Epidemiologic studies of uranium miners and other underground miners have consistently shown miners exposed to high levels of radon to be at increased risk of lung cancer. More recently, concern has arisen about lung cancer risks among people exposed to lower levels of radon in homes. The current Canadian guideline for residential radon exposure was set in 1988 at 800 Bq/m(3). Because of the accumulation of a considerable body of new scientific evidence on radon lung cancer risks since that time, Health Canada sponsored a workshop to review the current state-of-the-science on radon health risks. The specific objectives of the workshop were (1) to collect and assess scientific information relevant to setting national radon policy in Canada, and (2) to gather information on social, political, and operational considerations in setting national policy. The workshop, held on 3-4 March 2004, was attended by 38 invited scientists, regulators, and other stakeholders from Canada and the United States. The presentations on the first day dealt primarily with scientific issues. The combined analysis of North American residential radon and lung cancer studies was reviewed. The analysis confirmed a small but detectable increase in lung cancer risk at residential exposure levels. Current estimates suggest that radon in homes is responsible for approximately 10% of all lung cancer deaths in Canada, making radon the second leading cause of lung cancer after tobacco smoking. This was followed by a perspective from an UNSCEAR (United Nations Scientific Committee on the Effects of Atomic Radiation) working group on radon. There were two presentations on occupational exposures to radon and two presentations considered the possibility of radon as a causative factor for cardiovascular disease and for cancer in other organs besides the lung. The possible contribution of environmental tobacco smoke to lung cancers in nonsmokers was also considered. Areas for future research were identified. The second day was devoted to policy and operational issues. The presentations began with a perspective from the U.S. Environmental Protection Agency, followed by a history of radon policy development in Canada. Subsequent presentations dealt with the cost-effectiveness of radon mitigation, Canadian building codes and radon, and a summary of radon standards from around the world. Provincial representatives and a private consultant were given opportunities to present their viewpoints. A number of strategies for reducing residential radon exposure in Canada were recognized, including testing and mitigation of existing homes (on either a widespread or targeted basis) and changing the building code to require that radon mitigation devices be installed at the time a new home is constructed. The various elements of a comprehensive national radon policy were set forth.
To investigate the individual radiosensitivity of the human genome in long-term residents of areas with high radon concentration.
The materials used for this investigation were venous blood samples extracted from children living in the boarding school of Tashtagol (Kemerovo Region, Russia). Cytogenetic damage assessment was performed using the cytokinesis-block micronucleus assay (CBMN) on peripheral blood lymphocytes. PCR, gel electrophoresis and product detection using a transilluminator were used to determine polymorphisms in the genes ADPRT (rs 1136410), hOGG1 (rs 1052133), NBS1 (rs 1805794), XRCC1 (rs 25487), XpC (rs 2228001), XpD (rs 13181), and XpG (rs 17655). Statistical analysis was performed using nonparametric methods. To ensure accurate results, FDR-correction for multiple comparisons was performed.
We discovered a significant increase in the frequency of binucleated lymphocytes with micronuclei (MN) in carriers of the His/His genotype of the XpG gene Asp1104His polymorphism in comparison to heterozygous and homozygous carriers of the Asp allele. In addition, the Ala/Ala genotype for the ADPRT gene Val762Ala polymorphism and the Glu/Gln genotype for the NBS1 gene Glu185Gln polymorphism were associated with the elevated frequency of binucleated lymphocytes with nucleoplasmic bridges (NPB).
As a result of this study, the elevated frequency of cytogenetic damage in people with particular DNA-repair gene polymorphisms in response to chronic exposure to radon was demonstrated. It was shown that the genes and corresponding polymorphisms (the XpG gene Asp1104His polymorphism, the ADPRT gene Val762Ala polymorphism and the NBS1 gene Glu185Gln polymorphism) can be used as molecular genetic markers of increased individual radiosensitivity in long-term residents of areas with high concentrations of radon.
Indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. There is an increasing need among radiation practitioners to have numerical values of lung cancer risks for men and women, ever-smokers and never-smokers exposed to radon in homes. This study evaluates individual risks for the Canadian population exposed to radon in homes at different radon concentrations and for different periods of their lives.
Based on the risk model developed recently by U.S. Environmental Protection Agency (EPA), individual risks of radon-induced lung cancers are calculated with Canadian age-specific rates for overall and lung cancer mortalities (1996-2000) as well as the Canadian smoking prevalence data in 2002.
Convenient tables of lifetime relative risks are constructed for lifetime exposures and short exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 50 to 1000 Bq/m3.
