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Risk of incident diabetes in relation to long-term exposure to fine particulate matter in Ontario, Canada.

https://arctichealth.org/en/permalink/ahliterature114276
Source
Environ Health Perspect. 2013 Jul;121(7):804-10
Publication Type
Article
Date
Jul-2013
Author
Hong Chen
Richard T Burnett
Jeffrey C Kwong
Paul J Villeneuve
Mark S Goldberg
Robert D Brook
Aaron van Donkelaar
Michael Jerrett
Randall V Martin
Jeffrey R Brook
Ray Copes
Author Affiliation
Public Health Ontario, Toronto, Ontario, Canada.
Source
Environ Health Perspect. 2013 Jul;121(7):804-10
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Air Pollutants - analysis - toxicity
Cohort Studies
Diabetes Mellitus, Type 2 - chemically induced - epidemiology
Environmental Exposure
Environmental monitoring
Female
Follow-Up Studies
Humans
Incidence
Male
Middle Aged
Ontario - epidemiology
Particle Size
Particulate Matter - analysis - toxicity
Remote Sensing Technology
Risk factors
Abstract
Laboratory studies suggest that fine particulate matter (= 2.5 ?m in diameter; PM(2.5)) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating PM2.5 and diabetes is sparse, particularly for incident diabetes.
We conducted a population-based cohort study to determine whether long-term exposure to ambient PM(2.5) is associated with incident diabetes.
We assembled a cohort of 62,012 nondiabetic adults who lived in Ontario, Canada, and completed one of five population-based health surveys between 1996 and 2005. Follow-up extended until 31 December 2010. Incident diabetes diagnosed between 1996 and 2010 was ascertained using the Ontario Diabetes Database, a validated registry of persons diagnosed with diabetes (sensitivity = 86%, specificity = 97%). Six-year average concentrations of PM2.5 at the postal codes of baseline residences were derived from satellite observations. We used Cox proportional hazards models to estimate the associations, adjusting for various individual-level risk factors and contextual covariates such as smoking, body mass index, physical activity, and neighborhood-level household income. We also conducted multiple sensitivity analyses. In addition, we examined effect modification for selected comorbidities and sociodemographic characteristics.
There were 6,310 incident cases of diabetes over 484,644 total person-years of follow-up. The adjusted hazard ratio for a 10-?g/m(3) increase in PM(2.5) was 1.11 (95% CI: 1.02, 1.21). Estimated associations were comparable among all sensitivity analyses. We did not find strong evidence of effect modification by comorbidities or sociodemographic covariates.
This study suggests that long-term exposure to PM2.5 may contribute to the development of diabetes.
Notes
Cites: J Am Coll Cardiol. 2001 Mar 15;37(4):992-711263626
Cites: Environ Health Perspect. 2011 Mar;119(3):384-921118784
Cites: Diabetes Care. 2012 Jan;35(1):92-822074722
Cites: Environ Sci Technol. 2012 Jan 17;46(2):652-6022148428
Cites: Circulation. 2012 Feb 14;125(6):767-7222219348
Cites: Diabetologia. 1983 Jan;24(1):1-96131004
Cites: Diabetologia. 1983 Aug;25(2):73-76628876
Cites: Arch Intern Med. 1991 Jun;151(6):1141-72043016
Cites: Lancet. 1991 Sep 28;338(8770):774-81681160
Cites: Ann Intern Med. 1995 Apr 1;122(7):481-67872581
Cites: Circulation. 2005 Jun 7;111(22):2913-2015927967
Cites: Epidemiology. 2005 Nov;16(6):727-3616222161
Cites: Environ Res. 2006 Feb;100(2):255-6715982650
Cites: Nature. 2006 Dec 14;444(7121):860-717167474
Cites: N Engl J Med. 2007 Feb 1;356(5):447-5817267905
Cites: Lancet. 2007 Mar 3;369(9563):750-617336651
Cites: Environ Health Perspect. 2012 May;120(5):708-1422313724
Cites: Lancet. 2007 Sep 1;370(9589):797-917765529
Cites: N Engl J Med. 2001 Sep 13;345(11):790-711556298
Cites: Diabetes Care. 2002 Mar;25(3):512-611874939
Cites: JAMA. 2002 Mar 6;287(9):1132-4111879110
Cites: Am J Epidemiol. 2002 Nov 1;156(9):813-2312396999
Cites: Can J Cardiol. 2003 Aug;19(9):997-100412915926
Cites: JAMA. 2003 Nov 19;290(19):2581-714625335
Cites: Diabetes Care. 2004 May;27(5):1047-5315111519
Cites: Soc Sci Med. 2004 Oct;59(8):1613-2715279920
Cites: Diabetes Care. 2004 Oct;27(10):2478-8415451919
Cites: JAMA. 1979 May 11;241(19):2035-8430798
Cites: J Occup Environ Med. 2008 Jan;50(1):32-818188079
Cites: CMAJ. 2008 May 20;178(11):1429-3518490638
Cites: Eur Respir J. 2008 Oct;32(4):962-918579551
Cites: Circulation. 2009 Feb 3;119(4):538-4619153269
Cites: Rev Environ Health. 2008 Oct-Dec;23(4):243-9719235364
Cites: COPD. 2009 Oct;6(5):388-9419863368
Cites: Can Respir J. 2009 Nov-Dec;16(6):183-820011725
Cites: Circulation. 2010 Jun 1;121(21):2331-7820458016
Cites: Environ Health Perspect. 2010 Jun;118(6):847-5520519161
Cites: Environ Health Perspect. 2010 Sep;118(9):1273-920504758
Cites: BMC Health Serv Res. 2010;10:34721182790
Cites: Occup Environ Med. 2011 Dec;68(12):920-721610265
PubMed ID
23632126 View in PubMed
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Respiratory virus infection and risk of invasive meningococcal disease in central Ontario, Canada.

