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.. . ; ~° ,. Passive Smoking Alters Li!pid Profiles in Adolescents Q 3 Joseph Feldman, DrPH$;, I. Ronald Shenker, MD';, Ruth A. Etzel, MD, PhD§; Francis W. Spierto, PhD§;. David E. Lilienfield, MD, MPH,, MS, Engin1j; Michael Nussbaum, MD*; and Marc S, Jacobson, MD' From the 'Division of Ado/escenn. Medicine and Center for Atherosclerosis Prevenhon, Schneider Children's Hospital of Long Island Jewish Medical Center, the Long tsland campus for the AtbertEinstein College of, Medicine: New Hyde Park, New York; $Depar7ment of Preventive Medicine„ SUNY Heatth Seience Center of 6rooklyn, New York: §Center for Environmental Health and 1n1ury Control. Centers for Disease Control: Atlanta, Georgia; and, pDivision, of Environmental and OccupataonalMeorcine. Mt Snal School of Medicine, New York ABSTRACT. Although cigarette smoking is associated', with, elpvation of plasma lipid levels and changes in lipoprotein~di'stribution, it, is not known whether passive srnoking is associated with an~alteration in lipid'proftles. The relation between plasma cotinine.a marker of ex- posure to tobacco smoke, and lipid profiles was studied in healthv ad'olescents from a suburban New York high school district who were undergoing preparticipation sports physicals. Forty-four percent of the adolescentsreported that~ one or both parents currently smoked. Eleven percent of the adolescents had plasma cotinine concentrations ?2.5 ng/mL. the level considered indica- tive of exposure. Adolescents with two smoking parents had significantly, higher plasma cotinine concentrations aft,err adjustment for other factors than adolescents whose parents did not smoke. Plasma cotinine concentration ?2.5 ng/mL was associated with an 8.9°.o greater ratio of total cholesterol to high-density lipoprotein cholesterol (P <.003) and a 6.8 % lower high-density lipoprotein cholesterol (P'< .03). These results suggest that passive smoking, like active smoking,Jeadsto alterations in lipid profiles predictive of an increased risk of atherosclerosis. Pediatrics 1991;88:259-264; passive smoking, adolescents, cotinine, lipid pro/iles, cholesteroL ABBBEYIATIONS. TOTAL-C. total': cholesterol: HDL-C. hiahr density lipoprotein cholesterol: CV. coefficient of vanaaon: B1vlll bodv mass index: Cl, confidence intervall Received for publication Jul 9. 1990: accepted Oct 20. 1990: Reprint requests to IIv1.S.J.1 Center for Atherosclerosis Preven- tion. Schneideo Children's Hospital. Room 187. Long Island Jewish Medical Center, New H;vde Park. NY 11042. PEDIATRICS (ISSI: 0031 40051. Copyright Z 1991 by the American Academy of Pediatrics. Cigarette smoking is associated with elevation of' plasma lipid' levels and changes in lipoprotein dis- tribution,' including an elevated ratio of total cho- lesteroli (TOTAL,C) to liigh-density lipoprotein~ cholesterol (HDL-C).'-` The TOTAL-C/HDL-C ratio is a: powerful predictor of the risk of' athero- sclerotic cardiovascular disease and therefore itsrelationship to passive as well as active smokingg has implications for pediatric atherosclerosispre- vention.s.s The present, study investigated the relationship of passive smoking to lipid profidesin healthy ado. lpscents. Cotinine. a major metabolite of nicotine. was used as a rnarker of'passi~•e exposure to tobacco smoke. •6 We hypothesized that passive exposure to environmental tobacco smoke as indicated bs plasma cotinine concentration would be associated with an increase in the TOTAL-C/HDL-C ratlio. METHODS As part of a required health risk assessment and preparticipation sports physical examination non- fasting whole blood samples were obtained! from 444 students attending suburban New York high schools inlAugust 198T. Al] students trying out for an athletic team at the high schools took the phys- ical. Students were asked to complete self-admin- istered~ questionnaires abouv their cigarette smok- ing habits and diet. This questionnaire has previ- ousiv been found to be reliable.9 In addition, students were interviewed bv one of two~ authors (J.F., M.S:J.) regarding cigarette smoking habits of PEDIATRICS Vol. 88 No. 2 Augusti 19911 259

