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Biomedical subjects

J Q Koenig

Publications and source records attributed to J Q Koenig.

At least 37 records · Page 2Linked to original sources
PubMed1994

Wood smoke: emissions and noncancer respiratory effects.

In conclusion, this review reveals much about the constituents and fate of wood smoke but not enough about the health effects. Animal toxicological studies show that wood smoke exposure can disrupt cellular membranes, depress macrophage activity, destroy ciliated and secretory respiratory epithelial cells, and cause aberrations in biochemical enzyme levels. With respect to the human epidemiological data, the literature summarized in Table 4 shows a coherence of the data from young children, with 7/8 studies especially in children with asthma, reporting increased respiratory symptoms, lower respiratory infection, and decreased pulmonary function as a result of exposure to wood smoke. As Bates (6) has discussed, coherence of the data, although not amenable to statistical tests, carries the weight of linkage and plausibility. These adverse respiratory effects associated with wood smoke exposure also comply with many of Brandon Hill's aspects of association necessary to establish causation (40). There is strength of association, consistency (7/8 studies showing positive associations), temporality, plausibility, coherence, and analogy (using ETS exposure; 70, 94). A biological gradient has not been shown, although one is suggested in the study of pulmonary function in wildfire fighters. We conclude that the preponderance of the data suggest a causal relationship between elevated wood smoke levels and adverse respiratory health outcomes in young children.

Adolescent↗
PubMed1994

Inflammatory effects of ozone in the upper airways of subjects with asthma.

The objective of this study was to determine whether exposure to ozone causes inflammatory or functional changes in the upper or lower airways of asthmatic and nonasthmatic individuals. Ten asthmatic and eight nonasthmatic subjects were exposed to clean air, 120 ppb ozone, or 240 ppb ozone for 90 min during intermittent moderate exercise using a head dome exposure system. Pulmonary function tests, posterior rhinomanometry, and nasal lavage were performed before and after exposure. Leukocyte counts and chemotactic factors leukotriene B4 (LTB4), platelet-activating factor (PAF), and interleukin-8 (IL-8) were analyzed from nasal lavage fluid. In subjects with asthma, a significant increase (p < 0.05) in the number of white blood cells in lavage fluid was detected both immediately and 24 h after exposure to 240 ppb ozone, as was a significant increase in epithelial cells immediately after exposure (p < 0.05). No significant cellular changes were seen in nonasthmatic subjects. A significant correlation was observed between IL-8 and white blood cells counts after exposure to 240 ppb ozone (r = 0.76) in asthmatic subjects. No significant changes in pulmonary or nasal function or biochemical mediators were found in either the asthmatic or nonasthmatic subjects. These data indicate that asthmatic individuals are more sensitive to the acute inflammatory effects of ozone than nonasthmatic individuals.

Adolescent↗
PubMed1994

Oxidant and acid aerosol exposure in healthy subjects and subjects with asthma. Part I: Effects of oxidants, combined with sulfuric or nitric acid, on the pulmonary function of adolescents with asthma.

Both peak flow decrements in children at summer camps and increased hospital admissions for asthma have been associated with summer "acid haze," which is composed of ozone and various acidic species. The objective of this study was to investigate the pulmonary effects of acid summer haze in a controlled laboratory setting. Twenty-eight adolescent subjects with allergic asthma, exercise-induced bronchospasm, and a positive response to a standardized methacholine challenge enrolled in the study; 22 completed the study. Each subject inhaled one of four test atmospheres by mouthpiece on two consecutive days. The order of exposure to the four test atmospheres was assigned via a random protocol: air, oxidants (0.12 parts per million [ppm]* ozone plus 0.30 ppm nitrogen dioxide), oxidants plus sulfuric acid at 70 micrograms/m3 of air, or oxidants plus 0.05 ppm nitric acid. Exposure to each of the different atmospheres was separated by at least one week. The exposures were carried out during alternating 15-minute periods of rest and moderate exercise for a total exposure period of 90 minutes per day. Pulmonary function was measured before and after exposure on both test days and again on the third day as a follow-up measurement. A postexposure methacholine challenge was performed on Day 3. Low methacholine concentrations were chosen for the postexposure challenge to avoid provoking a response. The protocol was designed to detect subtle changes in airway reactivity. The statistical significance of the pulmonary function values was tested using paired t tests. First, we compared the difference between baseline and postexposure measurements after air exposure on Day 1 with the differences between baseline and postexposure measurements after Day 1 exposure to each of the other three atmospheres. Second, we compared the difference between baseline and postexposure measurements after the Day 2 air exposure with the differences between baseline and postexposure measurements after the Day 2 exposure to each of the pollutant atmospheres. Third, we compared the difference between baseline measurements on Day 1 of each exposure atmosphere with measurements after exposure to the same atmosphere on Day 2 to detect delayed effects. No changes in any of the pulmonary function parameters were statistically significant when compared with changes after clean air exposure. Six subjects left the study because of uncomfortable symptoms associated with the exposures. These all occurred after exposure to pollutant atmospheres and not after exposure to clean air.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid Rain↗
PubMed1993

