National Radon Action Month - January 2012

In 2012, January is National Radon Action Month According to Surgeon General and E.P.A.

envirolabs — Thu, 15 Dec 2011 06:04:53 +0000

The Environmental Protection Agency has designated January as National Radon Action Month. The Cancer Prevention Committee has published the following study:

According to recent reports from the World Health Organization, radon gas is responsible for approximately 20,000 deaths in the U.S. and 100,000 deaths worldwide each year. This equates to about 15% of all lung cancer deaths. Statistically, radon is the leading cause of lung cancer for non-smokers and the second leading cause for smokers. Learn more about radon gas at: http://www.MitigationSystem.comThe World Health Organization recently lowered their limit or “action level” for indoor radon levels from 4.0 to 2.7 (picocuries per liter) in response to several worldwide studies that point to health risks at lower exposure levels of the gas. More than 100 scientists from 30 countries participated in the World Health Organization International Radon Project and assisted in the publishing of the Handbook on Indoor Radon which was released earlier this year.

According to The Environmental Protection Agency, over 8 million U.S. homes have dangerous levels of radon gas. The Surgeon General is urging the media, state health departments, and the press to participate in National Radon Action Month by helping to promote awareness of this silent killer. Testing for radon is easy and inexpensive. “Radon test kits can be purchased from hardware stores, health departments, or online for around $20.00,” states Jamey Gelina; a certified radon mitigation specialist with SWAT Radon Mitigation. http://www.RadonMitigation.usMembers of the private sector are working side-by-side with government agencies to spread awareness of this cancer-causing threat. “By encouraging everyone to test their homes for radon and to take action when levels are elevated, we can all be a part this life-saving initiative” adds Ben Ingalls, who installs radon remediation systems throughout Colorado. “Radon problems can be fixed in most homes for under $1,000” he adds.January 2012 (which is National Radon Action Month) is the perfect time of year to test for radon gas. Testing in the summer time is difficult because occupants tend to keep windows and doors open for longer durations which could skew the results of the test. Since winter time is when people tend to spend more time indoors, it makes sense to test during this time. It’s a good idea to conduct a long-term or multiple short-term tests because radon levels can vary from season to season. You can also constantly monitor home’s radon levels with an electronic radon detector. Learn more at www.RadonMonitor.com.

All homes should be tested for radon regardless of the age of the home, geographic location, or type of construction. Radon problems have been found in every state in the U.S. and since you cannot see, smell, or taste radon, the only way to know if your home is affected is to conduct a test. The EPA recommends that you conduct a test at least once every two years because radon levels can fluctuate over time. If you find that your radon levels are above the World Health Organization limit of 2.7, a qualified contractor can install a radon reduction system to fix the problem. In most cases, the work can be completed in a single day.

Radon gas causes more deaths each year than any other in-home hazard including fires, carbon monoxide, drowning, poisoning, falls, and even guns! National Radon Action Month is an ideal time to make your household a safer place. You can learn more about 2012 National Radon Action Month and local activities that you can participate in and help create awareness about this deadly carcinogen at by calling 1-800-NO-RADON or by visiting http://www.RadonMonth.org

Radon Gas Identified As Leading Lung Cancer Cause in Non-Smokers. November is Lung Cancer Awareness Month

envirolabs — Mon, 28 Nov 2011 15:58:05 +0000

Recent studies point to radon gas as the #1 cause of lung cancer for non-smokers. Scientists have known for years that lung cancer is the leading cancer killer in the U.S. However, lung cancer victims were typically linked to cigarette smoke exposure. New research concludes that radon gas causes more deaths every year than any other in-home risk.

November was Lung Cancer Awareness Month in 2011. Lung cancer is a disease characterized by uncontrolled cell growth in tissues of the lung. If left untreated, this growth can spread beyond the lung in a process called metastasis into nearby tissue and, eventually into other parts of the body. Most cancers that start in lung, known as primary lung cancers, are carcinomas that derive from epithelial cells. Worldwide, lung cancer is the most common cause of cancer-related death in men and women, and is responsible for 1.3 million deaths annually, as of 2004, the most common symptoms are shortness of breath, coughing (including coughing up blood), and weight loss.

The main types of lung cancer are small-cell lung cancer (SCLC), also called oat cell cancer, and non-small-cell lung cancer (NSCLC). The most common cause of lung cancer is long-term exposure to tobacco smoke. Nonsmokers account for 15% of lung cancer cases, and these cases are often attributed to a combination of genetic factors, radon gas, asbestos, and air pollution including secondhand smoke.

Lung cancer may be seen on chest radiograph and computed tomography (CT scan). The diagnosis is confirmed with a biopsy. This is usually performed by bronchoscope or CT-guided biopsy. Treatment and prognosis depend on the histological type of cancer, the stage (degree of spread), and the patient’s general wellbeing, measured by performance status. Common treatments include surgery, chemotherapy, and radiotherapy. NSCLC is sometimes treated with surgery, whereas SCLC usually responds better to chemotherapy and radiation therapy. This is partly because SCLC often spreads quite early, and these treatments are generally better at getting to cancer cells that have spread to other parts of the body.

Survival of lung cancer depends on stage, overall health, and other factors, but overall 14% of people diagnosed with lung cancer survive five years after the diagnosis.

Radon is a chemical element with symbol Rn and atomic number 86. It is a radioactive, colorless, odorless, tasteless noble gas, occurring naturally as the decay product of uranium or thorium. Its most stable isotope, ²²²Rn, has a half-life of 3.8 days. Radon is one of the densest substances that remains a gas under normal conditions and is considered a health hazard due to its radioactivity. Intense radioactivity also hindered chemical studies of radon and only a few compounds are known.

Radon is formed as part of the normal radioactive decay chain of uranium and thorium. Uranium and thorium have been around since the earth was formed and their most common isotope has a very long half-life (4.5 billion years). Uranium and thorium, radium, and thus radon, will continue to occur for millions of years at about the same concentrations as they do now. As the radioactive gas of radon decays, it produces new radioactive elements called radon daughters or decay products. Radon daughters are solids and stick to surfaces such as dust particles in the air. If contaminated dust is inhaled, these particles can stick to the airways of the lung increasing your risk of developing lung cancer.^[2]

Radon is responsible for the majority of the 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.

Epidemiological studies have shown a clear link between breathing high concentrations of radon and incidence of lung cancer. Thus, radon is considered a significant contaminant that affects indoor air quality worldwide. According to the United States Environmental Protection Agency, radon is the second most frequent cause of lung cancer, after cigarette smoking, causing 21,000 lung cancer deaths per year in the United States. About 2,900 of these deaths occur among people who have never smoked. While radon is the second most frequent cause of lung cancer, it is the number one cause among non-smokers, according to EPA estimates.

Radon Gas Killed 20,000 Americans in 2010!

envirolabs — Wed, 22 Dec 2010 14:40:18 +0000

Environmental Protection Agency Designates January 2011 as National Radon Action Month

What is Radon?

Radon is naturally occurring, odorless, and colorless gas produced by the breakdown of uranium in soil, rock, and water. Because radon is a gas, it can enter buildings through openings or cracks in the foundation. The radon gas itself decays into radioactive solids, called radon daughters. The radon daughters attach to dust particles in the air, and can be inhaled. The inhalation of radon daughters has been linked to lung cancer.

Radon has been identified as the second leading cause of lung cancer in the United States (second only to smoking.) The Environmental Protection Agency reports that radon causes between 15,000 and 22,000 lung cancer deaths every year in the United States. These startling statistics have prompted the EPA to designate January as National Radon Action Month in the United States. View the E.P.A. Press Release Here: http://www.epa.gov/radon/nram/

Every home should be tested for radon regardless of where the home is located, the age of the home, foundation type, or whether or not the home is in an area where homes are “prone to having radon problems.” Homes with elevated radon levels have been found in practically every county in the United States.

The United States Environmental Protection Agency has established that if a home or building is found to have a radon level of 4 pCi/l or higher, action should be taken to reduce it. In most cases, radon levels can be reduced to 2 pCi/l or lower with the installation of an active (fan-assisted) venting system. As of September, 2009; The World Health Organization has established an action level of 2.7 pCi/l (100 Becquerel per cubic meter.)

Radon’s primary hazard is caused from inhalation of the gas and its highly radioactive heavy metallic decay products (Polonium, Lead, and Bismuth) which tend to collect on dust in the air. The problem arises when these elements stick to the delicate cells lining the passageways leading into the lungs.

