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lndian J Med Res [B] 96, Octobcr 1992, pd,2$2-287 NaS1 CC be ji1i5 t~tst~ ~. , t7~tN')~ pro~ w U S, Gl~de~. %W vh Serum lipids L& lipoprotein profiles of cigarette smokers 5" passive smokers ' . , - :J. Whig, C.B: Singh, G.L. Soni' dt A.X. Bansal•• Departmeat of Medicine, Dayatarld Medreil ColltP & Xotprtal; •Dcparuatttt of Microbioiogy, Panjab AQticttltural University, Ludhiana & ••Departmrnt of B;ocbemistry, GGS Medical College, Faridrot Acespted July 3, 1992 I M f 4aSS<890 ~~O'WON Setum Uptds snd Upoprotelos of $0 acttre .ad passl.e smokets were eontpared wtt6 le.eis in 25 ooatrd sYk/eets. Aetfre sawkSa= resWtld in at1 iserease in tOtal tholesl.rol (Tr) mW irlslyeerid• (Tw) Y eompared to cwatrol gottp. The paaslre stsokers also sbowad mlatd.ely bigher lesk but t!e d7.et was eot siVtlio,at. Aedvs sttTokiat ratied ttie low dettslty Upoptwtda ebo4es1rtal (LDL) aod wa7 b+r dmslq Mpopeotdn eboUesterol' (VLDL.) ir.eLt wherss 61s11 deashy tipopeoidr tAo3eaeror (H'DL) soeteat was lowered, thus resulting ia deQ.ased rtatJas of HDWr. and HDZ./LDL. The paastre amoken aJ.o sbowes a1YEhtlY higher levels of LDi" and VLDL but lower levels of HDL., a.d a bwet KDL/LDL ratlo. 0or Cadinp sauet thal smokln8 ahen the .erue. Uplds aed Upoproteies aed taeae chantes an related to the duratloo aed amoimt of amoklh=. Large prospective epidemiological studies have showtt strong association between cigarette amokiag xnd several diseases. The potential of developing eoronary artery disease in male eigaret?e smokers is approximately 2.14 times greater than in non-smokers'. 'The risk of infar,;ion for both men and women is eorrslated with the number of cigarettes smoked daily3. Asi<-~cimiosi oi cigarette smoking, aerum lipoproteins and eoronary artery disease has been repoeted by teveral workets'' `. Variutat reports suggest that involuntary in- halation of cigarette smoke by non-smokers causes disease, most notably lung diseases". The ubiquitousness of tobacco smoke in homes, work places and public areas maka exposure to environmenta] tobacco smoke unavoidable". 2E2 Asymptomatic non-smokers who are ehronieitly exposed to smoke contaminated air may develop small airway dy3funr:tion"10. Several studies suggest that passive smoking increaaes the risk for lung cancere and aggravates angina peetorisll. Very little attention has been paid to the effect of passive smoking on serum lipids and lipoproteins. In view of the fact that large population in India is exposed to passive smoldng, the present study has been undertaken to know the efTeet of passive smoking on serum lipids, and. lipoproteina compared to that in chronic amQkers and control subjectc. 1Kates{al ~ Methods A total of 7S subjects of tniddlb income group known to perform moderate physieal activity were ..~--~

WHIG et a1: SERVM LIPIDS iAt SMOXERS included iri the present study. Twenty five males who smoked more than 15 cigarettes a day for more than 5 consecutive years were taken as am4kcrs, 25 non-smokers who were ehronically ezpassd to smoke of atleast 20~eigarettes a day, in their homes and/or in work places in elosed environment of room (s)/ office (s) were taken as passive smokers. Similarly, 25 Inale non-smokers matched for age and physical activity were taken as control; these individuals lived with strict non- smokers at home and also ia their work plat:e. Subjects suffering from diseases which are known to alter the lipid profilc such as diabetes mcllitus, uremia, nephrotic syndrome, hypo- thyroidism, hypcrthyroidism and acromegaly, were excluded from the study. Alcoholics and subjects on steroids were also ercluded from the study. 