• Department

Erasmus MC,ofUniversity
Public Health
Medical
Sciences,
Centre
St Rotterdam,
George's Hospital
Sophia Medical
Children’s
School,
Hospital,
London,
Rotterdam,
UK. Netherlands
Health effects of passive smoking .5. Parental smoking and allergic sensitisation in children.

1. D P Strachan,
2. D G Cook
+Author Affiliations

Abstract
BACKGROUND: A systematic review was conducted of the effects of parental smoking on immunoglobulin (IgE) levels, skin prick positivity, and
allergic rhinitis or eczema in children. Asthma was excluded in order to distinguish more clearly the effect of passive smoke exposure on allergic
sensitisation. METHODS: Thirty six relevant publications were identified after consideration of 692 articles selected by electronic search of the
Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified nine
studies of IgE in neonates, eight of IgE in older children, 12 which included skin prick tests, and 10 describing symptoms of allergic disease other than
asthma or wheezing. A quantitative meta-analysis was possible only for the studies reporting skin prick tests. RESULTS: Several large studies failed to
confirm early reports of a substantial or statistically significant association of maternal smoking with concentrations of total serum IgE in neonates or in
older children. No consistent association emerged between parental smoking and allergic rhinitis or eczema. Few of these studies adjusted for
potential confounding variables. The quantity and quality of evidence was greatest for skin prick tests, and studies of parental smoking during
pregnancy or infancy were broadly consistent in showing no
adverse effect on prick positivity (pooled odds ratio 0.87, 95% confidence interval 0.62 to 1.24). There was much greater and statistically significant (p
= 0.002) heterogeneity of odds ratios relating current parental smoking to skin prick positivity. CONCLUSIONS: Parental smoking, either before or
immediately after birth, is unlikely to increase the risk of allergic sensitisation in children.

(9230 participants) and 14 papers on ETS and SPT (14 150 patients) met our inclusion criteria. ETS was shown to raise tIgE concentrations by 27.7 IU/mL (95% CI
7.8 to 47.7; I2=58%; results based on 3 studies) and to increase the risk of atopic sensitisation, as assessed by sIgE+ (OR=1.12, 95%CI 1.00 to 1.25; I2=54%; results
based on 4 studies) and SPT+ (OR=1.15; 95% CI 1.04 to 1.28; I2=0%; results based on 10 studies). In a subgroup analysis, this effect was most pronounced in
children <7 years (preschoolers) by OR=1.20; (95% CI 1.05 to 1.38) and OR=1.30 (95% CI 1.05 to 1.61), (for sIgE+ and SPT+, respectively).
Conclusions Current analysis supports an association between ETS exposure in early childhood and the increased risk of allergic sensitisation. Subgroup meta-
analyses demonstrate that younger children suffer the most from detrimental immunomodulating effects of ETS exposure. This study underscores ETS as an
important but avoidable risk factor for the development of allergic disease in children.

Adverse health effects of prenatal and postnatal

tobacco smoke exposure on children
1. W Hofhuis,
2. J C de Jongste,
3. P J F M Merkus
+Author Affiliations
1. Correspondence to:
Dr W Hofhuis
Erasmus MC, University Medical Centre Rotterdam, Sophia Children’s Hospital, Rotterdam, Netherlands; w.hofhuis@erasmusmc.nl
2. Accepted 15 March 2003

Abstract
Parents who choose to smoke are possibly not aware of, or deny, the negative effects of passive smoking on their offspring. This review summarises a
wide range of effects of passive smoking on mortality and morbidity in children. It offers paediatricians, obstetricians, specialists in preventive child
health care, general practitioners, and midwives an approach to promote smoking cessation in smoking parents before, during, and after pregnancy.

2. Cardiovascular Effects of Secondhand Smoke

Nearly as Large as Smoking

1. Joaquin Barnoya, MD, MPH;
• FromBACKGROUND
the Center for Tobacco Control Research and Education, Cardiovascular
2. Stanton A.Research Institute, and Division of
Glantz, PhD

+Author Affiliations

1. Reprint requests to Stanton A. Glantz, PhD, Professor of Medicine, University of California, San Francisco, 530 Parnassus,
Suite 366, San Francisco, CA 94143-1390. E-mail glantz@medicine.ucsf.edu

Abstract
Background— Secondhand smoke increases the risk of coronary heart disease by ≈30%. This effect is larger than one would expect on
the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers.
Methods and Results— We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the
cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of
active smoking. Evidence is rapidly accumulating that the cardiovascular system—platelet and endothelial function, arterial stiffness,
atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size—is exquisitely
sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large
(averaging 80% to 90%) as chronic active smoking.
Conclusions— The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in
epidemiological studies.

