Are Changes in Breathing Pattern on Exposure to Ozone Related to Changes in Pulmonary Surfactant?

Finlayson-Pitts, Barbara J.; Mautz, William J.; Lai, Ching-Yi; Bufalino, Charles; Messer, Karen; Mestas, J.; Koch, H. U.; Lucio, Lorena M.C.

doi:10.3109/08958379408995236

Cited by 10 publications

(10 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, at 1 .O ppm, following an initial, transient decline in V, a sustained slight increase in both frequency a n d V, was observed. This is not consistent with rapid/shallow breathing measured i n rats restrained in tube-type plethysmographs while exposed to 0.8 ppm (Mautz & Bufalino, 1989;Finlayson-Pitts et al, 1994). In addition, in the present study a rapid/shallow breathing pattern was observed in 4 non-test lactating rats exposed to 1.0 ppm ozone i n tube holders modified as flow plethysmographs (discussed later).…”

Section: Discussioncontrasting

confidence: 99%

Enhanced Pulmonary Inflammatory Response to Ozone During Lactation in Rats: Evaluation of the Influence of Inhaled Dose

Weideman

Chen

Gunnison

1996

Inhalation Toxicology

View full text Add to dashboard Cite

We previously demonstrated that rats in a late stage of pregnancy and throughout lactation were more susceptible to pulmonary inflammation induced by exposure to 1 ppm ozone than were age-matched virgin females or rats following lactation. The purpose of the study reported here was to extend the comparison of ozone-induced pulmonary inflammation in lactating and postlactating rats to lower concentrations of ozone and to investigate the hypothesis that the enhanced response demonstrated by lactating rats is attributable to a greater inhaled ozone dose. During pregnancy and lactation the metabolic demands on the female are substantially increased above prepregnancy levels. In response to this metabolic demand, it was shown in this study that the minute volume of air-breathing postpartum rats on day 73 of lactation increased to approximately 150% of that of age-matched postlactating rats with the same lung size. Heightened ventilation in lactating rats was maintained during exposure to 0.3, 0.5, and 1.0 ppm ozone for 6 h, resulting in greater inhaled ozone doses in lactating rats compared to postlactating rats exposed identically. The pulmonary inflammatory response to ozone was assessed in the same rats 18 h after expcsure by comparison of protein concentration and polymorphonuclear cell (PMN) numbers in bronchoalveolar lavage fluid ( B A LF).Both of these parameters were significantly greater m lactating than postlactating rats at 0.3, 0.5, and 1.0ppm ozone. Statistical analysis indicated that most or all of the greater BALF protein in lactating rats could be accounted for by their greater inhaled dose, whereas a significant portion of the enhanced PMN influx in lactating rats remained unexplained by inhaled ozone dose.A recent study from this laboratory demonstrated that acute exposure to 1 ppm ozone induced more severe pulmonary inflammation in late-stage pregnant and lactating rats than in age-matched virgin females or postlactating rats (Gunnison et al., 1992). The experiments described here were undertaken to confirm, at lower ozone concentrations, this earlier observation, and to explore the hypothesis that the enhanced inflammatory response of lactating rats relative to that of postlactating or virgin female rats is attributable to a greater inhaled dose in the lactating rats.

show abstract

Section: Discussioncontrasting

confidence: 99%

Enhanced Pulmonary Inflammatory Response to Ozone During Lactation in Rats: Evaluation of the Influence of Inhaled Dose

Weideman

Chen

Gunnison

1996

Inhalation Toxicology

View full text Add to dashboard Cite

show abstract

“…The fatty acid composition changed in favor of the saturated species. As the lavage of these rats did not contain elevated levels of proteins, changes in the fatty acid composition must result from direct reaction with 03 before epithelial damage has manifested [26]. There is substantial evidence that oxidation of unsaturated fatty acids in surfactant occurs in vivo [22].…”

