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PubMedDate not supplied

Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide.

Nitrogen dioxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system that also exhibits tolerance. It was found that when hamsters are preexposed daily to 10 ppm NO2, they develop tolerance for normally lethal concentrations of NO2, are protected against cytological injury from 10 ppm NO2, but are not protected from the cytotoxic effects of NO2 at concentrations greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytological injury induced by weekly exposures to 10 ppm NO2, but do develop tolerance for lethal concentrations of NO2. Thus, the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.

Animals↗
PubMedDate not supplied

Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide.

Nitrogen idoxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system which also exhibits tolerance. It was found that when hamsters are preexposured daily to 10 ppm NO2, they develop tolerance against normally lethal concentrations of NO2; are protected against further cytological injury from 10 ppmNO2; but are not protected from the cytotoxic effects of NO2 greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytotological injury induced byweekly exposures to 10 ppm NO2, but do develop tolerance against lethal concentrations of NO2. Thus the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.

Animals↗
PubMed1977

Some effects of nitrogen dioxide on the lung.

Nitrogen dioxide (NO2) when inhaled in different concentrations and for varying times produces pulmonary injuries which are dependent on the anatomic site in the lung and the duration of exposure. Single exposures to high concentrations of NO2 for 5-6 hr produce an intense cellular proliferation which regresses within 48 hr in all lung regions except the terminal respiratory bronchiole region and the alveoli where the proliferation persists for 4-7 days. This same delayed response is also observed in more chronic exposures. Histologically, the lesion in the terminal and respiratory bronchioles may resemble an obliterative bronchiolitis, but the lesion clears if further exposure is terminated. Prolonged exposure to 2 ppm NO2, 20-22 hr per day for 7 days per wk, produces an increase in total pulmonary upstream resistance in animals killed immediately after exposure; this resistence returns to normal values within 3 mo after removal from exposure. The internal surface area (ISA) is decreased after 12 mo exposure to NO2, but this loss of surface progresses during the recovery period in air, suggesting an autonomous progression of the tissue destructive process. Exposure to 3.64 ppm NO2 with and without fly ash for periods of 12-14 mo causes no increase in pulmonary resistance and no alteration in lung surface. Lung phospholipids and protein synthesis appear to be depressed following exposure to NO2. Lecithin is significantly increased. The synthesis of proteases by alveolar macrophages is increased during NO2 exposure. Pigmented alveolar macrophages present in animals exposed to NO2 simulate those found in human lungs of young cigarette smokers in the terminal and respiratory bronchioles. The mechanism of tissue injury by oxidants such as NO2 may involve free radical formation, and peroxidation of lipids or proteins.

Air Pollutants↗
PubMedDate not supplied

Effects of nitrogen dioxide on elastin and collagen contents of lung.

Male Syrian hamsters were exposed to 30 +/- 5 ppm nitrogen dioxide for 22 hr daily for 3 wk. Nitrogen dioxide-exposed hamsters sacrificed at various times during the 3 wk exposure showed a general loss of body weight and an increased dry lung weight when compared with the controls, which were housed in a similar, but nitrogen dioxide-free environment. Analysis of total lung collagen and total lung elastin revealed a net decrease in the moieties within 4 and 10 days, respectively, following commencement of nitrogen dioxide exposure. Total lung collagen returned toward pre-exposure levels by the 14th day of nitrogen dioxide exposure. Total lung elastin did not return toward normal until termination of nitrogen dioxide exposure. Recovery in room air for 3 wk following 21 days of nitrogen dioxide exposure restored the total pulmonary collagen and elastin to valutin and collagen degradation and synthesis differ during and after nitrogen dioxide exposure. Lung collagen loss was observed earlier and was restored to normal values during the continuation of nitrogen dioxide exposure. Lung elastin loss occurred later and persisted during the entire period of exposure but returned to normal after exposure was terminated.

Animals↗
PubMed1979

Combined exposure to ozone and nitrogen dioxide.

A study of rats acutely exposed to ozone (0.5--2.0 ppm) or nitrogen dioxide (2--20 ppm) for 2 hr and sacrificed immediately thereafter shows little similarity in the individual biochemical effects of these pollutants. No evidence of nitrogen dioxide-induced lipid peroxidation was observed. Of interest is the finding that inhalation of nitrogen dioxide increases the extent to which concanavalin A agglutinates alveolar macrophages while ozone has exactly the opposite effect.

Air Pollutants↗
PubMedDate not supplied

Histopathological and histochemical studies of the skin of guinea pigs after long-term exposure to nitrogen dioxide.

