Journal of Public Health Advance Access published June 14, 2015 Journal of Public Health | pp. 1–6 | doi:10.1093/pubmed/fdv083

Prenatal exposure to secondhand smoke may increase the risk of postpartum depressive symptoms Shama Khan, Ahmed A. Arif, James N. Laditka, Elizabeth F. Racine Department of Public Health Sciences, University of North Carolina at Charlotte, Charlotte, NC 28223, USA Address correspondence to Ahmed A. Arif, E-mail: [email protected]

A B S T R AC T

but there is little research on the association of secondhand smoke (SHS) exposure during pregnancy with PPDS. This study aimed to explore the relationship between prenatal exposure to SHS during pregnancy and PPDS. Methods The authors analyzed data from 6884 women who participated in the North Carolina Pregnancy Risk Assessment and Monitoring System survey (2004– 08). Data on the exposure ( prenatal SHS), outcome (PPDS) and covariates were obtained from self-reported questionnaires. Univariable and multivariable logistic regression was used for data analysis. Results The prevalence of PPDS was 16.5%. In the unadjusted analysis, women exposed to SHS during pregnancy had nearly twice the odds of PPDS than the unexposed (odds ratio, OR ¼ 1.90, 95% confidence interval, CI: 1.61–2.26). After adjusting for potential confounders, the association between SHS and PPDS was weakened but remained statistically significant (OR ¼ 1.49, 95% CI: 1.23– 1.80). A dose– response relationship was not evident in the analyses. Maternal smoking during pregnancy did not appear to modify the association between SHS and PPDS. Conclusions The current study identified a positive association between SHS and PPDS. Keywords NCPRAMS, postpartum depression, postpartum depression symptoms, secondhand smoke

Postpartum depression (PPD), also known as postnatal depression, is a serious mood disorder that can affect new mothers soon after delivery and up to 1 year post-delivery.1 It is a serious mental health problem that disrupts a woman’s life and can have a negative effect on the mother– child relationship, child development and the mother’s relationship with the partner/spouse.2 As of 2005, PPD affects 10 –15% of all childbearing women in the USA, although the actual number is estimated to be much higher.3 Based on the 2004 – 05 PPD prevalence data involving 17 states, North Carolina (NC) had the second highest rate of PPD at 19%, after New Mexico (20.4%).4 Secondhand smoke (SHS) contains almost all of the components of inhaled cigarette smoke including tar, nicotine, carbon monoxide and carbon dioxide.5 In the USA, SHS exposure is the third leading preventable cause of disability and early death. Over 65% of non-smokers in the US population, both children and adults, are regularly exposed to SHS.5 Most

exposure to SHS occurs in homes, workplaces, private vehicles and public places such as restaurants, bars and casinos.5 The prevalence of exposure to in-home SHS among NC adults is 9.5% (95% confidence interval, CI: 7.2 – 12.3).6 State-specific aggregate reports for 2008 indicated that 7.8% of North Carolina residents were exposed to SHS in their homes and 11.4% in their indoor workplaces.7 A number of studies have linked cigarette use in active smokers to chronic depression, but their findings were not specific to pregnant women.8 – 10 A few researchers have studied the relationship between SHS and risk of depression during pregnancy.11,12 However, to our knowledge, there are

Shama Khan, Graduate Student Ahmed A. Arif, Associate Professor of Public Health Sciences James N. Laditka, Associate Professor of Public Health Sciences Elizabeth F. Racine, Associate Professor of Public Health Sciences

# The Author 2015. Published by Oxford University Press on behalf of Faculty of Public Health. All rights reserved. For permissions, please e-mail: [email protected].

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Background The harmful effects of smoking during pregnancy on occurrence of postpartum depressive symptoms (PPDS) have been well studied,

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no studies that have examined the association between SHS and PPD. This study used data from the 2004 – 08 North Carolina Pregnancy Risk Assessment Monitoring System (NC PRAMS) to examine the association between SHS and PPD.

Methods

Measurement of exposure variable

The main exposure variable in this study was prenatal SHS exposure. Exposure status of the participants was determined based on their response to the question: ‘How many cigarette smokers, not including yourself, lived in your home during your most recent pregnancy?’ Women who replied ‘none’ or ‘zero’ to this question were considered as ‘unexposed’ and

Measurement of outcome variable

The outcome variable for this study was PPDS. The NC PRAMS asks two questions about mental health status and mood changes that the mother may have experienced since the birth of the baby. Two questions measured PPDS: (i) ‘Since your new baby was born, how often have you felt down, depressed, or hopeless?’ and (ii) ‘Since your new baby was born, how often have you had little interest or little pleasure in doing things?’ Responses for both questions included: always, often, sometimes, rarely and never. Women who answered ‘always’ or ‘often’ for either or both of these questions were categorized as positive for PPDS. Women who responded ‘sometimes’, ‘rarely’ or ‘never’ for both of these questions were categorized as negative for PPDS. The PRAMS survey did not include a physician diagnosis or standardized scale to evaluate PPD. However, this two-item questionnaire is reported to have a high degree of validity (sensitivity ¼ 96%, specificity ¼ 57%) and has been recommended as a case-finding instrument for depression in primary care settings.15 These two questions have been used to measure PPD in several studies.4,16 – 18 Measurement of covariates

Potential confounders for which this study controlled included maternal age, race/ethnicity, education level, marital status, income, participation in the Supplemental Nutrition Program for Women, Infants, and Children program (WIC), insurance coverage by Medicaid, alcohol consumption, smoking after pregnancy, pre-pregnancy body mass index (BMI), physical activity (PA) before and during pregnancy, maternal gestational weight gain, pre-existing diabetes, gestational diabetes, pregnancy-induced hypertension and timing of entry into prenatal care (PNC). Maternal smoking during pregnancy (coded as 1 ¼ yes and 0 ¼ no) was evaluated for effect modification using stratified analysis. Statistical analysis

Descriptive statistics were used to examine the sample characteristics and to estimate the prevalence of SHS and PPDS.

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The Pregnancy Risk Assessment and Monitoring System (PRAMS) is a state-specific, population-based surveillance effort of the Centers for Disease Control and Prevention (CDC) and state health departments. Its goal is to improve the health of mothers and infants by decreasing adverse pregnancy and birth outcomes.13 Currently, 40 states and New York City participate in the PRAMS, representing approximately three-quarters of all US births. The PRAMS questionnaire is self-administered. It includes a set of core questions to assess maternal attitudes and experiences before, during and shortly after pregnancy.13 Originating in 1997, the NC PRAMS is a joint initiative between the North Carolina State Center for Health Statistics (NCCHS) and the CDC.14 In North Carolina, 2400 new mothers are surveyed annually. Every month, 200 women who have recently given birth in the last 2 – 6 months are randomly selected from birth certificate files and are invited to participate in the study. To increase participation in the mailed survey, potential participants are contacted for a maximum of six times with a 7 –14 days gap between each contact period. Hence, the questionnaire is generally mailed within 2 –8 weeks from the time the women are selected to participate in the study. Potential participants are offered several incentives including coupons for certified birth certificates, participation in a raffle for a cash award, postage stamps, bibs, cash (a dollar bill) and magnetic picture frames.14 For this study, data were analyzed from the 2004 – 08 NC PRAMS survey. The total number of participants in this dataset was 10 585. Response rates for the years 2004, 2005, 2006, 2007 and 2008 were 71, 70, 59, 71 and 72%, respectively.14 Women who did not respond to the question that is represented in the outcome variable (PPD) were excluded from the analysis (n ¼ 3701). Therefore, a total of 6884 women were included in the final analysis.

women who replied ‘one’ or ‘two or more smokers’ were considered as ‘exposed’ to SHS during pregnancy. To examine a dose– response relationship between SHS exposure and postpartum depressive symptoms (PPDS), participants were categorized into three groups: women who were not exposed to SHS during pregnancy (coded as 0), women who were exposed to SHS generated by one cigarette smoker (coded as 1) and women who were exposed to SHS generated by two or more cigarette smokers (coded as 2).

SE CO ND HAN D SM OKE A N D PO STPA RTUM D EPRES SION

Table 1 Characteristics of the study sample participating in the North Carolina Pregnancy Risk Assessment Monitoring System, 2004 –08 Number (n)

Percentage (%)a

White

4886

73.3

Black

1697

22.25

Other

321

4.45

Characteristic Maternal race/ethnicity

Income ,$14 999

1920

28.63

$15 000– $24 999

1004

14.61

$25 000– $49 999

1319

19.39

.$50 000

2128

29.31

No

5953

86.52

Yes

912

13.23

Medicaid recipient

Physical activity during pregnancy ,1 day/week

3959

53.4

1– 4 days/week

2357

37.36

5 days/week

459

7.57

No

5530

85.91

Yes

1280

12.85

Pregnancy-induced hypertension

Results Table 1 provides a summary of descriptive statistics of the study population. The majority of the participants identified themselves as Whites (73.3%), followed by Blacks (22.3%). Other races including Hispanics, Asians and Native Americans constituted 4% of the total participants. Approximately 29% of participants reported an annual household income of ,$15 000 and an equal proportion reported an annual income of .$50 000. Thirteen percent of participants were Medicaid beneficiaries. About half of the participants reported exercising ,1 day/week during pregnancy. Moreover, almost 13% had pregnancy-induced hypertension. More than 80% received PNC services in their first trimester; ,1% had no PNC. Approximately 28% of the women were exposed to SHS during pregnancy. Finally, 16.5% of the participants experienced postpartum depressive symptoms. In the unadjusted analysis, reported in Table 2, women exposed to SHS during pregnancy had significantly higher odds of PPDS than the unexposed (odds ratio, OR ¼ 1.90, 95% CI: 1.61 –2.26). After adjusting for maternal race, income, Medicaid recipient status, physical activity during pregnancy, pregnancy-induced hypertension and timing of entry into PNC, the association between SHS and PPDS was weakened but remained statistically significant (adjusted OR ¼ 1.49, 95% CI: 1.23 – 1.80). A dose –response relationship was not apparent, because even though women exposed to SHS generated by two or more cigarette smokers had higher unadjusted odds of PPDS (OR ¼ 2.10, 95% CI: 1.60 – 2.73) than women exposed to SHS generated by one

Entry into prenatal care First trimester

5758

82.31

Second trimester

896

14.44

Third trimester

100

1.7

67

0.65

No

5645

83.48

Yes

1239

16.52

No

4754

69.94

Yes

1989

27.76

No prenatal care received Postpartum depressive symptoms

Exposure to secondhand smoke

a

Weighted percents.

cigarette smoker (OR ¼ 1.83, 95% CI: 1.51 – 2.22), the confidence intervals for these estimates overlapped. When adjusted for potential confounders, the odds ratio weakened, but the overall trend remained the same (Table 2). Table 3 presents the association between PPDS and SHS stratified by maternal smoking status during pregnancy and adjusted for potential confounding effects of maternal race, income, Medicaid recipient status, physical activity during pregnancy, pregnancy-induced hypertension and timing of entry into PNC. Maternal smoking during pregnancy did not modify the association between SHS and PPDS. Among women who did not smoke while pregnant (n ¼ 5770), those exposed to SHS had 30% higher odds of PPDS than the unexposed (95% CI: 1.03–1.64). Among those who smoked during pregnancy

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Unadjusted and adjusted odds ratios and 95% confidence intervals were calculated using univariable and multivariable logistic regression analyses. To select potential confounders, the approach of Hosmer and Lemeshaw was used.19 Initially, variables significant at P , 0.2 level in the univariable analysis were selected for inclusion in the multivariable logistic model. Next, the variables that were not significant at P , 0.05 were excluded one by one from the multivariable logistic model using the Wald test, where the variable with the highest P-value was the first to be dropped. All statistically significant variables (P , 0.05) were retained in the final logistic model. These included maternal race/ethnicity, income, receipt of Medicaid, PA during pregnancy, pregnancy-induced hypertension and entry into PNC. Stratified analysis was conducted to evaluate effect modification by maternal smoking during pregnancy. To account for the complex survey design and to incorporate sample weights, all analyses were performed using STATA statistical software, release 12, survey feature (STATA Corporation, College Station, TX, USA).

