Supervising Scientist Division

Explanatory notes on radon and radon progeny

Background

Radon-222 (radon) is a naturally occurring radioactive gas (half-life 3.8 days) formed through the decay of radium-226 in the uranium-238 decay series.

Because uranium-238 and radium-226 occur naturally at low concentrations in most rocks and soils, radon emanates from these materials, permeating through the soil pore space before being exhaled from the ground surface to the atmosphere where it is dispersed by diffusion and wind currents.

When radon in air decays, it forms a number of short-lived radioactive decay products (‘radon progeny’), which include polonium-218, lead-214, bismuth-214 and polonium-214. All are radioactive isotopes of heavy metal elements and all have half-lives that are much less than that of radon.

The concentration of radon progeny in air depends on the several factors:

The typical daily (diurnal) trend of radon progeny in air is for concentrations to peak in the early morning when atmospheric conditions tend to be most stable and then reduce during the day when air mixing increases through thermal convection and advection by wind.

Radon progeny concentrations in air may also vary seasonally. In the Top End of the Northern Territory the typical seasonal trend is for concentrations to be lower in the wet season due to rainfall suppression of radon exhalation from the ground surface and washout of radon progeny aerosols from the atmosphere. Higher concentrations are expected to occur in the dry season due to dry soils allowing greater permeation and exhalation of radon gas from the ground surface to the atmosphere.

Conversion of radon progeny PAEC to effective dose

Radon itself does not contribute much to dose since it is immediately exhaled from the lung before decaying. The main contribution to dose is from the inhalation of radon progeny in air. Some of the inhaled radon progeny are retained in the lung, with the subsequent alpha decays delivering a radiation dose.

Potential Alpha Energy Concentration (PAEC) gives a measure of the total alpha energy that may be emitted during the decay of radon progeny. The effective dose received by a member of the public via the inhalation pathway from exposure to radon progeny in air can be estimated from the PAEC as:

ERP = PAEC × HRP × t

With:

ERP (µSv) effective dose via the inhalation pathway from exposure to radon progeny in air

PAEC (µJ/m3) radon progeny potential alpha energy concentration

HRP (µSv per (µJh/m3)) dose coefficient for converting radon progeny PAEC to effective dose

t (hours) exposure time

The radon progeny dose coefficient HRP recommended by the International Commission on Radiological Protection (ICRP) for members of the public is 1.1 µSv per (µJh/m3) (ICRP 1993).

Anticipated change in radon progeny dose coefficient

The ICRP has recently published a report on lung cancer risk from the inhalation of radon and radon progeny (ICRP 2010). The report recommends changes to the dose conversion convention for estimating lung cancer risk from radon and radon progeny. These changes will result in new dose coefficients for inhalation of radon progeny, which are expected to be larger by a factor of two or more than the existing dose coefficient. Until such time as the ICRP publishes new dose coefficients for the inhalation of radon progeny, the existing dose coefficient of 1.1 µSv per (µJh/m3) for members of the public remains valid.

Estimate of total annual effective dose to the public at Jabiru town and Mudginberri community from radon progeny

For the 2011 calendar year, the total annual effective dose to the public at Jabiru town and Mudginberri community from radon progeny in air has been estimated to be 0.18 mSv and 0.21 mSv, respectively. This estimate has been made by calculating the hourly dose from the hourly PAEC, summing the hourly dose increments over the full year and then dividing by the percentage up time of the monitoring station to account for data gaps. The percentage up time of the Jabiru town and Mudginberri monitoring stations in 2011 was 67% and 60%, respectively. Most of the down time of the two monitoring stations occurred during the dry season, in May, June and October 2011. This, together with the long 2010–11 wet season, most likely lead to the low estimated total annual effective doses to the public from inhalation of radon progeny in air compared to previous years.

The estimated total annual effective dose is primarily due to radon progeny originating from the natural environment. The difference in dose levels between the two locations is caused by local meteorological conditions affecting radon exhalation and air mixing.

Contribution to annual effective dose from radon progeny originating from the Ranger mine

Previous research conducted by the Supervising Scientist Division suggests that the contribution to public dose at Jabiru town and Mudginberri community from radon progeny in air originating from the Ranger mine is a few percent or less of the annual dose limit of 1 mSv for full time occupancy at these locations. Although the dose limit applies to the sum of doses received from all exposure pathways, it is clear that there is no unacceptable radiation risk to the public at Jabiru town or Mudginberri community from radon progeny in air that may originate from the Ranger mine.

References

ICRP 1993. Protection against radon-222 at home and at work. ICRP Publication 65, Annals of the ICRP 23(2).

ICRP 2010. Lung cancer risk from radon and progeny and statement on radon. ICRP Publication 115, Annals of the ICRP 40(1).

Toxicity monitoring

Explanatory notes

Glossary