The immediate effect within minutes to hours of personal exposure to ambient fine particulate matter (PM 2.5 ) on cardiac autonomic function is limited, particularly at night. Our study aimed to assess the lagged association between personal exposure to PM 2.5 and nocturnal heart rate variability. Repeated measures panel study among 21 community adults recruited from a local health clinic during the period of March 1, 2004, to August 31, 2004, in Boston, Massachusetts, in the United States. Ambulatory electrocardiogram and continuous monitoring of personal exposure to PM 2.5 and were measured for up to 2 consecutive days. We calculated 5-minute time-specific average PM 2.5 exposure for each participant. Mixed-effects models were fit for 5-minute SD of normal-to-normal intervals (SDNN) and 5-minute heart rate in relation to 5-minute PM 2.5 exposure lagged in 5-minute intervals up to 4 hours. We found an 8.4% decrease in nocturnal SDNN (95% confidence interval [CI] −11.3% to −5.5%) and a 1.9% increase in nighttime heart rate (95% CI 1.1% to 2.7%) for an interquartile range increase in PM 2.5 (13.6 μg/m 3 ), after adjusting for confounders. Significant decreases in nocturnal SDNN associated with PM 2.5 exposure occurred within 2.5 hours. The largest decrease in nocturnal SDNN of −12.8% (95% CI −16.4 to −9.1%) that was associated with PM 2.5 exposure was found with a lag of 25 minutes. Rapid changes in nocturnal heart rate variability associated with personal PM 2.5 exposure occurred within the previous 2.5 hours, with the largest effects at 25 minutes, suggesting immediate cardiac autonomic effects of fine particulate exposure.
In 2012, the US Environmental Protection Agency strengthened the annual National Ambient Air Quality Standard for ambient fine particulate matter of <2.5 μm in mean aerodynamic diameter (PM 2.5 ) to 12 μg per cubic meter (μg/m 3 ) from 15 μg/m 3 in 1997 to protect public health. A body of epidemiologic evidence has demonstrated the association between exposure to PM 2.5 and cardiovascular events including ischemic heart disease, myocardial infarction, stroke, arrhythmia, and heart failure exacerbation. Cardiac autonomic function, mainly indicated by heart rate variability (HRV), has been suggested as one of the hypothesized mechanisms linking PM exposure with adverse cardiac events. These epidemiologic studies showed heterogeneous time-lagged effects of PM 2.5 exposure on reduced HRV. However, to our knowledge, studies have not yet explored the very acute effects of personal PM 2.5 exposure within minutes to hours on HRV. To provide further insights into the time course of the very acute effects of PM 2.5 exposure on cardiac autonomic function, the present study was designed to investigate the association between personal exposure to PM 2.5 lagged in 5-minute intervals up to 4 hours, and nocturnal HRV in a community-based general adult population; as nocturnal HRV better captured cardiac autonomic effects of personal PM 2.5 exposure in occupationally exposed and general population adults.
Methods
This repeated-measures panel study was designed to investigate the time course of the effects of personal PM 2.5 exposure on cardiac autonomic dysfunction. The study population has been described previously. Briefly, the study participants consisted of 21 adults, who did not have overt evidence of heart disease, that were recruited from a local health clinic in an inner city neighborhood of Boston, Massachusetts, during the period of March 1, 2004 to August 31, 2004. Each participant completed a modified American Thoracic Society questionnaire, which also included information on sociodemographic factors (age, gender, and smoking status) and medication use. Information on medication use included statins, nonteroidal anti-inflammatory drugs (NSAIDs), antihypertensive medications (β blocker, calcium channel blocker, or angiotensin-converting enzymeinhibitors/angiotensin receptor blockers), or aspirin which were taken at least once during the study period. All participants completed continuous monitoring of electrocardiogram (ECG) and personal PM 2.5 up to 2 consecutive days. The study was approved by the Institutional Review Boards of the Harvard School of Public Health and the Upham’s Corner Neighborhood Health Center. All subjects gave written informed consent before participate in the study.
