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Waste and materials management, land use planning, transportation and infrastructure including water and energy can have indirect or direct beneficial impacts on the environment and public health. The potential for impact, however, is rarely viewed in an integrated fashion. To facilitate such an integrated view in support of community-based policy decision making, we catalogued and evaluated associations between common, publically available, Environmental (e), Health (h), and Sustainability (s) metrics and sociodemographic measurements (n = 10) for 50 populous U.S. cities. E, H, S indices combined from two sources were derived from component (e) (h) (s) metrics for each city. A composite EHS Index was derived to reflect the integration across the E, H, and S indices. Rank order of high performing cities was highly dependent on the E, H and S indices considered. When viewed together with sociodemographic measurements, our analyses further the understanding of the interplay between these broad categories and reveal significant sociodemographic disparities (e.g., race, education, income) associated with low performing cities. Our analyses demonstrate how publically available environmental, health, sustainability and socioeconomic data sets can be used to better understand interconnections between these diverse domains for more holistic community assessments.
Jane E. Gallagher; Elaine Cohen Hubal; Laura Jackson; Jefferson Inmon; Edward Hudgens; Ann H. Williams; Danelle Lobdell; John Rogers; Timothy Wade. Sustainability, Health and Environmental Metrics: Impact on Ranking and Associations with Socioeconomic Measures for 50 U.S. Cities. Sustainability 2013, 5, 789 -804.
AMA StyleJane E. Gallagher, Elaine Cohen Hubal, Laura Jackson, Jefferson Inmon, Edward Hudgens, Ann H. Williams, Danelle Lobdell, John Rogers, Timothy Wade. Sustainability, Health and Environmental Metrics: Impact on Ranking and Associations with Socioeconomic Measures for 50 U.S. Cities. Sustainability. 2013; 5 (2):789-804.
Chicago/Turabian StyleJane E. Gallagher; Elaine Cohen Hubal; Laura Jackson; Jefferson Inmon; Edward Hudgens; Ann H. Williams; Danelle Lobdell; John Rogers; Timothy Wade. 2013. "Sustainability, Health and Environmental Metrics: Impact on Ranking and Associations with Socioeconomic Measures for 50 U.S. Cities." Sustainability 5, no. 2: 789-804.
Complex diseases are often difficult to diagnose, treat and study due to the multi-factorial nature of the underlying etiology. Large data sets are now widely available that can be used to define novel, mechanistically distinct disease subtypes (endotypes) in a completely data-driven manner. However, significant challenges exist with regard to how to segregate individuals into suitable subtypes of the disease and understand the distinct biological mechanisms of each when the goal is to maximize the discovery potential of these data sets.
ClarLynda R Williams-DeVane; David M Reif; Elaine Cohen Hubal; Pierre R Bushel; Edward E Hudgens; Jane E Gallagher; Stephen W Edwards. Decision tree-based method for integrating gene expression, demographic, and clinical data to determine disease endotypes. BMC Systems Biology 2013, 7, 119 -119.
AMA StyleClarLynda R Williams-DeVane, David M Reif, Elaine Cohen Hubal, Pierre R Bushel, Edward E Hudgens, Jane E Gallagher, Stephen W Edwards. Decision tree-based method for integrating gene expression, demographic, and clinical data to determine disease endotypes. BMC Systems Biology. 2013; 7 (1):119-119.
Chicago/Turabian StyleClarLynda R Williams-DeVane; David M Reif; Elaine Cohen Hubal; Pierre R Bushel; Edward E Hudgens; Jane E Gallagher; Stephen W Edwards. 2013. "Decision tree-based method for integrating gene expression, demographic, and clinical data to determine disease endotypes." BMC Systems Biology 7, no. 1: 119-119.
