Human Alveolar Macrophage Phagocytic Function is Impaired by Aggregates of Ultrafine Carbon Particles

Lundborg, Margot; Johard, Urban; Låstbom, Lena; Gerde, Per; Camner, Per

doi:10.1006/enrs.2001.4269

Cited by 98 publications

(57 citation statements)

References 17 publications

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“…Either of these possibilities may activate signaling in macrophages or epithelial cells, resulting in proinflammatory cytokine and chemokine production. Other possible explanations for the greater toxicity of ultrafine particles relative to fine particles include decreased ability of macrophages to phagocytose ultrafine particles (Kreyling and Scheuch 2000) or inhibition of phagocytosis by ultrafine particles Lundborg et al 2001). Renwick et al (2001) demonstrated that ultrafine TiO 2 particles impaired alveolar macrophage phagocytosis to a greater extent than did fine TiO 2 particles.…”

Section: Discussionmentioning

confidence: 99%

Airborne particles of the california central valley alter the lungs of healthy adult rats.

Smith

Kim

Recendez

et al. 2003

Environ Health Perspect

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Epidemiologic studies have shown that airborne particulate matter (PM) with a mass median aerodynamic diameter < 10 µm (PM 10 ) is associated with an increase in respiratory-related disease. However, there is a growing consensus that particles < 2.5 µm (PM 2.5 ), including many in the ultrafine (< 0.1 µm) size range, may elicit greater adverse effects. PM is a complex mixture of organic and inorganic compounds; however, those components or properties responsible for biologic effects on the respiratory system have yet to be determined. During the fall and winter of 2000-2001, healthy adult Sprague-Dawley rats were exposed in six separate experiments to filtered air or combined fine (PM 2.5 ) and ultrafine portions of ambient PM in Fresno, California, enhanced approximately 20-fold above outdoor levels. The intent of these studies was to determine if concentrated fine/ultrafine fractions of PM are cytotoxic and/or proinflammatory in the lungs of healthy adult rats. Exposures were for 4 hr/day for 3 consecutive days. The mean mass concentration of particles ranged from 190 to 847 µg/m 3 . PM was enriched primarily with ammonium nitrate, organic and elemental carbon, and metals. Viability of cells recovered by bronchoalveolar lavage (BAL) from rats exposed to concentrated PM was significantly decreased during 4 of 6 weeks, compared with rats exposed to filtered air (p < 0.05). Total numbers of BAL cells were increased during 1 week, and neutrophil numbers were increased during 2 weeks. These observations strongly suggest exposure to enhanced concentrations of ambient fine/ultrafine particles in Fresno is associated with mild, but significant, cellular effects in the lungs of healthy adult rats.

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Section: Discussionmentioning

confidence: 99%

Airborne particles of the california central valley alter the lungs of healthy adult rats.

Smith

Kim

Recendez

et al. 2003

Environ Health Perspect

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“…In lungs, UFPs are captured by alveolar macrophages and initiate inflammation, at least in part, by impairing alveolar macrophage phagocytosis and stimulating the release of inflammatory mediators from macrophages. 28,31,32 In the liver, however, the phagocytic activity of resident macrophages (Kupffer cells), ie, the kinetics of clearance of fluorescence-labeled circulating latex particles, was found to be comparable between the groups after infusion of either 5ϫ10 7 UFPs or vehicle, with 56Ϯ10% versus 58Ϯ1% moving particles at 1 minute, 38Ϯ7% versus 25Ϯ8% at 3 minutes, and 10Ϯ1% versus 17Ϯ4% at 5 minutes. This finding suggests that the accumulation of UFPs in the liver does not affect Kupffer cell function.…”

Section: Immunostaining For Fibrinogen Vwf and P-selectinmentioning

confidence: 98%

Ultrafine Particles Exert Prothrombotic but Not Inflammatory Effects on the Hepatic Microcirculation in Healthy Mice In Vivo

Khandoga¹,

Stampfl²,

Takenaka³

et al. 2004

Circulation

121

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Background-Air pollution episodes are strongly associated with increased cardiovascular morbidity and mortality. The effect of ultrafine particles (UFPs), when translocated after inhalation, on the microcirculation of extrapulmonary organs remains unclear. Methods and Results-In C57BL/6 mice, either carbon black UFPs (1ϫ10 7 and 5ϫ10 7 ) or vehicle was infused intra-arterially. Two hours after infusion, platelet-and leukocyte-endothelial cell interactions, sinusoidal perfusion, endothelial fibrin(ogen) deposition, and phagocytic activity of Kupffer cells were analyzed by intravital video fluorescence microscopy in the liver microvasculature. Expression of fibrin(ogen), von Willebrand factor (vWF), and P-selectin on hepatic endothelium was determined by immunostaining. Apoptotic cells were quantified in TUNELstained tissue sections. Application of UFPs caused significantly enhanced platelet accumulation on endothelium of postsinusoidal venules and sinusoids in healthy mice. UFP-induced platelet adhesion was not preceded by platelet rolling but was strongly associated with fibrin deposition and an increase in vWF expression on the endothelial surface. In contrast, inflammatory parameters such as the number of rolling/adherent leukocytes, P-selectin expression/ translocation, and the number of apoptotic cells were not elevated 2 hours after UFP exposure. In addition, UFPs did not affect sinusoidal perfusion and Kupffer cell function. Conclusions-UFPs

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“…34,35 Further, airway narrowing in patients with obstructive or restrictive lung disease (e.g. asthma) appears to enhance ultrafine particle deposition in the lung.…”

Section: Physicochemical Properties Of Biodiesel Exhaustmentioning

confidence: 99%

Biodiesel exhaust: The need for a systematic approach to health effects research

et al. 2015

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Biodiesel is a generic term for fuel that can be made from virtually any plant or animal oil via transesterification of triglycerides with an alcohol (and usually a catalyst). Biodiesel has received considerable scientific attention in recent years, as it is a renewable resource that is directly able to replace mineral diesel in many engines. Additionally, some countries have mandated a minimum biodiesel content in all diesel fuel sold on environmental grounds.When combusted, biodiesel produces exhaust emissions containing particulate matter, adsorbed chemicals and a range of gases. In many cases, absolute amounts of these pollutants are lower in biodiesel exhaust compared with mineral diesel exhaust, leading to speculation that biodiesel exhaust may be less harmful to health. Additionally, engine performance studies show that the concentrations of these pollutants vary significantly depending on the renewable oil used to make the biodiesel and the ratio of biodiesel to mineral diesel in the fuel mix. Given the strategic and legislative push towards the use of biodiesel in many countries, a concerning possibility is that certain biodiesels may produce exhaust emissions that are more harmful to health than others. This variation suggests that a comprehensive, systematic and comparative approach to assessing the potential for a range of different biodiesel exhausts to affect health is urgently required. Such an assessment could inform biodiesel production priorities, drive research and development into new exhaust treatment technologies, and ultimately minimize the health impacts of biodiesel exhaust exposure.

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Human Alveolar Macrophage Phagocytic Function is Impaired by Aggregates of Ultrafine Carbon Particles

Cited by 98 publications

References 17 publications

Airborne particles of the california central valley alter the lungs of healthy adult rats.

Airborne particles of the california central valley alter the lungs of healthy adult rats.

Ultrafine Particles Exert Prothrombotic but Not Inflammatory Effects on the Hepatic Microcirculation in Healthy Mice In Vivo

Biodiesel exhaust: The need for a systematic approach to health effects research

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