3.9 Increased susceptibility to infection in smokers

Smokers are at increased risk of infection, particularly respiratory infections.^1-3 People who smoke have an estimated 2.4-fold higher risk of pneumonia, a 1.8-fold higher of influenza and a 2-fold higher risk of other acute lower respiratory tract infections compared to never smokers.⁴ Smoking also increases the risk of dying from an infectious disease.⁵ People who are current smoke are approximately 3.7-fold times more likely to die from an infection compared to never-smokers, after adjustment for the effects of other risk factors.⁵

Smoking has substantial adverse effects on the immune system, both locally (such as in the respiratory tract and soft tissues in the lungs) and throughout the body. Inhaling the complex mixture of chemicals in tobacco smoke causes damage to the airways, directly affects invading pathogens and can reduce the effects of antibiotics.⁶ Smoking also causes diseases such as cancer (often requiring chemotherapy)⁷ and chronic obstructive pulmonary disease,⁸ which in turn can increase the risk of infections.

This Section examines evidence for the effects of smoking on acute respiratory infections: pneumonia, invasive pneumococcal disease, influenza, coronaviruses, as well as other types of infections, such as tuberculosis, meningococcal disease and HIV. Evidence regarding periodontitis is covered in Section 3.11.1 and surgical infection is discussed in Section 3.15.1. Chronic respiratory conditions such as chronic obstructive pulmonary disease and asthma are covered in Section 3.2.

3.9.1 Acute respiratory infections and the effects of smoke on immune responses

An acute respiratory infection is a sudden-onset infectious disease of the respiratory tract that may interfere with normal breathing. These infections include influenza, covid, respiratory syncytial virus (RSV), rhinovirus and whooping cough.⁹ Infections may occur in the upper respiratory tract, leading to symptoms in the nose, mouth, throat, sinuses or tonsils, or the lower respiratory tract, leading to bronchitis, bronchiolitis or pneumonia (infection of the lungs). Most acute infections of the respiratory tract are caused by viruses or bacteria, but some rarer infections are fungal or parasitic. Some of these infections spread to both upper and lower respiratory tracts. Specific acute infections of the respiratory tract are discussed in Sections 3.9.3, 3.9.4 and 3.9.12.

Exposure to tobacco smoke is a substantial risk factor for many acute respiratory infections. Both active and passive smoking increase the risk of respiratory infections.^1,10 Smoking can also increase the duration and/or severity of respiratory infections caused by numerous types of viruses and bacteria.¹¹ The incidences of respiratory infections are higher in people who smoke, taking into account potential confounding from sources such as socioeconomic status, age, ethnicity, alcohol and some other risk-taking activities. It is therefore likely that smoking has a causal role in acquiring acute respiratory infections. For people with sepsis, a life-threatening reaction to infection, the risk of dying from this condition is higher for people who smoke (see Section 3.9.11.2).¹²

The mechanisms causing the enhanced susceptibility to respiratory infections in people who smoke are multifactorial and include alterations in structural and immune defences.  The structural changes caused by smoking include inflammation, fibrosis (formation of disruptive scar tissue), changes to pathogen adherence and disruption of the respiratory epithelium (cells lining the surface of the respiratory system).¹ As described in Section 3.2.1.1, exposure to cigarette smoke disrupts the process of mucociliary clearance, which removes particles from the lungs. Immunological alternations are described below.

Exposure to tobacco smoke disrupts the normal functioning of the immune system that fights infection in the respiratory tract.¹ There is evidence that smoking disrupts innate immune responses (first-line defence) and adaptive immune responses (longer-term, more specific  defence) in the respiratory tract. Smoking may also have pathogen-related effects that increase infection rates. These likely include an increase in the virulence (harmfulness) of bacteria with smoke exposure, increase in the ability of pathogens to adhere to respiratory tract membranes and increase in resistance to antibiotics.¹³ There is evidence that people who smoke have changes to the balance of normal microbial communities (the microbiota) of the upper respiratory tract, which are thought to contribute to the prevalence of respiratory tract complications.^14,15

Smoking may cause an increase in the numbers of white blood cells (immune cells) in the blood and lung fluids, consistent with harmful effects of inflammation. Smoking also causes impairment of the normal functioning of immune cells such as neutrophils, lymphocytes, macrophages and natural killer cells, reducing their ability to clear infections.¹³ Smoking leads to a decrease in circulating antibodies and a depression of antibody responses, reducing the body’s ability to fight invading pathogens.¹

A considerable research effort has examined the changes caused by tobacco exposure on a molecular level that may be contributing to disrupted immune responses. Some examples of these changes are: suppression of RIG-I-initiated immune responses to influenza,¹⁶ suppression of NLF IL-6 nasal inflammatory and anti-viral responses,¹⁷ repression of responses to bacteria through NF-kappaB (a master regulator of critical defence genes),¹⁸ inhibition of pulmonary T-lymphocyte responses to influenza and tuberculosis,¹⁹ inhibition of type II interferon responses (antiviral mechanisms) in airway epithelial cells¹¹ and a decrease in the amount of intelectin 1 (an immune defence protein) in the airways.²⁰

3.9.2 Chronic respiratory infections

See Section 3.2.5 for discussion of chronic respiratory diseases such as chronic bronchitis and chronic obstructive pulmonary disease (COPD). Tuberculosis infection of the lungs is a chronic infectious disease that often lays dormant in the lungs for many years. See Section 3.9.5 for more information about tuberculosis.