There is sufficient evidence for the carcinogenicity of radon and its isotopic forms, radon-222 and radon-220, in experimental animals. When administered by inhalation, preceded by a single exposure to cerium hydroxide dust, radon induced pulmonary adenomas, adenocarcinomas, invasive mixed adenosquamous carcinomas, and squamous cell carcinomas in male rats. Extrapulmonary metastases occurred in only one animal. Most or all of the tumors were believed to be bronchiolar or bronchio-alveolar in origin. Radon decay products in combination with uranium-ore dust induced a progression of activity from single basal cell hyperplasia in bronchioles to malignant tumors in male hamsters when exposed by inhalation. Lung tumors observed were adenomas, adenocarcinomas, and squamous cell carcinomas; bronchiolar and alveolar metaplasia, adenomatous lesions, fibrosis, and interstitial pneumonia were also observed. When administered by inhalation in combination with decay products, uranium-ore dust, and cigarette smoke, radon-induced nasal carcinomas, epidermoid carcinomas, bronchio-alveolar carcinomas, and fibrosarcoma were observed in dogs of both sexes. In general, a significant increase was observed in respiratory tract tumors in rats and dogs in comparison with unexposed animals. A dose- response relationship was noted in those experiments with rats in which radon was tested. In most instances, tumors at sites other than the lung were not reported, but in one study, mention was made of tumors of the upper lip and urinary tract in rats.

An IARC Working Group reported that there is sufficient evidence for the carcinogenicity of radon and its decay products in humans. Increased incidences of lung cancer have been reported from numerous epidemiologic studies of groups occupationally exposed to high doses of radon, especially underground hard rock miners. These include particularly uranium miners, but also groups of iron-ore and other metal miners, and one group of fluorspar miners. Strong evidence for exposure response relationships has been obtained from several studies, in spite of uncertainties that affect estimates of the exposure of the study populations to radon decay products. Several small case-control studies of lung cancer have suggested a higher risk among individuals living in houses known or presumed to have higher levels of radon and its decay products than among individuals with lower presumed exposure in houses. The evidence on the interaction of radon and its decay products with cigarette smoking with regard to lung cancer does not lead to a simple conclusion. The data from the largest study are consistent with a multiplicative or submultiplicative model of synergisms and reject an additive model. In many studies of miners and in one of presumed domestic exposure, small cell cancers accounted for a greater proportion than expected of the lung cancer cases. In one population of uranium miners, this proportion has been declining with the passage of time. Because of the limited scale of epidemiologic studies of nonoccupational exposure to radon decay products available at the time reviews were made, quantification of risk has been based only on data of miners’ experience. An IARC Working Group considered that the epidemiologic evidence does not lead to a firm conclusion concerning the interaction between exposure to radon decay products and tobacco smoking. Most of the epidemiologic studies involve small numbers of cases, and the analytical approaches for assessing interaction have been variable and sometimes inadequate.

HOW RADON ENTERS

Radon moving through soil pore spaces and rock fractures near the surface of the earth usually escapes into the atmosphere. Where a house is present, however, soil air often flows toward its foundation for three reasons: (1) differences in air pressure between the soil and the house, (2) the presence of openings in the house’s foundation, and (3) increases in permeability around the basement (if one is present).

In constructing a house with a basement, a hole is dug, footings are set, and coarse gravel is usually laid down as a base for the basement slab. Then, once the basement walls have been built, the gap between the basement walls and the ground outside is filled with material that often is more permeable than the original ground. This filled gap is called a disturbed zone. Picture supplied by Radon Mitigation Colorado.

Radon moves into the disturbed zone and the gravel bed underneath from the surrounding soil. The backfill material in the disturbed zone is commonly rocks and soil from the foundation site, which also generate and release radon. The amount of radon in the disturbed zone and gravel bed depends on the amount of uranium present in the rock at the site, the type and permeability of soil surrounding the disturbed zone and underneath the gravel bed, and the soil’s moisture content.

The air pressure in the ground around most houses is often greater than the air pressure inside the house. Thus, air tends to move from the disturbed zone and gravel bed into the house through openings in the house’s foundation. All house foundations have openings such as cracks, utility entries, seams between foundation materials, and uncovered soil in crawl spaces and basements.

Most houses draw less than one percent of their indoor air from the soil; the remainder comes from outdoor air, which is generally quite low in radon. Houses with low indoor air pressures, poorly sealed foundations, and several entry points for soil air, however, may draw as much as 20 percent of their indoor air from the soil. Even if the soil air has only moderate levels of radon, levels inside the house may be very high.

Because radon is a gas, it has much greater mobility than uranium and radium, which are fixed in the solid matter in rocks and soils. Radon can more easily leave the rocks and soils by escaping into fractures and openings in rocks and into the pore spaces between grains of soil.

The ease and efficiency with which radon moves in the pore space or fracture effects how much radon enters a house. If radon is able to move easily in the pore space, then it can travel a great distance before it decays, and it is more likely to collect in high concentrations inside a building.

The method and speed of radon’s movement through soils is controlled by the amount of water present in the pore space (the soil moisture content), the percentage of pore space in the soil (the porosity), and the “interconnectedness” of the pore spaces that determines the soil’s ability to transmit water and air (called soil permeability).

Radon can move through cracks in rocks and through pore spaces in soils. Radon moves more rapidly through permeable soils, such as coarse sand and gravel, than through impermeable soils, such as clays. Fractures in any soil or rock allow radon to move more quickly.

Radon in water moves slower than radon in air. The distance that radon moves before most of it decays is less than 1 inch in water-saturated rocks or soils, but it can be more than 6 feet, and sometimes tens of feet, through dry rocks or soils. Because water also tends to flow much more slowly through soil pores and rock fractures than does air, radon travels shorter distances in wet soils than in dry soils before it decays.

For these reasons, homes in areas with drier, highly permeable soils and bedrock, such as hill slopes, mouths and bottoms of canyons, coarse glacial deposits, and fractured or cavernous bedrock, may have high levels of indoor radon. Even if the radon content of the air in the soil or fracture is in the “normal” range (200-2,000 pCi/L), the permeability of these areas permits radon-bearing air to move greater distances before it decays, and thus contributes to high indoor radon.

PROPERTIES

Radon was discovered in 1900 by Friedrich Ernst Dorn, (Germany). Named after the element “radium” (radon was called niton at first, from the Latin word “nitens” meaning “shining”) but has been called radon since 1923. It is an essentially inert, colorless, odorless gas at ordinary temperatures. Its melting point is 202 degrees K and the boiling point is 211 degrees K. When cooled below the freezing point radon exhibits a brilliant phosphorescence which becomes yellow as the temperature is lowered and orange-red at the temperature of liquid air.

The atomic radius is 1.34 angstroms and it is the heaviest known gas, being nine times denser than air. Because it is a single atom gas (unlike oxygen, O2, which is comprised of two atoms) it easily penetrates many common materials like paper, leather, low density plastic (like plastic bags, etc.) most paints, and building materials like gypsum board (sheetrock), concrete block, mortar, sheathing paper (tarpaper), wood paneling, and most insulation.

Radon is also fairly soluble in water and organic solvents. Although reaction with other compounds is comparatively rare, it is not completely inert and forms stable molecules with highly electronegative materials. Radon is considered a noble gas that occurs in several isotopic forms. Only two are found in significant concentrations in the human environment: radon-222, and radon-220. Radon-222 is a member of the radioactive decay chain of uranium-238, and radon-220 is formed in the decay chain of thorium-232. Radon-222 decays in a sequence of radionuclides called radon decay products, radon daughters, or radon progeny. It is radon-222 that most readily occurs in the environment. Atmospheric releases of radon-222 results in the formation of decay products that are radioisotopes of heavy metals (polonium, lead, bismuth) and rapidly attach to other airborne materials such as dust and other materials facilitating inhalation.

USE

Radon is a noble gas. Only two of its isotopic forms are found in significant concentrations in the human environment: radon-222 and radon-220. Their decay products are not gases and occur as unattached ions or atoms, condensation nuclei, or attached to particles. This decay product of uranium-238 is commonly found in uranium mines. Radon has been used in some spas for presumed medical effects. In addition, radon is used to initiate and influence chemical reactions and as a surface label in the study of surface reactions. It has been obtained by pumping the gases off of a solution of a radium salt, sparking the gas mixture to combine the hydrogen and oxygen, removing the water and carbon dioxide by adsorption, and freezing out the radon.

