Abstract
The United Kingdom's recently enacted Tobacco and Vapes Bill introduces a “generational smoking ban,” prohibiting tobacco sales to anyone born after 2008. While this landmark legislation is intended to reduce the country's burden of cancer, cardiovascular disease, and stroke, it also may have an unintentional impact on the incidence of Parkinson's disease (PD). Convergent data from observational and genetic studies indicate that non-smokers have approximately double the risk of developing PD compared to smokers. Together with preclinical data, these epidemiologic results support a potential neuroprotective effect of tobacco constituents. The new UK public health policy creates a valuable opportunity to assess prospectively whether reduction in smoking leads to a measurable increase in the age-adjusted incidence of PD, in addition to a much larger decrease in diseases known to be caused by smoking. This natural experiment may paradoxically help prevent PD, both in the long-term by enhancing our understanding of its causes, and in the short-term by motivating efforts to investigate candidate neuroprotective influences within smoked tobacco. Importantly, these benefits may be realized even if the results suggest a causal relationship between smoking and reduced PD risk. Ideally, the insights gained will accelerate development of targeted, non-toxic therapeutic interventions that slow PD without the adverse health consequences associated with tobacco use.
Keywords: smoking, tobacco, Parkinson's disease, epidemiology, quasi-experimental trial, public health policy, bioethics, monoamine oxidase, carbon monoxide, nicotine
Plain language summary
A Paradoxical Plus for Parkinson's in UK's New ‘Generational Smoking Ban’
The UK's new ban on tobacco sales for younger generations is intended to save lives by preventing cancer, heart disease, and stroke. The law will also provide an opportunity to understand how smoking may impact the risk of Parkinson's, which is less likely to occur among smokers.
Commentary
With his signature King Charles III granted Royal Assent for the Tobacco and Vapes Bill to become law in the United Kingdom on April 29, 2026. Its core restriction prohibiting sale of cigarettes and other tobacco products to anybody born after 2008 will begin on January 1, 2027 – and last in perpetuity. The law gradually increases the age at which adults will never be able to legally buy and smoke tobacco in the UK, without ever taking away an individual's existing right to smoke. While only the youngest adults won't be able to legally purchase cigarettes in the UK next year, by the turn of the century it will be illegal to sell them to any adult younger than ninety.
Given the incontrovertible evidence for the overall devastating effects of smoking on human health, this landmark law stands to meaningfully reduce the burden of diseases ranging from lung cancer to stroke for entire generations of UK citizens, with even greater potential benefit should these policies be adopted on a global scale. Nevertheless, this giant step forward for health has not been taken lightly nor has it been universally welcomed. In addition to the expected opposition from the tobacco industry, critics have objected to the law on grounds of liberty and equality (values that are themselves often used to justify such restrictions) among others.1,2
So how does Parkinson's disease (PD) figure into this debate? Smoking is consistently associated with a lower risk of developing PD.3–7 Epidemiological studies show smokers have about half the risk of developing PD compared to never-smokers, and studies using genetic instruments7–11 and other approaches 12 for causal inference support a potentially protective effect of smoking, despite its proven overall detrimental effects on health. Several groups have speculated that laudable reductions in global smoking rates, reducing exposure, may contribute as much as any other modifiable factor to a projected rise in the global burden of PD over the next 25 years, although simple demographic changes such as population aging are currently the most clearly established contributors.13,14
Opponents of the Tobacco and Vapes Bill might point to the substantially greater risk of PD among non-smokers to argue against the legislation, offsetting the substantial body of medical evidence for its future benefit. However, while the evidence for protection against PD from smoking is suggestive, it is inadequate to meaningfully diminish the overwhelming health benefit justifying a tobacco ban. Even if smoking were known to reduce the risk of PD, the magnitude of such a benefit would be greatly outweighed by the myriad harms of smoking. 15
Moreover, we contend that the smoking-PD link paradoxically strengthens the rationale for such a ban because it may provide a valuable opportunity to understand the causality of the link, provided that the ban remains in place over multiple decades – unlike New Zealand's smoking, which was enacted in 2022 but repealed before implementation by the country's next government. Public policy changes in environmental exposures and lifestyle behaviors constitute quasi-experimental trials that can directly address causality despite the lack of randomization, as long as good quality control data are collected in parallel regions or over time (e.g., as was used to demonstrate herpes zoster vaccination reduces dementia risk).16,17 To that end, we encourage adoption of complementary public health policies to ensure improved incidence surveillance systems (e.g., registries) to gather comparator data, not only in the countries implementing tobacco bans, but also in otherwise similar countries that do not implement them.
Finally, the long timeline of this proposed quasi-experimental study of smoking on PD incidence provides an impetus to prioritize research into multiple potential mechanisms (e.g., MAO-B inhibition, low-dose carbon monoxide, and nicotine) by which smoking may confer protection. 18 Prompted by the questions and opportunities raised by the UK's imminent generational tobacco ban, we may today accelerate our understanding of which constituents and biological pathways activated by cigarette smoke could account for its possible preventative influence on PD - well before future generations clarify the effects of reducing smoking rates on disease, including on Parkinson’s.
Footnotes
ORCID iDs: Michael A. Schwarzschild https://orcid.org/0000-0001-6019-8280
Eric A. Macklin https://orcid.org/0000-0003-1618-3502
Stephanie R. Morain https://orcid.org/0000-0001-7278-7517
Kjetil Bjornevik https://orcid.org/0000-0002-2892-6986
Xiqun Chen https://orcid.org/0000-0001-8582-8891
Petroula Proitsi https://orcid.org/0000-0002-2553-6974
Alastair J. Noyce https://orcid.org/0000-0003-3027-5497
Sirwan K. L. Darweesh https://orcid.org/0000-0002-4361-4593
Bastiaan R. Bloem https://orcid.org/0000-0002-6371-3337
Author contributions: MAS – concept, initial draft, critical review, editing
BB, SD, EAM – concept, critical review, editing
All others– critical review, editing
Funding: Supported by the Farmer Family Foundation for Parkinson's Research Initiative, and the Radboud University Excellence Initiative of Radboud University.
The authors report no conflict of interest with respect to the research, authorship, and/or publication of this article on the topic of commercial tobacco products. Dr. Gomperts reports being an inventor on intellectual property related to the development of low-dose carbon monoxide as a potential PD therapy; his immediate family members are also involved in its commercial development. Professor Bloem is editor-in-chief of the Journal of Parkinson's Disease but was in no way involved in the external peer review of this present article.
References
- 1.Schmidt AT. Freedom of choice and the tobacco endgame. Bioethics 2022; 36: 77–84. PMID: 34671993. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Doucet M. Trading one problem for two: the case against tobacco bans. Bioethics 2025; 39: 205–212. PMID: 39215766. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Ritz B, Ascherio A, Checkoway H, et al. Pooled analysis of tobacco use and risk of Parkinson disease. Arch Neurol 2007; 64: 990–997. PMID: 17620489. [DOI] [PubMed] [Google Scholar]
- 4.Noyce AJ, Bestwick JP, Silveira-Moriyama L, et al. Meta-analysis of early nonmotor features and risk factors for Parkinson disease. Ann Neurol 2012; 72: 893–901. PMID: 23071076. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Ascherio A, Schwarzschild MA. The epidemiology of Parkinson’s disease: risk factors and prevention. Lancet Neurol 2016; 15: 1257–1272. PMID: 27751556. [DOI] [PubMed] [Google Scholar]
- 6.Breckenridge CB, Berry C, Chang ET, et al. Association between Parkinson’s disease and cigarette smoking, rural living, well-water consumption, farming and pesticide use: systematic review and meta-analysis. PLoS One 2016; 11: e0151841. PMID: 27055126. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Grotewold N, Albin RL. Update: protective and risk factors for Parkinson disease. Parkinsonism Relat Disord 2024; 125: 107026. PMID: 38879999. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Domínguez-Baleón C, Ong JS, Scherzer CR, et al. Understanding the effect of smoking and drinking behavior on Parkinson’s disease risk: a Mendelian randomization study. Sci Rep 2021; 11: 13980. PMID: 34234189. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Heilbron K, Jensen MP, Bandres-Ciga S, et al. Unhealthy behaviours and risk of Parkinson’s disease: a Mendelian randomisation study. J Parkinsons Dis 2021; 11: 1981–1993. PMID: 34275906. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Domenighetti C, Sugier PE, Sreelatha AAK, et al. Mendelian randomisation study of smoking, alcohol, and coffee drinking in relation to Parkinson’s disease. J Parkinsons Dis 2022; 12: 267–282. PMID: 34633332. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Larsson SC, Burgess S. Appraising the causal role of smoking in multiple diseases: a systematic review and meta-analysis of Mendelian randomization studies. EBioMedicine 2022; 82: 104154. PMID: 35816897. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.O’Reilly EJ, Chen H, Gardener H, et al. Smoking and Parkinson’s disease: using parental smoking as a proxy to explore causality. Am J Epidemiol 2009; 169: 678–682. PMID: 19131566. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Rossi A, Berger K, Chen H, et al. Projection of the prevalence of Parkinson’s disease in the coming decades: revisited. Mov Disord 2017; 33: 156–159. PMID: 28590580. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Su D, Cui Y, He C, et al. Projections for prevalence of Parkinson’s disease and its driving factors in 195 countries and territories to 2050: modelling study of global burden of disease study 2021. Br Med J 2025; 388: e080952. PMID: 40044233. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Ahn SH, Kim DH, Park J, et al. Dynamic smoking patterns and risk of Parkinson disease and all-cause mortality: a competing risk analysis approach. Neurology 2026; 106: e214722. PMID: 41740083. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Eyting M, Xie M, Michalik F, et al. A natural experiment on the effect of herpes zoster vaccination on dementia. Nature 2025; 641: 438–446. PMID: 40175543. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Basu S, Meghani A, Siddiqi A. Evaluating the health impact of large-scale public policy changes: classical and novel approaches. Annu Rev Public Health 2017; 38: 351–370. PMID: 28384086. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Rose KN, Schwarzschild MA, Gomperts SN. Clearing the smoke: what protects smokers from Parkinson’s disease? Mov Disord 2024; 39: 267–272.. [DOI] [PMC free article] [PubMed] [Google Scholar]
