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Biomedical subjects

J R Balmes

Publications and source records attributed to J R Balmes.

At least 37 records · Page 2Linked to original sources
PubMed1995

Contribution of secretory leukocyte proteinase inhibitor to the antiprotease defense system of the peripheral lung: effect of ozone-induced acute inflammation.

Secretory leukocyte protease inhibitor (SLPI) and elafin are structurally similar, low-molecular-weight antiproteases produced in the lung. We have developed a simple method for distinguishing the antiprotease activities of SLPI and elafin in lung lavage fluid from those of alpha 1-antitrypsin (alpha 1-AT) that is based on the resistance of the low-molecular-weight antiproteases to inactivation by cetyltrimethylammonium bromide. In a study of 23 healthy, nonsmoking volunteers, we found that the low-molecular-weight antiproteases accounted for 22 +/- 2% (mean +/- SEM, n = 23) of the total neutrophil elastase-inhibitory capacity of human bronchoalveolar lavage fluid (BALF). Elafin activity was below the limit of detection. SLPI activity (as measured by inhibition of alpha-chymotrypsin) accounted for 72 +/- 4% (mean +/- SEM, n = 23) of the low-molecular-weight antiprotease activity in BALF. Measurements of SLPI in the lavage fluid samples by enzyme-linked immunosorbent assay (ELISA) agreed closely with values obtained by measuring the activity of this inhibitor. The activity of the low-molecular-weight antiproteases decreased significantly (p < 0.05), from 9.0 +/- 0.8 to 7.0 +/- 0.6 pmol of neutrophil elastase inhibited per mL (mean +/- SEM, n = 23), following acute ozone exposure.

Acute Disease↗
PubMed1995

Methacholine responsiveness is not associated with O3-induced decreases in FEV1.

STUDY OBJECTIVE: Controlled human exposure studies have suggested that the National Ambient Air Quality Standard for ozone (O3) may not provide a margin of safety to protect the most susceptible members of the population from adverse health effects. Although the subgroups of the population that are most susceptible to O3 have not been identified, recent work in our laboratory suggested that methacholine responsiveness might be an important determinant of susceptibility to O3. PATIENTS AND METHODS: To test the hypothesis that methacholine responsiveness is correlated with FEV1 response after O3 exposure, we conducted methacholine challenge tests and O3 (0.20 ppm) and filtered air exposures for 4 h with moderate exercise on 66 healthy individuals. RESULTS: Repeated measures analysis of variance demonstrated significant changes in FEV1 (-0.82 +/- 0.63 L), FVC (-0.69 +/- 0.48 L), and specific airway resistance (SRaw) (+1.5 +/- 1.1 L x cm H2O/L/s) across the O3 exposure that persisted after adjusting for responses to air. Baseline PC100 (the concentration of methacholine that caused a doubling of the baseline SRaw) was weakly associated with O3-induced increases in SRaw (F1.54 = 2.85, p = 0.09), but not O3-induced declines in FEV1 or FVC. There was a weak association (r = -0.29) between O3-induced responses for SRaw and FEV1. The FEV1 responses for O3 were weakly associated with the symptoms of cough (r = -0.37), wheeze (r = -0.29), chest pain on deep inspiration (r = -0.31), and shortness of breath (r = -0.37), but not with chest discomfort or sputum production. CONCLUSIONS: Although we were unable to find support for our hypothesis, we found, somewhat surprisingly, that respiratory symptoms were weakly associated or unassociated with FEV1 responses after O3 exposure. This finding implies that individuals may experience adverse effects, ie, respiratory symptoms, without large declines in lung function. Conversely, individuals may suffer large declines in lung function without prominent symptoms and, therefore, may remain in an unhealthy environment despite evidence of toxicity.

Adult↗
PubMed1994

Occupational factors in work-related inhalations: inferences for prevention strategy.

As part of a larger investigation of inhalational toxic exposures, we studied occupationally related cases in order to examine possible preventive strategies. We analyzed data from 224 structured interviews. Of the interviewed subjects, 48 (21%) reported closed space exposures and 44 (20%) concomitant skin exposure at the time of inhalation. Chlorine gas and bleach mixtures were the most common single reported exposure type, occurring in 54 (24%) of cases. The most common occupational groups represented were crafts workers, operatives, and laborers (n = 84, 38%), and service workers (n = 64, 29%). Adjusting for occupational group in a multiple logistic regression analysis that also included length of hire and access to personal respiratory protective equipment, report of prior specific chemical safety training was significantly protective against closed space inhalation (odds ratio (OR) = 0.2; 95% confidence interval (CI) 0.1-0.4) and concomitant skin exposure (OR = 0.3, 95% CI = 0.1-0.7). These data suggest that chemical safety training may be an effective preventive strategy for potentially high-risk inhalational exposure scenarios.

