Estimating deaths attributable to obesity in the United States

Estimates of deaths attributable to obesity in the United States rely on estimates from epidemiological cohorts of the relative risk of mortality associated with obesity. However, these relative risk estimates are not necessarily appropriate for the total US population, in part because of exclusions to control for baseline health status and exclusion or underrepresentation of older adults. Most deaths occur among older adults; estimates of deaths attributable to obesity can vary widely depending on the assumptions about the relative risks of mortality associated with obesity among the elderly. Thus, it may be difficult to estimate deaths attributable to obesity with adequate accuracy and precision. We urge efforts to improve the data and methods for estimating this statistic.     

Latency and the lung cancer epidemic among United States uranium miners

The latency of occupational cancer was a key factor in the recent epidemic of lung cancer among U.S. uranium miners. A review of the epidemic and analysis of latency periods with a near lifetime follow-up found that among former and nonsmokers, the mean mid-induction latent period is nearly a constant at about 25 y, regardless of age at starting or magnitude of exposure. Among cigarette smokers, the mean is shorter (about 19 y). It is not influenced by age at start of smoking, amount smoked, or magnitude of exposure, but there is a marked shortening as the age at start of radiation exposure rises. These latency variables affect lifetime risk models. By disregarding the European radon mine exposures and waiting for strong evidence of lung cancer among U.S. uranium miners (ignoring the exposures occurring while waiting during the latency period), the epidemic became inevitable.     

The impact of declining smoking on radon-related lung cancer in the United States

Objectives. We examined the effect of current patterns of smoking rates on future radon-related lung cancer.Methods. We combined the model developed by the National Academy of Science''s Committee on Health Risks of Exposure to Radon (the BEIR VI committee) for radon risk assessment with a forecasting model of US adult smoking prevalence to estimate proportional decline in radon-related deaths during the present century with and without mitigation of high-radon houses.Results. By 2025, the reduction in radon mortality from smoking reduction (15 percentage points) will surpass the maximum expected reduction from remediation (12 percentage points).Conclusions. Although still a genuine source of public health concern, radon-induced lung cancer is likely to decline substantially, driven by reductions in smoking rates. Smoking decline will reduce radon deaths more that remediation of high-radon houses, a fact that policymakers should consider as they contemplate the future of cancer control.The Environmental Protection Agency (EPA) estimates that radon in the home is responsible for over 21 000 lung cancer deaths annually among Americans, making radon the major cause of lung cancer after tobacco use. The agency considers radon a major public health problem and, since 1986, has mounted an aggressive campaign urging the public to test their homes for radon and take remedial actions when airborne concentrations of radon exceed 4 picocuries per liter of air (4 pCi/L).¹For its most current risk assessment, the EPA employed the BEIR VI model, developed by the Committee on Health Risks of Exposure to Radon (the BEIR VI committee) of the National Academy of Sciences (NAS).² The BEIR VI model''s calculation of radon-related risk (as was the case for its predecessor, BEIR IV) was estimated from data on miners, who are subject to much higher levels of radon than is the average population and have shown a significant correlation between lung cancer risk and radon exposure. Although the extrapolation of the results from miners to the much less exposed general public initially caused controversy, the BEIR VI implications of risk have been validated by recent case–control studies at the population level.^3–5 The BEIR VI model is thus broadly accepted as a valid predictor of the radon-related risk for typical individuals.The available data suggest a strong interaction effect between radon exposure and smoking status in the determination of lung cancer risk, which means that smokers are at a much higher risk of dying from radon-induced lung cancer than are nonsmokers. This interaction is recognized in the BEIR VI model, which postulates a superadditive (but less than multiplicative) interaction between smoking and radon. To appreciate the magnitude of this interaction, consider the fact that the background lung cancer risk ratio between ever and never smokers is 13 to 1.⁶ A multiplicative interaction between radon and smoking would imply that, at the same level of radon exposure, the ratio of radon-induced excess risk between ever and never smokers would be the same as the ratio of background lung cancer risks between those 2 groups (i.e., 13 to 1). On the other hand, an additive relationship between radon and smoking would imply that radon would add the same extra risk to ever and never smokers exposed to the same dosage, making the excess risks ratio between the 2 groups equal 1 to 1. Using the BEIR VI model, the EPA calculates that, at a radon level of 4 pCi/L, the lifetime risk of radon-induced lung cancer death is 62 per 1000 for ever smokers and 7 per 1000 for never smokers, yielding an excess risk ratio of 8.86 to 1 between the 2 groups.¹ As 8.86 falls between 1 and 13, the BEIR VI model implies that radon adds more risk to ever smokers than to never smokers, but that excess risk is less than proportional to the lung cancer background risk of those 2 groups, suggesting a submultiplicative (but superadditive) relationship between smoking and radon. The BEIR VI model does not distinguish between current and former smokers.Given this implied superadditive interaction, the number of future radon deaths will heavily depend on population smoking rates. As smoking rates in the United States have been falling for several decades and are expected to continue declining, the overall magnitude of the radon death toll is likely to decline as well. The question we try to address is what is the magnitude of this expected decline?We extend the EPA''s analysis by examining the sensitivity of radon-related lung cancer in the United States to future smoking rates. We estimate the proportional decline in the number of lung cancer deaths caused by radon for the period 2006 through 2100, assuming a likely scenario for smoking rates. We do not forecast specific numbers of radon-induced lung cancer deaths because these numbers will depend on many factors likely to change over such a long period of time. Instead, we concentrate on the relative impact of the smoking decline on the overall radon death toll and also examine the benefits of remediating houses with high radon levels given the results of our analysis. Following the EPA''s approach, in our computations, we employ the BEIR VI model, thereby assuming a submultiplicative relationship between smoking and radon. In the remaining sections of the report, we discuss the assumptions, models, and data employed in our analysis, our findings, and the implications of the results for both the magnitude of radon-related risk to the population and the effectiveness of housing remediation in reducing such risk.     

