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PubMed1991

A short-term diffusive sampler for nitrogen dioxide monitoring in epidemiology.

An automated timed exposure diffusive sampler (TEDS) for sampling nitrogen dioxide (NO2) was developed for use in epidemiological studies. The TEDS sequentially exposes four passive sampling devices (PSD) by microprocessor controlled valves while a pump and air flow guide prevent sampler "starvation." Two TEDS units and two portable, real-time NO2 monitors were tested for accuracy, precision, sensitivity, and linearity of response. The accuracy of the TEDS was within 10 percent of the calibrated NO2 values, and precision was within 10 percent of the means of the measured values. The TEDS sensitivity was 20 to 30 ppb-hour for NO2. Co-location of the TEDS with a chemiluminescent NOx monitor (EPA reference method) showed similar responses to ambient NO2 (R2 = 0.9991). TEDS allows better time resolution than traditional diffusive samplers (i.e., Palmes tube) while sharing their ability to sample a variety of gases.

Air Pollution↗

PubMedDate not supplied

Health effects resulting from nitrogen dioxide exposure in an indoor ice arena.

We investigated an outbreak of acute respiratory illness among adolescent ice-hockey players in an indoor ice arena in Stockholm that had a propane-powered ice-resurfacing machine. We administered questionnaires to all players, as well as to a reference group that had played ice hockey in indoor arenas with electric ice-resurfacing machines. In the exposed group, 55 subjects (55.6%) experienced acute respiratory symptoms, compared with 4 (7.1%) in the reference group (relative risk = 7.8; 95% confidence interval = 3.0, 20.3). The risk for pulmonary symptoms increased as time spent on the ice increased. Levels of nitrogen dioxide up to 2358 microg/m3 (1250 ppb) were detected during simulated conditions of the incident. The most likely cause of the outbreak was the high level of nitrogen dioxide that resulted from poor ventilation and a malfunctioning ice-resurfacing machine. Propane-fueled ice-resurfacing machines should not be used in indoor ice arenas.

Adolescent↗

PubMed1994

Carbon monoxide and nitrogen dioxide exposures in indoor ice skating rinks.

Exposures to carbon monoxide (CO) and nitrogen dioxide (NO2) were determined in seven enclosed ice skating rinks and an outdoor rink. The uptake of CO was also determined by the difference in alveolar CO concentration of the non-smoking hockey players before and after games. Carbon monoxide concentrations in enclosed rinks ranged from 4 to 117 ppm and NO2 concentrations from 342 to 2729 ppb for 2 h hockey games. The CO uptakes were linearly related to the ambient CO concentrations. Alveolar CO of the hockey players increased on average by 0.53 ppm per 1 ppm CO exposure over 2 h. Considering the CO and NO2 levels currently measured in enclosed ice skating rinks, indoor air quality guidelines or standards should be established. It is recommended that 1 h maximum allowable limits of 20 ppm CO and 250 ppb NO2 be established.

Absorption↗

PubMed1979

Effects of repeated exposures to peak concentrations of nitrogen dioxide and ozone on resistance to streptococcal pneumonia.

Exposures to various mixtures of nitrogen dioxide (NO2) and ozone (O3) reduced the resistance of mice to streptococcal pneumonia as evidenced by increased mortality rates and shortened survival time. Daily 3-h exposures (5 d/wk) for 2--6 mo to an air pollutant mixture consisting of 940 microgram/m3 (0.5 ppm) NO2 and 196 microgram/m3 (0.1 ppm) O3 were most effective in reducing the resistance to infection. The decrease in resistance to the infection occurred sooner than the mice continued to be exposed to the air pollutants instead of clean air for 14 d after the respiratory challenge with Streptococcus pyogenes aerosol. After 3 mo of exposure to the pollutant mixture, there was some decrease in the ability of mice to clear inhalated streptococci from their lungs. At the same time the total cell count in the fluid lavaged from the lungs of mice was markedly reduced, as were the viability and phagocytic activity of the alveolar macrophages. Exposure to the pollutants combined with challenge with Streptococcus aerosol resulted in marked morphological changes in lung tissues as seen by scanning electron microscopy.

