0
Article |

Breast-feeding and Environmental Tobacco Smoke Exposure FREE

Allan B. Becker, MD; Jure Manfreda, MD; Alexander C. Ferguson, MD; Helen Dimich-Ward, PhD; Wade T. A. Watson, MD; Moira Chan-Yeung, MD
[+] Author Affiliations

From the Section of Allergy and Clinical Immunology, Department of Pediatrics and Child Health (Drs Becker and Watson), and the Section of Respirology, Department of Medicine (Dr Manfreda), University of Manitoba, Winnipeg; the Division of Allergy and Clinical Immunology, Department of Pediatrics (Dr Ferguson), and the Division of Respirology, Department of Medicine (Drs Dimich-Ward and Chan-Yeung), University of British Columbia, Vancouver; and Inspiraplex: The Respiratory Health Network of Centres of Excellence (Drs Becker, Manfreda, and Chan-Yeung).


Arch Pediatr Adolesc Med. 1999;153(7):689-691. doi:10.1001/archpedi.153.7.689.
Text Size: A A A
Published online

Background  Exposure to environmental tobacco smoke is associated with adverse effects in infants and children.

Objective  To explore whether an increase in urinary cotinine fumarate level is caused by ingested nicotine and cotinine in breast-feeding infants.

Methods  We studied newborns at risk for developing asthma and allergies based on a strong family history. We measured urinary cotinine levels in the infants as a measure of environmental tobacco smoke exposure and cotinine levels in the breast milk of breast-feeding mothers.

Results  Of 507 infants, urinary cotinine levels during the first 2 weeks of life were significantly increased in infants whose mothers smoked. Breast-fed infants had higher cotinine levels than non–breast-fed infants, but this was statistically significant (P<.05) only if mothers smoked. Urinary cotinine levels were 5 times higher in breast-fed infants whose mothers smoked than in those whose mothers smoked but did not breast-feed.

Conclusions  Mothers should be encouraged to not smoke, and parents must be advised of the potential respiratory and systemic risks of environmental tobacco smoke exposure to their child, including the potential for future addiction to smoking.

EXPOSURE to environmental tobacco smoke (ETS) has been associated with multiple adverse health effects in infants and children. Maternal smoking during pregnancy is associated with premature delivery; intrauterine growth retardation; decreased birth weight, head circumference, and length; perinatal complications, including sudden infant death syndrome; and problems of neurodevelopmental impairment, attention-deficit/hyperactivity disorder, inflammatory bowel disease, and strabismus.111 Postnatal ETS exposure is associated with the increased occurrence of respiratory illnesses in infants.1217 Maternal smoking in the postnatal period has greater impact than paternal smoking on respiratory illnesses in infants.1214

We initiated a study of asthma prevention in newborns with a high risk for developing asthma and allergies, based on a strong immediate family history. As a component of this study, we measured their urinary cotinine fumarate levels as an indication of ETS exposure. We found that, in infants of mothers who smoked, urinary cotinine levels of breast-fed infants were much higher than of those not breast-fed. Therefore, we explored whether this increase was caused by ingested nicotine and cotinine in breast-feeding infants.

Urine samples were collected from 507 infants enrolled in an asthma and allergy prevention study during the first 2 weeks of life. After it became apparent that urine cotinine levels were markedly increased among breast-feeding infants whose mothers smoked, we obtained breast milk samples from 30 mothers who continued to breast-feed at the time of their next scheduled study visit (4 months after delivery). Five of these mothers also continued smoking. Among the 25 nonsmoking, breast-feeding mothers, 20 had no ETS exposure and 5 had some ETS exposure. Exposure to ETS was defined as the presence of a spouse or other individual who smoked in the home. Breast milk and urine samples were frozen at −20°C until they were assayed.

