Bronchoalveolar inflammation after exposure to diesel exhaust: comparison between unfiltered and particle trap filtered exhaust.

Rudell, Bertil; Blomberg, Anders; Helleday, Ragnberth; Ledin, M C; Lundbäck, Bo; Stjernberg, N; Hörstedt, Per; Sandström, Thomas

doi:10.1136/oem.56.8.527

Cited by 146 publications

(100 citation statements)

References 22 publications

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“…Numerous epidemiological studies have documented a detrimental relationship between exposure to particulate matter in urban air pollution and cardiopulmonary morbidity and mortality with both short-and long-term exposure [1][2][3][4][5]. Although the mechanism by which exposure to particles in urban air induces adverse cardiopulmonary effects remains unclear, several studies from the present authors' laboratory and others support a mechanism in which exposure to fine particles promotes inflammation in the lung [6][7][8][9][10][11] via activation of alveolar macrophages and lung epithelial cells [12][13][14][15][16]. Such exposure is also associated with a systemic inflammatory response [17][18][19][20], which in turn is associated with an increased presence of several cytokines (interleukin (IL)-6, IL-1b) in the bloodstream [21] as well as increased production and release of polymorphonuclear leukocytes (PMN) and monocytes from the bone marrow [17][18][19][20].…”

mentioning

confidence: 57%

Wood smoke exposure induces a pulmonary and systemic inflammatory response in firefighters

Swiston

Davidson²,

Attridge³

et al. 2008

Eur Respir J

202

172

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Epidemiological studies report an association between exposure to biomass smoke and cardiopulmonary morbidity. The mechanisms for this association are unclear. The aim of the present study was to characterise the acute pulmonary and systemic inflammatory effects of exposure to forest fire smoke.Seasonal forest firefighters (n552) were recruited before and/or after a day of fire-fighting. Exposure was assessed by questionnaires and measurement of carbon monoxide levels (used to estimate respirable particulate matter exposure). The pulmonary response was assessed by questionnaires, spirometry and sputum induction. Peripheral blood cell counts and inflammatory cytokines were measured to define the systemic response.Estimated respirable particulate matter exposure was high (peak levels .2 mg?m ). Serum interleukin (IL)-6, IL-8 and monocyte chemotactic protein-1 levels significantly increased following fire-fighting. There were no changes in band cells, IL-6, and IL-8 following strenuous physical exertion without fire-fighting. There was a significant association between changes in sputum macrophages containing phagocytosed particles and circulating band cells.In conclusion, acute exposure to air pollution from forest fire smoke elicits inflammation within the lungs, as well as a systemic inflammatory response.

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mentioning

confidence: 57%

Wood smoke exposure induces a pulmonary and systemic inflammatory response in firefighters

Swiston

Davidson²,

Attridge³

et al. 2008

Eur Respir J

202

172

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“…The presence of a neutrophilic inflammation has further been reported in BAL at 18 h after DE exposure [14,15]. Although the human data on the time course of the neutrophilic response to DE is limited, the results from these studies seem to suggest the peak response to occur sometime between 6 and 18 h following exposure.…”

Section: Discussionmentioning

confidence: 92%

“…In working environments, exposure to DE has been associated with various symptoms related to the eyes and airways [10±12]. In experimental chamber studies, DE has been shown to cause airway symptoms [13] and to induce an acute inflammatory response in human airways as reflected in bronchoalveolar lavage [14,15] and bronchial biopsy [16] samples. Further, local nasal challenge with DE particles has been reported to enhance immunoglobulin E production in the nose [17] and to cause an increased cytokine response in the nose of allergic subjects [18].…”

mentioning

confidence: 99%

Airway inflammation following exposure to diesel exhaust: a study of time kinetics using induced sputum