Health, socioeconomic, education, and environmental (e.g. air and water quality) indicators are often correlated and may serve as markers for other underlying community issues. These diverse measurements are usually not fully integrated and rarely evaluated in the context of sustainability metrics. We derived an integrated community health index (ICHI) for 50 of the most populous cities in the US using extant environmental, health and sustainability metrics and assessed relationships with sociodemographic measures. To derive the ICHI we used data from two sources: 1) SustainLane\'s (www.sustainlane.com) 2008 report card on urban sustainability which includes metrics such as energy and climate change policy, metro street congestion, metro transit ridership, and natural disaster risk, and 2) Earth Day Network\'s (www.eathday.net) Urban environmental report including a health metric which incorporates asthma, cardiovascular disease, diabetes, and obesity rates; and three environmental variables a) toxics and waste b) air quality c) drinking and surface water quality. Using these metrics we developed three separate indicators for health, sustainability and environment for each city. The ICHI was created by averaging across these three indicators. We used data from the 2010 Census (median family income, % of persons below the poverty level, % with a high school degree, % with college degree, and racial diversity (% White, nonwhite Black, Asian, and Hispanic) to assess relationships between the ICHI and sociodemographic characteristics. We compare mean values for various demographic measures for those cities with the "best" integrated community health index (highest 25th percentile) with those cities in the lower 25th percentile using t-tests. Cities with the better ICHI demonstrated 1) a higher % of persons with health insurance (20.1 vs 13.4 %; pth percentile) with those cities in the lowest 25thpercentile demonstrated 1) a lower score for toxic and waste (2.85 vs. 3.48; p
Jane Gallagher; Timothy Wade; Laura Jackson; Danelle Lobdell; Jyotsna Jagai; Jefferson Inmon; Elaine Cohen-Hubal. Correlates of Health, Sustainability and Environmental Metrics for 50 of the Most Populous U.S. Cities. Proceedings of The 1st World Sustainability Forum 2011, 1 .
AMA StyleJane Gallagher, Timothy Wade, Laura Jackson, Danelle Lobdell, Jyotsna Jagai, Jefferson Inmon, Elaine Cohen-Hubal. Correlates of Health, Sustainability and Environmental Metrics for 50 of the Most Populous U.S. Cities. Proceedings of The 1st World Sustainability Forum. 2011; ():1.
Chicago/Turabian StyleJane Gallagher; Timothy Wade; Laura Jackson; Danelle Lobdell; Jyotsna Jagai; Jefferson Inmon; Elaine Cohen-Hubal. 2011. "Correlates of Health, Sustainability and Environmental Metrics for 50 of the Most Populous U.S. Cities." Proceedings of The 1st World Sustainability Forum , no. : 1.
Asthma is a common complex disease responsible for considerable morbidity and mortality, particularly in urban minority populations. The Mechanistic Indicators of Childhood Asthma study was designed to pilot an integrative approach in children's health research. The study incorporates exposure metrics, internal dose measures, and clinical indicators to decipher the biological complexity inherent in diseases such as asthma and cardiovascular disease with etiology related to gene-environment interactions.
Jane Gallagher; Edward Hudgens; Ann Williams; Jefferson Inmon; Scott Rhoney; Gina Andrews; David Reif; Brooke Heidenfelder; Lucas Neas; Ronald Williams; Markey Johnson; Haluk Özkaynak; Stephen Edwards; Elaine Cohen Hubal. Mechanistic Indicators of Childhood Asthma (MICA) Study: piloting an integrative design for evaluating environmental health. BMC Public Health 2011, 11, 344 -344.
AMA StyleJane Gallagher, Edward Hudgens, Ann Williams, Jefferson Inmon, Scott Rhoney, Gina Andrews, David Reif, Brooke Heidenfelder, Lucas Neas, Ronald Williams, Markey Johnson, Haluk Özkaynak, Stephen Edwards, Elaine Cohen Hubal. Mechanistic Indicators of Childhood Asthma (MICA) Study: piloting an integrative design for evaluating environmental health. BMC Public Health. 2011; 11 (1):344-344.
Chicago/Turabian StyleJane Gallagher; Edward Hudgens; Ann Williams; Jefferson Inmon; Scott Rhoney; Gina Andrews; David Reif; Brooke Heidenfelder; Lucas Neas; Ronald Williams; Markey Johnson; Haluk Özkaynak; Stephen Edwards; Elaine Cohen Hubal. 2011. "Mechanistic Indicators of Childhood Asthma (MICA) Study: piloting an integrative design for evaluating environmental health." BMC Public Health 11, no. 1: 344-344.
Asthma and allergy represent complex phenotypes, which disproportionately burden ethnic minorities in the United States. Strong evidence for genomic factors predisposing subjects to asthma/allergy is available. However, methods to utilize this information to identify high risk groups are variable and replication of genetic associations in African Americans is warranted.
Bonnie R Joubert; David M Reif; Stephen W Edwards; Kevin A Leiner; Edward E Hudgens; Peter Egeghy; Jane E Gallagher; Elaine Cohen Hubal. Evaluation of genetic susceptibility to childhood allergy and asthma in an African American urban population. BMC Medical Genetics 2011, 12, 25 -11.
AMA StyleBonnie R Joubert, David M Reif, Stephen W Edwards, Kevin A Leiner, Edward E Hudgens, Peter Egeghy, Jane E Gallagher, Elaine Cohen Hubal. Evaluation of genetic susceptibility to childhood allergy and asthma in an African American urban population. BMC Medical Genetics. 2011; 12 (1):25-11.