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Table 2 Adjusted OR and 95% CI of the associations between SHS and

Table 3 Association of secondhand smoke and postpartum depressive

PPDS

symptoms, as modified by maternal smoking during pregnancy Unadjusted OR (95% CI) Adjusted ORa (95% CI)

Maternal smoking

Maternal smoking

during pregnancy

during pregnancy

(No) (n ¼ 5770)

(Yes) (n ¼ 1042)

Postpartum

Postpartum

depressive

depressive

symptoms

symptoms

ORa

95% CI

ORa

95% CI

No

1.00

Reference

1.00

Reference

Yes

1.30

1.03 –1.64

1.49

0.91 – 2.47

No smoker

1.00

Reference

1.00

Reference

1 smoker

1.32

1.03 –1.71

1.58

0.93 – 2.70

2 or more smokers

1.21

0.78 –1.88

1.36

0.77 – 2.41

Secondhand smoke No

Referent

Referent

Yes

1.90 (1.61 – 2.26)

1.49 (1.23 – 1.80)

No. of smokers at home No smoker

Referent

Referent

1 smoker

1.83 (1.51 – 2.22)

1.50 (1.22 – 1.85)

2 or more smokers 2.10 (1.60 – 2.73)

1.46 (1.08 – 1.96)

a

The odds ratio was adjusted for maternal race, income, Medicaid

Secondhand smoke

hypertension and timing of entry into prenatal care.

(n ¼ 1042), no significant association between SHS and PPDS was observed (adjusted OR ¼ 1.49, 95% CI ¼ 0.91–2.27). Similarly, the association between SHS and PPDS was not modified by the number of smokers in the home (Table 3).

No. of smokers at home

a

The odds ratio was adjusted for maternal race, income, Medicaid

recipient status, physical activity during pregnancy, pregnancy-induced hypertension and timing of entry into prenatal care.

Discussion Main findings of the study

In this study, prenatal SHS exposure was associated with almost twice the odds of PPDS. When the analysis was adjusted for confounding, the exposure –outcome relationship was weakened but remained statistically significant. A dose– response pattern was not evident in this study. Maternal smoking during pregnancy did not appear to modify the association between SHS and PPDS. What is already known on this topic

To the best of our knowledge, this study was the first to examine the association between SHS and depressive symptoms in the postpartum period. It was also the first study to analyze a dose– response relationship between SHS and PPDS. Although, not directly comparable, the results were consistent with previous studies of SHS and depressive symptoms in pregnant women.11,12 The current study found a modestly weaker association between SHS and depressive symptoms than the study by Tan et al. 12 The study by Tan and colleagues12 focused on minority pregnant women, whereas the current study examined a large, racially diverse group of women. Depression rates in the USA are greater for Hispanics and Blacks than Whites (6.3 versus 4.8%).20 Mbah et al. 11 reported higher mean Edinburg Perinatal Depression Scale scores for non-smokers exposed to SHS during pregnancy compared with those with no SHS exposure,

with an observed dose– response. Mbah et al. 11 used an objective, biological test (salivary cotinine) to measure SHS and smoking status, whereas the current study relied on selfreports. Although self-reported measures of SHS have a high degree of sensitivity (75%) and specificity (.85%) in comparison to clinical tests,21 the current study measured only residential SHS exposure and not exposure at work or other public places. The exact underlying biological mechanisms for the increased risk of perinatal depressive symptoms observed among pregnant women exposed to SHS remain unclear. However, non-smokers exposed to SHS have been shown to experience similar neurotransmitter pathways linked to depression as smokers.22 According to Wilkins and colleagues,23 nicotine exposure from cigarette smoke can raise circulating levels of corticotrophin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH). Increased levels of CRH and ACTH result in prolonged over activity of the hypothalamic-pituitary-adrenocortical axis and subsequent enlargement of the adrenals.24 This can lead to excess production of cortisol hormone which is responsible for altering mood, behavior and cognition.24 Similar to smokers, prolonged cigarette smoke exposure among passive smokers can also increase nicotine levels in the blood.25 This can lead to a decrease in dopamine levels and a subsequent decrease in gamma-amino butyric acid levels, which have been related to an increased risk for depression.25