Adult↗
PubMed1994

Persistent respiratory health effects after a metam sodium pesticide spill.

STUDY OBJECTIVE: To report the occurrence of persistent respiratory disorders, including irritant-induced asthma, among adults living and working near an environmental spill of the pesticide, metam sodium, after the derailment of a tank car. DESIGN: Retrospective clinical case series. SETTING: California communities situated within one-half mile of the Sacramento River, from Mt. Shasta City to Shasta Lake. PATIENTS: 197 adults referred to a university occupational/environmental health clinic or to a private occupational/environmental health practitioner for evaluation of health problems potentially related to the spill. MEASUREMENTS AND RESULTS: History, physical examination, review of medical records, spirometry, and methacholine challenge testing revealed 20 cases of persistent irritant-induced asthma and 10 cases of persistent exacerbation of asthma. CONCLUSIONS: This is the first reported series of cases of persistent irritant-induced asthma involving both community residents and occupationally exposed individuals.

Adult↗
PubMed1993

Effects of nitric acid gas alone or in combination with ozone on healthy volunteers.

Nitric acid (HNO3) is the most prevalent acid air pollutant in the western United States and has the potential to cause adverse respiratory effects through both acidification and oxidation reactions. To study this potential, we measured physiologic (specific airway resistance, SRaw, FEV1, and FVC) and bronchoalveolar lavage (total and differential cell counts, LDH, fibronectin, and total protein) end points in a group of 10 healthy, athletic subjects who were exposed to 500 micrograms/m3 of HNO3 gas or filtered air for 4 h during moderate exercise (ventilatory rate, 40 L/min) and underwent bronchoscopy 18 h later. Under an identical protocol, 10 healthy subjects were exposed to 500 micrograms/m3 of HNO3 gas plus 0.20 ppm ozone (O3) or 0.20 ppm O3 alone to determine if HNO3 might enhance the toxicity of O3. In addition to bronchoalveolar lavage (BAL), we employed the techniques of isolated left mainstem bronchial lavage and bronchial biopsy to determine if proximal airway injury was caused by pollutant exposure and whether there was any correlation with the degree of distal lung injury as assessed by BAL. We found no significant differences in pulmonary function tests or in the cellular or biochemical constituents in either the BAL or the left mainstem lavage fluids between the HNO3 and the air exposures. Similarly, there were no differences in these end points between the HNO3/O3 and the O3 exposures. Furthermore, there were no significant differences in the bronchial biopsy specimens between the HNO3 and air exposures or between the HNO3/O3 and O3 exposures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Ozone-induced airway inflammation in human subjects as determined by airway lavage and biopsy.

Ozone (O3) is a major constituent of urban air pollution. The acute effects of the inhalation of O3 at ambient or near-ambient concentrations on bronchoalveolar lavage (BAL) end points consistent with a distal lung inflammatory response have been well documented in human subjects. Animal toxicologic studies have shown that the airway is also a major site of O3-induced injury and inflammation. To date, no studies have confirmed this finding in human subjects. Effects of O3 on the proximal airways are not adequately studied by BAL, which is primarily influenced by events occurring in the terminal bronchioles and alveoli. We hypothesized that O3 causes injury and inflammation in the airways in addition to that previously documented to occur in the distal lung. We performed isolated lavage of the left mainstem bronchus and forceps biopsy of the bronchial mucosa in a group of 14 healthy, athletic subjects 18 h after exposure to 0.20 ppm O3 for 4 h during moderate exercise in order to assess this possibility. We followed an identical protocol in a similar group of 12 subjects exposed to filtered air. The mean (SD) total cell count and the lactate dehydrogenase (LDH) concentration in the isolated airway lavage were significantly greater after O3 than after air, 13.9 (20.5) versus 4.9 (5.4) cells/ml x 10(4) and 18.9 (11.2) versus 9.6 (9.0) U/L, respectively. Morphometry (2,070 neutrophils/cm2 of tissue for O3 and 330 neutrophils/cm2 of tissue for air) demonstrated that O3 exposure induced an acute inflammatory cell influx into the airway.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

The role of ozone exposure in the epidemiology of asthma.

