The residential radon-lung cancer association in U.S. counties: a commentary

There is little doubt that underground miners exposed to radon and its progeny have increased rates of lung cancer. Residential radon exposures should carry a possibly smaller risk of increased cancer. When it became possible to collect radon data in a large number of U.S. homes and the data were aggregated by counties, the apparent association with lung cancer was a negative one, even when many other variables were taken into account. Residential radon levels are higher in suburban residences leading to a negative association with population density. Population density is strongly positively associated with lung cancer. It follows that aggregate residential radon and lung cancer rates should be negatively associated for reasons having nothing to do with the possibility of radon being carcinogenic to the lung. A second problem presented by the data is the one of sampling bias since the county lung cancer data are from the whole county population, but only a few residences are tested. Examples of other inherent associations in environmental epidemiology are cited. One strategy is to study areas of the same population density but with radon exposure gradients. This is approximated by choice of rural high radon states. Counties in such states have weak and inconsistent associations between radon and lung cancer, some of which are positive. I conclude that counties are generally inappropriate units for study of radon and lung cancer associations.     

Smoking as a confounder in ecologic correlations of cancer mortality rates with average county radon levels

Cohen has reported a negative correlation between lung cancer mortality and average radon levels by county. In this paper, the correlation of U.S. county mortality rates for various types of cancers during the period 1970-1994 with Cohen's radon measurements is examined. In general, quantitatively similar, strongly negative correlations are found for cancers strongly linked to cigarette smoking, weaker negative correlations are found for cancers moderately increased by smoking, whereas no such correlation is found for cancers not linked to smoking. The results indicate that the negative trend previously reported for lung cancer can be largely accounted for by a negative correlation between smoking and radon levels across counties. Hence, the observed ecological correlation provides no substantial evidence for a protective effect of low level radon exposure.     

Epidemiological associations among lung cancer,radon exposure and elevation above sea level--a reassessment of Cohen''s county level radon study

Inhalation of radon (222Rn) decay products by persons living in homes has been associated with increased risk of lung cancer. Some epidemiological studies have shown a positive association between radon exposure and lung cancer rates. However, a large U.S.-wide ecological study (Cohen 1995) has shown a clear inverse association between average county radon concentration in homes and average lung cancer rates in the county. Cohen's strong inverse association between radon and lung cancer is surprising since there is no plausible biological reason for an inverse causal relationship between the two. We plot the county average lung cancer rate vs. the elevation above sea level (altitude) and show an inverse association between county average lung cancer rate and elevation. The elevation used for each county is the altitude of the most populous place in the county. We postulate that the decrease in lung cancer rates with higher elevations is caused by the carcinogenic effect of higher absolute oxygen concentration in the inspired air at lower elevations. Stratifying Cohen's lung cancer vs. radon data into ten groups of counties with similar elevations removes some, but not all, of his inverse association between radon and lung cancer.     

Association of lung cancer mortality with precambrian granite

Sixteen counties in New York, Pennsylvania, and New Jersey that are associated with the Reading Prong granite deposits have significantly higher age-adjusted lung cancer rates among whites of both sexes (1950-1979) than do 17 nearby control counties. Elevated radon daughter concentrations have been found in homes near the Reading Prong granites. Fraction of populations living in cities with over 5,000 persons, industrial centers, cities with populations above 20,000, and median incomes did not differ significantly for three county groups (those which include the granite, fringe area, and control areas). Weaknesses were inadequate home measurements of radon and lack of smoking information. Findings are consistent with several other studies relating radon in homes to lung cancer.     

Testing a BEIR-VI suggestion for explaining the lung cancer vs. radon relationship for U.S. counties

The BEIR-VI Report suggests that the large discrepancy between the observed lung cancer rate vs. radon exposure relationship for U.S. counties, and the predictions of linear no-threshold theory, may be explained by a strong negative correlation between smoking intensity and radon exposure. It proposes a model for testing that suggestion. We apply that model to the detailed data for U.S. counties; analysis shows that even a perfect negative correlation explains little more than half of the discrepancy, and the largest not-implausible correlation can explain less than a quarter of the discrepancy. We then extend the BEIR-VI suggestion to include a strong negative correlation between both the prevalence of smoking and the intensity of smoking. The largest not-implausible correlations can explain no more than 30% of the discrepancy. It is concluded that the previous interpretation of these data, that linear no-threshold theory fails this test, is sustained.     

