Maternal Smoke And Increased Risk Of Sudden Infant Essay
Maternal Smoke And Increased Risk Of Sudden Infant Essay
Question:
Answer:
Research Hypothesis
There will be no difference in the rate of infant death syndrome in relation to the rate of maternal smoking
Research Hypothesis Alternative
There will significant difference in the rate of infant death syndrome in relation to the rate of maternal smoking.
A Research Question Using PO
What is the rate of occurrence of infant mortality arising out of maternal smoking in Saudi-Arabia during the tenure of 2015 to 2017?
A Research Question Using PECO
What is the infant death syndrome (SIDS) risk among the smoking mother in comparison to the non-smoking mothers?
A Research Question Using PICO
| P (problem or patient or population) | Infant death syndrome |
| I (Intervention) | Prevention of maternal smoking (prenatal and post natal) |
| C (Comparison) | Reduced rate of smoking (prenatal and post natal) |
| O (Outcome) | Reduced rate of infant death syndrome |
Maternal smoking is detrimental to the development of fetuses and neonates. This meta-analysis was performed to measure the accumulated association of sudden infant death syndrome (SIDS) risk with both prenatal and postnatal maternal smoking. The odds ratio (OR) corresponding to the 95% confidence interval (CI) was used to assess the associations between maternal smoking and SIDS risk. The statistical heterogeneity among studies was assessed with the Q-test and I(2) statistics. Maternal Smoke And Increased Risk Of Sudden Infant Essay. The data for this meta-analysis were available from 35 case-control studies. The prenatal and postnatal maternal smoking was associated with a significantly increased risk of SIDS (OR=2.25, 95% CI=2.03-2.50 for prenatal maternal smoking analysis, and OR=1.97, 95% CI=1.77-2.19 for postnatal maternal smoking analysis, respectively) by random effects model. After stratified analyses, regardless of prenatal or postnatal smoking, heavy cigarette consumption increased the risk of SIDS and significantly elevated SIDS risk was found to be associated with co-sleeping with postnatal smoking mothers. Our results suggested that maternal smoking were associated with elevated SIDS risk, the effects were dose-dependent. In addition, SIDS risk was significantly increased in infants co-sleeping with postnatal smoking mothers.
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Early child neurodevelopment has major impacts on future human capital and health. However, not much is known about the impacts of prenatal risk factors on child neurodevelopment. This study evaluates the effects of maternal smoking during pregnancy on child neurodevelopment between 3 and 24 months of age and interactions with socioeconomic status (SES). Data from a unique sample of children from South America are employed. Smoking has large adverse effects on neurodevelopment, with larger effects in the low SES sample. The study results highlight the importance of early interventions beginning before and during pregnancy for enhancing child development and future human capital attainment.
I. Introduction
Maternal smoking during pregnancy contributes to a variety of infant health problems present at birth as well as long lasting behavioral and neurodevelopmental impairments, and remains arguably one of the most important modifiable risk behaviors for child and long-term health and human capital (Buka, Shenassa, and Niaura 2003; Dunn et al. 1976; Fried 1989; Fried and Watkinson 1988; Key et al. 2007; Lanting 2009; Obel et al. 1998; Olds, Henderson, and Tatelbaum 1994; Richardson, Walker, and Horne 2009; Weitzman, Gortmaker, and Sobol 1992). Maternal smoking increases the risk for several adverse birth outcomes including infant death, preterm birth, low birth weight and poor intrauterine growth (Buka et al. 2003; Dunn et al. 1976; Lanting 2009; Richardson et al. 2009; Weitzman et al. 1992)1. Further child health implications due to smoking during pregnancy may include respiratory problems and infections (DiFranza, Aligne, and Weitzman 2004; Weitzman et al. 1992)2. Maternal Smoke And Increased Risk Of Sudden Infant Essay.
