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t 1444 of urease; al1 these specimens yielded'a bavy growth of Cpylmid,k One-third'oftests were positive by 3 h and half.by 6 h: The advantage ofthis rapid test is the achievement ofadiagnais of C pyiaradis gastritis on the same day that patients attend for endoscopy, thus avoiding a second hoapital appointment. We have found' this very usefitl for the enrolment of patients into a therapeutic trui comparing medications. We rAaok' our colW gues for otxainrnt the bwpq umpla. Dep.rtmmr d MettidA4crabel6p, . Dudlry. Ra.d'HBsp,,.b QIODNA A. M. MCNULiT. avmaiRE.mata7QH: It. WtsE I.1a.#tn" M-L. Tf+pp GN: Sc6,pDe. MEl Rnsn P1GM.. 2anm HG C.mprlob.ctenLkt:xpurm u tle.owca of pw.metnd boit6y ,uG.+malL Lr+v.19a4; u I)4a. omprbb.ctal 2. 0- R1J Manm SR. axr P. Raod ~ YPdrayn- by M- /..m.14aS; h 111. l. C~ ST. Co.mR Snsl't mwul tw demfiQw dmrmcal'.1,~ 2nd d Cmb.dgc c,.e.daa uet.v.rr M1s, 1975: ss. CAMPYLOBACTER PYLORIDIS IN PEPTIC ULCER StR,-We read with interest Dr Rathbone and'collagues' letter (May 25; p 1217) in response to our Apti120 report and apologise for our failtue to make it clear that all peptic ulcer patients were diagnosed by endoscopy and that the sen studied were collected before tratment. The antibody assays were performed undencode. The 50~memben of laboratory stafTdi&not undergo endoscopy (for obvious reasons) nor have they been lhbelled' as a reference group. Similar remarks apply to the childten's sera, which were a general collection referred'to out hospital for viral studies. The purpose of our, c'ommuntcation was solely tt report the difference found between these cnhorts.'I2te data encourage speculation asso a link between Ccmpylobacrn pylorrdir and peptic ulcer. The raised titra in well people rnay be due ttsymptomless infection, perhaps a carrier state-thu is not unknown in infectious diseases and' has provided a stimulus tt epidemtologically based studies. Rythbane et al'suggest that under some circumstances a specific gut IgM response might occur without either an IgA or IgG response. This is at odtlt with generally accepted mecha nisttss of gut immunity, which regard IgA as the fint irnmunogltbulin of response in rthe gut. t' J. KAuxoR B. DsYER FurfisW lhfectrw D,usss.H<apusl. WEE TEE Furfisld.:Ystrau 707a. AuaralK PETE0.f1CGRTHY antl Alfred HdapualPW,M JAN WATSON I I Z'HLn rL'A: Hr,ne R..lm-Y.p.rf 1t+t porr.unetwt tnn ~ Pan I; J P.dw:•19TJ; ak s17-w. LIFETILME PASSIVE SMOKING AND CANCER RISK SiR,-Dr Sandler and colleagua(Feb 8,,p312), present results in their table l sho..ing that odds ratios for overall cancer risk increase markedly in relation to the number of' household members who smoke, and this increase is similu for active smokers as for non- smokers. Professor Burch (April 13, p 866) comments that this similarity, leads to the paradoxical conclusion that the average effects of active stnoking and passive smoking must be equaliand opposite. In reply, Sandler and colleagues point out that this equality is in reality a superficial averaging of two findings-a greater odds ratio for non-smokers than smokers in relation to passive smoking as an adult, and a greater odds ratio for smokers than non-smokers in relation to passive smoke exposure in child- hood Surely, however, the latter finding is even more implausible than equality of effecr in smoken and non-smokers. On any plausible model, the relative effect of passive smoking should be greater in non-smokers, who starrfrom a smaller backgroundlevelr than in smokers. Mathematically, ifjl is the background level of risk in the absence of passive smoke exposure and d'the increment in risk resulting from passive smoke esposure, the odds ratio (Ji+dya will tend to be smaller the greater the value of p. M TFIE IADtCET, jtl'NE 22.1985 Sandler's findings are implausible in other respects-notably the large effect claimed for passive smoking for a number