Transcript Second hand smoke exposure in children

Secondhand smoke exposure
in children focus on the cardiovascular system
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…dedicated to eliminating children’s exposure to tobacco
and secondhand smoke
Learning objectives
1) Understand tobacco smoking and SHS exposure as a
health disparity
2) Learn about epidemiological evidence of SHS
exposure and cardiovascular disease in adults.
3) Understand biological linkage between SHS exposure
and cardiovascular disease.
4) Learn how CVD precursors may be assessed during
childhood and adolescence.
SHS exposure as a health disparity
• Who is exposed to SHS?
• Overall, about 25% of US children
• Children in low-income homes – as high as 79%
• At least 50% of African American children
• More than 1/3 of children in low SES homes
• Low estimate (self report data only)
SHS exposure as a health disparity
• Who smokes?
• About 20% of US population, slightly lower rates
among women
• Geographical diversity
• (higher rates in Kentucky, West Virginia, lower in
California, Connecticut)
• Smoking rates inversely related to education &
income
• People who can least afford cigarettes & tobaccorelated disease
SHS as a health disparity
• Why does this matter?
• Concentration of multiple exposures among low SES
children
• Exposure throughout the lifespan
Childhood SHS exposure
• Most research on respiratory morbidity
• Diseases seen during childhood itself
Basic concepts of heart disease
• ‘Chronic inflammatory process’
• Immune mechanisms interact with metabolic risk
factors to initiate, maintain, & activate arterial lesions
• Adult cardiovascular disease begins & progresses
silently during childhood.
SHS exposure & cardiovascular disease
in adults
• 30,000 – 60,000 cardiovascular disease (CVD)
related deaths/year -- SHS exposure in non-smokers
• “causal relationship between SHS exposure &
increased risk for coronary heart disease morbidity &
mortality among men and women” (2006 Surgeon
General report)
SHS, heart disease & adults
• Risk of atherosclerotic heart disease in SHS exposed
non-smokers – 1.25
• Relative risk of acute cardiac syndrome (ACS)– 1.50
• Impact of smoking bans – natural observational
experiment
• hospital admissions for MI down almost 50%
(Montana)
• Scotland – ACS admissions down 17% after smokefree legislation.
What accounts for these observations?
• Not nicotine mediated
• SHS exposure – less than 1% of nicotine of active
smoker to 20 cigs/day
• Yet – 1.25 risk of CVD
• Blood levels of nicotine & CO are low in SHS exposed
non smokers
• Most likely cause- oxidant gas exposure
Animal Models of SHS exposure
• Exposure related to inflammation
• ↓ adiponectin (anti-inflammatory)
• ↑ TNF-α - pro-inflammatory
• ↑ IL-6 – pro-inflammatory
• ↑ CRP – pro-inflammatory
How can we assess pediatric precursors of
adult CVD?
• Inflammation
• CRP, other markers
• Endothelial dysfunction
• Multiple non-invasive reproducible methods
• All NO mediated, response to occlusion and reflow.
How can we assess pediatric precursors of
adult CVD?
• Endothelial stress
• s-ICAM (soluble intercellular adhesion molecule)
• One of family of molecules released from stressed
endothelial cells into blood
• Marker of endothelial stress
• Endothelial repair
• Endothelial progenitor cells (EPCs)
• Bone marrow derived cells
• “Patch” endothelium
The Endothelium and Endothelial Cells
Provide non-adherent, non-thrombotic
surface for blood flow
Endothelial cells maintain vascular
tone & hemostasis
Vasodilation & constriction modulated
by small molecules (nitric oxide,
prostacyclin and endothelin)
Endothelial dysfunction implicated in adult
conditions ---hypertension, obesity,
inflammation, diabetes, active & passive
smoking ----leading to atherosclerosis
Evidence that SHS exposure is related to
endothelial dysfunction
• Healthy SHS exposed non-smokers ages 18-35
• Impaired endothelial function measured by brachial
artery dilation in response to occlusion
• nitric oxide (NO) mediated
• Impairment similar to that seen among smokers
How does this happen with SHS exposure?
Combustion
products –
Oxidizing
gas
Oxidant
pathways
Direct
toxicity
Cell damage/stress
Inflammation
Endothelial dysfunction
In summary,
• Effect of SHS exposure on CV system is not nicotinemediated
• Believed to be due to oxidative stress leading to
inflammation with subsequent CVD
SHS and CVD precursors in children
• Children don’t have heart attacks – so what can we
measure?
• SHS exposure is directly related to inflammation in
children
• NHANES study
• Direct relationship between CRP and SHS (measured
by serum cotinine) in children
• Magnitude of association – same as adults
SHS and CVD precursors in children
• Endothelial function can be measured in children
• Non-invasive measurement in adults has direct
relationship w/coronary blood flow
• Dose dependent inverse relationship between SHS
exposure & endothelial function (11 year olds)
• CRP inversely related to endothelial function in healthy
children
What we don’t know:
• What happens to vascular system after years of SHS
exposure?
• What happens in the presences of another chronic
inflammatory state – obesity?
• What is impact of third hand smoke on inflammatory
pathways?
Summary
• SHS is linked to CVD in adults via oxidation and
inflammatory pathways
• Ultimately leads to endothelial dysfunction – a precursor
of CVD
• Effect supported by epidemiological data
• Effect supported by animal models
• Evidence in children that these changes are occurring
early in life
• One more reason that no child should have any SHS
exposure
Need more information?
The AAP Richmond Center
www.aap.org/richmondcenter
Audience-Specific Resources
State-Specific Resources
Cessation Information
Funding Opportunities
Reimbursement Information
Tobacco Control E-mail List
Pediatric Tobacco Control Guide