their parents, siblings, and friends. To improve reliability, the first 10 interviews conducted by each interviewer were observed by the other interviewer. The procedures followed were approved by the Hu- man Subjects Review Committee at Long Island Jewish~ Medical' Center. Passive exposure of tobacco smoke was grouped! into five mutually exclusive categories based on~the current cigarette smoking habits of the students' parents„siblings, andfriends. The first three groups below were based solely on exposure to parental' smoking without regard to sibs or friends. The five categories were as follows: (1)i mother smoked but father did not, (12) father smoke& but mother did not, (30' both, parents smoked, (4) siblings and/or friends only smoked. and (5) no parents, siblings, or friends smoked. Exposure from any parents not currentliv living with the subject was excluded', Ex- posure from smoking friends was excluded if the student reported'spending <_2 hours per week inn their company. Nonfasting plasma was collected by . venipuncture from seated subjects, centrifuged, and frozen until analysis. Cholesterol and triglycerides were assayed di- rectly from 10 µL of supernatant by a Kodak mu1- tiiaver film method. High-density lipoprotein cho- lesterol was determined by drawing 0.5 mL of plasma into tubes containing 50 000 molecular weight dextran sulfate-magnesium reagent and cen- trifuging the mixture at 1500 X g for 10 minutes to precipitate the very-low-density lipoprotein and low-densitv lipoprotein particles. The HDL-con- taining supernatant was then assayed directly for cholesterol' usiiig the Kodak multilaver film methodl We analk•zed 15 paired samples, both on a Kodak DT60 Analyzer and at Queens Hospital Center (New York)~Arterioscler-=is Research Lab- oraton•, which, is a participant n the Centers for Disease Control/National Heart, Lung, and~ Blood Instikute Lipid Standardization Program. Correla- tion coefficients were cholesterol = .99, triglycerides _ -9 7, and' HDL-C = .91. Total cholesterol and HDL-C were measured in 11 batches. The coefficient of variation (CV) of total cholesterol by batch ranged from 0.16 to 0.20 whereas for HDL-C: the CV ranged from 0:16 to 0:27. There were no significant differences in the average levels or the variation from the averages among the 11 batches in either males or females. Four hundred twenty-five of the students had'suf- ficient plasma remaining for cotinine analysis. Plasma cotinine analysis was performed at the Di- vision of Environmental Health Laboratory Sci- ences at the Centers for'SDisease Control using the radioimmuaoassay previously described by Knight et al.10 The level of detection for cotinine in this 260 PASSIVE SMOKING AND LIPfD LEVELS assay was 1.6 ng/mL. Cotinine and lipidiconcentra- tions were each determined without knowledge of reported exposure to tobacco smoke. Notched box plots in the Figure were use& to indicate the median cholesterol concentrations and the 95% confidence interval about the medians. If the notches in the boxes (ie, median ± 1.57x interquartile range/'.ln) do not overlap, this can be regard'e& as strong evidence that the popuiationn medians differ...... Hatched areas in the Figure denote the area between the 76th~and 25th per- centile (i.e; interquartile range)i Multiple linear analvses of covariance were per- formed using TOTAL-C, HDL-C, and ratio of TO- TAL-C/HDL-C as outcomes. Covariates included age, race, sex, triglyceride concentration, and bod,~ mass index (BMI). Body mass index was calculated byy dividing weight by the square of height. The predictor variables were plasma cotinine concentra- tions and self-reported passive tobacco smoke ex- posure. Inasmuch as the distributions of both cotin- ine and triglviceride concentrations were highl'y skewed, these data were logarithmically trans- formed. This transformation of the serum cotinine levels was also useful in testing, for differences among the exposure groups, inasmuch as the simi~ larity of the CV of cotinine among the exposure categories (from 1.6 to 2.4) suggested proportionall effects.'" We reporti both the arithmetic and geo- metric means of cotinine. The constant 0.05 was adde& to all' cotinine concentrations to avoid the logarithm of zero which is undefined. In addition„ 8 2 <2:5 ng/ml >2.5 ng/mli N W Figure. Lipid ratio in passive smoke-exposed andCA nonexposed adolescents. TC., total cholesterol; HDLC)-& high-density lipoprotein cholesterol; '. outlier values. N R COTININE

