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1.  Use of Satellite Observations for Long-Term Exposure Assessment of Global Concentrations of Fine Particulate Matter 
Environmental Health Perspectives  2014;123(2):135-143.
Background: More than a decade of satellite observations offers global information about the trend and magnitude of human exposure to fine particulate matter (PM2.5).
Objective: In this study, we developed improved global exposure estimates of ambient PM2.5 mass and trend using PM2.5 concentrations inferred from multiple satellite instruments.
Methods: We combined three satellite-derived PM2.5 sources to produce global PM2.5 estimates at about 10 km × 10 km from 1998 through 2012. For each source, we related total column retrievals of aerosol optical depth to near-ground PM2.5 using the GEOS–Chem chemical transport model to represent local aerosol optical properties and vertical profiles. We collected 210 global ground-based PM2.5 observations from the literature to evaluate our satellite-based estimates with values measured in areas other than North America and Europe.
Results: We estimated that global population-weighted ambient PM2.5 concentrations increased 0.55 μg/m3/year (95% CI: 0.43, 0.67) (2.1%/year; 95% CI: 1.6, 2.6) from 1998 through 2012. Increasing PM2.5 in some developing regions drove this global change, despite decreasing PM2.5 in some developed regions. The estimated proportion of the population of East Asia living above the World Health Organization (WHO) Interim Target-1 of 35 μg/m3 increased from 51% in 1998–2000 to 70% in 2010–2012. In contrast, the North American proportion above the WHO Air Quality Guideline of 10 μg/m3 fell from 62% in 1998–2000 to 19% in 2010–2012. We found significant agreement between satellite-derived estimates and ground-based measurements outside North America and Europe (r = 0.81; n = 210; slope = 0.68). The low bias in satellite-derived estimates suggests that true global concentrations could be even greater.
Conclusions: Satellite observations provide insight into global long-term changes in ambient PM2.5 concentrations. Satellite-derived estimates and ground-based PM2.5 observations from this study are available for public use.
Citation: van Donkelaar A, Martin RV, Brauer M, Boys BL. 2015. Use of satellite observations for long-term exposure assessment of global concentrations of fine particulate matter. Environ Health Perspect 123:135–143;
PMCID: PMC4314252  PMID: 25343779
2.  Traffic-related air pollution and health in Canada 
PMCID: PMC3855107  PMID: 24144607
3.  Household Cooking with Solid Fuels Contributes to Ambient PM2.5 Air Pollution and the Burden of Disease 
Environmental Health Perspectives  2014;122(12):1314-1320.
Background: Approximately 2.8 billion people cook with solid fuels. Research has focused on the health impacts of indoor exposure to fine particulate pollution. Here, for the 2010 Global Burden of Disease project (GBD 2010), we evaluated the impact of household cooking with solid fuels on regional population-weighted ambient PM2.5 (particulate matter ≤ 2.5 μm) pollution (APM2.5).
Objectives: We estimated the proportion and concentrations of APM2.5 attributable to household cooking with solid fuels (PM2.5-cook) for the years 1990, 2005, and 2010 in 170 countries, and associated ill health.
Methods: We used an energy supply–driven emissions model (GAINS; Greenhouse Gas and Air Pollution Interactions and Synergies) and source-receptor model (TM5-FASST) to estimate the proportion of APM2.5 produced by households and the proportion of household PM2.5 emissions from cooking with solid fuels. We estimated health effects using GBD 2010 data on ill health from APM2.5 exposure.
Results: In 2010, household cooking with solid fuels accounted for 12% of APM2.5 globally, varying from 0% of APM2.5 in five higher-income regions to 37% (2.8 μg/m3 of 6.9 μg/m3 total) in southern sub-Saharan Africa. PM2.5-cook constituted > 10% of APM2.5 in seven regions housing 4.4 billion people. South Asia showed the highest regional concentration of APM2.5 from household cooking (8.6 μg/m3). On the basis of GBD 2010, we estimate that exposure to APM2.5 from cooking with solid fuels caused the loss of 370,000 lives and 9.9 million disability-adjusted life years globally in 2010.
Conclusions: PM2.5 emissions from household cooking constitute an important portion of APM2.5 concentrations in many places, including India and China. Efforts to improve ambient air quality will be hindered if household cooking conditions are not addressed.
Citation: Chafe ZA, Brauer M, Klimont Z, Van Dingenen R, Mehta S, Rao S, Riahi K, Dentener F, Smith KR. 2014. Household cooking with solid fuels contributes to ambient PM2.5 air pollution and the burden of disease. Environ Health Perspect 122:1314–1320;
PMCID: PMC4256045  PMID: 25192243
4.  Proximity to Traffic, Ambient Air Pollution, and Community Noise in Relation to Incident Rheumatoid Arthritis 
Environmental Health Perspectives  2014;122(10):1075-1080.
Background: The risk of rheumatoid arthritis (RA) has been associated with living near traffic; however, there is evidence suggesting that air pollution may not be responsible for this association. Noise, another traffic-generated exposure, has not been studied as a risk factor for RA.
Objectives: We investigated proximity to traffic, ambient air pollution, and community noise in relation to RA in the Vancouver and Victoria regions of British Columbia, Canada.
Methods: Cases and controls were identified in a cohort of adults that was assembled using health insurance registration records. Incident RA cases from 1999 through 2002 were identified by diagnostic codes in combination with prescriptions and type of physician (e.g., rheumatologist). Controls were matched to RA cases by age and sex. Environmental exposures were assigned to each member of the study population by their residential postal code(s). We estimated relative risks using conditional logistic regression, with additional adjustment for median income at the postal code.
Results: RA incidence was increased with proximity to traffic, with an odds ratio (OR) of 1.37 (95% CI: 1.11, 1.68) for residence ≤ 50 m from a highway compared with residence > 150 m away. We found no association with traffic-related exposures such as PM2.5, nitrogen oxides, or noise. Ground-level ozone, which was highest in suburban areas, was associated with an increased risk of RA (OR = 1.26; 95% CI: 1.18, 1.36 per interquartile range increase).
Conclusions: Our study confirms a previously observed association of RA risk with proximity to traffic and suggests that neither noise levels nor traffic-related air pollutants are responsible for this relationship. Additional investigation of neighborhood and individual correlates of residence near roadways may provide new insight into risk factors for RA.
