Search

Background: Few longitudinal studies have examined the association between ultrafine particulate matter (UFP, particles < 0.1 μm aerodynamic diameter) exposure and cardiovascular disease (CVD) risk factors. We used data from 791 adults participating in the longitudinal Boston Puerto Rican Health Study (Massachusetts, USA) between 2004 and 2015 to assess whether UFP exposure was associated with blood pressure and high sensitivity C-reactive protein (hsCRP, a biomarker of systemic inflammation).Methods: Residential annual average UFP exposure (measured as particle number concentration, PNC) was assigned using a model accounting for spatial and temporal trends. We also adjusted PNC values for participants' inhalation rate to obtain the particle inhalation rate (PIR) as a secondary exposure measure. Multilevel linear models with a random intercept for each participant were used to examine the association of UFP with blood pressure and hsCRP.Results: Overall, in adjusted models, an inter-quartile range increase in PNC was associated with increased hsCRP (β = 6.8; 95% CI = - 0.3, 14.0%) but not with increased systolic blood pressure (β = 0.96; 95% CI = - 0.33, 2.25 mmHg), pulse pressure (β = 0.70; 95% CI = - 0.27, 1.67 mmHg), or diastolic blood pressure (β = 0.55; 95% CI = - 0.20, 1.30 mmHg). There were generally stronger positive associations among women and never smokers. Among men, there were inverse associations of PNC with systolic blood pressure and pulse pressure. In contrast to the primary findings, an inter-quartile range increase in the PIR was positively associated with systolic blood pressure (β = 1.03; 95% CI = 0.00, 2.06 mmHg) and diastolic blood pressure (β = 1.01; 95% CI = 0.36, 1.66 mmHg), but not with pulse pressure or hsCRP.Conclusions: We observed that exposure to PNC was associated with increases in measures of CVD risk markers, especially among certain sub-populations. The exploratory PIR exposure metric should be further developed. [ABSTRACT FROM AUTHOR]

Little is known about personal characteristics and systemic responses to particulate pollution in patients with COPD. Assess whether diabetes, obesity, statins and non-steroidal anti-inflammatory medications (NSAIDs) modify associations between indoor black carbon (BC) and fine particulate matter ≤2.5 μm in diameter (PM 2.5) on systemic inflammation and endothelial activation. 144 individuals with COPD without current smoking and without major in-home combustion sources were recruited at Veterans Affairs Boston Healthcare System. PM 2.5 and BC were measured in each participant's home seasonally for a week (up to 4 times; 482 observations) and plasma biomarkers of systemic inflammation [C-reactive protein (CRP); interleukin-6 (IL-6)] and endothelial activation [soluble vascular adhesion molecule-1 (sVCAM-1)] measured. Linear mixed effects regression with a random intercept was used, and effect modification assessed with multiplicative interaction terms and stratum specific estimates. Median (25%ile, 75%ile) indoor BC and PM 2.5 were 0.6 (0.5,0.7) μg/m3 and 6.8 (4.8,10.4) μg/m3, respectively. Although p-values for effect modification were not statistically significant, there were positive associations (%-increase/interquartile range; 95% CI) between CRP and BC greater among non-statin (18.8%; 3.6–36.3) than statin users (11.1%; 2.1–20.9). There were also positive associations greater among non-statin users between PM 2.5 and CRP. For IL-6, associations with BC and PM 2.5 were also greater among non-statin users. Associations between CRP and BC were greater (20.3%; 4.5–38.5) in persons with diabetes than without diabetes (10.3%; 0.92–20.6) with similar effects of PM 2.5. There were no consistent associations that differed based on obesity. Effect modification was not observed for NSAID use, or with any factor considered with sVCAM-1. Associations between indoor BC and PM 2.5 and CRP were greater in patients with diabetes and those not taking statins, and with IL-6 if not taking statins. These results suggest that these characteristics may modify the systemic response to indoor BC and PM 2.5 in persons with COPD. • Greater associations between in-home BC and PM2.5 with CRP in non-statin users. •Greater associations between in-home BC and PM2.5 with CRP and IL-6 in diabetics. •NSAID use and BMI ≥ 30 did not modify BC and PM2.5 and biomarker associations. •COPD patients not using statins or with diabetes may be more susceptible to BC/PM. [ABSTRACT FROM AUTHOR]