Philip Morris
Review 729 Subject Ref 8b 'childhood and Adolescent Passive Smoking and the Risk of Female Lung Cancer'
Fields
- Author
- Lee, P.N.
- Area
- SCIENCE & TECHNOLOGY-NEUCHATEL/STORAGE BAYS
- Type
- SCRT, REPORT, SCIENTIFIC
- CHAR, CHART, GRAPH, TABLE, MAPS
- Site
- E21
- Named Person
- Chilmonczyk
- Jarvis
- Wang, F.L.
- Jarvis
- Request
- Stmn/R2-038
- Document File
- 2028443175/2028443875/Peter Lee
- Named Organization
- 26th Annual Meeting Society for Epidemio
- American Journal of Epidemiology
- Chinese Journal of Preventive Medicine
- Intl Journal of Epidemiology
- American Journal of Epidemiology
- Litigation
- Stmn/Produced
- Characteristic
- CONF, CONFIDENTIAL
- Master ID
- 2028443187/3224
Related Documents: - Date Loaded
- 05 Jun 1998
- UCSF Legacy ID
- mwj24e00
Document Images
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R~EVIEW 729 CONFIDENTIAL
Subject ref 8b
"Childhood and adblescent passive smoking
and the risk of female lung cancer"
F-L Wang et ali
International Journal of Epidemiology (1994), 23, 223-230
In a paper published in 1989 in the Chinese Jiournal of Preventive
Medicine (2_3, 270-273) entitled "Analysis of risk factors for female lung
adenocarcinoma iin Harbini: Indoor air pollution", the same leading author,
based on the same study, reported that "no significant association with
cigarette smoking and indoor passive smoking was found",
major attention
being given to strong relationships of risk of adenocarcinoma with high
coal consumption, indoor smog pollution, and low ceiling height of the
living room, for all' of which odds ratios reported exceed'ed 10. No
relative risks were presented for passiive smoking.
The present paper, results from which had previously beenicite&in a
paper presented at the 26th Annual Meeting of the Society for
Epidemiol'ogic Research at Keystone, Colorado in June 1993 (American
Journal of Epidemiology, 1993, 1'38, 639), reports by contrast a
significant relationship between risk of lung cancer and exposure to ETS
in childhood, though no relationship between risk of lung cancer and
exposure to ETS in adulthood. Among,the 55 case-control pairs who had
never smoked, the key findings are summarized~below:

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Exposure period
(age in yearsJ
Relative risk
95% confidence level
P
0-6 1.6& 1.1i5-13.33' 0.012
7-1'4 3'.401 1.08-12.69 0.019
15-22 2'.43 0.88-7'.33 0.066
23-30 0.93 0.38-2.25 NS
31-69 0.9'1 0.32-2'.53 NS
The paper is based on al 1:1' paired case-control study conducted in
H'arbin; in China in 1985-86. There were 114 cases ini all, aged 30-69, with;
their hospital based non-cancer controls matche& on hospiital, age (+51
years), residential area,, and lifetime smoking status (ever/never). The
55; pairs who had never smoked are of most importance with regard to
assessing possible effects of ETS'.
Points to note about the study and its findings include the
following:
(i) The controls included 18% with
cardiovascular disease and 22% with
respiratory infections. They will certainly not be representative
of the popul'.ation in terms of smoking habits (since smoking,is
associated'with prevalence of these conditions) and may not be
representative in terms of ETS exposure. It would have been
preferable to include only controls with diseases not associlated
with smoking.
(ii) A remarkably similar relationship between ETS andilung,cancer was
seen in the smoking pairs (n-59) and the non-smoking pairs (na55)i-
see Table 5. Given the relatively wide confidence intervals, I find
it surprising that the results are so similar. Thus, for example,
for the exposure period 0-6 years, the ratio of relative risks for
non-smoking to smoking pairs is as close to 1 as 1.08 despite the

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fact that the 95% confidence interval for this ratio is of order
0.2 to 5.6!
(iiii) Althoughiquite large numbers of relative risks are cited, which
inter aliia show a dose response relationship with ETS exposure in
childhood (see Tables 6 and 7), only the results tabulated above
(taken from Tabl'e 5) are based on never smokers, as is
conventional for ETS analyses.
(iv) Despite the 1',989 paper pointing, out huge relationships of
adenocarcinoma risk with high coal consumption, indoor smog
pollution,, and low ceiling height, and despite about half the
lung cancers cases studied being adenocarcinoma, it is quitee
remarkable that no consideration at all is given to the possible
confounding effect of these variables. Indeed there is no mention
at all in the paper of these variables having been recorded in the
study!!
(v) The discussion concerning other evidence relating childhood ETS
exposure to risk of lung cancer in; adulthood is totally misleading.
For example, the statement on p228 that "findings from
epid'emiological studies7'910,1727' have provided further evidence
for the effect of PS in early life on cancer risk in adulthood"
includes reference to some studies (Chilmonczyk; Jarvis) that do
not even provide data on cancer risk in adulthood. Furthermore,
there is no reference at alil to studies reporting no association,
let alone the fact that the overall published evidence provides no
indicationiwhatsoever of an association between ETS exposure in

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ctlildhood and risk of lung cancer in lifelong non-smokers., The
results fromi this study do not affect the overall pictlure.,
P' N Le e
24.5.94
