EquinePhysiology
Human Studies:
| - Human
1-11 1: Environ Health Perspect 1998 Feb;106(2):93-9 Effects of ozone and other pollutants on the pulmonary function of adult hikers. Korrick SA, Neas LM, Dockery DW, Gold DR, Allen GA, Hill LB, Kimball KD, Rosner BA, Speizer FE. Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. This study evaluated the acute effects of ambient ozone (O3), fine particulate matter (PM2.5), and strong aerosol acidity on the pulmonary function of exercising adults. During the summers of 1991 and 1992, volunteers (18-64 years of age) were solicited from hikers on Mt. Washington, New Hampshire. Volunteer nonsmokers with complete covariates (n = 530) had pulmonary function measured before and after their hikes. We calculated each hiker's posthike percentage change in forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), the ratio of these two (FEV1/FVC), forced expiratory flow between 25 and 75% of FVC(FEF25-75%), and peak expiratory flow rate (PEFR). Average O3 exposures ranged from 21 to 74 ppb. After adjustment for age,sex, smoking status (former versus never), history of asthma or wheeze, hours hiked, ambient temperature, and other covariates, there was a 2.6% decline in FEV1 [95% confidence interval (CI), 0.4-4.7; p = 0.02] and a 2.2% decline in FVC (CI, 0.8-3.5; p =0.003) for each 50 ppb increment in mean O3. There were consistent associations of decrements in both FVC (0.4% decline; CI,0.2-0.6, p = 0.001) and PEFR (0.8% decline; CI, 0.01-1.6; p = 0.05) with PM2.5 and of decrements in PEFR (0.4% decline; CI, 0.1-0.7; p = 0.02) with strong aerosol acidity across the interquartile range of these exposures. Hikers with asthma or a history of wheeze (n = 40) had fourfold greater responsiveness to ozone than others. With prolonged outdoor exercise, low-level exposures to O3, PM2.5, and strong aerosol acidity were associated with significant effects on pulmonary function among adults. Hikers with a history of asthma or wheeze had significantly greater air pollution-related changes in pulmonary function. Publication Types: Clinical trial PMID: 9435151 [PubMed - indexed for MEDLINE]
1: Rev Epidemiol Sante Publique 1991;39(1):101-10 [The joint effects of various atmospheric pollutants: a meta-analysis]. [Article in French] Zmirou D, Dechenaux J. CAREPS (Centre Alpin de Recherche Epidemiologique et de Prevention Sanitaire), CHU, Grenoble. Epidemiological and experimental papers on respiratory effects of air pollution published between 1980 and 1988 were reviewed, using a meta-analytical approach. Forty epidemiological papers dealing with sulfur dioxide (SO2) and total suspended particles (TSP) were used to scrutinize the interaction between the two pollutants, and suggested that the effect of the acid gas was enhanced by the joint presence of TSP. Oxidant pollution combining O3 and NO2 was also found more noxious than ozone alone, using 32 experimental design papers. These results stem from the multivariate modelization of the relationship between the relative risk of cough or the relative decrease of FEV1.0, and the pollutants concentration, and illustrated some of the advantages of this quantitative approach to literature review. Underlying physiopathological processes are discussed, in the light of the important literature available on this topic. Publication Types: Meta-analysis PMID: 1827674 [PubMed - indexed for MEDLINE]
1: Allergy Proc 1989 May-Jun;10(3):209-14 Impact of air pollutants on athletic performance. Pierson WE. Univ. of Washington, Seattle 98105. Human controlled and observational studies both lead to the conclusion of air pollution adversely affecting athletic performance during training and competition. The dosage of various air pollutants during exercise is much higher due to the marked increase in ventilatory rate and concomitant nasal and oral breathing. This is particularly true for sulfur dioxide which is a highly water-soluble gas and is normally absorbed in the upper airway during nasal breathing. With heavy exercise, oral pharyngeal breathing is the predominant mode of breathing and much larger amounts of sulfur dioxide are delivered to the lower airway resulting in significant impact upon the lower respiratory tract. More recently, several controlled human studies have shown that a combination of exercise and air pollutants such as ozone (O3) or sulfur dioxides (SO2) cause a significant increase in bronchoconstriction and air flow obstruction when compared to the same exposure at rest. In strenuous athletic competition such as the Olympic Games where small increments of time often determine the ultimate success of athletes, the impact of air pollutants and subsequent adverse ventilatory changes can affect athletic performance. Publication Types: Review Review, tutorial PMID: 2670670 [PubMed - indexed for MEDLINE]
