nitrogen-dioxide and Lung-Diseases--Obstructive

This review presents a synthesis of studies published from 1962 to 2000 on the relations between air pollution and chronic obstructive pulmonary disease (COPD): 12 ecological epidemiological studies, 6 epidemiological panel studies, and 11 controlled human exposure trials. The controlled trials, ecological time-based epidemiological studies and panels are examined successively followed by a discussion of their methodology and results. The controlled trials either do no highlight effects or show effects having no clinical significance since variations are similar to physiological variability. For epidemiological studies reporting individual data, the results point to a particle effect (two studies). This effect of particles is found in ecological studies which also describe an impact of ozone, sometimes of sulfur dioxide and less often of nitrogen dioxide. In conclusion, patients suffering from COPD are generally regarded as a group sensitive to air pollution, as suggested by the results of numerous ecological epidemiological studies. Rare individual studies provide a few arguments supporting this assumption.

Topics: Air Pollutants; Air Pollution; Environmental Monitoring; Epidemiologic Studies; Epidemiological Monitoring; Humans; Lung Diseases, Obstructive; Nitrogen Dioxide; Ozone; Population Surveillance; Research Design; Sulfur Dioxide; Urban Health

Topics: Acids; Air Pollutants; Air Pollution; Animals; Asthma; Ecosystem; Environmental Monitoring; Epidemiological Monitoring; Humans; Hypersensitivity; Lung Diseases, Obstructive; Lung Neoplasms; Nitrogen Dioxide; Ozone; Prognosis; Respiratory Tract Diseases; Respiratory Tract Infections; Rhinitis; Sulfur Dioxide; Vehicle Emissions

Particles, SOx, and acid aerosols are a complex group of distinct pollutants that have common sources and usually covary in concentration. During the past two decades, the chemical characteristics and the geographic distribution of sulfur oxide and particulate pollution have been altered by control strategies, specifically taller stacks for power plants, put in place in response to air pollution regulations adopted in the early 1970s. While the increasing stack heights have lowered local ambient levels, the residence time of SOx and particles in the air have been increased, thereby promoting transformation to various particulate sulfate compounds, including acidic sulfates. These sulfate particles constitute a large fraction of the total mass of smaller particles (< 3 microns in aerodynamic diameter). Epidemiologic studies have consistently provided evidence of adverse health effects of these air pollutants. Particulate and SO2 pollution were strongly implicated in the acute morbidity and mortality associated with the severe pollution episodes in Donora (Pennsylvania), London, and New York in the 1940s, 1950s, and 1960s. There is new evidence that even current ambient levels of PM10 (30 to 150 micrograms/m3) are associated with increases in daily cardiorespiratory mortality and in total mortality, excluding accidental and suicide deaths. These associations have been shown in many different communities, as widely different in particle composition and climate as Philadelphia, St. Louis, Utah Valley, and Santa Clara County, California. It has recently been shown in a long-term prospective study of adults in the United States that chronic levels of higher PM10 pollution are associated with increased mortality after adjusting for several individual risk factors. Daily fluctuations in PM10 levels have also been shown to be related to acute respiratory hospital admissions in children, to school and kindergarten absences, to decrements in peak flow rates in normal children, and to increased medication use in children and adults with asthma. Although some epidemiologic studies suggest that acid aerosols are an important toxic component of PM10, other studies do not support this hypothesis. Dockery and Pope (408) recently reviewed the epidemiologic literature for adverse effects, assuming that reported associations can be attributed to acute particle mass exposures. Combined effects were estimated as percent increase in comparable measures of mortality and morbidit

Topics: Adult; Aerosols; Air Pollutants; Air Pollution; Animals; Asthma; Biomarkers; Bronchial Hyperreactivity; Carbon Monoxide; Cardiovascular Diseases; Cattle; Cells, Cultured; Child; Emergencies; Environmental Health; Female; Hospitalization; Humans; Lead; Lung Diseases, Obstructive; Male; Models, Biological; Nitrogen Dioxide; Occupational Health; Ozone; Pregnancy; Rabbits; Rats; Respiratory Function Tests; Respiratory Tract Diseases; Sulfur Dioxide; United States

Topics: Air Pollutants; Airway Resistance; Asthma; Bronchial Provocation Tests; Dose-Response Relationship, Drug; Humans; Lung; Lung Diseases, Obstructive; Lung Volume Measurements; Nitrogen Dioxide

Topics: Adolescent; Adult; Air Pollutants; Child; Child, Preschool; Europe; Humans; Lung Diseases, Obstructive; Nitrogen Dioxide; Nitrogen Oxides; Pneumonia; Respiratory Hypersensitivity; Risk Factors; United States