Estimating the cost of unmet HIV-prevention needs in the United States

BACKGROUND: Although new HIV infection cases have dropped from over 160,000 per year in the mid-1980s to 40,000 per year in the 1990s, HIV incidence has been relatively unchanged for a decade. This number of annual incident infections suggests that substantial, unmet HIV-prevention needs continue to fuel the HIV epidemic in the United States. OBJECTIVES: This study estimates the cost of addressing the unmet HIV-prevention needs in the United States and establishes a performance standard by estimating the number of HIV infections that would have to be prevented in order for these programs to be considered cost saving to society. METHODS: Standard methods of cost and threshold analysis were employed in this study. Interventions needed to address unmet behavioral risks include services to reduce sexual risk of HIV infection, services to provide access to sterile syringes for people who cannot stop injecting drugs, HIV counseling and testing, and intensive preventive services to help HIV-seropositive people avoid transmitting the virus to others. RESULTS: If brief interventions are utilized to address sexual behavior risk, the total program cost (over and above current resource levels) is just over $817 million; and if more expensive multisession, small-group interventions are used, the costs increase to over $1.85 billion. However, even the higher-cost program has a threshold of only 12,000 infections that must be prevented in order for the program to be considered a cost saving to society. CONCLUSIONS: Addressing the remaining unmet HIV-preventive needs in the United States will require a substantial commitment of resources. However, even a greatly expanded HIV-preventive program in the United States could pay for itself through savings in averted medical care costs.     

Environmental carcinogen releases and lung cancer mortality in rural-urban areas of the United States

Purpose: Environmental hazards are unevenly distributed across communities and populations; however, little is known about the distribution of environmental carcinogenic pollutants and lung cancer risk across populations defined by race, sex, and rural‐urban setting. Methods: We used the Toxics Release Inventory (TRI) database to conduct an ecological study at the county level (a total of 3,141 counties). Multiple linear regressions were used to assess the associations of carcinogenic discharges from TRI sites and lung cancer mortality rates at the county level in the United States during the years 1990 through 2007. Findings: We observed an excess risk of population lung cancer mortality associated with higher amounts of environmental carcinogen releases from TRI facilities in both males and females, and in both whites and African Americans. The strength of these associations tended to be stronger in African Americans. A significant dose‐response relationship was observed for the total volume of carcinogen releases or carcinogen releases to the air, but not releases to water. These associations appeared to be present within nonmetropolitan counties but not metropolitan counties, and to be concentrated in certain urban‐rural county typologies. Conclusions: Our results suggest that exposure to higher carcinogen releases from industrial or chemical facilities in rural areas may increase the risk of lung cancer mortality. Our findings add to the evidence for undertaking prudent efforts to limit the release of carcinogenic chemicals into the environment.     

