SEARCH · PubMed Health

Results for “NITROGEN DIOXIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

PubMed2003

Comparison of two manual methods of nitrogen dioxide determination in ambient air.

Sodium arsenite (modified Jacobs and Hochheiser method; hereafter referred as SA), the most widely used manual monitoring method for determination of nitrogen dioxide (NO2) in ambient air, particularly in developing countries has been evaluated and compared with US EPA recommended equivalent method of TGS-ANSA (hereafter referred as ANSA). NO2 concentrations generated from laboratory test atmosphere were analyzed by these two methods and were compared statistically. Laboratory evaluations showed that SA method has high sensitivity to different sampling conditions, which normally vary during actual field monitoring. Hence, correction factors for absorption efficiency were estimated for SA and ANSA methods. Absorption efficiency of NO2 in SA method was found to be much lower (64%) as against the reported value of 82% at the method recommended sampling conditions, whereas for ANSA method, it was found 1.0 as against the reported value of 0.93. After applying derived correction factors, both the methods produced almost similar concentration values of NO2.

Absorption↗

PubMed1984

A nitrosating agent from the reaction of atmospheric nitrogen dioxide (NO2) with methyl linoleate: comparison with a product from the skins of NO2-exposed mice.

We showed previously that exposure of mice to atmospheric nitrogen dioxide (NO2) leads to the formation of an ether-extractable nitrosating agent (NSA) in the skin, which produced N-nitrosomorpholine (NMOR) from morpholine in vitro but not in vivo (under our conditions). We now report that NO2 bubbled into hexane solutions of methyl linoleate (MLIN) produced a similar NSA that reacted with morpholine in dichloromethane solution to produce NMOR. The NSA yield increased sharply as MLIN concentration was raised, with a maximum 0.1% yield of NSA from MLIN. The NSA yield from MLIN was four times that from methyl oleate and seven times that from methyl stearate. The NSA derived from MLIN travelled on thin-layer chromatography more slowly than the main weight fraction; whereas TLC of NSA in the skin lipids of NO2-exposed mice and in untreated mouse skin lipids exposed in vitro to NO2 produced NSA that travelled more rapidly than the main weight fraction.

Air↗

PubMed1983

Long-term sequelae of bronchiolitis induced by nitrogen dioxide in hamsters.

The long-term consequences of acute lung injury during critical growth periods of the lung were evaluated by inducing mild bronchiolitis with nitrogen dioxide (NO2) in 3-day-old (newborn) and 21-day-old (young) hamsters. Hamsters were exposed to 30 ppm NO2 for 7 days. Age-matched animals exposed to room air served as controls. Lung volumes, static deflationary pressure-volume curves, mean linear intercept, and internal surface area were measured when the animals reached 1 yr of age. Newborns exposed to NO2 showed an increased volume at 25 cm H2O pressure (V25) adjusted for body weight, a decreased transpulmonary pressure at 60% of V25, and an increased mean linear intercept when compared with control animals. The internal surface area was less than that in the control animals; the difference approached significance. In the young exposed group there were no differences for any measurements when compared with the control group. These data indicate that a mild injury imposed during the newborn period may result in physiologic and morphometric changes that simulate mild emphysema in the mature animal.

Animals↗

PubMed1992

Effects of repeated exposure to 4 ppm nitrogen dioxide on bronchoalveolar lymphocyte subsets and macrophages in healthy men.

Following the basal descriptive studies of the bronchoalveolar inflammatory cell response induced by single exposure with nitrogen dioxide (NO2) in man, it was considered important to clarify the cell response to repeated exposure with NO2. This investigation was, therefore, undertaken with bronchoalveolar lavage (BAL) 3 weeks before and 24 h after six repeated exposures with 4 ppm NO2 (7 mg.m-3) in ten healthy volunteers. The exposures were performed during 20 min and every second day. Analysis of the recovered BAL fluid demonstrated that repeated exposures to NO2 caused a lung cell response different from that reported after a single exposure. Amounts of lavaged alveolar macrophages, B-cells, and natural killer (NK)-cells were decreased and the T-helper-inducer/cytotoxic-suppressor cell ratio was altered, but there was no lymphocytosis or mastocytosis as after single exposure. Lymphocyte numbers in peripheral blood were reduced after exposure. These results suggest that repeated exposure with NO2 adversely affects the immune defence. This could contribute to the increased susceptibility to airway infections reported to be associated with NO2 exposure.