Topics: Air Microbiology; Air Pollution; Female; Gambia; Humans; Kenya; Lung Diseases, Obstructive; Male; Netherlands; Nitrogen Dioxide; Smoke; Tobacco Smoke Pollution; Wood

Topics: Air Pollutants; Animals; Epidemiologic Methods; Europe; Humans; Lung Diseases, Obstructive; Nitrogen Dioxide; Ozone; Smoking; Sulfur

Topics: Air Pollutants; Bronchial Diseases; Chemical Phenomena; Chemistry; Environmental Exposure; Lung Diseases; Lung Diseases, Obstructive; Maximum Allowable Concentration; Nitrogen Dioxide; Nitrogen Oxides; Occupational Diseases; Smoking; Time Factors

Topics: Air Pollution; Arsenic Poisoning; Berylliosis; Cadmium Poisoning; Humans; Lung Diseases; Lung Diseases, Obstructive; Lung Neoplasms; Nitrogen Dioxide; Poisoning; Respiratory Tract Diseases; Solvents; Sulfur Dioxide

The aim of this study was to assess the effects of short-term exposure to low levels of nitrogen dioxide (NO2) on airway inflammation. We studied seven normal, eight mild asthmatic and seven chronic obstructive pulmonary disease (COPD) subjects. All subjects were exposed to air or to 0.3 parts per million (ppm) NO2 for 1 h, with moderate intermittent exercise, on different days and in random order. Before and 2 h after exposure, symptom score and results of pulmonary function tests (PFTs) were assessed. All subjects performed nasal lavage and hypertonic saline (HS) inhalation to collect sputum 2 h after both exposures. Asthmatic subjects had a higher percentage of eosinophils than normal and COPD subjects in HS-induced sputum after air (asthmatics: median 13 (range 0.4-37)%; normals: 0 (range 0-2)%; COPD 1.8 (range 0.1-19)%), whilst COPD patients showed a higher percentage of neutrophils than the two others groups. No significant differences in PFT values or percentages of inflammatory cells were observed in nasal lavage and in HS-induced sputum in normal, asthmatic and COPD subjects after NO2 exposure compared to air exposure, except for a mild decrease in forced expiratory volume in one second (FEV1) 2 h after NO2 exposure in COPD patients. Symptom score showed a mild increase after NO2 exposure both in normal subjects and in COPD patients. We conclude that short-term exposure to 0.3 ppm nitrogen dioxide does not induce an early detectable acute inflammation in proximal airways of normal subjects or of patients with asthma or chronic obstructive pulmonary disease.

Topics: Administration, Inhalation; Adult; Asthma; Bronchitis; Bronchoalveolar Lavage; Environmental Exposure; Eosinophils; Female; Forced Expiratory Volume; Humans; Leukocyte Count; Lung; Lung Diseases, Obstructive; Male; Middle Aged; Neutrophils; Nitrogen Dioxide; Nose; Oxidants, Photochemical; Physical Exertion; Saline Solution, Hypertonic; Single-Blind Method; Sputum; Time Factors; Vital Capacity

We combined field and laboratory experimentation to evaluate the effects of nitrogen dioxide in a panel of Los Angeles area residents with chronic respiratory illness, 15 men and 11 women aged 47 to 69. All had heavy smoking history, chronic symptoms, and low FEV1; some also had low FVC. During the fall-winter high-NO2 season, they monitored themselves for 2-wk periods using spirometers in the home, passive NO2 sampling badges, and diaries to record time and activity patterns and clinical status. In the middle of each self-monitoring week they were exposed in a chamber, once to clean air and once to 0.3 ppm NO2. Chamber exposures were double blind, lasted 4 h, and included four 7-min exercise sessions with average ventilation rates near 25 L/min. Symptom reports and hourly forced expiratory function tests showed no statistically significant differences between clean air and NO2 chamber exposures, although peak flow showed a approximately 3% loss with NO2 relative to clean air during the first 2 h of exposure only (p = 0.056). No significant overall differences were found between field self-measurements and measurements of lung function in the chamber or between field measurements in clean air and NO2 exposure weeks. Field data showed that group average lung function and symptom levels were worse in the morning than later in the day (p < 0.005) but otherwise were stable over 2 wk. Even though most subjects smoked and stayed indoors 80 to 90% of the time, personal NO2 exposures correlated significantly with outdoor NO2 concentrations as reported by local monitoring stations.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Air Pollutants; Female; Forced Expiratory Volume; Humans; Lung Diseases, Obstructive; Male; Maximal Midexpiratory Flow Rate; Middle Aged; Nitrogen Dioxide; Peak Expiratory Flow Rate; Respiratory Mechanics; Smoking; Vital Capacity

