The Chattanooga school children study: effects of community exposure to nitrogen dioxide. 1. Methods, description of pollutant exposure, and results of ventilatory function testing.
01 Aug 1970-Journal of the Air Pollution Control Association (Taylor & Francis Group)-Vol. 20, Iss: 8, pp 539-545
TL;DR: The data suggested that ventilatory performance was adversely affected only when an NO2 threshold was exceeded but that above this threshold no further impairment of performance could be detected.
Abstract: Elementary schools in four areas of Greater Chattanooga were selected for a study of the effects of community exposure to nitrogen dioxide. One area, in close proximity to a large TNT plant, had high NO2 exposure, another had relatively high suspended particulate exposure, and two areas served as “clean” controls. The similarity of the economic levels of the High-NO2 and Control areas and the moderately lower economic level of the High-Particulate area were documented. Pollutant concentrations for NO2 gas, suspended nitrates and sulfates, total suspended particulates, and soiling index were measured at stations located within the study areas. Ventilatory performance of second-grade school children in the High-NO2 exposure area was significantly lower than the performance of children in the Control areas. The data suggested that ventilatory performance was adversely affected only when an NO2 threshold was exceeded but that above this threshold no further impairment of performance could be detected.
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TL;DR: The incidence and duration of respiratory symptom episodes are likely associated with particulate concentrations and duration may be associated with NO2, according to a diary study conducted in two cities in Switzerland.
Abstract: A diary study on a random sample of 625 Swiss children aged 0 to 5 yr was conducted in two cities in Switzerland to investigate the association between air pollution and respiratory symptoms. Total suspended particulates (TSP), SO2 and NO2 were measured by city monitor. In addition, passive samplers inside and outside the home measured NO2 concentration during the 6 wk each child was on the diary. Diaries were filled out by parents, and 20% were validated with the attending pediatrician's case notes. Incidence and duration of symptom episodes were examined separately. The study included any episode, episodes of coughing without runny nose, upper respiratory episodes, and episodes of breathing difficulty. In regressions using 6-wk average pollution that controlled for medical history, NO2 measured outdoors but not indoors was associated with the duration of any symptom. Total suspended particulates were a more significant predictor of duration of any symptom than NO2. The 6-wk average TSP was significantly associated with incidence of coughing episodes and marginally significant as a predictor of upper respiratory episodes. Previous day's TSP was a significant predictor of incidence of upper respiratory symptoms. Annual average of NO2 was associated with the duration of any episode and of upper respiratory episodes. We conclude that the incidence and duration of respiratory symptom episodes are likely associated with particulate concentrations and duration may be associated with NO2.
285 citations
TL;DR: In this article, the instability of ordinary least squares estimates of linear regression coefficients is demonstrated for mortality rates regressed around various socioeconomic, weather and pollution variables, and two methods of variable elimination are compared.
Abstract: The instability of ordinary least squares estimates of linear regression coefficients is demonstrated for mortality rates regressed around various socioeconomic, weather and pollution variables. A ridge regression technique presented by Hoer1 and Kennard (Technometrics 12 (1970) 69–82) is employed to arrive at “stable” regression coefficients which, in some instances, differ considerably from the ordinary least squares estimates. In addition, two methods of variable elimination are compared—one based on total squared error and the other on a ridge trace analysis.
204 citations
TL;DR: A review of experimental studies of humans inhaling NO2 finds that a health-protective, short-term NO2 guideline level for susceptible (and healthy) populations would reflect a policy choice between 0.2 and 0.6 ppm, and indicates that there is no consistent evidence that NO2 concentrations below 2 ppm increase to viral infection.
Abstract: Nitrogen dioxide (NO2) is a ubiquitous atmospheric pollutant due to the widespread prevalence of both natural and anthropogenic sources, and it can be a respiratory irritant when inhaled at elevated concentrations. Evidence for health effects of ambient NO2 derives from three types of studies: observational epidemiology, human clinical exposures, and animal toxicology. Our review focuses on the human clinical studies of adverse health effects of short-term NO2 exposures, given the substantial uncertainties and limitations in interpretation of the other lines of evidence. We examined more than 50 experimental studies of humans inhaling NO2, finding notably that the reporting of statistically significant changes in lung function and bronchial sensitivity did not show a consistent trend with increasing NO2 concentrations. Functional changes were generally mild and transient, the reported effects were not uniformly adverse, and they were not usually accompanied by NO2-dependent increases in symptoms. The available human clinical results do not establish a mechanistic pathway leading to adverse health impacts for short-term NO2 exposures at levels typical of maximum 1-h concentrations in the present-day ambient environment (i.e., below 0.2 ppm). Our review of these data indicates that a health-protective, short-term NO2 guideline level for susceptible (and healthy) populations would reflect a policy choice between 0.2 and 0.6 ppm. EXTENDED ABSTRACT: Nitrogen dioxide (NO2) is a ubiquitous atmospheric pollutant due to the widespread prevalence of both natural and anthropogenic sources, and it can be a respiratory irritant when inhaled at elevated concentrations. Natural NO2 sources include volcanic action, forest fires, lightning, and the stratosphere; man-made NO2 