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OTHER HEALTH CONSIDERATIONS IN CHILDREN 269 15 Other Health Considerations in Children Several other health outcomes have been studied that relate to the growth and health of children. This chapter discusses studies of the influence of ETS exposure on birthweight of the offspring of nonsmoking pregnant women and its influence on childhood growth and ear infections. For all postnatal outcomes, it is often not possible to differentiate effects of in utero exposure to tobacco smoke constituent from subsequent childhood exposures to ETS. ENVIRONMENTAL TOBACCO SMOKE EXPOSURE BY NONSMOKING PREGNANT WOMEN The fetus of a smoking mother is exposed in a unique way to the chemicals produced in cigarette smoke. Many studies have documented the adverse effect this relationship has on intrauterine fetal growth, especially during the third trimester of pregnancy (U.S. Department of Health and Human Services, 1976). Maternal cigarette smoking apparently affects fetal oxygenation, due to high levels of carboxyhemoglobin in the blood of both mother and child (Abel, 1980). However, the effects on the fetus of a nonsmoking mother chronically exposed to ETS are not well documented. Some studies have indirectly approached this problem by evaluating paternal cigarette smoking and birth outcomes in nonsmoking pregnant women. Some early studies of paternal smoking and birthweight demonstrated a dose-response relationship that was discounted as
OTHER HEALTH CONSIDERATIONS IN CHILDREN 270 ânot easily acceptable as meaningful in terms of cause and effectâ (Yerushalmy, 1962). An interview survey of 982 pregnancies indicated a strong dose-response association between paternal cigarette smoking and the percent of infants weighing less than 5 pounds, 8 ounces (Yerushalmy, 1962). In a later prospective study of nearly 13,000 births, Yerushalmy (1971) reported that paternal smoking was more strongly associated with low birthweight than was maternal smoking. The healthiest low-birthweight infants were found for couples where the wife smoked and her husband did not; the highest mortality rate was found among infants produced by couples where the husband smoked and the wife did not. These latter couples also had increased risks of producing premature offspring. The possibility that these differences in smoking were associated with differences in social class was not explored. On the bases of these data, Yerushalmy (1971) inferred that paternal smoking may be incidental to birthweight. When the mother's smoking was considered, the importance of paternal smoking disappeared. In a study of 12,192 births, MacMahon et al. (1966) confirmed the negative association between maternal smoking and birthweight of offspring and also found that infants of fathers who smoked weighed about 3 ounces less than those of fathers who did not smoke. They attributed this finding to the correlation between husbands' and wives' smoking habits, or to chance. MacMahon et al. (1966) referred to Yerushalmy's (1962) observation of an association of father's smoking habits with infant weight as âbiologically nonsensical.â In a study of 175 normal neonates and 202 neonates with congenital malformations, Borlee et al. (1978) found that paternal smoking was independently and significantly associated with reduced birthweight and higher perinatal mortality. They speculated that the effect occurred through its association with another factor. Gibel and Blumberg (1973) reported on a study of 5,000 children in which children of nonsmoking mothers whose fathers smoked more than 10 cigarettes per day had higher perinatal mortality than children whose parents were both nonsmokers. The incidence of severe malformations in children of fathers who were heavy smokers was double that of children of nonsmoking fathers, independent of parental age and social class.
OTHER HEALTH CONSIDERATIONS IN CHILDREN 271 Using code sheets prepared at birth of 48,505 women in worldwide naval installations. Underwood et al. (1967) found that fathers' smoking habits influenced pregnancy outcome. However, this was attributed to the increased numbers of wives who smoked when husbands smoked. For paternal smoking in the absence of maternal smoking, no association was found. Holmberg and Nurminen (1980) and Hughes et al. (1982) also reported no association of paternal smoking with low birthweight in cross-sectional reviews of several thousand births. Rubin et al. (1986) provide a recent contribution to this subject based on a survey of 500 consecutive births. About two-fifths of the women reported smoking during pregnancy; 70 percent reported drinking. Paternal smoking was evaluated in terms of frequency and quantity of substance smoked, as reported in standardized interviews. They found that birthweight was reduced an average of 120 g per pack of cigarettes smoked per day by the father. This relationship remained statistically significant after controlling for relevant variables, including mother's age, parity, maternal smoking, and alcohol and tobacco consumption during pregnancy. The effect was greatest in the lower social classes. In a prospective study, Martin and Bracken (1986) studied 3,891 antenatal patients, 2,613 of whom did not smoke during pregnancy. One-third of the nonsmoking mothers (i.e., 906) were exposed to ETS for at least 2 hours per day. ETS exposure was related to lower birthweight in full-term babies (23.5 g, not significant). A logistic regression