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PubMed1990

Personal exposure to nitrogen dioxide and its association with respiratory illness in Hong Kong.

In 1985, 362 primary schoolchildren and their 319 mothers were surveyed in Hong Kong to study the possible relationship of air pollution to respiratory illnesses. Using nitrogen dioxide (NO2) measured by personal samplers as a measure of air pollution, the study aimed to identify the major sources of NO2 in the indoor environment and see whether its increased presence was associated with respiratory symptoms. The levels of NO2 among the mothers was found to increase by 21% if dust exposure was reported from the workplace, 18% if they used such cooking fuels as liquid petroleum gas or kerosene, 11% when kitchens did not have ventilating fans, and 10% when incense was burned at home. In terms of respiratory symptoms, an increase in NO2 levels of 19% was reported among those with allergic rhinitis and 18% among those with chronic cough. The levels of NO2 among children were correlated with levels measured in classrooms, all of which had opened windows so that the NO2 came from outdoors. No association was found between children's NO2 levels and respiratory symptoms. With the exception of smoking by the father and the children's NO2 levels, no association was found between smoking at home and NO2 levels.

Adult↗

PubMed2001

Personal and outdoor nitrogen dioxide concentrations in relation to degree of urbanization and traffic density.

To assess differences in exposure to air pollution from traffic in relation to degree of urbanization and traffic density, we measured personal and home outdoor nitrogen dioxide (NO(2)) concentrations for 241 children from six different primary schools in the Netherlands. Three schools were situated in areas with varying degrees of urbanization (very urban, fairly urban, and nonurban) and three other schools were located near highways with varying traffic density (very busy, fairly busy, and not busy). Weekly averaged measurements were conducted during four different seasons. Simultaneously, indoor and outdoor measurements were conducted at the schools. Personal and outdoor NO(2) concentrations differed significantly among children attending schools in areas with different degrees of urbanization and among children attending schools in areas close to highways with different traffic densities. For the children living near highways, personal and outdoor NO(2) concentrations also significantly decreased with increasing distance of the home address to the highway. Differences in personal exposures between children from the different schools remained present and significant after adjusting for indoor sources of NO(2). This study has shown that personal and outdoor NO(2) concentrations are influenced significantly by the degree of urbanization of the city district and by the traffic density of and distance to a nearby highway. Because NO(2) can be considered a marker for air pollution from traffic, the more easily measured variables degree of urbanization, traffic density, and distance to a nearby highway can all be used to estimate exposure to traffic-related air pollution.

Air Pollution↗

PubMed1992

Long-term effects of ozone and nitrogen dioxide on the metabolism and population of alveolar macrophages.

To investigate how alveolar macrophages adapt themselves to oxidative pollutants in the long term, rats were exposed to a strong oxidant, ozone (O3), or a weak oxidant, nitrogen dioxide (NO2), for a maximum duration of 12 wk. After exposures, alveolar macrophages were collected by pulmonary lavage. Throughout 11 wk of exposure to 0.2 ppm O3, the specific activities of glucose-6-phosphate dehydrogenase (G6PDH) and glutathione peroxidase of the peroxidative metabolic pathway and pyruvate kinase and hexokinase of the glycolytic pathway were 40-70% elevated over the controls in alveolar macrophages. The population of alveolar macrophages was consistently 60% higher than the controls. The small-sized macrophages, immature macrophages, preferentially increased. To the contrary, the thymidine incorporation per cell was always 20-30% lower than in the controls, although the total incorporation remained unchanged. No infiltration of polymorphonuclear leukocytes occurred. By 12 wk of exposures to 1.2 and 4.0 ppm NO2, the population of alveolar macrophages increased 30% over the control. Among the enzymes examined, however, only the G6PDH activity increased 10% for 4.0 ppm NO2. No increase in the enzyme activities occurred for 1.2 ppm NO2. Based on these results, alveolar macrophages adapt themselves to the long-term exposure of O3 or NO2 by recruiting immature macrophages through an apparent influx of monocytes. During the exposure to O3, the peroxidative metabolic and glycolytic pathways are enhanced persistently in alveolar macrophages, whereas both pathways were not enhanced by the exposures to NO2.

Adenosine Triphosphate↗

PubMed1996

Effect of subchronic in vivo exposure to nitrogen dioxide on lung tissue inflammation, airway microvascular leakage, and in vitro bronchial muscle responsiveness in rats.

