A systematic review of cardiovascular responses associated with ambient black carbon and fine particulate matter

Abstract

Background: Exposure to fine particulate matter (PM_2.5), an ambient air pollutant with mass-based standards promulgated under the Clean Air Act, and black carbon (BC), a common component of PM_2.5, are both associated with cardiovascular health effects.

Objectives: To elucidate whether BC is associated with distinct, or stronger, cardiovascular responses compared to PM_2.5, we conducted a systematic review. We evaluated the associations of short- and long-term BC, or the related component elemental carbon (EC), with cardiovascular endpoints including heart rate variability, heart rhythm, blood pressure and vascular function, ST segment depression, repolarization abnormalities, atherosclerosis and heart function, in the context of what is already known about PM_2.5.

Data sources: We conducted a stepwise systematic literature search of the PubMed, Web of Science and TOXLINE databases and applied Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines for reporting our results.

Study eligibility criteria: Studies reporting effect estimates for the association of quantitative measurements of ambient BC (or EC) and PM_2.5, with relevant cardiovascular endpoints (i.e. meeting inclusion criteria) were included in the review. Included studies were evaluated for risk of bias in study design and results.

Study appraisal and synthesis methods: Risk of bias evaluations assessed aspects of internal validity of study findings based on study design, conduct, and reporting to identify potential issues related to confounding or other biases. Study results are presented to facilitate comparison of the consistency of associations with PM_2.5 and BC within and across studies.

Results: Our results demonstrate similar associations for BC (or EC) and PM_2.5 with the cardiovascular endpoints examined. Across studies, associations for BC and PM_2.5 varied in their magnitude and precision, and confidence intervals were generally overlapping within studies. Where differences in the magnitude of the association between BC or EC and PM_2.5 within a study could be discerned, no consistent pattern across the studies examined was apparent.

Limitations: We were unable to assess the independence of the effect of BC, relative the effect of PM_2.5, on the cardiovascular system, nor was information available to understand the impact of differential exposure misclassification.

Conclusions: Overall, the evidence indicates that both BC (or EC) and PM_2.5 are associated with cardiovascular effects but the available evidence is not sufficient to distinguish the effect of BC (or EC) from that of PM_2.5 mass.

Keywords: Black carbon; Cardiovascular effects; Fine particulate matter.

Fig. 1.

Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) flow diagram summarizing the systematic literature search, inclusion and exclusion criteria for studies of cardiovascular responses included in this review. Note: mh = MeSH headings; n = number of records; tw = text words.

Fig. 2.

Risk of bias evaluation for epidemiologic studies of subclinical cardiovascular endpoints (a) Heart Rate Variability; (b) Arrhythmia; (c) Blood Pressure and Vascular Function; (d) Ischemia and Repolarization Abnormalities (e) Long-term Exposure. Note: Rich et al., 2016 report includes findings for the Augsburg Germany and REHAB (Rochester, NY) studies.

Fig. 3.

Association of short-term exposure to black carbon or elemental carbon (black circles) and particulate matter < 2.5 μm in diameter (open circles) with time domain measures of heart rate variability per interquartile range increase in mean (or median) pollutant concentration (in μg/m³). Studies are organized by endpoint (SDNN, rMSSD, pNN50), population type (i.e., healthy, pre-existing disease, older adults) and averaging time (i.e., shortest averaging time first). Circles represent point estimates and horizontal lines represent 95% confidence intervals. BC = black carbon; CAD = coronary artery disease; COPD = chronic obstructive pulmonary disease; CVD = cardiovascular disease; d = day; EC = elemental carbon; h = hour; IQR = interquartile range; MA = moving average; pNN50 = proportion of successive NNs that differ by > 50 ms; rMSSD = root mean-square of successive differences; SD: standard deviation; SDNN = standard deviation of all normal to-normal intervals.

Fig. 4.

Association of short-term exposure to black carbon or elemental carbon (black circles) and particulate matter < 2.5 μm in diameter (open circles) with frequency domain measures of heart rate variability per interquartile range increase in mean (or median) pollutant concentration (in μg/m³). Studies are organized by endpoint (LF, HF, LFHFR), population type (i.e., healthy, pre-existing disease, older adults) and averaging time. Circles represent point estimates and horizontal lines represent 95% confidence intervals. BC = black carbon; CAD = coronary artery disease; COPD = chronic obstructive pulmonary disease; CVD = cardiovascular disease; d = day; EC = elemental carbon; h = hour; HF = high frequency; IQR = interquartile range; LF = low frequency; LFHFR = low frequency high frequency ratio; MA = moving average.

Fig. 5.

Association of short-term exposure to black carbon or elemental carbon (black circles) and particulate matter < 2.5 μm in diameter (open circles) with arrhythmia recorded on implantable cardioverter defibrillator or electrocardiogram, per interquartile range increase in mean (or median) pollutant concentration (in μg/m³). Studies are organized by endpoint (VA, AF, SVE, discharges, any arrhythmia), population type (i.e., healthy, pre-existing disease, older adults) and averaging time. Circles represent point estimates and horizontal lines represent 95% confidence intervals. BC = black carbon; EC = elemental carbon; h = hour; IQR = interquartile range; MA = moving average; PM_2.5 = particulate matter < 2.5 μm in diameter; VA = ventricular arrhythmia; AF = atrial fibrillation; SVE = supraventricular ectopy; VE = ventricular ectopy.