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      Impact of neighborhood socioeconomic status, income segregation, and greenness on blood biomarkers of inflammation

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          Abstract

          Background:

          Neighborhood deprivation is linked with inflammation, which may explain poorer health across populations. Behavioral risk factors are assumed to largely mediate these relationships, but few studies have examined this. We examined three neighborhood contextual factors that could exert direct effects on inflammation: (1) neighborhood socioeconomic status, (2) an index of concentration at extremes (that measures segregation), and (3) surrounding vegetation (greenness).

          Methods:

          Using blood samples and addresses collected from prospective cohorts of 7,930 male (1990–1994) and 16,183 female (1986–1990) health professionals with at least one inflammatory marker, we prospectively linked neighborhood contextual factors to inflammatory biomarkers (adiponectin, C-reactive protein, interleukin-6, soluble tumor necrosis factor receptor-2). Log-transformed, z-scaled component measures were used to calculate an inflammation score. Neighborhood socioeconomic status and index of concentration of extremes were obtained from the 1990 decennial census and linked to participant addresses. Surrounding greenness was assessed from satellite data and focal statistics were applied to generate exposures within 270 m and 1230 m of the participants’ address. We fit multiple linear regression models adjusting for demographic, clinical, and behavioral risk factors.

          Results:

          Higher neighborhood socioeconomic status was associated with lower inflammation score in women (β for interquartile range increase = –27.7%, 95% CI: –34.9%, –19.8%) and men (β = –21.2%, 95% CI: –31.0%, –10.1%). Similarly, participants in neighborhoods with higher concentrations of high-income households were associated with lower inflammation score in women (β = –27.8%, 95% CI: –35.8%, –18.7%) and men (β = −16.4%, 95% CI: –29.7%, –0.56%). Surrounding greenness within 270 m of each participant’s address was associated with lower inflammation score in women (β = −18.9%, 95% CI: –28.9%, –7.4%) but not men. Results were robust to sensitivity analyses to assess unmeasured confounding and selection bias.

          Discussion:

          Our findings support the hypothesis that adverse neighborhood environments may contribute to inflammation through pathways independent of behavioral risk factors, including psychosocial stress and toxic environments.

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          Most cited references59

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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              Inflammation and Cancer: Triggers, Mechanisms, and Consequences

              Inflammation predisposes to the development of cancer and promotes all stages of tumorigenesis. Cancer cells as well as surrounding stromal and inflammatory cells engage in well-orchestrated reciprocal interactions to form an inflammatory tumor microenvironment (TME). Cells within the TME are highly plastic, continuously changing their phenotypic and functional characteristics. Here we review the origins of inflammation in tumors, and the mechanisms whereby inflammation drives tumor initiation, growth, progression and metastasis. We discuss how tumor promoting inflammation closely resembles inflammatory processes typically found during development, immunity, maintenance of tissue homeostasis or tissue repair, and illuminate the distinctions between tissue-protective and pro-tumorigenic inflammation, including spatio-temporal considerations. Defining the cornerstone rules of engagement governing molecular and cellular mechanisms of tumor-promoting inflammation will be essential for the further development of anti-cancer therapies. Grivennikov and Greten review the mechanisms underlying the initiation of pro-tumorigenic inflammatory responses, how these evolve throughout the different stages of tumor development and the plasticity of the cells within the tumor microenvironment.
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                Author and article information

                Journal
                7807270
                22115
                Environ Int
                Environ Int
                Environment international
                0160-4120
                1873-6750
                25 March 2022
                April 2022
                05 March 2022
                06 April 2022
                : 162
                : 107164
                Affiliations
                [a ]Division of Population Sciences, Dana-Farber Cancer Institute, Boston, USA
                [b ]Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, USA
                [c ]Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA
                [d ]Department of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, USA
                [e ]Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Healthcare, Boston, USA
                Author notes
                [* ]Corresponding author: Hari_Iyer@ 123456dfci.harvard.edu (H.S. Iyer).
                Article
                NIHMS1786670
                10.1016/j.envint.2022.107164
                8985077
                35255255
                ccb4aaa7-6017-412d-9b0d-6645683c66fa

                This is an open access article under the CC BY license ( http://creativecommons.org/licenses/by/4.0/).

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                Categories
                Article

                biomarkers,health behavior,residence characteristics,socioeconomic factors,inflammation,disparities

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