Examining the relationship between lung cancer and radon in small areas across Scotland

Numerous studies have suggested that long-term exposure to radon gas may be an important cause of lung cancer, yet the precise effects are still not fully understood, especially in residential settings. This paper considers whether there is a relationship between the distribution of naturally occurring radon gas and lung cancer incidence in Scotland, for the period 1988-1991. We use regression analysis to test whether exposure to radon was a significant cause of lung cancer in Scotland, once smoking and other possible confounding factors were controlled for. The results demonstrate that for the population aged over 54, there was no significant relationship between radon exposure and lung cancer incidence. However, for those aged less than 55, lung cancer rates were significantly higher in places expected to have the highest levels of radon. These results suggest that more research is needed into the relationship between exposure to naturally occurring radon gas and lung cancer in Scotland, particularly among younger age groups.     

Residential radon and risk of lung cancer: a combined analysis of 7 North American case-control studies

BACKGROUND: Underground miners exposed to high levels of radon have an excess risk of lung cancer. Residential exposure to radon is at much lower levels, and the risk of lung cancer with residential exposure is less clear. We conducted a systematic analysis of pooled data from all North American residential radon studies. METHODS: The pooling project included original data from 7 North American case-control studies, all of which used long-term alpha-track detectors to assess residential radon concentrations. A total of 3662 cases and 4966 controls were retained for the analysis. We used conditional likelihood regression to estimate the excess risk of lung cancer. RESULTS: Odds ratios (ORs) for lung cancer increased with residential radon concentration. The estimated OR after exposure to radon at a concentration of 100 Bq/m3 in the exposure time window 5 to 30 years before the index date was 1.11 (95% confidence interval = 1.00-1.28). This estimate is compatible with the estimate of 1.12 (1.02-1.25) predicted by downward extrapolation of the miner data. There was no evidence of heterogeneity of radon effects across studies. There was no apparent heterogeneity in the association by sex, educational level, type of respondent (proxy or self), or cigarette smoking, although there was some evidence of a decreasing radon-associated lung cancer risk with age. Analyses restricted to subsets of the data with presumed more accurate radon dosimetry resulted in increased estimates of risk. CONCLUSIONS: These results provide direct evidence of an association between residential radon and lung cancer risk, a finding predicted using miner data and consistent with results from animal and in vitro studies.     

Dose-response relationship for radiation carcinogenesis in the low-dose region

Evidence that low-level radiation substantially enhances the effectiveness of repair mechanisms is summarized. This finding destroys the theoretical basis (there is no other basis) for use of a linear-no threshold dose-response relationship to estimate the cancer risk of exposure to low-level radiation. Such a methodology will exaggerate the risk. This conclusion is further supported by epidemiological evidence and by studies of the effects of radon exposure in the home, which are reviewed.     

Estimated risks of radon-induced lung cancer for different exposure profiles based on the new EPA model

Radon is a naturally occurring radioactive gas. When inhaled, radon can cause mutations that lead to lung cancer. Some new epidemiologic studies indicate that indoor radon is a public health problem. The BEIR VI report outlined its preferred two risk models for the combined effects of smoking and exposure to radon progeny, and listed the estimated risk to ever-smokers and never-smokers of both sexes due to lifetime exposure. However, exposures for shorter periods of time are of practical interest since exposure to elevated levels of radon may occur and end at any age. This study aims to produce practical tables of lifetime relative risks for exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 100 to 1,000 Bq m(-3). The calculations are based on the risk model developed recently by U.S. Environmental Protection Agency. The EPA's risk model is a single model that gives risk values midway between those obtained from the two BEIR VI preferred models. The detailed tables provide a clearer view of the age groups at higher risk and the effect of exposure duration. The results will help radiation protection practitioners to better communicate indoor radon risk to members of the public.     

Residential radon exposure and risk of lung cancer in Missouri.

