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Indoor black carbon and biomarkers of systemic inflammation and endothelial activation in COPD patients.
Environmental Research 2018 August
RATIONALE: Evidence linking traffic-related particle exposure to systemic effects in chronic obstructive lung disease (COPD) patients is limited.
OBJECTIVES: Assess relationships between indoor black carbon (BC), a tracer of traffic-related particles, and plasma biomarkers of systemic inflammation and endothelial activation.
METHODS: BC was measured by reflectance in fine particle samples over a mean of 7.6 days in homes of 85 COPD patients up to 4 times seasonally over a year. After the completion of sampling, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular adhesion molecule-1 (sVCAM-1) were measured. Current smokers and homes with major sources of BC were excluded; therefore, indoor BC was primarily a measure of infiltrated outdoor BC. Mixed effects regression models with a random intercept for each participant were used to assess BC effects at different times (1-9 days before phlebotomy) and in the multi-day sample.
RESULTS: Measured median BC was 0.19 µg/m3 (interquartile range, IQR=0.22 µg/m3 ). Adjusting for season, race, age, BMI, heart disease, diabetes, ambient temperature, relative humidity, a recent cold or similar illness, and blood draw time, there was a positive relationship between BC and CRP. The largest effect size was for BC averaged over the previous seven days (11.8% increase in CRP per IQR; 95%CI = 1.8-22.9). Effects were greatest among non-statin users and persons with diabetes. There were positive effects of BC on IL-6 only in non-statin users. There were no associations with sVCAM-1.
CONCLUSIONS: These results demonstrate exposure-response relationships between indoor BC with biomarkers of systemic inflammation in COPD patients, with stronger relationships in persons not using statins and with diabetes.
OBJECTIVES: Assess relationships between indoor black carbon (BC), a tracer of traffic-related particles, and plasma biomarkers of systemic inflammation and endothelial activation.
METHODS: BC was measured by reflectance in fine particle samples over a mean of 7.6 days in homes of 85 COPD patients up to 4 times seasonally over a year. After the completion of sampling, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular adhesion molecule-1 (sVCAM-1) were measured. Current smokers and homes with major sources of BC were excluded; therefore, indoor BC was primarily a measure of infiltrated outdoor BC. Mixed effects regression models with a random intercept for each participant were used to assess BC effects at different times (1-9 days before phlebotomy) and in the multi-day sample.
RESULTS: Measured median BC was 0.19 µg/m3 (interquartile range, IQR=0.22 µg/m3 ). Adjusting for season, race, age, BMI, heart disease, diabetes, ambient temperature, relative humidity, a recent cold or similar illness, and blood draw time, there was a positive relationship between BC and CRP. The largest effect size was for BC averaged over the previous seven days (11.8% increase in CRP per IQR; 95%CI = 1.8-22.9). Effects were greatest among non-statin users and persons with diabetes. There were positive effects of BC on IL-6 only in non-statin users. There were no associations with sVCAM-1.
CONCLUSIONS: These results demonstrate exposure-response relationships between indoor BC with biomarkers of systemic inflammation in COPD patients, with stronger relationships in persons not using statins and with diabetes.
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