EXPOSURE

The primary routes of potential human exposure to radon are inhalation and ingestion. Radon in the ground, groundwater, or building materials enters working and living spaces and disintegrates into its decay products. In comparison with levels in outdoor air, the concentrations of radon and its decay products to which humans are exposed in confined air spaces, particularly in underground work areas such as mines and buildings, are elevated. Although high concentrations of radon in groundwater may contribute to human exposure through ingestion, the radiation dose to the body due to inhalation of radon released from water is usually more important. Concentrations of radon decay products measured in the air of underground mines throughout the world vary by several orders of magnitude. In countries for which data were available, concentrations of radon decay products in underground mines are now typically less than 1000 Bq/m3 EEC Rn (approx. 28 pCi/l). The average radon concentrations in houses are generally much lower than the average radon concentrations in underground ore mines. Workers are exposed to radon in several occupations. Underground uranium miners are exposed to the highest levels of radon and its decay products. Other underground workers and certain mineral processing workers may also be exposed to significant levels. Exhalation of radon from ordinary rock and soils and from radon- rich water can cause significant radon concentrations in tunnels, power stations, caves, public baths, and spas. Peripheral lymphocyte chromosomes from 80 underground uranium miners and 20 male controls in the Colorado plateau were studied. Taken into account were confounding factors such as cigarette smoking and diagnostic radiation. Groups that were increasingly exposed to radon and its decay products were selected. Significantly more chromosomal aberrations were observed among miners with atypical bronchial cell cytology, suspected carcinoma, or carcinoma in situ than among miners with regular or mildly atypical cells, as evaluated by sputum cell cytology.

The Environmental Protection Agency (U.S. E.P.A.) and the Surgeons General’s Office have urged widespread testing for radon. They estimated that as many as 20,000 lung cancer deaths are caused each year by radon. Next to smoking, radon is the second leading cause of lung cancer. EPA says that nearly 1 in 3 homes checked in seven states and on three Indian lands had screening levels over 4 pCi/L, the EPA’s recommended action level for radon exposure.

Radon is a national environmental health problem. Elevated radon levels have been discovered in virtually every state. The EPA estimates that as many as 8 million homes throughout the country have elevated levels of radon. State surveys to date show that 1 out of 5 homes have elevated radon levels. Radon seeps into homes from the surrounding soil through cracks and other openings in the foundation. Indoor radon has been judged to be the most serious environmental carcinogen to which the general public is exposed and which the EPA must address. Based on current exposure and risk estimates, radon exposure in single-family houses may be a causal factor in as many as 20,000 of the total lung cancer fatalities which occur each year. Radon decay products (polonium- 218 and polonium-214, solid form) can attach to the surface of aerosols, dusts, and smoke particles which may be inhaled, and become deeply lodged or trapped in the lungs. Once lodged, they can radiate and penetrate the cells of mucous membranes, bronchi, and other pulmonary tissues.

Some scientific studies of radon exposure indicate that children may be more sensitive to radon. This may be due to their higher respiration rate and their rapidly dividing cells, which may be more vulnerable to radiation damage.

National Radon Action Month is January, 2011. Take this opportunity to make sure your family is safe. Testing for radon is easy and inexpensive. If elevated levels of radon are detected, a radon mitigation system can be installed to fix the problem.

To learn more about radon gas, visit these informative websites:

Environmental Protection Agency
World Health Organization
Centers for Disease Control (CDC)
National Cancer Institute
American Lung Association
U.S. Surgeon General
American Cancer Society
Toxic Substances & Disease Registry

November 2010 is Lung Cancer Awareness Month: Test Your Home for Radon Gas

envirolabs — Sun, 14 Nov 2010 19:55:15 +0000

Radon Gas is The #2 Cause of Lung Cancer. November is Lung Cancer Awareness Month and A Perfect Time to Test Your Home for Radon Gas.

What is Radon?

Radon has been identified as the second leading cause of lung cancer in the United States (second only to smoking.) The Environmental Protection Agency reports that radon causes about 20,000 of the 160,000 lung cancer deaths every year in the United States. These startling statistics have prompted the declaration of November 2010 as National Lung Cancer Awareness Month.

HOW RADON ENTERS

PROPERTIES

USE

EXPOSURE

To learn more about radon gas, visit these informative websites:

Environmental Protection Agency
World Health Organization
Centers for Disease Control (CDC)
National Cancer Institute
American Lung Association
Radon Mitigation Systems
U.S. Surgeon General
American Cancer Society
Toxic Substances & Disease Registry

Radon Mitigation & Radon Remediation Systems

envirolabs — Tue, 09 Mar 2010 01:21:53 +0000

Radon Remediation / Radon Mitigation: When a building (or house) is found to have an elevated level of radon gas (defined by the U.S. Environmental Protection Agency as a radon result of 4.0 pCi/l or higher,) methods of reducing the radon levels can be applied to cure the problem. The most common method of radon mitigation (also known as radon remediation or radon gas abatement) is Active Soil Depressurization (ASD.) An ASD Radon Mitigation System utilizes PVC piping attached to an electric radon suction fan. The piping typically begins below the lowest floor of the structure’s foundation (penetrating the slab of the basement or the plastic membrane of the crawl space) and extends upward to an exit point above ground level. The inline radon fan is mounted in an inconspicuous location on the exterior or within an attic above the home. In cases where the radon fan is installed in the attic, the discharge pipe extends out through the roof so the radon gas can be released outdoors. Once radon is released into the atmosphere, it is no longer hazardous. Radon is only dangerous when trapped indoors.

Active (fan assisted) radon mitigation systems can reduce the radon gas entry by as much as 99%. A qualified radon contractor (also known as a radon mitigator or radon remediation specialist) can typically install a radon mitigation system in a home in less than a day. After the system is installed, the radon levels begin to drop almost immediately. Passive radon reduction techniques (such as sealing cracks or installing pipes without an inline radon fan) are rarely effective at reducing radon levels. The reason that these “passive” radon reduction techniques are ineffective is because radon gas is under pressure and must escape from the ground. It is a very inert, un-reactive gas that can be drawn up through the pours of concrete, around drains, utility penetrations, or expansion joints. Attempting to “seal out” radon is similar to trying to keep water out of a basement by painting the walls and floor with waterproofing paint. It may work temporarily if the problem is minor, but it wouldn’t keep standing water out. The only way to fix a water problem is to redirect the water somewhere else before it enters the home. The same principles apply to radon correction. Sealing cracks and openings is part of the radon mitigation process; however this is to prevent the downward draw of conditioned air from the home and to improve the pressure field extension of the system below the slab, not to “seal out” the radon.

Radon is a colorless, odorless, naturally occurring, radioactive noble gas that is formed from the decay of radium. Radon gas is one of the heaviest substances that remains a gas under normal conditions and is considered to be a health hazard. The most stable isotope, Rn222 (Radon Gas), has a half-life of 3.8 days and is used in radiotherapy. While having been less studied by chemists due to its radioactivity, there are a few known compounds of this generally un-reactive element.

Radon is a significant contaminant that affects indoor air quality worldwide. Radon gas from natural sources can accumulate in buildings, especially in confined areas such as the basement. Radon can be found in some spring waters and hot springs.

According to the United States Environmental Protection Agency, radon is reportedly the second most frequent cause of lung cancer, after cigarette smoking; and radon-induced lung cancer the 6th leading cause of cancer death overall. According to the same sources, radon reportedly causes 21,000 lung cancer deaths per year in the United States. Because of this, radon mitigation systems can be life-savers.

Indoor radon can be mitigated by sealing basement foundations, water drainage, or by sub-slab de-pressurization. In severe cases, radon mitigation can be achieved via air pipes and fans to exhaust sub-slab air to the outside. Indoor radon ventilation systems are less visible, but exterior radon systems can be more cost-effective in some cases. Modern construction that conserves energy by making homes air tight exacerbates the risks of radon exposure if radon is present in the home. Older homes with more porous construction are more likely to vent radon naturally. Ventilation systems can be combined with a heat exchanger to recover energy in the process of exchanging air with the outside. (This is more common with commercial and industrial radon mitigation.) Homes built on a crawl space can benefit from a radon collector installed under a radon barrier (a sheet of plastic that covers the crawl space).

The most common approaches are active soil depressurization (ASD) which utilizes a radon mitigation suction fan to pull the gas out from below the foundation of the home. The radon fan is attached in-line with a PVC pipe system running from the foundation to the roof of the home. Once the radon gas is discharged outdoors, it becomes diluted by the outdoor air to levels that are not hazardous.

