Passive Smoking During the First - NCBI

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Passive Smoking During the First Year of Life

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Robert A. Greenber, MD, MSPH, Karl E. Bauman, PhD, VictorJ. Strecher, PhD, MPH, Lynette L. Keyes, MS, MPH, Lucinda H. Glover, MPH, Nancy J. Haley, PhD, Helen C. Stedarn, BS, and FrankA Loda, MD

Inbrdudion Recognition of the adverse health effects of passive smoking in childhood, particularly during the first year of life,1-3 has led to efforts to reduce exposure to environmental tobacco smoke.4 To better inform such efforts, we previously reported the frequency of passive smoking and the circumstances in which it occurred in healthy neonates in central North Carolina.5 The observations from that research were extended by a one year follow-up of a sample of the original study infants. This paper reports the changes in tobacco smoke exposure and absorption during the first year of life, identifies selected correlates of these changes, and considers the implications of findings for prevention of passive smoking during infancy.

of age. The remainder of the control group (n = 152) constituted the study sample for the present paper. The mean number of adults living in study households was 2.3 at both enrollment and at one year. Seventy-five percent of the infants were living in twoparent families as neonates and 70 percent at one year. Table 1 describes the study sample. There were no significant differences between the 152 infants in the study sample and the remainder of the 1,096 infants who were eligible for enrollment in the gender of the infant, mother's age, mother's race, and smoking by the mother. The study population, however, included significantly more heads of household with more than a high school education (45 percent) than the remainder of the eligible population (34 percent).

Methods

Data Collection Procedures

Study Population The infants were enrolled at birth, from April 1986 to May 1987, in an experimental study of a program to reduce passive smoking and respiratory illness. To be eligible for enrollment, an infant had to have no significant postnatal problems, a birth weight of at least 2,000 gin, and reside in Alamance County or Chatham County in central North Carolina. Infants in the previous neonatal study5 were recruited from three hospitals where 433 mothers (40 percent of the 1,096 eligible) gave informed consent. Following data collection for those 433 infants, 216 infants began the passive smoking reduction program to which they had been randomly assigned and 217 remained in the control group. Sixty-five infants in the control group were lost to follow-up by one year

Data collectors visited the homes of enrolled infants when the infants were approximately three weeks of age [mean age (SD): 18 (seven) days, range: nine to 51 days] and before the family's assignment in the intervention trial. The follow-up visit for the data reported in this study was when the infants were approximately one year old [mean age (SD): 12.3 (0.6) From the University of North Carolina at Chapel Hill (Greenberg, Bauman, Strecher, Keyes, Glover, Stedman, Loda) and the American Health Foundation, Valhalla, NY (Haley). Address reprint requests to Robert A. Greenberg, MD, MSPH, Division of Community Pediatrics, CB #7225, Medical School Wing C, University of North Carolina, Chapel Hill, NC 27599-7225. This paper, submitted to the Journal April 23, 1990, was revised and accepted for publication September 20, 1990.

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Infant Passive Smoking

or elsewhere. A smoker was anyone who smoked at least one cigarette, cigar, or pipeful per day. Exposure to tobacco smoke was considered to occur when smoke was produced in the infant's presence, that is, in the same room or vehicle as the infant. The amount ofexposure was expressed as cigarettes per week smoked in the infant's presence. (See Appendix for method of measurement.) Smoke absorption was defined as sufficient airway contact with tobacco smoke to result in absorption of nicotine. It was measured by the urinary concentration of cotinine, a major metabolite of nicotine.2 Urine cotinine and our questionnaire measure of tobacco smoke exposure are related, but different measures of passive smoking. We have reported analyses of this relationship in infants elsewhere.5,6 (See Appendix for further discussion of measures of passive smoking.)

Infants of the nine mothers who smoked and breast-fed were eliminated from all analyses that used cotinine as a continuous variable because of the large amount of nicotine and cotinine absorbed through breast-feeding, relative to the amount absorbed through the airways.8

Stahstical Methods Distributions of categorical variables were compared by the chi-square statistic or the Fisher's Exact Test. The two-tailed Student t statistic was used to compare means of continuous variables for two groups. McNemar's test was used to assess changes between three weeks and one year of age in the proportion of infants exposed to tobacco smoke from different sources and the proportion excreting cotnine. Analyses of cotinine comparing smoke absorption at the two ages involved only the 114 infants who provided urine specimens at both data collection visits.

