Effects of NO 2 on Chronic Bronchitics

Abstract

The acute influence of NO2 on mechanics of breathing and respiratory gas exchange was investigated in a total of 111 subjects, aged 25 to 74 years, with chronic nonspecific lung disease (CNSLD). They breathed NO2-air mixtures containing 0.5 to 8.0 ppm NO2 for up to 15 to 60 min. Additionally in nine subjects the protective action of atropine, meclastine, and orciprenaline was investigated.While the alveolar P02 remained nearly constant during inhalation of 5 and 4 ppm NO2, a significant decrease of the arterial P02 and a corresponding increase of the arterial to alveolar P02 gradients occurred. Inhalation of 2 ppm NO2 had not such an effect.Inhalation of NO2 at concentrations down to 1.5 ppm resulted in a significant increase of airway resistance. Lower concentrations had no significant effect.Prolongation of the exposure period from 15 to 60 min at a NO2 concentration of 5 ppm did not result in a more pronounced disturbance of the respiratory gas exchange for oxygen beyond the extent observed after exposure to 5 ppm NO2 for 15 min.Meclastine, in comparison with orciprenaline and atropine, showed a pronounced protective effect on the negative impact of NO2 on respiratory gas exchange and airway resistance.It is concluded that NO2 may act by release of histamine, causing a bronchiolar, alveolar, and interstitial edema, thus differing from irritant air pollutants like SO2, where reflex bronchoconstriction causes in some bronchitics dramatic increases of airway resistance at similar low concentrations.

Nitrogen Dioxide Air Pollution near Ambient Levels is an Atherogenic Risk Primarily in Obese Subjects: A Brief Communication

“…In addition, levels as high as 0.5-0.6 ppm of nitrogen dioxide have been demonstrated in the vicinity of an operating gas stove (15). In the present study, it is striking that the atherogenic effects of nitrogen dioxide are shown primarily at a concentration of 0.16 ppm, which is near ambient levels, but less at higher toxic concentrations, Comparable results have been demonstrated by a previous human study: nitrogen dioxide exposure significantly increased airway resistance at a relatively low concentration (1.5 ppm), but not at higher concentrations up to 8.0 ppm (16). It has been reported that several of the dose-response curves for health effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin are It-shaped, which appears to result because the integrated toxicologic response depends on multiple underlying processes, each of which has a different relationship with respect to the pollutant (17).…”

Measurement of Respiratory Mechanics with Forced Oscillations

“…Recent reports confirmed the validity of this device in the area of bronchial challenges [1,17], in the study of bronchodilators [11,23] or its usefulness in pediatrics [2,9]. Furthermore, recent results point to the fact that a modification of the device reveals features typical of various lung diseases [12,13], Therefore, in our opinion the Siregnost FD 5 can be considered as a beneficial com pletion of the hitherto existing spirographic and body plethysmographic methods despite the limitations mentioned above.…”

Conceptual model for assessing criteria air pollutants in a multipollutant context: A modified adverse outcome pathway approach

“…SO 2 inhalation increased airway resistance, especially in adult asthmatics (Johns and Linn, 2011). Modest increases in airway resistance occurred in healthy humans exposed to O 3 (Hazucha et al, 1989) and in chronic bronchitics exposed to NO 2 (von Nieding and Wagner, 1979). Pharmacologic studies provided insight into the mechanisms underlying these responses.…”

“…Partial inhibition of SO 2 -induced increases in airway resistance by cromolyn sodium, a mast cell stabilizing agent, suggested that inflammatory mediators released by mast cells (e.g., histamine) also contributed to the response in asthmatics. Atropine inhibited O 3 -induced increases in airway resistance in healthy humans (Beckett et al, 1985), but failed to inhibit NO 2 -induced increases in airway resistance in chronic bronchitics (von Nieding and Wagner, 1979). However, a histamine-suppressing agent blocked the NO 2 response.…”