We assessed the association between psychosocial stress and preinvasive cervical neoplasia development controlling for HR-HPV infection.
This case-control study enrolled low-income women receiving family planning services at health department clinics. There were 59 cases with biopsy confirmed HSIL and 163 with low-grade SIL and 160 controls with normal cervical cytology. A modified SLE scale was used to measure stressful events and the perceived impact of the event in the prior 5 years. Unconditional logistic regression was used to assess SIL risk and stressful events scores and by subscales.
After adjusting for age, HR-HPV infection, and lifetime number of sex partners, the SLE count score was associated with an increased risk of SIL among white women (aOR = 1.20; 95% CI = 1.04, 1.38) yet not among African American women (aOR = 1.02; 95% CI = 0.87, 1.19). The relationship stress subscale (divorce, infidelity, an increase in the number of arguments, and psychological and physical partner violence) was the only one of four subscales (loss, violence, and financial stress) associated with SIL, again, only among white women (aOR = 1.54; 95% CI = 1.21, 1.96).
These data suggest that psychosocial stress may play a role in SIL development. Future studies are needed to confirm these findings, to explore racial difference in reporting stress, and to explore the mechanism through which psychosocial stress may affect cervical neoplasia risk.
From Department of Epidemiology (A.L.C.), University of Texas School of Public Health, Houston, Texas; School of Nursing (S.B.), Medical University of South Carolina, Charleston, South Carolina; Program in Epidemiology (M.M.M.), Fred Hutchinson Cancer Center, Seattle, Washington; Department of Health Promotion, Education, Behavior (K.L.), Norman J. Arnold School of Public Health; and Department of Pathology (L.P.), School of Medicine, University of South Carolina, Columbia, South Carolina
Address reprint requests to: Ann L. Coker, PhD, University of Texas School of Public Health 1200 Herman Pressler Dr., Rm. E-1009, PO Box 20186, Houston, TX 77225. Email: email@example.com
Received for publication May 2, 2001; revision received August 22, 2002.
This work was funded in part by National Cancer Institute Award R29-CA-57466 (to A.L. Coker), US Department of Defense Grant N00014-96-1-1298, and by a Fullerton Foundation grant to the Medical University of South Carolina.