Epidemiology and Air Pollution (1985) / Chapter Skim
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2 ASSESSMENT OF HEALTH EFFECTS
2 ASSESSMENT OF HEALTH EFFECTS
Pages 37-88
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From page 37... ...
Data of the second type, sometimes called subclinical or early marker data, are obtained by measuring physiologic, biochemical, or morphologic features or by analyzing symptoms reported on questionnaires. We do not address the problem of determining exactly what constitutes an adverse health effect in an epidemiologic study, a topic recently analyzed by a Committee of the American Thoracic Society, with reference to the Clean Air Act.1 Although annoyance or esthetic effects (such as odors or impaired visibility)
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From page 38... ...
HEALTH EFFECTS OF CONCERN This chapter focuses on respiratory effects, because clinical and epidemiologic studies and animal experiments have shown that the major effects of air pollutants are on the respiratory system. Health effects are divided into four categories: acute respiratory effects; chronic respiratory effects, excluding cancer; lung cancer; and effects on other organ systems.
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From page 39... ...
The purpose is not to determine whether existing evidence is conclusive, but rather to determine whether it is sufficient to warrant further study. ACUTE RESPIRATORY EFFECTS Asthma and Airway Hyperreactivity Asthma is characterized by intermittent obstruction of airflow that reverts either spontaneously or with treatment.
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From page 40... ...
Many different inhalants have been identified as primary sensitizers in asthma, including large complex proteins, such as ragweed and animal dander, and low-molecular-weight synthetic chemicals, such as toluene diisocyanate.131 Asthma that does not appear to be due to allergy to specific substances can arise from a complex set of genetic and environmental factors. Whatever its origin, asthma is often exacerbated by a variety of nonspecific stimuli, including respiratory infection, exercise, cold air, and emotional stress.
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From page 41... ...
did not seem to be more susceptible than healthy volunteers to the effects of ozone, O3, at low concentrations.99 151 However, SO2 at as low as 0.4 ppm and nitrogen dioxide, NO2, at as low as 0.3 ppm have induced symptoms or increased airway resistance in some asthmatics undergoing heavy exercise.14 100 Persons without respiratory disease generally do not show effects below 1 ppm.145 Good animal models of chronic human asthma do not exist, although acute episodes of bronchoconstriction can be induced in animals by inhalation of ambient air pollutants.59
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From page 42... ...
Early studies clearly demonstrated a link between high concentrations of reducing pollutants -- e.g., SO2 and total suspended particles (TSP) -- and respiratory infection in children.36 Several recent studies have shown that current concentrations of specific pollutants might also be associated with increases in respiratory infections and symptoms in exposed populations.
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From page 43... ...
Thus, the findings could be relevant to epidemiologic studies that show more respiratory infections in areas of greater air pollution, although such infections in humans are most often viral, rather than bacterial. Animal models for studying the effect of air pollutants on susceptibility to viral agents have not yet been developed.
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From page 44... ...
, diminished growth of lung function in children, and accelerated decrease in pulmonary function with age. Chronic Obstructive Pulmonary Disease The general use of the convenient, but imprecise, term chronic obstructive pulmonary disease and the widespread application of a single test of lung function, FEV1, combine to give a false impression of simplicity to the study of this disease.
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From page 45... ...
Chronic bronchitis is usually ascertained in epidemiologic studies when a productive cough (one that produces sputum or phlegm) is present for at least 3 consecutive months per year for at least 2 years, provided that it is not attributable to other lung or heart disease.68 Only in some people does chronic bronchitis lead to clinically important COPD, manifested by recurrent pulmonary infection, chronic airflow limitation, or both.
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From page 46... ...
Survival and morbidity are heavily influenced by the susceptibility of persons with COPD to respiratory infections, such as influenza, and those infections are likely to be more serious in them than in persons with normal lung function. Much has been learned about the components of COPD since the early 1950s, when chronic bronchitis was recognized clinically, but not considered important.
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From page 47... ...
Lower rates of increase in lung function are not synonymous with retardation of lung growth, but the terms are sometimes used interchangeably because lung function is the only readily measurable indicator of the growth process. Recent analyses from the Harvard Air Pollution Health Study indicate that increased exposure to some indoor air pollutants contributes to slower lung development in children between the ages of 6 and 12.154
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From page 48... ...
And some causes of COPD, especially smoking, are more likely than ambient air pollution. The extent to which specific air pollutants interact with other factors, including smoking, to contribute to the various components of COPD or to abnormal rates of change of lung function has not yet been determined.