Smoking and cancer in the United States

Based on the mortality experience of over one million Americans who have been followed in a prospective epidemiologic study since 1959, it is estimated that from 25 to 35% of cancer mortality in the U.S. male population and 5 to 10% in the female population are mainly due to smoking of tobacco products and cigarettes. These estimates are remarkably close to those derived from other U.S. studies and similar studies in the United Kingdom and Japan. While it is clear that several factors contribute to the causation of smoking-related cancer mortality, it is unlikely that the excess in deaths would occur in the absence of tobacco usage. The contribution of smoking is hence considered as the preponderant risk, and one that could be controlled by combined actions of individuals' responses to education, legislation, and modification of cigarettes toward less hazardous characteristics.     

Estimating the total number of newly-recognized silicosis cases in the United States

BACKGROUND: The US employer-based surveillance system for documenting occupational injuries and illnesses undercounts chronic diseases. We suggest a method to estimate the number of individuals who are newly-recognized with silicosis each year in the United States. METHODS: Data from US death certificates, the Michigan state-based surveillance system, and capture-recapture analysis were used to calculate national estimates of silicosis. RESULTS: From 1987 to 1996, 2,787 deaths occurred in the United States where silicosis was mentioned on the death certificates. During the same period, in Michigan 77% of death certificates with a mention of silicosis were confirmed as silicosis-related deaths and the ratio of the number of living to deceased confirmed silicosis cases was 6.44. The proportion of confirmed silicosis deaths, the ratio of the living to deceased silicosis cases and capture-recapture analysis from the Michigan surveillance system, were used to estimate that there were 3,600-7,300 cases per year of silicosis in the United States from 1987 to 1996. CONCLUSIONS: Our estimate of the annual number of newly-recognized silicosis cases is significantly larger than the estimate from the employer-based reporting system used for counting occupational disease in the United States. This employer-based surveillance system is inadequate for determining the frequency of occupational disease. Our analysis which combines a readily-available and relatively inexpensive national administrative database (i.e., death certificates) with a more costly state-based active surveillance system is a cost-effective model that could be used to provide better estimates of a number of different occupational diseases. Accurate estimates of occupational illnesses are essential to both determine temporal trends and evaluate efforts to prevent silicosis.     

Estimating risk from ambient concentrations of acrolein across the United States

BACKGROUND: Estimated ambient concentrations of acrolein, a hazardous air pollutant, are greater than the U.S. Environmental Protection Agency (EPA) reference concentration throughout the United States, making it a concern for human health. However, there is no method for assessing the extent of risk under the U.S. EPA noncancer risk assessment framework. OBJECTIVES: We estimated excess risks from ambient concentrations of acrolein based on dose-response modeling of a study in rats with a relationship between acrolein and residual volume/total lung capacity ratio (RV/TLC) and specific compliance (sC(L)), markers for altered lung function. METHODS: Based on existing literature, we defined values above the 90th percentile for controls as "adverse." We estimated the increase over baseline response that would occur in the human population from estimated ambient concentrations of acrolein, taken from the U.S. EPA's National-Scale Air Toxics Assessment for 1999, after standard animal-to-human conversions and extrapolating to doses below the experimental data. RESULTS: The estimated median additional number of adverse sC(L) outcomes across the United States was approximately 2.5 cases per 1,000 people. The estimated range of additional outcomes from the 5th to the 95th percentile of acrolein concentration levels across census tracts was 0.28-14 cases per 1,000. For RV/TLC, the median additional outcome was 0.002 per 1,000, and the additional outcome at the 95th percentile was 0.13 per 1,000. CONCLUSIONS: Although there are uncertainties in estimating human risks from animal data, this analysis demonstrates a method for estimating health risks for noncancer effects and suggests that acrolein could be associated with decreased respiratory function in the United States.     

Estimating the Prevalence of United States Women with Alcohol-exposed Pregnancies and Births

Aims

Researchers at the U.S. Centers for Disease Control and Prevention (CDC) recently estimated the number of women at risk for alcohol-exposed pregnancies (AEPs) as 3.3 million per month. The number of women at risk was widely interpreted as the actual number of AEPs. The actual number of AEPs may be easier to interpret and may be more a more relevant public health metric for evaluating efforts to reduce AEPs. We estimated the expected actual number of AEPs among U.S. women 15–44 years of age and the expected actual number of alcohol-exposed births (AEBs).