COTININE ASSAY

The samples of urine and breast milk were assayed for cotinine using a double antibody radioimmunoassay.18 Briefly, 0.1 mL of urine or 0.1 mL of cotinine standard (20-2000 pg) was added to a test tube followed by 0.1 mL of tritiated cotinine. Anticotinine antiserum, 0.1 mL, was added to each tube and mixed. The tubes were incubated at 37°C for 60 minutes. After incubation, 0.1 mL of diluted normal rabbit serum was added to each tube, followed by 0.1 mL of goat antirabbit gamma globulin. The tubes were centrifuged at 1000g for 45 minutes. The supernatant was removed, and the pellet was dissolved in 0.1 mL of 0.1-mol/L sodium hydroxide. Ecolume, 2.5 mL, was added, and the radioactivity was counted in a beta-counter. A standard curve was constructed, and the concentration of cotinine in the samples was read from the standard curve. Cotinine level was measured in the urine, and the results were expressed in nanograms per milligram of creatinine.

STATISTICAL ANALYSIS

A logarithmic transformation was applied to cotinine data because its distribution was not normal. Means of transformed data were compared with analysis of variance and t tests. Means and 95% confidence intervals were calculated using transformed data. Antilog values of transformed means (geometric means) and 95% confidence intervals were calculated to report data on the original scale. Statistical significance for the difference between 2 groups was set at P<.05; this condition was met when the 95% confidence interval of the 2 means compared did not overlap.

Results of urinary cotinine measurements in infants during the first 2 weeks of life are shown according to exposure to ETS and feeding in Table 1. Infants whose mothers smoked had significantly higher urinary cotinine levels than those whose mothers did not. Breast-fed infants had higher urinary cotinine levels than those not breast-fed, although this was statistically significant (P<.05) only if the mother smoked. For mothers who did not smoke, infants exposed to ETS had higher urinary cotinine levels than those with no exposure. However, this difference was also statistically significant (P<.05) only for breast-fed infants.

Table Graphic Jump LocationTable 1. Urinary Cotinine Levels in Infants (N = 507) by ETS Exposure and Breast-feeding Status*

Table 2 shows the results of breast milk cotinine measurements. Breast milk cotinine levels were significantly higher among mothers who smoked than those who did not. There was no significant difference (P<.05) in breast milk cotinine levels between mothers who did not smoke with ETS exposure and those without. The correlation between infant urinary cotinine level (obtained in the first 2 weeks of life) and their mother's breast milk cotinine level (obtained at the 4-month visit) was highly significant (r=0.93, P<.001).

Table Graphic Jump LocationTable 2. Cotinine Levels in Breast Milk*

We found increased urinary cotinine concentrations in infants with ETS exposure. Such levels were significantly higher among infants breast-fed by mothers who were exposed to ETS, particularly mothers who smoked. The extremely high level of urinary cotinine in breast-fed infants of mothers who smoked is likely to be a combination of inhaled and ingested nicotine and cotinine. Our data suggest that, among mothers who smoke and breast-feed, the elevated cotinine level in infants is caused by inhalation and ingestion. Also, breast milk is the major contributor to an infant's urinary cotinine level. In a recent study, Mascola et al19 demonstrated a similar dramatic increase in urinary cotinine levels in older infants who were breast-fed by mothers who were smokers. However, the researchers did not directly measure the levels of breast milk cotinine. In our study, the breast milk cotinine levels of mothers who smoked was high. Luck and Nau20,21 found that breast milk cotinine and nicotine levels were, on average, about 3 times higher than the plasma cotinine and nicotine levels determined simultaneously, suggesting that products of tobacco smoke are concentrated in breast milk. However, they did not demonstrate significant differences between infants exposed only by "passive smoking" from their mother and those breast-fed by mothers who smoked.21 In our study, levels of urinary cotinine in breast-fed infants whose mothers smoked were significantly increased and, on average, were 5 times higher than those whose mothers smoked but did not breast-feed. In fact, the lowest urinary cotinine level in a breast-fed infant whose mother smoked was substantially higher than the highest urinary cotinine level in an infant who was not breast-fed and whose mother smoked.

We demonstrated increased urinary cotinine levels in breast-fed infants whose mothers had passive ETS exposure compared with those who were breast-fed and whose mothers did not have ETS exposure. There was a trend of similar increases in urinary cotinine levels in infants who were not breast-fed but whose mothers had passive ETS exposure, although this did not reach levels of statistical significance. Cotinine levels in the breast milk of nonsmoking mothers with ETS exposure were not significantly elevated compared with those of nonsmoking mothers without ETS exposure. However, at the time we measured breast milk cotinine levels, there were only 5 mothers continuing to breast-feed who had passive ETS exposure. Thus, elevated cotinine concentrations in the urine of infants of nonsmoking mothers with ETS exposure may result more from inhalation than from ingestion.

