Association between coarse particulate matter and inflammatory and hemostatic markers in a cohort of midlife women

Abstract

Background Exposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; however, most studies have focused on fine particulate matter (PM2.5) exposure and CVD. Coarse particulate matter (PM10–2.5) exposure has not been extensively studied, particularly for long-term exposure, and the biological mechanisms remain uncertain. Methods We examined the association between ambient concentrations of PM10–2.5 and inflammatory and hemostatic makers that have been linked to CVD. Annual questionnaire and clinical data were obtained from 1694 women (≥ 55 years old in 1999) enrolled in the longitudinal Study of Women’s Health Across the Nation (SWAN) at six study sites from 1999 to 2004. Residential locations and the USEPA air monitoring network measurements were used to assign exposure to one-year PM10–2.5, as well as co-pollutants. Linear mixed-effects regression models were used to describe the association between PM10–2.5 exposure and markers, including demographic, health and other covariates. Results Each interquartile (4 μg/m3) increase in one-year PM10–2.5 exposure was associated with a 5.5% (95% confidence interval [CI]: 1.8, 9.4%) increase in levels of plasminogen activator inhibitor-1 (PAI-1) and 4.1% (95% CI: − 0.1, 8.6%) increase in high-sensitivity C-creative Protein (hs-CRP). Stratified analyses suggested that the association with PAI-1 was particularly strong in some subgroups, including women who were peri-menopausal, were less educated, had a body mass index lower than 25, and reported low alcohol consumption. The association between PM10–2.5 and PAI-1 remained unchanged with adjustment for PM2.5, ozone, nitrogen dioxide, and carbon monoxide. Conclusions Long-term PM10–2.5 exposure may be associated with changes in coagulation independently from PM2.5, and thus, contribute to CVD risk in midlife women.

Methylomic, proteomic, and metabolomic correlates of traffic-related air pollution: A systematic review, pathway analysis, and network analysis relating traffic-related air pollution to subclinical and clinical cardiorespiratory outcomes

“…Short-term exposure to PM 2.5 was associated with hypomethylation of the genes that encode plasminogen activator inhibitor type I ( SERPINE1 ), coagulation factor III ( F3 ), and coagulation factor II receptor ( F2R ), as well as hypermethylation of coagulation factor II ( F2 ) [38,46,120,142,157]. Within the proteomics literature, short-term exposure to PM 10 and PM 2.5-10 were associated with lower levels of the protein plasminogen activator inhibitor type 1, whereas long-term exposure to PM 2.5 , NO 2 , CO, and O 3 were associated with higher levels of this protein [69,71,73]. Additionally, short-term exposure to PM 2.5 , UFP, BC, NO 2 , and CO were associated with higher levels of coagulation factor III protein (F3) [123,132].…”

“…Short-term exposure to PM 2.5 was associated with hypomethylation of SERPINE1 [142]. Additionally, short-term exposure to PM 10 and PM 2.5-10 was associated with lower levels of the corresponding protein, whereas long-term exposure to PM 2.5 , PM 2.5-10 , NO 2 , CO, and O 3 were associated with higher levels [69,71,73]. Furthermore, short-term BC and NO 2 were associated with higher levels of insulin-like growth factor binding protein 1 and 3, while short-term diesel exhaust was associated with lower levels of insulin-like growth factor binding protein 2 and 14-3-3 protein sigma [79,126].…”

“…In our review, three methylomic markers, seven proteomic markers (including three overlapping methylomic-proteomic markers), and three metabolomic markers were represented in the KEGG pathway for asthma (Table 2). The overlapping markers included three inflammation and immunity markers (TNF, CD40LG, and IL-10); we described trends for these previously [58,69,88,91,113,115,120,124,141,205,206,206,209,235,255,269,277]. For the other proteomics markers, short-term PM 2.5 , PM 10 , NO 2 , CO, and SO 2 were inversely associated with IL-4, short-term CO was inversely associated with IL-13 [113,124,278]; and short-term NO 2 and diesel exhaust were positively associated with IL-5 [113,124].…”

“…For proteomic papers, serum and plasma were the most common biological matrices (34 and 21 papers, respectively). Nine proteomics papers used both serum and plasma, with the inclusion of plasma serving primarily to measure fibrinogen levels [69,72,78,89,[119][120][121][122][123]. Three proteomics papers used bronchoalveolar lavage fluid to understand the associations between TRAP and the bronchoalveolar proteome, serving as a more direct measure of TRAP's influence [124][125][126].…”

Coarse Particulate Matter and Markers of Inflammation and Coagulation in the Multi-Ethnic Study of Atherosclerosis (MESA) Population: A Repeat Measures Analysis

“…Although our findings are inconsistent with the toxicological research, the results are similar to some of the limited—and largely inconsistent 4 —epidemiological work that has evaluated and these markers, though the similarities differed by blood marker. For example, the cross-sectional 13 and longitudinal 30 studies that have evaluated longer-term and fibrinogen in different cohorts have also found lower levels of fibrinogen with higher concentrations, although all associations were imprecise. For CRP, studies have more consistently found some evidence that higher long-term concentrations led to increases in CRP.…”