Methods The cohort comprised 64 937 individuals ever employed at the study sites between 1946 and 2002, followed up to 2005; radiation exposures as measured by personal dosimeters (‘film badges’) were available for 42 426 individuals classified as ‘radiation workers’. Poisson regression models were used to investigate the relationship between excess mortality rates and cumulative radiation exposure, using both relative and additive risk models.

Results The cohort shows a pronounced ‘healthy worker’ effect. Overall, socio-economic status as indicated by employment status has a greater influence on mortality than does radiation exposure status. For male radiation workers, there is an apparent dose response for mortality from circulatory system disease [P < 0.001, ERR = 0.65 (90% CI 0.36–0.98) Sv^–1]. However there is evidence for inhomogeneity in the apparent dose response (P = 0.016), arising principally at cumulative doses in excess of 300 mSv, when the four categories of employment and radiation exposure status are examined separately.

Conclusions We have found evidence for an association between mortality from non-cancer causes of death, particularly circulatory system disease, and external exposure to ionizing radiation in this cohort. However, the tentative nature of biological mechanisms that might explain such an effect at low chronic doses and the above inhomogeneities in apparent dose–response, mean that the results of our analysis are not consistent with any simple causal interpretation. Further work is required to explain these inhomogeneities, and on the possible role of factors associated with socio-economic status and shift working, before any further conclusions can be drawn.

Methods Using the voters’ list as the selection frame, 148 173 men and women aged ≥35 years were recruited during 1991–97 in Mumbai city and were followed-up during 1997–2003.

Results During 774 129 person-years of follow-up, 13 261 deaths were observed. After adjusting for the potential confounders, increased mortality was observed in all under-weight categories [relative risk (RR) = 1.94 for BMI < 16.0 kg/m², 1.38 for BMI 16.0 to <17.0 and 1.24 for BMI 17.0 to <18.5 among women; the corresponding values for men were 2.24, 1.45 and 1.27, respectively] when compared with the rate in the normal weight category (BMI 18.5 to <25.0). Extremely thin (BMI < 16.0 kg/m²) cohort members were at highest risk for death due to tuberculosis (TB) (RR = 7.20 and 14.94 in women and men, respectively), cancer (RR = 1.87 and 2.44, respectively) and respiratory diseases (RR = 3.46 and 4.35, respectively). Subjects with above normal BMI had lower mortality risk than those with normal BMI values. Over-weight (BMI 25.0 to <30.0) women (RR = 0.89) and men (RR = 0.87) were at a lower risk; however, obese (BMI ≥ 30.0) men <60 years of age had an increased mortality risk (RR = 1.22).

Conclusion In Mumbai, under-weight was associated with an increased risk of pre-mature death. Despite the growing concerns regarding the gradual transition toward increasing rates of obesity, under-nutrition remains a major health problem in India. This study suggests the need for public health policies focusing on reducing under-nutrition.

Methods Information on smoking was collected from 10 areas in four continents among population-based, age-stratified random samples of women aged 15 years or older. HPV testing was performed using PCR-based enzyme immunoassay. Unconditional logistic regression was used to estimate odds ratios (OR) and corresponding 95% confidence intervals (CI) of being HPV-positive by smoking habits, adjusted for age and lifetime number of sexual partners.

Results Ten thousand five hundred and seventy-seven women (mean age 41.4 years) were included. Among current smokers, the risk of being HPV-positive increased with smoking intensity, after allowing for lifetime number of sexual partners: ORs for <5, 5–14 and ≥15 cigarettes per day were 1.21 (95% CI 0.95–1.54), 1.39 (95% CI 1.04–1.87) and 2.01 (95% CI 1.32–3.08), respectively, as compared with never-smokers. The risk among former smokers (OR = 0.95, 95% CI 0.73–1.23) was similar to that among never-smokers. Analyses stratified by lifetime number of sexual partners showed a significant trend in risk only for women with one lifetime sexual partner.

