Bryan Hubbell
United States Environmental Protection Agency
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Bryan Hubbell.
Environmental Health Perspectives | 2014
Richard T. Burnett; C. Arden Pope; Majid Ezzati; Casey Olives; Stephen S Lim; Sumi Mehta; Hwashin H. Shin; Gitanjali M. Singh; Bryan Hubbell; Michael Brauer; H. Ross Anderson; Kirk R. Smith; John R. Balmes; Nigel Bruce; Haidong Kan; Francine Laden; Annette Prüss-Üstün; Michelle C. Turner; Susan M. Gapstur; W. Ryan Diver; Aaron Cohen
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; http://dx.doi.org/10.1289/ehp.1307049
The Lancet | 2017
Aaron Cohen; Michael Brauer; Richard T. Burnett; H. Ross Anderson; Joseph Frostad; Kara Estep; Kalpana Balakrishnan; Bert Brunekreef; Lalit Dandona; Rakhi Dandona; Valery L. Feigin; Greg Freedman; Bryan Hubbell; Haidong Kan; Luke D. Knibbs; Yang Liu; Randall V. Martin; Lidia Morawska; C. Arden Pope; Hwashin Shin; Kurt Straif; Gavin Shaddick; Matthew L. Thomas; Rita Van Dingenen; Aaron van Donkelaar; Theo Vos; Christopher J. L. Murray; Mohammad H. Forouzanfar
Summary Background Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels. Methods We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM2·5) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure–response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure–response functions spanning the global range of exposure. Findings Ambient PM2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000–422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015. Interpretation Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction. Funding Bill & Melinda Gates Foundation and Health Effects Institute.
Risk Analysis | 2012
Neal Fann; Amy D. Lamson; Susan C. Anenberg; Karen Wesson; David Risley; Bryan Hubbell
Ground-level ozone (O(3)) and fine particulate matter (PM(2.5)) are associated with increased risk of mortality. We quantify the burden of modeled 2005 concentrations of O(3) and PM(2.5) on health in the United States. We use the photochemical Community Multiscale Air Quality (CMAQ) model in conjunction with ambient monitored data to create fused surfaces of summer season average 8-hour ozone and annual mean PM(2.5) levels at a 12 km grid resolution across the continental United States. Employing spatially resolved demographic and concentration data, we assess the spatial and age distribution of air-pollution-related mortality and morbidity. For both PM(2.5) and O(3) we also estimate: the percentage of total deaths due to each pollutant; the reduction in life years and life expectancy; and the deaths avoided according to hypothetical air quality improvements. Using PM(2.5) and O(3) mortality risk coefficients drawn from the long-term American Cancer Society (ACS) cohort study and National Mortality and Morbidity Air Pollution Study (NMMAPS), respectively, we estimate 130,000 PM(2.5) -related deaths and 4,700 ozone-related deaths to result from 2005 air quality levels. Among populations aged 65-99, we estimate nearly 1.1 million life years lost from PM(2.5) exposure and approximately 36,000 life years lost from ozone exposure. Among the 10 most populous counties, the percentage of deaths attributable to PM(2.5) and ozone ranges from 3.5% in San Jose to 10% in Los Angeles. These results show that despite significant improvements in air quality in recent decades, recent levels of PM(2.5) and ozone still pose a nontrivial risk to public health.
Air Quality, Atmosphere & Health | 2009
Neal Fann; Charles M. Fulcher; Bryan Hubbell
The benefit per ton (
American Journal of Agricultural Economics | 2000
Nii Adote Abrahams; Bryan Hubbell; Jeffrey L. Jordan
/ton) of reducing PM2.5 varies by the location of the emission reduction, the type of source emitting the precursor, and the specific precursor controlled. This paper examines how each of these factors influences the magnitude of the
Environmental Health Perspectives | 2004
Bryan Hubbell; Aaron Hallberg; Donald McCubbin; Ellen Post
/ton estimate. We employ a reduced-form air quality model to predict changes in ambient PM2.5 resulting from an array of emission control scenarios affecting 12 different combinations of sources emitting carbonaceous particles, NOx, SOx, NH3, and volatile organic compounds. We perform this modeling for each of nine urban areas and one nationwide area. Upon modeling the air quality change, we then divide the total monetized health benefits by the PM2.5 precursor emission reductions to generate
Environmental Health Perspectives | 2012
Douglas O. Johns; Lindsay Wichers Stanek; Katherine Walker; Souad Benromdhane; Bryan Hubbell; Mary Ross; Robert B. Devlin; Daniel L. Costa; Daniel S. Greenbaum
/ton metrics. The resulting
Risk Analysis | 2011
Neal Fann; Henry Roman; Charles M. Fulcher; Mikael A. Gentile; Bryan Hubbell; Karen Wesson; Jonathan I. Levy
/ton estimates exhibit the greatest variability across certain precursors and sources such as area source SOx, point source SOx, and mobile source NH3. Certain
Journal of Toxicology and Environmental Health | 2007
Kenneth Davidson; Aaron Hallberg; Donald McCubbin; Bryan Hubbell
/ton estimates, including mobile source NOx, exhibit significant variability across urban areas. Reductions in carbonaceous particles generate the largest
Environmental Science & Technology | 2011
A. Scott Voorhees; Neal Fann; Charles M. Fulcher; Patrick Dolwick; Bryan Hubbell; Britta G. Bierwagen; Philip E. Morefield
/ton across all locations.