Induction of Phosphorylated Tau Accumulation and Memory Impairment by Bisphenol A and the Protective Effects of Carnosic Acid in In Vitro and In Vivo.

Bisphenol A (BPA) is a component of polycarbonate plastics that has been implicated in memory impairment. The present study investigated the effect of carnosic acid (CA) on memory deficit induced by BPA and the role of Akt in this mechanism. First, SH-SY5Y cells were treated with 20 nM BPA and 1 µM CA for 12 h. The results showed that treatment of CA with BPA improved the alternation of IRS-1/Akt/GSK-3ß as well as the induction of ApoE and Ser396p-tau. Moreover, treatment of CA with BPA restored the signaling involved in long-term potentiation (LTP) effect, leading to induction of synaptic-related proteins, such as PSD-95, synapsin1a, and pro-BDNF. Wortmannin treatment alleviated the reversal by CA. Then, C57BL/6 J male mice were orally administered with CA to test the memory function in BPA treatment. The results showed that CA and RE can improve BPA-induced impairment of motor, recognition, and spatial memory by using open-field test (OFT), novel objective recognition test (NOR), and Y-maze test, respectively. Moreover, CA and RE improved the phosphorylation of tau and the reduction of PSD-95, synapsin1a, and pro-BDNF proteins induced by BPA. Therefore, the results indicated that CA decreased the phosphorylated tau and memory impairment induced by BPA through Akt pathway.

Factors affecting personal exposure to thoracic and fine particles and their components.

Central monitoring site (CMS) concentrations have been used to represent population-based personal exposures to particulate matter (PM) of ambient origin. We investigated the associations of the concentrations of PM(2.5) and PM(10) and their elemental components for elderly clinic patients with chronic obstructive pulmonary disease in two cities with different PM compositions, that is, New York City (NYC) and Seattle. Daily measurements of CMS, outdoor residential, and indoor PM(10) and PM(2.5) concentrations, as well as personal PM(10), were made concurrently for 12-consecutive winter days at 9 NYC and 15 Seattle residences, as well for 9 NYC residences in summer. Filters were analyzed for elemental components using X-ray fluorescence (XRF), and for black carbon (BC) by light reflectance, and outdoor-indoor-personal relationships of PM components were examined using mixed-effect models. Using sulfur (S) as a tracer of PM of ambient origin, the mean contributions of outdoor PM(2.5) was 55.2% of the indoor concentrations in NYC, and 80.0% in Seattle, and outdoor PM(2.5) in NYC and Seattle were 19.7 and 18.5% of personal PM(2.5) concentration. S was distributed homogeneously in both cities (R(2)=0.65), whereas nickel (R(2)=0.23) was much more spatially heterogeneous. Thus, CMS measurements can adequately reflect personal exposures for spatially uniform components, such as sulfate, but they are not adequate for components from more local sources.

Childhood exposure to fine particulate matter and black carbon and the development of new wheeze between ages 5 and 7 in an urban prospective cohort.

BACKGROUND: While exposures to urban fine particulate matter (PM(2.5)) and soot-black carbon (soot-BC) have been associated with asthma exacerbations, there is limited evidence on whether these pollutants are associated with the new development of asthma or allergy among young inner city children. We hypothesized that childhood exposure to PM(2.5) and the soot-BC component would be associated with the report of new wheeze and development of seroatopy in an inner city birth cohort. METHODS: As part of the research being conducted by the Columbia Center of Children's Environmental Health (CCCEH) birth cohort study in New York City, two-week integrated residential monitoring of PM(2.5), soot-BC (based on a multi-wavelength integrating sphere method), and modified absorption coefficient (Abs*; based on the smoke stain reflectometer) was conducted between October 2005 and May 2011 for 408 children at ages 5-6 years old. Residential monitoring was repeated 6 months later (n=262) to capture seasonal variability. New wheeze was identified through the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaires during up to 3 years of follow-up and compared to a reference group that reported never wheeze, remitted wheeze, or persistent wheeze. Specific immunoglobulin (Ig) E against cockroach, mouse, cat, and dust mite and total IgE levels was measured in sera at ages 5 and 7 years. RESULTS: PM(2.5), soot-BC, and Abs* measured at the first visit were correlated moderately with those at the second visit (Pearson r>0.44). Using logistic regression models, a positive association between PM(2.5) and new wheeze was found with adjusted odds ratio [95% confidence intervals] of 1.51 [1.05-2.16] per interquartile range (IQR). Positive but non-significant association was found between the development of new wheeze and soot-BC and (OR 1.40 [0.96-2.05]), and Abs* (OR 1.57 [0.91-2.68]); Significantly positive associations were found between air pollutant measurements and new wheeze when restricting to those participants with repeat home indoor measurements 6 months apart. Associations between pollutants and IgE levels were not detected. CONCLUSIONS: Our findings suggest that childhood exposure to indoor air pollution, much of which penetrated readily from outdoor sources, may contribute to the development of wheeze symptoms among children ages 5 to 7 years.

Residual oil combustion: a major source of airborne nickel in New York City.

On the basis of previous observations that: (1) both the nickel (Ni) concentration in ambient air fine particulate matter (PM(2.5)) and daily mortality rates in New York City (NYC) were much higher than in any other US city; and (2) that peaks in Ni concentration was strongly associated with cardiac function in a mouse model of atherosclerosis, we initiated a study of the spatial and seasonal distributions of Ni in NYC and vicinity to determine the feasibility of productive human population-based studies of the extent to which ambient fine particle Ni may account for cardiovascular health effects. Using available speciation data from previous studies at The New York University, Environmental Protection Agency's Speciation Trends Network; and the Interagency Monitoring of Protected Visual Environments network, we determined that Ni in NYC is on average 2.5 times higher in winter than in summer. This apparent seasonal gradient is absent, or much less pronounced, at NJ and CT speciation sites. Ni concentrations at a site on the east side of Manhattan and at two sites in the western portion of the Bronx were a factor of two higher than at a site on the west side of Manhattan, or at one at Queens College in eastern Queens County, indicating a strong spatial gradient within NYC. We conclude that the winter peaks of fine particle Ni indicate that space heating, which involves the widespread reliance on residual oil combustion in many older residential and commercial buildings in NYC, is a major source of ambient air Ni. Epidemiologic studies based on data generated by a network of speciation sites throughout NYC could effectively test the hypothesis that Ni could account for a significant portion of the excess mortality and morbidity that have been associated with elevated mass concentrations of PM(2.5).