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OBJECTIVE - We sought to determine the association of select clinical measures of asthma severity with percent predicted forced expiratory volume in one-second (%FEV1).
METHODS - We studied a prospective cohort of adult subjects (N = 129) with asthma exacerbations requiring hospital admission. Clinical data was acquired, including medical and social history, symptoms, vital signs, physical assessment, and spirometry. Predictor variables for this study included manually determined pulsus paradoxus (PP), percent predicted peak expiratory flow rate (%PEFR) and accessory muscle use. The outcome measure was %FEV1. Multiple linear regression analyses were performed to determine the independent associations between predictor variables and %FEV1.
RESULTS - In univariate analysis, %PEFR correlated with %FEV1 (rho = 0.77, P < .001) and PP correlated negatively with %FEV1 (rho = - 0.384, P < .001). %FEV1 was significantly lower in participants with accessory muscle use (Median %FEV1 = 37.5%, IQR: 27.0-49.0) than in those without accessory muscle use (Median %FEV1= 55.0%, IQR: 39.0-69.0), (P = .004). In multivariable analysis including the covariates %PEFR, accessory muscle use, PP, age, sex, heart rate and respiratory rate, %PEFR (P < .0001) and accessory muscle use (P = .003) remained significantly associated with %FEV1, whereas PP did not (P = .52).
STUDY OBJECTIVE - To determine whether increased exposure to particulate matter air pollution (PM), measured with personal, residential, or central site monitoring, was associated with pulmonary function decrements in either adults with COPD or children with asthma.
PARTICIPANTS - We studied 57 adults with or without COPD and 17 children aged 6 to 13 years with physician-diagnosed asthma in Seattle during a 3-year panel study.
STUDY DESIGN AND MEASUREMENTS - Indoor and outdoor PM measurements were made at subjects' homes. The subjects wore personal exposure monitors for 10 consecutive 24-h periods, and PM was also measured at a central outdoor location. We assessed the within-subject effect of particulate exposure on FEV(1) and peak expiratory flow (PEF) in adults, and maximal midexpiratory flow (MMEF), PEF, FEV(1), and symptoms in children.
RESULTS - FEV(1) decrements were associated with 1-day lagged central site PM = 2.5 microm in diameter (PM(2.5)) in adult subjects with COPD. In children not receiving antiinflammatory medication, same day indoor, outdoor, and central site exposures to PM(2.5) were associated with decrements in MMEF, PEF, and FEV(1). Associations with PM(2.5) and lung function decrements were also observed for 1-day lagged indoor (MMEF, PEF, FEV(1)) and personal (PEF only) exposures. Antiinflammatory medication use in children significantly attenuated the PM effect on airflow rates and volumes.
CONCLUSIONS - This study found consistent decrements in MMEF in children with asthma who were not receiving medications. It is notable that effects were observed even though PM exposures were low for an urban area. These findings suggest the need for future larger studies of PM effects in this susceptible population that repeatedly measure spirometry to include MMEF and potentially more sensitive markers of airway inflammation such as exhaled breath condensate and exhaled nitric oxide.
Information concerning the impact of environmental factors on cystic fibrosis (CF) is limited. We conducted a cohort study to assess the impact of air pollutants in CF. The study included patients over the age of 6 years enrolled in the Cystic Fibrosis Foundation National Patient Registry in 1999 and 2000. Exposure was assessed by linking air pollution values from the Aerometric Information Retrieval System with the patients' home zip code. After adjusting for confounders, a 10 microg/m(3) rise in particulate matter (both with a median aerodynamic diameter of 10 microm (PM(10)) or less and with an aerodynamic diameter of 2.5 microm or less (PM(2.5)) was associated with an 8% (95% confidence interval [CI], 2-15%) and 21% (95% CI, 7-33%) increase in the odds of two or more exacerbations, respectively; a 10-ppb rise in ozone was associated with a 10% (95% CI, 3-17%) increase in odds of two or more exacerbations. For every increase in PM(2.5) of 10 microg/m(3), there was an associated fall in FEV(1) of 24 ml (7-40) (95% CI) after adjusting for confounders. PM(2.5)'s association with mortality did not achieve statistical significance (adjusted RR = 1.32 per 10 microg/m(3) 0.91-1.93; 95% CI). Annual average exposures to particulate air pollution was associated with an increased risk of pulmonary exacerbations and a decline in lung function, suggesting a role of environmental exposures on prognosis in CF.
It is thought that reactive oxygen species (ROS) participate in the inflammation which characterizes asthma, but the evidence supporting this contention is incomplete. F(2)-isoprostanes (F(2)-IsoPs) are arachidonate products formed on membrane phospholipids by the action of ROS and thereby represent a quantitative measure of oxidant stress in vivo. Using a mass spectrometric assay we measured urinary release of F(2)-IsoPs in 11 patients with mild atopic asthma after inhaled allergen challenge. The excretion of F(2)-IsoPs increased at 2 h after allergen (1.5 +/- 0.2 versus 2.6 +/- 0.3 ng/mg creatinine) and remained significantly elevated in all urine collections for the 8-h period of the study (analysis of variance [ANOVA]). The measured compounds were of noncyclooxygenase origin because neither aspirin nor indomethacin given before challenge suppressed them. Urinary F(2)-IsoPs remained unchanged after inhaled methacholine challenge. In nine atopic asthmatics, F(2)-IsoPs were quantified in bronchoalveolar lavage fluid (BALF) at baseline values and in a separate segment 24 h after allergen instillation. F(2)-IsoPs were elevated late in the BALF (0.9 +/- 0.2 versus 11.4 +/- 3.0 pg /ml, baseline versus allergen, respectively, p = 0.007). The increase was inhibited by pretreatment of the subjects with inhaled corticosteroids. These findings provide a new evidence for a role for ROS and lipid peroxidation in allergen-induced airway inflammation.
Between 1982 and 1987, 139 patients with primary carcinoma of the lung were treated with pneumonectomy. Thirty-nine patients (28%) were in clinical stage I, 10 (7%) were in clinical stage II, and 90 (65%) were in clinical stage III. Overall actuarial 3-year survival was 33%. Actuarial 3-year survival for patients in clinical stage I was 44%; for those in clinical stage II, 48%; and for those in clinical stage III, 28%. Risk factors for operative mortality examined included preoperative forced vital capacity (FVC) of 2.13 L or less and forced expiratory volume in 1 second (FEV1) of 1.65 L or less, percent predicted FVC of 64% or less and FEV1 of 65% or less, predicted postoperative FVC of 1.31 L or less and FEV1 of 0.89 L or less, and predicted postoperative percent predicted FVC of 41% or less and FEV1 of 34% or less. Operative deaths occurred only in clinical stage III patients (7/90 or 8%). Patients with compromised pulmonary function based on one or more of the examined risk factors were at increased risk for death (2/10) compared with patients with better pulmonary function (5/80 or 6.25%). Actuarial 3-year survival for high-risk clinical stage III patients ranged from 0% to 16% compared with 28% for other clinical stage III patients. Thirty-day mortality for pathological stage III patients was 6.3% (5/79), and 3-year actuarial survival was 24%. No patient in pathological stage III who was at high risk survived beyond 3.1 years. Select individuals with adequate pulmonary function and stage III disease can achieve substantial long-term survival after pneumonectomy.(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise testing was performed on 37 patients with resectable lung lesions who were deemed inoperable because of any of the following risk factors: (1) FEV1 less than or equal to 40 percent of predicted; (2) radionuclide calculated postlobectomy FEV1 less than or equal to 33 percent of predicted; or (3) arterial PCO2 greater than or equal to 45 mm Hg. The patients who reached a peak level of oxygen consumption during exercise (VO2Peak) of greater than or equal to 15 ml/kg/min were offered surgical treatment. Patients with a VO2Peak of less than 15 ml/kg/min were referred for nonsurgical management and excluded from the study. Eight patients underwent lung resection. Their pulmonary function revealed a severe obstructive lung defect with a group mean predicted FEV1 of 40 +/- 6 percent, an FEV1/FVC ratio of 47 +/- 10, a radionuclide calculated postlobectomy FEV1 of 31 +/- 4 percent, and a mean arterial PCO2 of 44 +/- 6 mm Hg. No relationship was found between each patient's exercise performance and spirometric function. Six of the patients had an uncomplicated postoperative course. Two patients had complications but no patient died as a result of surgery or postoperative complications. All patients were discharged from the hospital within 22 days (mean = 9.8 days). We conclude that exercise testing is a useful complement to conventional cardiopulmonary evaluation used in selecting patients for lung resection.