Symptoms and changes in pulmonary function of subjects with chronic obstructive pulmonary disease (COPD) and elderly normal subjects, induced by a 4-h exposure to 0.3 ppm NO2, were investigated using a double-blind, crossover design with purified air. The 5-day experimental protocol required approximately 2 wk with at least a 5-day separation between randomized 4-h exposures to either NO2 or air which included several periods of exercise. Over a 2-yr period, COPD subjects, all with a history of smoking, consisting of 13 men and 7 women (mean age of 60.0 yr) and 20 elderly normal subjects of comparable age and sex were evaluated. During intermittent light exercise, COPD subjects demonstrated progressive decrements in FVC and FEV1 compared with baseline with 0.3 ppm NO2, but not with air. Differences in percent changes from baseline data (air-NO2) showed an equivocal reduction in FVC by repeated measures of analysis of variance and cross-over t tests (p less than 0.10). Subgroup analyses suggested that responsiveness to NO2 decreased with severity of COPD; in elderly normal subjects, NO2-induced reduction in FEV1 was greater among smokers than never-smokers. A comparison of COPD and elderly normal subjects also revealed distinctions in NO2-induced responsiveness.

Topics: Aged; Aging; Air Pollutants; Female; Forced Expiratory Volume; Humans; Lung Diseases, Obstructive; Male; Middle Aged; Nitrogen Dioxide; Reference Values; Respiratory Mechanics; Smoking; Vital Capacity

These studies were undertaken to evaluate short-term respiratory effects and identify markers of nitrogen dioxide toxicity during exposures designed to approximate realistic conditions. With the development of bronchoalveolar lavage as a clinical investigative technique, the evaluation focused on the assessment of effects induced at the alveolar level. The exposure protocols were designed to assess the duration of nitrogen dioxide-induced effects and determine exposure-response relationships. Groups of normal, nonsmoking volunteers of both sexes between the ages of 18 and 40 years, without airway hyperreactivity, constituted the study population. The exposure protocols required a total of three to five days for each subject, depending on the timing of bronchoalveolar lavage. Subjects were exposed to nitrogen dioxide or air for three hours in a double-blind, randomized fashion in a 45-m3 environmental chamber, with intermittent exercise sufficient to quadruple minute ventilation. Pulmonary function was measured during and after exposure, and airway reactivity to carbachol was assessed before and after exposure. Lavaged cells were examined for their capacity to inactivate influenza virus and secrete IL-1 in vitro. Cell-free lavage fluid was analyzed for total protein, albumin, alpha 2-macroglobulin, arylsulfatase, and alpha 1-protease inhibitor. The studies were undertaken in three phases, each of approximately one year's duration. In Phase 1, 15 subjects were exposed to a background concentration of 0.05 parts per million2 (ppm) nitrogen dioxide and to three 15-minute peaks of 2.0 ppm, and underwent bronchoalveolar lavage 3.5 hours after nitrogen dioxide exposure. During Phase 2, 8 subjects were exposed to continuous 0.60 ppm nitrogen dioxide and underwent bronchoalveolar lavage 18 hours later. Finally, in Phase 3, 15 subjects were exposed to continuous 1.5 ppm nitrogen dioxide and underwent bronchoalveolar lavage 3.5 hours after exposure. No significant symptomatic or pulmonary function changes could be detected in response to any of the nitrogen dioxide exposures. However, a small but significant increase in airway reactivity was observed in normal subjects after exposure to 1.5 ppm nitrogen dioxide. Following the highest dose of carbachol (10 mg/mL), the forced expiratory volume in one second decreased 7.5 +/- 1.1 percent after nitrogen dioxide exposure compared to 4.8 +/- 1.1 percent after exposure to air (p less than 0.05). No symptoms were induced in

Topics: Adolescent; Adult; Air Pollutants; Airway Resistance; Bronchoalveolar Lavage Fluid; Double-Blind Method; Female; Humans; Lung Diseases, Obstructive; Lung Volume Measurements; Macrophages, Alveolar; Male; Nitrogen Dioxide; Orthomyxoviridae

