Adolescent Environmental Tobacco Smoke Exposure Predicts Academic Achievement Test Failure

Article Outline

• Abstract
• Childhood ETS exposure
  • Purpose
• Methods
  • Sample and design
  • Outcome measure
  • Predictor variables
    • Maternal smoking during pregnancy
    • Offspring ETS exposure at age 16 years
  • Controlling variables
    • Maternal smoking before pregnancy with target offspring
    • Mother’s age during pregnancy with target offspring
    • Parental socioeconomic classification (SEC)
    • Offspring gender
    • Adolescent smoking status
  • Analysis
• Results
  • Characteristics of offspring and parents
  • O-Level achievement model
  • A-Level achievement model
• Discussion
  • Policy and treatment implications
• References
• Copyright

Abstract 

Purpose

Research has linked prenatal tobacco exposure to neurocognitive and behavioral problems that can disrupt learning and school performance in childhood. Less is known about its effects on academic achievement in adolescence when controlling for known confounding factors (e.g., environmental tobacco smoke [ETS]). We hypothesized that prenatal tobacco exposure would decrease the likelihood of passing academic achievement tests taken at 16 and 18 years of age.

Methods

This study was a longitudinal analysis of birth cohort data including 6,380 pregnant women and offspring from the 1958 National Child Development Study (NCDS). Academic pass/fail performance was measured on British standardized achievement tests (“Ordinary Level” [O-Level] and Advanced Level: [A-Level]). Prenatal tobacco exposure plus controlling variables (ETS, teen offspring smoking and gender, maternal age at pregnancy, maternal smoking before pregnancy, and socioeconomic status) were included in regression models predicting O- and A-Level test failure.

Results

Significant predictors of test failure in the O-Level model included exposure to maternal (OR = 0.71, p < .0001) and paternal (OR = 0.70, p < .0001) ETS, as well as teen smoking, female gender, and lower SES. Prenatal tobacco exposure did not influence failure. Similar factors emerged in the A-Level model except that male gender contributed to likelihood of failure. Prenatal exposure remained nonsignificant.

Conclusions

Our model suggests that adolescent exposure to ETS, not prenatal tobacco exposure, predicted failure on both O- and A-Level achievement tests when controlling for other factors known to influence achievement. Although this study has limitations, results bolster growing evidence of academic-related ETS consequences in adolescence.

Keywords: Adolescent, Environmental tobacco smoke, ETS, Academic achievement, Longitudinal

Both the United States and United Kingdom produce similar population data related to maternal smoking during pregnancy and children’s exposure to tobacco and its constituents. For example, approximately one third of women in their childbearing years are smokers, 10– 15% of women report smoking during pregnancy [1], [2] and up to 60% of children may be exposed to environmental tobacco smoke (ETS) in the home [3]. Smoking during pregnancy is an established risk factor for preterm birth, low birth weight, offspring’s delayed gross and fine motor coordination, and sudden infant death syndrome, accounting for 47% of all neonatal deaths [4], [5], [6], [7] Similarly, children’s ETS exposure has causal influence on child health problems, many of which influence future adolescent and adult health. A recent cross-sectional, cotinine-verified study of 5,400 children demonstrated health effects across the entire sample of 4- to 16-year-olds, whereby significant effects associated with high cotinine levels included wheezing, impaired lung function, and 6 or more days of absence from school within the last year [8]. Respiratory effects of ETS exposure and the development of respiratory symptoms have been demonstrated in both cross-sectional and longitudinal studies in 16- to 40-year-olds as well [9], [10], [11]. The consequences of prenatal and childhood exposure to ETS extend beyond health problems. The following sections highlight ETS-related academic achievement relationships.

Prenatal tobacco exposure may directly and indirectly affect academic achievement in childhood as evidenced by the higher risk among exposed versus nonexposed children of displaying cognitive and academic deficits, learning disabilities, impulsivity, auditory processing deficits, and decreased performance on intelligence tests [12], [13], [14], [15], [16], [17], [18], [19], [20], [21]. Such evidence has been extended by research on sibling pairs whose mother smoked during one pregnancy but not another [19]. Moreover, prenatal tobacco exposure-academic performance relationships may be mediated by offspring’s tobacco-related behavioral and psychological problems such as attention deficit disorder and conduct disorder [20], [22], [23], [24], [25].

Few studies have examined the effects of prenatal tobacco exposure on academic achievement or deficits related to achievement beyond childhood. Moreover, studies of prenatal exposure-related neurocognitive consequences [26], [27] often demonstrate less definitive results when controlling for confounding psychosocial and environmental factors. Martin et al [28] examined academic achievement-related effects of prenatal tobacco exposure longitudinally while controlling for confounding variables known to affect offspring development and academic performance. Their results indicated differential effects of prenatal tobacco exposure at infancy, preschool, and school age (age 12 years) [28].

Most relevant to the present paper, Martin et al [28] demonstrated that among offspring at age 12 years, teachers rated prenatal exposed versus non-exposed children as having greater distractibility, negative emotionality, and immaturity as well as less task-oriented behaviors likely to interfere with academic achievement. Direct measures of achievement at age 12 indicated that offspring of smoking mothers had significantly lower end-of-year summary grades than children of nonsmoking mothers.

Prenatal tobacco exposure clearly causes many health problems and increases risks of neurocognitive and behavioral problems that can undermine future academic achievement. However, many extant studies do not adequately control for confounding variables including offspring exposure to ETS during childhood [29].

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Childhood ETS exposure 

Evidence of postnatal ETS exposure effects on academic performance is sparse albeit expanding, in comparison to evidence of effects from prenatal exposure. Existing research suggests inverse relationships between recent ETS exposure and young children’s receptive vocabulary skills and reasoning tasks [12]. A review of 17 epidemiological studies that attempted to separate effects of prenatal versus childhood ETS exposure suggested subtle detrimental effects of ETS exposure on children’s neurodevelopment and behavior [15]. ETS exposure caused subtle changes in measures of neurocognitive development and behavior; however, results from many of these studies were difficult to interpret because of the colinearity of prenatal and postnatal exposure [15], as well as potential confounding psychosocial and demographic factors. These methodological issues, together with the relatively small number of ETS studies, make it difficult to determine the degree of influence of prenatal tobacco exposure versus ETS exposure on neurocognitive, behavioral, and academic outcomes. However, recent evidence from Yolton et al [30] examining the Third National Health and Nutrition Examination Survey (NHANES III) conducted between 1988 and 1994 in the U.S. [31] appear to strengthen the call to examine further the prenatal versus concurrent ETS exposure contributions to academic achievement deficits. Using data for 5,365 individuals 6–16 years old reporting recent tobacco abstinence, their results showed an inverse dose–response relationship between children’s cotinine levels and reading test scores, visuospatial reasoning skills, and math skills—with the negative effects of ETS on reading skills persisting even at low levels of exposure (<0.5 ng/mL) [30]. Moreover, a significant ETS-reading skills relationship remained when controlling for confounding effects of prenatal tobacco exposure, birth weight, and NICU admittance among a subsample of 1,266 children [30]. Although their ETS-related data were compelling, their data did not provide comparisons of retrospective, self-reported prenatal tobacco exposure and current ETS exposure effects on academic skills performance. To better understand academic-related tobacco exposure consequences, large, prospective birth cohort studies that include measures of prenatal and concurrent ETS exposure are needed.

Purpose 

Prenatal tobacco exposure–academic performance relationships remain inconclusive when controlling for known confounding factors such as ETS. Moreover, there are no studies that appropriately examine the effects of both prenatal tobacco and ETS exposure on late-adolescent academic achievement. These gaps are important to address, given that both tobacco exposure effects may manifest differently across age ranges. Therefore, while controlling for known confounding factors, we examined the influence of prenatal and adolescent ETS exposure on adolescent offspring achievement test performance. Based on existing evidence, we hypothesized that prenatal exposure to tobacco would significantly increase the likelihood of adolescent academic achievement test failure.

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Methods 

Sample and design 

Information was originally obtained from parents of 17,414 male and female children born in the U.K. March 3– 9, 1958, and from their surviving offspring during follow-up sweeps of survivors at ages 16 and 23 years. Follow-up sweeps reached 10,000-12,000 of the original cohort, with each sweep varying slightly in sample composition due to variable response rate. Data originated from the U.K.’s 1958 National Child Development Study (NCDS), an ongoing multidisciplinary investigation of a nationally representative cohort followed from birth into adulthood, with data collection on all study participants attempted at several follow-up “sweeps” by questionnaire, examination, or interview at varying ages between 1958 and 1991. These data are available for secondary analysis from the Data Archive at the University of Essex (http://www.data-archive.ac.uk/). Data obtained for this study were derived from parent and offspring reports when offspring were 16 and 23 years old, respectively.

Outcome measure 

Adolescent offspring academic achievement was measured by unverified, retrospective self-report when offspring were 23 years old (1981). Achievement was classified as pass versus fail, and was determined by performance on nationally standardized achievement tests taken at 16 years of age (“Ordinary Level” [O-Level]) and 18 years old (“Advanced Level” [A-Level]). In the U.S., these tests would be loosely akin to a general high school achievement test (O-Level) and a college entrance exam such as the Scholastic Achievement Test (SAT) (A-Level).

Predictor variables 

The only data available to determine fetal offspring exposure to tobacco was 1958 maternal report of smoking after the 4^th month of pregnancy. Smoking status, determined by unverified maternal self-report at the end of pregnancy, was coded dichotomously (smoker vs. nonsmoker).

Via an unverified maternal self-report in 1974, we included three variables to capture adolescents’ ETS exposure in the home, including daily maternal and/or paternal cigarette smoking (at least one smoker vs. nonsmoker), and daily paternal cigar/pipe smoking (yes vs. no).

Controlling variables 

A maternal self-report from 1958 provided information on maternal smoking (smoker vs. nonsmoker) before pregnancy with target offspring.

Because of nonproportionality across the age range, we constructed this variable to represent three age categories: <20 years, 21–24 years, and >24 years.

Data on parental SES were derived from self-report of paternal occupation and coded as SEC I-V according to the Registrar General’s Classification of Socioeconomic Status. Cases classified as unemployed or sick (n = 5) were excluded. The SEC variable used in the analysis was an average value including the observation taken at birth, and the two subsequent time points.

Gender was included to account for potential biases that could influence differential test performance between boys and girls.

Offspring report of smoking during adolescence was included to control for the influence of smoking on academic performance and to capture effects of latent adolescent psychosocial variables known to influence academic performance. We differentiated between light smoking and heavy smoking (< 10 vs. ≥ 10 cigarettes per day).

Analysis 

The overall analysis strategy was to model dichotomous, pass versus fail achievement (1, 0). The inclusion criterion was provision of self-report data at both follow-up time points (1974 and 1981). We conducted two logistic regression analyses to analyze test performance on the O- and A-Level examinations, respectively given that success on the O-Level is a prerequisite for taking the A-Level, thereby creating a smaller, subsample of students taking the A-Level examination. All analyses were conducted using Stata software (Stata Corporation, College Station, TX), and results are presented as odds ratios (OR) together with 95% confidence intervals. We used the cluster-correlated robust covariance to adjust standard errors for within-subject correlation.

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Results 

Characteristics of offspring and parents 

Every surviving offspring who provided complete self-report data at both follow-up time points were included in the study. For outcomes measured both at 16-year (1974) and 23-year (1981) follow-ups, this resulted in a final complete sample of n = 6380, representing approximately 41% of the original live births, and between 60% and 72% of the maximum number reached in follow-up sweeps. Table 1 compares the parental attributes of those in the final complete sample with those who were excluded for incomplete data.

Table 1. Parental attribute comparisons between complete and incomplete samples

Table 2 shows offspring demographic and smoking characteristics of the final sample¹ it also compares offspring characteristics of the final complete data sample and those excluded from the analyses.

Table 2. Offspring demographic and smoking characteristics of the final sample

	Level	(%)
		Incomplete	Complete
Sex	Male	52.61	49.99	x2(1)=11.45
	Female	47.39	50.01	p=.001
Marital status (1981)	Single, divorced, widowed	55.42	55.41	x2(1)=.00
	Legally married	44.58	44.59	p < 1.00
First job status at 23-year follow-up	Professional	2.41	3.34	x2(6)=38.65
	Intermediate	10.34	11.22	p < .0001
	Skilled nonmanual	36.72	39.23
	Skilled manual	25.38	24.43
	Semi-skilled nonmanual	3.46	2.92
	Semi-skilled manual	16.36	15.06
	Unskilled manual	5.33	3.81
Smoking status	Nonsmoker	65.15	69.38	x2(1)=24.27
	At 16-year follow-up			p < .0001
	Nonsmoker	38.32	43.86	x2(1)=27.51
	At 23-year follow-up			p < .0001
	Nonsmoker	64.16	70.16	x2(1)=45.70
	At 33-year follow-up			p < .0001
		Mean (SD)
Consumption among daily smokers	Cigarettes/day	15.64	15.34	t(5065)=1.20
	At 23-year follow-up	(8.88)	(8.81)	p=.23
	Cigarettes/day	16.83	16.11	t(3742)=2.31
	At 33-year follow-up	(9.36)	(9.61)	P=.02

O-Level achievement model 

Table 3 illustrates the O-Level test performance model. This model suggests that adolescents were more likely to fail the examination if they were exposed to maternal and paternal cigarette ETS, smoked cigarettes themselves (particularly 10 or more cigarettes/week), were female, had a younger mother, and had a lower SES status. Maternal smoking prior to pregnancy and smoking during pregnancy (offspring prenatal exposure) were not significant predictors of academic failure.

Table 3. Ordinary-Level (O-Level) examination failure model (n = 6380)

O-Level failure	OR	95% CI	p = z
Father’s socioeconomic classification	.64	.60,.67	.0001
Offspring gender (1 = female)	1.40	1.25,1.56	.0001
Mother young <23 years (ref. group)	1.00
Mother age ≥23 years	1.16	1.01,1.33	.03
Maternal smoking before pregnancy	.99	.95,1.05	.94
Maternal smoking late in pregnancy	.91	.74,1.13	.39
Mother smoked cigarettes (offspring ETS exposure)	.71	.61,.82	.0001
Father smoked cigarettes (offspring ETS exposure)	.70	.62,.79	.0001
Father smoked pipe (offspring ETS exposure)	1.10	.88,1.37	.42
Adolescent smoking <1/week (ref.)	1.00
Adolescent smoking 1–9/week	.55	.44,.69	.00001
Adolescent smoking ≥10/week	.33	.29,.37	.00001

LR chi²(10) = 1003.87; Prob > chi² = .00; Log likelihood = −3599.57; Pseudo R² = .12; CI = confidence interval; ETS = environmental tobacco smoke; OR = odds ratio.

A-Level achievement model 

Consistent with the O-Level model, prenatal tobacco exposure did not influence test performance on the A-Level examinations; however, ETS exposure did predict failure. Table 4 shows that adolescents were more likely to fail the A-Levels if they were exposed to maternal and paternal cigarette ETS, smoked cigarettes themselves (particularly ≥10 cigarettes/week), were male, had a younger mother, and had a lower social classification (SEC).

Table 4. Advanced-Level (A-Level) examination failure model completed by students previously passing the ordinary-Level (O-Level) examination (n = 4189)

A-Level failure	OR	95% CI	p = z
Father’s social class	.63	.59,.66	.00001
Sex female	.84	.74,.97	.01
Mother young <23 years (ref. group)	1.00
Mother ≥23 years	1.38	1.15,1.67	.001
Maternal smoking before pregnancy	1.02	.95,1.10	.58
Maternal smoking late in pregnancy	.82	.62,1.08	.16
Mother smoked (1974)	.76	.63,.92	.005
Father smoked (1974)	.73	.63,.85	.00001
Father smoked pipe (1974)	.92	.73,1.16	.47
Adolescent smoking <1/week (ref.)	1.00
Adolescent smoking 1–9/week	.75	.56,1.00	.05
Adolescent smoking ≥10/week	.29	.23,.36	.00001

LR chi² (10) = 597.21; Prob > chi² = .00; Log likelihood = −2447.62; Pseudo R² = .11; CI = confidence interval; OR = odds ratio.

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Discussion 

This study suggests that recent ETS exposure is a more important factor than prenatal tobacco exposure in predicting adolescent achievement test performance. Consistent in both regression models, exposure to both maternal and paternal cigarette smoke at age 16 years significantly predicted failure. Exposure to paternal cigar/pipe smoke did not influence test performance, perhaps due to the relatively small number of paternal (n = 974) cigar/pipe smokers compared to maternal (n = 4,992) and paternal (n = 5,457) cigarette smokers. Maternal smoking during pregnancy did not significantly contribute to the models of test failure.

Our results emphasize the importance of the inclusion of confounding variables such as ETS and other factors known to predict academic performance when assessing effects of prenatal tobacco exposure on offspring outcomes such as academic performance. Among other controlling variables in our models, teen smoking was a significant predictor of O- and A-Level performance, showing higher smoking rates increasing the likelihood of failure. SEC predicted failure on both examinations, with slightly greater effect on the A-Level tests. It is likely that both teen smoking and SEC capture latent biopsychosocial comorbidity factors that could influence offspring’s ability to pass the O-Levels and their choice to take, as well as their ability to pass, the A-Levels. Mother’s age at pregnancy was another such variable, with younger mothers delivering offspring that were more likely to fail in both models. The effect of mothers’ age could reflect differential parenting care affecting offspring academic performance.

Females in our sample were more likely to fail the O-Level tests, and males were more likely to fail the A-Level tests. The direction of this relationship was different than expected in the O-Level model, given that girls typically outperform boys in standardized achievement tests. Perhaps the direction of results with the O-Level tests reflects, in part, the sociocultural climate of 1950–1970 Britain wherein mid-20^th Century gender roles and expectations for girls’ career goals may have contributed to girls’ performance on or interest in the O-Levels.

Our study demonstrates the predictive effects of adolescent ETS exposure on adolescent achievement test failure. Nonetheless, there are several limitations to the present study. Primary limitations reflect the inherent constraints of the dataset. For example, maternal report of smoking during pregnancy was limited to answering whether she smoked after month 4 of pregnancy. It is impossible to determine from this variable whether offspring were exposed to tobacco in the first trimester, when tobacco-related neurocognitive damage would likely be the greatest, or the degree or dosages of exposure (e.g., number of weeks, etc.) Nonetheless, given that relatively few women in 1950s United Kingdom were likely warned about the dangers of smoking during pregnancy, it is safe to assume that smoking during the second trimester could relate to smoking in the other trimesters, although there is no way to be certain with the data available.

We were also limited to using a gross, dichotomous achievement outcome as opposed to a continuous measure, and there were no variables that would enable testing potential mechanisms of the relationship between ETS exposure and academic performance. We were unable to include potential moderator variables, such as maternal psychopathology during pregnancy or postpartum. However, the results from this study can stimulate future, more fine-grained analyses in this area of interest. Future studies also could attempt to disentangle ETS-related neurocognitive consequences from other biopsychosocial and environmental factors that affect academic performance and examine potential interactions of psychosocial and genetic factors in the expression of ETS exposure-related academic problems.

Also, our data consisted of unverified self-report. Although a limitation, the likelihood of misreporting could be considered low given that respondents had nothing to gain from misreporting and would have known their reports could be verified by existing test records. With regard to smoking behavior, evidence of the reliability of anonymous surveys of adolescent smoking behavior [32] suggests there is no specific reason to expect under-reporting of smoking. Likewise, we are not aware of any research that would increase concern of over-reporting of ETS exposure. Our data also lacked biochemical verification of maternal and offspring smoking, a considerable limitation by modern research standards that should be considered when interpreting these results. Also, the dataset did not provide data to examine potential variability in cumulative ETS exposure during childhood. Reported ETS exposure was only available at one time point, age 16 years. However, it is reasonable to assume that offspring were exposed to ETS throughout their childhood given the national smoking rates during the 1950s through 1970s and lack of information about deleterious effects of ETS.

Another argument could be made that all sample respondents would have been exposed to ETS on a daily basis throughout the community—as mothers and offspring. Indeed, this sample would have been exposed to a large lifetime dose of ETS in comparison to today (lower smoking rates, greater number of public smoking bans.) Thus ETS could have undermined all respondents’ academic performance. Because it is impossible to determine dosage effects with the data available, we cannot test this assumption. Therefore it is important to consider that direct exposure by parents can amplify ETS consequences that may exist with any exposure.

Final limitations include the dataset’s inability to determine how long smoking teens had been smoking before age 16 years and the decision to not include other risk factors such as maternal and offspring other substance use and psychopathology. However, it is well known that smoking is strongly correlated with substance use and psychopathology, and smoking would account for some of this latent variance in our models. Nonetheless it is impossible to disentangle these potential interrelationships and their effects on academic performance.

When considering these limitations for future studies, Wakschlag et al [20] provide appropriate guidelines for prospective studies to better enable interpretation of causality and to examine timing and dosage aspects of exposure and its academic consequences. The key challenge is following exposed offspring prenatally through adolescence to identify early versus concurrent versus cumulative exposure-related behavioral and neurocognitive vulnerabilities that may or may not cause adverse behavioral outcomes over time [20].

Despite the limitations stated above, a primary strength of this study is that it generates testable hypotheses for future research aimed to improve our understanding of relationships between ETS and adolescent academic performance. Future research could explore hypotheses within theoretical frameworks that can tease apart reciprocal interrelationships and interactions of the many biological and psychosocial factors that could account for the expression of academic deficits among tobacco exposed offspring beyond what was possible in this study. Biopsychosocial models provide such a framework for complex, multi-determined relationships between exposure and behavior. Within these models, direct and indirect effects of prenatal and childhood exposure to ETS on academic performance can be tested with other predictors, such as psychosocial (e.g., maternal psychopathology, parenting skills, etc.) and biological (e.g., fetal alcohol exposure, adolescent substance abuse, etc.) risk factors and potential mediating variables (e.g., cognitive ability, childhood externalizing disorders, ETS-related illness, etc.).

In this study, many of these “other,” etiologically important psychosocial and biological risk factors for academic failure would be considered latent variables in our model—we could not measure or capture them, yet their influence were likely captured because of their inter-relationships among variables that we could capture. Without the opportunity to enter important sources of heterogeneity such as developmental course, exposure dosage, and comorbidity in this study gives rise to opportunity for future researchers in this area who could consider using latent class or mixed models analyses to examine the complex set of multiple predictors and mediators that influence adolescent academic achievement.

To guide future research, we speculate that part of the influence of ETS may relate to health-related consequences of exposure. Research has established that ETS exposure increases incidence and severity of a variety of acute and chronic illness in children [33], [34], [35], [36] as well as adolescents and adults [9], [10], [11], [37]. Increased frequency and severity of illnesses would contribute to school absences and missed academic opportunities. ETS-related illness (e.g., otitis) could contribute to learning skills deficits (e.g., auditory processing) that could undermine academic skills development. Yet another factor that could mediate the ETS-academic performance link could be ETS-related behavioral problems that disrupt academic development and subsequent achievement [19].

Perhaps the teen smoking variables in our models capture variance of potential mediating factors such as conduct problems and other substance abuse that influence academic failure more than the ETS variables account for alone. For example, it is well known that tobacco use and individuals with nicotine dependence have increased risk for alcohol and illicit drug dependence, major depression, anxiety disorders, impulsivity, risk taking, and antisocial personality disorder [38], [39]. One feature of our models is that both ETS exposure and teen offspring smoking simultaneously related to academic failure when adjusting for the same confounding factors. These two variables may capture different, albeit overlapping, latent factors that influence academic failure. Bryant et al [40] tested a priori models of the interrelationships between academic achievement, social bonding, school misbehavior and cigarette use among adolescents from grades 8–12. Their models suggested that school misbehavior, low academic achievement, and cigarette use were interrelated.

This study gives rise to many opportunities for future studies to examine differential effects of prenatal tobacco versus ETS exposure on academic achievement within the context of other confounding factors. More current longitudinal studies could ensure appropriate measures of ETS exposure, and could examine potential differential age-related manifestations of tobacco exposure as well as ensure biochemically verified reports of smoking behavior.

Policy and treatment implications 

Our study supports growing evidence that ETS is an environmental toxin that affects academic performance. Evidence herein should further encourage multi-pronged efforts to reduce adolescents’ ETS exposure. This research points to the need to improve our understanding of the influence of ETS on neurocognitive systems, development, and subsequent academic performance—and how ETS exposure consequences might manifest differently at different age ranges during childhood and adolescence. Regarding implications for smoking treatment and ETS-exposure prevention, we emphasize that these data highlight the importance of helping smoking parents create smoke-free homes for their children—outcomes that can be achieved without requiring the immediate parental smoking cessation. Indeed, parental smoking cessation is the ideal outcome in reducing children’s ETS exposure. Nonetheless, health professionals are beginning to advocate for referrals to ETS reduction interventions as a positive alternative to smoking cessation treatment for those parents not willing or ready to consider abstinence-only treatment [41]. Finally, this study suggests the importance of addressing ETS exposure and parental smoking regardless of the child’s age.

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• 1 Although chi-square tests indicated that attributes differ across the two groups, an examination of the relative frequencies suggested that they are largely uniform across the data groups and that the statistical significance observed was due to the chi-square tests being overpowered as a result of the large sample size. For example, the significant 5.2 point difference in the percentage of mothers smoking late in pregnancy corresponds to an effect size of d = 0.0007, and the 2.7 point difference in the percentage males at birth corresponds to an effect size of d = 0.0004.