Quantifying the Distribution of Environmental Health Threats and Hazards in Washington State Using a Cumulative Environmental Inequality Index.

Background: Environmental racism, community stressors, and age-related susceptibility play a significant role in environmental inequality. The goal of this article was to use an inequality index (II) to assess the level of equality in environmental threats and hazards based on race, poverty, and age in Washington State. Methods: Using the Washington Environmental Health Disparities Map, we quantified the level of disproportionate burdens on communities with greater populations of people of color, people in poverty, children younger than 5, and people older than 65 using 3 cumulative environmental indices and 10 individual environmental indicators. Results: Census tracts with a higher proportion of people of color and those with people living below 185% federal poverty levels were found to be disproportionately burdened by environmental threats (II = -0.175 and II = -0.167, respectively, p < 0.001). Individual environmental indicators were found to disproportionately burden communities of color and low-income communities. Children younger than 5 were also disproportionately burdened by cumulative environmental indices (II = -0.076, p < 0.001) and individual indicators. Our analysis did not show disproportionate burden of environmental health threats based on the proportion of people older than 65 (II = 0.124, p < 0.001). Discussion: The disproportionate burden of the cumulative environmental threats on communities of color and low-income communities in this study corroborates similar analyses. These findings can be applied in policy and regulatory actions to correct the distributive environmental disparities. Conclusion: We found much higher burdens among historically marginalized communities and children who are more susceptible to environmental threats and hazards.

The Washington State Environmental Health Disparities Map: Development of a Community-Responsive Cumulative Impacts Assessment Tool.

Communities across Washington State have expressed the need for neighborhood-level information on the cumulative impact of environmental hazards and social conditions to illuminate disparities and address environmental justice issues. Many existing mapping tools have not explicitly integrated community voice and lived experience as an integral part of their development. The goals of this project were to create a new community-academic-government partnership to collect and summarize community concerns and to develop a publicly available mapping tool that ranks relative environmental health disparities for populations across Washington State. Using a community-driven framework, we developed the Washington Environmental Health Disparities Map, a cumulative environmental health impacts assessment tool. Nineteen regularly updated environmental and population indicators were integrated into the geospatial tool that allows for comparisons of the cumulative impacts between census tracts. This interactive map provides critical information for the public, agencies, policymakers, and community-based organizations to make informed decisions. The unique community-academic-government partnership and the community-driven framework can be used as a template for other environmental and social justice mapping endeavors.

Urinary metabolites of 1-nitropyrene in US-Mexico border residents who frequently cross the San Ysidro Port of Entry.

Diesel exhaust presents a community exposure hazard, but methods to measure internal exposure are lacking. We report results from a community-based study using 1-nitropyrene (1-NP) and its urinary metabolites as markers of exposure to traffic-related diesel particulate matter (DPM). The study participants were Tijuana, Mexico residents who commuted on foot into San Diego, California for work or school using the International San Ysidro Port of Entry, placing them within feet of idling traffic (referred to as border commuters). The comparison group (non-border commuters) was comprised of residents of south San Diego who did not commute into Mexico. Air concentration of 1-NP in fine particulate matter (PM2.5) was measured in personal samples from participants. Spot urine samples were analyzed for 1-NP urinary metabolites 8-hydroxy-1-nitropyrene (8-OHNP) and 8-hydroxy-N-acetyl-1-aminopyrene (8-OHNAAP). Compared with non-border commuters, border commuters had two- to threefold higher mean urinary concentrations for unadjusted and creatinine-adjusted 8-OHNP and 8-OHNAAP. Urinary 8-OHNAAP and the sum of 8-OHNP and 8-OHNAAP were both associated with personal exposure to 1-NP in the prior 24 h. These results suggest that 1-NP urinary metabolites reflect recent exposure to DPM-derived 1-NP in community settings and can be useful for exposure analysis.

Thirdhand smoke and exposure in California hotels: non-smoking rooms fail to protect non-smoking hotel guests from tobacco smoke exposure.

