Respiratory, cardiovascular and other physiological consequences of smoking cessation

Smoking cessation is associated with substantial reductions in tobacco-related morbidity and mortality. Based on the current literature, the beneficial effects of quitting are particularly evident on pulmonary and cardiovascular function, but the negative physiological effects of cessation are less well documented.

The objective of this article was to review systematically data on the physiological effects of smoking cessation. Articles based upon clinical trials, randomised controlled trials and meta-analyses were selected from titles and abstracts obtained via a MEDLINE search (May 2003-May 2008). Additional studies were identified from the bibliographies of reviewed literature.

Smoking cessation is associated with improved lung function and a reduction in the presence and severity of respiratory symptoms. These changes, apparent within months of quitting, are sustained with long-term abstinence. The underlying pathophysiologies of smoking-induced airway inflammation and endothelial dysfunction are partially reversed following cessation in healthy ex-smokers, but not in those with chronic obstructive pulmonary disease. Smoking cessation is also associated with substantially improved cardiovascular function and reduced risk of primary and secondary cardiovascular morbidity and mortality. Although the overall long-term health benefits are unquestionable, smoking cessation is also associated with other possible undesirable short-term physiological effects such as weight gain, hypertension, constipation and mouth ulcers; and altered activity of the enzyme cytochrome P450 1A2 (CYP1A2), which metabolises many commonly used drugs.

The negative physiological effects of smoking cessation may adversely affect a smoker's attempt to quit, and physicians should provide their smoking patients with motivation and regular encouragement and support when attempting to quit, whilst educating them on the health benefits of abstinence. Additionally, since cigarette smoke is a potent inducer of CYP1A2, patients attempting to quit smoking should have their dosages of drugs metabolised by this enzyme closely monitored.