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PubMedDate not supplied

Nocturnal uptake and assimilation of nitrogen dioxide by C3 and CAM plants.

In order to investigate nocturnal uptake and assimilation of NO2 by C3 and crassulacean acid metabolism (CAM) plants, they were fumigated with 4 microl l(-1) 15N-labeled nitrogen dioxide (NO2) for 8 h. The amount of NO2 and assimilation of NO2 by plants were determined by mass spectrometry and Kjeldahl-nitrogen based mass spectrometry, respectively. C3 plants such as kenaf (Hibiscus cannabinus), tobacco (Nicotiana tabacum) and ground cherry (Physalis alkekengi) showed a high uptake and assimilation during daytime as high as 1100 to 2700 ng N mg(-1) dry weight. While tobacco and ground cherry strongly reduced uptake and assimilation of NO2 during nighttime, kenaf kept high nocturnal uptake and assimilation of NO2 as high as about 1500 ng N mg(-1) dry weight. Stomatal conductance measurements indicated that there were no significant differences to account for the differences in the uptake of NO2 by tobacco and kenaf during nighttime. CAM plants such as Sedum sp., Kalanchoe blossfeldiana (kalanchoe) and Aloe arborescens exhibited nocturnal uptake and assimilation of NO2. However, the values of uptake and assimilation of NO2 both during daytime and nighttime was very low (at most about 500 ng N mg(-1) dry weight) as compared with those of above mentioned C3 plants. The present findings indicate that kenaf is an efficient phytoremediator of NO2 both during daytime and nighttime.

Aloe↗

PubMed2001

Vicinal nitrohydroxyeicosatrienoic acids: vasodilator lipids formed by reaction of nitrogen dioxide with arachidonic acid.

Nitric oxide (NO)-derived species could potentially react with arachidonic acid to generate novel vasoactive metabolites. We studied the reaction of arachidonic acid with nitrogen dioxide (NO2), a free radical that originates from NO oxidation. The reaction mixture contained lipid products that relaxed endothelium-removed bovine coronary arteries. Relaxation to the lipid mixture was inhibited approximately 20% by indomethacin and approximately 70% by a soluble guanylate cyclase (sGC) inhibitor (ODQ). Thus, novel lipid products, which activate sGC presumably through a mechanism involving NO, appeared to have contributed to the observed vasorelaxation. Lipids that eluted at 9 to 12 min during high-performance liquid chromatography fractionation accounted for about one-half of the vasodilator activity in the reaction mixture, which was inhibited by ODQ. Lipid products in fractions 9 to 12 were identified by electrospray tandem mass spectrometry to be eight isomers having molecular weight of 367 and a fragmentation pattern indicative of arachidonic acid derivatives containing nitro and hydroxy groups and consistent with the structures of vicinal nitrohydroxyeicosatrienoic acids. These lipids spontaneously released NO (183 +/- 12 nmol NO/15 min/micromol) as detected by head space/chemiluminescence analysis. Mild alkaline hydrolysis of total lipids extracted from bovine cardiac muscle followed by isotopic dilution gas chromatography/mass spectrometry analysis detected basal levels of nitrohydroxyeicosatrienoic acids (6.8 +/- 2.6 ng/g tissue; n = 4). Thus, the oxidation product of NO, NO2, reacts with arachidonic acid to generate biologically active vicinal nitrohydroxyeicosatrienoic acids, which may be important endogenous mediators of vascular relaxation and sGC activation.

8,11,14-Eicosatrienoic Acid↗

PubMed1996

Electrochemical nitric oxide and nitrogen dioxide analyzer for use with inhaled nitric oxide.

The use of inhaled nitric oxide (NO) in research and clinical applications requires the monitoring of NO and its autooxidation product nitrogen dioxide (NO2) in inspired gas and in the ambient environment. We describe an inexpensive electrochemical NO and NO2 analyzer that uses a critical orifice constant-flow controller and a microprocessor crossover correction for the measurement of NO and NO2 in the concentration range relevant to the use of inhaled NO. The analyzer proved to have good accuracy and precision for NO and NO2 in the range of concentrations relevant to studies of inhaled NO. In this range, the performance was similar to that of a chemiluminescence analyzer, and the response characteristics were not affected by varying the O2 concentration of the mixtures analyzed.