OBJECTIVES: In a previous study on bronchoalveolar lavage fluid from rats exposed in vivo for seven days to 10 ppm nitrogen dioxide (NO2), it has been shown that there is an influx of macrophages into the airways. The present study investigated the effect of seven day exposure to 10 ppm NO2, on: (a) lung tissue inflammation and morphology; (b) airway microvascular leakage; (c) in vitro contractile response of main bronchi. METHODS: Lung tissue was studied by light microscopy, after fixing the lungs by inflation with 4% formalin at a pressure of 20 cm H2O. Microvascular leakage was measured by extravasation of Evans blue dye in the larynx, trachea, main bronchi, and intrapulmonary airways. Smooth muscle responsiveness was evaluated by concentration-responses curves to acetylcholine (10(-9)-10(-3) M), serotonin (10(-9)-10(-4) M), and voltage-response curves (12-28 V) to electrical field stimulation. RESULTS: Histology showed an increased total inflammation at the level of respiratory bronchioles and alveoli. No influx of inflammatory cells was found in the main bronchi. A loss of cilia in the epithelium of small airways and ectasia of alveolar capillaries was also found. By contrast, no alterations to microvascular permeability or modification of bronchial smooth muscle responsiveness was found. CONCLUSIONS: Subchronic exposure to 10 ppm NO2 causes airway inflammation and structural damage, but does not cause any persistent alteration to microvascular permeability or bronchial smooth muscle responsiveness in rats.

Acetylcholine↗

PubMed1991

Effects of Mycoplasma pulmonis infection and exposure to nitrogen dioxide on activities of natural killer cells and macrophages of the mouse.

A marked enhancement was seen in activities of mouse splenic natural killer (NK) cells and macrophages one week after infection with Mycoplasma pulmonis (Mp) or exposure to nitrogen dioxide (NO2). Macrophage activity of the Mp-infected mouse showed further augmentation by exposure to NO2 while NK activity of Mp-infected mice was not affected by NO2-exposure.

Animals↗

PubMed2004

Product analyses of ozone mediated nitration of benzimidazole derivatives with nitrogen dioxide: formation of 1-nitrobenzimidazoles and conversion to benzotriazoles.

Several benzimidazole derivatives having electron-withdrawing or -donating substituent(s) at the benzene moiety were used as models of the imidazole moiety of purine bases and their nitration with nitrogen dioxide and ozone (so-called Kyodai nitration) were examined. Products were extracted from the reaction mixture with AcOEt and their structures were analyzed. 1-Nitrobenzimidazole derivatives and unexpected 1-nitrobenzotriazole derivatives were identified. Although the yields of 1-nitrobenzimidazole derivatives were quite low, these were all new compounds that could be obtained only by Kyodai nitration. It was speculated that benzotriazoles were formed via 1-nitrobenzimidazoles and subsequent nitration toward benzotriazoles resulted in the formation of 1-nitrobenzotriazoles.

Benzimidazoles↗

PubMedDate not supplied

Effect of ferrous sulfate aerosols and nitrogen dioxide on murine pulmonary defense.

A murine infectivity model was used to test the effect of exposure to atmospheres containing 290 +/- 50 microgram/m3 of respirable sized ferrous sulfate (FeSO4) particles (0.4 micron mass median aerodynamic diameter) and 1.0 ppm nitrogen dioxide (NO2) prior to infection with aerosols of Staphylococcus aureus or group C streptococci. Exposure to these combined pollutants for 24 or 48 hr did not impair pulmonary inactivation of S. aureus. Exposure to FeSO4 or NO2 for 48 hr, or to both pollutants for 24 or 48 hr, resulted in significant decreases in inactivation of inhaled group C streptococci. Mortality studies following pollutant exposure demonstrated earlier, but not an increased number of deaths. These studies demonstrate the importance of the test organism in assessing air quality standards with the infectivity model and enhanced toxicity and prolongation of exposure to relatively low levels of submicron-size particles of FeSO4 and NO2.

Aerosols↗

PubMed1997

Generation of nitrogen dioxide during nitric oxide therapy and mechanical ventilation of children with a Servo 900C ventilator.