plasma cotinine concentrations were categorized as <2.5 ng/mL', or ?2.5 ng/mL to indicate exposure based on previous work.is Interactions between the covariates and the predictor variables were exam- ine& and none was significant. The adequacy of the assumptions underlying the various models was assessed by examining various residual plots." Reanallysis omitting highly leveraged cases (ie„ dropping cases with a much greater than average impact on results) did not change any conclhsions, The actual computations were performed using Svstat.'6 Self-reported smokers (n- 7) were excluded. To reduce the possibility of including current smokers who did not report aceurately, students with~plasma cotinine concentrations of more than 25 ng/mL (in = 12) and nonresponders to the smoking question (n = 2) were also excluded.~ In addition„we excluded 7 adolescents on; cholesterol-lowering diets and 6 nonresponders to the diet question. The study sam- ple therefore consi'sted of 391 ad'olescents. The analyses in Tables 3' and 4 were also done excluding 5 adolescents with serum cotinine values of 11 to 25 to further reduce the possibility of misclassifi- cation of active smokers. The results were al'anost identicali and therefore are not shown. RESULTS The sample included274 boys (69.7So) and 117 girls (30.3 0); Two hundred seventy-eight (71.1cio) were white, 52' (113.2`-0Ywere black, 20 (5.1 %) were other races, and' 41 (110.5) o) did not indicate their race. The mean age was 14.8 ± 1.6 years; 34.3% of the adolescents reported no smokers among their parents, siblings, or friends; 115.1% reported that mother smoked but father did not; 17.4% reported' that father smoked but mother did not; 1'1.5°7o re- ported that both parents smoked;; and 21.7% re- ported': that siblings and/or friends only smoked. The arithmetic mean cotinine concentration was 11.39! ng/mL (SD = 4.70), which was not signifi- cantly different from the level of detection of the assay: Eleven percent (n = 44) of the adolescents had plasma cotinine concentrations -2.5 ng/mL, 89 0(n = 347) had'plasma cotinine concentrations <2.5 ng/mL. Both the geometric and arithmetic mean plasma cotinine concentrations were signifi- cantly higher among adolescents who reported that one or both parents smoked; the highest level was found among adolescents with two smoking parents (Table 1). Table 2 shows average levels of the ratio of TOTAL-C/HDL-C by reported exposure and category of serum cotinine concentration. The T0= TAL-C/HDL-C ratio was always higher in children whose serum cotinine level was >-2.5 ng/mL irre- spective of reported exposure. Despite the stat!isti- cally significant association between reponed ex- posure and' serum cotinine concentration, it was apparent that there was considerablp misclassifi- cation of exposure based on self-report. Fewer than 20rc of the students in anyy reported exposure cat- egory were classified as ezposed' based on serum cotinine levels greater than or equall to 2.5 ng/mL (Table 2). Mean TOTAL-C concentration was 154 mg/dL (SD1 = 27.2), mean HDL-C concentration was 44.6 mg/dL (SD = 10.0), and mean TOTAL-C/HDL-CC ratio was 3.58 (SD = 1.86), The Figure shows notched box plots for the ratio of TOTAL-CHDL- C by cotinine group with 95% confidence intervals about the medians. The asterisks in, the Figure indicate observations that fall outside the 95 t range of individual!values. The medlan TOTAL-C/ HDL-C ratio for the 44 adolescents with cotinine concentrations ?2.5 ng/mL was significantly . higher than that for the 347 adolescents with cotin- ine concentrations <2.5 ng/mL (P < .002). This was not true for HDL-C concentrations until' co- variates were taken into account as describe& later. In the analysis of covariance model with outcome equal to the ratio of TOTAL•C[H'DL-C; the inde- pendent variables BMI, log triglyceride lev.el, and log cotinine level were all significantll, associated