pregnant mothers and their children have reported a parallel increase in risk for childhood brain tumors (Bunin et al. 1994; Cordier et al. 1994; Efird et al. 2003; Holly et al. 1998). Speculation about farm-related exposures of interest for childhood brain tumors has cen- tered largely on agricultural pesticides and on farm animals [as a surrogate for an undeter- mined viral agent(s)]. Among the lymphomas, epidemiologic studies of risk associated with pesticide expo- sures have largely focused on non-Hodgkin lymphoma, and predominantly for cases diag- nosed in adults. In studies evaluating non- Hodgkin lymphoma diagnosed among children, Zahm and Ward (1998) noted that several reported an apparent dose response to both agricultural and residential pesticide exposures. The results for the few studies evaluating the possible risk associated with pesticide use and neuroblastomas in children have been equivocal; however, there is some evidence for an association for both occupational pesticide exposure of the parents and residential pesticide exposure of the family, particularly in studies that used speciﬁc pesticide exposure informa- tion rather than relying on parent’s job title (Daniels et al. 2001; Kristensen et al. 1996). Retinoblastoma is a very low-incidence childhood tumor. There are two recognized types of retinoblastoma: one linked to genetic mutations and the other related to sporadic tumors. The heritable forms of retinoblastoma tend to be bilateral and occur during the ﬁrst year of life. The sporadic nonheritable form is more likely to be unilateral and diagnosed after the ﬁrst year of life (Ries et al. 1999). Had the risk been conﬁned to children ≥ 1 year of age, this would have indicated that any putative association with agricultural pesticides is most relevant to the sporadic form; however, we saw increased risk estimates for the group < 1 year of age and up through 9 years of age. We also found a statistically significant association in this study for malignant melanoma. Reports indicate that incidence of this cancer has been increasing among children and adolescents in recent decades (Hamre et al. 2002; Strouse et al. 2005). Sun exposure (both intermittent and total accumulated) and number of melanocytic and dysplastic nevi are well-established risk factors for malignant melanoma in adults (Armstrong and English 1996) and also appear to be related to risk in children (Strouse et al. 2005). Many of the exposed counties in the study area were located in more northerly states not normally associ- ated with prolonged, intense sunlight exposure, so it seems unlikely that the increased risk would be attributed primarily to sun exposure. There has been an inconsistent pattern seen for melanoma risk associated with farmers and farming. Settimi et al. (1999, 2001) found an increased risk of melanoma in Italian farmers, but only among females. Another mortality study reported statistically signiﬁcant lowered mortality risk for melanoma among Wisconsin Agricultural pesticides and childhood cancers farmers (Hanrahan et al. 1996). Interestingly, a cancer mortality study among farmers in Iowa reported an increased mortality risk for melanoma, but only among younger farmers (20–64 years of age) (Cerhan et al. 1998). There has been some speculation that insecti- cides in particular may have a link with devel- opment of malignant melanoma, possibly by affecting melanocytic function (Burkhart and Burkhart 2000). Very little is known about the etiology of renal carcinomas, but there has been some indication of increased risk of Wilms’ tumor, the most common type of renal tumor in childhood, associated with possible occupa- tional pesticide exposures and home applica- tions (Sharpe et al. 1995; Zahm and Ward 1998). Similarly, because of the very few exist- ing studies, there is little evidence available to evaluate the potential for an association between pesticide exposures and risk of some of the rarer childhood