After Enstrom/Kabat did the data get better, Professor Stanton Glantz says so.

Yes, but not significantly. I am sure most of you are aware of the Enstrom/Kabat BMJ published Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98.

The conclusions were “The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.”

Enstrom/Kabat based their findings on “118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits.”

CPS I stands for Cancer Prevention Study I and there is now CPS II. As Enstrom and Kabat had come up with all the wrong results they were denied access to CPS II, but I have a copy.  😉  Strangely published in 1997 when E/K had just completed CPS I, three out of the four categories say SHS does not cause lung cancer and one barely statistically significant.  One of the co-authors is Dr. Michael Thun, M.D., M.S. Vice President of Epidemiology and Surveillance Research, American Cancer Society.

I had forgotten I had this but in 2007 Professor Stanton Glantz replied to my email on relative risk and commented.

“The Enstrom study is just the most recent time that the tobacco industry has financed analyses of the old CPS-I dataset. All those analyses failed to detect an increased risk. The main problem with using that dataset (as the Cancer Society told Enstrom) was that it was collected at a time when there was no meaningful “unexposed” group. The later, CPA-II (sic) dataset has better exposure assessment and reveals effects.”

The comment that sticks out for me is:”Although generally not statistically significant, these results agree with the EPA summary estimate that spousal smoking increases lung cancer risk by about 20 percent in never-smoking women. Even large prospective studies have limited statistical power to measure precisely the risk from ETS.”

Environmental tobacco smoke and lung cancer mortality in the American Cancer Society’s Cancer Prevention Study. II.

Source

Epidemiology Division, Rollins School of Public Health, Emory University, Atlanta, GA, USA.

Erratum in

  • Cancer Causes Control 1997 Jul;8(4):675.

Abstract

Environmental tobacco smoke (ETS) has been classified as a human lung carcinogen by the United States Environmental Protection Agency (EPA), based both on the chemical similarity of sidestream and mainstream smoke and on slightly higher lung cancer risk in never-smokers whose spouses smoke compared with those married to nonsmokers. We evaluated the relation between ETS and lung cancer prospectively in the US, among 114,286 female and 19,549 male never-smokers, married to smokers, compared with about 77,000 female and 77,000 male never-smokers whose spouses did not smoke. Multivariate analyses, based on 247 lung cancer deaths, controlled for age, race, diet, and occupation. Dose-response analyses were restricted to 92,222 women whose husbands provided complete information on cigarette smoking and date of marriage. Lung cancer death rates, adjusted for other factors, were 20 percent higher among women whose husbands ever smoked during the current marriage than among those married to never-smokers (relative risk [RR] = 1.2, 95 percent confidence interval [CI] = 0.8-1.6). For never-smoking men whose wives smoked, the RR was 1.1 (CI = 0.6-1.8). Risk among women was similar or higher when the husband continued to smoke (RR = 1.2, CI = 0.8-1.8), or smoked 40 or more cigarettes per day (RR = 1.9, CI = 1.0-3.6), but did not increase with years of marriage to a smoker. Most CIs included the null. Although generally not statistically significant, these results agree with the EPA summary estimate that spousal smoking increases lung cancer risk by about 20 percent in never-smoking women. Even large prospective studies have limited statistical power to measure precisely the risk from ETS.

http://www.ncbi.nlm.nih.gov/pubmed/9051323

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3 Responses to After Enstrom/Kabat did the data get better, Professor Stanton Glantz says so.

  1. The main problem with using that dataset (as the Cancer Society told Enstrom) was that it was collected at a time when there was no meaningful “unexposed” group.

    So glantz is telling us that because everyone was exposed and it showed no effect on anyone it was a faulty study………….hmm! but yet when they do a study with a supposed unexposed group it suddenly shows an effect small though it is!

    That kinda tells me shs/ets has a protection built into it from exposure!

  2. Klaus K says:

    Dave – are you aware of the dose-response manipulation in the Cardenas 1997 paper? This line in the abstract is very misleading:

    “Risk among women was similar or higher when the husband continued to smoke (RR = 1.2, CI = 0.8-1.8), or smoked 40 or more cigarettes per day (RR = 1.9, CI = 1.0-3.6),”

    As Jim Enstrom has shown in his Lysenko-article, the Cardenas 1997 paper is a (peer-reviewed!) re-write of Cardenas’ disseration from 1995:

    Enstrom: http://www.epi-perspectives.com/content/4/1/11 – please check table 1 and the accompanied text. The wording of the Cardenas 1997 abstract you link to should have been:

    “Risk among women was similar when the husband continued to smoke (RR = 1.2, CI = 0.8-1.8), but lower, when the husband smoked 40 or more cigarettes per day (RR = 0.9, CI = 0.2-3.9),”

    … in order to reflect the truth.

    Nevertheless the misleading dose-response figures are presented in all official reports, like IARC monograph 83, 2004. This according to Enstrom: “In other scientific fields, the type of data manipulation done in Cardenas’ Table 4 would most likely be treated as a serious ethical violation.”

  3. Mark1957 says:

    Not statistically significant? Then why are we discussing it? This is spin and spin only. Any self-respecting scientist would not even engage with such argument.

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