This project was undertaken to investigate symptom responses and changes in the pulmonary function of two susceptible groups--people with asthma and people with chronic obstructive pulmonary disease (COPD)--when exposed to 0.3 parts per million (ppm) (560 micrograms/m3) nitrogen dioxide. In these controlled clinical studies, a double-blind crossover design with purified air in a 45-m3 environmental chamber was used. Groups of non-respiratory-impaired (normal) subjects of a comparable age range and of both genders constituted controls for the asthmatic and COPD groups. The exposure protocol required five days: day 1, training and base-line preexposure measurements; day 2, a first exposure to 0.3 ppm nitrogen dioxide or air in a randomized sequence; day 3, 24-hour follow-up measurements of possible delayed effects; day 4, a second exposure; and day 5, a second 24-hour postexposure follow-up. All four-hour exposures included several predetermined periods of exercise and pulmonary function measurements. To examine changes in bronchial responsiveness and to aid in subject selection, bronchial challenges with carbachol and isoproterenol aerosol were used. The project was undertaken in four phases, each lasting approximately one year. In the first year, 20 normal non-smoking volunteers (10 women and 10 men) with an average age of 31.0 years were assessed. The second year, 20 non-smoking subjects with mild to moderate asthma were evaluated. This group was comparable in gender and age to the control group of normal volunteers. The third year, 20 subjects with COPD were studied. This group had a mean age of 60.0 years and consisted of 13 men and seven women. All subjects had a history of smoking. During the fourth and final year of the study, a group of 20 elderly normal volunteers similar in age and gender to the COPD group were evaluated. The main findings of the study were as follows. No significant symptomatic or physiologic responses to nitrogen dioxide could be detected in either the young or the elderly control group. Prior studies of asthmatic subjects had led us to hypothesize that 0.3 ppm nitrogen dioxide is close to the minimum level needed to produce significant functional deficits during moderate activity in this susceptible group. However, in this study the asthmatic group as a whole did not manifest significant reductions in lung function after exposure to 0.3 ppm nitrogen dioxide compared to their preexposure base-line data or to their responses aft

Topics: Adult; Aged; Asthma; Clinical Trials as Topic; Double-Blind Method; Exercise Test; Female; Humans; Lung; Lung Diseases, Obstructive; Male; Middle Aged; Nitrogen Dioxide; Respiratory Function Tests; Risk Factors

Nitrogen multiple-breath washout (N2 MBW) is a promising tool for assessing early lung damage in children with chronic obstructive pulmonary disease, but it can be a time-consuming procedure. We compared alternative test-shortening endpoints with the most commonly reported N2 MBW outcome, the lung clearance index, calculated as lung volume turnovers required to reach 2.5% of the starting N2 concentration (LCI2.5 ).. Cross-sectional study of triplicate N2 MBW measurements obtained in cystic fibrosis (CF) patients (N = 60), primary ciliary dyskinesia (PCD) patients (N = 28), and matched healthy controls (N = 48) aged 5-18 years. Bland-Altman analysis was used to compare LCI2.5 with earlier LCI endpoints (3%, 4%, 5%, 7%, and 9% of starting N2 concentration), Cn@TO6 (defined as % of N2 starting concentration when reaching six lung volume turnovers), and LCI derived from only two N2 MBW runs in each session. N2 MBW endpoints were analyzed as z-scores calculated from healthy controls.. In PCD, Cn@TO6 and LCI2.5 exhibited similar values (mean [95%CI] difference: 0.33 [-0.24; 0.90] z-scores), reducing the test duration by one-third (5.4 min; 95%CI: 4.0; 6.8). All other tested alternative endpoints exhibited increasing disagreement with increasing LCI2.5 . With an average reduction in test duration of 40%, LCI2.5 derived from two runs exhibited good agreement in all children.. Cn@TO6 may be suggested as a potential test-shortening endpoint in school children with PCD. In CF, early test termination may reduce measurement power with advancing pulmonary disease, suggesting differences in underlying pathophysiology. Two technically acceptable N2 MBW runs may be sufficient in school children irrespective of diagnosis with CF or PCD. Pediatr Pulmonol. 2016;51:624-632. © 2015 Wiley Periodicals, Inc.

Topics: Adolescent; Breath Tests; Child; Child, Preschool; Cross-Sectional Studies; Cystic Fibrosis; Female; Functional Residual Capacity; Humans; Lung; Lung Diseases, Obstructive; Male; Nitrogen Dioxide; Prospective Studies; Respiratory Function Tests; Tidal Volume; Total Lung Capacity

Air pollutants in Iceland's capital area include hydrogen sulfide (H2S) emissions from geothermal power plants, particle pollution (PM10) and traffic-related pollutants. Respiratory health effects of exposure to PM and traffic pollutants are well documented, yet this is one of the first studies to investigate short-term health effects of ambient H2S exposure.. The aim of this study was to investigate the associations between daily ambient levels of H2S, PM10, nitrogen dioxide (NO2) and ozone (O3), and the use of drugs for obstructive pulmonary diseases in adults in Iceland's capital area.. The study period was 8 March 2006 to 31 December 2009. We used log-linear Poisson generalized additive regression models with cubic splines to estimate relative risks of individually dispensed drugs by air pollution levels. A three-day moving average of the exposure variables gave the best fit to the data. Final models included significant covariates adjusting for climate and influenza epidemics, as well as time-dependent variables.. The three-day moving average of H2S and PM10 levels were positively associated with the number of individuals who were dispensed drugs at lag 3-5, corresponding to a 2.0% (95% confidence interval [CI] 0.4, 3.6) and 0.9% (95% CI 0.1, 1.8) per 10 μg/m3 pollutant concentration increase, respectively.. Our findings indicated that intermittent increases in levels of particle matter from traffic and natural sources and ambient H2S levels were weakly associated with increased dispensing of drugs for obstructive pulmonary disease in Iceland's capital area. These weak associations could be confounded by unevaluated variables hence further studies are needed.

Topics: Adult; Aged; Aged, 80 and over; Air Pollutants; Air Pollution; Anti-Asthmatic Agents; Asthma; Drug Utilization; Humans; Hydrogen Sulfide; Iceland; Inhalation Exposure; Lung Diseases, Obstructive; Middle Aged; Nitrogen Dioxide; Ozone; Particulate Matter; Poisson Distribution; Registries; Regression Analysis; Risk; Seasons; Urban Population; Weather

To investigate the relation between personal exposures to nitrogen dioxide, carbon monoxide, and PM(10), and exposures estimated from static concentrations of these pollutants measured within the same microenvironments, for healthy individuals and members of susceptible groups.. Eleven healthy adult subjects and 18 members of groups more susceptible to adverse health changes in response to a given level of exposure to nitrogen dioxide, carbon monoxide, and/or PM(10) than the general population (six schoolchildren, six elderly subjects, and six with pre-existing disease-two with chronic obstructive pulmonary disease (COPD), two with left ventricular failure (LVF), and two with severe asthma) were recruited. Daytime personal exposures were determined either directly or through shadowing. Relations between personal exposures and simultaneously measured microenvironment concentrations were examined.. Correlations between personal exposures and microenvironment concentration were frequently weak for individual subjects because of the small range in measured concentrations. However, when all subjects were pooled, excellent relations between measured personal exposure and microenvironment concentration were found for both carbon monoxide and nitrogen dioxide, with slopes of close to one and near zero intercepts. For PM(10), a good correlation was also found with an intercept of personal exposure (personal cloud) of 16.7 (SD 10.4) micro g/m(3). Modelled and measured personal exposures were generally in reasonably good agreement, but modelling with generic mean microenvironment data was unable to represent the full range of measured concentrations.. Microenvironment measurements of carbon monoxide and nitrogen dioxide can well represent the personal exposures of individuals within that microenvironment. The same is true for PM(10) with the addition of a personal cloud increment. Elderly subjects and those with pre-existing disease received generally lower PM(10) exposures than the healthy adult subjects and schoolchildren by virtue of their less active lifestyles.

Topics: Adult; Aged; Air Pollutants; Air Pollution, Indoor; Carbon Monoxide; Child; Environmental Exposure; Environmental Monitoring; Humans; Inhalation Exposure; Linear Models; Lung Diseases, Obstructive; Nitrogen Dioxide; Reproducibility of Results; Urban Health; Ventricular Dysfunction, Left

Topics: Air Pollutants; Cohort Studies; Humans; Lung Diseases, Obstructive; Nitrogen Dioxide; Spain; Sulfur Dioxide

Laboratory-based studies have shown that ozone and nitrogen dioxide can potentiate the effect of allergen in sensitized asthmatic subjects, but it is not known whether this interaction is important under natural exposure conditions. Thirty-five subjects with clinical diagnoses of asthma or chronic obstructive pulmonary disease and with a provocative dose causing a 20% fall in forced expiratory volume in one second methacholine <12.25 micromol (using the Yan method) kept peak expiratory flow (PEF) records for a 4-week period during late summer, with concurrent measurement of spore and pollen counts and pollution levels. Multiple regression analysis was then used to determine the effect on PEF of aeroallergen, and of the interaction between aeroallergen and pollutant levels. A statistically significant interaction was demonstrated between total spore count and ozone, but not nitrogen dioxide. Mean PEF fell in association with increasing spore count (same-day and 24-h lag level) and PEF variability increased with increasing spore count (24-h lag level only); both changes were greater the higher the prior ozone level. These results suggest that ozone can potentiate the effect of aeroallergens in subjects with bronchial hyperreactivity under natural exposure conditions. However, the effect was small, and the clinical significance of the interaction requires further study.

Topics: Adult; Aged; Air Pollutants; Allergens; Asthma; Bronchial Provocation Tests; Female; Forced Expiratory Flow Rates; Forced Expiratory Volume; Humans; Lung Diseases, Obstructive; Male; Methacholine Chloride; Middle Aged; Nitrogen Dioxide; Ozone; Peak Expiratory Flow Rate; Pollen; Spores, Fungal

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.

