Lung cancer mortality attributable to residential radon: a systematic scoping review.

After smoking, residential radon is the second risk factor of lung cancer in general population and the first in never-smokers. Previous studies have analyzed radon attributable lung cancer mortality for some countries. We aim to identify, summarize, and critically analyze the available data regarding the mortality burden of lung cancer due to radon, performing a quality assessment of the papers included, and comparing the results from different countries. We performed a systematic scoping review using the main biomedical databases. We included original studies with attributable mortality data related to radon exposure. We selected studies according to specific inclusion and exclusion criteria. PRISMA 2020 methodology and PRISMA Extension for Scoping Reviews requirements were followed. Data were abstracted using a standardized data sheet and a tailored scale was used to assess quality. We selected 24 studies describing radon attributable mortality derived from 14 different countries. Overall, 13 studies used risk models based on cohorts of miners, 8 used risks from residential radon case-control studies and 3 used both risk model options. Radon geometric mean concentration ranged from 11 to 83 Becquerels per cubic meter (Bq/m3) and the population attributable fraction (PAF) ranged from 0.2 to 26%. Studies performed in radon prone areas obtained the highest attributable mortality. High-quality publications reported PAF ranging from 3 to 12% for residential risk sources and from 7 to 25% for miner risk sources. Radon PAF for lung cancer mortality varies widely between studies. A large part of the variation is due to differences in the risk source used and the conceptual description of radon exposure assumed. A common methodology should be described and used from now on to improve the communication of these results.

M-mode echocardiographic changes in growing beagles.

Heart growth in 6 female beagle dogs was measured by using M-mode echocardiography at 4, 7, 10, 13, 17, and 21 mo of age. The same 6 dogs were evaluated throughout the study to establish when cardiac development ends in this breed. The following parameters were measured during systole and diastole: left ventricle posterior wall thickness, interventricular septal thickness, left ventricular internal dimension, left atrial dimension during ventricular systole, aortic root dimension at end diastole, E-point to septal separation, left ventricular preejection period, ejection time of the left ventricular outflow, and time between the cessation and onset of the mitral inflow intervals. The percentage of the left ventricle posterior wall thickening, fractional shortening, ejection fraction, left ventricular end systolic and end-diastolic volumes, ratio of the left atrial dimension to aortic root dimension, and the Tei index of myocardial performance were calculated. The heart rate was measured by cardiac auscultation. The influence of ageing on each echocardiographic parameter and relationships with body weight and surface were studied. Results show that cardiac development in female beagles can be considered finished by the age of 1 y, perhaps as soon as 7 mo. The cardiac indexes studied were unaffected by the age and corporal dimensions, confirming the usefulness of these parameters for evaluating cardiac functionality alterations independent of a dog's age and body weight or surface area.

Renal handling of calcium and phosphorus in experimental renal hyperparathyroidism in dogs.

Twenty-four hour urinary excretion, fractional excretion and the filtered load of calcium and phosphorus were monitored as hyperparathyroidism evolved in a model of progressive canine renal failure. Thirteen beagles of both sexes aged four and a half months were used. Nine of them were subjected to a renal damaging schedule (neomycine, 60 mg/kg/48 h, IM, 32 weeks) in order to induce chronic renal failure leading to secondary hyperparathyroidism (2HPT group). The remaining four were kept as the control group. The experiment was conducted over 32 weeks. Blood and 24 h urine were collected every four weeks. Calcium, phosphorus and creatinine were analyzed. Plasma parathormone and calcitonin were determined at weeks 0, 12, 24 and 32. The level of renal function in the 2HPT animals was reduced to 25% of that of the controls (endogenous creatinine clearance was 0.45 +/- 0.22 mL/min/kg as opposed to 1.81 +/- 0.54 mL/min/kg). Hyperparathyroidism was confirmed by a progressive increase in the levels of the parathyroid hormone. Calcitonin levels were not modified. A tendency to hypocalcaemia was observed, reaching statistically significant levels from the twenty-eighth week of the study, when hyperphosphataemia also became significant. Daily urinary excretion of calcium and phosphorus remained at values considered normal throughout the experiment with no alteration imputable to the impaired renal function. This is explained by the decrease in the filtered load of these elements (in both cases statistically significant from the 24th week on) being associated with an increase in their fractional excretion. Thus, calcium and phosphorus urinary excretion values could be maintained in a normal range up to the end of the experiment, showing that renal calcium handling in dogs with experimentally induced renal failure seems to differ from that observed in human patients.