PM 2.5 collected in a residential area induced Th1-type inflammatory responses with oxidative stress in mice

Park, Eun-Jung; Roh, Jinkyu; Kim, Younghun; Park, Kwangsik; Kim, Dae-Seon; Yu, Seong-Do

doi:10.1016/j.envres.2010.11.001

Cited by 47 publications

(33 citation statements)

References 40 publications

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“…However, in this study, the duration of exposure was probably too short to evoke a sufficient activation of those cytokines. This interpretation is supported by previous findings showing some increase in BALF IL-10, IL-12, and IFN-γ levels at 24 h after exposure to ambient air PM 2.5 samples (Park et al, 2011). Alternatively their manifestation would require use of a mice model that would be sensitive to allergic challenges (Stevens et al, 2009).…”

Section: Discussionsupporting

confidence: 73%

“…This is seen also in the present results where the IL-1β level correlated positively with neutrophil counts in the lungs of mice (Table 5). Similar IL-1β responses have also been seen after exposure of mice to urban air PM 2.5 (Park et al, 2011) and to diesel exhaust particles (Samuelsen et al, 2009). In contrast, Seagrave et al (2005) reported that after exposure to diesel exhaust and hardwood smoke samples the IL-1β concentrations in the BALF of rats and mice were too low to be analyzed.…”

Section: Discussionmentioning

confidence: 59%

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Acute systemic and lung inflammation in C57Bl/6J mice after intratracheal aspiration of particulate matter from small-scale biomass combustion appliances based on old and modern technologies

Uski

Happo

Jalava

et al. 2012

Inhalation Toxicology

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Inflammation is regarded as an important mechanism behind mortality and morbidity experienced by cardiorespiratory patients exposed to urban air particulate matter (PM). Small-scale biomass combustion is an important source of particulate air pollution. In this study, we investigated association between inflammatory responses and chemical composition of PM(1) emissions from seven different small-scale wood combustion appliances representing old and modern technologies. Healthy C57Bl/6J mice were exposed by intratracheal aspiration to single dose (10 mg/kg) of particulate samples. At 4 and 18 h after the exposure, bronchoalveolar lavage fluid (BALF) as well as serum was collected for subsequent analyses of inflammatory indicators (interleukin (IL)-6, IL-1β, IL-12, and IL-10; tumor necrosis factor-α (TNF-α); keratinocyte-derived chemoattractant (KC), and interferon-γ (IFN-γ)) in multiplexing assay. When the responses to the PM(1) samples were compared on an equal mass basis, the PM from modern technology appliances increased IL-6, KC, and IL-1β levels significantly in BALF at 4 and 18 h after the exposure. In contrast, these responses were seen only at 4 h time point in serum. Increased cytokine concentrations correlated with metal-rich ash related compounds which were more predominant in the modern technology furnaces emissions. These particles induced both local and systemic inflammation. Instead, polycyclic hydrocarbon (PAH) rich PM(1) samples from old technology (OT) evoked only minor inflammatory responses. In conclusion, the combustion technology largely affects the toxicological and chemical characteristics of the emissions. The large mass emissions of old combustion technology should be considered, when evaluating the overall harmfulness between the appliances. However, even the small emissions from modern technologies may pose significant toxic risks.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 59%

Acute systemic and lung inflammation in C57Bl/6J mice after intratracheal aspiration of particulate matter from small-scale biomass combustion appliances based on old and modern technologies

Uski

Happo

Jalava

et al. 2012

Inhalation Toxicology

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“…There is considerable toxicological evidence of adverse health effects of PM, including evidence of cytotoxicity and inflammatory effects through increased oxidative stress resulting from exposure to traffic-related particles such as PM 2.5 (Gualtieri et al 2010; Park et al 2011). However, there is also increasing evidence that coarse particles may activate inflammatory pathways (Graff et al 2009; Karlsson et al 2011), including an in vitro study that reported that coarse particles had an inflammatory potential similar to fine particles on an equal mass basis (Schwarze et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Associations between Fine and Coarse Particles and Mortality in Mediterranean Cities: Results from the MED-PARTICLES Project

Samoli

Stafoggia²,

Rodopoulou³

et al. 2013

Environ Health Perspect

216

112

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Background: Few studies have investigated the independent health effects of different size fractions of particulate matter (PM) in multiple locations, especially in Europe.Objectives: We estimated the short-term effects of PM with aerodynamic diameter ≤ 10 μm (PM10), ≤ 2.5 μm (PM2.5), and between 2.5 and 10 μm (PM2.5–10) on all-cause, cardiovascular, and respiratory mortality in 10 European Mediterranean metropolitan areas within the MED-PARTICLES project.Methods: We analyzed data from each city using Poisson regression models, and combined city-specific estimates to derive overall effect estimates. We evaluated the sensitivity of our estimates to co-pollutant exposures and city-specific model choice, and investigated effect modification by age, sex, and season. We applied distributed lag and threshold models to investigate temporal patterns of associations.Results: A 10-μg/m3 increase in PM2.5 was associated with a 0.55% (95% CI: 0.27, 0.84%) increase in all-cause mortality (0–1 day cumulative lag), and a 1.91% increase (95% CI: 0.71, 3.12%) in respiratory mortality (0–5 day lag). In general, associations were stronger for cardiovascular and respiratory mortality than all-cause mortality, during warm versus cold months, and among those ≥ 75 versus < 75 years of age. Associations with PM2.5–10 were positive but not statistically significant in most analyses, whereas associations with PM10 seemed to be driven by PM2.5.Conclusions: We found evidence of adverse effects of PM2.5 on mortality outcomes in the European Mediterranean region. Associations with PM2.5–10 were positive but smaller in magnitude. Associations were stronger for respiratory mortality when cumulative exposures were lagged over 0–5 days, and were modified by season and age.

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“…Although PM shares many of the same ingredients and characteristics as cigarette smoke, the M1 cytokines (IL-12 and IFN- γ ) are increased consistently in bronchoalveolar lavage fluid (BALF) from PM-exposed animals [63, 64] while the M2 cytokines (IL-4, IL-10, and IL-13) remain at lower levels [65]. Our group previously showed that primary cultured human AM, stimulated in vitro with urban PM 10 , produced an array of cytokines without significantly increased levels of IL-10 compared to nonstimulated AM [13].…”

Section: Response Of Lung Macrophages To Inhaled Air Pollutantsmentioning

confidence: 99%

Contribution of Lung Macrophages to the Inflammatory Responses Induced by Exposure to Air Pollutants

Hiraiwa

Eeden

2013

Mediators of Inflammation

210

135

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Large population cohort studies have indicated an association between exposure to particulate matter and cardiopulmonary morbidity and mortality. The inhalation of toxic environmental particles and gases impacts the innate and adaptive defense systems of the lung. Lung macrophages play a critically important role in the recognition and processing of any inhaled foreign material such as pathogens or particulate matter. Alveolar macrophages and lung epithelial cells are the predominant cells that process and remove inhaled particulate matter from the lung. Cooperatively, they produce proinflammatory mediators when exposed to atmospheric particles. These mediators produce integrated local (lung, controlled predominantly by epithelial cells) and systemic (bone marrow and vascular system, controlled predominantly by macrophages) inflammatory responses. The systemic response results in an increase in the release of leukocytes from the bone marrow and an increased production of acute phase proteins from the liver, with both factors impacting blood vessels and leading to destabilization of existing atherosclerotic plaques. This review focuses on lung macrophages and their role in orchestrating the inflammatory responses induced by exposure to air pollutants.

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PM 2.5 collected in a residential area induced Th1-type inflammatory responses with oxidative stress in mice

Cited by 47 publications

References 40 publications

Acute systemic and lung inflammation in C57Bl/6J mice after intratracheal aspiration of particulate matter from small-scale biomass combustion appliances based on old and modern technologies

Acute systemic and lung inflammation in C57Bl/6J mice after intratracheal aspiration of particulate matter from small-scale biomass combustion appliances based on old and modern technologies

Associations between Fine and Coarse Particles and Mortality in Mediterranean Cities: Results from the MED-PARTICLES Project

Contribution of Lung Macrophages to the Inflammatory Responses Induced by Exposure to Air Pollutants

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