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Community-based participatory research (CBPR) is increasingly being used by academics to address urban health and inequity. While its foundational literature emphasizes CBPR’s role in eschewing the traditional balance of power between communities and institutions, some scholars and grassroots activists note that it has not consistently delivered community-led, action-oriented strategies. Here we examine gaps between theory and current practice of CBPR. First, we assess its fundamental practices through social movement theory. Second, we examine narratives from grassroots leaders who have utilized CBPR in their environmental justice efforts. Three key facilitating factors are often cited for authentic applications of CBPR: (1) grounding research within community-specific opportunities for change, (2) collaborating with a strong community partner, and (3) facilitating flexibility in research processes. Building on previous scholarship, we investigate the complexity of CBPR implementation that may dampen its potency as a social change strategy and highlight the need for nuanced and critical application of best practices to suit local contexts. This is accomplished by pairing the theoretical framework with the experiences of four community leaders who are members of the Moving Forward Network (MFN). Narratives from their experiences with partnering with academic institutions speak to how theoretical complexities with CBPR occur in practice.

Purpose: This study evaluates and characterizes the choroid underlying congenital hypertrophy of the retinal pigment epithelium (CHRPE). Methods: Retrospective observational study of CHRPE at least 2 mm in diameter. Choroidal vascular architecture was qualitatively examined. Choroidal thickness was measured by 2 independent observers using enhanced depth imaging spectral domain optical coherence tomography. Results: Forty-six eyes of 46 patients with CHRPE were included. Thirty-two lesions had imaging sufficient for analysis. Haller’s layer was healthy in 18 (56%), thin in 13 (41%), and absent in 1 (2%). Sattler’s layer was atrophic in 30 (94%), and choriocapillaris was atrophic in 31 (97%). CHRPE with thinned Haller’s layer had significantly larger diameter. The mean sub-CHRPE choroidal thickness was 82.4 ± 7.9 µm, compared to a thickness of 148.4 ± 9.6 µm in the normal adjacent choroid (p < 0.0001). Mean retinal thickness overlying the CHRPE was 77.3 ± 4.3 µm, compared to a retinal thickness of 137.8 ± 2.9 µm overlying the normal adjacent choroid (p < 0.0001). Sub-CHRPE choroidal thickness was a mean of 56.2 ± 3.1% of the adjacent normal choroidal thickness. Conclusion: The underlying choroid CHRPE is thinner than the adjacent normal choroid. All layers of the choroid can be thin with a preference of the inner Sattler’s and choriocapillaris layers.

Background: Traffic-related air pollution (TRAP) has been associated with increased risk of airway inflammation in children with asthma. While epigenetic changes could potentially modulate TRAP-induced inflammatory responses, few studies have assessed the temporal pattern of exposure to TRAP, epigenetic changes and inflammation in children with asthma. Our goal was to test the time-lag patterns of personal exposure to TRAP, airway inflammation (measured as fractional exhaled nitric oxide, FeNO), and DNA methylation in the promoter regions of genes involved in nitric oxide synthesis among children with asthma.Methods: We measured personal exposure to black carbon (BC) and FeNO for up to 30 days in a panel of children with asthma. We collected 90 buccal cell samples for DNA methylation analysis from 18 children (5 per child). Methylation in promoter regions of nitric oxide synthase (NOS1, NOS2A, NOS3) and arginase (ARG1, ARG2) was assessed by bisulfite pyrosequencing. Linear-mixed effect models were used to test the associations of BC at different lag periods, percent DNA methylation at each site and FeNO level.Results: Exposure to BC was positively associated with FeNO, and negatively associated with DNA methylation in NOS3. We found strongest association between FeNO and BC at lag 0–6 hours while strongest associations between methylation at positions 1 and 2 in NOS3 and BC were at lag 13-24 hours and lag 0-24 hours, respectively. The strengths of associations were attenuated at longer lag periods. No significant associations between exposure to TRAP and methylation levels in other NOS and ARG isoforms were observed.Conclusions: Exposure to TRAP was associated with higher levels of FeNO and lower levels of DNA methylation in the promoter regions of the NOS3 gene, indicating that DNA methylation of the NOS3 gene could be an important epigenetic mechanism in physiological responses to TRAP in children with asthma.

Air concentrations of traffic-related air pollutants (TRAPs) vary in space and time within urban communities, presenting challenges for estimating human exposure and potential health effects. Conventional stationary monitoring stations/networks cannot effectively capture spatial characteristics. Alternatively, mobile monitoring approaches became popular to measure TRAPs along roadways or roadsides. However, these linear mobile monitoring approaches cannot thoroughly distinguish spatial variability from temporal variations in monitored TRAP concentrations. In this study, we used a novel mobile monitoring approach to simultaneously characterize spatial/temporal variations in roadside concentrations of TRAPs in urban settings. We evaluated the effectiveness of this mobile monitoring approach by performing concurrent measurements along two parallel paths perpendicular to a major roadway and/or along heavily trafficked roads at very narrow scale (one block away each other) within short time period (

Introduction. Ambient and traffic-related air pollution has been linked to exacerbation of asthma in adults and children. Our community-academic partnership is evaluating the effects of diesel emis...