Several studies have shown that the early physical health problems increased by smoking have adverse effects on human capital accumulation throughout life in both developed and less developed countries. For example, infants who are born at low birth weight have reduced educational achievement in the form of lower test scores, fewer school years completed, and higher rates of dropping out of school and lower economic performance in the form of lower income and living in areas with high poverty later in life (Button, Maughan, and McGuffin 2007; Case, Fertig, and Paxson 2005; Saigal and Rosenbaum 2007; Taylor et al. 2000; Victora et al. 2008).3 Some of the pathways through which early health conditions such as low birth weight reduce human capital are through increasing risks for developmental, behavioral and chronic health problems (Button et al. 2007; Case 2010; Saigal and Rosenbaum 2007; Taylor et al. 2000; Victora et al. 2008).4
In addition to affecting physical health, in utero exposure to maternal smoking may have adverse effects on cognitive ability, neurological health and behavior of infants and children. Neurodevelopment encompasses several neurological and psychomotor skills including fine and gross motor, language, and social adaptation skills and may be considered an early form of not only health but also human capital as several of these earlier skills are strongly predictive of standard measures of human capital such as education and cognitive performance later in life as highlighted below. The adverse effects of prenatal smoking on child neurodevelopment may include poor language development and reduction in cognitive functioning. Key et al. (2007) find that infants exposed to maternal smoking in utero have both delayed response to sound and a lower ability to discriminate between sounds after birth, which impact later language skills (Fried 1989; Molfese 2000). Maternal Smoke And Increased Risk Of Sudden Infant Essay, Prenatal exposure to smoking may also reduce the child’s motor performance, mental development (measured by the Bayley Scales of Infant Development), IQ scores, and language development through age three years (Fried 1989; Fried and Watkinson 1988; Gusella and Fried 1984; Obel et al. 1998; Richardson, Day, and Goldschmidt 1995).5
Prenatal smoking may also increase the risks of several child behavioral problems including externalization of aggressive and hyperactive behavior, prolonged periods of verbal or physical aggression and/or socially undesirable behavior (conduct disorder) throughout childhood, and delinquency in later childhood (Faden and Graubard 2000; Herrmann, King, and Weitzman 2008; Olds et al. 1994). Several of these behavioral health problems have adverse effects on future human capital. For example, Currie et al. (2010) report lower probability of 12th grade completion by age 17 years and increases in welfare use for children who had ADHD earlier in life compared to their siblings without ADHD.
There is evidence for long-lasting adverse effects of prenatal smoking on some human capital measures throughout childhood, adolescence and adulthood. Individuals who were exposed to maternal smoking in utero have lower scores on spelling, language and math assignments and tests through later childhood and teenage years (Bastra 2003) as well as deficits in auditory and visual processing (Fried 2002). Milberger et al. (1998)find that male children aged 6–17 years of women who smoked during pregnancy have significantly lower IQ scores overall compared to those who were born of non-smoking women. Case et al. (2005) report reduced employment at age 33 and 42 years among men exposed to moderate or heavy prenatal smoking. Other adverse long-term effects on human capital through increased prevalence of ADHD, externalizing behavior (Stene-Larsen 2009), criminal arrests, hospitalization for psychiatric disorders and conduct disorder (Wakschlag et al. 1997) are also found to have a dose-response relationship to maternal smoking during pregnancy (Brennan et al. 2002; Ernst, Moolchan, and Robinson 2001; Fergusson, Woodward, and Horwood 1998; Indredavik et al. 2007; Milberger 1998). It is also important to note that children of mothers who smoked during pregnancy are more likely to become smokers themselves later in life (Buka et al. 2003; Cornelius et al. 2000; Ernst et al. 2001).
In addition to the evidence linking prenatal smoking to measures of human capital at various ages either directly or indirectly through physical and behavioral health problems, a main motivation for studying child neurodevelopment as a form of early human capital is the strong evidence linking early neurodevelopmental skills to human capital attainment later in life. Suboptimal child neurodevelopment may reduce cognitive outcomes and educational achievement later in life (Capute et al. 1985; Fernald, Perfors, and Marchman 2006; Murray et al. 2007; Murray et al. 2006; Taanila et al. 2005) . Maternal Smoke And Increased Risk Of Sudden Infant Essay,Murray et al. (2006) find a significant relationship between the age at which a child learns to stand without aid – an important neurodevelopmental milestone – and performance on cognitive tasks involving categorization. Murray et al. (2007) find that earlier age at walking without aid and speaking names other than those of the parents is associated with higher IQ scores during childhood (age 8 years) and better reading comprehension and verbal ability during later adulthood. Suboptimal child neurodevelopment may increase the risks of mental health and behavioral problems later in adolescence and adulthood (Fergusson 1999; Fergusson, Horwood, and Lynskey 1993; Isohanni 2001; Jones 1994; Sigurdsson 1999; van Os 1997), which is expected to have adverse effects on human capital attainment.
