Ultrafine Particle Deposition in Humans During Rest and Exercise

Daigle, Christopher C.; Chalupa, David; Gibb, F.R.; Morrow, Paul E.; Oberdörster, Günter; Utell, Mark J.; Frampton, Mark W.

doi:10.1080/08958370304468

Cited by 427 publications

(249 citation statements)

References 20 publications

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“…The ultrafine particles had a predicted deposition fraction of 0.39 and the fine particles had a predicted deposition fraction of 0.47. Our ultrafine particle deposition fraction results were considerably higher than the predicted values (0.75 actual vs. 0.39 predicted), as we have seen to a lesser extent in our previous studies (25). Our fine particle number deposition fraction agreed better with the model (actual 0.34 vs. predicted 0.47), but the mass deposition fraction was undetermined in the study.…”

Section: Discussionsupporting

confidence: 55%

“…In a further study of breathing 25 g/m 3 ultrafine carbon particles during exercise, exposure was associated with reduced blood monocyte expression of intercellular adhesion molecule-1 in a concentration-related manner, evidence for transient reductions in parasympathetic influence on heart rate variability, a reduction in repolarization (QT) interval, and a small reduction in blood monocytes and activation of T lymphocytes in healthy women (25)(26)(27). However, no change in induced sputum cells was seen at 25 or 50 g/m 3 of ultrafine carbon particles (33).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Comparing Inhaled Ultrafine versus Fine Zinc Oxide Particles in Healthy Adults

Beckett

Chalupa

Pauly-Brown

et al. 2005

Am J Respir Crit Care Med

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149

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Rationale: Zinc oxide is a common, biologically active constituent of particulate air pollution as well as a workplace toxin. Ultrafine particles (Ͻ 0.1 m diameter) are believed to be more potent than an equal mass of inhaled accumulation mode particles (0.1-1.0 m diameter). Objectives: We compared exposure-response relationships for respiratory, hematologic, and cardiovascular endpoints between ultrafine and accumulation mode zinc oxide particles. Methods: In a human inhalation study, 12 healthy adults inhaled 500 g/m 3 of ultrafine zinc oxide, the same mass of fine zinc oxide, and filtered air while at rest for 2 hours. Measurements and Main Results: Preexposure and follow-up studies of symptoms, leukocyte surface markers, hemostasis, and cardiac electrophysiology were conducted to 24 hours post-exposure. Induced sputum was sampled 24 hours after exposure. No differences were detected between any of the three exposure conditions at this level of exposure. Conclusions: Freshly generated zinc oxide in the fine or ultrafine fractions inhaled by healthy subjects at rest at a concentration of 500 g/m 3 for 2 hours is below the threshold for acute systemic effects as detected by these endpoints.Keywords: air pollution; metal fume fever; particulate matter, ultrafine; zinc Ambient air pollution particles occur in three major size distributions. Common combustion processes generate some primary ultrafine particles (Ͻ 0.1 m diameter), which can rapidly coalesce into larger accumulation mode particles (0.1-1.0 m diameter). The third fraction is the coarse mode particles, from 1 to 100 m in diameter, which are often generated by mechanical breakdown of the earth's crustal minerals. A given mass of ultrafine particles has a markedly higher ratio of total surface area to weight than does the same mass of accumulation mode particles. In experimental animals, inhaled ultrafine particles exhibit greater lung inflammatory and systemic activity than an equal mass of larger particles, and these particles may also have greater effects in adult human subjects (1-3). With ambient particle air pollution exposure, certain respiratory effects have been more closely associated with the number of ultrafine particles than with the total mass of particle exposure (4).Zinc is a common element in the earth's crust and an essential mineral in human nutrition. Zinc oxide may be found in ambient air particles from combustion sources (5-7), and it is generated in high concentrations in industrial processes, such as brass founding and welding or cutting galvanized sheet metal. Actual exposures of welders and others depend on the conditions in the workplace, but the permissible exposure limit for occupational exposure to zinc oxide in the United States is 5.0 mg/m 3 respirable dust. Zinc is one of several transition metals that have been proposed to contribute to the biological activity of ambient combustion particles. Freshly generated zinc oxide causes a selflimited, febrile, and inflammatory response known as metal fume fever, subtle findings ...

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Comparing Inhaled Ultrafine versus Fine Zinc Oxide Particles in Healthy Adults

Beckett

Chalupa

Pauly-Brown

et al. 2005

Am J Respir Crit Care Med

Self Cite

149

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“…Increased pulmonary ventilation with physical activity leads to increased inhalation of air and therefore greater inhaled concentration (and potential dose) of TRAP (18). However, despite this possible increased dose, our findings suggest that physical activity may also offset the impact of TRAP on parasympathetic modulation of the heart at higher exposure levels.…”

Section: Discussionmentioning

confidence: 63%

Impact of traffic-related air pollution on acute changes in cardiac autonomic modulation during rest and physical activity: a cross-over study

