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Biomedical subjects

H B Newcombe

Publications and source records attributed to H B Newcombe.

14 recordsLinked to original sources
PubMed1991

Application of exact ODDS for partial agreements of names in record linkage.

Automated methods for linking records pertaining to the same individuals have in the past made only crude use of the name information. A perceptive filing clerk is more sophisticated because humans retain a lifetime memory of instances in which variant forms of names were employed interchangeably, and of synonyms that sometimes did not even resemble one another. This limitation of the machine can be rectified, but the body of knowledge required to serve as its memory must be large. The needed data have now been brought together on a suitable scale, from many past searches of Canada's Mortality Data Base. Described here are the development and use of the resulting tables of essentially exact discriminating powers (or ODDS) to do with comparisons of male given names. The aim is to reduce the proportion of ambiguously linked pairs of records requiring labor intensive clerical resolution. The tables are intended for general use in this country, and as a model for similar facilities appropriate to other populations.

Canada↗
PubMed1989

Discriminating powers of partial agreements of names for linking personal records. Part I: The logical basis.

Machines have difficulty when using people's names to link medical and other records pertaining to the same individuals because of nicknames, ethnic synonyms, truncations, misspellings and typographical errors. Present algorithms used to compute the discriminating powers (or ODDS) associated with partial agreements of names are based, inappropriately, on the degrees of outward similarity alone. They are particularly ineffective in dealing with names that look alike but are unrelated, and with related names that have little apparent similarity. A fundamentally different rationale is, therefore, proposed which, like the human mind, assesses the relatedness of two alternative forms of a name in terms of how often they are used, interchangeably in practice. This must be taken into account if the associated discriminating powers (ODDS) are to be correctly computed. A way of implementing this more precise approach is described and illustrated, using the given names on linked records from an earlier epidemiological study. This first study of two describes the logical basis for record linkage, a second one the empirical test.

Humans↗
PubMed1989

Discriminating powers of partial agreements of names for linking personal records. Part II: The empirical test.

The preceeding paper examined the logical basis of an exact way of calculating the discriminating powers of people's names when they only partially agree. The method has application to automated file searching and record linkage. The present account describes an empirical test of the approach. Use is made of some 2000 comparison pairs of male given names, obtained as a byproduct from an earlier linkage study. The test shows that exact value-specific ODDS can indeed be calculated for common names when compared with their accepted synonyms (e.g. JOSEPH versus JOE). Moreover, the use can be extended to include rare variants, by arranging these into groups defined in value-specific terms (e.g. as selected blocks in an alphabetically sequenced listing, or combinations of such blocks). A majority of all name comparisons may be handled in this manner. The added precision serves to reduce the numbers of records that are ambiguously linked and require labour intensive clerical resolution.

Humans↗
PubMed1988

Genetic disorders in children and young adults: a population study.

The data base of an ongoing population-based registry with multiple sources of ascertainment was used to estimate the present population load from genetic disease in more than 1 million consecutive live births. It was found that, before approximately age 25 years, greater than or equal to 53/1,000 live-born individuals can be expected to have diseases with an important genetic component. This total was composed of single-gene disorders (3.6/1,000), consisting of autosomal dominant (1.4/1,000), autosomal recessive (1.7/1,000), and X-linked recessive disorders (0.5/1,000). Chromosomal anomalies accounted for 1.8/1,000, multifactorial disorders (including those present at birth and those of onset before age 25 years) accounted for 46.4/1,000, and cases of genetic etiology in which the precise mechanism was not identified accounted for 1.2/1,000. Previous studies have usually considered all congenital anomalies (ICD 740-759) as part of the genetic load, but only those judged to fit into one of the above categories were included in the present study. Data for congenital anomalies are therefore also presented separately, to facilitate comparison with earlier studies. If all congenital anomalies are considered as part of the genetic load, then greater than or equal to 79/1,000 live-born individuals have been identified as having one or other genetic disorder before approximately age 25 years. These new data represent a better estimate of the genetic load in the population than do previous studies.

Adult↗
PubMed1987

Lung cancer mortality (1950-80) in relation to radon daughter exposure in a cohort of workers at the Eldorado Port Radium uranium mine: possible modification of risk by exposure rate.

A cohort study of 2,103 workers employed between 1942 and 1960 at a uranium mine in the Northwest Territories, Canada, was conducted. A total of 57 lung cancer deaths was observed (expected = 24.73, P less than .0001). There was a highly significant linear relationship between exposure and increased risk of lung cancer, giving estimates for the relative and attributable risk coefficients of 0.27 per working level month (WLM) and 3.10 per WLM per 10(6) person-years. These risk coefficients were substantially less than those estimated from the experience of miners in the Beaverlodge mine, which have previously been reported. Any biases in the present estimates are likely to have been upward, and therefore they probably represent an upper limit. The major difference between the two mine cohorts is in the exposure rate, since the Port Radium miners were exposed to much greater concentrations of radon daughters than the Beaverlodge miners. It is postulated that risk of lung cancer from radon daughter exposure may be modified by exposure rate, for which hypothesis there is some support from other epidemiologic data.

Humans↗
PubMed1986

Lung cancer mortality (1950-80) in relation to radon daughter exposure in a cohort of workers at the Eldorado Beaverlodge uranium mine.

A cohort study of 8,487 workers employed between 1948 and 1980 at a uranium mine in Saskatchewan, Canada, has been conducted. A total of 65 lung cancer deaths was observed (34.24 expected, P less than 10(-5)). There was a highly significant linear relationship between dose and increased risk of lung cancer giving estimates for the relative and attributable risk coefficients of 3.28% per working level month (WLM) and 20.8 per WLM per 10(6) person-years. Age at first exposure had a significant modifying effect on risk. The interaction of exposure with age at observation fits a relative risk model well. The similarity of these results to a recent study of Swedish iron miners with similar levels of relatively low exposure suggests that exposure to radon daughter products may be a major contributory factor to lung cancer occurring among nonsmokers in the general population. The results also reinforce concerns as to the appropriateness of present occupational exposure standards.

Age Factors↗
PubMed1979

Measuring the public health impact of the aneuploidies.

If the protection of man against mutagenic agents in general, and against those that cause aneuploidies in particular, is to have an increasingly rational basis with the passage of time, quantitative or at least semiquantitative assessments of risks are needed. These should take into account both the likely numbers of induced cases and the likely severities of the different conditions. In the past, quantitative data relating to severity have been limited or nonexistent, but the data sources exist by which follow-up studies may be carried out to determine age-specific and cumulative risks of hospitalization and death, the durations of hospital stays, and the economic burden to society which these represent. To illustrate the use of such sources, the cumulative risks of death in children with anomalies of the autosomes and of the sex chromosomes, over the first 19 years of life, are compared with those for other kinds of hereditary and environmentally caused handicaps that are reported in that age group.

Adolescent↗
PubMed1978

Problems or assessing the genetic impact of mutagens on man.

Available human data, of the kinds needed to assess the genetic harm to man from possible changes in his mutation rate, currently suffer from major limitations. In particular there is uncertainty about a) the total amount of hereditary disease, b) the fraction of this that is mutation-related and therefore likely to be increased in frequency as a result of exposures to elevated levels of environmental mutagens, and c) the severities of the mutation-related conditions and the collective public health importance of any anticipated increases in their frequencies. Standards of protection against environmental mutagens cannot be set on the basis of laboratory data alone, and more effort on the part of geneticists will need to be directed towards quantitative assessment of the impact of the mutagens in terms of human disease. The needs for relevant human data, and various deficiences in the statistical information that is currently available, are discussed.

Abnormalities, Multiple↗