Chicago/Turabian StyleBonnie R Joubert; David M Reif; Stephen W Edwards; Kevin A Leiner; Edward E Hudgens; Peter Egeghy; Jane E Gallagher; Elaine Cohen Hubal. 2011. "Evaluation of genetic susceptibility to childhood allergy and asthma in an African American urban population." BMC Medical Genetics 12, no. 1: 25-11.
The Mechanistic Indicators of Childhood Asthma (MICA) study in Detroit, Michigan introduced a participant-based approach to reduce the resource burden associated with collection of indoor and outdoor residential air sampling data. A subset of participants designated as MICA-Air conducted indoor and outdoor residential sampling of nitrogen dioxide (NO2), volatile organic compounds (VOCs), and polycyclic aromatic hydrocarbons (PAHs). This participant-based methodology was subsequently adapted for use in the Vanguard phase of the U.S. National Children’s Study. The current paper examines residential indoor and outdoor concentrations of these pollutant species among health study participants in Detroit, Michigan. Pollutants measured under MICA-Air agreed well with other studies and continuous monitoring data collected in Detroit. For example, NO2 and BTEX concentrations reported for other Detroit area monitoring were generally within 10–15% of indoor and outdoor concentrations measured in MICA-Air households. Outdoor NO2 concentrations were typically higher than indoor NO2 concentration among MICA-Air homes, with a median indoor/outdoor (I/O) ratio of 0.6 in homes that were not impacted by environmental tobacco smoke (ETS) during air sampling. Indoor concentrations generally exceeded outdoor concentrations for VOC and PAH species measured among non-ETS homes in the study. I/O ratios for BTEX species (benzene, toluene, ethylbenzene, and m/p- and o-xylene) ranged from 1.2 for benzene to 3.1 for toluene. Outdoor NO2 concentrations were approximately 4.5 ppb higher on weekdays versus weekends. As expected, I/O ratios pollutants were generally higher for homes impacted by ETS. These findings suggest that participant-based air sampling can provide a cost-effective alternative to technician-based approaches for assessing indoor and outdoor residential air pollution in community health studies. We also introduced a technique for estimating daily concentrations at each home by weighting 2- and 7-day integrated concentrations using continuous measurements from regulatory monitoring sites. This approach may be applied to estimate short-term daily or hourly pollutant concentrations in future health studies.
Markey M. Johnson; Ron Williams; Zhihua Fan; Lin Lin; Edward Hudgens; Jane Gallagher; Alan Vette; Lucas Neas; Haluk Özkaynak. Participant-based monitoring of indoor and outdoor nitrogen dioxide, volatile organic compounds, and polycyclic aromatic hydrocarbons among MICA-Air households. Atmospheric Environment 2010, 44, 4927 -4936.
AMA StyleMarkey M. Johnson, Ron Williams, Zhihua Fan, Lin Lin, Edward Hudgens, Jane Gallagher, Alan Vette, Lucas Neas, Haluk Özkaynak. Participant-based monitoring of indoor and outdoor nitrogen dioxide, volatile organic compounds, and polycyclic aromatic hydrocarbons among MICA-Air households. Atmospheric Environment. 2010; 44 (38):4927-4936.
Chicago/Turabian StyleMarkey M. Johnson; Ron Williams; Zhihua Fan; Lin Lin; Edward Hudgens; Jane Gallagher; Alan Vette; Lucas Neas; Haluk Özkaynak. 2010. "Participant-based monitoring of indoor and outdoor nitrogen dioxide, volatile organic compounds, and polycyclic aromatic hydrocarbons among MICA-Air households." Atmospheric Environment 44, no. 38: 4927-4936.
The interaction between air particulates and genetic susceptibility has been implicated in the pathogenesis of asthma. The overall objective of this study was to determine the effects of inhalation exposure to environmentally relevant concentrated air particulates (CAPs) on the lungs of ovalbumin (ova) sensitized and challenged Brown Norway rats. Changes in gene expression were compared with lung tissue histopathology, morphometry, and biochemical and cellular parameters in bronchoalveolar lavage fluid (BALF). Ova challenge was responsible for the preponderance of gene expression changes, related largely to inflammation. CAPs exposure alone resulted in no significant gene expression changes, but CAPs and ova-exposed rodents exhibited an enhanced effect relative to ova alone with differentially expressed genes primarily related to inflammation and airway remodeling. Gene expression data was consistent with the biochemical and cellular analyses of the BALF, the pulmonary pathology, and morphometric changes when comparing the CAPs-ova group to the air-saline or CAPs-saline group. However, the gene expression data were more sensitive than the BALF cell type and number for assessing the effects of CAPs and ova versus the ova challenge alone. In addition, the gene expression results provided some additional insight into the TGF-β–mediated molecular processes underlying these changes. The broad-based histopathology and functional genomic analyses demonstrate that exposure to CAPs exacerbates rodents with allergic inflammation induced by an allergen and suggests that asthmatics may be at increased risk for air pollution effects.
