T he environmental Kuznets curve posits an inverted-U relationship between pollution and economic development. Kuznets's name was apparently attached to the curve by Grossman and Krueger (1993), who noted its resemblance to Kuznets's inverted-U relationship between income inequality and development. In the first stage of industrialization, pollution in the environmental Kuznets curve world grows rapidly because people are more interested in jobs and income than clean air and water, communities are too poor to pay for abatement, and environmental regulation is correspondingly weak. The balance shifts as income rises. Leading industrial sectors become cleaner, people value the environment more highly, and regulatory institutions become more effective. Along the curve, pollution levels off in the middle-income range and then falls toward pre-industrial levels in wealthy societies. The environmental Kuznets curve model has elicited conflicting reactions from researchers and policymakers. Applied econometricians have generally accepted the basic tenets of the model and focused on measuring its parameters. Their regressions, typically fitted to cross-sectional observations across countries or regions, suggest that air and water pollution increase with development until per capita income reaches a range of $5000 to $8000. When income rises beyond that level, pollution starts to decline, as shown in the "conventional EKC" line in Figure 1. In developing countries, some policymakers have interpreted such results as conveying a message about priorities: Grow first, then clean up. Numerous critics have challenged the conventional environmental Kuznets curve, both as a representation of what actually happens in the development process and as a policy prescription. Some pessimistic critics argue that crosssectional evidence for the environmental Kuznets curve is nothing more than a

https://pubs.aeaweb.org/doi/pdfplus/10.1257/0895330027157

Confronting the Environmental Kuznets Curve

Recently, many researchers paid more attentions to the association between air pollution and respiratory system disease. In the past few years, levels of smog have increased throughout China resulting in the deterioration of air quality, raising worldwide concerns. PM2.5 (particles less than 2.5 micrometers in diameter) can penetrate deeply into the lung, irritate and corrode the alveolar wall, and consequently impair lung function. Hence it is important to investigate the impact of PM2.5 on the respiratory system and then to help China combat the current air pollution problems. In this review, we will discuss PM2.5 damage on human respiratory system from epidemiological, experimental and mechanism studies. At last, we recommend to the population to limit exposure to air pollution and call to the authorities to create an index of pollution related to health.

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The impact of PM2.5 on the human respiratory system.

This article briefly summarizes the epidemiology of the health effects of fine particulate air pollution, provides an early, somewhat speculative, discussion of the contribution of epidemiology to evaluating biologic mechanisms, and evaluates who's at risk or is susceptible to adverse health effects. Based on preliminary epidemiologic evidence, it is speculated that a systemic response to fine particle-induced pulmonary inflammation, including cytokine release and altered cardiac autonomic function, may be part of the pathophysiologic mechanisms or pathways linking particulate pollution with cardiopulmonary disease. The elderly, infants, and persons with chronic cardiopulmonary disease, influenza, or asthma are most susceptible to mortality and serious morbidity effects from short-term acutely elevated exposures. Others are susceptible to less serious health effects such as transient increases in respiratory symptoms, decreased lung function, or other physiologic changes. Chronic exposure studies suggest relatively broad susceptibility to cumulative effects of long-term repeated exposure to fine particulate pollution, resulting in substantive estimates of population average loss of life expectancy in highly polluted environments. Additional knowledge is needed about the specific pollutants or mix of pollutants responsible for the adverse health effects and the biologic mechanisms involved.

Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk?

About half of the world's population now lives in urban areas because of the opportunity for a better quality of life. Many of these urban centers are expanding rapidly, leading to the growth of megacities, which are defined as metropolitan areas with populations exceeding 10 million inhabitants. These concentrations of people and activity are exerting increasing stress on the natural environment, with impacts at urban, regional and global levels. In recent decades, air pollution has become one of the most important problems of megacities. Initially, the main air pollutants of concern were sulfur compounds, which were generated mostly by burning coal. Today, photochemical smog—induced primarily from traffic, but also from industrial activities, power generation, and solvents—has become the main source of concern for air quality, while sulfur is still a major problem in many cities of the developing world. Air pollution has serious impacts on public health, causes urban and regional haze, and has ...

/pdf/megacities-and-atmospheric-pollution-5by3o6aw1x.pdf

Megacities and atmospheric pollution

Ambient air pollution, climate change, and population health in China

The relationship between air pollution and daily mortality in 1989 was examined in two residential areas in Beijing, China. Very high concentrations of sulfur dioxide (SO2) (mean = 102 micrograms/m3, maximum = 630 micrograms/m3) and total suspended particulates (TSPs) (mean = 375 micrograms/m3, maximum = 1,003 micrograms/m3) were observed in these areas. Daily counts of deaths were regressed, using Poisson regression on the logarithm of (SO2) and/or TSPs controlling for effects of temperature, humidity, and day of week. A highly significant association was found between In(SO2) and daily mortality. The risk of total mortality was estimated to increase by 11% (95% confidence interval [95% CI] = 5%-16%) with each doubling in SO2 concentration. Separately, the association of In(TSP) with total daily mortality was positive but not significant (4% increase in mortality with each doubling in TSP; 95% CI = -2%-11%). When mortality was analyzed separately by cause, the association with a doubling in SO2 was significant for chronic obstructive pulmonary disease (29%), pulmonary heart disease (19%), and cardiovascular disease (11%), and marginally significant for the other nonmalignant causes (8%), but not statistically significant for cancer (2%). A similar association was noted for a doubling in TSP (4%, 38%, and 8% for total, chronic obstructive pulmonary disease, and pulmonary heart disease mortality, respectively), but the result was only statistically significant for chronic obstructive pulmonary disease. In the season-specific analysis, both SO2 and TSP were found to be significant predictors of total daily mortality in summer. In winter, SO2 was again significantly associated with increased mortality, but no positive association was found between TSP and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Douglas W. Dockery

Papers

Air Pollution and Daily Mortality in Residential Areas of Beijing,China (開発途上国における人口増加と地球環境問題の相互連関に関する基礎的研究)