OBJECTIVE: To determine the combinations of nitric oxide (NO), oxygen (O2), minute ventilation (MV) and total gas flow (TGF) which generate toxic concentrations of nitrogen dioxide (NO2) during mechanical ventilation with a Servo 900C ventilator. DESIGN: The measurement of NO2 generated with NO (20, 40, 60, 80, 100 ppm) and O2 [fractional inspired oxygen (FIO2) 0.21, 0.4, 0.6, 0.9] during mechanical ventilation with MVs of 2.5, 5.0 and 7.5 l/min and TGFs from 2 to 14 l/min. SETTING: Laboratory of intensive care unit in paediatric tertiary hospital. RESULTS: Toxic concentrations of NO2 (> 5 ppm) were generated in the ventilator circuit when NO was 80 ppm or 100 ppm in FIO2 of 0.6 or 0.9 with MVs of 2.5, 5.0 and 7.5 l/ min; and with 80 ppm NO in FIO2 of 0.6 at all TGFs from 2.0 to 13.6 l/min and MVs of 2.5, 5.0 and 7.5 l/min (TGF/MV 0.3-5.4). NO2 1.5-2.6 ppm was generated with 40 ppm NO in FIO2 of 0.6, TGFs 2.1-13.7 l/ min, and MVs 2.5, 5.0 and 7.5 l/min (TGF/MV 0.3-5.5). NO2 0.9-0.6 ppm was generated with 20 ppm NO in FIO2 of 0.6, TGFs 2.5-13.8 and MVs 2.5, 5.0 and 7.5 (TGF/MV 0.3-5.5). NO2 generation was not affected significantly by the TGF/MV ratio. CONCLUSIONS: The generation of NO2 in the ventilator circuit is directly proportional to concentration of NO and O2 and inversely proportional to the TGF and MV but uninfluenced by the TGF/MV ratio. NO 80 ppm, but neither 20 nor 40 ppm in FIO2 of 0.6, generates toxic NO2 irrespective of TGF, MV or the TGF/MV ratio.

Child↗

PubMed2005

Association between nitrogen dioxide and heart rate variability in a susceptible population.

BACKGROUND: Panel studies have shown a consistent association between changes in the cardiac autonomic nervous system with particulate matters (PM) but less with gaseous pollutants. This study examined the linkage between nitrogen dioxide (NO2) and heart rate variability (HRV) in a susceptible population. METHODS: We recruited a panel of 83 patients from the National Taiwan University Hospital Cardiology Clinic to measure their 24-h HRV by ambulatory electrocardiography. Thirty-nine patients had coronary heart disease (CHD) and another 44 patients had more than one major CHD risk factor. Ambient concentrations of NO2, sulphur dioxide (SO2), carbon monoxide (CO), ozone, and PM less than 10 microm in diameter (PM10) at each participant's close-by monitoring station were used to represent study participants' exposures. We used linear mixed-effects models to analyse the association between individual air pollutants and log10-transformed HRV, with key personal and environmental attributes and co-pollutants being adjusted. RESULTS: We found that an increase in 10 ppb NO2 at 4-h to 8-h moving averages was associated with 1.5-2.4% decreases in the standard deviation of all normal-to-normal intervals (SDNN) in our participants. For every 10 ppb NO2 at 5 and 7-h moving averages, our participants' low frequency was decreased by 2.2 and 2.5%, respectively. In contrast, HRV was not associated with PM10, CO, SO2, or O3. CONCLUSION: Increasing NO2 exposure was found to be associated with decreasing SDNN and low frequency in susceptible populations.

Adult↗

PubMed1992

Effect of in vitro nitrogen dioxide exposure on human bronchial smooth muscle response.

The aim of this study was to develop an in vitro system in which an isolated bronchus from human lung was exposed, during 30 min, to a constant flow of either air or nitrogen dioxide (NO2), and to examine subsequently the contractile response of airway smooth muscle rings to carbachol, histamine, and substance P. Two proximal bronchi were mounted in an organ bath, perfused externally with Krebs-Henseleit solution and ventilated with clean air, 1.0 or 2.0 ppm NO2. The exposed bronchi were then cut into rings and mounted in a computerized organ bath system. Contractile responses to agonists were measured isometrically. In each ring, a cumulative concentration response curve was obtained to the desired agonist. We found that in vitro exposure of human lumen bronchus to a constant flow of air did not alter the contractility of the smooth muscle. Whereas in vitro exposure of the bronchus to 1.0 ppm NO2 did not significantly increase the efficacy or the potency of carbachol, exposure to 2.0 ppm NO2 increased airway smooth muscle contractions in response to carbachol, histamine, and substance P. These results indicate that our experimental preparation is well suited to study the respiratory toxicity of inhaled pollutants in order to understand further the mechanisms underlying toxicant-induced airway hyperresponsiveness.

