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PubMed1990

Pulmonary arachidonic acid metabolism following acute exposures to ozone and nitrogen dioxide.

Ozone (O3) and nitrogen dioxide (NO2) are common air pollutants, and exposure to these gases has been shown to affect pulmonary physiology, biochemistry, and structure. This study examined their ability to modulate arachidonic acid metabolites (eicosanoids) in the lungs. Rabbits were exposed for 2 h to O3 at 0.1, 0.3, or 1 ppm; NO2 at 1, 3, or 10 ppm; or to a mixture of 0.3 ppm O3 and 3 ppm NO2. Groups of animals sacrificed either immediately or 24 h after each exposure underwent broncho-pulmonary lavage. Selected eicosanoids were assessed in lavage fluid by radioimmunoassay. Increases in prostaglandins E2 (PGE2) and F2 alpha (PGF2 alpha) were found immediately after exposure to 1 ppm O3. Exposure to 10 ppm NO2 resulted in a depression of 6-keto-PGF1 alpha, while thromboxane B2 (TxB2) was elevated after exposure to 1 ppm NO2 and depressed following 3 and 10 ppm. The O3/NO2 mixture resulted in synergistic increases in PGE2 and PGF2 alpha, with the response appearing to be driven by O3. This study has demonstrated that acute exposure to either O3 or NO2 can alter pulmonary arachidonic acid metabolism and that the responses to these oxidants differ, both quantitatively and qualitatively.

Air Pollutants↗

PubMedDate not supplied

Airway responses to 2.0 ppm nitrogen dioxide in normal subjects.

Nitrogen dioxide (NO2) is a common indoor air pollutant. To characterize the acute respiratory responses to this gas, 18 nonsmoking normal subjects (mean age +/- standard deviation [SD] = 25 +/- 4 yr) were exposed to filtered air or 2 ppm NO2 gas for 1 hr in a 30-m3 environmental chamber on different days, typically 1 wk apart, in a double-blind randomized fashion. Lung function tests included forced vital capacity, forced expiratory volume in one second, partial expiratory flow at 40% of vital capacity (Vp40), functional residual capacity, and specific airway conductance, and were measured before and after exposure. Airway reactivity to methacholine inhalation was determined within 45 min of each exposure. The dose of methacholine in mg/ml to cause a 40% decrease in specific airway conductance (PD40) was measured. Airway reactivity to methacholine aerosol increased significantly after NO2, which is shown by a decrease in the concentration of methacholine; PD40 (AIR) = 101 +/- 44, PD40 (NO2) = 81 +/- 45 mg/ml, p = .003. No significant changes were noted in the lung function tests after NO2 exposure. These findings indicate that normal nonsmokers exposed to 2.0 ppm NO2 for 1 hr develop an increase in airway reactivity to methacholine aerosol, which is not associated with changes in lung volumes, flow rates, or respiratory symptoms.

Adolescent↗

PubMed1998

Production of nitrogen dioxide in a delivery system for inhalation of nitric oxide: a new equation for calculation.

We have evaluated the kinetics of nitrogen dioxide production in a system for inhalation of nitric oxide. In addition to a small fraction of contamination of nitrogen dioxide in the nitric oxide stock gas, a considerable part of the total concentration of nitrogen dioxide is formed immediately after mixing of nitric oxide and oxygen. This initial build-up of nitrogen dioxide is followed by a linear, time-dependent increase in the concentration of nitrogen dioxide. An equation describing the concentration of nitrogen dioxide in the delivery system is formulated: [NO2] = kA x [NO] + kB x [NO]2 x [O2] + kC x t x [NO]2 x [O2], where nitrogen dioxide [NO2] and nitric oxide [NO] concentrations are in parts per million (ppm), oxygen concentration [O2] is expressed as a percentage and contact time (t) is in seconds. The rate constants are kA = 5.12 x 10(-3), kB = 1.41 x 10(-6) and kC = 0.86 x 10(-6). Calculated nitrogen dioxide values correlated well with measured concentrations. This new finding of an initial build-up of nitrogen dioxide has to be taken into consideration if the conversion of nitric oxide to nitrogen dioxide is to be calculated and in the safety guidelines for the use of nitric oxide.

Administration, Inhalation↗

PubMed1977

Some effects of nitrogen dioxide on the lung.

