Cardiovascular and lung function in relation to outdoor and indoor exposure to fine and ultrafine particulate matter in middle-aged subjects

Dorina Gabriela Karottki,Gabriel Bekö,Geo Clausen,Anne Mette Madsen,Zorana Jovanovic Andersen,Andreas Massling,Matthias Ketzel,Thomas Ellermann,Rikke Lund,Torben Sigsgaard,Peter Møller,Steffen Loft

doi:10.1016/j.envint.2014.08.019

Abstract

This cross-sectional study investigated the relationship between exposure to airborne indoor and outdoor particulate matter (PM) and cardiovascular and respiratory health in a population-based sample of 58 residences in Copenhagen, Denmark. Over a 2-day period indoor particle number concentrations (PNC, 10–300nm) and PM2.5 (aerodynamic diameter<2.5μm) were monitored for each of the residences in the living room, and outdoor PNC (10–280nm), PM2.5 and PM10 (aerodynamic diameter<10μm) were monitored at an urban background station in Copenhagen. In the morning, after the 2-day monitoring period, we measured microvascular function (MVF) and lung function and collected blood samples for biomarkers related to inflammation, in 78 middle-aged residents. Bacteria, endotoxin and fungi were analyzed in material from electrostatic dust fall collectors placed in the residences for 4weeks. Data were analyzed using linear regression with the generalized estimating equation approach. Statistically significant associations were found between indoor PNC, dominated by indoor use of candles, and lower lung function, the prediabetic marker HbA1c and systemic inflammatory markers observed as changes in leukocyte differential count and expression of adhesion markers on monocytes, whereas C-reactive protein was significantly associated with indoor PM2.5. The presence of indoor endotoxin was associated with lower lung function and expression of adhesion markers on monocytes. An inverse association between outdoor PNC and MVF was also statistically significant. The study suggests that PNC in the outdoor environment may be associated with decreased MVF, while PNC, mainly driven by candle burning, and bioaerosols in the indoor environment may have a negative effect on lung function and markers of systemic inflammation and diabetes.

Highlights

Long-term exposure to particulate air pollution from traffic and other combustion sources is associated with an increase in general mortality and morbidity from respiratory and cardiovascular diseases, especially among elderly and people with previous respiratory and cardiovascular diseases (Hoek et al, 2013)
Significant associations were found between indoor PNC, dominated by indoor use of candles, and lower lung function, the prediabetic marker HbA1c and systemic inflammatory markers observed as changes in leukocyte differential count and expression of adhesion markers on monocytes, whereas C-reactive protein was significantly associated with indoor PM2.5
We investigated inflammation markers in terms of C-reactive protein (CRP) and leukocyte counts, as well as expression levels of surface adhesion molecules on circulating monocytes by flow cytometry, because monocyte activation with attachment to the endothelium is an important event in the atherosclerotic process (Libby et al, 2002)

Summary

Introduction

Long-term exposure to particulate air pollution from traffic and other combustion sources is associated with an increase in general mortality and morbidity from respiratory and cardiovascular diseases, especially among elderly and people with previous respiratory and cardiovascular diseases (Hoek et al, 2013). Short-term exposure to elevated levels of outdoor air pollution, lasting hours to several days, has been linked to increased mortality and hospital admissions due to heart and lung diseases (Ruckerl et al, 2011). PM include pulmonary and systemic inflammation, oxidative stress, altered cardiac autonomic function, altered balance between coagulation and fibrinolysis, endothelial and microvascular dysfunction, atherosclerosis progression and plaque instability, as studied in panel and crosssectional studies with short-term exposure assessed from monitoring stations or after controlled exposure (Brook et al, 2010). Results have shown less consistency for prognostic markers for cardiovascular risk, including blood markers reflecting inflammation such as C-reactive protein (CRP) and circulating leukocyte counts, cell expression of adhesion molecules and impaired endothelial function (Li et al, 2012; Pope et al, 2011; Ruckerl et al, 2011)

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