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PubMed1994

Alcohol misuse and the predisposing environment.

In recent years, the aetiology of alcohol misuse has come to be conceptualised in terms of risk factor models. Risk can emanate from a number of sources ranging from the genetic to the sociostructural. This chapter reviews the major environmental risk factors under two broad headings--those that affect the availability of the agent and those that affect the vulnerability of the host. The former include a variety of economic, social and physical factors such as price, advertising and licensing laws. The latter include broad socioeconomic and sociocultural factors, as well as interpersonal influences such as family, peers, employment and stress. Practitioners (as distinct from policy-makers) concerned with prevention and treatment of alcohol misuse can most effectively intervene at the interpersonal level, and the paper concludes with a discussion of the implications for clinical practice of the research reviewed in this domain.

Alcoholic Beverages↗
PubMed1991

Lung cancer mortality and exposure to radon progeny in a cohort of New Mexico underground uranium miners.

A cohort of 3469 males with at least 1 y of underground uranium mining experience in New Mexico was assembled and mortality followed up through 31 December 1985. The mean and median cumulative exposures for the cohort were 0.39 J h m-3 and 0.12 J h m-3 (111.4 and 35.0 Working Level Months [WLM]), respectively. Overall, mortality in the cohort was significantly increased (standardized mortality ratio [SMR] = 1.1, 95% confidence interval [CI] = 1.02-1.2) relative to the general population of the state. By cause, significant increases were observed for lung cancer (SMR = 4.0, 95% CI 3.1-5.1) and for external causes of death (SMR = 1.5, 95% CI 1.3-1.7). The risk of lung cancer increased for exposure categories above 100 WLM; the excess relative risk increased by 0.5% per mJ h m-3, 95% CI 0.2-1.5 (1.8% per WLM, 95% CI 0.7-5.4). Data were consistent with a multiplicative interaction between smoking and exposure to Rn progeny in an exponential relative risk model. The risk of lung cancer varied substantially with age at observation; the odds ratios rose more steeply with exposure to Rn progeny for those less than age 55 y at observation.

Adult↗
PubMed2006

Estimation of Staphylococcus aureus growth parameters from turbidity data: characterization of strain variation and comparison of methods.

Turbidity methods offer possibilities for generating data required for addressing microorganism variability in risk modeling given that the results of these methods correspond to those of viable count methods. The objectives of this study were to identify the best approach for determining growth parameters based on turbidity data and use of a Bioscreen instrument and to characterize variability in growth parameters of 34 Staphylococcus aureus strains of different biotypes isolated from broiler carcasses. Growth parameters were estimated by fitting primary growth models to turbidity growth curves or to detection times of serially diluted cultures either directly or by using an analysis of variance (ANOVA) approach. The maximum specific growth rates in chicken broth at 17 degrees C estimated by time to detection methods were in good agreement with viable count estimates, whereas growth models (exponential and Richards) underestimated growth rates. Time to detection methods were selected for strain characterization. The variation of growth parameters among strains was best described by either the logistic or lognormal distribution, but definitive conclusions require a larger data set. The distribution of the physiological state parameter ranged from 0.01 to 0.92 and was not significantly different from a normal distribution. Strain variability was important, and the coefficient of variation of growth parameters was up to six times larger among strains than within strains. It is suggested to apply a time to detection (ANOVA) approach using turbidity measurements for convenient and accurate estimation of growth parameters. The results emphasize the need to consider implications of strain variability for predictive modeling and risk assessment.

Animals↗
PubMed2000

Parental transmission of type 2 diabetes: the Framingham Offspring Study.

