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PubMed1995

[Effects of the oxidizing agents ozone and nitrogen dioxide on the lung: studies of a cell culture model].

In experimental exposure studies with ozone or nitrogen dioxide a change in lung function and unspecific airway sensitivity was observed. These effects were paralleled by an induction of cellular and biochemical changes. The exposure of isolated cells in vitro led to a decrease in vitality, an increase in permeability and the secretion of mediators very similar to the composition found in bronchoalveolar lavage after in vivo exposure. The cell culture model, therefore, allows the study of the mechanism of these oxidative air pollutants and allows further the understanding of the influence of different cell types on the observed effects in vivo.

Cell Survival↗

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↗

PubMed1990

Nitrogen dioxide induces DNA single-strand breaks in cultured Chinese hamster cells.

Gaseous nitric oxide (NO) and nitrogen dioxide (NO2) were tested for their potential to induce DNA single-strand breaks (SSBs) in Chinese hamster cells (V79 cells). The alkaline elution assay was used for the detection of SSBs. V79 cells were exposed to NO and NO2 in N2 in varying concentrations (0-500 p.p.m.) and over varying periods (5-30 min). NO treatment did not result in any detectable DNA damage. NO2 led to a dose- and time-dependent increase of the rate of SSBs and the amount was dependent on concentration of NO2 and the length of exposure. The lowest observable effective concentration which was statistically different from control values was 10 p.p.m. exposed for 20 min. The metabolites of both gases, nitrite (NO2-) and nitrate (NO3-), had no DNA-damaging activity up to a concentration of 1 mM. The mechanism by which NO2 may generate SSBs is discussed.

Animals↗

PubMed1983

Effects of nitrogen dioxide exposure on prostacyclin synthesis in lung and thromboxane A2 synthesis in platelets in rats.

Effects of nitrogen dioxide (NO2) exposure on prostacyclin (PGI2) synthesis in the rat lung and thromboxane A2 (TXA2) synthesis in the platelets were studied. Male Wistar rats were exposed to 10 ppm NO2 for 1, 3, 5, 7 and 14 days. PGI2 synthesizing activity of homogenized lung decreased. The damage of PGI2 synthesizing activity reaches its maximum at 3 days. At 14 days, PGI2 synthesizing activity returned to the normal level. The activity of PGI2 synthetase decreased significantly. The formation of lipid peroxides due to NO2 exposure may cause the depression of PGI2 synthesizing activity of lung. On the other hand, platelet TXA2 synthesizing activity increased. This increased TXA2 synthesizing activity lasted at least till 3 days. Then, it returned to the normal level. The counts of platelet were decreased significantly by 1, 3, 5 and 7 days NO2 exposure. Then the decreased counts of platelet returned to the normal level at 14 days NO2 exposure. These results indicate that the depression of PGI2 synthesizing activity of lung by NO2 exposure cause an increase in TXA2 synthesizing activity of platelets. It may contribute to induce platelet aggregation and to the observed decrease in the number of platelets during NO2 exposure.

Animals↗

PubMed1988

Effects of nitrogen dioxide on Mycoplasma pulmonis infection and humoral immune responses in mice.

The effects of continuous exposure to nitrogen dioxide (NO2) on the pathologic and immunologic responses of ddY mice to the infection with Mycoplasma pulmonis were investigated. The organisms grew well in the trachea as early as 7 days after infection but barely grew in the lung even after 28 days, causing slight pneumonic lesions in only a few of the infected mice exposed to 1 and 5 ppm NO2. When mice were exposed to 10 ppm NO2 at or after the infection, however, mycoplasmal growth in the lung, but not in the trachea, was greatly enhanced, and pneumonic lesions were evident in the lung of almost all the mice examined. The serum antibody titers to M. pulmonis increased with time after infection regardless of the concentration of NO2 exposed or the mycoplasmal number in the respiratory tract in the infected mice. The in vitro immune responses of the spleen cells of the infected mice were significantly depressed by exposure to 10 ppm NO2 in not only mitogenic response to LPS and ConA but also antibody production to SRBC, whereas uninfected healthy mice were apparently not modulated except for a slight decrease in Con A response.

Animals↗

PubMed1982

Nitrogen dioxide exposure and alveolar macrophage elastase in hamsters.

