Hypoventilation and apnea in children during mechanically assisted ventilation.

Uncuffed tracheostomy tubes are used for long-term mechanical ventilation in children. However, upper airway mechanics differ between sleep and wakefulness; this may affect air leak around tracheostomies. We studied 19 children with high cervical spinal cord injury on portable positive pressure ventilators, age range birth to 19 years. Ventilator settings were adjusted while awake to achieve PaCO2 less than 45 mm Hg and PO2 greater than 90 mm Hg. Clinically several children with uncuffed tracheostomies became unstable at night with seizures and sleep disruption. Nine of 11 children on volume controlled systems were found to be inadequately ventilated during sleep. Substitution with a cuffed tracheostomy allowed adequate ventilation both awake and asleep, suggesting that inadequate ventilation during sleep was due to an uncompensated leak around the uncuffed tracheostomy. To avoid cuffed tracheostomies, eight children received pressure controlled ventilation. Gas exchange was adequate throughout the day and night. We conclude that children receiving volume controlled mechanical ventilation via uncuffed tracheostomy tubes can exhibit hypoventilation due to uncompensated air leak. Pressure controlled ventilation improves adequacy of gas exchange during sleep and wakefulness.

Short-term air pollution exposures and responses in Los Angeles area schoolchildren.

We studied 269 school children from three Southern California communities of contrasting air quality in two successive school years, to investigate short-term effects of ambient ozone (O3), nitrogen dioxide (NO2), or particulate matter (PM) on respiratory health. We measured lung function and symptoms twice daily for one week each in fall, winter and spring; and concurrently assessed time-activity patterns and personal exposures. Average daily personal exposures correlated with pollutant concentrations at central sites (r = 0.61 for O3, 0.63 for NO2, 0.48 for PM). Questionnaire-reported outdoor activity increased slightly in communities/seasons with higher pollution. Lung function differences between communities were explainable by age differences. Morning forced vital capacity (FVC) decreased significantly with increase in PM or NO2 measured over the preceding 24 hours. Morning-to-afternoon change of forced expired volume in one second (FEV1) became significantly more negative with increase in PM, NO2, or O3 on the same day. Predicted FVC or FEV1 loss on highest- vs lowest-pollution days was < 2%. Daily symptoms showed no association with current or prior 24-hour pollution, but increased with decreasing temperature. Parents' questionnaire responses suggested excess asthma and allergy in children from one polluted community while children in the other polluted community reported more symptoms, relative to the cleaner community. We conclude that Los Angeles area children may experience slight lung function changes in association with day-to-day air quality changes, reasonably similar to responses seen by others in less polluted areas. Although short-term pollution effects appear small, they should be assessed in longitudinal lung function studies when possible, to allow maximally accurate measurement of longer-term function changes.

Time-activity patterns and diurnal variation of respiratory status in a panel of asthmatics: implications for short-term air pollution effects.

To understand the short-term health risks to people from air pollution exposure, we investigated time-activity patterns and temporal variation of the respiratory status in 49 asthmatic Los Angeles area residents 18-50 years old. During the summer (May-September) and winter (November-March), subjects measured their lung function two to four times daily at home for one week periods, and every hour recorded their symptoms, medication, and activity hourly in diaries. Almost all subjects recorded heart rates (HR), which were converted to ventilation rate (VR) estimates using individual laboratory exercise data. Most subjects' lung function and symptoms varied diurnally, and were worst in early morning. For subjects with clinically mild asthma, diurnal forced expired volume in 1 sec (FEV1) changes averaged 7%, versus 12% in those with moderate symptoms, and 18% in severely asthmatic subjects. Lung function was similar in summer and winter, but symptoms and medication use decreased in winter. In the aggregate, subjects reported spending 75% of waking hours indoors at self-rated slow activity and 11% in vehicles. HR records usually corroborated reports of medium or fast activity. Mean estimated VR at slow, medium, and fast activity was 19, 37, and 61 L/min for men, and 16, 24, and 32 L/min for women. Outdoor fast activity, representing the greatest vulnerability to outdoor pollution, occupied approximately 0.2% of waking hours (2 min/day on average); outdoor medium activity occupied about 2% of waking hours (19 min/day on average). Estimated cumulative ventilation was higher than that of previous healthy panels because of asthmatics' higher VR at slow activity. If these activity patterns are typical, asthmatics may be especially vulnerable to pollutants with effects dependent on cumulative inhaled dose. Effects dependent on high inhaled dose rates over a short period, e.g., sulfur dioxide effects, would be unlikely, except perhaps for uncommonly active individuals in uncommonly polluted areas.