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From page 49... ...
, to respiratory infections in childhood, and to lower rates of lung growth in childhood. Why some smokers develop rapid deterioration in lung function while others with similar smoking patterns do not is a question of some relevance to air pollution epidemiology.
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From page 50... ...
Perhaps for that reason, published estimates of the fraction of lung cancer attributed to ambient air pollution have varied widely.35 83 Despite these uncertainties about the magnitude of the effect, several lines of evidence support the hypothesis that ambient air pollution contributes to the etiology of lung cancer.35 83 93 153 • Chemical analyses show carcinogens in polluted urban air, including polycyclic aromatic hydrocarbons (such as benzo[a] pyrene)
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From page 51... ...
.54 67 In summary, it is plausible that ambient air pollution causes some part of the lung cancer incidence in the United States, but the size of the fraction is still not known.83 153 NONRESPIRATORY END POINTS Although the Committee has elected to focus on respiratory end points, air pollution is either known or thought to be a causal factor in other major health problems, and epidemiologic studies will be necessary if these problems are pursued. These problems generate methodologic questions that are quite different from those emphasized in the remainder of the report.
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From page 52... ...
indicate that 3.9% of American children (18.6% of urban poor black children) between the ages of 6 months and 5 years examined in 1976-1980 had blood lead concentrations of 30 µg/dL or more,4 the concentrations considered indicative of increased lead absorption.
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From page 53... ...
Benzene and Leukemia Ambient air contains small amounts of many volatile organic chemicals that are known or suspected carcinogens. The data base for estimating the health effects of these exposures is far more extensive for benzene than for other substances.
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From page 54... ...
, and quarterly means as high as 400 µg/m3 have been noted.76 Benzene at ambient concentrations has not been demonstrated to cause leukemia or other cancers, nor is it likely that such an association could ever be directly demonstrated by epidemiologic study, given the generally low exposures, the almost total lack of information on past exposures, and the poor definition of confounding variables that are typical of community populations. Carbon Monoxide and Ischemic Heart Disease Tissue hypoxia is the principal toxic effect of carbon monoxide, CO.62 Inhaled CO binds tightly to circulating hemoglobin, producing carboxyhemoglobin, COHb, and thus reducing the ability of the blood to transport oxygen.113 159 The heart and brain are the organs most severely affected by CO.
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From page 55... ...
Exceptions might be made for heavily exposed populations, such as persons living near point sources of emission. Priority in future evaluations should be given to the development of methods for improved assessment of exposure and improved quantitation of toxic neurologic effects.10 SOURCES OF HEALTH EFFECT DATA Many kinds of data can be used to determine health status in an epidemiologic study.
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From page 56... ...
Detailed explanations of the testing procedures and the validity and reliability of items in the questionnaire are available in the literature.42 The revised version includes several items on asthma and pediatric respiratory diseases. Particular research applications might require the flexibility to alter some questions or to include more specific questions on some topics, such as occupational exposures.
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From page 57... ...
The reliability (reproducibility) of questionnaire responses of persons with chronic lung disease is also a matter of concern.136 Gandevia has recently discussed several innovative approaches to quantifying respiratory symptoms in epidemiologic studies of environmental inhalants.47 PULMONARY FUNCTION TESTING Pulmonary function tests of the mechanical aspects of airflow (spirometry)
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From page 58... ...
The most useful spirometric measurement is FEV1, which is the maximal amount of air that the subject can exhale in 1 second. The peak expiratory flow rate, measures of flow at various lung volumes, and forced vital capacity are also used often.
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From page 59... ...
In one such experiment, approximately 50% of the dust remained in the lungs of three smokers after 11 months, whereas only about 10% remained in the lungs of nine nonsmokers.27 Further research is needed to reduce the cost of this technique and to explore the relationship of clearance to deficits in other pulmonary functions. MORBIDITY AND MORTALITY RECORDS Death certificates are the standard source of mortality data, but sources and types of routinely collected morbidity data are varied.
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From page 60... ...
In respiratory diseases, there is an increasing trend toward use of "COPD," rather than the more specific "emphysema" or "chronic bronchitis," in hospital records and on death certificates; this is due in part to the decreasing rate of autopsy. Thus, apparent trends or geographic differences in COPD mortality might reflect changes in terminology or diagnostic practices.
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From page 61... ...
