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. 2005 Sep;59(9):755–760. doi: 10.1136/jech.2004.031674

Oil combustion and childhood cancers

E Knox 1
PMCID: PMC1733143  PMID: 16100313

Abstract

Study objectives: To identify specific toxic atmospheric emissions and their industrial sources in Great Britain. To link them with each other and with the birth addresses of children dying from cancer. To identify specific causal agents and sources.

Design: Birth and death addresses of children dying from cancer were linked to emissions hotspots for specific chemicals: and to related source installations. Among those who moved house, distances from each address to the nearest hazard were compared. Relative excesses of close-to-hazard birth addresses showed high prenatal or early postnatal risks. Relative risks for individual and for combined exposures were measured.

Setting and subjects: Atmospheric emissions hotspots (UK, 2001) published as maps on the internet, were converted to coordinates. Industrial sites were identified through trade directories and map inspections. Child cancer addresses for 1955–80 births were extracted from an earlier inquiry and their postcodes converted to map references.

Main results: There were excess relative risks (RR) within 0.3 km of hotspots for carbon monoxide, PM10 particles, nitrogen oxides, 1,3-butadiene, benzene, dioxins, benzo(a)pyrene, and volatiles; and within 1.0 km of bus stations, hospitals, heavy transport centres, railways, and oil installations. Some excesses were attributable to mutual confounding, but 1,3-butadiene and carbon monoxide, mainly derived from engine exhausts, were powerful independent predictors. They were strongly reinforced when associated with bus stations, hospitals, railways, oil installations, and industrial transport centres; RR = 12.6 for joint <0.5 km exposure to bus stations and 1,3-butadiene.

Conclusions: Childhood cancers are strongly determined by prenatal or early postnatal exposures to oil based combustion gases, especially from engine exhausts. 1,3-butadiene, a known carcinogen, may be directly causal.

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Selected References

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