Comparative pulmonary toxicity of inhaled nickel nanoparticles; role of deposited dose and solubility.

In this pilot study, we investigated which physicochemical properties of nickel hydroxide nanoparticles (nano-NH) were mainly responsible in inducing pulmonary toxicity. First, we studied the role of nickel ions solubilized from nano-NH by comparing the toxic effects of nano-NH to those of readily soluble nickel sulfate nanoparticles (nano-NS). Additionally, to test whether there was a non-specific stress response due to particle morphology, we compared the toxicity of nano-NH with that of carbon nanoparticles (nano-C) and titanium dioxide nanoparticles (nano-Ti), both of which had similar physical properties such as particle size and shape, to nano-NH.

Long-term inhalation exposure to nickel nanoparticles exacerbated atherosclerosis in a susceptible mouse model.

Background: Because associations have been reported between inhaled ambient ultrafine particles and increased risk of cardiopulmonary disease, it has been suggested that inhaled engineered nanoparticles (NPs) may also induce adverse effects on the cardiovascular system.

Objective: We examined the long-term cardiovascular effects of inhaled nickel hydroxide NPs (nano-NH) using a sensitive mouse model.

Methods: Hyperlipidemic, apoprotein E-deficient (ApoE-/-) mice were exposed to nano-NH at either 0 or 79 μg Ni/m3, via a whole-body inhalation system, for 5 hr/day, 5 days/week, for either 1 week or 5 months.

Age, strain, and gender as factors for increased sensitivity of the mouse lung to inhaled ozone.

Ozone (O(3)) is a respiratory irritant that leads to airway inflammation and pulmonary dysfunction. Animal studies show that neonates are more sensitive to O(3) inhalation than adults, and children represent a potentially susceptible population. This latter notion is not well established, and biological mechanisms underlying a predisposition to pollution-induced pulmonary effects are unknown.

Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice. VI. Gene expression in heart and lung tissue.

The purpose of this exploratory study within the integrated subchronic inhalation exposure study (Lippmann et al., 2005) was to identify genes in heart and lung tissue that changed in expression level as a result of subchronic exposure to concentrated ambient particles (CAPs). Identification of CAPs exposure-related changes in gene expression could serve in the formulation of mechanistic hypotheses and/or to suggest possible biomarkers of exposure.

O3-induced inflammation in prepregnant, pregnant, and lactating rats correlates with O3 dose estimated by 18O.

Previous studies have shown that rats late in pregnancy and throughout lactation are more susceptible to ozone (O3)-induced pulmonary inflammation than are prepregnant (virgin) or postlactating rats. The major aim of the present study was to determine whether these differences in response intensity could be accounted for by the O3 dose to the lower region of the lung. The relative O3 dose to the lower lung of groups of pregnant, lactating, and virgin female rats was estimated by measuring the incorporation of the 18O isotope into low-speed (cells) and high-speed (surfactant) pellets of bronchoalveolar lavage fluid immediately after acute exposure to 0.