Adult↗

PubMed1998

The Boston residential nitrogen dioxide characterization study: classification and prediction of indoor NO2 exposure.

Many epidemiological studies have used house characteristics associated with indoor sources as simplified proxies for personal nitrogen dioxide (NO2) exposure. Stove type and presence of a pilot light often been used as the two key characteristics, but significant overlaps have remained in the NO2 concentrations in the exposed and unexposed groups. This has contributed to inconsistencies in epidemiological findings, due to potential misclassification of exposure. In this study, other possible proxies were analyzed by cross-table analyses and were investigated in terms of improvements in both classification and predictive power. Adding building type to the above two proxies resulted in 0-5% of households with concentrations overlapping the observed range for the opposing stratum, compared with 22-42% for the two-proxy model. In spite of this performance, the predictive power of regression models for indoor NO2 was not improved by the addition of the third proxy, and the potential sample population was significantly limited. Using these analytical methods to choose descriptive proxies and evaluate the tradeoffs in their implementation can help epidemiological studies improve their designs and therefore optimize the robustness of their conclusions.

Air Pollution, Indoor↗

PubMed1989

Experimental exposures of young asthmatic volunteers to 0.3 ppm nitrogen dioxide and to ambient air pollution.

Asthmatic volunteers aged 8 to 16 (N = 34) were exposed on separate occasions to clean air (control), to 0.30 ppm nitrogen dioxide (NO2) in otherwise clean air, and to polluted Los Angeles area ambient air on summer mornings when NO2 pollution was expected. Exposures lasted 3 hr, with alternating 10-min periods of exercise and rest. In ambient pollution exposures, 3-hr average NO2 concentrations ranged from 0.01 to 0.26 ppm, with a mean of 0.09 ppm. Ambient exposures did not significantly affect lung function, symptoms, or bronchial reactivity to cold air, relative to the control condition. Responses to 0.3 ppm NO2 exposures were equivocal. Asthma symptoms were more severe during 1-week periods before 0.3 ppm exposures, and lung function was decreased immediately before 0.3 ppm exposures, compared to other conditions. Lung function declined slightly during the first hour at 0.3 ppm, but improved over the remaining 2 hr. Compared to other conditions, symptoms were not increased during 0.3 ppm exposures, but were increased during 1-week periods afterward. These observations may reflect untoward effects of 0.3 ppm NO2, or may reflect chance increases in asthma severity prior to 0.3 ppm exposures.

Adolescent↗

PubMed2005

The German view: effects of nitrogen dioxide on human health--derivation of health-related short-term and long-term values.

The presented overview concerning health relevant effects caused by nitrogen dioxide (NO2) resumes the current state of results from animal experiments and human studies (epidemiology and short-term chambers studies). NO2 concentrations applied in animal experiments were mostly considerably higher than in ambient air. Therefore, short- and long-term limit values were derived from human data. Experimental studies conducted with humans demonstrate effects after short-term exposure to concentrations at or above 400 microg NO2/m3. Effects on patients with light asthma could not be observed after short-term exposure to concentrations below 200 microg/m3. On basis of epidemiological long-term studies a threshold below which no effect on human health is expected could not be specified. Two short-term limit values have been proposed to protect public health: a 1-h value of 100 microg/m3 and a 24-h mean value of 50 microg/m3. Due to the limitations of epidemiological studies to disentangle effects of single pollutants, a long-term limit value cannot be easily derived. However, applying the precautionary principle, it is desirable to adopt an annual mean of 20 microg NO2/m3 as a long-term mean standard to protect public health.

Air Pollutants↗

PubMed1998

Exposure to nitrogen dioxide and the occurrence of bronchial obstruction in children below 2 years.

