Abstract:In spite of epidemiological evidence concerning vehicular air pollution and adverse respiratory/cardiovascular health, many athletic fields and school playgrounds are adjacent to high traffic roadways and could present long-term health risks for exercising children and young adults. Particulate matter (PM 1 ,0.02-1.0 µm diameter) number counts were taken serially at four elementary school athletic/playground fields and at one university soccer field. Elementary school PM 1 measurements were taken over 17 days;… Show more
“…Alternatively, particles in the Brook et al (2002) study were concentrated PM 2.5 , while the particles in our study were freshly generated particles from auto/truck emissions with a predominant size range in the ultrafine and nano fraction. We have recently measured the rate of particle decay with distance from a major highway (Rundell et al, 2006). We cannot rule out the influence of ozone, as ozone exposure has been shown to increase rate-pressure product and heart rate after inhalation (Gong et al, 1998).…”
Section: Discussionmentioning
confidence: 99%
“…Most studies documenting adverse health effects in relation to outdoor air pollutants have relied on measured concentrations from central monitoring stations, metrics of proximity to roads, or traffic volume estimates (Rundell et al, 2006;Zhu et al, 2002). Recent investigations support the notion that PM toxicity is highly influenced by number concentration and/or particle surface area (Oberdorster, 1996), and ambient particulate matter with median aerodynamic diameter less than 2.5 μm (PM 2.5 ) has been associated with cardiovascular events (Burnett et al, 1995;Peters et al, 2001;Ware, 2000).…”
This study investigated the effects of particulate matter (PM) with aerodynamic diameter 0.02-1 μm (noted as PM 1 ) inhalation during exercise on conduit artery and microvascular function. Inhalation of internal combustion-derived PM is associated with cardiovascular mortality and morbidity. Direct action of PM on the vascular endothelium is likely, as a substantial fraction of ultrafine PM translocates from the alveoli to the circulatory system. Sixteen intercollegiate athletes performed 30 min of exercise while inhaling low or high PM 1 . Flow-mediated brachial artery dilation (FMD) using high-resolution ultrasonography with simultaneous measurements of forearm oxygen kinetics using near infrared spectrophotometry (NIRS) was done before and after exercise. Basal brachial artery vasoconstriction was found after high PM 1 exercise (4.0%, 4.66 ± 0.609 to 4.47 ± 0.625 mm diameter; p = .0002), but not after low PM 1 exercise (−0.3%, 4.66 ± 0.626 to 4.68 ± 0.613 mm diameter). FMD was impaired after high PM 1 exercise (6.8 ± 3.58% for preexercise FMD and 0.30 ± 2.74% for postexercise FMD, p = .0001), but not after low PM 1 exercise (6.6 ± 4.04% for preexercise FMD and 4.89 ± 4.42% for postexercise FMD). Reduction in forearm muscle reperfusion estimated by reoxygenation slope-to-baseline after 4 min cuff ischemia was observed for high PM 1 exercise (55% vs. 3%, p = .0006); no difference was noted for low PM 1 exercise. Brachial artery FMD was significantly correlated to muscle reoxygenation slope-to-baseline (r = .50, p = .005). Acute inhalation of high [PM 1 ] typical of urban environments impairs both systemic conduit artery function and microcirculation. The observed decrease reoxygenation slope-to-baseline after cuff release is consistent with reduced blood flow in the muscle microvasculature.