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recipient status, physical activity during pregnancy, pregnancy-induced

SE CO ND HAN D SM OKE A N D PO STPA RTUM D EPRES SION

What this study adds

PPD is a public health concern, because it not only affects the mother, but the child and the spouse/partner as well. SHS has been linked to complications such as infertility, preterm delivery, stillbirth, low birth weight, sudden infant death syndrome and chronic respiratory disorders.26 Currently, there are no PNC guidelines in North Carolina that advise against SHS exposure. This study lends support for the role healthcare professionals can play encouraging women to avoid exposure to SHS during their preconception and prenatal period, which may minimize their risk of depression and other pregnancy-related complications.

There are several limitations in this study. There may have been selection bias in this study due to a relatively low response rate, ranging from 59 to 72%. Women who did not participate in the survey may have been different from those who responded, so any bias may have overestimated or underestimated the true association. To limit such bias, PRAMS uses weighted samples or adjustment factors for non-responders. The response rate was higher than that of other national datasets such as the Behavior Risk Factor Surveillance System (53.0% in 2011, 49.1% in 2012).27 There may have been a possibility of recall bias due to the self-report nature of the NC PRAMS questionnaire. Participants were contacted 2 –6 months after delivery and were asked to recall exposures during their pregnancy. Recall bias may also have occurred if women with PPDS were more likely to recall past exposures than women without PPDS. Use of self-reported SHS instead of an objective biological measure may have resulted in differential misclassification and an underestimation of the true association as some women may have given socially desirable answers. It is difficult to ascertain the risk of social desirability bias. The PRAMS question on SHS only measured exposure at home, not at work or other public places. This could have again underestimated the true association if some women who were not exposed at home, but were exposed at work or other public places. Since there is no reason to believe that such exposure misclassification affected women with PPDS differently than women without PPDS, any misclassification was most likely nondifferential. Another limitation in this study is that the definition of PPDS was based on the participants’ responses to two questions about ‘feeling depressed’ and ‘lack of interest’, instead of a physician diagnosis or a standardized scale like the Edinburgh Postnatal Depression Scale (EPDS). Although this two-item questionnaire has been used to measure postpartum depressive symptoms in several studies,16 – 18 it

provided no information on duration or intensity of depressive symptoms. Additionally, the use of self-reported PPDS may have been subject to misclassification if participants’ responses were affected by social desirability bias, as some women may not be willing to disclose depressive symptoms due to cultural and societal stigma surrounding depression. Previous studies used the EPDS to measure depressive symptoms.11 The EPDS asks about depressive symptoms within the last 7 days, whereas the current study asked about depressive symptoms since the new baby was born. Thus, results of the current study may be more representative of cumulative depressive symptoms in the postpartum period. In spite of the limitations, this study did have several strengths. This study had a large sample size (n ¼ 6884) which included a large, racially diverse group of women from varying socioeconomic and educational backgrounds. Therefore, the findings of the study are generalizable to all women in North Carolina, where both cigarette smoking and PPD prevalence rates are higher than the national average. Future studies should include objective measures of SHS such as salivary/blood/plasma cotinine test to avoid misclassification bias. In addition, information on frequency, duration and intensity of SHS as well as information on workplace exposures should be collected to further understand the relationship between SHS and PPD. Additional research should also identify the role of covariates such as a prior history of depression, pre-existing hypertension, birth anomalies, protective factors such as social support and social involvement in the exposure – outcome relationship. In conclusion, the current study found a positive association between prenatal exposure to SHS and the presence of postpartum depressive symptoms.

