# Association between air pollution and non-accidental mortality in Guiyang, China: a time-series analysis (2013–2023)

**Authors:** Xuanhao Chen, Minmin Su, Minlan Yuan, Zihai Jian, Dan Yang, Ruifang Liu, Hua Guo, Jianhua Zhang

PMC · DOI: 10.3389/fpubh.2025.1602900 · Frontiers in Public Health · 2025-07-16

## TL;DR

The study found that air pollution in Guiyang, China, is linked to increased non-accidental deaths, with different pollutants affecting mortality risks differently based on age, gender, and season.

## Contribution

This study provides new evidence on the specific health risks of various air pollutants in Guiyang, highlighting gender and age differences in susceptibility.

## Key findings

- SO₂ exposure was associated with a 3.18% increase in non-accidental mortality risk per 10 μg/m³.
- Females were more susceptible to SO₂, while males were more vulnerable to PM₂.₅.
- Individuals aged ≥65 years showed elevated risks across all pollutants, especially SO₂.

## Abstract

Air pollution remains one of the leading environmental risk factors for human health globally, significantly contributing to the burden of disease and premature mortality. The relationship between air pollutants and non-accidental deaths in Guiyang was unclear.

Descriptive analysis was conducted to characterize air pollutants and mortality trends during the study period. A time-stratified case-crossover design and a quasi-Poisson regression within a generalized additive model (GAM) framework were employed to examine the association between air pollution and mortality. The models incorporated a 7-day lag structure and adjusted for temporal trends, meteorological factors, and day of the week. Analyses were further stratified by cause-specific mortality, age group, sex, and seasonaty as an endpoint for acute health effects, stratified by cause-specific mortality, age, sex and season.

SO₂ exposure was associated with a 3.18% (95% CI: 1.95 to 4.42%) increase in excess risk (ER) for non-accidental mortality per 10 μg/m3 increase, with risks peaking at lag 1 and cumulative effects persisting beyond 7 days. NO₂ exposure resulted in a 2.87% (95% CI: 1.72 to 4.03%) ER increase, peaking at lag 1, with effects extending to lag 7. PM₂.₅ and PM₁₀ exposure resulted in ER increases of 1.42% (95% CI: 0.84 to 1.99%) and 0.86% (95% CI: 0.50 to 1.22%), respectively, peaking within 1–2 days. CO exposure was associated with a 1.64% (95% CI: 1.01 to 2.29%) ER increase per 0.1 mg/m3, with effects observed at lag 0. Females showed higher susceptibility to SO₂ (ER: 3.87, 95% CI: 2.05 to 5.72%), while males were more vulnerable to PM₂.₅ (ER: 1.80, 95% CI: 1.10 to 2.51%). Individuals aged ≥65 years exhibited elevated risks across all pollutants, particularly SO₂ (ER: 4.16, 95% CI: 2.73 to 5.61%). All pollutants contributed to excess mortality in the cold season.

Different pollutants exhibit different lag durations of excess risks and cumulative excess risks for non-accidental mortality and deaths related to circulatory and respiratory systems. Females showed greater susceptible to SO2, while males were more vulnerable to other pollutants. The individuals aged 65 years and older were particularly vulnerable populations.

## Linked entities

- **Chemicals:** CO (PubChem CID 281)

## Full-text entities

- **Diseases:** bronchitis (MESH:D001991), circulatory and respiratory system diseases (MESH:D015619), Deaths (MESH:D003643), Disease (MESH:D004194), cardiovascular (MESH:D002318), stroke (MESH:D020521), arrhythmia (MESH:D001145), coronary heart disease (MESH:D003327), respiratory inflammation (MESH:D007249), COVID-19 (MESH:D000086382), reduced lung function (MESH:D001523), respiratory and cardiovascular damage (MESH:D012140), airway irritation (MESH:D000402), hypoxia (MESH:D000860), toxicity (MESH:D064420)
- **Chemicals:** CO (MESH:D002248), water (MESH:D014867), NO2 (MESH:D009585), SO2 (MESH:D013458), oxygen (MESH:D010100), PM10 (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12307342/full.md

## References

33 references — full list in the complete paper: https://tomesphere.com/paper/PMC12307342/full.md

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Source: https://tomesphere.com/paper/PMC12307342