Nitrogen dioxide exposure: effects on airway and blood cells

Abstract

This study examined the effects of nitrogen dioxide (NO(2)) exposure on airway inflammation, blood cells, and antiviral respiratory defense. Twenty-one healthy volunteers were exposed on separate occasions to air and 0.6 and 1.5 ppm NO(2) for 3 h with intermittent moderate exercise. Phlebotomy and bronchoscopy were performed 3.5 h after each exposure, and recovered cells were challenged with respiratory viruses in vitro. Blood studies revealed a 4.1% NO(2) dose-related decrease in hematocrit (P = 0.003). Circulating total lymphocytes (P = 0.024) and T lymphocytes (P = 0.049) decreased with NO(2) exposure. Exposure to NO(2) increased the blood lymphocyte CD4(+)-to-CD8(+) ratio from 1.74 +/- 0.11 to 1.85 +/- 0.12 in males but decreased it from 1.88 +/- 0.19 to 1.78 +/- 0.19 in females (P < 0.001 for gender difference). Polymorphonuclear leukocytes in bronchial lavage increased with NO(2) exposure (P = 0.003). Bronchial epithelial cells obtained after exposure to 1.5 ppm NO(2) released 40% more lactate dehydrogenase after challenge with respiratory syncytial virus than with air exposure (P = 0.024). In healthy subjects, exposures to NO(2) at levels found indoors cause mild airway inflammation, effects on blood cells, and increased susceptibility of airway epithelial cells to injury from respiratory viruses.

Indoor NO2 air pollution and lung function of professional cooks

“…Frampton et al (35) found an inflammatory response that persisted at least 18 h after exposure, while Blomberg et al (36) demonstrated major decrements in FEV 1 just after exposure and this lung function indicator response was attenuated after repeated exposures, even in the presence of a persistent neutrophilic inflammation in the airways. They concluded that NO 2 is a proinflammatory air pollutant under conditions of repeated exposure.…”

“…Experimental studies on healthy nonsmoking subjects have shown that adverse inflammatory effects on the airways may occur due to acute exposure to NO 2 (2 ppm) and can be determined by bronchoalveolar lavage (35) and FEV 1 measurements (36). Frampton et al (35) found an inflammatory response that persisted at least 18 h after exposure, while Blomberg et al (36) demonstrated major decrements in FEV 1 just after exposure and this lung function indicator response was attenuated after repeated exposures, even in the presence of a persistent neutrophilic inflammation in the airways.…”

Exposure to air pollution and pulmonary function in university students

“…However, the mechanism of NO 2 toxicity on the airway is quite complex, and the toxicity varies depending on the dose, length, and the way of exposure. A meta-analysis of epidemiological studies for NO 2 effects reported that a 16-ppb increase in NO 2 level was associated with a 20% increase in the odds ratio of respiratory illness, whereas a clinical study indicates that a biologically effective dose of NO 2 was 600 ppb (Hasselblad et al 1992;Frampton et al 2002). NO 2 can reach the lower respiratory tract in the lung due to its limited solubility (Frampton et al 2002;Muller et al 1998).…”

“…A meta-analysis of epidemiological studies for NO 2 effects reported that a 16-ppb increase in NO 2 level was associated with a 20% increase in the odds ratio of respiratory illness, whereas a clinical study indicates that a biologically effective dose of NO 2 was 600 ppb (Hasselblad et al 1992;Frampton et al 2002). NO 2 can reach the lower respiratory tract in the lung due to its limited solubility (Frampton et al 2002;Muller et al 1998). Then, NO 2 could interact with the respiratory epithelial cell surface and produce reactive oxygen and nitrogen species (Persinger et al 2001;Frampton et al 2002).…”

“…NO 2 can reach the lower respiratory tract in the lung due to its limited solubility (Frampton et al 2002;Muller et al 1998). Then, NO 2 could interact with the respiratory epithelial cell surface and produce reactive oxygen and nitrogen species (Persinger et al 2001;Frampton et al 2002). Respiratory epithelial toxicity resulting from exposure to air pollutants may also be mediated by the products formed by NO 2 and epithelial lining fluids, rather than by direct interaction between NO 2 and the cell surface (van der Vliet and Cross 2000).…”