'fen ml of blood sample was collected after an overnight fast from each subject. The serum was separated by centrifugation at 3000 rpm for 10 min and was used for lipid and lipoprotein analysis. Total lipids were extracted from the serum1i and serum total cholesterol (Tc)D,serum triglycerides (Ti)1• in the extracted lipids, HDL,». LDL, and VLDL" were estimated. Student's 't' test was used for analysis of the data. Results Table I shows the comparison of T, and Tg of smokers and passive smokers with that of eontrol subjects. Significa.ntly higher levels of Te (P<0.05) 2i3 and T, (P<0.01) were observed in smokers whereas the passive smokers sbowed marginally higher levels but the values were statiatically insignificant when compared to controls. The active smokers had significantly higher levels of LDL. (P<0.0I) and VLDL (P<0.05) t&an controls, whereas these levels of passive smokers showed no significant difference (Table II). Tbe levels of HDL. in both groups were not significantly different when compar+ed with control. The ratios of HDLr/T, and HDL./LD" of smokers were eignificantJy lower (PC0.01) as compared to control group. Passive smokers, however, showed significantly lower (PC0.05) ratio of HDI../LDLc only (Table III). Table TV shows the Tt and Tr of moderate and heavy smokers of different durations. Moderate smokers (smoking 15 to 20 cigarettes/day) who were smoking for more than 15 yr and heary smokers (smoking more than 20 cigarettes/day) irrespective of the duration showed signifieaatly higher levels of T, (P<0.05) and Te (P<0.01) when compared to controls. LDL, of moderate and heavy smokers were also si"icantly higher (PC0.05): irrespective of duration of smoking, whereas no significant differencss were observed in HDL. of both groups as compared to control group (Table V). The levels of VLDL. were also significantly higher in moderate smokers who smoked for more thaa 15 yr and heavy imokers. Irrespective of the duration of smokiz4 both heavy and moderate smokers had significantly Tabl. I. Comparuon of tot.I cholaterot (T,) and trialycrrides (T,) of emol¢cn and palaNre smoken +.izh eaasmaker aontroia T, (ragldl) T, (mg/d1)' Range Mean ± SE Rang; 1rlcan t SE Co ntrol 1 A0-270 197.72 W126 100.16 (ns2S) ± 7.04 t 2" Smokers It0-300 233.21 96-1166 131.32 (n = 25). t S.B3•• t 3.7'7• Passire tmohers 146-2b6 202.00 a0• 131 106.00 (n=23) t4.62 S 2.76 P vaiun. •<0.01; ••<O.OS. at compared to controls

INDIAN J MED RES [B), OCTOfBR 1992 Tsbla 11. Cotaparizon of caolaste:ol of lipoprotcin fraezions in umoken aad pwive smokers with aontrols 2i4 HDL (maJdl), LDL (mi/dl) vLDL (mj/dA Range Meaa * SE Raape Maaa S SE Ran6c )Aeaa 3 SE Control it-74 53.2s 73-174 1I7:6i 17-2'9 21.76 (ai2S) tL60 fS.68 t0.69 Smokatt 40-76 52.98 116.221 133.52 11i-37 • 26.td (n a 23) t 1.61i f<.96' t 1.06•• Pauiw emoken 4C673 55.24 i3-170 123.72 16-32 22.{0 (p = 25) • f 1.72 t 3.11 t 0.72 PvaJua,'<0.01; ••<o.OS. ae eompared to controls Table m. Ratio of HDLr/T, aod HDL/LDL, of cmokets ud pa.fve smokers comparad vith costrolc HDI_lT. RDL/LDL Ran6e litcaa f SE Itang. Jr{eart * SE Control 0.25-036 0s30 0.3711.68 0411 (p=23) t0.006 f0.016 Smoken 0.17-0.2f 0.23 0.2a-0.s7 0.33 • (n-2,S) f0.006• t0.0I2• Paesive rmoken 0.11t-0.31 0.22 0.2a-0.6S 0.45 (n = 23) f 0.001 t 0.016•• t p val'ues, K0.01; •KO OS, as eompared to controL 1 TaYi. IV. T, aad T, of moderaa and 6eavy smoken of dilfsteat durarioor Dyri,aft'on T. (ma/ dl) T. (m.j/ dl) )Ran6s Msaa t SE ltatt6c Mean t SE Control 140-2?0 197.72 f 7.0s W120 100.16 ~ 1ai (n = 25) Moderate smokas < 15 1i0-246 21S.i8 f 6.92 f6-156 117.751 6.E2 . (15•30 (p. (i) eis./day), > 15 190-300 243.30 t 13.61•' 170-166 136.67 t 6,34• Heavy tmoksn (aw 6) < 13 210•265 2Zd0.13 t t.09•• 1WISS 137.30 t 6.?!• (<20 tis (as6) > 15 217•300 231.=o t 1!3.6]•• 11!0-136 13l10 t 7.a1• day): (o = 3) P vahxs, i<0:01; a" eompand to controls higher (P<0.o2) HD4/LD4 and HDI.JT, ratios the assoeiation of ci:.arette smokiaj, serum as compared to controls (Ta6ie VI). lipoproteuu and cardiovaicular diseasept'. In the DiscusalOe present study, the uruat lipids and lipoprotaini of ciSarette smokers and pauive imok.ers have been nere is increasing epidetniolagir.al erid'ence on compared with stsiet non-smokers. Comparison of

