Childhood cancers and atmospheric carcinogens

Abstract

Study objectives: To retest previous findings that childhood cancers are probably initiated by prenatal exposures to combustion process gases and to volatile organic compounds (VOCs); and to identify specific chemical hazards. Design: Birth and death addresses of fatal child cancers in Great Britain between 1966 and 1980, were linked with high local atmospheric emissions of different chemical species. Among migrant children, distances from each address to the nearest emissions ''hotspot'' were compared. Excesses of outward over inward migrations show an increased prenatal or early infancy risk. Setting and subjects: Maps of emissions of many different substances were published on the internet by the National Atmospheric Emissions Inventory and ''hotspots'' for 2001 were translated to map coordinates. Child cancer addresses were extracted from an earlier inquiry into the carcinogenic effects of obstetric radiographs; and their postcodes translated to map references. Main results: Significant birth proximity relative risks were found within 1.0 km of hotspots for carbon monoxide, PM10 particles, VOCs, nitrogen oxides, benzene, dioxins, 1,3-butadiene, and benz(a)pyrene. Calculated attributable risks showed that most child cancers and leukaemias are probably initiated by such exposures. Conclusions: Reported associations of cancer birth places with sites of industrial combustion, VOCs uses, and associated engine exhausts, are confirmed. Newly identified specific hazards include the known carcinogens 1,3-butadiene, dioxins, and benz(a)pyrene. The mother probably inhales these or related materials and passes them to the fetus across the placenta. P revious studies have shown (1) that childhood cancers and leukaemias in Great Britain exhibit geographical clustering of birth places: (2) they occur at increased densities around industrial sites with large scale combustion processes or using volatile organic compounds (VOCs), or which incinerate waste: (3) among children who moved house between birth and death the first addresses were closer to these hazards than were the later ones and migrations were more often directed away from a nearby hazard than towards one.

Reduced tumorigenesis in p53 knockout mice exposed in utero to low‐dose vitamin E

“…23,24 Conversely, prenatal folate and iron supplementation were associated with a reduced risk of acute lymphoblastic leukemia (ALL), 25 and prenatal multivitamin supplementation with a reduced risk of childhood brain tumors. 26,27 Similarly, neonatal twin studies suggest that some pediatric leukemias may be initiated in utero, 28 and ALL has been associated with chromosomal abnormalities, including high hyperdiploidy, that may reflect early initiating events in utero ( 29 and references therein).…”

Relationships between levels of volatile organic compounds in air and blood from the general population

“…Indeed, because personal air concentrations of VOCs are generally very low (p.p.b.) and poorly characterized in environmental epidemiology studies, the links between VOC exposures and environmental diseases, such as childhood asthma or leukemia, have not been well elucidated in the general population (Pappas et al, 2000;Duarte-Davidson et al, 2001;Delfino et al, 2003;Rumchev et al, 2004;Steffen et al, 2004;Knox, 2005;Elliott et al, 2006). Recent applications of passive monitors for measuring VOCs in ambient air suggest that it may be feasible to obtain personal exposure data from large numbers of subjects in future epidemiology studies of the general public Sexton et al, 2004).…”

Childhood Leukemia: A Preventable Disease

“…61,62 Studies of childhood brain tumors and other cancers also reported associations with ambient 3-butadiene, benzene, and particulate matter. 62,63 Overall, the similarity between tobacco smoke, ambient air pollutants, and paints and solvents in terms of mixtures of carcinogenic compounds and consistent tendencies to increase the risk of childhood leukemia is noteworthy, despite differences in exposure assessment (self-reports versus geocoding) and source of study participants. This observation lends further support for the probable role of volatile and persistent organic compounds in the development of the disease.…”