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Effect of cumulative ozone exposure on ozone-induced nasal epithelial hyperplasia and secretory metaplasia in rats.

Repeated exposure of rats to O3 induces proliferative and secretory metaplastic changes within nasal airway epithelia that may protect against subsequent exposures. Our study assessed the effect of different cumulative exposure times on O3-induced nasal epithelial hyperplasia and secretory metaplasia. Rats were exposed 6 h/day to air or to 0.8 ppm O3 and were sacrificed 18 h after the end of their last exposure. The rats were exposed to either air or 0.8 ppm O3 for 3 or 7 days, or to 0.8 ppm O3 for 3 days followed by a 4-day exposure to air. The effects of the exposures were determined by quantitating the hyperplastic (epithelial nuclei/mm basal lamina) and secretory metaplastic changes (volume densities of acidic and neutral mucosubstances) within the nasal nonciliated cuboidal epithelium (NNCE). There were no significant changes in NNCE cell numeric density, or in the volume density of intraepithelial mucus, compared to air-exposed control rats, in rats exposed to O3 for 3 days and sacrificed 18 h later. Compared to control rats, there was significant epithelial hyperplasia and secretory metaplasia within the NNCE of rats exposed to O3 either for 7 days or for 3 days followed by 4 days of exposure to air. There were no significant differences in NNCE cell hyperplasia or secretory metaplasia between these two experimental groups. Three 6 h/day exposures to 0.8 ppm O3 triggered hyperplastic and metaplastic changes within rat NNCE that were indistinguishable from those produced by seven 6 h/day exposures to the same concentration of O3. The data suggest that O3 is capable of rapidly inducing hyperplastic and metaplastic responses within rat NNCE, and that once initiated, development of the phenotypic changes within the epithelium does not require further O3 exposure.

Animals↗
PubMed1994

NTP Toxicology and Carcinogenesis Studies of Ozone (CAS No. 10028-15-6) and Ozone/NNK (CAS No. 10028-15-6/ 64091-91-4) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

