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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In October 1989, the Hungarian National Institute of Hygiene initiated the Children's Acute Respiratory Morbidity (CHARM) Surveillance System to assess the association between nine reportable respiratory diseases and air pollution. The weekly number of physician-diagnosed, reportable respiratory diseases among four age groups of children (less than 1, 1-2, 3-5, and 6-14 years) was tabulated for Sopron, a city with 60,000 residents. We calculated the proportion of diseases occurring during weeks with low, moderate, and high sulfur dioxide (SO2) and nitrogen dioxide (NO2) concentrations. The weekly averages of the 24-hour median SO2 concentrations were divided into thirds at less than or equal to 17.6, greater than 17.6 to less than or equal to 26.3, and greater than 26.3 micrograms/m3 (range: 0.9-79.6 micrograms/m3), and the NO2 concentrations at less than or equal to 29.8, greater than 29.8 to less than or equal to 44.1, and greater than 44.1 micrograms/m3 (range: 4.2-90.1 micrograms/m3). During 1990, 11,474 respiratory disease cases occurred among the 4,020 children less than 15 years of age living in Sopron and monitored by the CHARM system. The two most frequently reported disease categories were rhinitis/tonsillitis/pharyngitis (71.5%) and acute bronchitis (8.5%). Sixty-seven percent of pneumonia cases occurred when SO2 concentrations were highest. We found no association between levels of NO2 and respiratory diseases. The CHARM Surveillance System may characterize more fully which groups of children develop particular respiratory diseases following exposure to air pollution.
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PMID:Respiratory disease surveillance in Hungary. 152 85

Cause-specific deaths by day for the years 1973 to 1980 in Philadelphia, Pennsylvania, were extracted from National Center for Health Statistics mortality tapes. Death from accidents (International Classification of Disease, Revision 9 greater than or equal to 800) and deaths outside of the city were excluded. Daily counts of deaths were regressed using Poisson regression on total suspended particulate (TSP) and/or SO2 on the same day and on the preceding day, controlling for year, season, temperature, and humidity. A significant positive association was found between total mortality (mean of 48 deaths/day) and both TSP (second highest daily mean, 222 micrograms/m3) and SO2 (second highest daily mean, 299 micrograms/m3). The strongest associations were found with the mean pollution of the current and the preceding days. Total mortality was estimated to increase by 7% (95% CI, 4 to 10%) with each 100-micrograms/m3 increase in TSP, and 5% (95% CI, 3 to 7%) with each 100-micrograms/m3 increase in SO2. When both pollutants were considered simultaneously, the SO2 association was no longer significant. Mortality increased monotonically with TSP. The effect of 100 micrograms/m3 TSP was stronger in subjects older than 65 yr of age (10% increase) compared with those younger than 65 yr of age (3% increase). Cause-specific mortality was also associated with a 100-micrograms/m3 increase in TSP: chronic obstructive pulmonary disease (ICD9 490-496), +19% (95% CI, 0 to 42%), pneumonia (ICD9 480-486 & 507), +11% (95% CI, -3 to +27%), and cardiovascular disease (ICD9 390-448), +10% (95% CI, 6 to 14%). These results are somewhat higher than previously reported associations, and they add to the body of evidence showing that particulate pollution is associated with increased daily mortality at current levels in the United States.
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PMID:Increased mortality in Philadelphia associated with daily air pollution concentrations. 154 41

Airways and lungs are equipped with a highly effective defense mechanism. These can bei found damaged in the aged: Cough is weaker, mucociliary clearance and mucous production are irregular. This damage can bei caused and increased by smoking, recurrent infection, and some sorts of air pollution (SO2). We call it a primary infection, when the organ has been intact as well as the general condition (immune defense etc), and where the causative agent is a virus or virus-like organism. A secondary infection is conditioned by previous disease, and when the causative agents are bacilli. Finally, a tertiary infection is dependent on a defense failure of the body and on opportunistic organisms. For elderly patients, secondary infections outweight the others (recurrent purulent bronchitits). However, tertiary infections must also bei considered in bedridden or post-operative patients or in those with metabolic disease. Finally, pneumonia in the aged must be differentiated in terms of underlying carcinoma, infarction, aspiration and tuberculosis. Therapy of primary (viral)infection consists mainly in prophylaxis of bacterial secondary infection. The choice of drug, dosage and duration of treatment depends on the degree of previous damage to the organ, of complications and status of the whole body and it's defense mechanisms.
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PMID:[Therapeutic principles of bronchopulmonary infections in the aged]. 613 61

Automated measurements of respiratory gas exchange recently became available for the determination of oxygen uptake (VO2) in critically ill patients. Whereas these metabolic gas monitoring systems (MBM) are assumed to measure total body VO2, the reversed Fick method in principle excludes intrapulmonary VO2. Previous clinical reports comparing VO2 measured by the reversed Fick principle (VO2Fick) with VO2 measured by MBM (VO2MBM) found that VO2MBM was significantly greater than VO2Fick. It was suggested that these differences between methods represent VO2 of pulmonary and bronchial tissue, as intrapulmonary VO2 had been estimated to account for 15% of total body VO2 in dogs with experimental pneumonia. The objective of this study was to compare VO2Fick with VO2MBM in patients with and without pneumonia and to assess the reproducibility of both methods in critically ill patients. METHOD. With institutional approval nine critically ill patients with acute pneumonia were studied under controlled mechanical ventilation. The diagnosis of pneumonia was based on respective changes of chest X-rays, body temperature > 38 degrees C, and WBC counts > 12,000/mm3. Inspiratory oxygen fractions (FIO2) ranged from 0.3 to 0.6; all patients routinely received opioids and hypnotics. Complete muscle relaxation was achieved during the periods of measurement to avoid sudden changes in VO2 due to shivering or involuntary movements. Arterial and pulmonary-arterial blood samples were drawn simultaneously after aspiration of the sevenfold catheter dead space. Measurements of haemoglobin concentration (Hb), fractional oxygen saturation (SO2), and O2 partial pressure (PO2) were performed by use of a calibrated haemoximeter and blood gas analyser, respectively; 2 x 5 thermodilution measurements of cardiac output (CO) were spread randomly over the respiratory cycle for each determination of VO2Fick. To minimise systematic errors of CO measurements, the CO computer was calibrated in an extracorporeal flow model using an electromagnetic flowmeter. Calculations of VO2Fick were based on an oxygen binding capacity of 1.39 ml/g Hb. Simultaneous measurements of VO2MBM were obtained by use of a Datex Deltatrac MBM that had been validated in vitro with a gas dilution model of respiratory gas exchange. Calibration of the MBM was performed prior to each measurement. Gas supply of the respirator was provided by an external high-precision mixing device to reduce errors in VO2 measurements that may arise from short-term oscillations in FIO2. All patients with pneumonia were studied on three consecutive days; thus, measurements from 27 days could be analysed. On each day two sets of measurements were performed at an interval of 60 min to assess the reproducibility of differences between methods. During each set of measurements duplicate blood samples were drawn twice, before and after thermodilution measurements of CO, to evaluate the short-term repeatability of VO2Fick. The beginning and the end of each set of measurements were marked in the computer record of the MBM to assess the respective repeatability of VO2MBM. Fifty control measurements were performed in ten patients undergoing major neurosurgical procedures. None of these patients exhibited signs of pulmonary infection. Except for the number of repeated measures, all VO2 measurements were obtained in the same way as in the study group. Descriptive statistical analysis was performed according to Bland and Altman; comparisons between methods were done by multivariate analysis of variance for repeated measures. RESULTS. Neither in the study group nor in the control group could a significant difference between methods be demonstrated. In patients with pneumonia the mean difference between methods (VO2Fick-VO2MBM) was 15.2 ml/min (4.2%); the double standard deviation of differences (2 SD) was 59.2 ml/min (19.2%).
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PMID:[Inverse fick's principle in comparison to measurements of oxygen consumption in respiratory gases. Does intrapulmonary oxygen uptake account for differences shown by different system methods?]. 781 47

