Exposure to power frequency electric fields and the risk of childhood cancer in the UK

The United Kingdom Childhood Cancer Study, a population-based case-control study covering the whole of Great Britain, incorporated a pilot study measuring electric fields. Measurements were made in the homes of 473 children who were diagnosed with a malignant neoplasm between 1992 and 1996 and who were aged 0-14 at diagnosis, together with 453 controls matched on age, sex and geographical location. Exposure assessments comprised resultant spot measurements in the child's bedroom and the family living-room. Temporal stability of bedroom fields was investigated through continuous logging of the 48-h vertical component at the child's bedside supported by repeat spot measurements. The principal exposure metric used was the mean of the pillow and bed centre measurements. For the 273 cases and 276 controls with fully validated measures, comparing those with a measured electric field exposure >/=20 V m(-1) to those in a reference category of exposure <10 V m(-1), odds ratios of 1.31 (95% confidence interval 0.68-2.54) for acute lymphoblastic leukaemia, 1.32 (95% confidence interval 0.73-2.39) for total leukaemia, 2.12 (95% confidence interval 0.78-5.78) for central nervous system cancers and 1.26 (95% confidence interval 0.77-2.07) for all malignancies were obtained. When considering the 426 cases and 419 controls with no invalid measures, the corresponding odds ratios were 0.86 (95% confidence interval 0.49-1.51) for acute lymphoblastic leukaemia, 0.93 (95% confidence interval 0.56-1.54) for total leukaemia, 1.43 (95% confidence interval 0.68-3.02) for central nervous system cancers and 0.90 (95% confidence interval 0.59-1.35) for all malignancies. With exposure modelled as a continuous variable, odds ratios for an increase in the principal metric of 10 V m(-1) were close to unity for all disease categories, never differing significantly from one.     

Diet and cancer: Value of different types of epidemiological studies

Diet and nutrition are increasingly recognized as likely to be major determinants of cancer, notably cancers of the gastrointestinal tract, breast, endometrium, ovary, and prostate. Dietary factors may collectively account for a greater proportion of all cancers that occur in contemporary Western society than does any other category of environmental exposure (1). With the development of knowledge of the protective properties of certain components of food, links with diet have been suggested for other cancer sites (2).

The epidemiological evidence for the association of diet and cancer is, however, not uniformly convincing; also, the likely biological pathways are not always clear. In this paper, we comment on some current hypotheses in this area and examine the best epidemiological methods to test them.     

Minactivin expression in human monocyte and macrophage populations

Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or "tissue"-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone.     

Nuclear magnetic resonance in hypertrophic cardiomyopathy.

The large differences in the spin lattice relaxation times (T1) of blood and myocardium (measured by nuclear magnetic resonance) allow the heart to be visualised without the use of contrast media. The findings using nuclear magnetic resonance in 11 unselected patients with hypertrophic cardiomyopathy were compared with those in equal numbers of normal subjects and patients with electrocardiographic features of left ventricular hypertrophy. In patients with hypertrophic cardiomyopathy characteristic septal hypertrophy was noted together with variable and sometimes pronounced hypertrophy of the left ventricular free wall, which is consistent with the heterogeneous nature of this disease. The mean (SD) ratio of septal to free wall thickness was 1.5(0.8) for patients with hypertrophic cardiomyopathy, 0.8(0.2) for those with left ventricular hypertrophy, and 0.9(0.2) for normal subjects. Although septal measurements by nuclear magnetic resonance were greater than those obtained by echocardiography there was a significant correlation between the two. Septal and free wall area were significantly smaller in normal subjects. There were no differences in septal or free wall T1 values between the three groups. Non-gated nuclear magnetic resonance can detect septal and free wall hypertrophy. With the addition of multiple slice acquisition, rapid estimation of myocardial mass will be possible allowing the potentially important assessment of progression or regression of myocardial hypertrophy.     

Right ventricular performance during exercise in chronic obstructive pulmonary disease. The effects of oxygen

Radionuclide ventriculography allows non-invasive assessment of right ventricular performance. This study has confirmed that there is a modest reduction in right ventricular ejection fraction (RVEF) in patients with chronic obstructive pulmonary disease (COPD), as compared to normal subjects. However, occult right ventricular dysfunction also becomes apparent in these patients during exercise. The change in RVEF during exercise is related to the corresponding fall in arterial oxygen saturation in patients with COPD. Oxygen improves the response of the right ventricle to exercise, although the mechanism remains unclear. Long-term oxygen therapy, in patients with respiratory failure, does not appear to have any significant effect on RVEF.     

Are the clinical benefits of oral prenalterol in ischaemic heart failure due to beta blockade? A six month randomised double blind comparison with placebo.

The clinical effects of the oral beta 1 partial agonist, prenalterol, were investigated in 37 patients (29 male, eight female; mean age 57 years) with chronic ischaemic left ventricular failure using a placebo controlled randomised double blind protocol over six months. All patients were limited by dyspnoea (New York Heart Association class III) despite treatment with digoxin and diuretics. Twenty eight patients completed the protocol. Moderate clinical improvement was seen in the prenalterol group, whereas there was little change in the placebo group. Bicycle exercise capacity increased over six months in the prenalterol and placebo groups but only achieved statistical significance for prenalterol when compared with baseline values. Maximum exercise heart rate was significantly reduced in the prenalterol group compared with placebo. Radionuclide left ventricular ejection fraction at rest and during exercise and cardiothoracic ratio showed no significant improvement in either group over six months. Prenalterol was well tolerated and produced no increase in frequency of angina or ventricular arrhythmias. Prenalterol produced clinical benefits and improved exercise tolerance while reducing exercise heart rate. A moderate placebo response was noted. The apparent beta blocking effect of prenalterol may be as important as the beta 1 agonist effect in producing these benefits. Prenalterol has, however, been withdrawn because of side effects in animals.