A graphical analysis of the interrelationships among waterborne asbestos, digestive system cancer and population density

Our plain-English summary of A graphical analysis of the interrelationships among waterborne asbestos, digestive system cancer and population density, by M.E. Tarter, R.C. Cooper, W.R. Freeman (Environmental Health Perspectives, 1983).

The study

• Authors: M.E. Tarter, R.C. Cooper, W.R. Freeman
• Journal: Environmental Health Perspectives
• Published: 1983;53:79-89
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Five statistical procedures were used to partial the correlation between waterborne asbestos and digestive site cancer for the putative effects of population density. These include: analysis based on a data subset with roughly homogeneous population density; standard residual analysis (partial correlation); conditional probability integral transformation; analysis based upon ranked data, and use of logarithmic transformation. Nonparametric regression graphical techniques are applied to examine the nature or shape of the asbestos-cancer dose-response curve. Evidence is presented that suggests that there is considerable difference between analyses involving nonhigh-density tracts and non-San Francisco tracts. Evidence is also presented that the modal-type nonparametric regression curve forks or bifurcates when adjustment is made for population density.

In plain English

This article was a statistical reanalysis of data from an earlier study (Cooper et al., 1979) of asbestos in drinking water and cancer in San Francisco Bay Area census tracts. It tested whether population density explained the reported link between waterborne asbestos and excess digestive cancer in white males (observed minus expected cases). Asbestos was measured in fibers per liter; no fiber type was named. Across all tracts the correlation was 0.241. In low to moderate density tracts, with one outlying tract removed, it was 0.194. After statistical adjustment for population density in several ways, correlations ranged from 0.133 to 0.171. In 323 tracts outside San Francisco, the correlation with excess cancer fell to a non-significant 0.05. In the 99 San Francisco tracts alone it was minus 0.114, also not significant. The authors judged that the significant relationship came largely from low to moderately populated San Francisco tracts, and cautioned that their findings may not reflect a causal connection. They also concluded that the relationship came more clearly into focus once population density was taken into account.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Statistical reanalysis (follow-up investigation) of census-tract-level data from an earlier study, using correlation, partialling (adjustment), rank and log transformations, and nonparametric regression
• Who was studied: 426 census tracts from the Cooper et al. (1979) San Francisco Bay Area study. The outcome was white male all digestive site cancer per tract over a 6-year period. Subsets were 288 low to moderate density tracts, 323 non-San Francisco tracts and 99 San Francisco tracts.
• Exposure: Waterborne asbestos in drinking water, measured as asbestos exposure in fibers per liter ("gross mean"). Fiber type not specified.
• Main results:
  • For the entire data set of low, medium and high-density tracts, the correlation between asbestos exposure and excess morbidity was 0.241.
  • After removing all high-density tracts and one outlying tract, the correlation between asbestos exposure and excess cancer morbidity was 0.194.
  • The authors judged that excluding highly populated tracts would not change the original study's principal finding of a significant relationship between waterborne asbestos and digestive tract cancer.
  • In the low to medium density tracts, the nonparametric regression curve appeared to plateau at 27,500,000 fibers/L and 0.51 excess cases per census tract over a 6-year period.
  • After adjusting excess morbidity for population density by standard residual (partial correlation) analysis across all 426 tracts, the correlation was r = 0.171, significant at the 0.01 level.
  • With the conditional probability integral transformation adjustment, the correlation with asbestos exposure was r = 0.133.
  • With log-transformed and ranked population density adjustments, the correlations were r = 0.157 and r = 0.143.
  • In the 323 non-San Francisco tracts, the correlation between asbestos exposure and observed white male all digestive organ morbidity was r = 0.136.
  • In the 323 non-San Francisco tracts, once expected morbidity was subtracted, the correlation between asbestos exposure and excess morbidity dropped to a non-significant r = 0.05.
  • The authors attributed the significant relationship largely to low to moderately populated tracts located in San Francisco.
  • Among non-San Francisco tracts split at 3.6 million fibers/liter, the excess cancer frequency curves for the low-exposure group and the high-exposure group (estimated from only 45 observations) had almost the same mean, variance and shape.
  • Within the 99 San Francisco tracts alone, the correlation was negative (r = minus 0.114) but not significant.
  • After adjustment for population density using ranked data, the high-exposure tracts appeared to be made up of two distinct subpopulations.
• The authors' conclusion: The authors concluded that, rather than being an artifact of population density, the relationship between asbestos levels and excess cancer morbidity was brought more clearly into focus once population density was taken into account. They also cautioned that this may not reflect a causal connection.
• Limitations the authors state:
  • The authors stated that the finding may have nothing to do with a causal connection between asbestos and cancer.
  • The authors stated that the pattern may be a coincidence of higher-cancer tracts clustering in the part of the Bay Area with high exposure levels.
  • There were very few high-exposure tracts among the low to medium density tracts.
  • The authors stated it was too early to assess the statistical significance of the conditional probability integral transformation result.
  • The bimodal distribution of log population density questioned the assumed homogeneity of the low to moderate density tracts.

Topics

Medical terms in this study, explained in our Lexicon: Dose-response relationship.

Related studies

• Answers to some questions raised by the presentation on the graphical analysis of the interrelationships between waterborne asbestos, digestive system cancer and population density — M.E. Tarter (1983)
• Effect of population density on the results of the study of water supplies in five California counties — P.M. Conforti (1983)
• Additional comments on the study of the effect of population density on the results of the California Bay area study — P.M. Conforti (1983)
• Occupational asbestos exposure and digestive cancers - a cohort study — B. Clin, F. Morlais, et al. (2009)
• Digestive cancers and occupational asbestos exposure: incidence study in a cohort of asbestos plant workers — M. Boulanger, F. Morlais, et al. (2015)
• Incidence of digestive cancers and occupational exposure to asbestos — S. de La Provôté, N. Desoubeaux, et al. (2002)

Browse more research in Environmental Health Perspectives, or return to medical research.