Transformation and release of nanoparticle additives & byproducts from commercially available surface coatings on pressure treated lumber via dermal contact.

Production and marketing of "nano-enabled" products for consumer purchase has continued to expand. However, many questions remain about the potential release and transformation of these nanoparticle (NP) additives from products throughout their lifecycle. In this work, two surface coating products advertised as containing ZnO NPs as active ingredients, were applied to micronized copper azol (MCA) and aqueous copper azol (ACA) pressure treated lumber. Coated lumber was weathered outdoors for a period of six months and the surface was sampled using a method developed by the Consumer Product Safety Commission (CPSC) to track potential human exposure to ZnO NPs and byproducts through simulated dermal contact. Using this method, the total amount of zinc extracted during a single sampling event was <1 mg/m2 and no evidence of free ZnO NPs was found. Approximately 0.5% of applied zinc was removed via simulated dermal contact over 6-months, with increased weathering periods resulting in increased zinc release. XAFS analysis found that only 27% of the zinc in the as received coating could be described as crystalline ZnO and highlights the transformation of these mineral phases to organically bound zinc complexes during the six-month weathering period. Additionally, SEM images collected after sampling found no evidence of free NP ZnO release during simulated dermal contact. Both simulated dermal contact experiments, and separate leaching studies demonstrate the application of surface coating solutions to either MCA and ACA lumber will reduce the release of copper from the pressure treated lumber. This work provides clear evidence of the transformation of NP additives in consumer products during their use stage.

Release and transformation of ZnO nanoparticles used in outdoor surface coatings for UV protection.

A major area of growth for "nano-enabled" products has been the addition of nanoparticles (NPs) to surface coatings including paints, stains and sealants. Zinc oxide (ZnO) NPs, long used in sunscreens and sunblocks, have found growing use in surface coating formulations to increase their UV resistance, especially on outdoor products. In this work, ZnO NPs, marketed as an additive to paints and stains, were dispersed in Milli-Q water and a commercial deck stain. Resulting solutions were applied to either Micronized-Copper Azole (MCA) pressure treated lumber or a commercially available composite decking. A portion of coated surfaces were placed outdoors to undergo environmental weathering, while the remaining samples were stored indoors to function as experimental controls. Weathered and control treatments were subsequently sampled periodically for 6 months using a simulated dermal contact method developed by the Consumer Product Safety Commission (CPSC). The release of ZnO NPs, and their associated degradation products, was determined through sequential filtration, atomic spectroscopy, X-Ray Absorption Fine Structure Spectroscopy, and electron microscopy. Across all treatments, the percentage of applied zinc released through simulated dermal contact did not exceed 4%, although transformation and release of zinc was highly dependent on dispersion medium. For MCA samples weathered outdoors, water-based applications released significantly more zinc than stain-based, 180 ±â€¯28, and 65 ±â€¯9 mg/m2 respectively. Moreover, results indicate that the number of contact events drives material release.

Dermal transfer and environmental release of CeO2 nanoparticles used as UV inhibitors on outdoor surfaces: Implications for human and environmental health.

A major area of growth for "nano-enabled" consumer products have been surface coatings, including paints stains and sealants. Ceria (CeO2) nanoparticles (NPs) are of interest as they have been used as additives in these these products to increase UV resistance. Currently, there is a lack of detailed information on the potential release, and speciation (i.e., ion vs. particle) of CeO2 NPs used in consumer-available surface coatings during intended use scenarios. In this study, both Micronized-Copper Azole pressure-treated lumber (MCA), and a commercially available composite decking were coated with CeO2 NPs dispersed in Milli-Q water or wood stain. Coated surfaces were divided into two groups. The first was placed outdoors to undergo environmental weathering, while the second was placed indoors to act as experimental controls. Both weathered surfaces and controls were sampled over a period of 6months via simulated dermal contact using methods developed by the Consumer Product Safety Commission (CPSC). The size and speciation of material released was determined through sequential filtration, total metals analysis, X-Ray Absorption Fine Structure Spectroscopy, and electron microscopy. The total ceria release from MCA coated surfaces was found to be dependent on dispersion matrix with aqueous applications releasing greater quantities of CeO2 than stain based applications, 66±12mg/m2 and 36±7mg/m2, respectively. Additionally, a substantial quantity of CeO2 was reduced to Ce(III), present as Ce(III)-organic complexes, over the 6-month experimental period in aqueous based applications.

GABA-B Controls Persistent Na+ Current and Coupled Na+-Activated K+ Current.

The GABA-B receptor is densely expressed throughout the brain and has been implicated in many CNS functions and disorders, including addiction, epilepsy, spasticity, schizophrenia, anxiety, cognitive deficits, and depression, as well as various aspects of nervous system development. How one GABA-B receptor is involved in so many aspects of CNS function remains unanswered. Activation of GABA-B receptors is normally thought to produce inhibitory responses in the nervous system, but puzzling contradictory responses exist. Here we report that in rat mitral cells of the olfactory bulb, GABA-B receptor activation inhibits both the persistent sodium current (INaP) and the sodium-activated potassium current (IKNa), which is coupled to it. We find that the primary effect of GABA-B activation is to inhibit INaP, which has the secondary effect of inhibiting IKNa because of its dependence on persistent sodium entry for activation. This can have either a net excitatory or inhibitory effect depending on the balance of INaP/IKNa currents in neurons. In the olfactory bulb, the cell bodies of mitral cells are densely packed with sodium-activated potassium channels. These channels produce a large IKNa which, if constitutively active, would shunt any synaptic potentials traversing the soma before reaching the spike initiation zone. However, GABA-B receptor activation might have the net effect of reducing the IKNa blocking effect, thus enhancing the effectiveness of synaptic potentials.

Estimating dermal transfer of copper particles from the surfaces of pressure-treated lumber and implications for exposure.

Lumber pressure-treated with micronized copper was examined for the release of copper and copper micro/nanoparticles using a surface wipe method to simulate dermal transfer. In 2003, the wood industry began replacing CCA treated lumber products for residential use with copper based formulations. Micronized copper (nano to micron sized particles) has become the preferred treatment formulation. There is a lack of information on the release of copper, the fate of the particles during dermal contact, and the copper exposure level to children from hand-to-mouth transfer. For the current study, three treated lumber products, two micronized copper and one ionic copper, were purchased from commercial retailers. The boards were left to weather outdoors for approximately 1year. Over the year time period, hand wipe samples were collected periodically to determine copper transfer from the wood surfaces. The two micronized formulations and the ionic formulation released similar levels of total copper. The amount of copper released was high initially, but decreased to a constant level (~1.5mgm(-2)) after the first month of outdoor exposure. Copper particles were identified on the sampling cloths during the first two months of the experiment, after which the levels of copper were insufficient to collect interpretable data. After 1month, the particles exhibited minimal changes in shape and size. At the end of 2-months, significant deterioration of the particles was evident. Based on the wipe sample data, a playground visit may result in a potential exposure to 2.58mg of copper, which is near or exceeds the daily tolerable upper intake limits for children under the age of 8, if completely ingested through hand-to-mouth transfer. While nanoparticles were found, there is not enough information to estimate the exposure from the released particles due to a lack of published literature on copper carbonate.

Reassessment of the role of aromatic amino acid hydroxylases and the effect of infection by Toxoplasma gondii on host dopamine.

Toxoplasma gondii infection has been described previously to cause infected mice to lose their fear of cat urine. This behavioral manipulation has been proposed to involve alterations of host dopamine pathways due to parasite-encoded aromatic amino acid hydroxylases. Here, we report successful knockout and complementation of the aromatic amino acid hydroxylase AAH2 gene, with no observable phenotype in parasite growth or differentiation in vitro and in vivo. Additionally, expression levels of the two aromatic amino acid hydroxylases were negligible both in tachyzoites and in bradyzoites. Finally, we were unable to confirm previously described effects of parasite infection on host dopamine either in vitro or in vivo, even when AAH2 was overexpressed using the BAG1 promoter. Together, these data indicate that AAH enzymes in the parasite do not cause global or regional alterations of dopamine in the host brain, although they may affect this pathway locally. Additionally, our findings suggest alternative roles for the AHH enzymes in T. gondii, since AAH1 is essential for growth in nondopaminergic cells.