Nitrogen dioxide (NO2) when inhaled in different concentrations and for varying times produces pulmonary injuries which are dependent on the anatomic site in the lung and the duration of exposure. Single exposures to high concentrations of NO2 for 5-6 hr produce an intense cellular proliferation which regresses within 48 hr in all lung regions except the terminal respiratory bronchiole region and the alveoli where the proliferation persists for 4-7 days. This same delayed response is also observed in more chronic exposures. Histologically, the lesion in the terminal and respiratory bronchioles may resemble an obliterative bronchiolitis, but the lesion clears if further exposure is terminated. Prolonged exposure to 2 ppm NO2, 20-22 hr per day for 7 days per wk, produces an increase in total pulmonary upstream resistance in animals killed immediately after exposure; this resistence returns to normal values within 3 mo after removal from exposure. The internal surface area (ISA) is decreased after 12 mo exposure to NO2, but this loss of surface progresses during the recovery period in air, suggesting an autonomous progression of the tissue destructive process. Exposure to 3.64 ppm NO2 with and without fly ash for periods of 12-14 mo causes no increase in pulmonary resistance and no alteration in lung surface. Lung phospholipids and protein synthesis appear to be depressed following exposure to NO2. Lecithin is significantly increased. The synthesis of proteases by alveolar macrophages is increased during NO2 exposure. Pigmented alveolar macrophages present in animals exposed to NO2 simulate those found in human lungs of young cigarette smokers in the terminal and respiratory bronchioles. The mechanism of tissue injury by oxidants such as NO2 may involve free radical formation, and peroxidation of lipids or proteins.

Air Pollutants↗

PubMed1996

Antioxidant kinetics in lung lavage fluid following exposure of humans to nitrogen dioxide.

To determine if nitrogen dioxide (NO2), a gaseous free radical, modifies the protective antioxidant pool present in respiratory tract lining fluids, a random, double-blind study utilizing flexible fiberoptic bronchoscopy with bronchial and bronchoalveolar lavage was performed. Healthy, nonsmoking, asymptomatic subjects were exposed to filtered air and 2 ppm NO2 for 4 h on separate occasions. To examine the kinetics of the NO2-induced antioxidant reactions, 44 subjects were randomly assigned to one of three groups. Bronchoscopy was performed 1.5 h (group 1), 6 h (group 2) or 24 h (group 3) after each exposure. Reduced glutathione (GSH), uric acid, and ascorbic acid concentrations were determined in both bronchial and bronchoalveolar lavage fluid fractions. In addition, bronchoalveolar lavage fluid was screened for malondialdehyde as a marker of lipid peroxidation. Exposure to NO2 resulted in a rapid (1.5 h) loss of uric acid from the bronchial region, however by 6 h after exposure it had increased significantly above control uric acid concentration in this region. At 24 h after exposure, uric acid concentration had returned to the control level. A similar response of uric acid to NO2 was seen in the bronchoalveolar region. Ascorbic acid was also decreased in bronchial and bronchoalveolar lavage fluids 1.5 h after exposure to NO2, but returned to control values by 6 h. In marked contrast, significant increases in GSH concentration were seen at 1.5 and 6 h in bronchial lavage fluid after exposure to NO2, which subsequently returned to control levels by 24 h. No change in bronchoalveolar lavage fluid GSH concentration or malondialdehyde content was seen after NO2 exposure. These data support the view that antioxidants present in lung fluids react with, and hence modulate the impact of, NO2 on the lung.

Adult↗

PubMed1991

Experimental studies on tumor promotion by nitrogen dioxide.

