Abstract
Particle size and surface chemistry are potential determinants of silver nanoparticle (AgNP) respiratory toxicity that may also depend on the lung inflammatory state. We compared the effects of intratracheally-administered AgNPs (20nm and 110nm; polyvinylpyrrolidone (PVP) and citrate-capped; 0.1 mg/Kg) in Brown-Norway (BN) and Sprague-Dawley (SD) rats. In BN rats, there was both a neutrophilic and eosinophilic response, while in SD rats, there was a neutrophilic response at day 1, greatest for the 20nm citrate-capped AgNPs. Eosinophilic cationic protein was increased in bronchoalveolar lavage (BAL) in BN and SD rats on day 1. BAL protein and malondialdehyde levels were increased in BN rats at 1 and 7 days, and BAL KC, CCL11 and IL-13 levels at day 1, with increased expression of CCL11 in lung tissue. Pulmonary resistance increased and compliance decreased at day 1, with persistence at day 7. The 20nm, but not the 110 nm, AgNPs increased bronchial hyperresponsiveness on day 1, which continued at day 7 for the citrate-capped AgNPs only. The 20nm versus the 110 nm size were more proinflammatory in terms of neutrophil influx, but there was little difference between the citrate-capped versus the PVP-capped AgNPs. AgNPs can induce pulmonary eosinophilic and neutrophilic inflammation with bronchial hyperresponsiveness, features characteristic of asthma.
Highlights
Among the consumer products that contain engineered nanoparticles, one of the most common materials used is nanosilver [1, 2]
Eosinophillic Cationic Protein (ECP) in bronchoalveolar lavage (BAL) and lung In BN rats, BAL ECP levels increased following exposure to all AgNPs at day 1 except for Ag110cit, with levels returning to baseline by day 7, even though BAL eosinophils were persistently high at day 7 (Fig. 4C)
We investigated the impact of size and surface chemistry on the pulmonary toxicity of AgNPs by utilising well-dispersed AgNPs, with 20 and 110 nm diameters and two coating agents, PVP and citrate, designed to stabilise their dispersion
Summary
Among the consumer products that contain engineered nanoparticles, one of the most common materials used is nanosilver [1, 2]. There is growing concern that the widespread use of AgNPs in consumer products may impact negatively on human health, especially when these nanoparticles can be inhaled by workers handling these nanoparticles, and by domestic users and patients exposed to medical products containing AgNPs. The size and surface area of AgNPs are major determinants of pulmonary toxicity of AgNPs inhaled into the lungs that will affect bio-availability, surface charge and dissolution rates [6,7,8,9,10,11]. In vitro studies on pulmonary cells indicate that AgNPs can damage mitochondria and increase reactive-oxygen species [ROS] [22], leading to mitochondrial-dependent apoptosis [23]. How these contribute to the development of pulmonary inflammation and alterations in lung function remain unclear. To determine whether the pulmonary effects of intratracheally-instilled AgNPs administered at a single submaximal dose may be influenced by the pre-existing state of the lungs, we compared the responses of BN rats to the 20 nm AgNPs with those observed in the Sprague-Dawley (SD) rat [27]
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