The free radical theory of aging (FRTA) states that organisms age because cells accumulate free radical damage over time. A free radical is any atom or molecule that has a single unpaired electron in an outer shell. While a few free radicals such as melanin are not chemically reactive, most biologically relevant free radicals are highly reactive. For most biological structures, free radical damage is closely associated with oxidative damage. Antioxidants are reducing agents, and limit oxidative damage to biological structures by passivating them from free radicals.
Strictly speaking, the free radical theory is only concerned with free radicals such as superoxide ( O2− ), but it has since been expanded to encompass oxidative damage from other reactive oxygen species such as hydrogen peroxide (H2O2), or peroxynitrite (OONO−).
Denham Harman first proposed the free radical theory of aging in the 1950s, and in the 1970s extended the idea to implicate mitochondrial production of reactive oxygen species.
In some model organisms, such as yeast and Drosophila, there is evidence that reducing oxidative damage can extend lifespan. However, in mice, only 1 of the 18 genetic alterations (SOD-1 deletion) that block antioxidant defences, shortened lifespan. Similarly, in roundworms (Caenorhabditis elegans), blocking the production of the naturally occurring antioxidant superoxide dismutase has recently been shown to increase lifespan.
Whether reducing oxidative damage below normal levels is sufficient to
extend lifespan remains an open and controversial question.
Background
The free radical theory of aging was conceived by Denham Harman in the 1950s, when prevailing scientific opinion held that free radicals were too unstable to exist in biological systems. This was also before anyone invoked free radicals as a cause of degenerative diseases. Two sources inspired Harman: 1) the rate of living theory,
which holds that lifespan is an inverse function of metabolic rate
which in turn is proportional to oxygen consumption, and 2) Rebbeca
Gershman's observation that hyperbaric oxygen toxicity and radiation toxicity could be explained by the same underlying phenomenon: oxygen free radicals.
Noting that radiation causes "mutation, cancer and aging", Harman
argued that oxygen free radicals produced during normal respiration
would cause cumulative damage which would eventually lead to organismal
loss of functionality, and ultimately death.
In later years, the free radical theory was expanded to include not only aging per se, but also age-related diseases. Free radical damage within cells has been linked to a range of disorders including cancer, arthritis, atherosclerosis, Alzheimer's disease, and diabetes.
There has been some evidence to suggest that free radicals and some
reactive nitrogen species trigger and increase cell death mechanisms
within the body such as apoptosis and in extreme cases necrosis.
In 1972, Harman modified his original theory. In its current form, this theory proposes that reactive oxygen species that are produced in the mitochondria, causes damage to certain macromolecules including lipids, proteins and most importantly mitochondrial DNA. This damage then causes mutations which lead to an increase of ROS production and greatly enhance the accumulation of free radicals within cells. This mitochondrial theory has been more widely accepted that it could play a major role in contributing to the aging process.
Since Harman first proposed the free radical theory of aging,
there have been continual modifications and extensions to his original
theory.
Processes
In chemistry, a free radical is any atom, molecule, or ion with an unpaired valence electron
Free radicals are atoms or molecules containing unpaired electrons. Electrons normally exist in pairs in specific orbitals in atoms or molecules.
Free radicals, which contain only a single electron in any orbital, are
usually unstable toward losing or picking up an extra electron, so that
all electrons in the atom or molecule will be paired.
Note that the unpaired electron does not imply charge - free radicals can be positively charged, negatively charged, or neutral.
Damage occurs when the free radical encounters another molecule
and seeks to find another electron to pair its unpaired electron. The
free radical often pulls an electron off a neighboring molecule, causing
the affected molecule to become a free radical itself. The new free
radical can then pull an electron off the next molecule, and a chemical chain reaction of radical production occurs.
The free radicals produced in such reactions often terminate by
removing an electron from a molecule which becomes changed or cannot
function without it, especially in biology. Such an event causes damage
to the molecule, and thus to the cell that contains it (since the
molecule often becomes dysfunctional).
The chain reaction caused by free radicals can lead to
cross-linking of atomic structures. In cases where the free
radical-induced chain reaction involves base pair molecules in a strand of DNA, the DNA can become cross-linked.
DNA cross-linking can in turn lead to various effects of aging, especially cancer. Other cross-linking can occur between fat and protein molecules, which leads to wrinkles. Free radicals can oxidize LDL, and this is a key event in the formation of plaque in arteries, leading to heart disease and stroke. These are examples of how the free-radical theory of aging has been used to neatly "explain" the origin of many chronic diseases.
Free radicals that are thought to be involved in the process of aging include superoxide and nitric oxide.
Specifically, an increase in superoxide affects aging whereas a
decrease in nitric oxide formation, or its bioavailability, does the
same.
Antioxidants
are helpful in reducing and preventing damage from free radical
reactions because of their ability to donate electrons which neutralize
the radical without forming another. Ascorbic acid,
for example, can lose an electron to a free radical and remain stable
itself by passing its unstable electron around the antioxidant molecule.
This has led to the hypothesis that large amounts of antioxidants,
with their ability to decrease the numbers of free radicals, might
lessen the radical damage causing chronic diseases, and even radical
damage responsible for aging.
Evidence
Numerous studies have demonstrated a role for free radicals
in the aging process and thus tentatively support the free radical
theory of aging. Studies have shown a significant increase in superoxide radical (SOR) formation and lipid peroxidation in aging rats. Chung et al. suggest ROS production increases with age and indicated the conversion of XDH to XOD may be an important contributing factor. This was supported by a study that showed superoxide production by xanthine oxidase and NO synthase in mesenteric arteries was higher in older rats than young ones.
Hamilton et al. examined the similarities in impaired endothelial function in hypertension and aging in humans and found a significant overproduction of superoxide in both. This finding is supported by a 2007 study which found that endothelial oxidative stress develops with aging in healthy men and is related to reductions in endothelium-dependent dilation.
Furthermore, a study using cultured smooth muscle cells displayed
increased reactive oxygen species (ROS) in cells derived from older
mice. These findings were supported by a second study using Leydig cells isolated from the testes of young and old rats.
The Choksi et al. experiment with Ames dwarf (DW) mice suggests
the lower levels of endogenous ROS production in DW mice may be a factor
in their resistance to oxidative stress and long life. Lener et al. suggest Nox4 activity increases oxidative damage in human umbilical vein endothelial cells via superoxide overproduction.
Furthermore, Rodriguez-Manas et al. found endothelial dysfunction in
human vessels is due to the collective effect of vascular inflammation
and oxidative stress.
Sasaki et al. reported superoxide-dependent chemiluminescence was inversely proportionate to maximum lifespan in mice, Wistar rats, and pigeons. They suggest ROS signalling may be a determinant in the aging process. In humans, Mendoza-Nunez et al. propose an age of 60 years or older may be linked with increased oxidative stress. Miyazawa found mitochondrial superoxide anion production can lead to organ atrophy and dysfunction via mitochondrial- mediated apoptosis. In addition, they suggest mitochondrial superoxide anion plays an essential part in aging. Lund et al. demonstrated the role of endogenous extracellular superoxide dismutase in protecting against endothelial dysfunction during the aging process using mice.
Modifications of the free radical theory of aging
One
of the main criticisms of the free radical theory of aging is directed
at the suggestion that free radicals are responsible for the damage of biomolecules, thus being a major reason for cellular senescence and organismal aging. Several modifications have been proposed to integrate current research into the overall theory.
Mitochondrial theory of aging was first proposed in 1978, and shortly thereafter the Mitochondrial free radical theory of aging was introduced in 1980.
The theory implicates the mitochondria as the chief target of radical
damage, since there is a known chemical mechanism by which mitochondria
can produce Reactive oxygen species (ROS), mitochondrial components such as mtDNA
are not as well protected as nuclear DNA, and by studies comparing
damage to nuclear and mtDNA that demonstrate higher levels of radical
damage on the mitochondrial molecules. Electrons may escape from metabolic processes in the mitochondria like the Electron transport chain, and these electrons may in turn react with water to form ROS such as the superoxide radical, or via an indirect route the hydroxyl radical.
