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Alveolar and airway cell kinetics in the lungs of rats exposed to nitrogen dioxide, ozone, and a combination of the two gases.

Rats carrying minipumps filled with 5-bromo-2'deoxyuridine were exposed to ozone, NO2, or a mixture of the two gases using four different protocols: (A) ozone 0.2 ppm, NO2 3.6 ppm, or their mixture for 24 hr a day; (B) ozone 0.2 ppm, NO2 7.2 ppm, or their mixture for 12 hr per night; (C) ozone 0.6 ppm, NO2 10.8 ppm, or their mixture for 8 hr per night; and (D) ozone 0.8 ppm, NO2 14.4 ppm, or their mixture for 6 hr per night. After three consecutive daily exposures, the animals were returned to filtered air and killed 7 days after implantation of the minipump. Alveolar labeling indices were comparable to control values except in the group of animals exposed for 6 hr nightly to a combination of 0.8 ppm of ozone and 14.4 ppm of NO2. Labeling indices in the peripheral airways were the most sensitive exposure index since they were significantly increased over control values in all animals exposed to ozone, NO2, or a mixture of the two gases, regardless of concentration or exposure duration. Labeling indices increased with elevated dose rate, i.e., concentration of the gases in the inspired air. The response to the combined gases was greater than the calculated sum of the responses to the two individual gases for the three higher dose rates in the large airways and for the highest dose rate in the peripheral airways. The results led to the following conclusions: (1) By the criterion of analysis of cell kinetics in rat large and peripheral airways, neither ozone, NO2, nor their mixture follows Haber's law (c x t = k) over the concentration ranges studied; and (2) at the higher dose rates studied, there is a more than additive (synergistic) airway response to the combination of ozone and NO2.

Animals↗

Direct exposure to nitrogen dioxide fails to induce the expression of some inflammatory cytokines in an IC-21 murine macrophage cell model.

Biologically-active molecules secreted from alveolar macrophages, such as cytokines, have been proposed to be involved in the induction of pulmonary toxicity and inflammation in response to the inhalation of oxidant gas pollutants such as NO2 and O3. Despite this, mechanistic studies are hampered by the difficulty in obtaining control macrophages from human subjects, and the intrinsic variability of such primary cells. It is, thus, of importance to develop alternative models for such studies. Here, we have characterised expression kinetics of the mRNAs for tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), macrophage inflammatory protein-1 alpha (MIP-1 alpha) and macrophage inflammatory protein-1 beta (MIP-1 beta) in confluent cultures of the murine IC-21 macrophage line in response to LPS. The secretion of TNF-alpha protein into the medium, assayed by L-929 cell bioassay, closely followed the expression of its mRNA in response to the LPS stimulus. In contrast to LPS, the exposure of IC-21 cells to either air or various concentrations of NO2 in air between 2 and 20 ppm, in an inverted plate exposure model, failed to induce the expression of any of the cytokine mRNAs probed. We conclude that the IC-21 cell line may represent a suitable model for studying the role of stimulated cytokine gene expression in inflammation and that the early events in the pulmonary inflammatory response to the inhalation of NO2 do not involve stimulated release of TNF-alpha, IL-1 beta or MIP-1 alpha/MIP-1 beta from macrophages.

Actins↗

The effect of lung alpha-tocopherol content on the acute toxicity of nitrogen dioxide.