We used nocturnal HRV and nocturnal heart rate (HR), for a period of 7 hours from 00:00 a.m. to 07:00 a.m. , as measurements of cardiac autonomic response to PM 2.5 exposure. The ECG of each individual was measured continuously for up to 2 24-hour periods using a 5-lead ECG Holter monitor, Dynacord 3-Channel model 423 (Raytel Cardiac Services, Windsor, Connecticut). Of the 21 subjects, 18 subjects were monitored entire period and 3 subjects did not have nocturnal HRV ( Figure 1 ). The ECG monitoring protocol has been provided previously. Briefly, the Holter monitor was calibrated 15 minutes before placing electrodes. Separate electrodes were placed on the participant’s skin, and if necessary, the area was shaved for proper adhesion, and the leads were periodically checked by study staff. Each 24-hour recording was sent to Raytel Cardiac Services for processing and analysis using a StrataScan 563 (DelMar Avionics, Irvine, California) and then screened to correct data artifacts. A trained professional with no exposure information performed all analyses and edited all normal or abnormal findings on the basis of standard criteria. The mean of SD of normal-to-normal intervals (SDNN, in milliseconds), as a time-domain HRV measure, and the mean HR (in beats/min) were calculated in standard 5-minute segments throughout the entire recording and matched with the corresponding personal 5-minute PM 2.5 intervals.
Continuous real-time personal PM 2.5 concentrations were obtained for each individual with the TSI SidePak model AM510 Personal Aerosol Monitor, which uses light scattering technology to determine mass concentration (TSI Inc., Shoreview, Minnesota). Each SidePak was fit with a PM 2.5 inlet impactor. The air sample was drawn through a 1.2-m long Tygon tube into the impaction inlet at a flow rate of 1.7 L/min, adjusted using a DryCal DC-Lite Primary Air Flow Meter (BIOS, Butler, New Jersey). The PM 2.5 monitor was placed in a padded pouch, with the inlet tubing secured in the participant’s breathing zone, and attached to each participant. Participants were instructed to wear their monitors throughout the day and to place the monitor by their bed when sleeping at night. The monitor collected PM 2.5 concentrations every 10 seconds and reported 5-minute averages.
We analyzed data using PROC MIXED in the SAS statistical package, version 9.4, (SAS Institute Inc, Cary, North Carolina). We treated exposure (PM 2.5 ) and outcome variables (nocturnal SDNN and nocturnal HR) as repeated measurements in 5-minute segments. Dependent variables, 5-minute nocturnal SDNN, and 5-minute nocturnal HR, were log 10 transformed to improve normality and stabilize the variance. Linear mixed-effects models with random intercepts and unstructured covariance were used to estimate the percent changes as (10 [β×IQR] −1) × 100%, where β is the estimated regression coefficient and IQR is the interquartile range, in 5-minute SDNN and 5-minute HR for IQR increase in 5-minute PM 2.5 . To assess lagged effects of PM 2.5 , we used 5-minute lags up to 4 hours (total 48 lags calculated by 12 lags per hour × 4 hours) of PM 2.5 matched on the time of continuous ECG for each subjects. In these lag models, one lag indicates a 5-minute separation between the exposure and the outcome. We adjusted each model for age, gender, smoking status (current smoker and nonsmoker), use of statins, NSAIDs, antihypertensive medications (β blocker, calcium channel blocker, or angiotensin-converting enzyme inhibitors/angiotensin receptor blockers), and aspirin. Results are given as estimated percent changes with their 95% confidence intervals (CIs) in 5-minute HRV and 5-minute HR per IQR increase in 5-minute PM 2.5 exposure (13.6 μg/m 3 ).
Results
The demographic and clinical characteristics of each study participant are listed in Table 1 . Subjects were on average 44 years of age; 81% were women, 29% were current smokers, and 48% took regular medications including any of statin (10%), NSAIDs (29%), antihypertensive medications (43%), or aspirin (14%). Of the 21 participants, 15 participants (71%) had one or more diseases including diabetes (9.5%), chronic bronchitis (9.5%), asthma (33.3%), or hypertension (57.1%).
| Subject | Age | Gender | Race | Smoker | Statin | NSAIDs | Aspirin | AHT ∗ | SDNN (msec, mean±SD) | Heart rate (bpm, mean±SD) | PM 2.5 (μg/m 3 , mean±SD) | |||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Entire recording | Night | Entire recording | Night | Entire recording | Night | |||||||||
| 1 | 21 | F | B | N | – | – | – | – | 69.7±29.7 | 74.4±31.8 | 83.3±15.2 | 71.0±9.2 | 15.5±5.7 | 10.0±2.6 |
| 2 | 23 | M | B | N | – | – | – | – | 70.3±32.4 | 84.1±39.5 | 73.6±13.9 | 58.6±4.8 | 9.5±9.4 | 6.6±2.3 |
| 3 | 23 | F | B | N | – | – | – | – | 67.0±.25.5 | 74.0±24.3 | 82.9±15.7 | 69.7±5.7 | 18.1±4.2 | 20.5±4.1 |
| 4 | 25 | F | B | N | – | – | – | – | 68.7±23.2 | 77.8±26.2 | 71.6±10.8 | 57.3±4.7 | 12.8±24.4 | 6.4±1.3 |
| 5 | 26 | F | B | N | – | – | – | – | 102.5±24.7 | – | 66.2±10.0 | – | 8.8±15.6 | 4.1±0.6 |
| 6 | 33 | F | B | S | – | – | – | – | 28.6±12.0 | 35.9±13.2 | 101.2±13.4 | 86.8±5.5 | 52.4±97.3 | – |
| 7 | 39 | F | H | N | – | – | – | + | 41.0±25.4 | 57.9±19.7 | 74.7±10.1 | 66.4±5.7.3 | 10.3±13.9 | 4.1±3.5 |
| 8 | 41 | F | B | N | – | – | – | + | 54.0±22.0 | 60.0±27.8 | 79.3±14.6 | 63.7±8.5 | 6.4±4.7 | 6.3±1.5 |
| 9 | 43 | F | B | S | – | – | – | + | 41.3±19.4 | – | 88.1±13.0 | – | 175.8±88.9 | – |
| 10 | 45 | F | H | N | – | – | – | – | 57.4±21.0 | 58.4±22.4 | 84.1±12.3 | 81.0±11.3 | 4.6±6.3 | 0.4±0.3 |
| 11 | 45 | F | B | N | – | – | – | – | 46.9±16.4 | 52.6±17.4 | 82.9±12.6 | 72.1±5.9 | 6.1±8.1 | 3.2±0.6 |
| 12 | 45 | F | H | N | – | + | – | – | 42.7±17.6 | 54.7±25.5 | 83.6±12.6 | 66.0±4.3 | 18.8±72.4 | 2.1±0.6 |
| 13 | 46 | F | B | N | – | – | – | – | 54.0±20.6 | 52.9±23.3 | 83.4±12.8 | 76.3±19.3 | 13.4±48.2 | 3.5±1.3 |
| 14 | 47 | F | B | N | – | – | – | – | 29.9±11.6 | 34.2±13.3 | 98.2±10.1 | 87.3±7.9 | 9.7±8.6 | 6.6±4.6 |
| 15 | 51 | M | H | S | – | + | + | + | 28.4±17.9 | 55.4±19.3 | 96.4±10.8 | 79.2±6.4 | 24.9±50.7 | 21.9±12.6 |
| 16 | 54 | F | B | N | – | + | + | + | 34.5±14.2 | 37.4±16.8 | 94.7±12.4 | 84.4±10.0 | 63.5±58.7 | 9.3±6.6 |
| 17 | 55 | M | B | S | – | – | – | + | 36.8±29.4 | 55.2±55.5 | 78.4±7.6 | 75.0±7.4 | 64.7±86.7 | 49.7±22.9 |
| 18 | 61 | F | B | N | + | + | – | + | 54.5±23.6 | 56.9±32.1 | 79.5±10.6 | 66.9±4.3 | 12.6±27.9 | 7.2±0.9 |
| 19 | 66 | F | H | N | – | + | – | + | 50.4±19.7 | 48.1±25.8 | 70.1±6.5 | 69.5±6.4 | 13.5±5.2 | 12.3±2.6 |
| 20 | 68 | F | B | S | + | + | + | + | 34.3±10.3 | – | 76.1±6.1 | – | 26.7±51.3 | – |
| 21 | 69 | M | W | S | – | – | – | – | 30.8±11.9 | 27.5±10.9 | 82.4±6.4 | 85.8±5.1 | 218.6±251.4 | 12.8±30.1 |
| Mean | 44 | 49.6±27.2 | 55.2±30.0 | 82.8±14.8 | 73.4±12.3 | 29.8±77.7 | 10.7±15.0 | |||||||
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