1: Med Sci Sports Exerc 1986 Jun;18(3):322-7 Implications of air pollution effects on athletic performance. Pierson WE, Covert DS, Koenig JQ, Namekata T, Kim YS. Both controlled human studies and observational studies suggest that air pollution adversely affects athletic performance during both training and competition. The air pollution dosage during exercise is much higher than during rest because of a higher ventilatory rate and both nasal and oral breathing in the former case. For example, sulfur dioxide, which is a highly water-soluble gas, is almost entirely absorbed in the upper respiratory tract during nasal breathing. However, with oral pharyngeal breathing, the amount of sulfur dioxide that is absorbed is significantly less, and with exercise and oral pharyngeal breathing a significant decrease in upper airway absorption occurs, resulting in a significantly larger dosage of this pollutant being delivered to the tracheobronchial tree. Recently, several controlled human studies have shown that the combination of exercise and pollutant exposure (SO2 or O3) caused a marked bronchoconstriction and reduced ventilatory flow when compared to pollution exposure at rest. In a situation like the Olympic Games where milliseconds and millimeters often determine the success of athletes, air pollution can be an important factor in affecting their performance. This paper examines possible impacts of air pollution on athletic competition. PMID: 3088377 [PubMed - indexed for MEDLINE]
1: Allergy 1997;52(38 Suppl):37-44; discussion 57-8 Mechanisms of pollution-induced airway disease: in vivo studies. Peden DB. Center for Environmental Medicine & Lung Biology, University of North Carolina School of Medicine, Chapel Hill 27599-7310, USA. Several studies have investigated the effects of ozone, sulphur dioxide (SO2), and nitrogen dioxide (NO2) on lung function in normal and asthmatic subjects. Decreased lung function has been observed with ozone levels as low as 0.15 ppm-this effect is concentration dependent and is exacerbated by exercise. A number of lines of evidence suggest that the effect on lung function is mediated, at least in part, by neural mechanisms. In both normals and asthmatics, ozone has been shown to induce neutrophilic inflammation, with increased levels of several inflammatory mediators, including prostaglandin E2. However, in normal subjects, none of the markers of inflammation correlate with changes in lung function. The lung function changes in asthmatics may be associated with inflammatory effects; alternatively, ozone may prime the airways for an increased response to subsequently inhaled allergen. Indeed, an influx of both polymorphonucleocytes and eosinophils has been observed in asthmatic patients after ozone exposure. It has been suggested that the effect of ozone on classic allergen-induced bronchoconstriction may be more significant than any direct effect of this pollutant in asthmatics. SO2 does not appear to affect lung function in normal subjects, but may induce bronchoconstriction in asthmatics. Nasal breathing, which is often impaired in asthmatics, reduces the pulmonary effects of SO2, since this water-soluble gas is absorbed by the nasal mucosa. NO2 may also influence lung function in asthmatics, but further research is warranted. SO2 and NO2 alone do not seem to have a priming effect in asthmatics, but a combination of these two gases has resulted in a heightened sensitivity to subsequently inhaled allergen. Publication Types: Review Review, tutorial PMID: 9208058 [PubMed - indexed for MEDLINE]
1: Am J Respir Crit Care Med 1995 Aug;152(2):589-96 Proportion of moderately exercising individuals responding to low-level, multi-hour ozone exposure. McDonnell WF, Stewart PW, Andreoni S, Smith MV. Clinical Research Branch, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA. The purpose of this study was to describe the proportion of moderately exercising individuals experiencing significant respiratory responses to low-level, multi-hour ozone exposure as a function of ozone concentration and exposure duration. Sixty-eight healthy, nonsmoking adults, ages 18 to 34 yr, underwent two or more 6.6-h exposures to 0.0, 0.08, 0.10, or 0.12 ppm ozone. Five hours of exercise was performed during exposure, and lung function was measured before exposure and