INTRODUCTION: This study examined tobacco smoke pollution (also known as thirdhand smoke, THS) in hotels with and without complete smoking bans and investigated whether non-smoking guests staying overnight in these hotels were exposed to tobacco smoke pollutants. METHODS: A stratified random sample of hotels with (n=10) and without (n=30) complete smoking bans was examined. Surfaces and air were analysed for tobacco smoke pollutants (ie, nicotine and 3-ethynylpyridine, 3EP). Non-smoking confederates who stayed overnight in guestrooms provided urine and finger wipe samples to determine exposure to nicotine and the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone as measured by their metabolites cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), respectively. FINDINGS: Compared with hotels with complete smoking bans, surface nicotine and air 3EP were elevated in non-smoking and smoking rooms of hotels that allowed smoking. Air nicotine levels in smoking rooms were significantly higher than those in non-smoking rooms of hotels with and without complete smoking bans. Hallway surfaces outside of smoking rooms also showed higher levels of nicotine than those outside of non-smoking rooms. Non-smoking confederates staying in hotels without complete smoking bans showed higher levels of finger nicotine and urine cotinine than those staying in hotels with complete smoking bans. Confederates showed significant elevations in urinary NNAL after staying in the 10 most polluted rooms. CONCLUSIONS: Partial smoking bans in hotels do not protect non-smoking guests from exposure to tobacco smoke and tobacco-specific carcinogens. Non-smokers are advised to stay in hotels with complete smoking bans. Existing policies exempting hotels from complete smoking bans are ineffective.

Improved participation for blood lead screening with in-home phlebotomy.

Both nationally and within the State of California, it is unlikely that those children most susceptible to lead exposure are adequately screened for blood lead levels. New and creative approaches are necessary to reach these individuals. In-home phlebotomy was employed to test blood lead levels of 128 San Diego households containing Latino children aged 12-71 months. As part of a lead exposure study, these households were randomly selected from 12 census tracts in the downtown area during February-July, 2006. By employing a bicultural/bilingual phlebotomist, the participation rate for in-home phlebotomy was 89% among enrolled study participants. This rate is substantially higher than estimates for customary testing of similar underserved groups through physicians, has the advantage of reaching individuals without medical insurance, and contrasts favorably ($45 per individual test) with typical office visit costs. Culturally appropriate in-home phlebotomy may be a useful method for medical screening to meet the needs of underserved communities. Editors' Strategic Implications: The authors provide an excellent example of the importance of bringing prevention services to clients, literally in terms of the home visitation format but also with respect to the comfort level that may come from interacting with a bicultural and bilingual professional.

Genetic modifiers of the Drosophila blue cheese gene link defects in lysosomal transport with decreased life span and altered ubiquitinated-protein profiles.

Defects in lysosomal trafficking pathways lead to decreased cell viability and are associated with progressive disorders in humans. Previously we have found that loss-of-function (LOF) mutations in the Drosophila gene blue cheese (bchs) lead to reduced adult life span, increased neuronal death, and widespread CNS degeneration that is associated with the formation of ubiquitinated-protein aggregates. To identify potential genes that participate in the bchs functional pathway, we conducted a genetic modifier screen based on alterations of an eye phenotype that arises from high-level overexpression of Bchs. We found that mutations in select autophagic and endocytic trafficking genes, defects in cytoskeletal and motor proteins, as well as mutations in the SUMO and ubiquitin signaling pathways behave as modifiers of the Bchs gain-of-function (GOF) eye phenotype. Individual mutant alleles that produced viable adults were further examined for bchs-like phenotypes. Mutations in several lysosomal trafficking genes resulted in significantly decreased adult life spans and several mutants showed changes in ubiquitinated protein profiles as young adults. This work represents a novel approach to examine the role that lysosomal transport and function have on adult viability. The genes characterized in this study have direct human homologs, suggesting that similar defects in lysosomal transport may play a role in human health and age-related processes.