Donald H. Horstman

Comparison of Pulmonary Responses of Asthmatic and Nonasthmatic Subjects Performing Light Exercise While Exposed to a Low Level of Ozone

To determine if asthmatic subjects (ASTH, n = 17) experience greater O3 induced pulmonary decrements than nonasthmatic subjects (NONA, n = 13), both groups were exposed for 7.6 h to both clean air and 0.16 ppm 03. Exposures consisted of seven 50-min periods of light exercise (VE = 14.2 and 15.3 l/min/m2 for ASTH and NONA, respectively), each followed by 10 min rest. A 35-min lunch period followed the third exercise. Following 03 exposure, decrements in forced expiratory volume in one second (FEV1) and FEV1 divided by forced vital capacity (FVC), corrected for air exposure, for ASTH

Airway sensitivity of asthmatics to sulfur dioxide

The purpose of this study was to describe for asthmatic subjects the distribution of individual bronchial sensitivity to sulfur dioxide (SO2). Subjects were nonsmoking male asthmatics (n = 27) who were sensitive to inhaled methacholine. None of the subjects used corticosteroids or cromolyn sodium. Oral medications were with held for 48 hr, inhaled medications for 12 hr prior to all testing. Each subject participated in four separate randomly ordered 10 min exposures to 0.00, 0.25, 0.50 and 1.00 ppm SO2 at 26° C, 70% relative humidity. During exposures, subjects breathed naturally and performed moderate exercise (VE, normalized for body surface area = 21 l/m2 x min). Before and 3 min after exposure, specific airway resistance (SRaw) was measured by body plethysmography. Those subjects whose SRaw was not doubled by exposure to 1.00 ppm were also exposed to 2.00 ppm S02. Dose response curves (relative change in SRaw, corrected for change in clean air vs S02 concentration) were constructed for each subject. Bronchial sensi tivity to SO2 [PC(SO2)], defined as the concentration of S02 which provoked an increase in SRaw 100% greater than the response to clean air, was determined. Substantial variability in sensitivity was observed: for 23 subjects, PC(SO2) ranged between 0.28 and 1.90 ppm, while for the remaining 4 subjects, it was greater than 2.00- ppm S02. The median PC(SO2) was 0.75 ppm SO2, and 6 subjects had a PC(SO2) of less than 0.50 ppm. PC(SO2) was not related (r = 0.31) to airway sensitivity to methacholine.

Lack of effect of low levels of carboxyhemoglobin on cardiovascular function in patients with ischemic heart disease.

We studied 30 patients 38-75 yr of age who had ischemic heart disease to assess the effect of acute elevation of carboxyhemoglobin (COHb) concentration. Patients were nonsmokers with ischemia defined by exercise-induced ST depression (ST decreases)--25/30, angina--23/30, or abnormal ejection fraction (EF) response--18/30. After an initial familiarization and exercise session patients were exposed to air (carboxyhemoglobin [COHb] = 1.5 +/- 0.05%) and to carbon monoxide (CO) (100 ppm-COHb-average = 3.8 +/- 0.1%) on successive days in a double blind, randomized fashion. There was no significant difference in time to onset of angina (air = 312 sec, CO = 306 sec), maximal exercise time (air = 711 sec, CO = 702 sec), maximal ST decreases (1.5 mm for both), or time to significant ST decreases (air = 474 sec, CO = 475 sec). Double product at ST decreases and maximal double products were similar for both conditions. Resting ejection fraction was slightly but nonsignificantly higher after CO exposure (air = 53.9%, CO = 55.2%). Maximal ejection fraction was similar for both conditions (air = 57.4%, CO = 57.1%). Change in ejection fraction was slightly lower for CO exposure (air = 3.5%, CO = 2%), p = .049. In conclusion, there is no clinically significant effect of 3.8% COHb (representing a 2.2% increase from resting values) on the cardiovascular system in this study.

The Relationship Between Exposure Duration and Sulfur Dioxide-Induced Bronchoconstriction in Asthmatic Subjects

The purpose of this study was to determine the shortest duration of exposure to 1.0 ppm sulfur dioxide (SO2) sufficient to induce bronchoconstriction significantly greater than that observed with exposure to clean air (CA) in exercising SO2-sensitive asthmatics. Asymptomatic, nonmedicated, male asthmatics (n = 12) with airway hyperresponsiveness to both methacholine and SO2 were exposed in a chamber (20 degrees C, 40% relative humidity) for 0.0, 0.5, 1.0, 2.0 and 5.0 min to both CA and 1.0 ppm SO2 on separate days (10 exposures). Just prior to each exposure, subjects walked on a treadmill in CA for 5 min at a predetermined speed/elevation to elicit a target ventilation of about 40 L/min, i.e., a brisk pace up a slight incline. After this walk, subjects rapidly entered an adjoining exposure chamber containing either CA or SO2 and immediately walked at the same speed/elevation for the specified exposure duration. Subjects then rapidly exited the chamber. Specific airway resistance (SRaw) and ratings of respiratory symptoms associated with asthma [shortness of breath/chest discomfort (SB/CD) and wheezing (WHZ)] were measured prior to any exercise and following each exposure. Postexposure SRaw and symptom ratings increased with increased exposure duration in SO2; postexposure SRaw also was increased with increased exposure duration in CA but to a lesser extent. After adjusting for the CA response, significantly greater SO2-induced bronchoconstriction was observed for the 2.0 and 5.0 min exposures as indicated by substantially greater increases in SRaw and substantially higher ratings of respiratory symptoms. The authors conclude that with the above exposure conditions, on average, SO2-sensitive asthmatics exhibit significant bronchoconstriction at exposure durations of 2.0 min or more.