The effect of lung vitamin E content on early direct damage to lung by NO2 was studied by exposing three groups of rats differing in lung vitamin E content to 0, 10, 20, 30, and 40 ppm NO2 for 4 hr. Lung vitamin E contents of 3.24, 17.4, and 87.7 micrograms/lung were obtained by maintaining animals on semipurified diets containing 0, 10, or 1000 mg/kg of d-alpha-tocopherol acetate. Animals were sacrificed immediately after the 4-hr exposure and lung damage was assessed by assaying the lung lavage content of protein, sialic acid, lactate dehydrogenase (LDH), malate dehydrogenase (MDH), glucose-6-phosphate dehydrogenase (GDH), acid phosphatase (AP), and aryl sulfatase (AS), all of which increase in lavage fluid in a concentration-dependent manner over the range of NO2 concentrations used. Increases in lavagable protein, sialic acid, AP, and AS were not affected by the different vitamin E contents, while the increases in LDH, MDH, and GDH were significantly attenuated in the 1000-mg/kg diet group relative to the 0- and 10-mg/kg diet groups. Lipid peroxidation was not detectable in NO2-exposed lungs by either conjugated diene measurement or thiobarbituric-acid-reactive materials, with the exception of a slight increase in thiobarbituric-acid-reactive material in free cells. These results suggest two mechanisms of NO2 damage to lung. The attenuation of the appearance of some lavage parameters by high vitamin E is consistent with lipid peroxidation as a necessary event in the damage responsible for their appearance, although the lack of change in indicators of lipid peroxidation in the whole lung suggests that peroxidation occurs to only a very limited extent. The lavage parameters which are unaffected by lung vitamin E content apparently appear in airways as a result of events not involving lipid peroxidation.

Administration, Oral↗

Biochemical effects of combined gases of nitrogen dioxide and ozone. III. Synergistic effects on lipid peroxidation and antioxidative protective systems in the lungs of rats and guinea pigs.

Rats and guinea pigs were exposed continuously to 0.4 ppm NO2, 0.4 ppm O3 or a combination of the two gases for 2 weeks. The concentration of lipid peroxides in lungs of rats and guinea pigs exposed to NO2 alone or O3 alone did not change. The lipid peroxide level of rats inhaling the combined gases also did not change. However, the level of lipid peroxides in guinea pigs exposed to a combination of the two gases was increased to 2.2 times of the control level, showing a synergistic interaction. No increases of antioxidative protective enzyme activities and of antioxidants (such as NPSH, VE, VC) in guinea pigs exposed to NO2, O3 or the combined gases were found. In rats, no changes in enzyme activities and of the antioxidant contents were observed after NO2 alone, but O3 exposure produced slight increases of NPSH, VC, and GPx-H2O2. On the other hand, in rats exposed to the combined gases, marked synergistic increased of many antioxidative factors such as NPSH, VC, G6PD, GPx-cum.OOH and GPx-H2O2 were found. The results show that those animals which are able to increase antioxidative protective factors in the lung following exposure to the combined gases do not respond with a significant increase in lipid peroxides. On the other hand, in animals with poor induction-ability of these factors lipid peroxides are formed. This might explain why guinea pigs were the most sensitive to the effects of the combined gases. Furthermore, it was shown that in guinea pigs the increased level of lipid peroxides and that in rats the increased activities of antioxidative enzymes and the increased contents of the antioxidants were synergistic following exposure to the combined gases.

Animals↗

Exposure assessment approaches to evaluate respiratory health effects of particulate matter and nitrogen dioxide.

Several approaches can be taken to estimate or classify total personal exposures to air pollutants. While personal exposure monitoring (PEM) provides the most direct measurements, it is usually not practical for extended time periods or large populations. This paper describes the use of indirect approaches to estimate total personal exposure for NO2 and particulate matter (PM), summarizes the distributions of these estimates, and compares the effectiveness of these estimates with microenvironmental concentrations for evaluating effects on respiratory function and symptoms. Pollutant concentrations were measured at several indoor and outdoor locations for over 400 households participating in an epidemiological study in Tucson, Arizona. Central site monitoring data were significantly correlated with samples collected directly outside homes, but the former usually had higher pollutant concentrations. Integrated indices of daily total personal exposure were calculated using micro-environmental (ME) measurements or estimates and time-budget diary information. Peak expiratory flow rates (PEFR) were measured for up to four times a day during two-week study periods. In thirty children (ages 6-15 years) with current diagnosed asthma, a significant reduction in PEFR was associated with NO2 levels measured outside of their homes. Additional decrements of morning PEFR were found in those children sleeping in bedrooms with higher measured NO2 levels. Morning and noon PEFR decrements were also linked to higher morning NO2 levels that were measured at central monitoring stations. Effects of PM were also found, but were limited to morning PEFR. No effects were found in non-asthmatic children. The relationship of PEFR to the calculated indices of daily average total exposure were weaker than to the microenvironment concentrations. This suggests that diary and ME monitoring data need to yield better time resolution in order to incorporate short-term average exposures to higher concentrations into the exposure indices and into the analysis of within day health responses.

