Breath, urine, and blood measurements as biological exposure indices of short-term inhalation exposure to methanol.

Due to their transient nature, short-term exposures can be difficult to detect and quantify using conventional monitoring techniques. Biological monitoring may be capable of registering such exposures and may also be used to estimate important toxicological parameters. This paper investigates relationships between methanol concentrations in the blood, urine, and breath of volunteers exposed to methanol vapor at 800 ppm for periods of 0.5, 1, 2, and 8 h. The results indicate factors that must be considered for interpretation of the results of biological monitoring. For methanol, concentrations are not proportional to the exposure duration due to metabolic and other elimination processes that occur concurrently with the exposure. First-order clearance models can be used with blood, breath, or urine concentrations to estimate exposures if the time that has elapsed since the exposure and the model parameters are known. The 0.5 to 2-h periods of exposure were used to estimate the half-life of methanol. Blood data gave a half-life of 1.44+/-0.33 h. Comparable but slightly more variable results were obtained using urine data corrected for voiding time (1.55+/-0.67h) and breath data corrected for mucous membrane desorption (1.40+/-0.38 h). Methanol concentrations in blood lagged some 15-30 min behind the termination of exposure, and concentrations in urine were further delayed. Although breath sampling may be convenient, breath concentrations reflect end-expired or alveolar air only if subjects are in a methanol-free environment for 30 min or more after the exposure. At earlier times, breath concentrations included contributions from airway desorption or diffusion processes. As based on multicompartmental models, the desorption processes have half-lives ranging between 0.6 and 5 min. Preliminary estimates of the mucous membrane reservoir indicate contributions of under 10% for a 0.5-h exposure and smaller effects for longer periods of exposure.

Increased 5-lipoxygenase metabolism in the lungs of human subjects exposed to ozone.

The environmental pollutant ozone, at sufficiently high levels, is known to induce pulmonary inflammation with resultant airway obstruction in normal subjects. Eicosanoids comprise one group of mediators released from alveolar macrophages which are involved in the pathogenesis of inflammatory lung diseases. We compared the effects of 2-h exposures to 0.4 ppm ozone and filtered air on pulmonary function and eicosanoid levels in bronchoalveolar lavage fluid in 11 normal healthy volunteers. Subjects were exposed to a 6-fold increase in minute ventilation using an adjusted work load on a cycle ergometer. All subjects complained of cough and dyspnea, and demonstrated increased airway obstruction, and increased specific airway resistance following ozone exposure as compared to air exposure. Bronchoalveolar lavage cell count demonstrated a 9-fold increase in the number of neutrophils with a lesser reduction in the number of alveolar macrophages following ozone exposure. Notably, bronchoalveolar lavage fluid leukotriene (LT) C4 (8-fold) and to a lesser extent LTB4 (1.5-fold) levels were higher following ozone exposure compared to air control, with no change in prostaglandins. In a subset of four subjects, alveolar macrophage arachidonic acid metabolism was studied in vitro following separate in vivo exposures to both ozone and air. Alveolar macrophages obtained following ozone exposure released more 5-lipoxygenase (1.5-fold) metabolites, with no change in cyclooxygenase metabolites, than did cells obtained following air exposure. These observations document activation of the 5-lipoxygenase pathway in the lung following ozone exposure, and suggest that alveolar macrophages may participate in the generation of LT, whose actions promote airway inflammation and obstruction.

Mechanism of induction of asthmatic attacks initiated by the inhalation of particles generated by airbag system deployment.

OBJECTIVE: We have previously demonstrated that inhalation of the dust produced by dual frontal airbag deployment can result in significant bronchospasm in approximately 40% of mild to moderate asthmatics. This study was performed to determine the cause of the asthmatic response. DESIGN: Controlled laboratory study. MATERIALS AND METHODS: Asthmatics who were previously tested for their response to airbag effluents were exposed for twenty minutes to either 1) airbag effluents from airbag systems in which the airbag was insulated from the hot deployment module; 2) non-sulfur containing airbag effluents; 3) sodium chloride aerosol; or 4) sodium carbonate-bicarbonate aerosol (pH 10). Pre-exposure, post-exposure, and 2 hour post exposure pulmonary spirometry and mechanics were measured. Subject's filled out symptoms questionnaires before exposure, 2, 4, 8, 12, and 19 minutes into the exposure, immediately post-exposure, and 2 hours post-exposure. MEASUREMENTS AND MAIN RESULTS: Prevention of the pyrolysis of the passenger-side bag as it rested on the hot module after deployment did not diminish the asthmatic response. Removal of sulfur-containing oxidants from the airbag pyrotechnic chemistry, which may have led to sulfite production, similarly did not alleviate the asthmatic response to the airbag effluents. Lastly, when asthmatics were exposed to sodium chloride and sodium carbonate-bicarbonate aerosols at approximately the same concentration (approximately 220 mg/m3) as the airbag aerosol concentration that occurred in the in-car tests, they had responses similar to those produced by the airbag exposures. CONCLUSIONS: We conclude that the amount of soluble particulate contained in the aerosol discharged into the passenger compartment by dual frontal airbag deployment is largely the cause of the observed evoked asthmatic attacks. The alkaline pH of the airbag and carbonate aerosols may have added an additional degree of provocation.