OBJECTIVES: This study investigated residential radon exposure and lung cancer risk, using both standard radon dosimetry and a new radon monitoring technology that, evidence suggests, is a better measure of cumulative radon exposure. METHODS: Missouri women (aged 30 to 84 years) newly diagnosed with primary lung cancer during the period January 1, 1993, to January 31, 1994, were invited to participate in this population-based case-control study. Both indoor air radon detectors and CR-39 alpha-particle detectors (surface monitors) were used. RESULTS: When surface monitors were used, a significant trend in lung cancer odds ratios was observed for 20-year time-weighted-average radon concentrations. CONCLUSIONS: When surface monitors were used, but not when standard radon dosimetry was used, a significant lung cancer risk was found for radon concentrations at and above the action level for mitigation of houses currently used in the United States (148 Bqm-3). The risk was below the action level used in Canada (750 Bqm-3) and many European countries (200-400 Bqm-3).     

Lung cancer risk associated to exposure to radon and smoking in a case-control study of French uranium miners

A case-control study nested in the cohort of French uranium miners took smoking information into account in investigating the effect of radon exposure on lung cancer risk. This study included 100 miners who died of lung cancer and 500 controls matched for birth period and attained age. Data about radon exposure came from the cohort study, and smoking information was retrospectively determined from a questionnaire and occupational medical records. Smoking status (never vs. ever) was reconstructed for 62 cases and 320 controls. Statistical analyses used conditional logistic regression. The effect of radon exposure on lung cancer risk was assessed with a linear excess relative risk model, and smoking was considered as a multiplicative factor. Mean cumulative radon exposures were 114.75 and 70.84 Working Level Months (WLM) among exposed cases and controls, respectively. The crude excess risk of lung cancer per 100 WLM was 0.98 (95% CI: 0.18-3.08%). When adjusted for smoking, the excess risk was 0.85 per 100 WLM (95% CI: 0.12-2.79%), which is still statistically significant. The relative risk related to smoking was equal to 3.04 (95% CI: 1.20-7.70). This analysis shows a relative risk of lung cancer related to smoking similar to that estimated from previous miners' cohorts. After adjustment for smoking, the effect of radon exposure on lung cancer risk persists, and its estimated risk coefficient is close to that found in the French cohort without smoking information.     

Modeling joint exposures and health outcomes for cumulative risk assessment: the case of radon and smoking

Community-based cumulative risk assessment requires characterization of exposures to multiple chemical and non-chemical stressors, with consideration of how the non-chemical stressors may influence risks from chemical stressors. Residential radon provides an interesting case example, given its large attributable risk, effect modification due to smoking, and significant variability in radon concentrations and smoking patterns. In spite of this fact, no study to date has estimated geographic and sociodemographic patterns of both radon and smoking in a manner that would allow for inclusion of radon in community-based cumulative risk assessment. In this study, we apply multi-level regression models to explain variability in radon based on housing characteristics and geological variables, and construct a regression model predicting housing characteristics using U.S. Census data. Multi-level regression models of smoking based on predictors common to the housing model allow us to link the exposures. We estimate county-average lifetime lung cancer risks from radon ranging from 0.15 to 1.8 in 100, with high-risk clusters in areas and for subpopulations with high predicted radon and smoking rates. Our findings demonstrate the viability of screening-level assessment to characterize patterns of lung cancer risk from radon, with an approach that can be generalized to multiple chemical and non-chemical stressors.     

Measurement error in the explanatory variable of a binary regression: regression calibration and integrated conditional likelihood in studies of residential radon and lung cancer

In epidemiology, one approach to investigating the dependence of disease risk on an explanatory variable in the presence of several confounding variables is by fitting a binary regression using a conditional likelihood, thus eliminating the nuisance parameters. When the explanatory variable is measured with error, the estimated regression coefficient is biased usually towards zero. Motivated by the need to correct for this bias in analyses that combine data from a number of case-control studies of lung cancer risk associated with exposure to residential radon, two approaches are investigated. Both employ the conditional distribution of the true explanatory variable given the measured one. The method of regression calibration uses the expected value of the true given measured variable as the covariate. The second approach integrates the conditional likelihood numerically by sampling from the distribution of the true given measured explanatory variable. The two approaches give very similar point estimates and confidence intervals not only for the motivating example but also for an artificial data set with known properties. These results and some further simulations that demonstrate correct coverage for the confidence intervals suggest that for studies of residential radon and lung cancer the regression calibration approach will perform very well, so that nothing more sophisticated is needed to correct for measurement error.     

