ETS study confirms risks of low levels of particulate exposure to cardiovascular health

BrooklynDodger is not all that interested in environmental tobacco smoke as an environmental or occupational hazard, except as it informs understanding of particulate air pollution and industrially generated airborne particles in the workplace. Tobacco smoke is our best example of the high dose to low dose continuity of risk from direct smoking to ETS as a carcinogenic hazard. This paper demonstrates a mechanism for continuity in risk for cardiac effects. Decreased heart rate variability sounds like a good thing but is considered a bad thing, a risk for heart problems.

The abstract paraphrased: Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. ...ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers..Participants alternated 2 hr in nonsmoking and smoking areas. ... During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ... Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.

The RSP levels in µg/m3 were 24.74 in non smoking areas [the Dodger would not have permitted 4 significant figures if he were the reviewer or editor, nor allowed a table without a measure of variability, and would likely have insisted on a geometric mean and GSD] and 77.97 in the smoking area. The non-smoking area thus had exposures above the EPA annual averate permitted level for PM2.5; this high level would make it more difficult to see the effect if it were there.

Thus, cardiac effects of tobacco smoke may no longer be attributed solely to CO or nicotine.

EHP is available in full text via internet.

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Environ Health Perspect 109:711-716 (2001).

Acute Exposure to Environmental Tobacco Smoke and Heart Rate Variability

C. Arden Pope, III,1 Delbert J. Eatough,1 Diane R. Gold,2 Yanbo Pang,1 Karen R. Nielsen,3 Prema Nath,4 Richard L. Verrier,5 and Richard E. Kanner6

1Department of Chemistry & Biochemistry and Department of Economics, Brigham Young University, Provo, Utah; 2Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA; 3Cardiovascular Genetic Research Clinic, University of Utah School of Medicine, Salt Lake City, Utah, USA; 4University of Utah Hospital and Clinics, Salt Lake City, Utah, USA; 5Institute for Prevention of Cardiovascular Disease, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA; 6Division of Respiratory, Critical Care and Occupational Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA