4.11 Secondhand smoke and pregnancy

Compared to active smoking during pregnancy, few health effects of secondhand smoke exposure during pregnancy have been proven as causal. However, investigations continue into various health effects, particularly those that already have an established association with active smoking during pregnancy. Differentiating between the impacts of maternal secondhand smoke exposure, potential damage to sperm from paternal active smoking, and the influence of past maternal active smoking, when determining the cause of disease, can sometimes be difficult, particularly for rarer conditions such as birth defects or childhood cancers.

Biomarkers to determine exposure of neonates before birth to tobacco smoke can be measured in cord blood, or neonatal urine, hair, nails, amniotic fluid and meconium (the first faecal matter passed by the baby after birth). These samples are usually collected at or soon after birth. The metabolites of nicotine, in particular cotinine, are the biomarkers most commonly measured. Measuring biomarkers in cord blood and meconium are considered more adequate ways of distinguishing between foetuses whose mothers were exposed and not exposed to secondhand smoke. Biomarkers in cord blood indicate exposure to tobacco smoke in the few days before delivery, whereas biomarkers in meconium accumulate over several months of gestation.1


Some evidence suggests that exposure to secondhand smoke may be associated with reduced fertility or fecundity (rate of conception) in women, however these effects may be difficult to separate from the effects of active smoking on the partner's fertility.24 More research is required before these outcomes may be stated with certainty.3 In women undergoing IVF treatment, exposure to secondhand smoke may lead to a reduced chance of successful implantation,5 although this finding should also be considered preliminary.

4.11.2Low birthweight and preterm delivery

Exposure to secondhand smoke during pregnancy causes a small reduction in birthweight.6 Estimates of the mean decrease in weight calculated by various reviews range from around 30 g to 60 g, and birthweight decrements can range up to about 100 g.2,6,3,7 Further, one study examining women exposed to secondhand smoke who carried either one of two specific genotypes related to metabolising enzymes found that they delivered babies with mean birthweight decrements of around 160 g and 200 g.3 Therefore, there appears to be a sub-group of foetuses who are more susceptible to the effects of maternal secondhand smoke exposure.2

Mechanisms for lower birthweight in babies of non-smoking mothers exposed to secondhand smoke are likely to be similar to those that cause lower birthweight in infants of active smokers. Factors contributing to low birthweight may be preterm delivery, intrauterine growth retardation, or a combination of the two.6 Major reviews differ in their conclusions on the relationship of secondhand smoke exposure and preterm delivery. The California Environmental Protection Agency report (2005) concluded that secondhand smoke is a cause of preterm delivery, and may cause intrauterine growth retardation.2 The US Surgeon General's report (2006) concluded that the evidence for preterm delivery is mixed but 'suggestive' of causality.6 It also cited research suggesting that lower birthweight may be the result of reduced oxygen to the foetus.6 A meta-analysis (2010) found that duration of gestation and rates of preterm delivery among secondhand-smoke-exposed women were similar to unexposed women, although the exposed women's babies were lighter.7 Some studies have found that secondhand smoke exposure of the pregnant mother increases the risk for foetal growth restriction.8,9

4.11.3Lung development in the unborn child

There is clear evidence that smoking by a pregnant mother impairs foetal lung development.3,6,10 Animal studies suggest that maternal exposure to secondhand smoke also causes changes in foetal lung structure,6,10 including direct effects on the development of the alveoli in the lungs of the unborn child.11 One study on pregnant sheep indicated that maternal exposure to secondhand smoke may decrease blood flow and increase vascular resistance in the foetal lungs. It also appears to reduce the normal dilation of blood vessels in the foetal lungs in response to increased oxygen. These effects are associated with a marked decrease in oxygen within the foetus, and could potentially affect lung circulation at birth.12

4.11.4Spontaneous abortion (miscarriage) and stillbirth

Findings on an association between maternal exposure to secondhand smoke and an increased rate of spontaneous abortion are mixed, and further research is needed.2,6,3,13 A meta-analysis based on four studies showed that maternal secondhand smoke exposure was associated with an increased risk of stillbirth.13

