Abstract
BackgroundThe exact role of primary nanoparticle (NP) size and their degree of agglomeration in aerosols on the determination of pulmonary effects is still poorly understood. Smaller NP are thought to have greater biological reactivity, but their level of agglomeration in an aerosol may also have an impact on pulmonary response. The aim of this study was to investigate the role of primary NP size and the agglomeration state in aerosols, using well-characterized TiO2 NP, on their relative pulmonary toxicity, through inflammatory, cytotoxic and oxidative stress effects in Fisher 344 male rats.MethodsThree different sizes of TiO2 NP, i.e., 5, 10–30 or 50 nm, were inhaled as small (SA) (< 100 nm) or large agglomerates (LA) (> 100 nm) at 20 mg/m3 for 6 hours.ResultsCompared to the controls, bronchoalveolar lavage fluids (BALF) showed that LA aerosols induced an acute inflammatory response, characterized by a significant increase in the number of neutrophils, while SA aerosols produced significant oxidative stress damages and cytotoxicity. Data also demonstrate that for an agglomeration state smaller than 100 nm, the 5 nm particles caused a significant increase in cytotoxic effects compared to controls (assessed by an increase in LDH activity), while oxidative damage measured by 8-isoprostane concentration was less when compared to 10–30 and 50 nm particles. In both SA and LA aerosols, the 10–30 nm TiO2 NP size induced the most pronounced pro-inflammatory effects compared to controls.ConclusionsOverall, this study showed that initial NP size and agglomeration state are key determinants of nano-TiO2 lung inflammatory reaction, cytotoxic and oxidative stress induced effects.
Highlights
The exact role of primary nanoparticle (NP) size and their degree of agglomeration in aerosols on the determination of pulmonary effects is still poorly understood
With respect to hazard identification, our results indicate that even though large agglomerate (LA) aerosols induced an acute inflammatory response, which is reversible according to the literature [9,19,32,45,70,72], it cannot be concluded that these aerosols induce toxicity through the same mechanisms as SA aerosols, which showed clear oxidative stress damage in bronchoalveolar lavage fluids (BALF)
In summary, the results of this study suggest that the initial NP size and the agglomeration state are key determinants of nano-TiO2 lung inflammatory reaction, cytotoxic and oxidative stress induced effects
Summary
The exact role of primary nanoparticle (NP) size and their degree of agglomeration in aerosols on the determination of pulmonary effects is still poorly understood. Nanoparticles (NP) (< 100 nm) have attracted the increased attention of the industrial sector due to their unique physico-chemical properties and numerous applications Compared to their larger-sized counterparts, NP have improved and distinctive surface characteristics which are considered as the building blocks of nanotechnology. An increasing number of workers are Several toxicological studies have addressed the micro versus the nano size effect This has indicated at equivalent mass concentration that agglomerated NP produce greater pulmonary inflammation responses than micron size particles [4,5,6,7,8]. The biological reactivity of smaller NP is expected to be higher than that of larger NP [16] It is at approximately 20 nm that the highest relative deposition efficiency of NP in the alveolar region occurs [17,18]. This suggests that NP of different initial sizes could produce different biological responses [16,19]
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