We investigated the short-term effects of air pollution on hospital admissions for chronic obstructive pulmonary disease (COPD) in Europe. As part of a European project (Air Pollution and Health, a European Approach (APHEA)), we analysed data from the cities of Amsterdam, Barcelona, London, Milan, Paris and Rotterdam, using a standardized approach to data eligibility and statistical analysis. Relative risks for daily COPD admissions were obtained using Poisson regression, controlling for: seasonal and other cycles; influenza epidemics; day of the week; temperature; humidity and autocorrelation. Summary effects for each pollutant were estimated as the mean of each city's regression coefficients weighted by the inverse of the variance, allowing for additional between-cities variance, as necessary. For all ages, the relative risks (95% confidence limits (95% CL)) for a 50 microg x m(-3) increase in daily mean level of pollutant (lagged 1-3 days) were (95% CL): sulphur dioxide 1.02 (0.98, 1.06); black smoke 1.04 (1.01, 1.06); total suspended particulates 1.02 (1.00, 1.05), nitrogen dioxide 1.02 (1.00, 1.05) and ozone (8 h) 1.04 (1.02, 1.07). The results confirm that air pollution is associated with daily admissions for chronic obstructive pulmonary disease in European cities with widely varying climates. The results for particles and ozone are broadly consistent with those from North America, though the coefficients for particles are substantially smaller. Overall, the evidence points to a causal relationship but the mechanisms of action, exposure response relationships and pollutant interactions remain unclear.

https://erj.ersjournals.com/content/erj/10/5/1064.full.pdf

Air pollution and daily admissions for chronic obstructive pulmonary disease in 6 European cities: Results from the APHEA project

Ozone and the lung: a sensitive issue.

Integrated Science Assessment for Oxides of Nitrogen — Health Criteria

Ozone is one of the most toxic and ubiquitous air pollutants. This review focuses on the toxic effects of ozone in animals and on the similarities and disimilarities between the toxic effects in animals and humans. The molecular basis for the toxicity of ozone is discussed, based on the vigorous oxidizing properties of ozone. Despite the existence of anatomical differences between human, subhuman primate, and dog lungs versus common experimental rodent lungs, the anatomical lesion of ozone inhalation occurs at the functionally equivalent site of the junction between the conducting airway and the respiratory region. Ciliated cells of the upper airways and the type 1 cell of the centriacinar region are most affected. Type 2 cell proliferation is a hallmark of ozone toxicity. A wide variety of biochemical and physiological changes have been noted in several animal species and in humans. Considerable evidence for a free-radical-mediated or lipid peroxide-mediated toxicity is evident, especially in the induction of the glutathione peroxidase system and the protective effects of vitamins C and E. Ozone appears to be a weak mutagen and to produce chromosomal abnormalities. Defects in defense against airborne infection are present in animals, which are more susceptible to airborne infection after ozone exposure. Epidemiological studies, however, fail to detect increased respiratory infections in humans due to ozone. Despite the variety of toxic effects, few qualitative differences between species are apparent; rather, quantitative differences do occur. Ozone may thus be an ideal compound for quantitative extrapolation of toxicity from animals to humans.

Ozone: an overview of its toxicity in man and animals.

Nitrogen dioxide (NO2) is a product of combustion that has become recognized as a significant component of indoor air in some homes. Despite extensive study, it remains unresolved whether exposures to low levels of NO2 affect airway function or reactivity. These studies were designed to assess effects of various levels and patterns of NO2 exposure on pulmonary function and airway reactivity in normal humans. Normal volunteers screened for the absence of airway hyper-reactivity were exposed for 3 h in an environmental chamber to purified air or NO2, separated by at least 2 wk, according to three protocols: (1) continuous 0.60 ppm NO2, (2) baseline 0.05 ppm NO2 with intermittent peaks of 2.0 ppm, and (3) continuous 1.5 ppm NO2. Subjects exercised for 10 min of each 30 min at a level sufficient to result in a minute ventilation near 40 L/min. Pulmonary function was measured before, during, and after exposure. Airway reactivity to increasing doses of carbachol was assessed 30 min after exposure. NO2 did not d...

Effects of Nitrogen Dioxide Exposure on Pulmonary function and Airway Reactivity in Normal Humans

Effects of nitrogen dioxide on pulmonary function in human subjects: An environmental chamber study

Twenty healthy adults, 10 smokers and 10 nonsmokers, were exposed to 0.5 ppm of ozone for 6 hours in an environmental chamber. They engaged in two 15-min, medium-exercise stints on a bi· cycle ergometer during this period. The symptoms most commonly noted with exposure to ozone, dry cough and chest discomfort, were experienced by more nonsmokers than smokers. Subjects who experienced symptoms, in general, were those who developed objective evidence of decreased pul­ monary function. Significant changes from control values for the group as a whole with exposure to ozone were observed for the following pulmonary function tests: specific airway conductance, pul­ monary resistance, forced vital capacity, and 3-sec forced expiratory volume. No significant change was observed with respect to diffusing capacity for CO, static compliance, or the various tests de­ rived from the N2 elimination rate. In addition, nonsmokers exhibited a significant decrease in dynamic compliance after exposure to ozone. When the smokers were considered as a separate group, no significant decrease in pulmonary function was observed, although some individual smokers showed adverse functional changes.

Effects of ozone on pulmonary function in normal subjects. An environmental-chamber study.

Twenty healthy adults, 10 smokers and 10 nonsmokers, were exposed to 0.5 ppm of ozone for 6 hours in an environmental chamber. They engaged in two 15-min, medium-exercise stints on a bicycle ergometer during this period. The symptoms most commonly noted with exposure to ozone, dry cough and chest discomfort, were experienced by more nonsmokers than smokers. Subjects who experienced symptoms, in general, were those who developed objective evidence of decreased pulmonary function. Significant changes from control values for the group as a whole with exposure to ozone were observed for the following pulmonary function tests: specific airway conductance, pulmonary resistance, forced vital capacity, and 3-sec forced expiratory volume. No significant change was observed with respect to diffusing capacity for CO, static compliance, or the various tests derived from the N2 elimination rate. In addition, nonsmokers exhibited a significant decrease in dynamic compliance after exposure to ozone. When the smokers wer...

T. J. Kulle

Papers

Effects of nitrogen dioxide on pulmonary function in human subjects: An environmental chamber study

Effects of ozone on pulmonary function in normal subjects. An environmental-chamber study.

Effects of Ozone On Pulmonary Function in Normal Subjects1, 2