Effect of metaproterenol sulfate on mild asthmatics' response to sulfur dioxide exposure and exercise.

Twenty asthmatic volunteers, most with mild disease, underwent dose-response studies with sulfur dioxide (SO2) under three pretreatment conditions: (1) drug (metaproterenol sulfate in aerosolized saline solution), (2) placebo (aerosolized saline only), and (3) no pretreatment. Sulfur dioxide exposure concentrations were 0.0, 0.3, and 0.6 ppm. Experimental conditions were presented in random order at 1-wk intervals. Exposures lasted 10 min with heavy continuous exercise. Lung function was measured at baseline, after pretreatment (immediately pre-exposure), immediately post-exposure, and during a 2-hr follow-up. Subjects could elect to take bronchodilators during follow-up. Symptoms were monitored before, during, and for 1 wk after exposure. With no pretreatment, subjects exhibited typical exercise-induced bronchospasm at 0.0 ppm, slightly increased responses at 0.3 ppm, and more marked increases at 0.6 ppm. Seven subjects took bronchodilator after 0.6-ppm exposures, compared to 2 at lower concentrations. Within 30 min post-exposure, most subjects' symptoms and lung function had returned to near pre-exposure levels. A similar sequence was observed when subjects received placebo. Drug pretreatment improved lung function relative to baseline, prevented bronchoconstrictive responses at 0.0 and 0.3 ppm, and greatly mitigated responses at 0.6 ppm. Thus, typical bronchodilator usage by asthmatics is likely to reduce their response to ambient SO2 pollution.

Responses to sulfur dioxide and exercise by medication-dependent asthmatics: effect of varying medication levels.

Twenty-one volunteers with moderate to severe asthma were exposed to sulfur dioxide (SO2) at concentrations of 0 (control), 0.3, and 0.6 ppm in each of three medication states: (1) low (much of their usual asthma medication withheld), (2) normal (each subject on his own usual medication schedule), and (3) high (usual medication supplemented by inhaled metaproterenol before exposure). Theophylline, the medication usually taken by subjects, was often supplemented by beta-adrenergics. Exposures were for 10 min and were accompanied by continuous heavy exercise (ventilation approximately 50 l/min). Lung function and symptoms were measured before and after exposure. With normal medication, symptomatic bronchoconstriction occurred with exercise and was exacerbated by 0.6 ppm SO2, as reported for mildly unmedicated asthmatics studied previously. Both baseline and post-exposure lung function were noticeably worse in the low-medication state. High medication improved baseline lung function and prevented most bronchoconstrictive effects of SO2/exercise. High medication also increased heart rate and apparently induced tremor or nervousness in some individuals.

Changes in the health situation among the rural population and the challenges to the preventive services in China.

PIP: 80% of China's 1 billion population is rural. In response to the changing situation in rural health care work subsequent to profound economic rural structural reform, appropriate measures in Chinese rural health care work were taken. All levels of leaders in health care and other departments were instructed to continue the rural health care policy of "prevention first," and to expand the functions and tasks of prevention. Rural areas were to given top priority. To reform the current health organizational structure it was necessary to take into account several realities: The rural birth rate has dropped radically since liberation, as has the mortality rate. Life expectancy has increased, the combined effect being a population that is aging rapidly: people 65+ years old comprised 4.91% of the population in 1982. 32.2% of rural families are 1-child families, and the safeguarding of the health of children continues to be a high priority, as does the prevention of cardio- and cerebrovascular disease and malignant tumors, which as cause of 54.91% of mortality, has replaced infectious diseases as the main health threat. Occupational disease have become alarmingly more common as the effort to expand rural industry advances. The 3-level health care network is to continue to be reinforced: county facllities for training and care of complicated diseases, integrating multiple functions that were previously separate, township rural health centers for the development of prevention teams, and village level doctors. The rural medical system must, among other things, transform the medical model to a "biological, psychological, and social" medical model, mobilize various social sectors, and attempt to collect funds from various sources to support health care work and the prevention of disease.^ieng

Laboratory study of asthmatic volunteers exposed to nitrogen dioxide and to ambient air pollution.