Brooke L. Heidenfelder; David M. Reif; Jack R. Harkema; Elaine A. Cohen Hubal; Edward E. Hudgens; Lori A. Bramble; James G. Wagner; Masako Morishita; Gerald J. Keeler; Stephen W. Edwards; Jane E. Gallagher. Comparative Microarray Analysis and Pulmonary Changes in Brown Norway Rats Exposed to Ovalbumin and Concentrated Air Particulates. Toxicological Sciences 2009, 108, 207 -221.
AMA StyleBrooke L. Heidenfelder, David M. Reif, Jack R. Harkema, Elaine A. Cohen Hubal, Edward E. Hudgens, Lori A. Bramble, James G. Wagner, Masako Morishita, Gerald J. Keeler, Stephen W. Edwards, Jane E. Gallagher. Comparative Microarray Analysis and Pulmonary Changes in Brown Norway Rats Exposed to Ovalbumin and Concentrated Air Particulates. Toxicological Sciences. 2009; 108 (1):207-221.
Chicago/Turabian StyleBrooke L. Heidenfelder; David M. Reif; Jack R. Harkema; Elaine A. Cohen Hubal; Edward E. Hudgens; Lori A. Bramble; James G. Wagner; Masako Morishita; Gerald J. Keeler; Stephen W. Edwards; Jane E. Gallagher. 2009. "Comparative Microarray Analysis and Pulmonary Changes in Brown Norway Rats Exposed to Ovalbumin and Concentrated Air Particulates." Toxicological Sciences 108, no. 1: 207-221.
Asthma is a disorder characterized by inflammation of the airways. Oxidative stress may play a role in the pathophysiology of several diseases including asthma. Characterizing biomarkers of oxidative stress in the context of other systemic measures of immune function or inflammation could provide insight regarding underlying mechanisms inducing asthma. We evaluated whether oxidative stress in the form of plasma reactive oxidants differs between asthmatic and non-asthmatic children and elucidate relationships between plasma reactive oxidants and other asthma-related immunological markers. Plasma reactive oxidants, white blood cell counts, total serum immunoglobulin E (IgE), and a multi-allergen-specific IgE screen were measured in 74 asthmatic and 74 non-asthmatic children (9 to 13 years of age) from the Detroit, Michigan area. Plasma reactive oxidants were measured using a lucigenin-based chemiluminescence assay. Plasma reactive oxidants, eosinophils, and neutrophils (absolute counts and percent of total white blood cell counts), total IgE, and allergen-specific IgE levels were elevated in asthmatics after adjusting for age, gender, and ethnicity. IgE (total or allergen-specific), eosinophils and neutrophils were not significantly associated with plasma reactive oxidant levels. The association between plasma reactive oxidants and asthma status was similar when eosinophils, neutrophils, total IgE, or allergen-specific IgE were included as possible confounders in multivariate logistic regression models. In conclusion, plasma reactive oxidants are elevated in asthmatics and appear to be an independent predictor of asthma status. Measurement of plasma reactive oxidants may be a useful adjunct diagnostic tool and potential mechanistic indicator relevant to the study of asthma and asthma exacerbation.
Brooke Heidenfelder; Markey Johnson; Edward Hudgens; Jefferson Inmon; Robert G Hamilton; Lucas Neas; Jane E. Gallagher. Increased Plasma Reactive Oxidant Levels and Their Relationship to Blood Cells, Total IgE, and Allergen-specific IgE Levels in Asthmatic Children. Journal of Asthma 2009, 46, 687 -691.
AMA StyleBrooke Heidenfelder, Markey Johnson, Edward Hudgens, Jefferson Inmon, Robert G Hamilton, Lucas Neas, Jane E. Gallagher. Increased Plasma Reactive Oxidant Levels and Their Relationship to Blood Cells, Total IgE, and Allergen-specific IgE Levels in Asthmatic Children. Journal of Asthma. 2009; 46 (7):687-691.
