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The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55-70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p

The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies.This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air pollution.

Nitrogen dioxide exposure: effects on airway and blood cells. Am J Physiol Lung Cell Mol Physiol 282: L155-L165, 2002.--This study examined the effects of nitrogen dioxide (N[O.sub.2]) exposure on airway inflammation, blood cells, and antiviral respiratory defense. Twenty-one healthy volunteers were exposed on separate occasions to air and 0.6 and 1.5 ppm N[O.sub.2] for 3 h with intermittent moderate exercise. Phlebotomy and bronchoscopy were performed 3.5 h after each exposure, and recovered cells were challenged with respiratory viruses in vitro. Blood studies revealed a 4.1% N[O.sub.2] dose-related decrease in hematocrit (P = 0.003). Circulating total lymphocytes (P = 0.024) and T lymphocytes (P = 0.049) decreased with N[O.sub.2] exposure. Exposure to N[O.sub.2] increased the blood lymphocyte CD[4.sup.+]-to-CD[8.sup.+] ratio from 1.74 [+ or -] 0.11 to 1.85 [+ or -] 0.12 in males but decreased it from 1.88 [+ or -] 0.19 to 1.78 [+ or -] 0.19 in females (P < 0.001 for gender difference). Polymorphonuclear leukocytes in bronchial lavage increased with N[O.sub.2] exposure (P = 0.003). Bronchial epithelial cells obtained after exposure to 1.5 ppm N[O.sub.2] released 40% more lactate dehydrogenase after challenge with respiratory syncytial virus than with air exposure (P = 0.024). In healthy subjects, exposures to N[O.sub.2] at levels found indoors cause mild airway inflammation, effects on blood cells, and increased susceptibility of airway epithelial cells to injury from respiratory viruses. air pollution; influenza virus; respiratory syncytial virus; blood; epithelial cells

The article offers information on the relationship between exposure to ultrafine particles (UFPs) and mortality in people with fibrotic interstitial lung disease (fILD). Topics include the study's examination of two cohorts of fILD patients, the association of UFP exposure with increased mortality or transplant, and the reduction of forced vital capacity (FVC) associated with UFP exposure.

A study was conducted to test the hypothesis that lung cells secrete extracellular glutathione peroxidase (GPx), an antioxidant enzyme, into epithelial lining fluid (ELF). Immunoprecipitation techniques showed that ELF that 57% of ELF GPx activity was due to extracellular GPx and 40% due to cellular GPx. Similar results were observed in primary bronchial epithelial cells, primary alveolar macrophages and two human bronchial epithelial cell lines.

An analysis of the glycoproteins from samples of airway secretions from healthy individuals before and after exposure to sulphuric acid reveals that there is little change in the glycoproteins and related proteins. However, other factors such as mucus volume, mucus hydration and ciliary beating may be affected by exposure to acid or differences in substructures of glycoprotein are possible which require better detection methods. Glycoproteins in the mucin play an important role in the protection of airway mucus.

Frampton, Mark W., Andrew J. Ghio, James M. Samet, Johnny L. Carson, Jacqueline D. Carter, and Robert B. Devlin. Effects of aqueous extracts of [PM.sub.10] filters from the Utah Valley on human airway epithelial cells. Am. J. Physiol. 277 (Lung Cell. Mol. Physiol. 21): L960-L967, 1999.--We hypothesized that the reduction in hospital respiratory admissions in the Utah Valley during closure of a local steel mill in 1986-1987 was attributable in part to decreased toxicity of ambient air particles. Sampling filters for particulate matter [is less than] 10 [micro]m ([PM.sub.10]) were obtained from a Utah Valley monitoring station for the year before (year 1), during (year 2), and after (year 3) the steel mill closure. Aqueous extracts of the filters were analyzed for metal content and oxidant production and added to cultures of human respiratory epithelial (BEAS-2B) cells for 2 or 24 h. Year 2 dust contained the lowest concentrations of soluble iron, copper, and zinc and showed the least oxidant generation. Only dust from year 3 caused cytotoxicity (by microscopy and lactate dehydrogenase release) at 500 [micro]g/ml. Year 1 and year 3, but not year 2, dust induced expression of interleukin-6 and -8 in a dose-response fashion. The effects of ambient air particles on human respiratory epithelial cells vary significantly with time and metal concentrations. air pollution; metals; interleukin-6; interleukin-8; toxicity