COMMENT ON "HEALTH EFFECTS OF EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE"

CHAPTER 7
Carcinogenic Effects

7.3.2 Cervical Cancer

This report claims that "The epidemiological and biochemical evidence suggest that exposure to ETS may increase the risk of cervical cancer in nonsmokers" (7.5 Chapter Summary and Conclusions, page 7-52). We categorically reject this claim on the grounds that smoking does not cause cervical cancer even in active smokers. The statistical association between smoking and cervical cancer has been conclusively demonstrated to be the result of residual confounding. References: Bosch FX, de Sanjos S, Mu$oz N. (letter re Phillips & Davey Smith). Int J Epidemiol 1994 Oct;23(5):1100-1101. Phillips AN, Davey Smith G. Cigarette smoking as a potential cause of cervical cancer: Has confounding been controlled? Int J Epidemiol 1994 Feb; 23(1):42-49. Phillips AN, Davey Smith G. (reply to Whidden). Int J Epidemiol 1994 Oct;23(5):1100. Whidden P. (letter re Phillips & Davey Smith). Int J Epidemiol 1994 Oct; 23(5):1099.

This report also repeats the spurious claim that "Among women with cervical dysplasia, higher levels of mutagenicity in the cervical mucus of smokers compared to nonsmokers have been found (Holly et al., 1986)," and deceptively fudges that "this result has not been observed in studies of women without cervical dysplasia (Schiffman et al., 1987; Holly et al., 1993)." In fact, Schiffman (1987) admitted that bacterial infection was the real cause of the findings of mutagenicity. And Holly (1993) found that "About 4% of smokers and 8% of nonsmokers had positive mutagenicity test results."

7.4.1 Breast Cancer

This report states that "A large number of epidemiologic studies have investigated the association of active smoking and risk of breast cancer... and the results are inconclusive" (page 7-35). That there is no evidence of increased risk would be a better description. And, with no evidence of increased risk in active smokers, it should not merely be said that "There is insufficient evidence to draw any conclusion regarding the relationship between ETS exposure and cancers of the... breast ... at this time" (7.5 Chapter Summary and Conclusions, page 7-52), but that there is no ETS risk. Or is the anti-smoking movement going to attempt to make breast cancer the second known "disease with a "first-pass miss" phenomenon, affecting only the second-hand smoker?" (See Chapter 6, 6.1.3 Otitis Media (children)). Perhaps they believe that "If at first you don't succeed, try, try again."

7.4.2 Stomach Cancers

This report claims that "The epidemiological evidence in support of active smoking as a risk factor for stomach cancer is equivocal" (page 7-38). In fact, the International Agency for Research on Cancer (IARC) now considers Helicobacter pylori infection a major cause of stomach cancer. Also, there is good evidence that smokers and passive smokers, because they are socioeconomically disadvantaged with respect to non-smokers, are more likely to be infected by HP, and it can be presumed that therefore, the 1982 Surgeon General and 1986 IARC falsely blamed smoking for stomach cancer that was really caused by Helicobacter pylori. Yet this report fails to even mention the existence of Helicobacter pylori. There is no good excuse for this kind of slovenly research, only bad ones, such as anti-smoker conspiracy to deceive the public. And, with no evidence of increased risk in active smokers, it should not merely be said that "There is insufficient evidence to draw any conclusion regarding the relationship between ETS exposure and cancers of the... stomach ... at this time" (7.5 Chapter Summary and Conclusions, page 7-52), but that there is no ETS risk.

7.4.5 Lymphomas and Non-Hodgkin's Lymphomas

H pylori is also linked to primary gastric lymphoma. References: Bayerdrffer E, Neubauer A, Rudolph B, Thiede C, Lehn N, Eidt S, Stolte M, for MALT Lymphoma Study Group. Regression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure of Helicobacter pylori infection. Lancet 1995 Jun 24;345(8965):1591-1594. Boot H, de Jong D, van Heerde P, Taal B. (letter re Bayerdrffer) Role of Helicobacter pylori eradication in high-grade MALT lymphoma. Lancet 1995 Aug 12;346(8972):448-449. 5 cases. Cammarota C, Fedeli G, Montalto M, Tursi A, Renzi C, Papa A, Veccio FM, Branca G, Certo M, Gasbarrini G. Mucosa-associated lymphoid tissue in Helico- bacter pylori infection: frequency and response to therapy. Am J Gastroenterol 1994 Aug;89(8):1356 abstr 284. "Lymphoid follicles were found in 22 Hp+ pts (33.3%) and in 3 Hp- pts (8.33%) (p=0.005 chi-square). 10 treated, Hp & MALT disappeared. Also case report, abstr 285. Parsonnet J, Hansen S, Rodriguez L, Gelb AB, Warnke RA, Jellum E, Orentreich N, Vogelman JH, Friedman GD. Helicobacter pylori infection and gastric lymphoma. NEJM 1994 May 5;330(18):1267-1271. 2 cohorts, Kaiser Permanente & Janus (Norway), 230,593. 33 gastric, 31 non-gastric lymphoma. Gastric, HP 6.3 (2.0-19.9) caused 66% of cases. Other NHL sites 1.2 (0.5-3.0). "Had the ELISA for H. pylori been 100 percent sensitive and 100 percent specific, the odds ratio of lymphoma would have been approximately 25 percent higher." "Small intestinal lymphomas that develop from immunoproliferative small intestinal disease have previously been linked to bacterial infection. Other extranodal lymphomas (i.e., thyroid and salivary gland) have been linked to chronic inflammatory processes." Parsonnet J, Hansen S, Friedman GD. (reply to Mohandas). NEJM 1994 Sep 15;331(11):746. "low-grade lymphomas can be cured with therapy directed against the organism" [H pylori]. Weber DM, Dimopoulos MA, Anandu DP, Pugh WC, Steinbach G. Regression of gastric lymphoma of mucosa-associated lymphoid tissue with antibiotic therapy for Helicobacter pylori. Gastroenterol 1994 Dec;107(6):1835-1838. 1 case hx. Wotherspoon AC, Ortiz-Hidalgo C, Falzon MR, Isaacson PG. Helicobacter pylori-associated gastritis and primary B-cell gastric lymphoma. Lancet 1991 Nov 9;338:1175-1176. 450 HP gastritis, 110 gastric MALT lymphomas. "In the salivary gland and thyroid, MALT is acquired as a component of autoimmune disorders such as Sjogren's syndrome and Hashimoto's thyroiditis, and are necessary precursors for development of MALT lymphoma in these organs." Wotherspoon AC, Doglioni C, Diss TC, et al. (abstr) Regression of primary low-grade B cell gastric lymphoma of mucosa associated lymphoid tissue type after eradication of Helicobacter pylori. Lancet 1993;342:575-577.