Study of parental transmission of diabetes provides insight into the relative contributions of underlying maternal and paternal influences. We estimated risk for type 2 diabetes and milder degrees of glucose intolerance associated with parental diabetes among subjects of the population-based Framingham Offspring Study, in which participants are primarily Caucasian and at relatively low risk for diabetes and for which both parental and offspring phenotypes were ascertained by direct examination. Parental diabetes, assessed over 40 years of biennial follow-up, was defined by use of hypoglycemic drug therapy or a casual plasma glucose level > or = 11.1 mmol/l at any examination. Offspring glucose tolerance, assessed over 20 years of quadrennial follow-up, was defined by fasting plasma glucose levels > or = 7.8 mmol/l at any two examinations, use of hypoglycemic drug therapy at any examination, or with a 75-g oral glucose tolerance test (1980 World Health Organization criteria) at the most recent examination. We calculated odds ratios (ORs) and 95% CIs for offspring glucose tolerance status using generalized estimating equations to account for differential correlations within and between families. The 2,527 offspring came from 1,303 nuclear families, of which 77.6% had two or more siblings per family and in which the prevalence of parental diabetes was 24.6%. The mean offspring age was 54 years (range 26-82), 53% were women, 8.6% had diabetes, 11.4% had impaired glucose tolerance, 76.3% had no parental diabetes, 10.5% had maternal diabetes, 11.5% had paternal diabetes, and 1.7% had bilineal diabetes. Relative to individuals without parental diabetes, the age-adjusted ORs (95% CI) for offspring type 2 diabetes or abnormal glucose tolerance (fasting plasma glucose > or = 6.1 mmol/l or 2-h postchallenge glucose tolerance > or = 7.8 mmol/l) among individuals with maternal diabetes were 3.4 (2.3-4.9) and 2.7 (2.0-3.7), respectively; among individuals with paternal diabetes were 3.5 (2.3-5.2) and 1.7 (1.2-2.4), respectively; and among individuals with bilineal diabetes were 6.1 (2.9-13.0) and 5.2 (2.6-10.5), respectively. Although maternal and paternal diabetes conferred equivalent risk for offspring type 2 diabetes, offspring with maternal diabetes were slightly more likely to have abnormal glucose tolerance compared with those with paternal diabetes (OR 1.6, 95% CI 1.1-2.4). Offspring with maternal diabetes and an age of onset of <50 years had marked increased risk for both type 2 diabetes (9.7, 4.3-22.0) and abnormal glucose tolerance (9.0, 4.2-19.7). We conclude that risk ratios for offspring type 2 diabetes are consistent with a simple additive risk model, where risk when both parents are affected equals the sum of risk when either parent is affected. For maternal diabetes to confer excess risk for mild but not overt glucose intolerance, offspring of diabetic fathers may transit abnormal to impaired glucose tolerance relatively quickly, or diabetic mothers may transmit risk for a mild slowly progressive form of abnormal glucose tolerance in addition to overt diabetes. Very high risk for abnormal glucose homeostasis among offspring with young age-of-onset maternal diabetes is consistent with hypotheses that perinatal exposures increase diabetes risk. Given equivalent risk ratios for type 2 diabetes, fathers may transmit unique paternal genetic factors of similar strength to maternal environmental factors.

Adult↗
PubMed1999

Mortality rates after cataract extraction.

Senile cataract may be a marker of generalized tissue aging. We examined this hypothesis using population-based linked health data. We hypothesized that any such association would diminish with increased use of cataract surgery. Mortality rates of those 50-95 years of age undergoing cataract surgery in British Columbia during either 1985 or 1989 were compared with the provincial population of comparable age who did not undergo cataract surgery during the study period. The 1985 cohort included 8,262 patients undergoing surgery and a comparison population of 804,303, and the 1989 cohort included 11,952 patients and a comparison population of 839,393. Using Cox regression, for the 1985 cohort, the hazard ratios for dying during follow-up were 3.2 for males 50-54.9 years of age [95% confidence limits (CL) = 2.0, 5.0] and 3.3 for females (95% CL = 1.9, 5.7). Hazard ratios for older age groups decreased with age. We also fit an additive risk model that produced excess mortalities that were less age dependent. In the 1985 analysis, these ranged from +7.1 per 1,000 (95% CL = +0.44, +13.76) to +20.3 (95% CL = +13.24, +27.36) for males and -17.5 (95% CL = -28.28, -6.72) to +2.0 (95% CL = -2.12, +6.12) for females. Findings for the 1989 analyses were similar, indicating that the association between cataracts and generalized aging remained constant despite a large increase in the use of cataract surgery.

Age Distribution↗
PubMed1994

[Interaction among the relative risk factors of primary liver cancer in a case-control study].

This paper evaluates the combined effect of HBsAg, drinking water and aflatoxin B1 (AFB1) on the primary hepatocellular carcinoma (PHC) in a case-control study which was carried out in Fusui, Guangxi. We used relative risk model (from subadditive to supermultiplicative) to fit the relationship. The results showed that the combined effect of HBsAg infection and drinking pond-ditch water is nearly multiplicative, and the combined effect of HBsAg infection and AFB1 intake as well as drinking pond-ditch water and AFB1 intake were nearly additive.

Aflatoxin B1↗
PubMed1994

A test of the AIDS risk reduction model: psychosocial correlates of condom use in the AMEN cohort survey.

We examined the AIDS Risk Reduction Model (J. Catania, S. Kegeles, & T. Coates) in a sample of unmarried heterosexual adults with an HIV risk factor (n = 716). Labeling one's sexual behavior as risky was associated with having a history of sexually transmitted diseases, particularly genital herpes, and fewer stereotypic health beliefs. For people with secondary sexual partners, greater condom commitment was related to increased labeling, supportive condom norms, and greater enjoyment, and high levels of condom use were related to greater condom commitment, supportive norms, greater enjoyment, and health protective sexual communication. For people with primary partners, greater condom commitment was correlated with increased supportive condom norms, greater enjoyment, and having genital herpes, and high levels of condom use were correlated with greater condom commitment, greater enjoyment, and health protective sexual communication.