Conclusions Our study suggests that current, though not former, smoking is associated with an increased prevalence of HPV, after allowance for sexual covariates. Among current smokers, HPV prevalence increased with smoking intensity, but a clear dose–response relationship was exclusively seen among women who declared one lifetime sexual partner.

Method Three-year follow-up cross-sectional survey was carried out in 40 rural Ethiopian communities to evaluate the programme. Households were randomly selected and all children were invited for eye examination for active trachoma. In 2005, eye swabs were taken for Polymerase Chain Reaction (PCR) detection of ocular C. trachomatis DNA. Adult knowledge and behaviour related to trachoma were assessed.

Results Community summarized mean prevalence, overall, was 35.6% (SD = 17.6) for active trachoma, 34.0% (18.7) for trachomatous inflammation, follicular (TF) alone and 4.3% (5.3) for PCR positivity for C. trachomatis. After adjustment, odds of active trachoma were reduced in communities receiving antibiotics and one or two educational intervention components (OR = 0.35, 95% CI: 0.13–0.89 or OR = 0.31, 0.11–0.89, respectively). The odds of being PCR positive were lower in these intervention arms, compared with control (OR = 0.20, 0.06–0.62 and OR = 0.07, 0.02–0.30, respectively). Knowledge of treatment and preventative methods were reported with much higher frequency, compared with baseline.

Conclusions Trachoma remains a public health problem in Ethiopia. Antibiotic administration remains the most effective intervention but community-based health education programmes can impact, to additionally reduce prevalence of C. trachomatis.

Methods The source population has children aged 4–6 commencing school in the Australian Capital Territory from 2000 to 2005 inclusive. Over 80% of these children and their families completed a health questionnaire on asthma, other atopic disease and respiratory symptoms using some questions from the International Study of Asthma and Allergies in Childhood (n = 22 882). Current asthma has been previously validated against physician assessment in this setting.

Results The prevalence of current asthma declined (P < 0.001) but eczema ever increased (P < 0.001) from 2000 to 2005. The asthma decline was predominantly linear in form, and accompanied by a reduction in night cough and shortness of breath but not recent wheeze. Compared with Australian-born children, children from New Zealand and the United Kingdom had a similar prevalence of asthma, hay fever and eczema history. However, children born in other countries, such as Asia, generally had a lower prevalence of these disorders. The temporal trends for atopic disorders or respiratory symptoms did not differ for overseas-born compared with Australian-born children.

Conclusion The decline in current asthma prevalence from 2000 to 2005 was linear in form and appeared uncoupled from trends in child eczema. Country of birth was associated with marked variation in atopic disorder prevalence. The similar temporal trends for Australian vs overseas-born children indicate that the factors underlying the asthma prevalence decline are unlikely to be only in the pre-natal period.

Methods The International Study of Asthma and Allergies in Childhood (ISAAC) used a standard questionnaire to measure the 12-month period prevalence of asthma symptoms by parental report in 6–7 year olds in 40 countries, and by self-report in 13–14 year olds in 60 countries. The initial survey was in the mid 1990s (Phase One) and this was repeated in the early 2000s (Phase Three). We correlated the prevalence values of any wheeze and severe wheeze with national data on mortality and hospital admissions for asthma in 5–14 year olds.

Results All correlations with prevalence were positive. In 13–14 year olds, the correlations between severe wheeze in Phase One and contemporaneous mortality and hospital admission rates were r = 0.32 (P = 0.047) and r = 0.73 (P = 0.003), respectively. In 6–7 year olds in Phase One, the correlation with severe wheeze and mortality was r = 0.42 (P = 0.024). In 14 countries the correlation between admission and mortality rates in the 5–14 year age group was r = 0.53 (P = 0.054).

Conclusions There are consistently positive associations between asthma symptom prevalence, admissions and mortality. The prevalence of asthma symptoms in children obtained from local questionnaire studies may provide a guide to estimate the incidence of severe episodes of asthma in countries with incomplete data on hospital admissions or mortality, or vice versa.

