Interaction of nitrogen dioxide with cholesterol monomolecular films: effect of initial surface pressure, time of exposure, and concentration of nitrogen dioxide.
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Cholesterol↗
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Chronic effects of nitrogen dioxide on cilia in hamster bronchioles.
Nitrogen dioxide has been shown to have a deleterious effect on the structure and function of respiratory cilia. This study focuses on both the alterations of cilia morphology, and the ciliated cell response induced by nitrogen dioxide, in order to determine the mechanism(s) leading to ciliary dysfunction. Ciliated cells of the respiratory airways of hamsters, exposed to 30 ppm nitrogen dioxide for 5 months, 7 days/week, 22 hours/day, were examined ultrastructurally using Scanning Electron Microscopy (SEM) and Transmission Electron Microscopy (TEM) of thin sections, freeze-fracture replicas, and thin sections of tissues treated with cationized ferritin. SEM and TEM preparations appeared to show a generalized reduction in number and length of cilia. It was common to see basal bodies with no ciliary shaft and many cilia at different stages of growth. It was also apparent that the cilia were most fragile just below the ciliary necklaces. After breakage, the plasma membranes of the remaining ciliary stubs covered the exposed basal bodies. During the early stages of ciliary regeneration, freeze fracture replicas showed the emergence of membrane particles which appeared to correlate with cationized ferritin binding sites. As the cilia increased in length, the particles assembled into a necklace-like arrangement, varying in ring number and particle distribution as compared to the 5 to 7 well organized rings observed in controls. In corresponding thin sections, cationized ferritin appeared bound to sites in the region of the ciliary necklace particles. As the cilia developed further, the cationic ferritin binding at these sites diminished. This data suggests that nitrogen dioxide had an affect on the plasma membranes of ciliated cells. One of the major sites affected by the nitrogen dioxide was the ciliary necklace region. Exposure to nitrogen dioxide appeared to lead to increased ciliary fragility, stunted ciliary growth, and loss of ciliary motility. The rings of ciliary necklace particles exhibited an 8.4 degrees +/- 1.3 degree angle of pitch to a perpendicular through the longitudinal axis of the cilium. The measurable pitch and the identification of ciliary necklace "free ends" proximally and distally lead us to hypothesize that the particle arrangement of the ciliary necklace is that of a single spiral and not separate rings.
Animals↗
Effects of nitrogen dioxide on leaf chlorophyll and nitrogen content of soybean.
One-month-old soybean (Glycine max [L.] Merrill), cultivar 'Williams', plants were exposed to nitrogen dioxide (0.1, 0.2, 0.3 and 0.5 ppm) and carbon filtered air (control), 7 h per day, for 5 days, under a controlled environment. Leaf chlorophyll content (Ch a, Ch b, and total Ch content) and foliar nitrogen content (%N) were determined before and after the exposure. The influence of NO(2) treatments up to 0.3 ppm on leaf chlorophyll content was negligible although a stimulatory effect was evident in Ch a and total Ch content with 0.2 ppm NO(2). Marked decline in Ch content was observed with 0.5 ppm treatment; the reductions in Ch a and total Ch were 45% and 47%, respectively. Foliar-N contents of plants treated with 0.2 and 0.3 ppm NO(2) were higher than the control; plants exposed to 0.5 ppm NO(2) showed a 41% reduction in foliar-N compared to pre-exposure values.
Journal Article↗
Distributions of long-term household exposure of different population groups to nitrogen dioxide.
Exposure distributions to nitrogen dioxide in living rooms during the summer and winter were calculated for four groups of Zagreb inhabitants (high school students, university students, employed, and retired persons) using Duan's Cartesianization method. Households were classified into three categories according to fuel used for cooking and heating--electricity (or no gas use), propane-butane, and natural gas. The results showed a seasonally dependent contribution to exposure in households from outdoor sources through ventilation, while type of fuel used for heating and cooking, representing indoor pollution sources, had a predominant influence on exposure levels. Exposure distribution functions could be represented by lognormal, or summation by proportion of lognormal and normal distributions. A comparison of the results and the proposed exposure guideline value suggests that either the guideline value is too large, or a nitrogen dioxide exposure problem exists only in a small percentage of homes and is caused by the high rate of air exchange between the kitchen and living room.
Air Pollution, Indoor↗
Modulation of pulmonary defense mechanisms against viral and bacterial infections by acute exposures to nitrogen dioxide.
The scientific literature suggests that ambient levels of nitrogen dioxide increase susceptibility to respiratory infections. However, this association has not been conclusively demonstrated. The epidemiologic data regarding this relationship are inconclusive because these studies have used parameters of "acute respiratory illness" that are not necessarily related to infectious episodes. Previous animal studies have used either mortality after bacterial infection with virulent bacteria or decreased rate of intrapulmonary killing of bacteria with low virulence. Studies using appropriate bacterial and viral challenge organisms, with morbidity as an endpoint, provide a better basis for extrapolation to humans. The investigations in animals suggest a relationship between nitrogen dioxide and increased susceptibility to respiratory infection, but studies in which functional parameters of host resistance to such infections have been used are few. The aim of this work was to determine the threshold level of acute nitrogen dioxide exposure that would induce increased susceptibility to, and increased severity of, viral and bacterial infections. Physiologic parameters of host resistance to respiratory infections were used as endpoints. A composite picture was developed of dose-response relationships between nitrogen dioxide and the impairment of a spectrum of defense parameters in the murine respiratory tract against viral and bacterial challenges. The salient findings of this study are as follows: (1) the intrapulmonary killing of Staphylococcus aureus was impaired at 5 ppm of nitrogen dioxide; (2) this effect was found at 2.5 ppm or less when nitrogen dioxide exposure was superimposed on lungs predisposed to lowered resistance through immunosuppression with corticosteroids; (3) the adverse effect of nitrogen dioxide occurred at lower concentrations when exposure followed bacterial challenge; and (4) during the course of murine Sendai virus infection, exposure to nitrogen dioxide for four hours per day did not alter the infection in the lungs, but rather it enhanced lung pathology. The implications of these findings are that the antibacterial defenses of the lungs are susceptible to the inhibiting effects of short acute exposures of lower concentrations of nitrogen dioxide when the lungs are predisposed by bacteria present or, even more so, by immunosuppression. The alveolar macrophage phagocytic system is the defense component of the lungs that is most susceptible to the adverse effects of nitrogen dioxide. The finding that nitrogen dioxide increases virus-associated lung damage suggests that the increased severity of the disease process results from the proliferation of the virus to high titers, rather than from alterations of the infective process.
Animals↗
Altered susceptibility to viral respiratory infection during short-term exposure to nitrogen dioxide.
The studies reported here focus on the relation of nitrogen dioxide exposure to susceptibility to viral respiratory infection in a murine model of pneumonia, created by intratracheal inoculation of an endogenous murine pathogen, mouse cytomegalovirus. The purpose of this work is to clarify the potential role of nitrogen dioxide exposure in the pathogenesis of viral infection of the lower respiratory tract. Previous human epidemiologic studies have presented conflicting information about the relationship of nitrogen dioxide to acute, self-limited episodes of respiratory illness, which are characteristic of viral respiratory infection. Some studies have found an association between exposure to elevated ambient levels of nitrogen dioxide and increased occurrence of acute respiratory illness. In one study this association was found to be strongest in children in the first two years of life. However, other epidemiologic studies have failed to observe this relation. To determine if there is scientific evidence for the possible relation of nitrogen dioxide exposure to human respiratory infection, our studies were performed to assess the impact of nitrogen dioxide on respiratory tract susceptibility to initial, or primary, infection, as well as to recurrent infection, or reinfection, with the identical virus. The latter mechanism of viral respiratory infection is of particular interest, since reinfection is a common method for the development of infection of the lower respiratory tract during early childhood. Outbred CD-1 mice were exposed to either air or nitrogen dioxide for six hours a day on two consecutive days prior to inoculation with murine cytomegalovirus, and then were reexposed to the same level of nitrogen dioxide for six hours a day on four consecutive days, beginning the day after viral inoculation. Susceptibility to primary infection was determined by inoculating animals with an amount of virus (10(2) plaque-forming units) that is too small to produce viral infection in the lungs of normal animals. Mice exposed to 5 parts per million (ppm) nitrogen dioxide routinely developed viral replication in the lung and histologic evidence of pneumonitis after inoculation with this amount of virus, whereas air-exposed animals did not. Most importantly, animals exposed to 5 ppm nitrogen dioxide could be infected with a viral inoculum that was 100-fold smaller than that required to consistently produce viral infection in air-exposed mice. Enhanced susceptibility to infection was found after exposure to 5 ppm nitrogen dioxide, but was not observed with exposure to 2.5 or 1 ppm nitrogen dioxide.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Combined exposure to ozone and nitrogen dioxide.
