Subacute inhalation toxicity assessment of fly ash from industrial waste incinerators.

Fly ash from industrial waste incinerators has been a significant concern because of their constituent toxic heavy metals and organic compounds. The objective of this study was to identify the subacute inhalation toxicity of fly ash from industrial waste incinerators, using whole body inhalation exposure chambers. Male and female groups of Sprague-Dawley rats were exposed to fly ash by inhalation of concentrations of 0, 50, 100, 200 mg/m(3), for 6 h/day, 5 days/week for 4 weeks. There was no significant difference in body weight, and relative organ weight to body weight, between the exposure groups and the control group. Hematological examinations revealed a significant increase of monocyte counts in fly ash exposed rats and brown pigment laden macrophage was found in the lungs of rats exposed to high concentration of fly ash. A decrease of blood glucose levels and an increase in glutamate oxaloacetate transaminase activity were observed in fly ash treated rats. There was also a significant increase of lactate dehydrogenase levels in rat blood exposed fly ash. A significant dose-dependent increase of DNA damage was found in lymphocytes, spleen, bronchoalveolar lavage, liver, lung, and thymus of rats exposed to fly ash. In addition, the level of lipid peroxidation was increased in the plasma of rats exposed to a high concentration of fly ash. These results suggest that inhalation of fly ash from industrial waste incinerators can induce histopathologic, hematological, and serum biochemical changes and oxidative damage.

Multi-generational xenoestrogenic effects of Perfluoroalkyl acids (PFAAs) mixture on Oryzias latipes using a flow-through exposure system.

To elucidate the multi-generational estrogenic potential of Perfluoroalkyl acids (PFAAs) mixture, vitellogenin (VTG) expression, growth indices, histological alteration, fecundity, hatching rate, larval survival rate, and sex ratio of Japanese medaka (Oryzias latipes) were investigated by exposing the fish to a mixture of perfluorooctane sulfonate (PFOS), perfluroroctanoic acid (PFOA), perfluorobutane sulfonate (PFBS), and perfluorononanoic acid (PFNA) for three generations (238 days). Mixture composition is in the ratio of 1:1:1:1. In addition, whole body burden for each PFAA was analyzed. According to the results, concentrated levels of the PFAAs in both F1 and F2 generation O. latipes were ordered PFOS > PFNA > PFOA > PFBS at both low concentration (0.5 µg/L) and high concentration (5 µg/L), whereas a significant difference in whole body burden based on sex or generation was not detected. Significant induction of VTG expression in F2 and the decline of the gonad somatic index (GSI) in F1 were observed following PFAAs mixture exposure (p < 0.05, one-way ANOVA). Furthermore, suppression level of reproduction rate relative to the control increased as generation was transferred to the next in response to PFAAs mixture or 17 ß-estradiol exposure, with the inhibition of hatchability observed in the F1 generation. The PFAA high concentration caused significant alteration of F1 generation sex ratio, suggesting the adverse effect of PFAA in population level (Chi-square test, P > 0.05). Overall, this study demonstrated that PFAA mixture could have the potential of multi-generational endocrine disruptors in O. latipes.

Stepwise embryonic toxicity of silver nanoparticles on Oryzias latipes.

The developmental toxicity of silver nanoparticles (AgNPs) was investigated following exposure of Oryzias latipes (medaka) embryos to 0.1-1 mg/L of homogeneously dispersed AgNPs for 14 days. During this period, developmental endpoints, including lethality, heart rate, and hatching rate, were evaluated by microscopy for different stages of medaka embryonic development. To compare toxic sensitivity, acute adult toxicity was assessed. There was no difference in acute lethal toxicity between embryo and adult medaka. Interestingly, we found that the increase in stepwise toxicity was dependent on the developmental stage of the embryo. Lethal embryonic toxicity increased from exposure days 1 to 3 and exposure days 5 to 8, whereas there was no change from exposure days 3 to 5. In addition, 7 d exposure to 0.8 mg/L AgNPs resulted in significant heart beat retardation in medaka embryos. AgNPs also caused a dose-dependent decrease in the hatching rate and body length of larvae. These results indicate that AgNP exposure causes severe developmental toxicity to medaka embryos and that toxicity levels are enhanced at certain developmental stages, which should be taken into consideration in assessments of metallic NPs toxicity to embryos.