With the development of the National Death Index, researchers can now ascertain the fact and location of death from a central repository before requesting death certificates from individual states.166 Although mortality data are most useful for studies of lung cancer, they do provide a few important opportunities for studying the relationship of air pollution to other respiratory diseases when large data sets are available. The extent and nature of these opportunities have not been fully explored.
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From page 62... ...
Although biologic markers are commonly used in clinical research and in epidemiologic studies of infectious diseases, they have seldom been used for studying pulmonary effects. One reason is that spirometry has been extraordinarily useful in measuring pulmonary function.
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From page 63... ...
For example, studies examining alveolar inventory and fine structure in populations free of clinical lung disease (e.g., coroner's cases) are feasible.
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From page 64... ...
For example, it has been shown that ciliary beat frequency can be measured with a simple photoelectric device and that results obtained on samples from nasal mucosa are highly correlated with results from bronchoscopy.104 A recent study has shown that repeated nasal-brush sampling (even in children) is feasible and can be used to describe the evolution of changes in ciliary morphology before, during, and after acute viral infection or short-term exposure to O3.21 22 Blood and Urine Markers for COPD A task force of the National Institute of Environmental Health Sciences167 recently reported on investigations to determine early markers of COPD.
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From page 65... ...
Elastase has been assessed by measuring elastin fragments in serum with the use of antibodies to the various peptide fragments.114 Elastinderived peptides were detected in the serum of dogs that had been exposed to an elastase-containing aerosol to induce emphysema-like lesions. More recent clinical research has suggested that serum concentrations of these peptides are distinctly different between people with COPD and normal people and between heavy smokers without disease and nonsmokers.89 Assays for these fragments in urine have not yet been as successful.132 Detection of elastin fragments in serum might therefore provide the basis of an early biologic marker for emphysema that could be tested soon.
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From page 66... ...
The ratio and distribution of distinct types of collagen vary as a consequence of several disease states, and chronic lung disease induced in animals by long-term O3 exposure is associated with an increase in total lung collagen content.94 The specific collagens can be detected with immunochemical procedures.11 Furthermore, Michaeli and Fudenberg found that 70% of patients with emphysema had antibodies to denatured collagen in their serum, compared with 9% of control subjects.117 Antibody titers were also higher for the emphysema subjects. The amino acid hydroxyproline might also serve as an indicator of the status of lung connective tissue.
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From page 67... ...
Mahaffey. Blood Lead Levels for Persons 6 Months-74 Years, United States, 1976-1980.
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From page 68... ...
Sundell. Mining, lung cancer and smoking.
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From page 69... ...
Permutt. Evaluation of tests of lung function for "screening" for early detection of chronic obstructive lung disease, pp.
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From page 70... ...
Macklem. The relations between structural changes in small airways and pulmonary function tests.
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From page 71... ...
The UCLA population studies of chronic obstructive respiratory disease: 5. Agreement and disagreement of tests in identifying abnormal lung function.
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From page 72... ...
Turner-Warwick, Eds. Occupational Lung Diseases.
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From page 73... ...
Air pollution and chronic or repeated respiratory diseases: II. Results and discussion.
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From page 74... ...
Non-smoking wives of heavy smokers have a higher risk of lung cancer: A study from Japan.
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From page 75... ...
Thurlbeck. Site and nature of airway obstruction in chronic obstructive lung disease.
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From page 76... ...
Pulmonary functional impairment and symptoms in women in the Los Angeles Harbor Area.
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From page 77... ...
Short-term respiratory effects of 0.12 ppm ozone exposure in volunteers with chronic obstructive pulmonary disease.
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From page 78... ...
Effects of ozone on the pulmonary function of children, pp.
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From page 79... ...
115. Medical Research Council, Committee on the Aetiology of Chronic Bronchitis.
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From page 80... ...
Effect of urban ozone levels on laboratory-induced respiratory infections. Toxicol.
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From page 81... ...
Goldstein, Eds. Symposium Proceedings on Occupational Immunological Lung Disease, February 25, 1982.
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From page 82... ...
Lung Function Testing.
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From page 83... ...
The acute effects of 0.2 ppm ozone in patients with chronic obstructive pulmonary disease.
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From page 84... ...
The Health Consequences of Smoking: Chronic Obstructive Lung Disease, p.
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From page 85... ...
Gleser. Effects of carbon monoxide on oxygen transport during exercise.
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From page 86... ...
Correlation of mutagenic assessment of Houston air particulate extracts in relation to lung cancer mortality rates. Environ.
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From page 87... ...
87 Chapter 3 Exposure Assessment
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