Animals↗

PubMed1996

Distribution and determinants of personal exposure to nitrogen dioxide in school children.

OBJECTIVES: To assess the distribution of personal exposures to nitrogen dioxide (NO2) in school children, and to investigate factors that might influence personal exposure. METHODS: NO2 exposures were assessed by use of passive diffusion tubes for 46 children aged 9-11 years, selected from two Southampton schools. The tubes were worn for seven days, and parallel measurements were made with static samplers in the child's kitchen, living room, classroom, and playground. Information about potential exposures was collected by questionnaire. RESULTS: Personal exposures to NO2, averaged over seven days, ranged from 11 to 257 micrograms/m3 (6 to 137 ppb) with a geometric mean of 36 micrograms/m3 (19 ppb). Exposures correlated with concentrations of NO2 recorded in the home, but the relation was far from exact. Factors associated with increased personal exposure included the use of gas appliances in the home, living with one or more smokers, and travel to school by means other than a car. However, together these variables only explained a small part of the variation in personal exposures. CONCLUSIONS: These findings reinforce the need for personal monitoring of exposure in studies investigating potential health effects of NO2 in children.

Child↗

PubMed1997

Respiratory effects associated with indoor nitrogen dioxide exposure in children.

BACKGROUND: The human health effects of exposure to indoor nitrogen dioxide (NO2) are unclear, and few studies have examined the effects of short-term peak levels of exposure. METHODS: The association between indoor exposure to NO2 and respiratory illness was examined in 388 children aged 6-11 years. The NO2 levels were monitored during winter in 41 classrooms, from four schools with unflued gas heating and four schools with electric heating. Each classroom was monitored daily with 6-hour passive diffusion badge monitors over nine alternate weeks, and with hourly monitors over two of those weeks. Children living in homes with unflued gas appliances were also monitored daily over four evenings during times of gas use. RESULTS: Exposure to NO2 at hourly peak levels of the order of > or = 80 ppb, compared with background levels of 20 ppb, was associated with a significant increase in sore throat, colds and absences from school. An increase in cough with phlegm was marginally significant. Significant dose-response relationships were demonstrated for these four measures with increasing levels of NO2 exposure. CONCLUSIONS: Short-term peak levels of exposure are important to consider in relation to adverse respiratory effects associated with NO2 exposure.

Air Pollution, Indoor↗

PubMed2004

A comparison of indoor air pollutants in Japan and Sweden: formaldehyde, nitrogen dioxide, and chlorinated volatile organic compounds.

Indoor and outdoor concentrations of formaldehyde (HCHO), nitrogen dioxide (NO2), and selected chlorinated volatile organic compounds (chlorinated VOC) were measured in 37 urban dwellings in Nagoya, Japan, and 27 urban dwellings in Uppsala, Sweden, using the same sampling procedures and analytical methods. Indoor as well as outdoor air concentrations of HCHO, NO2, and chlorinated VOC were significantly higher in Nagoya than in Uppsala (P<0.01), with the exception of tetrachlorocarbon in outdoor air. In Nagoya, HCHO and NO2 concentrations were significantly higher in modern concrete houses than in wooden houses and higher in newer (less than 10 years) than in older dwellings (P<0.01), possibly due to less natural ventilation and more emission sources in modern buildings. Dwellings heated with unvented combustion sources had significantly higher indoor concentrations of NO2 than those with clean heating (P<0.05). Moreover, dwellings with moth repellents containing p-dichlorobenzene had significantly higher indoor concentrations of p-dichlorobenzene (P<0.01). In conclusion, there appear to be differences between Nagoya and Uppsala with respect to both indoor and outdoor pollution levels of the measured pollutants. More indoor pollution sources could be identified in Nagoya than in Uppsala, including construction and interior materials emitting VOC, use of unvented combustion space heaters, and moth repellents containing p-dichlorobenzene.

