The association of particulate air metal concentrations with heart rate variability.

Numerous studies show an association between particulate air pollution and adverse health effects. Particulate matter is a complex mixture of elemental carbon, ammonium, sulfates, nitrates, organic components, and metals. The mechanisms of action of particulate matter less than or equal to 2.5 micro m in mean aerodynamic diameter (PM(2.5)), as well as the constituents responsible for the observed cardiopulmonary health effects, have not been identified. In this study we focused on the association between the metallic component of PM(2.5) and cardiac autonomic function based on standard heart rate variability (HRV) measures in an epidemiologic study of boilermakers. Thirty-nine male boilermakers were monitored throughout a work shift. Each subject wore an ambulatory electrocardiogram (Holter) monitor and a personal monitor to measure PM(2.5). We used mixed-effects models to regress heart rate and SDNN index (standard deviation of the normal-to-normal) on PM(2.5) and six metals (vanadium, nickel, chromium, lead, copper, and manganese). There were statistically significant mean increases in the SDNN index of 11.30 msec and 3.98 msec for every 1 micro g/m(3) increase in the lead and vanadium concentrations, respectively, after adjusting for mean heart rate, age, and smoking status. Small changes in mean heart rate were seen with all exposure metrics. The results of this study suggest an association between exposure to airborne metals and significant alterations in cardiac autonomic function. These results extend our understanding of the adverse health effects of the metals component of ambient PM(2.5).

[1]  Frank E. Huggins,et al.  Characterization of Fine Particulate Matter Produced by Combustion of Residual Fuel Oil , 2000, Journal of the Air & Waste Management Association.

[2]  R. Devlin,et al.  Air pollution particles induce IL-6 gene expression in human airway epithelial cells via NF-kappaB activation. , 1998, American journal of respiratory cell and molecular biology.

[3]  U. Epa Air Quality Criteria for Particulate Matter , 1996 .

[4]  U. Kodavanti,et al.  Soluble transition metals mediate the acute pulmonary injury and airway hyperreactivity induced by residual oil fly ash particles. , 1996, Chest.

[5]  D. Costa,et al.  Bioavailable transition metals in particulate matter mediate cardiopulmonary injury in healthy and compromised animal models. , 1997, Environmental health perspectives.

[6]  J. Sarnat,et al.  Fine particulate air pollution and mortality in 20 U.S. cities. , 2001, The New England journal of medicine.

[7]  Ronald W. Williams,et al.  Daily variation of particulate air pollution and poor cardiac autonomic control in the elderly. , 1999, Environmental health perspectives.

[8]  C. A. Pope,et al.  Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk? , 2000 .

[9]  J Schwartz,et al.  Ambient pollution and heart rate variability. , 2000, Circulation.

[10]  A. Maseri,et al.  Additional predictive value of heart rate variability in high-risk patients surviving an acute myocardial infarction. , 1999, Cardiologia.

[11]  J Schwartz,et al.  Increased mortality in Philadelphia associated with daily air pollution concentrations. , 1992, The American review of respiratory disease.

[12]  D Kromhout,et al.  Heart rate variability from short electrocardiographic recordings predicts mortality from all causes in middle-aged and elderly men. The Zutphen Study. , 1997, American journal of epidemiology.

[13]  J. Bigger,et al.  Baroreflex sensitivity and heart-rate variability in prediction of total cardiac mortality after myocardial infarction , 1998, The Lancet.

[14]  J. Carter,et al.  Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent. , 1997, Toxicology and applied pharmacology.

[15]  J. Schwartz,et al.  Air Pollution and Hospital Admissions for Cardiovascular Disease in Tucson , 1997, Epidemiology.

[16]  C. Angle,et al.  Autonomic function in manganese alloy workers. , 1998, Environmental research.

[17]  K. Murata,et al.  Assessment of central, peripheral, and autonomic nervous system functions in lead workers: neuroelectrophysiological studies. , 1993, Environmental research.

[18]  C. Monn,et al.  Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air. , 1999, Toxicology and applied pharmacology.

[19]  C. Pope,et al.  Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk? , 2000, Environmental health perspectives.

[20]  D. Costa,et al.  Metal and sulfate composition of residual oil fly ash determines airway hyperreactivity and lung injury in rats. , 1997, Environmental research.

[21]  K. Murata,et al.  Autonomic nervous system dysfunction in workers exposed to lead, zinc, and copper in relation to peripheral nerve conduction: a study of R-R interval variability. , 1991, American journal of industrial medicine.

[22]  Thomas J. Smith,et al.  Association of Heart Rate Variability With Occupational and Environmental Exposure to Particulate Air Pollution , 2001, Circulation.

[23]  J. Schwartz,et al.  Association of fine particulate matter from different sources with daily mortality in six U.S. cities. , 2000, Environmental health perspectives.

[24]  J. Schwartz,et al.  Heart rate variability associated with particulate air pollution. , 1999, American heart journal.

[25]  D. Loring,et al.  Manual for the geochemical analyses of marine sediments and suspended particulate matter , 1992 .

[26]  F. Dominici,et al.  Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994. , 2000, The New England journal of medicine.

[27]  H Kasanuki,et al.  Idiopathic ventricular fibrillation induced with vagal activity in patients without obvious heart disease. , 1997, Circulation.

[28]  J. Paulauskis,et al.  Mediating phosphorylation events in the vanadium-induced respiratory burst of alveolar macrophages. , 1999, Toxicology and applied pharmacology.

[29]  J M Wolfson,et al.  Mechanisms of morbidity and mortality from exposure to ambient air particles. , 2000, Research report.