Asthma is a clinical condition characterized by intermittent respiratory symptoms, nonspecific airway hyperresponsiveness, and reversible airway obstruction. Although the pathogenesis of asthma is incompletely understood, it is clear that airway inflammation is a paramount feature of the condition. Because inhalation of ozone by normal, healthy subjects causes increased airway responsiveness and inflammation, it is somewhat surprising that most controlled human exposure studies that have involved asthmatic subjects have not shown them to be especially sensitive to ozone. The acute decrement in lung function that is the end point traditionally used to define sensitivity to ozone in these studies may be due more to neuromuscular mechanisms limiting deep inspiration than to bronchoconstriction. The frequency of asthma attacks following ozone exposures may be a more relevant end point. Epidemiologic studies, rather than controlled human exposure studies, are required to determine whether ozone pollution increases the risk of asthma exacerbations. Asthma affects approximately 10 million people in the United States and, thus, the answer to this question is of considerable public health importance. Both the prevalence and severity of asthma appear to be increasing in many countries. Although increased asthma morbidity and mortality are probably of multifactorial etiology, a contributory role of urban air pollution is plausible. The epidemiologic database to support an association between asthma and ozone exposure is limited, but the results of several studies suggest such an association. Some potential approaches to further investigation of the relationship between asthma and ozone, including those that would link controlled human exposures to population-based studies, are considered.

Adolescent↗
PubMed1993

Symptoms, lung function, and airway responsiveness following irritant inhalation.

STUDY OBJECTIVE: To estimate the incidence of respiratory symptoms and physiologic abnormalities after inhalation of common irritant chemicals. DESIGN: Structured interview of 12 months of poison control center (PCC) inhalation cases. Follow-up measurement of pulmonary function and airway responsiveness in a subgroup with symptoms 12 to 24 h postexposure. SETTING: A regional PCC and clinical pulmonary function laboratory. PATIENTS: Consecutive sample of 547 inhalation cases. Interviews of 299 subjects. Lung function follow-up in 10 subjects. MEASUREMENTS AND MAIN RESULTS: Immediate respiratory symptoms were reported by 262 (88 percent) subjects; 12 to 24 h postexposure symptoms were reported by 130 (44 percent). Cigarette smoking was significantly related to immediate onset of cough (relative risk [RR] = 1.3; 95 percent confidence interval [CI], 1.1 to 1.5); both smoking (RR = 1.6; 95 percent CI, 1.1 to 2.1) and prior asthma (RR = 1.3; 95 percent CI, 1.1 to 1.6) were associated with wheeze, exhibiting multiplicative combined risk (RR = 2.8; 95 percent CI, 1.9 to 4.3). Of 10 subjects studied, none had abnormal airflow or lung volumes 8 +/- 4 days postexposure; 8 demonstrated increased airway responsiveness to methacholine. By three months, only one subject's increased responsiveness reversed; in three others, symptoms resolved but increased responsiveness remained. CONCLUSIONS: Respiratory symptoms following irritant exposure are associated with smoking and asthma and typically resolve quickly. Continuing symptoms are associated with persistent increased airway responsiveness without other pulmonary function abnormalities. This may reflect newly induced airway changes or, alternatively, could represent underlying increased responsiveness in subjects symptomatic after irritant exposure.

Administration, Inhalation↗
PubMed1992

The effect of smoke inhalation on lung function and airway responsiveness in wildland fire fighters.

The current study was undertaken to evaluate the effect of smoke on forced expiratory volumes and airway responsiveness in wildland fire fighters during a season of active fire fighting. Sixty-three seasonal and full-time wildland fire fighters from five U.S. Department of Agriculture Forest Service (USDAFS) Hotshot crews in Northern California and Montana completed questionnaires, spirometry, and methacholine challenge testing before and after an active season of fire fighting in 1989. There were significant mean individual declines of 0.09, 0.15, and 0.44 L/s in postseason values of FVC, FEV1, and FEF25-75, respectively, compared with preseason values. There were no consistent significant relationships between mean individual declines of the spirometric parameters and the covariates: sex, smoking history, history of asthma or allergies, years as a fire fighter, upper/lower respiratory symptoms, or membership in a particular Hotshot crew. There was a statistically significant increase in airway responsiveness when comparing preseason methacholine dose-response slopes (DRS) with postseason dose-response slopes (p = 0.02). The increase in airway responsiveness appeared to be greatest in fire fighters with a history of lower respiratory symptoms or asthma, but it was not related to smoking history. These data suggest that wildland fire fighting is associated with decreases in lung function and increases in airway responsiveness independent of a history of cigarette smoking. Our findings are consistent with the results of previous studies of municipal fire fighters.