Nordenhäll¹,

Pourazar²,

Blomberg³

et al. 2000

Eur Respir J

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131

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The adverse health effects of particulate matter pollution are of increasing concern. In a recent bronchoscopic study in healthy volunteers, pronounced airway inflammation was detected following exposure to diesel exhaust (DE). The present study was conducted in order to evaluate the time kinetics of the inflammatory response following exposure to DE using induced sputum from healthy volunteers.Fifteen healthy nonsmoking volunteers were exposed to DE particles with a 50% cut-off aerodynamic diameter of 10 mm 300 mg . m -3 and air for 1 h on two separate occasions. Sputum induction with hypertonic saline was performed 6 and 24 h after each exposure. Analyses of sputum differential cell counts and soluble protein concentrations were performed.Six hours after exposure to DE, a significant increase was found in the percentage of sputum neutrophils (37.7 versus 26.2% p=0.002) together with increases in the concentrations of interleukin-6 (12.0 versus 6.3 pg . mL -1 , p=0.006) and methylhistamine (0.11 versus 0.12 mg . L -1 , p=0.024). Irrespective of exposure, a significant increase was found in the percentage of sputum neutrophils at 24 as compared to 6 h, indicating that the procedure of sputum induction itself may change the composition of sputum.This study demonstrates that exposure to diesel exhaust induces inflammatory response in healthy human airways, represented by an early increase in interleukin -6 and methylhistamine concentration and the percentage of neutrophils. Induced sputum provides a safe tool for the investigation of the inflammatory effects of diesel exhaust, but care must be taken when interpreting results from repeated sputum inductions. Eur Respir J 2000; 15: 1046±1051. The adverse health effects of particulate matter (PM) pollution are of increasing concern as several epidemiological studies have revealed an association between elevations in ground level PM concentrations and increased morbidity and mortality from cardiovascular and respiratory causes [1±7].Recently, attention has been directed towards the particulate air pollution emitted from diesel engines. The number of diesel-powered cars is rising and diesel engines emit up to 100 times more particles than petrol engines [8,9]. Diesel exhaust (DE) particles contain a carbonaceous core, which adsorbs various metals and organic compounds on its surface. Consequently, the biological effects of DE may be explained by not only the gases and pure particles but also by these surface components.The number of studies investigating the effects of DE has increased during recent years. In working environments, exposure to DE has been associated with various symptoms related to the eyes and airways [10±12]. In experimental chamber studies, DE has been shown to cause airway symptoms [13] and to induce an acute inflammatory response in human airways as reflected in bronchoalveolar lavage [14,15] and bronchial biopsy [16] samples. Further, local nasal challenge with DE particles has been reported to enhance immunoglobulin E production in the ...

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“…Numerous environmental pollutants can provoke an inflammatory response in patients with COPD (36)(37)(38). Importantly, epidemiologic studies have confirmed increased respiratory symptoms and mortality during times of increased air pollution (39)(40)(41).…”

Section: Pathogenesismentioning

confidence: 99%

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Martínez

2007

Proceedings of the American Thoracic Society

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Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the natural history of this chronic lung disorder. These events can be caused by a large number of infectious and noninfectious agents and are associated with an increased local and systemic inflammatory response. Their frequency and severity have been linked to progressive deterioration in lung function and health status. Infectious pathogens ranging from viral to atypical and typical bacteria have been implicated in the majority of episodes. Most therapeutic regimens to date have emphasized broad, nonspecific approaches to bronchoconstriction and pulmonary inflammation. Increasingly, therapy that targets specific etiologic pathogens has been advocated. These include clinical and laboratory-based methods to identify bacterial infections. Further additional investigation has suggested specific pathogens within this broad class. As specific antiviral therapies become available, better diagnostic approaches to identify specific pathogens will be required. Furthermore, prophylactic therapy for at-risk individuals during high-risk times may become a standard therapeutic approach. As such, the future will likely include aggressive diagnostic algorithms based on the combination of clinical syndromes and rapid laboratory modalities to identify specific causative bacteria or viruses.

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Bronchoalveolar inflammation after exposure to diesel exhaust: comparison between unfiltered and particle trap filtered exhaust.

Cited by 146 publications

References 22 publications

Wood smoke exposure induces a pulmonary and systemic inflammatory response in firefighters

Wood smoke exposure induces a pulmonary and systemic inflammatory response in firefighters

Airway inflammation following exposure to diesel exhaust: a study of time kinetics using induced sputum

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

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