Section: Stratospheric Generation Of 0 3 (Ozone Layer)mentioning

confidence: 93%

“…Plasma proteins present in edema are known to inhibit surfactant function [53,127]. Exposing rats to 0.8 ppm 03 for 4 h did not reveal any effect on surfactant function [26]. The fatty acid composition changed in favor of the saturated species.…”

Section: Stratospheric Generation Of 0 3 (Ozone Layer)mentioning

confidence: 99%

Toxic oxidant species and their impact on the pulmonary surfactant system

Putman

Golde

Haagsman

1997

Lung

View full text Add to dashboard Cite

In this review the effects of oxidant inhalation on the pulmonary surfactant system of laboratory animals are discussed. Oxidant lung injury is a complex phenomenon with many aspects. Inhaled oxidants interact primarily with the epithelial lining fluid (ELF), a thin layer covering the epithelial cells of the lung which contains surfactant and antioxidants. In the upper airways this layer is thick and contains high levels of antioxidants. Therefore oxidant injury in this area is rare and is more common in the lower airways where the ELF is thin and contains fewer antioxidants. In the ELF oxidants can react with antioxidants or biomolecules, resulting in inactivation of the biomolecules or in the formation of even more reactive agents. Oxidation of extracellular surfactant constituents may impair its function and affect breathing. Oxidized ELF constituents may promote inflammation and edema, which will impair the surfactant system further. Animal species differences in respiratory tract anatomy, ventilatory rate, and antioxidant levels influence susceptibility to oxidants. The oxidant exposure dose dictates injury, subsequent repair processes, and tolerance induction.

show abstract

“…O 3 and NO 2 however are known to alter the surfactant phospholipids chemically. As analysed in lavages from O 3 ‐exposed animals, the portion of unsaturated fatty acids in PC is decreased [ 73, 109–111]. However, opposite results were also reported [ 104].…”

Section: Toxicitymentioning

confidence: 99%

Effect of air pollutants on the pulmonary surfactant system

Müller

Seifart

Barth

1998

Eur J Clin Investigation

View full text Add to dashboard Cite

Air pollutants have been recognized to influence the structure and function of the surfactant system. Agents that have received the most attention include ozone, nitrogen dioxide, hyperoxia, diesel exhaust, tobacco smoke, silica and fibrous materials such as asbestos. The deleterious effects of air pollutants on the surfactant system depend on the size of the agent, on its solubility in aqueous solutions and chemical reactivity and on its concentration and the duration of exposure. Hereby the following general rules apply: the smaller the agent's size and the less water soluble the pollutant is, the greater the tendency to reach the alveoli during breathing. In addition, the reactivity also determines the depth of penetration into alveoli. Compounds with high reactivity such as O 3 , which also fulfil the earlier rules, will react with the upper respiratory tract compared with compounds with slightly reduced reactivity, such as NO 2 , which will penetrate the alveoli. The common consequence of exposure to air pollutants is an accumulation of surfactant phospholipids and surfactant-specific proteins in the bronchoalveolar lavage fluid. These components also are structurally altered, mainly by oxidant gases, resulting in impairment of their biological activity. Thus, for surfactant phospholipids, there is impaired adsorption to the air-liquid interface due to oxidation of their fatty acids. Also, surfactant protein A, regarded as a modulator of the surfactant system, shows impaired functions after exposure to oxidants. It is likely that in addition to the effects described in this review not all effects are known because the molecular effects of several key components (e.g SP-B and C) have not been well studied.

show abstract

Are Changes in Breathing Pattern on Exposure to Ozone Related to Changes in Pulmonary Surfactant?

Cited by 10 publications

References 54 publications

Enhanced Pulmonary Inflammatory Response to Ozone During Lactation in Rats: Evaluation of the Influence of Inhaled Dose

Enhanced Pulmonary Inflammatory Response to Ozone During Lactation in Rats: Evaluation of the Influence of Inhaled Dose

Toxic oxidant species and their impact on the pulmonary surfactant system

Effect of air pollutants on the pulmonary surfactant system

Contact Info

Product

Resources

About