Current understanding of how and why race influences the transition from acute to chronic pain following
traumatic injury remains limited. Traumatic injuries result in over 30 million emergency department visits and 2.5
million hospitalizations each year in the U.S. Risk for developing post-injury chronic pain is significantly greater
for non-Hispanic Black (NHB) patients compared to non-Hispanic White (NHW) patients with similar injuries.
Although NHB patients experience higher levels of acute post-injury pain and are more likely to transition to
chronic pain than NHW patients, the biobehavioral and social factors that influence this transition are not well
understood. The overall aim of this proposal is to improve understanding of the factors that influence the
transition to post-injury chronic pain and shape racial pain disparities. To address our aims, we will recruit 150
NHB and 150 NHW adults with traumatic orthopedic injuries from a level 1 trauma center and assess pain
outcomes during hospitalization and across monthly follow-ups. First, we will identity similarities and differences
in the extent to which biobehavioral factors explain post-injury chronic pain in NHB and NHW patients. We
hypothesize that greater pain sensitivity (assessed in hospital via quantitative sensory testing), elevated acute
inflammatory biomarkers (hsCRP, TNFa, IL1ß, IL-6), more negative cognitions (catastrophizing, pain/treatment
expectations), and higher depressive/posttraumatic stress symptoms will predict post-injury chronic pain (i.e.,
higher odds of chronic pain onset, greater pain intensity and interference) in both NHB and NHW patients. If
chronic pain risks are moderated by race, we hypothesize that worse post-injury chronic pain in NHB relative to
NHW patients will be explained, in part, by higher biobehavioral risk factors. Second, we will identify similarities
and differences in the extent to which social factors explain post-injury chronic pain in NHB and NHW patients.
We hypothesize that social risk factors (greater life and neighborhood stress, lower socioeconomic status) will
predict post-injury chronic pain in both NHB and NHW patients, and that social protective factors (higher social
support) will buffer against in the influence of social risk factors. If chronic pain risks are moderated by race, we
hypothesize that worse post-injury chronic pain in NHB relative to NHW patients will be explained, in part, by
higher levels of social risk factors. The comprehensive assessment of risk and protective factors across multiple
levels of the biopsychosocial model will advance understanding of the pathways that contribute to post-injury
chronic pain for both NHB and NHW adults, including factors implicated in racial differences in transition to
chronic pain. Evaluating in-hospital evoked pain sensitivity as a predictor of post-injury chronic pain development
represents a major innovation. This knowledge could spur the development of cost-effective, scalable screens
for hospital settings to redress racial disparities in pain. The investigators assembled for this multidisciplinary
team possess complementary skill sets in traumatic injury, chronic pain, quantitative sensory testing,
inflammation, pain-relevant biobehavioral and social factors, and racial disparities in chronic pain.