https://arctichealth.org/en/permalink/ahliterature139091
Source
PLoS One. 2010;5(11):e15493
Publication Type
Article
Date
2010
Author
Ashleigh R Tuite
Laura M Kinlin
Stefan P Kuster
Frances Jamieson
Jeffrey C Kwong
Allison McGeer
David N Fisman
Author Affiliation
Dalla Lana School of Public Health, University of Toronto, Toronto, Canada.
Source
PLoS One. 2010;5(11):e15493
Date
2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Child
Child, Preschool
Comorbidity - trends
Female
Humans
Incidence
Infant
Infant, Newborn
Influenza A virus - isolation & purification
Influenza B virus - isolation & purification
Influenza, Human - epidemiology - virology
Logistic Models
Male
Meningococcal Infections - epidemiology
Middle Aged
Multivariate Analysis
Odds Ratio
Ontario - epidemiology
Respiratory Syncytial Viruses - isolation & purification
Respiratory Tract Infections - chemically induced - epidemiology
Seasons
Young Adult
Abstract
In temperate climates, invasive meningococcal disease (IMD) incidence tends to coincide with or closely follow peak incidence of influenza virus infection; at a seasonal level, increased influenza activity frequently correlates with increased seasonal risk of IMD.
We evaluated 240 cases of IMD reported in central Ontario, Canada, from 2000 to 2006. Associations between environmental and virological (influenza A, influenza B and respiratory syncytial virus (RSV)) exposures and IMD incidence were evaluated using negative binomial regression models controlling for seasonal oscillation. Acute effects of weekly respiratory virus activity on IMD risk were evaluated using a matched-period case-crossover design with random directionality of control selection. Effects were estimated using conditional logistic regression.
Multivariable negative binomial regression identified elevated IMD risk with increasing influenza A activity (per 100 case increase, incidence rate ratio?=?1.18, 95% confidence interval (CI): 1.06, 1.31). In case-crossover models, increasing weekly influenza A activity was associated with an acute increase in the risk of IMD (per 100 case increase, odds ratio (OR) ?=?2.03, 95% CI: 1.28 to 3.23). Increasing weekly RSV activity was associated with increased risk of IMD after adjusting for RSV activity in the previous 3 weeks (per 100 case increase, OR?=?4.31, 95% CI: 1.14, 16.32). No change in disease risk was seen with increasing influenza B activity.
We have identified an acute effect of influenza A and RSV activity on IMD risk. If confirmed, these finding suggest that influenza vaccination may have the indirect benefit of reducing IMD risk.