WHIG et.t: SERUM LIPI'DS IN SMOKERS 285 taele V. Eomparuos of cholatcrol of l'ipoprotein fraetiotts of raoderate and heavy amokess of diffcrent duration with enntroli Duration. HD L (nt`/ dl) LDL. (n8ltS1) vLDL (m8/d1) yr Ranae Mean t SE Rutae Mean * SE Ranst Msan t SE Control 31-74 51.28tI.80 75- P74 1 l 7:6tt:5.68 17-29 . 21.7 6:1:0.69 (n=23) Moderau <1S 42-61 51.0Dt2.S8 120-177 141.1316.19•• 18-37 23.73*2.08 smokers (o = 8)' (1S-20 cia./dsy) > 1S 4L-" 59.33*4.37 116-201 157.33t 12.94•• 23-33 26:8331.33•' (n=6) Heavy < 1 S 4+f~S8 S 1.S0t2.39 134-1'80 1S1'.8'J:t6.29•• 22.37 27.30 12. 17•s' smokers (<20 efE•/day) (n s 6) > 1S 40-60 49.80t3.41 14b221 170.80213J3•• 27-36 31.20f1.71• Pvaluea„`<0.0U; ••<0.05, ae eompand to controls Table V1. Ratio of HDLIT. and HDI-lLDI. of moderate and beavy smokers of dUfersntduratioes eompared with control Durstion HDL./T. HDLILDL , yr Raage Mean S SY Raaae Mean t SE Control 0.25-0.36 0.30 = 0.006 0 37-0.6d 0.5 1 S 0.016 (e,- 25). Moderate <1S 0.1i-0.28 0.24s0.014• 0.25-0.44 0.37t0.021'8 smokers (13-20 eia.Jday) (n = a) > 15 0.21-0.23 0.24 f 0.012• 0.30-0.47 0.78 10.0248 (m+ 6) Heavy < 13 0:20-0.25 0.22 t 0.008• 0.29-0.39 0.3Y/ t 0.0r/oa tmokers (r = 6) (> 20 ci8./day) > 13 0:17-0.24 0.20 t 0.0i3• 0.2a-0Ji 0.30# 0.027• (n ' s) P values,, •<0,01,, ai compared to eontrois T, and Tr levels indicated that cigarette smoking raised To and Tj levelt. These findings are in accordance with the observations of other workers"-j', but contrary to a few who did not observe such an effcctz2. Since higher Tr and Ts levels are known to be responsible far the development of atherosclerosui3, it indicates that active cigarette smoking can be a major risk factor for coronary artery disease. Our findings of raised T, and Te levels in moderate smokers who had smoked for more than 15 •yr 3nt,1 in heavy smokers (7.e.,respective of the duratimi of smoking) are in agreement with the reports of a number of other workers trarrt different parts of the world""t'='. However, a few workers did not observe any change in Tf levels in smokersK 2s The levels of LDL and VLDL4 were higher in heavy arnokerc or those who had smoked for longer duration. The diffcrences observed in serum lipoproteint between smokers and non- smokers were in accordance with the observations of other workers"' _'' "' ". However, Howell" and Young'f did not observe any differenee. The HDL of smokers was lower than that of eontrol, and passive smokers. Recently, Rastoga' et a!" have also reported a similar effect on HDh in heavy smokers or those who were smoking for longer duration. The comparison of the ratios HDL.I'T.- and

286 INDIAN' I MfiD RES (,BJ. OCTOBER 1942 HDL,/LDI,K indicated that smokers had a significantly lower value. Investigators from the Framingham Heart Study=s have proposed' that these ratios may be better predictors of coronary risk than T, or any of the lipoprotein cholesterol levels alone. Lowering of this ratio is known to increase the risk of development of cardiovascular disease. It is thus clear that smoking is a great hazard with respect to cardiovascular diseases. Since the ratio of HDI:./LDL is also significantly lower amongst passive smokers, it indicates that not only active smokers hut also subjects who are in contact with active smokers are at a relatively higher risk of developing atherosclerosis. The