Citation: De Roos AJ, Koehoorn M, Tamburic L, Davies HW, Brauer M. 2014. Proximity to traffic, ambient air pollution, and community noise in relation to incident rheumatoid arthritis. Environ Health Perspect 122:1075–1080;
PMCID: PMC4181921  PMID: 24905961
5.  Residential Greenness and Birth Outcomes: Evaluating the Influence of Spatially Correlated Built-Environment Factors 
Environmental Health Perspectives  2014;122(10):1095-1102.
Background: Half the world’s population lives in urban areas. It is therefore important to identify characteristics of the built environment that are beneficial to human health. Urban greenness has been associated with improvements in a diverse range of health conditions, including birth outcomes; however, few studies have attempted to distinguish potential effects of greenness from those of other spatially correlated exposures related to the built environment.
Objectives: We aimed to investigate associations between residential greenness and birth outcomes and evaluate the influence of spatially correlated built environment factors on these associations.
Methods: We examined associations between residential greenness [measured using satellite-derived Normalized Difference Vegetation Index (NDVI) within 100 m of study participants’ homes] and birth outcomes in a cohort of 64,705 singleton births (from 1999–2002) in Vancouver, British Columbia, Canada. We also evaluated associations after adjusting for spatially correlated built environmental factors that may influence birth outcomes, including exposure to air pollution and noise, neighborhood walkability, and distance to the nearest park.
Results: An interquartile increase in greenness (0.1 in residential NDVI) was associated with higher term birth weight (20.6 g; 95% CI: 16.5, 24.7) and decreases in the likelihood of small for gestational age, very preterm (< 30 weeks), and moderately preterm (30–36 weeks) birth. Associations were robust to adjustment for air pollution and noise exposures, neighborhood walkability, and park proximity.
Conclusions: Increased residential greenness was associated with beneficial birth outcomes in this population-based cohort. These associations did not change after adjusting for other spatially correlated built environment factors, suggesting that alternative pathways (e.g., psychosocial and psychological mechanisms) may underlie associations between residential greenness and birth outcomes.
Citation: Hystad P, Davies HW, Frank L, Van Loon J, Gehring U, Tamburic L, Brauer M. 2014. Residential greenness and birth outcomes: evaluating the influence of spatially correlated built-environment factors. Environ Health Perspect 122:1095–1102;
PMCID: PMC4181932  PMID: 25014041
6.  A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010 
Lim, Stephen S | Vos, Theo | Flaxman, Abraham D | Danaei, Goodarz | Shibuya, Kenji | Adair-Rohani, Heather | Amann, Markus | Anderson, H Ross | Andrews, Kathryn G | Aryee, Martin | Atkinson, Charles | Bacchus, Loraine J | Bahalim, Adil N | Balakrishnan, Kalpana | Balmes, John | Barker-Collo, Suzanne | Baxter, Amanda | Bell, Michelle L | Blore, Jed D | Blyth, Fiona | Bonner, Carissa | Borges, Guilherme | Bourne, Rupert | Boussinesq, Michel | Brauer, Michael | Brooks, Peter | Bruce, Nigel G | Brunekreef, Bert | Bryan-Hancock, Claire | Bucello, Chiara | Buchbinder, Rachelle | Bull, Fiona | Burnett, Richard T | Byers, Tim E | Calabria, Bianca | Carapetis, Jonathan | Carnahan, Emily | Chafe, Zoe | Charlson, Fiona | Chen, Honglei | Chen, Jian Shen | Cheng, Andrew Tai-Ann | Child, Jennifer Christine | Cohen, Aaron | Colson, K Ellicott | Cowie, Benjamin C | Darby, Sarah | Darling, Susan | Davis, Adrian | Degenhardt, Louisa | Dentener, Frank | Des Jarlais, Don C | Devries, Karen | Dherani, Mukesh | Ding, Eric L | Dorsey, E Ray | Driscoll, Tim | Edmond, Karen | Ali, Suad Eltahir | Engell, Rebecca E | Erwin, Patricia J | Fahimi, Saman | Falder, Gail | Farzadfar, Farshad | Ferrari, Alize | Finucane, Mariel M | Flaxman, Seth | Fowkes, Francis Gerry R | Freedman, Greg | Freeman, Michael K | Gakidou, Emmanuela | Ghosh, Santu | Giovannucci, Edward | Gmel, Gerhard | Graham, Kathryn | Grainger, Rebecca | Grant, Bridget | Gunnell, David | Gutierrez, Hialy R | Hall, Wayne | Hoek, Hans W | Hogan, Anthony | Hosgood, H Dean | Hoy, Damian | Hu, Howard | Hubbell, Bryan J | Hutchings, Sally J | Ibeanusi, Sydney E | Jacklyn, Gemma L | Jasrasaria, Rashmi | Jonas, Jost B | Kan, Haidong | Kanis, John A | Kassebaum, Nicholas | Kawakami, Norito | Khang, Young-Ho | Khatibzadeh, Shahab | Khoo, Jon-Paul | Kok, Cindy | Laden, Francine | Lalloo, Ratilal | Lan, Qing | Lathlean, Tim | Leasher, Janet L | Leigh, James | Li, Yang | Lin, John Kent | Lipshultz, Steven E | London, Stephanie | Lozano, Rafael | Lu, Yuan | Mak, Joelle | Malekzadeh, Reza | Mallinger, Leslie | Marcenes, Wagner | March, Lyn | Marks, Robin | Martin, Randall | McGale, Paul | McGrath, John | Mehta, Sumi | Mensah, George A | Merriman, Tony R | Micha, Renata | Michaud, Catherine | Mishra, Vinod | Hanafiah, Khayriyyah Mohd | Mokdad, Ali A | Morawska, Lidia | Mozaff arian, Dariush | Murphy, Tasha | Naghavi, Mohsen | Neal, Bruce | Nelson, Paul K | Nolla, Joan Miquel | Norman, Rosana | Olives, Casey | Omer, Saad B | Orchard, Jessica | Osborne, Richard | Ostro, Bart | Page, Andrew | Pandey, Kiran D | Parry, Charles D H | Passmore, Erin | Patra, Jayadeep | Pearce, Neil | Pelizzari, Pamela M | Petzold, Max | Phillips, Michael R | Pope, Dan | Pope III, C Arden | Powles, John | Rao, Mayuree | Razavi, Homie | Rehfuess, Eva A | Rehm, Jürgen T | Ritz, Beate | Rivara, Frederick P | Roberts, Thomas | Robinson, Carolyn | Rodriguez-Portales, Jose A | Romieu, Isabelle | Room, Robin | Rosenfeld, Lisa C | Roy, Ananya | Rushton, Lesley | Salomon, Joshua A | Sampson, Uchechukwu | Sanchez-Riera, Lidia | Sanman, Ella | Sapkota, Amir | Seedat, Soraya | Shi, Peilin | Shield, Kevin | Shivakoti, Rupak | Singh, Gitanjali M | Sleet, David A | Smith, Emma | Smith, Kirk R | Stapelberg, Nicolas J C | Steenland, Kyle | Stöckl, Heidi | Stovner, Lars Jacob | Straif, Kurt | Straney, Lahn | Thurston, George D | Tran, Jimmy H | Van Dingenen, Rita | van Donkelaar, Aaron | Veerman, J Lennert | Vijayakumar, Lakshmi | Weintraub, Robert | Weissman, Myrna M | White, Richard A | Whiteford, Harvey | Wiersma, Steven T | Wilkinson, James D | Williams, Hywel C | Williams, Warwick | Wilson, Nicholas | Woolf, Anthony D | Yip, Paul | Zielinski, Jan M | Lopez, Alan D | Murray, Christopher J L | Ezzati, Majid
Lancet  2012;380(9859):2224-2260.
