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Increased in susceptibility to thrombotic disease may be associated with lower lung function.
These data thus suggest that higher systemic clotting pathway activity may be a modifiable risk factor for lower lung function.
Our original hypothesis was that higher levels of activation of blood coagulation would be associated with lower lung function.
[17] Similarly, Lewis negative or nonsecretor status was significantly associated with lower lung function, and higher prevalence of wheezing and asthma, in blood group O adults.
Cross-sectional studies have documented that increased systemic inflammation is associated with lower lung function in both healthy adults and patients with COPD [1], [2], [3], [21].
Indeed, obesity is associated with high CRP and fibrinogen [28] and lower lung function [29] and may provide another link between systemic inflammation and low lung function.
As air pollution is also a risk factor for lower lung function in children [20] it may impact on lung function by a vascular mechanism in addition to its direct toxic effects on the lungs.
This is consistent with the observation that individuals with lower lung function have a higher risk of myocardial infarction [17] – for which elevated D-dimer levels are an independent risk factor [14], [16].
ETS-exposure was associated with lower quality of life scores; greater rescue inhaler use; lower lung function; greater bronchodilator responsiveness; and greater risk for emergency room visits, hospitalization and intensive care unit admission.
An alternative explanation is that higher serum highly sensitive CRP is a biomarker for lower lung function and that the apparent associations between coagulation pathway activity and lung function that we have observed are in part a consequence of confounding.
For example, more missingness is anticipated in individuals with higher BMI or lower lung function measurements.
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