Chicago/Turabian StyleBrooke Heidenfelder; Markey Johnson; Edward Hudgens; Jefferson Inmon; Robert G Hamilton; Lucas Neas; Jane E. Gallagher. 2009. "Increased Plasma Reactive Oxidant Levels and Their Relationship to Blood Cells, Total IgE, and Allergen-specific IgE Levels in Asthmatic Children." Journal of Asthma 46, no. 7: 687-691.
Chronic high-dose inhalation of carbon black (CB) can produce carcinomas in rat lungs. The mechanisms underlying this response are uncertain. It has been hypothesized that chronic inflammation and cell proliferation may play a role in the development of tumors after high dose, long-term contact of the particles with lung epithelial cells. In this investigation, we analyzed the formation of a known mutagenic lesion [8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxo-dG)] in the lung DNA of rats following subchronic inhalation of CB (Printex-90 and Sterling V). Briefly, female Fischer 344 rats were exposed for 6 h/day, 5 days/week for 13 weeks to 1, 7, and 50 mg/m3 of Printex-90 (16 nm; specific surface area 300 m2/g) and to 50 mg/m3 of Sterling V CB (70 nm; surface area of 37 m2/g). The exposure concentration of Sterling V was selected to be equivalent in terms of retained mass in the lung to the high dose of Printex-90 at the end of exposure. However, in terms of retained particle surface area, the retained lung dose of Sterling V was equivalent to the mid-dose of Printex 90. This design allows comparison of results on the basis of retained particle mass as well as retained particle surface area between the two CB particles. The formation of 8-oxo-dG in the lung DNA was assessed using a reverse phase HPLC system coupled with UV and electrochemical (EC) detection. After 13 weeks of exposure, measurements were made on lung samples obtained at the end of the exposure and a 44-week recovery period in clean air. Lung burdens of CB were determined at both time points as well as differential cell populations from bronchoalveolar lavage fluid (BAL). The results indicate that lung particle overload was achieved after exposure to 7 and 50 mg/m3 (Printex-90) and 50 mg/m3 (Sterling V) but not at 1 mg/m3 (Printex-90). Consistent with these results, a significant increase (P < 0.05) in 8-oxo-dG induction was observed following 13 weeks of exposure to 50 mg/m3 Printex-90 and at 7 and 50 mg/m3 after the 44-week recovery period. Interestingly, no increase in 8-oxo-dG was observed for Sterling V CB at either time point despite lung particle overload. Although the retained mass dose of Sterling V at the end of exposure was even higher than for Printex 90 (50 mg/m3 exposure group) (∼7.6 vs 4.8 mg), the surface area of the retained Sterling V was similar to that of the retained Printex 90 of the mid-dose exposure (7 mg/m3) (∼0.2 m2 in both groups). Since both Sterling V (50 mg/m3) and Printex 90 (7 mg/m3) did not induce significant increases in 8-oxo-dG in the lung at the end of the 13-week exposure, this finding indicates that a retained large particle mass is not always correlated with similar adverse effects but that particle surface area is a better dose parameter. The lower effect per unit mass dose seen with Sterling V is consistent with earlier studies showing that particle surface area of low toxicity particles is a more appropriate dosemetric for induction of inflammation in the lungs than particle mass (Oberdörster et al., 1994, 2001; Brown et al. 2001; Donaldson et al., 2002). An increase (p < 0.05) in lung lavage neutrophils was observed at 7 mg/m3 (Printex-90) and 50 mg/m3 (Printex-90 and Sterling V) at the 13-week exposure period and again at 50 mg/m3 (Printex-90 and Sterling V, 44-week recovery period). Our current findings suggest that prolonged, high-dose exposure to CB can promote oxidative DNA damage that is consistent with the hypothesis that inflammatory cell-derived oxidants may play a role in the pathogenesis of rat lung tumors following long-term high-dose exposure to CB in rats.
J Gallagher; R Sams; J Inmon; R Gelein; A Elder; G Oberdörster; A.K Prahalad. Formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine in rat lung DNA following subchronic inhalation of carbon black. Toxicology and Applied Pharmacology 2003, 190, 224 -231.
AMA StyleJ Gallagher, R Sams, J Inmon, R Gelein, A Elder, G Oberdörster, A.K Prahalad. Formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine in rat lung DNA following subchronic inhalation of carbon black. Toxicology and Applied Pharmacology. 2003; 190 (3):224-231.
Chicago/Turabian StyleJ Gallagher; R Sams; J Inmon; R Gelein; A Elder; G Oberdörster; A.K Prahalad. 2003. "Formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine in rat lung DNA following subchronic inhalation of carbon black." Toxicology and Applied Pharmacology 190, no. 3: 224-231.