Administration, Inhalation↗

PubMedDate not supplied

Effects of exposure to 4 ppm nitrogen dioxide in healthy and asthmatic volunteers.

Healthy and asthmatic volunteer subjects (N = 25 and N = 23, respectively) were exposed twice each to purified air (control) and to 4 ppm nitrogen dioxide (NO2) in a controlled-environment chamber. Exposures lasted 75 min, and included 15 min each of light exercise (ventilation rate near 25 L/min) and heavy exercise (near 50 L/min). Compared to control, NO2 exposure produced no statistically significant untoward effects on airway resistance, symptoms, heart rate, skin conductance, or self-reported emotional state in normal or asthmatic subjects. Exercise was associated with significantly (P less than .001) increased airway resistance in both subject groups, although the increase in normals was small. In both groups, systolic blood pressure showed small but significant (P less than .01) decreases with NO2 exposure, compared to control. This effect, if real, may relate to formation of a vasodilating nitrite or nitrate from inhaled NO2. The lack of respiratory response contrasts with previous findings elsewhere; at present, this inconsistency is unexplained.

Adult↗

PubMed1995

[Effects of temperature and humidity on the stability of nitric oxide, and efficacy of soda lime as a selective absorber of nitrogen dioxide].

Although inhaled nitric oxide (NO) has attracted attention as a pulmonary vasodilator, little heed has been given to its potential toxicity. Nitric oxide is known to be rapidly oxidized to nitrogen dioxide (NO2), which may damage pulmonary tissue. We examined the effects of temperature and humidity on the production of NO2 from NO. We also evaluated the amount of NO2 absorbed by soda lime, which is usually placed in the inspiratory line. For this purpose, we measured changes over time in the concentrations of NO and NO2 in mixtures that included NO, oxygen, and nitrogen in various concentrations, and at different temperatures and humidities. We confirmed that the formation of NO2 from NO follows the equation: -d[NO]/dt = 2 k[NO]2 [O2], where k is the rate constant. We found that k was significantly smaller at 37 degrees C than at 25 degrees C but was not influenced by humidity (0%, 40% or 90%). Although soda lime was very effective in absorbing NO2 from the inspiratory line, NO was simultaneously absorbed at the same molar ratio when the two gases existed together in the line. We thus conclude that inhalation of NO at 37 degrees C is more desirable than inhalation at room temperature, to suppress the production of NO2. When soda lime is used in the inspiratory line, attention should be paid to the reduction in the concentration of NO in the line.

Absorption↗

PubMed1986

Nitrogen dioxide exposure and lung antioxidants in ascorbic acid-deficient guinea pigs.

We have previously found that ascorbic acid (AA) deficiency in guinea pigs enhances the pulmonary toxicity of nitrogen dioxide (NO2). The present study showed that exposure to NO2 (4.8 ppm, 3 hr) significantly increased lung lavage fluid protein (a sensitive indicator of pulmonary edema) only in guinea pigs fed rabbit chow (a diet not supplemented with vitamin C) for at least 7 days, at which time lung AA was about 50% of normal. The rabbit chow diet did not cause reduced body weight as did commercial synthetic scorbutic diets, even when they were supplemented with AA. After 14 days of feeding rabbit chow, lung AA was reduced to 15% of control. At this time, alpha-tocopherol (AT) in the same lungs was reduced to 85% of control, and lung nonprotein sulfhydryls (NPSH) were increased to 114% of control. Exposure of the guinea pigs to NO2 (4.5 ppm, 16 hr) increased wet lung weight and further altered the antioxidants in deficient (but not normally fed) animals in the following manner: NPSH content was increased to 130% of control, AT was decreased to 74% of control, and AA was increased from 15 to 50% of control. These findings suggest that depletion of AA in guinea pigs removes an important defense against NO2. The lung appears to be able to partially compensate for the dietary lack of antioxidant by accumulating AA from other tissues and by increasing NPSH concentrations. However, sufficient exposure to NO2 leads to oxidation of AT and pulmonary edema. Conditions in which NO2 produced edema were accompanied by only a slight consumption of AT, and no detectable oxidation of lung AA or NPSH.