Air Pollutants↗

PubMedDate not supplied

Exposures to nitrogen dioxide in EXPOLIS-Helsinki: microenvironment, behavioral and sociodemographic factors.

Personal exposures to nitrogen dioxide (NO(2)) were monitored for 176 randomly selected inhabitants (25-55 years old) of Helsinki Metropolitan area as a part of the EXPOLIS (Air Pollution Exposure Distributions Within Adult Urban Populations in Europe) study between October 1996 and December 1997. NO(2) measurements were 48-h averages collected by Palmes passive sampler tubes. Differences in personal exposures to NO(2) were analyzed between sub-populations stratified by microenvironment, behavioral, socioeconomic and demographic factors. Factors significantly associated with differences in exposures to NO(2) were home and work location, housing characteristics, traffic volume near home, season and keeping windows open at home. Exposure to environmental tobacco smoke (ETS) and use of gas stove were also associated with increased personal exposures, although only few participants had a gas stove in Helsinki, and other gas appliances are non-existent. Single adults had higher average exposures to NO(2) than married or cohabiting participants, suggesting differences in living conditions between these two groups. Increased education was associated with decreased exposures to NO(2) and employed men were more exposed than unemployed men. Increased exposures to NO(2) were not associated with age or occupational status in Helsinki. Thus, behavioral and sociodemographic factors may have significant impact on personal exposures to NO(2) and should be considered in addition to environmental determinants in any monitoring program.

Adult↗

PubMed1990

Chemoattractant and leukotriene B4 production from rat alveolar macrophages exposed to nitrogen dioxide.

The present study examined the hypothesis that exposure of alveolar macrophages to nitrogen dioxide (NO2) resulted in enhanced production of a lipophilic chemotactic agent for neutrophils, possibly leukotriene B4 (LTB4). Neutrophil migration was significantly increased in response to the reconstituted ethyl acetate extract of the medium surrounding macrophages exposed for 1 h to 5 or 20 ppm NO2. Compared with air-treated macrophages, production of LTB4 was found to be significantly increased by exposure to 5 ppm NO2, but unchanged by exposure to 20 ppm NO2. Treatment of macrophages with the calcium ionophore A23187 at a concentration of 2 microM for 15 min following a 1-h exposure to 5 ppm NO2 led to a significant increase in the production of LTB4 compared with A23187-treated air controls; however, LTB4 production in response to the calcium ionophore was unchanged following exposure to 20 ppm NO2. Thus, while increased neutrophil migration in response to products from macrophages exposed to 5 ppm NO2 correlated with the increased production of LTB4, increased migration in response to products from macrophages exposed to 20 ppm NO2 suggested the presence of another chemotactic lipid. Lipid peroxidation processes induced by NO2 at 5 ppm may lead to the formation of hydroperoxides that enhance the formation of LTB4; yet at 20 ppm, significantly higher concentrations of hydroperoxides may be responsible for impaired LTB4 formation. Phorbol ester-stimulated macrophage superoxide production was significantly inhibited in a dose-dependent manner following exposure to NO2 concentrations of 1, 5, or 20 ppm.

Animals↗

PubMedDate not supplied

Influence of ozone and nitrogen dioxide on hepatic microsomal enzymes in mice.

