Larry R. Sauder

Duration of pulmonary function adaptation to ozone in humans

The duration of pulmonary function adaptation subsequent to cessation of a 5-day repeated ozone (O3) exposure was studied in 24 nonsmoking human subjects. A three-week, 3 hr/day study was conducted. The subjects received filtered air on Week 1 and 0.4 ppm O3 on Week 2. During Week 3, 13 subjects were re-exposed to O3 on Friday and 11 were re-exposed to O3 on Tuesday. Spirometric measurements (FVC and FEV1) and bronchial reactivity to methacholine showed adaptation within 2-3 days of the repeated daily exposures (Week 2). Although the duration of adaptation seen with bronchial reactivity appears longer than 7-days, the FVC and FEV1 clearly demonstrated complete loss of adaptation by 7 days, with a trend toward significance by 4 days. We conclude, therefore, the loss of ozone adaptation in pulmonary function is a gradual phenomenon lasting less than 7 days following cessation of repeated daily exposures.

Acute Pulmonary Response of Asthmatics to 3.0 PPM Formaldehyde

Previous studies have failed to demonstrate bronchoconstriction in unselected asthmatics after brief (≤ 1/2-h), controlled exposures to formaldehyde (HCHO). This study was designed to evaluate the acute pulmonary response to 3 ppm HCHO in nine nonsmoking asthmatic volunteers over a more relevant exposure duration (3 hrs). Pulmonary function, nonspecific airway reactivity and symp toms were assessed before and at intervals during the exposure. No significant changes in pulmonary function (FVC, FEV 1 , FEF 25-27% , SGaw, or FRC) or airway reactivity were observed. There was a significant increase in nose/throat irritation at 30 min. (P < 0.05) and in eye irritation at 60 min (P < 0.05) and 180 min (P < 0.01). These results suggest that individuals with asthma will not expe rience significant bronchoconstriction when exposed at rest to 3 ppm HCHO; however, most will experience eye and upper respira tory tract irritation.

Formaldehyde dose-response in healthy nonsmokers.

Industrial, commercial, and domestic levels of formaldehyde exposure range from 5.0 ppm. Irritation of the eyes and upper respiratory tract predominate, and bronchoconstriction is described in case reports. However, pulmonary function and irritant symptoms together have not been assessed over a range of HCHO concentrations in a controlled environment. We investigated dose response in both symptoms and pulmonary function associated with 3-h exposures to 0.0-3.0 ppm HCHO in a controlled environmental chamber. Ten subjects were randomly exposed to 0.0, 0.5, 1.0, and 2.0 ppm HCHO at rest plus 2.0 ppm HCHO with exercise and nine additional subjects were randomly exposed to 0.0,1.0,2.0, and 3.0 ppm HCHO at rest plus 2.0 ppm HCHO with exercise. Significant dose-response relationships in odor and eye irritation were observed (p < 0.05). Nasal flow resistance was increased at 3.0 ppm (p < 0.01), but not at 2.0 ppm HCHO. There were no significant decrements in pulmonary function (FVC, FEV1, FEF25-75%, SGaw...

Tobacco Smoke Upper Respiratory Response Relationships in Healthy Nonsmokers

This study determined exposure-response relationships to side-stream tobacco smoke (2 hrs; 0, 1, 5, and 15 ppm CO) in 29 healthy nonsmoking young adults. Sixteen subjects had no history of environmental tobacco smoke rhinitis (ETS-NS) while 13 subjects had a history of ETS rhinitis (ETS-S). Eye irritation and odor perception showed a statistically significant exposure response in both groups; headache was significant in ETS-S and nose irritation was significant in ETS-NS subjects. Significant postexposure (P1) symptoms were first reported at 1 ppm CO among both groups, but in 3/9 symptoms were significantly greater at this exposure level in ETS-S subjects. Nasal congestion, rhinorrhea, and cough increased significantly at 15 ppm CO only. In ETS-S subjects, nasal volume decreased and nasal resistance increased in an exposure-response fashion. ETS-NS subjects had a qualitatively different shape to the exposure-response curve; significant dimensional reductions in mid- and posterior nasal volume occurred with exposure at 1 ppm CO but not at 5 ppm CO and reductions in posterior nasal volume occurred at 15 ppm CO exposure. These studies indicate subjective and objective response relationships with exposure to sidestream tobacco smoke at concentrations from 1 to 15 ppm CO. Some differences are noted among the two subject groups in the magnitude of some symptoms at the lowest exposure level and in the qualitative shape of the acoustic rhinometry and nasal resistance exposure-response curves.

