Cytotoxicity and Induction of Proinflammatory Cytokines from Human Monocytes Exposed to Fine (PM2.5) and Coarse Particles (PM10–2.5) in Outdoor and Indoor Air

Monn, Christian; Becker, Susanne

doi:10.1006/taap.1998.8591

Cited by 362 publications

(306 citation statements)

References 30 publications

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“…Our previous studies have shown that particles in the coarse PM 2.5-10 fraction alter the phenotype and phagocytic capability of these cells. PM 2.5 assessed simultaneously had no effect on phagocytosis or oxidant generation (13,15). Similarly, host defenses of mice exposed to PM 2.5 and PM 2.5-10 were found to be altered by PM 2.5-10 but not PM 2.5 (21).…”

Section: Discussionmentioning

confidence: 94%

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Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.

Harder

Soukup

Ghio

et al. 2001

Environ Health Perspect

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We tested the hypothesis that exposure of healthy volunteers to concentrated ambient air particles (CAPS) between 0.1 and 2.5 microm in diameter is associated with modulation of human alveolar macrophage (AM) function, cytokine production, and immune phenotype in both blood and lung. Thirty-eight volunteers were exposed to either filtered air or CAPS from the immediate environment of the U.S. Environmental Protection Agency human studies facility in Chapel Hill, North Carolina, USA. Particle concentrations in the chamber during the exposures ranged from 23.1 to 311.1 microg/m3. No symptoms were noted by volunteers after the exposure. Eighteen hours after exposure, analysis of cells obtained by bronchoalveolar lavage (BAL) showed a mild increase in neutrophils in both the bronchial (8.4 +/- 2%) and alveolar fractions (4.2 +/- 1.7%) in subjects exposed to the highest concentration of CAPS compared to neutrophils in the fluids of those exposed to filtered air (bronchial fraction 2.7 +/- 0.6%; alveolar fraction 0.8 +/- 0.3%). There was no change in the percentage of lymphocytes or AMs recovered in the lavage after inhalation of the highest particle levels (mean 207 microg/m3). There was also no change in the proportion of lymphocytes in the BAL expressing CD3, CD4, CD8, CD19, nor activation markers CD25 or CD69. Particle inhalation did not affect the expression of CD11b, CD64, CD16, CD14, CD71 on AM, nor was there an effect on phagocytosis or oxidant generation following stimulation with zymosan A. IL-6 and IL-8 levels detected by enzyme-linked immunoabsorbent assay in the BAL were unrelated to inhaled particle levels. The distribution of lymphocyte subsets in blood obtained 18 hr after exposure to CAPS did not differ from that found before exposure. We conclude that ambient air particles are capable of inducing a mild inflammation in the lower respiratory tract but have no effect on immune phenotype or macrophage function under the conditions tested.

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Section: Discussionmentioning

confidence: 94%

“…Furthermore, diesel particles have been shown to divert the immune response toward an allergic phenotype (9,10). In vitro studies with urban air particles have been shown to alter alveolar macrophage function in a manner promoting survival of microbes (11)(12)(13).…”

mentioning

confidence: 99%

Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.

Harder

Soukup

Ghio

et al. 2001

Environ Health Perspect

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“…algae, pollen, bacteria or fungi), affecting human health through inhalation. It has been established a correlation between particle size of PM and mortality [42][43][44]. In this sense, the different studies about As in the air consider total suspended particles (TSP), or particles with a certain aerodynamic diameter, expressed in microns (e.g.…”

Section: Sampling Of Particulate Mattermentioning

confidence: 99%

Analytical approaches for arsenic determination in air: A critical review

Sánchez-Rodas

Campa

Alsioufi

2015

Analytica Chimica Acta

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This review describes the different steps involved in the determination of arsenic in air, considering the particulate matter (PM) and the gaseous phase. The review focuses on sampling, sample preparation and instrumental analytical techniques for both total arsenic determination and speciation analysis. The origin, concentration and legislation concerning arsenic in ambient air are also considered. The review intends to describe the procedures for sample collection of total suspended particles (TSP) or particles with a certain diameter expressed in microns (e.g. PM10 and PM2.5), or the collection of the gaseous phase containing gaseous arsenic species. Sample digestion of the collecting media for PM is

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“…It seems that cardiopulmonary irritability associated with particulate air pollution may be induced through the sympathetic stress response or via inflammatory processes such as chemokine and cytokine production in respiratory or cardiac circulation [6][7][8]. It was also shown that the increased risk of cardiovascular mortality and morbidity following exposure to airborne particles can be caused by the progression of heart failure [9].…”

Section: Introductionmentioning

confidence: 99%

Comparison of heart rate variability and cardiac arrhythmias in polluted and clean air episodes in healthy individuals

Davoodi

Sharif

Kazemisaeid

et al. 2010

Environ Health Prev Med

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Objective Pathophysiological mechanisms and pathways linking cardiovascular mortality and morbidity with air pollution were recently hypothesized. The present study evaluated association between air pollution and changes in heart rate variability as a marker of cardiac autonomic function in healthy individuals, and also determined the frequency of cardiac arrhythmias and QT interval changes on polluted compared to unpolluted days. Methods Continuous Holter electrocardiography (ECG) monitoring was conducted on 21 young healthy individuals in the two episodes of clean air and elevated air pollution in Tehran. All subjects underwent a medical history review, a physical examination and echocardiography in order to rule out structural heart diseases. Measured pollutants and parameters included NO 2 , CO 2 , O 3 , SO 2 , and PM10, which all showed significantly higher concentrations on polluted days. Holter parameters were measured for 24-h time segments and compared. Results Maximum heart rate was significantly lower in polluted air conditions in comparison with clean air conditions (115.1 ± 32.2 vs. 128.9 ± 17.7), and the square root of the mean of squared differences between adjacent NN intervals (r-MSSD) was higher in polluted air compared to clean air (99.0 ± 58.2 vs. 58.5 ± 26.4). Also, the occurrence of nonsustained supraventricular tachycardia was reported in 42.9% of participants in air pollution episodes, whereas this arrhythmia was not seen in clear air conditions (p = 0.001).Conclusion Changes in air pollution indices may lead to the occurrence of nonsustained supraventricular tachycardia, a slight reduction in maximum heart rate, and an increase in r-MSSD in healthy individuals. Air quality monitoring in cities associated with a high exposure to air pollutants is recommended in order to prevent such events.

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Cytotoxicity and Induction of Proinflammatory Cytokines from Human Monocytes Exposed to Fine (PM2.5) and Coarse Particles (PM10–2.5) in Outdoor and Indoor Air

Cited by 362 publications

References 30 publications

Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.

Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.

Analytical approaches for arsenic determination in air: A critical review

Comparison of heart rate variability and cardiac arrhythmias in polluted and clean air episodes in healthy individuals

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