The relationship of beta-glucuronidase activity in crevicular fluid to probing attachment loss in patients with adult periodontitis. Findings from a multicenter study.

Analysis of gingival crevicular fluid (GCF) offers a non-invasive means of studying the host response in periodontal disease, and may provide an early indication of the patient at risk for active periodontitis. A number of host markers have been studied for their relationship to disease activity (probing attachment loss or PAL). GCF levels of the acid glycohydrolase beta-glucuronidase (beta G), a marker of primary granule release from polymorphonuclear leukocytes (PMN), have been shown to identify patients with periodontitis at risk for additional PAL. In this multicenter trial, we evaluated (a) the short-term effect of conservative periodontal therapy on beta G activity in GCF, and (b) the relationship of persistently elevated beta G activity to PAL in patients who were monitored for 6 months. The study population included a total of 140 patients with chronic adult periodontitis. 130 patients were on a regular recall schedule, and 10 were previously untreated. After collection of baseline clinical data at all sites, and analysis of beta G in GCF from one site (mesiobuccal) per tooth, the patients received a scaling and prophylaxis. Two weeks later patients were seen for collection of GCF. If elevated enzyme activity was found at 2 weeks, the patients were seen at 3 months for a clinical exam and GCF collection. Clinical parameters were collected from all patients at 6 months. Therapy tended to reduce beta G activity in GCF.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchoalveolar lavage neutrophilia in asthmatic and healthy volunteers after controlled exposure to ozone and filtered purified air.

STUDY OBJECTIVE: To characterize the pulmonary response of asthmatic and healthy nonsmoking adult men to 0.20 ppm ozone by controlled chamber exposure. DESIGN: A prospective, crossover study of five atopic asthmatic and five normal subjects randomly exposed to ozone and filtered purified air (FPA) for 6 h, consisting of 30-min alternating periods of rest and moderate exercise. The two exposures were separated by at least 30 days. SETTING: A controlled exposure in a stainless steel chamber. PATIENTS: Five atopic asthmatic and five normal subjects between 18 and 45 years of age. Treatment with medications was withheld from asthmatics prior to the exposures. All subjects were nonsmokers. INTERVENTIONS: Symptoms were assessed throughout the exposures. Pulmonary function was measured at baseline, hourly throughout an exposure, and after an exposure. Bronchoalveolar lavage (BAL) was performed 18 h after the completion of an exposure. The BAL fluid (BALF) was analyzed for cell count and differential; the cell-free supernatant was analyzed for albumin, tumor necrosis factor (TNF), interleukin 1 (IL-1), interleukin 6 (IL-6), and interleukin 8 (IL-8). RESULTS: There were statistically significant increases in IL-8 levels, as well as percent polymorphonuclear neutrophils (PMNs) and PMNs per milliliter of lavage in asthmatics exposed to ozone as compared with the same asthmatics exposed to FPA and the same normal subjects exposed to ozone and FPA. Interleukin 6 was also significantly increased in asthmatics exposed to ozone. The BALF albumin, TNF, and IL-1 levels were not significantly different among the four groups. There were no differences between asthmatics and healthy controls exposed to ozone or FPA in baseline to postexposure FEV1, FVC, FEV1/FVC, and sRaw. CONCLUSIONS: We conclude that asthmatics exposed to ozone develop a significant BALF neutrophilia and increased levels of the cytokines, IL-8 and IL-6. These BALF findings occur even though the level of ozone exposure was not significant enough to reduce pulmonary function.