These radicals then damage the mitochondria's DNA and proteins, and
these damage components in turn are more liable to produce ROS
byproducts. Thus a positive feedback loop
of oxidative stress is established that, over time, can lead to the
deterioration of cells and later organs and the entire body.
This theory has been widely debated and it is still unclear how ROS induced mtDNA mutations develop.
Conte et al. suggest iron-substituted zinc fingers may generate free
radicals due to the zinc finger proximity to DNA and thus lead to DNA
damage.
Afanas'ev suggests the superoxide dismutation activity of CuZnSOD
demonstrates an important link between life span and free radicals.
The link between CuZnSOD and life span was demonstrated by Perez et al.
who indicated mice life span was affected by the deletion of the Sod1
gene which encodes CuZnSOD.
Contrary to the usually observed association between
mitochondrial ROS (mtROS) and a decline in longevity, Yee et al.
recently observed increased longevity mediated by mtROS signaling in an
apoptosis pathway. This serves to support the possibility that observed
correlations between ROS damage and aging are not necessarily indicative
of the causal involvement of ROS in the aging process but are more
likely due to their modulating signal transduction pathways that are
part of cellular responses to the aging process.
Epigenetic oxidative redox shift (EORS) theory of aging
Brewer proposed a theory which integrates the free radical theory of aging with the insulin signalling effects in aging. Brewer's theory suggests "sedentary behaviour associated with age triggers an oxidized redox shift and impaired mitochondrial function". This mitochondrial impairment leads to more sedentary behaviour and accelerated aging.
Metabolic stability theory of aging
The
metabolic stability theory of aging suggests it is the cells ability to
maintain stable concentration of ROS which is the primary determinant
of lifespan.
This theory criticizes the free radical theory because it ignores that
ROS are specific signalling molecules which are necessary for
maintaining normal cell functions.
Mitohormesis
Oxidative stress may promote life expectancy of Caenorhabditis elegans by inducing a secondary response to initially increased levels of reactive oxygen species. In mammals, the question of the net effect of reactive oxygen species on aging is even less clear. Recent epidemiological
findings support the process of mitohormesis in humans, and even
suggest that the intake of exogenous antioxidants may increase disease prevalence
in humans (according to the theory, because they prevent the
stimulation of the organism's natural response to the oxidant compounds
which not only neutralizes them but provides other benefits as well).
Studies have demonstrated that calorie restriction displays positive
effects on the lifespan of organisms even though it is accompanied by
increases in oxidative stress. Many studies suggest this may be due to anti-oxidative action, oxidative stress suppression, or oxidative stress resistance
which occurs in calorie restriction. Fontana et al. suggest calorie
restriction influenced numerous signal pathways through the reduction of
insulin-like growth factor I (IGF-1). Additionally they suggest antioxidant SOD and catalase are involved in the inhibition of this nutrient signalling pathway.
The increase in life expectancy observed during some calorie
restriction studies which can occur with lack of decreases or even
increases in O2 consumption is often inferred as opposing the mitochondrial free radical theory of aging.However, Barja showed significant decreases in mitochondrial oxygen radical production (per unit of O2 consumed) occur during dietary restriction, aerobic exercise, chronic exercise, and hyperthyroidism.
Additionally, mitochondrial oxygen radical generation is lower in
long-lived birds than in short-lived mammals of comparable body size and
metabolic rate. Thus, mitochondrial ROS production must be regulated independently of O2 consumption in a variety of species, tissues and physiologic states.
Challenges to the free radical theory of aging
Naked Mole-rat
The naked mole-rat is a long-lived (32 years) rodent. As reviewed by Lewis et al., (2013), levels of reactive oxygen species (ROS) production in the naked mole rat are similar to that of another rodent, the relatively short-lived mouse
(4 years). They concluded that it is not oxidative stress that
modulates health-span and longevity in these rodents, but rather other
cytoprotective mechanisms that allow animals to deal with high levels of
oxidative damage and stress.
In the naked mole-rat, a likely important cytoprotective mechanism
that could provide longevity assurance is elevated expression of DNA repair genes involved in several key DNA repair pathways. Compared with the mouse, the naked mole rat had significantly higher
expression levels of genes essential for the DNA repair pathways of DNA mismatch repair, non-homologous end joining and base excision repair.
Birds
Among birds, parrots live about 5-times longer than quail. Reactive oxygen species (ROS)
production in heart, skeletal muscle, liver and intact erythrocytes was
found to be similar in parrots and quail and showed no correspondence
with longevity difference. These findings were concluded to cast doubt on the robustness of the oxidative stress theory of aging.
The mitochondrial theory of aging has two varieties: free radical and
non-free radical. The first is one of the variants of the free radical
theory of aging. It was formulated by J. Michel in 1980 and was
developed in the works of A. V. Linnan (1989). The second was proposed
by A. N. Lobachev in 1978.
The mitochondrial free radical theory of aging (MFRTA) proposes that free radicals produced by mitochondrial activity damage cellular components, leading to aging.
Free radicals damage mitochondria, which according to the mitochondrial free radical theory of aging, leads to ageing
Mitochondria are cellorganelles which function to provide the cell with energy by producing ATP (adenosine triphosphate). During ATP production electrons can escape the mitochondrion and react with water, producing reactive oxygen species, ROS for short. ROS can damage macromolecules, including lipids, proteins and DNA, which is thought to facilitate the process of ageing.
Electron Transport Chain in the Inner Mitochondrial Membrane
ROS are highly reactive, oxygen-containing chemical species, which include superoxide, hydrogen peroxide and hydroxyl radical.
If the complexes
of the ETC do not function properly, electrons can leak and react with
water, forming ROS. Normally leakage is low and ROS is kept at physiological levels, fulfilling roles in signaling and homeostasis. In fact, their presence at low levels lead to increased life span, by activating transcription factors and metabolic pathways involved in longevity. At increased levels ROS cause oxidative damage
by oxidizing macromolecules, such as lipids, proteins and DNA. This
oxidative damage to macromolecules is thought to be the cause of ageing.
Mitochondrial DNA is especially susceptible to oxidative damage, due to
its proximity to the site of production of these species.
Damaging of mitochondrial DNA causes mutations, leading to production
of ETC complexes, which don’t function properly, increasing ROS
production, increasing oxidative damage to macromolecules.
UPRmt
The mitochondrial unfolded protein response (UPRmt) is turned on in response to mitochondrial stress. Mitochondrial stress occurs when the proton gradient across the inner mitochondrial membrane is dissipated, mtDNA is mutated, and/or ROS accumulates, which can lead to misfolding and reduced function of mitochondrial proteins. Stress is sensed by the nucleus, where chaperones and proteases are upregulated, which can correct folding or remove damaged proteins, respectively. Decrease in protease levels are associated with ageing, as mitochondrial stress will remain, maintaining high ROS levels. Such mitochondrial stress and dysfunction has been linked to various age-associated diseases, including cardiovascular diseases, and type-2 diabetes.
Mitochondrial metabolites
As the mitochondrial matrix is where the TCA cycle takes place, different metabolites
are commonly confined to the mitochondria. Upon ageing, mitochondrial
function declines, allowing escape of these metabolites, which can
induce epigenetic changes, associated with ageing.
TCA cycle
Acetyl-coenzyme A (Acetyl-CoA) enters the TCA cycle in the mitochondrial matrix, and is oxidized in the process of energy production. Upon escaping the mitochondria and entering the nucleus, it can act as a substrate for histone acetylation. Histone acetylation is an epigenetic modification, which leads to gene activation.
At a young age, acetyl-CoA levels are higher in the nucleus and cytosol, and its transport to the nucleus can extend lifespan in worms.
Nicotinamide Adenine Dinucleotide (NAD+) is produced in the mitochondria and upon escaping to the nucleus, can act as a substrate for sirtuins. Sirtuins are family of proteins, known to play a role in longevity. Cellular NAD+ levels have been shown to decrease with age.
DAMPs
Damage-associated molecular patterns (DAMPs) are molecules that are released during cell stress.