How Radon Enters Your House

Radon is a Cancer-causing, Radioactive Gas

Radon is estimated to cause many thousands of lung cancer deaths each year. In fact, the Surgeon General has warned that radon is the second leading cause of lung cancer in the United States. Only smoking causes more lung cancer deaths. If you smoke and your home has high radon levels, your risk of lung cancer is especially high. If your test shows a level of 2.7 pCi/l or above, consider installing a radon remediation system.

What Do Your Radon Test Results Mean?

Selecting a Radon Test Kit

Before you’ll know if you need a radon mitigation system, you need to conduct a test. Since you cannot see or smell radon, special equipment is needed to detect it. When you’re ready to test your home, contact your state radon office (or visit our radon testing page for information on locating qualified test kits or qualified radon testers. You can also order test kits and obtain information from a radon hotline. There are two types of radon testing devices. Passive radon testing devices do not need power to function. These include charcoal canisters, alpha-track detectors, charcoal liquid scintillation devices, and electret ion chamber detectors. Both short- and long-term passive radon devices are generally inexpensive. Active radon testing devices require power to function and usually provide hourly readings and an average result for the test period. These include continuous radon monitors and continuous working level monitors, and these tests may cost more. A state or local official can explain the differences between radon devices and recommend ones which are more appropriate for your needs and expected testing conditions. Make sure to use a radon testing device from a qualified laboratory.

Any radon exposure has some risk of causing lung cancer. The lower the radon level in your home, the lower your family’s risk of lung cancer. A radon mitigation system installed by a qualified (radon certified) contractor could save your life. The amount of radon in the air is measured in “picocuries of radon per liter of air,” or “pCi/L.” Sometimes test results are expressed in Working Levels, “WL,” rather than picocuries per liter of air. A level of 0.016 WL is usually equal to about 4 pCi/L in a typical home. With this level, a radon abatement system would be recommended.

The U.S. Congress has set a long-term goal that indoor radon levels be no more than outdoor levels. About 0.4 pCi/L of radon is normally found in the outside air. EPA recommends fixing your home if the results one long-term test or the average of two short-term tests show radon levels of 4 pCi/L (or 0.016 WL) or higher. With today’s technology, radon levels in most homes can be reduced to 2 pCi/L or below. You may also want to consider radon mitigation if the level is between 2 and 4 pCi/L.

A short-term radon test remains in your home for 2 days to 90 days, whereas a long-term test remains in your home for more than 90 days. All radon tests should be taken for a minimum of 48 hours. A short-term test will yield faster results, but a long-term test will give a better understanding of your home’s year-round average radon level and indicate if a radon abatement or mitigation system is necessary.

The EPA recommends two categories of radon testing. One category is for concerned homeowners or occupants whose house is not for sale; refer to EPA’s A Citizen’s Guide to Radon for testing guidance. The second category is for radon testing and reduction in real estate transactions; refer to EPA’s Home Buyer’s and Seller’s Guide to Radon, which provides guidance and answers to some common questions.

Why Hire a Radon Contractor?

EPA recommends that you have a qualified radon mitigation contractor fix your home because lowering high radon levels requires specific technical knowledge and special skills. Without the proper equipment or technical knowledge, you could actually increase your radon level or create other potential hazards and additional costs. However, if you decide to do the work yourself, get information on appropriate training courses and copies of EPA’s technical guidance radon documents.

Will Any Radon Company Do?

EPA recommends that you use a state certified and/or qualified radon mitigation contractor trained to fix radon problems. You can determine a service provider’s qualifications to perform radon measurements or to mitigate radon from your home in several ways. First, check with your state radon office. Many states require radon professionals to be licensed, certified, or registered, and to install radon mitigation systems or conduct radon testing. Most states can provide you with a list of knowledgeable radon service providers doing business in the state. In states that don’t regulate radon services, ask the contractor if they hold a professional proficiency or certification credential, and if they follow industry consensus standards such as the American Society for Testing and Materials (ASTM) Standard Practice for Installing Radon Mitigation Systems in Existing Low-Rise Residential Buildings, E2121 (February 2003). You can contact private proficiency programs for lists of privately-certified professionals in your area. Such programs usually provide members with a photo-ID, which indicates their qualification(s) and the ID-card’s expiration date. For more information on private proficiency programs or contact your state radon office.

How To Select A Radon Mitigator

Get Estimates

Choose a radon contractor to fix the problem just as you would choose someone to do other home repairs. It is wise to get more than one estimate, to ask for references, and to contact some of those references to ask if they are satisfied with the radon mitigation company’s work. Also, ask your state radon office or your county/state consumer protection office for information about the radon companies.

Use this check-list when evaluating and comparing radon contractors and ask the following questions:

Radon is a naturally occurring radioactive gas produced by the breakdown of uranium in soil, rock, and water. Air pressure inside your home is usually lower than pressure in the soil around your home’s foundation. Because of this difference in pressure, your house acts like a vacuum, drawing radon in through foundation cracks and other openings. Radon Mitigation works by changing the pressure difference between the soil and the home. Radon gas may also be present in well water and can be released into the air in your home when water is used for showering and other household uses. In most cases, radon entering the home through water is a small risk compared with radon entering your home from the soil. Systems are available to reduce radon entry from water sources. In a small number of homes, the building materials (e.g., granite and certain concrete products) can give off radon, although building materials rarely cause radon problems by themselves. In the United States, radon gas in soils is the principal source of elevated radon levels in homes.

YES	NO
		Will the contractor provide references or photographs, as well as test results of ‘before’ and ‘after’ radon levels of past radon reduction work?
		Can the contractor explain what the work will involve, how long it will take to complete, and exactly how the radon mitigation system will work?
		Does the contractor charge a fee for any diagnostic tests? Although many contractors give free estimates, they may charge for diagnostic tests. These tests help determine what type of radon reduction system should be used and in some cases are necessary, especially if the contractor is unfamiliar with the type of house structure or the anticipated degree of difficulty. See “Radon Reduction Techniques” for more on diagnostic tests.
		Did the contractor inspect your home’s structure before giving you an estimate for radon mitigation?
		Did the contractor review the quality of your radon measurement results and determine if appropriate testing procedures were followed?

Compare the contractors’ proposed costs for the radon system and consider what you will get for your money, taking into account: (1) a less expensive system may cost more to operate and maintain; (2) a less expensive system may have less aesthetic appeal; (3) a more expensive system may be best for your house; and, (4) the quality of the building material will affect how long the radon mitigation system lasts.

Does the radon contractor‘s proposal and estimate include:

YES	NO
		Proof of state certification and/or professional proficiency or radon certification credentials?
		Proof of liability insurance and being bonded, and having all necessary licenses to satisfy local radon remediation requirements?
		Diagnostic testing prior to design and installation of a radon removal system?
		Installation of a warning device to caution you if the radon mitigation system is not working correctly?
		Testing after installation to make sure the radon reduction system works well?
		A guarantee to reduce radon levels to 4 pCi/L or below, and if so, for how long?

The Radon Abatement Contract

Ask the contractor to prepare a contract before any radon remediation work starts. Carefully read the contract before you sign it. Make sure everything in the contract matches the original proposal. The contract should describe exactly what work will be done prior to and during the installation of the radon system, what the system consists of, and how the system will operate. Many radon contractors provide a guarantee that they will adjust or modify the system to reach a negotiated radon level. Carefully read the conditions of the contract describing the guarantee. Carefully consider optional additions to your contract which may add to the initial cost of the radon removal system, but may be worth the extra expense. Typical options might include an extended warranty, a service plan, and/or improved aesthetics.

Important information that should appear in the radon abatement system contract includes:

	The total cost of the job, including all taxes and permit fees; how much, if any, is required for a deposit; and when payment is due in full.
	The time needed to complete the radon removal work.
	An agreement by the contractor to obtain necessary permits and follow required building codes for radon mitigation.
	A statement that the contractor carries liability insurance and is bonded and insured to protect you in case of injury to persons, or damage to property, while the radon work is done.
	A guarantee that the contractor will be responsible for damage and clean-up after the job.
	Details of any guarantee to reduce radon below a negotiated level.
	Details of warranties or other optional features associated with the hardware components of the mitigation system.
	A declaration stating whether any warranties or guarantees for the radon remediation work are transferable if you sell your home.
	A description of what the contractor expects the homeowner to do (e.g., make the work area accessible) before work begins.

