subsequent decades. 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, 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