3.9.3 Pneumonia and pneumococcal disease

3.9.3.1 Pneumonia

Pneumonia is an inflammatory disease of the lungs that is most often caused by acute infections. The pathogens causing pneumonia are usually bacterial or viral, sometimes fungal and, rarely, parasites. The most common bacterial infections causing pneumonia in adults is Streptococcus pneumoniae (pneumococcus). Rhinoviruses, influenza viruses, coronaviruses, adenoviruses and respiratory syncytial viruses are common causes of viral pneumonia, particularly in children. Hospital-acquired pneumonias are usually caused by bacterial infection, whereas community-acquired pneumonias are caused by infection with a wide range of different pathogens.²¹

Evidence from several studies confirms that smoking is significantly associated with the development of bacterial and viral pneumonia.^1,10,22,23 A 12-year study of over 340,000 people showed that people who smoke had a 2.4-fold higher risk of pneumonia compared to never-smokers.⁴ Exposure to tobacco smoke suppresses the activation of innate immune responses to bacterial infection; the front-line defence mechanism considered important in susceptibility to pneumonia.^24,25

Smoking is an especially prominent risk factor for pneumococcal pneumonia in patients with chronic obstructive pulmonary disease (COPD). But even without COPD, smoking remains a major risk factor.¹ There are reported estimates ranging from almost 2-fold to 4-fold increased odds of pneumococcal pneumonia among people who smoke. Exposure to secondhand smoke has been found to more than double the chances of this infection compared with non-exposed non-smokers.¹ A 2010 review indicates active smoking,²⁶ and other studies indicate secondhand smoke exposure^27,28 as factors that predispose the elderly population to pneumonia.^26,28

Exposure to tobacco smoke is significantly associated with the development of community-acquired pneumonia. People who currently smoke have a 2.8-fold increased risk of community-acquired pneumonia and former smokers have a 1.5-fold increased risk compared to people who have never smoked.²⁷ Evidence from several longitudinal studies conducted in large populations suggests a significant increase in pneumonia-associated mortality in people who smoke compared with non-smokers (but other evidence to-date from cross-sectional studies and meta-analyses is inconsistent).^2,29

There is evidence that smoking is an independent risk factor for Legionnaires disease, an atypical pneumonia that usually develops two to 14 days after exposure to L. pneumophila.^23,30

3.9.3.2 Invasive pneumococcal disease

Invasive pneumococcal disease, caused by S. pneumoniae, results in conditions such as pneumonia, bacteraemia (bacteria in the bloodstream) and meningitis (inflammation of the meninges, the membrane lining of the brain and spinal cord). A study from 2000 found a 4.1-fold increased chance of developing invasive pneumococcal disease for people who smoke compared to non-smokers.³¹ The chances of infection for people exposed to secondhand smoke were 2.5-fold higher than those unexposed.³¹ There was also a dose–dependent association for pack-years of smoking and time since quitting. This study found that 51% of cases of invasive pneumococcal disease could be attributed to smoking.³¹ A study of healthy young and middle-aged adults (up to the age of 64 years) also showed an increased risk of invasive pneumococcal disease associated with smoking. People who currently smoke had 2.6 times greater odds of infection compared to non-smokers^1,32 This study predicted that 31% of pneumococcal disease cases in this group could have been avoided if these people did not smoke.

3.9.4 Influenza

Influenza is a highly contagious acute viral infection of the upper and lower respiratory tracts. In severe cases, it causes fluid build-up in the lungs that makes breathing difficult and inhibits oxygen reaching the blood.

The 1964 US Surgeon General’s report found that people who smoke had a modestly increased risk of death from influenza.³³ The 2014 report of the US Surgeon General states that there is epidemiological evidence of increased risk of influenza in people who smoke.³⁴ An increased risk for young people who smoke during influenza epidemics has also been reported.^35,36 Whether smoking is a cause of this increased risk has not been assessed by Surgeon General reports.