Adolescent↗

A case study of personal exposure to nitrogen dioxide using a new high sensitive diffusive sampler.

Personal NO(2) exposure measurements were achieved during two campaigns in a large northern France city. These campaigns were following an innovating approach based on sequential exposure measurements by diffusive samplers distinguishing four categories of microenvironments ("home", "other indoor places", "transport" and "outdoors"). The objective of these campaigns was to obtain NO(2) personal exposure data in different microenvironments and to examine the determinants of personal exposure to this pollutant. Each campaign comprised two 24-h sampling periods: one during a working day and the second during the weekend. The average total NO(2) personal exposure ranged from 17 microg m(-3) for the summer weekend samplings to 38 microg m(-3) for the winter weekday samplings. The highest levels were found in transports and outdoors, the intermediate ones in other indoor places and the lowest in homes. Despite their weak levels, indoor environments contributed for more than 78% to total NO(2) personal exposure because of more time spent in these living places. A Multiple Correspondence Analysis (MCA) highlighted the determinants of NO(2) personal exposure in the "home" and "transport" microenvironments. This led to a classification of NO(2) personal exposure levels according to different means of transport: from the lowest to the highest exposure levels, train, tramway or underground, bicycle, car or motorcycle. In homes, the rise of NO(2) personal exposures is mainly due to the use of gas stoves and gas heating and the absence of automatic airing system. A classification of NO(2) personal exposure levels was set up according to the characteristics of homes. An analysis of correlations between the home NO(2) personal exposures and outdoor concentrations measured by fixed ambient air monitoring stations showed weak relations suggesting that the data of these stations are poor predictors of NO(2) personal exposures in homes.

Air Pollutants↗

Influence of environmental parameters on the accuracy of nitrogen dioxide passive diffusion tubes for ambient measurement.

Two studies at three sites in the UK provided confirmation that systematic positive bias in NO2 diffusion tube measurement occurred because of changes to "within-tube" chemistry, rather than eddy diffusion at the mouth of the tube. In the first study in Cambridge, UK, sampler overestimation for 1 and 2 week exposures was compared to corresponding time-averaged monitor measurements (NO-NO2-NOx, O3) and weather variables. Noninearity between sampler and monitor NO2 measurements was interpreted in terms of spatial and temporal variations in relative and absolute availability of NO, NO2 and O3 at the site. A maximum overestimation occurred for an exposure mean NO2/NOx approximately 0.5. The separate contributions of reduced NO2 photolysis and eddy diffusion were compared in Study II using samplers of two materials, acrylic and quartz, and of different lengths (40, 55, 71 and 120 mm) at three sites: Norwich background, Cambridge intermediate, London kerbside. For compared sites, NO2 measured by acrylic samplers was significantly higher than for equivalent quartz samplers. For quartz samplers [NO2]mean was only just above the monitor at Norwich and London; sampler/monitor NO2 = 1.04 (P = 0.59) and 1.01(P = 0.76), respectively. For acrylic samplers the order of [NO2]mean was 40 mm > 120 mm > 71 mm > or = 55 mm. Excepting 40 mm samplers, this accords with a chemical bias where co-diffusing NO and 03 molecules in longer tubes have more time to react to form excess NO2. Bias in 40 mm samplers is discussed. Eddy diffusion is negligible for standard samplers because [NO2]mean was equivalent for 55 mm and 71 mm acrylic samplers and close to monitor NO2 for 71 mm quartz tubes. Both studies showed that sampler accuracy was dependent on location. Significantly, overestimation was greatest (approximately 3-4 ppb) where the NO2 annual mean was approximately 20 ppb, close to the UK and EU air quality standard of 21 ppb.