Male guinea pigs were exposed to nitrogen dioxide (2 mg/m3) during 180 days (8 hours a day). Long-term exposure induced thickening of the corneal layer of the epidermis as well as inflammatory infiltrations in the proper skin. The following enzymes were estimated histochemically in skin samples of experimental and control animals: succinic dehydrogenase, NADH2-tetrazolium reductase, lactate dehydrogenase; alkaline phosphatase, acid phosphatase and adenosine triphosphatase. Chronic exposrue stimulated a decrease of NADH2-tetrazolium reductase in the epidermis and connective tissue components of proper skin and marked positive reaction of lactate dehydrogenase in epidermal cells and hair follicles. Increase of a diffuse reaction on adenosine triphosphatase in smooth muscles of the skin was found also in exposed animals.

Acid Phosphatase↗
PubMedDate not supplied

Experimental studies on human health effects of air pollutants. IV. Short-term physiological and clinical effects of nitrogen dioxide exposure.

Adult male volunteers were exposed to nitrogen dioxide (NO2) at 1.0 ppm in purified air under conditions simulating ambient photochemical smog exposures (2-hr exposure with intermittent light exercise at 31 degrees C and 35% relative humidity). Sham exposures to purified air alone served as controls. Exposure effects were assessed by pulmonary physiological tests and by a standardized clinical evaluation. No statistically physiological changes attributable to NO2 exposure were found except for a marginal loss in forced vital capacity after exposure on two successive days (1.5% mean decrease, P less than .05). Reported respiratory and other symptoms were slightly increased with exposure as compared to control, but the change was not significant. Short-term toxicity of NO2 at peak ambient concentrations appears to be substantially less than that of ozone in healthy people, but adverse NO2 effects in diseased people or in long-term exposures cannot be ruled out at present.

Adult↗
PubMed1977

Fate and distribution of inhaled nitrogen dioxide in rhesus monkeys.

The intra- and extrapulmonary distributions of inspired nitrogen dioxide (NO2) were studied by exposing rhesus monkeys to air mixtures containing concentrations slightly greater than ambient (0.56 to 1.71 mg per m3, or 0.30 to 0.91 ppm) of NO2 labeled with tracer quantities of NO2 containing nitrogen-13 dioxide (13NO2). The 13NO2 (half-time, 10 min) was synthesized by the oxygen-16 (P, alpha)13N nuclear reaction in an isochronous cyclotron. The intrapulmonary location and concentration of the inspired 13NO2 was detected continuously by external monitoring of the annihilation radiation consequent to positron emissions from disintegrating 13N. The 13N concentration of arterial blood was also measured at intervals, and the blood values were correlated with those from the lung. Chemical measurements of NO2 concentration in inspired and expired air were performed by the Saltman method. Control studies were performed with xenon-125 (125Xe) (halftime, 17 hours). The results demonstrated that 50 to 60% of the inspired pollutant was retained by the primate during quiet respiration; the gas was distributed throughout the lungs. Once absorbed, NO2 or chemical intermediates remained within the lungs for prolonged periods after cessation of exposure, and dissemination of the pollutant or its derivatives to extrapulmonary sites occurred via the blood stream. Indirect evidence indicated the probable reaction of NO2 with water in the nasopharynx and lungs to form nitric and nitrous acids. The reaction of these acids with pulmonary and extrapulmonary tissues probably accounts for the biologic toxicity of NO2.

Animals↗
PubMed1979

Effects of repeated exposures to peak concentrations of nitrogen dioxide and ozone on resistance to streptococcal pneumonia.

Exposures to various mixtures of nitrogen dioxide (NO2) and ozone (O3) reduced the resistance of mice to streptococcal pneumonia as evidenced by increased mortality rates and shortened survival time. Daily 3-h exposures (5 d/wk) for 2--6 mo to an air pollutant mixture consisting of 940 microgram/m3 (0.5 ppm) NO2 and 196 microgram/m3 (0.1 ppm) O3 were most effective in reducing the resistance to infection. The decrease in resistance to the infection occurred sooner than the mice continued to be exposed to the air pollutants instead of clean air for 14 d after the respiratory challenge with Streptococcus pyogenes aerosol. After 3 mo of exposure to the pollutant mixture, there was some decrease in the ability of mice to clear inhalated streptococci from their lungs. At the same time the total cell count in the fluid lavaged from the lungs of mice was markedly reduced, as were the viability and phagocytic activity of the alveolar macrophages. Exposure to the pollutants combined with challenge with Streptococcus aerosol resulted in marked morphological changes in lung tissues as seen by scanning electron microscopy.

Animals↗
PubMedDate not supplied

Nitrogen dioxide and pulmonary proteolytic enzymes. Effect on lung tissue and macrophages.