Adult male hamsters were exposed to 30 +/- 5 ppm nitrogen dioxide (NO2) for periods as long as 30 days. Alveolar macrophages obtained by lung lavage at 0, 2, 5, 14, and 30 days of exposure were present in increased amounts, with the greatest increase 8 times the control amount at 14 days of NO2 exposure. No elastolytic activity was observed in the cell-free lavage fluid. Alveolar macrophages were cultured in serum-free medium for 1 to 6 days. The mediums were collected and assayed for elastolytic activity using Sepharose-coupled [3H] soluble elastin as substrate. Elastolytic activity in the secretions increased significantly at days 2 and 5 but was greatest after 14 days of NO2 exposure. These observations indicate that the secretions of alveolar macrophages from hamsters exposed to NO2 increased elastolytic activity. This activity correlates with the duration of NO2 exposure for periods as long as 14 days. The increased elastolysis observed appears to be dependent on increased numbers of macrophages rather than on increased elastolytic secretion per cell. Inhibition studies with a battery of elastase inhibitors indicated that the elastase(s) secreted from NO2 and control alveolar macrophages have identical properties. The response of hamster macrophage elastase to inhibitors differs from that observed in the mouse and in humans in that it is not inhibited by EDTA, human serum or 1,10-phenanthroline.

Animals↗

PubMed1995

[In vitro exposure of a human bronchial epithelial cell line with nitrogen dioxide induces enhanced transcription and liberation of pro-inflammatory cytokines].

Studies of in vivo inhalation of nitrogen dioxide (NO2) have demonstrated a transient pulmonary inflammation. This study was done to determine the contribution of airway epithelial cells to the release of inflammatory mediators following NO2 exposure. Confluent cultures of the human bronchial epithelial cell line BEAS-2B on Transwell-Col filters were exposed for 1 h to air or NO2 up to 1.5 ppm with the apical fluids removed with 5% CO2 at 37 degrees C. The cells were hydrated with Hanks' Balanced Salt Solution (HBSS) in the basolateral compartment. Sequential reverse transcription and quantitative cDNA amplification (RT-PCR) was used to measure inflammatory mediator mRNA abundance in BEAS-2B cultures. When compared to air-exposed cells, NO2 induced increases in IL-6 (23.4-fold) and IL-8 (30.9-fold) mRNA abundance. The NO2-dependent increases in mRNA expression reached a maximum between 0 and 1 h post exposure and returned to baseline levels within 24 h. IL-6 and IL-8 proteins as measured by enzyme-linked immunosorbent assays (ELISA) were also elevated in supernatants recovered from NO2-exposed BEAS-2B cells. These studies suggest that exposure to NO2 induces the synthesis and release of inflammatory mediators from airway epithelial cells that may participate in the pathogenesis of airway disease.

Bronchi↗

PubMed1993

Effect of nitrogen dioxide on synthesis of inflammatory cytokines expressed by human bronchial epithelial cells in vitro.

Although studies of nitrogen dioxide (NO2) inhalation, in both animals and humans, have demonstrated that this agent can cause epithelial cell damage and inflammation of the airway epithelium, the mechanisms underlying these effects are not well understood. We have cultured human bronchial epithelial cells, as explant cultures from surgical tissue, and studied these firstly from their ability to constitutively synthesize specific proinflammatory cytokines and then investigated the effect of exposure to NO2 on the generation of these cytokines. Constitutive synthesis of cytokines was evaluated by analysis of both the expression of the mRNA for interleukin (IL)-1 beta, IL-4, IL-8, granulocyte/macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma), by the polymerase chain reaction (PCR), and by immunocytochemical staining for the presence of cell-associated IL-1 beta, IL-8, GM-CSF, TNF-alpha, and IFN-gamma, using specific monoclonal and polyclonal antibodies directed towards these cytokines. Release of IL-4, IL-8, GM-CSF, TNF-alpha, and IFN-gamma following exposure to 5% CO2 in air or 400 ppb and 800 ppb NO2 for 6 h was investigated by enzyme-linked immunosorbent assay. PCR demonstrated that the human bronchial epithelial cells expressed the mRNA for IL-1 beta, IL-8, GM-CSF, and TNF-alpha but not for IL-4 and IFN-gamma. Immunocytochemical staining confirmed the presence of endogenous IL-1 beta, IL-8, GM-CSF, and TNF-alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Molecular mechanisms of nitrogen dioxide induced epithelial injury in the lung.

