We found suggestive associations between several paternal hobbies and risk of a child developing MB or PNET in the first 6 years of life. The strongest associations were seen for lawn care with pesticides both during the pregnancy and after the child’s birth; however, no dose-response relationship was observed and there was evidence that recall bias might partly explain the association. Possible weak associations were seen for stripping paint from furniture or woodwork and for hunting.
The presumed exposures of interest for these hobbies are: pesticides from lawn care, solvents from stripping paint, and lead and cleaning solvents from hunting. The results of this study are consistent with and support findings from other studies that have looked at parental pesticide exposure and childhood brain tumors. Many pesticides readily cross the blood-brain barrier and are intentionally neurotoxic. Laboratory studies have shown that some pesticides can cross the placenta, damage DNA and initiate tumorigenic changes in fetal cells (reviewed in Baldwin & Preston-Martin, 2004 (3
)). A number of studies have found elevated risk for MB/PNET and other pediatric CNS cancers among children whose fathers have experienced pesticide exposures either occupationally or in the home (3
). However, null associations have also been found for both occupational and residential exposures (7
). Much of the research in this area has focused on occupational rather than residential exposures, but the strongest associations have been found for household pesticide use prior to or just after birth (3
). Most of the positive risk estimates for residential pesticide use have been on the order of 1.5 – 2.5 (7
), comparable to those found in this study.
The previous evidence for solvent and lead exposures has been less clear than that for pesticides. Mixed results have been found with some studies showing positive associations and others showing none (3
). This study adds to the suggestive but inconclusive evidence regarding solvent related exposures. To our knowledge, no previous studies have looked at possible associations between lead exposure and MB or PNET development. Lead is known to cross the developing blood-brain barrier (3
) and to induce potentially carcinogenic chromosomal aberrations (16
). In addition, occupational lead exposure has been shown to increase risk of brain tumors in adults (17
). Other research has shown significantly elevated levels of lead in the cerebral spinal fluid (CSF) of those with malignant tumors compared to control groups, with MB showing the highest mean CSF lead levels (19
More frequent hobby participation was not associated with higher risk estimates. There are a number of possible reasons for the lack of a dose-response relationship, including that small sample sizes limited the ability to detect these differences. It is also possible that the lack of a dose-response relationship is indicative of bias in the results rather than a true positive association.
The analyses by age of the child found generally higher odds ratios for the children who were older at diagnosis. This suggests that the environmental exposures measured here may manifest themselves primarily in older children, rather than in children diagnosed shortly after birth, possibly due to a necessary latency period between exposure and disease onset. However, these results must be interpreted with caution due to the small numbers and the lack of statistical significance.
The primary limitation of this study is the retrospective data collection based on paternal recall, which can result in recall bias or non-differential misclassification of exposure. There is some evidence from our analyses that recall bias was not a major concern here, but its effects on the results can not be ruled out. The presence of non-differential misclassification due to the time lag between exposures and reporting would generally be expected to bias the risk estimates towards the null.
Another limitation of this study was the broad nature of the questions. A father’s participation in a hobby could result in exposure to many substances. In addition, the exposures encountered during a hobby may not be the same for all participants. The broad nature of these questions would have acted to dilute risk estimates that may otherwise have been positive for specific exposures. On the other hand, asking such broad questions related to hobbies, rather than very detailed questions related to specific exposures, may have resulted in more accurate recall on the part of the study subjects. Data were not available on maternal hobbies or for either parent’s occupational exposures. Therefore, we can not account for exposures that may have resulted from maternal household activities or from either parent’s work-related exposures. This may have added to misclassification by exposure.
Further consideration must be given to the population used in these analyses. Only children who had been patients at a medical center participating in the CCG were enrolled in this study. Selection bias would have occurred if children with MB/PNET seen at CCG institutions differed from other children with MB/PNET. However, data were not available to assess potential differences and thus, we cannot assess the likelihood of selection bias due to case ascertainment through CCG. Further selection pressures arise from paternal response rates and use of mothers as proxy respondents. The overall response rate from fathers of identified eligible cases was 65%. Proxy interviews were conducted for a sizable minority of the fathers, particularly among controls. Use of these interviews could be expected to increase the probability of misclassification of exposure. Analyses were performed excluding proxy interviews and no differences from the reported results were seen.
These data on father’s hobbies prior to and after birth and his child’s risk of developing MB or PNET in the first 6 years of life provide some suggestive results and directions for future research. Combined with data from other studies, these results are suggestive of an association between residential pesticide exposures and brain tumor risk in children. This association was unlikely to have been entirely explained by confounders or bias, although these must be considered as possible explanations for the results. This study also suggests a possible role for stripping paint and hunting which should be further explored in future studies.