The effects of nitrogen dioxide (NO2) on promotion of lung tumorigenesis induced by N-bis(2-hydroxypropyl) nitrosamine (BHPN) were investigated in male Wistar rats. In a preliminary study, the highest non-effective dose of BHPN was found to be 0.5 g per kg body weight. Rats were given a single intraperitoneal injection of BHPN at a dose of 0.5 g per kg body weight or saline at 6 weeks of age, and then exposed to clean air, 0.04 ppm, 0.4 ppm or 4 ppm of NO2 for 17 months, respectively. The incidence of pulmonary tumors in rats exposed to BHPN plus 4 ppm of NO2 was 12.5%; the tumors were adenomas and adenocarcinomas. Adenomas were found in 4 out of 40 rats (10%) and adenocarcinomas were found in 1 out of 40 rats (2.5%). The tumor incidence in the lungs of rats kept in BHPN plus clean air and BHPN plus 0.04 ppm of NO2 was 2.5% (1/40). In both groups adenomas were found. There was no significant difference in tumor incidence between animals exposed to BHPN plus clean air and to BHPN plus 4 ppm of NO2. No lung tumors were found in the group of BHPN plus 0.4 ppm NO2 and in animals exposed to NO2 without BHPN treatment. A high incidence of alveolar cell hyperplasia was observed in the lungs of rats injected with BHPN, and the effect of NO2 on development of alveolar cell hyperplasia was slight. On the other hand, marked bronchiolar mucosal hyperplasia was found in 17 out of 40 rats (42.5%) in the group of BHPN plus 4 ppm of NO2, and in 1 out of 40 rats (2.5%) in each of the group exposed to clean air, 0.04 ppm or 0.4 ppm of NO2 with BHPN treatment, respectively. The hyperplasia in lungs of rats exposed to 4 ppm of NO2 without BHPN treatment was slighter than that in lung of rat exposed to 4 ppm of NO2 with BHPN treatment. On the other hand, tumor incidence in the nasal cavity of rats in each of group exposed to clean air and NO2 with BHPN treatment was 97-100%. Incidence of tumors in other organs in the groups exposed to clean air and NO2 with and without BHPN treatment was very low, and NO2 had no effect on tumor development in the nasal cavity and other organs whether animals were treated with BHPN or not.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗

PubMed1991

Association of indoor nitrogen dioxide with respiratory symptoms and pulmonary function in children.

The effect of indoor nitrogen dioxide on the cumulative incidence of respiratory symptoms and pulmonary function level was studied in a cohort of 1,567 white children aged 7-11 years examined in six US cities from 1983 through 1988. Week-long measurements of nitrogen dioxide were obtained at three indoor locations over 2 consecutive weeks in both the winter and the summer months. The household annual average nitrogen dioxide concentration was modeled as a continuous variable and as four ordered categories. Multiple logistic regression analysis of symptom reports from a questionnaire administered after indoor monitoring showed that a 15-ppb increase in the household annual nitrogen dioxide mean was associated with an increased cumulative incidence of lower respiratory symptoms (odds ratio (OR) = 1.4, 95% confidence interval (95% Cl) 1.1-1.7). The response variable indicated the report of one or more of the following symptoms: attacks of shortness of breath with wheeze, chronic wheeze, chronic cough, chronic phlegm, or bronchitis. Girls showed a stronger association (OR = 1.7, 95% Cl 1.3-2.2) than did boys (OR = 1.2, 95% Cl 0.9-1.5). An analysis of pulmonary function measurements showed no consistent effect of nitrogen dioxide. These results are consistent with earlier reports based on categorical indicators of household nitrogen dioxide sources and provide a more specific association with nitrogen dioxide as measured in children's homes.

Air Pollutants↗

PubMed1986

Toxicity of ozone and nitrogen dioxide to alveolar macrophages: comparative study revealing differences in their mechanism of toxic action.

The toxicity of ozone and nitrogen dioxide is generally ascribed to their oxidative potential. In this study their toxic mechanism of action was compared using an intact cell model. Rat alveolar macrophages were exposed by means of gas diffusion through a Teflon film. In this in vitro system, ozone appeared to be 10 times more toxic than nitrogen dioxide. alpha-Tocopherol protected equally well against ozone and nitrogen dioxide. It was demonstrated that alpha-tocopherol provided its protection by its action as a radical scavenger and not by its stabilizing structural membrane effect, as (1) concentrations of alpha-tocopherol that already provided optimal protection against ozone and nitrogen dioxide did not influence the membrane fluidity of alveolar macrophages and (2) neither one of the structural alpha-tocopherol analogs tested (phytol and the methyl ether of alpha-tocopherol) could provide a protection against ozone or nitrogen dioxide comparable to the one provided by alpha-tocopherol. It was concluded that reactive intermediates scavenged by alpha-tocopherol are important in the toxic mechanism of both ozone and nitrogen dioxide induced cell damage. However, further results presented strongly confirmed that the kind of radicals and/or reactive intermediates, and thus the toxic reaction mechanism involved, must be different in ozone- and nitrogen dioxide-induced cell damage. This was concluded from the observations that showed that (1) vitamin C provided significantly better protection against nitrogen dioxide than against an equally toxic dose of ozone, (2) glutathione depletion affected the cellular sensitivity toward ozone to a significantly greater extent than the sensitivity towards nitrogen dioxide, and (3) the scavenging action of alpha-tocopherol was accompanied by a significantly greater reduction in its cellular level during nitrogen dioxide exposure than during exposure to ozone. One of the possibilities compatible with the results presented in this study might be that lipid (peroxyl) free radicals formed in a radical-mediated peroxidative pathway, resulting in a substantial breakdown of cellular alpha-tocopherol, are involved in nitrogen dioxide-induced cell damage, and that lipid ozonides, scavenged by alpha-tocopherol as well, are involved in ozone-induced cell damage.

