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      The Inflammatory Bowel Diseases and Ambient Air Pollution: A Novel Association

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          Abstract

          OBJECTIVES:

          The inflammatory bowel diseases (IBDs) emerged after industrialization. We studied whether ambient air pollution levels were associated with the incidence of IBD.

          METHODS:

          The health improvement network (THIN) database in the United Kingdom was used to identify incident cases of Crohn's disease ( n=367) or ulcerative colitis ( n=591), and age- and sex-matched controls. Conditional logistic regression analyses assessed whether IBD patients were more likely to live in areas of higher ambient concentrations of nitrogen dioxide (NO 2), sulfur dioxide (SO 2), and particulate matter <10μm (PM 10), as determined by using quintiles of concentrations, after adjusting for smoking, socioeconomic status, non-steroidal anti-inflammatory drugs (NSAIDs), and appendectomy. Stratified analyses investigated effects by age.

          RESULTS:

          Overall, NO 2, SO 2, and PM 10 were not associated with the risk of IBD. However, individuals ≤23 years were more likely to be diagnosed with Crohn's disease if they lived in regions with NO 2 concentrations within the upper three quintiles (odds ratio (OR)=2.31; 95% confidence interval (CI)=1.25–4.28), after adjusting for confounders. Among these Crohn's disease patients, the adjusted OR increased linearly across quintile levels for NO 2 ( P=0.02). Crohn's disease patients aged 44–57 years were less likely to live in regions of higher NO 2 (OR=0.56; 95% CI=0.33–0.95) and PM 10 (OR=0.48; 95% CI=0.29–0.80). Ulcerative colitis patients ≤25 years (OR=2.00; 95% CI=1.08–3.72) were more likely to live in regions of higher SO 2; however, a dose–response effect was not observed.

          CONCLUSIONS:

          On the whole, air pollution exposure was not associated with the incidence of IBD. However, residential exposures to SO 2 and NO 2 may increase the risk of early-onset ulcerative colitis and Crohn's disease, respectively. Future studies are needed to explore the age-specific effects of air pollution exposure on IBD risk.

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          Most cited references21

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          Increased particulate air pollution and the triggering of myocardial infarction.

          Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown. We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass <2.5 microm (PM(2.5)), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 microg/m(3) PM(2.5) during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 microg/m(3) PM(2.5) in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively). The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.
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            Persistent endothelial dysfunction in humans after diesel exhaust inhalation.

            Exposure to combustion-derived air pollution is associated with an early (1-2 h) and sustained (24 h) rise in cardiovascular morbidity and mortality. We have previously demonstrated that inhalation of diesel exhaust causes an immediate (within 2 h) impairment of vascular and endothelial function in humans. To investigate the vascular and systemic effects of diesel exhaust in humans 24 hours after inhalation. Fifteen healthy men were exposed to diesel exhaust (particulate concentration, 300 microg/m(3)) or filtered air for 1 hour in a double-blind, randomized, crossover study. Twenty-four hours after exposure, bilateral forearm blood flow, and inflammatory and fibrinolytic markers were measured before and during unilateral intrabrachial bradykinin (100-1,000 pmol/min), acetylcholine (5-20 microg/min), sodium nitroprusside (2-8 microg/min), and verapamil (10-100 microg/min) infusions. Resting forearm blood flow, blood pressure, and basal fibrinolytic markers were similar 24 hours after either exposure. Diesel exhaust increased plasma cytokine concentrations (tumor necrosis factor-alpha and interleukin-6, p < 0.05 for both) but appeared to reduce acetylcholine (p = 0.01), and bradykinin (p = 0.08) induced forearm vasodilatation. In contrast, there were no differences in either endothelium-independent (sodium nitroprusside and verapamil) vasodilatation or bradykinin-induced acute plasma tissue plasminogen activator release. Twenty-four hours after diesel exposure, there is a selective and persistent impairment of endothelium-dependent vasodilatation that occurs in the presence of mild systemic inflammation. These findings suggest that combustion-derived air pollution may have important systemic and adverse vascular effects for at least 24 hours after exposure.
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              Which deprivation? A comparison of selected deprivation indexes.

              A number of indexes of deprivation which have been devised or adopted for use by the health services are examined in relation to their performance in explaining the variation observed in a range of health measures, using data for postcode sectors in Scotland. The Scottish deprivation score and the Townsend index are found to explain most variation, and to adhere most closely to the concept of material disadvantage. The Jarman score is less effective as a result of the inclusion of individual variables which are seen to correlate very weakly, even negatively, with the health indicators. The use of these measures in relation to resource allocation and the new GP contract is discussed.
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                Author and article information

                Journal
                Am J Gastroenterol
                The American Journal of Gastroenterology
                Nature Publishing Group
                0002-9270
                1572-0241
                November 2010
                29 June 2010
                : 105
                : 11
                : 2412-2419
                Affiliations
                [1 ]simpleDivision of Gastroenterology, Department of Medicine, University of Calgary , Calgary, Alberta, Canada
                [2 ]simpleDepartment of Community Health Sciences, University of Calgary , Calgary, Alberta, Canada
                [3 ]simpleMGH Crohn's and Colitis Center and Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School , Boston, Massachusetts, USA
                [4 ]simpleAir Health Science Division , Ottawa, Ontario, Canada
                [5 ]simplePopulation Studies Division, Health Canada , Ottawa, Ontario, Canada
                [6 ]simpleDalla Lana School of Public Health, University of Toronto , Ontario, Canada
                Author notes
                [* ]simpleDivision of Gastroenterology, Departments of Medicine and Community Health Sciences, University of Calgary, Teaching Research and Wellness Center , 3280 Hospital Drive NW, 6th Floor, Room 6D17, Calgary, AB, Canada, T2N 4N1. E-mail: ggkaplan@ 123456ucalgary.ca
                Article
                ajg2010252
                10.1038/ajg.2010.252
                3180712
                20588264
                a7fef7d3-f1c7-4f08-96e9-ee394986b857
                Copyright © 2010 American College of Gastroenterology

                This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

                History
                : 06 February 2010
                : 10 May 2010
                Categories
                Inflammatory Bowel Disease

                Gastroenterology & Hepatology
                Gastroenterology & Hepatology

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