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In 1880, coal was the primary energy source for everything from home heating to industry. Regions where coal was readily available, such as the Ruhr Valley in Germany and western Pennsylvania in the United States, witnessed exponential growth-yet also suffered the greatest damage from coal pollution.These conditions prompted civic activism in the form of \"anti-smoke\" campaigns to attack the unsightly physical manifestations of coal burning. This early period witnessed significant cooperation between industrialists, government, and citizens to combat the smoke problem. It was not until the 1960s, when attention shifted from dust and grime to hazardous invisible gases, that cooperation dissipated, and protests took an antagonistic turn.The Age of Smokepresents an original, comparative history of environmental policy and protest in the United States and Germany. Dividing this history into distinct eras (1880 to World War I, interwar, post-World War II to 1970), Frank Uekoetter compares and contrasts the influence of political, class, and social structures, scientific communities, engineers, industrial lobbies, and environmental groups in each nation. He concludes with a discussion of the environmental revolution, arguing that there were indeed two environmental revolutions in both countries: one societal, where changing values gave urgency to air pollution control, the other institutional, where changes in policies tried to catch up with shifting sentiments.Focusing on a critical period in environmental history,The Age of Smokeprovides a valuable study of policy development in two modern industrial nations, and the rise of civic activism to combat air pollution. As Uekoetter's work reveals, the cooperative approaches developed in an earlier era offer valuable lessons and perhaps the best hope for future progress.

In 1880, coal was the primary energy source for everything from home heating to industry. Regions where coal was readily available, such as the Ruhr Valley in Germany and western Pennsylvania in the United States, witnessed exponential growth-yet also suffered the greatest damage from coal pollution. These conditions prompted civic activism in the form of \\u201canti-smoke\\u201d campaigns to attack the unsightly physical manifestations of coal burning. This early period witnessed significant cooperation between industrialists, government, and citizens to combat the smoke problem. It was not until the 1960s, when attention shifted from dust and grime to hazardous invisible gases, that cooperation dissipated, and protests took an antagonistic turn. The Age of Smoke presents an original, comparative history of environmental policy and protest in the United States and Germany. Dividing this history into distinct eras (1880 to World War I, interwar, post-World War II to 1970), Frank Uekoetter compares and contrasts the influence of political, class, and social structures, scientific communities, engineers, industrial lobbies, and environmental groups in each nation. He concludes with a discussion of the environmental revolution, arguing that there were indeed two environmental revolutions in both countries: one societal, where changing values gave urgency to air pollution control, the other institutional, where changes in policies tried to catch up with shifting sentiments. Focusing on a critical period in environmental history, The Age of Smoke provides a valuable study of policy development in two modern industrial nations, and the rise of civic activism to combat air pollution. As Uekoetter's work reveals, the cooperative approaches developed in an earlier era offer valuable lessons and perhaps the best hope for future progress.

Regulatory oversight of toxic emissions from industrial plants and understanding about these emissions ' impacts are in their infancy. Applying a research design based on the openings and closings of 1,600 industrial plants to rich data on housing markets and infant health, we find that: toxic air emissions affect air quality only within 1 mile of the plant; plant openings lead to 11 percent declines in housing values within 0.5 mile or a loss of about $ 4.25 million for these households; and a plant's operation is associated with a roughly 3 percent increase in the probability of low birthweight within 1 mile.

AbstractObjectiveTo assess risks and costs of hospital admission associated with short term exposure to fine particulate matter with diameter less than 2.5 µm (PM2.5) for 214 mutually exclusive disease groups.DesignTime stratified, case crossover analyses with conditional logistic regressions adjusted for non-linear confounding effects of meteorological variables.SettingMedicare inpatient hospital claims in the United States, 2000-12 (n=95 277 169).ParticipantsAll Medicare fee-for-service beneficiaries aged 65 or older admitted to hospital.Main outcome measuresRisk of hospital admission, number of admissions, days in hospital, inpatient and post-acute care costs, and value of statistical life (that is, the economic value used to measure the cost of avoiding a death) due to the lives lost at discharge for 214 disease groups.ResultsPositive associations between short term exposure to PM2.5 and risk of hospital admission were found for several prevalent but rarely studied diseases, such as septicemia, fluid and electrolyte disorders, and acute and unspecified renal failure. Positive associations were also found between risk of hospital admission and cardiovascular and respiratory diseases, Parkinson’s disease, diabetes, phlebitis, thrombophlebitis, and thromboembolism, confirming previously published results. These associations remained consistent when restricted to days with a daily PM2.5 concentration below the WHO air quality guideline for the 24 hour average exposure to PM2.5. For the rarely studied diseases, each 1 µg/m3 increase in short term PM2.5 was associated with an annual increase of 2050 hospital admissions (95% confidence interval 1914 to 2187 admissions), 12 216 days in hospital (11 358 to 13 075), US$31m (£24m, €28m; $29m to $34m) in inpatient and post-acute care costs, and $2.5bn ($2.0bn to $2.9bn) in value of statistical life. For diseases with a previously known association, each 1 µg/m3 increase in short term exposure to PM2.5 was associated with an annual increase of 3642 hospital admissions (3434 to 3851), 20 098 days in hospital (18 950 to 21 247), $69m ($65m to $73m) in inpatient and post-acute care costs, and $4.1bn ($3.5bn to $4.7bn) in value of statistical life.ConclusionsNew causes and previously identified causes of hospital admission associated with short term exposure to PM2.5 were found. These associations remained even at a daily PM2.5 concentration below the WHO 24 hour guideline. Substantial economic costs were linked to a small increase in short term PM2.5.

