# Size-Segregated Incense Aerosols Drive ROS–Mitochondrial Dysfunction and Programmed Cell Death Across Human Cell Types

## TL;DR

Burning incense produces tiny particles that harm human cells by causing oxidative stress and mitochondrial damage, with the smallest particles being most harmful.

## Contribution

This study identifies ultrafine, lipophilic incense aerosol fractions as key drivers of cellular toxicity and establishes a size- and phase-resolved framework for assessing health risks.

## Key findings

- Ultrafine incense particles (0.18–0.10 μm and <0.10 μm) caused the strongest cytotoxicity and mitochondrial dysfunction.
- Sandalwood-dominant incense showed the highest toxicity across tested cell types.
- Incense particles <0.18 μm were enriched in organic-phase constituents and triggered apoptosis, pyroptosis, and autophagy.

## Abstract

Incense burning is
a major indoor source of fine and ultrafine
particulate matter (PM), yet the size–chemistry determinants
of its cellular toxicity remain underdefined. We characterized aerosols
from three commonly used incense types using Aerodynamics Particle
Sizer (APS)/Scanning Mobility Particle Sizer (SMPS) for sizing, Micro-Orifice
Uniform Deposit Impactor (MOUDI) for size segregation, and water-soluble
phase (WP) or organic-phase (OP) extraction to generate incense aerosol
extracts (IAEs). Across A549, HEK293T, and SH-SY5Y cells, OP-IAEs
from fraction III (0.18–0.10 μm) and IV (<0.10 μm)
exhibited the strongest cytotoxicity, oxidative responses, and mitochondrial
dysfunction. Type A incense (sandalwood-dominant) IAEs consistently
showed the highest potency among the investigated incenses. Mechanistic
assays revealed that ultrafine OP-IAEs, elevated intracellular H2O2, decreased mitochondrial membrane potential
(MMP), depleted ATP, and activated apoptosis (caspase-3), pyroptosis
(caspase-1), and autophagy-associated pathways. Moreover, ≥80%
of all emitted particles were <0.18 μm and were disproportionately
enriched in OP constituents across incense types. Collectively, these
results identify ultrafine, lipophilic aerosol fractions as key drivers
of oxidative–mitochondrial injury and programmed cell death,
establishing a size- and phase-resolved framework for assessing incense-related
health risks and for guiding exposure mitigation in incense-rich indoor
environments.