BACKGROUND: The objective of the investigation was to test the hypothesis that exposure to nitrogen dioxide (NO2) has a causal influence on the occurrence of bronchial obstruction in children below 2 years of age. METHODS: A nested case-control study with 153 one-to-one matched pairs was conducted within a cohort of 3754 children born in Oslo in 1992/93. Cases were children who developed > or = 2 episodes of bronchial obstruction or one episode lasting >4 weeks. Controls were matched for date of birth. Exposure measurements were performed in the same 14-day period within matched pairs. The NO2 exposure was measured with personal samplers carried close to each child and by stationary samplers outdoors and indoors. RESULTS: Few children (4.6%) were exposed to levels of NO2 > or = 30 microg/m3 (average concentration during a 14-day period). In the 153 matched pairs, the mean level of NO2 was 15.65 microg/m3 (+/-0.60, SE) among cases and 15.37 (+/-0.54) among controls (paired t = 0.38, P = 0.71). CONCLUSIONS: The results suggest that NO2 exposure at levels observed in this study has no detectable effect on the risk of developing bronchial obstruction in children below 2 years of age.

Air Pollution, Indoor↗

PubMed2002

Personal exposure of Paris office workers to nitrogen dioxide and fine particles.

AIMS: (1) To obtain an overall estimate of variability of personal exposure of Paris office workers to fine particles (PM(2.5)) and nitrogen dioxide (NO(2)), and to quantify their microenvironmental determinants. (2) To examine the role of potential determinants of indoor concentrations. METHODS: Sixty two office workers in a Paris municipal administration (all non-smokers) were equipped with personal samplers: passive samplers for 48 hours for NO(2) (n = 62), and active pumps for 24 hours for PM(2.5) (n = 55). Simultaneous measurements were performed in homes and offices; the local air monitoring network provided ambient concentrations. A time activity diary was used to weight measured concentrations by time spent in each microenvironment in order to estimate exposure concentrations. RESULTS: On average, PM(2.5) personal exposure (30.4 microg/m(3)) was higher than corresponding in-home (24.7 microg/m(3)) and ambient concentrations (16.7 microg/m(3)). Personal exposure to NO(2) (43.6 microg/m(3)) was significantly higher than in-home concentrations (35.1 microg/m(3)) but lower than the background outdoor level (60.1 microg/m(3)). Personal exposures to PM(2.5) and NO(2) were not significantly different from in-office concentrations. PM(2.5) and NO(2) personal exposures were not significantly correlated. In-home, in-office, in-transit, outdoor time weighted concentrations, and time spent in other indoor microenvironments explain respectively 86% and 78% of personal variations in PM(2.5) and NO(2). In-home PM(2.5) concentration was primarily influenced by exposure to environmental tobacco smoke, and secondly by the ambient level (R(2) = 0.20). NO(2) in-home concentration was affected mostly by the ambient level and gas cooking time (R(2) = 0.14). CONCLUSION: While results show the major contribution of in-home and in-office concentrations to both NO(2) and PM(2.5) personal exposures, the identification of indoor level determinants was not very conclusive.

Administrative Personnel↗

PubMed1997

Technical considerations for inhaled nitric oxide therapy: time response to nitric oxide dosing changes and formation of nitrogen dioxide.

UNLABELLED: The aim of the present study was to analyse the time response to nitric oxide (NO) dosing changes as well as the formation of nitrogen dioxide (NO2) with different ventilation systems, respirator settings and application sites during NO inhalation. The inspired NO and NO2 concentrations were continuously measured using chemiluminiscence within a dummy ventilatory system equipped with two different respirator systems (Siemens Servo 900c and Bear BP 2001). NO was either introduced into the afferent limb of the ventilatory circuit close to the endotracheal tube (site A) or into the so-called low pressure port of the Servo 900c respirator, far away from the endotracheal tube (site B). In addition, the decay of the inspired NO concentration after cessation of the NO gas flow was studied. This decay was considerably prolonged when NO was introduced at site B (time constants: tau = 7.19 min versus tau = 0.29 min). Within the concentration range studied (0-25 ppm NO) a linear correlation between the NO and NO2 concentration was found. At site A and an inspired oxygen concentration of > 0.95 NO2 formation amounts to 1.14% +/- 0.11% of the NO concentration. Using this value one can calculate the NO2 formation for a given NO dose. For example, when 40 ppm NO are applied, a concentration of 0.45 ppm NO2 can be expected, which is well below the relevant toxic concentrations. However, when NO was introduced at site B, NO2 formation was significantly increased to 1.61% +/- 0.16%. Passage of the ventilated gas through soda lime led only to a slight and insignificant reduction in NO2 concentration. The continuous flow respirator BP 2001 showed a significantly lower NO2 concentration when compared to the non-continuous flow respirator Servo 900c (0.64 +/- 0.11% vs.1.14 +/- 0.11%). CONCLUSION: The application of NO close to the endotracheal tube is associated with a much faster response of the actual inspired NO concentration to dosing changes and shows the lowest NO2 formation. In order to avoid toxic NO2 concentrations, an upper limit of 40 ppm NO is recommended for continuous NO inhalation.

Analysis of Variance↗

PubMed2006

Association of indoor nitrogen dioxide with respiratory symptoms in children: application of measurement error correction techniques to utilize data from multiple surrogates.

In 1991, Neas et al. reported that indoor nitrogen dioxide (NO(2)), a byproduct of high-temperature combustion, was significantly associated with lower respiratory symptoms among a cohort of 1,159 white children aged 7-11 years in six US cities studied from 1983 to 1988. For each 15 p.p.b. increment of NO(2), the multivariate adjusted odds ratio (OR) was 1.4 (95% confidence interval (CI)=[1.1, 1.7]). Although indoor NO(2) concentration in the ambient air was assessed only in a subset of the children, the prevalence of lower respiratory symptoms and surrogate exposure variables were available in all of the children at the time of the indoor monitoring program. This paper evaluates the effect of indoor NO(2) exposure on the annual risk of lower respiratory symptoms by applying a regression calibration method to the 2,891 children in the overall study with complete covariate and outcome data, 1,137 of whom had NO(2) directly measured and 1,754 of whom only surrogate exposure data were available. An estimate of the indoor annual NO(2) exposure effect (p.p.b.) is obtained, which is adjusted for measurement error induced by the use of surrogate NO(2) sources among the 1,754. These sources include the presence of a gas stove with or without a pilot light, the presence of a kerosene space heater, the presence of a wood stove, and the usage of a stove for heating, and residential characteristics, including fan usage for kitchen ventilation and the total number of rooms in the home. After adjusting for age, gender, city, parental history of respiratory diseases, and smoking inside the children's home (packs/day), a 15-p.p.b. increment in NO(2) exposure was found to be associated with a significant 50% increased annual risk of lower respiratory symptoms (OR=1.5, 95% CI=[1.2, 1.8]). Simulation results indicated that, under conditions similar to those observed in these data, the estimator is unbiased and has a coverage probability close to the nominal value. Using the methodology illustrated in this paper, it became possible to utilize all data available and obtain a 34% more precise estimate of the NO(2) exposure effect on lower respiratory symptoms, which was adjusted for measurement error due to using NO(2) surrogates instead of directly measured NO(2).

Air Pollution, Indoor↗

PubMed1997

Nitrogen dioxide production in a nitric oxide inhalation system using the Servo Ventilator 900C.

During nitric oxide (NO) inhalation therapy, toxicity may be produced by the reactive metabolite nitrogen dioxide (NO2). The purpose of the present study was to determine the NO2 concentration in a NO inhalation system used for respiratory failure in children at relatively low concentrations of NO (< 20 ppm). The production of NO2 in the NO inhalation system using the Servo Ventilator 900C connected to the test lung under each of 30 combinations of NO concentrations (0, 4, 8, 12, 16, and 19 ppm) and inspired oxygen (O2) concentrations (21, 40, 60, 80, and 100%). Pressure controlled ventilation was used with a respiratory rate of 20 breaths/min. NO and NO2 measurements were obtained on the inspiratory side of the Y-piece connected to the test lung. At a given NO level, increases in the concentration of inspired O2 resulted in increases in the concentration of NO2 produced, as did increases in the amount of NO at a given concentration of O2. The mean NO concentration at the inspiratory site of the Y-piece did not exceed 0.05 ppm (the limit of NO2 as an outdoor air pollutant in the United States) when the NO concentration did not exceed 8 ppm, regardless of the O2 concentration. NO inhalation therapy for children with severe respiratory failure using the Servo Ventilator 900C can be performed safely when the concentration of NO does not exceed 8 ppm.

Nitric Oxide↗

PubMed2006

A cohort study of indoor nitrogen dioxide and house dust mite exposure in asthmatic children.