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Limitations

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7 Centers for Disease Control and Prevention. State-specific secondhand smoke exposure and current cigarette smoking among adults United States, 2008. MMWR Morb Mortal Wkly Rep 2009;58: 1232 – 5. 8 Dierker LC, Avenevoli S, Stolar M et al. Smoking and depression: an examination of mechanisms of comorbidity. Am J Psychiatry 2002;159:947– 53.

Women in Hawaii: Pregnancy Risk Assessment Monitoring System (PRAMS), 2004 – 2007. Matern Child Health J 2010;14:765 – 73. 18 Lacoursiere DY, Baksh L, Bloebaum L et al. Maternal body mass index and self-reported postpartum depressive symptoms. Matern Child Health J 2006;10:385 – 90. 19 Hosmer DW, Lemeshow S. Applied Logistic Regression. New York: John Wiley & Sons, 2000.

9 Kendler KS, Neale MC, MacLean CJ et al. Smoking and major depression. A causal analysis. Arch Gen Psychiatry 1993;50:36– 43.

20 Pratt LA, Brody DJ. Depression in the United States household population, 2005 – 2006. NCHS Data Brief 2008;7:1 – 8.

10 Paperwalla KN, Levin TT, Weiner J et al. Smoking and depression. Med Clin North Am 2004;88:1483 – 94, x – xi.

21 Prochaska JJ, Grossman W, Young-Wolff KC et al. Validity of selfreported adult secondhand smoke exposure. Tob Control 2015;24: 48 –53.

11 Mbah AK, Salihu HM, Dagne G et al. Exposure to environmental tobacco smoke and risk of antenatal depression: application of latent variable modeling. Arch Womens Ment Health 2013;16:293 –302.

23 Wilkins JN, Carlson HE, Van Vunakis H et al. Nicotine from cigarette smoking increases circulating levels of cortisol, growth hormone, and prolactin in male chronic smokers. Psychopharmacology 1982;78:305– 8.

13 Centers for Disease Control and Prevention. Pregnancy Risk Assessment and Monitoring System. 2013. http://www.cdc.gov/ prams/ (9 September 2013, date last accessed).

24 Stokes PE. The potential role of excessive cortisol induced by HPA hyperfunction in the pathogenesis of depression. Eur Neuropsychopharmacol 1995;5 Suppl:77– 82.

14 North Carolina Department of Health and Human Services. North Carolina State Center for Health Statistics. 2013. http://www.schs. state.nc.us/units/stat/prams/ (9 September 2013, date last accessed).

25 Bandiera FC, Arheart KL, Caban-Martinez AJ et al. Secondhand smoke exposure and depressive symptoms. Psychosom Med 2010;72: 68 –72.

15 Whooley MA, Avins AL, Miranda J et al. Case-finding instruments for depression. Two questions are as good as many. J Gen Intern Med 1997;12:439– 45.

26 Leonardi-Bee J, Britton J, Venn A. Secondhand smoke and adverse fetal outcomes in nonsmoking pregnant women: a meta-analysis. Pediatrics 2011;127:734 –41.

16 Ersek JL, Brunner Huber LR. Physical activity prior to and during pregnancy and risk of postpartum depressive symptoms. J Obstet Gynecol Neonatal Nurs 2009;38:556 – 66.

27 Centers for Disease Control and Prevention. Behavioral Risk Factor and Surveillance System: Summary Data and Quality Report. 2012. http://www.cdc.gov/brfss/annual_data/2012/pdf/Summary DataQualityReport2012_20130712.pdf (28 October 2013, date last accessed).

17 Hayes DK, Ta VM, Hurwitz EL et al. Disparities in self-reported postpartum depression among Asian, Hawaiian, and Pacific Islander

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12 Tan S, Courtney LP, El-Mohandes AA et al. Relationships between self-reported smoking, household environmental tobacco smoke exposure and depressive symptoms in a pregnant minority population. Matern Child Health J 2011;15(Suppl. 1):S65 – 74.

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Prenatal exposure to secondhand smoke may increase the risk of postpartum depressive symptoms.

The harmful effects of smoking during pregnancy on occurrence of postpartum depressive symptoms (PPDS) have been well studied, but there is little res...
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