Animal Feed↗

PubMed1987

The effect of chlorphentermine pretreatment on the toxicity of nitrogen dioxide in mice.

Chlorphentermine HCl (CP) was used to induce preexisting alveolar alterations resembling a pulmonary lipidosis in mice to study these effects on the severity and duration of nitrogen dioxide (NO2) toxicity. Results indicated that a daily dose of 120 mg/kg for 14 days produced consistent histopathologic changes characterized by an accumulation of large foamy macrophages. Male Swiss-Webster mice were divided into a control and three treatment groups. Group 1 received 120 mg/kg CP po daily for 2 weeks followed by exposure to air for 48 hr. Group 2 received 20 ppm NO2 for 48 hr via whole-body inhalation, and group 3 received 120 mg/kg CP daily for 2 weeks followed by 20 ppm NO2 for 48 hr. The fourth group served as a nontreated control and received water in place of CP and air in place of NO2. All groups were compared by morphologic evaluation of pulmonary tissues at the light and electron microscopic levels at Days 0, 1, 3, 5, and 7 after the 48-hr exposure to air or NO2. In a second experiment using the same treatment groups, thin-section light microscopy was used to count the number of type I and type II cells and macrophages. NO2 exposure alone caused deaths in 20.8 and 18.5% of the mice in the two studies, but no deaths were seen in the combination groups from both experiments. Histopathologic evaluation showed a typical cellular response to the NO2 exposure, but differences were noted between the two groups receiving NO2 on this treatment. There was increased type II cell hyperplasia and terminal bronchiolitis on Days 0 and 1 but less on Days 3 to 7 in the combination group compared to the NO2 alone group. CP treatment prior to NO2 exposure caused less terminal bronchiolar epithelial hyperplasia and less pulmonary edema than was seen in the NO2 along group. The CP treatment appeared to protect against the lethal effects of NO2 at the concentration and time of exposure used and altered the cellular repair mechanism that occurs in response to NO2 toxicity. CP treatment prior to NO2 exposure caused significantly less loss of type I cells and less increase in type II cells due to NO2 damage. The combination treatment also caused an increase in macrophages greater than that seen in either individual treatment, and this number remained increased through 5 days post-NO2 exposure, whereas the NO2 alone caused a steady increase in macrophages following the exposure until Day 3.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1992

Silica-induced pulmonary inflammation and fibrosis in mice is altered by acute exposure to nitrogen dioxide.

The biologic impact of consecutive exposures to two environmental pollutants was examined in mice exposed to silica crystals (SI) by intratracheal (IT) injection followed by an inhalation exposure to nitrogen dioxide (NO2). C57Bl/6 mice received an IT injection of 2 mg SI or sterile saline (SAL) followed by a 2-h inhalation exposure to NO2 at 20 ppm either within 2 h of or 24 h after SI instillation. During acute inflammation (d 3 postsilica), mice exposed to NO2 at either time showed a dramatic and significant reduction in the number of lavaged alveolar neutrophils (PMN) when compared to silica/air-exposed mice. Animals exposed to NO2 24 h after silica also evidenced significant decreases in levels of lavage albumin and lactate dehydrogenase (LDH) 3 d after silica, as well as significant decreases in hydroxyproline content of the lung 30 and 60 d postsilica injection when compared to silica/air-exposed animals. NO2 administration 24 h after silica appeared to shift the appearance of PMN in the lung from d 3 to d 14, but did not otherwise alter chronic cellular inflammation. These data suggest that the marked neutrophil response and collagen deposition induced by SI can be modulated by NO2 exposure and that the time of oxidant gas exposure after silica administration is critical to this modulation.

Acute Disease↗

PubMedDate not supplied

Chronic obstructive pulmonary disease symptom effects of long-term cumulative exposure to ambient levels of total oxidants and nitrogen dioxide in California Seventh-Day Adventist residents.

