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Infant Morbidity and Mortality Attributable to Prenatal Smoking in the U.S.
Infant Morbidity and Mortality Attributable to Prenatal Smoking in the U.S. Patricia M. Dietz, DrPH, Lucinda J. England, MD, Carrie K. Shapiro-Mendoza, PhD, Van T. Tong, MPH, Sherry L. Farr, PhD, William M. Callaghan, MD Background: Although prenatal smoking continues to decline, it remains one of the most prevalent preventable causes of infant morbidity and mortality in the U.S.
Purpose: The aim of this study was to estimate the proportion of preterm deliveries, term low birth weight deliveries, and infant deaths attributable to prenatal smoking. Methods: Associations were estimated for prenatal smoking and preterm deliveries, term low birth weight (⬍2500 g) deliveries, sudden infant death syndrome (SIDS), and preterm-related deaths among 3,352,756 singleton, live births using the U.S. Linked Birth/Infant Death Data Set, 2002 birth cohort. The 2002 data set is the most recent, in which 49 states used the same standardized smoking-related question on the birth certifıcate. Logistic regression models estimated ORs of prenatal smoking for each outcome, and the prenatal smoking population attributable fraction was calculated for each outcome.
Results: Prenatal smoking (11.5% of all births) was signifıcantly associated with very (AOR⫽1.5, 95% CI⫽1.4, 1.6); moderate (AOR⫽1.4, 95% CI⫽1.4, 1.4); and late (AOR⫽1.2, 95% CI⫽1.2, 1.3) preterm deliveries; term low birth weight deliveries (AOR⫽2.3, 95% CI⫽2.3, 2.5); SIDS (AOR⫽2.7, 95% CI⫽2.4, 3.0); and preterm-related deaths (AOR⫽1.5, 95% CI⫽1.4, 1.6). It was estimated that 5.3%–7.7% of preterm deliveries, 13.1%–19.0% of term low birth weight deliveries, 23.2%–33.6% of SIDS, and 5.0%–7.3% of preterm-related deaths were attributable to prenatal smoking. Assuming prenatal smoking rates continued to decline after 2002, these PAFs would be slightly lower for 2009 (4.4%– 6.3% for preterm-related deaths, 20.2%–29.3% for SIDS deaths). Conclusions: Despite recent declines in the prenatal smoking prevalence, prenatal smoking continues to cause a substantial number of infant deaths in the U.S. (Am J Prev Med 2010;39(1):45–52) Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
Introduction
A
lthough smoking during pregnancy declined from 18.1% in 1991 to 11.4% in 2002, it remains one of the most prevalent and preventable causes of infant morbidity and mortality in the U.S.1 In two previous studies,2,3 5%– 6% of all infant deaths during 1995–1997 were estimated to be caused by prenatal smoking. However, a limitation of both of these studies is From the Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, CDC, Atlanta, Georgia Address correspondence to: Patricia M. Dietz, DrPH, Division of Reproductive Health, CDC, 4770 Buford Highway NE, MS K-22, Atlanta GA 30341. E-mail: [email protected]. The full text of this article is available via AJPM Online at www.ajpmonline.net. 0749-3797/$17.00 doi: 10.1016/j.amepre.2010.03.009
that the authors combined in their analyses all types of infant deaths, including those that were clearly unrelated to prenatal smoking (e.g., drowning). In addition, these studies were conducted before the publication of the 2004 Surgeon General’s report, The Health Consequences of Smoking. The report4 identifıed which infant outcomes are causally related to prenatal smoking following a review of all available scientifıc evidence. The Surgeon General’s report concluded that the evidence was suffıcient to infer a causal relationship between prenatal smoking and premature rupture of the membranes, placenta previa, placental abruption, preterm delivery, fetal growth restriction, and sudden infant death syndrome (SIDS). The underlying pathways for these outcomes have been reviewed extensively elsewhere.4,5 Using the most recent and complete U.S. vital statistics data on prenatal smok-
Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
Am J Prev Med 2010;39(1)45–52 45
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Dietz et al / Am J Prev Med 2010;39(1):45–52
ing, the current study provides updated estimates of the percentage of poor pregnancy outcomes and infant deaths attributable to prenatal smoking by using the outcomes identifıed as causally associated with prenatal smoking in the Surgeon General’s report.4
Methods In 2009, data from the U.S. Linked Birth/Infant Death (LBID) data set, 2002 birth cohort, were analyzed, which includes all births in the U.S. in 2002, and linked infant death certifıcates occurring among those live births. The 2002 LBID data set was analyzed because this is the most recent year where all states, with the exception of California, collected information on prenatal smoking in a similar format (using the 1989 version of the birth certifıcate). The 2003 birth certifıcate revision collects information on prenatal smoking in a different format and data from states using different versions of the certifıcate cannot be combined. As of January 1, 2008, this new 2003 certifıcate revision had been adopted by 27 states. The current study’s eligibility requirements included singleton births to U.S. residents, and information available on prenatal smoking and infant gestational age at delivery. All births from California (n⫽513,900) were excluded because prenatal smoking was not included on the state’s birth certifıcate, 22,620 additional births (⬍1% of births from the remaining states) were excluded because prenatal smoking status was missing, and 5253 births (⬍1%) were excluded because gestational age was missing. The fınal sample included 3,352,756 singleton live births. Live birth outcomes were grouped into fıve mutually exclusive categories of delivery: very preterm (ⱕ27 completed weeks of gestation); moderately preterm (28 –33 completed weeks); late preterm (34 –36 completed weeks); term low birth weight (ⱖ37 completed weeks and ⬍2500 g); and term normal birth weight (ⱖ37 completed weeks and ⱖ2500 g). The last menstrual period (LMP) was used to calculate gestational age when the LMP-based estimates were within 2 weeks of the clinical estimate. Otherwise, the clinical estimate was used to calculate gestational age. Infant deaths from preterm-related causes and SIDS were identifıed by using the ICD-10 underlying causes-of-death codes on the death certifıcates.6 SIDS deaths were identifıed by ICD-10 code R95. An expanded defınition of death from preterm delivery was used, as opposed to using only the ICD-10 codes for disorders related to short gestation and low birth weight. Preterm-related deaths were categorized on the basis of work by Callaghan and others (2006)7 and MacDorman and others (2007).8 The ICD-10 codes included K550, P000, P010, P011, P015, P020, P021, P027, P070 –P073, P102, P220 –229, P250 –279, P280, P281, P360 –P369, P520 –P523, and P77. The criteria that were developed to designate a death as preterm-related included delivery before 37 weeks of gestation and clinical evidence of a specifıc disease or condition that led to infant death that is caused by being preterm or caused the birth to be preterm. This preterm-related category included deaths from premature rupture of the membranes, placenta previa, and placental abruption. Prenatal smoking variables identifıed on the birth certifıcate included a yes or no response and the average number of cigarettes smoked during pregnancy per day. The number of cigarettes was categorized into four groups: 1–10, 11–20, ⱖ21, and unknown. In a bivariate analysis with categoric variables, chi-square tests for in-
