Comparison Of Risk Estimates Research Articles

Risk tolerance criteria for layers of protection analysis

AbstractLayers of protection analysis (LOPA) facilitates risk‐informed decision making by allowing comparison of risk estimates with risk tolerance criteria to determine if the risk is tolerable. Various types of risk criteria exist, and it is essential that LOPA practitioners match the type of risks calculated with the type of criteria used to ensure that valid comparisons are made and sound decisions are taken. A common error is to use individual risk criteria but calculate societal risk measures, which can lead to more stringent risk reduction measures than needed. Correct use of risk tolerance criteria is especially important when LOPA is used to determine safety integrity levels for safety instrumented functions to comply with industry standards for safety instrumented systems when critical decisions on process safety are made. This article describes the type of risk criteria that should be used with LOPA and contrasts risk measures calculated with LOPA and quantitative risk analysis. The concept of a representative receptor is introduced to allow the calculation of individual risk measures as well as societal risk measures. © 2011 American Institute of Chemical Engineers Process Saf Prog, 2011

A Comparison of Risk Estimates for the Effect of Short-Term Exposure to PM, NO2 and CO on Cardiovascular Hospitalizations and Emergency Department Visits: Effect Size Modeling of Study Findings

Although particulate matter (PM), nitrogen dioxide (NO2) and carbon monoxide (CO) typically exist as part of a complex air pollution mixture, the evidence linking these pollutants to health effects is evaluated separately in the scientific and policy reviews of the National Ambient Air Quality Standards (NAAQS). The objective of this analysis was to use meta-regression methods to model effect estimates for several individual yet correlated NAAQS pollutants in an effort to identify factors that explain differences in the effect sizes across studies and across pollutants. We expected that our consideration of the evidence for several correlated pollutants in parallel could lead to insights regarding exposure to the pollutant mixture. We focused on studies of hospital admissions for congestive heart failure (CHF) and ischemic heart disease (IHD), which have played an important role in the evaluation of the scientific evidence communicated in the PM, NO2, and CO Integrated Science Assessments (ISAs). Of the studies evaluated, 11 CHF studies and 21 IHD studies met our inclusion requirements. The size of the risk estimates was explained by factors related to the pollution mixture, study methods, and monitoring network characteristics. Our findings suggest that additional analyses focusing on understanding differences in effect sizes across geographic areas with different pollution mixtures and monitor network designs may improve our understanding of the independent and combined effects of correlated pollutants.

Consolidating Risk Estimates for Radiation-Induced Complications in Individual Patient: Late Rectal Toxicity

To test the feasibility of a new approach to synthesize published normal tissue complication data using late rectal toxicity in prostate cancer as an example. A data survey was performed to identify the published reports on the dose-response relationships for late rectal toxicity. The risk estimates for Grade 1 or greater, Grade 2 or greater, and Grade 3 or greater toxicity were obtained for a test cohort of patients treated at our institution. The influence of the potential factors that might have affected the reported toxicity levels was investigated. The studies that did not conform to the general data trends were excluded, and single, combined risk estimates were derived for each patient and toxicity level. A total of 21 studies of nonoverlapping patient populations were identified. Three studies provided dose-response models for more than one level of toxicity. Of these 21 studies, 6, 14, and 5 were used to derive the initial risk estimates for Grade 1, 2, and 3 or greater toxicity, respectively. A comparison of risk estimates between the studies reporting rectal bleeding and rectal toxicity (bleeding plus other symptoms) or between studies with follow-up <36 months and ≥36 months did not reveal significant differences (p ≥ .29 for all comparisons). After excluding three reports that did not conform to the general data trends, the combined risk estimates were derived from 5 reports (647 patients), 11 reports (3,369 patients), and 5 reports (1,330 patients) for Grade 1, 2, and 3 or greater toxicity, respectively. The proposed approach is feasible and allows for more systematic use of published dose-response data to estimate the complication risks for the individual patient.

Smoking as a risk factor for periodontitis: a literature review

Smoking is an important risk factor for periodontitis. The high prevalence of smokers in any population makes smoking a feasible target for intervention in public health. The magnitude of the associated risk between smoking and periodontitis varies among studies, and this variation is the result of the case definition adopted rather than the limitations of the population studies. A MEDLINE search was used to identify previous publications, and a literature review was developed based on the selected articles. Smoking was consistently identified as a risk factor for periodontitis, but the risk estimates varied between studies. The comparison of risk estimates between studies was affected by the lack of uniformity for case definitions of periodontitis and smoking status.

Quantitative comparisons of cancer induction in humans by internally deposited radionuclides and external radiation