Acetylcholine↗

PubMed2002

Photochemically catalyzed generation of site-specific 8-nitroguanine adducts in DNA by the reaction of long-lived neutral guanine radicals with nitrogen dioxide.

A novel photochemical approach is described for synthesizing site-specific 8-nitro-2'-deoxyguanosine (8-nitro-dG) adducts DNA. The method is based on the bimolecular reaction of a neutral, deprotonated guanine radical [G(-H)*] in DNA and nitrogen dioxide (*NO(2)) radicals. This approach is illustrated using the single-stranded oligodeoxyribonucleotide 5'-d(CCATCGCTACC) dissolved in an aqueous solution of nitrite and bicarbonate anions at pH 7.5. The photochemical synthesis was triggered by the selective photodissociation of persulfate anions to yield SO(4)(*-) radical anions by either 308 nm XeCl excimer laser pulses or by a continuous irradiation with 290-340 nm light from a 1000 W Xe lamp. The sulfate radicals formed generate the CO(3)(*-) and *NO(2) radicals by one-electron oxidation of the bicarbonate and nitrite anions. In turn, the CO(3)(*-) radicals site-selectively generate G(-H)* radicals in DNA that combine with *NO(2) to form 8-nitro-dG lesions in the oligonucleotide. The nitrated oligonucleotides were purified by reversed-phase HPLC techniques and are stable at 4 degrees C for at least 4 days, but depurinate at ambient temperatures of 23 degrees C at pH 7 with a half-life of approximately 20 h. The nature of the reaction and decomposition products were studied by a combination of ESI and MALDI-TOF mass spectrometric techniques.

DNA Adducts↗

PubMed2002

Measurements of children's exposures to particles and nitrogen dioxide in Santiago, Chile.

An exposure study of children (aged 10-12 years) living in Santiago, Chile, was conducted. Personal, indoor and outdoor fine and inhalable particulate matter (< 2.5 .m in diameter, PM2.5 and < 10 microm in diameter, PM10, respectively), and nitrogen dioxide (NO2) were measured during pilot (N = 8) and main (N = 20) studies, which were conducted during the winters of 1998 and 1999, respectively. For the main study, personal, indoor and outdoor 24-h samples were collected for five consecutive days. Similar mean personal, indoor and outdoor PM2.5 concentrations (69.5, 68.5 and 68.1 microg/m3, respectively) were found. However, for coarse particles (calculated as the difference between measured PM10 and PM2.5, PM2.5-10), indoor and outdoor levels (35.4 and 47.4 microg/m3) were lower than their corresponding personal exposures (76.3 microg/m3). Indoor and outdoor NO2 concentrations were comparable (35.8 and 36.9 ppb) and higher than personal exposures (25.9 ppb). Very low ambient indoor and personal O3 levels were found, which were mostly below the method's limit of detection (LOD). Outdoor particles contributed significantly to indoor concentrations, with effective penetration efficiencies of 0.61 and 0.30 for PM2.5 and PM2.5-10, respectively. Personal exposures were strongly associated with indoor and outdoor concentrations for PM2.5, but weakly associated for PM2.5-10. For NO2, weak associations were obtained for indoor-outdoor and personal-outdoor relationships. This is probably a result of the presence of gas cooking stoves in all the homes. Median I/O, P/I and P/O ratios for PM2.5 were close to unity, and for NO2 they ranged between 0.64 and 0.95. These ratios were probably due to high ambient PM2.5 and NO2 levels in Santiago, which diminished the relative contribution of indoor sources and subjects' activities to indoor and personal PM2.5 and NO2 levels.

Air Pollutants↗

PubMed2006

Simultaneous measurement of nitric oxide (NO) and nitrogen dioxide (NO2) in simulated automobile exhaust using medium pressure ionization-mass spectrometry.