The lung can be exposed to a variety of reactive nitrogen intermediates through the inhalation of environmental oxidants and those produced during inflammation. Reactive nitrogen species (RNS) include, nitrogen dioxide (.NO2) and peroxynitrite (ONOO-). Classically known as a major component of both indoor and outdoor air pollution, .NO2 is a toxic free radical gas. .NO2 can also be formed during inflammation by the decomposition of ONOO- or through peroxidase-catalyzed reactions. Due to their reactive nature, RNS may play an important role in disease pathology. Depending on the dose and the duration of administration, .NO, has been documented to cause pulmonary injury in both animal and human studies. Injury to the lung epithelial cells following exposure to .NO2 is characterized by airway denudation followed by compensatory proliferation. The persistent injury and repair process may contribute to airway remodeling, including the development of fibrosis. To better understand the signaling pathways involved in epithelial cell death by .NO2 or otherRNS, we routinely expose cells in culture to continuous gas-phase .NO2. Studies using the .NO2 exposure system revealed that lung epithelial cell death occurs in a density dependent manner. In wound healing experiments, .NO2 induced cell death is limited to cells localized in the leading edge of the wound. Importantly, .NO2-induced death does not appear to be dependent on oxidative stress per se. Potential cell signaling mechanisms will be discussed, which include the mitogen activated protein kinase, c-Jun N-terminal Kinase and the Fas/Fas ligand pathways. During periods of epithelial loss and regeneration that occur in diseases such as asthma or during lung development, epithelial cells in the lung may be uniquely susceptible to death. Understanding the molecular mechanisms of epithelial cell death associated with the exposure to .NO2 will be important in designing therapeutics aimed at protecting the lung from persistent injury and repair.

Air Pollutants↗

PubMed1996

In vivo formation of mutagens by intraperitoneal administration of polycyclic aromatic hydrocarbons in animals during exposure to nitrogen dioxide.

Consumption of fossil fuels has increased indoor and outdoor concentrations of polycyclic aromatic hydrocarbons (PAHs) and nitrogen dioxide (NO2). To study the combined effect of PAH administration and NO2 exposure on mutagenicity of urine from animals we injected 400 mg/kg body wt i.p. one of five kinds of PAH (pyrene, fluoranthene, fluorene, anthracene and chrysene) into ICR mice, Wistar rats, Syrian golden hamsters or Hartley guinea pigs after exposure to 20 p.p.m. NO2 gas for 24 h and then exposed the animals to NO2 gas for an additional 24 h. During the latter 24 h we collected the urine and assayed its mutagenicity with the Ames Salmonella strains after treatment with beta-glucuronidase and arylsulfatase and extraction with dichloromethane. The urine from mice treated with both PAH and NO2 showed high mutagenicity for Salmonella typhimurium strains TA98 and TA100, whereas the urine from mice treated with PAH and air showed almost no mutagenic activity. The mutagenicity was decreased in nitroreductase- and acetyltransferase-deficient strains TA98NR and TA98/1,8-DNP6 respectively. Treatment with a mixture of 20% of each of the five kinds of PAH and NO2 augmented the urinary mutagenicity of mice 1.5-fold. The urine from hamsters treated with pyrene or fluoranthene and NO2 was also highly mutagenic, but that from rats or guinea pigs was not very mutagenic. The mutagenicity was also decreased in strains TA98NR and TA98/1,8-DNP6. These results suggest that the urine contains nitro compounds and that the nitration of PAHs occurs in the body of animals under exposure to NO2 gas. Actually, the nitrated metabolites of pyrene, 1-nitro-6/8-hydroxypyrene and 1-nitro-3-hydroxypyrene, were detected in the urine from mice treated with pyrene under exposure to NO2 gas. To elucidate the mechanism of in vivo nitration, NO2 (20 p.p.m.) was bubbled through 50 mM Tris-HCl buffer (pH 7.4) or dichloromethane solution containing pyrene or 1-hydroxypyrene (10 microg/ml). Pyrene was not nitrated by NO2 in either aqueous or organic solutions. However, 1-hydroxypyrene was changed to nitrohydroxypyrenes by NO2 in the Tris-HCl buffer, but not in the organic solution. Ascorbic acid, alpha-tocopherol, glutathione oleic acid and hemoglobin were found to inhibit the nitration of 1-hydroxypyrene in aqueous solution. The urinary mutagenicity of mice treated with both pyrene and NO2 was also decreased by oral administration of ascorbic acid and alpha-tocopherol. These results suggest that 1-hydroxypyrene is nitrated by an ionic reaction in the animal body after hydroxylation of pyrene in the liver.

