Population disparities in asthma.
ABSTRACT The prevalence of asthma in the United States is higher than in many other countries in the world. Asthma, the most common chronic disease of childhood in the United States, disproportionately burdens many socioeconomically disadvantaged urban communities. In this review we discuss hypotheses for between-country disparities in asthma prevalence, including differences in "hygiene" (e.g., family size, use of day care, early-life respiratory infection exposures, endotoxin and other farm-related exposures, microbial colonization of the infant bowel, exposure to parasites, and exposure to large domestic animal sources of allergen), diet, traffic pollution, and cigarette smoking. We present data on socioeconomic and ethnic disparities in asthma prevalence and morbidity in the United States and discuss environmental factors contributing to asthma disparities (e.g., housing conditions, indoor environmental exposures including allergens, traffic air pollution, disparities in treatment and access to care, and cigarette smoking). We discuss environmental influences on somatic growth (low birth weight, prematurity, and obesity) and their relevance to asthma disparities. The relevance of the hygiene hypothesis to the U.S. urban situation is reviewed. Finally, we discuss community-level factors contributing to asthma disparities.
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ABSTRACT: Racial/ethnic minorities are 1.5 to 2.0 times more likely than whites to have most of the major chronic diseases. Chronic diseases are also more common in the poor than the nonpoor and this association is frequently mediated by race/ethnicity. Specifically, children are disproportionately affected by racial/ethnic health disparities. Between 1960 and 2005 the percentage of children with a chronic disease in the United States almost quadrupled with racial/ethnic minority youth having higher likelihood for these diseases. The most common major chronic diseases of youth in the United States are asthma, diabetes mellitus, obesity, hypertension, dental disease, attention-deficit/hyperactivity disorder, mental illness, cancers, sickle-cell anemia, cystic fibrosis, and a variety of genetic and other birth defects. This review will focus on the psychosocial rather than biological factors that play important roles in the etiology and subsequent solutions to these health disparities because they should be avoidable and they are inherently unjust. Finally, this review examines access to health services by focusing on health insurance and dental insurance coverage and access to school health services.BioMed Research International 09/2013; 2013:787616. DOI:10.1155/2013/787616 · 2.71 Impact Factor
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ABSTRACT: Alarming disparities in population health and wellness in the United States have led to multidisciplinary research efforts to create health equity. Identifying disparities, elucidating the etiological bases of disparities, and implementing solutions to eliminate disparities are part of the U.S. national health agenda. Racial and ethnic disparities have been identified throughout the cancer control continuum, in cardiovascular disease, diabetes and a multitude of other conditions. The causes of disparities are complex, condition specific, and conjectured to result from combinations of biological and socio-behavioral factors. Racial and ethnic health disparities within the vast incarcerated communities have been excluded from most studies, yet are of significant ethical and fiscal concern to inmates, governing bodies, and non-incarcerated communities into which inmates return. Importantly, research on racial and ethnic disparities in this unique population may shed light on the relative etiologies of health disparities and solutions for creating health equity throughout the general population in the United States.01/2012; 5(2):92-100.
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ABSTRACT: A new monoclonal antibody (mAb), specific for human IgE, the central mediator of immediate-type hypersensitivity reactions, has been shown to possess a unique set of binding specificities. The mAb, 8D6, binds to a conformational epitope on the CH3 domain of human e immunoglobulin and can compete with omalizumab for binding to IgE. Like omalizumab, it does not bind to IgE bound by the high-affinity IgE.Fc receptor (FcɛRI) on basophils and mast cells. It also does not cause activation and degranulation of IgE-pulsed, human FcɛRI-expressing rat basophilic leukemic cells (RBL SX-38). The mAb can inhibit IgE binding to recombinant α chain of human FcɛRI in ELISA and to human FcɛRI-expressing RBL SX38 cells in fluorescence flow cytometric analysis. However, unlike omalizumab, 8D6 can bind to IgE already bound by the low-affinity IgE.Fc receptors (FcɛRII, or CD23), as revealed in ELISA with recombinant CD23 and in flow cytometric analysis with human B cells. Since earlier investigators have shown that anti-CD23 mAbs can inhibit the synthesis of IgE in lymphocyte culture in vitro and can down-regulate IgE production in treated patients, 8D6 may offer pharmacological mechanisms in addition to those mediated by omalizumab, for controlling IgE in patients with allergic diseases.Immunobiology 11/2011; 217(7):676-83. DOI:10.1016/j.imbio.2011.11.006 · 3.18 Impact Factor