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Biomedical subjects

M T Kleinman

Publications and source records attributed to M T Kleinman.

At least 19 recordsLinked to original sources
PubMed1992

Valuing the health benefits of clean air.

An assessment of health effects due to ozone and particulate matter (PM10) suggests that each of the 12 million residents of the South Coast Air Basin of California experiences ozone-related symptoms on an average of up to 17 days each year and faces an increased risk of death in any year of 1/10,000 as a result of elevated PM10 exposure. The estimated annual economic value of avoiding these effects is nearly $10 billion. Attaining air pollution standards may save 1600 lives a year in the region.

Air Pollutants↗
PubMed1991

The effects of exercise on dose and dose distribution of inhaled automotive pollutants.

The purpose of this study was to determine how changes in ventilation rate and in the entry route of air pollutants into the respiratory tract (nose versus mouth breathing) affected the respiratory tract uptake and penetration of inhaled gaseous and particulate pollutants associated with automobile emissions. Experiments were performed with female beagle dogs exposed while standing at rest or while exercising on a treadmill at 5 km/hour and a 7.5 percent grade. Dogs were exposed to nitrogen dioxide at concentrations of 1 and 5 parts per million (ppm), to formaldehyde at 2 and 10 ppm, and to an aerosol of ammonium nitrate particles (0.3 micron mass median aerodynamic diameter) at 1 mg/m3. Total respiratory system uptake and effects on breath time, expired tidal volume, fractional expiration time, minute ventilation, respiratory gas exchange, ventilation equivalents for oxygen and carbon dioxide, and dynamic pulmonary resistance and compliance were measured in exercising and resting dogs exposed for two hours to 5 ppm nitrogen dioxide and 10 ppm formaldehyde in combination with 1 mg/m3 of ammonium nitrate particles. Regional penetration of pollutants through oral and nasal airways and pollutant uptake in the lung were measured in a separate group of six tracheostomized dogs standing at rest while being exposed to nitrogen dioxide, formaldehyde, and ammonium nitrate particles. Hypercapnic stimulation was used to modify ventilation rates in the tracheostomized dogs while pollutant penetration and uptake were measured. Dogs exposed to 5 ppm of nitrogen dioxide at rest tended to breathe more rapidly (p less than 0.05) and more shallowly (a nonsignificant trend) than dogs exposed to purified air. The changes observed were similar in direction, but of smaller magnitude, to changes observed when the same dogs were exposed during exercise to ozone at 0.6 ppm in a separate study. Rapid-shallow breathing was not observed when the dogs were exposed during exercise to 5 ppm nitrogen dioxide. Dogs exposed to a mixture of 10 ppm formaldehyde and 1 mg/m3 ammonium nitrate particles during exercise showed a shift to larger tidal volume breathing, but the response was much less pronounced than the slow-deep breathing pattern response observed in a separate study of dogs exposed to 10 ppm formaldehyde alone. The total respiratory system uptake of formaldehyde from the formaldehyde and ammonium nitrate mixture was larger than that measured for 10 ppm of formaldehyde alone in another exercise and exposure study.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Effects of ozone on pulmonary function: the relationship of response to dose.

A dose-response relationship for the effects of ozone on pulmonary function in humans has been derived using the concept of internal thoracic dose. This quantity, which represents the dose of inhaled pollutant capable of reaching and affecting target sites in the lower respiratory tract, was estimated using a mathematical model derived in part from theory and in part from data obtained using human and animal subjects. The model was applied to ozone exposures of individuals ranging in age from infants to adults over age 65 and for exercise conditions ranging from rest to heavy exercise (greater than 6 times resting minute ventilation). The dose model was successfully used to compare results from clinical studies in which subjects were exposed under disparate conditions of exercise, exposure concentration and exposure duration. The model can also be applied to estimate doses to populations exposed to ambient pollution. The effects of ozone on pulmonary function in adults and children were evaluated using the model. On the basis of dose of ozone (micrograms O3 per kg body mass), children, aged 8 to 15 years, and adults were equally sensitive. When dose is analyzed as a function of age, the data suggest that children, under the age of 6 years, receive greater doses to respiratory tract tissues than do older children or adults, under equivalent conditions of exposure.

Administration, Inhalation↗
PubMed1989

Health effects of acid aerosols formed by atmospheric mixtures.