What to Look for in a Radon Reduction System

In selecting a radon reduction method for your home, you and your contractor should consider several things, including: how high your initial radon level is, the costs of installation and system operation, your house size and your foundation type.

Installation and Operating Costs of Radon Ventilation Equipment

Most types of radon reduction systems cause some loss of heated or air conditioned air, which could increase your utility bills. How much your utility bills will increase will depend on the climate you live in, what kind of reduction system you select, and how your house is built. Systems that use fans are more effective in reducing radon levels; however, they will slightly increase your electric bill. The “Installation and Operating Cost Table” lists the installation and average operating costs for different radon reduction systems and describes the best use of each method.

Radiation risk to low fluences of particles may be greater than we thought

envirolabs — Sun, 07 Mar 2010 03:16:22 +0000

Radiation risk to low fluences of particles may be
greater than we thought
Hongning Zhou*, Masao Suzuki*†, Gerhard Randers-Pehrson*, Diane Vannais‡§, Gang Chen¶, James E. Trosko¶,
Charles A. Waldren‡§, and Tom K. Hei***
*Center for Radiological Research, College of Physicians and Surgeons, and Environmental Health Sciences, School of Public Health, Columbia University,
New York, NY 10032; ‡Department of Radiological Health Science, Colorado State University, Fort Collins, CO 80523; and ¶Department of Pediatrics
Human Development, Michigan State University, East Lansing, MI 48824
Communicated by Richard B. Setlow, Brookhaven National Laboratory, Upton, NY, October 3, 2001 (received for review August 18, 2001)
Based principally on the cancer incidence found in survivors of the
atomic bombs dropped in Hiroshima and Nagasaki, the International
Commission on Radiation Protection (ICRP) and the United
States National Council on Radiation Protection and Measurements
(NCRP) have recommended that estimates of cancer risk for low
dose exposure be extrapolated from higher doses by using a linear,
no-threshold model. This recommendation is based on the dogma
that the DNA of the nucleus is the main target for radiationinduced
genotoxicity and, as fewer cells are directly damaged, the
deleterious effects of radiation proportionally decline. In this
paper, we used a precision microbeam to target an exact fraction
(either 100% or <20%) of the cells in a confluent population and
irradiated their nuclei with exactly one particle each. We found
that the frequencies of induced mutations and chromosomal
changes in populations where some known fractions of nuclei
were hit are consistent with non-hit cells contributing significantly
to the response. In fact, irradiation of 10% of a confluent mammalian
cell population with a single particle per cell results in a
mutant yield similar to that observed when all of the cells in the
population are irradiated. This effect was significantly eliminated
in cells pretreated with a 1 mMdose of octanol, which inhibits gap
junction-mediated intercellular communication, or in cells carrying
a dominant negative connexin 43 vector. The data imply that the
relevant target for radiation mutagenesis is larger than an individual
cell and suggest a need to reconsider the validity of the
linear extrapolation in making risk estimates for low dose, high
linear-energy-transfer (LET) radiation exposure.
Radiation can cause as well as cure cancer. The risk of
developing radiation-induced cancer has traditionally been
estimated from cancer incidence among survivors of the atomic
bombs dropped in Hiroshima and Nagasaki in 1945. These data
provide the best estimate of human cancer risk over the dose
range from 20 to 250 cGy for low linear energy transfer radiation
such as X- or -rays. The cancer risk at doses below 20 cGy,
however, is uncertain and has been the subject of controversy for
decades. Both the International Commission on Radiation Protection
and the U.S. National Council on Radiation Protection
and Measurements have recommended using a linear nothreshold
extrapolation from higher doses where more accurate
risk estimates are available (1, 2). However, this approach has
drawn criticisms for being too strict on the one hand and too
conservative on the other (3). A better understanding of the
mechanisms of radiobiological effects at low doses would shed
light on the validity of the currently used model and provide a
rationale for the best estimates of risk.
Ever since X-rays were shown to induce mutation in Drosophila
and maize, it has been accepted dogma that the deleterious
effects of radiation, such as mutation and carcinogenesis, were
due mainly to direct damage to DNA. Evidence is now emerging
that extranuclear or extracellular targets are extremely important
in mediating the genotoxic effects of radiation (4–16). We
showed, for example, that irradiation of just the cellular cytoplasm
could induce mutation in the nucleus of the target cells by
a process involving oxyradicals (11). Furthermore, very low
doses of particles induced significantly higher levels of p53 in
populations of human fibroblasts than expected from the number
of cells that had actually been hit by an particle (5). The
excess in the fraction of responding cells, which received no
radiation exposure, were termed ‘‘bystanders.’’ It has been
difficult to measure the induction of mutations in populations of
mammalian cells where only a small fraction were traversed by
an exact number of particles. Here, we used a precision charged
particle beam to deliver exactly one particle through the nuclei
of a known proportion of human-hamster hybrid AL cells to
clearly ascertain the magnitude of this bystander mutagenic
effect. We found that cells irradiated with a single particle can
induce bystander mutagenic response in nonirradiated neighboring
cells, and that gap junction cell–cell communication plays
a critical role in mediating that bystander mutagenesis. Furthermore,
irradiation of 10% of a population resulted in a mutagenic
yield that was similar to when all of the cells in the population
were hit. These results are of considerable importance in reassessing
the potential genotoxic effect of low dose radiation and
suggest that the assumption of direct proportionality in radiation
risk assessment is seriously in error.
Materials and Methods
Cell and Culture Conditions. The human–hamster hybrid AL cells
containing a standard set of Chinese hamster ovary-K1 (CHO
K1) chromosomes plus a single copy of human chromosome 11
were used in this study. Chromosome 11 encodes cell surface
antigens (CD59) that render AL cells sensitive to killing by
specific monoclonal antibody E7.1 in the presence of complement.
Rabbit serum complement was from HRP (Denver, PA).
Antibody specific to the CD59 antigen was produced from
hybridoma cultures as described (17, 18). Cells were maintained
in Ham’s F-12 medium supplemented with 8% heatinactivated
FBS, 25 gml gentamycin, and 2 104Mglycine
at 37°C in a humidified 5% CO2 incubator, and passaged as
described (19, 20).
Irradiation Procedure. Approximately 500 exponentially growing
AL cells in 0.5 l volume were inoculated into each of a series of
microbeam dishes constructed by drilling a 14 inch hole in the
center of 60-mm diameter non-tissue-culture dishes as described
Abbreviations: CX10, AH1-9 cells carrying connexin 43 overexpressing construct; G2 PCC, G2
phase premature chromosome condensation.
†Present address: National Institute of Radiological Health Sciences, 4-9-1 Anagawa,
Inage-ku, Chiba, Japan.
§Present address: Radiation Effects Research Foundation (RERF), 5-2 Hijiyama Koen,
Minami-ku, Hiroshima, Japan.
**To whom reprint requests should be addressed at: Center for Radiological Research,
Vanderbilt Clinic 11-218, College of Physicians and Surgeons, Columbia University, 630
West 168th Street, New York, NY 10032. E-mail: TKH1@Columbia.edu.
The publication costs of this article were defrayed in part by page charge payment. This
article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C.
§1734 solely to indicate this fact.
14410–14415 PNAS December 4, 2001 vol. 98 no. 25 www.pnas.orgcgidoi10.1073pnas.251524798
(11, 13, 19). A 3.8-m-thick polypropylene film was epoxied over
the bottom of the hole, creating a miniwell that was then coated
with Cel-Tak (BD Biosciences, Bedford, MA) to enhance cell
attachment. Two days after plating, when the number of attached
cells reached an average of 2,000 per dish with 70% of
the attached cells in contact with neighboring cells, the nuclei of
attached cells were stained with a 50 nM solution of Hoechst
33342 dye for 30 min. The image analysis system then located the
centroid of each nucleus and irradiated some or all of them
randomly, one at a time, with an exact number of particles.
After irradiation, cells were maintained in the dishes for 3 days
