Altogether 238 759 miners employed by the National Coal Board were examined in the third of the Board's radiological surveys from 1969 to 1973 inclusive. Excluding those diagnosed as having progressive massive fibrosis (PMF) on that occasion, 210 847 were in collieries still operating at the time of the fourth survey four to five years later; 132 728 attended for radiography at the same colliery on the second occasion, and were used to study the attack rate of PMF. In all groups in the age range 35-54 and having category 2 simple pneumoconiosis (SPN) or less, 80 % or more had a second radiograph. It was found that the probability of developing PMF increased sharply with rising category of SPN; however, half the cases occurred in men having SPN categories 0 or 1, who were in the majority. Current coalface work had no significant effect on the attack rate. Age increased the attack rate of PMF within each major SPN category (0, 1, 2, and 3), especially the higher categories. All or part of this effect may have been due to the fact that SPN in younger men with categories 1 and 2 tends to lie in the lower range within these categories. Similarly, a lower distribution of SPN within each category associated with a low overall local prevalence may account wholly or in part for the great difference between the attack rates of PMF supervening on each category of SPN in Scotland and South Wales. The rank (quality) of coal mined had no effect on the attack rate.

As part of the Periodic X-ray Scheme of the National Coal Board (NCB), a comparison is made between the previous and new films of all miners who were face-workers on the former occasion, five years earlier. This assessment is made by distributing the films randomly to all the NCB readers. This paper compares the rank of coal mined in each colliery with each colliery's percentage prevalence of pneumoconiosis of at least ILO category 1 in the films of previous faceworkers obtained during the third survey round . Of the NCB's 291 collieries in Britain, information enabling a rank classification to be made was available for 250, employing 62 362 face-workers. In these 250 mines a progressive and five-fold increase in prevalence was observed from collieries mining low-rank (bituminous) coal to those mining coal of high ranks (anthracite and high-grade steam and coking ccal). A possible reascn for this is that, in the past, high-rank collieries may have had the highest mass-concentrations of respirable dust.

Background Inflammatory bowel disease (IBD) is characterized by chronic inflammation, which can progress to colorectal cancer, with duration of disease being the most important risk factor. Although many factors are involved, the pathogenic link between inflammation and cancer and the role played by the lymphatic system have not been fully investigated. This project uses lymphatic-deficient mice (Angiopoietin-2 [Ang2] knockout) to examine the lymphatic system in the progression of IBD to colorectal cancer. Methods Angiopoietin-2 wild-type, heterozygote, and knockout mice received a single injection of the procarcinogen azoxymethane and had an IBD-promoting chemical irritant (dextran sodium sulfate) added to their drinking water over a 7-week period. We measured disease activity (weight loss, stool consistency, fecal occult blood) during the study and at sacrifice, collected blood for cytokine/biomarker (Ang2, interleukin [IL] 1-β, IL-6, tumor necrosis factor α [TNFα], and VEGF-C) enzyme-linked immunosorbent assay analysis, measured colon length, and assessed tumor burden. Results Ang2 knockout (KO) mice exhibited reduced (55%) survival vs wild-type (100%) and heterozygotes (91%; P < 0.01 and P < 0.0001, respectively). Most (>89%) mice developed tumors, and the incidence of colorectal cancer did not differ among the genotypes (P = 0.32). The tumor area was significantly increased in KO mice (P = 0.004). Of the biomarkers measured in the serum, Ang2 and TNF-α concentrations were significantly different among the genotypes (P = 3.35e-08 and P = 0.003 respectively). Disease activity was significantly increased in KO mice compared with wild-type and heterozygote mice (P = 0.033). Conclusions Lymphatic deficiency, defective lymphangiogenesis, and impaired lymphatic-generated inflammation did not protect against clinical IBD or progression to colorectal cancer in this experimental model.