“…Alternatively, particles in the Brook et al (2002) study were concentrated PM 2.5 , while the particles in our study were freshly generated particles from auto/truck emissions with a predominant size range in the ultrafine and nano fraction. We have recently measured the rate of particle decay with distance from a major highway (Rundell et al, 2006). We cannot rule out the influence of ozone, as ozone exposure has been shown to increase rate-pressure product and heart rate after inhalation (Gong et al, 1998).…”
Section: Discussionmentioning
confidence: 99%
“…Most studies documenting adverse health effects in relation to outdoor air pollutants have relied on measured concentrations from central monitoring stations, metrics of proximity to roads, or traffic volume estimates (Rundell et al, 2006;Zhu et al, 2002). Recent investigations support the notion that PM toxicity is highly influenced by number concentration and/or particle surface area (Oberdorster, 1996), and ambient particulate matter with median aerodynamic diameter less than 2.5 μm (PM 2.5 ) has been associated with cardiovascular events (Burnett et al, 1995;Peters et al, 2001;Ware, 2000).…”
This study investigated the effects of particulate matter (PM) with aerodynamic diameter 0.02-1 μm (noted as PM 1 ) inhalation during exercise on conduit artery and microvascular function. Inhalation of internal combustion-derived PM is associated with cardiovascular mortality and morbidity. Direct action of PM on the vascular endothelium is likely, as a substantial fraction of ultrafine PM translocates from the alveoli to the circulatory system. Sixteen intercollegiate athletes performed 30 min of exercise while inhaling low or high PM 1 . Flow-mediated brachial artery dilation (FMD) using high-resolution ultrasonography with simultaneous measurements of forearm oxygen kinetics using near infrared spectrophotometry (NIRS) was done before and after exercise. Basal brachial artery vasoconstriction was found after high PM 1 exercise (4.0%, 4.66 ± 0.609 to 4.47 ± 0.625 mm diameter; p = .0002), but not after low PM 1 exercise (−0.3%, 4.66 ± 0.626 to 4.68 ± 0.613 mm diameter). FMD was impaired after high PM 1 exercise (6.8 ± 3.58% for preexercise FMD and 0.30 ± 2.74% for postexercise FMD, p = .0001), but not after low PM 1 exercise (6.6 ± 4.04% for preexercise FMD and 4.89 ± 4.42% for postexercise FMD). Reduction in forearm muscle reperfusion estimated by reoxygenation slope-to-baseline after 4 min cuff ischemia was observed for high PM 1 exercise (55% vs. 3%, p = .0006); no difference was noted for low PM 1 exercise. Brachial artery FMD was significantly correlated to muscle reoxygenation slope-to-baseline (r = .50, p = .005). Acute inhalation of high [PM 1 ] typical of urban environments impairs both systemic conduit artery function and microcirculation. The observed decrease reoxygenation slope-to-baseline after cuff release is consistent with reduced blood flow in the muscle microvasculature.
“…They are often acutely exposed to exhaust from combustion engines during exercising or commuting and this may therefore represent an important fraction of their daily exposure to outdoor particulate pollution. The total number of particles deposited in the lungs increases in proportion to minute ventilation and the deposition fraction nearly doubles from rest to intense exercise [Rundell et al, 2006;Daigle et al, 2003]. In New York City runners, after 30 min of exercise near busy roadways, an acute rise in blood carboxyhaemoglobin from 1.7% to 5.1% occurred, a concentration similar to those found in regular cigarette smokers [Nicholson, 1983].…”
Section: Short-term Exposure To Air Pollutants Effects On the Cardiovmentioning
“…Other environmental triggers include chlorine in swimming pools [13,14] chemicals from resurfacing ice hockey rinks [15], and in urban areas from automobile exhaust [16]. EIB may be underestimated as athletes have been shown to be poor perceivers of bronchospasm [17,18] and lack awareness of symptoms [19,20].…”
Breathing concerns in athletes are common and can be due to a wide variety of pathology. The most common etiologies are exercise-induced bronchoconstriction (EIB) and paradoxic vocal fold movement disorder (PVFMD). Although some patients may have both, PVFMD is often misdiagnosed as EIB, which can lead to unnecessary treatment. The history and physical exam are important to rule out life threatening pulmonary and cardiac causes as well as common conditions such as gastroesophageal reflux disease, sinusitis, and allergic etiologies. The history and physical exam have been shown to be not as vital in diagnosing EIB and PVFMD. Improvement in diagnostic testing with office base spirometry, bronchoprovocation testing, eucapnic voluntary hyperpnea (EVH) and video laryngoscopy are essential in properly diagnosing these conditions. Accurate diagnosis leads to proper management, which is essential to avoid unnecessary testing and save healthcare costs. Also important to the physician treating dyspnea in athletes is knowing regulations on medications, drug testing, and proper documentation needed for certain organizations. The differential diagnosis of dyspnea is broad and is not limited to EIB and PVFMD. Ruling out life threatening cardiac and pulmonary causes with a proper history, physical, and appropriate testing is essential. The purpose of this review is to highlight recent literature on the diagnosis and management of EIB and PVFMD as well as discuss other potential causes for dyspnea in the athlete.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.