Surgical smoke and ultrafine particles

© 2008 Brüske-Hohlfeld et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Immediate ozone effects on heart rate and repolarisation parameters in potentially susceptible individuals

Elevated ozone levels have been associated with cardiovascular morbidity and mortality. We investigated the effects of ozone on heart rate (HR) and repolarisation parameters in potentially susceptible populations

Hourly exposure to ultrafine particle metrics and the onset of myocardial infarction in Augsburg, Germany

BACKGROUND: Epidemiological evidence on the health effects of ultrafine particles (UFP) remains insufficient to infer a causal relationship that is largely due to different size ranges and exposure metrics examined across studies. Moreover, evidence regarding the association between UFP and cardiovascular disease at a sub-daily timescale is lacking.OBJECTIVE: We investigated the relationship between different particle metrics, including particle number (PNC), length (PLC), and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale.METHODS: We collected hourly air pollution and meteorological data from fixed urban background monitoring sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during 2005-2015. We conducted a time-stratified case-crossover analysis with conditional logistic regression to estimate the association between hourly particle metrics and MI cases, adjusted for air temperature and relative humidity. We also examined the independent effects of a certain particle metric in two-pollutant models by adjusting for copollutants, including particulate matter (PM) with an aerodynamic diameter of >= 10 mu m or 2.5 mu m (PM10 and PM2.5, respectively), nitrogen dioxide, ozone, and black carbon.RESULTS: Overall, a total of 5,898 cases of nonfatal MI cases were recorded. Exploratory analyses showed similar associations across particle metrics in the first 6-12 h. For example, interquartile range increases in PNC within the size range of 10-100 nm, PLC, and PSC were associated with an increase of MI 6 h later by 3.27% [95% confidence interval (CI): 0.27, 6.37], 5.71% (95% CI: 1.79, 9.77), and 5.84% (95% CI: 1.04, 10.87), respectively. Positive, albeit imprecise, associations were observed for PNC within the size range of 10-30 nm and 100-500 nm. Effect estimates for PLC and PSC remained similar after adjustment for PM and gaseous pollutants.CONCLUSIONS: Transient exposure to particle number, length, and surface area concentrations or other potentially related exposures may trigger the onset of nonfatal myocardial infraction

Short-term effects of air pollution: a panel study of blood markers in patients with chronic pulmonary disease

<p>Abstract</p> <p>Background</p> <p>Growing evidence indicates that ambient air pollution is associated with exacerbation of chronic diseases like chronic pulmonary disease. A prospective panel study was conducted to investigate short-term changes of blood markers of inflammation and coagulation in response to daily changes in air pollution in Erfurt, Germany. 12 clinical visits were scheduled and blood parameters were measured in 38 male patients with chronic pulmonary disease during winter 2001/2002. Additive mixed models with random patient intercept were applied, adjusting for trend, weekday, and meteorological parameters. Hourly data on ultrafine particles (UFP, 0.01-0.1 μm), accumulation mode particles (ACP, 0.1-1.0 μm), PM₁₀(particulate matter <10 μm in diameter), elemental (EC) and organic carbon (OC), gaseous pollutants (nitrogen monoxide [NO], nitrogen dioxide [NO₂], carbon monoxide [CO], and sulphur dioxide [SO₂]) were collected at a central monitoring site and meteorological data were received from an official network. For each person and visit the individual 24-hour average of pollutants immediately preceding the blood withdrawal (lag 0) up to day 5 (lag1-4) and 5-day running means were calculated.</p> <p>Results</p> <p>Increased levels of fibrinogen were observed for an increase in one interquartile range of UFP, PM₁₀, EC, OC, CO, and NO revealing the strongest effect for lag 3. E-selectin increased in association with ACP and PM₁₀with a delay of one day. The ACP effect was also seen with the 5-day-mean. The pattern found for D-dimer was inconsistent. Prothrombin fragment 1+2 decreased with lag 4 consistently for all particulate pollutants. Von Willebrand factor antigen (vWF) showed a consistent decrease in association with almost all air pollutants with all lags except for lag 0. No associations were found for C-reactive protein, soluble intercellular adhesion molecule 1, serum amyloid A and factor VII.</p> <p>Conclusion</p> <p>These results suggest that elevated concentrations of air pollution are associated with changes in some blood markers of inflammation and coagulation in patients with chronic pulmonary disease. The clinical implications of these findings need further investigation.</p

Impact of meteorological conditions on airborne fine particle composition and secondary pollutant characteristics in urban area during winter-time

The assessment of airborne fine particle composition and secondary pollutant characteristics in the case of Augsburg, Germany, during winter (31 January–12 March 2010) is studied on the basis of aerosol mass spectrometry (3 non-refractory components and organic matter, 3 positive matrix factorizations (PMF) factors), particle size distributions (PSD, 5 size modes, 5 PMF factors), further air pollutant mass concentrations (7 gases and VOC, black carbon, PM10, PM2.5) and meteorological measurements, including mixing layer height (MLH), with one-hourly temporal resolution. Data were subjectively assigned to 10 temporal phases which are characterised by different meteorological influences and air pollutant concentrations. In each phase hierarchical clustering analysis with the Ward method was applied to the correlations of air pollutants, PM components, PM source contributions and PSD modes and correlations of these data with all meteorological parameters. This analysis resulted in different degrees of sensitivities of these air pollutant data to single meteorological parameters. It is generally found that wind speed (negatively), MLH (negatively), relative humidity (positively) and wind direction influence primary pollutant and accumulation mode particle (size range 100–500 nm) concentrations. Temperature (negatively), absolute humidity (negatively) and also relative humidity (positively) are relevant for secondary compounds of PM and particle (PM2.5, PM10) mass concentrations. NO, nucleation and Aitken mode particle and the fresh traffic aerosol concentrations are only weakly dependent on meteorological parameters and thus are driven by emissions. These daily variation data analyses provide new, detailed meteorological influences on air pollutant data with the focus on fine particle composition and secondary pollutant characteristics and can explain major parts of certain PM component and gaseous pollutant exposure