dependence were calculated. Based on previous literature, the following potential confounders were selected for inclusion in adjusted models: maternal race or ethnicity; age; education; parity; average weekly weight gain during pregnancy (for all outcomes except SIDS); gestational age (adjusted in the SIDS analysis only); trimester of entry into prenatal care; marital status; and infant gender.2,3 Weight gain during pregnancy was categorized as low if the weekly average weight gain was less than 0.30 lbs (equivalent to total weight gain ⬍11 lbs at 37 weeks’ gestation) and as high if the weekly average weight gain was greater than 1.1 lbs (equivalent to ⬎40 lbs at 37 weeks’ gestation), based on the 2009 IOM recommendations. Polytomous logistic regression was used with backward elimination to estimate the AOR and 95% CIs as measures of the associations among prenatal smoking and the fıve-level live birth outcomes (very preterm, moderately preterm, late preterm, term low birth weight, and term normal birth weight deliveries). Term normal birth weight infants were the reference group. For infant deaths due to SIDS compared to all infant births that did not result in SIDS, the adjusted odds of death from prenatal smoking were estimated by using logistic regression with backward elimination. The same method was used when estimating the logistic model for preterm-related deaths. The prenatal smoking population attributable fraction (PAF) for each poor pregnancy outcome was estimated using an equation incorporating the prevalence of smoking and the prenatal smoking AOR for each outcome (formula [pd(RR–1/RR)], where pd⫽ proportion of cases exposed to the risk factor and RR⫽relative risk).9 The OR was presumed to estimate the relative risk because the prevalence of each outcome was less than 10%. Because prenatal smoking may be under-reported on the birth certifıcate, two PAFs per outcome were estimated. For the fırst PAF calculation, the prenatal smoking prevalence was based on self-reported smoking from the birth certifıcate. For the second PAF calculation, a prevalence estimate 45% higher than that reported was used. The high estimate was based on a previous population-based study of live births in 24 states, which found that birth certifıcates underreported prenatal smoking by 45% compared to a combined estimate of prenatal smoking from a self-administered questionnaire and birth certifıcate.10
Results Overall, 11.5% of singleton, live infants born in 2002 were exposed to prenatal smoking (n⫽386,262). Compared with women who did not smoke, women who smoked during pregnancy were more likely to be younger, unmarried, less educated, and non-Hispanic white, and have had three or more previous live births, have initiated prenatal care after the fırst trimester, and have had low or high weight gain during pregnancy (Table 1). In 2002, the percentage of live births occurring at less than 28 weeks of gestation was 0.6%; those between 28 and 33 weeks was 2.2%, and those between 34 and 36 weeks was 7.5%; and 2.2% of births were term low birth weight. Among women with adverse pregnancy outcomes, prenatal smoking prevalence ranged from 13.7% among mothers who delivered late preterm infants to www.ajpm-online.net
Dietz et al / Am J Prev Med 2010;39(1):45–52
Table 1. Characteristics of women with live births in 2002 by prenatal smoking status
Characteristic
Prenatal smokers Nonsmokers (nⴝ386,262) (nⴝ2,966,674)
Age (years) ⬍20
16.0
10.5*
20–24
37.8
24.5
25–34
37.0
51.4
9.2
13.6
ⱖ35 Education (years) ⬍12
35.9
18.7*
12
43.5
30.1
ⱖ13
20.6
51.2
Non-Hispanic white
80.6
58.7*
Non-Hispanic black
12.0
16.2
Hispanic
4.7
19.6
Other
2.7
5.5
0
34.6
41.3*
1–2
31.1
32.8
ⱖ3
34.2
25.9
1st trimester
75.6
84.2*
2nd trimester
18.3
12.3
6.2
3.4
9.0
6.3*
Maternal race/ethnicity
Parity
Entry into prenatal care
3rd trimester/no care Weight gain during pregnancy (lbs per week) ⬍0.30 0.30–1.1
67.5
72.8
⬎1.1
19.0
14.8
4.6
6.0
Unmarried
58.9
31.1*
Married
41.1
68.9
Unknown Marital status
Note: Values are percentages. *p⬍0.001
23.4% among mothers who delivered term low birth weight infants (Table 2). Women who delivered normalweight term infants had the lowest prenatal smoking prevalence of 10.9%. The distributions of maternal charJuly 2010
47
acteristics varied according to birth outcome. Women who delivered preterm or term low birth weight infants were more likely to be aged ⬍20 years, have less than 12 years of education, and have entered prenatal care later than women who delivered normal-weight term infants. The SIDS mortality rate was 0.57 for every 1000 singleton live births in 2002. Of women who delivered infants who died of SIDS, 36.8% smoked during pregnancy (Table 3). Compared to women whose infants did not die or whose infants died from causes other than SIDS, women whose infants died of SIDS were more likely to be aged ⬍35 years, unmarried, and non-Hispanic black, and have less than 13 years of education, have had three or more previous live births, have entered prenatal care after the fırst trimester, and have had low weight gain during pregnancy. The preterm-related mortality rate was 2 for every 1000 live singleton births in 2002. Of women who delivered infants who died from a preterm-related death, 15.7% smoked during pregnancy (Table 3). Compared to women whose infants did not die or whose infants died from non–preterm-related causes, women whose infants died from preterm-related causes were more likely to be aged ⬍20 years, non-Hispanic black, nulliparous, and unmarried, and to have less than 13 years of education, have had low weight gain, and have had no prenatal care or entry into prenatal care in the third trimester. Prenatal smoking was associated with very (AOR⫽1.5, 95% CI⫽1.4, 1.6); moderate (AOR⫽1.4, 95% CI⫽1.4, 1.4); and late (AOR⫽1.2, 95% CI⫽1.2, 1.3) preterm deliveries and term low birth weight deliveries (AOR⫽2.3, 95% CI⫽2.3, 2.5) compared to term ⱖ2500-g deliveries (Table 4). Prenatal smoking was also associated with SIDS (AOR⫽2.7, 95% CI⫽2.4, 3.0) and preterm-related deaths (AOR⫽1.5, 95% CI⫽1.4, 1.6). A dose response of daily average cigarettes smoked was found for all poor birth and infant outcomes, and smoking at least 21 cigarettes each day had the strongest association with poor pregnancy and infant outcomes (Table 4). When using the smoking prevalence reported on the birth certifıcates, the fraction of adverse birth outcomes attributable to prenatal smoking was 5.3% for very, 4.6% for moderate, and 2.6% for late preterm deliveries (Table 4). The fraction of term low birth weight deliveries attributable to prenatal smoking was 13.1%. When a 45% higher smoking prevalence estimate was used, the estimated PAFs were 7.7%, 6.7%, 3.7%, and 19.0%, respectively. Preterm-related deaths and SIDS deaths attributed to prenatal smoking was 5.0% and 23.2%, respectively. Using higher smoking prevalence estimates, the PAF estimates were 7.3% and 33.6%, respectively. The fraction of all infant deaths attributable to prenatal smoking was estimated to be 2.8%– 4.1%.
