Lung cancer remains one of the deadliest diseases globally, with causes rooted in both lifestyle and environmental exposures. Two of the most well-established risk factors are cigarette smoking and asbestos exposure. While each poses a substantial risk on its own, the combined effect of smoking and asbestos exposure dramatically elevates lung cancer risk beyond either factor alone. This combined risk is known as a synergistic effect.
Asbestos is a naturally occurring mineral used extensively throughout the 20th century in construction, shipbuilding, and industry due to its durability and fire resistance. When disturbed, asbestos fibers can become airborne and are easily inhaled. Once inhaled, these fibers embed in lung tissue, causing inflammation, cellular damage, and long-term changes that can lead to asbestosis, mesothelioma, and lung cancer.
Cigarette smoke, meanwhile, contains thousands of chemicals, including potent carcinogens such as polycyclic aromatic hydrocarbons and nitrosamines. These substances damage lung cells directly, causing mutations that can eventually result in cancer.
Historically, the risk of lung cancer from smoking and asbestos was described as multiplicative—meaning the combined risk was much greater than the sum of individual risks. Seminal studies such as the one by Hammond et al. in the 1970s suggested that while asbestos exposure alone increased lung cancer risk fivefold and smoking elevenfold, the combination could raise risk up to 55-fold.
More recent research, however, reveals a more nuanced picture. In a 2015 meta-analysis, Ngamwong et al. reported that the synergy between smoking and asbestos was additive, not multiplicative, in most modern cohorts. The combined risk was greater than either exposure alone, but not exponentially so.
What explains the difference? The answer likely lies in exposure intensity.
The Impact of High vs. Low Exposure
Older studies involved workers in environments with extremely high fiber concentrations—such as shipyards, insulation work, or textile plants—combined with heavy smoking. These workers often inhaled large volumes of asbestos over decades. In such cases, the interaction appears multiplicative.
Contemporary studies often include workers in lower-risk environments or with less intense exposures. In these groups, the data support an additive risk model. However, in environments where asbestos exposure remains high—such as unregulated chrysotile factories in developing nations—recent studies still show near-multiplicative risk levels:
Wang et al. (2012) followed Chinese chrysotile workers for 37 years and found a lung cancer hazard ratio (HR) of 17.35 for workers who smoked and were exposed to asbestos, compared to non-smoking controls.
Suraya et al. (2020) in Indonesia reported an odds ratio (OR) of 8.70 for combined smoking and asbestos exposure, with both additive and multiplicative synergy indices confirming elevated risk.
These findings suggest that synergy varies by exposure level:
Low to moderate exposure: Additive synergy.
High, prolonged exposure: Multiplicative or near-multiplicative synergy.
Several mechanisms help explain the interaction:
Impaired clearance: Smoking damages the lung's natural defenses (e.g., cilia), reducing the ability to clear inhaled asbestos fibers.
Increased fiber retention: Smokers retain more asbestos fibers, increasing long-term damage.
Co-carcinogenesis: Asbestos fibers may act as carriers for tobacco carcinogens, delivering them deeper into lung tissue.
Genetic damage: Both asbestos and tobacco cause mutations in tumor suppressor genes like p53 and K-ras.
Chronic inflammation: Both exposures create oxidative stress and inflammation, increasing cancer risk.
While smoking significantly increases the risk of lung cancer in asbestos-exposed individuals, it does not cause mesothelioma. Mesothelioma is caused by asbestos exposure alone. Smoking does not increase the incidence of mesothelioma, though it may worsen overall respiratory health.
For individuals exposed to asbestos, smoking cessation is one of the most powerful tools to reduce the risk of lung cancer. Even if asbestos exposure occurred decades ago, quitting smoking can meaningfully lower ongoing cancer risk.
Employers and policymakers must ensure strict asbestos controls and smoking cessation programs for at-risk workers. Medical surveillance, early detection, and education are critical for high-risk populations.
The synergy between asbestos exposure and smoking in the development of lung cancer is well established—but the degree of synergy depends on exposure intensity. At low levels, the risk is additive. At high levels, especially in historically or currently unregulated environments, the risk becomes multiplicative.
No one should assume smoking alone caused their lung cancer if they were ever exposed to asbestos. And no one exposed to asbestos should ignore the profound impact that quitting smoking can have on reducing their cancer risk.
Ngamwong Y, et al. Additive Synergism between Asbestos and Smoking in Lung Cancer Risk: A Systematic Review and Meta-Analysis. PLoS ONE. 2015;10(8):e0135798. doi:10.1371/journal.pone.0135798.
Wang X, et al. A 37-year observation of mortality in Chinese chrysotile asbestos workers. Thorax. 2012;67(2):106–110. doi:10.1136/thoraxjnl-2011-200169.
Suraya A, et al. Asbestos-Related Lung Cancer: A Hospital-Based Case-Control Study in Indonesia. Int J Environ Res Public Health. 2020;17(2):591. doi:10.3390/ijerph17020591.
Hammond EC, Selikoff IJ, Seidman H. Asbestos exposure, cigarette smoking and death rates. Ann N Y Acad Sci. 1979;330:473–490. doi:10.1111/j.1749-6632.1979.tb18755.x.
