Air Pollution and Health

Robert L. Maynard, Stephen T. Holgate, Hillel S. Koren, Jonathan M. Samet, Robert L. Maynard, Stephen T. Holgate, Hillel S. Koren, Jonathan M. Samet

• Verlag: Academic Press
• Jahr: 1999
• ISBN:
  9780080526928
• Thema: Tecnología e ingeniería
• Thema: Seguridad y salud industriales

Concern about the impact of air pollution has led governments and local authorities across the world to regulate, among other things, the burning of fossil fuels, industrial effluence, cigarette smoke, and aerosols. This legislation has often followed dramatic findings about the impact of pollution on human health. At the same time there have been significant developments in our ability to detect and quantify pollutants and a proliferation of urban and rural air pollution networks to monitor levels of atmospheric contamination.
Air Pollution and Health is the first fully comprehensive and current account of air pollution science and it impact on human health. It ranges in scope from meteorology, atmospheric chemistry, and particle physics to the causes and scope of allergic reactions and respiratory, cardiovascular, and related disorders. The book has substantial international coverage and includes sections on cost implications, risk assessment, regulation, standards, and information networks. The multidisciplinary approach and the wide range of issues covered makes this an essential book for all concerned with monitoring and regulating air pollution as well as those concerned with its impact on human health.

• Only comprehensive text covering all the important air pollutants and relating these to human health and regulatory bodies
• Brings together a wide range of issues concerning air pollution in an easily accessible format
• Contributions from government agencies in the US and UK provide information on public policy and resource networks in the areas of health promotion and environmental protection

1

Introduction

DAVID V. BATES,     University of British Columbia, Vancouver, BC, Canada

It is not surprising that the study of the effects of air pollution on human populations began with major episodes of increased mortality, in which the cause and effect relationship between the dramatic episode and its consequences could not be doubted. The episodes in the Meuse Valley in 1930, in the small town of Donora in Pennsylvania in 1948, and the London episode of December 1952 provided unequivocal evidence of that kind. The city Ordinance against air pollution passed in Pittsburgh in 1946 was carried through by concerned citizens, but no scientific evidence of the impact of current air pollution levels on the population had been secured (Bates, 1994).

The development of epidemiological studies can be properly dated from the London episode; it was natural to ask the question of what effects, other than acute mortality, the air pollution might be causing. A linkage between air pollution levels in different parts of the London Metropolitan region, and the occurrence of bronchitis quickly emerged, but it was not until 1965 that Holland and Reid established the model for many future studies. This was a cross-sectional comparison of lung function of postal workers in London compared with that of others in different country towns in which the pollution level was known to be much lower. The socioeconomic level of the workers was the same in both locations; non-smokers, ex-smokers, and smokers at three different levels of intensity were characterized; and there were no climatic differences between the different regions. The results showed a clear decrement of function in all of these categories between the London and provincial workers.

We now know that the forced expiratory volume in 1 s (FEV₁), which with the peak expiratory flow rate (PEFR), was the test used in that study to characterize function, is closely related to survival; hence we can now infer that residence in more polluted regions of Britain involved a lower survival expectancy. Recent studies of non-smoking women in Beijing, and early cross-sectional studies in France, both showed decrements of FEV₁ in those living in more polluted regions, but we still do not have a precise interpretation of what this finding means in structural terms. Is there a higher degree of airway responsiveness? Is the induced bronchitis responsible for small airway disease? Is the degree of emphysema more severe? It is also quite possible that the lower FEV₁ in adults in more polluted regions is due to the fact that growing up in such locations meant that lung growth was altered, so that the initial FEV₁ (say at age 18) was never as high as it was in those growing up in cleaner locations.