Dietz et al / Am J Prev Med 2010;39(1):45–52
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Table 2. Characteristics of women delivering live births by infant gestational age and birth weight (g), U.S., 2002 <27 weeks’ gestation (nⴝ20,594)
28–33 weeks’ gestation (nⴝ75,594)
34–36 weeks’ gestation (nⴝ260,821)
>37 weeks’ gestation and <2500 g (nⴝ77,555)
>37 weeks’ gestation and >2500 g (nⴝ2,918,192)
Yes
15.5
15.9
13.7
23.4
10.9*
No
84.5
84.1
86.3
76.6
89.1
None
84.5
84.1
86.3
76.6
89.1*
1–10
10.0
10.2
8.8
14.5
7.1
11–20
3.0
3.3
2.9
5.5
2.2
ⱖ21
0.4
0.4
0.4
0.7
0.2
Unknown
2.0
1.9
1.6
2.6
1.3
⬍20
17.4
16.7
13.1
16.5
10.6*
20–24
27.5
27.2
26.9
30.6
25.8
25–34
41.5
42.0
46.1
40.7
50.6
ⱖ35
13.6
14.2
13.9
12.3
13.0
⬍12
27.4
28.4
24.4
28.9
19.9*
12
36.7
35.2
33.5
36.0
31.2
ⱖ13
35.8
36.3
42.1
35.1
48.9
Non-Hispanic white
40.3
47.9
55.3
50.0
62.6*
Non-Hispanic black
39.7
28.4
21.2
27.0
14.4
Hispanic
16.1
19.0
18.7
16.8
17.8
3.9
4.7
4.9
6.2
5.2
0
49.9
43.4
39.5
48.7
40.3*
1–2
24.3
27.3
30.8
26.1
33.1
ⱖ3
25.8
29.3
29.7
25.2
26.6
1st trimester
77.2
74.8
80.2
77.6
83.9*
2nd trimester
13.5
18.0
14.7
16.6
12.6
9.3
7.2
5.1
5.9
3.5
Characteristic Prenatal smoking
Daily average cigarettes smoked
Age (years)
Education (years)
Maternal race/ethnicity
Other Parity
Entry into prenatal care
3rd trimester/no care Weight gain during pregnancy (lbs per week) ⬍0.30
16.7
8.1
7.8
11.2
0.30–1.1
53.2
63.8
65.8
72.9
73.1
⬎1.1
13.7
18.6
19.5
8.7
15.0
Unknown
16.4
9.5
6.8
7.2
5.6
Unmarried
54.9
49.9
40.5
49.2
32.8*
Married
45.1
50.1
59.5
50.8
67.2
6.3*
Marital status
Note: Values are percentages. *p⬍0.001
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Dietz et al / Am J Prev Med 2010;39(1):45–52
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Table 3. Characteristics of women by infant death, U.S., 2002 SIDS death (nⴝ1926)
No SIDS death (nⴝ3,350,999)
Preterm-related death (nⴝ6703)
No preterm-related death (nⴝ3,346,163)
Yes
36.8
11.5*
15.7
11.5*
No
63.2
88.5
84.3
88.5
None
63.1
88.5*
84.3
88.5*
1–10
24.2
7.5
9.9
7.5
11–20
7.9
2.3
3.4
2.3
ⱖ21
1.1
0.3
0.4
0.3
Unknown
3.7
1.4
2.1
1.4
⬍20
23.2
11.1*
17.3
11.1*
20–24
39.9
26.0
27.9
26.0
25–34
32.0
49.8
41.2
49.8
4.9
13.1
13.5
13.1
Characteristic Prenatal smoking
Daily average cigarettes smoked
Age (years)
ⱖ35 Education (years) ⬍12
38.7
20.7*
26.4
20.7*
12
39.7
31.6
38.9
31.6
ⱖ13
21.6
47.7
34.6
47.7
Non-Hispanic white
56.9
61.3*
41.2
61.3*
Non-Hispanic black
Maternal race/ethnicity
29.2
15.7
40.9
15.7
Hispanic
9.6
17.9
14.2
17.9
Other
4.3
5.1
3.7
5.1
Parity 0
29.7
40.5*
51.2
40.5*
1–2
32.8
32.6
23.9
32.6
ⱖ3
37.4
26.9
24.9
26.9
1st trimester
69.6
83.2*
78.7
83.2*
2nd trimester
22.2
13.0
11.0
13.0
8.2
3.7
10.4
3.7
6.6*
21.4
Entry into prenatal care
3rd trimester/no care Weight gain during pregnancy (lbs per week) ⬍0.30
11.2
0.30–1.1
64.0
72.2
50.2
72.2
⬎1.1
16.6
15.3
9.0
15.3
7.8
5.8
19.3
5.8
Unmarried
62.0
34.3*
54.6
34.3*
Married
38.0
36.7
45.4
64.7
Unknown
6.6*
Marital status
Note: Values are percentages. *p⬍0.001 SIDS, sudden infant death syndrome
July 2010
Dietz et al / Am J Prev Med 2010;39(1):45–52
50
Table 4. AOR (95% CI) and population-attributable fraction of pregnancy and infant outcomes attributable to prenatal smoking, U.S., 2002
Characteristic
>37 weeks’ <27 weeks’ 28–33 weeks’ 34–36 weeks’ gestation and gestationa gestationa gestationa <2500 ga
Prenatal smoking
1.5 (1.4, 1.6)
1.4 (1.4, 1.4)
1.2 (1.2, 1.3)
1–10
1.5 (1.4, 1.5)
1.4 (1.3, 1.4)
11–20
1.6 (1.5, 1.8)
ⱖ21 Unknown
SIDSb
Preterm-related deathsb
2.3 (2.3, 2.5)
2.7 (2.4, 3.0)
1.5 (1.4, 1.6)
1.2 (1.2, 1.2)
2.3 (2.3, 2.4)
2.7 (2.4, 3.0)
1.4 (1.3, 1.5)
1.6 (1.5, 1.6)
1.3 (1.3, 1.4)
3.1 (3.0, 3.2)
2.9 (2.4, 3.5)
1.6 (1.4, 1.9)
2.1 (1.7, 2.7)
1.9 (1.7, 2.1)
1.6 (1.5, 1.7)
4.0 (3.6, 4.3)
3.9 (2.5, 6.0)
1.9 (1.3, 2.7)
0.7 (0.5, 0.9)
0.7 (0.6, 0.8)
0.7 (0.7, 0.8)
0.6 (0.5, 0.6)
0.6 (0.4, 1.0)
0.8 (0.7, 0.8)
Prenatal smoking reported on birth certificate
5.3
4.6
2.6
13.1
23.2
5.0
Prenatal smoking 45% higher than reported on birth certificate
7.7
6.7
3.7
19.0
33.6
7.3
Daily average cigarettes smoked
Population-attributable fraction
Note: Adjusted for maternal age, education, race/ethnicity, marital status, parity, infant gender, weight gain during pregnancy (except SIDS) and entry in prenatal care, and gestational age (SIDS only) a Compared to infants ⱖ37 weeks gestation and ⱖ2500 g b Compared to all other infants born in 2002 SIDS, sudden infant death syndrome
Discussion Prenatal smoking continues to contribute to poor pregnancy and infant outcomes in the U.S. Among 2002 births, the present study estimated that 5%– 8% of very and moderately preterm births and 3%– 4% of late preterm births were attributed to prenatal smoking. Assuming the risk of preterm delivery for smokers could be decreased to that of nonsmokers, these preterm births would be prevented. Similarly, 13%–19% of term low birth weight deliveries potentially could have been prevented. Among infant deaths, 5%–7% of preterm-related deaths and 23%–34% of SIDS deaths potentially could have been avoided. The high PAF level among SIDS deaths is especially striking and suggests that tobacco control and SIDS prevention activities should be coordinated. Infants born preterm or term low birth weight may encounter challenging short- and long-term health problems, including neurologic, developmental, and neurosensory morbidities. In 2001, the hospitalization costs in the fırst year of life for all preterm low birth weight infant admissions in the U.S. totaled $5.8 billion.11 Even using a conservative PAF estimate of 4% for preterm delivery, preventing women from smoking during pregnancy could have substantial cost savings (approximately $232
million annually) in addition to overall improved health for mothers and their children. The estimated associations in the present study between prenatal smoking and SIDS and between prenatal smoking and early preterm births are consistent with those found in a previous study that used 1995–1996 data.2,3 The estimates are also consistent with previous studies conducted at different times and in different geographic locations.12,13 The consistency of these associations over time suggests that states interested in estimating the state-specifıc PAF of adverse birth outcomes due to prenatal smoking can use their state-specifıc prevalence of prenatal smoking and the AORs found in the present study. The current study makes two new contributions to the literature. As previously stated, it restricts infant deaths to those for which prenatal smoking has an established causal relationship. Second, it assesses the association of prenatal smoking with preterm-related deaths, a relatively new construct that is now used by NCHS to calculate national preterm-related death rates.8 The defınition of a preterm-related infant death is based on a paradigm that identifıes deaths among infants born preterm according to ICD-10 codes that reflect reasons for death that occur almost exclusively among preterm infants, or www.ajpm-online.net
Dietz et al / Am J Prev Med 2010;39(1):45–52
codes that characterize the cause of death according to the reason for the preterm birth.8 Preterm-related deaths account for at least one third of all infant deaths, and they are most likely to occur at the very earliest gestation.7 Some of these deaths could be prevented by eliminating smoking during pregnancy. The present study’s estimates of prenatal smoking and the PAFs of poor pregnancy and infant outcomes are subject to several limitations. Prenatal smoking data recorded on the birth certifıcate are presumed to be selfreported at delivery or taken from the medical record (when the woman reported smoking to her prenatal healthcare provider). Both of these scenarios are likely to lead to under-reporting. Conversely, birth certifıcates may capture a disproportionate percentage of heavier smokers because light smokers may be less likely to report smoking to their prenatal healthcare providers. This would lead to an overestimation of the strength of the association between prenatal smoking and adverse outcomes (given the dose response found in the current study). Uncontrolled confounding could have biased the fındings because smokers may differ from nonsmokers in factors that contribute to poor birth outcomes for factors not available in the data set. Two possible confounders not available on birth and death certifıcates are infant sleep position and exposure to secondhand smoke, both of which increase the risk of SIDS. However, at least one study found no association between sleep position and prenatal smoking behaviors.14 Finally, recent studies have questioned the accuracy and consistency of the reporting of SIDS as a cause-of-death determination on the death certifıcate. Without a thorough case investigation, it is diffıcult to distinguish a SIDS case from a suffocation case.15,16 However, any outcome misclassifıcation would, most likely, bias results toward the null. Other potential uncontrolled confounders include other substance abuse and psychiatric disorders that could negatively influence benefıcial health behaviors.17 Despite the inability to adjust for all potential confounders, the consistency of the results with multiple studies that were conducted over several decades in a variety of geographic locations and diverse populations and the clear dose–response relationship between cigarettes smoked and adverse outcomes support the validity of the results.12,13 Overall, the current study’s fındings are generalizable to births in the U.S., excluding California. According to the California Maternal and Infant Health Assessment, 9% of women in California smoked during pregnancy in 2002.18 This level of smoking is slightly lower than the average of all other states for 2002 (11.5%). Given that California births represented 13% of all births in 2002, the July 2010
51
U.S. smoking prevalence during pregnancy may be slightly lower at approximately 11.2% based on birth certifıcate estimates. The effect of adding California to the analysis on the PAF would be minimal. For example, the PAF for prenatal smoking attributable to SIDS would decrease from 23.2% to 22.6%. Ideally, this analysis would have been conducted with more-recent vital statistics data; however, use of different versions of the birth certifıcate in different states after 2002 prevented this. It does appear that prenatal smoking prevalence has decreased slightly since 2002. NCHS reported for 2005 births the prenatal smoking rate for states using the 1989 version of the birth certifıcate (10.7% smoked during pregnancy vs 11.7% in 2002 among these same states). If one assumes that the estimated 2002 U.S. prenatal smoking rate of 11.2% (including California) declined at a similar rate as these states (annual decrease of .014%), then the estimated U.S. 2009 prenatal smoking rate would be approximately 10.0%, and the PAFs would be slightly lower than what was estimated for 2002 in the present study at 4.4%– 6.3% for preterm-related deaths and 20.2%–29.3% for SIDS deaths. The current study found that prenatal smoking continues to contribute to a substantial proportion of avoidable cases of infant morbidity and mortality in the U.S. Prenatal smoking prevalence is decreasing; however, in some states prenatal smoking prevalence is as high as 36%, more than three times the national average.19 In addition, pregnant women with Medicaid report a higher smoking prevalence (24%) compared to women with private insurance (7%).20 Smoking prevalence can be reduced through sustained and comprehensive tobacco control activities, such as promoting policies that establish smokefree environments in public places and the workplace, increasing tobacco excise taxes, banning all forms of tobacco advertisement, and ensuring adequate healthcare insurance for cessation services.21 On the clinical level, prenatal care providers can assess smoking status, offer smoking cessation interventions, or refer patients who smoke to effective cessation services.22 As of 2007, a total of 43 state Medicaid programs covered some form of tobacco-dependence treatment, yet only two states had no restrictions on this coverage such as copayments, limits on number of treatment courses, and coverage of types of treatments.23 The Public Health Service’s Clinical Practice Guidelines recommend comprehensive insurance coverage of tobacco-dependence treatments without barriers to care. Maternal and child healthcare providers need to work in concert with state tobacco control professionals to improve access to comprehensive insurance coverage and to strengthen state
52
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tobacco control policies to reduce prenatal smoking rates and prevent the harm smoking causes to both mother and child. The fındings and conclusions in this article are those of the authors and do not necessarily represent the offıcial position of the CDC. No fınancial disclosures were reported by the authors of this paper.
References 1. Mathew TJ, Rivera CC. Smoking during pregnancy—U.S., 1990 –2002. MMWR Morb Mortal Wkly Rep 2004;53(39):911–5. 2. Salihu HM, Aliyu MH, Pierre-Louis BJ, Alexander GR. Levels of excess infant deaths attributable to maternal smoking during pregnancy in the U.S. Matern Child Health J 2003;7(4):219 –27. 3. Pollack H, Lantz PM, Frohna JG. Maternal smoking and adverse birth outcomes among singletons and twins. Am J Public Health 2000;90(3):395– 400. 4. USDHHS. The health consequences of smoking: a report of the Surgeon General. Atlanta GA: USDHHS, CDC, National Center for Chronic Disease Prevention and Health Promotion, Offıce on Smoking and Health, 2004:576. 5. Cnattingius S. The epidemiology of smoking during pregnancy: smoking prevalence, maternal characteristics, and pregnancy outcomes. Nicotine Tob Res 2004;6(2S):S125– 40. 6. WHO. International statistical classifıcation of diseases and related health problems, 10th revision. Geneva: WHO, 1992. 7. Callaghan WM, MacDorman MF, Rasmussen SA, Qin C, Lackritz EM. The contribution of preterm birth to infant mortality rates in the U.S. Pediatrics 2006;118(4):1566 –73. 8. MacDorman MF, Callaghan WM, Mathews TJ, Hoyert DL, Kochanek KD. Trends in preterm-related infant mortality by race and ethnicity, U.S., 1999 –2004. Int J Health Serv 2007;37(4):635– 41. 9. Rockhill B, Newman B, Weinberg C. Use and misuse of population attributable fractions. Am J Public Health 1998;88(1):15–9.
10. Allen AM, Dietz PM, Tong VT, England L, Prince CB. Prenatal smoking prevalence ascertained from two population-based data sources: birth certifıcates and PRAMS questionnaires, 2004. Public Health Rep 2008;123(5):586 –92. 11. Russell RB, Green NS, Steiner CA, et al. Cost of hospitalization for preterm and low birth weight infants in the U.S. Pediatrics 2007; 120(1):e1–9. 12. Shah NV, Bracken MB. A systematic review and meta-analysis of prospective studies on the association between maternal cigarette smoking and preterm delivery. Am J Obstet Gyecol 2000;182(2): 465–72. 13. Anderson HR, Cook DG. Passive smoking and sudden infant death syndrome: review of the epidemiological evidence. Thorax 1997;52: 1003–9. 14. Pollack H, Lantz PM, Frohna JG. Infant sleep placement after the back to sleep campaign. Pediatrics 2002;109(4):608 –14. 15. Shapiro-Mendoza CK, Tomashek KM, Anderson RN, Wingo J. Recent national trends in sudden, unexpected infant deaths: more evidence supporting a change in classifıcation or reporting. Am J Epidemiol 2006;163(8):762–9. 16. Malloy MH, MacDorman M. Changes in the classifıcation of sudden unexpected infant deaths: U.S., 1992–2001. Pediatrics 2005;115(5): 1247–53. 17. Gilman SE, Breslau J, Subramanian SV, Hitsman B, Koenen KC. Social factors, psychopathology, and maternal smoking during pregnancy. Am J Public Health 2007;97(8):15–20. 18. California Department of Health Services. Smoking during pregnancy. 2006. www.dhs.ca.gov/tobacco. 19. Tong VT, Jones J, D’Angelo D, Bombard J, Dietz PM. Trends in smoking before, during, and after pregnancy 2000 –2005: PRAMS. MMWR Surveill Summ 2009;58(4):1–29. 20. CDC. Preventing smoking and exposure to secondhand smoke before, during, and after pregnancy. 2007. www.cdc.gov/chronicdieases/ resources/publications/fact_sheets/smoking.htm. 21. Hopkins DP, Briss PA, Ricard CJ, et al. Reviews of evidence regarding interventions to reduce tobacco use and exposure to environmental tobacco smoke. Am J Prev Med 2001;20(2S):16 – 66. 22. Fiore MC, Bailey WC, Cohen SJ, Dorfman SF, Goldstein MG, Gritz ER. Treating tobacco use and dependence. In: Clinical practice guideline. Rockville MD: USDHHS Public Health Service, 2008. 23. McMenamin SB, Halpin HA, Bellows NM, et al. State Medicaid coverage for tobacco-dependence treatments—U.S., 2007. MMWR Morb Mortal Wkly Rep 2009;58(43):1199 –204.
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Purpose: The aim of this study was to estimate the proportion of preterm deliveries, term low birth weight deliveries, and infant deaths attributable to prenatal smoking. Methods: Associations were estimated for prenatal smoking and preterm deliveries, term low birth weight (⬍2500 g) deliveries, sudden infant death syndrome (SIDS), and preterm-related deaths among 3,352,756 singleton, live births using the U.S. Linked Birth/Infant Death Data Set, 2002 birth cohort. The 2002 data set is the most recent, in which 49 states used the same standardized smoking-related question on the birth certifıcate. Logistic regression models estimated ORs of prenatal smoking for each outcome, and the prenatal smoking population attributable fraction was calculated for each outcome.
Results: Prenatal smoking (11.5% of all births) was signifıcantly associated with very (AOR⫽1.5, 95% CI⫽1.4, 1.6); moderate (AOR⫽1.4, 95% CI⫽1.4, 1.4); and late (AOR⫽1.2, 95% CI⫽1.2, 1.3) preterm deliveries; term low birth weight deliveries (AOR⫽2.3, 95% CI⫽2.3, 2.5); SIDS (AOR⫽2.7, 95% CI⫽2.4, 3.0); and preterm-related deaths (AOR⫽1.5, 95% CI⫽1.4, 1.6). It was estimated that 5.3%–7.7% of preterm deliveries, 13.1%–19.0% of term low birth weight deliveries, 23.2%–33.6% of SIDS, and 5.0%–7.3% of preterm-related deaths were attributable to prenatal smoking. Assuming prenatal smoking rates continued to decline after 2002, these PAFs would be slightly lower for 2009 (4.4%– 6.3% for preterm-related deaths, 20.2%–29.3% for SIDS deaths). Conclusions: Despite recent declines in the prenatal smoking prevalence, prenatal smoking continues to cause a substantial number of infant deaths in the U.S. (Am J Prev Med 2010;39(1):45–52) Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
Introduction
A
lthough smoking during pregnancy declined from 18.1% in 1991 to 11.4% in 2002, it remains one of the most prevalent and preventable causes of infant morbidity and mortality in the U.S.1 In two previous studies,2,3 5%– 6% of all infant deaths during 1995–1997 were estimated to be caused by prenatal smoking. However, a limitation of both of these studies is From the Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, CDC, Atlanta, Georgia Address correspondence to: Patricia M. Dietz, DrPH, Division of Reproductive Health, CDC, 4770 Buford Highway NE, MS K-22, Atlanta GA 30341. E-mail: [email protected]. The full text of this article is available via AJPM Online at www.ajpmonline.net. 0749-3797/$17.00 doi: 10.1016/j.amepre.2010.03.009
that the authors combined in their analyses all types of infant deaths, including those that were clearly unrelated to prenatal smoking (e.g., drowning). In addition, these studies were conducted before the publication of the 2004 Surgeon General’s report, The Health Consequences of Smoking. The report4 identifıed which infant outcomes are causally related to prenatal smoking following a review of all available scientifıc evidence. The Surgeon General’s report concluded that the evidence was suffıcient to infer a causal relationship between prenatal smoking and premature rupture of the membranes, placenta previa, placental abruption, preterm delivery, fetal growth restriction, and sudden infant death syndrome (SIDS). The underlying pathways for these outcomes have been reviewed extensively elsewhere.4,5 Using the most recent and complete U.S. vital statistics data on prenatal smok-
Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
Am J Prev Med 2010;39(1)45–52 45
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Dietz et al / Am J Prev Med 2010;39(1):45–52
ing, the current study provides updated estimates of the percentage of poor pregnancy outcomes and infant deaths attributable to prenatal smoking by using the outcomes identifıed as causally associated with prenatal smoking in the Surgeon General’s report.4
Methods In 2009, data from the U.S. Linked Birth/Infant Death (LBID) data set, 2002 birth cohort, were analyzed, which includes all births in the U.S. in 2002, and linked infant death certifıcates occurring among those live births. The 2002 LBID data set was analyzed because this is the most recent year where all states, with the exception of California, collected information on prenatal smoking in a similar format (using the 1989 version of the birth certifıcate). The 2003 birth certifıcate revision collects information on prenatal smoking in a different format and data from states using different versions of the certifıcate cannot be combined. As of January 1, 2008, this new 2003 certifıcate revision had been adopted by 27 states. The current study’s eligibility requirements included singleton births to U.S. residents, and information available on prenatal smoking and infant gestational age at delivery. All births from California (n⫽513,900) were excluded because prenatal smoking was not included on the state’s birth certifıcate, 22,620 additional births (⬍1% of births from the remaining states) were excluded because prenatal smoking status was missing, and 5253 births (⬍1%) were excluded because gestational age was missing. The fınal sample included 3,352,756 singleton live births. Live birth outcomes were grouped into fıve mutually exclusive categories of delivery: very preterm (ⱕ27 completed weeks of gestation); moderately preterm (28 –33 completed weeks); late preterm (34 –36 completed weeks); term low birth weight (ⱖ37 completed weeks and ⬍2500 g); and term normal birth weight (ⱖ37 completed weeks and ⱖ2500 g). The last menstrual period (LMP) was used to calculate gestational age when the LMP-based estimates were within 2 weeks of the clinical estimate. Otherwise, the clinical estimate was used to calculate gestational age. Infant deaths from preterm-related causes and SIDS were identifıed by using the ICD-10 underlying causes-of-death codes on the death certifıcates.6 SIDS deaths were identifıed by ICD-10 code R95. An expanded defınition of death from preterm delivery was used, as opposed to using only the ICD-10 codes for disorders related to short gestation and low birth weight. Preterm-related deaths were categorized on the basis of work by Callaghan and others (2006)7 and MacDorman and others (2007).8 The ICD-10 codes included K550, P000, P010, P011, P015, P020, P021, P027, P070 –P073, P102, P220 –229, P250 –279, P280, P281, P360 –P369, P520 –P523, and P77. The criteria that were developed to designate a death as preterm-related included delivery before 37 weeks of gestation and clinical evidence of a specifıc disease or condition that led to infant death that is caused by being preterm or caused the birth to be preterm. This preterm-related category included deaths from premature rupture of the membranes, placenta previa, and placental abruption. Prenatal smoking variables identifıed on the birth certifıcate included a yes or no response and the average number of cigarettes smoked during pregnancy per day. The number of cigarettes was categorized into four groups: 1–10, 11–20, ⱖ21, and unknown. In a bivariate analysis with categoric variables, chi-square tests for in-
dependence were calculated. Based on previous literature, the following potential confounders were selected for inclusion in adjusted models: maternal race or ethnicity; age; education; parity; average weekly weight gain during pregnancy (for all outcomes except SIDS); gestational age (adjusted in the SIDS analysis only); trimester of entry into prenatal care; marital status; and infant gender.2,3 Weight gain during pregnancy was categorized as low if the weekly average weight gain was less than 0.30 lbs (equivalent to total weight gain ⬍11 lbs at 37 weeks’ gestation) and as high if the weekly average weight gain was greater than 1.1 lbs (equivalent to ⬎40 lbs at 37 weeks’ gestation), based on the 2009 IOM recommendations. Polytomous logistic regression was used with backward elimination to estimate the AOR and 95% CIs as measures of the associations among prenatal smoking and the fıve-level live birth outcomes (very preterm, moderately preterm, late preterm, term low birth weight, and term normal birth weight deliveries). Term normal birth weight infants were the reference group. For infant deaths due to SIDS compared to all infant births that did not result in SIDS, the adjusted odds of death from prenatal smoking were estimated by using logistic regression with backward elimination. The same method was used when estimating the logistic model for preterm-related deaths. The prenatal smoking population attributable fraction (PAF) for each poor pregnancy outcome was estimated using an equation incorporating the prevalence of smoking and the prenatal smoking AOR for each outcome (formula [pd(RR–1/RR)], where pd⫽ proportion of cases exposed to the risk factor and RR⫽relative risk).9 The OR was presumed to estimate the relative risk because the prevalence of each outcome was less than 10%. Because prenatal smoking may be under-reported on the birth certifıcate, two PAFs per outcome were estimated. For the fırst PAF calculation, the prenatal smoking prevalence was based on self-reported smoking from the birth certifıcate. For the second PAF calculation, a prevalence estimate 45% higher than that reported was used. The high estimate was based on a previous population-based study of live births in 24 states, which found that birth certifıcates underreported prenatal smoking by 45% compared to a combined estimate of prenatal smoking from a self-administered questionnaire and birth certifıcate.10
Results Overall, 11.5% of singleton, live infants born in 2002 were exposed to prenatal smoking (n⫽386,262). Compared with women who did not smoke, women who smoked during pregnancy were more likely to be younger, unmarried, less educated, and non-Hispanic white, and have had three or more previous live births, have initiated prenatal care after the fırst trimester, and have had low or high weight gain during pregnancy (Table 1). In 2002, the percentage of live births occurring at less than 28 weeks of gestation was 0.6%; those between 28 and 33 weeks was 2.2%, and those between 34 and 36 weeks was 7.5%; and 2.2% of births were term low birth weight. Among women with adverse pregnancy outcomes, prenatal smoking prevalence ranged from 13.7% among mothers who delivered late preterm infants to www.ajpm-online.net
Dietz et al / Am J Prev Med 2010;39(1):45–52
Table 1. Characteristics of women with live births in 2002 by prenatal smoking status
Characteristic
Prenatal smokers Nonsmokers (nⴝ386,262) (nⴝ2,966,674)
Age (years) ⬍20
16.0
10.5*
20–24
37.8
24.5
25–34
37.0
51.4
9.2
13.6
ⱖ35 Education (years) ⬍12
35.9
18.7*
12
43.5
30.1
ⱖ13
20.6
51.2
Non-Hispanic white
80.6
58.7*
Non-Hispanic black
12.0
16.2
Hispanic
4.7
19.6
Other
2.7
5.5
0
34.6
41.3*
1–2
31.1
32.8
ⱖ3
34.2
25.9
1st trimester
75.6
84.2*
2nd trimester
18.3
12.3
6.2
3.4
9.0
6.3*
Maternal race/ethnicity
Parity
Entry into prenatal care
3rd trimester/no care Weight gain during pregnancy (lbs per week) ⬍0.30 0.30–1.1
67.5
72.8
⬎1.1
19.0
14.8
4.6
6.0
Unmarried
58.9
31.1*
Married
41.1
68.9
Unknown Marital status
Note: Values are percentages. *p⬍0.001
23.4% among mothers who delivered term low birth weight infants (Table 2). Women who delivered normalweight term infants had the lowest prenatal smoking prevalence of 10.9%. The distributions of maternal charJuly 2010
47
acteristics varied according to birth outcome. Women who delivered preterm or term low birth weight infants were more likely to be aged ⬍20 years, have less than 12 years of education, and have entered prenatal care later than women who delivered normal-weight term infants. The SIDS mortality rate was 0.57 for every 1000 singleton live births in 2002. Of women who delivered infants who died of SIDS, 36.8% smoked during pregnancy (Table 3). Compared to women whose infants did not die or whose infants died from causes other than SIDS, women whose infants died of SIDS were more likely to be aged ⬍35 years, unmarried, and non-Hispanic black, and have less than 13 years of education, have had three or more previous live births, have entered prenatal care after the fırst trimester, and have had low weight gain during pregnancy. The preterm-related mortality rate was 2 for every 1000 live singleton births in 2002. Of women who delivered infants who died from a preterm-related death, 15.7% smoked during pregnancy (Table 3). Compared to women whose infants did not die or whose infants died from non–preterm-related causes, women whose infants died from preterm-related causes were more likely to be aged ⬍20 years, non-Hispanic black, nulliparous, and unmarried, and to have less than 13 years of education, have had low weight gain, and have had no prenatal care or entry into prenatal care in the third trimester. Prenatal smoking was associated with very (AOR⫽1.5, 95% CI⫽1.4, 1.6); moderate (AOR⫽1.4, 95% CI⫽1.4, 1.4); and late (AOR⫽1.2, 95% CI⫽1.2, 1.3) preterm deliveries and term low birth weight deliveries (AOR⫽2.3, 95% CI⫽2.3, 2.5) compared to term ⱖ2500-g deliveries (Table 4). Prenatal smoking was also associated with SIDS (AOR⫽2.7, 95% CI⫽2.4, 3.0) and preterm-related deaths (AOR⫽1.5, 95% CI⫽1.4, 1.6). A dose response of daily average cigarettes smoked was found for all poor birth and infant outcomes, and smoking at least 21 cigarettes each day had the strongest association with poor pregnancy and infant outcomes (Table 4). When using the smoking prevalence reported on the birth certifıcates, the fraction of adverse birth outcomes attributable to prenatal smoking was 5.3% for very, 4.6% for moderate, and 2.6% for late preterm deliveries (Table 4). The fraction of term low birth weight deliveries attributable to prenatal smoking was 13.1%. When a 45% higher smoking prevalence estimate was used, the estimated PAFs were 7.7%, 6.7%, 3.7%, and 19.0%, respectively. Preterm-related deaths and SIDS deaths attributed to prenatal smoking was 5.0% and 23.2%, respectively. Using higher smoking prevalence estimates, the PAF estimates were 7.3% and 33.6%, respectively. The fraction of all infant deaths attributable to prenatal smoking was estimated to be 2.8%– 4.1%.
Dietz et al / Am J Prev Med 2010;39(1):45–52
48
Table 2. Characteristics of women delivering live births by infant gestational age and birth weight (g), U.S., 2002 <27 weeks’ gestation (nⴝ20,594)
28–33 weeks’ gestation (nⴝ75,594)
34–36 weeks’ gestation (nⴝ260,821)
>37 weeks’ gestation and <2500 g (nⴝ77,555)
>37 weeks’ gestation and >2500 g (nⴝ2,918,192)
Yes
15.5
15.9
13.7
23.4
10.9*
No
84.5
84.1
86.3
76.6
89.1
None
84.5
84.1
86.3
76.6
89.1*
1–10
10.0
10.2
8.8
14.5
7.1
11–20
3.0
3.3
2.9
5.5
2.2
ⱖ21
0.4
0.4
0.4
0.7
0.2
Unknown
2.0
1.9
1.6
2.6
1.3
⬍20
17.4
16.7
13.1
16.5
10.6*
20–24
27.5
27.2
26.9
30.6
25.8
25–34
41.5
42.0
46.1
40.7
50.6
ⱖ35
13.6
14.2
13.9
12.3
13.0
⬍12
27.4
28.4
24.4
28.9
19.9*
12
36.7
35.2
33.5
36.0
31.2
ⱖ13
35.8
36.3
42.1
35.1
48.9
Non-Hispanic white
40.3
47.9
55.3
50.0
62.6*
Non-Hispanic black
39.7
28.4
21.2
27.0
14.4
Hispanic
16.1
19.0
18.7
16.8
17.8
3.9
4.7
4.9
6.2
5.2
0
49.9
43.4
39.5
48.7
40.3*
1–2
24.3
27.3
30.8
26.1
33.1
ⱖ3
25.8
29.3
29.7
25.2
26.6
1st trimester
77.2
74.8
80.2
77.6
83.9*
2nd trimester
13.5
18.0
14.7
16.6
12.6
9.3
7.2
5.1
5.9
3.5
Characteristic Prenatal smoking
Daily average cigarettes smoked
Age (years)
Education (years)
Maternal race/ethnicity
Other Parity
Entry into prenatal care
3rd trimester/no care Weight gain during pregnancy (lbs per week) ⬍0.30
16.7
8.1
7.8
11.2
0.30–1.1
53.2
63.8
65.8
72.9
73.1
⬎1.1
13.7
18.6
19.5
8.7
15.0
Unknown
16.4
9.5
6.8
7.2
5.6
Unmarried
54.9
49.9
40.5
49.2
32.8*
Married
45.1
50.1
59.5
50.8
67.2
6.3*
Marital status
Note: Values are percentages. *p⬍0.001
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49
Table 3. Characteristics of women by infant death, U.S., 2002 SIDS death (nⴝ1926)
No SIDS death (nⴝ3,350,999)
Preterm-related death (nⴝ6703)
No preterm-related death (nⴝ3,346,163)
Yes
36.8
11.5*
15.7
11.5*
No
63.2
88.5
84.3
88.5
None
63.1
88.5*
84.3
88.5*
1–10
24.2
7.5
9.9
7.5
11–20
7.9
2.3
3.4
2.3
ⱖ21
1.1
0.3
0.4
0.3
Unknown
3.7
1.4
2.1
1.4
⬍20
23.2
11.1*
17.3
11.1*
20–24
39.9
26.0
27.9
26.0
25–34
32.0
49.8
41.2
49.8
4.9
13.1
13.5
13.1
Characteristic Prenatal smoking
Daily average cigarettes smoked
Age (years)
ⱖ35 Education (years) ⬍12
38.7
20.7*
26.4
20.7*
12
39.7
31.6
38.9
31.6
ⱖ13
21.6
47.7
34.6
47.7
Non-Hispanic white
56.9
61.3*
41.2
61.3*
Non-Hispanic black
Maternal race/ethnicity
29.2
15.7
40.9
15.7
Hispanic
9.6
17.9
14.2
17.9
Other
4.3
5.1
3.7
5.1
Parity 0
29.7
40.5*
51.2
40.5*
1–2
32.8
32.6
23.9
32.6
ⱖ3
37.4
26.9
24.9
26.9
1st trimester
69.6
83.2*
78.7
83.2*
2nd trimester
22.2
13.0
11.0
13.0
8.2
3.7
10.4
3.7
6.6*
21.4
Entry into prenatal care
3rd trimester/no care Weight gain during pregnancy (lbs per week) ⬍0.30
11.2
0.30–1.1
64.0
72.2
50.2
72.2
⬎1.1
16.6
15.3
9.0
15.3
7.8
5.8
19.3
5.8
Unmarried
62.0
34.3*
54.6
34.3*
Married
38.0
36.7
45.4
64.7
Unknown
6.6*
Marital status
Note: Values are percentages. *p⬍0.001 SIDS, sudden infant death syndrome
July 2010
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50
Table 4. AOR (95% CI) and population-attributable fraction of pregnancy and infant outcomes attributable to prenatal smoking, U.S., 2002
Characteristic
>37 weeks’ <27 weeks’ 28–33 weeks’ 34–36 weeks’ gestation and gestationa gestationa gestationa <2500 ga
Prenatal smoking
1.5 (1.4, 1.6)
1.4 (1.4, 1.4)
1.2 (1.2, 1.3)
1–10
1.5 (1.4, 1.5)
1.4 (1.3, 1.4)
11–20
1.6 (1.5, 1.8)
ⱖ21 Unknown
SIDSb
Preterm-related deathsb
2.3 (2.3, 2.5)
2.7 (2.4, 3.0)
1.5 (1.4, 1.6)
1.2 (1.2, 1.2)
2.3 (2.3, 2.4)
2.7 (2.4, 3.0)
1.4 (1.3, 1.5)
1.6 (1.5, 1.6)
1.3 (1.3, 1.4)
3.1 (3.0, 3.2)
2.9 (2.4, 3.5)
1.6 (1.4, 1.9)
2.1 (1.7, 2.7)
1.9 (1.7, 2.1)
1.6 (1.5, 1.7)
4.0 (3.6, 4.3)
3.9 (2.5, 6.0)
1.9 (1.3, 2.7)
0.7 (0.5, 0.9)
0.7 (0.6, 0.8)
0.7 (0.7, 0.8)
0.6 (0.5, 0.6)
0.6 (0.4, 1.0)
0.8 (0.7, 0.8)
Prenatal smoking reported on birth certificate
5.3
4.6
2.6
13.1
23.2
5.0
Prenatal smoking 45% higher than reported on birth certificate
7.7
6.7
3.7
19.0
33.6
7.3
Daily average cigarettes smoked
Population-attributable fraction
Note: Adjusted for maternal age, education, race/ethnicity, marital status, parity, infant gender, weight gain during pregnancy (except SIDS) and entry in prenatal care, and gestational age (SIDS only) a Compared to infants ⱖ37 weeks gestation and ⱖ2500 g b Compared to all other infants born in 2002 SIDS, sudden infant death syndrome
Discussion Prenatal smoking continues to contribute to poor pregnancy and infant outcomes in the U.S. Among 2002 births, the present study estimated that 5%– 8% of very and moderately preterm births and 3%– 4% of late preterm births were attributed to prenatal smoking. Assuming the risk of preterm delivery for smokers could be decreased to that of nonsmokers, these preterm births would be prevented. Similarly, 13%–19% of term low birth weight deliveries potentially could have been prevented. Among infant deaths, 5%–7% of preterm-related deaths and 23%–34% of SIDS deaths potentially could have been avoided. The high PAF level among SIDS deaths is especially striking and suggests that tobacco control and SIDS prevention activities should be coordinated. Infants born preterm or term low birth weight may encounter challenging short- and long-term health problems, including neurologic, developmental, and neurosensory morbidities. In 2001, the hospitalization costs in the fırst year of life for all preterm low birth weight infant admissions in the U.S. totaled $5.8 billion.11 Even using a conservative PAF estimate of 4% for preterm delivery, preventing women from smoking during pregnancy could have substantial cost savings (approximately $232
million annually) in addition to overall improved health for mothers and their children. The estimated associations in the present study between prenatal smoking and SIDS and between prenatal smoking and early preterm births are consistent with those found in a previous study that used 1995–1996 data.2,3 The estimates are also consistent with previous studies conducted at different times and in different geographic locations.12,13 The consistency of these associations over time suggests that states interested in estimating the state-specifıc PAF of adverse birth outcomes due to prenatal smoking can use their state-specifıc prevalence of prenatal smoking and the AORs found in the present study. The current study makes two new contributions to the literature. As previously stated, it restricts infant deaths to those for which prenatal smoking has an established causal relationship. Second, it assesses the association of prenatal smoking with preterm-related deaths, a relatively new construct that is now used by NCHS to calculate national preterm-related death rates.8 The defınition of a preterm-related infant death is based on a paradigm that identifıes deaths among infants born preterm according to ICD-10 codes that reflect reasons for death that occur almost exclusively among preterm infants, or www.ajpm-online.net
Dietz et al / Am J Prev Med 2010;39(1):45–52
codes that characterize the cause of death according to the reason for the preterm birth.8 Preterm-related deaths account for at least one third of all infant deaths, and they are most likely to occur at the very earliest gestation.7 Some of these deaths could be prevented by eliminating smoking during pregnancy. The present study’s estimates of prenatal smoking and the PAFs of poor pregnancy and infant outcomes are subject to several limitations. Prenatal smoking data recorded on the birth certifıcate are presumed to be selfreported at delivery or taken from the medical record (when the woman reported smoking to her prenatal healthcare provider). Both of these scenarios are likely to lead to under-reporting. Conversely, birth certifıcates may capture a disproportionate percentage of heavier smokers because light smokers may be less likely to report smoking to their prenatal healthcare providers. This would lead to an overestimation of the strength of the association between prenatal smoking and adverse outcomes (given the dose response found in the current study). Uncontrolled confounding could have biased the fındings because smokers may differ from nonsmokers in factors that contribute to poor birth outcomes for factors not available in the data set. Two possible confounders not available on birth and death certifıcates are infant sleep position and exposure to secondhand smoke, both of which increase the risk of SIDS. However, at least one study found no association between sleep position and prenatal smoking behaviors.14 Finally, recent studies have questioned the accuracy and consistency of the reporting of SIDS as a cause-of-death determination on the death certifıcate. Without a thorough case investigation, it is diffıcult to distinguish a SIDS case from a suffocation case.15,16 However, any outcome misclassifıcation would, most likely, bias results toward the null. Other potential uncontrolled confounders include other substance abuse and psychiatric disorders that could negatively influence benefıcial health behaviors.17 Despite the inability to adjust for all potential confounders, the consistency of the results with multiple studies that were conducted over several decades in a variety of geographic locations and diverse populations and the clear dose–response relationship between cigarettes smoked and adverse outcomes support the validity of the results.12,13 Overall, the current study’s fındings are generalizable to births in the U.S., excluding California. According to the California Maternal and Infant Health Assessment, 9% of women in California smoked during pregnancy in 2002.18 This level of smoking is slightly lower than the average of all other states for 2002 (11.5%). Given that California births represented 13% of all births in 2002, the July 2010
51
U.S. smoking prevalence during pregnancy may be slightly lower at approximately 11.2% based on birth certifıcate estimates. The effect of adding California to the analysis on the PAF would be minimal. For example, the PAF for prenatal smoking attributable to SIDS would decrease from 23.2% to 22.6%. Ideally, this analysis would have been conducted with more-recent vital statistics data; however, use of different versions of the birth certifıcate in different states after 2002 prevented this. It does appear that prenatal smoking prevalence has decreased slightly since 2002. NCHS reported for 2005 births the prenatal smoking rate for states using the 1989 version of the birth certifıcate (10.7% smoked during pregnancy vs 11.7% in 2002 among these same states). If one assumes that the estimated 2002 U.S. prenatal smoking rate of 11.2% (including California) declined at a similar rate as these states (annual decrease of .014%), then the estimated U.S. 2009 prenatal smoking rate would be approximately 10.0%, and the PAFs would be slightly lower than what was estimated for 2002 in the present study at 4.4%– 6.3% for preterm-related deaths and 20.2%–29.3% for SIDS deaths. The current study found that prenatal smoking continues to contribute to a substantial proportion of avoidable cases of infant morbidity and mortality in the U.S. Prenatal smoking prevalence is decreasing; however, in some states prenatal smoking prevalence is as high as 36%, more than three times the national average.19 In addition, pregnant women with Medicaid report a higher smoking prevalence (24%) compared to women with private insurance (7%).20 Smoking prevalence can be reduced through sustained and comprehensive tobacco control activities, such as promoting policies that establish smokefree environments in public places and the workplace, increasing tobacco excise taxes, banning all forms of tobacco advertisement, and ensuring adequate healthcare insurance for cessation services.21 On the clinical level, prenatal care providers can assess smoking status, offer smoking cessation interventions, or refer patients who smoke to effective cessation services.22 As of 2007, a total of 43 state Medicaid programs covered some form of tobacco-dependence treatment, yet only two states had no restrictions on this coverage such as copayments, limits on number of treatment courses, and coverage of types of treatments.23 The Public Health Service’s Clinical Practice Guidelines recommend comprehensive insurance coverage of tobacco-dependence treatments without barriers to care. Maternal and child healthcare providers need to work in concert with state tobacco control professionals to improve access to comprehensive insurance coverage and to strengthen state
52
Dietz et al / Am J Prev Med 2010;39(1):45–52
tobacco control policies to reduce prenatal smoking rates and prevent the harm smoking causes to both mother and child. The fındings and conclusions in this article are those of the authors and do not necessarily represent the offıcial position of the CDC. No fınancial disclosures were reported by the authors of this paper.
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