Under ambient conditions, sulfur and nitrogen oxides can react with photochemical products and airborne particles to form acidic vapors and aerosols. Inhalation toxicological studies were conducted, exposing laboratory animals, at rest and during exercise, to multicomponent atmospheric mixtures under conditions favorable to the formation of acidic reaction products. Effects of acid and ozone mixtures on early and late clearance of insoluble radioactive particles in the lungs of rats appeared to be dominated by the oxidant component (i.e., the mixture did cause effects that were significantly different from those of ozone alone). Histopathological evaluations showed that sulfuric acid particles alone did not cause inflammatory responses in centriacinar units of rat lung parenchyma (expressed in terms of percent lesion area) but did cause significant damage (cell killing followed by a wave of cell replication) in nasal respiratory epithelium, as measured by uptake of tritiated thymidine in the DNA of replicating cells. Mixtures of ozone and nitrogen dioxide, which form nitric acid, caused significant inflammatory responses in lung parenchyma (in excess of effects seen in rats exposed to ozone alone), but did not damage nasal epithelium. Mixtures containing acidic sulfate particles, ozone, and nitrogen dioxide damaged both lung parenchyma and nasal epithelia. In rats exposed at rest, the response of the lung appeared to be dominated by the oxidant gas-phase components, while responses in the nose were dominated by the acidic particles. In rats exposed at exercise, however, mixtures of ozone and sulfuric acid particles significantly (2.5-fold) elevated the degree of lung lesion formation over that seen in rats exposed to ozone alone under an identical exercise protocol.

Acid Rain↗
PubMed1988

Effects of exercise exposure on toxic interactions between inhaled oxidant and aldehyde air pollutants.

Respiratory tract injury resulting from inhalation of mixtures of ozone (O3) and nitrogen dioxide (NO2) and of O3 and formaldehyde (HCHO) was studied in Sprague-Dawley rats under exposure conditions of rest and exercise. Focal inflammatory injury induced in lung parenchyma by O3 exposure was measured morphometrically and HCHO injury to the nasal respiratory epithelium was measured by cell turnover using tritium-labeled thymidine. Mixtures of O3 (0.35 or 0.6 ppm) with NO2 (respectively 0.6 or 2.5 ppm) doubled the level of lung injury produced by O3 alone in resting exposures to the higher concentrations and in exercising exposures to the lower concentrations. Formaldehyde (10 ppm) mixed with O3 (0.6 ppm) resulted in reduced lung injury compared to O3 alone in resting exposures, but exercise exposure to the mixture did not show an antagonistic interaction. Nasal epithelial injury from HCHO exposure was enhanced when O3 was present in a mixture. Mixtures of O3 and NO2 at high and low concentrations formed respectively 0.73 and 0.02 ppm nitric acid (HNO3) vapor. Chemical interactions among the oxidants, HNO3, and other reaction products (N2O5 and nitrate radical) and lung tissue may be the basis for the O3-NO2 synergism. Increased dose and dose rate associated with exercise exposure may explain the presence of synergistic interaction at lower concentrations than observed in resting exposure. No oxidation products were detected in O3-HCHO mixtures, and the antagonistic interaction observed in lung tissue during resting exposure may result from irritant breathing pattern interactions.

Air Pollutants↗
PubMed1987

Tracheal and bronchoalveolar permeability changes in rats inhaling oxidant atmospheres during rest or exercise.

Permeability of tracheal and bronchoalveolar airways of rats was measured and used to examine the effects of inhaled oxidant-containing atmospheres. The atmospheres studied were (a) ozone (O3) at 0.6 ppm (1.2 mg/m3) or 0.8 ppm (1.6 mg/m3); (b) nitrogen dioxide (NO2) at 6 ppm (11.3 mg/m3) or 12 ppm (22.6 mg/m3); (c) O3 + NO2 at 0.6 ppm (1.2 mg/m3) and 2.5 ppm (4.7 mg/m3), respectively; and (d) a 7-component particle and gas mixture (complex atmosphere) representing urban air pollution in a photochemical environment. The rats were exposed for 2 h. The effects of exercise during exposure were evaluated by exposing additional groups in an enclosed treadmill. Exposure of resting rats to 0.8 ppm O3 increased tracheal permeability to DTPA and bronchoalveolar permeability to diethylenetriamine pentaacetate (DTPA) and bovine serum albumin (BSA) at 1 h after the exposure. Bronchoalveolar, but not tracheal, permeability remained elevated at 24 h after the exposure. Exercise during exposure to O3 increased permeability to both tracers in the tracheal and the bronchoalveolar zones, and prolonged the duration of increased permeability in the tracheal zone from 1 h to 24 h, and in the bronchoalveolar zone from 24 h to 48 h. Permeability in the tracheal and bronchoalveolar zones of rats exposed at rest to 6 or 12 ppm NO2 did not differ from controls. However, rats exposed during exercise to 12 ppm NO2 for 2 h developed a significant increase in tracheal and bronchoalveolar permeability to DTPA and BSA at 1 h, but not at 24 or 48 h, after exposure. Exposure at rest to 0.6 ppm O3 plus 2.5 ppm NO2 significantly increased bronchoalveolar permeability at 1 and 24 h after exposure, although exposure at rest to 0.6 ppm O3 alone increased bronchoalveolar permeability only at 1 h after exposure. Exposure to O3 + NO2 during exercise led to significantly greater permeability to DTPA than did exercising exposure to O3 alone. Resting rats exposed to a complex gas/aerosol atmosphere composed of the above O3 and NO2 concentrations, plus 5 ppm (13.1 mg/m3) sulfur dioxide (SO2) and an aerosol of insoluble colloidal Fe2O3 with an aerosol of manganese, ferric, and ammonium salts, demonstrated increased permeability at 1 and 24 h after exposure. Nitric acid vapor was formed in both the O3 + NO2 atmosphere and the complex gas/aerosol atmosphere.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗
PubMed1986

