Diesel exhaust enhances airway responsiveness in asthmatic subjects

Nordenhäll, Charlotta; Pourazar, Jamshid; Ledin, M C; Levin, Jan‐Olof; Sandström, Thomas; Ädelroth, E

doi:10.1183/09031936.01.17509090

Cited by 166 publications

(117 citation statements)

References 35 publications

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“…Most studies generally did not found effects on lung function parameters in relation to short-term air pollution chamber exposure [9][10][11][12][13][14]. Compared with the chamber studies, our study explored the pulmonary effects in the natural environment, where more complex traffic-related air pollutants existed, this may lead to the discrepancies between the findings of the chamber studies and our own.…”

Section: Discussioncontrasting

confidence: 48%

“…Acute respiratory effects of exposure to diesel exhaust have also been studied in controlled chamber studies [9][10][11][12][13][14][15]. Most studies generally did not found effects on lung function parameters in relation to short-term air pollution chamber exposure [9][10][11][12][13][14].…”

Section: Discussionmentioning

confidence: 99%

“…Acute effects on pulmonary function of exposure to traffic exhaust have been studied in controlled chamber studies [9][10][11][12][13][14][15]. However, considering the realworld exposure where mixtures of pollutants are more complex, the results of chamber studies may have some difficulties when applied to the exposure in real-world traffic micro-environment.…”

Section: Introductionmentioning

confidence: 99%

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Acute effects on pulmonary function in young healthy adults exposed to traffic-related air pollution in semi-closed transport hub in Beijing

Huang

Deng

et al. 2016

Environ Health Prev Med

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Objectives Transport hub is an important part of urban comprehensive transportation system. Traffic-related air pollution can reach high level because of difficulty of diffusion and increase of emission in transport hub. However, whether exposure in this semi-closed traffic microenvironment causes acute changes in pulmonary function of commuters still needs to be explored. Methods Forty young healthy adults participated in this randomized, crossover study. Each participant underwent 2 h exposure in a designated transport hub and, on a separate occasion, in an appointed park. Personal exposures to fine particulate matter (PM 2.5 ), black carbon (BC) and carbon monoxide (CO) were measured. Forced expiratory volume in 1 s (FEV 1 ) and peak expiratory flow (PEF) were assessed pre-, during and post-exposure. Mixed linear models were used to analyze the pulmonary effects of traffic-related air pollutants. Results Participants had significantly higher exposures to PM 2.5 , BC and CO in the transport hub than in the park. Exposure in transport hub induced significant reductions in FEV 1 and PEF compared with the park during exposure 1 and 2 h. The reductions were significant associated with traffic-related air pollutants. For instance, per 10 lg/m 3 increment in PM 2.5 was associated with -0.15 % (95 % CI -0.28, -0.02 %) reduction in FEV 1 during exposure 2 h. However, effects became attenuate after 2 h exposure. Conclusions Short-term exposure in transport hub had acute reduction effects on pulmonary function. More attention should be paid to the health effects of exposure in the semi-closed traffic micro-environment.

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Section: Discussioncontrasting

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acute effects on pulmonary function in young healthy adults exposed to traffic-related air pollution in semi-closed transport hub in Beijing

Huang

Deng

et al. 2016

Environ Health Prev Med

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“…For instance, it is capable of inducing AHR in naïve mice in the absence of allergen [62,108]. It has also been demonstrated that DEP alone can induce increased AHR in asthmatic individuals [109]. While these effects may be related to PM effects on the immune system, the particles and their components may directly contribute to increased AHR during asthma attack [110][111][112].…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

802

529

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Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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“…(2010), whole body plethysmography is “a rather crude indicator of pulmonary function”, and as they did not use confirmatory methods of lung function assessment based on physical principles, their “pulmonary responsiveness” data should be viewed with some caution 32 . In saying this, it is well established that influenza infection results in pulmonary hyper‐reactivity in mice 24 and humans, 33 and that diesel exposure causes airway hyper‐reactivity in humans 34 . Interestingly, Gowdy et al.…”

Section: Introductionmentioning

confidence: 99%

Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function

Larcombe

Foong

Boylen

et al. 2012

Influenza Resp Viruses

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Please cite this paper as: Larcombe et al. (2012) Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function. Influenza and Other Respiratory Viruses DOI:10.1111/irv.12012. Background Exposure to diesel exhaust particles (DEP) is thought to exacerbate many pre‐existing respiratory diseases, including asthma, bronchitis and chronic obstructive pulmonary disease, however, there is a paucity of data on whether DEP exacerbates illness due to respiratory viral infection. Objectives To assess the physiological consequences of an acute DEP exposure during the peak of influenza‐induced illness. Methods We exposed adult female BALB/c mice to 100 μg DEP (or control) 3·75 days after infection with 104·5 plaque forming units of influenza A/Mem71 (or control). Six hours, 24 hours and 7 days after DEP exposure we measured thoracic gas volume and lung function at functional residual capacity. Bronchoalveolar lavage fluid was taken for analyses of cellular inflammation and cytokines, and whole lungs were taken for measurement of viral titre. Results Influenza infection resulted in significantly increased inflammation, cytokine influx and impairment to lung function. DEP exposure alone resulted in less inflammation and cytokine influx, and no impairment to lung function. Mice infected with influenza and exposed to DEP had higher viral titres and neutrophilia compared with infected mice, yet they did not have more impaired lung mechanics than mice infected with influenza alone. Conclusions A single dose of DEP is not sufficient to physiologically exacerbate pre‐existing respiratory disease caused by influenza infection in mice.

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Diesel exhaust enhances airway responsiveness in asthmatic subjects

Cited by 166 publications

References 35 publications

Acute effects on pulmonary function in young healthy adults exposed to traffic-related air pollution in semi-closed transport hub in Beijing

Acute effects on pulmonary function in young healthy adults exposed to traffic-related air pollution in semi-closed transport hub in Beijing

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function

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