Cancer in miners ). 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, Saxony, Germany. Given that the
type locality of the important uranium ore
pitchblende is in the
Ore Mountains and that region was the most important German speaking mining area at the time, it is likely the radon-induced lung cancers were associated with uranium. 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. Modern mining techniques, including better ventilation for underground mines, routine radiation monitoring as well as technologies like
in-situ leaching have helped decrease the incidence of radon exposure among miners in 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. 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. 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. 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. 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 escalator. 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, 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. 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. 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 Since radon is generally associated with diseases that are not detected until many years after elevated exposure, the public may not consider the implications of radon exposure during childhood. Aside from the exposure in the home, one of the major contributors to radon exposure in children are schools. 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. 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, 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. 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 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. ==Studies on domestic exposure==