Passive Smoking and Impaired Endothelium-

Dependent Arterial Dilatation in Healthy Young
Adults
David S. Celermajer, Ph.D., Mark R. Adams, M.B., B.S., Peter Clarkson, M.B., B.S., Jacqui
Robinson, R.N., Robyn McCredie, B.Sc., Ann Donald, and John E. Deanfield, M.B., Ch.B.
N Engl J Med 1996; 334:150-155January 18, 1996DOI: 10.1056/NEJM199601183340303
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Abstract
Article
References
Citing Articles (297)
Letters
Passive Smoking and Heart DiseaseMechanisms and Risk
Stanton A. Glantz, PhD; William W. Parmley, MD
JAMA. 1995;273(13):1047-1053. doi:10.1001/jama.1995.03520370089043.
 Text Size: A A A
Article
References

ABSTRACT

ABSTRACT | REFERENCES
Objective. —Recent clinical, laboratory, and epidemiological evidence that passive smoking causes heart disease was reviewed,
with particular emphasis on understanding the underlying physiological and biochemical mechanisms.
Data Sources. —Publications in the peer-reviewed literature were located via MEDLINE, citation in other relevant articles, and
appropriate reports by scientific agencies. Greatest emphasis was given to work published since 1990.
Conclusions. —Passive smoking reduces the blood's ability to deliver oxygen to the heart and compromises the myocardium's
ability to use oxygen to create adenosine triphosphate. These effects are manifest as reduced exercise capability in people
breathing secondhand smoke. Secondhand smoke increases platelet activity, accelerates atherosclerotic lesions, and increases
tissue damage following ischemia or myocardial infarction. The effects of secondhand tobacco smoke on the cardiovascular
system are not caused by a single component of the smoke, but rather are caused by the effects of many elements, including carbon
monoxide, nicotine, polycyclic aromatic hydrocarbons, and other, not fully specified elements in the smoke. Nonsmokers exposed
to secondhand smoke in everyday life exhibit an increased risk of both fatal and nonfatal cardiac events.(JAMA. 1995;273:1047-
1053)

The impact of passive smoking: cancer deaths among nonsmoking women.

(PMID:2224913)
• Abstract
• Citations
 • BioEntities

• Related Articles

• External Links

Miller GH
Studies on Smoking, Inc., Edinboro, PA 16412.
Cancer Detection and Prevention [1990, 14(5):497-503]
Type: Journal Article, Research Support, Non-U.S. Gov't
Abstract Highlight Terms
Gene Ontology(1) Diseases(4) Species(1)
In order to obtain an estimate of the impact of passive smoking on cancer mortality, a retrospective study was conducted
examining the cancer mortality of nonsmoking wives with no known or minimal exposure in contrast to nonsmoking wives
with moderate to life-time exposure to tobacco smoke. The study was based on the data from 906 deceased nonsmoking
women who resided in Erie County, Pennsylvania, who were divided into the following three categories: 1. No known
exposure. 2. Exposed nonemployed. 3. Employed (assumed to be exposed to environmental tobacco smoke in the
workplace). The data were analyzed by the retrospective case-control method using cancer deaths as the cases and non-
cancer related deaths as the controls. Also, the data from 401 smoking women were used for comparative purposes of the
total percentage of cancer deaths among three groups: 1. Nonsmoking, nonexposed women. 2. Combined nonsmoking
unemployed and employed exposed women. 3. Smoking women. The major findings from the study are: 1. Only (2.2%) of
the total deathsreported among the nonsmoking women with no known or minimal exposure to tobacco smoke were due
to cancer of any site. 2. No cases of lung cancer deaths were reported for the nonexposed, nonsmoking women, and
eight lung cancer deaths were reported among the nonsmoking women who were exposed to passive smoking. Also, for
this small group of 170 nonsmoking nonexposed women, there were no reported cases of breast cancer, genitourinary
or lymphatic cancer. 3. Employed nonsmoking women experienced proportionately more cancer deaths (34.3%) than both
nonexposed (2.2%) and exposed nonemployed wives (18.9%). The combined groups of exposed nonsmoking wives
(nonemployed and employed) contracted 25.5% cancer deaths. 4. Age-adjusted data showed similar trends.
5. Cancer death rates for women smokers was 35.5% of the total deaths of women smokers. Public health officials should
consider requiring that the workplace be free from tobaccosmoke since these data imply that passive smoking has a very
detrimental effect upon nonsmokers. Also, smokers should be made aware of the potential damage they inflict on others in
their home as well as the workplace.

The impact of passive smoking: cancer deaths among nonsmoking women.

(PMID:2224913)
• Abstract
• Citations

• BioEntities

• Related Articles

• External Links

Miller GH
Studies on Smoking, Inc., Edinboro, PA 16412.
Cancer Detection and Prevention [1990, 14(5):497-503]
Type: Journal Article, Research Support, Non-U.S. Gov't
Abstract Highlight Terms
Gene Ontology(1) Diseases(4) Species(1)