lower degree of risk amongst passive smokers compared to that amongst active smokers could be due to the filteration of smoke in thc lungs of the smokers. Some of the eornponents like nicotine and taz are deposited in the lungs of active smokers and therefore the passive smokers are exposed to. a lower density of harraful' components. Swendsen er aR' conducted the multiple risk factor intervention tria!' to study the effects of passive smoking and the data from their istudy suggeited that passive exposure to cigarette smoke may have a deleterious impact on the health of no"moker: and the non-smokers may be at an increased risk of death through passive exposure to cigarette smoke. Our findings also -suport this, as the levels of serum lipidi and lipoproteins were altered in passive smokers in such a manner that it may have a deleterious effect on cardiovaacular system. The fulS impact of smoking on cardiovascular disease may not be revealed by available epidemiological surveys as risk ratios derived from these surveys do not neceuarily reveal all of the cardiovaacuiar consequences of smoking. It hat been demonstrated that heavy imokers are at a higher risk than light smokers2. ln conclusion, our findings suggest that smoking alters the serum lipid and lipaproteins and these changes become more marked with duration and amount of smoking. The passive smokers also ahow relatively less altered lipid and lipoproteins, in a trend similar to that of smokers. The alteration in the individual value of lipids and lipoproteins is not significant in case of passive smokers but the results are significant only in case of ratios of HDL,/T, and HDL/ LDI.r. As decrease in this ratio is responsible for the development of atherosclerosis, thc results indieate that even the passive smokers arc at a relatively higher risk of developing coronary heart disease. R eferenee: 1. Sliapiro. S., Weinbl.tt, E., Frank. C.W. and Sager. R.V. lneideneo of coronary heart disease ih a population insured for medical ure (HIP): myorardial infarction, angina pectoris and possible myowdial infaretion. Am J Public HeslN Si Suppl (1969) 1. 2 Kaufman. D.W., Helatrich. S.P., Rosenberg, L... Miettinen, O.S. and Shapiro. S. Nieotine and carbon monoxide eoetent of eisareue smoke and the risk of myocardial infaraion Ih young men. N EAdJ J Med 343 (19s3) 409. 3. Brischetto, C.S.. Connor, W.E.. Connor, S.L and Msr-•2--o, J.D. Plasma lipid and lipoproteio profiles of eiaaretta imoksrs from randomly seleeted families: enhanr.ement of Eyperlipidtmia aed deprmslon of hi&kt deDCiey lipoprottia. Am J Cirdiol63 (1983) 675. 4. Stamler. J: Primary prevendon of coronary haart di.e„e. The Itvt m years. Am J C.r,dior 47 (1991) 7zz S. Akiba. S., raio, H. and Blot, WJ. Passive ctnokina and luna eanesr amons Japaneae women. Cancer Ro 46 (1986) 4EOt.. 6. Dimiuioa. T.. Kalandidi„ A.. Sparroa, 1., and MacMahoa, 8. Lung cancer and pwive smoking. lnr J CAn=r 27 (1901)1. 7. Tagcr, l.a., Wei.., S.T., Ro.ner. a. and Spriser, F.E. Effeet of parsntal cigarctte smoking on the pLllnonary function of ehildrea. Am J FpedemiaJ'11G(1979) 15. i. Weisa, S.T. Passive smoking aod luoa canocr. What ia the rak7 Am Rer Respir Dir 1]3 (19i6) 1. 9. xauffmann, F., Tessier, J.F. aad Oriot. r. Adult paaalve smoking in the home eoviroameot: a risk factor for ehronk airflow lindtation. Am J'F.pidemlol 117 (19t3) 269. White, J.RL and•Froeb, H.P. Stnall-airrays dysfunetion in nonsmokers chronically exposed to tobacro stnoke. N Ensl J Med 762 (19io) 7'0: , 11. Aronew, W.S. ERect of paa.ive smoking on aetSina peetoria. N Rnaf J A(ed 2" (1978) 21'. 12. Foklti. J., Lees. M. and SJoane-Stanley, O.H. A timpk method for tbe isolation and purif,catioa of total llpidi from utimsl tusuea. J Bio! Cbem 236 (1957) a97.