Exposure to ETS primarily by inhalation has been associated with the increased occurrence of respiratory illnesses,1217 decreased pulmonary function,1217,22 and increased bronchial responsiveness.2224 It is not clear whether ingested tobacco products play any role in these problems. In a recent study,13 maternal smoking was associated with an increased risk for respiratory illness during the first year of life. However, the risk for respiratory illness was 7 times higher in infants not breast-fed compared with those breast-fed whose mothers smoked. This suggests that the ingested components of tobacco products from breast milk do not place infants at greater risk for respiratory complications and that breast-feeding is protective against respiratory illness.

Little is known about the effect of ETS exposure during pregnancy and infancy on the child's subsequent smoking behavior. Results of a recent study25 demonstrated that maternal smoking during pregnancy increased the probability of smoking in adolescent girls, after adjusting for postnatal smoke exposure. Another study26 found that the risk of adolescents taking up smoking was related to cotinine content in their saliva 6 years earlier, which was unrelated to the number of smokers in the home. These data suggest that the systemic effects of ETS exposure during pregnancy, and possibly early in life, may lead to an increased risk of addiction to tobacco. Also, ETS exposure during pregnancy and early in childhood has been associated with systemic, nonrespiratory health effects such as neurodevelopmental delay, attention-deficit/hyperactivity disorder, inflammatory bowel disease, and strabismus.611 It is not clear how much postnatal ingested nicotine products play a role in these developmental problems.

We conclude that it is important for women to stop smoking from the time of conception to protect their children from the long-lasting harmful effects of prenatal and postnatal exposure. There is strong public awareness of the risks of smoking during pregnancy, but mothers may once again start smoking after the birth of the child. Mothers should be encouraged to breast-feed yet discouraged from smoking. Parents who smoke must be advised of the potential increased risk to their child, not only for respiratory problems but also the risk for systemic problems, including neurodevelopmental abnormalities and the potential for the future addiction of that child to smoking.

Accepted for publication November 12, 1998.

The cotinine radioimmunoassay kit was provided by Helen van Vunakis, PhD, Brandeis University, Waltham Mass.

Reprints: Allan B. Becker, MD, Children's Hospital of Winnipeg, 820 Sherbrook St, Room AE101, Winnipeg, Manitoba, Canada R3A 1R9 (e-mail: becker@cc.umanitoba.ca).

Editor's Note: I hope no one interprets this study as a reason to discourage breast-feeding among mothers who smoke. It is better to use the study to convince mothers who breast-feed to not smoke.—Catherine D. DeAngelis, MD

