Research Shows That Ozone Induces Inflammation
In the s, one other response to exposure has been identified and acknowledged as important in the medical literature. This involves inflammationthe body’s response to trauma, infection, or irritation. At rest, exposure results in biochemical changes that stimulate the production of neutrophil cells and mediators of inflammation in the nasal cavity and upper airways, because as much as of inspired ozone collects at those sites during quiet nose breathing.
During exercise, inflammation also may occur deeper in the lung. A recent study attempted to clarify the unexplained relationship between O-induced airway inflammation and decreased inspiratory capacity. Ten test subjects consumed either the nonsteroidal anti-inflammatory drug ibuprofen or a placebo pill, ath before and at the midpoint of each experiment. The pollutant exposure for included of intermittent exercise. Although ibuprofen had no effect on neutrophil production, it significantly reduced the levels of known mediators of inflammation prostaglandin E, thromboxane B and the levels of interleukin-, a protein that enhances immmune responses. Because these changes were concurrent with a blunting of the usual decrease in FEVP this study supported a connection between the natural compounds that mediate inflammation and pulmonary impairment.
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With regard to exposure levels, it has been shown that exercising exposure to for and exposure to forh both resulted in biochemical changes similar to those described above. In the latter condition, increases in lung fluid neutrophils, prostaglandin E, fibronectin, interleukin-, and a decrease in the phagocytic engulfing activity of alveolar macrophage cells all indicated obvious inflammatory and immune system reactions to ozone in the lung. This concentration is considered to be a low-level, prolonged exposure that would be common in most large cities around the world.- It also suggests that virtually all previous exercise studies have induced some degree of inflammation in bronchial tubes or lung tissue, because these studies have utilized levels ranging fromto and have involved increased ventilation fromh to h, indicating large effective doses.’
Could inflammatory responses be involved in some aspects of the O-induced impairment of pulmonary function, maximal exercise performance, or VO max? Yes but clarification of the exact mechanisms awaits future research. It also is possible that edema fluid accumulation, swelling, a hallmark of inflammation, may be involved. An early report suggested that some pulmonary edema occurred after a exposure to ozone in concentrations of Exercise-induced increases in blood pressure could further increase fluid movements into the space between cells interstitial space or into/between alveoli, thereby potentially impairing oxygen and carbon dioxide gas diffusion across alveolar capillary membranes.
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