Methods To examine if pre-natal exposure to paracetamol is associated with the risk of asthma or wheezing in early childhood, we selected 66 445 women from the Danish National Birth Cohort for whom we had information on paracetamol use during pregnancy and who participated in an interview when their children were 18-months-old and 12 733 women whose children had reached the age of 7 and estimated the prevalence of physician-diagnosed asthma and wheezing at the ages of 18 months and 7 years. We also linked our population to the Danish National Hospital Registry to record all hospitalizations due to asthma up to age of 18 months.

Results Paracetamol use during any time of pregnancy was associated with a small but statistically significant increased risk of physician-diagnosed asthma or bronchitis among children at 18 months [relative risk (RR) = 1.17, 1.13–1.23)], hospitalizations due to asthma up to 18 months (hazard ratio = 1.24, 1.11–1.38) and physician-diagnosed asthma at 7 years (RR = 1.15, 1.02–1.29). The highest risks were observed for paracetamol use during the first trimester of pregnancy and persistent wheezing (wheezing at both 18 months and 7 years) (RR = 1.45, 1.13–1.85).

Conclusion Paracetamol use during pregnancy was associated with an increased risk of asthma and wheezing in childhood. If this association is causal, we may need to revisit the clinical practice on use of paracetamol during pregnancy.

Methods Of the GAZEL cohort, 14 445 participants aged 39–54 years in 1993 and followed-up over 12.7 years, completed the Bortner-Type-A-scale, the Buss-Durkee-Hostility-Inventory and the Grossarth-Maticek and Eysenck-Personality-Stress-Inventory. Indicators of SEP, such as father's social class, education, occupational grade and income, were assessed at baseline. Relative indices of inequality in Cox regression models were used to estimate associations.

Results In age-adjusted analyses, risk of death was inversely associated with SEP among men and women. Among men, the attenuation in this association depended on the measures of SEP and was 28–29% for ‘neurotic-hostility’, 13–22% for ‘anti-social’ and 13–16% for ‘CHD-prone’ personality. In women, the attenuation was evident only for type-A-behaviour, by 11%. After controlling simultaneously for all personality factors that predicted mortality, associations between SEP and mortality were attenuated in men: by 34% for education, 29% for occupational position and 28% for income; but were only attenuated by 11% for income in women. For cardiovascular mortality, the corresponding percentages of reduction were 42, 31 and 44% after adjustment for ‘CHD-prone’ personality in men.

Conclusions Personality measures explained some of the mortality gradients observed for measures of adult socioeconomic position in men, but had little explanatory power in women. Whether personality represents a predictor or an outcome of social circumstances needs further research.

Methods In 1996, 2338 adult offspring of participants of the 1970s Renfrew/Paisley study took part in a screening examination. They provided information on sociological, behavioural and clinical risk factors, as their parents had done 20 years previously. Social class and father's social class were available, enabling their influence on risk factors to be investigated.

Results Generally risk factors improved for offspring compared with parents, except for Body mass index and obesity, which worsened. Risk factors were less favourable in manual compared with non-manual offspring, and were more closely related to own than father's social class. There was a large amount of upward social mobility involving 35% of sons and 50% of daughters. Risk factors for the upwardly mobile tended to be more favourable than the class they left behind but less favourable than the class they joined.

Conclusions The concomitants of social mobility may reflect behavioural choices, such as smoking, and adverse factors, which are more difficult to leave behind. The relatively fast changes in social class profile may not be reflected in as quick changes in population health, as the upwardly mobile bring their earlier life adversities with them.

Methods We investigated the association between education and lifetime smoking patterns in a birth cohort established in 1959 and followed through adulthood (n = 1311). We controlled for a wide range of potential confounders that were measured prior to school entry, and also estimated sibling fixed effects models to control for unmeasured familial vulnerability to smoking.

