Search PubMed⌕ Search

Biomedical subjects

Richard W Hyde

Publications and source records attributed to Richard W Hyde.

4 recordsLinked to original sources
PubMed2006

Changes in markers of epithelial permeability and inflammation in chronic smokers switching to a nonburning tobacco device (Eclipse).

Eclipse, produced by R. J. Reynolds Tobacco Company, is a potential reduced exposure product (PREP) that heats rather than burns tobacco. We hypothesized that switching to Eclipse would result in relative normalization of pulmonary epithelial permeability, airway inflammation, and blood leukocyte activation in current smokers. We assessed 10 healthy smokers (aged 21-50 years, 19+/-8 pack-years) at baseline and after 2 and 4 weeks of switching to Eclipse, for symptoms, pulmonary function, airway inflammation, lung clearance of (99m)technicium-diethylenetriaminepentaacetic acid, and blood leukocyte activation and production of reactive oxygen species. Values were compared before and after Eclipse use and with those of healthy, lifetime nonsmokers (aged 18-53 years). Compared with baseline values before switching to Eclipse, lung permeability half-time increased from 33+/-3 to 43+/-6 min (p = .017) after 2 weeks and to 44+/-7 min (p = .10) after 4 weeks of Eclipse use. Carboxyhemoglobin levels increased from 5%+/-2% to 7%+/-2% (p<.01) at 4 weeks. Compared with smoking the usual brand of cigarettes, after smoking Eclipse the percentage of natural killer cells, the expression of intercellular adhesion molecule-1 on monocytes, and the expression of CD45RO on T cells showed significant improvement. However, expression of other surface markers, notably CD23 on monocytes, became more abnormal. Production of reactive oxygen species by smokers' neutrophils and monocytes increased further with Eclipse use. We found no significant effects on pulmonary function, cells in induced sputum, or exhaled nitric oxide. Switching to Eclipse reduces alveolar epithelial injury in some smokers but may increase carboxyhemoglobin levels and oxidative stress.

Adult↗
PubMed2004

Pulmonary function, diffusing capacity, and inflammation in healthy and asthmatic subjects exposed to ultrafine particles.

Particulate air pollution is associated with asthma exacerbations and increased morbidity and mortality from respiratory causes. Ultrafine particles (particles less than 0.1 microm in diameter) may contribute to these adverse effects because they have a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity when compared with larger particles on a mass basis. We hypothesized that ultrafine particle exposure would induce airway inflammation in susceptible humans. This hypothesis was tested in a series of randomized, double-blind studies by exposing healthy subjects and mild asthmatic subjects to carbon ultrafine particles versus filtered air. Both exposures were delivered via a mouthpiece system during rest and moderate exercise. Healthy subjects were exposed to particle concentrations of 10, 25, and 50 microg/m(3), while asthmatics were exposed to 10 microg/m(3). Lung function and airway inflammation were assessed by symptom scores, pulmonary function tests, and airway nitric oxide parameters. Airway inflammatory cells were measured via induced sputum analysis in several of the protocols. There were no differences in any of these measurements in normal or asthmatic subjects when exposed to ultrafine particles at concentrations of 10 or 25 microg/m(3). However, exposing 16 normal subjects to the higher concentration of 50 microg/m(3) caused a reduction in maximal midexpiratory flow rate (-4.34 +/- 1.78% [ultrafine particles] vs. +1.08 +/- 1.86% [air], p =.042) and carbon monoxide diffusing capacity (-1.76 +/- 0.66 ml/min/mm Hg [ultrafine particles] vs. -0.18 +/- 0.41 ml/min/mm Hg [air], p =.040) at 21 h after exposure. There were no consistent differences in symptoms, induced sputum, or exhaled nitric oxide parameters in any of these studies. These results suggest that exposure to carbon ultrafine particles results in mild small-airways dysfunction together with impaired alveolar gas exchange in normal subjects. These effects do not appear related to airway inflammation. Additional studies are required to confirm these findings in normal subjects, compare them with additional susceptible patient populations, and determine their pathophysiologic mechanisms.

Adult↗