| 1. |
- Amato, Fulvio, et al.
(författare)
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Urban air quality : The challenge of traffic non-exhaust emissions
- 2014
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Ingår i: Journal of Hazardous Materials. - : Elsevier BV. - 0304-3894 .- 1873-3336. ; 275, s. 31-36
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Tidskriftsartikel (refereegranskat)abstract
- About 400,000 premature adult deaths attributable to air pollution occur each year in the European Region. Road transport emissions account for a significant share of this burden. While important technological improvements have been made for reducing particulate matter (PM) emissions from motor exhausts, no actions are currently in place to reduce the non-exhaust part of emissions such as those from brake wear, road wear, tyre wear and road dust resuspension. These "non-exhaust" sources contribute easily as much and often more than the tailpipe exhaust to the ambient air PM concentrations in cities, and their relative contribution to ambient PM is destined to increase in the future, posing obvious research and policy challenges.This review highlights the major and more recent research findings in four complementary fields of research and seeks to identify the current gaps in research and policy with regard to non-exhaust emissions. The objective of this article is to encourage and direct future research towards an improved understanding on the relationship between emissions, concentrations, exposure and health impact and on the effectiveness of potential remediation measures in the urban environment.
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| 2. |
- Baloch, Ramen Munir, et al.
(författare)
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Indoor air pollution, physical and comfort parameters related to schoolchildren's health : Data from the European SINPHONIE study
- 2020
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Ingår i: Science of the Total Environment. - : ELSEVIER. - 0048-9697 .- 1879-1026. ; 739
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Tidskriftsartikel (refereegranskat)abstract
- Substantial knowledge is available on the association of the indoor school environment and its effect among schoolchildren. In the same context, the SINPHONIE (School indoor pollution and health: Observatory network in Europe) conducted a study to collect data and determine the distribution of several indoor air pollutants (IAPs), physical and thermal parameters and their association with eye, skin, upper-, lower respiratory and systemic disorder symptoms during the previous three months. Finally, data from 115 schools in 54 European cities from 23 countries were collected and included 5175 schoolchildren using a harmonized and standardized protocol. The association between exposures and the health outcomes were examined using logistic regression models on the environmental stressors assessed in classroom while adjusting for several confounding factors; a VOC (volatile organic compound) score defined as the sum of the number of pollutants to which the children were highly exposed (concentration > median of the distribution) in classroom was also introduced to evaluate the mul tiexposu re - outcome association. Schoolchildren while adjusting for several confounding factors. Schoolchildren exposed to above or equal median concentration of PM2.5, benzene, limonene, ozone and radon were at significantly higher odds of suffering from upper, lower airways, eye and systemic disorders. Increased odds were also observed for any symptom (sick school syndrome) among schoolchildren exposed to concentrations of limonene and ozone above median values. Furthermore, the risks for upper and lower airways and systemic disorders significantly increased with the VOCs score. Results also showed that increased ventilation rate was significantly associated with decreased odds of suffering from eye and skin disorders whereas similar association was observed between temperature and upper airways symptoms. The present study provides evidence that exposure to IAPs in schools is associated with various health problems in children. Further investigations are needed to confirm our findings. (C) 2020 Elsevier B.V. All rights reserved.
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| 3. |
- Bølling, Anette Kocbach, et al.
(författare)
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Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines.
- 2012
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Ingår i: Particle and fibre toxicology. - : Springer Science and Business Media LLC. - 1743-8977. ; 9:1
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Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT: BACKGROUND: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in northern countries during the winter season. The overall aim of this study was therefore to investigate the cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. RESULTS: WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. CONCLUSION: The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
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| 4. |
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| 5. |
- Gerlofs-Nijland, Miriam E., et al.
(författare)
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Inhalation toxicity profiles of particulate matter : a comparison between brake wear with other sources of emission
- 2019
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Ingår i: Inhalation Toxicology. - : Taylor & Francis. - 0895-8378 .- 1091-7691. ; 31:3, s. 89-98
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Tidskriftsartikel (refereegranskat)abstract
- Objective: There is substantial evidence that exposure to airborne particulate matter (PM) from road traffic is associated with adverse health outcomes. Although it is often assumed to be caused by vehicle exhaust emissions such as soot, other components may also contribute to detrimental effects. The toxicity of fine PM (PM2.5; <2.5 µm mass median aerodynamic diameter) released from brake pads was compared to PM from other sources.Materials and methods: PM2.5 of different types of brake pads (low-metallic, semi-metallic, NAO and ECE-NAO hybrid), tires and road pavement, poultry as well as the combustion of diesel fuel and wood (modern and old-fashioned stove technologies) were collected as suspensions in water. These were subsequently aerosolized for inhalation exposures. Female BALB/cOlaHsd mice were exposed for 1.5, 3, or 6 hours by nose-only inhalation up to 9 mg/m 3 .Results: Neither cytotoxicity nor oxidative stress was observed after exposure to any of the re-aerosolized PM2.5 samples. Though, at similar PM mass concentrations the potency to induce inflammatory responses was strongly dependent on the emission source. Exposure to most examined PM2.5 sources provoked inflammation including those derived from the poultry farm, wear emissions of the NAO and ECE-NAO hybrid brake pads as well as diesel and wood combustion, as indicated by neutrophil chemoattractant, KC and MIP-2 and lung neutrophil influx.Discussion and conclusions: Our study revealed considerable variability in the toxic potency of brake wear particles. Understanding of sources that are most harmful to health can provide valuable information for risk management strategies and could help decision-makers to develop more targeted air pollution regulation.
