Testicular nonseminoma and seminoma in relation to perinatal characteristics.

BACKGROUND: Testicular cancer incidence peaks during the third decade of life, and an increasing trend in the occurrence of this disease has been seen in many countries. Few risk factors have been established for testicular cancer, but evidence suggests that causal factors operate early in life, perhaps even in utero.
PURPOSE: We performed a case-control study to evaluate specific perinatal characteristics as risk factors for the two main histopathologic types of testicular cancer: seminomas and nonseminomas.
METHODS: Two hundred thirty-two case patients with invasive testicular cancer and 904 individually matched control subjects (all singleton births), nested in a cohort of men born at 10 hospitals in Sweden from 1920 through 1978, were included in the study. Perinatal information about the study subjects and their parents was obtained from birth records. For the mothers, information was recorded concerning age at menarche, marital status, parity, age at delivery, maternal weight at delivery and at first visit to a maternal-care center, education and/or profession, and any medical problems encountered during pregnancy or after delivery. For the fathers, information was obtained concerning age at delivery and education and/or profession. For the study subjects, information was recorded about the following: gestational age, birth length and weight, placental weight, method of delivery (normal, cesarean section, or with forceps or vacuum extractor), medical problems during hospital stay, presence of jaundice, method of feeding at discharge, and duration of hospital stay after birth. Individuals diagnosed with testicular cancer were identified through the Swedish National Cancer Registry and the Uppsala Regional Cancer Registry. The data were analyzed by use of conditional logistic regression modeling.
RESULTS: When testicular cancer was modeled as a single entity, significantly elevated risks were associated with neonatal jaundice (adjusted odds ratio [OR] = 2.30; 95% confidence interval [CI] = 1.07-4.94) and with either low (< 2500 g) or high (> or = 4000 g) birth weight (OR = 2.59; 95% CI = 1.05-6.38 and OR = 1.58; 95% CI = 1.10-2.29, respectively). When seminomas and nonseminomas were analyzed separately, high maternal socioeconomic status (OR = 2.54; 95% CI = 1.05-6.12), neonatal jaundice (OR = 3.96; 95% CI = 1.47-10.69), and low birth weight (OR = 7.62; 95% CI = 1.59-36.60) were associated with nonseminomas, whereas high placental weight (OR = 3.50; 95% CI = 0.97-12.62) suggested increased risk for seminomas. CONCLUSIONS AND IMPLICATIONS: Perinatal exposures appear to influence the risk of testicular cancer, and seminomas and nonseminomas may have somewhat different risk profiles. Future epidemiologic studies should consider the possibility of etiologic heterogeneity in the development of seminomas and nonseminomas.