Purpose: To compare quantitative estimates of lifetime cancer risk in humans for exposures to internally deposited radionuclides and external radiation. To assess the possibility that risks from radionuclide exposures may be underestimated.Materials and methods: Risk estimates following internal exposures can be made for a small number of alpha-particle-emitting nuclides. (1) Lung cancer in underground miners exposed by inhalation to radon-222 gas and its short-lived progeny. Studies of residential 222Rn exposure are generally consistent with predictions from the miner studies. (2) Liver cancer and leukaemia in patients given intravascular injections of Thorotrast, a thorium-232 oxide preparation that concentrates in liver, spleen and bone marrow. (3) Bone cancer in patients given injections of radium-224, and in workers exposed occupationally to 226Ra and 228Ra, mainly by ingestion. (4) Lung cancer in Mayak workers exposed to plutonium-239, mainly by inhalation. Liver and bone cancers were also seen, but the dosimetry is not yet sufficiently good enough to provide quantitative estimates of risks. Comparisons can be made between risk estimates for radiation-induced cancer derived for radionuclide exposure and those derived for the A-bomb survivors, exposed mainly to low-LET (linear energy transfer) external radiation. Data from animal studies, using dogs and rodents, allow comparisons of cancer induction by a range of alpha- and beta-/gamma-emitting radionuclides. They provide information on relative biological effectiveness (RBE), dose-response relationships, dose-rate effects and the location of target cells for different malignancies.Results: For lung and liver cancer, the estimated values of risk per Sv for internal exposure, assuming an RBE for alpha-particles of 20, are reasonably consistent with estimates for external exposure to low-LET radiation. This also applies to bone cancer when risk is calculated on the basis of average bone dose, but consideration of dose to target cells on bone surfaces suggests a low RBE for alpha-particles. Similarly, for leukaemia, the comparison of risks from alpha-irradiation (232Th and progeny) and external radiation suggest a low alpha RBE; this conclusion is supported by animal data. Risk estimates for internal exposure are dependent on the assumptions made in calculating dose. Account is taken of the distribution of radionuclides within tissues and the distribution of target cells for cancer induction. For the lungs and liver, the available human and animal data provide support for current assumptions. However, for bone cancer and leukaemia, it may be that changes are required. Bone cancer risk may be best assessed by calculating dose to a 50 µ;m layer of marrow adjacent to endosteal (inner) bone surfaces rather than to a single 10 µ;m cell layer as currently assumed. Target cells for leukaemia may be concentrated towards the centre of marrow cavities so that the risk of leukaemia from bone-seeking radionuclides, particularly alpha emitters, may be overestimated by the current assumption of uniform distribution of target cells throughout red bone marrow.Conclusions: The lifetime risk estimates considered here for exposure to internally deposited radionuclides and to external radiation are subject to uncertainties, arising from the dosimetric assumptions made, from the quality of cancer incidence and mortality data and from aspects of risk modelling; including variations in baseline rates between populations for some cancer types. Bearing in mind such uncertainties, comparisons of risk estimates for internal emitters and external radiation show good agreement for lung and liver cancers. For leukaemia, the available data suggest that the assumption of an alpha-particle RBE of 20 can result in overestimates of risk. For bone cancer, it also appears that current assumptions will overestimate risks from alpha-particle-emitting nuclides, particularly at low doses.

Issues in the Comparison of Risk Estimates for the Population in the Techa River Region and Atomic Bomb Survivors

Plutonium production in the former Soviet Union began in 1949 at the Mayak Production Association located between the cities of Chelyabinsk and Ekaterinbourg in the southern Ural mountains about 1200 km east to Moscow. During the first few years of Mayak's operation, almost 30,000 people living on the banks of the Techa River received significant internal and external exposures as a consequence of the release of large quantities of radioactive materials from Mayak. Studies of levels of radioactive contamination and health effects in this population began in the early 1950s. A systematic follow-up of a fixed cohort that includes all people who were living in Techa River villages in 1949 was begun about 30 years ago. In this paper we describe the Techa River cohort, outline the nature of the exposures and discuss the status of follow-up for the period from 1950 through 1989. While noting the limitations of the current epidemiological follow-up data, we also compare the demographic and mortality structure of the Techa River cohort with the Life Span Study cohort of Japanese atomic bomb survivors. It is seen that, despite a number of limitations, the current data suggest that the risks of mortality from leukemia and other cancers increase with increasing radiation dose in the Techa River cohort. This finding suggests that, with continued improvements in the quality of the follow-up and dosimetry, the Techa River cohort has the potential to provide quantitative estimates of the risks of chronic low-dose-rate radiation exposures for an unselected general population that will be an important complement to the estimates based on the Life Span Study that are used as the primary basis for numerical assessments of radiation risk.

Cancer and Non-Cancer Controls in Studies on the Effect of Tobacco and Alcohol Consumption

A comparison of risk estimates using controls with other cancers versus controls with acute diseases unrelated to tobacco and alcohol consumption in the study of the effect of these two factors has been performed using data on tumours of the oral cavity and pharynx from an ongoing case-control surveillance programme in Northeastern Italy. Similar results were obtained using either type of controls: as compared to never smokers, moderate smokers (less than or equal to 14 cigarettes/day) showed age- and sex-adjusted odds ratio (OR) = 5.2 (95% confidence interval (CI): 2.9-9.2) when using cancer controls and 5.8 (95% CI: 3.3-10.1) when using non-cancer controls. Similarly, those who had smoked for 40 years or longer showed ORs of 7.4 (95% CI: 4.0-13.6) and 8.8 (95% CI: 4.9-15.6), respectively, using cancer and non-cancer controls. For moderate drinkers of alcoholic beverages (21-34 drinks/week) and heavy drinkers (greater than or equal to 84 drinks/week) the ORs, as compared to individuals who drank less than 21 drinks/week, were 1.9 (95% CI: 1.0-3.6) and 2.2 (95% CI: 1.2-4.0) and 10.6 (95% CI: 5.5-20.6) and 11.4 (95% CI: 6.0-21.4) using cancer and non-cancer controls, respectively. The same comparability of ORs for tobacco- and alcohol-related variables using either type of controls was observed when separate analyses of the two sexes were performed. The close similarity between cancer and non-cancer controls in studies on tobacco- and alcohol-related risks may be exploited when the choice of other types of controls would increase the costs and the feasibility of the study, and thus hamper its statistical power.(ABSTRACT TRUNCATED AT 250 WORDS)