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Neupane B.,McMaster University | Jerrett M.,University of California at Berkeley | Burnett R.T.,Environmental Health Directorate | Marrie T.,University of Alberta | And 2 more authors.
American Journal of Respiratory and Critical Care Medicine | Year: 2010

Rationale: Little is known about the long-term effects of air pollution on pneumonia hospitalization in the elderly. Objectives: To assess the effect of long-term exposure to ambient nitrogen dioxide, sulfur dioxide, and fine particulate matter with diameter equal to or smaller than 2.5 μm(PM 2.5) on hospitalization for community-acquired pneumonia in older adults. Methods: We used a population-based case-control study in Hamilton, Ontario, Canada.Weenrolled 345 hospitalized patients aged 65 years or more for community-acquired pneumonia and 494 control participants, aged 65 years and more, randomly selected from the same community as cases from July 2003 to April 2005. Health data were collected by personal interview. Annual average levels of nitrogen dioxide, sulfur dioxide, and PM2.5 before the study period wereestimatedat the residential addresses of participantsbyinverse distance weighting, bicubic splinedandland use regressionmethods and merged with participants' health data. Measurements and Main Results: Long-term exposure to higher levels of nitrogen dioxide and PM2.5 was significantly associated with hospitalization for community-acquired pneumonia (odds ratio [OR], 2.30; 95% confidence interval [CI], 1.25 to 4.21; P = 0.007 and OR, 2.26; 95% CI, 1.20 to 4.24; P = 0.012, respectively, over the 5th-95th percentile range increase of exposure). Sulfur dioxide did not appear to have any association (OR, 0.97; 95% CI, 0.59 to 1.61; P = 0.918). Results were somewhat sensitive to the choice of methods used to estimate air pollutant levels at residential addresses, although all risks from nitrogen dioxide and PM 2.5 exposure were positive and generally significant. Conclusions: In older adults, exposure to ambient nitrogen dioxide and PM2.5 was associated with hospitalization for community-acquired pneumonia.


Kish L.,University of Alberta | Hotte N.,University of Alberta | Kaplan G.G.,University of Calgary | Vincent R.,Environmental Health Directorate | And 7 more authors.
PLoS ONE | Year: 2013

Background:Particulate matter (PM) is a key pollutant in ambient air that has been associated with negative health conditions in urban environments. The aim of this study was to examine the effects of orally administered PM on the gut microbiome and immune function under normal and inflammatory conditions.Methods:Wild-type 129/SvEv mice were gavaged with Ottawa urban PM10 (EHC-93) for 7-14 days and mucosal gene expression analyzed using Ingenuity Pathways software. Intestinal permeability was measured by lactulose/mannitol excretion in urine. At sacrifice, segments of small and large intestine were cultured and cytokine secretion measured. Splenocytes were isolated and incubated with PM10 for measurement of proliferation. Long-term effects of exposure (35 days) on intestinal cytokine expression were measured in wild-type and IL-10 deficient (IL-10-/-) mice. Microbial composition of stool samples was assessed using terminal restriction fragment length polymorphism. Short chain fatty acids were measured in caecum.Results:Short-term treatment of wild-type mice with PM10 altered immune gene expression, enhanced pro-inflammatory cytokine secretion in the small intestine, increased gut permeability, and induced hyporesponsiveness in splenocytes. Long-term treatment of wild-type and IL-10-/- mice increased pro-inflammatory cytokine expression in the colon and altered short chain fatty acid concentrations and microbial composition. IL-10-/- mice had increased disease as evidenced by enhanced histological damage.Conclusions:Ingestion of airborne particulate matter alters the gut microbiome and induces acute and chronic inflammatory responses in the intestine. © 2013 Kish et al.


Su J.G.,University of California at Berkeley | Jerrett M.,University of California at Berkeley | Beckerman B.,University of California at Berkeley | Verma D.,McMaster University | And 5 more authors.
Atmospheric Environment | Year: 2010

More than 25 studies have employed land use regression (LUR) models to estimate nitrogen oxides and to a lesser extent particulate matter indicators, but these methods have been less commonly applied to ambient concentrations of volatile organic compounds (VOCs). Some VOCs have high plausibility as sources of health effects and others are specific indicators of motor vehicle exhaust. We used LUR models to estimate spatial variability of VOCs in Toronto, Canada. Benzene, n-hexane and total hydrocarbons (THC) were measured from July 25 to August 9, 2006 at 50 locations using the TraceAir organic vapor monitors. Nitrogen dioxide (NO2) was also sampled to assess its spatial pattern agreement with VOC exposures. Buffers for land use, population density, traffic density, physical geography, and remote sensing measures of greenness and surface brightness were also tested. The remote sensing measures have the highest correlations with VOCs and NO2 levels (i.e., explains >36% of the variance). Our regression models explain 66-68% of the variance in the spatial distribution of VOCs, compared to 81% for the NO2 model. The ranks of agreement between various VOCs range from 48 to 63% and increases substantially - up to 75% - for the top and bottom quartile groups. Agreements between NO2 and VOCs are much smaller with an average rank of 36%. Future epidemiologic studies may therefore benefit from using VOCs as potential toxic agents for traffic-related pollutants. © 2010 Elsevier Ltd.