Animals↗

PubMedDate not supplied

Anaerobic ammonia oxidation with nitrogen dioxide by Nitrosomonas eutropha.

Nitrosomonas eutropha, an obligately lithoautotrophic bacterium, was able to nitrify and denitrify simultaneously under anoxic conditions when gaseous nitrogen dioxide (NO2) was supplemented to the atmosphere. In the presence of gaseous NO2, ammonia was oxidized, nitrite and nitric oxide (NO) were formed, and hydroxylamine occurred as an intermediate. Between 40 and 60% of the produced nitrite was denitrified to dinitrogen (N2). Nitrous oxide (N2O) was shown to be an intermediate of denitrification. Under an N2 atmosphere supplemented with 25 ppm NO2 and 300 ppm CO2, the amount of cell protein increased by 0.87 mg protein per mmol ammonia oxidized, and the cell number of N. eutropha increased by 5.8 x 10(9) cells per mmol ammonia oxidized. In addition, the ATP and NADH content increased by 4.3 micromol ATP (g protein)-1 and 6.3 micromol NADH (g protein)-1 and was about the same in both anaerobically and aerobically grown cells. Without NO2, the ATP content decreased by 0.7 micromol (g protein)-1, and the NADH content decreased by 1.2 micromol (g protein)-1. NO was shown to inhibit anaerobic ammonia oxidation.

Adenosine Triphosphate↗

PubMed1982

Protection with cycloheximide or emetine against pulmonary edema induced by ozone or nitrogen dioxide.

Pretreatment with cycloheximide or emetine provided significant protection against pulmonary edema in rats exposed to ozone or nitrogen dioxide. Other inhibitors of protein-synthesis, actinomycin D or puromycin, failed to show such effects. Possible actions of these agents as well as the doses and times that afforded the significant protection were investigated. These agents, by themselves, did not alter the water content of the lungs. In vitro study revealed that both cycloheximide and emetine hardly acted as scavengers of oxidant. Pretreatment with either agent was associated with a significant increase in the activity of glucose 6-phosphate dehydrogenase of the lungs, but the increase did not necessarily coincide with the protection. Activity levels of non-protein SH, glutathione-peroxidase and -reductase in the lungs of rats treated with either agent were scarcely altered. The effect of these agents administered in vivo or in vitro on the in vitro lipid peroxidation by air was also investigated. Other possible mechanisms of these agents responsible for the protective effect against pulmonary edema induced by oxidants were also discussed.

Animals↗

PubMed1986

Effects of nitrogen dioxide exposure on the contents of prostaglandins and thromboxane B2 in broncho alveolar lavage.

Effects of 10 ppm nitrogen dioxide (NO2) exposure on the contents of prostaglandins (PGs) and thromboxane (TX) B2 in bronchoalveolar lavage (BAL) of rats were studied. In the BAL of normal rats, the amounts of PGs and TXB2 in the whole lavage were 6-keto-PGF1 alpha (38.0 +/- 6.4 ng) greater than TXB2 (11.8 +/- 4.0 ng) greater than PGF2 alpha (5.7 +/- 1.6 ng) much greater than PGE (0.5 +/- 0.3 ng). Rats were exposed to NO2 for 1,3,5,7 and 14 days. The NO2 exposure decreased in the level of 6-keto-PGF1 alpha by about 35% throughout the exposure. The level of TXB2 was higher in the day 5 exposure group (155%). The contents of PGF2 alpha and PGE first, decreased and then transiently increased on days 3 and 5. PG 15-hydroxy-dehydrogenase activity of lung homogenate decreased correspondingly on day 3 and 5. Then the contents PGF2 alpha and PGE decreased on day 7 and 14. 6-keto-PGF1 alpha and TXB2 are stable metabolites of PGI2, a strong bronchorelaxant and TXA2, a strong bronchoconstrictor respectively. Therefore the results suggested that the decrease in 6-keto-PGF1 alpha, a major prostanoid in the BAL and the increase in TXB2 may correlate with broncho constriction by NO2 exposure.

6-Ketoprostaglandin F1 alpha↗

PubMed1992

Biochemical and histological alterations in rats after acute nitrogen dioxide intoxication.