Since ambient concentrations of ozone and nitrogen dioxide increase drug-induced sleeping time in female mice, potential mechanisms were sought by investigating the effects of these gases on hepatic microsomal mixed-function oxidases in female CD-1 mice. A 3-h exposure to 9800 microgram O3/m3 (5 ppm) or 9400 microgram NO2/m3 (5 ppm) did not change the concentration of cytochrome P-450 significantly. Aniline hydroxylase, but not aminopyrine N-demethylase or p-nitroanisole O-demethylase, activities were increased following a 3-h exposure to 9400 microgram O3/m3 (5 ppm). Aniline hydroxylase activity was also increased after a 2-d (5 h/d) exposure to 1960 microgram O3/m3 (1 ppm). None of these enzyme activities were affected by a 3-h exposure to 9400 microgram NO2/m3 (5 ppm). In these studies, O3 sometimes increased wet liver weight, and thus additional experiments were conducted. A 5-h exposure to 1960 microgram O3/m3 (1 ppm) caused a lesser decrease in body weight than the decrease observed after a similar air exposure. Liver wet weights were elevated after O3 exposure. However, there were no significant changes in liver dry weight, liver dry-to-wet-weight ratio, or ratios of liver (wet or dry) weight to body weight. From these data, it is concluded that mechanisms other than those investigated are responsible for the effect of O3 and NO2 on drug-induced sleeping time. However, the activity of one mixed-function oxidase was slightly increased by O3, indicating a hitherto unrecognized systemic effect of O3 exposure.

Animals↗

PubMed1980

Exposure of nitrous oxide to X-rays. Production of nitric oxide and nitrogen dioxide.

X-radiation has been shown to produce nitric oxide (NO) and nitrogen dioxide (NO2) in the presence of nitrous oxide (N2O). The purpose of the present study was to confirm how much NO and NO2 was produced when constant amounts of nitrous oxide were exposed to constant X-radiation. Twenty polyethylene bottles (capacity 10 litres) were filled with nitrous oxide alone. Another 20 bottles were filled with nitrous oxide and 30% oxygen. Each bottle was placed at a distance of 30 cm from the X-ray tube and they were directly in the line of the X-ray beam at a setting of 90 kV at 0.5 mA, a standard setting for chest fluoroscopy. The range of duration of X-ray exposure was from 0 (control), to 2, 3, and 5 minutes in five bottles each, respectively. A colorimetric recording method (Saltzman) and a chemiluminescent monitor were used for measurement of NO and NO2. In the bottles filled with nitrous oxide alone, the production of NO was not affected by the duration of X-ray exposure, but the longer duration of X-ray exposure produced a larger amount of NO2. In the bottles filled with nitrous oxide and 30% oxygen, the longer duration of X-ray exposure produced larger amounts of both NO and NO2. These finding confirmed a previous investigation in which nitrous oxide was not inert under X-ray exposure. As the presence of oxygen plays an important role in the oxidation of nitrous oxide under X-ray, this study suggests another potentially hazardous interaction that may occur secondary to the administration of an anaesthetic in the presence of X-irradiation such as pulmonary angiography, cardiac catheterisation, and fluoroscopic bronchoscopy or biopsy.

Nitric Oxide↗

PubMed1997

Nitrogen dioxide in indoor ice skating facilities: an international survey.

An international survey of nitrogen dioxide (NO2) levels inside indoor ice skating facilities was conducted. One-week average NO2 concentrations were measured inside and outside of 332 ice rinks located in nine countries. Each rink manager also completed a questionnaire describing the building, the resurfacing machines, and their use patterns. The (arithmetic) mean NO2 level for all rinks in the study was 228 ppb, with a range of 1-2,680 ppb, based on a sample collected at breathing height and adjacent to the ice surface. The mean of the second indoor sample (collected at a spectator's area) was 221 ppb, with a range of 1-3,175 ppb. The ratio of the indoor to outdoor NO2 concentrations was above 1 for 95% of the rinks sampled, indicating the presence of an indoor NO2 source (mean indoor:outdoor ratio = 20). Estimates of short-term NO2 concentrations indicated that as many as 40% of the sampled rinks would have exceeded the World Health Organization 1-hour guideline value of 213 ppb NO2 for indoor air. Statistically significant associations were observed between NO2 levels and the type of fuel used to power the resurfacer, the absence of a catalytic converter on a resurfacer, and the use of an ice edger. There were also indications that decreased use of mechanical ventilation, increased number of resurfacing operations per day, and smaller rink volumes were associated with increased NO2 levels. In rinks where the main resurfacer was powered by propane, the NO2 concentrations were higher than in those with gasoline-powered resurfacers, while the latter had NO2 concentrations higher than in those using diesel. Rinks where the main resurfacer was electric had the lowest indoor NO2 concentrations, similar to the levels measured outdoors.

