Tobacco Documents Online

3 convincing. In conclusion, this study does not clearly demonstrate a clear effect of ETS exposure in nonsmokers on risk of NPC, and the overall evidence remains far from convincing. P N Lee 16.1.01. Reference List 1. Yu MC, Mo CC, Chong WX, Yeh FS, Henderson BE. Preserved foods and nasopharyngeal carcinoma: a case-control study in Guangxi, China. Cancer Res 1988;48:1954-9. 2. Vaughan TL, Shapiro JA, Burt RD, Swanson GM, Berwick M, Lynch CF, et al. Nasopharyngeal cancer in a low-risk population: defining risk factors by histological type. Cancer Epidemiol Biomarkers Prev 1996;5:587-93. 3. Yu MC, Garabrant DH, Huang TB, Henderson BE. Occupational and other non-dietary risk factors for nasopharyngeal carcinoma in Guangzhou, China. Int J Cancer 1990;45 :1033-9. 4. Cheng Y-J, Hildesheim A, Hsu M-M, Chen I-H, Brinton LA, Levine PH. Cigarette smoking, alcohol consumption and risk of nasopharyngeal carcinoma in Taiwan. Cancer Causes Control 1999;10:201-7. 5. Yuan J-M, Wang X-L, Xiang Y-B, Gao Y-T, Ross RK, Yu MC. Non-dietary risk factors for nasopharyngeal carcinoma in Shanghai, China. Int J Cancer 2000;85:364-9.

2 simultaneously fitted for active smoking, parental smoking for smokers and for parental smoking for nonsmokers. Such an analysis would not necessarily give the same results. Why the estimated effect (after adjustment for diet) should be somewhat greater for parental smoking in nonsmokers than for active smoking (2.28 vs 1.82) is difficult to explain, especially bearing in mind the much higher exposure to smoke constituents inthe active smokers. There are four limitations of the study and the paper that merit comment: 1) The analysis and presentation is very limited. There is no attempt to obtain any information on dose-response relationships. Furthermore, one is given no background data on the numbers of cases and controls subdivided by whether they smoked and whether they were exposed to passive smoking in childhood. Results are also not given for the sexes separately. 2) The possibility of recall bias exists given the subjects knew the diagnosis when they answered the questions. 3) Only 282 of 530 identified cases were interviewed, partly because of non-response but mainly because many had died or were too ill. The study is not of cases interviewed soon after the cancer was diagnosed, but over-represents cases who survive better. Factors associated with a propensity for better survival could, in this study, be wrongly interpreted as being factors associated with disease incidence. Also there was a moderate refusal rate (10%) among the controls, and this was noted not to be random, being higher in affluent neighbourhoods. Again the possibility of selection bias exists. 4) The authors state that their findings "confirm the finding of Yu et al' that exposure to parental smoking during childhood plays a role." However that paper did not report results for nonsmokers, and three studies that didZ-" found no association ofNPC with any index of ETS exposure. A further study'reported an association in nonsmoking women, not in nonsmoking men but, as I discuss elsewhere in Review 1113, this is far from

I REVIEW 1135 Subj_ect ref 8b g6a CONFIDENTIAL "Nasopharyngeal carcinoma in Malaysian Chinese: occupational exposures to particles, formaldehyde and heat R W Armstrong et al International Journal of Epidemiology (2000), 29, 991-998 This paper describes the results of a study conducted in Malaysian Chinese in 1990-92 involving 282 cases (195 male, 87 female) of histologically confirmed squamous carcinoma of the nasopharynx (NPC) and 282 individually age and sex matched population controls. Data were collected on occupational history (in a very detailed manner), diet, alcohol consumption, tobacco smoking and childhood exposure to parental smoking. The authors report that history of active cigarette smoking for more than 6 months was associated with NPC, citing an odds ratio of 1.66 (p=0.012) in the text on page 993, but odds ratios of 2.86 (95% CI 1.42-5.76) unadjusted for diet and 1.82 (0.78-4.23) adjusted for diet in Table 2. These somewhat conflicting results suggest that dietary differences between smokers and nonsmokers explain a substantial part of the excess risk associated with active smoking. The text on page 993 also notes that after adjustment for active cigarette smoking, exposure to passive parental smoking during childhood was also associated with NPC, citing an odds ratio of 1.54 (p=0.040) which presumably applies to smokers and nonsmokers combined. In Table 2 they resent the results of more detailed analyses, which report odds ratios, adjusted for diet, of 0.74 (0.34-1.59) for parental smoking for smokers and 2.28 (1.21-4.28) for parental smoking for nonsmokers, odds ratios which show significant (p=0.028) interaction between the effects of active smoking and parental smoking during childhood. It is not clear to me that in fact the estimate of 2.28 was actually based on an analysis restricted to nonsmokers, as it should be for conventional assessment of ETS effects. It seems quite likely that in fact Table 2 presents the results of a single analysis based on the whole study population in which terms were