Hamsters were exposed to 30 ppm nitrogen dioxide (NO2) for 2 and 50 days and sacrificed. Pulmonary lavage was carried out on a portion of each group to obtain an alveolar macrophage fraction. Proteolytic activity (P.A.), as measured by caseinolysis at pH 3.0 and pH 5.0, increased nearly twofold in the 2-day NO2 lung extracts and fourfold in the 50-day NO2 samples. P.A. in macrophage extract at pH 3.0 increased tenfold with both 2- and 50-day NO2 exposure. Lung extract hydrolysis of specific esterase and amidase substrates and susceptibility to activators and inhibitors of proteolytic enzymes are consistent with the presence of lysosomal cathepsin A, B1, B2, C, D, and E. The lack of NO2-induced increases in P.A. at physiologic values of pH may be the basis of the lack of significant pulmonary tissue destruction observed in rodents exposed to NO2 for 2 and 50 days.

Animals↗
PubMed1979

Dysfunction of small airways following pulmonary injury due to nitrogen dioxide.

Serial physiologic studies were performed to characterize both the immediate and delayed effects of a single occupational exposure to nitrogen dioxide in a nonsmoker. During the initial acute stage of pulmonary edema, the abnormal static pressure-volume curve and decreased static compliance corresponded to a reduction in pulmonary volume. During the delayed acute stage, elastic recoil and properties of resistance to flow were normal, but dynamic compliance was reduced and dependent on respiratory frequency, and oxygen transport was abnormal during exercise, which is consistent with dysfunction of the small airways.

Forced Expiratory Flow Rates↗
PubMed1979

The relation between respiratory illness in primary schoolchildren and the use of gas for cooking--II. Factors affecting nitrogen dioxide levels in the home.

The study was designed to determine whether there was an association between indoor levels of nitrogen dioxide (NO2) and respiratory illness and lung function in schoolchildren. NO2 was measured for one week in the winter outside and inside the homes of children aged 6-7 years living and attending primary schools in a defined 4 square km area in Middlesbrough, Cleveland, UK. Outdoor levels of NO2 measured at 75 points within the area ranged from 14-24 ppb weekly average. Measurements were also made in 428 kitchens with gas cookers, range 5-317 ppb, mean 112.2 ppb, and in 87 kitchens with electric cookers, range 6-188 ppb, mean 18.0 ppb. In a random subsample of homes the range of NO2 levels in 107 children's bedrooms in homes where gas was used for cooking was 4-169 ppb, mean 30.5 ppb, in 18 bedrooms in electric cooking homes the range was 3-37 ppb, mean 13.9 ppb. NO2 levels in the gas cooking kitchens were positively related to the presence of pilot lights, use of gas fires for main heating, number of regular smokers, and the number of people in the home. Information from 29 homes with the highest kitchen NO2 levels paired with 29 low NO2 gas cooking homes showed that the daily number of meals eaten and the frequency with which the cooker was used for heating and drying clothes were significantly greater in the high NO2 homes.

Air Pollutants↗
PubMedDate not supplied

Nitrogen dioxide inhalation and human blood biochemistry.

Blood from ten young adult male humans, exposed to 1 ppm or 2 ppm nitrogen dioxide (NO2) for 2.5--3.0 hr, was examined for evidence of biochemical changes. The experiments lasted three days. The subjects entered an environmental chamber, performed mild exercise, and completed a series of measurements of pulmonary physiology while breathing filtered air. Blood samples were then taken and analyzed. This regimen was repeated on the second and third day, except that the chamber atmosphere now contained 1 ppm or 2 ppm NO2. Paired group analyses were performed on the data. A statistically significant decrease was observed in the activity of the erythrocyte membrane enzyme acetylcholinesterase at both NO2 levels. Levels of peroxidized red blood cell lipids showed statistically significant elevations after inhalation of 2 ppm NO2 but not 1 ppm. Glucose-6-phosphate dehydrogenase was significantly elevated only after the second 2-ppm NO2 exposure. Small but statistically significant decreases were observed in both hemoglobin and hematocrit values after exposure to both NO2 levels. The experiment was repeated with NO2, (i.e., three days of filtered air) to detect possible effects of the experimental procedure. Decreases were again seen in hemoglobin and hematocrit, and acetyecholinesterase, although of smaller magnitude than when NO2 was inhaled. Other data showed random variations that were not additive over the three-day sham exposure period. It was concluded that significant blood biochemical changes resulted from NO2 inhalation, although the three-day experimental regimen independently produced changes that account for some of the apparent response.

Acetylcholinesterase↗
PubMed1978

Influence of 0.5 ppm nitrogen dioxide exposure of mice of macrophage congregation in the lungs.