Mitochondrial DNA is a DAMP, which only becomes available during
mitochondrial damage. Blood mitochondrial DNA levels become elevated
with age, contributing to inflamm-aging, a chronic state of inflammation characteristic of advanced age.
Mitochondrial-derived peptides
Mitochondrial
DNA has been known to encode 13 proteins. Recently, other short protein
coding sequences have been identified, and their products are referred
to as mitochondria-derived peptides.
MOTS-c has been shown to prevent age-associated insulin resistance, the main cause of type 2 diabetes.
Humanin and MOTS-c levels have been shown to decline with age, and their activity seems to increase longevity.
Mitochondrial membrane
Almaida-Pagan and coworkers found that mitochondrial membrane lipid composition changes with age, when studying Turquoise killifish. The proportion of monosaturatedfatty acids decreased with age, and the proportion of polysaturated fatty acids increased. The overall phospholipid content also decreased with age.
History
In 1956 Denham Harman first postulated the free radical theory of ageing, which he later modified to the mitochondrial free radical theory of ageing (MFRTA).
He found ROS as the main cause of damage to macromolecules, known as
“ageing”. He later modified his theory because he found that
mitochondria were producing and being damaged by ROS, leading him to the
conclusion that mitochondria determine ageing. In 1972, he published
his theory in the Journal of the American Geriatrics Society.
Evidence
It has been observed that with age, mitochondrial function declines and mitochondrial DNA mutation increases in tissue
cells in an age-dependent manner. This leads to increase in ROS
production and potential decrease in the cell’s ability to remove ROS.
Most long-living animals have been shown to be more resistant to
oxidative damage and have lower ROS production, linking ROS levels to
lifespan. Overexpression of antioxidants, which function to remove ROS has also been shown to increase lifespan.
Bioinformatics
analysis showed that amino acid composition of mitochondrial proteins
correlate with longevity (long-living species are depleted in cysteine and methionine), linking mitochondria to the process of ageing.By studying expression of certain genes in C. elegans, Drosophila, and mice it was found that disruption of ETC complexes can extend life – linking mitochondrial function to the process of ageing.
Evidence supporting the theory started to crumble in the early 2000s.
Mice with reduced expression of the mitochondrial antioxidant, SOD2, accumulated oxidative damage and developed cancer, but did not live longer than normal life. Overexpression of antioxidants reduced cellular stress, but did not increase mouse life span. The naked mole-rat, which lives 10-times longer than normal mice, has been shown to have higher levels of oxidative damage.
Radon (/ˈreɪdɒn/) is a radioactive, colorless, odorless, tasteless noble gas, occurring naturally as the decay product of radium.
It is one of the densest substances that remains a gas under normal
conditions, and is considered to be a health hazard due to its
radioactivity. Its most stable isotope, 222Rn, has a half-life of 3.8 days. Due to its high radioactivity, it has been less well-studied by chemists, but a few compounds are known.
Radon is formed as part of the normal radioactive decay chain of uranium into 206Pb. Uranium has been present since the earth was formed and its most common isotope
has a very long half-life (4.5 billion years), which is the time
required for one-half of uranium to break down. Thus, uranium and radon,
will continue to occur for millions of years at about the same
concentrations as they do now.
Radon is responsible for the majority of the mean public exposure to ionizing radiation.
It is often the single largest contributor to an individual's
background radiation dose, and is the most variable from location to
location. Radon gas from natural sources can accumulate in buildings,
especially in confined areas such as attics, and basements. It can also
be found in some spring waters and hot springs.
According to a 2003 report EPA's Assessment of Risks from Radon in Homes from the United StatesEnvironmental Protection Agency, epidemiological evidence shows a clear link between lung cancer and high concentrations of radon, with 21,000 radon-induced U.S. lung cancer deaths per year—second only to cigarette smoking. Thus in geographic areas where radon is present in heightened concentrations, radon is considered a significant indoor air contaminant.
210Pb is formed from the decay of 222Rn. Here is a typical deposition rate of 210Pb as observed in Japan as a function of time, due to variations in radon concentration.
Radon concentration is usually measured in the atmosphere in becquerels per cubic meter (Bq/m3), which is an SI derived unit. As a frame of reference, typical domestic exposures are about 100 Bq/m3 indoors and 10-20 Bq/m3 outdoors. In the US, radon concentrations are often measured in picocuries per liter (pCi/l), with 1 pCi/l = 37 Bq/m3.
The mining industry traditionally measures exposure using the working level (WL) index, and the cumulative exposure in working level months (WLM): 1 WL equals any combination of short-lived 222Rn progeny (218Po, 214Pb, 214Bi, and 214Po) in 1 liter of air that releases 1.3 × 105 MeV of potential alpha energy; one WL is equivalent to 2.08 × 10−5 joules per cubic meter of air (J/m3).[1] The SI unit of cumulative exposure is expressed in joule-hours per cubic meter (J·h/m3). One WLM is equivalent to 3.6 × 10−3 J·h/m3. An exposure to 1 WL for 1 working month (170 hours) equals 1 WLM cumulative exposure.
A cumulative exposure of 1 WLM is roughly equivalent to living one year in an atmosphere with a radon concentration of 230 Bq/m3.
The radon (222Rn) released into the air decays to 210Pb and other radioisotopes. The levels of 210Pb can be measured. The rate of deposition of this radioisotope is dependent on the weather.
Natural
Radon concentration next to a uranium mine
Radon concentrations found in natural environments are much too low to be detected by chemical means: for example, a 1000 Bq/m3 (relatively high) concentration corresponds to 0.17 pico-gram per cubic meter. The average concentration of radon in the atmosphere is about 6×10−20 atoms of radon for each molecule in the air, or about 150 atoms in each ml of air.
The entire radon activity of the Earth's atmosphere at a time is due to
some tens of grams of radon, consistently replaced by decay of larger
amounts of radium and uranium. Concentrations can vary greatly from place to place. In the open air, it ranges from 1 to 100 Bq/m3, even less (0.1 Bq/m3) above the ocean. In caves, aerated mines, or in poorly ventilated dwellings, its concentration can climb to 20-2,000 Bq/m3.
In mining contexts, radon concentrations can be much higher.
Ventilation regulations try to maintain concentrations in uranium mines
under the "working level", and under 3 WL (546 pCi 222Rn per liter of air; 20.2 kBq/m3 measured from 1976 to 1985) 95 percent of the time.
The concentration in the air at the (unventilated) Gastein Healing Gallery averages 43 kBq/m3 (about 1.2 nCi/L) with maximal value of 160 kBq/m3 (about 4.3 nCi/L).
Radon emanates naturally from the ground and from some building materials all over the world, wherever traces of uranium or thorium can be found, and particularly in regions with soils containing granite or shale, which have a higher concentration of uranium. Every square mile of surface soil, to a depth of 6 inches (2.6 km2 to a depth of 15 cm), contains approximately 1 gram of radium, which releases radon in small amounts to the atmosphere Sand used in making concrete is the major source of radon in buildings.
On a global scale, it is estimated that 2,400 million curies (91
TBq) of radon are released from soil annually. Not all granitic regions
are prone to high emissions of radon. Being a rare gas, it usually
migrates freely through faults and fragmented soils, and may accumulate
in caves or water. Due to its very small half-life (four days for 222Rn), its concentration decreases very quickly when the distance from the production area increases.
Its atmospheric concentration varies greatly depending on the
season and conditions. For instance, it has been shown to accumulate in
the air if there is a meteorological inversion and little wind.
Because atmospheric radon concentrations are very low, radon-rich water exposed to air continually loses radon by volatilization. Hence, ground water generally has higher concentrations of 222Rn than surface water, because the radon is continuously produced by radioactive decay of 226Ra
present in rocks. Likewise, the saturated zone of a soil frequently has
a higher radon content than the unsaturated zone because of diffusional
losses to the atmosphere. As a below-ground source of water, some springs—including hot springs—contain significant amounts of radon. The towns of Boulder, Montana; Misasa; Bad Kreuznach, Germany; and the country of Japan
have radium-rich springs which emit radon. To be classified as a radon
mineral water, radon concentration must be above a minimum of 2 nCi/L
(74 Bq/L). The activity of radon mineral water reaches 2,000 Bq/L in Merano and 4,000 Bq/L in the village of Lurisia (Ligurian Alps, Italy).
