Human Alveolar Macrophage Responses to Air Pollution Particulates Are Associated with Insoluble Components of Coarse Material, Including Particulate Endotoxin

Soukup, Joleen M.; Becker, Susanne

doi:10.1006/taap.2000.9096

Cited by 252 publications

(187 citation statements)

References 39 publications

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“…An important determinant of the acute inflammatory response appears to be the dose of bio-available transition metals (such as copper, vanadium, chromium, nickel, cobalt and iron), organic compounds (such as polycyclic aromatic hydrocarbons) and biological fractions (such as endotoxins) [35,36]. The oxidative stress mediated by particulate matter (PM) may arise from: direct generation of reactive oxygen species (ROS) from the surface of soluble compounds; altered function of mitochondria or reduced nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase; and activation of inflammatory cells capable of generating ROS and reactive nitrogen species (RNS), as well as oxidative DNA damage [37,38].…”

Section: Biological and Epidemiological Evidencementioning

confidence: 99%

Air pollution, oxidative stress and dietary supplementation: a review

Romieu

Castro-Giner²,

Künzli³

et al. 2007

Eur Respir J

223

157

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The aim of the present review was to provide an up-to-date overview of the biological and epidemiological evidence of the role of oxidative stress as a major underlying feature of the toxic effect of air pollutants, and the potential role of dietary supplementation in enhancing antioxidant defences.A bibliographic search was conducted through PubMed. The keywords used in the search were ''air pollutant'', ''oxidative stress'', ''inflammation'', ''antioxidant polyunsaturated fatty acids'' and ''genetics''. In addition, the authors also searched for biomarkers of oxidative stress and nutrients.The review presents the most recent data on: the biological and epidemiological evidence of the oxidative stress response to air pollutants; the role of dietary supplementation as a modulator of these effects; and factors of inter-individual variation in human response. The methodology for further epidemiological studies will be discussed in order to improve the current understanding on how nutritional factors may act.There is substantial evidence that air pollution exposure results in increased oxidative stress and that dietary supplementation may play a modulating role on the acute effect of air pollutants. Further epidemiological studies should address the impact of supplementation strategies in the prevention of air-pollution-related long-term effects in areas where people are destined to be exposed for the distant future.

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Section: Biological and Epidemiological Evidencementioning

confidence: 99%

Air pollution, oxidative stress and dietary supplementation: a review

Romieu

Castro-Giner²,

Künzli³

et al. 2007

Eur Respir J

223

157

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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: 97%

“…However, this effect on macrophages resides in the coarse particle fraction (2.5-10 µm) rather than in the fine fraction (14,15).…”

mentioning

confidence: 98%

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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“…The exact constituents of PM air pollution that induce disease and the mechanisms involved are unknown. Studies to determine the components of PM that contribute to airway inflammation and irritation have been attempted (Bonner et al 1998;Donaldson and MacNee 2001;Soukup and Becker 2001;Boehlecke et al 2003). Aerodynamic size fractions of PM have been studied including coarse (PM 10−2.5 ) and fine (PM 2.5 ), and recently fine and submicrometer fractions (Pope 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Aerodynamic size fractions of PM have been studied including coarse (PM 10−2.5 ) and fine (PM 2.5 ), and recently fine and submicrometer fractions (Pope 2000). Yet the coarse PM fraction remains recognized as being associated with significant adverse effects on the bronchiolar region of conducting airways that remains the primary site of asthma and associated airway inflammation (Monn and Becker 1999;Soukup and Becker 2001). Although bioaerosols have been identified and linked to adverse health effects, they have not been extensively studied for their prevalence in ambient PM.…”

Section: Introductionmentioning

confidence: 99%

The Measurement of Ambient Bioaerosol Exposure

Menetrez¹,

Foarde²,

Esch³

et al. 2007

Aerosol Science and Technology

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Monitoring of ambient bioaerosol concentrations through the characterization of outdoor particulate matter (PM) has only been performed on a limited basis in North Carolina (NC) and was the goal of this research. Ambient samples of PM 2.5 (fine) and PM 10−2.5 (coarse) were collected for a six-month period and analyzed for mold, endotoxins and protein. PM 2.5 and PM 10−2.5 concentrations of these bioaerosols were reported as a function of PM mass, as well as volume of air sampled. The mass of PM 2.5 was almost twice that of the PM 10−2.5 ; however, the protein and endotoxin masses were greater in the coarse than the fine PM indicating an enrichment in the coarse PM. The protein and mold results demonstrated a seasonal pattern, both being higher in the summer than in the winter. Except for an occasional excursion, the endotoxin data remained fairly constant throughout the six months of the study.

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Human Alveolar Macrophage Responses to Air Pollution Particulates Are Associated with Insoluble Components of Coarse Material, Including Particulate Endotoxin

Cited by 252 publications

References 39 publications

Air pollution, oxidative stress and dietary supplementation: a review

Air pollution, oxidative stress and dietary supplementation: a review

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

The Measurement of Ambient Bioaerosol Exposure

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