Chen H.,McGill University | Goldberg M.S.,McGill University | Crouse D.L.,McGill University | Burnett R.T.,Environmental Health Directorate | And 6 more authors.
Atmospheric Environment | Year: 2010

Land use regression has been used in epidemiologic studies to estimate long-term exposure to air pollution within cities. The models are often developed toward the end of the study using recent air pollution data. Given that there may be spatially-dependent temporal trends in urban air pollution and that there is interest for epidemiologists in assessing period-specific exposures, especially early-life exposure, methods are required to extrapolate these models back in time. We present herein three new methods to back-extrapolate land use regression models. During three two-week periods in 2005-2006, we monitored nitrogen dioxide (NO2) at about 130 locations in Montreal, Quebec, and then developed a land-use regression (LUR) model. Our three extrapolation methods entailed multiplying the predicted concentrations of NO2 by the ratio of past estimates of concentrations from fixed-site monitors, such that they reflected the change in the spatial structure of NO2 from measurements at fixed-site monitors. The specific methods depended on the availability of land use and traffic-related data, and we back-extrapolated the LUR model to 10 and 20 years into the past. We then applied these estimates to residential information from subjects enrolled in a case-control study of postmenopausal breast cancer that was conducted in 1996. Observed and predicted concentrations of NO2 in Montreal decreased and were correlated in time. The estimated concentrations using the three extrapolation methods had similar distributions, except that one method yielded slightly lower values. The spatial distributions varied slightly between methods. In the analysis of the breast cancer study, the odds ratios were insensitive to the method but varied with time: for a 5ppb increase in NO2 using the 2006 LUR the odds ratio (OR) was about 1.4 and the ORs in predicted past concentrations of NO2 varied (OR∼1.2 for 1985 and OR∼1.3-1.5 for 1996). Thus, the ORs per unit exposure increased with time as the range and variance of the spatial distributions decreased, and this is due partly to the regression coefficient being approximately inversely proportional to the variance of exposure. Changing spatial variability complicates interpretation and this may have important implications for the management of risk. Further studies are needed to estimate the accuracy of the different methods. © 2010 Elsevier Ltd.


Salim S.Y.,University of Alberta | Jovel J.,University of Alberta | Wine E.,University of Alberta | Kaplan G.G.,University of Calgary | And 4 more authors.
Inflammatory Bowel Diseases | Year: 2014

Background: Epidemiological associations between early-life air pollution exposure and increased risk of inflammatory bowel diseases have been shown. Our aim was to determine if exposure to airborne particulate matter (PM10) during the neonatal period would alter colitis in the interleukin (IL)-10-/- mouse model. Methods: IL-10-/- pregnant dams and pups were fed chow ± PM10 (9 μg/g) and pups were studied at 10, 14, and 20 weeks. Twenty-week-old mice were given 2% dextran sodium sulfate. Metagenomic analysis of stool was performed. Bacterial translocation was assessed by serum lipopolysaccharide and culturing bacteria from mesenteric lymph nodes and spleen. Cytokine expression was measured in gut homogenates using the MesoScale discovery platform. PM10 was applied to CMT93 cells±J744 macrophages, and resistance and cytokine secretion were assessed. THP-1 macrophages were incubated with Escherichia coli HB101±PM10 for assessment of uptake and killing. Results: PM10 exposure increased colonic proinflammatory cytokines and bacterial translocation into mesenteric lymph nodes, whereas IL-17A levels were reduced in PM 10-fed 10-week-old mice. Bifidobacterium was decreased in mice fed PM10, whereas serum lipopolysaccharide was increased. PM10 interfered with phagocytosis and killing in THP-1 cells. In coculture, PM 10 increased tumor necrosis factor a and fluorescein isothiocyanate-dextran flux. After dextran sodium sulfate treatment, PM 10-fed mice responded with increased colonic tumor necrosis factor α and IL-1β and α larger percentage of PM10-fed mice had live bacteria in the mesenteric lymph nodes. Conclusions: Our data suggest that early exposure to pollution particulates can result in an earlier onset of intestinal disease in genetically susceptible hosts and can alter responses to gut injury in later life. Copyright © 2014 Crohn's & Colitis Foundation of America, Inc.

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