Airway and systemic inflammatory responses to ultrafine carbon black particles and ozone in older healthy subjects

• Published in: Journal of Toxicology and Environmental Health, Part A Vol. 81; no. 13; pp. 576 - 588
• Main Authors: Holz, Olaf, Heusser, Karsten, Müller, Meike, Windt, Horst, Schwarz, Katharina, Schindler, Christoph, Tank, Jens, Hohlfeld, Jens M., Jordan, Jens
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis Ltd 01.01.2018
• Subjects: Air pollution; Black carbon; Carbon; Carbon black; Cardiovascular diseases; Contaminants; Exposure; Health risks; Inflammation; Inflammatory response; Interleukin 6; Leukocytes (neutrophilic); Markers; Matrix metalloproteinase; Metalloproteinase; Neutrophils; Ozone; Pollutants; Proteins; Respiratory tract; Sputum; Subgroups
• ISSN: 1528-7394; 1087-2620; 2381-3504
• DOI: 10.1080/15287394.2018.1463331

Increased adverse health effects in older subjects due to exposure to ambient air pollutants may be related to the inflammatory response induced by these contaminants. The aim of this study was to assess airway and systemic inflammatory responses in older healthy subjects to a controlled experimental exposure with spark-generated elemental carbon black ultrafine particles (cbUFPs) and ozone (O ). Twenty healthy subjects, age 52-75 years, were exposed on three occasions separated by at least 8 weeks. The exposures to filtered air (FA), to cbUFP (50 μg/m ), or to cbUFP in combination with 250 ppb ozone (cbUFP + O ) for 3 h with intermittent exercise were performed double blind, and in random order. Sputum and blood samples were collected 3.5 h after each exposure. Exposure to cbUFP + O significantly increased plasma club cell protein 16 (CC16), the number of sputum cells, the number and percent of sputum neutrophils, and sputum interleukin 6 and matrix metalloproteinase 9. Exposure to cbUFP alone exerted no marked effect, except for an elevation in sputum neutrophils in a subgroup of 13 subjects that displayed less than 65% sputum neutrophils after FA exposure. None of the inflammatory markers was correlated with age, and serum cardiovascular risk markers were not markedly affected by cbUFP or cbUFP + O . Exposure to cbUFP+O induced a significant airway and systemic inflammatory response in older healthy volunteer subjects. The effects induced by cbUFP alone suggest that the inflammation was predominantly mediated by O , although one cannot rule out that the interaction of cbUFP and O played a role.