1. In previous studies a rat inhalation model was developed to investigate the treatment of acute nitrogen dioxide (NO2) intoxication. 2. Biochemical parameters, which may be important for the evaluation of lung injury and repair, were reviewed and compared with the histology. 3. After exposure to high NO2 concentrations (75 ppm, 125 ppm or 175 for 10 min) the lung injury observed by light microscope was most pronounced after 24 h and became worse with increasing concentration. 4. The most sensitive indicators for lung injury in the broncho-alveolar lavage fluid (BAL) were protein and albumin concentrations, angiotensin converting enzyme activity, beta-glucuronidase activity and the presence of neutrophil leucocytes. The changes observed in these variables were dose-dependent. Following exposure to 175 ppm the protein and albumin concentrations and the angiotensin converting enzyme activity showed a 100-fold increase, while the beta-glucuronidase activity showed a 10-fold increase. 5. Glucose-6-phosphate dehydrogenase and glutathione peroxidase in the supernatant of lung homogenate and gamma-glutamyl transferase activity in BAL are likely to be the most practical parameters for monitoring the phase of repair because their activities were maximal at the moment histological changes were reduced in intensity. 6. Repair was almost complete 7 d following exposure.

Administration, Inhalation↗

PubMed1981

Mutagenicity of nitro derivatives induced by exposure of aromatic compounds to nitrogen dioxide.

Mutagenic nitro derivatives were readily induced when 6 kinds of chemicals were exposed to 10 ppm of nitrogen dioxide (NO2). Single nitro derivatives were formed from pyrene, phenanthrene, fluorene or chrysene. Carbazole and fluoranthene each produced 2 derivatives substituted with nitro groups at different positions. The formation of nitro derivatives was enhanced by exposure of pyrene to NO2 containing nitric acid (HNO3, less than 100-fold enhancement) or sulphur dioxide (SO2, less than 15-fold enhancement). After 24 h of exposure the yields of the nitro derivative were 0.02% with 1 ppm of NO2 in air and 2.85% with NO2 (1 ppm) containing traces of HNO3. The nitro derivatives from all but phenanthrene and carbazole were chemically identified by means of gas chromatography (GC) and mass spectrometry (MS), and the mutagenicity of the 4 kinds of authentic nitro derivatives was tested by using Salmonella strains TA98 and TA1538 with or without the S9 fraction from rat liver treated with Aroclor 1254. The nitro derivative induced from pyrene was determined to be 1-nitropyrene; that of chrysene was 6-nitrochrysene; that of fluorene was 2-nitrofluorene; and those of fluoranthene were 3-nitrofluoranthene, and 8-nitrofluoranthene. Tested with strain TA98 in the absence of the S9 fraction, the first 4 of these derivatives yielded, respectively, 3050, 269, 433 and 13 400 revertants per nmole. Thus, each nitro derivative formed was potentially a direct-acting frameshift-type mutagen. Each compound exposed to NO2 showed a decreased mutagenic activity when tested in the presence of S9 mix. A possible explanation comes from experiments in which 1-nitropyrene was incubated with the S9 mix at 37 degree C for 10 min, and 1-aminopyrene was formed. The mutagenic activity of 1-aminopyrene was appreciable, but only about one-tenth of that of 1-nitropyrene in the Ames test.

Heterocyclic Compounds↗

PubMed2000

Personal exposures of children to nitrogen dioxide relative to concentrations in outdoor air.

OBJECTIVES: To investigate the relation between fluctuations in personal exposure to nitrogen dioxide (NO(2)) in school children and changes in outdoor NO(2) concentrations. METHODS: 114 Asthmatic school children aged 7-12 years were recruited from the Southampton area. Weekly average personal exposures to NO(2) were measured over a 13 month period with passive diffusion tubes. At the same time, outdoor NO(2) concentrations were monitored at a fixed site in the centre of Southampton. Correlations between weekly personal exposures and mean outdoor concentrations during the same periods were examined. RESULTS: Mean duration of follow up was 32 weeks. Measurements of weekly mean personal NO(2) exposures were generally low and ranged from 2.47 to 1751 [corrected] micrograms/m(3) with a geometric mean of 60 [corrected] micrograms/m(3). Substantial variation in personal exposures occurred between children and more especially within individual children from week to week. Daily outdoor concentrations of NO(2) ranged from 15.2 to 105.2 [corrected] micrograms/m(3), with a geometric mean of 43.4 [corrected] micrograms/m(3). There was no evidence of seasonal variation in outdoor concentrations. No significant correlation was found between each child's weekly mean personal exposures to NO(2) and mean outdoor concentrations for the corresponding periods. CONCLUSION: At low outdoor NO(2) concentrations, fluctuations in NO(2) in outdoor air as measured at a central monitoring station do not contribute importantly to variations in personal exposure when averaged over a week.

