The association between secondhand smoke exposure and accelerated biological aging: A population-based study and...

Area of Science:

• Environmental Health
• Gerontology
• Metabolic Diseases

Background:

• Aging is a complex biological process influenced by oxidative stress.
• Direct smoking's impact on aging is known, but secondhand smoke (SHS) effects are less understood.
• SHS exposure is linked to chronic inflammation and oxidative stress, potentially accelerating aging.

Purpose of the Study:

• To investigate the association between SHS exposure and biological aging.
• To explore the mediating role of diabetes in the SHS-aging relationship.
• To establish a causal link between SHS exposure and biological aging using genetic methods.

Main Methods:

• Analysis of NHANES data (1999-2010) using serum cotinine for SHS exposure and phenotypic age for biological aging.
• Multifactorial linear regression and restricted cubic splines to assess dose-response relationships.
• Two-sample Mendelian randomization (MR) using GWAS data to determine causality between workplace SHS exposure and age acceleration.

Main Results:

• SHS exposure was associated with increased biological aging (0.37 years for low, 0.76 years for high exposure).
• A U-shaped dose-response curve was observed between SHS exposure and biological aging.
• Diabetes mediated 31.25% of the SHS-aging association; MR confirmed a causal link between workplace SHS and accelerated aging (3.05 years).

Conclusions:

• Secondhand smoke exposure significantly accelerates biological aging.
• Diabetes plays a mediating role in the relationship between SHS exposure and accelerated aging.
• Genetic evidence supports a causal effect, highlighting the critical need to minimize SHS exposure to prevent premature aging.