Pulmonary function changes in children associated with fine particulate matter.

During winter months many neighborhoods in the Seattle metropolitan area are heavily affected by particulate matter from residential wood burning. A study was conducted to investigate the relationship between fine particulate matter and pulmonary function in young children. The subjects were 326 elementary school children, including 24 asthmatics, who lived in an area with high particulate concentrations predominantly from residential wood burning. FEV1 and FVC were measured before, during and after the 1988-1989 and 1989-1990 winter heating seasons. Fine particulate matter was assessed using a light-scattering instrument. Analysis of the relationship between light scattering and lung function indicated that an increase in particulate air pollution was associated with a decline in asthmatic children's pulmonary function. FEV1 and FVC in the asthmatic children dropped an average of 34 and 37 ml respectively for each 10(-4) m-1 increase in sigma sp. This sigma sp increase corresponds to an increase in PM2.5 of 20 micrograms/m3. It is concluded that fine particulate matter from wood burning is significantly associated with acute respiratory irritation in young asthmatic children.

Air Pollutants↗
PubMed1993

Particulate air pollution and hospital emergency room visits for asthma in Seattle.

Recent studies have associated short-term exposure to respirable particulate matter (PM10) exposure with peak flow decrements, increased symptoms of respiratory irritation, increased use of asthma medications, and increased hospitalization for asthma. Increased mortality from chronic respiratory disease has also been reported. To help confirm whether PM10 exposure is a risk factor for the exacerbation of asthma, we compiled daily records of asthma emergency room visits from eight hospitals in the Seattle area. In Poisson regressions controlling for weather, season, time trends, age, hospital, and day of the week, the daily counts of emergency room visits for persons under age 65 were significantly associated with PM10 exposure on the previous day. The mean of the previous 4 days' PM10 was a better predictor (p < 0.005). The relative risk for a 30 micrograms/m3 increase in PM10 was 1.12 (95% confidence interval 1.20 to 1.04). Daily PM10 concentrations never exceeded 70% of the current ambient air quality standards during the period. The consistency of investigations of the health effects of PM10 suggest that increased attention should be given to the control of particulate matter air pollution.

Adolescent↗
PubMed1992

Respiratory effects of air pollution on allergic disease.

Allergic patients have an increased susceptibility to the adverse effects of both natural and man-made air pollutants. This goes for both indoor and outdoor air pollutants and manifests itself with biochemical, cellular, and pathophysiologic expressions of adverse health effects in allergic individuals. Also occupationally induced allergic diseases will remain very important. This area has been reviewed recently by Cullen et al. Since allergic patients comprise somewhere between 15% and 20% of the population, this increased susceptibility is of crucial importance not only for medical care and research but for legislative and regulatory consideration to protect these vulnerable individuals.

Air Pollutants↗
PubMed1992

Theophylline mitigates the bronchoconstrictor effects of sulfur dioxide in subjects with asthma.

The objective of the study was to investigate the ability of a sustained-release (SR) theophylline tablet (Uniphyl; Purdue Frederick Co., Norwalk, Conn.) to block or mitigate sulfur dioxide (SO2)-induced bronchoconstriction in adult subjects with asthma. Eight subjects participated in a double-blind, crossover study with a 400 mg theophylline tablet or placebo once a day for a week before a 10-minute SO2 challenge. FEV1 and total respiratory resistance (RT) were measured before and after the SO2 challenge and on a different day before and after an air exposure. After exposure to SO2, average values of FEV1 dropped 16% after placebo treatment and 7% after theophylline treatment. The corresponding percentages for RT were a 37% increase after placebo and a 7% increase after theophylline treatment. Analysis of variance demonstrated a significant difference between the SO2-induced decrease in FEV1 and increase in RT after SR theophylline treatment compared with that of placebo treatment. Thus, we conclude that SR theophylline tablets, taken at this concentration for 1 week, mitigate SO2-induced bronchoconstriction.