Notes
Cites: Annu Rev Public Health. 2000;21:193-22110884952
Cites: JAMA. 2010 Mar 10;303(10):943-5020215608
Cites: N Engl J Med. 2001 May 3;344(18):1378-8811333996
Cites: Aust N Z J Public Health. 2002;26(3):212-812141615
Cites: Eur J Epidemiol. 2004;19(2):181-715074574
Cites: N Engl J Med. 1972 Jul 6;287(1):5-94623954
Cites: Am J Epidemiol. 1991 Jan 15;133(2):144-531985444
Cites: Lancet. 1991 Aug 31;338(8766):554-71678811
Cites: Int J Biometeorol. 1992 Mar;36(1):18-291582720
Cites: J Infect Dis. 1992 Sep;166(3):542-51500737
Cites: Clin Infect Dis. 1993 Jul;17(1):126-328353232
Cites: FEMS Immunol Med Microbiol. 1999 Feb;23(2):115-2410076908
Cites: Infect Immun. 1999 Jun;67(6):3082-610338524
Cites: J Indian Med Assoc. 1963 Feb 1;40:113-513928180
Cites: PLoS Med. 2005 Jan;2(1):e615696216
Cites: Eur J Epidemiol. 2006;21(6):465-816835720
Cites: Annu Rev Public Health. 2007;28:127-4317222079
Cites: Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5692-717369367
Cites: Ann Epidemiol. 2007 Sep;17(9):654-6217555986
Cites: Am J Epidemiol. 2009 Mar 1;169(5):588-9519164421
Cites: Vaccine. 2009 Mar 10;27(11):1735-4019186206
Cites: Ecohealth. 2008 Dec;5(4):482-9019370300
Cites: Environ Health Perspect. 2009 Jul;117(7):1049-5219654911
Cites: Infect Immun. 2009 Sep;77(9):3588-9519528219
Cites: Ann Epidemiol. 2009 Oct;19(10):681-9119700344
Cites: Science. 2009 Sep 25;325(5948):1705-819696313
Cites: BMC Infect Dis. 2009;9:19619961583
Cites: Lancet Infect Dis. 2010 Feb;10(2):112-2420113980
Cites: Epidemiology. 2001 Mar;12(2):186-9211246579
PubMed ID
21103353 View in PubMed
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Spatial association between ambient fine particulate matter and incident hypertension.

https://arctichealth.org/en/permalink/ahliterature106335
Source
Circulation. 2014 Feb 4;129(5):562-9
Publication Type
Article
Date
Feb-4-2014
Author
Hong Chen
Richard T Burnett
Jeffrey C Kwong
Paul J Villeneuve
Mark S Goldberg
Robert D Brook
Aaron van Donkelaar
Michael Jerrett
Randall V Martin
Alexander Kopp
Jeffrey R Brook
Ray Copes
Author Affiliation
From Public Health Ontario, Toronto, Ontario, Canada (H.C., J.C.K., R.C.); Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada (H.C., J.C.K., P.J.V., R.C.); Institute for Clinical Evaluative Sciences, Toronto, Ontario, Canada (H.C., J.C.K., A.K.); Population Studies Division, Health Canada, Ottawa, Ontario, Canada (R.T.B.); Department of Family and Community Medicine, University of Toronto, Toronto, Ontario, Canada (J.C.K.); Department of Health Sciences, Carleton University, Ottawa, Ontario, Canada (P.J.V.); Department of Medicine, McGill University, Montreal, Quebec, Canada (M.S.G.); Division of Clinical Epidemiology, McGill University Health Centre, Montreal, Quebec, Canada (M.S.G.); Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor (R.D.B.); Department of Physics and Atmospheric Science, Dalhousie University, Halifax, Nova Scotia, Canada (A.v.D., R.V.M.); Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley (M.J.); Harvard-Smithsonian Center for Astrophysics, Cambridge, MA (R.V.M.); and Air Quality Research Division, Environment Canada, Toronto, Ontario, Canada (J.R.B.).
Source
Circulation. 2014 Feb 4;129(5):562-9
Date
Feb-4-2014
Language
English
Publication Type
Article
Keywords
Adult
Cohort Studies
Environmental Exposure - analysis
Female
Follow-Up Studies
Health Surveys - methods
Humans
Hypertension - diagnosis - epidemiology
Incidence
Male
Middle Aged
Ontario - epidemiology
Particulate Matter - adverse effects
Population Surveillance - methods
Abstract
Laboratory studies suggest that exposure to fine particulate matter (=2.5 µm in diameter) (PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension.
We assembled a cohort of 35 303 nonhypertensive adults from Ontario, Canada, who responded to 1 of 4 population-based health surveys between 1996 and 2005 and were followed up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants' postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adjusting for various individual and contextual risk factors including body mass index, smoking, physical activity, and neighbourhood-level unemployment rates. We conducted various sensitivity analyses to assess the robustness of the effect estimate, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time. Between 1996 and 2010, we identified 8649 incident cases of hypertension and 2296 deaths. For every 10-µg/m(3) increase of PM2.5, the adjusted hazard ratio of incident hypertension was 1.13 (95% confidence interval, 1.05-1.22). Estimated associations were comparable among all sensitivity analyses.
This study supports an association between PM2.5 and incident hypertension.
PubMed ID
24190962 View in PubMed
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