Source-specific fine particulate air pollution and systemic inflammation in ischaemic heart disease patients

Abstract

ObjectiveTo compare short-term effects of fine particles (PM2.5; aerodynamic diameter <2.5 µm) from different sources on the blood levels of markers of systemic inflammation.MethodsWe followed a panel of 52 ischaemic heart disease patients from 15 November 2005 to 21 April 2006 with clinic visits in every second week in the city of Kotka, Finland, and determined nine inflammatory markers from blood samples. In addition, we monitored outdoor air pollution at a fixed site during the study period and conducted a source apportionment of PM2.5 using the Environmental Protection Agency's model EPA PMF 3.0. We then analysed associations between levels of source-specific PM2.5 and markers of systemic inflammation using linear mixed models.ResultsWe identified five source categories: regional and long-range transport (LRT), traffic, biomass combustion, sea salt, and pulp industry. We found most evidence for the relation of air pollution and inflammation in LRT, traffic and biomass combustion; the most relevant inflammation markers were C-reactive protein, interleukin-12 and myeloperoxidase. Sea salt was not positively associated with any of the inflammatory markers.ConclusionsResults suggest that PM2.5 from several sources, such as biomass combustion and traffic, are promoters of systemic inflammation, a risk factor for cardiovascular diseases.

TP53-dependent autophagy links the ATR-CHEK1 axis activation to proinflammatory VEGFA production in human bronchial epithelial cells exposed to fine particulate matter (PM2.5)

“…Additionally, many in vitro studies have focused on the upregulation and release of proinflammatory cytokines, such as IL1B, IL6, CXCL8 and TNF, by airway epithelial cells in response to PM2.5 exposure due to the critical role of these cytokines in the initiation and resolution of inflammation. [4][5][6] In fact, elevation of these cytokines has also been observed in the bronchial alveolar lavage fluid of animals, 28 further confirming the results obtained from the in vitro studies. In this work, to explore the inflammatory responses induced by the particles, the expression levels of several inflammatory factors were analyzed.…”

“…The induction or exacerbation of airway inflammation is considered a common mechanism underlying the particle exposure-induced development of various adverse health effects in the respiratory and cardiovascular systems. [1][2][3][4][5][6] Thus, understanding how particulate matter triggers inflammatory reactions in the airway is a central issue in particle toxicology.…”

“…The release of these molecules then facilitates a pulmonary inflammatory response within a short time, which exacerbates the airway symptoms, especially in vulnerable populations with preexisting cardiopulmonary diseases and the elderly. 2,[4][5][6] When the response is sustained for a longer period, proinflammatory factors may move to the systemic circulation from the lungs and then cause adverse effects on the cardiovascular system. 2,3,6 Therefore, control of the inflammatory response may allow for more effective strategies to abate the cardiopulmonary dysfunctions induced by PM2.5.…”

“…2,[4][5][6] When the response is sustained for a longer period, proinflammatory factors may move to the systemic circulation from the lungs and then cause adverse effects on the cardiovascular system. 2,3,6 Therefore, control of the inflammatory response may allow for more effective strategies to abate the cardiopulmonary dysfunctions induced by PM2.5. Unfortunately, the mechanisms underlying the association between air particles and increased airway inflammatory response have not been clearly defined.…”

Long-term effects of elemental composition of particulate matter on inflammatory blood markers in European cohorts

“…No significant associations of transition metals were observed for fibrinogen. A recent study, investigated short-term effects of PM 2.5 sources, resulting from source apportionment, on inflammatory blood markers (Siponen et al, 2015). The authors detected increased CRP concentrations in association with elevated levels of PM 2.5 sources related to long-range transport and biomass combustion but no effects on fibrinogen.…”