Canadian individual risks of radon-induced lung cancer for different exposure profiles

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.     

Pesticide sales and adult male cancer mortality in Brazil

In Brazil, where the use of pesticide grows rapidly, studies that evaluate the impact of pesticide exposure on cancer incidence and mortality are very scarce. In this study, we evaluated the degree of correlation between pesticide sales in 1985 in eleven Brazilian states and cancer mortality rates during 1996-1998. Information of all cancer deaths occurred in men 30-69 years old from 1996 to 1998 were collected from National Mortality System. Single and multiple linear regression coefficients were obtained to assess the relationship between per capita sales of pesticides in 1985, specific-site cancer mortality rates (prostate, soft tissue, larynx, leukemia, lip, esophagus, lung, pancreas, bladder, liver, testis, stomach, brain, non-Hodgkin's lymphoma, and multiple myeloma) during 1996-1998, and several covariates. In addition, states were stratified into three groups according to tertiles of pesticides sales and cancer mortality rate ratios (MRR) were then calculated using first tertile as reference. Finally, a factor analysis was performed to reveal unapparent relationships between pesticide use and cancer mortality. Pesticide sales showed statistically significant correlation with the mortality rates for the cancers of prostate (r=0.69; p=0.019), soft tissue (r=0.71; p=0.015), leukemia (r=0.68; p=0.021), lip (r=0.73; p=0.010), esophagus (r=0.61; p=0.046), and pancreas (r=0.63; p=0.040). Moderate to weak correlations were observed for the cancers of larynx, lung, testis, bladder, liver, stomach, brain, and NHL and multiple myeloma. In addition, correlation between pesticide sales and specific-site cancer mortality rates was reinforced by multiple regression analysis. For all specific-sites, cancer mortality rates were significantly higher in the states of moderate (2nd tertile) and high (3rd tertile) pesticide sales, with MRR ranging from 1.11 to 5.61. Exploring hidden relationships between pesticide sales and cancer mortality in Brazil, through a factor analysis, revealed that affluence; public policies and lifestyle behaviors may explain almost 70% of the variance of the studied association. The results suggest that population exposure to pesticides in the 1980s in some Brazilian States may have been associated with selected cancer sites observed a decade later.     

Exposure to atmospheric radon.

We measured radon (222Rn) concentrations in Iowa and Minnesota and found that unusually high annual average radon concentrations occur outdoors in portions of central North America. In some areas, outdoor concentrations exceed the national average indoor radon concentration. The general spatial patterns of outdoor radon and indoor radon are similar to the spatial distribution of radon progeny in the soil. Outdoor radon exposure in this region can be a substantial fraction of an individual's total radon exposure and is highly variable across the population. Estimated lifetime effective dose equivalents for the women participants in a radon-related lung cancer study varied by a factor of two at the median dose, 8 mSv, and ranged up to 60 mSv (6 rem). Failure to include these doses can reduce the statistical power of epidemiologic studies that examine the lung cancer risk associated with residential radon exposure.     

The Montana Radon Study: Social Marketing via Digital Signage Technology for Reaching Families in the Waiting Room