Quantification of the disease burden caused by different risks informs prevention by providing an account of health loss different to that provided by a disease-by-disease analysis. No complete revision of global disease burden caused by risk factors has been done since a comparative risk assessment in 2000, and no previous analysis has assessed changes in burden attributable to risk factors over time.
We estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. We estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specific deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden.
In 2010, the three leading risk factors for global disease burden were high blood pressure (7·0% [95% uncertainty interval 6·2–7·7] of global DALYs), tobacco smoking including second-hand smoke (6·3% [5·5–7·0]), and alcohol use (5·5% [5·0–5·9]). In 1990, the leading risks were childhood underweight (7·9% [6·8–9·4]), household air pollution from solid fuels (HAP; 7·0% [5·6–8·3]), and tobacco smoking including second-hand smoke (6·1% [5·4–6·8]). Dietary risk factors and physical inactivity collectively accounted for 10·0% (95% UI 9·2–10·8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily affect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient deficiencies, fell in rank between 1990 and 2010, with unimproved water we and sanitation accounting for 0·9% (0·4–1·6) of global DALYs in 2010. However, in most of sub-Saharan Africa childhood underweight, HAP, and non-exclusive and discontinued breastfeeding were the leading risks in 2010, while HAP was the leading risk in south Asia. The leading risk factor in Eastern Europe, most of Latin America, and southern sub-Saharan Africa in 2010 was alcohol use; in most of Asia, North Africa and Middle East, and central Europe it was high blood pressure. Despite declines, tobacco smoking including second-hand smoke remained the leading risk in high-income north America and western Europe. High body-mass index has increased globally and it is the leading risk in Australasia and southern Latin America, and also ranks high in other high-income regions, North Africa and Middle East, and Oceania.
Worldwide, the contribution of different risk factors to disease burden has changed substantially, with a shift away from risks for communicable diseases in children towards those for non-communicable diseases in adults. These changes are related to the ageing population, decreased mortality among children younger than 5 years, changes in cause-of-death composition, and changes in risk factor exposures. New evidence has led to changes in the magnitude of key risks including unimproved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollution. The extent to which the epidemiological shift has occurred and what the leading risks currently are varies greatly across regions. In much of sub-Saharan Africa, the leading risks are still those associated with poverty and those that affect children.
Bill & Melinda Gates Foundation.
PMCID: PMC4156511  PMID: 23245609
7.  Exposure assessment for estimation of the global burden of disease attributable to outdoor air pollution 
Ambient air pollution is associated with numerous adverse health impacts. Previous assessments of global attributable disease burden have been limited to urban areas or by coarse spatial resolution of concentration estimates. Recent developments in remote sensing, global chemical-transport models, and improvements in coverage of surface measurements facilitate virtually complete spatially resolved global air pollutant concentration estimates. We combined these data to generate global estimates of long- term average ambient concentrations of fine particles (PM2.5) and ozone at 0.1° × 0.1° spatial resolution for 1990 and 2005. In 2005, 89% of the world’s population lived in areas where the World Health Organization Air Quality Guideline of 10 μg/m3 PM2.5 (annual average) was exceeded. Globally, 32% of the population lived in areas exceeding the WHO Level 1 Interim Target of 35 μg/m3; driven by high proportions in East (76%) and South (26%) Asia. The highest seasonal ozone levels were found in North and Latin America, Europe, South and East Asia, and parts of Africa. Between 1990 and 2005 a 6% increase in global population-weighted PM2.5 and a 1% decrease in global population- weighted ozone concentrations was apparent, highlighted by increased concentrations in East, South and Southeast Asia and decreases in North America and Europe. Combined with spatially resolved population distributions, these estimates expand the evaluation of the global health burden associated with outdoor air pollution.
PMCID: PMC4043337  PMID: 22148428
8.  Long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study 
BMJ Open  2014;4(4):e004743.
Epidemiological studies have demonstrated associations between long-term exposure to traffic-related air pollution and coronary heart disease (CHD). Atherosclerosis is the principal pathological process responsible for CHD events, but effects of traffic-related air pollution on progression of atherosclerosis are not clear. This study aimed to investigate associations between long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis.
Healthy volunteers in metropolitan Vancouver, Canada.
Participants and outcome measures
509 participants aged 30–65 years were recruited and followed for approximately 5 years. At baseline and end of follow-up, participants underwent carotid artery ultrasound examinations to assess atherosclerosis severity, including carotid intima-media thickness, plaque area, plaque number and total area. Annual change of each atherosclerosis marker during the follow-up period was calculated as the difference between these two measurements divided by years of follow-up. Living close to major roads was defined as ≤150 m from a highway or ≤50 m from a major road. Residential exposures to traffic-related air pollutants including black carbon, fine particles, nitrogen dioxide and nitric oxide were estimated using high-resolution land-use regression models. The data were analysed using general linear models adjusting for various covariates.
At baseline, there were no significant differences in any atherosclerosis markers between participants living close to and those living away from major roads. After follow-up, the differences in annual changes of these markers between these two groups were small and not statistically significant. Also, no significant associations were observed with concentrations of traffic-related air pollutants including black carbon, fine particles, nitrogen dioxide and nitric oxide.
This study did not find significant associations between traffic-related air pollution and progression of carotid artery atherosclerosis in a region with lower levels and smaller contrasts of ambient air pollution.
PMCID: PMC3987708  PMID: 24710134
Occupational & Industrial Medicine; Epidemiology; Public Health; Preventive Medicine
9.  An Integrated Risk Function for Estimating the Global Burden of Disease Attributable to Ambient Fine Particulate Matter Exposure 
Environmental Health Perspectives  2014;122(4):397-403.
Background: Estimating the burden of disease attributable to long-term exposure to fine particulate matter (PM2.5) in ambient air requires knowledge of both the shape and magnitude of the relative risk (RR) function. However, adequate direct evidence to identify the shape of the mortality RR functions at the high ambient concentrations observed in many places in the world is lacking.
Objective: We developed RR functions over the entire global exposure range for causes of mortality in adults: ischemic heart disease (IHD), cerebrovascular disease (stroke), chronic obstructive pulmonary disease (COPD), and lung cancer (LC). We also developed RR functions for the incidence of acute lower respiratory infection (ALRI) that can be used to estimate mortality and lost-years of healthy life in children < 5 years of age.
Methods: We fit an integrated exposure–response (IER) model by integrating available RR information from studies of ambient air pollution (AAP), second hand tobacco smoke, household solid cooking fuel, and active smoking (AS). AS exposures were converted to estimated annual PM2.5 exposure equivalents using inhaled doses of particle mass. We derived population attributable fractions (PAFs) for every country based on estimated worldwide ambient PM2.5 concentrations.
Results: The IER model was a superior predictor of RR compared with seven other forms previously used in burden assessments. The percent PAF attributable to AAP exposure varied among countries from 2 to 41 for IHD, 1 to 43 for stroke, < 1 to 21 for COPD, < 1 to 25 for LC, and < 1 to 38 for ALRI.
Conclusions: We developed a fine particulate mass–based RR model that covered the global range of exposure by integrating RR information from different combustion types that generate emissions of particulate matter. The model can be updated as new RR information becomes available.
Citation: Burnett RT, Pope CA III, Ezzati M, Olives C, Lim SS, Mehta S, Shin HH, Singh G, Hubbell B, Brauer M, Anderson HR, Smith KR, Balmes JR, Bruce NG, Kan H, Laden F, Prüss-Ustün A, Turner MC, Gapstur SM, Diver WR, Cohen A. 2014. An integrated risk function for estimating the global burden of disease attributable to ambient fine particulate matter exposure. Environ Health Perspect 122:397–403;
PMCID: PMC3984213  PMID: 24518036
10.  GSTP1 and TNF Gene Variants and Associations between Air Pollution and Incident Childhood Asthma: The Traffic, Asthma and Genetics (TAG) Study 
Environmental Health Perspectives  2014;122(4):418-424.
Background: Genetics may partially explain observed heterogeneity in associations between traffic-related air pollution and incident asthma.
Objective: Our aim was to investigate the impact of gene variants associated with oxidative stress and inflammation on associations between air pollution and incident childhood asthma.
Methods: Traffic-related air pollution, asthma, wheeze, gene variant, and potential confounder data were pooled across six birth cohorts. Parents reported physician-diagnosed asthma and wheeze from birth to 7–8 years of age (confirmed by pediatric allergist in two cohorts). Individual estimates of annual average air pollution [nitrogen dioxide (NO2), particulate matter ≤ 2.5 μm (PM2.5), PM2.5 absorbance, ozone] were assigned to each child’s birth address using land use regression, atmospheric modeling, and ambient monitoring data. Effect modification by variants in GSTP1 (rs1138272/Ala114Val and rs1695/IIe105Val) and TNF (rs1800629/G-308A) was investigated.
Results: Data on asthma, wheeze, potential confounders, at least one SNP of interest, and NO2 were available for 5,115 children. GSTP1 rs1138272 and TNF rs1800629 SNPs were associated with asthma and wheeze, respectively. In relation to air pollution exposure, children with one or more GSTP1 rs1138272 minor allele were at increased risk of current asthma [odds ratio (OR) = 2.59; 95% CI: 1.43, 4.68 per 10 μg/m3 NO2] and ever asthma (OR = 1.64; 95% CI: 1.06, 2.53) compared with homozygous major allele carriers (OR = 0.95; 95% CI: 0.68, 1.32 for current and OR = 1.20; 95% CI: 0.98, 1.48 for ever asthma; Bonferroni-corrected interaction p = 0.04 and 0.01, respectively). Similarly, for GSTP1 rs1695, associations between NO2 and current and ever asthma had ORs of 1.43 (95% CI: 1.03, 1.98) and 1.36 (95% CI: 1.08, 1.70), respectively, for minor allele carriers compared with ORs of 0.82 (95% CI: 0.52, 1.32) and 1.12 (95% CI: 0.84, 1.49) for homozygous major allele carriers (Bonferroni-corrected interaction p-values 0.48 and 0.09). There were no clear differences by TNF genotype.
Conclusions: Children carrying GSTP1 rs1138272 or rs1695 minor alleles may constitute a susceptible population at increased risk of asthma associated with air pollution.
Citation: MacIntyre EA, Brauer M, Melén E, Bauer CP, Bauer M, Berdel D, Bergström A, Brunekreef B, Chan-Yeung M, Klümper C, Fuertes E, Gehring U, Gref A, Heinrich J, Herbarth O, Kerkhof M, Koppelman GH, Kozyrskyj AL, Pershagen G, Postma DS, Thiering E, Tiesler CM, Carlsten C, TAG Study Group. 2014. GSTP1 and TNF gene variants and associations between air pollution and incident childhood asthma: the traffic, asthma and genetics (TAG) Study. Environ Health Perspect 122:418–424;
PMCID: PMC3984232  PMID: 24465030
13.  A longitudinal analysis of associations between traffic-related air pollution with asthma, allergies and sensitization in the GINIplus and LISAplus birth cohorts 
PeerJ  2013;1:e193.