Acute pulmonary response of asthmatics to aerosols and gases generated by airbag deployment.

The purpose of this study was to determine whether the aerosols and gases that vent into an automobile's passenger compartment after airbag deployment pose a risk to the asthmatic population. After baseline pulmonary function measurements were taken, 24 diagnosed asthmatic subjects were placed in the rear seat of an automobile, and a driver-passenger airbag system was deployed. Subjects remained in the vehicle with the windows closed and no ventilation for 20 min or until they perceived or demonstrated signs of chest tightness and bronchoconstriction. They then exited the vehicle and were retested immediately after exposure and 2 and 4 h after exposure. Ten of the 24 subjects demonstrated clinically significant bronchoconstrictive episodes, three of which required medical intervention. These three events were quickly reversed by beta-agonist therapy. When eight of the responding subjects were reexposed at later dates to the same supplemental inflatable restraints emissions while wearing a high-efficiency particulate absolute respirator, which prevented inhalation of the particles but allowed passage of the gases, the pulmonary response was essentially eliminated. We conclude that the aerosols generated by deployment of automotive driver-passenger airbag systems can induce significant asthmatic reactions in some individuals.

The relationship of beta-glucuronidase activity in crevicular fluid to clinical parameters of periodontal disease. Findings from a multicenter study.

Previous reports have suggested that persistently elevated levels of the acidic glycohydrolase beta-glucuronidase (beta G) in gingival crevicular fluid (GCF) can identify patients with chronic adult periodontitis who are at risk for future probing attachment loss (PAL). To comprehensively study beta G activity in GCF, a multicenter trial examining the relationship of the enzyme in GCF to traditional clinical parameters of periodontal disease and PAL was conducted. In this report, the baseline data was used to evaluate the relationship of beta G activity in GCF to traditional parameters of periodontal disease. The study group included 130 patients who had been treated for periodontal disease and were on a regular recall schedule, and 10 patients with chronic adult periodontitis who had never received treatment. Upon entering the longitudinal trial, the patients were examined, and a standardized 30-s GCF sample was collected from the mesiobuccal crevice of all study teeth. As a control, GCF samples and clinical data were collected from 62 patients with a healthy periodontium or mild inflammatory gingivitis without loss of probing attachment. At baseline, beta G activity for the periodontitis patients ranged from 0 to 1704 Units (U), with a median of 32 U. beta G could not be detected in 0.2% of samples (activity < or = 2.0 U). The 90% cumulative relative frequency was 139 U. For the healthy/gingivitis subjects beta G activity ranged from 0 to 504 U, with a median of 22 U. Enzyme was not detectable in 0.4% of samples. Only 0.9% of samples contained greater than 139 U. beta G activity in GCF was not related to gender or age. For the periodontitis patients, elevated enzyme activity (> or = 140 U) was most often associated with molar teeth, followed by maxillary bicuspids. Maxillary central incisors, and mandibular central and lateral incisors displayed the lowest frequency of elevated enzyme activity. The relationship of beta G activity to the traditional parameters of probing depth and bleeding on probing was assessed. For shallow sites (1.0-1.5 mm, 2.0-2.5 mm probing depth), the large majority of GCF samples contained low enzyme activity (90% of samples < 50 U). Descriptive indicators demonstrated a trend of increased beta G activity with increased probing depth. The median beta G activity shifted from 15 U for the shallowest sites (1.0-1.5 mm) to 127 U for the deepest sites (5-8 mm). However, this was due to a broadening of the distribution rather than representing a shift in the distribution profile.(ABSTRACT TRUNCATED AT 400 WORDS)

Effectiveness of antimicrobial mouthrinses on aerosols produced by an air polisher.