Objectives. I tested a social marketing intervention delivered in health department waiting rooms via digital signage technology for increasing radon program participation among priority groups.Methods. I conducted a tri-county, community-based study over a 3-year period (2010–2013) in a high-radon state by using a quasi-experimental design. We collected survey data for eligible participants at the time of radon test kit purchase.Results. Radon program participation increased at the intervention site (t₃₈ = 3.74; P = .001; 95% confidence interval [CI] = 4.8, 16.0) with an increase in renters (χ²_1,228 = 4.3; P = .039), Special Supplementary Nutrition Program for Women, Infants, and Children families (χ²_1,166 = 3.13; P = .077) and first-time testers (χ²_1,228 = 10.93; P = .001). Approximately one third (30.3%; n = 30) attributed participation in the radon program to viewing the intervention message. The intervention crossover was also successful with increased monthly kit sales (t₃₇ = 2.69; P = .01; 95% CI = 1.20, 8.47) and increased households participating (t₂₃ = 4.76; P < .001; 95% CI = 3.10, 7.88).Conclusions. A social marketing message was an effective population-based intervention for increasing radon program participation. The results prompted policy changes for Montana radon programming and adoption of digital signage technology by 2 health departments.Indoor radon exposure accounts for 21 000 deaths (15% of lung cancer deaths) in the United States each year and is the second leading cause of lung cancer behind smoked tobacco.1 Radon causes 100 times more deaths than carbon monoxide poisoning2 and is the leading environmental cause of cancer in North America.3 Although lung cancer can be treated, the survival rate is one of the lowest for all cancer types. The estimate that Americans spend more than 90% of their time indoors further underscores the need to reduce residential exposures.4Montana, like other states in the Rocky Mountain Region, is a high-radon geographic area with all but 7 of Montana’s 56 counties designated by the Environmental Protection Agency as having the most serious radon risk (i.e., Zone 1).5 Although 49 of Montana’s 56 counties share the Zone 1 designation, only 4 have a Montana Department of Environmental Quality–funded radon program. Started in 1993, these state funds were appropriated to the health departments in the 4 fastest-growing counties in the state: Gallatin, Ravalli, Flathead, and Missoula counties. Health department administrators used these funds to purchase radon test kits, provide education and outreach, and manage a database of reported radon concentrations.A recent evaluation of the Gallatin County radon program showed that participants were predominantly nonsmoking, older, well-educated, and middle-class homeowners.6 A social marketing campaign was identified as a potential way to expand radon program participation to other high-priority groups. Social marketing is a strategy that has been effective across a wide range of topics, settings, and audiences including sexual health,7,8 asthma in older adults,9 and fruit and vegetable consumption in Special Supplementary Nutrition Program for Women, Infants, and Children (WIC) participants.10 Health department WIC clinics were identified as an ideal place to reach younger, lower-income families with children, and renters—subgroups not well represented among baseline radon program participants. In support of the goal to expand radon program participation to priority groups, the aim of the Montana Radon Study (MRS) was to test the efficacy of a social marketing intervention for increasing radon program participation by lower-income families, first-time testers, and families who rented their homes. Although current and former smokers are the groups at greatest risk of radon-related lung cancer, they were not specifically addressed in this intervention message designed to appeal to all residents of high-radon counties.     

Mortality of a cohort of tin miners 1941-86.

The mortality patterns of United Kingdom tin miners were examined in relation to calendar period and duration of underground work with particular attention to lung cancer and exposure to radon. Subjects were all men who had worked for at least one year between 1941 and 1984 at one of two United Kingdom tin mines and for whom a complete work history could be constructed from mine records. Standardised mortality ratios (SMRs) were calculated using national (England and Wales) rates. The pattern of SMRs in relation to potential explanatory variables was analysed using Poisson regression methods. Mortalities from lung cancer and silicosis (including silicotuberculosis) were significantly raised and showed a significant relation with duration of underground work (mortality from stomach cancer was raised in both underground and surface workers, but not significantly). Excess mortality from silica related disease declined steeply from 35% among workers first exposed before 1920 to 1% among those first exposed after 1950. Thirteen surface workers with known exposure to arsenic had high rates of lung and stomach cancer. The SMR for lung cancer showed a consistent pattern in relation to duration of underground exposure, rising from 83 (observed/expected = 8/9.6) for surface workers (without exposure to arsenic) to 447 (15/3.4) for workers with more than 30 years underground exposure. Examination of the SMR for lung cancer by total underground exposure, age, and time since last exposure gave rise to a model for the expression of risk which depends only on total exposure and time since exposure. The fitted model implies that the effect of exposure to radon in a given year has no effect on risk for 10 years, then rapidly rises to a maximum from which the excess risk then declines, halving every 4.3 years. There were no direct measurements of historic radon levels. A conservative estimate based on measurements taken since 1969 by the National Radiological Protection Board and the Mines and Quarries Inspectorate is that the annual dose to an underground worker was about 10 working level months (WLM). Given this assumption, the risk/exposure slope implied by the present data, and the model fitted to it, was somewhat lower than that given in the fourth Committee on the Biological Effects of Ionisation Radiation (BEIR IV) report (about 40% lower for lifetime exposures). The present data also imply different risks depending on the age at exposure, with relatively higher lifetime risks for exposure at older ages, and relatively lower risks for exposures at younger ages. In conclusion, there was a clear relation between exposure to radon and death from lung cancer. The relative risk of lung cancer due to exposure to radon was not constant in cessation of exposure. The lifetime excess risk of lung cancer implied by these data for 40 years exposure at the current statutory limit of four WLM a year starting at age 20, was about 8% (79 excess deaths per 1000 exposed), assuming average smoking habits among the exposed workers. Control of dust concentrations in the mines has substantially reduced--and may have eliminated--direct mortality from silica related disease.     