Laboratory Procedures

months, range: 11.5 to 14.9 months]. Before beginning the interview, the data collector placed a urine collection bag on the infant and explained to the mother that the urine would be analyzed for tobacco smoke products to determine whether the baby had been exposed to smoke. The mother was then asked to describe the smoking habits of all household members and any recent exposure of the infant to tobacco smoke.

Definitons of Variables An infant was considered to have contact with smokers if the infant lived in the same household as a smoker or was in the same place, at the same time, as a nonhousehold smoker, either in the house

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The urine samples were frozen and shipped to the American Health Foundation, in Valhalla, NY. Researchers there analyzed each specimen without knowing the exposure status of the infant. Cotinine concentration was quantitated by radioimmunoassay with a modification of the method originally described by Langone, et al.7 This protocol uses specific antisera produced by rabbits and has interassay and intraassayvariations of 8 percent, with a sensitivity of 1 ng/ml (6 nmol/L). Levels less than 2 ng/ml (12 nmol/L) were reported as below limits of reliable detection. Creatinine was measured by dry chemistry methods on a Kodak Ektachem 400 analyzer (Eastman Kodak Company, Rochester, NY). The cotinine was divided by the creatinine concentration to adjust the data to reflect the concentration of the urine sample.

Resuits Exposure to Tobacco Smoke Between three weeks and one year of the proportion of infants reportedly exposed to tobacco smoke from any source increased from 39 percent to 63 percent (Table 2). The proportion of infants exposed to tobacco smoke produced by their mothers, by nonmatemal household members, by nonhousehold smokers, and by more than one of these sources, increased significantly during the first year of life. The greatest increase (157 percent) was in the proportion of infants exposed to smoke produced by nonhousehold smokers. Very similar results were found when the data analyses for Table 2 were repeated for just the 114 infants who provided urine specimens for cotinine analysis. One infant was in day care at 3 weeks of age. By one year, 90 (58 percent) of the 152 study infants were in day care and 17 (19 percent) of those in day care were exposed there. Only six infants had their only exposure in day care. The median amount of exposure for the 39 percent of infants who were exposed to any source of smoke at three weeks was 36 cigarettes per week per infant, with a range from two to 250 cigarettes per week. When these exposed three-week-old infants became one-yearolds the median amount of exposure was still 36 and the range was zero to 343 cigarettes per week. age,

American Journal of Public Health 851

Greenbeirg et al.

Our findings support vigorous early and continued efforts to prevent infant passive smoking. The larger study from which the data reported here are derived is evaluating one such effort.9 [1

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Acknowledgments

Among exposed three-week-old infants, the mother contributed, on the average, 34 percent of the cigarettes per week to which an infant was exposed. All household members other than the mother contributed 42 percent and nonhousehold smokers contributed, on the average, 23 percent to the total amount of an infant's exposure. Among exposed one-year-old infants, the mother contnbuted, on the average, 33 percent; nonmaternal household members, 38 percent; and nonhousehold smokers, 28 percent.

Absorption of Tobacco Smoke At three weeks of age, 53 percent of the infants had cotinine in their urine. By one year, the proportion excreting cotinine increased to 77 percent (95% CI of difference: 14, 35). For the infants excreting cotinine at three weeks, the median cotinine concentration was 79 ng/mg of creatinine (51 nmoVmmol) with a range of 9-643 ng/mg (6-413 nmollmmol). The median among the same infants at one yearwas 127 ng/mg of creatinine (82 nmollmmol), range 0-714 ng/mg (0-458 nmol/mmol). Among individual infants, the difference between the urine concentrations at the two ages varied considerably. Although the mean difference was only 11 ng/mg of creatinine (7 nmoVmmol), the 95% CI of the difference was wide: -40 ng/mg (-26 nmol/mmol), 62 ng/mg (40 nmoVmmol). Table 3 contains the distribution of infants by smoke absorption status at one year, according to smoke absorption status at three weeks. Almost all infants (92 percent) absorbing tobacco smoke at three weeks were also absorbing smoke at one year. In contrast, only 39 percent of infants who were not absorbing smoke at three weeks were still not absorbing smoke at one year. We compared the characteristics of these 21 infants with the 33 infants who also were not absorbing smoke at three weeks, but who became

852 American Joumal of Public Health

tobacco smoke absorbers by one year. The latter infants were more likely to live in a household with smokers, 30 percent compared with only 5 percent of infants who continued to not absorb smoke at one year. The two groups of infants did not differ by educational level of the head of household, race, or the proportion attending day care at one year.

