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Coggon D.,MRC Lifecourse Epidemiology Unit | Coggon D.,University of Southampton | Ntani G.,University of Southampton | Harris E.C.,University of Southampton | Palmer K.T.,University of Southampton
American Journal of Epidemiology | Year: 2014

The International Agency for Research on Cancer controversially has classified formaldehyde as causing nasopharyngeal carcinoma and myeloid leukemia. To provide further information on this question, we extended follow-up of a cohort of 14,008 chemical workers at 6 factories in England and Wales, covering the period 1941-2012. Mortality was compared with national death rates for England and Wales, and associations with incident upper airway cancer and leukemia were explored in nested case-control analyses. We observed excess deaths from cancers of the esophagus (100 observed vs. 93.1 expected), stomach (182 vs. 141.4), rectum (107 vs. 86.8), liver (35 vs. 26.9), and lung (813 vs. 645.8), but none of these tumors exhibited a clear exposure-response relationship. Nested case-control analyses of 115 men with upper airway cancer (including 1 nasopharyngeal cancer), 92 men with leukemia, and 45 men with myeloid leukemia indicated no elevations of risk in the highest exposure category (high exposure for ≥1 year). When the 2 highest exposure categories were combined, the odds ratio for myeloid leukemia was 1.26 (95% confidence interval: 0.39, 4.08). Our results provide no support for an increased hazard of myeloid leukemia, nasopharyngeal carcinoma, or other upper airway tumors from formaldehyde exposure. These results indicate that any excess risk of these cancers, even from relatively high exposures, is at most small. © 2014 The Author 2014. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. Source


Palmer K.T.,University of Southampton | Palmer K.T.,MRC Lifecourse Epidemiology Unit
British Medical Bulletin | Year: 2012

Background: The prevalence of knee osteoarthritis (OA) is rising and the search for interventions to mitigate risk is intensifying. This review considers the contribution of occupational activities to disease occurrence and the lessons for prevention.Sources: Systematic search in Embase and Medline covering the period 1996 to November 011.Areas of agreement: Reasonably good evidence exists that physical work activities (especially kneeling, squatting, lifting and climbing) can cause and/or aggravate knee OA. These exposures should be reduced where possible. Obese workers with such exposures are at additional risk of knee OA and should therefore particularly be encouraged to lose weight.Areas of uncertainty/research need: Workplace interventions and policies to prevent knee OA have seldom been evaluated. Moreover, their implementation can be problematic. However, the need for research to optimize the design of work in relation to knee OA is pressing, given population trends towards extended working life. © 2012 The Author. Source


Krishnaveni G.V.,Epidemiology Research Unit | Veena S.R.,Epidemiology Research Unit | Karat S.C.,Epidemiology Research Unit | Yajnik C.S.,Diabetes Unit | Fall C.H.D.,MRC Lifecourse Epidemiology Unit
Diabetologia | Year: 2014

Aims/hypothesis: In an Indian birth cohort, higher maternal homocysteine concentration in pregnancy was associated with lower birthweight of the offspring. Lower maternal vitamin B12 and higher folate concentrations were associated with higher offspring insulin resistance. Disordered one-carbon metabolism during early development may increase later metabolic risk. We explored these associations in another birth cohort in India at three age points. Methods: We measured plasma vitamin B12, folate and homocysteine concentrations at 30 ± 2 weeks' gestation in 654 women who delivered at one hospital. Neonatal anthropometry was recorded, and the children's glucose and insulin concentrations were measured at 5, 9.5 and 13.5 years of age. Insulin resistance was estimated using HOMA of insulin resistance (HOMA-IR). Results: Maternal homocysteine concentrations were inversely associated with all neonatal anthropometric measurements (p < 0.05), and positively associated with glucose concentrations in the children at 5 (30 min; p = 0.007) and 9.5 years of age (120 min; p = 0.02). Higher maternal folate concentrations were associated with higher HOMA-IR in the children at 9.5 (p = 0.03) and 13.5 years of age (p = 0.03). Maternal vitamin B12 concentrations were unrelated to offspring outcomes. Conclusions/interpretation: Maternal vitamin B12 status did not predict insulin resistance in our cohort. However, associations of maternal homocysteine and folate concentrations with birth size, and with childhood insulin resistance and glycaemia in the offspring, suggest a role for nutritionally driven disturbances in one-carbon metabolism in fetal programming of diabetes. © 2013 The Author(s). Source


Grant
Agency: GTR | Branch: MRC | Program: | Phase: Intramural | Award Amount: 920.94K | Year: 2010

The mission of the MRC Lifecourse Epidemiology Unit is to provide a centre of excellence which uses epidemiological methods to promote human health by delineating the environmental and occupational causes throughout the lifecourse of: (1) chronic musculoskeletal disorders (osteoporosis, osteoarthritis and sarcopenia); and (2) metabolic disorders (diabetes mellitus, obesity and cardiovascular disease). Through understanding these causes, we aim to develop population-based and high risk preventive strategies against these disorders. This programme will explore the contributions made by maternal undernutrition to the origins of later diabetes and heart disease in the offspring. It is based in India, and includes a series of observational studies and trials.


Luyckx V.A.,University of Alberta | Bertram J.F.,Monash University | Brenner B.M.,Harvard University | Fall C.,MRC Lifecourse Epidemiology Unit | And 3 more authors.
The Lancet | Year: 2013

Summary Developmental programming of non-communicable diseases is now an established paradigm. With respect to hypertension and chronic kidney disease, adverse events experienced in utero can affect development of the fetal kidney and reduce final nephron number. Low birthweight and prematurity are the most consistent clinical surrogates for a low nephron number and are associated with increased risk of hypertension, proteinuria, and kidney disease in later life. Rapid weight gain in childhood or adolescence further compounds these risks. Low birthweight, prematurity, and rapid childhood weight gain should alert clinicians to an individual's lifelong risk of hypertension and kidney disease, prompting education to minimise additional risk factors and ensuring follow-up. Birthweight and prematurity are affected substantially by maternal nutrition and health during pregnancy. Optimisation of maternal health and early childhood nutrition could, therefore, attenuate this programming cycle and reduce the global burden of hypertension and kidney disease in the future. © 2013 Elsevier Ltd. Source

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