to control for gestational age, parity, ethnicity, and maternal age produced a significantly increased risk of delivering a low-birthweight baby, i.e., less than 2,500 g at birth for ETS-exposed mothers (relative risk=2.17, p<0.05). The retardation in fetal growth rate is small but appears to be clinically meaningful at the low end of the birthweight distribution. That is, exposure to ETS increases the risk that the infant will weigh less than 2,500 g and, therefore, will have a higher perinatal mortality. GROWTH IN CHILDREN A few studies have examined possible relationships between chronic exposure to ETS by children and parameters of growth and development. Many studies have demonstrated that smoking during pregnancy results in newborns who are lighter and shorter than other infants, even when gestational age has been taken into
OTHER HEALTH CONSIDERATIONS IN CHILDREN 272 account (Meredith, 1975; U.S. Department of Health and Human Services, 1976). This deficit in height and weight appears to persist into infancy and childhood (Goldstein, 1971; Butler and Goldstein, 1973; Dunn et al., 1976; Miller et al., 1976; Rantakallio, 1983). Current smoking status of the mother also has been associated with decreased attained height (Rona et al., 1981; Berkey et al., 1984), although growth rate was not slower among these children (Berkey et al., 1984). These studies, however, did not differentiate between smoking during pregnancy and subsequent exposures during infancy and preschool years. Rona and colleagues (1985) reanalyzed data from the National Study of Health and Growth (England) for a sample of 5,903 children aged 5 to 11 years, separating the effects of smoking during pregnancy from those of later smoking. After adjusting the data for social class and other social factors, they found that reduced height was associated with increasing numbers of cigarettes smoked in the home, regardless of whether the mother smoked during pregnancy and regardless of which parent smoked. There remained a small but significant effect on height âa reduction of approximately 0.05 standard deviations of height (approximately 0.3 cm) for each 20 cigarettes consumed daily in the home. To verify this small change in height, other studies of comparable magnitude are needed. Growth is an especially difficult phenomenon to study. Many factors, such as genetics, nutrition, social class, and ethnicity play important roles, and it is difficult to assign proportionate causality to each factor. Recall bias in the mothers of school-age children regarding their smoking habits during the pregnancy may produce unreliable results, especially in light of the increasing publicity regarding ill effects on the fetus of maternal smoking during pregnancy. Moreover, height and weight ratios and other growth measures are not reliably obtained in standard pediatric surveys. CHRONIC EAR INFECTIONS A number of studies have linked household exposure to ETS with increased rates of chronic ear infections and effusions in children. Chronic ear infections or effusions in young children can lead to hearing loss and consequent speech pathology. Kraemer and colleagues (1983) conducted a hospital-based case-control study of 76 children with persistent middle-ear effusions contrasted with 76
OTHER HEALTH CONSIDERATIONS IN CHILDREN 273 children admitted for other types of surgery who were matched for age, sex, season, and surgical ward. They found that the daily exposure to ETS was greater among cases. They also reported that middle-ear effusions clear less readily in children heavily exposed to ETS. They concluded that a combination of several factors increased the risk of persistent middle-ear effusions, including recurrent otitis media, nasal catarrh, cigarette smoke exposure, and nasal allergies that chronically inflame the nasal and middle-ear cavities, causing persistent eustachian tube dysfunction. For children with regular exposure to ETS, atopy, and congestion, the relative risk for PPME was 6.3 (95% confidence interval, 1.9â21.1). In another case-control study of 150 children hospitalized for chronic middle-ear effusions and 150 children hospitalized for other reasons (Black, 1985), the odds ratio for parental smoking was found to be significantly elevated (1.6). This effect was consistent across age groups, and became more evident in older children where effusions are less common. Pukander et al. (1985) reported that ETS was a significant risk factor for acute otitis media in 2-and 3-year-old children. They evaluated a number of important indoor environmental conditions, including relative humidity, carbon dioxide, and temperature. In this study, children of smoking parents also had 60% more middle-ear effusions than children of nonsmoking parents. SUMMARY AND RECOMMENDATIONS For all postnatal outcomes among children, it is difficult to differentiate effects of in utero exposure to tobacco smoke constituents from subsequent childhood exposures to ETS. However, for the above outcomes, there are indications that exposures to ETS may have effects on the fetus or child. What Is Known 1. Evidence has accumulated indicating that nonsmoking pregnant women exposed to ETS on a daily basis for several hours are at increased risk for producing low-birthweight babies, through mechanisms which are, as yet, unknown. Recent studies show a dose-response relationship between the number of cigarettes smoked by the father and birthweight of the children of nonsmoking pregnant women.
