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  • 1
    Language: English
    In: American journal of public health, December 2011, Vol.101 Suppl 1, pp.S94-101
    Description: Genetic factors, other exposures, individual disease states and allostatic load, psychosocial stress, and socioeconomic position all have the potential to modify the response to environmental exposures. Moreover, many of these modifiers covary with the exposure, leading to much higher risks in some subgroups. These are not theoretical concerns; rather, all these patterns have already been demonstrated in studies of the effects of lead and air pollution. However, recent regulatory impact assessments for these exposures have generally not incorporated these findings. Therefore, differential risk and vulnerability is a critically important but neglected area within risk assessment, and should be incorporated in the future.
    Subject(s): Genetic Predisposition to Disease ; Stress, Psychological ; Environmental Exposure -- Analysis ; Hazardous Substances -- Toxicity
    ISSN: 0090-0036
    E-ISSN: 1541-0048
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  • 2
    Language: English
    In: American journal of public health, December 2011, Vol.101 Suppl 1, pp.S102-9
    Description: Several methodological issues have been identified in analysis of epidemiological data to better assess the distributional effects of exposures and hypotheses about effect modification. We discuss the hierarchical mixed model and some more complex methods. Methods of capturing inequality are a second dimension of risk assessment, and simulation studies are important because plausible choices for air pollution effects and effect modifiers could result in extremely high risks in a small subset of the population. Future epidemiological studies should explore contextual and individual-level factors that might modify these relationships. The Environmental Protection Agency should make this a standard part of their risk assessments whenever the necessary information is available.
    Subject(s): Disease Susceptibility ; Environmental Exposure -- Analysis ; Hazardous Substances -- Toxicity ; Risk Assessment -- Methods
    ISSN: 0090-0036
    E-ISSN: 1541-0048
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  • 3
    Language: English
    In: American journal of public health, December 2011, Vol.101 Suppl 1, pp.S88-93
    Description: The central paradigm of the Environmental Protection Agency is risk assessment. We examined how differential responses across population groups could be better integrated into the environmental risk assessment process, providing tools to achieve greater equity in health status in addition to risk reduction. Such integration was difficult with paradigms like reference dose and was easier with consideration of dose-response curves, which incorporated nontrivial effects observed at low doses for common exposures. We identified 6 assumptions implicit in standard chemical risk assessments that should changed: (1) risk independence, (2) risk averaging, (3) risk nontransferability, (4) risk synchrony, (5) risk accumulation and chaining, and (6) quantification of numbers of persons above certain thresholds or limit values sufficient to characterize risk.
    Subject(s): Disease Susceptibility ; Risk Assessment ; Vulnerable Populations ; Environmental Exposure -- Analysis
    ISSN: 0090-0036
    E-ISSN: 1541-0048
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  • 4
    Language: English
    In: Analytical Biochemistry, 01 July 2014, Vol.456, pp.38-42
    Description: Prior observations that questioned the validity of kinetic exclusion assays were based on the mistaken assumption that the assays quantified the fraction of those antibody molecules that had unoccupied binding sites. Instead, the standard KinExA assay quantifies the fraction of total antibody binding sites that are unoccupied, regardless of the number of unoccupied sites on each antibody molecule. Although the standard KinExA analysis assumes that there is only a small probability of antibody-site capture by the affinity matrix, the results of numerical simulations demonstrate the reliability of dissociation constants obtained by the standard KinExA analysis for capture probabilities as high as 30%. This finding further strengthens the potential of kinetic exclusion assays as the procedure of choice for the rapid and accurate characterization of immunochemical reactions that forms part of screening processes in the search for therapeutic antibodies.
    Subject(s): Antigen–Antibody Interactions ; Antibody Bivalence ; Kinetic Exclusion Assay ; Antigen–Antibody Interactions ; Antibody Bivalence ; Kinetic Exclusion Assay ; Chemistry ; Anatomy & Physiology
    ISSN: 0003-2697
    E-ISSN: 1096-0309
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  • 5
    Language: English
    In: American journal of public health, July 2014, Vol.104(7), pp.1230-9
    Description: We present a system dynamics model that quantifies the energy imbalance gap responsible for the US adult obesity epidemic among gender and racial subpopulations. We divided the adult population into gender-race/ethnicity subpopulations and body mass index (BMI) classes. We defined transition rates between classes as a function of metabolic dynamics of individuals within each class. We estimated energy intake in each BMI class within the past 4 decades as a multiplication of the equilibrium energy intake of individuals in that class. Through calibration, we estimated the energy gap multiplier for each gender-race-BMI group by matching simulated BMI distributions for each subpopulation against national data with maximum likelihood estimation. No subpopulation showed a negative or zero energy gap, suggesting that the obesity epidemic continues to worsen, albeit at a slower rate. In the past decade the epidemic has slowed for non-Hispanic Whites, is starting to slow for non-Hispanic Blacks, but continues to accelerate among Mexican Americans. The differential energy balance gap across subpopulations and over time suggests that interventions should be tailored to subpopulations' needs.