Animals↗

PubMed1993

Nitrogen dioxide and respiratory illness in children. Part I: Health outcomes.

We have carried out a prospective cohort study to test the hypothesis that exposure to nitrogen dioxide increases the incidence and severity of respiratory infections during the first 18 months of life. Between January 1988 and June 1990, 1,315 infants were enrolled into the study at birth and followed with prospective surveillance for the occurrence of respiratory infections and monitoring of nitrogen dioxide concentrations in their homes. The subjects were healthy infants from homes without smokers; they were selected with stratification by type of cooking stove at a ratio of four to one for gas and electric stoves. Illness experience was monitored by a daily diary of symptoms completed by the mother and a telephone interview conducted every two weeks. Illnesses with wheezing or wet cough were classified as involving the lower respiratory tract; all other respiratory illnesses were designated as involving the upper respiratory tract. Exposure to nitrogen dioxide was estimated by two-week average concentrations measured in the subjects' bedrooms with passive samplers. This analysis is limited to the 1,205 subjects completing at least one month of observation; of these, 823 completed the full protocol, contributing 82.8% of the total number of days during which the subjects were under observation. Incidence rates for all respiratory illnesses, all upper respiratory illness, all lower respiratory illnesses, and lower respiratory illness further divided into those with any wheezing, or wet cough without wheezing, were examined within strata of nitrogen dioxide exposure at the time of the illness, nitrogen dioxide exposure during the prior month, and type of cooking stove. Consistent trends of increasing illness incidence rates with increasing exposure to nitrogen dioxide were not evident for either the lagged or unlagged exposure variables. The effect of nitrogen dioxide exposure on illness occurrence during at-risk intervals of two weeks' duration was examined using the generalized estimating equation approach. In these multivariate analyses, none of the odds ratios was significantly elevated for unlagged nitrogen dioxide exposures, lagged nitrogen dioxide exposures, or stove type. Duration of illness was assessed in relation to the same exposure variables; illness duration and nitrogen dioxide exposure were not associated. We have found that indoor exposure to nitrogen dioxide is associated with neither the incidence nor the duration of respiratory illnesses. The study was designed to have sufficient power to detect effects of nitrogen dioxide exposure of magnitudes previously reported and in a range relevant to public health concern; the lack of association cannot be attributed to potential bias from misclassification of outcome or exposure.(ABSTRACT TRUNCATED AT 400 WORDS)

Air Pollutants↗

PubMedDate not supplied

Effects of acute exposure to nitrogen dioxide on primary antibody response.

The effects of acute exposure to nitrogen dioxide on primary humoral antibody response to sheep red blood cells in mice were studied. Mice were exposed to 5 ppm, 20 ppm, and 40 ppm nitrogen dioxide for 12 hr. An exposure of 20 ppm or 40 ppm resulted in a significant suppression of antibody responses, but 5 ppm did not affect antibody response. This immunosuppression resulting from nitrogen dioxide exposure was more apparent in males than females. Exposures to 20 ppm nitrogen dioxide for various time intervals revealed that the strongest suppression effect was observed in the group exposed 2 days after antigen injection. A decreased total cell number in the spleen, and more strikingly, in the thymus, was also caused by acute exposure to nitrogen dioxide.

Animals↗

PubMed1998

Evaluation of nitrogen dioxide scavengers during delivery of inhaled nitric oxide.

