PMID- 15923244
OWN - NLM
STAT- MEDLINE
DCOM- 20050627
LR  - 20181113
IS  - 0040-6376 (Print)
IS  - 1468-3296 (Electronic)
IS  - 0040-6376 (Linking)
VI  - 60
IP  - 6
DP  - 2005 Jun
TI  - Traffic related pollution and heart rate variability in a panel of elderly 
      subjects.
PG  - 455-61
AB  - BACKGROUND: Particulate air pollution has been associated with increased 
      cardiovascular deaths and hospital admissions. To help understand the mechanisms, 
      the types of particles most involved, and the types of persons most susceptible, 
      the association between exposure to summertime air pollution and heart rate 
      variability (HRV) was examined in a panel study of 28 elderly subjects. METHODS: 
      Subjects were seen once a week for up to 12 weeks and HRV (SDNN, r-MSSD, PNN50, 
      low frequency/high frequency ratio (LFHFR)) was measured for approximately 30 
      minutes at each session using a defined protocol. Temperature, day of the week, 
      and hour of the day were controlled, and dummy variables for each subject were 
      controlled for subject specific risk factors. RESULTS: PM2.5 was associated with 
      r-MSSD (-10.1% change for an interquartile range (IQR) increase in exposure (95% 
      CI -2.8 to -16.9)) and PNN50, but stronger associations were seen with black 
      carbon, an indicator of traffic particles, which was also associated with SDNN 
      (-4.6% per IQR (95% CI -2.0 to -7.2)) and LFHFR. Secondary particles were more 
      weakly associated with r-MSSD, as was ozone. No associations were seen with SO2 
      or NO2. CO had similar patterns of association to black carbon, which disappeared 
      after controlling for black carbon. Black carbon had a substantially higher 
      effect on SDNN in subjects who had had a previous myocardial infarction (-12.7%, 
      95% CI -5.7 to -19.25). CONCLUSIONS: Particles, especially from traffic, are 
      associated with disturbances of autonomic control of the heart.
FAU - Schwartz, J
AU  - Schwartz J
AD  - Department of Environmental Health, Environmental Epidemiology Program, Harvard 
      School of Public Health, 401 Park Drive,P O Box 15677, Landmark Center, Suite 
      415, Boston, MA 02215, USA. jschwrtz@hsph.harvard.edu
FAU - Litonjua, A
AU  - Litonjua A
FAU - Suh, H
AU  - Suh H
FAU - Verrier, M
AU  - Verrier M
FAU - Zanobetti, A
AU  - Zanobetti A
FAU - Syring, M
AU  - Syring M
FAU - Nearing, B
AU  - Nearing B
FAU - Verrier, R
AU  - Verrier R
FAU - Stone, P
AU  - Stone P
FAU - MacCallum, G
AU  - MacCallum G
FAU - Speizer, F E
AU  - Speizer FE
FAU - Gold, D R
AU  - Gold DR
LA  - eng
GR  - 5 P01 ES09825/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Thorax
JT  - Thorax
JID - 0417353
RN  - 0 (Vehicle Emissions)
RN  - 0UZA3422Q4 (Sulfur Dioxide)
RN  - 66H7ZZK23N (Ozone)
RN  - 7440-44-0 (Carbon)
RN  - 7U1EE4V452 (Carbon Monoxide)
RN  - S7G510RUBH (Nitrogen Dioxide)
SB  - IM
CIN - Thorax. 2005 Jun;60(6):441-2. PMID: 15923240
MH  - Aged
MH  - Aged, 80 and over
MH  - Arrhythmias, Cardiac/*chemically induced
MH  - Carbon/adverse effects/analysis
MH  - Carbon Monoxide/analysis/toxicity
MH  - Electrocardiography, Ambulatory
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nitrogen Dioxide/analysis/toxicity
MH  - Ozone/analysis/toxicity
MH  - Sulfur Dioxide/analysis/toxicity
MH  - Vehicle Emissions/analysis/*toxicity
PMC - PMC1747419
EDAT- 2005/06/01 09:00
MHDA- 2005/06/28 09:00
PMCR- 2008/06/01
CRDT- 2005/06/01 09:00
PHST- 2005/06/01 09:00 [pubmed]
PHST- 2005/06/28 09:00 [medline]
PHST- 2005/06/01 09:00 [entrez]
PHST- 2008/06/01 00:00 [pmc-release]
AID - 60/6/455 [pii]
AID - 10.1136/thx.2004.024836 [doi]
PST - ppublish
SO  - Thorax. 2005 Jun;60(6):455-61. doi: 10.1136/thx.2004.024836.