The lungs of 12 mice, half of which were exposed to continuous 0.5 ppm nitrogen dioxide for 3 weeks, were explanted in culture, and the instances of macrophage congregation were quantitated according to numbers of target cells involved, categories of congregation from three to 11 or more, numbers of macrophages participating in each category for the total cultures, and the influence of delaying explantation for 24 and 96 hr. A total of 9042 macrophages and 2140 epithelial and spindle target cells were counted in the outgrowths from 306 explants. The incidence of macrophage congregation (or numbers of target cells) was greater for the cultures from the NO2-exposed animals, both with respect to total incidences between groups (p leads to) and the 0-hr (p less than 0.001) and 24-hr (p less than 0.01) culture subgroups. In addition, the values for T3 to T6 macrophage congregation were individually and consistently greater for the exposed animal group. Postmortem interval stress at 96 hr appeared to result in large colonies, but they were reduced greatly in number. Also the incidence of macrophage congregation fell by 28% as compared to 0-hr and 24-hr subgroups.

Animals↗
PubMed1975

Nitrogen dioxide and the erythrocyte redox state.

Normal human erythrocytes were exposed for two hours at 38 C to an atmosphere of air containing variable concentrations of nitrogen dioxide, in order to detect any primary cytoplasmic effect of NO2 on the calculated oxidation-reduction (redox) ratio ([NAD+]/[NADH]) of a mitochondria-free cell. Substantial increases in the redox ratio were noted only when NO2 concentrations exceeded 15 ppm. In the range of 15 to 500 ppm NO2, the increase in the redox ratio significantly correlated with the NO2 concentration (r=.71; p less than .01). Intracellular to extracellular anion distribution ratios for chloride, lactate, and pyruvate were similar in NO2 and non-NO2 exposed cells, suggesting absence of a substantial hemolytic effect. These data identify a direct cytoplasmic NO2-induced biochemical change that may be mediated by a mechanism other than lipid peroxidation. Alteration of hemoglobin or NAD-NADH-dependent enzyme activity is suggested.

Cell Fractionation↗
PubMed1979

Proliferation of lung and airway cells induced by nitrogen dioxide.

Proliferation of lung cells of Chinese hamsters was examined in several regions of the lung parenchyma and ciliated airway epithelium after a 24-h exposure to 28.2 mg/m3 (15 ppm) nitrogen dioxide (NO2). Label was retained 3 wk after the injection of [3H]thymidine, and autoradiographic methods were used to localize the site of retention. By 24 h after administration of [3H]thymidine, parenchymal areas, exclusive of airways, showed an increased labeling index, indicative of cell death and replacement. This increase in the number of labeled cells persisted for 3 wk. Type II cells were labeled twice as frequently in regions of the terminal bronchiole than in other alveolar areas. Type II cell cycle time was reduced from 26 to 3 d after NO2 exposure. Alveolar macrophages were significantly labeled in the alveolar areas during the thymidine pulse at the end of the exposure episode and retained label for 3 wk. Airway epithelia showed no labeling in the trachea and progressively greater labeling in increasingly small er airways. Epithelial cells lining the small airways and alveoli showed greater susceptibility to NO2 injury than cells lining the bronchi or trachea. Nonciliated or basal cells serve as a precursor of ciliated cells in the epithelium of small airways (0.35 mm) and bronchi.

Animals↗
PubMed1979

The relation between respiratory illness in primary schoolchildren and the use of gas for cooking--III. Nitrogen dioxide, respiratory illness and lung infection.

We examined the relation between lung function and respiratory illness in a population of 808 primary school children aged 6-7 years and the levels of nitrogen dioxide (NO2) in the kitchens and bedrooms in their homes. Complete data were collected on about 66% of the population. The children lived in a defined 4 square km area in Middlesbrough, Cleveland, UK. One week average outdoor levels of NO2 varied little over the area (14-24 ppb); The prevalence of respiratory illness was higher in children from gas than electric cooking homes (p approximately or equal to 0.1). Although prevalence was not related to kitchen NO2 levels (range 5-317 ppb) it increased with increasing levels of NO2 in the children's bedrooms in gas cooking homes (range 4-169 ppb, p approximately or equal to 0.1). Symptoms in siblings and parents were not related to kitchen NO2 levels. Lung function was not related to NO2 levels in the kitchen or bedroom. Because of the very low levels of NO2 at which an association with illness was observed and the inconsistency between our results in the UK and those from several studies in the US, it is possible that the NO2 levels were a proxy for some other factor more directly related to respiratory disease such as temperature or humidity.

Air Pollutants↗