Background. There is a need to study whether the adverse effects of traffic-related air pollution (TRAP) on childhood asthma and allergic diseases documented during early-life persist into later childhood. This longitudinal study examined whether TRAP is associated with the prevalence of asthma, allergic rhinitis and aeroallergen sensitization in two German cohorts followed from birth to 10 years.
Materials. Questionnaire-derived annual reports of doctor diagnosed asthma and allergic rhinitis, as well as eye and nose symptoms, were collected from 6,604 children. Aeroallergen sensitization was assessed for 3,655 children who provided blood samples. Associations between these health outcomes and nitrogen dioxide (NO2), particles with aerodynamic diameters less than 2.5 µg/m3 (PM2.5) mass, PM2.5 absorbance and ozone, individually estimated for each child at the birth, six and 10 year home addresses, were assessed using generalized estimation equations including adjustments for relevant covariates. Odds ratios [95% confidence intervals] per increase in interquartile range of pollutant are presented for the total population and per geographical area (GINI/LISA South, GINI/LISA North and LISA East, Germany).
Results. The risk estimates for the total population were generally null across outcomes and pollutants. The area-specific results were heterogeneous. In GINI/LISA North, all associations were null. In LISA East, associations with ozone were elevated for all outcomes, and those for allergic rhinitis and eyes and nose symptom prevalence reached statistical significance (1.30 [1.02, 1.64] and 1.35 [1.16, 1.59], respectively). For GINI/LISA South, two associations with aeroallergen sensitization were significant (0.84 [0.73, 0.97] for NO2 and 0.87 [0.78, 0.97] for PM2.5 absorbance), as well as the association between allergic rhinitis and PM2.5 absorbance (0.83 [0.72, 0.96]).
Conclusions. This study did not find consistent evidence that TRAP increases the prevalence of childhood asthma, allergic rhinitis or aeroallergen sensitization in later childhood using data from birth cohort participants followed for 10 years in three locations in Germany. Results were heterogeneous across the three areas investigated.
PMCID: PMC3828611  PMID: 24255809
Asthma; Allergies; Air pollution; Birth cohort; Children; Long-term exposure; Traffic
14.  Evaluation of a Wildfire Smoke Forecasting System as a Tool for Public Health Protection 
Environmental Health Perspectives  2013;121(10):1142-1147.
Background: Exposure to wildfire smoke has been associated with cardiopulmonary health impacts. Climate change will increase the severity and frequency of smoke events, suggesting a need for enhanced public health protection. Forecasts of smoke exposure can facilitate public health responses.
Objectives: We evaluated the utility of a wildfire smoke forecasting system (BlueSky) for public health protection by comparing its forecasts with observations and assessing their associations with population-level indicators of respiratory health in British Columbia, Canada.
Methods: We compared BlueSky PM2.5 forecasts with PM2.5 measurements from air quality monitors, and BlueSky smoke plume forecasts with plume tracings from National Oceanic and Atmospheric Administration Hazard Mapping System remote sensing data. Daily counts of the asthma drug salbutamol sulfate dispensations and asthma-related physician visits were aggregated for each geographic local health area (LHA). Daily continuous measures of PM2.5 and binary measures of smoke plume presence, either forecasted or observed, were assigned to each LHA. Poisson regression was used to estimate the association between exposure measures and health indicators.
Results: We found modest agreement between forecasts and observations, which was improved during intense fire periods. A 30-μg/m3 increase in BlueSky PM2.5 was associated with an 8% increase in salbutamol dispensations and a 5% increase in asthma-related physician visits. BlueSky plume coverage was associated with 5% and 6% increases in the two health indicators, respectively. The effects were similar for observed smoke, and generally stronger in very smoky areas.
Conclusions: BlueSky forecasts showed modest agreement with retrospective measures of smoke and were predictive of respiratory health indicators, suggesting they can provide useful information for public health protection.
Citation: Yao J, Brauer M, Henderson SB. 2013. Evaluation of a wildfire smoke forecasting system as a tool for public health protection. Environ Health Perspect 121:1142–1147;
PMCID: PMC3801470  PMID: 23906969
15.  A new exposure metric for traffic-related air pollution? An analysis of determinants of hopanes in settled indoor house dust 
Environmental Health  2013;12:48.
Exposure to traffic-related air pollution (TRAP) can adversely impact health but epidemiologic studies are limited in their abilities to assess long-term exposures and incorporate variability in indoor pollutant infiltration.
In order to examine settled house dust levels of hopanes, engine lubricating oil byproducts found in vehicle exhaust, as a novel TRAP exposure measure, dust samples were collected from 171 homes in five Canadian cities and analyzed by gas chromatography–mass spectrometry. To evaluate source contributions, the relative abundance of the highest concentration hopane monomer in house dust was compared to that in outdoor air. Geographic variables related to TRAP emissions and outdoor NO2 concentrations from city-specific TRAP land use regression (LUR) models were calculated at each georeferenced residence location and assessed as predictors of variability in dust hopanes.
Hopanes relative abundance in house dust and ambient air were significantly correlated (Pearson’s r=0.48, p<0.05), suggesting that dust hopanes likely result from traffic emissions. The proportion of variance in dust hopanes concentrations explained by LUR NO2 was less than 10% in Vancouver, Winnipeg and Toronto while the correlations in Edmonton and Windsor explained 20 to 40% of the variance. Modeling with household factors such as air conditioning and shoe removal along with geographic predictors related to TRAP generally increased the proportion of explained variability (10-80%) in measured indoor hopanes dust levels.
Hopanes can consistently be detected in house dust and may be a useful tracer of TRAP exposure if determinants of their spatiotemporal variability are well-characterized, and when home-specific factors are considered.
PMCID: PMC3711892  PMID: 23782977
Air pollution; Dust; Exposure assessment; Hopanes; Land use regression; Traffic
16.  Maternal Exposure to Particulate Air Pollution and Term Birth Weight: A Multi-Country Evaluation of Effect and Heterogeneity 
Environmental Health Perspectives  2013;121(3):267-373.
Background: A growing body of evidence has associated maternal exposure to air pollution with adverse effects on fetal growth; however, the existing literature is inconsistent.
Objectives: We aimed to quantify the association between maternal exposure to particulate air pollution and term birth weight and low birth weight (LBW) across 14 centers from 9 countries, and to explore the influence of site characteristics and exposure assessment methods on between-center heterogeneity in this association.
Methods: Using a common analytical protocol, International Collaboration on Air Pollution and Pregnancy Outcomes (ICAPPO) centers generated effect estimates for term LBW and continuous birth weight associated with PM10 and PM2.5 (particulate matter ≤ 10 and 2.5 µm). We used meta-analysis to combine the estimates of effect across centers (~ 3 million births) and used meta-regression to evaluate the influence of center characteristics and exposure assessment methods on between-center heterogeneity in reported effect estimates.
Results: In random-effects meta-analyses, term LBW was positively associated with a 10-μg/m3 increase in PM10 [odds ratio (OR) = 1.03; 95% CI: 1.01, 1.05] and PM2.5 (OR = 1.10; 95% CI: 1.03, 1.18) exposure during the entire pregnancy, adjusted for maternal socioeconomic status. A 10-μg/m3 increase in PM10 exposure was also negatively associated with term birth weight as a continuous outcome in the fully adjusted random-effects meta-analyses (–8.9 g; 95% CI: –13.2, –4.6 g). Meta-regressions revealed that centers with higher median PM2.5 levels and PM2.5:PM10 ratios, and centers that used a temporal exposure assessment (compared with spatiotemporal), tended to report stronger associations.
Conclusion: Maternal exposure to particulate pollution was associated with LBW at term across study populations. We detected three site characteristics and aspects of exposure assessment methodology that appeared to contribute to the variation in associations reported by centers.
PMCID: PMC3621183  PMID: 23384584
air pollution; fetal growth; heterogeneity; ICAPPO; low birth weight; meta-analysis; meta-regression; multi-center study; particulate matter; pregnancy
17.  Satellite-based Estimates of Ambient Air Pollution and Global Variations in Childhood Asthma Prevalence 
Environmental Health Perspectives  2012;120(9):1333-1339.
Background: The effect of ambient air pollution on global variations and trends in asthma prevalence is unclear.
Objectives: Our goal was to investigate community-level associations between asthma prevalence data from the International Study of Asthma and Allergies in Childhood (ISAAC) and satellite-based estimates of particulate matter with aerodynamic diameter < 2.5 µm (PM2.5) and nitrogen dioxide (NO2), and modelled estimates of ozone.
Methods: We assigned satellite-based estimates of PM2.5 and NO2 at a spatial resolution of 0.1° × 0.1° and modeled estimates of ozone at a resolution of 1° × 1° to 183 ISAAC centers. We used center-level prevalence of severe asthma as the outcome and multilevel models to adjust for gross national income (GNI) and center- and country-level sex, climate, and population density. We examined associations (adjusting for GNI) between air pollution and asthma prevalence over time in centers with data from ISAAC Phase One (mid-1900s) and Phase Three (2001–2003).
Results: For the 13- to 14-year age group (128 centers in 28 countries), the estimated average within-country change in center-level asthma prevalence per 100 children per 10% increase in center-level PM2.5 and NO2 was –0.043 [95% confidence interval (CI): –0.139, 0.053] and 0.017 (95% CI: –0.030, 0.064) respectively. For ozone the estimated change in prevalence per parts per billion by volume was –0.116 (95% CI: –0.234, 0.001). Equivalent results for the 6- to 7-year age group (83 centers in 20 countries), though slightly different, were not significantly positive. For the 13- to 14-year age group, change in center-level asthma prevalence over time per 100 children per 10% increase in PM2.5 from Phase One to Phase Three was –0.139 (95% CI: –0.347, 0.068). The corresponding association with ozone (per ppbV) was –0.171 (95% CI: –0.275, –0.067).
Conclusion: In contrast to reports from within-community studies of individuals exposed to traffic pollution, we did not find evidence of a positive association between ambient air pollution and asthma prevalence as measured at the community level.
PMCID: PMC3440118  PMID: 22548921
air pollution; asthma prevalence; children; epidemiology; global; nitrogen dioxide; ozone; particulate matter; satellite observations
18.  Risk of Nonaccidental and Cardiovascular Mortality in Relation to Long-term Exposure to Low Concentrations of Fine Particulate Matter: A Canadian National-Level Cohort Study 
Environmental Health Perspectives  2012;120(5):708-714.
Background: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM2.5)]. This is the first national-level cohort study to investigate these risks in Canada.
Objective: We investigated the association between long-term exposure to ambient PM2.5 and cardiovascular mortality in nonimmigrant Canadian adults.
Methods: We assigned estimates of exposure to ambient PM2.5 derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models.
Results: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m3 increase in concentrations of PM2.5. Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities.
Conclusions: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM2.5. Associations were observed with exposures to PM2.5 at concentrations that were predominantly lower (mean, 8.7 μg/m3; interquartile range, 6.2 μg/m3) than those reported previously.
PMCID: PMC3346774  PMID: 22313724
Canada; cardiovascular mortality; cohort study; fine particulate matter
19.  Estimated Global Mortality Attributable to Smoke from Landscape Fires 
Environmental Health Perspectives  2012;120(5):695-701.
Background: Forest, grass, and peat fires release approximately 2 petagrams of carbon into the atmosphere each year, influencing weather, climate, and air quality.
Objective: We estimated the annual global mortality attributable to landscape fire smoke (LFS).
Methods: Daily and annual exposure to particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) from fire emissions was estimated globally for 1997 through 2006 by combining outputs from a chemical transport model with satellite-based observations of aerosol optical depth. In World Health Organization (WHO) subregions classified as sporadically affected, the daily burden of mortality was estimated using previously published concentration–response coefficients for the association between short-term elevations in PM2.5 from LFS (contrasted with 0 μg/m3 from LFS) and all-cause mortality. In subregions classified as chronically affected, the annual burden of mortality was estimated using the American Cancer Society study coefficient for the association between long-term PM2.5 exposure and all-cause mortality. The annual average PM2.5 estimates were contrasted with theoretical minimum (counterfactual) concentrations in each chronically affected subregion. Sensitivity of mortality estimates to different exposure assessments, counterfactual estimates, and concentration–response functions was evaluated. Strong La Niña and El Niño years were compared to assess the influence of interannual climatic variability.
