Newswise — WASHINGTON, D.C. — Increased exposure to traffic-related air pollution during pregnancy was associated with a higher incidence of acute lymphoblastic leukemia and two rare childhood cancers, according to data presented at the AACR Annual Meeting 2013, held in Washington, D.C., April 6-10.
“The main reason for undertaking this study was that we know much more about the causes of adult cancers than we do of the causes of childhood cancers,” said Julia Heck, Ph.D., M.P.H., assistant researcher in the Department of Epidemiology at the University of California, Los Angeles School of Public Health. “We studied pregnancy exposures because the fetus is likely to be more vulnerable to environmental factors during that time, and we also know that certain childhood cancers originate in utero.”
Heck and her colleagues identified 3,590 children from the California Cancer Registry born between 1998 and 2007 who could be linked to a California birth certificate. Children were five years of age or younger at diagnosis. Researchers selected controls at random from 80,224 children listed on California birth rolls. They used the California Line Source Dispersion Modeling Version 4 (CALINE4) to generate estimates of local traffic exposure at the mother’s home during each trimester of pregnancy and during the child’s first year of life. Estimates were based on local traffic emissions of gasoline vehicles and diesel trucks within a 1,500-meter radius buffer and included traffic volumes, roadway geometry, vehicle emission rates and meteorology.
Each interquartile range increase in exposure to traffic-related pollution was associated with an increased risk for developing acute lymphoblastic leukemia (4 percent), retinoblastoma (14 percent for all cases of the disease; 11 percent for retinoblastoma affecting just one eye and 19 percent for retinoblastoma affecting both eyes) and germ cell tumors (17 percent).
Because CALINE4 estimates were highly correlated across trimesters and during the first year of life, the researchers were not able to determine the most important period in terms of exposure.
“This is the first study that’s ever been reported on air pollution as it relates to rarer pediatric cancers, so it needs to be replicated in other states or in other countries,” Heck said. “It would be interesting to determine if there are specific pollutants like benzene or polycyclic aromatic hydrocarbons that are driving these associations.”
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Abstract Number: 2531
Presenter: Julia Heck, Ph.D., M.P.H.
Title: Childhood cancer and traffic-related air pollution exposure in pregnancy and early life
Authors: Julia E. Heck1, Jun Wu2, Travis J. Meyers1, Michelle Wilhelm1, Myles Cockburn3, Beate Ritz1. 1UCLA, Los Angeles, CA; 2UC Irvine, Irvine, CA; 3University of Southern California, Los Angeles, CA
Background: The literature on traffic-related air pollution and childhood cancers presents a mixture of findings, likely due to variations in exposure assessment methods, differing time periods in the children’s lives that were considered with regard to exposures, and often, small sample sizes which necessitated the grouping together of disparate cancer types. To date, few studies used a sophisticated emissions-based model to assess pollution exposures in pregnancy and early childhood.
Methods: The present study included children younger than age 6 identified in the California cancer registry (born 1998-2007) who could be linked to a California birth certificate (N=3590). Controls were selected at random from California birthrolls (N=80,224). CAlifornia LINE Source Dispersion Modeling, version 4 (CALINE4) was used to generate estimates of local traffic exposures at the child’s residence during each trimester of pregnancy and in the first year of life. Model inputs were based on local traffic emissions of both gasoline vehicles and diesel trucks within a 1500m radius buffer, and included traffic volumes, roadway geometry, vehicle emission rates, and meteorology. Unconditional logistic regression was used to estimate cancer risk.Results: A per interquartile range increase in exposure to traffic-related pollution from CALINE4 was associated with increases in acute lymphoblastic leukemia, germ cell tumors, and retinoblastoma, particularly bilateral. CALINE4 estimates were highly correlated across trimesters and the 1st year of life (r~0.96-0.98), making it difficult to discern the most important period for exposure.
Conclusions: Our findings support a relation between traffic pollution and several childhood cancers. As this is the first study to report upon traffic pollution in relation to retinoblastoma or germ cell tumors, and both are rare, these findings require replication in other studies.