cancers we evaluated, including soft-tissue sarcomas, malignant bone tumors, germ cell tumors, and hepatic tumors (Nasterlack 2006; Zahm and Ward 1998). Several limitations to our approach must be considered when interpreting the data. The exposure variable used is an imprecise surrogate for agriculturally related chemical exposures. However, of the 563 counties we categorized as exposed using this surrogate (i.e., having ≥ 20% of their total acreage in cropland), 332 (59%) had > 50% of their total county acreage in cropland, and 124 (22%) had a full Table 5. Estimated ORsa (95% CIs) for childhood cancers associated with speciﬁc crops, NAACCR, 1995–2001, ICCC major sites and selected subgroups. Cancer type All cancers Leukemias Lymphoid leukemias Acute myeloid leukemias Lymphomas and reticuloendothelial Hodgkin lymphomas Non-Hodgkin lymphomas Central nervous system Astrocytomas PNET Sympathetic nervous system tumors Neuroblastomas Retinoblastoma Renal tumors Wilms’ tumor Renal carcinoma Hepatic tumors Hepatoblastoma Malignant bone tumors Osteosarcoma Ewing’s sarcoma Soft-tissue sarcomas Rhabdomyosarcomas Germ cell, etc.b Carcinomas and otherc Thyroid carcinoma Malignant melanoma Other and unspeciﬁed Barley 0.9 (0.8–1.0) 1.0 (0.8–1.2) 1.0 (0.8–1.2) 1.0 (0.6–1.5) 1.1 (0.8–1.4) 1.0 (0.6–1.6) 1.0 (0.6–1.5) 0.8 (0.7–1.0) 0.7 (0.6–1.0) 0.8 (0.6–1.1) 0.8 (0.6–1.1) 0.8 (0.6–1.1) 0.9 (0.6–1.6) 0.9 (0.6–1.3) 0.9 (0.6–1.4) 4.7 (0.7–33.3) 0.6 (0.3–1.0) 0.6 (0.3–1.1) 1.3 (0.8–2.2) 1.3 (0.7–2.5) 1.1 (0.5–2.4) 0.9 (0.7–1.3) 1.2 (0.7–2.0) 0.7 (0.5–1.1) 1.0 (0.6–1.6) 1.7 (0.6–4.9) 1.3 (0.6–2.9) 1.1 (0.3–3.9) Corn 1.0 (0.9–1.0) 1.0 (0.9–1.1) 1.0 (0.9–1.1) 1.2 (1.0–1.5) 1.2 (1.0–1.4) 1.2 (1.0–1.5) 1.5 (1.1–1.8) 1.0 (0.9–1.1) 1.1 (1.0–1.3) 1.1 (0.9–1.3) 1.3 (1.1–1.5) 1.3 (1.1–1.5) 1.2 (0.9–1.5) 1.3 (1.1–1.6) 1.4 (1.1–1.7) 1.2 (0.6–2.6) 1.2 (0.8–1.7) 1.3 (0.9–1.9) 1.2 (1.0–1.4) 1.3 (1.0–1.7) 1.4 (1.0–2.0) 1.1 (1.0–1.3) 1.3 (1.0–1.6) 1.3 (1.0–1.7) 1.1 (0.9–1.4) 1.6 (1.1–2.3) 1.3 (0.8–2.0) 1.6 (0.8–3.0) Cotton 1.0 (0.9–1.1) 1.1 (1.0–1.3) 1.1 (0.9–1.3) 1.0 (0.7–1.5) 1.0 (0.8–1.3) 0.8 (0.5–1.2) 0.9 (0.6–1.3) 0.9 (0.7–1.1) 0.8 (0.6–1.1) 0.8 (0.6–1.2) 1.0 (0.7–1.4) 1.0 (0.7–1.3) 1.0 (0.6–1.7) 0.8 (0.6–1.1) 0.8 (0.6–1.1) 6.9 (1.4–34.0) 0.6 (0.3–1.3) 0.5 (0.2–1.1) 0.8 (0.5–1.1) 0.7 (0.5–1.2) 0.6 (0.3–1.2) 0.9 (0.6–1.2) 0.9 (0.6–1.5) 1.0 (0.7–1.6) 1.1 (0.8–1.6) 0.5 (0.2–1.3) 0.6 (0.3–1.3) 0.2 (0.0–0.5) Oats 1.0 (0.9–1.1) 1.1 (1.0–1.3) 1.2 (1.0–1.4) 1.1 (0.8–1.5) 1.2 (1.0–1.4) 1.2 (0.9–1.7) 1.5 (1.1–2.1) 1.1 (1.0–1.3) 1.3 (1.0–1.6) 1.5 (1.1–2.0) 1.1 (0.9–1.4) 1.1 (0.9–1.4) 1.6 (1.1–2.3) 1.0 (0.8–1.3) 1.1 (0.8–1.4) 2.2 (0.8–5.7) 1.4 (0.9–2.3) 1.7 (1.0–2.8) 1.3 (1.0–1.8) 1.4 (0.9–2.0) 2.3 (1.4–3.7) 1.2 (0.9–1.5) 1.2 (0.9–1.7) 2.6 (1.6–4.0) 1.3 (1.0–1.8) 2.0 (1.2–3.4) 2.4 (1.3–4.5) 3.2 (1.3–7.8) Soybean 1.0 (1.0–1.1) 1.0 (0.9–1.1) 1.0 (0.9–1.0) 1.4 (1.1–1.7) 1.2 (1.1–1.4) 1.4 (1.1–1.8) 1.3 (1.0–1.7) 1.0 (0.9–1.1) 1.0 (0.9–1.2) 1.2 (1.0–1.5) 1.3 (1.1–1.6) 1.3 (1.1–1.6) 1.4 (1.1–1.8) 1.4 (1.2–1.7) 1.4 (1.1–1.7) 2.0 (0.8–5.0) 1.1 (0.8–1.7) 1.1 (0.7–1.7) 1.2 (1.0–1.4) 1.4 (1.1–1.9) 1.3 (1.0–1.8) 1.2 (1.0–1.4) 1.3 (1.0–1.7) 1.2 (0.9–1.5) 1.3 (1.0–1.6) 1.4 (1.0–2.1) 1.2 (0.8–1.9) 1.0 (0.5–1.7) PNET, primitive ectodermal tumor. Referent category is counties with no acreage in the speciﬁc crop being evaluated and total percent cropland < 20%. aORs adjusted for age and sex. bGerm cell, trophoblastic, and other gonadal neoplasms. cCarcinomas and other malignant epithelial neoplasms. Environmental Health Perspectives • VOLUME 116 | NUMBER 4 | April 2008 Wheat 1.1 (1.0–1.2) 1.0 (0.9–1.2) 1.0 (0.9–1.1) 0.9 (0.6–1.2) 1.0 (0.8–1.3) 1.1 (0.7–1.6) 0.8 (0.6–1.1) 1.1 (0.9–1.2) 0.9 (0.8–1.2) 0.9 (0.6–1.1) 0.9 (0.7–1.2) 0.9 (0.7–1.2) 0.6 (0.4–1.0) 0.9 (0.6–1.1) 0.8 (0.6–1.1) 0.3 (0.0–2.0) 0.6 (0.3–1.2) 0.4 (0.2–0.7) 0.9 (0.7–1.3) 0.8 (0.6–1.2) 0.4 (0.3–0.7) 0.9 (0.7–1.1) 0.9 (0.6–1.3) 1.1 (0.7–1.7) 0.9 (0.6–1.2) 0.4 (0.3–0.7) 0.4 (0.2–0.8) 0.3 (0.2–0.7) 563