WHIO er al; SERUM LIPTDS IN SMOT.ERS 13. Zlatkis, A., Zak, B. and Boyk., A.J: A new method for thc dirsct dctcrmination of servm eholeueroL J Lab CUa Med 4] (1933) 486. 14. 'J-%a iiandel. E. and Zilversrnit, D.B. Micromethod for 3 r1e dlrect determinatibn of serstm trislyoterides. J Lab Clin Mrd S0 (1957) 152. 15. Lopa-Virella, M.F., Stone, P., 611it, S, and Colvrcll, J.A, Cholesuroll detcrrainativn in hlaL detuity lipo- proteins eepantad by three difien;nt methods. Cfin Cbcm Zl (l'977) 8&2 16. Wilson. D.E. and Spiger, MJ. A dual pROipitation method for quantitailve plasma lipoproteia tneasurv menu without ultraaeatrifugation., J Lab pin Alted 82 (1973) 473. 17. Gnuady, S.M., Oreenland, P., Hard, A., Huebeeh, J.A., Jones, R.J., Mitchell. J.H. and Sehleat, It.C. Cardio- vueular and rieli factor evaJuation of healthy Ameritan adults. Circulatlon 75 (1987) I340A. 2=7 21. Richmood, W., Scviour. F.W., Taal„'T.K. and Elkelat, R.S. lmpairsd iatnvueular 1'ipolytu with chan,6a In eonoentrations of hian dentity lipoprotaLn sub.dassa in young tmokea. Br Mod J 2" (19E7) 245. 22. Kontinen, A. and Rajasalami, M. Effect of hsavy cijarette smoYina en poetprand'uJ trijlycssidea, free fatty acidt and chokstsrol. Br Med J 1(1963) t30, 23. •Keys, A. Coronary bean disease In seven eountrue, Grculst7on 41 Suppl (1970) 1. .24. Billitaoria, J.D., Pozaer, H., Meuelaar, B., Best, F.W. and James, D.C. Pffem of cisaretts smoking on Ilpids, lipoproteina, blood eoasul.tlon„fibrinolysie and tsUular eumponenra of human blood. AtherosrJerartt 31' (1975) 61. I!. y'outu, D.L. Rslatfonship betwecn eijaatts tmoldn=, oral wntrasptivtx and platma vitamins A, E, C and plasma trialyoerldes aad ehoksterol. Am J Clia Nutr 29 (11976) 1216. 18. Baltlwa, V.S., Gupta, !w(.C., Mahabwari, V.D. and 26. Rastosi, R, SLrixastava, S.S.L. Mehrotta, T.N:, Slajh, Bhantali, A. Effect of prolonged smoldaj and aleohol on lipid profile, aeparately and in oombinatioa. J Amor Fhyrslciaru lndi.31 (1953) 573. 27. V.S. and Getpta, M.K. L.ipid profile in emohers. JAuoe Pllytlusar l.od3a 37 (19e9) 764. Howell, R. W. Smoitina habits and laboratory twu. 19. Freedatan, D.S„ Sriitivasaa, S.R., Shear, C.L., Httater, Lacer Y (1l70), 131 S. M,. Craft, J.B., Wtbber, LS. and' Berettson, G.S. 28. Wilson, P.W.. Garrison, RJ., Cutelli, W.P., Ftdnleib, 0. Cigarette smoking initiation and lo4tuditaakehaagss in serurn lipids an& lipoproteins in sariy adulthood: the Bojalusa heart study. Am J Epid'emlo1134 (191i6) 207. Gar=, J.P., Gupta, R.S„ Aaar.val. M.P. and' Bhandati, M., McNamara. P.M. and 1Cannel, W:B. Prevalenoe of coroaary heart diseue in the Framinaliam offisptiaj study: role of lipoprouin eholeatuolt. Am J CardioJ 46 (t9i0) 649. V.rit: Effect of smoking on serum lipids and'lipoproteint 29. Svendsen, [.H.; Kulkr. LH., Martin. MJ. and Oebene, in healthy eubjetts and patients of o/d myoeardial! intarstien and liypauneion. 6ndisn J Rfd Sd 37 (1993) 63. J.K. Effecu of pauive smoking in ths multiple riik factor intsrventlon trial. Am JFpidemiol'1126 (1987) 793. Repnne rrquesu: DrJ. w+hig. Dcparteneot of Meateine, Da ay nand; Mediei! College arta Mpviuj Ludhiana 141001 ,