It was the concomitant increase in cigarette smoking in most countries that confused the understanding of air pollution effects. Indeed, the relevant literature of the period might be interpreted as showing that all chronic lung disease was attributable to cigarette smoking, and that air pollution only exerted an effect by increasing the mortality in acute episodes. Although this is biologically inherently unlikely to be true, it was the study of Holland and Reid that first indicated that air pollution might be causing long-term chronic effects of some significance. We can now summarize the effects of air pollution due to uncontrolled coal burning as being responsible for enhancing the risk of chronic obstructive pulmonary disease in smokers and its severity, increasing the prevalence of chronic bronchitis and sputum production, and possibly, as discussed below, increasing the risk of lung cancer. Surprisingly, the prevalence of asthma does not seem to be related to this type of air pollution. Acute episodes in which particulates and acid aerosols are at high levels increase mortality from respiratory disease in all age groups.

It was in 1952, the year of the major London episode, that Hagen-Smidt in Los Angeles showed that tropospheric ozone was formed when oxides of nitrogen and hydrocarbons were both in the air and subjected to sunlight. He was investigating the adverse effects of photochemical air pollution on citrus fruit. The study of the acute effects of ozone on lung function did not start until 10 years later, but by 1970 it had become clear that ozone was an intensely irritant gas, and that normal subjects showed a wide variation in sensitivity to it. Ten years after that, a series of studies of children at summer camps documented the fall in lung function that commonly occurred in summer outdoor conditions. Two other developments were crucial in establishing the importance of ozone as an air pollutant. One was the demonstration that an induced fall in forced vital capacity (FVC) after ozone breathing was accompanied by evidence from bronchial lavage that inflammation had occurred in the lung; and the other was the study of large banks of hospital admission data that showed a significant association between summer ozone levels and hospital admissions for acute respiratory disease. In the northeast of North America, where these studies were conducted, ozone was closely correlated with aerosol sulfates in the summer.

The difficulty with ozone is that any biological effect or mechanism is theoretically possible. Increased airway reactivity, small airway inflammation, pneumonia, damage from oxygen radicals, and even induced neoplasia can all be postulated. Interference with normal lung growth is also a possibility. The main acute effects that have been demonstrated are acute reductions in lung function, aggravation of asthma (an effect still ignored in much contemporary literature), an increased risk of pneumonia in the elderly, and hospital admissions for acute respiratory disease in all age groups, including those in infants under the age of 1 year. As far as chronic effects are concerned, we have evidence from one study of incoming Berkeley students that lifetime ozone exposure might be associated with a significant reduction in terminal airflow velocity (Kunzli et al., 1997). More work on possible chronic effects of ozone exposure must be done before we can be confident that our knowledge is complete.

Finally, the past 10 years have seen a remarkable ‘avalanche’ of studies incriminating urban particles in the respirable range (less than 10 µm in diameter, or PM₁₀). The first data showed that in time-series analysis, there was an association between daily mortality, excluding accidents and suicides, and the level of PM₁₀ prior to the relevant date. This association has now been shown to be robust to different methods of accounting for weather variations; in many different populations (over 30 at last count); and when other pollutants such as SO₂ or ozone or acid aerosols are virtually absent. There is also striking coherence, in that PM₁₀ levels have been shown to be associated with function test decline in children, hospital admissions for respiratory disease, aggravation of asthma, increased school absences, and lower lung function in children. There is general evidence – not complete because of the relative scarcity of monitoring data – that all of these associations are stronger if PM_2.5 instead of PM₁₀ is considered.

In contrast to the situation with regard to ozone, the mechanism of these effects is not precisely understood. Although the associations have been shown to occur when pollution levels never exceed a PM₁₀ value of 150 µg/m³ for any hour in the monitoring period, these are still very low levels of exposure compared with those to which workers in many occupations are exposed. Indoor PM₁₀ is increased considerably when there is a cigarette smoker in the house, and there is a possibility that it is the particulate component which is responsible for these effects.

The observation that exposure to passive cigarette smoke increases the risk of lung cancer in non-smokers is one of the pieces of information that suggests that outdoor exposure to particles derived from combustion products emitted from vehicles might also increase the risk of lung cancer. So powerful is the effect of cigarette smoking in increasing the risk of lung cancer that the unequivocal demonstration of an enhancement of risk by air pollutants is difficult. The evidence on which such an opinion must be based is drawn together in this book.