Adult volunteers with moderate to severe asthma (N = 59) underwent dose-response studies to assess their reactivity to nitrogen dioxide (NO2) in otherwise clean air. Exposure concentrations were 0.0 (control), 0.3 and 0.6 ppm. A subgroup (N = 36) also underwent exposures to Los Angeles area ambient air at times when NO2 pollution was expected. Concentrations of NO2 during ambient exposures were 0.086 +/- 0.024 ppm (mean +/- s.d.). All exposures took place in a movable chamber/laboratory facility. Each study lasted 2 hr, with alternating 10 min periods of exercise (mean ventilation rate 40 L/min) and rest. Lung function was measured prior to exposure and after 10 min, 1 hr and 2 hr of exposure. Symptoms were recorded prior to exposure, during exposure and for 1 week afterward. In some subjects bronchial reactivity to cold air was measured 1 hr after the end of exposure and again 24 hr later. Different exposure conditions were presented in randomized order, 1 week apart. No pollutant exposure produced statistically significant changes in lung function, symptoms, or bronchial reactivity, relative to clean air. Ambient air exposures produced the largest (still nonsignificant) mean changes in some lung function tests. Given the physiological and atmospheric variability, negative statistical results do not rule out a small unfavorable effect of ambient pollution on lung function. If any such effect occurred, it was not likely caused by NO2. Statistical results remained negative when the analysis was restricted to the 20 subjects with most severe lung dysfunction. In conclusion at least in the Los Angeles area, sensitivity to ambient concentrations of NO2 is not common, even among adult asthmatics with moderate to severe disease.

Replicated dose-response study of sulfur dioxide effects in normal, atopic, and asthmatic volunteers.

To help assess respiratory health risks from sulfur dioxide (SO2) air pollution, we studied 24 normal, 21 atopic, 16 minimal/mild asthmatic, and 24 moderate/severe, medication-dependent asthmatic subjects classified according to history, lung function, allergy skin tests, serum IgE level, and airway reactivity to methacholine. All were exposed in a chamber (21 degrees C, 50% humidity) to 0.0, 0.2, 0.4, and 0.6 ppm SO2 in random order at 1-wk intervals; then exposures were repeated to test consistency of response. The 1-h exposures included three 10-min exercise periods (ventilation approximately 40 L/min). Physiologic response was measured early (approximately 15 min) and late (approximately 55 min) in exposure. Symptoms were evaluated during exposure and for 1 wk afterward. Normal and most atopic subjects showed little response at these SO2 levels. A few atopic subjects and many asthmatics developed bronchoconstriction and respiratory symptoms, but most were able to maintain their exercise. Effects were not markedly different between early and late measurements, nor between the first and second round of studies; however, late and second-round responses appeared slightly more favorable. No statistically significant effect of SO2 on symptoms was found 1 day or 1 wk after exposure. Minimal/mild asthmatics showed, on the average, slight responses at 0.0 ppm (attributable to exercise) and increasing responses at increasing SO2 concentrations. Moderate/severe asthmatics reacted more at 0.0 ppm, but their increments in response with increasing SO2 concentration were roughly similar to those of minimal/mild asthmatics. Thus, responses to SO2 per se were not strongly dependent on clinical severity of asthma, nor on SO2 exposure history during previous weeks.

Respiratory responses of young asthmatic volunteers in controlled exposures to sulfuric acid aerosol.

Thirty-two asthmatic volunteers 8 to 16 yr of age, recruited through local schools and private physicians, were exposed in a chamber to clean air (control condition) and to sulfuric acid aerosol at a "low" concentration (46 +/- 11 micrograms/m3; mean +/- SD) and at a "high" concentration (127 +/- 21 micrograms/m3). Acid aerosols had mass median aerodynamic diameters near 0.5 microns with geometric standard deviations near 1.9. Temperature was 21 degrees C, and relative humidity was near 50%. Subjects were exposed with unencumbered oronasal breathing for 30 min at rest plus 10 min at moderate exercise (ventilation rate approximately 20 L/min/m2 of body surface). A subgroup (21 subjects) were exposed similarly to clean air and to "high" acid (134 +/- 20 micrograms/m3) with 100% oral breathing. Increased symptoms and bronchoconstriction were found after exercise under all exposure conditions. For the group, symptom and lung function responses were not statistically different during control and during acid exposures with unencumbered breathing or with oral breathing. By contrast, other investigators have reported statistically significant lung function disturbances in groups of young asthmatics exposed similarly with oral breathing. A minority of our subjects showed possibly meaningful excess bronchoconstriction with "high" acid exposure relative to control with both routes of breathing. This could be the result of chance, or it could suggest the existence of an acid-sensitive subpopulation of young asthmatics.

Effects of prolonged, repeated exposure to ozone, sulfuric acid, and their combination in healthy and asthmatic volunteers.