Cole‐Hunter

Weichenthal

Kubesch

et al. 2015

J Expo Sci Environ Epidemiol

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People are often exposed to traffic-related air pollution (TRAP) during physical activity but it is not clear if physical activity modifies the impact of TRAP on cardiac autonomic modulation. We conducted a panel study among 28 healthy adults in Barcelona, Spain to examine how physical activity may modify the impact of TRAP on cardiac autonomic regulation. Participants completed four two-hour exposure scenarios that included either rest or intermittent exercise in high and low-traffic environments. Time-and frequencydomain measures of heart rate variability (HRV) were monitored during each exposure period along with continuous measures of TRAP. Linear mixed-effects models were used to estimate the impact of TRAP on HRV as well as potential effect modification by physical activity. Exposure to TRAP was associated with consistent decreases in HRV; however, exposure-response relationships were not always linear over the broad range of exposures. For example, each 10 µg/m 3 increase in black carbon was associated with a 23% (95% CI: -31, -13) decrease in high frequency power at the low-traffic site whereas no association was observed at the high-traffic site. Physical activity modified the impact of TRAP on HRV at the high-traffic site and tended to weaken inverse associations with measures reflecting parasympathetic modulation (p≤0.001). Evidence of effect modification at the low-traffic site was less consistent. The strength and direction of the relationship between TRAP and HRV may vary across exposure gradients. Physical activity may modify the impact of TRAP on HRV, particularly at higher concentrations.3

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“…Despite overall similar average concentrations, it is possible that the PM characteristics may differ between the bedroom and living areas. Furthermore, the main living area may represent the location where subjects are awake and active, therefore having higher minute ventilation and increased particle deposition (32), and subsequently increased susceptibility to adverse effects of pollutant exposure. We found no link between pollutant concentrations and changes in lung function, similar to results of previous studies showing no clear association between indoor PM and lung function in few patients with COPD (27,28).…”

Section: Discussionmentioning

confidence: 99%

In-Home Air Pollution Is Linked to Respiratory Morbidity in Former Smokers with Chronic Obstructive Pulmonary Disease

Hansel¹,

McCormack²,

Belli³

et al. 2013

Am J Respir Crit Care Med

100

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Rationale: The effect of indoor air pollutants on respiratory morbidity among patients with chronic obstructive pulmonary disease (COPD) in developed countries is uncertain. Objectives: The first longitudinal study to investigate the independent effects of indoor particulate matter (PM) and nitrogen dioxide (NO 2 ) concentrations on COPD morbidity in a periurban community. Methods: Former smokers with COPD were recruited and indoor air was monitored over a 1-week period in the participant's bedroom and main living area at baseline, 3 months, and 6 months. At each visit, participants completed spirometry and questionnaires assessing respiratory symptoms. Exacerbations were assessed by questionnaires administered at clinic visits and monthly telephone calls. Measurements and Main Results: Participants (n ¼ 84) had moderate or severe COPD with a mean FEV 1 of 48.6% predicted. The mean (6 SD) indoor PM 2.5 and NO 2 concentrations were 11.4 6 13.3 µg/m 3 and 10.8 6 10.6 ppb in the bedroom, and 12.2 6 12.2 µg/m 3 and 12.2 6 11.8 ppb in the main living area. Increases in PM 2.5 concentrations in the main living area were associated with increases in respiratory symptoms, rescue medication use, and risk of severe COPD exacerbations. Increases in NO 2 concentrations in the main living area were independently associated with worse dyspnea. Increases in bedroom NO 2 concentrations were associated with increases in nocturnal symptoms and risk of severe COPD exacerbations. Conclusions: Indoor pollutant exposure, including PM 2.5 and NO 2 , was associated with increased respiratory symptoms and risk of COPD exacerbation. Future investigations should include intervention studies that optimize indoor air quality as a novel therapeutic approach to improving COPD health outcomes.Keywords: indoor air; chronic obstructive pulmonary disease; particulate matter; nitrogen dioxide; exacerbations Chronic obstructive pulmonary disease (COPD), the third leading cause of death in the United States and the fifth leading cause worldwide, is expected to become increasingly prevalent in upcoming decades (1, 2). Most COPD is caused by environmental exposures; in developed countries, this exposure is primarily cigarette smoke. After COPD begins, evidence indicates that it can be worsened by other environmental exposures. For example, outdoor particulate matter (PM) concentrations have been associated with an increase in COPD hospitalizations and mortality (3, 4). Similarly, outdoor nitrogen dioxide (NO 2 ) exposure has been linked to worse COPD morbidity, including higher rates of exacerbations (4-6).Although substantial evidence shows that outdoor air pollutants impact COPD, there is much less evidence for the impact of indoor air on COPD, especially in developed countries. Although the Global Initiative for Chronic Obstructive Lung Disease guidelines identify indoor air pollution resulting from burning wood and other biomass fuels as a major risk factor for COPD (7), exposures under these conditions are two to three orders of magnitude higher ...

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Ultrafine Particle Deposition in Humans During Rest and Exercise

Cited by 427 publications

References 20 publications

Comparing Inhaled Ultrafine versus Fine Zinc Oxide Particles in Healthy Adults

Comparing Inhaled Ultrafine versus Fine Zinc Oxide Particles in Healthy Adults

Impact of traffic-related air pollution on acute changes in cardiac autonomic modulation during rest and physical activity: a cross-over study

In-Home Air Pollution Is Linked to Respiratory Morbidity in Former Smokers with Chronic Obstructive Pulmonary Disease

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