Alcohol, tobacco and breast cancer: should alcohol be condemned and tobacco acquitted?

British Journal of Cancer (2002) 87, 1195–1196. doi:10.1038/sj.bjc.6600633 www.bjcancer.co

Potential Residential Exposure to Toxics Release Inventory Chemicals during Pregnancy and Childhood Brain Cancer

BACKGROUND: Although the susceptibility of the developing fetus to various chemical exposures is well documented, the role of environmental chemicals in childhood brain cancer etiology is not well understood. OBJECTIVES: We aimed to evaluate whether mothers of childhood brain cancer cases had greater potential residential exposure to Toxics Release Inventory (TRI) chemicals than control mothers during pregnancy. METHODS: We included 382 brain cancer cases diagnosed at < 10 years of age from 1993 through 1997 who were identified from four statewide cancer registries. One-to-one matched controls were selected by random-digit dialing. Computer-assisted telephone interviews were conducted. Using residential history of mothers during pregnancy, we measured proximity to TRI facilities and exposure index, including mass and chemicals released. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression to estimate brain cancer risk associated with TRI chemicals. RESULTS: Increased risk was observed for mothers living within 1 mi of a TRI facility (OR = 1.66; 95% CI, 1.11–2.48) and living within 1 mi of a facility releasing carcinogens (OR = 1.72; 95% CI, 1.05–2.82) for having children diagnosed with brain cancer before 5 years of age, compared to living > 1 mi from a facility. Taking into account the mass and toxicity of chemical releases, we found a nonsignificant increase in risk (OR = 1.25; 95% CI, 0.67–2.34) comparing those with the lowest versus highest exposure index. CONCLUSIONS: Risk of childhood brain cancers may be associated with living near a TRI facility; however, this is an exploratory study and further studies are needed

The risk linked to ionizing radiation: an alternative epidemiologic approach.

Radioprotection norms have been based on risk models that have evolved over time. These models show relationships between exposure and observed effects. There is a high level of uncertainty regarding lower doses. Recommendations have been based on the conservative hypothesis of a linear relationship without threshold value. This relationship is still debated, and the diverse observations do not allow any definitive conclusion. Available data are contradictory, and various interpretations can be made. Here we review an alternative approach for defining causation and reconciling apparently contradictory conclusions. This alternative epidemiologic approach is based on causal groups: Each component of a causal group is necessary but not sufficient for causality. Many groups may be involved in causality. Thus, ionizing radiation may be a component of one or several causal groups. This formalization reconciles heterogeneous observations but implies searching for the interactions between components, mostly between critical components of a causal profile, and, for instance, the reasons why specific human groups would not show any effect despite exposure, when an effect would be expected

Follow-up of blood-pressure lowering and glucose control in type 2 diabetes.

BACKGROUND In the Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) factorial trial, the combination of perindopril and indapamide reduced mortality among patients with type 2 diabetes, but intensive glucose control, targeting a glycated hemoglobin level of less than 6.5%, did not. We now report results of the 6-year post-trial follow-up. METHODS We invited surviving participants, who had previously been assigned to perindopril–indapamide or placebo and to intensive or standard glucose control (with the glucose-control comparison extending for an additional 6 months), to participate in a post-trial follow-up evaluation. The primary end points were death from any cause and major macrovascular events. RESULTS The baseline characteristics were similar among the 11,140 patients who originally underwent randomization and the 8494 patients who participated in the post-trial follow-up for a median of 5.9 years (blood-pressure–lowering comparison) or 5.4 years (glucose-control comparison). Between-group differences in blood pressure and glycated hemoglobin levels during the trial were no longer evident by the first post-trial visit. The reductions in the risk of death from any cause and of death from cardiovascular causes that had been observed in the group receiving active blood-pressure–lowering treatment during the trial were attenuated but significant at the end of the post-trial follow-up; the hazard ratios were 0.91 (95% confidence interval [CI], 0.84 to 0.99; P=0.03) and 0.88 (95% CI, 0.77 to 0.99; P=0.04), respectively. No differences were observed during follow-up in the risk of death from any cause or major macrovascular events between the intensive-glucose-control group and the standard-glucose-control group; the hazard ratios were 1.00 (95% CI, 0.92 to 1.08) and 1.00 (95% CI, 0.92 to 1.08), respectively. CONCLUSIONS The benefits with respect to mortality that had been observed among patients originally assigned to blood-pressure–lowering therapy were attenuated but still evident at the end of follow-up. There was no evidence that intensive glucose control during the trial led to long-term benefits with respect to mortality or macrovascular events

Random walk generated by random permutations of {1,2,3, ..., n+1}

We study properties of a non-Markovian random walk $X^{(n)}_l$, $l =0,1,2, >...,n$, evolving in discrete time $l$ on a one-dimensional lattice of integers, whose moves to the right or to the left are prescribed by the \text{rise-and-descent} sequences characterizing random permutations $\pi$ of $[n+1] = \{1,2,3, ...,n+1\}$. We determine exactly the probability of finding the end-point $X_n = X^{(n)}_n$ of the trajectory of such a permutation-generated random walk (PGRW) at site $X$, and show that in the limit $n \to \infty$ it converges to a normal distribution with a smaller, compared to the conventional P\'olya random walk, diffusion coefficient. We formulate, as well, an auxiliary stochastic process whose distribution is identic to the distribution of the intermediate points $X^{(n)}_l$, $l < n$, which enables us to obtain the probability measure of different excursions and to define the asymptotic distribution of the number of "turns" of the PGRW trajectories.Comment: text shortened, new results added, appearing in J. Phys.