We have analysed the ability of three nitrogen dioxide absorbing materials (soda lime, noXon and zeolite) to act as nitrogen dioxide scavengers during delivery of inhaled nitric oxide. Different mixtures of gas were produced in a ventilator (Servo Ventilator 300) and passed through an inspiratory tube. Concentrations of nitrogen dioxide and nitric oxide were measured in the distal part of the tube, with and without the gas having passed through a canister containing the different filter materials. Our findings indicated that nitrogen dioxide was absorbed effectively by all filter materials but that there was re-formation of nitrogen dioxide from nitric oxide and oxygen in or immediately after the canister. This initial production of nitrogen dioxide was very rapid and could not be prevented by the use of scavengers. Thus soda lime and zeolite had no practical effect as scavengers in this delivery system, and the effect of noXon was very slight.

Absorption↗

PubMed1991

Histamine of mouse lungs after single exposure to nitrogen dioxide.

Pulmonary histamine and the weight of lungs were studied in mice, exposed to a single one-hour effect of high concentrations of edemagenic gas nitrogen dioxide in a metabolic chamber. Nitrogen dioxide concentrations were chosen according to the results of nitrogen dioxide analysis of the mining atmosphere immediately after the mining blasts. The results were estimated by the method of paired comparison with the findings registered in mice, exposed to the effect of air atmosphere under identical experimental conditions. The intervals following immediately the exposure and 5 hours after were chosen for the evaluation, with regard to the dynamics of the early and late stages of hypersensitivity of the first type. i) Immediately after the exposure to the concentrations of 43, 250, 387 and 540 mg.m-3, no significant differences were observed in the amount of pulmonary histamine. In concentrations higher than 43 mg.m-3, the weight of lungs increased (the proportion of pulmonary water and the dry tissue). ii) Five hours after the exposure (nitrogen dioxide concentrations 66, 130, 137 and 270 mg.m-3), pulmonary histamine decreased, at the concentration of 137 mg.m-3 in a significant way, on the other hand, it increased significantly at the concentration of 270 mg.m-3. Both concentrations higher than 130 mg.m-3 manifested an increased weight of lungs (increased proportion of dry tissue and pulmonary water). The obtained data do not allow to establish unambiguously the part of histamine on the pulmonary changes following the effect of nitrogen dioxide. The edemagenic effect of nitrogen dioxide estimated after one-hour influence can be considered as reversible up to five hours after the exposure in concentrations lower than 130 mg.m-3. The metodical part of the study gives detailed description of exposure technique and it brings a survey of methods of histamine determination in blood and tissues.

Animals↗

PubMed1994

[In vitro studies of modification of mucociliary clearance by guinea pig tracheas by exposure to air pollutants of sulfur or nitrogen dioxide].

We studied the effect of sulfur dioxide (SO2) and nitrogen dioxide (NO2) on mucociliary activity (MCA) and ciliary beat frequency (CBF) in 63 guinea pig tracheas. The tracheas were placed in a gas cylinder and exposed for 30 minutes to SO2 concentrations ranging from 2.5 to 12.5 ppm or to NO2 concentrations ranging from 3.0 to 15.0 ppm. Control experiments were performed with exposure of the tracheas to synthetic air. MCA was measured by recording the light reflected from ciliated mucous membranes using an infrared barcode reader and CBF using video-interference microscopy. The exposure to 2.5 ppm SO2 caused a reduction in mean MCA of 63% and no significant changes in CBF. Higher SO2 concentrations caused a further impairment of MCA as well as a dose-dependent decrease in CBF. 10.0 or 12.5 ppm SO2 induced a decrease from baseline values to approximately 20% in MCA and to roughly 30% in mean CBF. The exposure to NO2 at concentrations ranging from 3.0 to 15.0 ppm did not induce any changes in MCA or CBF of the guinea pig tracheas. Our results show that exposure to SO2 for 30 minutes is able to depress the mucociliary clearance of guinea pig tracheas, whereas the exposure to equivalent NO2 concentrations for the same time do not alter the mucociliary transport.

Air Pollutants↗

PubMed1987

Comparison between aqueous-phase and gas-phase exposure protocols for determining the mutagenic potential of nitrogen dioxide and the gas fraction of welding fumes.

Nitrogen dioxide and the gas fraction of welding fumes, a complex gas mixture which contains high concentrations of nitrogen dioxide, were tested for mutagenicity in Salmonella typhimurium tester strains, TA1535 and TA1538. A comparison between 2 exposure protocols, aqueous phase and gas phase, was made to evaluate the sensitivity of each in measuring the mutagenic potential of the gases. In the aqueous-phase exposure, a suspension of cells in an isotonic salt solution was exposed by bubbling the gas through the culture. In the gas-phase exposure, the plated cells were exposed to the gas in a chamber. For both gases tested, the gas-phase exposure resulted in a higher reversion frequency than the aqueous-phase exposure. Furthermore, we found that nitrogen dioxide accounted for only a fraction of the mutagenicity observed for the gas fraction of welding fumes.

