Search

Adverse cardiovascular effects are associated with both diesel exhaust and road traffic noise, but these exposures are hard to disentangle epidemiologically. We used an experimental setup to evaluate the impact of diesel exhaust particles and traffic noise, alone and combined, on intermediary outcomes related to the autonomic nervous system and increased cardiovascular risk. In a controlled chamber 18 healthy adults were exposed to four scenarios in a randomized cross-over fashion. Each exposure scenario consisted of either filtered (clean) air or diesel engine exhaust (particle mass concentrations around 300 µg/m3), and either low (46 dB(A)) or high (75 dB(A)) levels of traffic noise for 3 h at rest. ECG was recorded for 10-min periods before and during each exposure type, and frequency-domain heart rate variability (HRV) computed. Endothelial dysfunction and arterial stiffness were assessed after each exposure using EndoPAT 2000. Compared to control exposure, HRV in the high frequency band decreased during exposure to diesel exhaust, both alone and combined with noise, but not during noise exposure only. These differences were more pronounced in women. We observed no synergistic effects of combined exposure, and no significant differences between exposure scenarios for other HRV indices, endothelial function or arterial stiffness. Three-hour exposure to diesel exhaust, but not noise, was associated with decreased HRV in the high frequency band. This indicates activation of irritant receptor-mediated autonomic reflexes, a possible mechanism for the cardiovascular risks of diesel exposure. There was no effect on endothelial dysfunction or arterial stiffness after exposure. [ABSTRACT FROM AUTHOR]

Context: Professional ski waxers are exposed to particulate matter (PM) during work, but little is known about untoward pulmonary effects. Objectives: The aim was to study lung function and pneumoproteins in professional ski waxers before and during exposure to PM generated during ski waxing and ski preparation. Material and methods: Forty-five male professional ski waxers examined on an exposure-free day in the morning and at least 6 h later were re-examined during ski waxing 2 d later in a cross-shift study. Pulmonary function and gas diffusion capacity were measured and Clara cell protein 16 (CC-16), surfactant protein A and D (SP-A and SP-D), and C-reactive protein (CRP) were determined in serum. PM was collected by personal sampling. Results: The mean PM concentrations in the respirable and in the inhalable aerosol fraction in air samples collected during waxing were 3.1 mg/m3 and 6.2 mg/m3, respectively. The mid expiratory flow (MEF75%) was significantly lower during exposure. The concentrations of CRP increased significantly by more than 100% during ski waxing, and SP-D and CC-16 were significantly lower during the exposed day as compared with the non-exposed day. The results further suggest that SP-D and CC-16 in serum are affected by diurnal variations. No significant alterations were observed for the lung diffusion capacity. Discussion and conclusions: The results suggest that exposure to PM generated during ski waxing may induce pulmonary inflammation with reduced flow in small airways. The increased CRP concentrations indicate the induction of systemic inflammation in ski waxers during exposure. [ABSTRACT FROM AUTHOR]

Context: Urban particulate air pollution is associated with cardiovascular diseases and mortality, possibly mediated through systemic inflammation and increased blood viscosity. Objectives: To examine short-term effects of exposure to urban air pollution on blood biomarkers for systemic inflammation and coagulation in a panel of healthy adults living in Gothenburg, Sweden. Materials and methods: The 16 volunteers, all non-smokers, median age 35 years, were called for blood sampling the morning after a day with high levels of urban particulate matter (PM10 > 30 µg/m3) or a day with low levels (PM10 < 15 µg/m3 and NO2 < 35 µg/m3). Associations between exposure to air pollution and each biomarker (C-reactive protein, fibrinogen, serum amyloid A, coagulation factor VIII, plasminogen activator inhibitor-1, p-selectin, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, Clara cell protein 16 and surfactant protein D) were examined using a linear mixed-effects model. Results: In total, 12 sampling sessions were performed, six after high-pollution and six after low-pollution days, over 21 months. The ratio of air pollution levels between high- and low-pollution days was five for PM10 (median: 49 and 10 µg/m3) and two for NO2 (median: 47 and 24 µg/m3). No significant increase in blood levels of any of the biomarkers were seen after days with high air pollution levels compared with low levels. Conclusion: Biomarkers of inflammation and coagulation were not found to be significantly increased in the mornings after days with elevated levels of urban air pollution compared with low levels when performing repeated blood samplings in healthy volunteers. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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 PM2.5 were 295 µg/m3 and 146 µg/m3, number concentrations 140 000/cm3 and 100 000/cm3. 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. [ABSTRACT FROM AUTHOR]

