PubMed Health⌕ Search

Biomedical subjects

Alan Rogers

Publications and source records attributed to Alan Rogers.

8 recordsLinked to original sources
PubMed2006

Reply to comments on "Derivation of numerical values for the World Health Organization guidelines for recreational waters".

The contribution addressed reveals an optimistic design philosophy likely to systematically underestimate risk in epidemiologic studies into the health effects of bathing water exposures. The authors seem to recommend that data on the 'exposure' measure (i.e. water quality) in such studies should be acquired in a similar manner to that used for regulatory sampling. This approach may compromise the quality of the epidemiologic investigations undertaken. It may result in imprecise estimates of exposure because it ignores the fact that regulatory timescales and spatial resolution (even if artificially compressed to a bathing day) can mask large spatial and temporal variability in water quality. If this variability is ignored by taking some mean value and attributing that to all of those exposed in a period at a study location, many bathers may be misclassified and the studies may be biased to a 'no-effect' conclusion. A more appropriate approach is to maximise the precision of the epidemiologic investigations by measurement of individual exposure (or water quality) at the place and time of the exposure, as has been done in randomised volunteer studies in the UK and Germany. The precise epidemiologic relationships linking 'exposure' with 'illness' can then be related to the probability of exposure to particular water quality by a 'normal bather' using the known probability distribution of the exposure variable (i.e. faecal indicator concentration) in the regulated bathing waters. We suggest that any research protocol where poor sampling design for water quality assessment is justified because regulatory monitoring is equally imprecise may be fundamentally flawed. The rationale for this assessment is that the epidemiology is the starting point and evidence-base for 'standards'. If precision is not maximised at this stage in the process it compromises the credibility of the standards design process. The negative effects of the approach advocated in this 'comment' are illustrated using published research findings used to derive the figures illustrated in Wymer et al. [2005. Comment on derivation of numerical values for the World Health Organization guidelines for recreational waters. Water Research 39, 2774-2777].

Environmental Exposure↗
PubMed2004

Silicosis and lung cancer: a mortality study of compensated men with silicosis in New South Wales, Australia.

BACKGROUND: Lung cancer mortality has been found to be in excess in several groups with silicosis, but allowance for smoking was not always possible. We investigated the lung cancer mortality in men with silicosis in New South Wales, Australia, who were compensated, making allowance for smoking habits. METHODS: A mortality study of 1467 men with silicosis in New South Wales who were compensated was carried out comparing observed mortality with that expected from the New South Wales death rates adjusting for age and period. Their smoking habits were compared with national survey smoking rates and the expected number of lung cancer deaths adjusted for smoking. Cases were coded for occupation and industry. RESULTS: The observed mortality was higher than expected, but the only site of cancer showing a significant excess was the lung. The group with silicosis had smoked more than the national rates. After adjusting for smoking the standardized mortality ratio for lung cancer was 1.9 (95% confidence interval 1.5-2.3). Although there were differences in lung cancer mortality between industries and occupations, these differences were not statistically significant. CONCLUSIONS: The excess lung cancer death rate may not be entirely due to silica exposure because compensation may have been influenced by the presence of chronic obstructive respiratory disease and there is some evidence that the presence of this disease increases lung cancer risk independently of smoking.

Aged↗
PubMed2004

Derivation of numerical values for the World Health Organization guidelines for recreational waters.

In April 2001, draft 'Guidelines' for safe recreational water environments were developed at a World Health Organization (WHO) expert consultation. Later the same month, these were presented and discussed at the 'Green Week' in Brussels alongside the on-going revision of the European Union Bathing Water Directive 76/160/EEC. The WHO Guidelines cover general aspects of recreational water management as well as define water quality criteria for various hazards. For faecal pollution, these include faecal indicator organism concentrations and an assessment of vulnerability to faecal contamination. Central to the approach set out in the WHO Guidelines are: (i) the concept of beach profiling to produce a 'sanitary inspection category' which implies a priori hazard assessment as a core management tool and (ii) the prediction of poor water quality to assist in real time risk assessment and public health protection. These management approaches reflect a harmonized approach towards the assessment and management of risk for water-related infectious disease being applied by WHO. Numerical microbiological criteria for intestinal enterococci are proposed in the new Guidelines. These were developed using a novel approach to disease burden assessment, which has been applied to both recreational waters and urban air quality. This paper explains the scientific rationale and mathematical basis of the new approach, which is not presented in the WHO Guidelines for recreational waters.

Cities↗
PubMed2002

Sequence variations in the public human genome data reflect a bottlenecked population history.

Single-nucleotide polymorphisms (SNPs) constitute the great majority of variations in the human genome, and as heritable variable landmarks they are useful markers for disease mapping and resolving population structure. Redundant coverage in overlaps of large-insert genomic clones, sequenced as part of the Human Genome Project, comprises a quarter of the genome, and it is representative in terms of base compositional and functional sequence features. We mined these regions to produce 500,000 high-confidence SNP candidates as a uniform resource for describing nucleotide diversity and its regional variation within the genome. Distributions of marker density observed at different overlap length scales under a model of recombination and population size change show that the history of the population represented by the public genome sequence is one of collapse followed by a recent phase of mild size recovery. The inferred times of collapse and recovery are Upper Paleolithic, in agreement with archaeological evidence of the initial modern human colonization of Europe.

Databases, Nucleic Acid↗
PubMed2002

The matrix coalescent and an application to human single-nucleotide polymorphisms.

The "matrix coalescent" is a reformulation of the familiar coalescent process of population genetics. It ignores the topology of the gene tree and treats the coalescent as a Markov process describing the decay in the number of ancestors of a sample of genes as one proceeds backward in time. The matrix formulation of this process is convenient when the population changes in size, because such changes affect only the eigenvalues of the transition matrix, not the eigenvectors. The model is used here to calculate the expectation of the site frequency spectrum under various assumptions about population history. To illustrate how this method can be used with data, we then use it in conjunction with a set of SNPs to test hypotheses about the history of human population size.

Data Interpretation, Statistical↗