In previous papers we have demonstrated two different, two-color resonance-enhanced multiphoton ionization (REMPI) schemes for the simultaneous measurement of trace amounts (ppbV to pptV) of nitrogen monoxide (NO) and nitrogen dioxide (NO(2)). The goal of this study is to provide a laser ionization-mass spectrometric scheme capable of measuring ppmV to ppthV concentrations of NO and NO(2) within vehicle exhaust containing up to ppthV of aromatic hydrocarbons and a time frame of seconds. Two ionization schemes are used here to measure NO and NO(2) in simulated automobile exhaust with three different sources. REMPI Scheme 1 uses broad-bandwidth light and an effusive source to measure NO (limit of detection (LOD) 300 ppmV), NO(2) (LOD 100 ppmV), and aromatic hydrocarbons (via photoionization) along with fragments (via electron impact). REMPI Scheme 2 uses narrow-bandwidth light and a medium pressure laser ionization (MPLI) source to measure NO (LOD 60 ppmV), NO(2) (LOD 3 ppmV), and fragments (via electron impact). The LOD is determined using 10-second sampling times. A newly developed delayed-ion extraction technique for MPLI is then applied to REMPI Scheme 2, dramatically reducing the electron impact signal, so that only NO and NO(2) are observed. We conclude that Scheme 2 with delayed-electron extraction is best suited for measuring in situ NO and NO(2) within engine exhaust.

Algorithms↗

PubMed1996

Scavenging of nitrogen dioxide, thiyl, and sulfonyl free radicals by the nutritional antioxidant beta-carotene.

Mechanisms of free radical scavenging by the nutritional antioxidant beta-carotene have been investigated by pulse radiolysis. Free radicals, which can initiate the chain of lipid peroxidation, including nitrogen dioxide (NO2.), thiyl (RS.), and sulfonyl (RSO2.) radicals, are rapidly scavenged by beta-carotene. Absolute rate constant k[NO2. + beta-carotene] = (1.1 +/- 0.1) x 10(8) m-1 s-1 and for the glutathione thiyl radical k[GS. + beta-carotene] = (2.2 +/- 0.1) x 10(8) m-1 s-1 have been determined. The mechanisms however are mutually exclusive, the former involving electron transfer to generate the radical-cation [ beta-carotene]+. and the latter by radical-addition to generate an adduct-radical [RS... beta-carotene].. Rate constants for thiyl radical-addition reactions vary from 10(6) to 10(9) m-1 s-1 and correlate with the lipophilicity of the thiyl radical under study. Sulfonyl radicals undergo both electron abstraction, [ beta-carotene]+. and radical-addition, [RSO2... beta-carotene]. in an approximate 3:1 ratio. The beta-carotene radical-cation and adduct-radicals are highly resonance stabilized and undergo slow bimolecular decay to non-radical products. These carotenoid-derived radicals react differently with oxygen, a factor which is expected to influence the antioxidant activity of beta-carotene within tissues of varying oxygen tension in vivo.

Antioxidants↗

PubMed2001

Effects of nitrogen dioxide exposure and ascorbic acid supplementation on exhaled nitric oxide in healthy human subjects.

BACKGROUND: Nitric oxide (NO) is detectable in the exhaled breath, is involved in airway defence and inflammation, and probably modulates bronchial smooth muscle tone. Given the sensitivity of nitrogen oxides to local redox conditions, we postulated that exposure to oxidant or antioxidant compounds could alter concentrations of NO in the exhaled breath (eNO). We assessed the effect of nitrogen dioxide (NO(2)) and ascorbic acid exposure on eNO in healthy human subjects. METHODS: Ten healthy subjects were randomised to undergo a 20 minute single blind exposure to NO(2) (1.5 parts per million) or medical air in a crossover fashion. Exhaled NO and pulmonary function were measured before and for 3 hours after exposure. In a separate double blind crossover study 20 healthy subjects received ascorbic acid 500 mg twice daily or placebo for 2 weeks with a 6 week interim washout. Serum ascorbic acid levels and eNO were measured before and after each supplementation phase. RESULTS: NO(2) induced a decrease of 0.62 (95% CI 0.32 to 0.92) ppb in the mean post-exposure eNO (p<0.01) with no change in forced expiratory volume in 1 second (FEV(1)). Oral supplementation with ascorbic acid increased the mean serum ascorbic acid concentration by 7.4 (95% CI 5.1 to 9.7) microg/ml (63%) but did not alter eNO. CONCLUSIONS: NO(2) exposure causes a decrease in eNO, an effect which may be mediated through changes in epithelial lining fluid redox state or through a direct effect on epithelial cells. In contrast, ascorbic acid does not appear to play a significant role in the metabolism of NO in the epithelial lining fluid.

