Friday, 11 March 2011 16:26


Rate this item
(1 Vote)

Most of the radiation that a human being will be exposed to during a lifetime comes from natural sources in outer space or from materials present in the earth’s crust. Radioactive materials may affect the organism from without or, if inhaled or ingested with food, from within. The dose received may be very variable because it depends, on the one hand, on the amount of radioactive minerals present in the area of the world where the person lives—which is related to the amount of radioactive nuclides in the air and the amount found both in food and especially in drinking water—and, on the other, on the use of certain construction materials and the use of gas or coal for fuel, as well as the type of construction employed and the traditional habits of people in the given locality.

Today, radon is considered the most prevalent source of natural radiation. Together with its “daughters," or radionuclides formed by its disintegration, radon constitutes approximately three fourths of the effective equivalent dose to which humans are exposed due to natural terrestrial sources. The presence of radon is associated with an increase in the occurrence of lung cancer due to the deposition of radioactive substances in the bronchial region.

Radon is a colourless, odourless and tasteless gas seven times as heavy as air. Two isotopes occur most frequently. One is radon-222, a radionuclide present in the radioactive series from the disintegration of uranium-238; its main source in the environment is the rocks and the soil in which its predecessor, radium-226, occurs. The other is radon-220 from the thorium radioactive series, which has a lower incidence than radon-222.

Uranium occurs extensively in the earth’s crust. The median concentration of radium in soil is in the order of 25 Bq/kg. A Becquerel (Bq) is the unit of the international system and it represents a unit of radionuclide activity equivalent to one disintegration per second. The average concentration of radon gas in the atmosphere at the surface of the earth is 3 Bq/m3, with a range of 0.1 (over the oceans) to 10 Bq/m3. The level depends on the porousness of the soil, the local concentration of radium-226 and the atmospheric pressure. Given that the half-life of radon-222 is 3.823 days, most of the dosage is not caused by the gas but by radon daughters.

Radon is found in existing materials and flows from the earth everywhere. Because of its characteristics it disperses easily outdoors, but it has a tendency to become concentrated in enclosed spaces, notably in caves and buildings, and especially in lower spaces where its elimination is difficult without proper ventilation. In temperate regions, the concentrations of radon indoors are estimated to be in the order of eight times higher than the concentrations outdoors.

Exposure to radon by most of the population, therefore, occurs for the most part within buildings. The median concentrations of radon depend, basically, on the geological characteristics of the soil, on the construction materials used for the building and on the amount of ventilation it receives.

The main source of radon in indoor spaces is the radium present in the soil on which the building rests or the materials employed in its construction. Other significant sources—even though their relative influence is much less—are outside air, water and natural gas. Figure 1 shows the contribution that each source makes to the total.

Figure 1. Sources of radon in the indoor environment.


The most common construction materials, such as wood, bricks and cinder blocks, emit relatively little radon, in contrast to granite and pumice-stone. However, the main problems are caused by the use of natural materials such as alum slate in the production of construction materials. Another source of problems has been the use of by-products from the treatment of phosphate minerals, the use of by-products from the production of aluminium, the use of dross or slag from the treatment of iron ore in blast furnaces, and the use of ashes from the combustion of coal. In addition, in some instances, residues derived from uranium mining were also used in construction.

Radon can enter water and natural gas in the subsoil. The water used to supply a building, especially if it is from deep wells, may contain significant amounts of radon. If this water is used for cooking, boiling can free a large part of the radon it contains. If the water is consumed cold, the body eliminates the gas readily, so that drinking this water does not generally pose a significant risk. Burning natural gas in stoves without chimneys, in heaters and in other home appliances can also lead to an increase of radon in indoor spaces, especially dwellings. Sometimes the problem is more acute in bathrooms, because radon in water and in the natural gas used for the water heater accumulates if there is not enough ventilation.

Given that the possible effects of radon on the population at large were unknown just a few years ago, the data available on concentrations found in indoor spaces are limited to those countries which, because of their characteristics or special circumstances, are more sensitized to this problem. What is known for a fact is that it is possible to find concentrations in indoor spaces that are far above the concentrations found outdoors in the same region. In Helsinki (Finland), for instance, concentrations of radon in indoor air have been found that are five thousand times higher than the concentrations normally found outdoors. This may be due in large part to energy-saving measures that can noticeably favour the concentration of radon in indoor spaces, especially if they are heavily insulated. Buildings studied so far in different countries and regions show that the concentrations of radon found within them present a distribution that approximates the normal log. It is worth noting that a small number of the buildings in each region show concentrations ten times above the median. The reference values for radon in indoor spaces, and the remedial recommendations of various organizations are given in “Regulations, recommendations, guidelines and standards” in this chapter.

In conclusion, the main way to prevent exposures to radon is based on avoiding construction in areas that by their nature emit a greater amount of radon into the air. Where that is not possible, floors and walls should be properly sealed, and construction materials should not be used if they contain radioactive matter. Interior spaces, especially basements, should have an adequate amount of ventilation.



