Smoking and air pollution

Key points

Although becoming less popular, one-fifth of the UK population still smokes tobacco, and worldwide, the number of smokers is increasing.
Smoking involves the regular inhalation of a variety of toxic compounds that stimulate airway irritant receptors and activate inflammatory pathways in the lung.
The effects of passive smoking begin in utero, when lung development is impaired, leaving the infant susceptible to lower respiratory tract illness for the first few years of life.
Air pollution with carbon monoxide, ozone, nitrogen dioxide and particulate matter can occur either indoors or outside, and is associated with a variety of respiratory diseases and symptoms.

The air we breathe is rarely a simple mixture of oxygen, nitrogen and water vapour. For much of the world’s population, air also contains a variety of other, more noxious, gases and particles. In addition, a substantial proportion of people choose to further contaminate the air that they, and others, breathe with tobacco smoke.

Tobacco smoke

In the Americas tobacco was used for medicinal purposes for many centuries before being introduced from the New World into Europe in the 16th century. Through his acquaintance with Queen Elizabeth I, Sir Walter Raleigh made smoking tobacco an essential fashionable activity of every gentleman. Thereafter the practice steadily increased in popularity until the explosive growth of the habit after the First World War (1914–1918).

There have always been those opposed to smoking, and King James I (1603–1625) described it as ‘a custom loathsome to the eye, hateful to the nose, harmful to the brain and dangerous to the lungs’. However, firm evidence to support his last conclusion was delayed by some 350 years. Only relatively recently did it become clear that smokers had a higher mortality, and that the causes of the excess mortality included many respiratory diseases. There are currently over a billion smokers worldwide. In high-income countries, the proportion of the population that smokes has generally declined since evidence of serious health consequences emerged; in the UK and the US this is now around 20%. Globally, however, the number of smokers is increasing. The health costs of tobacco smoking are enormous: over 80% of smokers are in low- and middle-income countries, where the smoking prevalence amongst males may exceed 70%. Worldwide, one-third of people who smoke will die as a result of their habit, and it is estimated that during this century smoking will cause 1000 million premature deaths.

Constituents of tobacco smoke

More than 2000 potentially noxious constituents have been identified in tobacco smoke, some in the gaseous phase and others in the particulate or tar phase. The particulate phase is defined as the fraction eliminated by passing smoke through a filter of pore size 0.1 µm. This is not to be confused with the ‘filter tip’, which allows passage of considerable quantities of particulate matter.

There is great variation in the yields of the different constituents between different brands and different types of cigarettes. This is achieved by using leaves of different species of plants, by varying the conditions of curing and cultivation and by using filter tips. Ventilated filters have a ring of small holes in the paper between the filter tip and the tobacco. These holes admit air during a puff, and dilute all constituents of the smoke.

Gaseous phase

Carbon monoxide (CO) is present in cigarette smoke at a concentration issuing from the butt of the cigarette during a puff of around 1% to 5%, which is far into the toxic range. A better indication of the extent of CO exposure is the percentage of carboxyhaemoglobin in blood. For nonsmokers, the value is normally less than 1.5%, but is influenced by exposure to air pollution and other people’s cigarette smoke (see later). Typical values for smokers range from 2% to 12%. The value is influenced by the number of cigarettes smoked, the type of cigarette and the pattern of inhalation of smoke.

Tobacco smoke also contains very high concentrations (about 400 parts per million [ppm]) of nitric oxide (NO) and trace concentrations of nitrogen dioxide, the former being slowly oxidized to the latter in the presence of oxygen. The toxicity of these compounds is well known. Nitrogen dioxide hydrates in alveolar lining fluid to form a mixture of nitrous and nitric acids. In addition, the nitrite ion converts haemoglobin to methaemoglobin.

Other constituents of the gaseous phase include hydrocyanic acid, cyanogen, aldehydes, ketones, nitrosamines and volatile polynuclear aromatic hydrocarbons (PAHs).

Particulate phase

The material removed by a Cambridge filter is known as the ‘total particulate matter’, with an aerosol particle size in the range of 0.2 to 1 µm. The particulate phase comprises water, nicotine and ‘tar’. Nicotine ranges from 0.05 to 2.5 mg per cigarette, and ‘tar’ from 0.5 to 35 mg per cigarette.