To assess the risk of chronic obstructive pulmonary disease symptoms due to long-term exposure to ambient levels of total oxidants and nitrogen dioxide (NO2), symptoms were ascertained using the National Heart, Lung, and Blood Institute (NHLBI) respiratory symptoms questionnaire. A total of 7,445 Seventh-day Adventist (SDA) nonsmokers who were 25 yr of age or older and had resided at least 11 yr in areas of California with high to low photochemical air pollution were included in this study. Cumulative exposures to each pollutant in excess of four thresholds were estimated for each participant, using zip codes for months of residence and interpolated dosages from state air-monitoring stations. Multiple logistic regression analyses were conducted individually and together for pollutants and included eight covariables, including passive smoking. A statistically significant association with chronic symptoms was seen for total oxidants above 10 pphm (196 mcg/m3) (p less than .004, relative risk of 1.20 for 750 hr/yr). Chronic respiratory disease symptoms were not associated with relatively low NO2 exposure levels in this population. When these pollutant exposures were studied with exposures to total suspended particulates (TSP) and sulfur dioxide (SO2), only TSP exposure above 200 mcg/m3 showed statistical significance (p less than .01). Exposure to TSP is either more strongly associated with symptoms of chronic obstructive pulmonary disease than the other measured exposures or is the best single surrogate representing the mix of pollutants present.

Adult↗

PubMed1995

The effect of 1 ppm nitrogen dioxide on bronchoalveolar lavage cells and inflammatory mediators in normal and asthmatic subjects.

Several studies have suggested that patients with bronchial asthma are more susceptible to the potential effects of nitrogen dioxide (NO2) than healthy subjects, with respect to airway responsiveness and lung function. We investigated whether these differences are paralleled by differences in the cellular and biochemical response within the airway lumen. Twelve subjects with mild extrinsic asthma and eight normal subjects breathed either filtered air or 1 ppm NO2 in a single-blind manner during intermittent exercise for 3 h. Bronchoscopy with bronchoalveolar lavage (BAL) was performed one hour after each exposure, and on a third day without exposure (baseline day). Prostanoids, leukotrienes and histamine were analysed in BAL fluid, and the cellular composition of BAL fluid was assessed. In the asthmatic subjects, NO2 induced a small mean drop in forced expiratory volume in one second (FEV1). Differential cell counts in BAL fluid did not reveal significant effects of NO2. Levels of 6-keto-prostaglandin1 alpha (6-keto-PGF1 alpha) were decreased, and levels of thromboxane B2 (TxB2) and prostaglandin D2 (PGD2) in BAL fluid were increased after NO2 compared to filtered air exposure; whereas, prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), histamine and leukotriene levels did not change significantly. The normal subjects showed no change in lung function parameters and a small increase in TxB2 after breathing NO2. We conclude that in subjects with mild asthma NO2 is capable of inducing an activation of cells, which is compatible with enhancement of airway inflammation, even if lung function parameters and cellular composition of BAL fluid are not markedly affected.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2001

Effect of ozone and nitrogen dioxide on the release of proinflammatory mediators from bronchial epithelial cells of nonatopic nonasthmatic subjects and atopic asthmatic patients in vitro.

BACKGROUND: Although studies have suggested that ozone (O3) and nitrogen dioxide (NO2) may play a role in the pathogenesis of asthma, the underlying mechanisms are not clear. OBJECTIVE: We aimed to investigate the effects of O3 and NO2 on the release of IL-8, GM-CSF, RANTES, and soluble intercellular adhesion molecule 1 (sICAM-1) from human bronchial epithelial cells (HBECs) of nonatopic nonasthmatic subjects (nonasthmatic subjects) and atopic subjects with mild asthma (asthmatic subjects) in vitro. METHODS: We cultured HBECs from bronchial biopsy specimens of nonasthmatic and asthmatic subjects; exposed these for 6 hours to air, 10 to 100 ppb O3, or 100 to 400 ppb NO2; and analyzed the release of IL-8, GM-CSF, RANTES, and sICAM-1 after 24 hours' incubation. RESULTS: There was no significant difference between the constitutive release of IL-8, GM-CSF, and sICAM-1 from HBECs of asthmatic and nonasthmatic subjects. RANTES was detected only in HBECs derived from asthmatic subjects. Exposure of HBECs of asthmatic subjects to both 50 to 100 ppb O3 and 200 to 400 ppb NO2 significantly increased the release of IL-8, GM-CSF, RANTES, and sICAM-1 from these cells after 24 hours of incubation. However, 50 to 100 ppb O3 and 200 to 400 ppb NO2 led to a significant increase in release of only IL-8 and sICAM-1 from HBECs of nonasthmatic subjects after 24 hours' incubation. A comparison between the pollutant-induced release of mediators demonstrated that 100 ppb O3-induced release of GM-CSF and sICAM-1 was significantly greater in HBECs of asthmatic subjects (medians, 0.59 and 27.4 pg/microg cellular protein, respectively) than in HBECs of nonasthmatic subjects (medians, 0.27 and 14.4 pg/microg cellular protein, respectively; P < .02). CONCLUSION: These results suggest that O3 and NO2 may modulate airway diseases, such as asthma, by increasing the release of inflammatory mediators from bronchial epithelial cells and that the cells of asthmatic subjects may be more susceptible to the adverse effects of these pollutants.