Relative permeability of nasal, tracheal, and bronchoalveolar mucosa to macromolecules in rats exposed to ozone.

Nasal, tracheal and bronchoalveolar injuries resulting from acute ozone exposure of rats were investigated by permeability changes. 99mTc-labeled diethylenetriaminepentaacetate (DPTA) and 125I-labeled bovine serum albumin (BSA) were selectively instilled into localized airway regions of anesthetized rats exposed to 0.8 ppm 03 or clean air for 2 h. Transmucosal transfer of the radiolabeled tracers was detected by counting the radioactivity in blood samples collected at short postinstillation time intervals. Permeability measurements were made on d 0, 1, and 2 after O3 exposure to analyze the extent and persistence of tissue injury in the nasal, tracheal, and bronchoalveolar regions. Normal mucosal permeability was low in nose, intermediate in bronchoalveolar zone, and high in trachea. The O3-related injury, reflected by elevated permeability, was substantial in the trachea and bronchoalveolar zone but was minimal in the nose immediately after the exposure. Abnormal permeability persisted for less than 24 h in the trachea but for more than 24 h in the bronchoalveolar zone. The results are consistent with the properties of O3 of causing greater injury in the smaller airways and the alveolar zone than in the trachea.

Animals↗
PubMed1984

Respiratory responses of humans exposed to an aerosol-gas pollutant mixture: multivariate contrast of a complex atmosphere to clean air and sodium chloride aerosol controls.

Data from a group of 20 subjects with normal baseline pulmonary function, who were exposed for 2 h to a test atmosphere containing a complex mixture of pollutants, have been contrasted with data from two other groups exposed to presumably non-toxic control atmospheres. Group 1 was exposed to clean air, group 2 was exposed to clean air containing sodium chloride aerosol at 270 micrograms m-3, and group 3 was exposed to the complex atmosphere containing sodium chloride (332 micrograms m-3) and zinc ammonium sulfate (23 micrograms m-3) aerosols plus nitrogen dioxide (0.5 ppm) and sulfur dioxide (0.5 ppm). These atmospheres (ranked according to the presumed relative toxicities of the components; clean air = 0, sodium chloride = 1, complex mixture = 2) were contrasted using multiple regression and partial correlation analyses. The effects of exposure to the complex gas-aerosol mixture on forced expiratory performance were not significantly different from those observed in subjects exposed to clean air or to sodium chloride aerosol.

Adolescent↗
PubMed1979

Controlled exposures of human volunteers to sulfate aerosols. Health effects and aerosol characterization.

Our laboratory has undertaken the study of possible acute adverse health effects of sulfate aerosols through controlled exposures of volunteer human subjects. Both healthy and asthmatic adult men were exposed for 2-hour periods (with intermittent exercise) to ammonium sulfate, ammonium bisulfate, and sulfuric acid of particle size distributions and concentrations intended to simulate "worst case" exposures during Los Angeles smog episodes. Lung function tests were performed by the subjects on entering and before exiting from a carefully controlled environmental chamber. Subject symptoms were evluated in a standardized manner. Aerosol concentrations and size distributions were determined by an on-line computer/aerometric monitoring system; gravimetric and chemical analyses were performed on impactor and total filter samples after test exposures. We found little or no evidence of adverse health effects from 2-hour multiple-day exposures to any of the compounds at "worst case" ambient concentrations.

Aerosols↗