“Personal Freedom, Personal Choice”

Myth 1

By Steve Cross
10th December 2006

’30 minutes exposure to second hand smoke increases your likelihood of heart attack.’

A Japanese study of 30 men (15 smokers and 15 non-smokers) conducted in 2000 “Acute Effects of Passive Smoking on the Coronary Circulation in Healthy Young Adults” concluded:

“Passive smoking substantially reduced CFVR in healthy nonsmokers. This finding provides direct evidence that passive smoking may cause endothelial dysfunction of the coronary circulation in nonsmokers.”

From the above paragraph hundreds of anti-smoking groups around the world have made claims along the lines of the title of this article but can exposure to extremely dilute and tiny quantities of particles put you at risk of heart attack after just 30 minutes?

Firstly we need to know three things from the conclusions made;

1. What does a ‘substantially reduced CFVR’ actually mean and how does it affect health?

2. What is ‘endothelial dysfunction’ and how does it occur?

3. Could endothelial dysfunction occur in 30 minutes and give you a heart attack?


CFVR; is Coronary Flow Velocity Reserve which is the measure of how the lining of the coronary arteries is able to respond to certain stressful conditions. It is a purely academic measurement and its significance to the causes of heart disease is not known.

Reduced CFVR, such as found in this research, is not a permanent condition and is quite normal after activities such as eating a high fat meal; furthermore it does not affect normal functioning of the coronary system. The research does conclude however that CFVR may lead to endothelial dysfunction.

Endothelial Dysfunction; is abnormal functioning of the cells in the lining of the artery indicating that this research may show a reduced dilation of the coronary arteries; this however does not affect blood flow and is therefore not in itself a risk of ‘heart attack’.

Under normal circumstances the cells within the artery lining release chemicals that cause expansion of the artery however, certain stimulants contained in food and pollutants can cause endothelial dysfunction by restricting these chemicals. The condition is also temporary with the endothelial cells returning to normal after the ‘stimulant’ is removed.

Dysfunction To Heart Attack; the question remaining then is, how can endothelial dysfunction lead to a heart attack?

Endothelial dysfunction cannot in itself cause a heart attack as has already been pointed out. There is no impairment of ability to deliver blood from a reduced CFVR; a blockage or rupture of the artery is necessary for heart attack to occur, additionally both temporary endothelial dysfunction and reduced CFVR are normal. However ‘Chronic’ endothelial dysfunction over many years can lead to hardening of the arteries and this is where the claims arise.

The main problems with the anti-smoking claims are that of dosage and duration. We don’t see otherwise healthy people falling down with heart attacks after eating a couple of cheeseburgers, nor do we see healthy non-smokers collapsing in smoky bars; the dosage and duration are simply not anywhere near enough to cause cellular damage in either of those circumstances. The fact is that obese people and heavy smokers are at higher risk from this type of cellular damage only after chronic exposure over many years.


A research containing 15 people in each of two groups is certainly not comprehensive enough to make any major assumptions.

However; contrary to the anti-smoking claims, the research actually shows normal bodily response after exposure to certain stimulants namely a reduced CFVR; it did not find direct evidence of endothelial dysfunction, only that a reduced CFVR indicates that dysfunction “may” occur. None of this means that there will be hardening of the arteries, decreased actual blood flow or any other compromise to the heart.

Given that direct smokers are exposed to high doses with high frequency and over very long periods before hardening of the arteries occurs, dosage and frequency to a ‘passive smoker’ would have to be as high as that of a direct smoker over a period of many years to achieve a similar response. Additionally many other confounders would be involved such as diet, genetics and exercise.

It is therefore highly implausible that levels of passive smoke such as those found in modern ventilated bars could lead to an increased risk of heart attacks even over many years of exposure let alone within 30 minutes.

This myth is busted.