    Subject(s): Diet ; Models, Theoretical ; Obesity -- Epidemiology
    ISSN: 0090-0036
    E-ISSN: 1541-0048
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  • 6
    Language: English
    In: Social Psychiatry and Psychiatric Epidemiology, 2014, Vol.49(3), pp.467-475
    Description: Byline: Kara E. Rudolph (1,2), Elizabeth A. Stuart (2,3), Thomas A. Glass (1), Kathleen R. Merikangas (4) Keywords: Adolescent; Mental health; Psychiatric epidemiology; Neighborhood; Propensity score; Survey Abstract: Purpose Inconsistent evidence of a relationship between neighborhood disadvantage and adolescent mental health may be, in part, attributable to heterogeneity based on urban or rural residence. Using the largest nationally representative survey of US adolescent mental health available, we estimated the association between neighborhood disadvantage and adolescent emotional disorders and the extent to which urbanicity modified this association. Methods The National Comorbidity Survey Replication Adolescent Supplement (NCS-A) sampled adolescents aged 13--17 years (N = 10,123). Households were geocoded to Census tracts. Using a propensity score approach that addresses bias from non-random selection of individuals into neighborhoods, logistic regression models were used to estimate the relative odds of having a DSM-IV emotional disorder (any past-year anxiety disorder, major depressive disorder or dysthymia) comparing similar adolescents living in disadvantaged versus non-disadvantaged neighborhoods in urban center, urban fringe, and non-urban areas. Results The association between neighborhood disadvantage and emotional disorder was more than twice as large for adolescents living in urban centers versus non-urban areas. In urban centers, living in a disadvantaged neighborhood was associated with 59 % (95 % confidence interval 25--103) increased adjusted odds of emotional disorder. Conclusions Urbanicity modifies the relationship between neighborhood disadvantage and emotional disorder in adolescents. This effect modification may explain why evidence of a relationship between neighborhood disadvantage and adolescent mental health has been inconsistent. Recognizing the joint influence of neighborhood socioeconomic context and urbanicity may improve specificity in identifying relevant neighborhood processes. Author Affiliation: (1) Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, E6541, Baltimore, MD, 21205, USA (2) Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA (3) Department of Mental Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA (4) Genetic Epidemiology Research Branch, National Institute of Mental Health, Bethesda, MD, USA Article History: Registration Date: 27/05/2013 Received Date: 16/03/2013 Accepted Date: 27/05/2013 Online Date: 11/06/2013 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00127-013-0725-8) contains supplementary material, which is available to authorized users.
    Subject(s): Adolescent ; Mental health ; Psychiatric epidemiology ; Neighborhood ; Propensity score ; Survey
    ISSN: 0933-7954
    E-ISSN: 1433-9285
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  • 7
    Language: English
    In: Pediatrics, April 2014, Vol.133(4), pp.668-76
    Description: Childhood attention-deficit/hyperactivity disorder (ADHD) has been associated with childhood and adult obesity, and stimulant use with delayed childhood growth, but the independent influences are unclear. No longitudinal studies have examined associations of ADHD diagnosis and stimulant use on BMI trajectories throughout childhood and adolescence. We used longitudinal electronic health record data from the Geisinger Health System on 163,820 children ages 3 to 18 years in Pennsylvania. Random effects linear regression models were used to model BMI trajectories with increasing age in relation to ADHD diagnosis, age at first stimulant use, and stimulant use duration, while controlling for confounding variables. Mean (SD) age at first BMI was 8.9 (5.0) years, and children provided a mean (SD) of 3.2 (2.4) annual BMI measurements. On average, BMI trajectories showed a curvilinear relation with age. There were consistent associations of unmedicated ADHD with higher BMIs during childhood compared with those without ADHD or stimulants. Younger age at first stimulant use and longer duration of stimulant use were each associated with slower BMI growth earlier in childhood but a more rapid rebound to higher BMIs in late adolescence. The study provides the first longitudinal evidence that ADHD during childhood not treated with stimulants was associated with higher childhood BMIs. In contrast, ADHD treated with stimulants was associated with slower early BMI growth but a rebound later in adolescence to levels above children without a history of ADHD or stimulant use. The findings have important clinical and neurobiological implications.
    Subject(s): BMI ; Adolescent ; Attention Deficit Disorder With Hyperactivity ; Central Nervous System Stimulants ; Child ; Epidemiology ; Longitudinal Studies ; Body Mass Index ; Attention Deficit Disorder With Hyperactivity -- Drug Therapy ; Central Nervous System Stimulants -- Therapeutic Use
    ISSN: 00314005
    E-ISSN: 1098-4275
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  • 8
    Article
    Article
    2004
    ISSN: 0002-9262 
    In: American Journal of Epidemiology, 2004, Vol.160(5), pp.503-504
    Description: Glass reviews Health Inequalities: Lifecourse Approaches edited by George Davey Smith.
    Subject(s): Nonfiction ; Health Care ; Inequality;
    ISSN: 0002-9262
    E-ISSN: 1476-6256
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  • 9
    In: Social Psychiatry and Psychiatric Epidemiology, 2013, pp.1-9
    Subject(s): Adolescent ; Mental Health ; Neighborhood ; Propensity Score ; Psychiatric Epidemiology ; Survey
    ISSN: 09337954
    E-ISSN: 14339285
    Source: Scopus (Elsevier B.V)〈img src="http://exlibris-pub.s3.amazonaws.com/Scopus.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Article
    Article
    2006
    ISSN: 0300-5771 
    In: International Journal of Epidemiology, 2006, Vol.35(2), pp.259-261
    Subject(s): Medicine ; Public Health;
    ISSN: 0300-5771
    E-ISSN: 1464-3685
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