The throat consists of two major parts: the pharynx (back of the throat) and the larynx, commonly known as the voice box, which is an organ within the throat. The pharynx consists of the nasopharynx (behind the nose), oropharynx (behind the mouth) and hypopharynx (also called the laryngopharynx, which connects to the oesophagus and larynx).1
Throat cancer is most common in the oropharynx.2-4 There were 1,055 people diagnosed with oropharyngeal cancer in Australia in 2024 and 247 who died from this cancer, with 73.6% of people surviving for five years after diagnosis (from 2016–2020 data).2-4 There were an estimated 200 people diagnosed with cancer of the nasopharynx, with 86 dying from this cancer in 2024 and a five-year survival rate of 67.1%. For hypopharyngeal cancer, 173 people were diagnosed in 2024, with 79 dying and a relatively low five-year survival rate of 38.4%.2-4
In 2024 573 people who were diagnosed with cancer of the larynx (voice box) in Australia.2 An estimated 187 people died from laryngeal cancer that year, with 64.8% of those diagnosed surviving for at least five years (from 2016–2020 data).3,4
Treatment for throat or voice box cancer has many side effects that make the lived experience of this cancer very difficult. These include chemotherapy and radiotherapy as well as surgical removal of part of the throat or voice box, leaving people unable to speak naturally.5
3.5.2.1 Risk associated with smoking
Smoking causes cancer of the pharynx and the larynx.6,7
Pharyngeal cancer (throat cancer)
The 2004 US Surgeon General’s report found that the evidence is sufficient to conclude that smoking is a cause of pharyngeal cancer.6 This finding is supported by a meta-analysis of studies from 1961 to 2003, which concluded that people with a history of smoking had a 6.8-fold higher risk of pharyngeal cancer compared to non-smokers.8 A 2017 meta-analysis of 17 case-control and 4 cohort studies determined that smokers had significantly higher odds of nasopharyngeal cancer than non-smokers. This study found a dose-dependent relationship where the risk estimate rose by 15% with every additional 10 pack-years of smoking.9
Based on its exhaustive review of available studies, the 2004 International Agency for Research on Cancer (IARC) report also found sufficient evidence to conclude that tobacco smoking causes cancer of the naso-, oro- and hypopharynx.7
Laryngeal cancer (voice box cancer)
Smoking is a cause of laryngeal cancer.6,7 The 2004 US Surgeon General’s report concluded that there was sufficient evidence to infer a causal relationship between smoking and cancer of the larynx, and that smoking and alcohol cause most cases of this cancer in the US.6
The larynx is directly exposed to tobacco smoke when it is inhaled through the space between the vocal chords, and smoking is a particularly strong risk factor for cancer of the larynx. A meta-analysis of 85 studies found that the risk of laryngeal cancer was nine times greater for current smokers than never smokers.10 Risks have been reported in some studies at 20-fold higher for people who smoke are compared to non-smokers.6 In Australia, the risk of laryngeal cancer for smokers was estimated to be 11.3-fold higher than for non-smokers, for people 45 years and above.11 The risk of laryngeal cancer for people who smoke rises with greater exposure; there was a 19-fold increased risk for heavy smokers and 7.66-fold risk for lighter smokers compared to people who never smoked.6,10
3.5.2.2 How tobacco smoke causes throat and voice box cancers
The cells lining the pharynx and larynx are directly exposed to tobacco smoke and can also be affected by chemicals from smoke that have entered the bloodstream via the lungs and circulated to all parts of the body. Carcinogens and other toxic chemicals from tobacco smoke can damage DNA as well as disrupt various cellular processes, leading to the formation of cancer. See Section 3.5.1.2 for a brief summary of the effects of carcinogens on cells in the airways.
Exposure to carcinogens from tobacco smoke leads to DNA mutations, chromosomal changes, and disruption of cellular process, culminating in formation of cancer. DNA adducts and damage associated with the carcinogens in smoke have been found in pharynx and larynx cells. Numerous studies have demonstrated that smokers have higher levels of DNA adducts in their larynx tissue samples than non-smokers.12,13 People who smoked more heavily had higher levels of DNA adducts in laryngeal cells.13 In one study, mutations caused by DNA adducts were found in pharynx and larynx tissue samples from smokers are were more prominent in larynx samples.14
Polycyclic aromatic hydrocarbons (PAHs) are cancer-causing chemicals (carcinogens) found in tobacco smoke. PAHs are predicted to cause mutations in the influential TP53 gene, found in laryngeal tumours.12 Reactive oxygen species (see Section 3.5.1.2) are present in tobacco smoke are implicated as a cause of squamous cell carcinoma of larynx.15
3.5.2.3 Factors affecting risk
Intensity and duration of smoking
Both the duration of smoking and the intensity of smoking (number of cigarettes per day) can increase the risks of pharyngeal and laryngeal cancer.16
A study that pooled data for oral and throat cancers also found that both intensity and duration of smoking increased the risks of these cancers, but that duration of smoking had a stronger effect than number of cigarettes per day.17 Longer duration and higher intensity smoking was found to be associated with increased risks of nasopharyngeal cancer18 as well as all pharyngeal cancers.16
A pooled analysis of 15 case–control studies found that the risk of laryngeal cancer was more strongly associated with greater intensity of smoking (cigarettes per day) than the duration of smoking.16
Viral infections
Human papilloma virus (HPV) infection is a known cause of cervical cancer (see Section 3.5.5.3). A 2016 meta-analysis concluded that there is a potentially significant casual relation between HPV infection and oropharyngeal cancers.19 It estimated that 12% of all pharyngeal cancers and 30–60% of oropharyngeal carcinomas are caused by HPV infection.20 HPV infection is associated with an increased risk of oropharyngeal cancer in people with and without a history of smoking.21
HPV-driven oropharyngeal cancer patients generally have a better prognosis than those who do not have the infection. However, smoking increases the risk of poor outcomes and mortality among these people.22,23 People with HPV-driven oropharyngeal cancers associated with smoking have poorer treatment responses and worse survival rates.22,24 People who smoke heavily (≥20 per day) who had HPV had over twice the risk of cancer recurrence and of mortality from oropharyngeal cancer compared with those who did not have HPV.25
Epstein Barr virus (EBV) usually causes infection with few symptoms and is latently carried by most people. EBV infection is an established cause of some types of cancer.26 Some studies suggest that early infection with EBV may play a causal role in nasopharyngeal cancer.27 One study has proposed that smoking could increase nasopharyngeal carcinoma risk by repeatedly reactivating latent EBV.28 However, smoking and EBV infection have been shown in another study to be independent risk factors for nasopharyngeal cancer.18 The relationship between smoking, EBV infection and nasopharyngeal cancer needs further investigation.
Alcohol consumption
Alcohol consumption is a risk factor for and cause of numerous cancers including pharyngeal and laryngeal cancers.29
A synergistic effect of tobacco and alcohol on the risk of laryngeal cancer has been found, where the risk from both is greater than addition of the individual risks.30 One study found that the risk of pharyngeal cancer from alcohol alone was 1.3-fold above non-drinkers, the risk from smoking alone was about 2-fold higher compared to non-smokers and the risks from drinking and smoking were 5.4-fold higher compared to that for people who abstained from both. The effects for laryngeal cancer were even greater for both risks factors: alcohol alone increased the risk 1.2-fold and smoking 6.7-fold, whereas those who both smoked and consumed alcohol had a 14-fold higher risk compared to abstainers.30
Smoking cessation
Smoking cessation reduces the risks of cancers of the pharynx and larynx.31 The excess risks of laryngeal and pharyngeal cancer are approximately halved within 10 years of cessation. Compared with continuing smoking, the excess risks for former smokers were reduced by approximately 30% within 5 years of cessation, 50% from 5 to 9 years after cessation and 80% by 20 or more years after smoking cessation.31 In 2007, the International Agency for Research on Cancer reported that, even after a long period of abstinence, the risks for laryngeal and oesophageal cancer do not return to that of never smokers.32
In one study, smoking cessation was associated with increased odds of survival for people with oropharyngeal cancer compared to continued smoking.33
3.5.2.4 Impact of smoking on prognosis
As described above in Section 3.5.1.4, smoking is associated with poor treatment outcomes and higher risk of dying from head and neck cancers (oral, nasal, sinus, laryngeal and pharyngeal cancers).
People who smoke at the time of diagnosis with either pharyngeal or laryngeal cancer have an increased chance of dying from that cancer over the next five years.23,34 A study that investigated the reasons for lower survival rates among people with oropharyngeal cancer found that smoking, as well as lower socioeconomic status, were influential factors, regardless of whether these people’s cancer was caused by HPV infection.35 One study has found that people with a higher intensity of smoking (25 pack-years or more) had a higher risk of their oropharyngeal cancer returning after initial treatment.36
People who continued to smoke after diagnosis with early-stage oral, laryngeal or pharyngeal cancer had an almost twice the risk of dying from that cancer compared to those who ceased smoking in one study.37
Related reading
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References
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