To evaluate effects of "acid summer haze" on individuals who exercise extensively outdoors, we exposed 45 adult volunteers (15 normal or atopic, 30 asthmatic) in a chamber to a mixture of 0.12 ppm ozone (O3) and approximately 100 micrograms/m3 of respirable sulfuric acid aerosol (H2SO4). On separate occasions we exposed the same subjects to O3 alone, to H2SO4 alone, and to clean air. In exposures involving H2SO4, excess acid was generated to consume ammonia released by the subjects, and the aerosol therefore contained ammonium salts in addition to H2SO4. Subjects were exposed to each atmosphere on two successive days, for 6.5 h/d, with six 50-min exercise periods at ventilation rates averaging 29 L/min. Exposures were conducted during four successive weeks, in random order. Lung function and symptoms were measured before exposure and hourly during exposure. Bronchial reactivity to inhaled methacholine was measured just after the end of each exposure. Exposure to H2SO4 alone caused no significant changes in lung function, symptoms, or bronchial reactivity relative to clean air. Exposure to O3 alone or O3 + H2SO4 caused a progressive, statistically significant (p < 0.05) decline in forced expiratory function, smaller on the second day than the first, as previously found by others for O3 exposure. Bronchial reactivity increased significantly after exposure to O3 with or without H2SO4. Changes in mean lung function and bronchial reactivity with O3 + H2SO4 exposure were modestly larger than changes with O3 exposure, but the differences were nonsignificant or marginally significant. A minority of individual asthmatic and nonasthmatic subjects showed substantially greater declines in function with exposure to O3 + H2SO4 relative to O3 alone. Repeat exposure studies of these subjects again showed an excess response to O3 + H2SO4 on the average, but there was no significant correlation between the excess responses of individual subjects in the original and repeat studies. We conclude that for typical healthy or asthmatic adults heavily exposed to acid summer haze, O3 is more important than H2SO4 as a cause of short-term respiratory irritant effects.

Effect of droplet size on respiratory responses to inhaled sulfuric acid in normal and asthmatic volunteers.

We exposed groups of healthy and asthmatic volunteers to sulfuric acid aerosols with volume median droplet diameters of approximately 20, 10, and 1 microns, at nominal concentrations of 2,000 micrograms/m3, and exposed them similarly to aerosols of purified water as a control. Exposures lasted 1 h each, and included three 10-min periods of exercise (ventilation rate typically 40 to 45 L/min). Exposures occurred in randomized order 7 days apart. Temperature was 10 degrees C, relative humidity was approximately 100% in 20- and 10-microns (fog) exposures, and approximately 75 to 80% in 1-micron aerosol exposures. Healthy subjects showed no statistically significant changes in lung function or in bronchial reactivity to methacholine attributable to acid exposures. They showed significant increases in lower and upper respiratory irritant symptoms when exposed to 20- or 10-microns acid fog, but not when exposed to 1-micron acid aerosol. Asthmatics showed significant excess decreases in forced expiratory performance, increases in airway resistance, and increases in irritant symptoms during acid exposures, relative to control conditions. Lung function changes in asthmatics tended to increase with time during exposure; they did not vary significantly with acid droplet size. Symptoms in asthmatics were slightly worse with 10- or 20-microns fog as compared with 1-micron aerosol. In a few instances, symptoms and lung function decrements necessitated stopping exercise or terminating the exposure early. Thus, asthma is a risk factor for unfavorable physiologic response to sulfuric acid at occupational exposure concentrations. Large droplet size (i.e., fog) tends to exacerbate short-term symptomatic response, but we have not been able to demonstrate a consistent effect of droplet size on physiologic response.

Repeated laboratory ozone exposures of volunteer Los Angeles residents: an apparent seasonal variation in response.

This study was intended to help explain individual differences in susceptibility to irritant effects of ozone (O3), by determining whether prior ambient O3 exposures and/or recent acute respiratory illness modified response to laboratory O3 exposures. Response was measured in terms of lung function changes and irritant symptoms. Initially, 59 adult volunteer Los Angeles area residents underwent screening exposures in spring, before the season of frequent high ambient O3 levels. Unusually responsive and nonresponsive individuals (N = 12 and 13 respectively) underwent followup exposures in autumn (late in the high-O3 season) and in winter (low-O3 season). All exposures were to 0.18 ppm O3 for 2 hr with intermittent heavy exercise at 31 degrees C and 35% relative humidity. Nonresponders tended to remain nonresponsive throughout. In fall, responders had lost much of their reactivity, as if they had "adapted" to summer ambient O3 exposures. They did not regain reactivity by winter. Clinical laboratory findings suggestive of acute respiratory illness did not appear to correlate with O3 response. Eight responders and 9 nonresponders underwent another followup exposure in spring, about 1 yr after screening. By that time most responders had regained their reactivity; individual function changes were significantly correlated with changes 1 yr earlier. These results suggest that response to O3 is a persistent individual characteristic, but can be modified by repeated ambient exposures.