Tager  IBNgo  LHanrahan  JP Maternal smoking during pregnancy: effects on lung function during the first 18 months of life. Am J Respir Crit Care Med. 1995;152977- 983
Wang  XWypij  DGold  DR  et al.  A longitudinal study of the effects of parental smoking on pulmonary function in children 6-18 years. Am J Respir Crit Care Med. 1994;1491420- 1425
Stick  SMBurton  PRGurrin  LSly  PDLeSouëf  P Effects of maternal smoking during pregnancy and a family history of asthma on respiratory function in newborn infants. Lancet. 1996;3481060- 1064
Milberger  SBiederman  JFaraone  SVChen  LJones  J Is maternal smoking during pregnancy a risk factor for attention deficit hyperactivity disorder in children? Am J Psychiatry. 1996;1531138- 1142
Eskenazi  BBergmann  J Passive and active maternal smoking during pregnancy, as measured by serum cotinine and postnatal smoke exposure, I: effects on physical growth at age 5 years. Am J Epidemiol. 1995;142(suppl)S10- S18
Blair  PSFleming  PJBensley  D  et al.  Smoking and the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. BMJ. 1996;313195- 198
Fleming  PJBlair  PSBacon  C  et al.  Environment of infants during sleep and risk of the sudden infant death syndrome: results of 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. BMJ. 1996;313191- 195
Lashner  BAShaheen  NJHanauer  SBKirschner  BS Passive smoking is associated with an increased risk of developing inflammatory bowel disease in children. Am J Gastroenterol. 1993;88356- 359
Hakim  RBTieslsch  JM Maternal cigarette smoking during pregnancy: a risk factor for childhood strabismus. Arch Ophthalmol. 1992;1101459- 1462
McCartney  JSFried  PAWatkinson  B Central auditory processing in school-age children prenatally exposed to cigarette smoke. Neurotoxicol Teratol. 1994;16269- 276
Olds  DLHenderson  CR  JrTatelbaum  R Intellectual impairment in children of women who smoke cigarettes during pregnancy. Pediatrics. 1994;93221- 227
Weiss  STTager  IBSchenker  MSpeizer  FE The health effects of involuntary smoking. Am Rev Respir Dis. 1983;128933- 942
Woodward  ADouglas  RMGraham  NMHMiles  H Acute respiratory illness in Adelaide children: breast feeding modifies the effect of passive smoking. J Epidemiol Community Health. 1990;44224- 230
Ey  JLHolberg  CJAldous  MBWright  ALMartinez  FDTaussig  LM Passive smoke exposure and otitis media in the first year of life. Pediatrics. 1995;95670- 677
Ehrlich  RIToit  DJordaan  E  et al.  Risk factors for childhood asthma and wheezing. Am J Respir Crit Care Med. 1996;154681- 688
Ehrlich  RIDu Toit  DJordaan  E  et al.  Risk factors for childhood asthma and wheezing: importance of maternal and household smoking. Am J Respir Crit Care Med. 1996;154681- 688
Fergusson  DMHorwood  LJ Parental smoking and respiratory illness during early childhood: a six year longitudinal study. Pediatr Pulmonol. 1985;199- 106
Langine  JJvan Vunakis  H Radioimmune assay of nicotine, cotinine and alpha-(3 pyridyl)-oxo-N-methylbutylamide. Methods Enzymol. 1982;83628- 640
Mascola  MAvan Vunakis  HTager  IBSpeizer  FEHanrahan  JP Exposure of young infants to environmental tobacco smoke: breastfeeding among smoking mothers. Am J Public Health. 1998;88893- 896
Luck  WNau  H Nicotine and cotinine concentrations in serum and milk of nursing smokers. Br J Clin Pharmacol. 1984;189- 16
Luck  WNau  H Nicotine and cotinine concentrations in serum and urine of infants exposed via passive smoking or milk from smoking mothers. J Pediatr. 1985;107816- 820
Tager  IWeiss  STMunoz  ARosner  BSpeizer  F Longitudinal study of the effects of maternal smoking on pulmonary function in children. N Engl J Med. 1983;309699- 703
Murray  ABMorrison  BJ The effect of cigarette smoke from the mother on bronchial responsiveness and severity of symptoms in children with asthma. J Allergy Clin Immunol. 1986;77575- 581
Frischer  TKuehr  JMeinert  R  et al.  Maternal smoking in early childhood: a risk factor for bronchial responsiveness to exercise in primary-school children. J Pediatr. 1992;12117- 22
Kandel  DBWu  PDavies  M Maternal smoking during pregnancy and smoking by adolescent daughters. Am J Public Health. 1994;841407- 1413
Becklake  MRGhezzo  Hvan Vliet  PErnst  P Is salivary cotinine a biomarker of lung susceptibility to inhaled pollutants? Am J Respir Crit Care Med. 1995;155A550

Figures

Tables

Table Graphic Jump LocationTable 1. Urinary Cotinine Levels in Infants (N = 507) by ETS Exposure and Breast-feeding Status*
Table Graphic Jump LocationTable 2. Cotinine Levels in Breast Milk*