Results In the full sample of participants, regression analyses adjusting for multiple childhood factors (including socioeconomic status, IQ, behavioural problems, and medical conditions) indicated that the number of pack-years smoked was higher among individuals with less than high school education [rate ratio (RR) = 1.58, confidence interval (CI) = 1.31, 1.91]. However, in the sibling fixed effects analysis the RR was 1.23 (CI = 0.80, 1.93). Similarly, adjusted models estimated in the full sample showed that individuals with less than high school education had fewer short-term (RR = 0.40; CI = 0.23, 0.69) and long-term (RR = 0.59; CI = 0.42, 0.83) quit attempts, and were less likely to quit smoking (odds ratio = 0.34; CI = 0.19, 0.62). The effects of education on quitting smoking were attenuated in the sibling fixed effects models that controlled for familial vulnerability to smoking.

Conclusions A substantial portion of the education differential in smoking that has been repeatedly observed is attributable to factors shared by siblings that contribute to shortened educational careers and to lifetime smoking trajectories. Reducing disparities in cigarette smoking, including educational disparities, may therefore require approaches that focus on factors early in life that influence smoking risk over the adult life span.

Methods Literature search for review and research articles on temporal trends in US breast cancer incidence during the past 25 years, starting in the mid-1980s, when extant epidemiologic evidence had already indicated that HT increased risk of breast cancer.

Results Among the 21 articles identified, spanning from 1987 to 2007, nine included no mention of HT as a possible factor contributing to the steep rise in breast cancer incidence in the 1980s, seven included a minor mention and only five (one published in 2003, the others in 2006 and 2007) provided any substantive discussion of this issue—but only in relation to current trends and not the 1980 rise in breast cancer incidence.

Conclusion A critical appraisal of the epidemiologic literature highlights important gaps in explanations for breast cancer incidence trends and also how current and changing population patterns of disease distribution are ultimately what put our aetiologic explanations to the test.

Methods The P-value is by far the most commonly used measure, but requires careful calibration when the a priori probability of an association is small, and discards information by not considering the power associated with each test. The q-value is a frequentist method by which the false discovery rate (FDR) may be controlled.

Results We advocate the use of the Bayes factor as a summary of the information in the data with respect to the comparison of the null and alternative hypotheses, and describe a recently-proposed approach to the calculation of the Bayes factor that is easily implemented. The combination of data across studies is straightforward using the Bayes factor approach, as are power calculations.

Conclusions The Bayes factor and the q-value provide complementary information and when used in addition to the P-value may be used to reduce the number of reported findings that are subsequently not reproduced.

Methods A systematic literature review identified nine diseases with sufficient evidence of a causal relationship with UVR exposure and for which the population attributable fraction (PAF) for UVR could be estimated. For cutaneous malignant melanoma and cataract, the PAF was directly applied to disease burdens already calculated by WHO. For seven other diseases, we developed population-level exposure–disease relationships and used these to calculate disease incidence and mortality, and thence disease burden. We also estimated the disease burden from rickets, osteomalacia and osteoporosis that might result if global UVR exposure was reduced to very low levels.

Results UVR exposure is a minor contributor to the world's disease burden, causing an estimated annual loss of 1.6 million DALYs; i.e. 0.1% of the total global disease burden. A markedly larger annual disease burden, 3.3 billion DALYs, might result from reduction in global UVR exposure to very low levels.

Conclusions Sun protection messages are important to prevent diseases of UVR exposure. However, without high dietary (or supplemental) intake of vitamin D, some sun exposure is essential to avoid diseases of vitamin D insufficiency.

Methods In this analysis of the Copenhagen City Heart Study, in which alcohol intake was measured four times, 9318 Danish women with no previous diagnosis of cancer were followed for breast cancer for 27 years, from 1976 to 2002. During follow-up, breast cancer was diagnosed in 476 women.

Results The association between alcohol intake at first measurement (baseline alcohol intake) and breast cancer was positive and approximately linear. When alcohol intake was updated during follow-up, no association was observed between breast cancer and alcohol intake. It is suggested that this difference in results may be attributable to long latency time between alcohol intake and breast cancer occurrence, because a markedly increased risk was estimated on the basis of direct lagging of risk time.

Conclusions Our results support the hypothesis that baseline alcohol intake is more strongly associated with breast cancer risk than updated intake, and we suggest that this is due to the long latency between alcohol intake and breast cancer.