before being removed by trypsinization and replated into culture
flasks. After culture for 4–5 days, the cells were trypsinized and
replated to measure the mutant fraction as described (19, 20).
Cytotoxicity of a Single Particle Traversal Through the Nucleus.
Conditions for assessing the clonogenic survival of cells irradiated
with a single particle have previously been described (19).
Briefly, irradiated and control cells in a series of miniwells were
trypsinized and replated into 60-mm-diameter Petri dishes for
colony formation. After incubating for 7–9 days, cultures were
fixed with formaldehyde and stained with Giemsa. The number
of colonies was counted to determine the surviving fraction as
described (11, 13, 19).
Quantification of CD59 Mutants. Determination of the mutant
fraction was carried out as described (11, 17–20). Briefly, 5 104
cells were plated into each of six 60-mm dishes in 2 ml of growth
medium, and the cultures were incubated for 2 h to allow for cell
attachment, after which 0.3% CD59 antiserum (E7.1) and 1.5%
(volvol) freshly thawed complement were added to each dish as
described (19, 20). The cultures were further incubated for 7–8
days for colony formation. At this time, the cells were fixed and
stained, and the number of CD59 mutant colonies was scored.
Controls included sets of dishes containing antiserum alone,
complement alone, or neither agent. Mutant yields in the
cultures derived from each radiation group were determined for
two consecutive weeks to ensure full expression of the mutations.
The mutant fraction at each dose was calculated as the number
of surviving colonies divided by the total number of cells plated
after correction for any nonspecific killing because of complement
alone and was expressed as the number of mutants per 105
clonogenically viable cells.
Prediction of the Mutant Yields. Predictions of the yield of mutants
where a known fraction of the cells was irradiated through the
nucleus with exactly one particle were made based on the
assumption of no bystander mutagenic effect. Mathematically,
we can predict the mutant fraction in a culture where a known
fraction of cells has been irradiated as follows.
The number of cells that were irradiated, survived, and formed
mutants is given as: FNP.E.IRMIR where F is the fraction
of cells irradiated with exactly one particle, N is the total
number of cells in the population, P.E.IR and MIR are the plating
efficiency and mutant fraction where 100% of cells have been
irradiated with exactly one particle, respectively.
The number of cells that were not irradiated, that were
attached, and that produced mutants is given as: (1 F) N
P.E.c Mc where P.E.c, and Mc are the plating efficiency and
mutant fraction of the controls, respectively.
The expected mutant fraction in population where a known
fraction (F) of cells was irradiated by a single particle is
therefore:
F N P.E.IR MIR 1 F N P.E.c Mc
F N P.E.IR 1 F N P.E.c
.
Cancel out N and divide all terms by P.E.c, then the formation
becomes
F S.F.IR MIR 1 F Mc
F S.F.IR 1 F
,
where S.F.IR is the survival fraction where 100% of the cells have
been irradiated with exactly one particle.
Treatment with Octanol. Octanol, an effective inhibitor of gap
junction communication (21), was used to investigate the role of
gap junction-mediated cell–cell communication in bystander
mutagenesis. Cells were treated with a 1-mM dose of octanol 2 h
before and maintained until 3 days after the irradiation. After
treatment, cultures were washed, trypsinized, and replated for
survival and mutagenesis as described above.
Bystander Mutagenesis in Cells Genetically Deficient in Gap Junction-
Mediated Cell–Cell Communication. To further investigate the role
of cell–cell communication in bystander mutagenesis, we transfected
AH1-9 cells (a variant of AL cells containing a hygromycin
resistant marker on chromosome 11) with either a dominant
negative connexin 43 vector or with connexin 43 expressing
vector and repeated the bystander mutagenic studies. Connexin
43 is the principal protein component of gap junctions (22).
There is good evidence that connexin of itself (assembled in a
lipid bilayer) is sufficient and necessary for the generation of gap
junction channels (23, 24). The scrape-loading assay (25) was
used to test the existence of gap junction-mediated intercellular
communication in the AH1-9-transfected cells. Briefly, confluent,
density-inhibited cells were scraped with a scalpel blade,
exposed to Lucifer yellow (0.05%) and Rhodamine dextran
solution (0.05%) for 3 min, and washed with PBS three times,
and the distance traveled by the migrating dye was determined
under a fluorescent microscope.
Detection of Chromosomal Damage. The use of premature chromosome
condensation to analyze the frequency of chromatid
break as an index of chromosomal damage has been described
(26). We chose to use a Calyculin A-inducedG2 phase premature
chromosome condensation (G2 PCC) assay to detect chromatid
damage instead of the conventional metaphase spread because
of its higher sensitivity. Immediately after irradiation, cells were
treated with Calyculin A at a final concentration of 50 nM for 30
min at 37°C. The PCC samples were prepared according to
conventional cytogenetic procedure (26, 27). Briefly, cells were
treated with 75 mM KCl for 20 min at 37°C and fixed in
methanolacetic acid (3:1). The cell suspension was dropped on
ethanol-cleaned slides, air-dried, stained with 5% Giemsa solution,
and scored under a microscope. Chromatid-type breaks,
which included chromatid breaks and acentric fragments, were
scored from a minimum of 50 G2 PCC samples per experiment.
The estimated chromatid-type breaks per cell, assuming no
interaction between irradiated and nonirradiated cells, were
similarly calculated as described above. To assess the role of gap
junctions in mediating the bystander process, lindane (40 M) or
octanol (1 mM) was added to the cultures 2 h before irradiation
as described (13).
Statistical Analysis. Data were calculated as means and standard
deviations. Comparisons of surviving fractions and induced
mutant fractions between treated groups and controls were
made by Student’s t test. A P value of 0.05 or less between groups
was considered to be significant.
Zhou et al. PNAS December 4, 2001 vol. 98 no. 25 14411
CELL BIOLOGY
Results
Bystander Mutagenesis in AL Cells Induced by a Single Particle
Through the Nucleus. Consistent with our previous finding, traversal
of the nucleus with a single particle was only slightly
cytotoxic to AL cells, resulting in a surviving fraction 0.79
0.05 (19). The yield of CD59 mutants induced in populations of
AL cells in which 5, 10, 20, or 100% of the cells had received
exactly one particle through the nucleus is shown in the upper
curve of Fig. 1. The mutant fractions (MF) predicted, assuming
no bystander interaction between the irradiated and nonirradiated
cells, are shown in the lower curve. The experimental curve
is significantly different from that expected. For example, the
mutant fraction when 5% of the cells had been irradiated was
58% of that when all of the cells were irradiated (induced mutant
fractions were 57 and 98 per 105 survivors, respectively). It is of
interest to note that there was little change in the yield of mutants
when the fraction of irradiated cells increased from 10 to 100%.
This result could be a reflection that the percentage of irradiated
cells in the population that were in direct contact with non-hit
cells in mediating the bystander response had reached a plateau
at 10% level and that further increases in the proportion of
irradiated cells would not enhance the bystander response.
Because the range of secondary electrons from particles of this
energy is 0.25 m (28), it is highly unlikely that direct radiation
damage to the nontargeted cells by secondary electrons contributes
to the bystander effect.
Involvement of Gap Junction-Mediated Cell–Cell Communication in
Bystander Mutagenesis. Because a high cell density implies cell–
cell contact in the process, we investigated the relationship
between gap junctional activity and particle-induced bystander
mutagenic effect in two ways: (i) the use of octanol to inhibit gap
junction-mediated intercellular communication (21) and (ii) the
use of genetically engineered cells that lack gap junctions. In our
first set of studies, we treated AL cells with a nontoxic and largely
nonmutagenic dose of octanol (1 mM) beginning 2 h before and
until 3 days after irradiation. As shown in Fig. 2, octanol reduced
the yield of induced CD59 mutants from 92 35 to 16 3 per
105 survivors. Treatment of octanol alone resulted in an induced
mutant fraction of 10 4 per 105 survivors. Although this
result indicates a role of gap junctions in the bystander mutagenic
response, the effects of octanol are not limited to gap
junctions but can affect other cellular structures and functions,
including membrane fluidity (29). Therefore, to investigate more