Results: Our principal estimate for the average mortality attributable to LFS exposure was 339,000 deaths annually. In sensitivity analyses the interquartile range of all tested estimates was 260,000–600,000. The regions most affected were sub-Saharan Africa (157,000) and Southeast Asia (110,000). Estimated annual mortality during La Niña was 262,000, compared with 532,000 during El Niño.
Conclusions: Fire emissions are an important contributor to global mortality. Adverse health outcomes associated with LFS could be substantially reduced by curtailing burning of tropical rainforests, which rarely burn naturally. The large estimated influence of El Niño suggests a relationship between climate and the burden of mortality attributable to LFS.
PMCID: PMC3346787  PMID: 22456494
air pollution; biomass burning; carbon cycle; deforestation; global burden of disease; landscape fire smoke; mortality
20.  Spatiotemporal air pollution exposure assessment for a Canadian population-based lung cancer case-control study 
Environmental Health  2012;11:22.
Few epidemiological studies of air pollution have used residential histories to develop long-term retrospective exposure estimates for multiple ambient air pollutants and vehicle and industrial emissions. We present such an exposure assessment for a Canadian population-based lung cancer case-control study of 8353 individuals using self-reported residential histories from 1975 to 1994. We also examine the implications of disregarding and/or improperly accounting for residential mobility in long-term exposure assessments.
National spatial surfaces of ambient air pollution were compiled from recent satellite-based estimates (for PM2.5 and NO2) and a chemical transport model (for O3). The surfaces were adjusted with historical annual air pollution monitoring data, using either spatiotemporal interpolation or linear regression. Model evaluation was conducted using an independent ten percent subset of monitoring data per year. Proximity to major roads, incorporating a temporal weighting factor based on Canadian mobile-source emission estimates, was used to estimate exposure to vehicle emissions. A comprehensive inventory of geocoded industries was used to estimate proximity to major and minor industrial emissions.
Calibration of the national PM2.5 surface using annual spatiotemporal interpolation predicted historical PM2.5 measurement data best (R2 = 0.51), while linear regression incorporating the national surfaces, a time-trend and population density best predicted historical concentrations of NO2 (R2 = 0.38) and O3 (R2 = 0.56). Applying the models to study participants residential histories between 1975 and 1994 resulted in mean PM2.5, NO2 and O3 exposures of 11.3 μg/m3 (SD = 2.6), 17.7 ppb (4.1), and 26.4 ppb (3.4) respectively. On average, individuals lived within 300 m of a highway for 2.9 years (15% of exposure-years) and within 3 km of a major industrial emitter for 6.4 years (32% of exposure-years). Approximately 50% of individuals were classified into a different PM2.5, NO2 and O3 exposure quintile when using study entry postal codes and spatial pollution surfaces, in comparison to exposures derived from residential histories and spatiotemporal air pollution models. Recall bias was also present for self-reported residential histories prior to 1975, with cases recalling older residences more often than controls.
We demonstrate a flexible exposure assessment approach for estimating historical air pollution concentrations over large geographical areas and time-periods. In addition, we highlight the importance of including residential histories in long-term exposure assessments.
For submission to: Environmental Health
PMCID: PMC3372423  PMID: 22475580
Air pollution; Canada; Exposure assessment; Lung cancer; Residential mobility; Spatiotemporal
21.  Health Impacts of the Built Environment: Within-Urban Variability in Physical Inactivity, Air Pollution, and Ischemic Heart Disease Mortality 
Environmental Health Perspectives  2011;120(2):247-253.
Background: Physical inactivity and exposure to air pollution are important risk factors for death and disease globally. The built environment may influence exposures to these risk factors in different ways and thus differentially affect the health of urban populations.
Objective: We investigated the built environment’s association with air pollution and physical inactivity, and estimated attributable health risks.
Methods: We used a regional travel survey to estimate within-urban variability in physical inactivity and home-based air pollution exposure [particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5), nitrogen oxides (NOx), and ozone (O3)] for 30,007 individuals in southern California. We then estimated the resulting risk for ischemic heart disease (IHD) using literature-derived dose–response values. Using a cross-sectional approach, we compared estimated IHD mortality risks among neighborhoods based on “walkability” scores.
Results: The proportion of physically active individuals was higher in high- versus low-walkability neighborhoods (24.9% vs. 12.5%); however, only a small proportion of the population was physically active, and between-neighborhood variability in estimated IHD mortality attributable to physical inactivity was modest (7 fewer IHD deaths/100,000/year in high- vs. low-walkability neighborhoods). Between-neighborhood differences in estimated IHD mortality from air pollution were comparable in magnitude (9 more IHD deaths/100,000/year for PM2.5 and 3 fewer IHD deaths for O3 in high- vs. low-walkability neighborhoods), suggesting that population health benefits from increased physical activity in high-walkability neighborhoods may be offset by adverse effects of air pollution exposure.
Policy implications: Currently, planning efforts mainly focus on increasing physical activity through neighborhood design. Our results suggest that differences in population health impacts among neighborhoods are similar in magnitude for air pollution and physical activity. Thus, physical activity and exposure to air pollution are critical aspects of planning for cleaner, health-promoting cities.
PMCID: PMC3279444  PMID: 22004949
active travel; air quality; environmental planning; infill; risk assessment; urban form
22.  Proximity of public elementary schools to major roads in Canadian urban areas 
Epidemiologic studies have linked exposure to traffic-generated air and noise pollution with a wide range of adverse health effects in children. Children spend a large portion of time at school, and both air pollution and noise are elevated in close proximity to roads, so school location may be an important determinant of exposure. No studies have yet examined the proximity of schools to major roads in Canadian cities.
Data on public elementary schools in Canada's 10 most populous cities were obtained from online databases. School addresses were geocoded and proximity to the nearest major road, defined using a standardized national road classification scheme, was calculated for each school. Based on measurements of nitrogen oxide concentrations, ultrafine particle counts, and noise levels in three Canadian cities we conservatively defined distances < 75 m from major roads as the zone of primary interest. Census data at the city and neighborhood levels were used to evaluate relationships between school proximity to major roads, urban density, and indicators of socioeconomic status.