Mortality of a cohort of tin miners 1941-86

The mortality patterns of United Kingdom tin miners were examined in relation to calendar period and duration of underground work with particular attention to lung cancer and exposure to radon. Subjects were all men who had worked for at least one year between 1941 and 1984 at one of two United Kingdom tin mines and for whom a complete work history could be constructed from mine records. Standardised mortality ratios (SMRs) were calculated using national (England and Wales) rates. The pattern of SMRs in relation to potential explanatory variables was analysed using Poisson regression methods. Mortalities from lung cancer and silicosis (including silicotuberculosis) were significantly raised and showed a significant relation with duration of underground work (mortality from stomach cancer was raised in both underground and surface workers, but not significantly). Excess mortality from silica related disease declined steeply from 35% among workers first exposed before 1920 to 1% among those first exposed after 1950. Thirteen surface workers with known exposure to arsenic had high rates of lung and stomach cancer. The SMR for lung cancer showed a consistent pattern in relation to duration of underground exposure, rising from 83 (observed/expected = 8/9.6) for surface workers (without exposure to arsenic) to 447 (15/3.4) for workers with more than 30 years underground exposure. Examination of the SMR for lung cancer by total underground exposure, age, and time since last exposure gave rise to a model for the expression of risk which depends only on total exposure and time since exposure. The fitted model implies that the effect of exposure to radon in a given year has no effect on risk for 10 years, then rapidly rises to a maximum from which the excess risk then declines, halving every 4.3 years. There were no direct measurements of historic radon levels. A conservative estimate based on measurements taken since 1969 by the National Radiological Protection Board and the Mines and Quarries Inspectorate is that the annual dose to an underground worker was about 10 working level months (WLM). Given this assumption, the risk/exposure slope implied by the present data, and the model fitted to it, was somewhat lower than that given in the fourth Committee on the Biological Effects of Ionisation Radiation (BEIR IV) report (about 40% lower for lifetime exposures). The present data also imply different risks depending on the age at exposure, with relatively higher lifetime risks for exposure at older ages, and relatively lower risks for exposures at younger ages. In conclusion, there was a clear relation between exposure to radon and death from lung cancer. The relative risk of lung cancer due to exposure to radon was not constant in cessation of exposure. The lifetime excess risk of lung cancer implied by these data for 40 years exposure at the current statutory limit of four WLM a year starting at age 20, was about 8% (79 excess deaths per 1000 exposed), assuming average smoking habits among the exposed workers. Control of dust concentrations in the mines has substantially reduced--and may have eliminated--direct mortality from silica related disease.     

Small-area incidence trends in breast cancer

BACKGROUND: During the past 2 decades, the observed incidence of in situ and early-stage invasive breast cancer has increased substantially as a result of increased use of mammography. Geographic variability in the increase in breast cancer incidence has been observed among large areas. Examining the variability among small areas in the incidence over time will facilitate appropriate geographic allocation of resources aimed at increasing screening. METHODS: We examined county-specific increases in breast cancer incidence over time, specifically the variability and spatial correlation in the increase in breast cancer incidence. The analyses were based on county-level data (1973-1997) from the Iowa Surveillance, Epidemiology, and End Results program. A spatiotemporal hierarchical Bayesian model was used to examine variability in county-specific rates (intercepts, slopes, and spatial correlations) among white women at least 40 years of age. RESULTS: Posterior values indicate there was little variability among counties in the change in breast cancer incidence over time (slope) but substantial variation among intercepts. There was considerable spatial correlation among the county-specific intercepts but a lack of a spatial correlation among the county-specific slopes. There was no correlation between the county-specific intercept and slope. CONCLUSIONS: Breast cancer incidence increased over time, but county-specific rates increased independently relative to their neighboring counties or their initial rate.