Objective. The objective of this study is to examine the influence of storage time at −20°C on the concentration of albumin, γ-glutamyl transpeptidase (γ-GT), N-acetyl-β--glucosaminidase (NAG), α1-microglobulin (A1M) and creatinine in a large sample of healthy children. Material and methods. The New England Children's Amalgam Trial followed 534 children, aged 6-10 at baseline, for 5 years, with annual urine collections. Urine samples were analysed for creatinine, albumin, γ-GT, NAG and A1M concentrations. Repeated measures analysis of covariance was used to model the effect of storage time on these concentrations. Results. The γ-GT concentration decreased significantly with storage time at −20°C. There was also a limited decrease in NAG. Albumin, A1M and creatinine concentrations did not appear to be affected by storage time at −20°C. Conclusions. If it is necessary to interpret results from samples stored for a long time at −20°C, it is advisable to account for storage time in statistical models. [ABSTRACT FROM AUTHOR]

Objective: To provide recommendations for design and analysis of studies using urine specimens to evaluate renal function or mercury excretion in children. Methods: An analysis of mercury, albumin, γ-glutamyl transpeptidase (γ-GT) and N-acetyl-β-D-glucosaminidase (NAG) concentrations was carried out. Results: Mercury concentration and creatinine-corrected renal markers were higher in daytime compared with overnight samples. Excretion rates increased with urinary flow rate. γ-GT and NAG concentrations decreased with storage time at −20°C. Differences by age, sex and race were noted. Conclusions: We recommend use of these creatinine-corrected markers and collection of timed overnight urine samples, stored at −70°C, with control for urinary flow rate, age, sex and race in statistical models. [ABSTRACT FROM AUTHOR]

Pneumoproteins, biomarkers of systemic inflammation and endothelial activation were studied across a season in 72 asphalt pavers, 32 asphalt plant operators and 19 asphalt engineers. Smokers had lower concentrations of Clara cell protein (CC-16) and surfactant protein A, but higher concentrations of surfactant protein D, interleukin 6, C-reactive protein, fibrinogen and intercellular adhesion molecule (ICAM)-1 than non-smokers. Smokers reporting wheezing had lower mean CC-16 concentration than smokers not reporting wheezing (5.7 vs 8.6 µg l−1; p = 0.05). Cholesterol, P-selectin and ICAM-1 were lower in pavers and operators at the end compared with the start of the season. This may be related to increased physical activity during the season. [ABSTRACT FROM AUTHOR]

Urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) is widely used as a marker of oxidative stress. Here we report the comparison of two, distinct chromatographic assays with an enzyme-linked immunosorbent assay (ELISA). The chromatographic assays displayed good agreement (r =:0.89, p < 0.0001), whereas there was markedly worse, albeit still significant, agreement with the ELISA (high-pressure liquid chromatography followed by gas chromatography (HPLC-GC/MS), r = 0.43; HPLC with electrochemical detection (HPLC-EC), r = 0.56; p < 0.0001). Mean values differed significantly between the chromatographic assays and the ELISA (HPLC-GC/MS 3.86, HPLC-EC 4.20, ELISA 18.70 ng mg-1 creatinine; p < 0.0001). While it is reassuring to note good agreement between chromatographic assays, this study reveals significant short-comings in the ELISA, which brings into question its continued use in its present form. [ABSTRACT FROM AUTHOR]

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 μ g / m 3 , and number concentrations were 95,000–180,000/ cm 3 . About half of the particles were ultrafine ( 2α , a major F 2 -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. [ABSTRACT FROM AUTHOR]

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 PM 2.5 and PM 1 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 μm), as well as nitrous oxides, CO 2 , 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 μg/m 3 ) was in the PM 1 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. [ABSTRACT FROM AUTHOR]

Examines the kinetics of mercury (Hg) in blood and urine after metallic vapor exposure. Consideration on choice of starting point for decay calculations; Effect of B-Hg decline on kidney; Factors contributing to interindividual variation of U-Hg decay.