Fast phasic release properties of dopamine studied with a channel biosensor.

Few other neurotransmitters are of as intense interest to neuropsychiatry and neurology as dopamine, yet existing techniques to monitor dopamine release leave an important spatiotemporal gap in our understanding. Electrochemistry and fluorescence imaging tools have been developed to fill the gap, but these methods have important limitations. We circumvent these limitations by introducing a dopamine-gated chloride channel into rat dorsal striatal medium spiny neurons, targets of strong dopamine innervation, thereby transforming dopamine from a slow transmitter into a fast transmitter and revealing new opportunities for studying moment-to-moment regulation of dopamine release. We demonstrate pharmacological and biophysical properties of the channel that make it suitable for fast, local dopamine measurements, and we demonstrate for the first time spontaneous and evoked responses to vesicular dopamine release in the dorsal striatum. Evoked dopamine currents were separated into a fast, monosynaptic component and a slower-rising and decaying disynaptic component mediated by nicotinic receptor activation. In summary, LGC-53 represents a dopamine biosensor with properties suitable for temporal separation of distinct dopamine signals in targets of dopamine innervation.

The Parkinsonian mimetic, 6-OHDA, impairs axonal transport in dopaminergic axons.

6-hydroxydopamine (6-OHDA) is one of the most commonly used toxins for modeling degeneration of dopaminergic (DA) neurons in Parkinson's disease. 6-OHDA also causes axonal degeneration, a process that appears to precede the death of DA neurons. To understand the processes involved in 6-OHDA-mediated axonal degeneration, a microdevice designed to isolate axons fluidically from cell bodies was used in conjunction with green fluorescent protein (GFP)-labeled DA neurons. Results showed that 6-OHDA quickly induced mitochondrial transport dysfunction in both DA and non-DA axons. This appeared to be a general effect on transport function since 6-OHDA also disrupted transport of synaptophysin-tagged vesicles. The effects of 6-OHDA on mitochondrial transport were blocked by the addition of the SOD1-mimetic, Mn(III)tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP), as well as the anti-oxidant N-acetyl-cysteine (NAC) suggesting that free radical species played a role in this process. Temporally, microtubule disruption and autophagy occurred after transport dysfunction yet before DA cell death following 6-OHDA treatment. The results from the study suggest that ROS-mediated transport dysfunction occurs early and plays a significant role in inducing axonal degeneration in response to 6-OHDA treatment.

Rapid adaptation to mammalian sociality via sexually selected traits.

BACKGROUND: Laboratory studies show that the components of sexual selection (e.g., mate choice and intrasexual competition) can profoundly affect the development and fitness of offspring. Less is known, however, about the total effects of sexual selection on offspring in normal social conditions. Complex social networks, such as dominance hierarchies, regulate the opportunity for mating success, and are often missing from laboratory studies. Social selection is an extended view of sexual selection that incorporates competition during sexual and nonsexual interactions, and predicts complex evolutionary dynamics. Whether social selection improves or constrains offspring fitness is controversial. RESULTS: To identify fitness consequences of social selection, wild-derived mice that had bred under laboratory conditions for eight generations were re-introduced to naturalistic competition in enclosures for three consecutive generations (promiscuous line). In parallel, a control lineage bred in cages under random mate assignment (monogamous line). A direct competition experiment using second-generation animals revealed that promiscuous line males had greater reproductive success than monogamous line males (particularly during extra-territorial matings), in spite of higher mortality and equivalent success in social dominance and sperm competition. There were no major female fitness effects (though promiscuous line females had fewer litters than monogamous line females). This result suggested that selection primarily acted upon a sexually attractive male phenotype in the promiscuous line, a hypothesis we confirmed in female odor and mating preference trials. CONCLUSIONS: We present novel evidence for the strength of sexual selection under normal social conditions, and show rapid male adaptation driven largely by sexual trait expression, with tradeoffs in survivorship and female fecundity. Re-introducing wild-derived mice to competition quickly uncovers sexually selected phenotypes otherwise lost in normal colony breeding.