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Rats were exposed to nickel oxide nanoparticles (NiO-NP) inhalation at 0.23 ± 0.01 mg/m3 for 4 h a day 5 times a week for up to 10 months. The rat organism responded to this impact with changes in cytological and some biochemical characteristics of the bronchoalveolar lavage fluid along with a paradoxically little pronounced pulmonary pathology associated with a rather low chronic retention of nanoparticles in the lungs. There were various manifestations of systemic toxicity, including damage to the liver and kidneys; a likely allergic syndrome as indicated by some cytological signs; transient stimulation of erythropoiesis; and penetration of nickel into the brain from the nasal mucous membrane along the olfactory pathway. Against a picture of mild to moderate chronic toxicity of nickel, its in vivo genotoxic effect assessed by the degree of DNA fragmentation in nucleated blood cells (the RAPD test) was pronounced, tending to increasing with the length of the exposure period. When rats were given orally, in parallel with the toxic exposure, a set of innocuous substances with differing mechanisms of expected bioprotective action, the genotoxic effect of NiO-NPs was found to be substantially attenuated.

We studied differences between phagocytic responses to nanoparticles (NPs) versus microparticles in the pulmonary region by synthesizing magnetite of different sizes and instilling suspensions of these particles intratracheally into rats' lungs. Ten and 50 nm particles caused a greater increase in cell counts of the bronchoalveolar lavage fluid (BALF) than the instillation of microparticles. The response to 10 nm particles was weaker than to 50 nm ones, and the smaller NPs were more cytotoxic; both were more cytotoxic than the microparticles. Phagocytic activity was also studied using optical and atomic force microscopy. Phagocytes were more "loaded" in the lungs instilled with 10 nm particles as compared with those instilled with 50 nm particles; NPs of both sizes were engulfed more avidly than microparticles. We found in a separate comparative experiment that magnetite NPs were more cytotoxic than titanium dioxide and quartz suspensions having particle size distribution typical of industrial dusts.

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Environment chemical pollution can be persistent, and even virtually irremovable. For some chemicals in the workplace environment reliably safe low exposure levels are technically unattainable or presumably nonexistent. As a supplement to decreasing harmful exposures to as low levels as possible, the "biological prophylaxis" aims at enhancing host's protective mechanisms. During over 30 years in animal experiments modeling isolated or combined chronic or subchronic exposures to silica, asbestos, monazite, lead, chromium, arsenic, manganese, nickel, vanadium, nanosilver, nanocopper, formaldehyde, phenol, naphthalene, benzo(a)pyrene we tested so-called "bioprophylatic complexes" (BPCs) comprising innocuous substances with theoretically expected beneficial influence on the toxicokinetics and/or toxicodynamics of those toxics. The BPCs proved protectively effective in animal experiments were then subjected to controlled field trials on restricted groups of volunteers. Once the effectiveness and safety of a BPC was established, it was recommended for practical use, first of all, in the most vulnerable population groups (children, pregnant women) and in the most harmful occupations. At each stage of this work the effectiveness of the bioprophylactic approach to chemical risks management was successfully demonstrated. The BPCs tested up to now proved capable of mitigating systemic toxicity, cytotoxicity, fibrogenicity, and mutagenicity of the above-listed chemicals. B. A. Katsnelson et al.