Air Pollution, Indoor↗

PubMed1988

Effect of nitrogen dioxide on surface membrane fluidity and insulin receptor binding of pulmonary endothelial cells.

Nitrogen dioxide (NO2), an environmental oxidant pollutant, is known to peroxidize membrane lipids of lung cells. We evaluated the ability of NO2 to alter the surface membrane fluidity, lipid composition, and insulin receptor binding of porcine pulmonary artery endothelial cells in culture. After 3- to 24-hr exposure to 5 ppm NO2, cells were labeled with either 1-(4-trimethylaminophenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH), a cationic fluorescent aromatic hydrocarbon that anchors at the lipid-water interface, or fluorescamine, a fluorescent molecular probe that covalently binds with amino groups of surface phospholipids and proteins. Membrane fluidity was measured by monitoring changes in the steady-state fluorescence anisotropies (rs) for TMA-DPH and fluorescamine. Insulin specific receptor binding was monitored by measuring time-dependent binding of 125I-insulin. Following NO2 exposure, rs values for TMA-DPH and fluorescamine were increased significantly in a time-dependent fashion, with maximum increases at 24 hr (P less than 0.001). Similar increases in rs values were observed in isolated plasma membranes as well as in lipid vesicles prepared from total lipid extracts of endothelial cells or their plasma membranes. Phosphatidylethanolamine plus phosphatidylserine content in lipid extracts from 24-hr but not 3- to 12-hr NO2-exposed cells was increased significantly (P less than 0.01) compared to control cells. Specific binding of 125I-insulin to cells exposed to NO2 for 12 and 24 hr (but not 3 and 6 hr) was reduced significantly (P less than 0.05) compared to binding in control cells. Scatchard analysis of the binding data indicated that NO2 exposure caused a 5-fold reduction in insulin receptor binding sites in endothelial cells. Recovery was achieved 24 hr after NO2 exposure with, but not without, changing culture medium. These results indicate that NO2 exposure causes reversible changes in the physical state of lipids in the superficial lipid domains of the pulmonary endothelial cell plasma membrane, and these alterations may interfere with plasma membrane-dependent functions such as receptor-ligand interaction.

Amino Acids↗

PubMed1986

Effects of subchronic inhalation of low concentrations of nitrogen dioxide. I. The proximal alveolar region of juvenile and adult rats.

Inhalation of nitrogen dioxide (NO2) produces injury to the epithelium of terminal airways and the alveoli proximal to the airways. Techniques were devised to isolate alveolar tissue from this region for morphometric studies to define the extent of alveolar septal injury caused by NO2. One-day-old and six-week-old rats were exposed to either room air or 0.5 ppm NO2 for 23 hr per day 7 days per week for 6 weeks. An additional group of 6-week-old rats were exposed to 2.0 ppm NO2 for the same duration. Two daily hour spikes to three times the background concentrations (0.5 to 1.5 ppm and 2.0 to 6.0 ppm) were applied Monday through Friday. At the end of the exposure, rat lungs were fixed by intratracheally infusing buffered 2% glutaraldehyde. Pieces of lung tissue were embedded in large plastic blocks which were softened with heat and thin (0.3 mm) sliced. Terminal bronchioles and their corresponding proximal alveolar regions were identified from the thin plastic slices, removed, and glued to cylindrical EM blocks for thin sectioning. Morphometric analysis revealed that epithelial injury occurred in all exposed animals. The juvenile rats which had been exposed to 0.5 ppm NO2 since 1 day of age exhibited changes in the characteristics of type II epithelial cells. These cells spread to cover more alveolar surface and became thinner. Adult animals exposed to 0.5 and 2.0 ppm NO2 showed changes in alveolar macrophages and in the alveolar interstitium in addition to changes in the epithelium. Animals exposed to 0.5 ppm NO2 showed spreading and hypertrophy of type II epithelial cells. Those animals exposed to the higher concentration of NO2 had similar changes in type II epithelial cells and in addition showed an increase in type I cell number. The type I epithelial cells were smaller and covered less alveolar surface area than normal type I cells, suggesting a regenerating population of type I cells. These results suggest that prolonged exposure to low concentrations of NO2 can cause injury to the alveolar epithelium indicated initially by spreading and hypertrophy of type II cells followed by differentiation into type I cells to compensate and repair the injury. Adult rats were as sensitive or more sensitive to NO2 injury than were juvenile rats.