The aim of this ecological study was to investigate the effect of outdoor air pollution on the mortality risk of metropolitan inhabitants in Santiago de Chile. Cause-specific deaths by the day for the years 1988-1991 in Santiago de Chile were extracted from mortality data tapes of the National Center for Statistics. Deaths from accidents were excluded. Total and some specific respiratory diseases deaths were compared calculating the risk of death by municipality and month of the year using age-adjusted standardized mortality ratios (SMRs) controlling for socioeconomic level. Daily counts of deaths were regressed using a Poisson model on the total and fine suspended particles, SO2, CO and ozone on the preceding day, controlling for temperature and humidity. A clear pattern in the geographical distribution of risk of death, both for general mortality and specific respiratory causes (pneumonia, COPD and asthma) was found using SMR, with higher values in the most polluted areas regardless of socioeconomic and living conditions. A highly significant positive association was found between total mortality and both fine suspended particles and CO level. The association remained significant for those days with fine suspended particles levels below 150 micrograms/dl suggesting a no-threshold effect for the total number of deaths. These results are in agreement with previously reported associations, and they add to the body of evidence showing that particulate pollution is associated with increases daily mortality.
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PMID:The effect of outdoor air pollution on mortality risk: an ecological study from Santiago, Chile. 858 29

We examined the relation of invasive pneumococcal disease to season, atmospheric conditions, and the rate of respiratory virus isolation in a community-wide surveillance program in Houston. Among adults, the number of cases of pneumococcal bacteremia peaked in midwinter and declined strikingly in midsummer, indicating a high degree of inverse correlation with the ambient temperature. We detected significant correlations between the occurrence of pneumococcal disease and the isolation of respiratory syncytial virus (P < .001), influenza virus (P < .001), and all viruses except influenza virus (P < .001), as well as with air pollution, as measured by SO2 levels (P < .001). In contrast, the rate of invasive pneumococcal disease among infants and children was relatively more sustained from October through May, with a notable decrease in summer months; the incidence of pneumococcal disease was therefore less strongly correlated with cold weather and less closely associated with the isolation of respiratory syncitial virus or influenza virus. However, pneumococcal disease among infants and children was associated with isolation of these viruses after a 4-week lag period as well as with isolation of adenovirus and ragweed pollen counts. The finding, with regard to children, that correlations tended to be stronger for events that occurred 1 month previously than for those that occurred contemporaneously is consistent with the concept that viral or allergic events predispose to otitis media with effusion, which becomes suppurative and leads to pneumococcal bacteremia or meningitis. For adults, a more immediate predisposition to pneumococcal pneumonia and bacteremia because of viral infection or air pollution was suggested.
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PMID:Association of invasive pneumococcal disease with season, atmospheric conditions, air pollution, and the isolation of respiratory viruses. 882 73

On a temporal basis, air has immense capacity for moving a large mass of pollutants. Mammals and birds are exposed to pollutants in air by the inhalation (nose and mouth), cutaneous or ocular routes. Most laboratory studies on air pollutants have been limited to single air pollutants and very little research has been done on the complex mixture of compounds that exist in ambient air. Complex mixtures are further complicated by dynamic chemical reactions that occur after the emissions leave point sources. Exposure parameters are also important in the toxicity of air pollutants. Intermittent exposure of monkeys to ozone increased the adverse pulmonary effects. Superimposing spikes of 0.8 ppm nitrogen dioxide on a baseline of 0.2 ppm, as occurs on a calm winter day, increased the susceptibility of mice to bacteria-induced pneumonia. Sulfur dioxide at concentrations of 5 ppm increased pulmonary resistance by 39%. Sulfuric acid is the predominate acid particle in the atmosphere. Exposure for 1 h to > 200 micrograms sulfuric acid/m3 depressed bronchomucociliary clearance. Concentrations of 100 micrograms/m3 of photochemical products caused headaches and 510 micrograms/m3 produced cough and chest pain. For chemical interactions in dose response, nitrogen dioxide is synergistic with ozone and ammonium sulfate. When all 3 chemicals are used in mixture, the response was 340%. Atmospheric conditions, such as fog, can alter the toxicity of air pollutants. The dose response to a single chemical can be altered by chemical mixtures and pre-existing disease conditions. Understanding these relationships is important for establishing no observable adverse effect levels. Mechanisms for multiple chemical interactions are multifaceted. One chemical may interfere with the metabolism or detoxification of another. Others may interact at cell receptors. To understand the effects of multiple chemical interactions of air pollutants, there is a need for a blend of epidemiological, laboratory and field studies. Studies are expensive. In the rural agricultural settings, the economic and environmental health risks are high. Should field observations and chemical problems be used as "red flags" for action?
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PMID:A review of the toxicology of air pollutants: toxicology of chemical mixtures. 888 47

