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Biomedical subjects

J R Balmes

Publications and source records attributed to J R Balmes.

At least 55 records · Page 3Linked to original sources
PubMed1991

Computed tomography of asbestos-related pulmonary parenchymal and pleural diseases.

Computed tomography has acquired an increasingly central role in the evaluation of asbestos-exposed individuals. The advantages of increased contrast resolution and axial image display have extended our ability to interrogate areas of the pulmonary parenchyma and pleura that are inadequately seen on chest radiographs. The additional information to be gained from CT evaluation must be balanced by the additional expense and time required, particularly in view of the large numbers of asbestos-exposed individuals who will undergo screening over the coming decades. Ideally, imaging strategies that include CT should emphasize those problematic situations in which additional information will serve a differential or diagnostic function, alter the management or habits of the individuals, modify the working environment, or improve our understanding of asbestos-induced diseases. The chest radiograph is the mainstay in the imaging evaluation of asbestos-exposed individuals, providing an inexpensive and rapid appraisal of the presence of both focal and diffuse abnormalities of the pleura and lung parenchyma. Conventional (whole-thorax) CT may be an important adjunct in the following situations: (1) to clarify the presence of pleural thickening, particularly in distinguishing pleural disease from normal extrapleural soft tissues; (2) to stage and determine tumor extent in malignant pleural mesothelioma; (3) to identify optimal sites for biopsy of suspicious pleural changes; and (4) to detect and characterize lung cancers or other focal masses that may be obscured by extensive pleural or parenchymal fibrosis. Limited HRCT studies are roughly competitive in time and cost with four-view radiographic examinations. There is growing evidence that HRCT can detect interstitial disease in advance of conventional clinical or radiographic studies. However, the application of limited HRCT for large-scale screening is controversial. This issue will be resolved as we gain greater understanding of the specificity of HRCT and establish guidelines for standardizing the technique and image interpretation. At present, limited HRCT scans can supplement the evaluation of subjects in whom there is equivocal parenchymal or pleural disease on radiographs or unexplained abnormalities on pulmonary function tests. In individuals with significant pleural disease, HRCT can effectively define the presence and extent of interstitial fibrosis. In individuals with combined cigarette smoking-asbestos exposure in whom symptoms or functional abnormalities are present, HRCT may play a central role in distinguishing emphysematous lung destruction from the peripheral interstitial changes of asbestosis.

Asbestosis↗
PubMed1990

Acid fog-induced bronchoconstriction. The role of hydroxymethanesulfonic acid.

Hydroxymethanesulfonate (HMSA), the bisulfite (HSO3-) adduct of formaldehyde (CH2O), is a common constituent of California acid fogs. HMSA, most stable in a fog pH range of 3 to 5, dissociates at 6.6, the pH of the fluid lining human airways. The dissociation of inhaled HMSA should theoretically generate sulfur dioxide and CH2O, both of which have bronchoconstrictor potential. Thus, we hypothesized that HMSA may have a specific bronchoconstrictor effect independent of its strength as an acid. To determine whether HMSA has such an effect, 19 subjects with mild to moderate asthma were studied using two different protocols. Initially, a mouthpiece study was performed in which 9 subjects, on 2 separate days, inhaled five aerosols containing either sequentially increasing concentrations (0, 30, 100, 300, and 1000 microM) of HMSA in 50 microM sulfuric acid (H2SO4) or 50 microM H2SO4 alone. The subjects inhaled each aerosol for 3 min during tidal breathing at rest. Specific airway resistance (SRaw) was measured before and after each 3-min exposure. There were no significant differences in the mean changes in SRaw among the various aerosol exposures. To confirm this lack of bronchoconstrictor effect of HMSA, we then performed a chamber study in which 10 freely breathing, intermittently exercising subjects were exposed to fog containing either 1 mM HMSA in 5 mM H2SO4 or 5 mM H2SO4 alone for 1 h. SRaw was measured before, during, and at the end of the 1-h exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1989

Prospective study of respiratory effects of formaldehyde among healthy and asthmatic medical students.

