear, associations were found between mobilized mercury and the premobilization mercury levels in plasma and urine, but not with the duration of occupational exposure or the rough estimate of the integrated function of blood levels vs time. The present data indicate that mercury mobilized after a single DMPS dose in close connection with exposure is mainly an index of recent exposure and is not significantly affected by slow body pools or long-term exposure.

Cerebrospinal fluid was examined for 23 patients with chronic toxic encephalopathy after heavy exposure to organic solvents and 23 healthy age-matched referents. No differences were found between the patients and referents with respect to the levels of albumin, immunoglobulin, prealbumin, alpha-1-antitrypsin, beta-2-microglobulin, haptoglobin, or the astroglial cell proteins S100 and glial fibrillary acidic protein in the cerebrospinal fluid. The albumin ratio was normal for both the patients and the referents. The patient group had had heavy exposure to organic solvents, but its members had not been exposed for at least one year before the study. It was concluded that, if exposure to organic solvents affects proteins in cerebrospinal fluid, such effects are probably reversible.

The monitoring of exposure to mercury in the Swedish chloralkali industry started in 1946 and became common in the 1960s. During the 1970s both urinary and blood mercury (U-Hg, B-Hg) concentrations decreased substantially. The mean (geometric) U-Hg was 500-700 nmol l.-1 in the 1960s as compared with 150 nmol l.-1 today. During the 1970s the mean (geometric) B-Hg declined from about 100 to 40 nmol l.-1. Nowadays high values, U-Hg greater than 1500 nmol l.-1 or B-Hg greater than 600 nmol l.-1, are very rare whereas in the 1950s and the 1960s such peak values were found among 30% of the workers. The most effective measures taken were the reduction of the hydrogen discharges from the process and the replacement of graphite anodes by dimensionally stable anodes which require less frequent maintenance. Today efficient cleaning and continuous monitoring make it possible to keep the exposure levels low. The use of respiratory protection equipment is, however, still necessary during certain maintenance operations.

The characteristics of airborne dust in a soft paper production plant have been characterized by scanning and transmission electron microscopy. A combination of X-ray diffraction, electron diffraction and energy-dispersive X-ray flouresence spectroscopy (EDX) was used to determine the structure and composition of the different components. Size distribution determination and phase identification were carried out. Besides the cellulose fibres, fibres of kaolinite, wollastonite, talc and other silicates were also identified. Gravimetric analysis and fibre counting by optical phase contrast microscopy were used to determine total dust and fibre concentrations. Total dust exposure at the plant was generally below 3 mg m-3. The respirable fraction of the total dust concentrations varied from 15 to 70%. The inorganic dust was 36 +/- 15% of the total dust. The ratio of inorganic fibres to total fibre concentration at the plant varied between 10 and 15%.

The aim of the present cross-sectional study was to investigate whether long-term exposure to soft paper dust causes impairment of lung function. Exposed workers (n = 287) and referents (n = 79) were investigated, using spirometry and questionnaires. Personal samplings of total dust showed that the actual mean concentrations did not exceed 3 mg/m3. The exposed subjects were divided into three categories according to historical and present exposure to paper dust; low exposure, moderate exposure and high exposure. The study did not show any lung function impairment due to exposure to paper dust. However, the exposed subjects had a significantly increased prevalence of symptoms from both the upper and lower airways as well as an increased prevalence of reported asthma. On the basis of our study, we conclude that lung function impairment does not occur among workers exposed to mean levels of soft paper dust below 5 mg/m3.

The method is demonstrated in connection with a study of lung cancer among metal-workers exposed to oil mist. As exposure to oil mist is uncommon and lung cancer is common, the cohort study is the method of choice. Estimation of exposure, problems of selection, calculation of person-years etc is discussed. There was no increased morbidity from lung cancer.

Floorlayers and age matched carpenters with long (greater than or equal to 20 years) and short (5-10 years) occupational experience were compared with respect to chronic and acute neuropsychiatric, neuropsychological, and general health effects as related to different types of solvent exposure. An increased prevalence of neuropsychiatric illness occurred among floorlayers with long occupational experience, possibly caused by high levels of exposure which were present until the 1970s. The disease appears partly reversible since, at the time of the investigation, all had essentially recovered. Some impairment of performance in psychological tests was seen, however, in this group. Visuoanalytical impairment was associated with indices of exposure to glues based on alcohols whereas contact adhesives appeared more deleterious to perceptual functions. The increased prevalence of neuropsychiatric symptoms among the floorlayers was interpreted to reflect mainly acute effects on the central nervous system.

Analysis of data obtained by linking the 1960 Swedish Census and the Swedish Cancer Registry has demonstrated an increased risk of pleural mesothelioma among pulp and paper workers. The present study was undertaken with the aim of revealing possible environmental risk factors. The work histories of the 25 cases identified earlier were reviewed. "Certain" or "probable" exposure to asbestos was found among 70% of these workers. The study illustrates how linkage of official registers can be used to identify new risk environments and encourage the establishment of preventive measures.