The study of the adverse health effects of air pollution has come a long way since 1952. Much more powerful tools are available for data collection and analysis; far more data are available; there is a much greater understanding of the power and limitations of statistical methods; and the economic costs of increasingly strict regulation are such that there is a willingness (albeit reluctant) to invest in research programs designed to answer some of the outstanding important questions. Although it can point to an honorable past, environmental epidemiological studies of air pollution and its effects can be expected to have a distinguished future. One of the reasons why research in this field is such an interesting challenge is that the field has such breadth that many disciplines are involved in its full understanding. This is well exemplified by the multi-disciplinary focus of the different sections in this book. In some scientific fields, the contemporary focus seems to get narrower and narrower; but an understanding of the effects of air pollutants on the human respiratory, and possibly also cardiovascular systems, necessitates a broadening of the approach as the complexity of the questions becomes apparent. It is this aspect of the field that ensures its continuing interest.

REFERENCES

Bates, DV, Environmental Health Risks and Public Policy; Decision-making in Free Societies, Seattle, Washington University Press, 1994:117.

Holland, WW, Reid, DD. The urban factor in chronic bronchitis. Lancet. 1965;1:445–448.

Kunzli, N, Lurmann, F, Segal, M, et al. Association between lifetime ambient ozone exposure and pulmonary function in college freshmen–results of a pilot study. Environ Res. 1997;72:8–23.

2

Air Pollution and Health History

PETER BRIMBLECOMBE, School of Environmental Sciences, University of East Anglia, Norwich, UK

INTRODUCTION

Recent times have seen startling changes in the way we view our environment. This has made it easy to forget that concern over air pollution and health is not restricted to the late twentieth century. A study of the environmental problems of the past is useful because it brings new perspectives to the issue. The unfamiliar historical context can often help to throw the causal features into sharper relief.

This chapter focuses on the historical developments in the UK where there is, unfortunately or not, a long history of environmental contamination. The account will stop in the 1950s with the development of modern research, much of which was initiated in response to the deadly London smog of 1952 and the growing problems in Los Angeles.

EVIDENCE OF INDOOR AIR POLLUTION IN ANTIQUITY

It is likely that indoor air pollution has a history much longer than documentary records. Archaeological evidence suggests that it was widely experienced in the distant past. Mummified lung tissue provides the most useful source of information on prehistoric exposure to particulate materials, but this can be found only where it has been preserved by tanning, freezing or desiccation. Such mummification may be deliberate or accidental, but the geographical extent is broad, covering many drier and colder regions. Palaeopathological samples of lung tissue can be examined after rehydration (Reyman and Dowd, 1980), which allows subsequent treatment to be similar to that for fresh tissue. Thus, microscopic examination enables solid deposits in the lung to be readily identified.

The dry climate of Egypt with its associated high concentrations of wind-blown sand may have been responsible for the occurrence of pneumoconiosis in the mummies examined by Cockburn et al. (1975), although these authors are careful to point out that these individuals are unlikely to have suffered from any resultant disability. Early examples of industrial lung diseases caused by exposure to mineral dusts (pneumoconiosis and silicosis) are found in the lung tissue of a sixteenth century Peruvian miner and among East Anglian flint-knappers (Shaw, 1981). The more general occurrence of anthracotic deposits in ancient lung tissue is assumed to be the result of lifelong exposure to smoke indoors.

Less direct evidence of polluted interiors may be found in skeletal materials. Wells (1977) examined many skulls from early burial grounds in the British Isles. Although diseases of the maxillary antrum or sinus had long been recognized by palaeopathologists, technical problems meant that the incidence and range had remained uncertain. The development of the antroscope allowed sinusitis to be detected in complete skulls by looking for osteitic changes in the floor of the antrum. These are seen as a roughening of the bone, which in severe cases becomes pitted with holes some 1–3 mm in diameter. Maxillary sinusitis is a common disease today and was routinely present in ancient populations. In ancie...