Acute pulmonary response in healthy, nonsmoking adults to inhalation of formaldehyde and carbon.

Formaldehyde (HCHO) is a common chemical found in occupational and residential environments and has been suggested as a cause of asthmalike symptoms in some individuals. Clinical and animal studies suggest that HCHO adsorbed on respirable particles may elicit a greater pulmonary physiologic and inflammatory effect than gaseous HCHO alone. The purpose of this study was to determine if respirable carbon particles have a synergistic effect on the acute symptomatic and pulmonary physiologic response to HCHO inhalation. We randomly exposed 24 normal, nonsmoking, methacholine-nonreactive subjects to 2 h each of clean air, 3 ppm formaldehyde, 0.5 mg/m3 respirable activated carbon aerosol, and the combination of 3 ppm formaldehyde plus activated carbon aerosol. The subjects engaged in intermittent heavy bicycle exercise (VE = 57 l/min) for 15 min each half hour. Measures of response included symptom questionnaires, spirometry, body plethysmography, and postexposure serial peak flows. Formaldehyde exposure was associated with significant increases in reported eye irritation, nasal irritation, throat irritation, headache, chest discomfort, and odor. We observed synergistic increases in cough, but not in other irritant respiratory tract symptoms, with inhalation of formaldehyde and carbon. Small (less than 5%) synergistic decreases in FVC and FEV3 were also seen. We observed no HCHO effect on FEV1; however, we did observe small (less than 10%) significant decreases in FEF25-75% and SGaw which may be indicative of increased airway tone. Overall, our results demonstrated synergism, but the effect is small and its clinical significance is uncertain.

Pulmonary function adaptation to ozone in subjects with chronic bronchitis.

Twenty smokers with chronic bronchitis were exposed to 0.41 ppm ozone for 3 hr-day for 5 consecutive days and reexposed 4 days later to determine (1) if they are sensitive to ozone, (2) if they adapt, and (3) if the adaptation lasts longer than 4 days. There were significant decrements in forced vital capacity (FVC) and forced expiratory volume in 3 sec ( FEV3 ) on the first day of the 5-day repeated exposures and also on reexposure 4 days following cessation of the sequential exposures. Symptoms experienced were mild and did not predominate on any exposure days. These results suggest that individuals with chronic bronchitis adapt rapidly to ozone and lose this adaptive phenomenon within 4 days. The small decreases seen in FVC and FEV3 (less than or equal to 3%) appear to impose no more than minimal limitations on their daily activities.

Sulfur Dioxide and Ammonium Sulfate Effects on Pulmonary Function and Bronchial Reactivity in Human Subjects

The effect of exposures to 1 ppm sulfur dioxide (SO2) and 500 micrograms/m3 respirable ammonium sulfate [(NH4)2SO4] was studied in 20 nonsmoking subjects to determine if a response can be measured at these atmospheric levels and if the response is additive or synergistic. Four-hour separate and combined exposures were employed. Each subject acted as his or her own control and performed two light-to-moderate exercise stints (612 kg-m/min) for 15 minutes on each days confinement in the environmental chamber. Pulmonary function tests (body plethysmography and spirometry) and bronchial reactivity to methacholine were performed to assess the response of these exposures. No significant changes in pulmonary function or bronchial reactivity were observed in the individual exposures [(NH4)2SO4 or SO2], the combined exposure [(NH4)2SO4 and SO2], or 24 hours post-exposure. This study design and the observed results did not demonstrate any readily apparent risk to healthy subjects with these exposures. Since no significant changes were measured, it was not possible to conclude if these two pollutants in combination produce an additive or synergistic response.