Experimental exposures of young asthmatic volunteers to 0.3 ppm nitrogen dioxide and to ambient air pollution.

Asthmatic volunteers aged 8 to 16 (N = 34) were exposed on separate occasions to clean air (control), to 0.30 ppm nitrogen dioxide (NO2) in otherwise clean air, and to polluted Los Angeles area ambient air on summer mornings when NO2 pollution was expected. Exposures lasted 3 hr, with alternating 10-min periods of exercise and rest. In ambient pollution exposures, 3-hr average NO2 concentrations ranged from 0.01 to 0.26 ppm, with a mean of 0.09 ppm. Ambient exposures did not significantly affect lung function, symptoms, or bronchial reactivity to cold air, relative to the control condition. Responses to 0.3 ppm NO2 exposures were equivocal. Asthma symptoms were more severe during 1-week periods before 0.3 ppm exposures, and lung function was decreased immediately before 0.3 ppm exposures, compared to other conditions. Lung function declined slightly during the first hour at 0.3 ppm, but improved over the remaining 2 hr. Compared to other conditions, symptoms were not increased during 0.3 ppm exposures, but were increased during 1-week periods afterward. These observations may reflect untoward effects of 0.3 ppm NO2, or may reflect chance increases in asthma severity prior to 0.3 ppm exposures.

Controlled exposures of volunteers to respirable carbon and sulfuric acid aerosols.

Respirable carbon or fly ash particles are suspected to increase the respiratory toxicity of coexisting acidic air pollutants, by concentrating acid on their surfaces and so delivering it efficiently to the lower respiratory tract. To investigate this issue, we exposed 15 healthy and 15 asthmatic volunteers in a controlled-environment chamber (21 degrees C, 50 percent relative humidity) to four test atmospheres: (i) clean air; (ii) 0.5-microns H2SO4 aerosol at approximately 100 micrograms/m3, generated from water solution; (iii) 0.5-microns carbon aerosol at approximately 250 micrograms/m3, generated from highly pure carbon black with specific surface area comparable to ambient pollution particles; and (iv) carbon as in (iii) plus approximately 100 micrograms/m3 of ultrafine H2SO4 aerosol generated from fuming sulfuric acid. Electron microscopy showed that nearly all acid in (iv) became attached to carbon particle surfaces, and that most particles remained in the sub-micron size range. Exposures were performed double-blind, 1 week apart. They lasted 1 hr each, with alternate 10-min periods of heavy exercise (ventilation approximately 50 L/min) and rest. Subjects gargled citrus juice before exposure to suppress airway ammonia. Lung function and symptoms were measured pre-exposure, after initial exercise, and at end-exposure. Bronchial reactivity to methacholine was measured after exposure. Statistical analyses tested for effects of H2SO4 or carbon, separate or interactive, on health measures. Group data showed no more than small equivocal effects of any exposure on any health measure.(ABSTRACT TRUNCATED AT 250 WORDS)

Exposures of older adults with chronic respiratory illness to nitrogen dioxide. A combined laboratory and field study.

We combined field and laboratory experimentation to evaluate the effects of nitrogen dioxide in a panel of Los Angeles area residents with chronic respiratory illness, 15 men and 11 women aged 47 to 69. All had heavy smoking history, chronic symptoms, and low FEV1; some also had low FVC. During the fall-winter high-NO2 season, they monitored themselves for 2-wk periods using spirometers in the home, passive NO2 sampling badges, and diaries to record time and activity patterns and clinical status. In the middle of each self-monitoring week they were exposed in a chamber, once to clean air and once to 0.3 ppm NO2. Chamber exposures were double blind, lasted 4 h, and included four 7-min exercise sessions with average ventilation rates near 25 L/min. Symptom reports and hourly forced expiratory function tests showed no statistically significant differences between clean air and NO2 chamber exposures, although peak flow showed a approximately 3% loss with NO2 relative to clean air during the first 2 h of exposure only (p = 0.056). No significant overall differences were found between field self-measurements and measurements of lung function in the chamber or between field measurements in clean air and NO2 exposure weeks. Field data showed that group average lung function and symptom levels were worse in the morning than later in the day (p < 0.005) but otherwise were stable over 2 wk. Even though most subjects smoked and stayed indoors 80 to 90% of the time, personal NO2 exposures correlated significantly with outdoor NO2 concentrations as reported by local monitoring stations.(ABSTRACT TRUNCATED AT 250 WORDS)