Air Pollutants↗

[Elimination of nitrogen dioxide and nitric oxide by soda lime and its components].

OBJECTIVES: To investigated the efficacy of soda lime and its components in absorbing NO2 and NO. METHODS: VIP BIRD ventilator was connected with Siemens test lung. While the concentration of inhaled NO was 80 mg/L, the inspired gas passed through soda lime or its component. NO and NO2 were measured before and after testing materials in the circuit. Test 1, the soda lime canister sequentially was filled with smaller particle soda lime 500, 250, 125, 62.5, 39, 20, 10 and 0 g, to determine weight-efficacy relationship of the soda lime. Test 2, the canister sequentially was filled with bigger particle soda lime 500, 62.5, 30, 20 and 10 g, for comparing effective absorption of NO and NO2 between the two types of soda lime Test 3, 1.0 g methyl orange was added to smaller particle soda lime 10 g and 20 g respectively to observe its effect on eliminating NO and NO2. Test 4, silica gel tube was filled with smaller particle soda lime 10 g, KOH 10 g, NaOH 10 g, Ca(OH)2 2.5 g, and methly orange 0.5 g respectively for observing their ability of eliminating NO and NO2. RESULTS: The two types soda lime had the ability to eliminating NO and NO2 from inspired gas with a positive relationship with its weight. Both KOH and NaOH did not eliminate NO and NO2 Ca(OH)2 and methyl orange had a week ability. Methyl orange did not affect the ability of soda lime to eliminate NO2, but decreased its ability to eliminate NO. During 240 min, the eliminating NO2 ability of soda lime did not change, but the eliminating NO ability was reduced from 30% to 19% after 60 min. CONCLUSIONS: The effective components to eliminate NO and NO2 in soda lime are Ca(OH)2 and NaOH. Their ability to eliminate NO and NO2 increases with increase in their weight. The ability to eliminate NO decreases with increase in the contacting time with NO.

Calcium Compounds↗

Biochemical effects of combined gases of nitrogen dioxide and ozone. IV. Changes of lipid peroxidation and antioxidative protective systems in rat lungs upon life span exposure.

Lipid peroxide production, antioxidant contents and activities of antioxidative protective enzymes were examined in lungs of rats exposed to clean air (control group), 0.05 ppm O3, 0.05 ppm O3 + 0.04 ppm NO2 and 0.05 ppm O3 + 0.4 ppm NO2 for 22 months. The results were compared with our previous data in rats exposed to 0.04 ppm NO2, 0.4 ppm NO2 and 4 ppm NO2 for their life span (Sagai et al., Toxicol. Appl. Pharmacol., 73, (1984) 444-456). TBA values used as an index of lipid peroxidation in the lungs were increased maximally at 9 months, but were decreased below control values in animals exposed for 18 and 22 months. Nonprotein sulfhydryl (NPSH) contents were increased maximally at 9 months, and after 18 and 22 months were decreased significantly below control values. Vitamin E (VE) contents showed a similar trend. On the other hand, enzyme activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione peroxidase measured by using cumene hydroperoxide (cum.OOH) substrate (GPx-cum.OOH), glutathione peroxidase measured by using H2O2 as a substrate (GPx-H2O2), glutathione S-transferase (GSH-Tase) and superoxide dismutase (SOD) did not show any significant changes during this experiment. The results show that lipid peroxidation in lungs was increased synergistically by a combination of NO2 and O3 at ambient levels, and that the time of maximum lipid peroxide production was shorter than with NO2 alone. The protective ability against lipid peroxides was higher with increased lipid peroxide levels, but the inducibility was not maintained through a life span exposure to the combined gases. Additionally, two small adenomas were observed in 2 out of 18 rats in the 0.05 ppm O3 + 0.04 ppm NO2 group and a large adenoma was observed in 1 out of 18 animals in the 0.05 ppm + 0.4 ppm NO2 group exposed for 22 months.

Adenoma↗

Evaluation of method of preparation of passive diffusion tubes for measurement of ambient nitrogen dioxide.

This study was carried out in response to suggestions that the measurement of NO(2) by Palmes-type passive diffusion tubes (PDT) is affected by the method of preparation of the triethanolamine (TEA) absorbent coating on the grids. The following combinations of factors were investigated: TEA solvent (acetone or water), volume composition of TEA in solvent (50% or 20%), and grid coating method (dipping in solution prior to assembly or pipetting solution on after assembly). Duplicate PDTs prepared by each of the 8 methods were exposed in parallel, in urban air, for a total of 80 separate 1 week exposures. NO(2) concentrations derived from PDTs prepared by pipetting methods were significantly less precise than concentrations from dipping methods, with mean RSDs for duplicate measurements of 13.8% and 8.5%, respectively (n= 316 each category). Pipetting methods using solutions of 50% TEA composition were particularly imprecise (mean RSD 17.2%). Data from PDTs prepared by pipetting methods were systematically more poorly correlated with each other and with data from co-located chemiluminescence analysers, than corresponding data from PDTs prepared by dipping methods, indicating that more consistent accuracy was also obtained by the latter PDTs. The statistical evidence suggested that PDTs prepared by pipetting 50% TEA in water generally gave lower NO(2) concentrations. Although this is in agreement with a previous study, it is also possible that such an observation here may be a statistical artefact given the demonstrably poorer precision of this method. The general tendency of PDTs to show positive bias in NO(2) measurement in urban air in 1 week exposures was again evident in this study (mean biases at roadside and urban centre locations of +35% (n= 475) and +18% (n= 112), respectively) consistent with augmentation of within-tube NO(2) flux by chemical reaction between co-diffusing NO and O(3). Overall, it is recommended that the pipetting method of PDT grid preparation is avoided, or at least investigated further, because of the apparent degradation in precision and accuracy of NO(2) measurement. Potential reasons for the effect are discussed.

Adsorption↗

Current asthma and respiratory symptoms among pupils in Shanghai, China: influence of building ventilation, nitrogen dioxide, ozone, and formaldehyde in classrooms.

We investigated 10 naturally ventilated schools in Shanghai, in winter. Pupils (13-14 years) in 30 classes received a questionnaire, 1414 participated (99%). Classroom temperatures were 13-21 degrees C (mean 17 degrees C), relative air humidity was 36-82% (mean 56%). The air exchange rate was 2.9-29.4 ac/h (mean 9.1), because of window opening. Mean CO2 exceeded 1000 ppm in 45% of the classrooms. NO2 levels were 33-85 microg/m3 indoors, and 45-80 microg/m3 outdoors. Ozone were 1-9 microg/m3 indoors and 17-28 microg/m3 outdoors. In total, 8.9% had doctors' diagnosed asthma, 3.1% wheeze, 23.0% daytime breathlessness, 2.4% current asthma, and 2.3% asthma medication. Multiple logistic regression was applied. Observed indoor molds was associated with asthma attacks [odds ratio (OR) = 2.40: P < 0.05]. Indoor temperature was associated with daytime breathlessness (OR = 1.26 for 1 C; P < 0.001), and indoor CO2 with current asthma (OR = 1.18 for 100 ppm; P < 0.01) and asthma medication (OR = 1.15 for 100 ppm; P < 0.05). Indoor NO2 was associated with current asthma (OR = 1.51 for 10 microg/m3; P < 0.01) and asthma medication (OR = 1.45 for 10 microg/m3; P < 0.01). Outdoor NO2 was associated with current asthma (OR = 1.44 for 10 microg/m3; P < 0.05). Indoor and outdoor ozone was negatively associated with daytime breathlessness. In conclusion, asthma symptoms among pupils in Shanghai can be influenced by lack of ventilation and outdoor air pollution from traffic. Practical Implications Most urban schools in Asia are naturally ventilated buildings, often situated in areas with heavy ambient air pollution from industry or traffic. The classes are large, and window opening is the only way to remove indoor pollutants, but this results in increased exposure to outdoor air pollution. There is a clear need to improve the indoor environment in these schools. Building dampness and indoor mold growth should be avoided, and the concept of mechanical ventilation should be introduced. City planning aiming to situate new schools away from roads with heavy traffic should be considered.

Adolescent↗

In vivo effects of nitrogen dioxide on membrane constituents in lung and liver of rats.

When rats were exposed to 10 ppm NO2 for 7 days, the succinate-cytochrome c reductase activity, the rate-limiting step of mitochondrial succinoxidase, of the liver decreased progressively, reaching 77% (P less than 0.01) of the control level by the fifth day. By contrast, this activity was gradually increased by a 10-day exposure to 4 ppm NO2 and reached 1.14-fold that of the control level at the seventh day. A reduction in the components of electron-transport systems in liver microsomes was found during exposure to NO2 at both concentrations. This reduction was preferential for components of drug-metabolizing systems. The NADPH-cytochrome c reductase activity and the cytochrome P-450 content were decreased to 82% (P less than 0.05) and 76% (P less than 0.05), respectively, at the fifth day of exposure to 10 ppm NO2. Exposure to 4 ppm NO2 also caused a significant decrease in the NADPH-cytochrome c reductase and the cytochrome P-450 content, which were lowered to 84% (P less than 0.05) of the control level at the fourth and seventh days, respectively. Reduction in these components appears to occur even at the concentration of 0.4 ppm at the seventh day. Alterations in the components of mitochondria and microsomes of the lung were considerably different from those of the liver. The protein content of the lung increased to 1.18 (P less than 0.05)- and 1.14 (P less than 0.05)-fold that of the control during exposure to 10 and 4 ppm NO2, respectively. The succinate-cytochrome c reductase activity showed a reduced value, which was 73% (P less than 0.01) of the control level, 1 day after exposure to 10 ppm NO2, Subsequently, the activity increased to 1.14-fold that of the control during exposure to 10 (at the fifth day) and 4 ppm (at the fourth day) NO2. Components of microsomal electron-transport systems also showed a slightly elevated value during exposure to 4 ppm NO2. Seven days after exposure, the cytochrome P-450 content was decreased to 61% (P less than 0.01) of the control level, while other components were retained at control levels. A significant reduction in the cytochrome P-450 content was also observed at the exposure concentration of 1.2 ppm, but not of 0.4 ppm, at the seventh day.

Animals↗

Effects of nitrogen dioxide on red blood cells of rats: alterations of cell membrane components and populational changes of red blood cells during in vivo exposure to NO2.

Male Wistar rats were exposed to 4 ppm NO2 for 10 days in order to examine the relationship between the changes in components of red cell membranes and alterations of erythrocyte population. Na+, K+-ATPase activity of red blood cell membranes of exposed animals showed a significantly higher value than that of the control at the first and fourth days of exposure and then decreased to under the control value at the seventh day. In order to examine changes in erythrocyte population, red blood cells were fractionated into four fractions according to their density using Dextran density centrifugation. The alteration of the percentage of lowest-density cells (fraction IV) of exposed animals was completely consistent with that of Na+,K+-ATPase activity in addition to that of the sialic acid content as described in a previous report (K. Kaya, T. Miura, and K. Kubota (1980). Environ. Res. 23, 397-409.). The percentage of fraction IV was 1.43- (P less than 0.05) and 1.68-fold (P less than 0.01) those of the control at the first and fourth days of exposure, respectively, and then decreased to under the control value at the seventh day. This decrease accompanied increases in the percentages of higher-density cells (fractions I and II). Examination of subfractions of red blood cells showed that Na+,K+-ATPase activity and the sialic acid content of three fractions with lower densities have higher values in exposed animals than in the control 1 day after exposure to NO2. Based on these results, it is concluded that increases in Na+,K+-ATPase activity and the sialic acid content occurring 1 day after exposure to 4 ppm NO2 were caused by elevated levels of these components in three fractions with lower densities as well as by an increase in the percentage of lowest-density cells in the erythrocyte population. It was also suggested that NO2 inhalation accelerated aging of erythrocytes with respect to density. The change in Ca2+,Mg2+-ATPase activity, in addition to that in the hexose content as described in a previous report (Kaya et al., 1980), was different from those in the sialic acid content and Na+,K+-ATPase activity. Ca2+,Mg2+-ATPase activity and the hexose content of exposed animals showed slightly reduced values 1 day after exposure to NO2. In all subfractions of red blood cells these values were slightly lower in exposed animals than in the controls. Therefore, reduction in Ca2+,Mg2+-ATPase activity and the hexose content is not due to changes in erythrocyte population.

Animals↗

[The effects of occupational exposure to nitrogen dioxide (NO2) on the immunological parameters in workers].

The study of T-cell subpopulation: T CD3+, T CD4+, T CD8+; NK CD16+ and B CD19+ cells as well as of serum concentrations of immunoglobulins G, A, M, E, complement components C3c and C4, total circulating immune complexes (CIC), CRP, haptoglobin, ceruloplasmin and transferin, was carried out in 16 males, smokers and non-smokers. The control group of smokers and non-smokers comprised 36 males not exposed to any chemical compound. The study was performed also in two groups of non-smokers: 5 workers occupationally exposed and 7 non-exposed controls. For the determination of T-cells, NK- and B CD19+ cells populations monoclonal antibodies were used in indirect immunofluorescence tests. Passive sampling spectrophotometric method was employed to determine NO2 and NO concentrations in the work environment air. Their mean values were 0.0867 +/- 0,0585 mg x m-3 (from 0.0165 to 0.1960) and 0.0614 +/- 0.0263 mg x m-3 (from 0.0220 to 0.1090), respectively. The number of total leucocytes and lymphocytes in the group of 16 smokers and non-smokers exposed to NO2 and NO was increased. Stimulation T-cells line in the men exposed to NO2 and NO was evidenced by an increased number of T CD3+ cells, about two-fold increase in absolute number of T CD4+ cells (p < 0.001), an increased number of T CD8+ cells (p < 0.001) and by an enhanced value (by 24.7%) of the T CD4+/T CD8+ ratio. In the group of 16 persons exposed to NO2 and NO serum IgG concentration was elevated (p < 0.01), C3c C4 decreased (p < 0.001), and serum CIC enhanced by about two times (p < 0.001). Stimulation T-cells line in the groups of 5 non-smoking workers exposed to NO2 and NO was evidenced by an increased number of T CD3+ (p < 0.05), T CD4+ (p < 0.05) and T CD8+ cells but without any change in the value of the T CD4+/T CD8+ ratio. In addition, decreased serum C3c and C4 levels together with serum CIC elevated by 76.7% (p < 0.05) were evidenced in this group on non-smokers. Moreover, significant positive correlations between NO2 concentrations in the air and the numbers of total lymphocytes, T CD3+, TCD4+, T CD8+ cells or IgG: (magnitude of r in the range between 0.31 and 0.71), as well as significant negative correlations between NO2 concentrations in the air and C3c (r = 0.44) in the group of 16 smoking and non-smoking workers were calculated. In this group significant positive correlation between NO concentrations in the air of the workplace and counts of T CD3+, T CD8+, B CD19+ (magnitude of r in the range between 0.51 and 0.63), haptoglobin and ceruloplasmin (magnitude of r from 0.37 to 0.58), as well as significant negative correlation between NO concentrations in the air and serum levels of IgG, IgA and IgM (magnitude of r from -0.67 to -0.47) and CIC (magnitude of r = -0.39) were also observed. In the group of 5 exposed non-smoking workers, the values of correlation coefficients magnitude of r between NO2 and NO concentrations in the work environment air and immunological parameters were similar to those in the whole group. The results obtained suggest that during occupational exposure NO2 may play a more important role mainly in the process of inflammation but exogenous NO seems to act as modulating factor of this proinflammatory NO2 effect through a greater and exposure-dependent influence mainly on B CD19+ cells and other parameters of humoral immunity.