Published after the 2014 US Surgeon General’s report, two meta-analyses have found an increased risk of influenza infection for smokers. The first of these studies found a 5.7-fold higher chance of developing influenza for people who currently smoked compared to non-smokers.³⁷ People who smoke also had a 1.34-fold higher chance of developing influenza-like illness compared to non-smokers. The second study found a 1.5-fold increase in hospital admissions and 2.2-fold increase in admissions to intensive care after influenza infection for people with a history of smoking (>100 cigarettes) compared to never-smokers.³⁸ This study also found some evidence that children under 15 exposed to secondhand smoke had a higher chance being treated in hospital after influenza infection. A 2023 study of over 340,000 people has found a 1.8-fold higher risk of influenza for people who smoke compared to never-smokers.⁴

3.9.5 Tuberculosis

3.9.5.1 Smoking increases the risk of tuberculosis

Tuberculosis is a chronic infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis. It typically attacks the lungs but can also affect other parts of the body. Globally, tuberculosis is one of the top 10 causes of death and the leading cause from a single infectious agent.³⁹ Approximately a quarter of the world’s population are believed to have been infected, but most of these people have latent tuberculosis – they do not have symptoms or spread the disease, but there is a risk that the disease could be activated, leading to active tuberculosis illness. In high-income countries, tuberculosis is controlled by effective public health systems. However, in countries where symptomatic disease is endemic, control remains a huge challenge; one that is exacerbated as multidrug-resistant strains continue to evolve.⁴⁰ Australia has one of the lowest incident rates of tuberculosis in the world at 5.8 cases per 100,000 people in 2018.⁴¹ Most cases (86 to 89%) occurred in people born overseas.⁴¹

Globally, Indigenous peoples generally have a higher prevalence of tuberculosis, and are more likely to experience risk factors for tuberculosis than non-Indigenous people, such as smoking.⁴² Aboriginal and Torres Strait Islander peoples have a 4-fold higher incidence of active tuberculosis than non-Indigenous Australians.⁴¹

The US Surgeon General’s report in 2014 was the first in its series to address the evidence regarding smoking and risk of tuberculosis. It concluded that smoking causes both an increased risk of tuberculosis illness (from M. tuberculosis infection) and increased risk of mortality from tuberculosis. Smoking was also suggested as causing an increased risk of recurrence of symptomatic tuberculosis.³⁴

A meta-analysis found that people who currently smoke have approximately double the risk of active tuberculosis and double the risk of latent tuberculosis compared to non-smokers.⁴³ Some studies estimate that at least one in five deaths from tuberculosis could be avoided if these people were non-smokers.^44-46 There is also evidence that smoking is associated with a delay in diagnosis with tuberculosis and it increases the severity of tuberculosis illness.^47,48

Exposure to secondhand smoke is also a risk factor for the development of tuberculosis,⁴⁹ especially in children.⁴³

A meta-analysis has shown that former smokers had a 1.7-fold increased risk of active tuberculosis compared to non-smokers, which is a lower estimate of risk than those for active smoking.⁴³ Quitting smoking and prevention of exposure to secondhand smoke are therefore both important measures in the control of tuberculosis.^23,50

3.9.5.2 Smoking increases the risk of poor treatment outcomes for tuberculosis

Smoking increases the risk of a poor treatment outcome for tuberculosis.^51,52 A meta-analysis has shown that the risk of a poor treatment outcome (treatment failure or death) is higher for people who smoke compared to non-smokers.⁵¹ The effect was worse in low-income countries with a 1.74-fold increased risk for people who smoke, compared to 1.34-fold increased risk in high-income countries.⁵¹ A meta-analysis has found a 2.1-fold increased risk of tuberculosis recurrence (reactivation of the disease after successful treatment) for people who smoke compared to non-smokers.⁵³ Smoking also increased the risk of diagnosis with secondary multidrug-resistant tuberculosis.⁵⁴

3.9.5.3 How smoking affects the risk of tuberculosis

Smoking may increase the access of tuberculosis bacteria to the lungs. In people who smoke, the protective actions of muco-ciliary clearance (see Section 3.2.1.1) are reduced, which increases the chances of particles reaching the lungs. Exposure to cigarette smoke can also weaken the defences of the macrophages in the lungs – the cells in which the tuberculosis bacteria enter and live for a long time.⁴⁷ 

3.9.6 Risks for and complications of HIV

Human Immunodeficiency Virus (HIV) infection causes Acquired Immunodeficiency Syndrome (AIDS) if untreated. HIV is transmitted via unsafe sex, sharing of contaminated needles, breastfeeding, or medical procedures using contaminated equipment or blood. By the end of 2023, there were an estimated 39.9 million people living with HIV, with over 42.3 million lives claimed by the disease in total.⁵⁵ In high-income countries, most people infected with HIV are successfully treated with antiretroviral drugs, preventing development of AIDS and reducing transmission of the virus. The situation in low- and middle-income countries is improving thanks to international efforts to address the pandemic. In 2018, an estimated 62% of adults and 54% of children living with HIV in low- and middle-income countries were receiving lifelong treatment with antiretroviral drugs. Worldwide, an estimated 630,000 people died from HIV-related causes in 2023 and 1.3 million were infected that year.⁵⁵ Australia’s incidence of HIV remains relatively low, with 2.2 notifications of infection per 100,000 people in 2022.⁵⁶

People with HIV are known to have a higher prevalence of smoking than the general population. However, smoking is not generally considered to be a risk factor for HIV infection as it is also associated with other risk-taking activities that may increase the risk of infection.⁵⁷ The authors of a 2007 systematic review suggest that smoking may be an independent risk factor for acquiring HIV infection⁵⁸ but this finding is inconsistent with other reviews.² Research into the association between smoking and HIV disease progression has produced inconsistent findings.⁵⁹

Effective antiretroviral therapy has greatly improved the lives of people with HIV, who now have a life-expectancy approaching that of people without HIV if they are treated.⁶⁰ However, HIV-positive people have an increased risk of ageing-related diseases such as cancer, liver disease and cardiovascular disease. The higher rates of smoking and use of alcohol and other drugs by people with HIV are likely to contribute to this increased morbidity, as well as other factors associated with HIV and its treatment.⁶¹ Studies have found that the life-expectancy of HIV-positive people who smoke is reduced by an estimated 16 years.^61,62

Among people with HIV, smoking may increase the risk of developing oral candidiasis (a fungal infection) and bacterial pneumonia.³⁴ Women with HIV who smoke also have a higher risk of infection with high-risk HPV strains (see Section 3.5.5.3) that can lead to cervical cancer.⁶³ A review concluded that social class, intravenous drug use and compliance with the antiretroviral treatment program are factors that may interact with smoking behaviour, and the independent role of these factors may be difficult to assess in relation to the outcome of HIV infection.²  

People with HIV who smoke are at increased risk of the HIV complication HAND (HIV-Associated Neurocognitive Disorder) which is characterised by disruption of the blood-brain barrier and cognitive impairment. There is some evidence that nicotine from tobacco exposure is involved in the development of HAND in HIV-positive people who smoke.⁶⁴ 

3.9.7 Other viral infections

Secondhand smoking increases the risks of otitis media (middle ear inflammation and infections) in children. Otitis media disproportionately affects Aboriginal and Torres Strait Islander children and leads to high rates of disability and learning difficulties—see Section 8.7.4. Both viral and bacterial infections are common in this condition.^13,65 Tobacco smoke is predicted to delay or worsen the recovery of otitis media by causing inflammation and swelling in the Eustachian tubes.⁶⁶ See Section 4.17.6 for more information about secondhand smoke and otitis media.

Smoking may indirectly lead to adverse outcomes such as the increased risk of hepatocellular carcinoma (cancer of the liver) due to smoking-related progression of chronic viral hepatitis.²

People who smoke are more likely to have infections with Epstein Barr Virus (EBV) and cytomegalovirus (CMV).⁶⁷ Whether smoking causes these infections is currently unknown.

3.9.8 Infections of the reproductive system

A small number of studies have investigated the association between smoking and infections of the reproductive system.

Bacterial vaginosis (a bacterial infection of the vagina) can cause considerable discomfort. It may lead to more serious infections such as septicaemia and increase the risk of poor pregnancy outcomes. A review found that smoking is significantly associated with bacterial vaginosis, typically being around twice as common in women who smoke as non-smokers, with a greater prevalence noted in young women.⁶⁸ Tobacco use was also independently associated with a higher prevalence of sexually transmitted chlamydia and gonorrhoea (both bacterial infections).²³

Human papillomavirus (HPV) is a highly contagious virus spread by sexual contact. Most infected people do not have symptoms or long-term consequences. However, for some people, infection with high-risk strains of HPV causes cancers of the cervix, vulva, vagina, penis and anus, or throat.⁶⁹ Cervical cancer incidence in Australia has dropped from 14 cases per 100,000 females in 1982 to 3.8 per 100,000 females in 2024, after the screening program for HPV infection was introduced in 1991.⁷⁰ Increasing the duration of high-risk HPV infection of the cervix is predicted to be one way in which smoking increases the risk of cervical cancer.^71,72 See Sections 3.5.2 and 3.5.5 for more information about throat cancer and cervical cancer associated with smoking and HPV infection.

3.9.9 Periodontitis (see Section 3.11.1)  

3.9.10 Surgical infections (see Section 3.15.1)

3.9.11 Other types of infections

3.9.11.1 Meningococcal disease

Meningococcal disease describes infections caused by Neisseria meningitidis, also known as meningococcal bacteria. Meningococcal bacteria are a cause of meningitis (infection and inflammation of the membrane lining of the brain and spinal cord). Meningococcal bacteria are also one of several pathogens that can cause septicaemia (blood poisoning) and sepsis (see below at 3.9.11.2).⁷³ Although meningococcal disease is rare in Australia, it has a high mortality rate. There were 142 notifications of invasive meningococcal disease in Australian in 2023.⁷⁴ Approximately 10% of infected people die from this disease, and 10–20% of survivors had long-term health problems.⁷⁵

