Air Research
Black Carbon Health Effects
In the PM family, black carbon is a major contributor to the fine particle (PM2.5) burden in the air. It is small enough to be easily inhaled into the lungs and has been associated with adverse health effects. Whether black carbon is itself toxic or functions as an indicator of other co-pollutants is currently under debate. But, clearly, black carbon is associated with asthma, and other respiratory problems, low birth weights, heart attacks and lung cancer. EPA scientists study the effects of particles including black carbon on human health through clinical and animal testing.
Using human and animal exposure data, researchers can estimate the amount of black carbon deposited into lungs under a variety of breathing conditions. When compared with lung tissue samples from coal miners, smokers and nonsmokers, correlations and predictions can be drawn between the exposure and potential risk of adverse lung outcomes. Such research has contributed to global awareness of black carbon's health effects.
Research to investigate children's asthma in Detroit, Michigan, is examining the impact of diesel exhaust from roadways. As part of this research effort, the Near-Road EXposures to Urban Air Pollutants Study (NEXUS) is evaluating the impact of vehicle emissions, including black carbon, on near-road exposures and asthma outcomes.
Similarly, controlled clinical studies in adults are being conducted to examine the health effects from exposure to different air quality scenarios: diesel exhaust, clean air, ozone, or a mixture of diesel exhaust and ozone.
Peat-burning wildfires, as occurred in a large wildfire in the summer of 2008 in rural eastern North Carolina, released enormous amounts of PM, especially black carbon, which were linked to increased risk of heart failure and respiratory hospital visits in the affected region.
EPA research will continue to evaluate the health effects wildfires, involving black carbon, have on disadvantaged groups.
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Effect of inhaled carbon ultrafine p... [Environ Health Perspect. 2008] - PubMed - NCBI
Effect of inhaled carbon ultrafine particles on reactive hyperemia in healthy human subjects.
Abstract
BACKGROUND:
Ultrafine particles (UFP) may contribute to the cardiovascular effects of exposure to particulate air pollution, partly because of their relatively efficient alveolar deposition and potential to enter the pulmonary vascular space.
OBJECTIVES:
This study tested the hypothesis that inhalation of elemental carbon UFP alters systemic vascular function.
METHODS:
Sixteen healthy subjects (mean age, 26.9 +/- 6.5 years) inhaled air or 50 microg/m3 elemental carbon UFP by mouthpiece for 2 hr, while exercising intermittently. Measurements at preexposure baseline, 0 hr (immediately after exposure), 3.5 hr, 21 hr, and 45 hr included vital signs, venous occlusion plethysmography and reactive hyperemia of the forearm, and venous plasma nitrate and nitrite levels.
RESULTS:
Peak forearm blood flow after ischemia increased 3.5 hr after exposure to air but not UFP (change from preexposure baseline, air: 9.31 +/- 3.41; UFP: 1.09 +/- 2.55 mL/min/100 mL; t-test, p = 0.03). Blood pressure did not change, so minimal resistance after ischemia (mean blood pressure divided by forearm blood flow) decreased with air, but not UFP [change from preexposure baseline, air: -0.48 +/- 0.21; UFP: 0.07 +/- 0.19 mmHg/mL/min; analysis of variance (ANOVA), p = 0.024]. There was no UFP effect on pre-ischemia forearm blood flow or resistance, or on total forearm blood flow after ischemia. Venous nitrate levels were significantly lower after exposure to carbon UFP compared with air (ANOVA, p = 0.038). There were no differences in venous nitrite levels.
CONCLUSIONS:
Inhalation of 50 microg/m3 carbon UFP during intermittent exercise impairs peak forearm blood flow during reactive hyperemia in healthy human subjects.
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