Topics: Air Pollution; Climate; Europe; Humans; Lung Diseases, Obstructive; Nitrogen Dioxide; Ozone; Patient Admission; Population Surveillance; Regression Analysis; Risk; Smoke; Sulfur Dioxide

We investigated the association between air pollution and hospital admissions for chronic obstructive pulmonary disease and pneumonia among the elderly in Minneapolis-St. Paul, MN, and Birmingham, AL, over the period January 1, 1986, to December 31, 1991. Pollutants included in our analyses were PM10 (particulate matter less than 10 microns in aerodynamic diameter), SO2, NO2, O3, and CO in Minneapolis-St. Paul, and PM10, O3, and CO in Birmingham. After adjusting for temperature, day of week, season, and temporal trends, we found little evidence of association between air pollution and hospital admissions for respiratory causes in Birmingham. In contrast, we found that air pollution was associated with hospital admissions for respiratory causes in Minneapolis-St. Paul. Among the individual pollutants, O3 was most strongly associated with admissions (estimated increase in hospital admissions associated with a 15-parts-per-billion increase in O3 on the previous day = 5.15%; 95% confidence interval = 2.36-7.94%), and this association was robust in the sense that it was little affected by the simultaneous consideration of other pollutants. PM10, SO2, and NO2 were also associated with hospital admissions, although none could be singled out as being more important than the others.

Topics: Aged; Air Pollution; Alabama; Carbon Monoxide; Confidence Intervals; Humans; Lung Diseases, Obstructive; Minnesota; Models, Statistical; Nitrogen Dioxide; Ozone; Particle Size; Patient Admission; Pneumonia; Regression Analysis; Retrospective Studies; Sulfur Dioxide; Temperature; Time Factors

A study was undertaken to investigate the relationship between air pollution levels and respiratory symptoms and peak expiratory flow rate (PEFR) in subjects with chronic obstructive pulmonary disease (COPD) living in Christchurch, New Zealand.. Forty subjects aged over 55 years with COPD completed twice daily diaries for three months during the winter of 1994. Subjects recorded respiratory symptoms, PEFR, outdoor activity, visits to doctor or hospital, and medication use. All were resident within a 5 km radius of the regional council's air pollution monitoring site. Daily and hourly mean pollutant levels (particulates (PM10, nitrogen dioxide (NO2), sulphur dioxide (SO2) and carbon monoxide (CO)) were measured at the monitoring site.. Pollution levels were generally low relative to those recorded in previous years. The New Zealand Ministry for the Environment guidelines for PM10 were exceeded on five occasions, and for CO six times. No association was found between PEFR and any of the pollution variables. A rise in the PM10 concentration equivalent to the interquartile range was associated with an increase in night time chest symptoms (relative risk 1.38, 95% CI 1.07 to 1.78). A rise in NO2 concentrations equivalent to the interquartile range was associated with increased reliever inhaler use (relative risk 1.42, 95% CI 1.13 to 1.79) and for 24 hour lag analysis with increased nebuliser use (relative risk 2.81, 95% CI 1.81 to 4.39). There was no increase in the relative risk of other symptoms in relation to pollution levels.. These effects, demonstrated in a small susceptible group of subjects with COPD, indicate that adverse outcomes can be measured in response to pollution levels that are within current guidelines.

Topics: Aged; Aged, 80 and over; Air Pollutants; Bronchodilator Agents; Carbon Monoxide; Cohort Studies; Female; Humans; Lung; Lung Diseases, Obstructive; Male; Middle Aged; Nebulizers and Vaporizers; Nitrogen Dioxide; Peak Expiratory Flow Rate; Regression Analysis; Risk

Exposure to polluted air can cause respiratory symptoms in subjects with airflow limitation. Twelve COPD (chronic obstructive pulmonary disease) patients with mild to moderate obstructive ventilatory defects were exposed on separate occasions to fresh ambient air and polluted air collected from the Lin-Sun S. Road tunnel in Taipei City. Concentrations of SO2 and NO2 were 85-121 ppb and 449-502 ppb, respectively, and were 4-fold and 10-fold, respectively, higher than those of out-door air in the city. Twenty healthy adult volunteers served as the control group. Maximal expiratory flow-volume determination, respiratory resistance (Rrs) and methacholine bronchial challenges were completed before and after inhalation of polluted air for 20 minutes. No difference in FVC (forced vital capacity), FEV1 (1 second forced expiratory volume), Rrs and bronchial reactivity was noted for normal subjects after inhaling polluted air and ambient air. For patients with COPD, there was a small but significant decrease in FEV1 after exposure. The elevation in Rrs was prominent, and there was also a significant increase in bronchial sensitivity to methacholine (decrease in cumulative provocation dose, DA) in positive responders. We conclude that short-term exposures to moderate polluted air can affect lung function and increase bronchial sensitivity to methacholine in COPD patients.