Addresses were obtained for 1,556 public elementary schools, 95% of which were successfully geocoded. Across all 10 cities, 16.3% of schools were located within 75 m of a major road, with wide variability between cities. Schools in neighborhoods with higher median income were less likely to be near major roads (OR per $20,000 increase: 0.81; 95% CI: 0.65, 1.00), while schools in densely populated neighborhoods were more frequently close to major roads (OR per 1,000 dwellings/km2: 1.07; 95% CI: 1.00, 1.16). Over 22% of schools in the lowest neighborhood income quintile were close to major roads, compared to 13% of schools in the highest income quintile.
A substantial fraction of students at public elementary schools in Canada, particularly students attending schools in low income neighborhoods, may be exposed to elevated levels of air pollution and noise while at school. As a result, the locations of schools may negatively impact the healthy development and academic performance of a large number of Canadian children.
PMCID: PMC3283477  PMID: 22188682
23.  Built Environment Influences on Healthy Transportation Choices: Bicycling versus Driving 
A growing body of evidence links the built environment to physical activity levels, health outcomes, and transportation behaviors. However, little of this research has focused on cycling, a sustainable transportation option with great potential for growth in North America. This study examines associations between decisions to bicycle (versus drive) and the built environment, with explicit consideration of three different spatial zones that may be relevant in travel behavior: trip origins, trip destinations, and along the route between. We analyzed 3,280 utilitarian bicycle and car trips in Metro Vancouver, Canada made by 1,902 adults, including both current and potential cyclists. Objective measures were developed for built environment characteristics related to the physical environment, land use patterns, the road network, and bicycle-specific facilities. Multilevel logistic regression was used to model the likelihood that a trip was made by bicycle, adjusting for trip distance and personal demographics. Separate models were constructed for each spatial zone, and a global model examined the relative influence of the three zones. In total, 31% (1,023 out of 3,280) of trips were made by bicycle. Increased odds of bicycling were associated with less hilliness; higher intersection density; less highways and arterials; presence of bicycle signage, traffic calming, and cyclist-activated traffic lights; more neighborhood commercial, educational, and industrial land uses; greater land use mix; and higher population density. Different factors were important within each spatial zone. Overall, the characteristics of routes were more influential than origin or destination characteristics. These findings indicate that the built environment has a significant influence on healthy travel decisions, and spatial context is important. Future research should explicitly consider relevant spatial zones when investigating the relationship between physical activity and urban form.
PMCID: PMC3005092  PMID: 21174189
Bicycle; Built environment; Physical activity; Urban form; Non-motorized transportation
24.  Otitis media incidence and risk factors in a population-based birth cohort 
Paediatrics & Child Health  2010;15(7):437-442.
Otitis media is the main reason young children receive antibiotics and is the leading reason for physician visits.
To characterize the incidence, recurrence and risk factors for otitis media in a population-based birth cohort.
All children born in southwestern British Columbia during 1999 to 2000 were followed until the age of three years. Otitis media was defined using The International Classification of Diseases, Ninth Revision coding of physician visits, and linked with antibiotic prescription data. Information on sex, birth weight, gestational age, Aboriginal status, maternal age, older siblings, maternal smoking during pregnancy, breastfeeding initiation, neighbourhood income, female education and rural residence were obtained from vital statistics, birth hospitalizations, perinatal registry and census data.
Complete risk factor information was available for 50,474 children (86% of all births). Nearly one-half of the children (48.6%) had one or more physician visits for otitis media during follow-up, and 3952 children (7.8%) met the definition for recurrent otitis media. Of the children with at least three visits during follow-up (n=7571), 73% had their initial visit during the first year of life. Aboriginal status, maternal age younger than 20 years, male sex and older siblings were the strongest risk factors identified in the adjusted conditional logistic regression models.
The present study established a population-based birth cohort by linking multiple administrative databases to characterize the incidence of and risk factors for otitis media. Although the incidence of otitis media is generally low in southwestern British Columbia, important risk factors continue to be young maternal age, mothers who smoke during pregnancy and children with Aboriginal ancestry.
PMCID: PMC2948776  PMID: 21886448
Birth cohort; Incidence; Otitis media; Risk factors
25.  Three Measures of Forest Fire Smoke Exposure and Their Associations with Respiratory and Cardiovascular Health Outcomes in a Population-Based Cohort 
Environmental Health Perspectives  2011;119(9):1266-1271.
Background: During the summer of 2003 numerous fires burned in British Columbia, Canada.
Objectives: We examined the associations between respiratory and cardiovascular physician visits and hospital admissions, and three measures of smoke exposure over a 92-day study period (1 July to 30 September 2003).
Methods: A population-based cohort of 281,711 residents was identified from administrative data. Spatially specific daily exposure estimates were assigned to each subject based on total measurements of particulate matter (PM) ≤ 10 μm in aerodynamic diameter (PM10) from six regulatory tapered element oscillating microbalance (TEOM) air quality monitors, smoke-related PM10 from a CALPUFF dispersion model run for the study, and a SMOKE exposure metric for plumes visible in satellite images. Logistic regression with repeated measures was used to estimate associations with each outcome.
Results: The mean (± SD) exposure based on TEOM-measured PM10 was 29 ± 31 μg/m3, with an interquartile range of 14–31 μg/m3. Correlations between the TEOM, smoke, and CALPUFF metrics were moderate (0.37–0.76). Odds ratios (ORs) for a 30-μg/m3 increase in TEOM-based PM10 were 1.05 [95% confidence interval (CI), 1.03–1.06] for all respiratory physician visits, 1.16 (95% CI, 1.09–1.23) for asthma-specific visits, and 1.15 (95% CI, 1.00–1.29) for respiratory hospital admissions. Associations with cardiovascular outcomes were largely null.
Conclusions: Overall we found that increases in TEOM-measured PM10 were associated with increased odds of respiratory physician visits and hospital admissions, but not with cardiovascular health outcomes. Results indicating effects of fire smoke on respiratory outcomes are consistent with previous studies, as are the null results for cardiovascular outcomes. Some agreement between TEOM and the other metrics suggests that exposure assessment tools that are independent of air quality monitoring may be useful with further refinement.
PMCID: PMC3230386  PMID: 21659039
biomass smoke; cohort study; exposure assessment; particulate matter; population-based

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