General air pollution and cancer in the United States

General air pollution may be defined as a body of contaminated air extending over a population area of appreciable size (a town, city, etc.). It excludes occupational, personal, or neighborhood pollution exposure to dusts or fumes. In the American Cancer Society's study of a half million men, subjects who had lived in the same neighborhood for at least 10 years were classified into various categories by place of residence, and whether or not they were occupationally exposed to dusts, fumes, or vapors. Lung cancer rates were computed standardized by age and smoking habits. Men who said they were occupationally exposed had mortality rates of lung cancer 14% greater than the nonexposed. Among those not exposed, there were little or no differences in mortality ratios by urban-rural place of residence, in Los Angeles and nearby counties; by whether they lived in cities with high, medium, or low levels of total suspended particulate matter or benzene-soluble organic matter. We conclude the general air pollution at present has very little effect, if any, on the lung cancer death rate.     

Breast cancer screening legislation in the United States.

We discuss some of the issues emerging from a powerful legislative movement for preventive services over the past three years. During this time an increasing number of states passed, considered, or are currently developing breast cancer screening legislation. Most of these laws require some form of third party payment for mammography or establish breast cancer screening programs. The legislation varies markedly with regard to periodicity of examinations, ages covered, type and extent of third party coverage, dosage regulation, and radiographic equipment standards. This shows a need for common standards. Legislation provides an essential incentive for a public health response to a serious problem, but more than laws are needed. Health care providers and the general public need to be aware and take advantage of the coverage provided as a result of legislation. Moreover, public health officials need to be aware that such legislation may lead to a demand for services that exceeds present capacity to deliver them.     

Estimating Populations of Men Who Have Sex with Men in the Southern United States

Population estimates of men who have sex with men (MSM) by state and race/ethnicity are lacking, hampering effective HIV epidemic monitoring and targeting of outreach and prevention efforts. We created three models to estimate the proportion and number of adult males who are MSM in 17 southern states. Model A used state-specific census data stratified by rural/suburban/urban area and national estimates of the percentage MSM in corresponding areas. Model B used a national estimate of the percentage MSM and state-specific household census data. Model C partitioned the statewide estimates by race/ethnicity. Statewide Models A and B estimates of the percentages MSM were strongly correlated (r = 0.74; r-squared = 0.55; p < 0.001) and had similar means (5.82% and 5.88%, respectively) and medians (5.5% and 5.2%, respectively). The estimated percentage MSM in the South was 6.0% (range 3.6–13.2%; median, 5.4%). The combined estimated number of MSM was 2.4 million, including 1,656,500 (69%) whites, 339,400 (14%) blacks, 368,800 (15%) Hispanics, 34,600 (1.4%) Asian/Pacific Islanders, 7,700 (0.3%) American Indians/Alaska Natives, and 11,000 (0.5%) others. The estimates showed considerable variability in state-specific racial/ethnic percentages MSM. MSM population estimates enable better assessment of community vulnerability, HIV/AIDS surveillance, and allocation of resources. Data availability and computational ease of our models suggest other states could similarly estimate their MSM populations.     

Estimating future hepatitis C morbidity, mortality, and costs in the United States

OBJECTIVES: This study estimated future morbidity, mortality, and costs resulting from hepatitis C virus (HCV). METHODS: We used a computer cohort simulation of the natural history of HCV in the US population. RESULTS: From the year 2010 through 2019, our model projected 165,900 deaths from chronic liver disease, 27,200 deaths from hepatocellular carcinoma, and $10.7 billion in direct medical expenditures for HCV. During this period, HCV may lead to 720,700 years of decompensated cirrhosis and hepatocellular carcinoma and to the loss of 1.83 million years of life in those younger than 65 at a societal cost of $21.3 and $54.2 billion, respectively. In sensitivity analysis, these estimates depended on (1) whether patients with HCV and normal transaminase levels develop progressive liver disease, (2) the extent of alcohol ingestion, and (3) the likelihood of dying from other causes related to the route of HCV acquisition. CONCLUSIONS: Our results confirm prior Centers for Disease Control and Prevention projections and suggest that HCV may lead to a substantial health and economic burden over the next 10 to 20 years.