Hourly Exposure to Ultrafine Particle Metrics and the Onset of Myocardial Infarction in Augsburg, Germany

BACKGROUND: Epidemiological evidence on the health effects of ultrafine particles (UFP) remains insufficient to infer a causal relationship that is largely due to different size ranges and exposure metrics examined across studies. Moreover, evidence regarding the association between UFP and cardiovascular disease at a sub-daily timescale is lacking. OBJECTIVE: We investigated the relationship between different particle metrics, including particle number (PNC), length (PLC), and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale. METHODS: We collected hourly air pollution and meteorological data from fixed urban Background: monitoring sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during 2005-2015. We conducted a time-stratified case-crossover analysis with conditional logistic regression to estimate the association between hourly particle metrics and MI cases, adjusted for air temperature and relative humidity. We also examined the independent effects of a certain particle metric in two-pollutant models by adjusting for copollutants, including particulate matter (PM) with an aerodynamic diameter of >= 10 mu m or 2.5 mu m (PM10 and PM2.5, respectively), nitrogen dioxide, ozone, and black carbon. RESULTS: Overall, a total of 5,898 cases of nonfatal MI cases were recorded. Exploratory analyses showed similar associations across particle metrics in the first 6-12 h. For example, interquartile range increases in PNC within the size range of 10-100 nm, PLC, and PSC were associated with an increase of MI 6 h later by 3.27% [95% confidence interval (CI): 0.27, 6.37], 5.71% (95% CI: 1.79, 9.77), and 5.84% (95% CI: 1.04, 10.87), respectively. Positive, albeit imprecise, associations were observed for PNC within the size range of 10-30 nm and 100-500 nm. Effect estimates for PLC and PSC remained similar after adjustment for PM and gaseous pollutants. CONCLUSIONS: Transient exposure to particle number, length, and surface area concentrations or other potentially related exposures may trigger the onset of nonfatal myocardial infraction

Changes in deceleration capacity of heart rate and heart rate variability induced by ambient air pollution in individuals with coronary artery disease

<p>Abstract</p> <p>Background and Objective</p> <p>Exposure to ambient particles has been shown to be responsible for cardiovascular effects, especially in elderly with cardiovascular disease. The study assessed the association between deceleration capacity (DC) as well as heart rate variability (HRV) and ambient particulate matter (PM) in patients with coronary artery disease (CAD).</p> <p>Methods</p> <p>A prospective study with up to 12 repeated measurements was conducted in Erfurt, Germany, between October 2000 and April 2001 in 56 patients with physician-diagnosed ischemic heart disease, stable angina pectoris or prior myocardial infarction at an age of at least 50 years. Twenty-minute ECG recordings were obtained every two weeks and 24-hour ECG recordings every four weeks. Exposure to PM (size range from 10 nm to 2.5 μm), and elemental (EC) and organic (OC) carbon was measured. Additive mixed models were used to analyze the association between PM and ECG recordings.</p> <p>Results</p> <p>The short-term recordings showed decrements in the high-frequency component of HRV as well as in RMSSD (root-mean-square of successive differences of NN intervals) in association with increments in EC and OC 0-23 hours prior to the recordings. The long-term recordings revealed decreased RMSSD and pNN50 (% of adjacent NN intervals that differed more than 50 ms) in association with EC and OC 24-47 hours prior to the recordings. In addition, highly significant effects were found for DC which decreased in association with PM_2.5, EC and OC concurrent with the ECG recordings as well as with a lag of up to 47 hours.</p> <p>Conclusions</p> <p>The analysis showed significant effects of ambient particulate air pollution on DC and HRV parameters reflecting parasympathetic modulation of the heart in patients with CAD. An air pollution-related decrease in parasympathetic tone as well as impaired heart rate deceleration capacity may contribute to an increased risk for cardiac morbidity and sudden cardiac death in vulnerable populations.</p

The procoagulant effects of fine particulate matter in vivo

Inhalation of fine particulate matter (<2.5 μm; fine PM) has been shown to increase the risk for cardiovascular events. In this letter, we reappraise the role of tissue factor (TF) antigen and we also summarize changes in measured coagulation proteins in humans and rodents by other studies with fine PM. By considering all studies including ours, we conclude that monitoring the overall coagulation state by measuring capacity assays such as thrombin generation, and quantification of TF activity would be more suitable than determining single coagulation proteins (such as TF antigen) in order to better assess the systemic prothrombotic effects of fine PM

Polygenic Parkinson's Disease Genetic Risk Score as Risk Modifier of Parkinsonism in Gaucher Disease

Background: Biallelic pathogenic variants in GBA1 are the cause of Gaucher disease (GD) type 1 (GD1), a lysosomal storage disorder resulting from deficient glucocerebrosidase. Heterozygous GBA1 variants are also a common genetic risk factor for Parkinson's disease (PD). GD manifests with considerable clinical heterogeneity and is also associated with an increased risk for PD. Objective: The objective of this study was to investigate the contribution of PD risk variants to risk for PD in patients with GD1. Methods: We studied 225 patients with GD1, including 199 without PD and 26 with PD. All cases were genotyped, and the genetic data were imputed using common pipelines. Results: On average, patients with GD1 with PD have a significantly higher PD genetic risk score than those without PD (P = 0.021). Conclusions: Our results indicate that variants included in the PD genetic risk score were more frequent in patients with GD1 who developed PD, suggesting that common risk variants may affect underlying biological pathways. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA