SERIES “THE GLOBAL BURDEN OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE” 

Edited by K.F. Rabe and J.B. Soriano 

Number 2 in this Series 

### Summary

⇓Information about the comparative magnitude of the burden from various diseases and injuries is a critical input into building the evidence base for health policies and programmes. Such information should be based on a critical evaluation of all available epidemiological data using standard and comparable procedures across diseases and injuries, including information on the age at death and the incidence, duration and severity of cases who do not die prematurely from the disease. A summary measure, disability-adjusted life yrs (DALYs), has been developed to simultaneously measure the amount of disease burden due to premature mortality and the amount due to the nonfatal consequences of disease. 

Approximately 2.7 million deaths from chronic obstructive pulmonary disease (COPD) occurred in 2000, half of them in the Western Pacific Region, with the majority of these occurring in China. About 400,000 deaths occur each year from COPD in industrialised countries. The increase in global COPD deaths between 1990 and 2000 (0.5 million) is likely to be partly real, and partly due to better methods and more extensive data availability in 2000. The regional (adult) prevalence in 2000 varied from 0.5% in parts of Africa to 3–4% in North America.

### Introduction

Health systems must increasingly address a broad spectrum of health issues, ranging from epidemic outbreaks to advanced therapeutic care. They must, or should, also support disease prevention and health-promotion activities. Recognising that resources for health were unlikely to grow as quickly as demand, in 1993, the World Bank proposed a series of intervention packages for countries at different stages of development which, if implemented, would probably lead to the greatest gains in population health at affordable cost. The evidence for these recommendations was based …

https://erj.ersjournals.com/content/erj/27/2/397.full.pdf

Chronic obstructive pulmonary disease: current burden and future projections

This article summarizes epidemiological evidence of health effects of particulate air pollution. Acute exposure to elevated levels of particulate air pollution has been associated with increased cardiopulmonary mortality, increased hospitalization for respiratory disease, exacerbation of asthma, increased incidence and duration of respiratory symptoms, declines in lung function, and restricted activity. Small deficits in lung function, higher risk of chronic respiratory disease and symptoms, and increased mortality have also been associated with chronic exposure to respirable particulate air pollution. Health effects have been observed at levels common to many U.S. cites and at levels below current US. National Ambient Air Quality Standards. Although the biological mechanisms involved are poorly understood, recent epidemiological evidence supports the hypothesis that respirable particulate air pollution is an important risk factor for respiratory disease and cardiopulmonary mortality.

Review of epidemiological evidence of health effects of particulate air pollution

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?

Over the last decade or so, a large number of studies have investigated the possible adverse effects of ambient air pollution on birth outcomes. We reviewed these studies, which were identified by a systematic search of the main scientific databases. Virtually all reviewed studies were population based, with information on exposure to air pollution derived from routine monitoring sources. Overall, there is evidence implicating air pollution in adverse effects on different birth outcomes, but the strength of the evidence differs between outcomes. The evidence is sufficient to infer a causal relationship between particulate air pollution and respiratory deaths in the postneonatal period. For air pollution and birth weight the evidence suggests causality, but further studies are needed to confirm an effect and its size and to clarify the most vulnerable period of pregnancy and the role of different pollutants. For preterm births and intrauterine growth retardation (IUGR) the evidence as yet is insufficient to infer causality, but the available evidence justifies further studies. Molecular epidemiologic studies suggest possible biologic mechanisms for the effect on birth weight, premature birth, and IUGR and support the view that the relation between pollution and these birth outcomes is genuine. For birth defects, the evidence base so far is insufficient to draw conclusions. In terms of exposure to specific pollutants, particulates seem the most important for infant deaths, and the effect on IUGR seems linked to polycyclic aromatic hydrocarbons, but the existing evidence does not allow precise identification of the different pollutants or the timing of exposure that can result in adverse pregnancy outcomes.

Ambient air pollution and pregnancy outcomes: a review of the literature.

Air pollution episodes have been associated with increased cardiovascular hospital admissions and mortality in time-series studies. We tested the hypothesis that patients with implanted cardioverter defibrillators experience potentially life-threatening arrhythmias after such air pollution episodes. We compared defibrillator discharge interventions among 100 patients with such devices in eastern Massachusetts, according to variations in concentrations of particulate matter, black carbon, and gaseous air pollutants that were measured daily for the years 1995 through 1997. A 26-ppb increase in nitrogen dioxide was associated with increased defibrillator interventions 2 days later (odds ratio = 1.8; 95% confidence interval = 1.1-2.9). Patients with ten or more interventions experienced increased arrhythmias in association with nitrogen dioxide, carbon monoxide, black carbon, and fine particle mass. These results suggest that elevated levels air pollutants are associated with potentially life-threatening arrhythmia leading to therapeutic interventions by an implanted cardioverter defibrillator.

Air pollution and incidence of cardiac arrhythmia.

The relationship between daily mortality of elderly (65+ y) persons and air pollution in the metropolitan area of Sao Paulo, Brazil, for the period May 1990 to April 1991 was evaluated by time series regression, controlling for season, weather, and other factors. Mortality was associated with respirable particles (PM10), nitrogen oxides (NOx), sulfur dioxide (SO2), and carbon monoxide (CO). The association with PM10 was most statistically significant, robust, and independent of other air pollutants. An increase in PM10 equal to 100 micrograms/m3 was associated with an increase in overall mortality equal to approximately 13%. This association was consistent across various model specifications and estimation techniques. The dose-response relationship between mortality and respirable particulate pollution was almost linear, with no evidence of a "safe" threshold level. The results were similar to those observed in London and several U.S. cities. The results were also supportive of recent animal studies that have observed adverse health outcomes in experimental animals exposed to air pollution in Sao Paulo.

I.A. Barone

Papers

Air Pollution and Mortality in Elderly People: A Time-Series Study in Sao Paulo, Brazil

Association between Air Pollution and Mortality Due to Respiratory Diseases in Children in São Paulo, Brazil: A Preliminary Report

Air pollution and mortality in elderly people: a time series study in Sao Paulo, Brazil