Adolescent↗
PubMed1992

Response of young asthmatic patients to inhaled sulfuric acid.

The intent of this study was to explore the effects of inhalation of [H+] defined here as acid airborne particles at near ambient concentrations on the pulmonary function of adolescent asthmatic subjects. During rest and exercise, 22 adolescent asthmatic subjects inhaled atmospheres containing either clean air or sulfuric acid particles (H2SO4) through a mouthpiece. The concentration of hydrogen ion at the mouthpiece ([H+]) ranged from 1.18 to 3.59 mumol/m3 (51 to 176 micrograms/m3 of H2SO4). The lower range of [H+] is near the peak values measured during the summer months in the eastern United States and Canada. Pulmonary function and oral ammonia levels were measured before and after exposure in all subjects. Significant group responses to [H+] were seen in FEV1 (p = 0.016) and FVC (p = 0.039) measured 2 to 3 min post-exposure. Also, the slopes of the change in pulmonary function versus [H+] were computed for each subject. The slopes of changes in FEV1 and Vmax50 and Vmax75 versus [H+] were related to the subject's response to a standard exercise treadmill test, specifically to the subject's percentage decrease in FEV1 after exercise challenge. Pulmonary function changes 20 min postexposure did not show a significant group response to [H+] exposure; however, the relationship between percentage FEV1 decrease after exercise and the individual slopes of Vmax50 and Vmax75 persisted for at least 20 min after exposure.

Adolescent↗
PubMed1992

Respiratory effects from the inhalation of hydrogen chloride in young adult asthmatics.

Almost no human data exist from controlled studies using low levels of hydrogen chloride (HCl), and, with no existing HCl ambient standards in the United States, the need for human health effects research is evident. In this study, five female and five male 18 to 25-year-old asthmatic subjects were exposed to filtered air, 0.8 ppm and 1.8 ppm HCl while wearing half-face masks, during three separate 45-minute experimental sessions involving 15 minutes exercise (treadmill walking), 15 minutes rest, followed again by exercise. Baseline and postexposure pulmonary function measurements were taken including forced expiratory volume in 1 second (FEV1), forced expiratory volume (FVC), maximal flow at 50% of expired vital capacity (Vmax50), maximal flow at 75% of expired vital capacity (Vmax75), and total respiratory resistance as well as peak flow. Nasal work of breathing and oral ammonia levels also were measured preexposure and postexposure. No significant pulmonary effects were found at these HCl concentrations and exposure duration. Nasal power showed no significant differences between test atmospheres; however, in isolation a significant decrease (P less than .01) was found in measurements of inspiration with exposure to 0.80 ppm. Ammonia levels showed a significant rise postexposure after both concentrations of HCl (paired t test, (P less than .01)), not seen after air exposure. In summary, the asthmatic subjects in this study showed no adverse respiratory health effects of inhalation of low concentrations of HCl.

Administration, Inhalation↗
PubMed1991

Acute pulmonary effects of nitrogen dioxide exposure during exercise in competitive athletes.

The acute pulmonary responses of athletes after short-term exposure to ambient concentrations of NO2 during heavy exercise have been examined. Intercollegiate male athletes were screened for history of cardiac disease, respiratory disease, allergic conditions and extensive exposure to pollutants. After completion of serum IgE level determination, exercise tolerance test and methacholine challenge test with normal results, nine healthy subjects 18 to 23 years of age were exposed to filtered air and to 0.18 and 0.30 ppm NO2 for 30 min on different days while exercising on a treadmill. Pulmonary function parameters were measured before and after each exposure. In this study, no statistically significant changes were observed in FEV1, RT PEFR, and Vmax50% after exposure to 0.18 and 0.30 ppm NO2. For these selected healthy athletes, short-term exposure to ambient NO2 levels during heavy exercise does not affect adversely the pulmonary function.

Adult↗
PubMed1991

Air pollutants and the respiratory system: toxicity and pharmacologic interventions.