There is evidence that tobacco smoke exposure is associated with an increased risk of developing meningococcal disease.^2,76,77 A meta-analysis found that young people (15 to 24 years) had a 1.5-fold increased chance of meningococcal disease if exposed to active or passive smoking.⁷⁷ However, a high risk of bias and a lack of prospective studies in this meta-analysis means that more research is required to confirm this association.⁷⁷

 One study found that children under 18 years of age had almost four times the odds of acquiring meningococcal disease if they were exposed to maternal smoking. All age groups had more than a doubling of odds from active smoking or from exposure to secondhand smoke compared to no exposure. There was a dose–response relationship between exposure to secondhand smoke and the risk of meningococcal disease in all age groups.⁷⁶ Smoking also was found to be a risk factor for an outbreak of meningococcal disease in adults in Italy in 2015.⁷⁸

3.9.11.2 Sepsis

Sepsis is a serious condition that arises from infection, where the body is damaged by strong immune responses. The initial infection could be viral, bacterial or fungal in origin. A 10-year follow-up study found that people who smoke had a higher risk of sepsis.⁷⁹ In this study, both people who currently smoked and former smokers had higher risks, and those who smoked with greater intensity had higher risk compared to lesser intensity.⁷⁹ A meta-analysis has shown that, when patients are followed up for at least 2 months, the risk of death for sepsis is 2.3-fold higher for people who smoke compared to non-smokers.¹² Sepsis patients also needed a longer hospital stay and were more likely to need mechanical ventilation if they smoked.⁸⁰

3.9.11.3 Other types of bacterial infections

There is evidence that smoking may cause an increased risk of peptic ulcer disease owing to an increased susceptibility for Helicobacter pylori infection.^2,81 See Section 3.12.1 for more information.

Tobacco smoke may be directly affecting bacteria, making it easier for them to grow on biological and non-living surfaces, in microbial communities called biofilms. There is evidence that tobacco smoke chemicals alter the surface of bacteria and promote biofilm formation, increasing the growth of several important human pathogens.⁸² These include Staphylococcus aureus (known as “Golden Staph” which can cause serious infections spread through hospitals), Streptococcus mutans (which can cause tooth decay), Klebsiella pneumonia (causes pneumonia, urinary tract infections, infected wounds and other problems), Porphyromonas gingivalis (involved in periodontal disease and also found  in the gastrointestinal tract) and Pseudomonas aeruginosa (causes a serious hospital-acquired pneumonia).⁸²

3.9.11.4 Fungal infections

A meta-analysis has found a 2.15-fold increased risk of oral infection with Candida species for people who smoke, compared to non-smokers. There was also a 1.8-fold increased risk for those who used smokeless tobacco. Whether tobacco use is a cause of this increased risk requires further research.⁸³

Invasive fungal disease is a serious risk for people who are immunocompromised – such as people who take medications after transplant surgery or for autoimmune diseases. Invasive fungal diseases are caused by fungal infections, such as Candida and Aspergillus species, in deep-seated tissues. A meta-analysis has found that people who smoke are at 1.4-fold increased risk of invasive fungal disease compared to non-smokers.⁸⁴ The studies covered in this meta-analysis included a broad range of people in both community and hospital settings, many of which were immunocompromised and others who were not. There is some evidence that non-immunocompromised people who smoke are at higher risk of invasive fungal disease than non-smokers.⁸⁵

3.9.12 Coronaviruses and the COVID-19 pandemic

Coronaviruses are a broad group of related viruses that cause respiratory tract infections with varying severity. There are four strains of coronavirus that usually cause disease of low severity and three that have caused recent outbreaks with significant morbidity and mortality. Coronaviruses with low virulence cause illnesses such as the common cold, whereas more dangerous forms cause severe respiratory syndromes such as Middle East Respiratory Syndrome (MERS), with a 35% mortality rate. About 15% of common colds are estimated to result from coronavirus infections. Aside from the common cold coronaviruses sometimes infect the lower respiratory tract, leading to pneumonia, bronchitis, bronchiolitis and croup.⁸⁶ Three coronaviruses that infect both the upper and lower respiratory tracts have been responsible for serious outbreaks with high mortality rates: SARS-CoV-1, (causing the 2002-2004 Severe Acute Respiratory Syndrome (SARS) outbreak), MERs-CoV (causing MERS outbreaks from 2012) and SARS-CoV-2 (causing the COVID-19 pandemic).^87,88 People infected with SARS or MERS viruses have symptoms ranging from mild to severe.