Adult↗
PubMed1992

Occupational asthma.

The Council on Scientific Affairs of the California Medical Association presents the following inventory of items of progress in chest diseases. Each item, in the judgment of a panel of knowledgeable physicians, has recently become reasonably firmly established, both as to scientific fact and important clinical significance. The items are presented in simple epitome, and an authoritative reference, both to the item itself and to the subject as a whole, is generally given for those who may be unfamiliar with a particular item. The purpose is to assist busy practitioners, students, researchers, or scholars to stay abreast of these items of progress in chest diseases that have recently achieved a substantial degree of authoritative acceptance, whether in their own field of special interest or another. The items of progress listed below were selected by the Advisory Panel to the Section on Chest Diseases of the California Medical Association, and the summaries were prepared under its direction.

Asthma↗
PubMed1992

Atopy and airways reactivity in animal health technicians. A pilot study.

Smoking, response to allergen skin testing, and nonspecific airways reactivity in students entering a career program for animal health technicians (AHT) were studied at their entrance and 7 months into the program to determine whether such persons provide a suitable cohort to overcome the selection biases accompanying investigations of occupational asthma. Previous occupational exposure to animals (65%) was associated positively with allergic symptoms but negatively with skin response to animal allergens and to airway hyperreactivity (AR). AHTs remaining in the program were more likely than those dropping out to have (1) worked with animals, (2) positive skin responsiveness to animal allergens, and (3) AR; the latter was significantly associated with positive skin-test responses to animal allergen testing. This study demonstrates that significant exposure to animals may have occurred among workers entering animal-handling careers. Additionally, competing "healthy" and "resistant" worker effects operate among AHTs to influence the prevalence of occupational asthma in this population.

Adult↗
PubMed1991

The effects of sequential exposure to acidic fog and ozone on pulmonary function in exercising subjects.

In Southern California coastal regions, morning fog is often acidified by the presence of nitric acid (HNO3). Peak exposure to ozone (O3) usually occurs in the afternoon and evening, after the fog has dissipated. To determine whether fog containing HNO3 might enhance pulmonary responses to O3, we studied a group of healthy, athletic subjects selected for lung function sensitivity to O3. On 3 separate days, the subjects exercised for 2 h in atmospheres containing HNO3 fog (0.5 mg/ml), H2O fog, or clean, filtered air. After a 1-h break, they exercised for an additional 3 h in an atmosphere containing 0.20 ppm O3. Surprisingly, the mean O3-induced decrements in FEV1 and FVC were smaller after exercise in each fog-containing atmosphere than they were after exercise in clean, filtered air. The mean (+/- SEM) O3-induced decrements in FEV1 were 26.4 +/- 5.3% after air, 17.1 +/- 3.7% after H2O fog, and 18.0 +/- 4.3% after HNO3 fog, and in FVC they were 19.9 +/- 4.7% after air, 13.6 +/- 2.8% after H2O fog, and 13.6 +/- 4.2% after HNO3 fog.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Lack of bronchoconstrictor response to sulfuric acid aerosols and fogs.

Sulfuric acid (H2SO4) is the most common acid air pollutant in the United States and is thought to have adverse respiratory effects. Sulfuric acid exists in polluted air as a dissolved solute in both small (haze) and large (fog) particles. Previous work in our laboratory has failed to demonstrate bronchoconstriction after near ambient, large-particle H2SO4 exposure in subjects with asthma. However, other investigators have found slight but significant changes in lung function following inhalation of small-particle or small-particle, low-relative-humidity (RH) H2SO4 aerosols, leading us to hypothesize that particle size and/or RH may be important variables in acid aerosol exposure. We initially studied the effects of resting inhalation of large-particle (volume median diameter, VMD, approximately equal to 6 microns) and small-particle (VMD approximately equal to 0.4 microns) aerosols with an H2SO4 concentration of 3 mg/m3 through a mouthpiece and found no effect on specific airway resistance (SRaw) or symptom scores. In a second mouthpiece study designed to compare high-RH (100%), large-particle (VMD approximately equal to 6 microns) and low-RH (less than 10%), small-particle (VMD approximately equal to 0.3 microns) aerosols with an H2SO4 concentration of 3 mg/m3, we again found no effect of either aerosol. We then examined the effects of small-particle aerosols inhaled in dry air during moderate exercise. Although breathing low-RH air during exercise provoked increases in SRaw in almost all subjects, this could not be attributed to H2SO4 since low-RH saline aerosol produced a similar result.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