Asthma↗

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↗

PubMed1968

Lipoperoxidation of lung lipids in rats exposed to nitrogen dioxide.

Absorption spectra characteristic of diene conjugation and typical for peroxidized polyenoic fatty acids can be induced in rat lung lipids after the rats have been exposed to a scant amount of nitrogen dioxide (1 part per million) for 4 hours. The peroxidative changes do not occur immediately but appear to reach a maximum between 24 and 48 hours after exposure. The prooxidant effect of this atmospheric pollutant in rat lung lipids may be partially prevented by prior treatment of the animal with large doses of alpha-tocopherol.

Alkenes↗

PubMed1991

Inflammatory cell response in bronchoalveolar lavage fluid after nitrogen dioxide exposure of healthy subjects: a dose-response study.

The combination of environmental chamber exposure and bronchoalveolar lavage (BAL) was used to study the effects of the common air pollutant nitrogen dioxide (NO2). Eighteen healthy nonsmokers were exposed to NO2 during 20 min in an exposure chamber during light bicycle ergometer work. All subjects were examined with BAL at least 3 wks before exposure, as a reference. The subjects were re-examined with BAL, in groups of eight, 24 h after exposure to 4, 7 and 10 mg NO2.m.3 (2.25, 4.0 and 5.5 ppm), respectively. An inflammatory cell response was found after exposure to all concentrations. An increase in the number of lymphocytes in BAL fluid was observed after 7 and 10 mg.m.3 (p less than 0.05 and 0.02, respectively). An increase in the number of mast cells, that appears to be dose-dependent, was found after exposure to all concentrations. The proportion of lysozyme positive alveolar macrophages was elevated after exposure to 7 mg.m.3. The inflammatory mediators fibronectin, hyaluronan, angiotensin converting enzyme (ACE) and beta 2-microglobulin were unchanged by exposure. Due to the findings of inflammatory cell changes far below the peak exposure limits for work places in industrialized countries, 9-18 mg.m.3, the safety of these limits is questioned. Studies are in progress in our laboratory using BAL to evaluate the effects of repeated NO2 exposure.

Adult↗

PubMed2002

Effect of ozone and nitrogen dioxide on the permeability of bronchial epithelial cell cultures of non-asthmatic and asthmatic subjects.

BACKGROUND: Although epidemiological as well as in vivo exposure studies suggest that ozone (O3) and nitrogen dioxide (NO2) may play a role in airway diseases such as asthma, the underlying mechanisms are not clear. OBJECTIVE: Our aim was to investigate the effect of O3 and NO2 on the permeability of human bronchial epithelial cell (HBEC) cultures obtained from non-atopic non-asthmatic (non-asthmatics) and atopic mild asthmatic (asthmatics) individuals. METHODS: We cultured HBECs from bronchial biopsies of non-asthmatics and asthmatics, and exposed these for 6 h to air, 10 to 100 parts per billion (p.p.b.) O3, or to 100 to 400 p.p.b. NO2, and assessed changes in electrical resistance (ER) and movement of 14C-BSA across the cell cultures. RESULTS: Although exposure to either O3 or NO2 did not alter the permeability of HBEC cultures of non-asthmatics, 10 to 100 p.p.b. O3 and 400 p.p.b. NO2 significantly decreased the ER of HBEC cultures of asthmatics, when compared with exposure to air. Additionally, 10, 50 and 100 p.p.b. O3 led to a significant increase in the movement of 14C-BSA across asthmatic HBEC cultures, after 6 h of exposure (medians = 1.73%; P < 0.01, 1.50%; P < 0.05 and 1.53%, P < 0.05, respectively), compared with air exposed cultures (median = 0.89%). Similarly, exposure for 6 h to both 200 and 400 p.p.b. NO2 significantly increased the movement of 14C-BSA across asthmatic HBEC cultures, when compared with air exposure. A comparison of data obtained from the two study groups demonstrated that 10 to 100 p.p.b. O3- and 200 to 400 p.p.b. NO2-induced epithelial permeability was greater in cultures of asthmatics compared with non-asthmatics. CONCLUSION: These results suggest that HBECs of asthmatics may be more susceptible to the deleterious effects of these pollutants. Whether in patients with asthma the greater susceptibility of bronchial epithelial cells to O3 and NO2 contributes to the development of the disease, or is a secondary characteristic of this condition, remains to be determined.