Read 6629 times Last modified on Friday, 12 August 2011 20:52

" DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."


Indoor Air Quality References

American Conference of Governmental Industrial Hygienists (ACGIH). 1989. Guidelines for the Assessment of Bioaerosols in the Indoor Environment. Cincinnati, Ohio: ACGIH.

American Society for Testing Materials (ASTM). 1989. Standard Guide for Small-Scale Environmental Determinations of Organic Emissions from Indoor Materials/Products. Atlanta: ASTM.

American Society of Heating Refrigerating and Air Conditioning Engineers (ASHRAE). 1989. Ventilation for Acceptable Indoor Air Quality. Atlanta: ASHRAE.

Brownson, RC, MCR Alavanja, ET Hock, and TS Loy. 1992. Passive smoking and lung cancer in non-smoking women. Am J Public Health 82:1525-1530.

Brownson, RC, MCR Alavanja, and ET Hock. 1993. Reliability of passive smoke exposure histories in a case-control study of lung cancer. Int J Epidemiol 22:804-808.

Brunnemann, KD and D Hoffmann. 1974. The pH of tobacco smoke. Food Cosmet Toxicol 12:115-124.

—. 1991. Analytical studies on N-nitrosamines in tobacco and tobacco smoke. Rec Adv Tobacco Sci 17:71-112.

COST 613. 1989. Formaldehyde emissions from wood based materials: Guideline for the determination of steady state concentrations in test chambers. In Indoor Air Quality & Its Impact On Man. Luxembourg: EC.

—. 1991. Guideline for the characterization of volatile organic compounds emitted from indoor materials and products using small test chambers. In Indoor Air Quality & Its Impact On Man. Luxembourg: EC.

Eudy, LW, FW Thome, DK Heavner, CR Green, and BJ Ingebrethsen. 1986. Studies on the vapour-particulate phase distribution of environmental nicotine by selective trapping and detection methods. In Proceedings of the Seventy-Ninth Annual Meeting of the Air Pollution Control Association, June 20-27.

Feeley, JC. 1988. Legionellosis: Risk associated with building design. In Architectural Design and Indoor Microbial Pollution, edited by RB Kundsin. Oxford: OUP.

Flannigan, B. 1992. Indoor microbiological pollutants—sources, species, characterisation: An evaluation. In Chemical, Microbiological, Health and Comfort Aspects of Indoor Air Quality—State of the Art in SBS, edited by H Knöppel and P Wolkoff. Dordrecht: Kluwer.

—. 1993. Approaches to the assessment of microbial flora of buildings. Environments for People: IAQ ’92. Atlanta: ASHRAE.

Freixa, A. 1993. Calidad Del Aire: Gases Presentes a Bajas Concentraciones En Ambientes Cerrados. Madrid: Instituto Nacional de Seguridad e Higiene en el Trabajo.

Gomel, M, B Oldenburg, JM Simpson, and N Owen. 1993. Work-site cardiovascular risk reduction: A randomized trial of health risk assessment, education, counselling and incentives. Am J Public Health 83:1231-1238.

Guerin, MR, RA Jenkins, and BA Tomkins. 1992. The Chemistry of Environmental Tobacco Smoke. Chelsea, Mich: Lewis.

Hammond, SK, J Coghlin, PH Gann, M Paul, K Taghizadek, PL Skipper, and SR Tannenbaum. 1993. Relationship between environmental tobacco smoke and carcinogen-hemoglobin adduct levels in non-smokers. J Natl Cancer Inst 85:474-478.

Hecht, SS, SG Carmella, SE Murphy, S Akerkar, KD Brunnemann, and D Hoffmann. 1993. A tobacco-specific lung carcinogen in men exposed to cigarette smoke. New Engl J Med 329:1543-1546.

Heller, W-D, E Sennewald, J-G Gostomzyk, G Scherer, and F Adlkofer. 1993. Validation of ETS-exposure in a representative population in Southern Germany. Indoor Air Publ Conf 3:361-366.

Hilt, B, S Langard, A Anderson, and J Rosenberg. 1985. Asbestos exposure, smoking habits and cancer incidence among production and maintenance workers in an electrical plant. Am J Ind Med 8:565-577.

Hoffmann, D and SS Hecht. 1990. Advances in tobacco carcinogenesis. In Handbook of Experimental Pharmacology, edited by CS Cooper and PL Grover. New York: Springer.

Hoffmann, D and EL Wynder. 1976. Smoking and occupational cancer. Prevent Med 5:245-261.
International Agency for Research on Cancer (IARC). 1986. Tobacco Smoking. Vol. 38. Lyon: IARC.

—. 1987a. Bis(Chloromethyl)Ether and Chloromethyl Methyl Ether. Vol. 4 (1974), Suppl. 7 (1987). Lyon: IARC.

—. 1987b. Coke Production. Vol. 4 (1974), Suppl. 7 (1987). Lyon: IARC.