Adult↗
PubMed2005

Evaluation of physiologically based pharmacokinetic models in risk assessment: an example with perchloroethylene.

One of the more problematic aspects of the application of physiologically based pharmacokinetic (PBPK) models in risk assessment is the question of whether the model has been adequately validated to provide confidence in the dose metrics calculated with it. A number of PBPK models have been developed for perchloroethylene (PCE), differing primarily in the parameters estimated for metabolism. All of the models provide reasonably accurate simulations of selected kinetic data for PCE in mice and humans and could thus be considered to be "validated" to some extent. However, quantitative estimates of PCE cancer risk are critically dependent on the prediction of the rate of metabolism at low environmental exposures. Recent data on the urinary excretion of trichloroacetic acid (TCA), the major metabolite of PCE, for human subjects exposed to lower concentrations than those used in previous studies, make it possible to compare the high- to low-dose extrapolation capability of the various published human models. The model of Gearhart et al., which is the only model to include a description of TCA kinetics, provided the closest predictions of the urinary excretion observed in these low-concentration exposures. Other models overestimated metabolite excretion in this study by 5- to 15-fold. A systematic discrepancy between model predictions and experimental data for the time course of the urinary excretion of TCA suggested a contribution from TCA formed by metabolism of PCE in the kidney and excreted directly into the urine. A modification of the model of Gearhart et al. to include metabolism of PCE to TCA in the kidney at 10% of the capacity of the liver, with direct excretion of the TCA formed in the kidney into the urine, markedly improved agreement with the experimental time-course data, without altering predictions of liver metabolism. This case study with PCE demonstrates the danger of relying on parent chemical kinetic data to validate a model that will be used for the prediction of metabolism.

Animals↗
PubMedDate not supplied

[The relative biological effectiveness of alpha-radiation during human lung exposure to irradiation].

The assessment of the relative biological effectiveness (RBE) for alpha-radiation was held in the cases of inhalation of radon progeny and incorporation of plutonium in lungs. It is based on simulation of lung cancer radiation risk for different types of radiation. Specific radiation risk models developed according to the results of direct epidemiological studies are used for the simulation. These include two published risk models for uranium miners and nuclear workers of the Mayak facilities in the former Soviet Union. Additionally two lung cancer risk models are developed and described for the following cases: population indoor radon exposure and low-linear-energy-transfer reference radiation exposure. By the results of lifetime lung cancer risk simulation the RBE values range from 11 to 12 and from 1.7 to 4.9 for the cases of plutonium incorporation and of radon progeny exposure accordingly. The significant uncertainty of radiation risk models results in significant variation of RBE assessments. Rough estimations of RBE values 90% confidence interval are from unit fraction to 25 and from 2 to 50 for the cases of radon progeny exposure and plutonium incorporation accordingly.

Alpha Particles↗
PubMed1981

Some practical problems arising from use of the gamma multihit model for risk estimation.

The Scientific Committee of the Food Safety Council recently recommended use of the gamma multihit model for risk assessment. Some practical problems arising from the use of this model are presented. In some instances the model produces what appear to be unreasonably high "safe dose" estimates. In other instances the estimates appear unrealistically low. Neither the original "standard" nor the "conservative" confidence limits seem adequate for practical application. The assumptions leading to the use of Abbott's correction are difficult to verify, but have a great effect on safe dose estimates. Indeed, the introduction of as little as 1% additive background into the gamma multihit model leads to safe dose estimates closer to those produced by the Armitage-Doll model than to those of the pure gamma multihit model.

Aflatoxin B1↗
PubMed2000

Modelling the cumulative risk for a false-positive under repeated screening events.

Screening examinations are widely utilized in detecting the presence of medical disorders, for instance, screening mammograms and clinical breast examinations for detection of breast cancer. Such procedures are invaluable in enabling early treatment but produce the possibilities of false-positive and false-negative diagnoses. Focusing on false-positive results, with increasing number of screening events, it is clear that the risk of a false-positive increases. The objective of this paper is to quantify the cumulative risk associated with repeated screening. We provide a very general framework within which to investigate this risk, both at the population and the individual level. The latter allows incorporation of evolving patient medical history to permit individualized assessment of risk. We model cumulative risk in terms of the number of screening events until first false-positive. We develop models which are essentially familiar actuarial models for life table data adding a Cox regression to enable individual level modelling. Because it offers several advantages, we employ a Bayesian inference framework and apply our modelling to the analysis of 9773 screening mammograms collected from 2227 women at an HMO serving nearly 300000 adults in and around Boston, MA.

Adult↗