Diwussion Although passive smoking was already common at three weeks ofage, there was a large increase in the prevalence of passive smoldng by one year, an increase found in both the proportion of infants exposed to smoke and in the proportion absorbing nicotine. The large number of infants eligible for enrollment who were not in the study sample may limit the generalizability of our results. For example, because the heads of household ofinfants not included in the study had less education and were therefore more likely to smoke, the extent of passive smoking among study infants may be an underestimate for infants in the entire community. Our analysis of smoking by household members suggests that the increase in prevalence ofpassive smoking might be reduced by urging smokers who are already in contact with infants, but not smoking in their presence, to continue to refrain after the newborn period. Considering the large increase during the first year of life in the proportion of infants exposed to smoke produced by nonhousehold smokers, parents should be encouraged to limit contact between their infants and nonhousehold smokers. Mothers may be unaware of all contacts their infants have with smokers, however: 24 percent of the three-week-old and 49 percent of the one-year-old infants in our study were reported to have no contact with smokers but had cotinine in their urine.

This research was funded by Grant No. 28895 from the National Heart, Lung, and Blood Institute, National Institutes of Health. We are grateful to the pediatricians ofAlamance County and Chatham County, North Carolina, for supporting our study of their patients. The cooperation of the administrative and nursing staff of Alamance County Hospital, Alamance Memorial Hospital, and North Carolina Memorial Hospital is also greatly appreciated. We thank the staff of the Infant Health Study, whose work made this study possible.

References 1. US Department of Health and Human Services: The Health Consequences of Involuntary Smoking: A report of the Surgeon General. DHHS Pub. No. (CDC) 878398. Washington, DC: Govt Printing Office, 1986; 38-49, 58-59, 127-132. 2. National Research Council: Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: National Academy Press, 1986; 137146, 269-276. 3. Fielding JE, Phenow KJ: Health effects of involuntary smoking. N Engl J Med 1988; 319:1452-1460. 4. Perry CL, Silvis GL: Smoking prevention: Behavioral prescriptions for the pediatrician. Pediatrics 1987; 79:790-799. 5. Greenberg RA, Bauman KE, Glover LH, etaL Ecology of passive smoking byyoung infants. J Pediatr 1989; 114:774-780. 6. Bauman KE, Greenberg RA, Strecher VJ, Haley NJ: A comparison of biochemical and interview measures of the exposure of infants to environmental tobacco smoke. Eval Health Prof 1989; 12:179-191. 7. Langone JJ, Gjika HB, Van Vunakis H: Nicotine and its metabolites: Radioimmunoassays for nicotine and cotinine. Biochemistry 1973; 12:5025-5030. 8. Schwartz-Bickenbach D, Schute-Hobein B, Abt S, Plum C, Nau H: Smoking and passive smoking during pregnancy and early infancy: Effects on birth weight, lactation period, and cotinine concentrations in mother's milk and infant's urine. Toxicol Lett 1987; 35:73-81. 9. Strecher VJ, Bauman KE, Boat B, Fowler MG, Greenberg RA, Stedman H: The development and formative evaluation of a home-based intervention to reduce passive smoking by infants. Health Educ Res 1989; 4:225-232. 10. Coutas DB, Samet JM, McCarthy JF, Spengler JD: A personal monitoring study to assess workplace exposure to environmental tobacco smoke. Am J Public Health 1990; 80:988-990. 11. Benowitz NL, Jacob P: Daily intake of nicotine during cigarette smoking. Clin Pharmacol Ther 1984; 35:499-504.

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Infant Passive Smoking

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American Journal of Public Health 853