The Near-Road Exposures and Effects of Urban Air Pollutants Study (NEXUS) was designed to examine the relationship between near-roadway exposures to air pollutants and respiratory outcomes in a cohort of asthmatic children who live close to major roadways in Detroit, Michigan USA. From September 2010 to December 2012 a total of 139 children with asthma, ages 6–14, were enrolled in the study on the basis of the proximity of their home to major roadways that carried different amounts of diesel traffic. The goal of the study was to investigate the effects of traffic-associated exposures on adverse respiratory outcomes, biomolecular markers of inflammatory and oxidative stress, and how these exposures affect the frequency and severity of respiratory viral infections in a cohort of children with asthma. An integrated measurement and modeling approach was used to quantitatively estimate the contribution of traffic sources to near-roadway air pollution and evaluate predictive models for assessing the impact of near-roadway pollution on children’s exposures. Two intensive field campaigns were conducted in Fall 2010 and Spring 2011 to measure a suite of air pollutants including PM2.5 mass and composition, oxides of nitrogen (NO and NO2), carbon monoxide, and black carbon indoors and outdoors of 25 participants’ homes, at two area schools, and along a spatial transect adjacent to I-96, a major highway in Detroit. These data were used to evaluate and refine models to estimate air quality and exposures for each child on a daily basis for the health analyses. The study design and methods are described, and selected measurement results from the Fall 2010 field intensive are presented to illustrate the design and successful implementation of the study. These data provide evidence of roadway impacts and exposure variability between study participants that will be further explored for associations with the health measures.

BackgroundOver the past twenty years, racial/ethnic disparities between late-stage diagnoses and mortality outcomes have widened due to disproportionate medical benefits that different racial/ethnic groups have received. Few studies to date have examined the spatial relationships of racial/ethnic disparities between breast cancer late-stage diagnosis and mortality as well as the impact of socioeconomic status (SES) on these two disparities at finer geographic scales.MethodsThree methods were implemented to assess the spatial relationship between racial/ethnic disparities of breast cancer late-stage diagnosis and morality. First, this study used rate difference measure to test for racial/ethnic disparities in both late-stage diagnosis and mortality of female breast cancer in Texas during 1995-2005. Second, we used linear and logistic regression models to determine if there was a correlation between these two racial/ethnic disparities at the census tract level. Third, a geographically-weighted regression analysis was performed to evaluate if this correlation occurred after weighting for local neighbors.ResultsThe spatial association of racial disparities was found to be significant between late-stage diagnosis and breast cancer mortality with odds ratios of 33.76 (CI: 23.96-47.57) for African Americans and 30.39 (CI: 22.09-41.82) for Hispanics. After adjusting for a SES cofounder, logistic regression models revealed a reduced, although still highly significant, odds ratio of 18.39 (CI: 12.79-26.44) for African-American women and 11.64 (CI: 8.29-16.34) for Hispanic women. Results of the logistic regression analysis indicated that census tracts with low and middle SES were more likely to show significant racial disparities of breast cancer late-stage diagnosis and mortality rates. However, values of local correlation coefficients suggested that the association of these two types of racial/ethnic disparities varied across geographic regions.ConclusionsThis study may have health-policy implications that can help early detection of breast cancer among disadvantaged minority groups through implementing effective intervention programs in targeted regions.

Previous studies have reported that lower-income and minority populations are more likely to live near major roads. This study quantifies associations between socioeconomic status, racial/ethnic variables, and traffic-related exposure metrics for the United States. Using geographic information systems (GIS), traffic-related exposure metrics were represented by road and traffic densities at the census tract level. Spearman's correlation coefficients estimated relationships between socio-demographic variables and traffic-related exposure metrics, and ANOVA was performed to test for significant differences in socio-demographic variables for census tracts with low and high traffic-related metrics. For all census tracts in the United States, %Whites, %Blacks, and %Hispanics (percent of tract population) had correlation coefficients greater than 0.38 and 0.16 with road density and traffic density, respectively. Regions and states had correlation coefficients as high as 0.78. Compared with tracts with low road and traffic densities (<25th percentile), tracts with high densities (>75th percentile) had values of %Blacks and %Hispanics that were more than twice as high, 20% greater poverty levels, and one-third fewer White residents. Census tracts that had mid-level values for road and traffic densities had the most affluent characteristics. Results suggest that racial/ethnic and socioeconomic disparities exist on national level with respect to lower-income and minority populations living near high traffic and road density areas.

Viroids are circular noncoding RNAs that infect plants. Without encoding any protein, these noncoding RNAs contain the necessary genetic information for propagation in hosts. Nuclear-replicating viroids employ DNA-dependent RNA polymerase II (Pol II) for replication, a process that makes a DNA-dependent enzyme recognize RNA templates. Recently, a splicing variant of transcription factor IIIA (TFIIIA-7ZF) was identified as essential for Pol II to replicate potato spindle tuber viroid (PSTVd). The expression of TFIIIA-7ZF, particularly the splicing event, is regulated by a ribosomal protein (RPL5). PSTVd modulates its expression through a direct interaction with RPL5 resulting in optimized expression of TFIIIA-7ZF. This review summarizes the recent discoveries of host factors and regulatory mechanisms underlying PSTVd-templated transcription processes and raises new questions that may help future exploration in this direction. In addition, it briefly compares the machinery and the regulatory mechanism for PSTVd with the replication/transcription system of human hepatitis delta virus.