Aryl hydrocarbon hydroxylase in asbestos workers

Our plain-English summary of Aryl hydrocarbon hydroxylase in asbestos workers, by S.M. Naseem, P.V. Tishler, H.A. Anderson, et al (The American Review of Respiratory Disease, 1978).

The study

• Authors: S.M. Naseem, P.V. Tishler, H.A. Anderson, I.J. Selikoff
• Journal: The American Review of Respiratory Disease
• Published: 1978;118(4):693-700
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy.

Abstract

Aryl hydrocarbon hydroxylase (AHH) activity and inducibility were studied in the lymphoblasts of 47 asbestos workers and 31 control subjects. Mean inducibility (3-methylcholanthrene [MC]-or dibenz(a,h,)anthracene [DBA]-induced divided by basal enzyme activity) was greater in the occupationally exposed subjects than in the control subjects. The estimated estimated change in mean value (+/- SE) of MC inducibility was 0.88 +/- 0.21 (P less than 0.001), and that of DBA inducibility was 1.59 +/- 0.56 (P less than 0.01). Differences in inducibility values were particularly apparent in 12 pairs of spouses, in all of whom the inducibility values of the occupationally exposed subjects exceeded those of their spouses. The differences in inducibility of AHH resulted from increases in induced activity, not from any appreciable change in basal activities. They were independent of subject age, sex, smoking status, year of first exposure to asbestos, yield of lymphoblasts, or the rate of blastogenesis as measured by the incorporation of tritiated thymidine into nucleic acid. Increased AHH inducibility may bear some relation to the greatly increased risk of bronchogenic carcinoma in asbestos workers who smoke cigarettes.

In plain English

This laboratory study measured an enzyme, aryl hydrocarbon hydroxylase (AHH), in cultured white blood cells from 47 asbestos-exposed men and 31 controls. The men were insulators in New York City and Newark, N.J., or former asbestos factory workers in Paterson, N.J. Forty-one had X-ray evidence of asbestosis. None had lung cancer when studied, though one had undergone partial lung removal for it 4 years earlier. Controls were 20 relatives (12 spouses) and 11 clinic employees. Inducibility (the enzyme's response to two test chemicals, MC and DBA) was higher in the exposed men. The estimated differences, with standard errors, were 0.88 plus or minus 0.21 for MC (P less than 0.001) and 1.59 plus or minus 0.56 for DBA (P less than 0.01). Baseline activity did not differ significantly. In all 12 spouse pairs, the worker's value exceeded the spouse's. Age and smoking status did not explain the differences. The authors suggested this may bear some relation to the high lung cancer risk of asbestos workers who smoke, but cautioned it could not be assigned directly and solely to asbestos.

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: Laboratory comparison of enzyme (AHH) activity and inducibility in cultured lymphoblasts (white blood cells) from asbestos-exposed workers and from control subjects, each sampled once
• Who was studied: The exposed group was 47 men, aged 33 to 78. Forty-one had radiographic evidence of asbestosis. None had lung cancer at the time of study, although one had had a partial pneumonectomy for lung cancer 4 years earlier. The 31 controls (11 men, 20 women) were 20 relatives of the workers (12 of them spouses) and 11 employees of the health clinic the workers attended. Blood was drawn on six examination dates in 1976 and 1977.
• Exposure: Occupational asbestos exposure. The men were members of the Heat and Frost Insulators and Asbestos Workers union in New York City and Newark, N.J., or former employees of an asbestos factory in Paterson, N.J. Fiber types are not specified. All had begun exposure at least 14 years before the study, and 45 more than 20 years before.
• Main results:
  • AHH inducibility was higher in the asbestos-exposed subjects than in the controls. The estimated difference in mean, plus or minus its standard error, was 0.88 plus or minus 0.21 for MC inducibility (P less than 0.001) and 1.59 plus or minus 0.56 for DBA inducibility (P less than 0.01).
  • The differences in inducibility did not result from significant changes in basal (uninduced) enzyme activity.
  • Induced enzyme activity was greater in the asbestos-exposed group for both MC and DBA. The difference was significant for MC-induced activity (+0.113 plus or minus 0.047, P less than 0.025).
  • In all 12 spouse pairs, the asbestos-exposed worker's inducibility ratio was greater than the spouse's.
  • Inducibility in the spouse controls, who were probably exposed to lesser amounts of asbestos at home, did not differ significantly from that of the unrelated controls.
  • Smoking status made no significant difference to inducibility in either the exposed group or the control group.
  • The exposed group was older than the controls (mean age 56.1 plus or minus 9.5 years versus 48.4 plus or minus 14.0 years, P less than 0.025). However, no significant age-related differences in AHH were found within either group.
• The authors' conclusion: The authors concluded that AHH inducibility appeared to be increased in asbestos-exposed workers. They stated that this may bear some relation to the greatly increased risk of bronchogenic carcinoma in asbestos workers who smoke cigarettes.
• Limitations the authors state:
  • The data cannot definitively assign the effect on AHH directly and solely to asbestos.
  • The results conflict with the few animal studies of this relationship, so conclusions about cause and mechanism are premature.
  • The subjects may have had inherently high AHH inducibility before their asbestos exposure.
  • Environmental factors that are not yet recognized may be involved.
  • The relation of inducibility to the total duration of asbestos exposure could not be analyzed.
  • Thymidine incorporation was measured at only one examination. Large variances and few observations meant that the differences found there were not significant.

Topics

Medical terms in this study, explained in our Lexicon: Bronchogenic Carcinoma.

Related studies

• Aryl hydrocarbon hydroxylase induction in mitogen-stimulated lymphocytes by benzanthracene or cigarette tars adsorbed to asbestos fibers — T.L. McLemore, W.T. Jenkins, et al. (1979)
• Effect of asbestos fibers on aryl hydrocarbon hydroxylase and aminopyrine N-demethylase activities of rat liver microsomes — C. Kandaswami, M. Rahimtula, et al. (1986)
• Worker exposure to asbestos during removal of sprayed material and renovation activity in buildings containing sprayed material — N.W. Paik, R.J. Walcott, et al. (1983)
• Effects of particulate matter on rates of membrane uptake of polynuclear aromatic hydrocarbons — D.R. Bevan, S.C. Riemer, et al. (1981)
• A summary of asbestos fibre counting experience in seven countries — G.W. Gibbs, P. Baron, et al. (1977)
• Industrial trials with the Vickers M88 rapid asbestos fibre counter — A.D. Jones, R.W. Gale (1982)

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