Aging↗

PubMed1994

Lung injury following exposure of rats to relatively high mass concentrations of nitrogen dioxide.

Human inhalation exposures to relatively high mass concentrations of the oxidant gas nitrogen dioxide (NO2) can result in a variety of pulmonary disorders, including life-threatening pulmonary edema, pneumonia, and bronchiolitis obliterans. Inasmuch as most experimental studies to date have examined NO2-induced lung injury following exposures to near ambient or supra-ambient concentrations of NO2, e.g., < or = 50 ppm, little detailed information about the pulmonary injurious responses following the acute inhalation of higher NO2 concentrations that are more commensurate with some actual human exposure conditions is currently available. Described in this report are the results from a series of investigations in which various aspects of the inhalation toxicity of high concentrations of NO2 have been examined in laboratory rats. In the first component of our study, we characterized the kinetic course of development of lung injury following acute exposures to high concentrations of NO2 delivered over varying durations, and we assessed the relative importance of NO2 exposure concentration versus exposure time in producing lung injury. For a given exposure duration, the resulting severity of lung injury was found to generally scale proportionately with inhaled mass concentration, whereas for a given concentration of inhaled NO2, the magnitude of resulting injury was not directly proportional to exposure duration. Moreover, evidence was obtained that indicated exposure concentration is more important than exposure time when high concentrations of NO2 are inhaled. In a second component of our investigation, we assessed the pulmonary injurious response that occurs when NO2 is inhaled during very brief, 'high burst' exposures to very high concentrations of NO2. Such exposures resulted in significant lung injury, with the magnitude of such injury being directly proportional to exposure concentration. Comparisons of results obtained from this and the first component studies additionally revealed that brief exposures to the very high concentrations of NO2 are more hazardous than longer duration exposures to lower concentrations. In a third study series, we examined pre-exposure, exposure, and post-exposure modifiers of NO2-induced lung injury, including dietary taurine, minute ventilation, and post-exposure exercise. Results from these studies indicated: (i) dietary taurine does not protect the rat lung against high concentration NO2 exposure, (ii) the severity of acute lung injury in response to NO2 inhalation is increased by an increase in minute ventilation during exposure, and (iii) the performance of exercise after NO2 exposure can significantly enhance the injurious response to NO2.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗

PubMed2000

An ex post cost-benefit analysis of the nitrogen dioxide air pollution control program in Tokyo.