with the ratio (not shown). Together the variables accounted f'or 28% of the variation in the ratio of TOTAL-C/HDL-C, with triglyceride concentration an& BMI accounting for 97 c7c of that amount. Re- sults of analysis with cotinine grouped into two categories are shown in Table 3. Cotinine level wass significantly associated with the ratio of TOTAL- C/HDL-C (P'<.003). IThe regression equation wass ratio = -.60 + .038' (BMI) + ..771 ln (triglyceride) - .324 (if cotinine level <2.5 ng/tnL) + .379 (if white).) For the group with cotinine levels >-2.5 ng/ mL„the ratio of TOTAL-C/HDL-C on average was .324 or 8:9 0(955o confidence interval) [C1J 6:9 % to 11.0~'0) higher than if the cotinine level was <2.5 ng/mL. Cotinine level was significantly associated with lower HDL-C concentration (P < .03)' (Table 4). [HDL-C = 77.8' - 5.4 In (trig)viceride) - 0:48 (BMI) + 3.0 (if cotinine leveli <2.5 ng/mLl - 2.56 (if male).J The HDL-C level, in adolescents with plasma cotinine concentratios>-2.5 ng/mL was 3.0 mg/dL or 6.8P (95 o C1 4.6/ to 8.9ro) lower than in those with pl'asma cotinine concentration <2.5 ng/rnL after adjustment for other factors. The association of serum cotinine concentration with the ratio of TOTAL-C/HDL-C was examined separatel~, . for whites with similar results ( P=.001); as well as for boys (P = .014) and girls (P =.001). ARTICLES 261

TABLE 1. Arithmetic and Geometric Mean Levels and 95 % Confidence Intervals (CI) for Serum Cotinine Levels by Reported Exposure Reported Exposure n Arithmetic Mean l95"c CIl' Geometric Mean (95 c CI) None Friends/sibs only 134 8 7 0.55 (0.40-0.69') 1.35 (0.66-2.03) 0.07, 0.07 (0.04-0:11) (0.04-0:14') Mother, not father 59 1.06 (0.49-1.62) 0.13 (0.0L-0:26)1 Father, not mother 66 1.39'(0.75-2.02) 0.21 (0.11-0:39); Both~mother and father F ratio 4.386 dJ 45 2.15(0.81-3.49) 3:65 0.35 4.48 (0.17-0:'4)' P value 0.006 0.001 TABLE 2. Ratio of Total Choiesterol to High-Density Lipoprotein Cholesterol by Serum Cotinine Group and Reported Exposure Reported Exposure Serum Cotinine Concentration <2.5 ng/mL i''_'.5 ng mL n Ratio SD n Ratio SD ?V one 1124 3:47, 0.8-1 10 3.77, 0:76 Friends/sibs only 71 3.55 0.90 16 3."0 1.13 Mother, not father 49: 3.34 0.55 10 4.06 1.02 Father. not mother 33'. 3.64 0.78 13 4.22 1.04. Both mother, and: father 37 3.68 0.85 8 3.91 1.02 TABLE 3. Multiple Regression Analysis of Ratio of Total Cholesterol to High-Density Lipoprotein Cholesterol by Plasma Cotinine Concentration. Grouped, Adjusted for Several Covariates' Source of Variation, SS. df F Ratio P Value Race 1."2 2 1.81 .165 Body mass index 6:64. 1 13.99 .000. Cotinine grouped: <2.5 ng/mL vs _2:5 ng/mL 4.27 11 9.01 .003 Log triglyceride 44.W 11 92.79 .000 Error 160.29 338 ' SS = sum of squares; N = 344: r = .54. Forty•seven patients with missing data on any of the above variables are excluded. TABLE 4. Multiple Regression Analysis of High-Density Lipoprotein Cholesterol by Grouped Plasma Cotinine Levels Adjusted'for Several Covariates' Source of'Variation SS d/, F Ratio P Value Sex 515.20 1 5.-7 .01 -1 Log triglyceride 2346.87 1 26.27 .000 Bod'y mass index 1452.40 1 12.90 .000 Cotinine grouped: <2:5 ng/mL or >_2.5 ng/mL 427.50 1 4.79 .030 Error 34041.56 381 ' N = 386; r=.35. Five patients with data missing on any of these variables are excluded. The relationship betweem reported smoking hab- its of parents, siblings, and friends and the ratio of' TOTP.L-C/HDL-C was not statistically significant (P =.18). There was a significant difference in the ratio of TOTAL-C/HDL-C of adolescents whose fathers smoked' compared with others (P' <_ .04). When adjusted for multiple comparison bias, this finding was no longer statistically significant. There was no difference in the ratio of TOTAL-C/ H'DL-C of adolrescents whose mothers smoked com- pared with others. DISCUSSION In this sample, passive exposure to tobacco smoke as indicated by plasma cotinine coneentra- tiom was associated with a higher ratio of TOTAL, C/HDL-C and with a lower HDL-C concentration. 262 PASSIVE SMOKING AND LIPID~ LEVELS

