Association of heart rate variability with occupational and environmental exposure to particulate air pollution

Citation
Sr. Magari et al., Association of heart rate variability with occupational and environmental exposure to particulate air pollution, CIRCULATION, 104(9), 2001, pp. 986-991
Citations number
15
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
0009-7322 → ACNP
Volume
104
Issue
9
Year of publication
2001
Pages
986 - 991
Database
ISI
SICI code
0009-7322(20010828)104:9<986:AOHRVW>2.0.ZU;2-F
Abstract
Background-Airborne particulate matter has been linked to excess morbidity and mortality. Recent attention has focused on the effects of particulate e xposure on cardiac autonomic control. Inhaled particulates may affect the a utonomic nervous system either directly, by eliciting a sympathetic stress response, or indirectly, through inflammatory cytokines produced in the lun gs and released into the, circulation. Methods and Results-This longitudinal study examined the association of par ticulates less than or equal to2.5 mum in diameter (PM2.5) with heart rate variability (HRV) in an occupational cohort (N = 40). Continuous monitoring of exposure and HR was performed during and away from work. PM2.5 levels w ere higher than ambient levels typically reported in Boston, 0.167 +/- 3.20 5 mg/m(3) (geometric mean geometric SD). We found a 2.66% decrease (95% CI, -3.75% to -1.58%) in the 5-minute SD of normal RR intervals (SDNN) for eve ry 1 mg/m(3) increase in the 4-hour moving PM2.5 average and a 1.02% increa se (95% CI, 0.59% to 1.46%) in HR after adjusting for potential confounding factors. The decrease in SDNN became larger as the averaging interval incr eased. Conclusions-Workers experienced altered cardiac autonomic control after exp osure to occupational and environmental PM2.5. There appears to be either a long-acting (several hours) and a short-acting (several minutes) component to the mechanism of action that may be related to the production of cytoki nes and the sympathetic stress response, respectively, or a cumulative effe ct that begins shortly after exposure begins. The clinical significance of these effects in a healthy working population is unclear.