Radon is also found in some petroleum. Because radon has a
similar pressure and temperature curve as propane, and oil refineries
separate petrochemicals based on their boiling points, the piping
carrying freshly separated propane in oil refineries can become
partially radioactive due to radon decay particles. Residues from the oil and gas
industry often contain radium and its daughters. The sulfate scale from
an oil well can be radium rich, while the water, oil, and gas from a
well often contains radon. The radon decays to form solid radioisotopes
which form coatings on the inside of pipework. In an oil processing
plant, the area of the plant where propane is processed is often one of the more contaminated areas, because radon has a similar boiling point as propane.
Accumulation in dwellings
Typical Lognormal radon distribution in dwellings
Typical domestic exposures are of around 100Bq/m3
indoors, but specifics of construction and ventilation strongly affect
levels of accumulation; a further complications for risk assessment is
that concentrations in a single location may differ by a factor of two
over an hour, and concentrations can vary greatly even between two
adjoining rooms in the same structure.
The distribution of radon concentrations tends to be asymmetrical
around the average, the larger concentrations have a disproportionately
greater weight. Indoor radon concentration is usually assumed to follow
a lognormal distribution on a given territory. Thus, the geometric mean is generally used for estimating the "average" radon concentration in an area.
The mean concentration ranges from less than 10 Bq/m3 to over 100 Bq/m3 in some European countries. Typical geometric standard deviations found in studies range between 2 and 3, meaning (given the 68-95-99.7 rule) that the radon concentration is expected to be more than a hundred times the mean concentration for 2 to 3% of the cases.
The so-called "Watras incident" in 1984 (named for
American construction engineer Stanley Watras), in which Watras, an
employee at a U.S. nuclear power plant, triggered radiation monitors
while leaving work over several days — despite the fact that the plant
had not yet been fueled, and despite Watras being decontaminated and
sent home "clean" each evening — pointed to a source of contamination
outside the power plant, which turned out to be radon levels of 100,000 Bq/m3 (2.7 nCi/L)
in the basement of his home. He was told that living in the home was
the equivalent of smoking 135 packs of cigarettes a day, and he and his
family had increased their risk of developing lung cancer by 13 or 14
percent. The incident dramatized the fact that radon levels in particular dwellings can occasionally be orders of magnitude higher than typical. Radon soon became a standard homeowner concern,
though typical domestic exposures are two to three orders of magnitude lower (100 Bq/m3, or 2.5 pCi/L), making individual testing essential to assessment of radon risk in any particular dwelling.
Radon exists in every U.S. state, and approximately 6% of all American houses have elevated levels. The highest average radon concentrations in the United States are found in Iowa and in the Appalachian Mountain areas in southeastern Pennsylvania. Some of the highest readings have been recorded in Mallow, County Cork, Ireland. Iowa has the highest average radon concentrations in the United States due to significant glaciation that ground the granitic rocks from the Canadian Shield and deposited it as soils making up the rich Iowa farmland. Many cities within the state, such as Iowa City, have passed requirements for radon-resistant construction in new homes. In a few locations, uraniumtailings have been used for landfills and were subsequently built on, resulting in possible increased exposure to radon.
Jewelry contamination
In the early 20th century, 210Pb-contaminated gold, from gold seeds that were used in radiotherapy which had held 222Rn, were melted down and made into a small number of jewelry pieces, such as rings, in the U.S.
Wearing such a contaminated ring could lead to a skin exposure of 10 to 100 millirad/day (0.004 to 0.04 mSv/h).
Health effects
Cancer in miners
Relative
risk of lung cancer mortality by cumulative exposure to radon decay
products (in WLM) from the combined data from 11 cohorts of underground
hard rock miners. Though high exposures (>50 WLM) cause statistically
significant excess cancers, the evidence on small exposures (10 WLM) is
inconclusive and appears slightly beneficial in this study (see radiation hormesis).
The health effects of high exposure to radon in mines, where exposures reaching 1,000,000 Bq/m3 can be found, can be recognized in Paracelsus' 1530 description of a wasting disease of miners, the mala metallorum.
Though at the time radon itself was not understood to be the
cause—indeed, neither it nor radiation had even been
discovered—mineralogist Georg Agricola recommended ventilation of mines to avoid this mountain sickness (Bergsucht).
In 1879, the "wasting" was identified as lung cancer by Herting and
Hesse in their investigation of miners from Schneeberg, Germany.
Beyond mining in general, radon is a particular problem in the mining of uranium;
significant excess lung cancer deaths have been identified in epidemiological studies of uranium miners and other hard-rock miners employed in the 1940s and 1950s. Residues from processing of uranium ore can also be a source of radon. Radon resulting from the high radium content in uncovered dumps and tailing ponds can be easily released into the atmosphere.
The first major studies with radon and health occurred in the context of uranium mining, first in the Joachimsthal region of Bohemia and then in the Southwestern United States during the early Cold War. Because radon is a product of the radioactive decay of uranium, underground uranium mines may have high concentrations of radon. Many uranium miners in the Four Corners region contracted lung cancer
and other pathologies as a result of high levels of exposure to radon
in the mid-1950s. The increased incidence of lung cancer was
particularly pronounced among Native American and Mormon miners, because those groups normally have low rates of lung cancer.
Safety standards requiring expensive ventilation were not widely implemented or policed during this period.
In studies of uranium miners, workers exposed to radon levels of 50 to 150 picocuries of radon per liter of air (2000–6000 Bq/m3) for about 10 years have shown an increased frequency of lung cancer.
Statistically significant excesses in lung cancer deaths were present after cumulative exposures of less than 50 WLM.
There is, however, unexplained heterogeneity in these results (whose confidence interval do not always overlap).
The size of the radon-related increase in lung cancer risk varied by
more than an order of magnitude between the different studies.
Heterogeneities are possibly due to systematic errors in exposure
ascertainment, unaccounted for differences in the study populations
(genetic, lifestyle, etc.), or confounding mine exposures. There are a number of confounding factors
to consider, including exposure to other agents, ethnicity, smoking
history, and work experience. The cases reported in these miners cannot
be attributed solely to radon or radon daughters but may be due to
exposure to silica, to other mine pollutants, to smoking, or to other
causes.
The majority of miners in the studies are smokers and all inhale dust
and other pollutants in mines. Because radon and cigarette smoke both
cause lung-cancer, and since the effect of smoking is far above that of
radon, it is complicated to disentangle the effects of the two kinds of
exposure; misinterpreting the smoking habit by a few percent can blur
out the radon effect.
Since that time, ventilation and other measures have been used to
reduce radon levels in most affected mines that continue to operate. In
recent years, the average annual exposure of uranium miners has fallen
to levels similar to the concentrations inhaled in some homes. This has
reduced the risk of occupationally induced cancer from radon, although
it still remains an issue both for those who are currently employed in
affected mines and for those who have been employed in the past.
The power to detect any excess risks in miners nowadays is likely to be
small, exposures being much smaller than in the early years of mining.
A confounding factor with mines is that both radon concentration
and carcinogenic dust (such as quartz dust) depend on the amount of
ventilation.
This makes it very difficult to state that radon causes cancer in
miners; the lung cancers could be partially or wholly caused by high
dust concentrations from poor ventilation.
Health risks
Radon-222 has been classified by International Agency for Research on Cancer as being carcinogenic to humans.
In September 2009, the World Health Organization released a
comprehensive global initiative on radon that recommended a reference
level of 100 Bq/m3 for radon, urging establishment or
strengthening of radon measurement and mitigation programs as well as
development building codes requiring radon prevention measures in homes
under construction.
Elevated lung cancer rates have been reported from a number of cohort
and case-control studies of underground miners exposed to radon and its
decay products but the main confounding factor in all miners' studies is
smoking and dust. Up to the most of regulatory bodies there is
sufficient evidence for the carcinogenicity of radon and its decay
products in humans for such exposures. However, the discussion about the opposite results is still going on,
especially a recent retrospective case-control study of lung cancer
risk showed substantial cancer rate reduction between 50 and 123 Bq per
cubic meter relative to a group at zero to 25 Bq per cubic meter.