—. 1987c. Environmental Carcinogens: Methods of Analysis and Exposure. Vol. 9. Passive smoking. IARC Scientific Publications, no. 81. Lyon: IARC.

—. 1987d. Nickel and Nickel Compounds. Vol. 11 (1976), Suppl. 7 (1987). Lyon: IARC.

—. 1988. Overall Evaluation of Carcinogenicity: An Updating of IARC Monographs 1 to 42. Vol. 43. Lyon: IARC.

Johanning, E, PR Morey, and BB Jarvis. 1993. Clinical-epidemiological investigation of health effects caused by Stachybotrys atra building contamination. In Proceedings of Sixth International Conference On Indoor Air Quality and Climate, Helsinki.

Kabat, GC and EL Wynder. 1984. Lung cancer incidence in non-smokers. Cancer 53:1214-1221.

Luceri, G, G Peiraccini, G Moneti, and P Dolara. 1993. Primary aromatic amines from sidestream cigarette smoke are common contaminants of indoor air. Toxicol Ind Health 9:405-413.

Mainville, C, PL Auger, W Smorgawiewicz, D Neculcea, J Neculcea, and M Lévesque. 1988. Mycotoxines et syndrome d’extrême fatigue dans un hôpital. In Healthy Buildings, edited by B Petterson and T Lindvall. Stockholm: Swedish Council for Building Research.

Masi, MA et al. 1988. Environmental exposure to tobacco smoke and lung function in young adults. Am Rev Respir Dis 138:296-299.

McLaughlin, JK, MS Dietz, ES Mehl, and WJ Blot. 1987. Reliability of surrogate information on cigarette smoking by type of informant. Am J Epidemiol 126:144-146.

McLaughlin, JK, JS Mandel, ES Mehl, and WJ Blot. 1990. Comparison of next of kin with self-respondents regarding question on cigarette, coffee and alcohol consumption. Epidemiology 1(5):408-412.

Medina, E, R Medina, and AM Kaempffer. 1988. Effects of domestic smoking on the frequency of infantile respiratory diseases. Rev Chilena Pediatrica 59:60-64.

Miller, JD. 1993. Fungi and the building engineer. Environments for People: IAQ ’92. Atlanta: ASHRAE.

Morey, PR. 1993a. Microbiological events after a fire in a high-rise building. In Indoor Air ’93. Helsinki: Indoor Air ‘93.

—. 1993b. Use of hazard communication standard and general duty clause during remediation of fungal contamination. In Indoor Air ‘93. Helsinki: Indoor Air ‘93.

Nathanson, T. 1993. Indoor Air Quality in Office Buildings: A Technical Guide. Ottawa: Health Canada.

New York City Department of Health. 1993. Guidelines On Assessment and Remediation of Stachybotrys Atra in Indoor Environments. New York: New York City Department of Health.

Pershagen, G, S Wall, A Taube, and I Linnman. 1981. On the interaction between occupational arsenic exposure and smoking and its relationship to lung cancer. Scand J Work Environ Health 7:302-309.

Riedel, F, C Bretthauer, and CHL Rieger. 1989. Einfluss von paasivem Rauchen auf die bronchiale Reaktivitact bei Schulkindern. Prax Pneumol 43:164-168.

Saccomanno, G, GC Huth, and O Auerbach. 1988. Relationship of radioactive radon daughters and cigarette smoking in genesis of lung cancer in uranium miners. Cancer 62:402-408.

Sorenson, WG. 1989. Health impact of mycotoxins in the home and workplace: An overview. In Biodeterioration Research 2, edited by CE O’Rear and GC Llewellyn. New York: Plenum.

Swedish Work Environment Fund. 1988. To Measure or to Take Direct Remedial Action? Investigation and Measurement Strategies in the Working Environment. Stockholm: Arbetsmiljöfonden [Swedish Work Environment Fund].

US Environmental Protection Agency (US EPA). 1992. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. Washington, DC: US EPA.

US National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effect. Washington, DC: National Academy of Sciences.

US Surgeon General. 1985. The Health Consequences of Smoking: Cancer and Chronic Lung Disease in the Workplace. Washington, DC: DHHS (PHS).

—. 1986. The Health Consequences of Involuntary Smoking. Washington, DC: DHHS (CDC).

Wald, NJ, J Borcham, C Bailey, C Ritchie, JE Haddow, and J Knight. 1984. Urinary cotinine as marker of breathing other people’s tobacco smoke. Lancet 1:230-231.

Wanner, H-U, AP Verhoeff, A Colombi, B Flannigan, S Gravesen, A Mouilleseux, A Nevalainen, J Papadakis, and K Seidel. 1993. Biological Particles in Indoor Environments. Indoor Air Quality and Its Impact On Man. Brussels: Commission of the European Communities.

White, JR and HF Froeb. 1980. Small airway dysfunction in non-smokers chronically exposed to tobacco smoke. New Engl J Med 302:720-723.

World Health Organization (WHO). 1987. Air Quality Guidelines for Europe. European Series, no. 23. Copenhagen: WHO Regional Publications.