The risk of developing lung cancer from residential radon exposure increases with radon concentration and exposure duration. For short exposure periods, such as 10 or 20 years, risks are higher in middle age groups (30-50) compared especially to the later years. Individuals could lower their risks significantly by reducing radon levels earlier in life. The tables could help radiation protection practitioners to better communicate indoor radon risk to members of the public.
Exposure to indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. Canadian population risk of radon induced lung cancer was assessed in 2005 with the radon distribution characteristics determined from a radon survey carried out in the late 1970s in 19 cities. In that survey, a grab sampling method was used to measure radon levels. The observed radon concentration in 14,000 Canadian homes surveyed followed a log-normal distribution with a geometric mean (GM) of 11.2 Bq m(-3) and a geometric standard deviation (GSD) of 3.9. Based on the information from that survey, it was estimated that ~10 % of lung cancers in Canada resulted from indoor radon exposure. To gain a better understanding of radon concentrations in homes across the country, a national residential radon survey was launched in April 2009. In the recent survey, long-term (3 month or longer) indoor radon measurements were made in roughly 14 000 homes in 121 health regions across Canada. The observed radon concentrations follow, as expected, a log-normal distribution with a GM of 41.9 Bq m(-3) and a GSD of 2.8. Based on the more accurate radon distribution characteristics obtained from the recent cross-Canada radon survey, a re-assessment of Canadian population risk for radon induced lung cancer was undertaken. The theoretical estimates show that 16 % of lung cancer deaths among Canadians are attributable to indoor radon exposure. These results strongly suggest the ongoing need for the Canadian National Radon Program. In particular, there is a need for a focus on education and awareness by all levels of government, and in partnership with key stakeholders, to encourage Canadians to take action to reduce the risk from indoor radon exposure.
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A cohort study of the mortality experience (1950-1984) of 1,772 Newfoundland underground fluorspar miners occupationally exposed to high levels of radon daughters (mean dose = 382.8 working levels months) has been conducted. Observed numbers of cancers of the lung, salivary gland, and buccal cavity and pharynx were significantly elevated among these miners. A highly significant relation was noted between radon daughter exposure and risk of dying of lung cancer; the small numbers of salivary gland (n = 2) and buccal cavity and pharynx (n = 6) cancers precluded meaningful analysis of dose response. Attributable and relative risk coefficients for lung cancer were estimated as 6.3 deaths per working level month per million person-years and 0.9% per working level month, respectively. Relative risk coefficients were highest for those first exposed before age 20 years. Cigarette smokers had relative and attributable risk coefficients comparable to those of nonsmokers. Relative risks fell sharply with age, whereas attributable risks were lowest in the youngest and oldest age groups. The results suggest that efforts to raise existing occupational exposure standards may be inappropriate.
A cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.
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Relation between the risk of lung cancer and combined home and work indoor radon exposure was studied on the example of the population of Lermontov town (Stavropol Region, Russia). The town is situated in the former uranium mining area. Case (121 lung cancer cases) and control (196 individuals free of lung cancer diagnosis) groups of the study included both ex-miners and individuals that were not involved in the uranium industry. Home and work radon exposures were estimated using archive data as well as contemporary indoor measurements. The results of our study support the conclusion about the effect of radon exposure on the lung cancer morbidity.
Public concern was expressed regarding the possibility of adverse health effects with the disposal of radioactive waste in Port Hope, Ontario. A case-control study was carried out to estimate the relative importance of domestic radon gas exposure in the causation of lung cancer in the town over a ten-year period. Twenty-seven cases met the entry criteria. Statistical analyses of results did not provide conclusive results that linked an increased risk of lung cancer and elevated domestic alpha radiation levels, when all factors were considered. However, a very strong association was demonstrated between cigarette smoking and lung cancer.
A case-control study of lung cancer in relation to exposure to radon in homes in Winnipeg, Manitoba, Canada, was conducted during 1983-1990. In total, 738 individuals with histologically confirmed incident cases of lung cancer were interviewed, along with 738 controls matched on age (+/- 5 years) and sex. Radon dosimeters were placed in all residences in which the study subjects had reported living within the Winnipeg metropolitan area for at least 1 year. Radon dosimetry was done by means of integrated alpha-track measurements over a 1-year period. In the homes monitored, the average level of radon-222 was about 120 becquerels (Bq)/m3 in the bedroom area and 200 Bq/m3 in the basement. After adjusting for cigarette smoking and education, no increase in the relative risk for any of the histologic types of lung cancer observed among the cases was detected in relation to cumulative exposure to radon.
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