Adult↗

Exchanges of oxygen, carbon dioxide, nitrogen and water in the caecilian Dermophis mexicanus.

Oxygen consumption was measured in five Dermophis mexicanus and averaged (+/- SEM) 0.047 +/- 0.004 ml O2 g(-1) x h(-1). Carbon dioxide production averaged 0.053 +/- 0.005 ml CO2 g(-1) x h(-1) in the same five animals 1 week later. This metabolic rate is similar to metabolic rates of other Gymnophionans but lower than metabolic rates reported for Anurans and Urodeles. Total nitrogen excretion averaged 1.37 micromol N g(-1) x h(-1) which is higher than that found for other amphibians. Of this, 82.5% (1.13 micromol N g(-1) x h(-1)) was in the form of urea while 17.5% (0.24 micromol N g(-1) h(-1)) was in the form of NH3 + NH4+. Such ureotelism is typical of terrestrial amphibians like D. mexicanus. Osmotic water flux averaged 0.0193 ml g(-1) x h(-1) in control (sham injected) animals and was not significantly altered by injection of either arginine vasotocin or mesotocin. This osmotic flux is similar to osmotic fluxes found for other terrestrial amphibians. The combined data suggest that metabolism in D. mexicanus is, like most other Gymnophionans, lower than other amphibians. The high rates of nitrogen (especially urea) excretion suggests that this fossorial animal accumulates urea like other burrowing amphibians.

Amphibians↗

Intestinal perfusion during pneumoperitoneum with carbon dioxide, nitrogen, and nitric oxide during laparoscopic surgery.

OBJECTIVE: To find out what effect insufflation pressure and type of gas have on intestinal perfusion during pneumoperitoneum. DESIGN: Randomized, controlled, prospective, experimental study. SETTING: University affiliated animal experimental laboratory, Sweden. ANIMALS: Fasted, anaesthetised, domestic pigs of both sexes operated on laparoscopically (n = 7, weight 26-31 kg). INTERVENTIONS: Insufflation of carbon dioxide (CO2), nitric oxide (NO), or nitrogen (N2) at intra-abdominal pressures of 0, 5, 10, 15 and 20 mm Hg. MAIN OUTCOME MEASURES: Cardiac output, portal blood flow, and jejunal mucosal perfusion. RESULTS: Cardiac output decreased during N2 and NO (15, 20 mm Hg) but not during CO2 insufflation because of an accompanying tachycardia. Portal flow decreased during insufflation with N2 and NO (15, 20 mm Hg) and CO2 (20 mm Hg). Jejunal perfusion was reduced during N2 and NO insufflation (5-20 mm Hg) but remained unchanged during CO2 insufflation (5-20 mm Hg). CONCLUSIONS: Insufflation with CO2 maintained jejunal mucosal perfusion, probably as a result of hypercarbia as N2 at equal pressures reduced mesenteric flow. The vasodilator NO provided no haemodynamic benefit.

Abdomen↗