specifically the role of gap junction-mediated cell–cell communication
with particle-induced bystander mutagenicity, we
used cells in which gap junctional activity was suppressed by a
dominant negative connexin construct.
AL-AH1-9 Cells Genetically Deficient in Connexin 43 Demonstrate No
Bystander Mutagenesis. We transfected AH1-9 cells with either a
connexin 43 overexpressing or a dominant negative construct. By
using the standard scrape-loading test as a measure of gap
junction activity (22), we found that the migration of Lucifer
yellow was completely blocked in cells carrying the dominant
negative connexin 43 vector (Fig. 3B, DN6). In contrast, the dye
was found to migrate many cell layers in distance among cells
carrying connexin 43 overexpressing construct (Fig. 3A, CX10).
Parental AL cells and AH1-9 cells showed a moderate migration
of Lucifer yellow (data not shown). Significantly, AH1-9 cells
containing the connexin 43 expressing vector showed a higher
bystander mutagenic yield than that of vector control (Fig. 4,
Table 1). In contrast, there was little, if any, bystander effect
among AH1-9 cells carrying the dominant negative vector (Table
1). These data clearly show that gap junction intercellular
communication is critical in mediating the bystander mutagenesis,
although the nature of the signaling molecules involved in
the communication between particle-traversed and nontraversed
cells remains to be established.
Using Chromatid Breakage as an Endpoint To Assess the Bystander
Effect. In addition to gene mutations, chromosomal aberrations
are an important class of DNA damages induced by particles.
Therefore, we further compared the incidence of chromatid-type
breaks induced in AL cells where a single particle was delivered
to the nucleus in either 20 or 100% of the cultures. As shown in
Fig. 5B, in population where every cell had been irradiated, 93%
of the cells contained three or more chromatid breaks. This
result was in sharp contrast to the control where only 10% of the
cells contained one break (Fig. 5A). When 20% of the cells in a
population were irradiated with a single particle, 75% of the cells
were expected to contain no breaks if one assumed there was no
interaction between the irradiated and nonirradiated cells (Fig.
5C). In actuality, only 36% of the cells in this population showed
no chromatid breaks (Fig. 5D). Furthermore, the profile of
chromatid breaks was very different from that in which 100% of
the cells in the population were hit. Addition of octanol (1 mM)
Fig. 1. Induced CD59 mutant fractions per 105 survivors obtained from
populations of AL cells in which 0, 5, 10, 20, or 100% had been irradiated with
exactly one particle through its nucleus. Induced mutant fraction total
mutant fraction minus background incidence, which was 4610 mutants per
105 clonogenic survivors in AL cells used in these experiments. Data are pooled
from three to seven independent experiments. Error bars representSD. The
calculated curve deviates slightly from a straight line fitting because of the
slight cytotoxic effect of single particle traversal among the irradiated cells.
Fig. 2. Effect of octanol treatment (1 mM, 2 h before and maintained until
3 days after irradiation) on mutant fractions of AL cell population of which
20%had been irradiated with a single particle through the nucleus. Data are
from three independent experiments. Error bars represent SD.
14412 www.pnas.orgcgidoi10.1073pnas.251524798 Zhou et al.
or lindane (40 M) to the 20% irradiated culture likewise
obliterated the increase in chromatid breaks resulting from the
bystander effects to a profile similar to that shown in Fig. 5C
(data not shown).
Discussion
Both epidemiological and experimental animal studies have
indicated an association between exposure to radon ( particles)
and the incidence of lung cancer (see ref. 30 for review).
Although the mechanisms of radiation carcinogenesis have not
been elucidated, there is good evidence that radiation-induced
genetic changes such as chromosomal aberrations, gene mutations,
and genomic instability play a critical role in the
process. Because direct epidemiological studies on indoor
radon exposure and lung cancer are equivocal, risk for low
level of exposure received by the general population have been
based on extrapolation from higher exposures in studies of
underground miners assuming a linear, no-threshold doseresponse
relationship. This model for cancer estimation, however,
has been a subject of controversy for decades because
there is insufficient observational basis to confirm the model
(3, 31). Moreover, application of this model as a basis of
radioprotection and risk assessment by no means signifies its
validity, merely a precautionary necessity.
It has always been accepted that most of the deleterious
effects of ionizing radiation including particles are attributable
to direct nuclear hits. Recent evidence, however, indicates
that extranuclear or extracellular events are also important
in mediating the genotoxic effects of particles. Early
investigations of the radiation-induced bystander effect measured
the frequency of sister chromatid exchanges (SCE) in
populations of cells exposed to low fluencies of particles. It
was found that SCE levels were significantly higher than
expected from target theory calculations of the number of cells
that had actually been hit by an particle (4, 6). Furthermore,
such biological effects as induction of micronuclei (10), gene
Fig. 3. The scrape-loading assay (20) was used to evaluate levels of gap
junction-mediated intercellular communication inAL-AH1-9-transfected cells.
In connexin 43 overexpressing (CX10) cells (A), Lucifer yellow migrated a
distance of several cell layers away from the scrape. In contrast, in cells
transfected with the dominant negative vector (DN6) cells (B), there was no
migration of the dye (200).
Fig. 4. Mutation fraction (MF) from population of AL-AH1-9 cells transfected
with connexin 43 overexpressing vector (CX10), a dominant negative connexin
43 vector (DN6), or vector alone (CXV2). Data are from three to four independent
experiments. Error bars represent SD. The populations of AH1-9 cells
used in these experiments have higher mutant induction as well as background
mutant level than the parental AL cells.
Zhou et al. PNAS December 4, 2001 vol. 98 no. 25 14413
CELL BIOLOGY
mutation (12, 13), and expression of stress-related genes (5, 9,
15) can occur in a significantly higher proportion of cells than
in those traversed by an particle. There is also evidence that
bystander effects are involved in malignant transformation of
mammalian cells in vitro (16).
By using a precision charged-particle microbeam, we reported
that cells that had been lethally irradiated with particles could
induce mutagenesis in neighboring cells not directly hit by the
particles, and that mutant induction depended on cell–cell
communication (13). However, exposure to high dose of
particles is an unlikely scenario in environmental exposures to
radon. To extend this observation, we show here that a single
particle traversal of a small fraction ofAL cells (10–20%) induces
a mutagenic response similar to that occurring when 100% of the
cells in the population are hit, and that gap junction-mediated
cell–cell communication plays an important role in the process.
Although it is not clear whether directly irradiated cells are
equally responsive to the bystander effect observed in nonirradiated
cells, it is likely that, when cells are directly hit, they
initiate a series of self-preservation mechanisms including DNA
repair and a cell-signaling process that diminish their ability to
respond to bystander signaling. In other words, irradiated cells
behave differently from bystander, nonirradiated cells in their
collective response to mutagenic signals.
Two important questions need to be addressed: (i) What are
the mechanism(s) of the bystander mutagenic process, and (ii)
what is the implication of the present findings to low dose
radiation risk assessment? Based on the literature, it is likely that
at least two pathways are involved in mediating radiationinduced
bystander effects (see ref. 32 for review). In sparsely
populated cultures, any induction of a bystander response clearly
requires the presence of oxyradicals or other soluble mediators
(10). In contrast, studies (including ours) with confluent monolayers
have implicated gap junctional activities (12–15). These
latter findings are consistent with our result that certain cytotoxic
factor(s), such as cytokines and reactive oxygen or nitrogen
species released into the culture medium from irradiated cells,
have little, if any, effect on bystander mutagenesis (33). Furthermore,
pretreatment of cells with the intracellular radical
scavenger, N-acetyl cysteine (10 mM) had little effect on bystander
mutagenic yield (data not shown). However, there is
evidence that, among confluent human fibroblast cultures, secretion
of cytokines or other growth-promoting factors by irradiated