There is widespread concern over the health effects of oxidant air pollutants. The state of California and the Health Effects Institute (HEI) (a nonprofit research institute funded jointly by the U.S. Environmental Protection Agency [USEPA] and combustion engine manufacturers) nominated ozone for evaluation in long-term animal studies. The NTP study designs were a result of a series of meetings at the NIEHS with scientists from NIEHS, USEPA, and HEI, as well as experts from academic institutions working in the area of air pollutants. Male and female F344/N rats and B6C3F1 mice were exposed to ozone by inhalation for 4 weeks, 2 years, or for 124 weeks (rats) or 130 weeks (mice). The oxygen used to generate the ozone was greater than 99.9% pure. Additional groups of male F344/N rats were administered injections of 4-(N-methyl-Nnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (~99% pure) 3 times per week for 20 weeks and exposed to ozone by inhalation for 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium. 4-WEEK OZONE STUDY IN RATS: Groups of five male and five female F344/N rats were exposed to 0, 0.5, or 1.0 ppm ozone by inhalation 6 hours per day, 5 days per week, for a total of 20 days. All rats survived to the end of the study. The final mean body weights and mean body weight gains of 0.5 ppm males and females and of 1.0 ppm females were similar to those of the controls. The final mean body weight of 1.0 ppm males was 7% lower than that of the controls. Clinical findings included hypoactivity in 1.0 ppm males and females and ruffled fur in exposed groups of males. Male and female rats exposed to 0.5 or 1.0 ppm developed multifocal lesions of the lung, which consisted of infiltration of granulocytes and macrophages with extension of the bronchial epithelium into the alveolar ducts. Female rats exposed to ozone developed minimal squamous metaplasia of the laryngeal epithelium at the base of the epiglottis. Absolute and relative lung weights of all exposed groups of males and females were greater than those of the controls, and absolute and relative thymus weights of all exposed groups were generally lower than those of the controls. 4-WEEK OZONE STUDY IN MICE: Groups of five male and five female B6C3F1 mice were exposed to 0, 0.5, or 1.0 ppm ozone by inhalation 6 hours per day, 5 days per week, for a total of 20 days. All mice survived to the end of the study. The final mean body weights and body weight gains of all exposed groups of mice were less than those of the controls. Hypoactivity was observed in 1.0 ppm mice. Male and female mice exposed to 0.5 or 1.0 ppm ozone developed patchy, multifocal lesions of the lung, which consisted of infiltration of granulocytes and macrophages with extension of the bronchial epithelium into the alveolar ducts. The relative lung weight of 1.0 ppm males was significantly greater than that of the controls. There were no other statistically significant differences in absolute or relative organ weights in males or females. 2-YEAR OZONE STUDY IN RATS: The 2-year study was designed to include the present USEPA standard (0.12 ppm), the maximum concentration believed compatible with long-term survival (1.0 ppm), and an intermediate concentration (0.5 ppm). Groups of 50 male and 50 female F344/N rats were exposed to 0, 0.12, 0.5, or 1.0 ppm ozone by inhalation for 6 hours per day, 5 days per week, for 105 weeks. Survival, Body Weights, and Clinical Findings: Survival of exposed groups of rats was similar to that of the controls at the end of the study. The mean body weights of 0.12 and 0.5 ppm males and females were similar to those of the controls throughout the study. The mean body weights of 1.0 ppm males and females were slightly lower than those of the controls throughout the study. Hypoactivity was observed in male and female rats exposed to ozone. Pathology Findings: Increased incidences of ozone-induced metaplasia occurred in the nose and lung of rats exposed to 0.5 or 1.0 ppm ozone. The lesions in the nose were characterized by an increase in the number of goblin the number of goblet cells in the respiratory epithelium with mild squamous metaplasia of the cuboidal epithelium on the lateral wall. The increase in the number of goblet cells was found primarily in level I and II epithelium occurring along the lateral wall and on the maxilloturbinates and nasoturbinates. The metaplasia in the lung was a patchy multifocal lesion consisting of extension of the bronchial epithelium into the alveoli of the centriacinar region. This may represent more an extension of the bronchial epithelium into the pulmonary parenchyma than an actual transition of one epithelial cell type into another. There were increased incidences of squamous metaplasia at the base of the epiglottis characterized by one or more layers of flattened epithelial cells where low cuboidal cells are normally found. There were no increases in the incidences of alveolar/bronchiolar adenoma or carcinoma in either males or females exposed to ozone. LIFETIME OZONE STUDY IN RATS: For this study, rats were exposed to 0.5 and 1.0 ppm ozone for an additional 6 months to determine the effect of extended exposure on neoplasm incidence. Groups of 50 male and 50 female F344/N rats were exposed to 0, 0.5, or 1.0 ppm ozone by inhalation for 6 hours per day, 5 days per week, for 125 weeks. Survival, Body Weights, and Clinical Findings: Survival rates of exposed rats were similar to those of the controls. The mean body weights of 0.5 ppm males and females were similar to those of the controls throughout the study. The mean body weights of 1.0 ppm males and females were slightly lower than those of the controls for the first two years of the study. Hypoactivity was observed in exposed groups of males and females. Pathology Findings: Increased incidences of metaplasia occurred in the nose, larynx, and lung of rats exposed to 0.5 or 1.0 ppm ozone. The lung lesions were multifocal, centriacinar and were characterized by the presence of cuboidal epithelium (ciliated and nonciliated) along the alveolar ducts where type I epithelium is normally present. Inflammation (histiocytic infiltration) and interstitial fibrosis were observed in the lung of exposed males and females, and hyperplasia was observed in the nose of exposed male and female groups. There were no ozone-related increased incidences of neoplasms. 