Risk factors for cerebral glioma in adults: a case-control study in an Italian population

Abstract

A case-control study on risk factors for cerebral tumors was conducted on an adult Italian population by the four Neurosurgical Departments of the Veneto Region, i.e. Padua, Treviso, Verona and Vicenza. The study recruited 195 cases of histologically-confirmed cerebral glioma. One hospital control was selected for each case. Cases and controls were matched for age, sex, data of hospitalization and residence. Information on both cases and controls was obtained from a relative. Uninvolved interviewers administered a structured questionnaire including items on the subject's education, occupation, lifestyle, medical history, exposure to radiation for diagnosis or therapy, head trauma and blood group and the medical history of family members. The series of cerebral tumors was first considered as an indistinct set: none of the risk factors examined showed a statistically significant association. A positive association was found with blood group A (OR = 6) when low-grade astrocytomas (n = 41) were considered separately. As for the malignant astrocytomas (n = 132), there was a suggestive but not statistically significant association with the presence of CNS tumors among first- and second-degree relatives (OR = 7.0). On the whole, this study yielded no clear and meaningful association for the various risk factors analyzed.

Association of adult glioma with medical conditions, family and reproductive history

“…One study demonstrated significantly more cases that were blood group A or AB (Selverstone and Cooper, 1961), while in another study, a significant excess of individuals with blood group A was observed in males but not in females (Garcia et al, 1963). However, our findings are consistent with several studies that showed no difference in the distribution of blood groups between cases and controls with glioma (Choi et al, 1970;Zampieri et al, 1994).…”

“…While some evidence exists implicating certain work chemicals (Burch et al, 1987;Preston-Martin and Mack, 1991;Morrison et al, 1992), investigations of a wide range of genetic and environmental factors have been inconclusive (Burch et al, 1987;Wrensch and Barger, 1990;Schiffer, 1991;Ryan et al, 1992;Zampieri et al, 1994).…”

“…A wide range of genetic and environmental factors have been investigated. While some evidence exists implicating certain work chemicals (Burch et al, 1987;Preston-Martin and Mack, 1991;Morrison et al, 1992), investigations of a wide range of genetic and environmental factors have been inconclusive (Burch et al, 1987;Wrensch and Barger, 1990;Schiffer, 1991;Ryan et al, 1992;Zampieri et al, 1994).A role has been suggested for genetic factors in the aetiology of glioma (Schiffer, 1991;Wrensch and Barger, 1990), but this is not consistent in all studies (Choi et al, 1970). This is based on the following: the difference in distribution of ABO blood groups between brain tumour patients and controls (Selverstone and Cooper, 1961;Zampieri et al, 1994), the association of brain tumours with genetically determined disorders (Schiffer, 1991), some evidence of familial aggregation of brain tumours (Schiffer, 1991) and familial clustering of brain tumours with breast and lung cancers (Wrensch and Barger, 1990;Zampieri et al, 1994).…”

Descriptive Epidemiology of Cerebral Gliomas in Northwest Greece and Study of Potential Predisposing Factors, 2005–2007

“…Inskipp et al [12] suggested that severe head trauma slightly increases the overall risk of brain tumors. Similarly, Salvati et al [21] believe in an etiological association between severe head trauma and glioma development whereas others [22][23][24] consider that there is no clear correlation between cranial trauma and subsequent glioma formation. However, these studies included all types of head injuries (mild, moderate and severe) and could not rule out the possible effect of a severe cranial trauma.…”

Smoking and risk of glioma: a meta-analysis

“…Three studies were considered to be ineligible for inclusion in the analysis for the following reasons: (i) in one study, the definition of exposure to smoking was based on a high dose (C20 cigarettes/day) only [24]; (ii) another study [25] was based on the same study population as that of a later study [14], which provided a more comprehensive analysis of smoking and glioma; (iii) an additional study was excluded because the odds ratios for the smoking variables were not presented, but simply described as ''at unity,'' with no confidence intervals or p values [12].…”