Additionally, the meta-analysis of many radon studies, which
independently show radon risk increase, gives no confirmation of that
conclusion: the joined data show log-normal distribution with the
maximal value in zero risk of lung cancer below 800 Bq per cubic meter.
The primary route of exposure to radon and its progeny is
inhalation. Radiation exposure from radon is indirect. The health hazard
from radon does not come primarily from radon itself, but rather from
the radioactive products formed in the decay of radon. The general effects of radon to the human body are caused by its radioactivity and consequent risk of radiation-induced cancer.
Lung cancer is the only observed consequence of high concentration
radon exposures; both human and animal studies indicate that the lung
and respiratory system are the primary targets of radon daughter-induced
toxicity.
Radon has a short half-life (3.8 days) and decays into other solid particulate radium-series radioactive nuclides.
Two of these decay products, polonium-218 and 214, present a significant radiologic hazard.
If the gas is inhaled, the radon atoms decay in the airways or the
lungs, resulting in radioactive polonium and ultimately lead atoms
attaching to the nearest tissue. If dust or aerosol is inhaled that
already carries radon decay products, the deposition pattern of the
decay products in the respiratory tract depends on the behaviour of the
particles in the lungs. Smaller diameter particles diffuse further into
the respiratory system, whereas the larger — tens to hundreds of
micron-sized — particles often deposit higher in the airways and are
cleared by the body's mucociliary staircase. Deposited radioactive atoms
or dust or aerosol particles continue to decay, causing continued
exposure by emitting energetic alpha radiation with some associated gamma radiation too, that can damage vital molecules in lung cells,
by either creating free radicals or causing DNA breaks or damage,
perhaps causing mutations that sometimes turn cancerous. In addition,
through ingestion and blood transport, following crossing of the lung
membrane by radon, radioactive progeny may also be transported to other
parts of the body.
The risk of lung cancer caused by smoking is much higher than the
risk of lung cancer caused by indoor radon. Radiation from radon has
been attributed to increase of lung cancer among smokers too. It is
generally believed that exposure to radon and cigarette smoking are
synergistic; that is, that the combined effect exceeds the sum of their
independent effects. This is because the daughters of radon often become
attached to smoke and dust particles, and are then able to lodge in the
lungs.
It is unknown whether radon causes other types of cancer, but
recent studies suggest a need for further studies to assess the
relationship between radon and leukemia.
The effects of radon, if found in food or drinking water, are
unknown. Following ingestion of radon dissolved in water, the biological
half-life for removal of radon from the body ranges from 30 to 70
minutes. More than 90% of the absorbed radon is eliminated by exhalation
within 100 minutes, By 600 minutes, only 1% of the absorbed amount
remains in the body.
Health risks in children
While
radon presents the aforementioned risks in adults, exposure in children
leads to a unique set of health hazards that are still being
researched. The physical composition of children leads to faster rates
of exposure through inhalation given that their respiratory rate is
higher than that of adults, resulting in more gas exchange and more
potential opportunities for radon to be inhaled.
The resulting health effects in children are similar to those of
adults, predominantly including lung cancer and respiratory illnesses
such as asthma, bronchitis, and pneumonia.
While there have been numerous studies assessing the link between radon
exposure and childhood leukemia, the results are largely varied. Many
ecological studies show a positive association between radon exposure
and childhood leukemia; however, most case control studies have produced
a weak correlation.
Genotoxicity has been noted in children exposed to high levels of
radon, specifically a significant increase of frequency of aberrant
cells was noted, as well as an “increase in the frequencies of single
and double fragments, chromosome interchanges, [and] number of
aberrations chromatid and chromosome type”.
Childhood exposure
Because radon is generally associated with diseases that are not
detected until many years after elevated exposure, the public may not
consider the amount of radon that children are currently being exposed
to. Aside from the exposure in the home, one of the major contributors
to radon exposure in children are the schools in which they attend
almost every day. A survey was conducted in schools across the United
States to detect radon levels, and it was estimated that about one in
five schools has at least one room (more than 70,000 schoolrooms) with
short-term levels above 4pCi/L.
Many states have active radon testing and mitigation programs in
place, which require testing in buildings such as public schools.
However, these are not standardized nationwide, and the rules and
regulations on reducing high radon levels are even less common. The
School Health Policies and Practices Study (SHPPS), conducted by the CDC
in 2012, found that of schools located in counties with high predicted
indoor radon levels, only 42.4% had radon testing policies, and a mere
37.5% had policy for radon-resistant new construction practices. Only about 20% of all schools nationwide have done testing, even though the EPA recommends that every school be tested.
These numbers are arguably not high enough to ensure protection of the
majority of children from elevated radon exposures. For exposure
standards to be effective, they should be set for those most
susceptible.
Effective dose and cancer risks estimations
UNSCEAR recommends a reference value of 9 nSv (Bq·h/m3)−1.
For example, a person living (7000 h/year) in a concentration of 40 Bq/m3 receives an effective dose of 1 mSv/year.
Studies of miners exposed to radon and its decay products provide
a direct basis for assessing their lung cancer risk. The BEIR VI
report, entitled Health Effects of Exposure to Radon, reported an excess relative risk from exposure to radon that was equivalent to 1.8% per megabecquerel hours per cubic meter (MBq·h/m3) (95% confidence interval: 0.3, 35) for miners with cumulative exposures below 30 MBq·h/m3. Estimates of risk per unit exposure are 5.38×10−4 per WLM; 9.68×10−4/WLM for ever smokers; and 1.67×10−4 per WLM for never smokers.
According to the UNSCEAR modeling, based on these miner's
studies, the excess relative risk from long-term residential exposure to
radon at 100 Bq/m3 is considered to be about 0.16 (after
correction for uncertainties in exposure assessment), with about a
threefold factor of uncertainty higher or lower than that value.
In other words, the absence of ill effects (or even positive hormesis effects) at 100 Bq/m3 are compatible with the known data.
The ICPR 65 model follows the same approach, and estimates the relative lifelong risk probability of radon-induced cancer death to 1.23 × 10−6 per Bq/(m3·year).
This relative risk is a global indicator; the risk estimation is
independent of sex, age, or smoking habit. Thus, if a smoker's chances
of dying of lung cancer are 10 times that of a nonsmoker's, the relative
risks for a given radon exposure will be the same according to that
model, meaning that the absolute risk of a radon-generated cancer for a
smoker is (implicitly) tenfold that of a nonsmoker.
The risk estimates correspond to a unit risk of approximately 3–6 × 10−5 per Bq/m3, assuming a lifetime risk of lung cancer of 3%. This means that a person living in an average European dwelling with 50 Bq/m3 has a lifetime excess lung cancer risk of 1.5–3 × 10−3. Similarly, a person living in a dwelling with a high radon concentration of 1000 Bq/m3 has a lifetime excess lung cancer risk of 3–6%, implying a doubling of background lung cancer risk.
The BEIR VI model proposed by the National Academy of Sciences of the USA
is more complex. It is a multiplicative model that estimates an excess
risk per exposure unit. It takes into account age, elapsed time since
exposure, and duration and length of exposure, and its parameters allow
for taking smoking habits into account.
In the absence of other causes of death, the absolute risks of lung
cancer by age 75 at usual radon concentrations of 0, 100, and 400 Bq/m3
would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong
nonsmokers, and about 25 times greater (10%, 12%, and 16%) for cigarette
smokers.
There is great uncertainty in applying risk estimates derived
from studies in miners to the effects of residential radon, and direct
estimates of the risks of residential radon are needed.
As with the miner data, the same confounding factor of other carcinogens such as dust applies.
Radon concentration is high in poorly ventilated homes and buildings
and such buildings tend to have poor air quality, larger concentrations
of dust etc. BEIR VI did not consider that other carcinogens such as
dust might be the cause of some or all of the lung cancers, thus
omitting a possible spurious relationship.
