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Low-moderate urine arsenic and biomarkers of thrombosis and inflammation in the
Strong Heart Study.
Authors Moon KA, Navas-Acien A, Grau-P茅rez M, Francesconi KA, Goessler W, Guallar E,
Umans JG, Best LG, Newman JD
Submitted By Jonathan Newman on 2/5/2019
Status Published
Journal PLoS ONE
Year 2017
Date Published
Volume : Pages 12 : e0182435
PubMed Reference
Abstract The underlying pathology of arsenic-related cardiovascular disease (CVD) is
unknown. Few studies have evaluated pathways through thrombosis and inflammation
for arsenic-related CVD, especially at low-moderate arsenic exposure levels
(<100 碌g/L in drinking water). We evaluated the association of chronic
low-moderate arsenic exposure, measured as the sum of inorganic and methylated
arsenic species in urine (SAs), with plasma biomarkers of thrombosis and
inflammation in American Indian adults (45-74 years) in the Strong Heart Study.
We evaluated the cross-sectional and longitudinal associations between baseline
SAs with fibrinogen at three visits (baseline, 1989-91; Visit 2, 1993-95, Visit
3, 1998-99) using mixed models and the associations between baseline SAs and
Visit 2 plasminogen activator inhibitor-1 (PAI-1) and high sensitivity
C-reactive protein (hsCRP) using linear regression. Median (interquartile range)
concentrations of baseline SAs and fibrinogen, and Visit 2 hsCRP and PAI-1 were
8.4 (5.1, 14.3) 碌g/g creatinine, 346 (304, 393) mg/dL, 44 (30, 67) mg/L, and 3.8
(2.0, 7.0) ng/mL, respectively. Comparing the difference between the 75th and
the 25th percentile of SAs (14.3 vs. 5.1 碌g/g creatinine), SAs was positively
associated with baseline fibrinogen among those with diabetes (adjusted
geometric mean ratio (GMR): 1.05, 95% CI: 1.02, 1.07) not associated among those
without diabetes (GMR: 1.01, 95% CI: 0.99, 1.02) (p-interaction for diabetes =
0.014), inversely associated with PAI-1 (GMR: 0.94, 95% CI: 0.90, 0.99), and not
associated with hsCRP (GMR: 1.00, 95% CI: 0.93, 1.08). We found no evidence for
an association between baseline SAs and annual change in fibrinogen over
follow-up (p-interaction = 0.28 and 0.12 for diabetes and non-diabetes,
respectively). Low-moderate arsenic exposure was positively associated with
baseline fibrinogen in participants with diabetes and unexpectedly inversely
associated with PAI-1. Further research should evaluate the role of
prothrombotic factors in arsenic-related cardiovascular disease.

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