Whemotlier factors were adjusted, passive exposure to tobacco smoke was associated~ with an increased ratio of TOTAL-C/HDL-C and decreased~ HDL-C concentration of between 7% an& 9%. However, compared~ with other factors such as BMI or tri- glycerid'e concentration, the impact of passive smoking on the ratio of TOTAL-C/HDL-C was relativelv small. We did not measure socioeconomic status of sub- jects or obtain detailed dietary histories and there- fore could not control for these variables. It is possible that parents of lower economic status smoked more frequently and~ provided their chil- dren diets higher in cholesterol and saturated fats, resulting in a secondary association ~ between serum cotinine concentration and lipid! ratios. This seems an unlikelv explanationl however, because the stu- dents came from a relatively homogeneous com- munity. The association of lipid profiles with reported smoking habits of parents. siblings, and''friends was not statistically significant. There was an associa- tion for adolescents whose fathers smoked com- pared with~ others. But there was no association with mothers" smoking. We did not predict this pattern initially and the observation is inconsistent with other reports, which have found a stronger association with mothers' smoking." The most likely explanatiom for thib pattern is a spurious association. Parentheticalh•, this pattern' also di- minishes the likelihood that the observed associa- tion between the lipid ratio and cotinine concentra- t~ion was due to smoking mothers' providing a more atherogenic diet. The association of passive expo- sure to tobacco smoke with reduced HDL ,C and elevated ratio of TOTAL-C/HDL-C is biologically plausible, inasmuch as several investigators have found that cigarette smoking results in~a lowering of HDL-C.'-8-`-2' In one longitudinal study of' 36 female volunteers, investigators found that HDL-C levels fluctuated with smoking status, increasing when smoking ceased and decreasing when smoking resumed." In another study, investigators reported a dose-response relationship between smoking and ratio of TOITAL-C/HDL-C:' The age- and weight- adjusted ratio of TOTAL-C/HDL-C among 233 randomly selected families was 1,3% higher for smokers than for nonsmokers, about 1.5 times that seen in this study. Several investigators have foun& suggestive evi- dence of an increased risk of coronarv heart disease mortality among adults passively exposed to to- bacco smoke. Helsing et al-= found that death rates from atherosclerotic heartdisease were 24 o to 31% higher for nonsmokers living with smokers com- pared with those living with nonsmokers. In a study of nonsmoking women 50 to 79'years old! in south- ern Calif'ornia, those whose husband's smoked had a: 10-year mortalitv from ischemic heart disease that was 2.1 times higher than those whose husband's never smoked~ (P'< .10)~=''` In the Multiple Risk Factor Intervention Trial, the effect of exposure t~o tobacco smoke was assessed among 1245 married' men aged 35 to 57, years.''' The relative risk for nonsmoking men with smoking wives compared~ with those with nonsmoking wives was 2.1 f'or cor- onary heart disease death ('.P = .19): and 1.48 for f'atal or nonfatal coronar_v heart disease events 1 P _ .13). A recent study in 216 families of preadolescent children fromithe Medical Colleage of Virainia twin study found that children in the 105 families of smoking parents had significantly lower HDL-C and higher whole blood 2,3,d-phosphoglN•eerate lev- els thanichildTen in the 1111 nonsmoking families.=" The authors concluded that children, with long- termlexposure to passive smoke may be at elevated risk for the development of premature coronam~ heart disease. The effect ofltobacco on lipi& levels provides one plausible mechanism (among others such as platelet aggregation, vasoactivity; and compromised oxygen, transport) for the well-established' elevation of cor- onary heart disease risk among smokers and' sug- gests a mechanism for the possible increased coro- nary heart' disease risk in passive smokers. ACKNOWLEDGMENTS Partial support was received from National Institute of Environmental Health Sciences grants F+;08-F.S00161 and P30-E500928. We thank Paul'Samuel. N1D. S. Bader. F. H. 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