Air pollution remains a major aggravation of respiratory symptoms and disease. Sulfur dioxide, ozone, sulfuric acid, particulate matter such as the fine particles from wood smoke, and nitrogen dioxide all produce significant effects when investigated in laboratory or field studies. These effects are decreases in pulmonary function and evidence of inflammation as well as suggestions of increases in chronic respiratory disease. Asthmatic subjects may be the group at greatest risk from air pollutants. Common medications used to treat asthma have varying effects on blocking or mitigating these pollutant-induced effects.

Air Pollutants↗
PubMed1990

Prior exposure to ozone potentiates subsequent response to sulfur dioxide in adolescent asthmatic subjects.

The objective of this study was to test whether prior exposure to a low concentration of ozone (120 ppb) would condition airways in asthmatic subjects to respond to a subthreshold concentration of sulfur dioxide (100 ppb). Eight male and five female subjects 12 to 18 yr of age participated. They all had allergic asthma and exercise-induced bronchospasm. Subjects were exposed to three test atmosphere sequences during intermittent moderate exercise (a 45-min exposure to one pollutant followed by a 15-min exposure to the second pollutant). The sequences were: air followed by 100 ppb SO2, 120 ppb O3 followed by 120 ppb O3, and 120 ppb O3 followed by 100 ppb SO2. The pulmonary function measurements assessed were FEV1, total respiratory resistance (RT), and maximal flow (Vmax50). Air-SO2 and O3-O3 exposures did not cause significant changes in pulmonary function. On the other hand, exposure to 100 ppb SO2 after a 45-min exposure to 120 ppb O3 caused a significant (8%) decrease in FEV1 (p = 0.046), a significant (19%) increase in RT (p = 0.048), and a significant (15%) decrease in Vmax50 (p = 0.008). It is concluded that prior O3 exposure increased bronchial hyperresponsiveness in these subjects such that they responded to an ordinarily subthreshold concentration of SO2. These data suggest that assessment of pulmonary changes to single pollutant challenges overlooks the interactive effects of common coexisting or sequentially occurring air pollutants.

Adolescent↗
PubMed1989

Pulmonary effects of sulfur dioxide exposure and ipratropium bromide pretreatment in adults with nonallergic asthma.

In this study we examined the potential short-term effect of sulfur dioxide (SO2) on total respiratory resistance and forced expiratory volume in patients with nonallergic asthma. A group of nine adult subjects with nonallergic asthma, 55 years of age or older, were exposed to SO2 at 0, 0.5, and 1.0 ppm for 20 minutes at rest followed by 10 minutes during light-moderate exercise. The measures of pulmonary function assessed were FEV1, specific total respiratory resistance (SRT), and maximal expiratory flow rates at 50% (Vmax50) and 75% (Vmax75) of expired vital capacity. Measurements were made before exposure to SO2 (baseline), postresting exposure, postexercising exposure, and at 30 minutes thereafter (recovery). Repeat measure analysis of variance revealed a statistically significant dose-response effect of SO2 inhalation on FEV1 (p = 0.008), SRT (p = 0.033), Vmax50 (p = 0.017), and Vmax75 (p = 0.048). Eight subjects had repeat exposure to SO2 at 1.0 ppm after treatment with either placebo or ipratropium bromide, 60 micrograms by metered-dose inhaler. Inpratropium bromide treatment, compared to placebo treatment, resulted in a statistically significant improvement in all baseline measures of pulmonary function: FEV1 (p = 0.017), SRT (p = 0.027), Vmax50 (p = 0.018), and Vmax75 (p = 0.035). However, this drug did not significantly alter the proportionate change in pulmonary function caused by SO2 inhalation in these subjects. These findings indicate that adults with nonallergic asthma are sensitive to short-term low-level SO2 exposure and that treatment with 60 micrograms of ipratropium bromide causes significant bronchodilation but does not protect, completely, these patients from the effect of SO2 inhalation.

Aged↗
PubMed1989

Effects of inhalation of acidic compounds on pulmonary function in allergic adolescent subjects.