3.9.12.1 SARS and MERS outbreaks since 2002

Recombination events, that mix the genetic material of viruses, are predicted to have given rise to new forms of coronaviruses that cause serious outbreaks. The pathogenic SARS-CoV and MERS-CoV viruses are predicted to have recent origins in animals such as bats (SARS) and camels (MERS).^88-90 The 2002-2004 SARS-CoV outbreak had a reported total of over 8,000 cases and 774 deaths. The outbreak had a case fatality rate of 9.6%. Cases were reported in 29 countries with the vast majority in China and Hong Kong.⁹¹ MERS outbreaks have occurred in 2012, 2015 and 2018, with most cases in the Middle East and South Korea. From 2012 to April 2020, 2,494 cases have been reported in over 27 countries, with 858 deaths. This is a case fatality rate of 34.4%.⁹² Strict public health measures, contact tracing and surveillance were used to control these epidemics.

Australia has been affected by six suspected cases of SARS from the 2002–2004 outbreak but no cases of MERS as of 2020.^93 94 There have been no deaths from MERS or the SARS 2002–2004 outbreak reported in Australia.

Smoking is predicted to be a risk factor for MERS-CoV infection.⁹⁵ Whether smoking was a risk factor for SARS-CoV during the 2002­–2004 epidemic has not been definitively reported.

3.9.12.2 COVID-19 pandemic

The COVID-19 pandemic was caused by an outbreak of the new SARS-CoV-2 virus, originating in China in late 2019.^96,97 Spreading worldwide, the COVID-19 pandemic has caused over 670 million reported infections and led to over 6.8 million deaths (as of January 2025).⁹⁸ Effective public health measures such as the vaccination rollout have led to a relatively low number of deaths and low case fatality rate in Australia compared to many other countries. As of January 2025, there have been over 11.4 million reported infections and 19,578 deaths from the COVID-19 pandemic in Australia.⁹⁸

3.9.12.3 Association of smoking with the incidence of COVID-19

The effects of smoking on COVID-19 infection have been subject to hundreds of studies and numerous meta-analyses. Overall, smoking does not increase the risk of covid-19 infection and people who smoke are less likely to get COVID-19 than non-smokers. However, many of the studies described below are potentially affected by bias, which may have distorted the results. In particular, there is evidence that people who smoke are more likely to be tested for COVID-19 infection than non-smokers. There is little high-quality research to support a specific protective mechanism by which covid might be reducing the risk of covid infection.⁹⁹  

A publication in the Lancet Infectious Diseases journal in May 2020 aimed to determine risk factors for COVID-19 diagnosis.¹⁰⁰ Among the factors associated with increased risk were age, ethnicity, obesity and living in urban and underprivileged areas. In this study, active smoking was associated with a lower odds of diagnosis. People who smoked had approximately half the chance of testing positive. Several plausible explanations for this are proposed, including issues with study bias and accuracy of testing, as well as the possibility that smoking is protective against infection. The study authors state that their “findings should not be used to conclude that smoking prevents SARS-CoV-2 infection, or to encourage ongoing smoking, particularly given the well documented harms to overall health from smoking, the potential for smoking to increase COVID-19 disease severity, and the possible alternative explanations for these findings.”¹⁰⁰ 

Multiple studies from at least 20 countries have similar findings, summarised in a living rapid evidence review.¹⁰¹ These studies generally support a lower-than-expected current smoking prevalence in people diagnosed with COVID-19 disease. The relative risk of COVID-19 diagnosis for current compared to never smokers was 0.67. The prevalence of former smokers was more similar to the population prevalence in these studies, with a relative risk of diagnosis for former compared to never smokers of 0.99.

Two studies have examined smoking rates among Australians hospitalised with COVID-19. Among 172 critically ill COVID-19 patients, 12.2% reported a history of smoking.¹⁰² In this cohort, people who smoked were older and had a higher incidence of chronic comorbidities. Although this rate of smoking is lower than that among equivalent (COVID-19-negative) intensive care patients (20.3%), it’s similar to the current population prevalence of smoking in Australia. A second Australian study identifying COVID-19-positive people among those presenting to emergency departments also found a rate of smoking prevalence among those testing positive for SARS-CoV-2 that was similar to smoking prevalence among the total Australian population—about 10%.¹⁰³ Interestingly, in this study of over 30,000 presentations, non-smoking status was reported to be a risk factor for COVID-19 infection. Smoking prevalence in those presenting with COVID-19 was 10%, compared to 38% for people presenting without the infection. Together, these studies indicate that the prevalence of smoking in people hospitalised with COVID-19 in Australia is very similar to the Australian population prevalence of smoking, but lower than expected for those admitted to hospital.

Given the effects of smoking in causing lung damage, weakening the immune system and increasing susceptibility to lung infections, the lower prevalence of smoking in people diagnosed with COVID-19 indicated in these studies was unexpected. A number of issues complicate interpretation of the current results, as described by the living review authors.¹⁰¹ Certain groups of people, based on age, gender, geographical location and socioeconomic status, are more likely to be exposed to the virus at different times during the pandemic. These groups of people have different levels of smoking. It’s possible that people who were more likely to be exposed were less likely to smoke. Younger people, who are less likely to smoke, may be less likely to have symptoms, meaning that they are less likely to be tested for infection. More than half of these studies have collected data from hospitalised patients only. This is a source of potential bias, such as collider bias (see Griffith et al 2020 and Tattan-Birth et al 2020)^104,105 which may have distorted the results indicating association of current and former smoking with COVID-19 diagnosis.