Adult↗

PubMed1985

Biochemical assessment of acute nitrogen dioxide toxicity in rat lung.

The early primary biochemical response of lung to NO2 was studied separately from the later secondary responses of inflammation and proliferation by measuring several biochemical parameters in lungs of rats immediately following a 4-hr exposure to nitrogen dioxide (NO2) at concentrations of 10, 20, 30, and 40 ppm. Cell-free lavage fluid contained elevated amounts of lactate dehydrogenase (LDH), malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), glucose-6-phosphate dehydrogenase (GDH), acid phosphatase (AP), and aryl sulfatase (AS) after 30 or 40 ppm NO2. Total protein and sialic acid were increased in cell-free lavage after 20, 30, or 40 ppm NO2. The amounts of protein, sialic acid, and acid phosphatase recovered by airway lavage were equal to the amounts found in 0.7 ml of plasma, consistent with transudation of this volume of plasma into airways as a source of these parameters. The plasma activity of the other parameters measured was too low to account for their increase in lavage fluid by plasma leakage into airways. Decrease in the number and enzyme content of lavagable cells indicated damage to free cells in the airways. The amount of the decrease in enzyme content of the lavagable cell fraction was similar to the increase in the cell-free lavage for all of the measured enzymes except acid phosphatase, suggesting the release of these enzymes into airways as a result of damage to free cells. However, the LDH isoenzyme profile in cell-free lavage after exposure is inconsistent with free cells as the source of this enzyme. No changes were observed in the whole-lung homogenate content of protein, DNA, lipid, LDH, MDH, IDH, GDH, AP, AS, glutathione reductase, NADPH cytochrome c, or succinate cytochrome c reductase immediately after NO2 exposure. This study indicates that initial acute damage to lung by NO2 results in translocation of enzymes, proteins, and sialic acid into airways. Plasma is a likely source of translocated protein, sialic acid, and acid phosphatase. The sources of the other enzyme activities remain to be identified, with lung parenchyma and free cells as likely sources.

Animals↗

PubMed1997

Front-door concentrations and personal exposures of Danish children to nitrogen dioxide.

The aims of the study were to evaluate the front-door concentration of traffic exhaust fumes as a surrogate for the personal exposure of children and to study factors in the behavior and the environment of children that affect their personal exposure to nitrogen dioxide (NO(2)). The exposure to NO(2) of 103 children living in Copenhagen and 101 children living in rural areas of Denmark was studied by measuring average concentrations over 1 week with diffusive badge samplers placed outside the front door of the home, inside the child's bedroom, and on each child. Detailed information about the activities of the children involving potential exposure to NO(2) was noted in diaries. The results indicated that the front-door concentration of traffic pollution might be used to classify the personal exposure of urban children, although misclassification would be introduced. Multiple regression analysis showed several factors that affected the personal NO(2) exposure of the children independently, including the front-door concentration, the bedroom concentration, time spent outdoors, gas appliances used at home, passive smoking, and burning candles.

Air Pollutants↗

PubMed1982

Immunocytochemical studies of APUD cells in airways: effects of nitrosodiethylamine and nitrogen dioxide.

The amine precursor uptake and decarboxylase (APUD) cells and neuroepithelial bodies (NEBs) in airways of adult rats have been studied by immunocytochemical methods for the presence of adrenocorticotropic hormone (ACTH), growth hormone (hGH), calcitonin, and bombesin in control animals and following exposure to nitrosodiethylamine and nitrogen dioxide (NO2). Calcitonin-like immunoreactivity (CLIR) is present in APUD cells of the trachea and bronchioles and in NEBs in the lung. Rats treated with nitrosodiethylamine and NO2 exhibit increased numbers of argyrophilic cells but no increase in cells containing specific intracytoplasmic CLIR. The presence of ACTH, hGH, and bombesin in respiratory tract APUD cells was not observed. These studies indicate that APUD cells in the trachea and bronchioles of adult rats harbor endocrine cells with immunohistochemical characteristics similar to C cells of the thyroid, and that these cell do not appear to be altered in number when rats are treated with agents known to produce an increase in APUD cells.

APUD Cells↗