Modifications of carbon black nanoparticle surfaces modulate type II pneumocyte homoeostasis.

ABSTRACT

Inhalation uptake of carbon black nanoparticles (CBNP) bears the risk of morphological and functional lung impairment attributed to the highly reactive particle surface area. Chemical particle surface modifications might affect particle-cell interactions; however, thus far these alterations have not been determined. This is the first in vivo study comparing particle-induced acute lung injury using Printex(®)90 (Pr90, 7 µg), Printex®90 covered by benzo[a]pyrene or 9-nitroanthracene (BaP-Pr90, NA-Pr90, 7 µg, 15% BaP or NA by weight), and acetylene carbon black (CB) with polycyclic aromatic hydrocarbons (PAH-AB, 7 µg, 20% PAH by weight). All particles were suspended in distilled water with bovine serum albumin (BSA). In addition, the influence of suspension media was tested using Printex®90 suspended without BSA (Pr90(-BSA), 7 µg). Quartz (DQ12, 7 µg), 70 µl saline (NaCl), and distilled water with or without BSA (H2O(+/-BSA)) were used as reference and controls. It was postulated that CBNP surface modifications trigger pulmonary responses. After oropharyngeal particle aspiration, lung functions were measured 2 d postexposure, followed by lung preparation for histological or bronchoalveolar lavage fluid (BALF) examinations and type II pneumocyte isolation on d 3. Head-out body plethysmography revealed reduced flow rates induced by PAH-AB. Examinations of BALF demonstrated reduced influx of macrophages after exposure to Pr90(-BSA) and decreased lymphocyte levels after Pr90(+BSA) or BaP-Pr90 treatment. Further, CBNP induced changes in mRNA expressions (surfactant proteins) in type II pneumocytes. These findings indicate that CBNP surface area and media modulate interactions between NP and lung cells in short-term experiments.