OBJECTIVE: The purpose of this study was to investigate dose-response relationships between asthma symptoms and indoor nitrogen dioxide (NO2) and house dust mite allergen (HDM) in children. METHODS: Asthmatic children from 18 primary schools in Adelaide, Australia, kept a daily symptoms diary over 12 weeks. Home and classroom NO2 levels were measured repeatedly in winter 2000. HDM levels were obtained from beds. Lung function tests were performed at the beginning and at the end of the study period. RESULTS: Data on exposure and respiratory outcomes were gathered for 174 children. For school exposure, the estimated relative symptom rate (RR) for a 10-ppb increase in NO2 for difficulty breathing during the day was 1.09 (95% confidence interval [CI] = 1.03-1.15), at night 1.11 (95% CI = 1.05-1.18), and for chest tightness at night 1.12 (95% CI = 1.07-1.17). Significant symptom rate increases were also found for kitchen NO2 exposure. This was supported by a negative dose-response relationship between percentage predicted forced expiratory volume in 1 second and NO2 (-0.39%; 95% CI = -0.76 to -0.02) for kitchen exposure. Significant threshold effects using a 10-microg/g cutoff point for HDM exposure were established in the sensitized children for nighttime wheeze (RR = 3.62, 95% CI = 1.49-8.77), daytime cough (RR = 1.64, 95% CI = 1.14-2.36), and daytime asthma attack (RR = 1.95, 95% CI = 1.06-3.60). CONCLUSION: This study has established reliable risk estimates for exacerbations of asthma symptoms in children based on dose-response investigations of indoor NO2 and HDM.

Adolescent↗

PubMed1999

Effects of nitrogen dioxide exposure on Clara cell proliferation and morphology.

The present study was performed to relate Clara cell proliferation and Clara cell morphology to duration and intensity of nitrogen dioxide (NO2) exposure as a model of lung injury in rats. Male Sprague-Dawley rats were exposed to 5, 10 and 20 ppm NO2 for three (short term exposure) and 25 days (long term exposure). Epithelial proliferation was immunohistochemically assessed by BrdU-incorporation into the bronchial and bronchiolar epithelium. Clara cell specific 10 kD protein was detected using an antibody versus recombinant protein. Following short term exposure Clara cells showed a significant alteration of their morphology: the cells lost the apical intraluminal projections, and the damaged epithelium was covered by a layer of CC10 reactive material. After long term exposure the Clara cell morphology was indistinguishable from that of unexposed controls. In all short term exposure groups cellular proliferation was higher in the bronchiolar epithelium than in the bronchial epithelium. Whereas short term exposure to 5 ppm NO2 sufficed to induce a maximum epithelial proliferation of the bronchiolar epithelium, long term exposure to 5 ppm NO2 yielded no significant increase in the epithelial proliferation, a finding reflecting the adaptation of the airway epithelium to oxidative stress. Long term exposure to 10 and 20 ppm NO2 resulted in a dosilinear increase of cell proliferation in the bronchial and bronchiolar epithelium. Double labelling of CC10 and BrdU showed that BrdU uptake and hence proliferation were restricted to Clara cells. We conclude that changes of the Clara cell morphology are closely related to the extent of inhalative stress and functional status of the Clara cell. The results are in keeping with the assumption that the Clara cell exerts progenitor cell functions in the airway epithelium.

Animals↗

PubMed1989

Effects of nitrogen dioxide and ozone in combination on xenobiotic metabolizing activities of rat lungs.