The respiratory responses of subjects with allergic rhinitis to ozone exposure and their relationship to nonspecific airway reactivity.

Ozone exposure in man produces changes in respiratory function and symptoms. There is a large degree of unexplained intersubject variability in the magnitude of these responses. There is concern that individuals with chronic respiratory diseases may also be more responsive to ozone than normal individuals. The purpose of this study was to describe the responses of subjects with allergic rhinitis to ozone exposure and to compare these responses to those pre viously observed in normal individuals. A further purpose was to measure the association of baseline nonspecific airway reactivity with changes in lung function and respiratory symptoms following ozone exposure. A group of 26 nonasthmatic subjects with allergic rhinitis performed a bronchial inhalation challenge with histamine and subsequently underwent two hour exposures to both clean air and to 0.18 part per million ozone with alternating periods of rest and heavy exercise. The airway reactivity of this group of subjects was no greater than that of a comparable group of subjects without allergic rhinitis. The respiratory responses of these subjects to ozone exposure were similar to those previously reported for sub jects without allergic rhinitis with the exception that the allergic rhinitis subjects appeared to have a modestly increased broncho constrictor response compared to normals. Furthermore, we observed no significant relationships between nonspecific airway reactivity and response to ozone as measured by changes in lung function or the induction of symptoms.

Effects of submicronic sulfuric acid aerosol on human pulmonary function

The effects of a 4-hr exposure in an environmental chamber to an average 108 micrograms/m3 sulfuric acid (H2SO4 (MMAD, 0.5 micrograms)] on pulmonary function were examined in healthy young men. Subjects were randomly assigned to either experimental (N = 18) or control (N = 17) groups. All subjects were exposed to clean air on the first day. On the second day, experimental subjects were exposed to H2SO4 while control subjects were re-exposed to air. Subjects exercised for 15 min at 1.5 and 3.5 hr of exposure at an intensity equivalent to 75% of predicted maximal heart rate. Ventilation was monitored during the initial 14 min of each exposure. Pulmonary function was assessed prior to, and 2 hr and 4 hr of each exposure. Exposure to H2SO4 had no significant effect on minute ventilation, respiratory frequency, or tidal volume, nor did it affect pulmonary function as assessed by measures of airway resistance, specific airway conductance, forced vital capacity (FVC), forced expiratory flow in 1 sec (FEV 1.0), FEV 1.0/FVC, mean expiratory flow rate between 25% and 75% FVC, and expiratory flow rate at 50% and 25% FVC. It was concluded that no changes in pulmonary function resulted from exposure to H2SO4 under the above conditions.

Exposure to Nitric Acid Stimulates Human Alveolar Macrophage Function But Does Not Cause Inflammation or Changes in Lung Function

AbstractNitric acid (HNO3) is common component of air pollution possibly associated with increased risk for airway infection, airway injury, and inflammation. Jo experimentally address this question, we exposed 9 healthy nonsmoking volunteers once to HNO3 vapor (200 μg/m3, 0.08 ppm), and once to filtered air, for 2 h with 100 min of moderate intermittent exercise (ventilation rate 39 L/min). Pulmonary functions (spirometry and airway resistance) were measured, as were subjective symptoms of response. Bronchoaiveolar lavage (BAL) was performed 18 h after exposure, and cells and fluid were analyzed for indicators of airway injury and inflammation. As a measure of host defense capability against infectious disease, alveolar macrophages (AM) were tested for phagocytosis of Candida albicans and for susceptibility to infection with respiratory syncytial virus (RSV). Exposure to HNO3 did not change pulmonary function nor measures of symptoms. Compared to air-exposed BAL, there was no significant increase in prot...

Red Blood Cell Antioxidants in Human Volunteers Exposed to Ozone

Indices of red blood cell (RBC) antioxidant capacity can undergo changes upon exposure to oxidants, either acutely or chronically. To investigate whether these changes might provide a biochemical marker for acute environmental ozone exposure, we assessed RBC glutathione (GSH) and catalase (CAT) responses in seven normal volunteers exposed to 0.16 ppm ozone for 7.5 hours compared to the same measurements following sham exposure to clean air. For each subject, an interim period of two weeks separated the two exposure studies. Investigators performing the RBC assays were unaware of the environmental conditions. No changes in either GSH or CAT were observed for any study condition when compared to pre-study values. Our conclusion is that RBC antioxidants do not accurately reflect in vivo exposure to ozone at concentrations readily attainable during periods of heavy urban pollution. Our data dispute the value of these indices as markers of acute environmental photochemical oxidant exposure.