Heart rate variability associated with particulate air pollution

Pope, C. Arden; Verrier, Richard L.; Lovett, Eric G.; Larson, Andrew C.; Raizenne, Mark; Kanner, Richard E.; Schwartz, Joel; Villegas, G. Martin; Gold, Diane R.; Dockery, Douglas W.

doi:10.1016/s0002-8703(99)70014-1

Cited by 527 publications

(350 citation statements)

References 27 publications

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“…These studies have found that the elderly with or without cardiovascular conditions, hypertension or diabetes may be more responsive to airborne particle exposure and have a larger reduction of the HRV in relation to an increase in PM 2.5 ambient concentrations (Liao et al, 1999;Pope et al, 1999Pope et al, , 2004bGold et al, 2000;Holguı´n et al, 2003). Our findings are consistent with those even though we studied young healthy adults; as expected, the magnitude of association was larger in those studies where susceptible individuals were included than in ours.…”

Section: Discussionsupporting

confidence: 92%

“…Some studies have used time domain indexes with 24 h ambulatory ECG. One included seven participants and involved monitoring only PM 10 (Pope et al, 1999). Another study estimated the effect of average levels of PM 2.5 and ozone over the previous 4 h on SDNN and rMSSD (Gold et al, 2000), and a study in Utah that included 88 participants examined PM's influence on cardiac autonomic function as measured by HRV (SDNN and rMSSD) and blood markers of inflammation (Pope et al, 2004 b).…”

Section: Discussionmentioning

confidence: 99%

“…These researches in susceptible groups have helped to explain the short-term effects of PM 2.5 air pollution and possible mechanisms of mortality displacement after pollution episodes as the 1952 ''4 days fog'' event in London with an increase in morbidity and mortality related to respiratory or cardiovascular disease (Logan et al, 1953;Bell and Davis, 2001). The possible mechanisms for the acute cardiovascular effects may include endothelial cell, platelet and leukocyte activation as part of inflammatory response, along with increased blood viscosity (Pope et al, 1999(Pope et al, , 2004a and physiological changes such as acute arterial constriction responses (Brook et al, 2002) that may trigger acute cardiovascular events.…”

Section: Discussionmentioning

confidence: 99%

“…Most air pollution research has measured the exposure with fix monitors, in some cases data were taken from the environmental monitor network, which is known to be a good estimate but may be altered by weather conditions such as wind, rain or RH (Pope et al, 1999, Gold et al, 2000, Park et al, 2005. Other studies have used fixed indoor monitors (Liao et al, 1999;Holguı´n et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

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Ambient fine particles modify heart rate variability in young healthy adults

Vallejo

Ruiz

Hermosillo

et al. 2005

J Expo Sci Environ Epidemiol

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Particulate air pollution has been related with cardiopulmonary morbidity and mortality. Recent studies have shown that an increase in particulate matter (PM) 2.5 ambient concentrations was associated with a decrease in heart rate variability (HRV) in the elderly with cardiovascular conditions, which could increase the risk of death. In order to assess if this association could also be observed in young adults, we studied 40 young healthy residents of the Mexico City Metropolitan Area (MCMA) who underwent 13 h Holter electrocardiographic and PM 2.5 personal monitoring. HRV was evaluated in time domain: the standard deviation of normal RR intervals (SDNN) and the percentage of differences between adjacent normal RR intervals larger than 50 ms (pNN50). In multivariate analysis with mixed effects models, a significant negative association of pNN50 with PM 2.5 accumulative exposure was found. An increase in 30 mg/m 3 of the average PM 2.5 personal exposure in the previous 2 h decreased the pNN50 in 0.08% (P ¼ 0.01). This observation revealed an acute effect related to environmental exposure to PM 2.5 with regard to HRV in normal youngsters. The long-term health consequences of this association in young healthy adults remain to be clarified.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Ambient fine particles modify heart rate variability in young healthy adults

Vallejo

Ruiz

Hermosillo

et al. 2005

J Expo Sci Environ Epidemiol

View full text Add to dashboard Cite

show abstract

“…Epidemiological studies indicate that peaks of ambient particulate air pollution are associated with an increase in pulmonary and cardiovascular morbidity and mortality (Samet et al, 2000). In fact, more people seem to die from cardiovascular than from pulmonary diseases during episodes of urban air pollution (Pope et al, 1999). In addition, the short-term effects of exposure to these particles have been recently described and include an increased susceptibility to ischemia (Pekkanen et al, 2002) and the occurrence of myocardial infarction (Peters et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Translocation Pathway of the Intratracheally Instilled Ultrafine Particles from the Lung into the Blood Circulation in the Mouse

et al. 2006

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Recently, it has been demonstrated that ultrafine particles (UFPs) are able to translocate from the lung into the systemic circulation. Precise mechanisms of the anatomical translocation (crossing the air-blood barrier) of inhaled UFPs at the alveolar wall are not fully understood. In this study, we examined the translocation pathway of the intratracheally instilled ultrafine carbon black (UFCB) from the lung into the blood circulation in mouse. Electron microscopy demonstrated accumulation of intratracheally instilled UFCB in the large-sized gaps developing between the cytoplasmic processes of the alveolar epithelial cells, possibly as a result of shrinkage of cytoplasm, by receiving stimulus/signals generated and released following UFCB attachment on the alveolar epithelial cells. Occasional penetration of the accumulated UFCB into the alveolar basement membrane, exposing to the air space, was observed at the gap. These results suggest that inhaled UFPs may, in part, pass the air-blood barrier through the large-sized gap formed between the alveolar epithelial cells.

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