PURPOSE: The purpose of this examiner-blind investigation was to study the effect of two antimicrobial mouthrinses on the quantity and potential respiratory-penetrating ability of microorganisms generated by an air-abrasive polisher. METHODS: Forty-five adult subjects were randomly assigned to one of three groups and asked to rinse for 30 seconds with 15 ml of either a 0.12% chlorhexidine rinse, an essential oil mouthrinse, or water prior to air polishing. Prior to treatment, microbes in ambient air were collected for five minutes using an Andersen air sampler. This device simulates the human respiratory system and collects airborne microbes by means of blood agar plates stacked in a cascade impact system. Bacteria found at stages two, four, and six--representing the pharynx, bronchi, and alveoli-were collected and counted in this study. During three minutes of air-abrasive instrumentation and two minutes immediately following, airborne microbes were again collected. Agar plates removed from the sampler were incubated for 24 hours at 37 degrees C. Colony-forming units per cubic foot of air (CFUs/ft(3)) were enumerated using a Lab Line colony counter. Data were analyzed using a two-factor repeated measure ANOVA and Dunn's multiple mean comparison techniques. RESULTS: Results showed no significant effect of prerinsing among treatment groups. An increase in CFUs/ft(3) was found at each sequential stage of the air sampler, resulting in a statistically significant within-group effect (p< or =.05). Additionally, a significant interaction was found between prerinse treatment and respiratory stage (p< or =.05) . CONCLUSION: While the air-abrasive polisher produced significant amounts of deeply penetrating bacterial aerosol, differences in CFUs/ft(3) generated following the antimicrobial prerinsing tested are of little clinical significance.

Effects of air-powder polishing on the bond strength of orthodontic bracket adhesive systems.

PURPOSE: The purpose of this in vitro investigation was to evaluate the effects of air-powder polishing on the shear bond strength of two adhesive systems used for direct orthodontic bracket bonding. METHODS: Ninety-six third molar teeth were randomly assigned to be bonded with metal brackets using either a no-mix (System 1+) or a two-paste (Concise) orthodontic adhesive resin. Twelve samples in each test group were air-powder polished for either 0, 15, 30, or 60 seconds. The shear bond strength was determined for each bracket using the Instron. Scanning electron microscopy determined bond fracture patterns of tested samples. RESULTS: Mean shear bond strength values from baseline to 60 seconds varied from 22.9+/-1.9 megapascal units (MPa) to 18.2+/-4.1 MPa for Concise and from 15.5+/-2.1 MPa to 14.6+/-1.9 MPa for System 1+. A two-factor analysis of variance showed air-powder polishing significantly affected the mean shear bond strength of one adhesive. Results showed a significant decrease (p < or = .05) in the mean shear bond strength of the Concise adhesive at 60 seconds of air-powder polishing when compared to the 0-, 15-, and 30-second treatments. No significant within group time effect of air-powder polishing was found for System 1+. Differences in the fracture pattern of the Concise 60-second air-powder polishing group may account for the decrease in mean bond strength seen after treatment. CONCLUSION: Although in vitro results showed decreased bond strength for Concise, these values were well above the minimum values needed for successful bonding. Therefore, use of air-powder polishing on orthodontic bracket adhesive systems does not appear to be contraindicated.

Aerosol generation by two ultrasonic scalers and one sonic scaler. A comparative study.

The purposes of this study were to compare the amount of aerosols generated from ultrasonic and sonic scalers and to measure the potential depth of respiratory tract penetration. Forty subjects were randomly assigned to receive instrumentation with the magnetostrictive, piezoelectric, or air turbine scaler. The Anderson Air Sampler collected total baseline airborne microbes for 20 minutes prior to treatment and for 20 minutes during instrumentation. This cascade impactor system measures the degree of microbial penetration in a simulated respiratory system. Blood agar plates from the sampler were incubated for 24 hours at 37 degrees C. Colony forming units per cubic foot of air (CFUs/cu. ft.) were enumerated by one blind examiner using a Lab Line Colony Counter. Data for total microbial CFUs/cu.ft. and CFUs/cu.ft. by sampler level were analyzed on the log-transformed data using ANCOVA. Baseline values of airborne bacteria served as the covariate. Results showed no significant difference in mean combined total CFUs/cu.ft. for the magnetostrictive, piezoelectric, or air turbine sonic scalers. The magnetostrictive scaler generated the lowest CFUs/cu.ft. at the deepest level of penetration; however, no significant difference in level of penetration was found among the three scalers.

Lack of blood formate accumulation in humans following exposure to methanol vapor at the current permissible exposure limit of 200 ppm.