We conducted a prospective evaluation of pulmonary function and respiratory symptoms among 103 medical students exposed to formaldehyde over a 7-month period to determine the incidence of bronchoconstriction and respiratory symptoms in response to exposure. Time-weighted average formaldehyde exposures were generally less than 1 part per million (ppm) and peak exposures were less than 5 ppm. Acute symptoms of eye and upper respiratory irritation were significantly associated with exposure. There was no pattern of bronchoconstriction in response to exposure after either 2 weeks or 7 months. Twelve subjects had a history of asthma; they were no more likely to have symptoms of respiratory irritation or changes in pulmonary function than those without such a history. These findings are consistent with previous case reports that indicate exposure to formaldehyde vapor at levels that are commonly encountered in occupational and residential settings do not commonly cause significant bronchoconstriction, even among subjects with preexisting asthma.

Adult↗
PubMed1989

Potential bronchoconstrictor stimuli in acid fog.

Acid fog is complex and contains multiple stimuli that may be capable of inducing bronchoconstriction. These stimuli include sulfuric and niric acids, the principal inorganic acids present; sulfites, formed in the atmosphere as a reaction product of sulfur dioxide and water droplets; fog water itself, a hypoosmolar aerosol; the organic acid hydroxymethanesulfonate, the bisulfite adduct of formaldehyde; and gaseous pollutants, e.g., sulfur dioxide, oxides of nitrogen, ozone. Given this complexity, evaluation of the respiratory health effects of naturally occurring acid fog requires assessment of the bronchoconstrictor potency of each component stimulus and possible interactions among these stimuli. We summarize the results of three studies that involve characterization of the bronchoconstrictor potency of acid fog stimuli and/or their interaction in subjects with asthma. The results of the first study indicate that titratable acidity appears to be a more important stimulus to bronchoconstriction than is pH. The results of the second study demonstrate that sulfite species are capable of inducing bronchoconstriction, especially when inhaled at acid pH. The results of the third study suggest that acidity can potentiate hypoosmolar fog-induced bronchoconstriction.

Acid Rain↗
PubMed1988

Acidity potentiates bronchoconstriction induced by hypoosmolar aerosols.

Naturally occurring fogs are usually hypoosmolar with respect to body fluids and can be quite acidic. Because both hypoosmolarity and acidity can cause bronchoconstriction, we studied whether there was a positive interaction between these stimuli in 12 subjects with asthma. We administered the following aerosols: hypoosmolar saline (30 mOsm) at pH 5.5, 3 hypoosmolar acids (0.005 M H2SO4, 0.01 M HNO3 and a 1:1 mixture of 0.005 M H2SO4 and 0.01 M HNO3, all 30 mOsm) at pH 2, and isoosmolar 0.005 M H2SO4 (300 mOsm) at pH 2. Each aerosol was administered on a separate day and was inhaled through a mouthpiece during tidal breathing. Specific airway resistance (SRaw) was measured before and after the subjects inhaled aerosols delivered at as much as 5 doubling nebulizer outputs. For each aerosol challenge, an output-response curve was generated, and the nebulizer output required to increase SRaw by 100% above baseline (PO100) was calculated. Mean values of PO100 were significantly lower for each of the hypoosmolar acids than for hypoosmolar saline (1.65 + 0.43 g/min [mean + SEM] for saline compared with 0.95 + 0.11, 1.05 + 0.20, and 0.90 + 0.14 for H2SO4, HNO3, and a 1:1 mixture of the two; all p values less than 0.025). Mean values of PO100 did not differ among the 3 acids studied. For 7 of 12 subjects, all 3 acids caused a leftward shift in the output-response curve from the curve generated for hypoosmolar saline aerosol. Isoosmolar H2SO4 did not increase SRaw by 100% in any subjects, even at the maximal nebulizer output that delivered a concentration of H2SO4 in excess of 40 mg/m3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Hypokalemia induced by inhaled bronchodilators.

Since parenteral beta 2-adrenergic stimulation can induce hypokalemia, we postulated that administration of beta 2 adrenoreceptor agonists by inhalation could induce the same. We administered the usual clinical doses of three commonly used bronchodilators to each of six subjects receiving assisted mechanical ventilation in line with the ventilator: two beta 2-adrenoreceptor agonists, metaproterenol, 5 percent solution, and isoetharine, 1 percent solution; and the anticholinergic agent atropine as a control. Each bronchodilator was nebulized over 10 to 15 minutes in random order, four hours apart, and given to every subject. Plasma potassium was measured at five-minute intervals and arterial blood gases at 15-minute intervals, for a total of 50 minutes after administration of each bronchodilator. Following administration of each drug, plasma potassium showed an average decline. The mean decline in plasma potassium from baseline was statistically significant for metaproterenol (p = 0.04) and atropine (p = 0.001) but not for isoetharine (p = 0.09). Although there were no statistically significant differences among the declines in plasma potassium induced by the three drugs, metaproterenol caused the greatest decline (-0.6 mEq/L).

Administration, Inhalation↗
PubMed1988

Airway inflammation and occupational asthma.

Airway inflammation due to exposure to a wide variety of agents encountered in the workplace is a major cause of occupational asthma. This article reviews major examples of occupational asthma linked to airway inflammation, including their epidemiology, pathophysiology, and clinical course.

Asthma↗
PubMed1987

Respiratory effects of cotton dust exposure in the cotton garnetting industry.

We measured exposures to total dust, vertically elutriated dust, and endotoxin and studied acute pulmonary responses among 128 workers in the cotton garnetting and mattress assembly industries. Previous studies in this segment of industry have not characterized endotoxin exposures or related them to pulmonary responses. The median 8-hour time-weighted average total dust was 0.72 mg/m3, the median vertically elutriated dust was 0.22 mg/m3, and the median endotoxin concentration was 5.2 ng/m3. Ten percent of the subjects reported chest tightness or dyspnea on Mondays. Thirteen percent of the subjects reported symptoms of chronic bronchitis. Although there was no relationship between changes in pulmonary function across the workshift and either total dust, vertically elutriated dust, or endotoxin exposure, 13% of the subjects had greater than 5% decrements in FEV1 over the workshift.

Adult↗
PubMed1987

Symptomatic bronchoconstriction after short-term inhalation of sulfur dioxide.

We studied the relationship between duration and concentration of exposure in SO2-induced bronchoconstriction in 8 asthmatic subjects. On separate days, we administered SO2 in humidified air through a mouthpiece at 2 concentrations (0.5 and 1.0 ppm) for 3 time periods (1, 3, and 5 min) during eucapnic hyperpnea (60 L/min). Humidified air was administered for 5 min as a control. Bronchoconstriction was assessed by measurement of specific airway resistance (SRaw). The magnitude of the bronchoconstrictor response to both concentrations of SO2 increased progressively over the 3 time periods studied. The mean (+/- SE) increase in SRaw (in L x cm H2O/L/s) and percent increase above baseline (in parentheses) after each exposure to SO2 were as follows: 2.5 +/- 0.3 (34%) after 0.5 ppm for 1 min; 7.5 +/- 4.7 (93%) after 1.0 ppm for 1 min; 13 +/- 3.2 (173%) after 0.5 ppm for 3 min; 31.4 +/- 7.4 (395%) after 1.0 ppm for 3 min; 19.6 +/- 4.0 (234%) after 0.5 ppm for 5 min; 44.1 +/- 9.8 (580%) after 1.0 ppm for 5 min; 3.5 +/- 1.5 (46%) after humidified air for 5 min. For the group, the increases in SRaw caused by inhalation of both concentrations of SO2 for 1 min were small. However, 2 of 8 subjects did develop large increases in SRaw and chest tightness after inhalation of 1.0 ppm for 1 min. Seven of 8 subjects developed wheezing, chest tightness, or dyspnea and used an inhaled bronchodilator after inhalation of 0.5 ppm for 3 and 5 min and 1.0 ppm for 3 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1987

Chronic beryllium disease in a precious metal refinery. Clinical epidemiologic and immunologic evidence for continuing risk from exposure to low level beryllium fume.

Five workers at a precious metal refinery developed granulomatous lung disease between 1972 and 1985. The original diagnosis was sarcoidosis, but 4 of the workers were subsequently proved to have hypersensitivity to beryllium by in vitro proliferative responses of lymphocytes obtained by bronchoalveolar lavage. Review of medical records of coworkers and extensive industrial hygiene surveillance of the plant demonstrated that 4 cases occurred in the furnace area where air concentrations of beryllium fume were consistently below the permissible exposure limit of 2 micrograms/M3. A single case has been recognized from parts of the refinery where exposures to cold beryllium dust often exceeded the standard by as much as 20-fold. These data demonstrate that chronic beryllium disease still occurs and confirm the importance of specific immunologic testing in patients suspected of having sarcoidosis but with potential exposure to beryllium. The data raise concern about the adequacy of modern industrial controls, especially in the setting of exposure to highly respirable beryllium fume.