of ancen (breast, thyroid, lettkaemia/lymphotna) ~that are generally believed to have little or no relationship to active smoking-and attention must inevitably centre on ahe adequacy of the study methods used. The choice of controls used in this study, a ttsiinure of friends or acquaintattces of' patients and people randomly selected byy systematic telephone sampling, is certaihly unusual!and seems very open to question. Sandlu and colleagues admit that the study cannot be used to relate active smoking to risk of cancer,, since estimates will be biased by the similanty of active smoking habits of friends. Surely, since active atxl' passive smoking ue strongly cornlatedi bias in studying thrrelatiottship of passive smoking to risk of cancer will also arise. Btaa may also, anse because of the dllTerenez in method of appro.ch. 'Ibua, in a separate paper,' Sandler et ai note that the proponion of subjects ttot' answering questions on marital status was over three times greater in controli than in cases. If there are highly significant differences in the proportion of cenain questions being answered u all,,how does one know that there are nortiighly signifiant difTerettess in the way the passive smoking questiotts are dealt with? Given that sctive smokers receive substantial passive smoke exposure from their own agarates, it is a priori implausible that passive smoking should increase risk of cancers thau are not asaociated with active smoking. Seen in this light,,a mueh tmre appropriate analysis of Sandler't dita would be to treat patients with smoking-related cancers as casa and patients acith non-stnoking- related mncers aa controls. Calculations from data presented in table in of their Lanoa paper itxlicate that there is no significant relation between passive smoking and cancer risk if the data are analysed in this way. This is a more plausible firtding,.nd consistent with the results ofmy 1984 reviewi which concluded that there is as yet no convincing evidence that passive smoking results in any material risk of serious health ha2ards. P. N. lu< k+mo -d Campunna. L3 4 25 Cidv Ru.d.. Sutcod Sunr SM2 sDG PETER N. LEE I. S.ndtv DP, E.ersn Rl. OJcos Al. Parw ®o4na ,e adultbood ad rsca.rut Aw 7 .EPi.rl 19e9.. 121: 37-48 2. t<t P4. P~.. ~mor,a{. la: cumauey0. sotrtµerc G, e& S.okme ted te. ro.R Pknum.. Vi. York..IN61. StR,-In their reply accompanying my letter of April 13 (p 866) Dr Sandler and colleagues misrepresent me as arguing that "smoking is protective". In fact I pointed to three possible interpretations of their findings and concluded that "active smoking has Uttle or no net carcinogenic action". The new breakdown oftheir findings does not eliminate the paradoxes implicit in the aggregate data. Dep.nmmtoi:.Medr•at Phwa. CitMral IndltmiM. u.m tsl oE!e P. R. J. &utteH BENZTROPINE I1VHI33ITS TOXICITY OF MPTP ISl MICE S[R,-TAe discovery thar MPTP (1-methyll4-phenvl-l,2,3,6b tetnhvdropyridine) causes irreversible parkinsonism in man and otherpriantes has provided new clues as to the cause of Parkinson!s disase.,-IZte ability of MPTP to produce a relatively specific destruction of dopamutergic nigrostriatal!neurons can be prevented by inhibitors of the enzyme manoamine ozidase B, including deprenyl;, in priautal'a and mice.3 Deprenyl (selegiline hydrochloride) has been in use in, Etuope for some ytars as an adjunct to levodopa treatment because of its ability to inhibit dopamine catabolism in the brain. Now it is suggested that early treatment with deprenyl might slow or even preventprogression of Parkinson's disease by preventing toxicity of some MPPP-like substance conceived as responsible for Parkinson's disease. MPTP is not neuroto:ic; its oxidation product MPP' (1-methyl- 4-phenylpyridine) is.4 MPP' accumulates in nigrostriatal neurons via the dopamine neuronal uptake system; MPP' uptake into rat str¢atal!synaptossomes is inhibited by dopamute uptake inhibitors