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      Energy savings, emission reductions, and health co-benefits of the green building movement

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          Abstract

          Buildings consume nearly 40% of primary energy production globally. Certified green buildings substantially reduce energy consumption on a per square foot basis and they also focus on indoor environmental quality. However, the co-benefits to health through reductions in energy and concomitant reductions in air pollution have not been examined.We calculated year by year LEED (Leadership in Energy and Environmental Design) certification rates in six countries (the United States, China, India, Brazil, Germany, and Turkey) and then used data from the Green Building Information Gateway (GBIG) to estimate energy savings in each country each year. Of the green building rating schemes, LEED accounts for 32% of green-certified floor space and publically reports energy efficiency data. We employed Harvard's Co-BE Calculator to determine pollutant emissions reductions by country accounting for transient energy mixes and baseline energy use intensities. Co-BE applies the social cost of carbon and the social cost of atmospheric release to translate these reductions into health benefits. Based on modeled energy use, LEED-certified buildings saved $7.5B in energy costs and averted 33MT of CO2, 51 kt of SO2, 38 kt of NOx, and 10 kt of PM2.5 from entering the atmosphere, which amounts to $5.8B (lower limit = $2.3B, upper limit = $9.1B) in climate and health co-benefits from 2000 to 2016 in the six countries investigated. The U.S. health benefits derive from avoiding an estimated 172-405 premature deaths, 171 hospital admissions, 11,000 asthma exacerbations, 54,000 respiratory symptoms, 21,000 lost days of work, and 16,000 lost days of school. Because the climate and health benefits are nearly equivalent to the energy savings for green buildings in the United States, and up to 10 times higher in developing countries, they provide an important and previously unquantified societal value. Future analyses should consider these co-benefits when weighing policy decisions around energy-efficient buildings.

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          Most cited references16

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          Increased particulate air pollution and the triggering of myocardial infarction.

          Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown. We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass <2.5 microm (PM(2.5)), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 microg/m(3) PM(2.5) during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 microg/m(3) PM(2.5) in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively). The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.
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            Ozone and short-term mortality in 95 US urban communities, 1987-2000.

            Ozone has been associated with various adverse health effects, including increased rates of hospital admissions and exacerbation of respiratory illnesses. Although numerous time-series studies have estimated associations between day-to-day variation in ozone levels and mortality counts, results have been inconclusive. To investigate whether short-term (daily and weekly) exposure to ambient ozone is associated with mortality in the United States. Using analytical methods and databases developed for the National Morbidity, Mortality, and Air Pollution Study, we estimated a national average relative rate of mortality associated with short-term exposure to ambient ozone for 95 large US urban communities from 1987-2000. We used distributed-lag models for estimating community-specific relative rates of mortality adjusted for time-varying confounders (particulate matter, weather, seasonality, and long-term trends) and hierarchical models for combining relative rates across communities to estimate a national average relative rate, taking into account spatial heterogeneity. Daily counts of total non-injury-related mortality and cardiovascular and respiratory mortality in 95 large US communities during a 14-year period. A 10-ppb increase in the previous week's ozone was associated with a 0.52% increase in daily mortality (95% posterior interval [PI], 0.27%-0.77%) and a 0.64% increase in cardiovascular and respiratory mortality (95% PI, 0.31%-0.98%). Effect estimates for aggregate ozone during the previous week were larger than for models considering only a single day's exposure. Results were robust to adjustment for particulate matter, weather, seasonality, and long-term trends. These results indicate a statistically significant association between short-term changes in ozone and mortality on average for 95 large US urban communities, which include about 40% of the total US population. The findings indicate that this widespread pollutant adversely affects public health.
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              A roadmap for rapid decarbonization

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                Author and article information

                Journal
                Journal of Exposure Science & Environmental Epidemiology
                J Expo Sci Environ Epidemiol
                Springer Nature
                1559-0631
                1559-064X
                January 30 2018
                :
                :
                Article
                10.1038/s41370-017-0014-9
                29382929
                a137fcb4-ddf7-4cd1-a639-8fd08b78aba0
                © 2018

                http://www.springer.com/tdm

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