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We obtained lifetime occupational and residential histories by telephone interview with 622 mesothelioma patients (512 men, 110 women) and 1420 population controls. Odds ratios (ORs) were converted to lifetime risk (LR) estimates for Britons born in the 1940s. Male ORs (95% confidence interval (CI)) relative to low-risk occupations for 410 years of exposure before the age of 30 years were 50.0 (25.8 -96.8) for carpenters (LR 1 in 17), 17.1 (10.3 -28.3) for plumbers, electricians and painters, 7.0 (3.2 -15.2) for other construction workers, 15.3 (9.0 -26.2) for other recognised high-risk occupations and 5.2 (3.1 -8.5) in other industries where asbestos may be encountered. The LR was similar in apparently unexposed men and women (B1 in 1000), and this was approximately doubled in exposed workers' relatives (OR 2.0, 95% CI 1.3 -3.2). No other environmental hazards were identified. In all, 14% of male and 62% of female cases were not attributable to occupational or domestic asbestos exposure. Approximately half of the male cases were construction workers, and only four had worked for more than 5 years in asbestos product manufacture. (Hodgson et al, 2005), or about 1 in 170 of all deaths. Substantial exposure to asbestos dust continued until about 1970 in parts of the asbestos industry, and until the early 1980s in the much larger workforce in construction and other occupations in which asbestos lagging was applied or asbestos insulation board (AIB) was sawn. The death rate is still increasing above 60 years of age, but the reduction in asbestos use since the mid-1970s has been followed 20 years later by a rapid fall in the number of mesothelioma deaths at 35 -49 years of age in British men

Survivors of hereditary retinoblastoma who are not exposed to high-dose radiotherapy have a high lifetime risk of developing a late-onset epithelial cancer. Most of the excess cancer risks in hereditary retinoblastoma survivors might be preventable by limiting exposures to DNA damaging agents (radiotherapy, tobacco, and UV light).

on behalf of the ARTISTIC Trial Study GroupHow to obtain copies of this and other HTA programme reports An electronic version of this publication, in Adobe Acrobat format, is available for downloading free of charge for personal use from the HTA website (www.hta.ac.uk). A fully searchable CD-ROM is also available (see below).Printed copies of HTA monographs cost £20 each (post and packing free in the UK) to both public and private sector purchasers from our Despatch Agents.Non-UK purchasers will have to pay a small fee for post and packing. For European countries the cost is £2 per monograph and for the rest of the world £3 per monograph.You can order HTA monographs from our Despatch Agents:-fax (with credit card or official purchase order) -post (with credit card or official purchase order or cheque) -phone during office hours (credit card only).Additionally the HTA website allows you either to pay securely by credit card or to print out your order and then post or fax it. Contact details are as follows: Payment methods Paying by chequeIf you pay by cheque, the cheque must be in pounds sterling, made payable to Direct Mail Works Ltd and drawn on a bank with a UK address. Paying by credit cardThe following cards are accepted by phone, fax, post or via the website ordering pages: Delta, Eurocard, Mastercard, Solo, Switch and Visa. We advise against sending credit card details in a plain email. Paying by official purchase orderYou can post or fax these, but they must be from public bodies (i.e. NHS or universities) within the UK. We cannot at present accept purchase orders from commercial companies or from outside the UK. How do I get a copy of HTA on CD?Please use the form on the HTA website (www.hta.ac.uk/htacd.htm). Or contact Direct Mail Works (see contact details above) by email, post, fax or phone. HTA on CD is currently free of charge worldwide.The website also provides information about the HTA programme and lists the membership of the various committees. combination with HPV; it is highly effective as primary screening but HPV testing has twin advantages of high negative predictive value and automated platforms enabling high throughput. HPV primary screening would require major contraction and reconfiguration of laboratory services. Follow-up continues in ARTISTIC while maintaining concealment for a further 3-year round of screening, which will help in screening protocol development for the post-vaccination era.

Cytology and histology records and cervical samples for HPV assay were obtained from a prospective cohort of 49 655 women attending clinics for routine cervical cytology in or near Manchester between 1988 and 1993. The women were followed up for cytological abnormality and neoplasia through the cytology laboratory's records. HPV at entry was assayed in an age-and periodstratified random sample of 7278 women and in prevalent and incident CIN3 cases. The prevalence of newly diagnosed CIN3 increased with time since last normal smear, indicating that most cases persist for several years. CIN3 prevalence did not increase further for screening intervals exceeding 5 years, however, suggesting that CIN3 eventually regresses cytologically. CIN2 prevalence increased less steeply with screening interval, while the prevalence of lesser abnormality was almost independent of screening interval. The prevalence of oncogenic HPV at entry declined from 19% among women aged under 25 to less than 3% at age 40 or above. Oncogenic HPV infection was strongly predictive of subsequent CIN3 (OR 17.2, 95% CI 10.4 -28.4), but only weakly related to CIN2 (OR 2.3, 95% CI 0.5 -10.7) and lesser abnormality (OR 1.4, 95% CI 0.8 -2.5). At current incidence rates, the lifetime risk of developing CIN3 will be 9% in this population. The cumulative risk of CIN3 diagnosis among cytologically normal women with oncogenic HPV detected at entry was 28% (CI 18 -43%) after 14 years. Persistence of oncogenic HPV may be more sensitive and specific than cytology for early detection of CIN3 and invasive cancer. Population-based prospective data on cervical neoplasia rates in relation to age, screening interval and history of type-specific HPV infection are still limited. Few cohorts are representative of regularly screened women in the general population, and those using the Bethesda system under which the high-grade category (HSIL) includes both CIN2 and CIN3 (Solomon et al, 2002) have often not analysed CIN2 and CIN3 separately. There is a strong and consistent association of genital HPV infection with cervical intraepithelial neoplasia (CIN) and cancer. CIN3 is almost always preceded by persistently detectable oncogenic HPV (Nobbenhuis et al, 1999), and HPV DNA was present in virtually all (99.7%) of a large sample of cervical cancers obtained from populations worldwide . Uninfected women, including those with abnormal cytology, are thus at negligible risk of invasive cancer. Follow-up studies indicate that most HPV infections are transient (Hildesheim et al, 1994;Remmink et al, 1995;Ho et al, 1998;Liaw et al, 1999;Nobbenhuis et al, 1999), but women with persistent HPV are at high risk of developing CIN3 (Nobbenhuis et al, 1999(Nobbenhuis et al, , 2001. HPV testing could thus be superior to cytology in routine cervical screening (Nobbenhuis et al, 1999;Cuzick et al, 2003).This report describes the relationship between HPV detection at entry and cytological and histological follow-up based on routine laboratory records in a prospective population-based cohort...