Air Pollution↗

PubMed1987

Acute effect of nitrogen dioxide exposure on the functional activity of alpha-1-protease inhibitor in bronchoalveolar lavage fluid of normal subjects.

Nitrogen dioxide is one form of an oxidizing free radical that is sufficiently stable to exist in relatively high concentrations in ambient air and cigarette smoke. We examined the effect of NO2 exposure on the functional activity against pancreatic elastase of alpha-1-protease inhibitor (alpha 1PI) in bronchoalveolar lavage (BAL) fluid of nonsmoking subjects. Ten nonsmokers (mean age, 25 +/- 2 SE yr) were exposed to NO2 (3 or 4 ppm) for 3 h with intermittent exercise. Seven nonsmokers (mean age, 24 +/- 2 SE yr) underwent a similar protocol but were exposed to NO2-free air and served as control subjects. Bronchoalveolar lavage was performed 3.5 to 4 h after the end of exposure. Exposure to NO2 caused a 45% decrease in functional activity of alpha 1PI in BAL. There was no significant difference in immunoreactive alpha 1PI between the groups whether expressed as micrograms per 100 ml of recovered fluid or per milligram of albumin. This inactivation of alpha 1PI was not associated with any neutrophil migration into the air spaces of the lung. The "elastaselike" activity of BAL using synthetic elastinlike chromophore substrate succinyl-trialanine-nitroanilide showed no significant difference between the NO2-exposed group (221 +/- 39 SE ng/dl BAL) and the control group (196 +/- 61 SE ng/dl BAL). Assay for human leukocyte elastase (HLE) in concentrated BAL using the synthetic substrate Methoxysuc-Ala3-Pro-Val-aminomethylcoumarin did not detect any HLE activity in the BAL. These results showed that nonsmoking subjects exposed to relatively low concentrations of NO2 for a short time have a significant inactivation of alpha 1PI in the lower respiratory tract fluid than did nonsmoking control subjects.

Adult↗

PubMed2005

A miniaturized active sampler for the assessment of personal exposure to nitrogen dioxide.

A personalized, miniaturized air sampling system was evaluated to estimate the daily exposure of pediatric asthmatics to nitrogen dioxide (NO2). The lightweight device (170 g) uses a sampling pump connected to a solid sorbent tube containing triethanolamine (TEA)-impregnated molecular sieve. The pump is powered by a 9 V battery and samples air over a 24 h period at a collection rate of 0.100 L/min. After exposure, the solid sorbent is removed from the tubes for spectrophotometric analysis (Griess Assay). The lower detection limit of the overall method for NO2 is 11 microg/m3. The linearity, precision and accuracy of the sampler was evaluated. Different NO2 concentrations generated in the laboratory (range: 50 to 340 microg/m3) were simultaneously measured by the TEA tube samplers and colocated continuous chemiluminescent NO(x) analyzers (reference method). The coefficient of determination for the laboratory test derived from ordinary linear regression (OLR) was r2 = 0.99 (y(OLR) = 0.94 x -4.58) and the precision 3.6%. Further, ambient NO2 concentrations in the field (range: 10-120 microg/m3) were verified with continuous chemiluminescent monitors next to the active samplers. Re-weighted least squares analysis (RLS) based on the least median squares procedure (LMS) resulted in a correlation of r2 = 0.68 for a field comparison in Riverside, CA (y(RLS) = 1.01 x -0.94) and r2 = 0.92 in Los Angeles, CA (y(RLS) = 1.31 x -7.12). The precision of the TEA tube devices was 7.4% (at 20-60 microg/m3 NO2) under outdoor conditions. Data show that the performance of this small active sampling system was satisfactory for measuring environmental concentrations of NO2 under laboratory and field conditions. It is useful for personal monitoring of NO2 in environmental epidemiology studies where daily measurements are desired.

Air Pollutants↗