The combined effects of ozone and nitrogen dioxide were assessed in an in vitro test system utilizing human red cells. In general, these two pollutants had additive effects on the parameters measured which included osmotic fragility, acetylcholinesterase activity, lipid peroxidation, reduced glutathione and methemoglobin levels. However, at lower pollutant doses a synergistic increase in lipid peroxides was noted while at higher doses the effect became less than additive. Further studies of this observation suggested that ferrous hemoglobin potentiates ozone-induced lipid peroxidation while methemoglobin, resulting primarily from nitrogen dioxide, inhibits this process. Ozone was also found to potentiate the methemoglobinemic effects of nitrogen dioxide, particularly in sequential studies in which ozone exposure preceded nitrogen dioxide. Inasmuch as the effects of these two pollutants vary from protective to synergistic depending on the pollutant concentration, duration and sequence of exposure, as well as on the parameter assayed, it would appear that the approach to in vivo study of the combined effects of ozone and nitrogen dioxide should be aimed at simulating ambient conditions as closely as possible.
Acetylcholinesterase↗
The use of simple diffusion tube samplers for the measurement of nitrogen dioxide in an operating room using nitrogen oxide as an anaesthetic (July - November 1999).
Estimates have been made of the amounts of nitrogen dioxide (NO2) in the operating room of University of Benin Teaching Hospital (UBTH) where nitrous oxide (N2O) a potential source of NO is used as an anaesthetic agent Measurements were made using palmes diffusion tubes, a device which is capable of taking samples of NO2 gas from the atmosphere through diffusion or permeation of this compound to the interior and subsequently trapping it by means of adsorption on reactive material, but which does not involve the active movement of the gas through the sampler. Results obtained indicate a low concentration of NO2 in the operating room with a minimum of 5.83 microg/m3 and a maximum concentration of 6.22 microg/m3 NO2. This result therefore suggests that the use of nitrous oxide in the operating room does not contribute significantly to the concentration of NO2.
Adsorption↗
Effect of domestic concentrations of nitrogen dioxide on airway responses to inhaled allergen in asthmatic patients.
Nitrogen dioxide is a common indoor pollutant. In the light of suggestions that outdoor air pollution can harm people with asthma, we investigated the effect of 1 h exposures to domestic concentrations of nitrogen dioxide on the airway response to house-dust mite (HDM) allergen in ten patients with mild asthma. Each subject breathed air, 100 ppb nitrogen dioxide, or 400 ppb nitrogen dioxide for 1 h, in double-blind, random order, then immediately underwent a fixed-dose HDM challenge. Baseline forced expiratory volume in 1 s (FEV1) was not affected by any of the gas mixtures. The mean early asthmatic response (maximum percentage change in FEV1 during first 2 h after challenge) was -14.62% (SD 8.03) after air, -14.41% (7.86) after 100 ppb nitrogen dioxide, and -18.64% (7.28) after 400 ppb nitrogen dioxide. The difference between air and 400 ppb (-4.01%) was significant (95% CI -1.34 to -6.69%, p < 0.009), but those between air and 100 ppb and between 100 and 400 ppb were not (0.21 [-3.10 to 3.53]% and -4.23 [-8.75 to 0.29]%). The mean late asthmatic response (maximum percentage change in FEV1) to challenge after air was -2.85% (3.95), after 100 ppb nitrogen dioxide -7.76% (6.92), and after 400 ppb -8.13% (6.64). The difference in means between the air and 400 ppb exposures was significant (-5.28 [-0.73 to -9.83]%, p < 0.02) but those between air and 100 ppb (-4.90 [-10.60 to 0.78]%) and 100 and 400 ppb (0.37 [3.06 to 3.80]%) were not. These findings suggest that nitrogen dioxide, at concentrations encountered in the home environment, can potentiate the specific airway response of patients with mild asthma to inhaled HDM allergen, although the effect is small.