following each hour of exposure. For each combination of concentration and duration, each individual was determined to either have or not have experienced a 10% or greater decrement in FEV1. A logistic function was used to model the proportion of individuals experiencing such a decrement as a function of concentration and exposure duration. Bootstrap 90% confidence intervals (CIs) were calculated around the predictions. The model was found to give predictions that were in good agreement with observed data. The lowest level of exposure (C x T) for which the 90% CI excluded zero was approximately 0.2 ppm-h. For exposure to 0.12 ppm ozone for 6.6 h, 47% (90% CI = 30 to 65%) of exposed individuals were predicted to experience a 10% decrement in FEV1. A greater proportion of younger adults than of older adults were found to experience a given effect for a given exposure. PMID: 7633712 [PubMed - indexed for MEDLINE]
1: Inhal Toxicol 2000 Mar;12(3):151-67 Time course of response to ozone exposure in healthy adult females. Folinsbee LJ, Hazucha MJ. National Center for Environmental Assessment, United States Environmental Protection Agency, MD 52, Research Triangle Park, NC 27711, USA. Folinsbee.Lawrence@epa.gov Ozone exposure causes acute decrements in pulmonary function, increases airway responsiveness, and changes the breathing pattern. We examined these responses in 19 ozone-responsive (DeltaFEV(1) > 5%) young females exposed to both air and 0.35 ppm ozone. The randomized 75-min exposures included two 30-min exercise periods at V(E) approximately 40 L/min. Responses were measured before, during, and after exposure and at 18 and 42 h postexposure. FVC, FEV(1), and FIV(0.5) decreased (p <.01) immediately postexposure by 13.2%, 19.9%, and 20.8%, respectively, and the airway responsiveness was significantly increased. Raw increased (p <.05), while TGV remained essentially unchanged. At 18 h postexposure, the airways were still hyperresponsive and FEV(1) and FIV(0.5) were still 5% below the preexposure levels. There were no residual effects in any of the variables at 42 h postexposure. During exercise in ozone the tidal volume was decreased (-14%) and respiratory frequency increased (+15%). The changes in airway responsiveness were not related to changes in spirometric measurements. We found no significant differences between postair and postozone mouth occlusion pressure (Pm(0.1)) and the hypercapnic response to CO(2) rebreathing. We conclude that ozone induced typical acute changes in airway responsiveness and that ventilatory (exercise), spirometric (inspiratory and expiratory), and plethysmographic pulmonary function may show some residual effects for up to 18 h after exposure. The ozone-induced alteration in breathing pattern during exercise does not appear to be related to a change in ventilatory drive. Publication Types: Clinical trial Randomized controlled trial PMID: 10715622 [PubMed - indexed for MEDLINE]
1: Am J Respir Crit Care Med 1994 Sep;150(3):642-7 Lung function response of healthy women after sequential exposures to NO2 and O3. Hazucha MJ, Folinsbee LJ, Seal E, Bromberg PA. Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill 27599-7310. Since NOx emissions bear a precursor-product relation with ambient ozone (O3) levels, the sequence of peak ambient concentrations is first nitrogen dioxide (NO2) followed later in the day by ozone (O3). We ascertained whether preliminary exposure to 0.6 parts per million (ppm) NO2 would affect the lung function response to subsequent exposure to 0.3 ppm O3. Twenty-one healthy young nonsmoking women (18 to 35 yr of age) underwent two sets of exposures on two different days separated by a minimum of 2 wk. On one day, subjects were exposed to air for 2 h followed 3 h later by a 2-h exposure to O3. On the other day, the first exposure was to NO2; order of the days was randomized. During each exposure subjects intermittently exercised, alternating 15 min of rest with 15 min of exercise (Ve approximately 40 L/min). Spirometry was performed before the first exposure and at 1-h intervals until the end of the 2-h (O3) exposure. Plethysmography measurements were made before and after NO2 and O3 exposures. Nonspecific airway reactivity (AR) was determined at least 1 wk prior to the first exposure and following each O3 exposure. AR to methacholine (MCh) was expressed as dose required to decrease FEV1 by 10% (PD10FEV1). Nitrogen dioxide exposure alone did not reduce FEV1 but did significantly enhance O3-induced spirometric changes. No significant effects were observed in plethysmography. On both exposure days, the median PD10FEV1 was significantly reduced (p < 0.05) from control PD10FEV1 (14.3 mg/ml).(ABSTRACT TRUNCATED AT 250 WORDS) Publication Types: Clinical trial Randomized controlled trial PMID: 8087332 [PubMed - indexed for MEDLINE]