Accumulation of formate, the putative toxic metabolite of methanol, in the blood and the relationship between pulmonary intake and blood methanol concentration were investigated in six human volunteers following a 6-hr exposure to 200 ppm methanol (the current Occupational Safety and Health Administration 8-hr time-weighted average permissible exposure limit). At the end of a 6-hr exposure to 200 ppm methanol at rest, the blood methanol concentration was increased from a mean of 1.8 micrograms/mL to 7.0 micrograms/mL. Under light exercise, the total amount of methanol inhaled during the 6-hr exposure period was 1.8 times that inhaled at rest. However, no statistically significant increase in blood methanol concentration was observed under exercise: the concentrations averaged 8.1 micrograms/mL. Formate did not accumulate in the blood above its background level following the 6-hr exposures to 200 ppm methanol whether subjects were exposed at rest or during exercise. Unlike the data collected from epidemiologic studies, the authors' results were obtained under well-controlled methanol exposure conditions and by using appropriate dietary restrictions. The data show that (1) the biological load of methanol would be the same regardless of whether workers are engaged in light physical activity when they are exposed to methanol vapors below 200 ppm and (2) the formate that is associated with acute methanol toxicities in humans does not accumulate in blood when methanol exposure concentrations are below 200 ppm.

Pulmonary responses of asthmatic and normal subjects to different temperature and humidity conditions in an environmental chamber.

Determining the possible adverse health effects of air pollutants can be complicated by differences in the environmental conditions of temperature and humidity. To evaluate the potentially confounding effects of differences in temperature and humidity, we exposed 8 normal male subjects and 8 male subjects with asthma to the extremes in temperature and humidity that could be maintained in an environmental chamber. We performed serial pulmonary function tests for these subjects before and during 6 hr exposure periods on 5 separate occasions: cold, dry (10 degrees C, 10% relative humidity); cold, humid (10 degrees C, 50% relative humidity); normal ambient (22 degrees C, 40% relative humidity); hot, dry (37 degrees C, 15% relative humidity); and hot, humid (37 degrees C, 60% relative humidity). The exposure period included a 12 min exercise on a cycle ergometer. We found no significant change in spirometry, airways resistance, or diffusing capacity for either group of subjects at rest alone over the 6 hr period of exposure for any exposure condition. However, there were changes in spirometry and airways resistance as a result of the 12 min period of exercise. The subjects with asthma had significant decreases in forced expiratory volume in 1 sec (FEV1) (20-21%) and increases in specific airways resistance when exercising in conditions of cold and dry, cold and humid, and hot and dry. The normal subjects had an average increase in FEV1 of approximately 6% when exercising in the hot and humid conditions. We found significant correlations for the changes in FEV1 with the water content of the exposure conditions for both groups of subjects. We also found that the work performance (expressed as the external work performed divided by the oxygen consumed) was decreased for the subjects in both groups at the conditions of the higher temperature (37 degrees C) compared with the lower temperature (10 degrees C). These results confirm that controlling for the conditions of temperature and humidity is essential in chamber studies, field studies, or epidemiologic evaluations determining the adverse effect of an air pollutant.

Effectiveness of chlorhexidine and sodium fluoride in reducing dentin hypersensitivity.

This investigation was conducted to evaluate the effect of chlorhexidine, sodium fluoride, and sequential rinses of chlorhexidine (Cx) and sodium fluoride (NaF) on dentin hypersensitivity. Forty-four adult patients with dentin hypersensitivity on three teeth were randomly assigned to receive one of four treatment rinses: (1) placebo; (2) 0.12% Cx; (3) 0.2% NaF; or (4) 0.12% Cx plus 0.2 NaF. Patients' responses to cold stimulation were recorded at baseline, two weeks, and four weeks. Pain response was quantified by applying successively decreasing temperature intervals of water (20 degrees C, 15 degrees C, 10 degrees C, 5 degrees C, and 0 degrees C) to exposed dentin. Plaque Index (Silness and Löe) was recorded at baseline only. Data on dentin sensitivity over time were analyzed using a repeated measures ANOVA. This ANOVA was conducted to generate an error term for calculation of Dunn's multiple mean comparison test. A Spearman rank order test was computed to assess correlation between plaque and hypersensitivity at baseline. Results showed the Cx and NaF rinses alone significantly reduced hypersensitivity (p less than .01) at four weeks compared to baseline. Sequential Cx and NaF rinses significantly decreased sensitivity (p less than .01) at both the two- and four-week intervals compared to baseline. At the four-week interval, the sequential Cx/NaF rinse group showed a significantly greater reduction (p less than .01) in hypersensitivity response when compared to placebo. Cx alone, or NaF alone groups. A moderate, positive correlation (r = 0.55) was demonstrated between plaque and dentin hypersensitivity. This was statistically significant at the (p less than .05) level.

Integrating dental and medical care for the chronic bulimia nervosa patient: a case report.