Adolescent↗
Nitrogen dioxide in Australian homes: levels and sources.
Indoor nitrogen dioxide exposure has been associated with respiratory symptoms in children in many studies, but in Australia, levels and sources of nitrogen dioxide in homes have not been well-characterized. Therefore, as part of a larger indoor environmental study, conducted in the Latrobe Valley, Victoria, nitrogen dioxide was monitored using passive samplers in 80 homes. Samples were collected on five occasions over one year. Mean indoor levels were higher than outdoor levels, and a seasonal variation was evident, with highest levels recorded in winter. The overall median level was 11.6 micrograms/m3 (6.0 ppb), ranging from < 0.7 to 246 micrograms/m3 (128 ppb). Major indoor nitrogen dioxide sources were: gas stoves, vented gas heaters, and smoking. Some 67% of variation in indoor nitrogen dioxide levels could be explained by presence of major sources, house age, and outdoor levels. Gas stoves were the main contributors.
Adolescent↗
Nitrogen dioxide modifies allergic inflammation in tracheal mucosa.
Our study was designed to investigate the possible role of nitrogen dioxide exposure in respiratory allergic disorders. Guinea pigs were treated with a combination of passive sensitization, antigen challenge and nitrogen dioxide exposure. Nitrogen dioxide accumulated eosinophils to the epithelium of the trachea. Neither passive sensitization nor antigen challenge with nitrogen dioxide exposure developed more prominent pathological changes than nitrogen dioxide exposure alone. However, antigen--antibody interaction with nitrogen dioxide exposure resulted in a disruption of epithelial cells so prominent that the basement membrane was denuded in areas. Activated eosinophils and free eosinophil-specific granules were considered to be responsible for the extreme epithelial injury. In conclusion, nitrogen dioxide exposure does not cause prominent epithelial injury by itself, but could be a trigger for hyperresponsiveness in allergic airways, and is probably involved in the pathogenesis of airway allergic disorders.
Air Pollutants↗
Reduction in nitrogen dioxide concentration by soda lime preparations during simulated nitric oxide inhalation.
Nitrogen dioxide is formed during delivery of inhaled nitric oxide for the treatment of patients with pulmonary hypertension. Soda lime has been shown to absorb nitrogen dioxide. We tested three different commercially available soda lime preparations (Sodasorb, Drägersorb 800 and Sofnolime) for their efficacy in absorbing nitrogen dioxide and nitric oxide during simulated nitric oxide inhalation. All soda lime preparation absorbed nitrogen dioxide (15%, 24% and 34%, respectively). To test if this difference could be attributed to the potassium hydroxide (KOH) content of the different preparations, two other preparations with a higher (3.0% and 7.3% w/w, respectively) KOH content were tested and we found an increase in nitrogen dioxide removal up to 47% and 46%, respectively. We conclude that soda lime absorbed nitrogen dioxide during nitric oxide inhalation. This effect seemed to be moderate under simulated clinical conditions, but increased using soda lime with a higher KOH content. Nevertheless, we recommend continuous monitoring of inspired nitrogen dioxide concentration during clinical inhalation of nitric oxide.
Absorption↗
Nitrogen dioxide exposure alters neonatal development.
Nitrogen dioxide (NO2) is one of the commonly encountered environmental contaminants. Experiments were carried out to test for neonatal behavioral alterations associated with prenatal NO2 exposure. Pregnant CD-1 mice were exposed in environmental chambers to 0, 22, or 45 ppm of NO2 in air from gestation day 7 to 18. The gas-air flow was set at 450 ml/min. Food and water were available at all times. The dams were allowed to deliver and neonatal behavioral development of the pups was studied. Nitrogen dioxide exposure did not affect the number of live pups born/litter; however, it significantly decreased their birth weight. Prenatal NO2 exposure at both levels significantly altered the righting reflex and aerial righting score of the pups on postnatal days 1 and 12, respectively. Prenatal NO2 exposure did not affect negative geotaxis and activity scores of pups on postnatal day 10 and 28, respectively. The data suggest that maternal NO2 exposure at low levels can affect neuromuscular coordination and thus produce deficits in the functional capability of the offspring.
Animals↗
Ventilation in public housing: implications for indoor nitrogen dioxide concentrations.
UNLABELLED: Although elevated nitrogen dioxide (NO2) exposures may exacerbate asthma, few studies have examined indoor NO2 levels in low-income, urban neighborhoods, where asthma prevalence is high. As part of the Healthy Public Housing Initiative, NO2 was measured in 77 homes within three Boston public housing developments, using Palmes tubes placed in the kitchen, living room, and outdoors. Air exchange rates (AERs) were assessed using a perfluorocarbon tracer technique. Overall NO2 levels were [mean (ppb)+/-s.d.]: kitchen (43+/-20, n=100), living room (36+/-17, n=102), outdoor (19+/-6, n=91). Indoor NO2 levels were significantly higher in the heating season (living room: 43 ppb vs. 26 ppb, kitchen: 50 ppb vs. 33 ppb), while AERs were significantly lower in the heating season (medians 0.49/h vs. 0.85/h). Significant univariate predictors of indoor concentrations include: outdoor NO2 levels, AERs, and occupancy. AERs and outdoor NO2 remained significant in multivariate models (P<0.05). A dummy variable for supplemental heating with gas stove was not significant (P=0.14), but had a large, positive coefficient. Indoor NO2 levels in this cohort are higher than those generally reported in residential US settings, associated in part with increased gas stove usage and decreased AERs during the heating season. PRACTICAL IMPLICATIONS: Indoor air quality is mainly a function of outdoor concentrations, indoor sources, ventilation, and residential behavior. Indoor exposures to nitrogen dioxide and other combustion pollutants may be elevated within low-income housing developments due to the presence of multiple sources, poor ventilation, small apartment size, and behavioral responses to apartment conditions (e.g. supplemental heating with gas stove). This information may be used by housing authorities and other landlords to decrease potential environmental stressors, through interventions such as source substitution and improved ventilation, particularly for sensitive sub-populations such as asthmatics.
Air Pollution, Indoor↗
Uptake by macrophages of low-density lipoprotein damaged by nitrogen dioxide in air.
In order to know whether nitrogen dioxide, an environmental and endogenous free radical toxin, can participate in the formation of atherosclerotic lesions, damage to low-density lipoprotein (LDL) by nitrogen dioxide and uptake of the damaged LDL by macrophages were investigated. A solution of LDL at pH 7.5 was exposed to an atmosphere of nitrogen dioxide (70 ppm) in air at 37 degrees C for 5 or 10 h. Lipid oxidation was induced by the exposure as assessed by the formation of thiobarbituric acid reactive substances. Apolipoprotein B was covalently cross-linked via nondisulfide bonds. Fluorescence analysis showed that tryptophan residues were extensively decreased, and amino acid analysis indicated that the contents of histidine, lysine, and tyrosine residues were decreased by 30-40, 10-20, and 20-30%, respectively. Binding of LDL to thioglycolate-induced mouse peritoneal macrophages was markedly increased by the exposure as observed by the binding of mouse erythrocytes coated with LDL. The activity of LDL to convert macrophages into lipid-laden foam cells was also increased by the exposure. Modification of lysine residues of apo B with lipid oxidation products formed by the exposure may be responsible for the uptake by macrophages. The results suggest the possibility that exposure of LDL in vivo to nitrogen dioxide participates in the formation of atherosclerotic lesions.
Air Pollutants↗
Effects of nitrogen dioxide on alveolar epithelial barrier properties.
This study analyzed the effects of nitrogen dioxide (NO2) on alveolar epithelial permeability and transport properties. Primary cultured monolayers of rat Type II pneumocytes, cultured on both nonporous and porous surfaces, were used as models of isolated alveolar epithelium for in vitro exposure to nitrogen dioxide. The effects of nitrogen dioxide exposure for monolayers cultured on nonporous substrata were monitored by observing the changes in the net volume of fluid under the monolayer; for cells cultured on porous substrata, alterations in tissue bioelectric properties were noted. As a first step, primary cultured monolayers of rat Type II pneumocytes plated on nonporous plastic Petri dishes were used to investigate the effects of nitrogen dioxide on alveolar epithelial barrier properties. Such monolayers form fluid filled domes that are thought to result from active solute transport from medium to substratum, with water following passively. We used dome formation as a transport marker. Five-day-old cultures were directly exposed to 30 ppm NO2 in 5 percent CO2 in air at 25 degrees C, by cyclically tilting culture plates from side to side, so that both halves of the monolayer were exposed during each cycle. Exposures consisted of 10 cycles of four minutes each (two minutes per side), for a cell exposure time of 20 minutes. Control plates were simultaneously exposed to 5 percent CO2 in air under identical conditions. One day after the exposure, nitrogen dioxide-exposed monolayers exhibited significant decreases in dome density and individual dome volume, compared to the controls. By 48 hours post-exposure, differences between nitrogen dioxide-exposed and control monolayers were less, but remained significant. These results showed that short-term sublethal exposures to nitrogen dioxide produce a decrease in dome formation in Type II alveolar epithelial cell monolayers. This finding is most likely due to a decrease in the active transepithelial sodium transport rate, or an increase in the permeability of cell membranes or tight junctions, or both. Addition of vitamin E-containing liposomes to the culture media 24 hours pre-exposure did not affect the nitrogen dioxide-induced decrease in dome formation, indicating that under these circumstances no protective effect was provided by the antioxidant.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Explanation of pressure effects on a nitrogen dioxide (NO2) sampler.
When nitrogen dioxide (NO2) samplers were exposed at several reduced pressures, it was found that the sampling rate was correspondingly decreased; that finding did not agree with accepted diffusional theory. When the experiments were repeated using water vapor as the gas and molecular sieve as the sorbent, the observed sampling rates were in very good agreement with diffusional theory. These findings demonstrated that the pressure effect was not common to all diffusional samplers and suggested that there might be an alternate explanation for the results with NO2-triethanolamine (TEA). The best possibility appeared to be the dehydration of TEA that takes place at reduced pressures. That this is a very significant factor was demonstrated by simultaneous exposure to identical concentrations of NO2 at 1 atm and 50% or 0% relative humidity. In dry air the sampling rate was equivalent to that found previously at about 1/10 atm. The earlier results can be satisfactorily explained as indirect rather than direct effects of reduced pressure.
Diffusion↗
Airway responses to nitrogen dioxide in asthmatic subjects.
Nitrogen dioxide is a common indoor air pollutant. In order to characterize the respiratory responses to this gas, 10 asthmatics (mean age +/- SD = 30 +/- 8 yrs) were exposed to air and 0.5 ppm NO2 gas for 1 h in a 30-m3 environmental chamber on different days in a double-blind randomized fashion. The forced vital capacity, (VC), functional residual capacity, forced expiratory volume in 1 s, partial expiratory flow at 40% VC (Vp 40), and specific airway conductance were measured before and after exposure. Airway reactivity to methacholine inhalation was determined after each exposure. The dose of methacholine in milligrams per milliliter to cause a 40% decrease in Vp 40 was measured. None of the subjects reported any significant symptoms after exposure. Significant potentiation of airway reactivity was noted after NO2 exposure in asthmatic subjects as a group [PD40(AIR) = 9.2 +/- SD 15.0 versus PD40(NO2) = 4.6 +/- SD 8.2 mg/ml, p = 0.042]. No significant changes were noted in other lung functions after NO2 exposure. These findings indicate that asthmatics exposed to 0.5 ppm NO2 develop heightened airway reactivity.
Adult↗