It is generally well accepted that prenatal factors such as maternal smoking, nutrition, and body size influence fetal adaptive responses and subsequently have significant impacts on the risk of disease throughout life (Gluckman et al. 2008). One of the mechanisms by which smoking during pregnancy is thought to affect child neurodevelopment is by restricting fetal access to oxygen-rich blood, leading to fetal neurodevelopment impairments (Ernst et al. 2001; Gennser, Marsal, and Brantmark 1975; Maritz 2008). This is thought to occur through impacting uterine blood flow and the level of carboxyhemoglobin (hemoglobin with carbon monoxide) in both the infant’s and mother’s blood (Morrow, Ritchie, and Bull 1988; Soothill et al. 1996).6 In addition, toxins introduced into the mother’s body via smoking readily cross the placenta during gestation and are absorbed easily by the developing fetus (Matta et al. 2007). Some of the early detrimental smoking effects may involve changes in brain activation that affect children’s ability to appropriately respond to stimuli (Bennett et al. 2009).
Given the importance of early child health in general and neurodevelopment specifically for future human capital and that neurodevelopment may be considered an early form of human capital, identifying the effects of maternal risk behaviors during pregnancy, such as smoking, on early child neurodevelopment becomes essential for identifying ways to improve not only neurodevelopment but also human capital throughout life. Therefore, studying the effects of prenatal smoking on neurodevelopment has direct implications for identifying early determinants of human capital that can be addressed by interventions very early in life, including during pregnancy. Identifying these effects may allow for developing such interventions that can have positive multiplicative lifetime effects on health and human capital. Prenatal interventions that improve early child neurodevelopment are likely to be cost-effective and result in large social returns due to the self-producing effects of child developmental skills over time and their complementarity effects with investments later in life (Cunha and Heckman 2007; Doyle et al. 2009). In other words, early child development has direct positive (self-producing) effects on development later in life and may also enhance the effects of later investments. For example, children who have acquired more skills earlier in life may benefit more from later investments compared to those who have acquired fewer skills. Maternal Smoke And Increased Risk Of Sudden Infant Essay.
The increasing knowledge and publicity of the negative smoking effects on health have resulted in reductions in maternal smoking over the past two decades, though only small reductions during certain periods (CDC 2009; Ebrahim 2000).7 Nonetheless, the rates of smoking among women of childbearing age and prenatal smoking are still high worldwide. For example, about 12% of women reported smoking during pregnancy in 2005 in the US and about 22.4% of women of reproductive age continue to smoke (CDC 2008, 2009).8
This study assesses the effects of maternal smoking during pregnancy on child neurodevelopment between ages 3 to 24 months. The study evaluates the smoking effects both pooled and stratified by socioeconomic status (SES), which is a significant predictor of smoking participation and intensity. The paper contributes significantly to understanding the impacts of smoking as a major maternal risk behavior on early child neurodevelopment as a form of human capital. Previous studies of smoking effects during pregnancy on early life neurodevelopment are limited by fairly small sample sizes and descriptive statistical methods that do not account for unobserved confounders that may correlate with both smoking and child neurodevelopment. Another limitation in several studies is relying on maternal report of child developmental measures, which may be biased. Further, previous studies of prenatal smoking effects on child neurodevelopment in populations from less developed countries such as in South America are rare. Such studies are essential given the comparable, and in certain countries, higher prenatal smoking rates compared to developed countries (Bloch et al. 2008).
We address these limitations by studying a unique and large sample of children from South America with systematic neurodevelopmental screening measurements by trained physicians for all sample children. The study estimates the smoking effects accounting for several observed relevant factors and evaluates the potential effects of maternal self-selection into smoking, based on unobserved relevant factors, on the estimated smoking effects.
II. Methods
A. Analytical Framework
The study follows the standard health production approach that has been employed in several previous seminal studies of child health production (such as Rosenzweig and Schultz, 1983; Grossman and Joyce, 1990). The model is based on a maternal utility function U during pregnancy that includes “anticipated” child’s health/development and other utility-enhancing constructs and consumption (Z), which may include maternal health (H), smoking (S), and others as follows:
Child development (D) is produced by maternal inputs and investments (I) during pregnancy such as nutrition and prenatal care use and by maternal health. D is also impacted by smoking but also by other behavioral factors (B) of Z such as alcohol use, stress, exercise, and others, and by exogenous technological factors such as genetic factors (T). Maternal Smoke And Increased Risk Of Sudden Infant Essay. The child development production function can be specified as follows:
The mother maximizes her utility during pregnancy subject to the child development production function (2) and to the following budget constraint of income (G) being equal to expenditures on utility-enhancing consumption and inputs of child health development:
where p are prices. Utility maximization allows deriving reduced-form functions for Z, Iand D that include prices, income, “unobserved” utility-function preferences (R) and “unobserved” exogenous genetic endowments T, assumed known, at least partially, to the mother. For example, the reduced-form function for smoking is as follows:
As shown in Rosenzweig and Schultz (1983), the presence of T in the reduced-form function for behavioral factors such as smoking complicates the estimation of the child development function. Mothers may decide to continue or quit smoking during pregnancy in part because of their perceptions of T based on informal and formal risk indicators such as her and her family’s history of health problems, health professionals’ assessments and recommendations and other indicators that are largely unobserved. For example, mothers who perceive larger developmental risks (lower T) may decide to quit smoking. If so, standard estimation of input effects, even if all relevant inputs are observed, reflects the real effects in equation (2), the impacts of T on development and the relationships between inputs and T and results, therefore, in biased estimates of input effects.
Of course, it is virtually impossible to observe all relevant production inputs, which further biases the classical estimations and results in a theoretically ambiguous net bias. For example, in this study, we do not observe prenatal nutritional inputs and healthcare inputs. Maternal smoking may be correlated with unobserved inputs and risk behaviors that may impact child neurodevelopment. Maternal Smoke And Increased Risk Of Sudden Infant Essay. Specifically, the “unobserved” maternal preferences for child development and for risk taking (R) that impact the smoking decision may also impact other prenatal investments such as prenatal care use and nutrition and risk behaviors such as alcohol use and others, which are unobserved. This “omitted variable” bias due to unobserved preferences and inputs may result in a negative bias in smoking effects on development (i.e. overestimation of adverse smoking effects), as smoking may be positively correlated with risky behaviors that have adverse effects on development. Conversely, smoking may be negatively correlated with healthy behaviors that enhance development. However, the bias due to unobserved endowments T is likely to result in an opposite bias (i.e. a positive bias or underestimation of the adverse smoking effects), as women who perceive larger fetal health and developmental risks face a larger incentive to avoid smoking during pregnancy, but may be more likely to have children with neurodevelopmental problems due to these health risks. Therefore, the net bias is a function of the relative contribution of each of these self-selection biases.
B. Empirical Model and Study Measures
We employ a quasi-structural child development production function that includes development production inputs and exogenous factors that may relate to maternal preferences towards development as follows:
The observed production inputs are maternal smoking during pregnancy (S) and maternal health status (M), measured by the mother having chronic physical and mental health conditions. We also include maternal socioeconomic status (E), defined below in detail, as it may have direct effects on development by impacting maternal self-esteem and efficiency in health/development production (Currie 2009; Grossman 1972), beyond its effects on income. However, as discussed below, we evaluate the model sensitivity to this assumption. Also included are demographic characteristics (H) including the child’s ethnic ancestry, maternal age and marital status, and number of child’s older siblings, which are assumed to impact maternal preferences for development and to modify child development production. Maternal Smoke And Increased Risk Of Sudden Infant Essay. Further, given that we employ a multiple-country sample as described below, the model includes country fixed effects (C) in order to account for differences in child neurodevelopment production between the sample countries. We describe below how evaluate the sensitivity of the smoking effects to the model specification.
B.1 Neurodevelopment
We measure neurodevelopment based on the child’s performance on the Bayley Infant Neurodevelopmental Screener (BINS) (Aylward 1995).9 The BINS screens children between the age of 3 and 24 months for risk of neurodevelopmental problems by evaluating cognitive processes, receptive functions, expressive functions and basic neurological functions. The BINS predicts child’s development assessed using diagnostic instruments including as the McCarthy Scales of Children’s Abilities and the Bayley-II very well (Aylward 1995, 2004; Aylward and Verhulst 2000). The BINS has 11–13 items based on age which are scored 1 if the child performs the task or 0 if the child does not perform the task. The items are summed to obtain a total score, which may be classified into a three- (high, moderate, low) or two-category (high versus low) risk status for neurodevelopmental delay based on the instrument norms (Aylward 1995; Aylward and Verhulst 2000). The study physicians administered the BINS to all the study children.
This study employs two neurodevelopment measures based on the BINS score. The first measure is a binary risk status of high versus low risk for neurodevelopmental delay based on the instrument norms. The second measure is a continuous measure of the child’s neurodevelopment relative to the sample average neurodevelopment. Specifically, this measure is the percentage deviation of each child’s total bins score from the sample mean of the BINS score for the child’s age, and is therefore referred to here as the child neurodevelopment rate. Unlike the binary risk status measure, this sample-based measure is “norm-free” as it does not utilize the BINS population norms, which are developed based on a sample from the United States. Since the study sample is from South America, we employ this “norm-free” measure in part to evaluate if the smoking effects are sensitive to employing norms from another population. Maternal Smoke And Increased Risk Of Sudden Infant Essay. The sign of the smoking effect is expected to be positive for the binary risk status measure and negative for the child neurodevelopment rate, which unlike the binary
B.2 Smoking
Smoking is measured by smoking participation during pregnancy (after pregnancy occurrence) and by the number of cigarettes smoked per day, based on maternal self-report. We do not observe maternal smoking post birth at the time of measuring child’s neurodevelopment. If postnatal smoking impacts neurodevelopment, the estimated prenatal smoking effects reflect both the “prenatal smoking” effect and the “postnatal smoking” effect, as well as changes in smoking status between the two periods. However, the evidence is still unclear in terms of the importance of postnatal smoking on neurodevelopment at the ages evaluated in this study (Faden and Graubard 2000; Herrmann et al. 2008).
B.3 Socioeconomic Status
SES is measured by an index of maternal human capital and household wealth using principal component analysis (Kolenikov 2004). Maternal human capital is measured by ordinal scales for education and employment/occupational status. Household wealth is measured by asset ownership and housing quality conditions.10 The index uses the first principal component scoring coefficients as weights for the index variables.11 The first principal component explains about 30.5% of the variation in the asset ownership, housing quality and human capital indicators. In order to better interpret the socioeconomic status index, Table A1 in the Appendixreports the distribution of the index variables for the low and high SES groups that are identified based on having negative and positive SES index values, respectively. As expected, there are marked differences in the distribution of the index variables between the two groups with greater assets and improved household quality conditions in the high SES group. We also estimate an alternative specification of the child neurodevelopment function that includes indicators for maternal education and employment/occupational level in order to evaluate their direct effects on development, and a wealth index using PCA that includes the asset ownership and household quality conditions. Maternal Smoke And Increased Risk Of Sudden Infant Essay.
Table 1 includes the distribution of the study variables.
Table 1
Distribution of study variables
| Variable | Mean (SD)
|
||
|---|---|---|---|
| Total | Low SES | High SES | |
| Child developmental risk status (high versus low)a | 0.181 (0.395) | 0.217 (0.142) | 0.145 (0.352) |
| Child neurodevelopment ratea | 0.00 (14.581) | −1.596 (15.157) | 1.620 (13.793) |
| Maternal smoking during pregnancy | 0.109 (0.311) | 0.154 (0.361) | 0.062 (0.242) |
| Number of cigarettes per day during pregnancy | 0. 754 (3.007) | 1.175 (3.827) | 0.326 (1.733) |
| African ancestry | 0.154 (0.361) | 0.211 (0.408) | 0.097 (0.296) |
| Native ancestry | 0.426 (0.495) | 0.451 (0.498) | 0.399 (0.490) |
| Birth weight (in 100 grams) | 33.47 (4.26) | 33.30 (4.31) | 33.64 (4.21) |
| Gestational age (in weeks) | 39.3 (1.05) | 39.39 (1.04) | 39.21 (1.05) |
| Socioeconomic status index | −0.002 (1.238) | −0.954 (0.819) | 0.965 (0.741) |
| Completed primary schoolb | 0.298 (0.458) | 0.530 (0.500) | 0.062 (0.242) |
| Incomplete secondary schoolb | 0.199 (0.399) | 0.274 (0.447) | 0.122 (0.328) |
| Complete secondary schoolb | 0.306 (0.461) | 0.177 (0.382) | 0.438 (0.496) |
| Attended universityb | 0.197 (0.398) | 0.019 (0.136) | 0.378 (0.485) |
| Unemployedc | 0.639 (0.480) | 0.801 (0.400) | 0.475 (0.500) |
| Unskilled blue collar workerc | 0.074 (0.263) | 0.109 (0.312) | 0.039 (0.195) |
| Skilled blue collar workerc | 0.042 (0.201) | 0.021 (0.144) | 0.064 (0.244) |
| Independent workerc | 0.042 (0.201) | 0.023 (0.149) | 0.062 (0.242) |
| Clerkc | 0.136 (0.343) | 0.045 (0.208) | 0.229 (0.420) |
| Wealth index | 0.038 (0.981) | −0.624 (0.87) | 0.71 (0.524) |
| Maternal mental health problems | 0.037 (0.188) | 0.045 (0.208) | 0.028 (0.165) |
| Maternal chronic physical health problems | 0.052 (0.222) | 0.050 (0.218) | 0.053 (0.225) |
| Maternal age | 27.076 (6.571) | 25.197 (6.267) | 28.985 (6.322) |
| Maternal age squared | 776.287 (376.990) | 674.099 (345.748) | 880.036 (379.256) |
| Mother is single | 0.169 (0.374) | 0.212 (0.409) | 0.125 (0.330) |
| Mother is in a stable relationship | 0.409 (0.492) | 0.509 (0.500) | 0.308 (0.462) |
| Number of older child’s siblings | 1.007 (1.368) | 1.214 (1.553) | 0.796 (1.111) |
| Area smoking rate | 0.109 (0.070) | 0.120 (0.072) | 0.097 (0.066) |
| Area smoking rate squared | 0.016 (0.017) | 0.020 (0.019) | 0.014 (0.015) |
| Area-level average cigarette number | 0.754 (0.740) | 0.875 (0.793) | 0.63 (0.66) |
| Cesarean delivery rate | 0.385 (0.153) | 0.361 (0.158) | 0.410 (0.143) |
| Average number of prenatal visits | 6.997 (1.589) | 6.864 (1.592) | 7.129 (1.577) |
| Average number of weeks delayed before initiating prenatal care | 13.046 (2.745) | 13.364 (2.885) | 12.726 (2.561) |
| Average number of ultrasounds during pregnancy | 2.287 (1.012) | 2.207 (1.057) | 2.367 (0.959) |
| Medication use rate during pregnancy | 0.715 (0.281) | 0.684 (0.286) | 0.747 (0.272) |
| Immunization rate during pregnancy | 0.548 (0.294) | 0.581 (0.277) | 0.516 (0.308) |
| Brazild | 0.331 (0.471) | 0.381 (0.486) | 0.281 (0.450) |
| Chiled | 0.245 (0.430) | 0.167 (0.373) | 0.321 (0.468) |
Note: The table reports the means and standard deviation of the study variables.
C. Study Sample
The study sample includes 1,584 children between ages 3 and 24 months who attended 24 pediatric practices in Argentina (671 infants), Brazil (525 infants) and Chile (388 infants) for routine well-child care in 2005 and 2006. These children participated in a study of child neurodevelopment in South America, which was part of the Global Network for Women’s and Children’s Health Research study (Wehby et al. 2006; McCarthy 2010).Maternal Smoke And Increased Risk Of Sudden Infant Essay. Given its focus on normal development, the main study that provides the data for this paper included only children with normal birth outcomes and without major health complications such as requiring oxygen after birth, hospitalization for more than 5 days before hospital discharge after birth, or admission to the intensive neonatal care unit. Also for this purpose, the main study did not enroll children who are low birth weight (<2500 grams) and born prematurely (<37 weeks).12The study physicians, the majority of whom were pediatricians, were affiliated with a longstanding epidemiological research and surveillance program in South America, ECLAMC, which has been conducting infant health studies in South America for over three decades (Castilla and Orioli 2004; Wehby, Castilla, and Lopez-Camelo 2010; Wehby et al. 2009). As part of their involvement with ECLAMC, these physicians are routinely involved in infant health research studies.
The study physicians administered the BINS to evaluate neurodevelopment for all study children and obtained data on other characteristics using the same instruments and study questionnaires across all study sites. Before initiating data collection, the study investigators provided training to the study physicians in how to administer the BINS and assessed their reliability in using the instrument. The average physicians’ agreement with the gold standard scores for BINS case studies during the training was 84%. The physicians also received standardized training in data collection and study procedures. The mothers were interviewed by study physicians and staff for household demographic and socioeconomic characteristics, health conditions and behaviors using the same instruments and data collection procedures across all sites.
D. Model Estimation
The child neurodevelopment production function is first estimated treating smoking as exogenous with probit regression for the binary child neurodevelopment risk status and ordinary least squares (OLS) for the child neurodevelopment rate.Maternal Smoke And Increased Risk Of Sudden Infant Essay. These models are estimated for the total sample and separately for individuals with low and high SES, given the strong SES effects on smoking in this sample. For the purposes of this estimation, low SES and high SES are assigned for negative (798 children) and positive (786 children) SES index values, respectively.
In order to evaluate the potential bias due to maternal self-selection into smoking based on unobserved factors as described above, the neurodevelopment production function is also estimated treating smoking as endogenous. For smoking participation, the sample rate of smoking during pregnancy at each of the study sites (clinics), excluding the individual’s smoking status, is employed as an instrument. For each mother in the study sample, we estimate the smoking rate among the mothers of the other children recruited at the same study site (total of 24 sites), and use that as an instrument. This measure is expected to be a good proxy for the smoking rate in the community where the mother lives. Community smoking rates reflect the effects of local cigarette prices and smoking-related policies, but may also have direct effects on the mother’s propensity to smoke by representing the social acceptability of smoking during pregnancy.
The conditions under which the used area-level instruments provide consistent estimates of the mother’s smoking effects are that the area-level smoking measures based on the other mothers’ smoking status are not related to: 1- the unobserved child’s own developmental endowments (T) that may affect the mother’s smoking behaviors and 2- the mother’s own preferences for risk taking, healthy behaviors, and child health (R). Under these conditions, the area-level instruments as constructed are not expected to affect the child’s neurodevelopment other than through affecting the child’s mother propensity to smoke by reflecting area differences in smoking regulations and cigarette prices/costs. Maternal Smoke And Increased Risk Of Sudden Infant Essay.
The first condition is likely to hold given that it is not expected that the behaviors of other mothers affect or are related to the child’s neurodevelopmental endowments. The second condition holds if mothers do not sort themselves into areas based on either their smoking status or their smoking-related preferences for risk taking, child health, and health behaviors that are relevant for child neurodevelopment. Of course, “general” preferences for health, wellbeing and risk taking such as for area and neighborhood safety and quality certainly affect residential choice. However, it seems reasonable to assume that the mother’s own smoking status and her “specific” preferences for smoking are not “major” determinants of self-selection into areas defined by the study sites. Individuals may choose their “neighborhood” based on certain physical characteristics that relate to smoking such as the concentration of bars, restaurants and nightclubs. However, the “area” measure employed in this study reflects a wider geographic area than a single residential neighborhood and each “area” likely encompasses multiple neighborhoods that differ in their physical characteristics that may relate to smoking. Therefore, while some self-sorting may occur between neighborhoods within a certain study area based on neighborhood-physical characteristics related to smoking, it is expected that such characteristics vary less between than within the area-levels at which we calculate the instruments. For example, most areas are expected to have neighborhoods with bars, restaurants and nightclubs. Of course, we cannot completely verify the assumption that the area-level instruments do not affect child neurodevelopment other than through maternal smoking behaviors due to the lack of data on neighborhood selection within the study areas and on area and neighborhood physical characteristics. However, we describe below several checks that we employ to further evaluate the instrument exogeneity.
The square of the smoking rate is also added as an instrument given the likely diminishing marginal effects of community smoking rates on individual smoking propensity. Similar instruments for smoking and other risk behaviors have been employed in other studies (Fang, Ali, and Rizzo 2009; Morris 2006). For cigarette number, we use the average number of cigarettes smoked per day at the individual’s community (defined at the study site level), excluding the individual’s cigarette number, as an instrument. We also include an interaction between the area cigarette number average and the individual’s SES index, given that increasing SES may lessen the adverse area-level effects such as tobacco advertisements, may change sensitivity to prices and taxes, and may increase access to available resources to reduce or quit smoking.
We find these instruments to be significantly related to smoking participation and cigarette number, with F-statistics of 10 for smoking participation and 42 for cigarette number in the total sample.13 Smaller but significant F-statistics are observed in the samples stratified by SES, which we account for by employing weak-instrument robust inference as described below. The only exception is for cigarette number in the high SES subsample, where the instruments have insignificant effects. Maternal Smoke And Increased Risk Of Sudden Infant Essay. The reason is the very limited distribution and variation of cigarette number in this subsample. Therefore, we only estimate models assuming exogenous cigarettes when using the cigarette number in this subsample. Commonly used instruments such as local cigarette prices/taxes and smoking policy measures are not available for use as instruments due to the lack of data.
When treating smoking as endogenous, the child neurodevelopment risk status function (the first binary development measure) is estimated with conditional maximum likelihood (Wooldridge 2002). The model estimates simultaneously the neurodevelopment risk function and the smoking/cigarette function, which includes the instruments and other model variables. The model is estimated by bivariate probit regression when measuring smoking by participation status, and by instrumental variables (IV) probit regression when measuring smoking by the number of cigarettes. The neurodevelopment rate function (second development measure) is estimated using two-stage least squares (2SLS) when treating smoking as endogenous. Given that the instrument F-statistics for smoking participation are less than 10 in the subsamples stratified by SES, we estimate 95% confidence bounds for the 2SLS smoking participation effects that are robust for weak instruments using the conditional Likelihood Ratio (CLR) statistic (Andrews, Moreira, and Stock 2006; Finaly and Magnusson 2009). Standard over-identification tests are employed in the IV probit and 2SLS models to evaluate if the instruments fit the over-identification restrictions.14Evaluating the over-identification restrictions for the bivariate probit model is less straightforward – the model may be identified without instruments. Therefore, 2SLS is used to test the over-identification restrictions in the model of child neurodevelopment risk status and smoking participation.
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We estimate the variance-covariance matrices for all models with a Huber-type estimator that accounts for the clustering of the sample across the study clinics (Wooldridge 2002). We assume that the error term is correlated for children from the same area (clinic site) due to area-level “random effects” that are not related to smoking behaviors and the instruments and not due to non-random effects that vary systematically with smoking behavior. In other words, these random effects are assumed to be not correlated to maternal preferences for smoking, smoking status, and average smoking rates, and may include some unobserved area characteristics that affect child health and neurodevelopment such as transportation costs. Under this assumption, the Huber-type estimator accounting for clustering by study area is expected to provide more accurate estimates of the standard errors than those assuming classical error terms given the clustered nature of the sample and that certain covariates are measured at the area-level (Moulton 1986). Clustering the standard errors would contradict the assumptions needed for the validity of the instruments if the shared cluster-level error term is related to the mother’s smoking behaviors and to the instruments (i.e. if non-random effects resulted in correlations between the error terms of individuals in the same area). However, the inference of the results as a whole is generally unaffected by clustering the standard errors, which suggests that the unobserved cluster-level effects in the error term are less relevant and overall unrelated to the instruments. We note below when differences in significance levels are observed between clustered and classical standard errors. Maternal Smoke And Increased Risk Of Sudden Infant Essay.
E. Further Instrument Checks
In addition to the standard over-identification tests described below for evaluating the excludability of instruments from the development function, we further evaluate the exogeneity of the constructed area-level instruments by assessing their relationships with the model control variables. The expectation is that the instruments should not be systematically related to the individual-level characteristics that are related to the individual-level smoking measures. Therefore, we regress both the area-level instruments and the individual-level smoking measures on the model control variables and compare the effects of these variables on the area- and individual-level smoking measures. Table 2 reports the effects of the individual-level characteristics on the area- and individual-level smoking measures. The area-level smoking rate is not systematically related to the individual-level characteristics as is individual-level smoking participation. Individual-level smoking participation significantly increases with mental health problems, being unmarried, and with the number of children, and decreases with socioeconomic status and maternal age. However, none of these characteristics is significantly related to the area-level smoking rate, which is only significantly and positively related to maternal chronic physical health conditions. Individual-level cigarette number decreases significantly with socioeconomic status and maternal age and increases with the number of children. However of these variables, only maternal age is significantly and negatively related to the area-level cigarette number average, which is also positively related to maternal chronic physical health conditions. Maternal Smoke And Increased Risk Of Sudden Infant Essay.