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| 6. |
- Gerlofs-Nijland, Miriam E, et al.
(författare)
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Toxicity of coarse and fine particulate matter from sites with contrasting traffic profiles.
- 2007
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Ingår i: Inhalation Toxicology. - : Taylor & Francis. - 0895-8378 .- 1091-7691. ; 19:13, s. 1055-69
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Tidskriftsartikel (refereegranskat)abstract
- Residence in urban areas with much traffic has been associated with various negative health effects. However, the contribution of traffic emissions to these adverse health effects has not been fully determined. Therefore, the objective of this in vivo study is to compare the pulmonary and systemic responses of rats exposed to particulate matter (PM) obtained from various locations with contrasting traffic profiles. Samples of coarse (2.5 mu m-10 mu m) and fine (0.1 mu m-2.5 mu m) PM were simultaneously collected at nine sites across Europe with a high-volume cascade impactor. Six PM samples from various locations were selected on the basis of contrast in in vitro analysis, chemical composition, and traffic profiles. We exposed spontaneously hypertensive (SH) rats to a single dose (3 mg PM/kg body weight or 10 mg PM/kg body weight) of either coarse or fine PM by intratracheal instillation. We assessed changes in biochemical markers, cell differentials, and histopathological changes in the lungs and blood 24 h postexposure. The dose-related adverse effects that both coarse and fine PM induced in the lungs and vascular system were mainly related to cytotoxicity, inflammation, and blood viscosity. We observed clear differences in the extent of these responses to PM from the various locations at equivalent dose levels. There was a trend that suggests that samples from high-traffic sites were the most toxic. It is likely that the toxicological responses of SH rats were associated with specific PM components derived from brake wear (copper and barium), tire wear (zinc), and wood smoke (potassium).
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| 7. |
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| 8. |
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| 9. |
- Langrish, Jeremy P., et al.
(författare)
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Controlled exposures to air pollutants and risk of cardiac arrhythmia
- 2014
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Ingår i: Journal of Environmental Health Perspectives. - : Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 122:7, s. 747-753
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Epidemiological studies have reported associations between air pollution exposure and increases in cardiovascular morbidity and mortality. Exposure to air pollutants can influence cardiac autonomic tone and reduce heart rate variability, and may increase the risk of cardiac arrhythmias, particularly in susceptible patient groups. OBJECTIVES: We investigated the incidence of cardiac arrhythmias during and after controlled exposure to air pollutants in healthy volunteers and patients with coronary heart disease. METHODS: We analyzed data from 13 double-blind randomized crossover studies including 282 participants (140 healthy volunteers and 142 patients with stable coronary heart disease) from whom continuous electrocardiograms were available. The incidence of cardiac arrhythmias was recorded for each exposure and study population. RESULTS: There were no increases in any cardiac arrhythmia during or after exposure to dilute diesel exhaust, wood smoke, ozone, concentrated ambient particles, engineered carbon nanoparticles, or high ambient levels of air pollution in either healthy volunteers or patients with coronary heart disease. CONCLUSIONS: Acute controlled exposure to air pollutants did not increase the short-term risk of arrhythmia in participants. Research employing these techniques remains crucial in identifying the important pathophysiological pathways involved in the adverse effects of air pollution, and is vital to inform environmental and public health policy decisions.
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| 10. |
- Lucking, Andrew J, et al.
(författare)
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Diesel exhaust inhalation increases thrombus formation in man
- 2008
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 29:24, s. 3043-3051
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: Although the mechanism is unclear, exposure to traffic-derived air pollution is a trigger for acute myocardial infarction (MI). The aim of this study is to investigate the effect of diesel exhaust inhalation on platelet activation and thrombus formation in men. METHODS AND RESULTS: In a double-blind randomized crossover study, 20 healthy volunteers were exposed to dilute diesel exhaust (350 microg/m(3)) and filtered air. Thrombus formation, coagulation, platelet activation, and inflammatory markers were measured at 2 and 6 h following exposure. Thrombus formation was measured using the Badimon ex vivo perfusion chamber. Platelet activation was assessed by flow cytometry. Compared with filtered air, diesel exhaust inhalation increased thrombus formation under low- and high-shear conditions by 24% [change in thrombus area 2229 microm(2), 95% confidence interval (CI) 1143-3315 microm(2), P = 0.0002] and 19% (change in thrombus area 2451 microm(2), 95% CI 1190-3712 microm(2), P = 0.0005), respectively. This increased thrombogenicity was seen at 2 and 6 h, using two different diesel engines and fuels. Diesel exhaust also increased platelet-neutrophil and platelet-monocyte aggregates by 52% (absolute change 6%, 95% CI 2-10%, P = 0.01) and 30% (absolute change 3%, 95% CI 0.2-7%, P = 0.03), respectively, at 2 h following exposure compared with filtered air. CONCLUSION: Inhalation of diesel exhaust increases ex vivo thrombus formation and causes in vivo platelet activation in man. These findings provide a potential mechanism linking exposure to combustion-derived air pollution with the triggering of acute MI.
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