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Parkinson's disease was found to be linked to nitrogen dioxide (NO₂) exposure, an air contaminant produced mainly by burning fossil fuels in cars and power plants, according to a retrospective study.

People living in districts with the highest NO₂ exposure had a 41% higher risk of newly diagnosed Parkinson's disease than people who lived with the least exposure (HR 1.41, 95% CI 1.02-1.95, P for trend=0.045), reported Sun Ju Chung, MD, PhD, of the University of Ulsan in Seoul, South Korea, and co-authors.

"This finding suggests the role of air pollutants in Parkinson's disease development, advocating for the need to implement a targeted public health policy," Chung and colleagues wrote in .

Exposures to environmental contaminants including pesticides, metals, and air pollution have been associated with Parkinson's and other neurologic diseases. A recent evaluation of Medicare beneficiaries in the U.S., for example, showed that was tied to increased risks of first hospital admission with Parkinson's disease and Alzheimer's disease.

"Beyond loose epidemiological ties, the pathology and clinical features of Parkinson disease also implicate air pollution," noted E. Ray Dorsey, MD, of the University of Rochester in New York, and co-authors, in an .

Degeneration in many forms of Parkinson's disease, Dorsey and colleagues observed.

"Pathological studies have found that the with misfolded alpha-synuclein and that Lewy bodies in the olfactory bulb precede those in the intracerebral basal ganglia structures," they wrote.

"Moreover, among the earliest and most common features of the disease is a loss of smell," they added. "Experts have speculated that this hyposmia could be linked to air pollution."

In their study, Chung and co-authors followed 78,830 adults over age 40 without Parkinson's disease who lived in Seoul from 2002 to 2006, monitoring air quality in the districts where they lived. Over a median 8.6 years (from 2007 to 2015), 338 people were diagnosed with Parkinson's disease.

Mean age of the entire group was about 54 at baseline, and 52% were women. Compared with the total study population, people who developed Parkinson's were significantly older (mean 54.4 vs 66.5 years, P<0.001).

Links between Parkinson's disease and NO₂ were evident when exposure was greater than 0.038 ppm. This relationship continued even after adjusting for age, sex, insurance type, comorbidities, and lifestyle.

However, no statistically significant associations emerged between Parkinson's and other air pollutants like particulate matter (PM_2.5 and PM₁₀), ozone, sulfur dioxide, and carbon monoxide, in both unadjusted and adjusted analyses.

The researchers' conclusion about other air contaminants is problematic, the editorialists noted.

"The concern is their conclusion that not observing an association is the equivalent of no association," Dorsey and co-authors wrote. "This finding fails to take into account the challenges inherent in assessing the relationship between air pollution and disease."

Quantifying individual pollution exposure is difficult, as is accounting for interactions and confounding factors, they pointed out. The time between exposure and outcome is long (like smoking and lung cancer), and Parkinson's diagnoses are imperfect.

Mixed results shouldn't obscure the possibility that ambient pollution is partly fueling the rise of Parkinson's disease, Dorsey and colleagues said.

"In contrast to the large risks (e.g., 100% or more) associated with other environmental pollutants that can be inhaled, such as the pesticide and the industrial solvent , the effect size of air pollution may be modest," they wrote.

"However, air pollution, which is often concentrated in densely populated urban areas, may affect hundreds of millions of people, so small increases in risk can have large effects."

The study had several limitations, Chung and co-authors acknowledged. Ambient air pollution was measured outdoors only and may not reflect indoor concentrations. Occupational exposure to pollution like heavy metals, pesticides, and trichloroethylene was also not considered. In addition, 8.6 years of follow-up may have been insufficient.

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