2-YEAR OZONE/NNK STUDY IN MALE RATS: An intermediate concentration of 0.5 ppm ozone was combined with exposure to two levels of a known carcinogen (0.1 and 1.0 mg NNK/kg body weight) in order to determine if ozone promotes the carcinogenic process or acts as a cocarcinogen. Groups of 48 male F344/N rats were exposed to 0 or 0.5 ppm ozone by inhalation, 6 hours per day, 5 days per week for 105 weeks. During the first 20 weeks of the study, these rats were subcutaneously injected with 0, 0.1, or 1.0 mg NNK per kg body weight in trioctanoin three times weekly. Survival and Body Weights: Two-year survival rates of male rats were similar in all groups. Final mean body weights of all males exposed to NNK alone or NNK and ozone were similar to that of the controls, with the exception of rats exposed to 1.0 mg NNK/kg body weight and 0.5 ppm ozone. Hypoactivity was observed in males exposed to NNK and ozone, in those exposed to NNK without ozone, and in those exposed to ozone only. Pathology Findings: Alveolar epithelial metaplasia and interstitial fibrosis occurred in all groups of rats exposed to ozone or to NNK and ozone, but not in those exposed to NNK without ozone. Increased incidences of hyperplasia occurred in groups of rats exposed to NNK or to ozone and NNK. Incidences of hyperplasia were similar among groups of rats exposed to NNK only. An increased incidence of alveolar/bronchiolar adenoma or carcinoma (combined) occurred in rats administered 1.0 mg/kg NNK, with or without ozone. The administration of ozone did not affect the occurrence of pulmonary neoplasms or nonneoplastic lesions in rats administered NNK. 2-YEAR OZONE STUDY IN MICE: The 2-year study was designed to include the present USEPA standard (0.12 ppm), the maximum concentration believed compatible with long-term survival (1.0 ppm), and an intermediate concentration (0.5 ppm). Groups of 50 male and 50 female B6C3F1 mice were exposed to 0, 0.12, 0.5, or 1.0 ppm ozone by inhalation for 6 hours per day, 5 days per week, for 105 weeks. Survival, Body Weights, and Clinical Findings: Survival rates of exposed mice were generally similar to those of the controls; the 2-year survival rate of 1.0 ppm females was greater than that of the controls. The mean body weights of 0.12 and 0.5 ppm males were similar to that of the controls throughout the study; the mean body weights of 1.0 ppm males and of all exposed groups of females were generally lower than those of the controls throughout the study. Hypoactivity was observed in male and female mice exposed to ozone. Pathology Findings: Increased incidences of metaplasia occurred in the nose and lung of mice exposed to 0.5 or 1.0 ppm ozone. The metaplasia in the nose consisted of increased thickening and extension of the squamous epithelium in the anterior portion of the nasal passage. The metaplasia in the lung consisted of extension of the bronchial epithelium into the alveoli of the centriacinar region. There were increased incidences of hyperplasia in the nose characterized by thickening of the noncuboidal (transitional) epithelium. There were increased incidences of hyperplasia in the epiglottis of female mice, a change that was characterized by a minimal increase in the thickness of the epithelium. Incidences of alveolar/bronchiolar adenoma or carcinoma (combined) were marginally increased in 0.5 and 1.0 ppm males (0 ppm, 14/50; 0.12 ppm, 13/50; 0.5 ppm, 18/50; 1.0 ppm, 19/50) and were increased in 1.0 ppm females (6/50, 7/50, 9/49, 16/50). LIFETIME OZONE STUDY IN MICE: For this study, mice were exposed to 0.5 and 1.0 ppm ozone for 30 months to determine the effect of extended exposure on neoplasm incidence. Groups of 50 male and 50 female B6C3F1 mice were exposed to 0, 0.5, or 1.0 ppm ozone by inhalation for 6 hours per day, 5 days per week, for 130 weeks. Survival and Body Weights: Survival rates of exposed mice were similar to those of the controls. The mean body weights of 0.5 ppm males and females were similar to those of the controls throughout the study. The mean body weights of 1.0 ppm males and females were generally lower than those of the controls throughout the study. Hypoactivity was observed in male and female mice exposed to ozone. Pathology Findings: The incidences of alveolar/bronchiolar adenoma and carcinoma (combined) were marginally increased in exposed males (0 ppm, 16/49; 0.5 ppm, 22/49; 1.0 ppm, 21/50) and in exposed females (6/50, 8/49, 12/50). Increased incidences of metaplasia occurred in the nose, larynx, and lung of exposed groups of males and females, and the incidences of hyperplasia were increased in the larynx and nose of exposed mice. The morphology of the lesions was similar to that seen in the 2-year study. There were no ozone-related increases in alveolar epithelial hyperplasia. GENETIC TOXICOLOGY: Ozone was mutagenic in Salmonella typhimurium strain TA102, with and without S9 metabolic activation. CONCLUSIONS: Under the conditions of these 2-year and lifetime inhalation studies, there was no evidence of carcinogenic activity of ozone in male or female F344/N rats exposed to 0.12, 0.5, or 1.0 ppm. There was equivocal evidence of carcinogenic activity of ozone in male B6C3F1 mice based on increased incidences of alveolar/bronchiolar adenoma or carcinoma. There was some evidence of carcinogenic activity of ozone in female B6C3F1 mice based on increased incidences of alveolar/bronchiolar adenoma or carcinoma. There was no evidence that exposure to 0.5 ppm ozone enhanced the incidence of NNK-induced pulmonary neoplasms in male rats. Exposure of male and female rats to ozone for 2 years or 125 weeks was associated with goblet cell hyperplasia and squamous metaplasia in the nose, squamous metaplasia in the larynx, and metaplasia (extension of bronchial epithelium into the centriacinar alveolar ducts) and interstitial fibrosis in the lung. Exposure of male and female mice to ozone for 2 years or 130 weeks was associated with hyperplasia and squamous metaplasia in the nose and inflammation (histiocytic infiltration) and metaplasia (extension of bronchial epithelium into the centriacinar alveolar ducts) of the lung.