emissions derive from fossil fuel combustion and incineration. The current National Ambient Air Quality Standard (NAAQS) for NO2, initially established in 1971, is 0.053 ppm (annual average). Ambient concentrations monitored in urban areas in the United States are approximately 0.015 ppm, as an annual mean, i.e., below the current NAAQS. Short-term (1-h peak) NO2 concentrations outdoors are not likely to exceed 0.2 ppm, and even 1-h periods exceeding 0.1 ppm are infrequent. Inside homes, 1-h NO2 peaks, typically arising from gas cooking, can range between 0.4 and 1.5 ppm. The health effects evidence of relevance to ambient NO2 derives from three lines of investigation: epidemiology studies, human clinical studies, and animal toxicology studies. The NO2 epidemiology remains inconsistent and uncertain due to the potential for exposure misclassification, residual confounding, and co-pollutant effects, whereas animal toxicology findings using high levels of NO2 exposure require extrapolation to humans exposed at low ambient NO2 levels. Given the limitations and uncertainties in the other lines of health effects evidence, our review thus focused on clinical studies where human volunteers (including asthmatics, children, and elderly) inhaled NO2 at levels from 0.1 to 3.5 ppm during short-term ((1/2)-6-h) exposures, often combined with exercise, and occasionally combined with co-pollutants. We examined the reported biological effects and classified them into (a) lung immune responses and inflammation, (b) lung function changes and airway hyperresponsiveness (AHR), and (c) health effects outside the lungs (extrapulmonary). We examined more than 50 experimental studies of humans inhaling NO2, finding that such clinical data on short-term exposure allowed discrimination of NO2 no-effect levels versus lowest-adverse-effects levels. Our conclusions are summarized by these six points: For lung immune responses and inflammation: (1) healthy subjects exposed to NO2 below 1 ppm do not show pulmonary inflammation; (2) at 2 ppm for 4 h, neutrophils and cytokines in lung-lavage fluid can increase, but these changes do not necessarily correlate with significant or sustained changes in lung function; (3) there is no consistent evidence that NO2 concentrations below 2 ppm increase susceptibility to viral infection; (4) for asthmatics and individuals having chronic obstructive pulmonary disease (COPD), NO2-induced lung inflammation is not expected below 0.6 ppm, although one research group reported enhancement of proinflammatory processes at 0.26 ppm. With regard to NO2-induced AHR: (5) studies of responses to specific or nonspecific airway challenges (e.g., ragweed, methacholine) suggest that asthmatic individuals were not affected by NO2 up to about 0.6 ppm, although some sensitive subsets may respond to levels as low as 0.2 ppm. And finally, for extra-pulmonary effects: (6) such effects (e.g., changes in blood chemistry) generally required NO2 concentrations above 1-2 ppm. Overall, our review of data from experiments with humans indicates that a health-protective, short-term-average NO2 guideline level for susceptible populations (and healthy populations) would reflect a policy choice between 0.2 and 0.6 ppm. The available human clinical results do not establish a mechanistic pathway leading to adverse health impacts for short-term NO2 exposures at levels typical of maximum 1-h concentrations in the present-day ambient environment (i.e., below 0.2 ppm).
200 citations
TL;DR: Key elements of further studies are the assessment of total exposure to the different pollutants (occurring from indoor and outdoor source) and the interactive effects of pollutants, which will be extremely useful additions to standard physiological, immunological, and clinical instruments, and the understanding of biological plausibility.
Abstract: Environmental epidemiological studies of the health effects of air pollution have been major contributors to the understanding of such effects. The chronic effects of atmospheric pollutants have been studied, but, except for the known respiratory effects of particulate matter (PM), they have not been studied conclusively. There are ongoing studies of the chronic effects of certain pollutant classes, such as ozone, acid rain, airborne toxics, and the chemical form of PM (including diesel exhaust). Acute effects on humans due to outdoor and indoor exposures to several gases/fumes and PM have been demonstrated in epidemiological studies. However, the effects of these environmental factors on susceptible individuals are not known conclusively. These acute effects are especially important because they increase the human burden of minor illnesses, increase disability, and are thought to decrease productivity. They may be related to the increased likelihood of chronic disease as well. Further research is needed in this latter area, to determine the contributions of the time-related activities of individuals in different microenvironments (outdoors, in homes, in transit). Key elements of further studies are the assessment of total exposure to the different pollutants (occurring from indoor and outdoor source) and the interactive effects of pollutants. Major research areas include determination of the contributions of indoor sources and of vehicle emissions to total exposure, how to measure such exposures, and how to measure human susceptibility and responses (including those at the cellular and molecular level). Biomarkers of exposures, doses and responses, including immunochemicals, biochemicals and deoxyribonucleic acid (DNA) adducts, are beginning to promote some basic knowledge of exposure-response, especially the mechanisms. These will be extremely useful additions to standard physiological, immunological, and clinical instruments, and the understanding of biological plausibility. The outcomes of all this work will be the management of risks and the prevention of respiratory diseases related to air pollution.
139 citations
TL;DR: Animal and human population studies suggest that the greatest risk from low-dose long-term exposure is reduced host resistance to viral and bacterial respiratory tract infections, and the present national ambient air quality standard does not provide a large safety margin for this latter effect.
122 citations