Airway inflammatory response to diesel exhaust generated at urban cycle running conditions

Sehlstedt, Maria; Behndig, Annelie F.; Boman, Christoffer; Blomberg, Anders; Sandström, Thomas; Pourazar, Jamshid

doi:10.3109/08958378.2010.529181

Cited by 38 publications

(31 citation statements)

References 21 publications

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“…When it comes to respiratory effects of diesel exhaust generated during idling and transient driving, so far only one study has been performed using the transient driving condition. It showed that the airway inflammatory response may be less pronounced compared with after idling (Salvi et al, 1999;Sehlstedt et al, 2010). It is plausible that differences in particle deposition and the characteristics investigated in this study (size, morphology, volatile vs. core mass fraction, etc.)…”

Section: Implications For Health Effectsmentioning

confidence: 67%

Experimental determination of deposition of diesel exhaust particles in the human respiratory tract

Rissler

Swietlicki

Bengtsson

et al. 2012

Journal of Aerosol Science

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128

104

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a b s t r a c tDiesel emissions are a major contributor to combustion-generated airborne ambient particles. To understand the role of diesel particulate emissions on health effects, it is important to predict the actual particulate dose deposited in the human respiratory tract, with respect to number, surface area and mass. This is complicated by the agglomerate nature of some of these particles. In this study the respiratory tract deposition fraction in the size range 10-500 nm, was determined for 10 healthy volunteers during both idling and transient engine running conditions of a heavy duty diesel engine. The aerosol was characterized with respect to both chemical and physical properties including size resolved particle effective density. The dominating part of the emitted particles had an agglomerate structure. For those formed during transient running conditions, the relationship between particle mass and mobility diameter could be described by a power law function. This was not the case during idling, most likely because of volatile compounds condensing on the agglomerates. The respiratory tract particle deposition revealed large intra-subject variability with some subjects receiving a dose that was twice as high as that of others, when exposed to the same particle concentration. Associations were found between total deposited fractions (TDF), and breathing pattern. There was a difference between the idling and transient cycle with TDF being higher with respect to number during idling. The measured size-dependent deposition fraction of the agglomerated exhaust particles from both running conditions was nearly identical and closely resembled that of spherical hydrophobic particles, if plotted as a function of mobility diameter. Thus, for the size range covered, the mobility diameter could well describe the diameter-dependent particle respiratory tract deposition probability, regardless of the agglomeration state of the particles. Whilst mobility diameter well describes the deposition fraction, more information about particle characteristics is needed to convert this to volume equivalent diameter or estimate dose with respect to surface area or mass. A methodology is presented and applied to calculate deposited dose by surface area and mass of agglomerated particles. The methodology may be useful in similar studies estimating dose to the lung, deposition onto cell cultures and in animal studies.

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Section: Implications For Health Effectsmentioning

confidence: 67%

Experimental determination of deposition of diesel exhaust particles in the human respiratory tract

Rissler

Swietlicki

Bengtsson

et al. 2012

Journal of Aerosol Science

Self Cite

128

104

View full text Add to dashboard Cite

show abstract

“…(76–77) Another recent study examined diesel exhaust produced under realistic conditions to simulate actual driving conditions and emissions. (79) Evaluating inflammatory markers 6 hours after a 1 hour exposure, they found increased expression of p-selectin (p=0.036) and vascular cell adhesion molecule-1 (p=0.030) in bronchial mucosal biopsies as well as the novel finding of increased eosinophils in bronchial alveolar lavage (p=0.017), not previously seen under idling engine conditions. The implications for diesel potentiation of allergic respiratory disease are substantial, especially in light of previous experimental work.…”

Section: Mechanistic Insightmentioning

confidence: 88%

Respiratory health effects of air pollution: Update on biomass smoke and traffic pollution