Journal Article↗
PubMed1994

Effects of ozone on managed pasture: I. Effects of open-top chambers on microclimate, ozone flux, and plant growth.

Open-top chambers (OTC) were established in a field of managed pasture, and environmental parameters were recorded inside and outside to study the influence of OTCs on radiation, air temperature (T(air)), saturation vapour pressure deficit (svpd), and soil water content in relationship to plant growth and yield. Canopy development in OTCs supplied with non-filtered air (NF) and in ambient (AA) plots was followed by measuring leaf area index (LAI). The dry matter yield was determined after three growth periods in each of two consecutive seasons. Boundary layer conductance (g(bw)) and wind speed (u) were measured along a vertical profile, and day-time flux were measured along a vertical profile, and day-time flux of O(3) was estimated throughout the experiment on the basis of a mass balance. The vertical profile of u showed values in the range 1-1.2 m s(-1) at the top of the canopy, and maximum g(bw) was 20-25 mm s(-1). Average reduction in global radiation in OTCs was 25%, and volumetric soil water content was reduced by about 5%. Daily mean T(air) was increased by 1.3 degrees C, mean daily maximum svpd by 0.08 kPa, and the temperature sum (degree days with base temperature of +5 degrees C) by 12%. Fluctuations in the difference in daily mean T(air) and svpd during the daytime between OTCs and ambient air were related to canopy structure. Differences were largest after each cut and declined with increasing LAI. A small effect of changes in LAI on T(air) and svpd occurred during periods with low soil water content. The flux of O(3) in OTCs was largest (>100 microg m(-2) min(-1)) before and smallest (<20 microg m(-2) min(-1)) after each cut. Calculated deposition velocities for O(3) (nu(d)) in the range 0-3 cm s(-1) were generally higher than those measured under most field conditions. Overall, in OTCs the deficit in soil and atmospheric moisture was larger than in the open field, and the increase in daily mean T(air) was strongly influenced by the stage of canopy development. Changes in microclimate and incoming radiation affected pasture development. LAI was slightly reduced in OTCs as compared to AA plots. The total accumulated dry matter yield for all six growth periods was only about 7% lower in OTCs, but the contribution of clover to total forage mass declined during the experiment. OTCs had no significant effect on weeds. The results indicate that OTCs reduced the competitiveness of clover, and that the increase in growth of grasses compensates for the loss in clover yield. The shift in species composition caused by OTCs must be considered when studying the effect of pollutants on pasture.

Journal Article↗