Filtration↗

PubMed1995

Curcumin inhibits nitrogen dioxide induced oxidation of hemoglobin.

Curcumin protects hemoglobin from nitrogen dioxide induced oxidation. Curcumin was also found to scavenge nitrogen dioxide in a concentration dependent way. The study also explains the ability of curcumin to protect hemoglobin from nitrite induced oxidation, where nitrogen dioxide is a key intermediate.

Curcumin↗

PubMed1982

[Dynamic studies on inhaled 15N-labelled nitrogen dioxide (15NO2)].

The dynamic pathway of inhaled nitrogen dioxide was investigated in rats exposed to 15NO2 for the specified experimental period. After exposure, various organs, blood and urine were taken out, dried by lyophilization, and then digested by the semi-micro Kjeldahl method. Determination of 15N was performed by mass-spectrometry. The 15N content (atom % excess) of each sample was calculated by subtracting the natural 15N content which was separately estimated from normal rats. The 15N content was relatively high in urine, plasma and kidneys, and low in liver, trachea, heart and brain. It was concluded that the inhaled nitrogen dioxide was quickly absorbed into blood and was excreted into urine. Nitrite was detected in the plasma obtained from the rats exposed to 15NO2 at levels higher than 10 ppm, and a significant correlation was found between the concentration of nitrite and the exposure concentration of 15NO2.

Animals↗

PubMed1985

Recommendations for air quality standards for nitrogen dioxide and ozone.

The acute health effects of nitrogen dioxide and ozone critical to the general population are summarized. For long-term exposures to the former in the outdoor environment a six-month average limit value of 80 micrograms/m3 is recommended for the wintertime. When "new" residential areas are planned or when the limit value is used as an air quality standard for the nonindustrial indoor environment, the adequate six-months' average limit value for the winter would be 50 micrograms/m3. For short-term exposures to nitrogen dioxide outdoors a limit value of 320 micrograms/m3 (1-h average) is recommended, not to be exceeded more than 12 h per year, each time during a maximum of 2 h. This value should apply only to "old" residential areas in which nitrogen dioxide pollution cannot be reduced without large economical and practical consequences. The value 190 micrograms/m3 (1-h average), not to be exceeded more than 12 h per year, should apply to most residential areas, to recreational areas, and to all nonindustrial indoor environments. For short-term exposures to photochemical oxidants, as represented by ozone in nonindustrial outdoor environments, the acceptable short-term limit value should be 120 micrograms/m3 (1-h average), not to be exceeded more than 12 h per year. An additional 1-h outdoor ceiling value of 200 micrograms/m3 is recommended, not to be exceeded. For the nonindustrial indoor environment a 1-h ceiling value of 100 micrograms/m3 is recommended, not to be exceeded.

Air Pollutants↗

PubMed1989

Mutagenic activity of ultraviolet-irradiated mixtures of nitrogen dioxide and propene or butadiene.

The mutagenic activities of mixtures of nitrogen dioxide and 1,3-butadiene or propene were investigated after uv-irradiation in a small, laboratory-bench scale flow-through gas exposure system. The tester organism was Salmonella typhimurium, principally strain TA100. The photoreaction products from 1,3-butadiene and nitrogen dioxide were more mutagenic than those from propene and nitrogen dioxide. Approximately 0.25 ppm butadiene, compared to 100 ppm propene, was needed to give a significant mutagenic effect with 0.25 ppm NO2 after 6 hr exposure. The influence of different experimental conditions on mutagenic activity was studied using propene plus nitrogen dioxide. Increasing the mean reaction time from 40 min to 1 hr 20 min or 3 hr 20 min by reduction of the flow rate through the 20-liter reaction vessel did not appreciably increase the sensitivity of the system, nor did humidification of the air, omission of the metabolic system (S9 mix), or spreading of the bacteria on the agar surface. Prolongation of the exposure time from 6 to 16 or 24 hr did, however, give an increased mutagenic response. With prolonged exposure, a slight mutagenic effect could also be detected with ethene + NO2 + uv. Ozone addition did not appreciably enhance the mutagenic response.

Alkenes↗