4.11.5Birth defects

A meta-analysis (2011) showed that maternal secondhand smoke exposure was associated with an increased risk of birth defects, although it did not have the power to determine specific congenital abnormalities.13 A few studies support an increased risk of oral clefts with paternal smoking, although it is not clear whether this is due to exposure of the mother to secondhand smoke or if it is due to the effects of tobacco smoke on sperm.3

4.11.6Cardiovascular effects

An autopsy study indicated that the foetuses of women exposed to secondhand smoke were more likely to have lesions in the walls of the foetal artery and adjoining vessels, which are the initial stages of atherosclerosis (narrowing of the arteries by fatty deposits).14

For more information on the effects of active maternal smoking and pregnancy, see Chapter 3.7. The link between parental smoking and development of childhood cancers is discussed in Chapter 4.9.9.

Recent news and research

For recent news items and research on this topic, click here (Last updated January 2017 


1. Llaquet H, Pichini S, Joya X, Papaseit E, Vall O, Klein J, et al. Biological matrices for the evaluation of exposure to environmental tobacco smoke during prenatal life and childhood. Analytical and Bioanalytical Chemistry 2009;396(1):379–99. Available from: http://www.springerlink.com/content/4960m70q40652246/fulltext.html

2. Office of Environmental Health Hazard Assessment and California Air Resources Board. Health effects of exposure to environmental tobacco smoke: final report, approved at the Panel's June 24, 2005 meeting. Sacramento: California Environmental Protection Agency, 2005. Available from: http://www.oehha.ca.gov/air/environmental_tobacco/2005etsfinal.html

3. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html

4. Peppone LJ, Piazza KM, Mahoney MC, Morrow GR, Mustian KM, Palesh OG, et al. Associations between adult and childhood secondhand smoke exposures and fecundity and fetal loss among women who visited a cancer hospital. Tobacco Control 2009;18(2):115-20. Available from: http://tobaccocontrol.bmj.com/cgi/content/abstract/18/2/115

5. Neal M, Hughes E, Holloway A and Foster W. Sidestream smoking is equally as damaging as mainstream smoking on IVF outcomes.2005. Human Reproduction 2005;20(9):2531-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15919779

6. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm

7. Salmasi G, Grady R, Jones J and McDonald S. Environmental tobacco smoke exposure and perinatal outcomes: a systematic review and meta-analyses. Acta Obstetricia et Gynecologica Scandinavica 2010;89(4):423-41. Available from: http://informahealthcare.com/doi/full/10.3109/00016340903505748

8. Reeves S and Bernstein I. Effects of maternal tobacco-smoke exposure on fetal growth and neonatal size. Expert Reviews in Obstetrics and Gynecology 2008;3(6):719-30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19881889

9. Varvarigou A, Fouzas S and Beratis N. Effect of prenatal tobacco smoke exposure on fetal growth potential. Journal of Perinatal Medicine 2010;38(6):683–7. Available from: http://www.reference-global.com/doi/pdf/10.1515/JPM.2010.101

10. Joad JP. Smoking and pediatric respiratory health. Clinics in Chest Medicine 2000;21(1):37-46, vii-viii. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10763088

11. Zhong C-Y, Zhou Y, Joad J and Pinkerton K. Environmental tobacco smoke suppresses nuclear factor-{kappa}B signaling to increase apoptosis in infant monkey lungs. American Journal of Critical Care Medicine 2006;174(4):428-36. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16709937

12. Houfflin-Debarge V, Sabbah-Briffaut E, Aubry E, Deruelle P, Alexandre C and Storme L. Effects of environmental tobacco smoke on the pulmonary circulation in the ovine fetus. American Journal of Obstetrics and Gynecology 2011;204(5):450 e8-14. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21333966

13. Leonardi-Bee J, Britton J and Venn A. Secondhand smoke and adverse fetal outcomes in nonsmoking pregnant women: a meta-analysis. Pediatrics 2011;127(4):734-41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21382949

14. Mecchia D, Lavezzi AM, Mauri M and Matturri L. Feto-placental atherosclerotic lesions in intrauterine fetal demise: role of parental cigarette smoking. Open Cardiovascular Medicine Journal 2009;June 11(3):51–6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19572018

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