Interaction Between Cigarette Smoking and PARK16 on Parkinson's Disease.
- 1Department of Neurology, National Neuroscience Institute, Singapore General Hospital Campus, Singapore 168581, Singapore.
- 2Duke-NUS Medical School, Singapore 169857, Singapore.
- 3Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 308232, Singapore.
Abstract
Parkinson's disease (PD) is influenced by genetic and environmental factors. Epidemiological evidence indicates that smoking is associated with reduced PD risk, potentially through oxidative stress-related pathways. PARK16 is a PD-susceptibility locus also implicated in oxidative stress regulation. This study examined gene-environment interaction involving smoking and a PARK16 single nucleotide polymorphism (SNP). A case-control study involving 999 Chinese subjects (497 cases, 502 controls) was conducted. PARK16 SNP rs6679073 (NC_000001.11:g.205787356C>A) was identified in a genome-wide association study in an Asian population. Logistic regression estimated adjusted odds ratios (ORs), controlling for age, sex, family history, and comorbidities. Gene-environment interactions were assessed using both additive (RERI, AP, and S) and multiplicative models. Smoking was not significantly associated with PD risk in the cohort (adjusted OR 0.78, 95% CI 0.54-1.12, and p = 0.179). rs6679073 was significantly associated with increased PD risk under the recessive model (AA vs. CC/CA: adjusted OR 1.47, 95% CI 1.11-1.93, and p = 0.007). An additive interaction between rs6679073 and smoking was observed (RERI 0.85, 95% CI 0.21-1.50; AP 0.51, 95% CI 0.12-0.89). These findings suggest a biologically plausible interaction between PARK16 rs6679073 and cigarette smoking in modulating PD risk and warrants further investigation. Understanding gene-environment interactions may inform the design of mechanistic studies and contribute to risk stratification in susceptible populations.
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BibTeX
@article{chong2026interaction,
title = {{Interaction Between Cigarette Smoking and PARK16 on Parkinson's Disease.}},
author = {Tze Tsung Chong and Jia Dong James Wang and Ebonne Yu-Lin Ng and Qiao-Yang Sun and Eng-King Tan},
journal = {International journal of molecular sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27198556},
url = {https://europepmc.org/article/MED/42883802},
note = {CC BY},
}
RIS
TY - JOUR
TI - Interaction Between Cigarette Smoking and PARK16 on Parkinson's Disease.
AU - Tze Tsung Chong
AU - Jia Dong James Wang
AU - Ebonne Yu-Lin Ng
AU - Qiao-Yang Sun
AU - Eng-King Tan
PY - 2026
DA - 2026/09/24
JO - International journal of molecular sciences
DO - 10.3390/ijms27198556
UR - https://europepmc.org/article/MED/42883802
AB - Parkinson's disease (PD) is influenced by genetic and environmental factors. Epidemiological evidence indicates that smoking is associated with reduced PD risk, potentially through oxidative stress-related pathways. PARK16 is a PD-susceptibility locus also implicated in oxidative stress regulation. This study examined gene-environment interaction involving smoking and a PARK16 single nucleotide polymorphism (SNP). A case-control study involving 999 Chinese subjects (497 cases, 502 controls) was conducted. PARK16 SNP rs6679073 (NC_000001.11:g.205787356C>A) was identified in a genome-wide association study in an Asian population. Logistic regression estimated adjusted odds ratios (ORs), controlling for age, sex, family history, and comorbidities. Gene-environment interactions were assessed using both additive (RERI, AP, and S) and multiplicative models. Smoking was not significantly associated with PD risk in the cohort (adjusted OR 0.78, 95% CI 0.54-1.12, and p = 0.179). rs6679073 was significantly associated with increased PD risk under the recessive model (AA vs. CC/CA: adjusted OR 1.47, 95% CI 1.11-1.93, and p = 0.007). An additive interaction between rs6679073 and smoking was observed (RERI 0.85, 95% CI 0.21-1.50; AP 0.51, 95% CI 0.12-0.89). These findings suggest a biologically plausible interaction between PARK16 rs6679073 and cigarette smoking in modulating PD risk and warrants further investigation. Understanding gene-environment interactions may inform the design of mechanistic studies and contribute to risk stratification in susceptible populations.
SN - 1422-0067
ER -