Individual smoke exposure

Individual smoke exposure is a complex function of the quantity of cigarettes that are smoked and the pattern of inhalation.

Quantifying cigarettes smoked

Exposure is usually quantified in ‘pack-years’. This equals the product of the number of packs (20 cigarettes) smoked per day, multiplied by the number of years that that pattern was maintained. The totals for each period are then summated for the lifetime of the subject.

Pattern of inhalation

There are very wide variations in patterns of smoking. Air is normally drawn through the cigarette in a series of ‘puffs’ with a volume of about 25 to 50 mL per puff. The puff may be simply drawn into the mouth and rapidly expelled without appreciable inhalation. However, the habituated smoker will either inhale the puff directly into the lungs or, more commonly, pass the puff from the mouth to the lungs by inhaling air either through the mouth or else through the nose while passing the smoke from the mouth into the pharynx by apposing the tongue against the palate, obliterating the gas space in the mouth. The inspiration is often especially deep, to flush into the lung any smoke remaining in the dead space.

The quantity of nicotine, tar and CO obtainable from a single cigarette is therefore variable, and the number and type of cigarettes smoked are not the sole determinants of effective exposure. Habituated smokers adjust their smoking pattern to maintain a particular blood level of nicotine. For example, after changing to a brand with a lower nicotine yield, it is common practice to modify the pattern of inhalation to maximize nicotine absorption.

Respiratory effects of smoking

Cigarette smoking has extensive effects on respiratory function, and is clearly implicated in the aetiology of a number of respiratory diseases, particularly chronic obstructive pulmonary disease (COPD) and bronchial carcinoma, which are discussed in Chapters 28 and 30 , respectively. Why only around one-fifth of smokers go on to develop COPD remains uncertain, but is likely to relate to a genetic susceptibility to the effect of tobacco smoke (page 331). Studies of the modification of the expression of several genes in smokers via methylation of DNA have identified associations with this and a decline in lung function, the development of COPD and lung cancer. Pulmonary endothelial cell injury because of cigarette smoke includes barrier dysfunction, endothelial inflammation, apoptosis and altered vasoactive mediator production. These processes are implicated in the development of conditions including acute respiratory distress syndrome (ARDS), emphysema and vascular remodeling in COPD.

Airway mucosa

There are conflicting laboratory reports regarding the sensitivity of airway reflexes in smokers, with increased sensitivity demonstrated in response to inhalation of small concentrations of ammonia vapour and decreased sensitivity in response to capsaicin. There are also variable effects of smoking cessation on the cough reflex. There is, however, general agreement that smokers have hyperresponsive airway reflexes secondary to airway inflammation, probably caused by increased excitability of vagal sensory nerves in response to inflammatory mediators.

Ciliary movement is inhibited by both particulate and gas phase compounds in vitro, but in vivo studies have shown contradictory results, with some studies showing increased ciliary activity in response to cigarette smoke. Ciliary structure may be abnormal, with some work showing smoking reduces the length of cilia by reducing expression of the intraflagellar transport gene responsible for normal ciliary production. A small reduction in ciliary length may significantly impair its mucus-clearing function (page 166).

There is agreement that mucus production is increased in long-term smokers, who have hyperplasia of submucosal glands and increased numbers of goblet cells even when asymptomatic. Mucus clearance is universally found to be impaired in smokers, which, coupled with increased mucus production and airway sensitivity, gives rise to the normally productive smoker’s cough. Three months after smoking cessation, many of these changes are reversed, except in those patients who have developed airway damage from long-term airway inflammation.

Airway diameter

Airway diameter is reduced acutely with smoking as a result of reflex bronchoconstriction in response to inhaled particles and the increased mucus production already described. Long-term small airway inflammation causes chronic airway narrowing that has a multitude of effects on lung function. Airway narrowing promotes premature airway closure during expiration, which results in an increase in closing volume and disturbed ventilation/perfusion relationships. Distribution of inspired gas as indicated by the single-breath nitrogen test (page 92) is therefore often abnormal in smokers. Small airway narrowing over many years gives rise to a progressive reduction in the forced expiratory volume in one second (FEV ₁ ), described later. Many of these changes are at an advanced stage before smokers develop respiratory symptoms.

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