Excessive tooth erosion and resulting sensitivity and esthetic concerns are well-documented problems in patients with eating disorders. Several techniques for restoring lost tooth structure have been reported in the literature. However, the potential significant role of dental care in the comprehensive treatment of the chronically bulimic patient has received little attention. Integration and coordination of dental treatment with medicopsycho-social therapy of the bulimic patient may enhance the patient's success in combating this complex disorder. The key to proper dental management is a definitive approach to data collection and close coordination among all health care personnel providing primary health care therapy. A specific dental approach model is recommended in this report of a patient with a 15-year history of bulimia.

The effect of ozone inhalation on metabolic functioning of vascular endothelium and on ventilatory function.

The primary purpose of this research was to determine the effect of ozone inhalation on pulmonary vascular endothelium. Male Fischer-344 rats were exposed to 0.5 or 0.7 ppm ozone, 20 hr/day for 7 days. Lungs were excised and perfused with Krebs medium containing [14C]serotonin or [14C]hippurylhistidylleucine (HHL). When compared to controls, the animals exposed to the lower ozone concentration showed no statistically significant changes in serotonin removal. In contrast, the higher ozone concentration resulted in a 32% decrease (p less than 0.0001) in serotonin removal, but had no effect on HHL. Rats similarly exposed to 0.7 ppm ozone but allowed to recover for 14 days in clean air showed no decrease in serotonin removal compared to their controls. Animals exposed sequentially to 0.5 ppm ozone for 7 days and then to 0.7 ppm for 7 days showed no alteration in serotonin metabolism, suggesting the development of tolerance initiated by the lower dose. After 7 days exposure to 0.7 ppm ozone, lung ventilatory function measurements revealed small though significant decreases in several parameters. Electron microscopic evaluation of lung capillary endothelium from animals exposed to the 0.7 ppm ozone showed no changes. Positive control animals exposed to greater than 95% oxygen, 20 hr/day for 2 days showed a 23% decrease in serotonin removal (p less than 0.03) and a 12% decrease in HHL removal (p less than 0.017). These studies indicate that inhalation of ozone can induce functional alterations in the lung endothelium, and that this effect occurs at a dosage of ozone that produces minimal ventilatory changes and no observable endothelial ultrastructural changes.

Inhalation of an alkaline aerosol by subjects with mild asthma does not result in bronchoconstriction.

Although it is recognized that inhalation of acid aerosols by subjects with asthma can cause bronchoconstriction, the effects of the inhalation of an alkaline aerosol are unknown. When supplemental inflatable restraints (automobile air bags) are deployed an alkaline aerosol is released. This aerosol is composed of particles of sodium carbonate and sodium bicarbonate with some sodium hydroxide. The mass median aerodynamic diameter (MMAD) of the aerosol is approximately 1 micron, and the pH of the aerosol is 9.8 to 10.3. A group of 14 volunteer male subjects with mild asthma inhaled increasing concentrations of this aerosol for 20-min periods of mouth-only tidal ventilation. Pulmonary function tests were performed at baseline (preexposure), after inhalation of room air alone (control), and after each period of inhalation of the aerosol. A total of 5 subjects inhaled aerosols at nominal concentrations of 10, 20, and 40 mg/m3, whereas 11 subjects inhaled aerosols concentrations of approximately 30, 60, and 120 mg/m3. The mean changes in FEV1 and specific airways resistance (SRaw) for the 11 subjects who inhaled the higher concentrations (average highest concentration 126.6 +/- 7.5 mg/m3, mean +/- SEM) were -1.4 +/- 1.9 and +17.5 +/- 8.5%, respectively. Neither change in lung function was clinically or statistically significant. We conclude that the inhalation of relatively high concentrations of this alkaline aerosol by subjects with mild asthma does not result in bronchoconstriction.

Indomethacin does not inhibit the ozone-induced increase in bronchial responsiveness in human subjects.