Male Jcl:Wistar rats were exposed continuously to 0.2 ppm ozone (O3) and 4 ppm nitrogen dioxide (NO2), alone and in combination, for 1 and 2 months to examine the effects of combined gas on the xenobiotic metabolizing systems of lung microsomes. The cytochrome P-450 content increased to 200% and 253% of the control values during 2-month exposures to O3, while it was not increased by NO2 exposures. Addition of NO2 to O3 reduced the increased level of cytochrome P-450 to 179% and 178% of the control values. The activities of cytochrome P-450-dependent monooxygenase, benzo[a]pyrene hydroxylase and 7-ethoxycoumarin O-deethylase were changed in the same fashion by exposures to NO2 and O3. The 7-ethoxycoumarin O-deethylase activity was increased to 147% and 142% of the control values by O3 exposure, whereas it was decreased to 71% and 75% of the control values by NO2 exposures. This activity was decreased to 124% and 97% of the control values by combination of O3 with NO2 after 1 and 2 months, respectively. Similarly, the benzo[a]pyrene hydroxylase activity was increased to 157% and 153% of the control values during O3 exposures, while it was not changed by NO2 exposures. Addition of NO2 to O3 reduced the activity to 140% and 115% of the control values after 1 and 2 months, respectively. The alteration of coumarin hydroxylase activity was different from those of others. This activity decreased to 44% and 29% of the control values after 1- and 2-month exposures to NO2, respectively, and was also decreased by O3 exposures. However, the magnitude of decrease was not reinforced by combination of NO2 with O3. These results indicate that an increased level of xenobiotic metabolizing activity produced by O3 exposures is lowered by combination with NO2. These phenomena may be antagonistic effects of these gases on the xenobiotic metabolizing systems of lung microsomes.

7-Alkoxycoumarin O-Dealkylase↗

PubMed1980

The McConnell missile accident. Clinical spectrum of nitrogen dioxide exposure.

Twenty-four men were refueling a missile when a large spill of oxidizer occurred. Three crewmen were exposed to very high concentrations of the oxides of nitrogen. One died within minutes. Severe respiratory distress syndrome developed in the other two, one of whom survived. Twenty-one other workers were exposed to minimal to moderate concentrations of the gas. Most remained asymptomatic while six had shortness of breath, cough, or hemoptysis. The three with persistent symptoms received corticosteroid therapy; the complaints resolved in two. Corticosteroid therapy for four asymptomatic patients who had moderate hypoxemia two weeks after the accident may have aborted the second stage of nitrogen dioxide injury. Six patients with minimal exposure had persisting headaches, visual disturbances, and emotional difficulties. These latter findings may represent an unusual complication of exposure to these gases.

Accidents, Occupational↗

PubMed1986

Identification of cholesterol as a mouse skin lipid that reacts with nitrogen dioxide to yield a nitrosating agent, and of cholesteryl nitrite as the nitrosating agent produced in a chemical system from cholesterol.

The skin lipids of mice exposed to nitrogen dioxide (NO2) and mouse skin lipids exposed in vitro to NO2 contain nitrosating agents (NSAs), that react with amines to produce nitrosamines. This situation represents a potential hazard of exposure to NO2. A principal NSA precursor in mouse skin lipids was purified by thin-layer and high-performance liquid chromatography. Each fraction was assayed by bubbling in NO2 and determining NSA. The precursor was identified as cholesterol on the basis of its chromatographic behavior and spectral properties. In a chemical system, cholesterol reacted with NO2 to give 13% yields of an NSA, which was identified from its spectral properties as the previously known compound, cholesteryl-3-beta-nitrite. These findings and the chromatographic behavior of a major NSA in the skin lipids of NO2-exposed mice suggested that this NSA was cholesteryl nitrite.

Animals↗

PubMed2000

Effect of an imidazolineoxyl nitric oxide on prostaglandin synthesis in experimental shock: possible role of nitrogen dioxide in prostacyclin synthase inactivation.

The effect of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a nitric oxide (NO) scavenger that yields nitrogen dioxide (NO(2)) in a rat endotoxemia model was investigated. Endotoxin (lipopolysaccharide [LPS]) increased NO synthase (NOS) activity and inducible NOS expression measured in lung and plasma levels of nitrite/nitrate, 6-oxo-prostaglandin (PG) F(1alpha), thromboxane B(2), and PGF(2alpha). Infusion of cPTIO significantly reduced LPS-induced mean arterial blood pressure decline and mortality and selectively reduced LPS-induced 6-oxo-PGF(1alpha) plasma levels and prostacyclin synthase (PGIS) activity measured in the lung and aorta. In vitro, PGIS activity in aorta rings was not modified by SNAP (NO donor), cPTIO slightly inhibited the enzyme but not in the presence of L-N(G)-monomethyl arginine, and SNAP in combination with cPTIO significantly inhibited PGIS. Thus, cPTIO may be beneficial in endotoxic shock because of NO scavenging and PGIS inactivation, which could be mediated by NO(2).

6-Ketoprostaglandin F1 alpha↗