Many of the studies of COVID-19 diagnosis suffer from selection bias. This occurs because the people being tested are not usually chosen at random; they present at clinics for testing for a variety of reasons. One type of selection bias is that people who smoke are more likely to be tested than non-smokers, possibly because they tend to suffer more frequent coughs and other respiratory symptoms. This would mean that tests of people who smoke are over-represented in the samples of these studies. This could increase the denominator in studies that measure the rate of positive tests, artificially decreasing the rate of testing positive for people who smoke. This hypothesis is supported by three studies. In a study of US military veterans an overall average of 23.8% of the sample received a COVID-19 test, but 42.3% of people who currently smoked received the test.¹⁰⁶ A study from the UK found that current (1.29-fold) and former smokers (1.44-fold) were more likely to receive a test in a multivariable analysis.¹⁰⁷ In an Australian rapid assessment screening clinic, of all those who attended the clinic, current compared with former or never smokers may have been less likely to have met criteria for (i.e. to have been deemed sufficiently at risk to require) a test (RR = 0.93, 95% CI = 0.86-1.0, p = 0.045).¹⁰⁸

In contrast, two cohort studies—one in the UK^109,110 and in one China¹¹¹ have suggested that smoking is a risk factor for COVID-19 incidence, not a protective factor. However, the body of evidence to date suggests that smoking is not a risk factor for covid.¹⁰¹

3.9.12.4 Association of smoking with the severity of COVID-19 disease

Severity of COVID-19 disease is often measured as the need for hospitalisation, intensive care admission, use of ventilation, death or a combination of these measures. Overall, there is evidence that a history of smoking is a risk factor for the severity of COVID-19 disease. However, a trend in the data indicates a greater risk for former smokers than for people who currently smoke.

A living rapid evidence review combined data from multiple studies to assess COVID-19 disease severity in current, former and never-smokers.¹⁰¹ Current and former smokers were at increased risk of hospitalisation with COVID-19, but the evidence was not conclusive for current smokers. Current and former smokers had a higher risk of severe COVID disease compared to never-smokers. These results showed a small but important increase in the risk of severe disease for people who currently smoke. Both current and former smokers were at increased risk of dying from COVID disease but the evidence was inconclusive for current smokers.¹⁰¹ As described above, numerous issues, such as potential collider bias, complicate the interpretation of these results.

Other meta-analyses assessing the association of smoking with COVID-19 severity have had mixed results. A meta-analysis of 18 studies, including over 5,000 people, found that people with COVID-19 who smoked were less likely to be hospitalised (OR = 0.18).¹¹² However, a meta-analysis of 60 studies, with over 50,000 people in 13 countries showed a higher in-hospital mortality risk for smoking (OR = 1.6).¹¹³ Smoking was more strongly associated with mortality for people 60 years of age and under. People who currently smoke also had an increased risk of severe COVID-19 disease (RR 1.80) in a meta-analysis of 47 studies, reporting on >32,000 hospitalised people with COVID-19 disease.¹¹⁴ People with a history of smoking had an increased risk of severe disease (RR =  1.29) and death (RR = 1.28) in a large meta-analysis of 77 studies, including almost 39,000 people. However, this meta-analysis did not consider current and former smokers separately and included many studies that did not examine other factors that could potentially explain the relationship.¹¹⁵ A number of longitudinal studies have also shown an increase risk of severe disease and hospitalisation among people with COVID-19 who smoke.^116,117,118

3.9.12.5 Smoking and COVID-19 disease severity in people with other serious illnesses

Smoking appears to be associated with poor outcomes for people with COVID-19 together with other serious illnesses. A meta-analysis of 15 studies, including 2,473 COVID-19 patients, showed that people with chronic obstructive pulmonary disease (COPD) who smoked were at greater risk of severe complications or death from COVID-19 compared to former or never smokers with COPD.¹¹⁹ COPD was also associated with poor outcomes in a pooled analysis of data from over 4,000 people.¹²⁰ A study of 928 patients from the US, Canada and Spain with a range of cancers showed that smoking status was also associated with more severe COVID-19 disease or death.¹²¹ A registry-based study of people with thoracic cancer and COVID-19 infection showed that a history of smoking was independently associated with increased risk of death from COVID-19. People in this study with a history of smoking had a 3.18-fold higher odds of dying, compared to never smokers.¹²² In a study from the US, people with lung cancer and COVID-19 were almost 3-fold more likely to have severe disease if they had a history of smoking.¹²³ Smoking was strongly associated with mortality for people with COVID-19 who had urgent surgery for hip fractures.¹²⁴ Diabetes is consistently associated with poorer outcomes from COVID-19. A more recent meta-analysis of studies using multivariate analysis showed that diabetes and age were associated with death from COVID-19 but that smoking was not.¹²⁵

