Radon carcinogenesis: risk data and cellular hits

Abstract

Abundant epidemiological data are now available (2008) on the human lung cancer response for lifetime radon gas exposure to residential concentrations of 100 Bq m(-3), equal to 22 working level months over 40 y. We combined published pooled epidemiological data and dosimetric calculations of alpha particle hits to target basal or mucous cell nuclei in bronchial epithelium. This yields an estimate that about 10,000 basal nuclei (target) cell hits per cm2 per person over a lifetime are involved in radon-related lung cancer. The DNA target cell area (cross section) for a hit is about 2 bp. The present epidemiology indicates that 1000 persons need to be exposed to this hit rate for observable cancers to be detected. The mechanism proposed is that the extensive prior DNA damage in smokers, followed by alpha particle damage to a critical site in checkpoint genes, accounts for the greater lung cancer response in smokers.

Tracing the sources of gaseous components (222Rn, CO2 and its carbon isotopes) in soil air under a cool-deciduous stand in Sapporo, Japan

“…Potential risk to human health by radon has been reported at many locations in the world (Darby et al 2005;Harley et al 2008). Authors in Slovenia have surveyed radon in public buildings including schools and hospitals for many years (Vaupotič 2003).…”

Using risk model judgements to better understand perceptions of synergistic risks

“…More specifically, in contrast to the alcohol-driving combination, (a) the risk of combining radon and tobacco has not been highlighted by widespread public campaigns, (b) the combination is not prohibited in law and (c) the underlying mechanism for the radon-tobacco synergistic risk is unlikely to be understood by the participants, as the mechanistic process is complex and not yet fully understood by scientists (Harley, Chittaporn, Heikkinen, Meyers, & Robbins, 2008).…”

“…The extent to which the synergistic risk attributable to radon-tobacco would be familiar to the participants is unclear. More specifically, in contrast to the alcohol-driving combination: (1) the risk of combining radon and tobacco has not been highlighted by widespread public campaigns; (2) the combination is not prohibited in law; and (3) the underlying mechanism for the radontobacco synergistic risk is unlikely to be understood by the participants, as the mechanistic process is complex and not yet fully understood by scientists (Harley, Chittaporn, Heikkinen, Meyers, & Robbins, 2008). However, authors of both US-and UK-based studies, each employing different response metrics, have reported that participants judged the risk attributable to the radon-tobacco combination as synergistic (Eiser, Reicher, & Podpadec, 1995;Hampson et al, 2000).…”

Air Pollution and Its Effects in the Respiratory System

“…The cancer risk from radon increases the risk from smoking. Radon induces damage to a checkpoint tumor suppressor gene such as Tp53 (which codes for p53) since alpha particle radiation is a key mechanism for radonrelated lung cancer (Harley et al, 2008;Bissett & McLaughlin 2010). Some studies suggest a relationship between the AGGARG-ATGMET transversion in codon 249 of P53 from people exposed to high radon concentrations (Ruano-Ravina et al, 2009).…”