Cadmium, total mercury, and lead in blood and associations with diet, sociodemographic factors, and smoking in Swedish adolescents.

BACKGROUND: Despite their vulnerability to the toxic effects of certain metals, biomonitoring data on adolescents are limited. In the present study, we assessed blood concentrations of toxic metals (cadmium [Cd], total mercury [Hg], and lead [Pb] in a national representative sample of Swedish adolescents. We also examined the associations of Cd, total Hg and Pb with habitual intakes of major energy-providing food groups and other possible determinants such as age, sex, household education, Nordic or non-Nordic origin, and smoking. METHODS: We analysed blood concentrations of Cd, total Hg, and Pb in a sample of 1099 adolescents from the Riksmaten Adolescents 2016-17 study in three age groups (mean age of 12, 15, and 18 years) using inductively coupled plasma mass spectrometry. The participants completed web-based questionnaires on food consumption frequency, sociodemographic factors and health status. Dietary data from two web-based 24-h dietary recalls were used to estimate the habitual intake of 10 major food groups. RESULTS: Almost all participants had detectable concentrations of Cd, total Hg, and Pb in whole blood. The median blood concentrations were 0.12 µg/L for Cd, 0.72 µg/L for total Hg, and 7.1 µg/L for Pb. Higher blood concentrations of Cd were observed in girls than in boys, whereas concentrations of total Hg and Pb were higher in boys. We observed an inverse association between Cd and meat intake. Total Hg concentrations were positively associated with intakes of fish, eggs, meat, and vegetables, and Pb concentrations were inversely associated with intakes of dairy products. Furthermore, smokers had higher concentrations of Cd and Pb. CONCLUSIONS: We found that fish was a potentially important source of exposure to total Hg in Swedish adolescents. No other food group was identified to have a strong impact on the blood levels of Cd, total Hg and Pb. Thirteen per cent of the adolescents had blood Pb concentrations above 12 µg/L, the reference point used in the risk assessment of Pb by the European Food Safety Authority (EFSA).

Roof cavity dust as an exposure proxy for extreme air pollution events.

Understanding exposure to air pollution during extreme events such as fire emergencies is critical for assessing their potential health impacts. However, air pollution emergencies often affect places without a network of air quality monitoring and characterising exposure retrospectively is methodologically challenging due to the complex behaviour of smoke and other air pollutants. Here we test the potential of roof cavity (attic) dust to act as a robust household-level exposure proxy, using a major air pollution event associated with a coal mine fire in the Latrobe Valley, Australia, as an illustrative study. To assess the relationship between roof cavity dust composition and mine fire exposure, we analysed the elemental and polycyclic aromatic hydrocarbon composition of roof cavity dust (<150µm) from 39 homes along a gradient of exposure to the mine fire plume. These homes were grouped into 12 zones along this exposure gradient: eight zones across Morwell, where mine fire impacts were greatest, and four in other Latrobe Valley towns at increasing distance from the fire. We identified two elements-barium and magnesium-as 'chemical markers' that show a clear and theoretically grounded relationship with the brown coal mine fire plume exposure. This relationship is robust to the influence of plausible confounders and contrasts with other, non-mine fire related elements, which showed distinct and varied distributional patterns. We conclude that targeted components of roof cavity dust can be a useful empirical marker of household exposure to severe air pollution events and their use could support epidemiological studies by providing spatially-resolved exposure estimates post-event.

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.

Short-term chamber exposure to low doses of two kinds of wood smoke does not induce systemic inflammation, coagulation or oxidative stress in healthy humans.

INTRODUCTION: Air pollution increases the risk of cardiovascular diseases. A proposed mechanism is that local airway inflammation leads to systemic inflammation, affecting coagulation and the long-term risk of atherosclerosis. One major source of air pollution is wood burning. Here we investigate whether exposure to two kinds of wood smoke, previously shown to cause airway effects, affects biomarkers of systemic inflammation, coagulation and lipid peroxidation. METHODS: Thirteen healthy adults were exposed to filtered air followed by two sessions of wood smoke for three hours, one week apart. One session used smoke from the start-up phase of the wood-burning cycle, and the other smoke from the burn-out phase. Mean particle mass concentrations were 295 µg/m³ and 146 µg/m³, and number concentrations were 140,000/cm³ and 100,000/cm³, respectively. Biomarkers were analyzed in samples of blood and urine taken before and several times after exposure. Results after wood smoke exposure were adjusted for exposure to filtered air. RESULTS: Markers of systemic inflammation and soluble adhesion molecules did not increase after wood smoke exposure. Effects on markers of coagulation were ambiguous, with minor decreases in fibrinogen and platelet counts and mixed results concerning the coagulation factors VII and VIII. Urinary F2-isoprostane, a consistent marker of in vivo lipid peroxidation, unexpectedly decreased after wood smoke exposure. CONCLUSIONS: The effects on biomarkers of inflammation, coagulation and lipid peroxidation do not indicate an increased risk of cardiovascular diseases in healthy adults by short-term exposure to wood smoke at these moderate doses, previously shown to cause airway effects.

Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans.

INTRODUCTION: Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. MATERIALS AND METHODS: Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM(2.5) were 295 µg/m(3) and 146 µg/m(3), number concentrations 140 000/cm(3) and 100 000/cm(3). Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. RESULTS: After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. CONCLUSIONS: The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.