The benefits and costs of past nitrogen dioxide (NO2) control policies were calculated for Tokyo, Japan, using environmental, economic, political, demographic, and medical data from 1973 to 1994. The benefits of NO2 control were estimated as medical expenses and lost work time due to hypothetical no-control air concentrations of NO2. Direct costs were calculated as annualized capital expenditures and 1 year's operating costs for regulated industries plus governmental agency expenses. The major findings were as follows: (1) Using Tokyo's average medical cost of pollution-related illness, the best net estimate of the avoided medical costs due to incidence of phlegm and sputum in adults was 730 billion yen ($6.08 billion; 1 U.S. dollar = 120 yen). (2) The best net estimate of the avoided medical costs due to incidence of lower respiratory illness in children was 93 billion yen ($775 million). (3) Using Tokyo's average duration of pollution-related illness and average wages, the best net estimate of the avoided costs of lost wages in workers was 760 billion yen ($6.33 billion). (4) The best net estimate of the avoided costs of lost wages in mothers caring for their sick children was 100 billion yen ($833 million). (5) Using Tokyo-specific data, the best net costs were estimated as 280 billion yen ($2.33 billion). (6) Using human health and productivity benefits, and annualized capital cost and operating cost estimates, the best net benefits-to-costs ratio was 6:1 (upper limit 44:1; lower limit 0.3:1). Benefit calculations were sensitive to assumptions of mobile source emissions and certain health impacts that were not included. Cost calculations were highly dependent on assumptions of flue gas volume and fuel use. For comparative purposes, we identified other studies for air pollution-related illness. Assumptions that formed the basis for most of the inputs in the present study, such as duration of illness, medical treatment costs, per person illness in children, and lost wages for working mothers, were similar to those recommended in the literature. Lost wages in sick workers and per capita illness incidence in adults were higher than numbers reported elsewhere. Further advances in cost-benefit analysis (CBA) procedures to evaluate the economic effectiveness of NO2 controls in Tokyo are recommended to estimate impacts and values for additional human health benefits, ecosystem health and productivity effects, and nonliving system effects, as well as benefits of ancillary reductions in other pollutants. The present study suggests that Tokyo's past NO2 control policies in total were economically quite effective.

Adult↗

PubMed1989

Effects of nitrogen dioxide on growth and yield of black turtle bean (Phaseolus vulgaris L.) cv. 'Domino'.

Twenty-six-day-old black turtle bean cv. 'Domino' plants were exposed to nitrogen dioxide (0.0, 0.025, 0.05 and 0.10 microl liter(-1)), 7 h per day for 5 days per week for 3 weeks, under controlled environment. Data were collected on net photosynthesis rate (PN), stomatal resistance (SR), and dark respiration rate (DR), immediately after exposure, 24 h after the termination of exposure and at maturity (when the leaves had just started turning yellow), using a LICOR 6000 Portable Photosynthesis System. Chlorophyll-a (Ch-a), chlorophyll-b (Ch-b), total chlorophyll (tot-Ch) and leaf nitrogen were measured immediately after exposure and at maturity. Growth characteristics-relative growth rate (RGR), net assimilation rate (NAR), leaf area ratio (LAR) and root: shoot ratio (RSR)-were computed for treated plants. Net photosynthesis rate increased by 53% in 0.10 microl liter(-1) NO2 treated plants immediately after exposure compared to control plants. Dark respiration rates were also higher in treated plants. Ch-a, Ch-b and tot-Ch showed significant increases with 0.1 microl liter(-1) NO2 treatment immediately after exposure. Foliar nitrogen content showed an increase in treated plants both immediately after exposure and at maturity. Increases were also seen in RGR and NAR. Plant yield increased by 86% (number of pods), 29% (number of seeds) and 46% (weight of seeds), respectively. Nitrogen dioxide stimulated the overall plant growth and crop yield.

Journal Article↗

PubMed2004

Atmospheric concentrations of sulfur dioxide, nitrogen oxides, ammonia, hydrogen chloride, nitric acid, formic and acetic acids in the south of Vietnam measured by the passive sampling method.

A passive sampling method was applied to measure the concentrations of air pollutants, such as sulfur dioxide, nitrogen oxides, ammonia, hydrogen chloride, and nitric, formic and acetic acids, in the ambient air at four test sites in the southern region of Vietnam. The monthly averages and the average concentrations of air pollutants during the period from July 2001 to September 2002 are reported here. The concentrations of air pollutants varied widely, depending on the test sites and the sampling periods. The average concentrations of sulfur dioxide in the air during the period from July 2001 to September 2002 at the four test sites were 3.3-16.9 ppb, and those of nitrogen dioxide were 5.4-12.8 ppb. The concentrations of nitrogen monoxide and hydrogen chloride were very low at all of the test sites. The observed concentrations of all of the above-mentioned pollutants were lower than those of the Vietnamese standards of air pollutants.

Journal Article↗