OTHER HEALTH CONSIDERATIONS IN CHILDREN 274 2. A few studies have reported that children of smokers have reduced growth and development. These require further corroboration to differentiate in utero exposure from subsequent childhood exposures. 3. Household exposure to ETS is linked with increased rates of chronic ear infections and middle-ear effusions in young children. For children with nasal allergies and recurrent otitis media, ETS exposure may synergistically increase their risk of persistent middle-ear effusions. What Scientific Information Is Missing 1. Experimental studies should be developed to articulate possible mechanisms through which paternal smoking adversely effects fetal growth in nonsmoking pregnant women. Special emphasis should be placed on identifying relevant effects of pregnancy on excretion and absorption of ETS, including transplacental metabolism. 2. Additional study is needed to corroborate one finding of a dose-response relationship between reduced height of children and increasing numbers of cigarettes smoked in the home, regardless of whether the mother smoked during pregnancy and regardless of which parent smoked. 3. Research should be conducted to explore the mechanisms by which exposure to ETS might adversely affect the functioning of the ear and to study possible long-term consequences of ETS exposure for the auditory apparatus. REFERENCES Abel, E.L. Smoking during pregnancy: A review of effects on growth and development of offspring. Hum. Biol. 52:593â625, 1980. Berkey C.S., J.H.Ware, F.E.Speizer, and B.G.Ferris, Jr. Passive smoking and height growth of preadolescent children. Int. J. Epidemiol. 13:454â458, 1984. Black, N. The aetiology of glue earâA case-control study. Int. J. Pediatr. Otorhinolaryngol. 9:121â133, 1985. Borlee, I., A.Bouckaert, M.F.Lechat, and C.B.Mission. Smoking patterns during and before pregnancy: Weight, length and head circumference of progeny. Eur. J. Obstet. Gynecol Reprod. Biol. 8:171â177, 1978. Butler, N.R., and H.Goldstein. Smoking in pregnancy and subsequent child development. Br. Med. J. 4:573â575, 1973.
OTHER HEALTH CONSIDERATIONS IN CHILDREN 275 Dunn, H.G., A.K.McBurney, S.Ingram, and C.M.Hunter. Maternal cigarette smoking during pregnancy and child's subsequent development. I. Physical growth to the age of 6 1/2 years. Can J. Public Health 67:499â505, 1976. Gibel, W., and H.-H.Blumberg. Die Auswirkungen der Rauchgewohnheiten von Eltern auf das ungeborene und neugeborene Kind. Z. Ãrztl. Fortbild. 73:341â342, 1973. Goldstein, H. Factors influencing the height of seven year old childrenâResults from the National Child Development Study. Hum. Biol. 43:92â111, 1971. Hughes, J.R., L.H.Epstein, F.Andrasik, D.F.Neff, and D.S.Thompson. Smoking and carbon monoxide levels during pregnancy. Addict. Behav. 7:271â276, 1982. Holmberg, P.C., and M.Nurminen. Congenial defects of the central nervous system and occupational factors during pregnancy. A case- referrent study. Am. J. Ind. Med. 1:167â176, 1980. Kraemer, M.J., M.A.Richardson, N.S.Weiss, C.T.Furukawa, G.G.Shapiro, W.E.Pierson, and W.Bierman. Risk factors for persistent middle-ear effusions. Otitis media, catarrh, cigarette smoke exposure and atopy. JAMA 249:1022â1025, 1983. MacMahon, B., M.Alpert, and E.J.Salber. Infant weight and parental smoking habits. Am. J. Epidemiol. 82:247â261, 1966. Martin, T.R., and M.B.Bracken. Association of low birth weight with passive smoke exposure in pregnancy. Am. J. Epidemiol. 124:633â642, 1986. Meredith, H.V. Relation between tobacco smoking of pregnant women and body size of their progeny: A compilation of published studies. Hum. Biol. 47:451â472, 1975. Miller, H.C., K.Hassanein, and P.A.Hensleigh. Fetal growth retardation in relation to maternal smoking and weight gain in pregnancy. Am J. Obstet. Gynecol. 125:55â60, 1976. Pukander, J., J.Lustonen, M.Timore, and P.Karma. Risk factors affecting the occurrence of acute otitis media among two and three year old urban children. Acta Otolaryngol. 100:260â265, 1985. Rantakallio, P. A follow-up study up to the age of 14 of children whose mothers smoked during pregnancy. Acta Paediatr. Scand. 72:747â753, 1983. Rona, R.J., C.Du Ve Florey, G.C.Clarke, and S.Chinn. Parental smoking at home and height of children. Br. Med. J. 283:1363, 1981. Rona, R.J., S.Chinn, and C.Du Ve Florey. Exposure to cigarette smoking and children's growth. Int. J. Epidemiol. 14:402â409, 1985. Rubin, D.H., P.A.Krasilnikoff, J.M.Leventhol, B.Weile, and A.Berget. Effect of passive smoking on birth-weight. Lancet 2:415â417, 1986. Underwood, P.B., K.F.Kesler, J.M.O'Lane, and D.A.Collagan. Parental smoking empirically related to pregnancy outcome. Obstet. Gynecol. 29:1â8, 1967. U.S. Department of Health and Human Services. The Health Consequences of Smoking. Selected Chapters from the 1971â1975 Report. Report of the Surgeon General Publ. No. CDC 78â8357. Washington, D.C.: U.S. Department of Health, Education, and Welfare, Public Health Service, Office on Smoking and Health, 1976. 657 pp.
OTHER HEALTH CONSIDERATIONS IN CHILDREN 276 Yerushalmy, J. Statistical considerations and evaluation of epidemiological evidence. In G.James, Ed. Tobacco and Health. Springfield, Illinois: Charles C Thomas, 1962. Yerushalmy, J. The relationship of parents' cigarette smoking to outcome of pregnancyâImplications as to the problem of inferring causation from observed associations. Am. J. Epidemiol. 93:443â456, 1971.