Laumbach

Kipen

2012

Journal of Allergy and Clinical Immunology

397

244

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Mounting evidence suggests that air pollution contributes to the large global burden of respiratory and allergic diseases including asthma, chronic obstructive pulmonary disease, pneumonia and possibly tuberculosis. Although associations between air pollution and respiratory disease are complex, recent epidemiologic studies have led to an increased recognition of the emerging importance of traffic-related air pollution in both developed and less-developed countries, as well as the continued importance of emissions from domestic fires burning biomass fuels primarily in the less-developed world. Emissions from these sources lead to personal exposures to complex mixtures of air pollutants that change rapidly in space and time due to varying emission rates, distances from source, ventilation rates, and other factors. Although the high degree of variability in personal exposure to pollutants from these sources remains a challenge, newer methods for measuring and modeling these exposures are beginning to unravel complex associations with asthma and other respiratory disease. These studies indicate that air pollution from these sources is a major preventable cause of increased incidence and exacerbation of respiratory disease. Physicians can help to reduce the risk of adverse respiratory effects of exposure to biomass and traffic air pollutants by promoting awareness and supporting individual and community-level interventions.

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“…Healthy and asthmatic volunteers were exposed in an exposure chamber to either DE concentrations of 300 μg/m 3 (measured as PM 10 ) for 1 h [17-19] or 100 μg/m 3 for 2 h [20,21]. The results demonstrated that DE exposure caused inflammatory responses at 6 h and 18 h. This was indicated by increased cell counts (neutrophils, B lymphocytes and eosinophils) and concentrations of fibronectin and methyl histamine in airway lining fluid, as well as increase neutrophils and mast cells, up-regulation of endothelial adhesion molecules and interleukins in bronchial biopsies [17-19,22]. In one experiment, this airway inflammation was also followed by an increase of neutrophils and platelets in peripheral blood [19].…”

Section: Introductionmentioning

confidence: 99%

Effects of diesel exposure on lung function and inflammation biomarkers from airway and peripheral blood of healthy volunteers in a chamber study

Barregård

Nielsen³

et al. 2013

Part Fibre Toxicol

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BackgroundExposure to diesel exhaust causes inflammatory responses. Previous controlled exposure studies at a concentration of 300 μg/m3 of diesel exhaust particles mainly lasted for 1 h. We prolonged the exposure period and investigated how quickly diesel exhaust can induce respiratory and systemic effects.MethodsEighteen healthy volunteers were exposed twice to diluted diesel exhaust (PM1 ~300 μg/m3) and twice to filtered air (PM1 ~2 μg/m3) for 3 h, seated, in a chamber with a double-blind set-up. Immediately before and after exposure, we performed a medical examination, spirometry, rhinometry, nasal lavage and blood sampling. Nasal lavage and blood samples were collected again 20 h post-exposure. Symptom scores and peak expiratory flow (PEF) were assessed before exposure, and at 15, 75, and 135 min of exposure.ResultsSelf-rated throat irritation was higher during diesel exhaust than filtered air exposure. Clinical signs of irritation in the upper airways were also significantly more common after diesel exhaust exposure (odds ratio=3.2, p<0.01). PEF increased during filtered air, but decreased during diesel exhaust exposure, with a statistically significant difference at 75 min (+4 L/min vs. -10 L/min, p=0.005). Monocyte and total leukocyte counts in peripheral blood were higher after exposure to diesel exhaust than filtered air 20 h post-exposure, and a trend (p=0.07) towards increased serum IL-6 concentrations was also observed 20 h post-exposure.ConclusionsDiesel exhaust induced acute adverse effects such as symptoms and signs of irritation, decreased PEF, inflammatory markers in healthy volunteers. The effects were first seen at 75 min of exposure.

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Airway inflammatory response to diesel exhaust generated at urban cycle running conditions

Cited by 38 publications

References 21 publications

Experimental determination of deposition of diesel exhaust particles in the human respiratory tract

Experimental determination of deposition of diesel exhaust particles in the human respiratory tract

Respiratory health effects of air pollution: Update on biomass smoke and traffic pollution

Effects of diesel exposure on lung function and inflammation biomarkers from airway and peripheral blood of healthy volunteers in a chamber study

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