Adult↗

PubMed1994

Personal exposure to nitrogen dioxide in the Los Angeles Basin.

A large scale study of human exposure to nitrogen dioxide (NO2) was conducted in the Los Angeles Basin, the only metropolitan area in the United States that exceeds the NO2 NAAQS. Data are available for a population representative sample of 482 households and 682 individuals. Personal exposures, as well as indoor and outdoor home levels, were monitored using passive time-integrating filter badges. Monitoring extended over a one-year period (May 1987 to May 1988), with each individual providing two consecutive days of data. Information was also collected on activity patterns, household and personal characteristics, and spatial and temporal variables. This paper describes the study design, summarizes the sample characteristics and representativeness, and presents the distribution of personal, indoor, and outdoor NO2 concentrations recorded by the monitors. Over the entire sample, median personal and outdoor levels were 35 ppb; median indoor levels were 24 ppb. Personal exposures for those in homes with gas ranges with pilot lights average 10 ppb greater than those with electric ranges, and 4 ppb greater than those with gas ranges without pilot lights. Forty percent of the variation in indoor concentrations is explained by outdoor levels; 59 percent of the variation in personal exposures is explained by indoor levels; and 48 percent of the variation in personal exposures is explained by outdoor levels.

Adolescent↗

PubMed2002

Sum-frequency-generation system for differential absorption lidar measurement of atmospheric nitrogen dioxide.

A sum-frequency-generation system for differential absorption lidar measurement of atmospheric nitrogen dioxide in the lower troposphere was developed. The system uses a combination of a pair of KD*P crystals and a tunable dye laser with LDS 765 dye pumped by the second harmonic of a Nd:YAG laser to generate lambdaon and lambdaoff alternatively. Compared with the conventional system that uses Coumarin 445 dye pumped by the third harmonic, the output energy and long-term stability were improved. By use of this system, atmospheric NO2 concentrations of approximately 10-50 ppb were measured, with an instrumental error of approximately 7 ppb.

Journal Article↗

PubMed1993

Near-lifetime exposure of the rat to a simulated urban profile of nitrogen dioxide: pulmonary function evaluation.

To investigate the potential for up to a near-lifetime exposure to high-ambient levels of nitrogen dioxide (NO2) to induce functional lung damage, groups of rats were exposed to air or a simulated urban profile of NO2 (0.5 ppm background, 1.5 ppm peak) for 1, 3, 13, 52, or 78 weeks. The dynamic, static, and diffusional characteristics of the lung were evaluated postexposure in anesthetized rats. Furthermore, for the 13-, 52-, and 78-week groups, additional animals were tested after a 6-, 26-, or 17-week period in filtered air, respectively. No significant NO2 differences between exposed and control animals were found for the nitrogen washout, compliance, lung volume, or diffusion capacity of carbon monoxide measurements. At 78 weeks, however, a reduction in delta FEF25%, an estimate of convexity in the later portion of the forced expiratory flow volume curve, was observed. Breathing patterns and mechanisms were also assessed postexposure in a parallel group of similarly exposed unanesthetized rats. These rats were examined during a filtered air, 4 and 8% carbon dioxide (CO2) challenge. In the unanesthetized rat, frequency of breathing was significantly decreased and tidal volume, expiratory resistance, and inspiratory and expiratory times tended to increase. For several of these variables, the largest response also occurred at 78 weeks and seemed to be exacerbated by CO2 challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