There is concern about the human health effects of inhalation of acid compounds found in urban air pollution. It was the purpose of this study to investigate three of these acid compounds, sulfur dioxide (SO2), sulfuric acid (H2SO4), and nitric acid (HNO3) in a group of allergic adolescent subjects. Subjects were exposed during rest and moderate exercise to 0.7 mumole/m3 (68 micrograms/m3) H2SO4, 4.0 mumole/m3 (0.1 ppm) SO2, or 2.0 mumole/m3 (0.05 ppm) HNO3. Pulmonary functions (FEV1, total respiratory resistance, and maximal flow) were measured before and after exposure. Preliminary analysis based on nine subjects indicates that exposure to 0.7 mumole/m3 H2SO4 alone and in combination with SO2 caused significant changes in pulmonary function, whereas exposure to air or SO2 alone did not. FEV1 decreased an average of 6% after exposure to H2SO4 alone and 4% when the aerosol was combined with SO2. The FEV1 decrease was 2% after both air and SO2 exposures. Total respiratory resistance (RT) increased 15% after the combined H2SO4 exposures, 12% after H2SO4 alone, and 7% after exposure to air. After exposures to HNO3 alone, FEV1 decreased by 4%, and RT increased by 23%. These results are preliminary; final conclusions must wait for completion of the study.

Acid Rain↗
PubMed1989

Human nasal epithelium: characterization and effects of in vitro exposure to sulfur dioxide.

Human nasal turbinate tissue from surgical specimens was dissected free of connective tissue, and primary epithelial cultures were established by explant techniques. Transmission electron microscopy revealed that cultured cells retained homogeneous cytoplasmic granules, tonofilaments, and desmosomes and formed a homogeneous monolayer. The epithelial cells stained positively with cytokeratin antibodies AE1, AE3, and 35BH11 but failed to stain with two other cytokeratin antibodies, AE2 and 34BE12. Staining was also positive with anti-desmoplakin I and II but negative with antivimentin (43BE8), anti-desmin, and anti-human factor VIII antibodies. Cultured cells were exposed to filtered air or sulfur dioxide at 1-5 ppm for 30-60 min. Although there was no increase in cell lysis as measured by chromium-51 release, SO2 exposure significantly inhibited [3H]leucine incorporation compared to air exposure. This effect was dependent on both SO2 concentration and exposure duration. Control experiments revealed that these SO2 effects were not caused by the [H+] load produced by SO2 exposure. Electron microscopy of cells exposed to air or SO2 did not show any significant morphological differences.

Adolescent↗
PubMed1989

Potential adverse health effects of wood smoke.

The use of wood stoves has increased greatly in the past decade, causing concern in many communities about the health effects of wood smoke. Wood smoke is known to contain such compounds as carbon monoxide, nitrogen oxides, sulfur oxides, aldehydes, polycyclic aromatic hydrocarbons, and fine respirable particulate matter. All of these have been shown to cause deleterious physiologic responses in laboratory studies in humans. Some compounds found in wood smoke--benzo[a]pyrene and formaldehyde--are possible human carcinogens. Fine particulate matter has been associated with decreased pulmonary function in children and with increased chronic lung disease in Nepal, where exposure to very high amounts of wood smoke occurs in residences. Wood smoke fumes, taken from both outdoor and indoor samples, have shown mutagenic activity in short-term bioassay tests. Because of the potential health effects of wood smoke, exposure to this source of air pollution should be minimal.

Humans↗
PubMed1989

Studies of neutrophil chemotactic factor of anaphylaxis in metabisulfite sensitivity.

The mechanism(s) of adverse reactions to sulfites remains unclear. To determine whether mast cell degranulation is involved in sulfite sensitivity, we performed single-blind, placebo-controlled oral aqueous challenges with potassium metabisulfite in 13 patients with histories suggestive of sulfite sensitivity. Ten patients were also skin tested with potassium metabisulfite at 10 mg/mL and all had negative reactions. Serum samples were obtained from all the patients before the challenge and for 180 minutes after the challenge. The samples were tested for the presence of neutrophil chemotactic factor of anaphylaxis, using both a 51chromium microchamber chemotaxis assay and a leukocyte polarization technique. Six of 13 patients had positive challenges as defined by a fall equal to or greater than 20% in their forced expiratory volume in one second. No significant increase in neutrophil chemotactic factor activity was detected in the postchallenge serum samples from patients who experienced positive or negative challenges. We conclude that sensitivity to aqueous metabisulfite is not associated with mast cell degranulation in metabisulfite skin test-negative patients.

Adult↗