References

Tager  IBNgo  LHanrahan  JP Maternal smoking during pregnancy: effects on lung function during the first 18 months of life. Am J Respir Crit Care Med. 1995;152977- 983
Wang  XWypij  DGold  DR  et al.  A longitudinal study of the effects of parental smoking on pulmonary function in children 6-18 years. Am J Respir Crit Care Med. 1994;1491420- 1425
Stick  SMBurton  PRGurrin  LSly  PDLeSouëf  P Effects of maternal smoking during pregnancy and a family history of asthma on respiratory function in newborn infants. Lancet. 1996;3481060- 1064
Milberger  SBiederman  JFaraone  SVChen  LJones  J Is maternal smoking during pregnancy a risk factor for attention deficit hyperactivity disorder in children? Am J Psychiatry. 1996;1531138- 1142
Eskenazi  BBergmann  J Passive and active maternal smoking during pregnancy, as measured by serum cotinine and postnatal smoke exposure, I: effects on physical growth at age 5 years. Am J Epidemiol. 1995;142(suppl)S10- S18
Blair  PSFleming  PJBensley  D  et al.  Smoking and the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. BMJ. 1996;313195- 198
Fleming  PJBlair  PSBacon  C  et al.  Environment of infants during sleep and risk of the sudden infant death syndrome: results of 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. BMJ. 1996;313191- 195
Lashner  BAShaheen  NJHanauer  SBKirschner  BS Passive smoking is associated with an increased risk of developing inflammatory bowel disease in children. Am J Gastroenterol. 1993;88356- 359
Hakim  RBTieslsch  JM Maternal cigarette smoking during pregnancy: a risk factor for childhood strabismus. Arch Ophthalmol. 1992;1101459- 1462
McCartney  JSFried  PAWatkinson  B Central auditory processing in school-age children prenatally exposed to cigarette smoke. Neurotoxicol Teratol. 1994;16269- 276
Olds  DLHenderson  CR  JrTatelbaum  R Intellectual impairment in children of women who smoke cigarettes during pregnancy. Pediatrics. 1994;93221- 227
Weiss  STTager  IBSchenker  MSpeizer  FE The health effects of involuntary smoking. Am Rev Respir Dis. 1983;128933- 942
Woodward  ADouglas  RMGraham  NMHMiles  H Acute respiratory illness in Adelaide children: breast feeding modifies the effect of passive smoking. J Epidemiol Community Health. 1990;44224- 230
Ey  JLHolberg  CJAldous  MBWright  ALMartinez  FDTaussig  LM Passive smoke exposure and otitis media in the first year of life. Pediatrics. 1995;95670- 677
Ehrlich  RIToit  DJordaan  E  et al.  Risk factors for childhood asthma and wheezing. Am J Respir Crit Care Med. 1996;154681- 688
Ehrlich  RIDu Toit  DJordaan  E  et al.  Risk factors for childhood asthma and wheezing: importance of maternal and household smoking. Am J Respir Crit Care Med. 1996;154681- 688
Fergusson  DMHorwood  LJ Parental smoking and respiratory illness during early childhood: a six year longitudinal study. Pediatr Pulmonol. 1985;199- 106
Langine  JJvan Vunakis  H Radioimmune assay of nicotine, cotinine and alpha-(3 pyridyl)-oxo-N-methylbutylamide. Methods Enzymol. 1982;83628- 640
Mascola  MAvan Vunakis  HTager  IBSpeizer  FEHanrahan  JP Exposure of young infants to environmental tobacco smoke: breastfeeding among smoking mothers. Am J Public Health. 1998;88893- 896
Luck  WNau  H Nicotine and cotinine concentrations in serum and milk of nursing smokers. Br J Clin Pharmacol. 1984;189- 16
Luck  WNau  H Nicotine and cotinine concentrations in serum and urine of infants exposed via passive smoking or milk from smoking mothers. J Pediatr. 1985;107816- 820
Tager  IWeiss  STMunoz  ARosner  BSpeizer  F Longitudinal study of the effects of maternal smoking on pulmonary function in children. N Engl J Med. 1983;309699- 703
Murray  ABMorrison  BJ The effect of cigarette smoke from the mother on bronchial responsiveness and severity of symptoms in children with asthma. J Allergy Clin Immunol. 1986;77575- 581
Frischer  TKuehr  JMeinert  R  et al.  Maternal smoking in early childhood: a risk factor for bronchial responsiveness to exercise in primary-school children. J Pediatr. 1992;12117- 22
Kandel  DBWu  PDavies  M Maternal smoking during pregnancy and smoking by adolescent daughters. Am J Public Health. 1994;841407- 1413
Becklake  MRGhezzo  Hvan Vliet  PErnst  P Is salivary cotinine a biomarker of lung susceptibility to inhaled pollutants? Am J Respir Crit Care Med. 1995;155A550

Correspondence

CME
Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).
Submit a Comment

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Topics
PubMed Articles