Studies on domestic exposure
Average
radiation doses received in Germany. Radon accounts for half of the
background dose; and medical doses reach the same levels as background
dose.
The largest natural contributor to public radiation dose is radon, a
naturally occurring, radioactive gas found in soil and rock, which comprises approximately 55% of the annual background dose.
Radon gas levels vary by locality and the composition of the underlying soil and rocks.
Radon (at concentrations encountered in mines) was recognized as
carcinogenic in the 1980s, in view of the lung cancer statistics for
miners' cohorts.
Although radon may present significant risks, thousands of persons
annually go to radon-contaminated mines for deliberate exposure to help
with the symptoms of arthritis without any serious health effects.
Radon as a terrestrial source of background radiation
is of particular concern because, although overall very rare, where it
does occur it often does so in high concentrations. Some of these areas,
including parts of Cornwall and Aberdeenshire
have high enough natural radiation levels that nuclear licensed sites
cannot be built there—the sites would already exceed legal limits before
they opened, and the natural topsoil and rock would all have to be
disposed of as low-level nuclear waste.
People in affected localities can receive up to 10 mSv per year background radiation.
This led to a health policy problem: what is the health impact of exposure to radon concentrations (100 Bq/m3) typically found in some buildings?
Detection methods
When
exposure to a carcinogenic substance is suspected, the cause/effect
relationship on any given case can never be ascertained. Lung cancer
occurs spontaneously, and there is no difference between a "natural"
cancer and another one caused by radon (or smoking). Furthermore, it
takes years for a cancer to develop, so that determining the past
exposure of a case is usually very approximative. The health effect of
radon can only be demonstrated through theory and statistical
observation.
The best proofs come from observations of cohorts
(predetermined populations with known exposures and exhaustive
follow-up), such as those on miners, or on Hiroshima and Nagasaki
survivors. Such studies are efficient, but very costly
when the population needs to be a large one. Such studies can only be
used when the effect is strong enough, hence, for high exposures.
Alternate proofs are case-control studies
(the environment factors of a "case" population is individually
determined, and compared to that of a "control″ population, to see what
the difference might have been, and which factors may be significant),
like the ones that have been used to demonstrate the link between lung
cancer and smoking. Such studies can identify key factors when the
signal/noise ratio is strong enough, but are very sensitive to selection
bias, and prone to the existence of confounding factors.
Lastly, ecological studies
may be used (where the global environment variables and their global
effect on two different populations are compared). Such studies are
"cheap and dirty": they can be easily conducted on very large
populations (the whole USA, in Dr Cohen's study), but are prone to the
existence of confounding factors, and exposed to the ecological fallacy problem.
Furthermore, theory and observation must confirm each other for a
relationship to be accepted as fully proven. Even when a statistical
link between factor and effect appears significant, it must be backed by
a theoretical explanation; and a theory is not accepted as factual
unless confirmed by observations.
Epidemiology studies of domestic exposures
A controversial epidemiological study, unexpectedly showing decreased cancer risk vs. radon domestic exposure (5 pCi/L ≈ 200 Bq/m3).
This study lacks individual level controls for smoking and radon
exposure, and therefore lacks statistical power to draw definitive
conclusions. Because of this, the error bars (which simply reflect the
raw data variability) are probably too small. Among other expert panels, the WHO's International Agency for Research on Cancer concluded that these analyses "can be rejected."
Cohort studies are impractical for the study of domestic radon
exposure. With the expected effect of small exposures being very small,
the direct observation of this effect would require huge cohorts: the
populations of whole countries.
Several ecological studies
have been performed to assess possible relationships between selected
cancers and estimated radon levels within particular geographic regions
where environmental radon levels appear to be higher than other
geographic regions.
Results of such ecological studies are mixed; both positive and negative
associations, as well as no significant associations, have been
suggested.
The most direct way to assess the risks posed by radon in homes is through case-control studies.
The studies have not produced a definitive answer, primarily
because the risk is likely to be very small at the low exposure
encountered from most homes and because it is difficult to estimate
radon exposures that people have received over their lifetimes. In
addition, it is clear that far more lung cancers are caused by smoking
than are caused by radon.
Epidemiologic radon studies have found trends to increased lung
cancer risk from radon with a no evidence of a threshold, and evidence
against a threshold above high as 150 Bq/m3 (almost exactly the EPA's action level of 4 pCi/L).
Another study similarly found that there is no evidence of a threshold
but lacked the statistical power to clearly identify the threshold at
this low level. Notably, the latter deviance from zero at low level convinced the World Health Organization
that, "The dose-response relation seems to be linear without evidence
of a threshold, meaning that the lung cancer risk increases
proportionally with increasing radon exposure."
The most elaborate case-control epidemiologic radon study performed by R. William Field and colleagues identified a 50% increased lung cancer risk with prolonged radon exposure at the EPA's action level of 4 pCi/L.
Iowa has the highest average radon concentrations in the United States
and a very stable population which added to the strength of the study.
For that study, the odds ratio was found to be increased slightly above
the confidence interval (95% CI) for cumulative radon exposures above 17
WLM (6.2 pC/L=230 Bq/m3 and above).
The results of a methodical ten-year-long, case-controlled study
of residential radon exposure in Worcester County, Massachusetts, found
an apparent 60% reduction in lung cancer risk amongst people exposed to low levels (0–150 Bq/m3) of radon gas; levels typically encountered in 90% of American homes—an apparent support for the idea of radiation hormesis. In that study, a significant result (95% CI) was obtained for the 75-150 Bq/m3 category.
The study paid close attention to the cohort's
levels of smoking, occupational exposure to carcinogens and education
attainment. However, unlike the majority of the residential radon
studies, the study was not population-based. Errors in retrospective
exposure assessment could not be ruled out in the finding at low levels.
Other studies into the effects of domestic radon exposure have not
reported a hormetic effect; including for example the respected "Iowa
Radon Lung Cancer Study" of Field et al. (2000), which also used
sophisticated radon exposure dosimetry.
Intentional exposure
"Radon therapy" is an intentional exposure to radon
via inhalation or ingestion. Nevertheless, epidemiological evidence
shows a clear link between breathing high concentrations of radon and
incidence of lung cancer.
Arthritis
In the late 20th century and early 21st century, some "health mines" were established in Basin, Montana, which attracted people seeking relief from health problems such as arthritis through limited exposure to radioactive mine water and radon. The practice is controversial because of the "well-documented ill effects of high-dose radiation on the body." Radon has nevertheless been found to induce beneficial long-term effects.
Bathing
Radioactive water baths have been applied since 1906 in Jáchymov, Czech Republic, but even before radon discovery they were used in Bad Gastein, Austria. Radium-rich springs are also used in traditional Japaneseonsen in Misasa, Tottori Prefecture. Drinking therapy is applied in Bad Brambach, Germany. Inhalation therapy is carried out in Gasteiner-Heilstollen, Austria, in Kowary, Poland and in Boulder, Montana, United States. In the United States and Europe there are several "radon spas",
where people sit for minutes or hours in a high-radon atmosphere in the
belief that low doses of radiation will invigorate or energize them.
Radon has been produced commercially for use in radiation therapy,
but for the most part has been replaced by radionuclides made in
accelerators and nuclear reactors. Radon has been used in implantable
seeds, made of gold or glass, primarily used to treat cancers.
The gold seeds were produced by filling a long tube with radon pumped
from a radium source, the tube being then divided into short sections by
crimping and cutting. The gold layer keeps the radon within, and
filters out the alpha and beta radiations, while allowing the gamma rays
to escape (which kill the diseased tissue). The activities might range
from 0.05 to 5 millicuries per seed (2 to 200 MBq). The gamma rays are produced by radon and the first short-lived elements of its decay chain (218Po, 214Pb, 214Bi, 214Po).
Radon and its first decay products
being very short-lived, the seed is left in place. After 11 half-lives
(42 days), radon radioactivity is at 1/2000 of its original level. At
this stage, the predominant residual activity is due to the radon decay product210Pb, whose half-life (22.3 year) is 2000 times that of radon, and its descendants 210Bi and 210Po, totaling 0.03% of the initial seed activity.