3.9.12.6 The effect of smoking on COVID-19 vaccination

There are a number of effective vaccines for SARS-CoV-2 that have been taken by millions of people worldwide. COVID-19 vaccination induces long-lived immune responses that reduce the chances of being infected with the virus, reduce the chances of severe disease and death for those who do become infected,¹²⁶ and reduce the chances of long covid.¹²⁷

The two main types of immune responses induced by COVID-19 vaccines, as well as most vaccines, are antibody production and T-cell responses to the virus.^128-130 Studies have shown that the immune mechanisms that underlie covid vaccine efficacy are multifactorial, including antibodies, which drop in level after vaccination, and T-cell response that provide more durable and cross-reactive immunity against different strains of the virus.¹³¹ Factors that reduce the immune responses to the COVID-19 virus have the potential to reduce the effectiveness of COVID-19 vaccines. The effects of smoking on vaccinated people have been studied for numerous COVID-19 vaccines.^132,133

Antibody responses to the covid virus in vaccinated people

A systematic review of effects of smoking on antibody production found that most (17 out of 23) studies showed that vaccinated people who smoked had much lower antibody concentrations, or more rapid lowering of the vaccine-induced antibodies over time, compared with non-smokers.¹³² However, most the studies looked at total antibody concentration, not specifically at neutralising antibodies, which would be more effective. Most of these studies examined antibody levels in people who had two doses of the Pfizer mRNA virus, the Sinovac whole-inactivated virus or the Astra Zeneca adenoviral vaccine. For the Pfizer vaccine, many studies have shown that the total antibody concentration, or concentration antibodies targeting the receptor binding site of the virus spike protein, were lower in people who smoked than non-smokers. The association of smoking with lower antibody levels remained apparent once other potential risk factors were taken into account.^134-139 One study measured neutralising antibody activity in 587 health care workers in Spain who had either Pfizer or Moderna mRNA vaccines. This study showed that smoking was associated with lower neutralising Ab levels compared to non-smokers, after taking into account the effects of other risk factors.¹³⁹

In a study of 55 Japanese people who smoked, the concentration of antibodies that target the receptor binding domain of the COVID-19 spike protein was lower in people with higher nicotine dependence, but not with serum cotinine, a biomarker for nicotine intake. These results indicate that stronger smoking dependence may have a greater effect on reducing antibody levels after mRNA vaccination, however more studies are required to confirm this result.¹⁴⁰

Whilst the mechanism by which smoking reduces the production of antibodies after COVID-19 vaccination is unknown, this phenomenon is consistent with a diminished antibody response to vaccines for numerous other pathogens.^141-144

T-cell responses to the covid virus in vaccinated people

T-cell immunity to the covid-19 virus has been studied for the Pfizer BNT162b2 vaccine. Unexpectedly, in one study the people who currently smoke had a greater chance of increased duration of T-cell responses compared to people who never smoked.¹⁴⁵ Another study of T-cell responses for people who had that same vaccine did not find a correlation of T-cell activity and smoking for people with detectable T-cell responses.¹⁴⁶ But a high proportion (67%) of those without detectable T-cell responses smoked, indicating that smoking might be a factor that affects the establishment of a T-cell response.¹⁴⁶ Given the apparent conflicting results of these two studies, more research is needed to determine the effects of smoking on T-cell responses for covid-19 vaccines.

3.9.12.7 Association of smoking and “long covid”

A subset of people infected with the COVID-19 virus develop a longer-term condition characterised by persistent symptoms, called “long covid”. The results of a number of large studies indicate that smoking may be a risk factor for developing long covid. In study of over 600,000 people infected with COVID-19 in England, smoking was associated with persistent covid symptoms lasting 12 weeks or more.¹⁴⁷ A study of over 500,000 adults with covid infection (and a control group with over million people) found that smoking was a risk factor for developing long covid with symptoms extending beyond 12 weeks after infection.¹⁴⁸ A study of over 100,000 US adults found that both current and former smokers had 1.2-fold increased chances of getting long covid.¹²⁷  

3.9.12.8 Potential mechanisms for the effect of smoking on COVID-19 infection and outcomes  

As described in 3.9.12.4, smoking appears be a risk factor for COVID-19 disease severity. There are numerous possible mechanisms by which smoking may be increasing risk. Smoking has a strong negative effect on respiratory health, causing chronic inflammation and reducing immune responses. Older age and underlying health problems are common in those with more severe COVID-19 disease and mortality. Smoking causes several conditions that are independently associated with poor outcomes from COVID-19. These include COPD, diabetes and cardiovascular diseases.³⁴ These pre-existing conditions seem to increase the vulnerability of patients to COVID-19 severity. By increasing the rates of COPD and cardiovascular diseases in people who smoke, smoking is likely to indirectly increase COVID-19 disease severity and mortality.

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