Particles with diameters ranging from less than 0.02 to more than 100 microns and in concentration up to 120 micrograms/m3 daily average TSP (total suspended particles) are measurable in the air of Swiss cities and responsible for the decrease of visibility on the Swiss Plateau and south of the Alps. The particle size shows a typical distribution: the coarse particles (> 2.5 microns mass median diameter) are mostly of natural origin (plants, pollen, earth particles) and are deposited in the upper airways. The fine particles (PM2.5 < 2.5 microns) are predominantly deposited into the alveolar space. These fine and ultrafine particles (< 0.02 microns) are produced by the burning of fossil fuels or by photochemical reactions. By bypassing the mucociliary and cellular defense mechanisms, fine particles can invade the lung parenchyma and cause an inflammatory response. The additional chemical layering of a carbon core by nitrates, sulfates and other organic materials and metals such as iron cause greater local oxidative and/or carcinogenic damage than in the vaporized state. In comparing worldwide epidemiological studies, there seems to be a cohesive and consistent relationship between increases of particle concentration and the increase of mortality (mostly among patients over 65 with concomitant lung and heart diseases and among smokers) and morbidity (bronchitis, pneumonia, COPD, and, less convincingly, asthma). An increase in daily average PM10 (particles < 10 microns) is correlated with an increase in mortality not related to accidents and suicides of 1.0% for the same and/or the following days. In Switzerland, mean annual concentrations of 14-53 micrograms/m3 TSP or 10-33 micrograms/m3 PM10, well below the national standard (annual mean TSP 70 micrograms/m3) have been measured in rural and urban areas. Even at these concentrations an increase in respiratory symptoms and a decrease in lung function, without evidence for a "safe" threshold, have been observed in the Swiss study of air pollution and lung diseases in adults (SAPALDIA). Although the noxious effects of the particles cannot be clearly separated from the effect of other pollutants (e.g. NOx, SO2, ozone) in complex pollutant mixtures, the emission standards and national standards for ambient air should be revised, in particular by adding a standard for fine particles (e.g. PM10 or PM2.5).
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PMID:[Are inhaled dust particles harmful for our lungs?]. 900 26

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.
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PMID:Air pollution and hospital admissions for respiratory causes in Minneapolis-St. Paul and Birmingham. 920 44

We conducted a prospective study of a cohort of 3091 nonsmokers, ages 27 to 87 years, to evaluate the association between long-term ambient ozone exposure and development of adult-onset asthma. Over a 15-year period, 3.2% of males and 4.3% of females reported new doctor diagnoses of asthma. For males, we observed a significant relationship between report of doctor diagnosis of asthma and 20-year mean 8-h average ambient ozone concentration (relative risk (RR)=2.09 for a 27 ppb increase in ozone concentration, 95% CI=1.03 to 4.16). We observed no such relationship for females. Other variables significantly related to development of asthma were a history of ever-smoking for males (RR=2.37, 95% CI=1.13 to 4.81), and for females, number of years worked with a smoker (RR=1.21 for a 7-year increment, 95% CI=1.04 to 1.39), age (RR=0.61 for a 16-year increment, 95% CI=0.44 to 0.84), and a history of childhood pneumonia or bronchitis (RR=2.96, 95% CI=1.68 to 5.03). Addition of other pollutants (PM10, SO4, NO2, and SO2) to the models did not diminish the relationship between ozone and asthma for males. These data suggest that long-term exposure to ambient ozone is associated with development of asthma in adult males.
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PMID:Long-term ambient ozone concentration and the incidence of asthma in nonsmoking adults: the AHSMOG Study. 1009 2


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