Health policies
Current policy in the U.S.A.
Federal Radon Action Plan
The Federal Radon Action Plan, also known as FRAP, was created in 2010 and launched in 2011.
It was piloted by the U.S. Environmental Protection Agency in
conjunction with the U.S. Departments of Health and Human Services,
Agriculture, Defense, Energy, Housing and Urban Development, the
Interior, Veterans Affairs, and the General Services Administration. The
goal set forth by FRAP was to eliminate radon induced cancer that can
be prevented by expanding radon testing, mitigating high levels of radon
exposure, and developing radon resistant construction, and to meet
Healthy People 2020 radon objectives.
They identified the barriers to change as limited public knowledge of
the dangers of radon exposure, the perceived high costs of mitigation,
and the availability of radon testing. As a result, they also identified
major ways to create change: demonstrate the importance of testing and
the ease of mitigation, provide incentives for testing and mitigation,
and build the radon services industry.
To complete these goals, representatives from each organization and
department established specific commitments and timelines to complete
tasks and continued to meet periodically. However, FRAP was concluded in
2016 as The National Radon Action Plan took over. In the final report
on commitments, it was found that FRAP completed 88% of their
commitments. They reported achieving the highest rates of radon mitigation and new construction mitigation in the United States as of 2014.
FRAP concluded that because of their efforts, at least 1.6 million
homes, schools, and childcare facilities received direct and immediate
positive effects.
National Radon Action Plan
The National Radon Action Plan, also known as NRAP, was created in 2014 and launched in 2015.
It is led by The American Lung Association with collaborative efforts
from the American Association of Radon Scientists and Technologists,
American Society of Home Inspectors, Cancer Survivors Against Radon,
Children’s Environmental Health Network, Citizens for Radioactive Radon
Reduction, Conference of Radiation Control Program Directors,
Environmental Law Institute, National Center for Healthy Housing, U.S.
Environmental Protection Agency, U.S. Department of Health and Human
Services, and U.S. Department of Housing and Urban Development. The
goals of NRAP are to continue efforts set forth by FRAP to eliminate
radon induced cancer that can be prevented by expanding radon testing,
mitigating high levels of radon exposure, and developing radon resistant
construction. NRAP also aims to reduce radon risk in 5 million homes, and save 3,200 lives by 2020.
To complete these goals, representatives from each organization have
established the following action plans: embed radon risk reduction as a
standard practice across housing sectors, provide incentives and support
to test and mitigate radon, promote the use of certified radon services
and build the industry, and increase public attention to radon risk and
the importance of reduction.
The NRAP is currently in action, implementing programs, identifying
approaches, and collaborating across organizations to achieve these
goals.
= Policies and scientific modelling worldwide
Dose-effect model retained
The
only dose-effect relationship available are those of miners cohorts
(for much higher exposures), exposed to radon. Studies of Hiroshima and
Nagasaki survivors are less informative (the exposure to radon is
chronic, localized, and the ionizing radiations are alpha rays).
Although low-exposed miners experienced exposures comparable to
long-term residence in high-radon dwellings, the mean cumulative
exposure among miners is approximately 30-fold higher than that
associated with long-term residency in a typical home. Moreover, the
smoking is a significant confounding factor in all miners' studies. It
can be concluded from miner studies that when the radon exposure in
dwellings compares to that in mines (above 1000 Bq/m3), radon
is a proven health hazard; but in the 1980s very little was known on
the dose-effect relationship, both theoretically and statistical.
Studies have been made since the 1980s, both on epidemiological studies and in the radiobiology field.
In the radiobiology and carcinogenesis
studies, progress has been made in understanding the first steps of
cancer development, but not to the point of validating a reference
dose-effect model. The only certainty gained is that the process is very
complex, the resulting dose-effect response being complex, and most
probably not a linear one.
Biologically based models have also been proposed that could project
substantially reduced carcinogenicity at low doses.
In the epidemiological field, no definite conclusion has been reached.
However, from the evidence now available, a threshold exposure, that is,
a level of exposure below which there is no effect of radon, cannot be
excluded.
Given the radon distribution observed in dwellings, and the
dose-effect relationship proposed by a given model, a theoretical number
of victims can be calculated, and serve as a basis for public health
policies.
With the BEIR VI model, the main health effect (nearly 75% of the
death toll) is to be found at low radon concentration exposures,
because most of the population (about 90%) lives in the 0-200 Bq/m3 range.
Under this modeling, the best policy is obviously to reduce the radon
levels of all homes where the radon level is above average, because this
leads to a significant decrease of radon exposure on a significant
fraction of the population; but this effect is predicted in the 0-200
Bq/m3 range, where the linear model has its maximum
uncertainty. From the statistical evidence available, a threshold
exposure cannot be excluded; if such a threshold exists, the real radon
health effect would in fact be limited to those homes where the radon
concentrations reaches that observed in mines — at most a few percent.
If a radiation hormesis
effect exists after all, the situation would be even worse: under that
hypothesis, suppressing the natural low exposure to radon (in the 0-200
Bq/m3 range) would actually lead to an increase of cancer
incidence, due to the suppression of this (hypothetical) protecting
effect. As the low-dose response is unclear, the choice of a model is
very controversial.
No conclusive statistics being available for the levels of exposure
usually found in homes, the risks posed by domestic exposures is usually
estimated on the basis of observed lung-cancer deaths caused by higher
exposures in mines, under the assumption that the risk of developing
lung-cancer increases linearly as the exposure increases. This was the basis for the model proposed by BEIR IV in the 1980s. The linear no-threshold model has since been kept in a conservative approach by the UNSCEAR report and the BEIR VI and BEIR VII publications, essentially for lack of a better choice:
Until the [...] uncertainties on low-dose response are resolved, the Committee believes that [the linear no-threshold model]
is consistent with developing knowledge and that it remains,
accordingly, the most scientifically defensible approximation of
low-dose response. However, a strictly linear dose response should not
be expected in all circumstances.
The BEIR VI committee adopted the linear no-threshold
assumption based on its understanding of the mechanisms of radon-induced
lung cancer, but recognized that this understanding is incomplete and
that therefore the evidence for this assumption is not conclusive.
Death toll attributed to radon
In
discussing these figures, it should be kept in mind that both the radon
distribution in dwelling and its effect at low exposures are not
precisely known, and the radon health effect has to be computed (deaths
caused by radon domestic exposure cannot be observed as such). These
estimations are strongly dependent on the model retained.
According to these models, radon exposure is thought to be the second major cause of lung cancer after smoking.
Iowa has
the highest average radon concentration in the United States; studies
performed there have demonstrated a 50% increased lung cancer risk with
prolonged radon exposure above the EPA's action level of 4 pCi/L.
Based on studies carried out by the National Academy of Sciences in the United States, radon would thus be the second leading cause of lung cancer after smoking, and accounts for 15,000 to 22,000 cancer deaths per year in the US alone.
The United States Environmental Protection Agency (EPA) says that radon is the number one cause of lung cancer among non-smokers.
The general population is exposed to small amounts of polonium as a radon daughter in indoor air; the isotopes 214Po and 218Po are thought to cause the majority of the estimated 15,000–22,000 lung cancer deaths in the US every year that have been attributed to indoor radon.
The Surgeon General of the United States has reported that over 20,000 Americans die each year of radon-related lung cancer.
In the United Kingdom, residential radon would be, after
cigarette smoking, the second most frequent cause of lung cancer deaths:
according to models, 83.9% of deaths are attributed to smoking only,
1.0% to radon only, and 5.5% to a combination of radon and smoking.
The World Health Organization has recommended a radon reference concentration of 100 Bq/m3 (2.7 pCi/L). The European Union recommends that action should be taken starting from concentrations of 400 Bq/m3 (11 pCi/L) for older dwellings and 200 Bq/m3 (5 pCi/L) for newer ones. After publication of the North American and European Pooling Studies, Health Canada proposed a new guideline that lowers their action level from 800 to 200 Bq/m3 (22 to 5 pCi/L).
