Secondhand smoke exposure in children -

focus on the cardiovascular system

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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 & tobacco-related 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 smoke-free 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 flowEndothelial cells maintain vascular tone & hemostasisVasodilation & 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?

Cell damage/stressInflammationEndothelial dysfunction

Combustionproducts –Oxidizing gas

Oxidant pathwaysDirect toxicity

In summary,

• Effect of SHS exposure on CV system is not nicotine-mediated

• 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

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