1: J Appl Physiol 1989 Oct;67(4):1535-41 Mechanism of action of ozone on the human lung. Hazucha MJ, Bates DV, Bromberg PA. Center for Environmental Medicine and Lung Biology, School of Medicine, University of North Carolina, Chapel Hill 27599-7310. Fourteen healthy normal volunteers were randomly exposed to air and 0.5 ppm of ozone (O3) in a controlled exposure chamber for a 2-h period during which 15 min of treadmill exercise sufficient to produce a ventilation of approximately 40 l/min was alternated with 15-min rest periods. Before testing an esophageal balloon was inserted, and lung volumes, flow rates, maximal inspiratory (at residual volume and functional residual capacity) and expiratory (at total lung capacity and functional residual capacity) mouth pressures, and pulmonary mechanics (static and dynamic compliance and airway resistance) were measured before and immediately after the exposure period. After the postexposure measurements had been completed, the subjects inhaled an aerosol of 20% lidocaine until response to citric acid aerosol inhalation was abolished. All of the measurements were immediately repeated. We found that the O3 exposure 1) induced a significant mean decrement of 17.8% in vital capacity (this change was the result of a marked fall in inspiratory capacity without significant increase in residual volume), 2) significantly increased mean airway resistance and specific airway resistance but did not change dynamic or static pulmonary compliance or viscous or elastic work, 3) significantly reduced maximal transpulmonary pressure (by 19%) but produced no changes in inspiratory or expiratory maximal mouth pressures, and 4) significantly increased respiratory rate (in 5 subjects by more than 6 breaths/min) and decreased tidal volume.(ABSTRACT TRUNCATED AT 250 WORDS) Publication Types: Clinical trial Randomized controlled trial PMID: 2793755 [PubMed - indexed for MEDLINE]
1: J Appl Physiol 1987 Apr;62(4):1671-80 Relationship between ozone exposure and pulmonary function changes. Hazucha MJ. A detailed comparison of literature-reported averaged decrements in pulmonary function of normal subjects exposed to O3 has been undertaken. The data base was formed by including data published during the past 20 yr from studies that reported at least one of the pulmonary function variables (forced vital capacity, forced expiratory volume at 1 s, mean forced expiratory flow between 25 and 75% of forced vital capacity, and airway resistance) acquired at 2 h of exposures utilizing either original or modified Bates-Hazucha (intermittent exercise) protocol and that satisfied selection criteria. The final set of data (24 studies involving 299 subjects) was divided by ventilation rate (exercise loads) into four categories: light, moderate, high, and very high ventilation level. For each pulmonary function variable and ventilation level a quadratic function has been fitted to the data using regression procedures. The curve parameter estimates have been computed, tabulated, and statistically evaluated. The slope (quadratic coefficient) for each variable within a group and almost all variables between groups were significantly different from zero and from each other at P less than or equal to 0.0001. Publication Types: Review PMID: 3298195 [PubMed - indexed for MEDLINE]
1: Bol Asoc Med P R 1990 Dec;82(12):517-22 [Performance of athletes exercising in ozone polluted air]. [Article in Spanish] Morales Cardona T. Departamento de Farmacologia, Escuela de Medicina, San Juan, Puerto Rico. The literature on the performance of those exercising in air containing ozone was examined. The action of ozone is mediated by muscarinic receptors and others of unknown nature localized, apparently, over the respiratory epithelium of gaseous transport. Due to its action on those receptors the inspiratory phase of the pulmonary ventilation is reduced in an effect associated with pain and, simultaneously, the resistance to the pass of air is increased. If exercise increases ventilation to 90 or more liters per minute the effective dose of ozone increases potentiating its effect on the inspiration and the resistance. The potentiated reduction of the inspiratory phase and the associated pain (a) strongly antagonize the ventilatory effort of exercise and (b) reduced the capacity of response to the increase in resistance with augmented inspirations. In this way an important decrease in performance appears. Publication Types: Review Review, tutorial PMID: 2078253 [PubMed - indexed for MEDLINE]