cells leads to enhanced production of reactive oxygen
species in bystander cells (6, 7). These two observations among
confluent cultures are not necessarily mutually exclusive because
there is evidence that radiation induces long-lived organic
radicals that persist for hours (34).
We also found that the gap junction inhibitor octanol significantly
decreased the mutant yield. These results were further
confirmed in transfected cells carrying a dominant negative
connexin that reduced the mutation frequency of the cell
Fig. 5. Induction of chromatid-type breaks per cell from populations of AL cells in which 0, 20 or 100% of cells were traversed by exactly one particle through
the nucleus. The data are from three to four independent experiments. Bars represent SD.
Table 1. Comparison of mutant fractions (MF) in population of
AL-AH1-9 cells transfected with either connexin 43
overexpressing vector (CX10), dominant negative
vector (DN6), or with vector alone (CXV2)
Cell line
Level of
GJCC* Induced MF
† Predicted MF
MF because
of bystander‡
CX10 High 467 97 370
CXV2 Moderate 346 123 223
DN6 None 149 141 8
*GJCC, gap junction-mediated cell–cell communication.
†Mutant fraction, number of CD59 mutants per 105 survivors.
‡Bystander mutagenic yield induced MF minus predicted MF, assuming no
interaction between irradiated and nonirradiated cells.
14414 www.pnas.orgcgidoi10.1073pnas.251524798 Zhou et al.
populations to the level expected assuming no bystander effect.
The gap junction channels have an apparent selectivity based
principally on molecular size, allowing the movement of molecules
smaller than 1,000 Da, such as cAMP, but preventing the
movement of proteins or nucleic acids. These findings show that
gap junction intercellular communication plays a critical role in
bystander mutagenesis when cells are in close contact, although
the nature of the signaling molecules involved in the communication
between particle-traversed and nontraversed cells remains
to be established.
Our G2 PCC studies indicated that bystander effect could also
be demonstrated at the chromosomal level. Compared with the
traditional mitotic preparation based on metaphase spread, the
use of chemically induced PCC provides a more sensitive and
easier approach to score chromatid damage in mammalian cells
(26). For example, in Calyculin A-treated cells, theG2 PCC index
was found to be seven times higher than the mitotic index after
a comparable treatment with colcemid (26). It should be noted
that the profile of chromatid breaks found in populations where
100% of cells were hit was very different from that in which only
20% of cells received a hit. The findings are consistent with the
observations that (i) high linear-energy-transfer radiation produces
multiple damaged sites in the nucleus of hit cells (35) and
(ii) the type of mutations induced as a result of the bystander
effect is qualitatively different from that of direct nuclear hit (12,
13). The findings that, in the presence of octanol or lindane, the
profile of chromatid breaks in this latter population resembled
that found in controls suggest that gap junctions are indeed
involved in the bystander phenomenon.
Our studies provide clear evidence that a single particle can
induce mutations and chromosome aberrations in cells that
received no direct radiation exposure to their DNA. These
findings imply that the target for radiation-induced genetic
damage is larger than an individual cell. The observation is
important in formulating risk assessment models because, for
particles, a cell cannot receive a dose lower than a single traversal
and these hit cells are a minority population in lung tissue
exposed to environmental radon. The observation that irradiation
of as few as 10% of a cell population results in a mutagenic
yield similar to that when all of the cells in the population are hit
indicates that low dose particle irradiation can induce a huge
bystander mutagenic response in neighboring cells not directly
traversed by particles. The genotoxic risk at such a low dose
region, therefore, may be significantly underestimated based on
current practice. Because radiation-induced bystander response
(mainly cell killing and genomic instability) has been demonstrated
with low linear-energy-transfer radiation such as X- or
-rays (8, 32), our findings may not be inconsistent with the
recent study of radiation-related cancer risk among A-bomb
survivors at the dose range of 0.15–0.30 Sv (36). Results of our
present studies cast doubt on the dose at which dose linearity
would be expected, a strong indication that the models presently
used in predicting radiation risk at low doses are inadequate and
need to be reexamined.
We thank Drs. Eric Hall and Charles Geard for helpful discussion and
Dr. Hiroshi Yamasaki for providing the dominant negative connexin 43
plasmids. This work was supported by National Cancer Institute Grants
CA75384, 49062, and 36447 and by National Cancer Institute Research
Resource Grant RR 11623.
1. International Commission on Radiological Protection (1991) Recommendations
(Pergamon, New York), Report no. 60.
2. National Council on Radiation Protection and Measurements. (1993) Report
116 (Natl. Counc. Radiat. Prot. Meas., Bethesda).
3. Strom, D. J., Cameron, J. R. & Cohen, B. L. (1998) Med. Phys. 25, 273–278.
4. Nagasawa, H. & Little, J. B. (1992) Cancer Res. 52, 6394–6396.
5. Hickman, A. W., Jaramillo, R. J., Lechner, J. F. & Johnson, N. F. (1994) Cancer
Res. 54, 5797–5800.
6. Deshpande, A., Goodwin, E. H., Bailey, S. M., Marrone, B. L. & Lehnert, B. E.
(1996) Radiat. Res. 145, 260–267.
7. Narayanan, P. K., Goodwin, E. H. & Lehnert, B. E. (1997) Cancer Res. 57,
3963–3971.
8. Mothersill, C. & Seymour, C. B. (1998) Radiat. Res. 149, 256–262.
9. Azzam, E. I., de Toledo, S. M., Gooding, T. & Little, J. B. (1998) Radiat. Res.
150, 497–504.
10. Prise, K. M., Belyakov, O. V., Folkard, M. & Michael, B. D. (1998) Int. J.
Radiat. Biol. 74, 793–798.
11. Wu, L. J., Randers-Pehrson, G., Xu, A., Waldren, C. A., Geard, C. R., Yu, Z.
& Hei, T. K. (1999) Proc. Natl. Acad. Sci. USA 96, 4959–4964.
12. Nagasawa, H. & Little, J. B. (1999) Radiat. Res. 152, 552–557.
13. Zhou, H., Randers-Pehrson, G., Waldren, C. A., Vannais, D., Hall, E. J. & Hei,
T. K. (2000) Proc. Natl. Acad. Sci. USA 97, 2099–2104. (First Published
February 11, 2000; 10.1073pnas.030420797)
14. Bishayee, A., Hill, H. Z., Stein, D., Rao, D. V. & Howell, R. W. (2001) Radiat.
Res. 155, 335–344.
15. Azzam, E. I., de Toledo, S. M. & Little, J. B. (2001) Proc. Natl. Acad. Sci. USA
98, 473–478. (First Published January 9, 2001; 10.1073pnas.011417098)
16. Sawant, S. G., Randers-Pehrson, G., Geard, C. R., Brenner, D. J. & Hall, E. J.
(2001) Radiat. Res. 155, 397–401.
17. Waldren, C. A., Jones, C. & Puck, T. T. (1979) Proc. Natl. Acad. Sci. USA 76,
1358–1362.
18. Waldren, C. A., Correll, L., Sognier, M. A. & Puck, T. T. (1986) Proc. Natl.
Acad. Sci. USA 83, 4839–4843.
19. Hei, T. K., Wu, L. J., Liu, S. X., Vannais, D.&Waldren, C. A. (1997) Proc. Natl.
Acad. Sci. USA 94, 3765–3770.
20. Hei, T. K., Piao, C. Q., He, Z. Y., Vannais, D. & Waldren, C. A. (1992) Cancer
Res. 52, 6305–6309.
21. Princen, F., Robe, P., Lechanteur, C., Mesnil, M., Rigo, J., Gielen, J., Merville,
M. & Bours, V. (1999) Clin. Cancer Res. 5, 3639–3643.
22. Bruzzone, R. & Meda, P. (1998) Eur. J. Clin. Invest. 18, 13–21.
23. Bruzzone, R., White, T. W. & Goodenough, D. A. (1996) BioEssays. 18, 709–718.
24. Trosko, J. E. (1998) Environ. Health Perspect. 106, Suppl. 1, 331–339.
25. El-Fouly, M. H., Trosko, J. E. & Chang, C. C. (1987) Exp. Cell Res. 168, 422–430.
26. Masao, S., Piao, C. Hall, E. J. & Hei, T. K. (2001) Radiat. Res. 155, 432–439.
27. Durante, M., Furusawa, Y., Majima, J., Kawata, T. & Gotoh, E. (1999) Radiat.
Res. 151, 670–676.
28. Magee, J. & Chatterjee, A. (1980) J. Phys. Chem. 84, 3529–3536.
29. Sikkema, J., de Bont, J. A. & Poolman, B. (1994) J. Biol. Chem. 269, 8022–8028.
30. National Research Council Committee on Health Risk of Exposure to Radon
(BEIR VI) (1994) Health Effects of Exposure to Radon: Time for Reassessment
(Natl. Acad. Press, Washington, DC).
31. Kellerer, A. M. (2000) Radiat. Environ. Biophys. 39, 17–24.
32. Mothersill, C. & Seymour, C. (2001) Radiat. Res. 155, 759–767.
33. Zhou, H., Suzuki, M., Geard, C. & Hei, T. K. (2002) Mutat. Res., in press.
34. Koyama, S., Kodama, S., Suzuki, K., Matsumoto, T., Miyazaki, T. & Watanabe
M. (1998) Mutat. Res. 421, 45–54.
35. Goodhead, D. T. (1994) Int. J. Radiat. Biol. 65, 7–17.
36. Pierce, D. A. & Preston, D. L. (2000) Radiat. Res. 154, 178–186.
Zhou et al. PNAS December 4, 2001 vol. 98 no. 25 14415
CELL BIOLOGY

Radon Gas Killed 20,000 Americans in 2009

envirolabs — Fri, 08 Jan 2010 14:44:11 +0000

Environmental Protection Agency Designates January 2010 as National Radon Action Month

What is Radon?

HOW RADON ENTERS

PROPERTIES

USE

EXPOSURE

To learn more about radon gas, visit these informative websites: