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American Journal of Epidemiology Advance Access published online on September 18, 2008
American Journal of Epidemiology, doi:10.1093/aje/kwn223
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American Journal of Epidemiology Published by the Johns Hopkins Bloomberg School of Public Health 2008.

Original Contribution

Dose-Response Associations Between Maternal Smoking During Pregnancy and Subsequent Childhood Obesity: Effect Modification by Maternal Race/Ethnicity in a Low-Income US Cohort

Andrea J. Sharma, Mary E. Cogswell and Ruowei Li

Correspondence to Dr. Andrea J. Sharma, Centers for Disease Control and Prevention, 4770 Buford Highway, Mailstop K-25, Atlanta, GA 30341-3724 (e-mail: AJSharma{at}cdc.gov).

Received for publication December 14, 2007. Accepted for publication June 26, 2008.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Studies suggest that children exposed to cigarette smoke in utero are at risk of becoming obese. Few researchers have evaluated the dose-response association between maternal smoking during pregnancy and childhood obesity or whether this association varies by maternal race/ethnicity. The authors obtained retrospective cohort data by linking records from the Pregnancy Nutrition Surveillance System and the Pediatric Nutrition Surveillance System on 155,411 low-income children born during 1995–2001 in 9 US states and 2 tribal nations. The authors examined maternal smoking status, duration of smoking, quantity of smoking, and both duration and quantity combined. Childhood obesity was based on a body mass index greater than or equal to the 95th percentile for sex and age, assessed at age 2–4 years. Maternal race/ethnicity modified the association between smoking during pregnancy and childhood obesity. Among non-Hispanic White mothers, both duration and quantity of smoking were positively associated with childhood obesity in a dose-response manner. Among non-Hispanic Black mothers, only heavy smoking was positively associated with childhood obesity. Among Hispanics, American Indians/Alaska Natives, and Asians/Pacific Islanders, smoking was not associated with childhood obesity. The inconsistent association between smoking during pregnancy and childhood obesity across race/ethnicity categories merits further investigation into potential explanations for this variation, which may include confounding, reporting bias, or unexplored biologic mechanisms.

child; ethnic groups; obesity; pregnancy; prenatal exposure delayed effects; smoking

Abbreviations: BMI, body mass index; PedNSS, Pediatric Nutrition Surveillance System; PNSS, Pregnancy Nutrition Surveillance System; WIC, Special Supplemental Nutrition Program for Women, Infants, and Children


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Childhood obesity is a leading public health concern in the United States (1). The prevalence of obesity among 2- to 5-year-old US children increased from 10.3% to 13.9% from 1999 to 2004 (2). This is a disturbing trend, because obese children are more likely to become obese adults (3, 4) and to develop a spectrum of morbidities (5, 6).

Fetal growth retardation has been suggested as a risk factor for later obesity (7). Smoking during pregnancy is a known cause of reduced fetal growth (8). Investigators from several studies have reported a positive association between smoking during pregnancy and subsequent child obesity (9–22). However, because of the observational nature of these studies, whether this association is causal remains unclear. Two criteria which lend support for a causal relation are dose-response and consistency (23).

Limited information exists on the dose-response relation between maternal smoke exposure in utero and child obesity. Of the 3 studies that have examined smoking duration, researchers in 2 concluded that the greatest risk of child obesity is associated with smoking throughout pregnancy (13, 19), while researchers in the other study concluded that increased risk is associated with first-trimester exposure (12). In comparison, daily quantity of cigarettes smoked during pregnancy is consistently associated with childhood obesity (10, 13, 19, 24). Furthermore, in all but 2 studies (15, 19), study populations consisted predominately of White women. Heavy smoking during pregnancy (≥20 cigarettes daily) is more common among White women (25); thus, associations observed among White smokers may not be generalizable to all smokers if smoking patterns differ across racial/ethnic groups. Examination of both smoking duration and quantity smoked during pregnancy and the variation (or lack thereof) by racial/ethnic group would increase our understanding of the consistency of the association. To our knowledge, no published studies to date have examined associations between smoking patterns across diverse racial/ethnic groups or have simultaneously examined duration and quantity.

In this study, we examined the dose-response and consistency of associations between maternal smoking during pregnancy and subsequent obesity among low-income preschoolers. We additionally examined the potentially mediating role of birth weight.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
We used data on mothers and children from the Centers for Disease Control and Prevention's Pregnancy Nutrition Surveillance System (PNSS) and Pediatric Nutrition Surveillance System (PedNSS) (26). These are voluntary program-based state surveillance systems that monitor the nutritional status of low-income infants, children, and women who participate in federally funded maternal and child health programs—primarily the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC). PNSS data are collected on pregnant women during an initial prenatal visit (usually entry into the WIC program) and during a postpartum visit. PedNSS data are collected on children, twice a year on average; height and weight are measured each time.

The study was determined to be exempt from review by the Centers for Disease Control and Prevention's institutional review board. Nine states and 2 tribal nations had PNSS records which could be linked to PedNSS for children aged 2–4 years during 2000–2003. To link records (Figure 1), we identified PNSS records of singleton births occurring in 1995–2001. Duplicate records were excluded. PedNSS records were identified for children who were aged 2–4 years during 2000–2003. Each child may have had up to 3 records during this period. State/tribal identification number and child's identification number and date of birth were used to link 739,107 PedNSS and PNSS records. Of these, records with missing data on maternal smoking, child body mass index (BMI; weight (kg)/height (m)2), or covariates (described below) were excluded. Approximately 21% of excluded records were attributed to mothers’ participating in WIC postpartum; thus, prenatal smoking data had not been collected. Of 290,630 records with complete data, 1 record per child was randomly chosen, leaving 160,851 unique children. Mothers and children included in the study sample were similar to those excluded (Table 1). Individual identifiers were removed before transmission of the data to researchers.


Figure 1
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  		Figure 1. Selection of the study sample through linkage of mothers from the Pregnancy Nutrition Surveillance System (PNSS) with children from the Pediatric Nutrition Surveillance System (PedNSS), United States, 1995–2003. Includes only the 9 states and 2 tribal nations which had linkable PNSS and PedNSS records. PNSS contains 1 maternal record per pregnancy, and PedNSS contains 1 child record per year. ID, identification number.

 

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  		Table 1. Select Characteristics of Mothers and Children Included In and Excluded From the Study Sample After Linkage of Records From the Pregnancy Nutrition Surveillance System and the Pediatric Nutrition Surveillance System, United States, 1995–2003a

 
We used data collected at the prenatal and postpartum visits to define mother's smoking status during pregnancy. For the basic smoking measure, mothers were categorized as nonsmokers, smokers, or quitters. At the initial visit, which could have occurred at any time during pregnancy, mothers were asked about the number of cigarettes they had smoked daily during the 3 months before pregnancy and the number they were smoking currently. At the postpartum visit, mothers were asked about the number of cigarettes they had smoked daily during the last 3 months of pregnancy. Mothers who reported no smoking at all 3 time points were categorized as nonsmokers and were considered the referent group. Mothers who reported smoking 1 or more cigarettes daily at all 3 time points were categorized as smokers. Mothers who reported smoking before pregnancy but not during the last 3 months of pregnancy, regardless of their smoking status at the first prenatal visit, were categorized as quitters. Mothers who started to smoke during pregnancy (i.e., not smoking during the 3 months before pregnancy but smoking at the prenatal visit or during the last 3 months of pregnancy; n = 2,041) or who relapsed during pregnancy (i.e., smoking during the 3 months before pregnancy, not smoking at the prenatal visit, and then smoking during the last 3 months of pregnancy; n = 3,399) were excluded because of the small samples within each racial/ethnic group. Our final sample included 155,411 children.

To examine duration of smoking, we expanded the basic smoking measure by categorizing mothers who stopped smoking during pregnancy as early quitters or late quitters using gestational age and smoking status at the time of the first prenatal visit. Among mothers categorized as quitters, those seen at ≤13 weeks’ gestation who reported not currently smoking were categorized as early quitters; those seen at >13 weeks’ gestation who reported currently smoking 1 or more cigarettes daily were categorized as late quitters. The timing of smoking cessation could not be determined for mothers categorized as quitters who were seen at ≤13 weeks’ gestation and reported currently smoking or who were seen at >13 weeks’ gestation and reported not currently smoking. We categorized these mothers as unknown quitters and expected their results to fall between those of early and late quitters.

To examine quantity of smoking, we used smoking habits reported for the 3 months before pregnancy, for 2 reasons. First, smoking habits have been shown to fluctuate throughout pregnancy (27, 28). We considered smoking habits reported for the 3 months before pregnancy to be a more stable indicator of usual smoking habits in the early weeks of pregnancy, and at least 1 study has shown that the first trimester may be the critical period of exposure (12). Second, the time period, the 3 months before pregnancy, is consistent across all mothers. Because mothers can enter WIC at any time during pregnancy, gestational age at the time of the prenatal visit varies; similarly, gestational age during the last 3 months of pregnancy depends on gestational age at birth.

To examine both duration and quantity simultaneously, we created a new variable that combined the basic smoking measure and the number of cigarettes smoked per day during the 3 months before pregnancy. The categories of the duration-quantity variable were defined as: nonsmoker, quitter (1–9 cigarettes/day), quitter (10–19 cigarettes/day), quitter (≥20 cigarettes/day), smoker (1–9 cigarettes/day), smoker (10–19 cigarettes/day), and smoker (≥20 cigarettes/day).

Age- and sex-specific BMI percentiles using the 2000 Centers for Disease Control and Prevention growth reference (29, 30) are reported in each child's PedNSS record. We defined obesity (formerly referred to as overweight (31)) among children as a BMI greater than or equal to the 95th percentile (32). Obesity was set to missing if a child had an implausible BMI-, height-, or weight-for-age z score (defined as a BMI-for-age z score less than –4 or greater than 5, a height-for-age z score less than –5 or greater than 3, or a weight-for-age z score less than –5 or greater than 5 (www.cdc.gov/pednss/pop-ups/biv_pednss.htm)) (29, 30). Self-reported maternal race/ethnicity was categorized as non-Hispanic White, non-Hispanic Black, Hispanic, American Indian/Alaska Native, or Asian/Pacific Islander. Maternal age at the child's birth was calculated, as was child's age at each anthropometric assessment. Maternal prepregnancy BMI was calculated from self-reported prepregnancy weight and measured height. Gestational age at birth was calculated from the date of the mother's last menstrual period. Self-reported household income and size were used to calculate the poverty index ratio as the ratio of household income to the annual poverty-threshold value for a given household size (33). The mother self-reported information on her weight gain during pregnancy, her education, the child's birth weight and sex, and whether the child had ever been breastfed.

We examined variation in maternal and child characteristics across maternal racial/ethnic groups using analysis of variance for continuous variables and {chi}2 statistics for categorical variables. Because quantities of cigarettes reported for the 3 months before pregnancy, at the prenatal visit, and over the last 3 months of pregnancy were not normally distributed, we log-transformed these data before analyzing heterogeneity. We examined Spearman rank correlations between reported quantities of cigarettes smoked daily during the 3 months before pregnancy and quantities reported at the prenatal visit and for the last 3 months of pregnancy.

We examined associations between childhood obesity and maternal smoking status (nonsmoker, quitter, smoker), duration (nonsmoker, early quitter, unknown quitter, late quitter, smoker), quantity (0, 1–9, 10–19, or ≥20 cigarettes/day), and duration and quantity combined in both univariate and multivariate analyses. We used logistic regression to test whether associations between smoking during pregnancy and childhood obesity were modified by maternal race/ethnicity by including an interaction term in each model. To test whether childhood obesity increased with duration, quantity, or both duration and quantity, we calculated a contrast with equally spaced coefficients for each category (test of linear trend), using a contrast statement in SAS with the GENMOD procedure (SAS Institute Inc., Cary, North Carolina). Final models were adjusted for the child's age, sex, gestational age, and ever being breastfed and the mother's age, education, poverty index ratio, prepregnancy BMI, and weight gain during pregnancy. Because birth weight (a proxy measure of fetal growth) may lie within the causal pathway between maternal smoking and childhood obesity, we analyzed an additional model including child's birth weight to examine how the inclusion of birth weight affected the association of maternal smoking with childhood obesity. If the association was mediated through birth weight, we would expect the inclusion of birth weight to change the relation.

We identified 12% of our subjects as siblings; thus, we employed generalized estimating equations (34), implemented using the SAS procedure GENMOD, and specified an exchangeable working correlation matrix to account for correlated data (SAS, version 9.0). We assessed statistical significance at P < 0.05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
We analyzed data for 145,835 mothers and 155,411 children. Of the children, 53.0% were born to non-Hispanic White mothers, 20.4% to non-Hispanic Blacks, 22.1% to Hispanics, 1.4% to American Indians/Alaska Natives, and 3.1% to Asians/Pacific Islanders. Maternal race/ethnicity was associated with maternal and child characteristics in our study (Table 2). Overall, 13.4% of children were obese, with the lowest prevalence being observed among children born to non-Hispanic White mothers and the highest being observed among children born to Hispanics.


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  		Table 2. Characteristics of 155,411 Children Included in the Study Sample and Their Mothers According to Maternal Race/Ethnicity, United States, 1995–2003a

 
Among all children, 71.3% were born to nonsmokers, 14.5% to mothers who quit smoking during pregnancy, and 14.1% to mothers who smoked throughout pregnancy; the distribution of children born to nonsmokers, quitters, and smokers varied significantly by maternal race/ethnicity (Table 3). The prevalence of smoking during pregnancy was greatest among non-Hispanic White mothers and lowest among Asians/Pacific Islanders. Similarly, the daily number of cigarettes smoked before and during pregnancy varied by race/ethnicity, with the highest median and interquartile range being observed among non-Hispanic Whites. Across all racial/ethnic groups, smokers, on average, reported smoking fewer cigarettes per day during pregnancy than before pregnancy, even if they smoked throughout pregnancy. Spearman rank correlations between cigarettes smoked daily during the 3 months before pregnancy and cigarettes being smoked daily at the prenatal visit ranged from 0.15 to 0.34 among mothers who quit during pregnancy and from 0.40 to 0.57 among mothers who smoked throughout pregnancy. Among mothers who smoked throughout pregnancy, correlations between cigarettes smoked daily during the 3 months before pregnancy and cigarettes smoked daily during the last 3 months of pregnancy ranged from 0.05 to 0.47. The weakest correlations were observed among Asians/Pacific Islanders.


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  		Table 3. Prevalence of Maternal Smoking and Quantity of Cigarettes Smoked Per Day Before and During Pregnancy, by Maternal Race/Ethnicity and Smoking Status, United States, 1995–2003

 
A significant interaction between maternal race/ethnicity and each smoking variable was observed (all P’s < 0.0001); thus, analyses were stratified by race/ethnicity. After adjustment for covariates, smoking status during pregnancy was associated with childhood obesity only among children born to non-Hispanic Whites and non-Hispanic Blacks (Table 4). Among non-Hispanic Whites, the odds of obesity were 42% greater for children born to smokers and 23% greater for children born to quitters than for children born to nonsmokers. Among non-Hispanic Black mothers, the odds of obesity were 19% greater for children born to smokers than for children born to nonsmokers and 5% greater (not significant) for children born to quitters than for children born to nonsmokers.


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  		Table 4. Odds Ratios for Childhood Obesity According to Maternal Smoking Status During Pregnancy, by Maternal Race/Ethnicity, United States, 1995–2003

 
After further categorization of quitters as early, unknown, or late quitters (Table 5), duration of smoking during pregnancy in adjusted analyses was associated with obesity among children born to non-Hispanic White mothers. The odds of obesity rose with increasing duration of smoking during pregnancy (P for trend < 0.0001).


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  		Table 5. Odds Ratios for Childhood Obesity According to Duration of Maternal Smoking During Pregnancy, by Maternal Race/Ethnicity, United States, 1995–2003

 
The quantity of cigarettes smoked during the 3 months before pregnancy was associated with obesity only among children born to non-Hispanic White mothers (Table 6). Similarly, when duration and quantity were combined, smoking during pregnancy was associated with obesity only among children born to non-Hispanic White mothers (Figure 2). Compared with children of nonsmokers, the odds of obesity among children exposed to any smoking during pregnancy increased with both duration and quantity of smoking. There was a suggestion of an increase in the odds of obesity with increasing duration and quantity of smoking among non-Hispanic Black mothers, but the odds of obesity were significantly higher only among children born to mothers who smoked throughout pregnancy and smoked 20 or more cigarettes daily during the 3 months before pregnancy.


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  		Table 6. Odds Ratios for Childhood Obesity According to Number of Cigarettes Smoked Daily During the 3 Months Before Pregnancy, by Maternal Race/Ethnicity, United States, 1995–2003

 

Figure 2
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  		Figure 2. Adjusted odds ratios for childhood obesity according to both duration of smoking and quantity of cigarettes smoked daily during the 3 months before pregnancy, by maternal race/ethnicity, United States, 1995–2003. The study sample was selected through linkage of mothers from the Pregnancy Nutrition Surveillance System with children from the Pediatric Nutrition Surveillance System. Odds ratios are presented on a log scale and are adjusted for child's age, sex, gestational age, and ever breastfeeding and mother's age, education, poverty index ratio, prepregnancy body mass index, and weight gain during pregnancy. NS, nonsmoker. Bars, 95% confidence interval (CI).

 
Across all indicators of maternal smoking (i.e., status, duration, and timing), adding birth weight to the models strengthened the positive associations between maternal smoking and childhood obesity (Tables 4–6). However, evidence of a statistical association was observed only among children born to non-Hispanic Whites and non-Hispanic Blacks. Among models with duration and quantity combined, on average, odds ratios increased from 2% to 10% after adjustment for birth weight (data not shown). Positive trends were observed only among non-Hispanic Whites and non-Hispanic Blacks.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
In a cohort of low-income preschool-aged children, we observed associations between smoking during pregnancy and subsequent childhood obesity that varied across maternal racial/ethnic groups. Among non-Hispanic White mothers, our data suggested that any smoking during pregnancy may increase the likelihood that the infant will be obese as a child; quitting or reducing the level of smoking may reduce this risk. Among non-Hispanic Black mothers, heavy smoking in early pregnancy with continued smoking throughout pregnancy may increase the likelihood that the child will be obese, but we found no increased risk among children born to Black mothers who quit smoking during pregnancy or smoked fewer than 20 cigarettes daily early in pregnancy. We observed null associations between smoking during pregnancy and childhood obesity among children born to mothers categorized as Hispanic, American Indian/Alaska Native, or Asian/Pacific Islander.

Our observations for the non-Hispanic White and Black subgroups generally agree with results of previous studies that examined predominantly White (9–14, 16–18, 20–22) or Black (19) populations, where smoking during pregnancy and the quantity of cigarettes smoked were positively associated with childhood obesity. Of these studies, only 3 examined the association between duration of smoking exposure and childhood obesity; in 1 (12), the investigators suggested that exposure to tobacco smoke early in pregnancy is critical for the development of childhood obesity, and in the others (13, 19), they suggested that the odds of obesity are higher only among children born to mothers who smoked throughout pregnancy. Our data among children born to non-Hispanic White mothers suggest a cumulative effect of in utero exposure to tobacco smoke on childhood obesity that begins early in pregnancy and increases with the duration of smoking. Our observations do not agree with those of the only earlier study (15) to examine an American Indian/Alaska Native population, as we did not observe an association between maternal smoking and obesity among children born to mothers from this population. To our knowledge, our study is the first to have specifically examined these associations among children born to Hispanic and Asian/Pacific Islander mothers.

We suggest 4 possible explanations for the differences found by maternal race/ethnicity. First, different genetic polymorphisms affecting nicotine metabolism have been identified among different racial/ethnic groups (35). Tobacco toxins, including nicotine, readily cross the placenta (36); variations in enzyme activity may alter toxic effects on the fetus. Second, dose per cigarette may vary by race/ethnicity because of differences in the types of tobacco products consumed (e.g., light, herbal, menthol). Preferences for certain types of cigarettes differ by race/ethnicity (37); thus, the same quantity of cigarettes may not equal the same dose of toxins across racial/ethnic groups. Third, cultural biases in reporting of smoking habits during pregnancy may lead to differential misclassification, limiting the ability to detect associations in some subgroups. Although studies of the validity of self-reported smoking habits demonstrate that pregnant women tend to underreport smoking (38), we found no published studies assessing the validity of self-reported smoking habits during pregnancy specifically among American Indian/Alaska Native, Hispanic, or Asian/Pacific Islander mothers in the United States. Fourth, maternal smoking may be a marker for an obesogenic home environment, but the dynamics of these environments may differ by race/ethnicity. Although we adjusted for many potentially confounding sociodemographic factors, there may be residual confounding related to behavioral or dietary factors that we were not able to capture.

In our analysis, we examined models with and without birth weight. Adjustment for birth weight must be interpreted carefully, since birth weight may be in the causal pathway. Smoking during pregnancy is a well-established risk factor for reduced birth weight (39). Although some researchers have reported an association between low birth weight and later obesity (40–42), the majority have observed birth weight to be positively associated with later obesity (43). Adjusting for birth weight consistently shifted the association between maternal smoking and childhood obesity in a positive direction. This suggests that birth weight has a suppression effect (44) and that maternal smoking may affect childhood obesity through more than 1 mechanism. Maternal smoking may indirectly reduce the odds of childhood obesity by decreasing birth weight, as well as increase the odds of childhood obesity through a separate biologic mechanism associated with maternal smoking exposure (e.g., rapid postnatal growth). While the effect of maternal smoking on childhood obesity, independent of birth weight, can be interpreted from a model that controls for birth weight, the total effect of maternal smoking on childhood obesity includes all effects (45), which we believe should be interpreted from a model that does not control for birth weight.

The biologic mechanisms by which smoking during pregnancy may influence the child's weight are not fully understood. Studies suggest that fetal malnutrition may increase the risk of developing obesity later in life, particularly when it is followed by postnatal catch-up growth (46); smoking may mimic fetal malnutrition by reducing the mother's food intake (47) or by reducing blood supply to the fetus via the vasoconstrictive effects of nicotine (48). Although birth weight is significantly reduced by maternal smoking, longitudinal studies show that children born to smokers experience more postnatal catch-up growth, particularly in weight, than do children born to nonsmokers (49, 50). Perhaps children exposed to maternal smoking in utero mimic an effect seen in adults: Adult smokers are thinner than nonsmokers but gain weight when they stop smoking (51).

Our study had several strengths. First, it was longitudinal, with data on maternal smoking being measured during prenatal and postpartum visits and childhood anthropometric data being collected at age 2–4 years. Some other studies have relied on maternal smoking data that were recalled several years after pregnancy. Second, the large sample of more than 155,000 low-income children allowed us to examine the consistency of associations by race/ethnicity and associations in a population at greater risk for maternal smoking exposure (52) and childhood obesity (53). Third, we were able to control for several important covariates associated with maternal smoking and childhood obesity. Finally, our analysis was one of the few that had data with which to examine associations with duration of smoking and was the first to report the dose-response relation with duration and quantity combined.

Our study also had limitations. First, maternal smoking information was based on self-report. Substantial underreporting would have biased results toward the null value and caused us to underestimate the true association. Second, we could not fully characterize smoking intensity throughout pregnancy because of limited data on daily exposure. Different patterns of timing, duration, type, and quantity of maternal smoking may alter the effect of smoking on children's outcomes, and we know that smoking habits during pregnancy fluctuate substantially within individual smokers (27). Third, we had relatively few American Indian/Alaska Native or Asian/Pacific Islander mothers in some categories when we examined duration or quantity of smoking; thus, our statistical power in this regard was limited. Fourth, we could not control for the child's caloric intake and physical activity, since these data were not collected. Finally, our study sample consisted of low-income mothers and children participating in the WIC program; thus, generalizability was limited to this population.

In conclusion, public health recommendations already discourage smoking during pregnancy because it increases the risk of low birth weight and other undesirable outcomes for infants (54). Although an association with childhood obesity would provide another reason to promote the prevention of smoking and encouragement of cessation during pregnancy, further investigations are warranted to evaluate whether the racial/ethnic differences observed in our study can be explained by differences in biologic mechanisms, smoking habits, the validity of self-reported smoking data, or uncontrolled confounding.


   ACKNOWLEDGMENTS
 
Author affiliations: Epidemic Intelligence Service, Office of Career and Workforce Development, Centers for Disease Control and Prevention, Atlanta, Georgia (Andrea J. Sharma) and Division of Nutrition, Physical Activity, and Obesity, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention Atlanta, Georgia (Andrea J. Sharma, Mary E. Cogswell, Ruowei Li).

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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