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- Ozone 1: J Appl Physiol 1989 Oct;67(4):1535-41 Mechanism of action of ozone on the human lung. Hazucha MJ, Bates DV, Bromberg PA. Center for Environmental Medicine and Lung Biology, School of Medicine, University of North Carolina, Chapel Hill 27599-7310. Fourteen healthy normal volunteers were randomly exposed to air and 0.5 ppm of ozone (O3) in a controlled exposure chamber for a 2-h period during which 15 min of treadmill exercise sufficient to produce a ventilation of approximately 40 l/min was alternated with 15-min rest periods. Before testing an esophageal balloon was inserted, and lung volumes, flow rates, maximal inspiratory (at residual volume and functional residual capacity) and expiratory (at total lung capacity and functional residual capacity) mouth pressures, and pulmonary mechanics (static and dynamic compliance and airway resistance) were measured before and immediately after the exposure period. After the postexposure measurements had been completed, the subjects inhaled an aerosol of 20% lidocaine until response to citric acid aerosol inhalation was abolished. All of the measurements were immediately repeated. We found that the O3 exposure 1) induced a significant mean decrement of 17.8% in vital capacity (this change was the result of a marked fall in inspiratory capacity without significant increase in residual volume), 2) significantly increased mean airway resistance and specific airway resistance but did not change dynamic or static pulmonary compliance or viscous or elastic work, 3) significantly reduced maximal transpulmonary pressure (by 19%) but produced no changes in inspiratory or expiratory maximal mouth pressures, and 4) significantly increased respiratory rate (in 5 subjects by more than 6 breaths/min) and decreased tidal volume. (ABSTRACT TRUNCATED AT 250 WORDS) Publication Types: Clinical trial Randomized controlled trial PMID: 2793755 [PubMed - indexed for MEDLINE]
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| - Airports 1: Occup Environ Med 1999 Feb;56(2):118-23 Pulmonary function and respiratory symptoms in a population of airport workers. Tunnicliffe WS, O'Hickey SP, Fletcher TJ, Miles JF, Burge PS, Ayres JG. Heartlands Research Institute, Heartlands Hospital, Green East, Birmingham, UK. OBJECTIVES: To assess the prevalence of respiratory symptoms and to measure spirometry in a sample of employees of Birmingham International Airport, United Kingdom, to examine whether occupational exposure to aircraft fuel or jet stream exhaust might be associated with respiratory symptoms or abnormalities of lung function. METHODS: Cross sectional survey by questionnaire and on site measurement of lung function, skin prick tests, and exhaled carbon monoxide concentrations. Occupational exposure was assigned by job title, between group comparison were made by logistic regression analysis. RESULTS: 222/680 full time employees were studied (mean age 38.6 y, 63% male, 28% current smokers, 6% self reported asthma, 19% self reported hay fever). Upper and lower respiratory tract symptoms were common and 51% had one or more positive skin tests. There were no significant differences in lung function tests between exposure groups. Between group comparisons of respiratory symptoms were restricted to male members of the medium and high exposure groups. The adjusted odds ratio (OR) for cough with phlegm and runny nose were found to be significantly associated with high exposure (OR 3.5, 95% confidence interval (95% CI) 1.23 to 9.74 and 2.9, 1.32 to 6.40 respectively) when the measured confounding effects of age and smoking, and in the case of runny nose, self reported hay fever had been taken into account. There was no obvious association between high exposure and the presence of shortness of breath or wheeze, or for the symptoms of watering eyes or stuffy nose. CONCLUSIONS: These findings support an association in male airport workers, between high occupational exposures to aviation fuel or jet stream exhaust and excess upper and lower respiratory tract symptoms, in keeping with a respiratory irritant. It is more likely that these effects reflect exposure to exhaust rather than fuel, although the effects of an unmeasured agent cannot be discounted. PMID: 10448317 [PubMed - indexed for MEDLINE]
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