Adult↗
PubMed1984

Exercise testing in occupational lung diseases.

The authors discuss the value of exercise testing in two areas of importance in occupational pulmonary disease: (1) the surveillance of worker populations in order to gain epidemiologic and physiologic understanding of disease and (2) the assessment of work capacity in individual patients.

Asbestosis↗
PubMed1982

Lung cancer: a persistent challenge.

The most frequently diagnosed type of lung cancer now is probably adenocarcinoma. This cell type is not clearly related to smoking, but may reflect environmental and occupational factors. Staging systems assess the extent of primary and metastatic disease, aid in determining appropriate treatment, and suggest prognosis. Clinical stage correlates with survival rate, but most staging systems underestimate the extent of metastases in lung cancer.

Adenocarcinoma↗
PubMed1981

Lipoid pneumonia caused by oil mist exposure from a steel rolling tandem mill.

Five of nine active tandem mill operators exposed at work to aerosolized hydrocarbon mist were referred for evaluation of respiratory complaints. The worker with the longest exposure had reduced lung volumes; he was admitted to the hospital for detailed study. Exercise studies revealed work load limited by ventilation and arterial oxygen desaturation. Flexible fiberoptic bronchoscopy with bronchoalveolar lavage and transbronchial biopsy revealed evidence of lipoid pneumonia. Assessment of the mill revealed levels of respirable oil mist by personal samplers throughout the area far below the currently accepted standard of 5 mg/M3. These findings confirm a 20-year-old hypothesis of J.G. Jones regarding the hazard of oil mist in this industrial setting.

Adult↗
PubMedDate not supplied

A comparison of two methods for determining nasal irritant sensitivity.

Nasal irritation and irritant-induced reflexes (rhinorrhea and congestion) are prominent symptoms associated with indoor and ambient air pollution, and marked heterogeneity in individual sensitivity has been suggested. Nevertheless, there is currently no generally accepted functional index of nasal irritant sensitivity available for clinical use. To address this issue, we compared two objective measures of nasal irritant sensitivity: a CO2 detection task, and CO2-induced transient disruption of respiratory pattern (pulsed CO2 acting as an odorless irritant). Using a respiratory flow thermocouple to produce a continuous recording of respiratory pattern, we challenged 20 normal adult volunteers (13 males and 7 females, average age 39.4 years) with brief (approximately 3 second) pulses of the odorless irritant carbon dioxide. Increasing levels of CO2 (10-70%, vol/vol), paired with filtered air in random order, were presented unilaterally by nasal cannula of fixed geometry, synchronized with the inspiratory phase of the respiratory cycle. All subjects yielded CO2 detection thresholds, whereas within the constraints of the testing method (subjective irritation rating < or = "very strong"), only 13 of 20 subjects (65%) exhibited transient disruption of their breathing pattern. Further, although decreased respiratory volume (indirectly measured) appeared to be a common feature, several distinct patterns of respiratory alteration were observed, rendering objective scoring more difficult. Finally, some subjects showed CO2-induced respiratory disruption intermittently from trial to trial, implying that rapid adaptation occurs. Determination of the CO2 detection threshold therefore appears to be the more objective and consistently applicable endpoint for determining individual nasal irritant sensitivity.

Adult↗
PubMedDate not supplied

Surveillance for occupational asthma.

Medical surveillance programs can be established either for identification of workers potentially at risk for developing occupational asthma or for early detection of occupational asthma so that appropriate interventions can be made to prevent further cases. The author describes several tests used for the early detection of occupational asthma. These include respiratory and allergic symptom questionnaires, cross-shift spirometry, serial measurement of peak expiratory flow rates and/or serial methacholine challenge, and serial skin or serum testing for specific sensitization. Available data suggest that medical surveillance programs for early case detection and removal of affected workers from further exposure can be effective in preventing persistent asthma.

Asthma↗
PubMedDate not supplied

Medical surveillance for pulmonary endpoints.

The institution of workplace medical surveillance for pulmonary endpoints assumes the following conditions: that occupational lung diseases can be detected in early or preclinical stages; that early detection with appropriate intervention can lead to reduced morbidity; and that early detection and appropriate intervention are both feasible. The author of this chapter points out that, unfortunately, very few occupational settings meet these conditions.

Environmental Monitoring↗