Topics: Aged; Air Pollution; Bronchi; Female; Humans; Lung; Lung Diseases, Obstructive; Male; Middle Aged; Nitrogen Dioxide; Sulfur Dioxide

The effects of ozone (O3) and nitrogen dioxide (NO2) on the solubility and proteolytic susceptibility of elastin were examined to better understand how these oxidant air pollutants might damage the lung. In vitro O3 exposures at pH 7.4 resulted in the complete solubilization of elastin, but NO2 had no effect on solubility. The initial solubilization rate was 65 micrograms/mumol of O3, which increased to 150 micrograms/mumol in the midregion of a sigmoidal solubilization curve. Peptide fragments of the O3-solubilized elastin ranged in size from 5 to 20 kD. The conversion of insoluble elastin into soluble fragments by O3 was not due to the destruction of desmosine crosslinks. The effect of O3 on the proteolytic susceptibility of elastin was measured using insoluble elastin recovered from exposures that resulted in 5.3%, 12.8%, and 26.3% solubilization. Human neutrophil elastase (HNE) digested the remaining insoluble elastin samples 4.3, 6.0, and 9.8 times faster than unexposed elastin. In contrast, NO2-exposed elastin was no more susceptible to digestion by HNE. Ascorbate, EDTA, and uric acid reduced the proteolytic susceptibility of O3-exposed elastin, but mannitol afforded no protection. These findings indicate that the inhalation of O3 may contribute to lung disease by directly damaging elastin and by increasing its susceptibility to proteolysis, whereas NO2 probably damages lungs via alternative mechanisms.

Topics: Air Pollutants; Animals; Antioxidants; Cattle; Elastin; Humans; In Vitro Techniques; Leukocyte Elastase; Lung Diseases, Obstructive; Neutrophils; Nitrogen Dioxide; Ozone; Pancreatic Elastase; Peptide Fragments; Solubility

This project tested the hypothesis that inhaled oxidants could cause lung damage by inactivating the proteinase inhibitors that normally protect the lung from proteolysis. Rat alpha-1-proteinase inhibitor (alpha 1-PI)2 was purified from blood plasma, and antibodies to this inhibitor were prepared. The activity of alpha 1-PI in lung lavage fluids from rats was measured by elastase inhibition, and the immunological concentration of alpha 1-PI was quantified in an enzyme-linked immunoassay. The ratio of the amount of active alpha 1-PI relative to its immunological concentration was examined as a measure of the inhibitor's functional activity. This ratio and the ratio of the immunological concentration of alpha 1-PI to the total protein concentration were determined in lung lavage fluids from rats exposed to air, 10 parts per million (ppm) nitrogen dioxide, and diesel emissions (3.5 mg/m3 particulates) for 12, 18, and 24 months. Only diesel exposures resulted in a statistically significant reduction in the functional activity of alpha 1-PI of 30 percent (p less than 0.05). Similar studies were performed on rats exposed to nitrogen dioxide (0.5 ppm background with peaks of 1.5 ppm) and ozone (0.06 ppm background with peaks of 0.25 ppm) for 12 and 18 months. No statistically significant effects were observed in the functional activity of alpha 1-PI or its immunological concentration. In other protocols, rats were acutely exposed to 0.8 ppm or 1.2 ppm ozone for two, four, or eight hours, and to 0.5 ppm or 0.8 ppm ozone in conjunction with 8 percent carbon dioxide for two or seven hours. Although these acute exposure conditions did not reduce the functional activity of alpha 1-PI, the immunological concentration of alpha 1-PI and the elastase inhibitory activity, relative to other proteins, were significantly increased in relation to the total amount of ozone inhaled. The functional activity of alpha 1-PI also was measured in the bronchoalveolar lavage fluids of human subjects exposed to nitrogen dioxide (0.05 ppm with 2 ppm peaks, or to 1.5 ppm continuously) for three hours and to ozone (0.4 ppm) for two hours during exercise. These exposures did not result in significant changes in the functional activity of alpha 1-PI or its immunological concentration.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Air Pollutants; alpha 1-Antitrypsin; Animals; Bronchoalveolar Lavage Fluid; Exercise Test; Humans; Leukocytes; Lung; Lung Diseases, Obstructive; Male; Mast Cells; Nitrogen Dioxide; Oxidants, Photochemical; Ozone; Pancreatic Elastase; Peptide Hydrolases; Protease Inhibitors; Rats; Rats, Inbred F344; Vehicle Emissions

