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.
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
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.
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
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.).
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.