Association of Heart Rate Variability With Occupational and Environmental Exposure to Particulate Air Pollution

Abstract

Background-Airborne particulate matter has been linked to excess morbidity and mortality. Recent attention has focused on the effects of particulate exposure on cardiac autonomic control. Inhaled particulates may affect the autonomic nervous system either directly, by eliciting a sympathetic stress response, or indirectly, through inflammatory cytokines produced in the lungs and released into the circulation. Methods and Results-This longitudinal study examined the association of particulates Յ2.5 m in diameter (PM 2.5 ) with heart rate variability (HRV) in an occupational cohort (Nϭ40). Continuous monitoring of exposure and HR was performed during and away from work. PM 2.5 levels were higher than ambient levels typically reported in Boston, 0.167Ϯ3.205 mg/m 3 (geometric meanϮgeometric SD). We found a 2.66% decrease (95% CI, Ϫ3.75% to Ϫ1.58%) in the 5-minute SD of normal RR intervals (SDNN) for every 1 mg/m 3 increase in the 4-hour moving PM 2.5 average and a 1.02% increase (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 increased. Conclusions-Workers experienced altered cardiac autonomic control after exposure to occupational and environmental PM 2.5 . 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 cytokines and the sympathetic stress response, respectively, or a cumulative effect that begins shortly after exposure begins. The clinical significance of these effects in a healthy working population is unclear.

Cardiovascular changes in workers exposed to fine particulate dust

“…In their previous study concerning 40 boilermakers, Magari et al have found, that the increase in occupational air pollution correlated with the decrease in SDANN [49].…”

Air Pollution Exposure and Osteoporosis among Retired Workers with Chronic Obstructive Pulmonary Disease

“…The possibility of this finding was that it was caused by the different spatial representativeness of air monitoring stations for NO 2 and other air pollutants [23]. We correlated yearly concentrations of PM10, NO 2 , O 3 , SO 2 and CO measured at one air monitoring station with those measured at 9 air monitoring stations and found that NO2 had the highest correlation coefficients (r=0.87) compared to PM10 (r=0.57), O 3 (r=0.72), SO 2 , (r=0.42) and CO (0.55).…”

“…We correlated yearly concentrations of PM10, NO 2 , O 3 , SO 2 and CO measured at one air monitoring station with those measured at 9 air monitoring stations and found that NO2 had the highest correlation coefficients (r=0.87) compared to PM10 (r=0.57), O 3 (r=0.72), SO 2 , (r=0.42) and CO (0.55). It is possible that PM10, O 3 , SO 2 and CO measured at the air monitoring station may not properly represent participants' long-term air pollution exposures. The association of incident osteoporosis with PM10, O 3 , SO 2 and CO may be biased towards the null due to misclassification [24].…”

“…Occupational and environmental exposure to air pollution has been documented as a risk factor for cardiopulmonary effects [1,2]. The presence of preexisting chronic respiratory diseases may also increase cardiopulmonary mortality risk [3].…”

Tracheal instillation of urban PM2.5 suspension promotes acute cardiac polarization changes in rats

“…Epidemiologic studies have also demonstrated a consistent link between sudden cardiac death and particulate air pollution (16), with changes such as increased QRS duration and arrhythmias (17), alteration of heart rate variability (HRV) (18,19) and repolarization abnormalities (20)(21)(22)(23) increasing morbidity and mortality. Previous epidemiological studies have shown that daily variations in particulate air pollution induced a decrease of HRV (24,25) and an increase of arrhythmias (26). Studies focusing on the onset of myocardial infarction in patients exposed to traffic in their routine activities indicated that the most critical time window is within one hour of the onset of clinical manifestations (27).…”