Short-time exposure to air pollutants and in particular to sulfur dioxide, nitrogen oxides and photochemical oxidants may cause respiratory symptoms similar to acute bronchial asthma. In healthy adults however the concentrations required to evoke significant bronchial obstruction lie still above the level of atmospheric air pollution usually observed in our country. In contrast patients with preexisting pulmonary diseases or with impaired bronchopulmonary defense mechanisms may show harmful reactions even at concentrations which actually occur in urban and rural atmospheres. In addition there is evidence of on increased prevalence of chronic obstructive pulmonary diseases in countries with high chemical pollution indicating that long-term exposure of ambient air pollution may cause chronic illness as well. Since air pollution is accepted to produce adverse health effects, emergent efforts are required to improve air quality in order to avoid further injuries in man.

Topics: Adult; Aged; Air Pollutants; Asthma; Bronchitis; Humans; Lung Diseases; Lung Diseases, Obstructive; Middle Aged; Nitric Oxide; Nitrogen Dioxide; Ozone; Risk; Smoking; Sulfur Dioxide; Switzerland

Questionnaires, spirometry, and the single-breath nitrogen test were administered to 3,192 participants 25 to 39 yr of age in area exposed to low concentrations of all pollutants (Lancaster, California) and to 2,369 similar participants living in an area exposed to high concentrations of photochemical oxidants, nitrogen dioxide, and sulfates (Glendora, California). The prevalence of symptoms and results in the majority of the tests were worse in the polluted area between current and never smokers and men and women. Those tests associated primarily with small airways (Vmax50, Vmax75, delta N 2(750-1250) showed little or no difference between areas. The difference in the prevalence of participants with a poor FEV1 and/or poor FEV1 and/or poor FVC and in the mean Vmax and closing volume was greater between areas than between smoking categories. These results suggest that long-term exposure to high concentrations of photochemical oxidants, NO2, and sulfates at place of residence may result in measurable impairment in both current smokers and never smokers. Firmer documentation of this effect will require following these populations for changes in lung function that correlate with pollutant exposures.

Topics: Adult; Air Pollutants; California; Female; Humans; Lung Diseases, Obstructive; Male; Middle Aged; Nitrogen Dioxide; Oxidants, Photochemical; Pulmonary Ventilation; Smoking; Spirometry; Sulfates; Time Factors

Topics: Accidents, Occupational; Airway Obstruction; Animals; Bronchitis; Cricetinae; Fires; Humans; Infections; Lung Diseases, Obstructive; Nitrogen Dioxide; Rabbits; Rats

Air pollution referable to increased ambient levels of sulfur dioxide and suspended particulates is associated with increased episodes of acute bronchitis and is also causally related to some cases of chronic bronchitis. Oxidant air pollution is associated with abnormalities of pulmonary function in children and is a major contributory factor in COP, especially bronchitis, in some areas of the United States. The relationship of nitrogen dioxide atmospheric contamination to COPD is still controversial. In our opinion, the epidemiologic studies conducted to date have been inadequate and further elucidation is indicated. Cadmium fumes and compounds have been found to be instrumental in the development of some cases of chronic bronchitis and emphysema in Sweden. This association is unproved in the United States and warrants a thorough clinical and epidemiologic evaluation.

Topics: Air Pollutants; Cadmium; Carbon Monoxide; Chlorine; Chronic Disease; Humans; Lung; Lung Diseases, Obstructive; Nitrogen Dioxide; Ozone; Sulfur Dioxide

Topics: Humans; Lung Diseases, Obstructive; Nitrogen Dioxide; Nitrogen Oxides; Smoking

Topics: Lung; Lung Diseases, Obstructive; Nitrogen Dioxide; Ozone; Smoking

Topics: Adrenergic beta-Agonists; Air Pollution; Bronchi; Histamine; Humans; Lung Diseases, Obstructive; Nitrogen Dioxide; Ozone; Parasympatholytics; Sulfur Dioxide; Time Factors; Work of Breathing

Topics: Acetylcholine; Air Pollution; Animals; Asthma; Congresses as Topic; Dogs; Epidemiologic Methods; Histamine; Humans; Lung Diseases, Obstructive; Methods; Netherlands; Nitrogen Dioxide; Respiratory Function Tests; Rural Population; Seasons; Sensory Receptor Cells; Sulfur Dioxide; Temperature

Topics: Adult; Age Factors; Air Pollution; California; Environment, Controlled; Environmental Exposure; Environmental Health; Female; Histamine; Humans; Lung Diseases; Lung Diseases, Obstructive; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Sex Factors; Smoking; Sputum; Styrenes; Toluene; Urban Population