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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.

Objectives: To describe the process for obtaining mercury and the historical exposure of Almadén miners to mercury., Methods: Information on every workplace and historical data on production, technological changes in the productive process and biological and environmental values of mercury was collected. A job-exposure matrix was built with these values and the exposure to inorganic mercury was estimated quantitatively as mug/l of urine mercury. A cumulative exposure index was calculated for every worker by adding the estimates for every year in the different workplaces., Results: In the mine, the highest exposures occurred during drilling, with values up to 2.26 mg/m3 in air, 2194 microg/l in urine and 374 microg/l in blood. Furnace operation and cleaning were the tasks with the highest values in metallurgy, peaking up to 3.37 mg/m3. The filling of bottles with mercury by free fall gave values within a range of 1.13-2.43 mg/m3 in air; these values dropped to 0.32-0.83 mg/m3 after introducing a new ventilation system. The toxicity effects of high doses of inorganic mercury on the central nervous and urinary systems have been known for decades., Conclusions: The exposure of the workers in Almadén mines to mercury has been very high. The extremely high content cinnabar ore of the mine explains the increased concentrations of mercury in air at the work places. This, together with inadequate working conditions, explains the high mercury levels found in blood and urine during the study period.

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.

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.

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.

Objective: The aim was to study whether functional impairment of the pituitary, thyroid, testes, and adrenal glands of humans occupationally exposed to mercury (Hg) vapour can be shown as a result of accumulation of Hg in these glands., Methods: Basal concentrations of thyrotrophin (TSH), prolactin, free thyroxine (free T4), free 3,5,3'-triiodothyronine (free T3), antibodies against thyroperoxidase, and testosterone in serum, as well as cortisol in morning urine were measured in 41 chloralkali workers exposed (10 years on average) to Hg vapour, and in 41 age matched occupationally unexposed referents. The chloralkali workers had a mean urinary Hg concentration (U-Hg) of 15 nmol/mmol (27 micrograms/g) creatinine, and a mean blood Hg concentration (B-Hg) of 46 nmol/l. For the reference group U-Hg and B-Hg were 1.9 nmol/mmol (3.3 micrograms/g) creatinine and 17 nmol/l respectively., Results: The serum free T4 concentration and the ratio free T4/free T3 were slightly, but significantly, higher in the subgroups with the highest exposure, and the serum free T3 was inversely associated with cumulative Hg exposure. This indicates a possible inhibitory effect of mercury on 5'-deiodinases, which are responsible for the conversion of T4 to the active hormone T3. Serum total testosterone, but not free testosterone, was positively correlated with cumulative Hg exposure. Prolactin, TSH and urinary cortisol concentrations were not significantly associated to exposure., Conclusion: Apart from inhibition of the deiodination of T4 to T3, the endocrine functions studied seem not to be affected by exposure to Hg vapour at the exposure levels of the present study. Growth hormone secretion was not studied.

The elimination of mercury (Hg) in urine was investigated in 12 former chloro-alkali workers exposed to metallic Hg vapour for two to 18 (median five) years. Morning urine samples were taken on several (median 9) occasions after change of employment or retirement. The median follow up time was 28 months. The decrease in concentration of Hg in urine (U-Hg) was well characterised by a one compartment model. Three different regression methods were used; non-linear least squares regression (NLSR), weighted non-linear least squares regression (WNLSR), and linear least squares regression (LLSR) after log transformation of the U-Hg data. The median half life from the WNLSR method was 55 days. There were no large differences in the half life estimates given by the WNLSR or the NLSR methods, but for five subjects the LLSR method gave poor fits. There was a non-significant tendency towards longer half lives with higher initial U-Hg. About three years after the cessation of occupational exposure a mobilisation test with 2,3-dimercaptopropane-1-sulphonate (DMPS) was performed on seven subjects. Excretion of Hg, copper (Cu), and zinc (Zn) in urine was estimated before and after the ingestion of 300 mg of DMPS. Treatment with DMPS increased 24 hour urinary excretion by a factor of 7.6 for Hg, 12 for Cu, and 1.5 for Zn. The relative increase in U-Hg was not significantly higher than that obtained in a previous study of an occupationally unexposed group. A major proportion (62%) of Hg excreted during 24 hours after DMPS appeared in the first six hours.