The United States Environmental Protection Agency (EPA) strongly recommends action for any dwelling with a concentration higher than 148 Bq/m3 (4 pCi/L),
and encourages action starting at 74 Bq/m3 (2 pCi/L).
EPA recommends that all homes should be monitored for radon. If
testing shows levels less than 4 picocuries radon per liter of air (160
Bq/m3), then no action is necessary. For levels of 20 picocuries radon per liter of air (800 Bq/m3) or higher, the home owner should consider some type of procedure to decrease indoor radon levels.
For instance, as radon has a half-life of four days, opening the
windows once a day can cut the mean radon concentration to one fourth of
its level.
The United States Environmental Protection Agency
(EPA) recommends homes be fixed if an occupant's long-term exposure
will average 4 picocuries per liter (pCi/L) that is 148 Bq/m3. EPA estimates that one in 15 homes in the United States has radon levels above the recommended guideline of 4 pCi/L.
EPA radon risk level tables including comparisons to other risks encountered in life are available in their citizen's guide.
The EPA estimates that nationally, 8% to 12% of all dwellings are above
their maximum "safe levels" (four picocuries per liter—the equivalent to
roughly 200 chest x-rays). The United States Surgeon General and the
EPA both recommend that all homes be tested for radon.
The limits retained do not correspond to a known threshold in the
biological effect, but are determined by a cost-efficiency analysis.
EPA believes that a 150 Bq/m3 level (4 pCi/L) is achievable
in the majority of homes for a reasonable cost, the average cost per
life saved by using this action level is about $700,000.
For radon concentration in drinkable water, the World Health Organization issued as guidelines (1988) that remedial action should be considered when the radon activity exceeded 100 kBq/m3 in a building, and remedial action should be considered without long delay if exceeding 400 kBq/m3.
There are relatively simple tests for radon gas. Radon test kits are
commercially available. The short-term radon test kits used for
screening purposes are inexpensive, in many cases free. In the United
States, discounted test kits can be purchased online through The
National Radon Program Services at Kansas State University or through
state radon offices. Information about local radon zones and specific state contact information can be accessed through the Environmental Protection Agency (EPA) Map. The kit includes a collector that the user hangs in the lowest livable floor of the dwelling for 2 to 7 days. Charcoal canisters are another type of short-term radon test, and are designed to be used for 2 to 4 days.
The user then sends the collector to a laboratory for analysis. Both
devices are passive, meaning that they do not need power to function.
The accuracy of the residential radon test depends upon the lack
of ventilation in the house when the sample is being obtained. Thus, the
occupants will be instructed not to open windows, etc., for ventilation
during the pendency of test, usually two days or more.
Long-term kits, taking collections for 3 months up to one year, are also available. An open-land test kit can test radon emissions from the land before construction begins. A Lucas cell
is one type of long-term device. A Lucas cell is also an active device,
or one that requires power to function. Active devices provide
continuous monitoring, and some can report on the variation of radon and
interference within the testing period. These tests usually require
operation by trained testers and are often more expensive than passive
testing. The National Radon Proficiency Program (NRPP) provides a list of radon measurement professionals.
Radon levels fluctuate naturally. An initial test might not be an
accurate assessment of a home's average radon level. Transient weather
can affect short term measurements. Therefore, a high
result (over 4 pCi/L) justifies repeating the test before undertaking
more expensive abatement projects. Measurements between 4 and 10 pCi/L
warrant a long-term radon test. Measurements over 10 pCi/L warrant only
another short-term test so that abatement measures are not unduly
delayed. Purchasers of real estate are advised to delay or decline a
purchase if the seller has not successfully abated radon to 4 pCi/L or
less.
Since radon concentrations vary substantially from day to day,
single grab-type measurements are generally not very useful, except as a
means of identifying a potential problem area, and indicating a need
for more sophisticated testing.
The EPA recommends that an initial short-term test be performed in a
closed building. An initial short-term test of 2 to 90 days allows
residents to be informed quickly in case a home contains high levels of
radon. Long-term tests provide a better estimate of the average annual
radon level.
Transport of radon in indoor air is almost entirely controlled by the
ventilation rate in the enclosure. Since air pressure is usually lower
inside houses than it is outside, the home acts like a vacuum, drawing
radon gas in through cracks in the foundation or other openings such as
ventilation systems. Generally, the indoor radon concentrations increase as ventilation rates decrease. In a well ventilated place, the radon concentration tends to align with outdoor values (typically 10 Bq/m3, ranging from 1 to 100 Bq/m3).
Radon levels in indoor air can be lowered in several ways, from
sealing cracks in floors and walls to increasing the ventilation rate of
the building. Listed here are some of the accepted ways of reducing the
amount of radon accumulating in a dwelling:
Improving the ventilation of the dwelling and avoiding the transport of radon from the basement, or ground, into living areas;
Installing crawlspace or basement ventilation systems;
Installing sub-slab depressurization radon mitigation systems, which vacuum radon from under slab-on-grade foundations;
Installing sub-membrane depressurization radon mitigation systems,
which vacuum radon from under a membrane that covers the ground used in
crawlspace foundations;
Installing a radon sump system in the basement;
Sealing floors and walls (not a stand-alone solution); and
Installing a positive pressurization or positive supply ventilation system.
The half-life for radon is 3.8 days, indicating that once the source
is removed, the hazard will be greatly reduced within approximately one
month (seven half-lives).
Positive-pressure ventilation systems can be combined with a heat
exchanger to recover energy in the process of exchanging air with the
outside, and simply exhausting basement air to the outside is not
necessarily a viable solution as this can draw radon gas into a dwelling. Homes built on a crawl space
may benefit from a radon collector installed under a "radon barrier, or
membrane" (a sheet of plastic or laminated polyethylene film that
covers the crawl space floor).
ASTM E-2121 is a standard for reducing radon in homes as far as practicable below 4 picocuries per liter (pCi/L) in indoor air.
In the US, approximately 14 states have a state radon programs
which train and license radon mitigation contractors and radon
measurement professionals. To determine if your state licenses radon
professionals contact your state health department. The National
Environmental Health Association and the National Radon Safety Board
administer voluntary National Radon Proficiency Programs for radon
professionals consisting of individuals and companies wanting to take
training courses and examinations to demonstrate their competency.
Without the proper equipment or technical knowledge, radon levels can
actually increase or create other potential hazards and additional
costs. A list of certified mitigation service providers is available through state radon offices, which are listed on the EPA website.
Indoor radon can be mitigated by sealing basement foundations, water
drainage, or by sub-slab, or sub-membrane depressurization. In many
cases, mitigators can use PVC piping and specialized radon suction fans
to exhaust sub-slab, or sub-membrane radon and other soil gases to the
outside atmosphere. Most of these solutions for radon mitigation require
maintenance, and it is important to continually replace any fans or
filters as needed to continue proper functioning.
Since radon gas is found in most soil and rocks, it is not only
able to move into the air, but also into underground water sources.
Radon may be present in well water and can be released into the air in
homes when water is used for showering and other household uses.
If it is suspected that a private well or drinking water may be
affected by radon, the National Radon Program Services Hotline at
1-800-SOS-RADON can be contacted for information regarding state radon
office phone numbers. State radon offices can provide additional
resources, such as local laboratories that can test water for radon.
If it is determined that radon is present in a private well,
installing either a point-of-use or point-of-entry solution may be
necessary.
Point-of-use treatments are installed at the tap, and are only helpful
in removing radon from drinking water. To address the more common
problem of breathing in radon released from water used during showers
and other household activities, a point-of-entry solution may be more
reliable.
Point-of-entry systems usually involve a granular activated carbon
filter, or an aeration system; both methods can help to remove radon
before it enters the home’s water distribution system.
Aeration systems and granular activation carbon filters both have
advantages and disadvantages, so it is recommended to contact state
radon departments or a water treatment professional for specific
recommendations.
Detractors
The high cost of radon remediation in the 1980s led to detractors arguing that the issue is a financial boondoggle reminiscent of the swine flu scare of 1976.
They further argued that the results of mitigation are inconsistent
with lowered cancer risk, especially when indoor radon levels are in the
lower range of the actionable exposure level.
