A new analysis of over 500,000 people suggests higher exhaled carbon monoxide—even among never-smokers—was associated with about a 30% lower Parkinson's risk, offering one possible explanation for the long-observed inverse link between smoking and Parkinson's. Researchers also point to nicotine and other tobacco compounds as potential protective factors. Experts stress this finding is not a recommendation to smoke; smoking causes substantial and well-documented harms, and further research is needed to isolate any safe, protective mechanisms.
New Study Points to Carbon Monoxide as a Possible Reason Smokers Have Lower Parkinson’s Risk
Stock photo: A woman is smoking at a table, holding her cigarette over an ashtray.
Multiple large-scale studies have observed that cigarette smokers and some tobacco users develop Parkinson's disease at lower rates than the general population. A recent large analysis offers a possible biological explanation: low-level carbon monoxide exposure may be linked to a reduced Parkinson's risk.
What the Evidence Shows
Decades of epidemiological research report an inverse association between smoking and Parkinson's disease—meaning smokers have been found less likely to develop Parkinson's than lifelong non-smokers. A 65-year follow-up of more than 30,000 British doctors, published in Neurology (2020), found smokers had a 30–40% lower risk compared with never-smokers. A 2002 Neurology study of identical twins reached similar conclusions.
On Sept. 8, a new JAMA Neurology analysis of more than 500,000 participants reported that never-smokers who exhaled elevated carbon monoxide (CO) levels—about 3 parts per million (ppm) or higher—had roughly a 30% lower risk of Parkinson's. The authors suggest that the link between smoking and lower Parkinson's risk may be driven in part by CO exposure rather than by tobacco use itself.
Possible Biological Mechanisms
Carbon monoxide is a colorless, odorless gas that is toxic at high concentrations but also produced in small amounts by the body as a signaling molecule. At low concentrations, CO can influence oxidative stress, inflammation and cell survival—pathways that might protect dopamine-producing neurons implicated in Parkinson's.
Several white smokeless tobacco pouches (snus) scattered on a reflective black surface next to an open round container.
"We normally think of carbon monoxide as a poison, and at high levels it absolutely is, but our bodies also produce small amounts of it naturally as a signaling molecule," said Dr. Michael Okun, Professor of Neurology at the University of Florida.
Other tobacco-related hypotheses remain plausible. Studies of smokeless tobacco (for example, Swedish moist snuff) have also reported lower Parkinson's risk, suggesting non-smoke constituents of tobacco might be relevant. Researchers have proposed nicotine and compounds that inhibit monoamine oxidase B (MAO-B) as candidate protective agents—both could preserve dopamine signaling or improve neuron survival.
Experts’ Caution and Public-Health Context
Experts emphasize that an association does not prove causation. Observational links point to biological clues worth pursuing, but do not justify smoking. The Centers for Disease Control and Prevention (CDC) reports that more than 16 million Americans live with a smoking-related disease, and smoking plus secondhand smoke contribute to over 480,000 U.S. deaths annually. Smoking remains a leading cause of cancer, heart disease, stroke, lung disease, type 2 diabetes and other harms.
"This does not prove carbon monoxide prevents Parkinson's, but it gives us a specific biological clue to chase," Okun said. "If we can identify exactly what appears protective and separate it from the enormous harms of tobacco, we may uncover new targets for preventing or slowing Parkinson's."
What This Means Going Forward
The new findings point researchers toward measurable biological pathways—CO signaling, nicotine action at nicotinic acetylcholine receptors, MAO-B inhibition and possibly other tobacco constituents. Some carbon monoxide–based approaches are already entering early clinical testing, but further laboratory and clinical research is needed to confirm mechanisms and to develop safe, targeted interventions that do not carry the risks of smoking.
Bottom line: The link between smoking and lower Parkinson's risk is an important scientific puzzle. It could reveal new preventive or therapeutic targets, but smoking itself is dangerous and should not be used as a means of prevention.
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