The entire Medicare population was used to establish a relationship between all-cause mortality and small particulate matter in the air. Even at concentrations below current air-quality standards, higher levels of particulate matter were associated with higher rates of death. The adverse health effects associated with long-term exposure to air pollution are well documented. 1 , 2 Studies suggest that fine particles (particles with a mass median aerodynamic diameter of less than 2.5 μm [PM 2.5 ]) are a public health concern, 3 with exposure linked to decreased life expectancy. 4 – 6 Long-term exposure to ozone has also been associated with reduced survival in several recent studies, although evidence is sparse. 4 , 7 – 9 Studies with large cohorts have investigated the relationship between long-term exposures to PM 2.5 and ozone and mortality 4 , 9 – 13 ; others have estimated the health effects of fine particles at . . .

The transboundary health impacts of air pollution associated with the international trade of goods and services are greater than those associated with long-distance atmospheric pollutant transport. The international air pollution trade Air quality and mortality are affected by local air pollution, but not all local air pollution comes from local emissions. It is also fed by atmospheric transport of pollutants from distant sources, and some of the pollution in one region is due to the production of goods for consumption in another. This study investigates the effect of these two remote pollution sources on premature mortality linked to fine particulate matter pollution. Qiang Zhang et al . find that, in 2007, about 12 per cent of premature deaths related to fine particulate matter were attributed to air pollutants from distant sources and about 22 per cent were associated with goods and services produced in one region for consumption in another. The findings suggest that the health impacts of pollution associated with international trade are greater than those associated with long-distance atmospheric pollutant transport. Millions of people die every year from diseases caused by exposure to outdoor air pollution 1 , 2 , 3 , 4 , 5 . Some studies have estimated premature mortality related to local sources of air pollution 6 , 7 , but local air quality can also be affected by atmospheric transport of pollution from distant sources 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 . International trade is contributing to the globalization of emission and pollution as a result of the production of goods (and their associated emissions) in one region for consumption in another region 14 , 19 , 20 , 21 , 22 . The effects of international trade on air pollutant emissions 23 , air quality 14 and health 24 have been investigated regionally, but a combined, global assessment of the health impacts related to international trade and the transport of atmospheric air pollution is lacking. Here we combine four global models to estimate premature mortality caused by fine particulate matter (PM 2.5 ) pollution as a result of atmospheric transport and the production and consumption of goods and services in different world regions. We find that, of the 3.45 million premature deaths related to PM 2.5 pollution in 2007 worldwide, about 12 per cent (411,100 deaths) were related to air pollutants emitted in a region of the world other than that in which the death occurred, and about 22 per cent (762,400 deaths) were associated with goods and services produced in one region for consumption in another. For example, PM 2.5 pollution produced in China in 2007 is linked to more than 64,800 premature deaths in regions other than China, including more than 3,100 premature deaths in western Europe and the USA; on the other hand, consumption in western Europe and the USA is linked to more than 108,600 premature deaths in China. Our results reveal that the transboundary health impacts of PM 2.5 pollution associated with international trade are greater than those associated with long-distance atmospheric pollutant transport.

Short-term exposure to ambient air pollution has been associated with lower lung function. Few studies have examined whether these associations are detectable at relatively low levels of pollution within current U.S. Environmental Protection Agency (EPA) standards. To examine exposure to ambient air pollutants within EPA standards and lung function in a large cohort study. We included 3,262 participants of the Framingham Offspring and Third Generation cohorts living within 40 km of the Harvard Supersite monitor in Boston, Massachusetts (5,358 examinations, 1995-2011) who were not current smokers, with previous-day pollutant levels in compliance with EPA standards. We compared lung function (FEV1 and FVC) after previous-day exposure to particulate matter less than 2.5 μm in diameter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) in the \"moderate\" range of the EPA Air Quality Index to exposure in the \"good\" range. We also examined linear relationships between moving averages of pollutant concentrations 1, 2, 3, 5, and 7 days before spirometry and lung function. Exposure to pollutant concentrations in the \"moderate\" range of the EPA Air Quality Index was associated with a 20.1-ml lower FEV1 for PM2.5 (95% confidence interval [CI], -33.4, -6.9), a 30.6-ml lower FEV1 for NO2 (95% CI, -60.9, -0.2), and a 55.7-ml lower FEV1 for O3 (95% CI, -100.7, -10.8) compared with the \"good\" range. The 1- and 2-day moving averages of PM2.5, NO2, and O3 before testing were negatively associated with FEV1 and FVC. Short-term exposure to PM2.5, NO2, and O3 within current EPA standards was associated with lower lung function in this cohort of adults.

Investigation of premature mortality by seven emission sources of atmospheric pollutants shows that outdoor air pollution, mostly by fine particulate matter, leads to more than three million premature deaths per year worldwide, which could double by 2050. Links between air pollution and premature mortality Premature mortality can be linked to a wide range of causes including the effect of outdoor air pollutants such as ozone and fine particulate matter on human health. This paper investigates the link between premature mortality and seven sources of atmospheric pollutants in urban and rural environments. Jos Lelieveld et al . find that outdoor air pollution, mostly by fine particulate matter, leads to around three million premature deaths per year worldwide. Emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest effect on premature mortality globally. In large areas of the United States and a few other countries, emissions from traffic and power generation are important, whereas in the eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to fine particulate matter, with the overall health effect depending on assumptions regarding particle toxicity. Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes 1 , 2 , 3 , 4 , 5 , including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM 2.5 ) 3 , 4 , 5 , 6 , 7 , 8 , 9 . It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary 10 . Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5 ), we calculate that outdoor air pollution, mostly by PM 2.5 , leads to 3.3 (95 per cent confidence interval 1.61–4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic 5 , but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM 2.5 , with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.

In this large study, the mortality benefits of reducing levels of fine particulate matter air pollution were greater for low-income and higher-income Black persons and for low-income White persons than for higher-income White persons.