Exposure of human subjects to sufficiently high levels of ozone can result in reversible changes in lung function (restrictive in nature) and increases in nonspecific airway responsiveness. Several studies have implicated products of cyclooxygenase metabolism in the mediation of these changes. The purpose of this study was to determine if indomethacin (a cyclooxygenase inhibitor) would alter the changes in the ozone-induced increase in responsiveness to methacholine or the ozone-induced decrease in lung function. Thirteen male subjects underwent three randomly assigned 2-h exposure to 0.4 ppm ozone with alternating 15-min periods of rest and exercise on a cycle ergometer (30 L/min/m2, body surface area). For the 4 days before each of the exposures, the subjects received either indomethacin (150 mg/day) or placebo, or no modification. Of the 13 subjects, only seven had both detectable indomethacin serum levels on the indomethacin Study Day and a significant increase in bronchial responsiveness to methacholine on the No Medication Day. For this group of seven subjects, we found that indomethacin did not alter the ozone-induced increase in bronchial responsiveness to methacholine (decrease in PC100SRaw for the different study days: no medication, -78.4 +/- 5.3% [mean +/- SEM]; placebo, -48.9 +/- 12.2%; indomethacin, -64.5 +/- 6.3%; p greater than 0.2), although indomethacin did attenuate the ozone-induced decrease in lung function. The decrease in the FEV1 for the different study days was as follows: no medication, -20.7 +/- 5.0% (mean +/- SEM); placebo, -19.2 +/- 6.3%; indomethacin, -4.8 +/- 3.7% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of exposures to ambient ozone on ventilatory lung function in children.

This study was undertaken to determine if the ventilatory capacity of children is affected by hourly concentrations of ozone inhaled during their daily activity. Over a 3-wk period (June-July 1987) children who were attending a summer camp in the San Bernardino mountains of California performed spirometry up to three times per day during their stay at the camp. A total of 43 children were tested a total of 461 times. Ozone, oxides of nitrogen, sulfur dioxide, temperature, and relative humidity were measured continuously. Daily average measurements of total suspended particulate and the PM10 particulate fraction (less than or equal to 10 microns) were also made. Hourly ozone concentrations at the time of testing varied between 20 and 245 ppb. Regressions of each individual's FEV1 and FVC supported the view that high ozone levels reduced these lung function parameters. The average regression coefficient for FEV1 on ozone was -0.39 ml/ppb (SEM = 0.12) and for FVC -0.44 ml/ppb (SEM = 0.15), both of which were significantly different from zero. Statistical allowance for temperature and humidity increased the magnitude of these slopes. Nitrogen dioxide never exceeded 40 ppb during the time of testing and averaged 13 ppb. Sulfur dioxide's highest measurement was 8 ppb and often was at the limit of detection. Neither NO2 nor SO2 was considered in the statistical modeling. Data were divided based on whether each subject had been exposed to levels of ozone in excess of the National Ambient Air Quality Standard (NAAQS) during the several hours previous to being tested. Exposures exceeding the NAAQS indicated a significant negative relationship between ozone and FEV1, FVC, and PEFR. Data for nonexceedance periods did not indicate this negative relationship for any of the three lung function parameters, but it could not be determined if this was due to an absence of an ozone effect or to a combination of the increased variability and decreased size of this data subset. These data indicate that lung function changes on a daily basis relate in a negative fashion to ambient ozone levels. The magnitude of the changes are small and are reversed as ambient ozone decreases.

Assessment of curette sharpness.

Nothing to date has appeared in the literature addressing the relationship of specific bevel dimension and clinical sharpness of curette blades. This study investigated the degree of clinical sharpness of Gracey curettes following four periods of simulated root planning and, using the scanning electron microscope (SEM), determined the approximate number of strokes at which loss of clinical sharpness became apparent. Seventy-five new stainless steel curette blades were standardized and randomly assigned to one of five groups: control, 30-stroke, 50-stroke, 70-stroke, and 90-stroke. With the exception of the control group, blades underwent a simulated root-planing procedure, on extracted, periodontally involved teeth, which employed a device to standardize pressure and stroke length. Blades were then tested for clinical sharpness using light reflection, with two degrees of magnification; and plastic stick, a tactile evaluation. Blades were photographed under the SEM at a magnification of x1,000. Bevel width was measured at 10 standardized locations on the photomicrographs, and a mean was calculated. Nonparametric data were analyzed using the Kruskal-Wallis statistical test and SEM parametric data using ANOVA and post hoc Newman-Kuels tests. Results showed no significant differences among treatment groups when either tactile or magnification sharpness tests were used. Analysis of the SEM data showed no statistically significant differences among bevel dimensions for any of the five groups. A Spearman rank order correlation, used to compare the clinical data to the SEM bevel measurements, showed no correlation of clinical sharpness and SEM-determined bevel dimension.