# Ambient Air Pollution and Cardiometabolic Health in the Tehran Lipid and Glucose Study: A Scoping Review of Two Decades of Evidence

**Authors:** Amir Hossein Hasanpour, Mohammad Javad Mansourzadeh, Alireza Khajavi, Fereidoun Azizi, Farzad Hadaegh

PMC · DOI: 10.5812/ijem-166630 · International Journal of Endocrinology and Metabolism · 2025-10-30

## TL;DR

A review of 20 years of data from Tehran shows that air pollution is linked to higher blood pressure, bad cholesterol, and increased heart disease risk.

## Contribution

The study provides a comprehensive synthesis of air pollution's heterogeneous effects on cardiometabolic health in a single population over two decades.

## Key findings

- Short-term exposure to PM₁₀ and SO₂ is associated with elevated systolic and diastolic blood pressure.
- Long-term exposure to PM₁₀ and SO₂ increases the risk of hypertension and dysglycemia.
- CO and SO₂ are linked to adverse lipid profiles and higher cardiovascular disease hospitalization risks.

## Abstract

This scoping review investigates the association between ambient air pollution and cardiometabolic outcomes using data from the Tehran Lipid and Glucose Study (TLGS), a population-based cohort initiated in 1999.

Five TLGS studies were included, each examining associations between ambient air pollutants and cardiometabolic outcomes such as hypertension (HTN), dyslipidemia, diabetes, cardiovascular morbidity, and mortality. Due to overlapping populations but differing outcome measures across studies, a meta-analysis was not feasible. Instead, a narrative synthesis was conducted, with results organized into a comparative matrix to facilitate cross-study evaluation.

The findings reveal heterogeneous effects of ambient air pollutants on cardiometabolic health across both short- and long-term pathways. Short-term exposures to nitrogen dioxide (NO₂) and particulate matter ≤ 10 µm in diameter (PM₁₀) were linked to higher systolic blood pressure (SBP), while sulfur dioxide (SO₂) was associated with elevated diastolic pressure. For lipid parameters, carbon monoxide (CO) and SO₂ corresponded with higher total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol (non-HDL-C) levels. Cardiovascular outcomes also worsened, as increases in the Air Quality Index (AQI), PM₁₀, SO₂, and CO were associated with higher risks of cardiovascular disease (CVD) hospitalization and mortality. Long-term exposures to ozone (O₃), PM₁₀, and SO₂ predicted incident HTN (strongest for PM₁₀), while CO was associated with elevated TC, TG, and adverse dyslipidemia phenotypes but not high LDL-C. Sulfur dioxide, O₃, and PM₁₀ also increased risks of dysglycemia, though no consistent associations with type 2 diabetes incidence or long-term mortality were observed.

This review underscores the substantial influence of ambient air pollution on metabolic and cardiovascular health in Tehran. Short-term exposure to pollutants such as PM₁₀, SO₂, and CO is associated, either immediately or with lagged effects, with increased blood pressure, adverse lipid changes, and heightened cardiovascular risk, while long-term exposure to PM₁₀ and SO₂ exacerbates HTN and impairs glucose metabolism. These findings highlight the need for stricter air quality regulations and further investigation into the cumulative, long-term effects of air pollution in the metropolitan city of Tehran.

## Linked entities

- **Chemicals:** nitrogen dioxide (PubChem CID 3032552), sulfur dioxide (PubChem CID 1119), carbon monoxide (PubChem CID 281), ozone (PubChem CID 24823)
- **Diseases:** dyslipidemia (MONDO:0002525), diabetes (MONDO:0005015), cardiovascular disease (MONDO:0004995)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** TC (MESH:C535937), HF (MESH:D006333), peripheral artery disease (MESH:D058729), T2D. (MESH:D003924), TLGS (MESH:D011017), glucose intolerance (MESH:D018149), atherosclerosis (MESH:D050197), Death (MESH:D003643), HTN (MESH:D006973), thrombosis (MESH:D013927), DBP (MESH:D006337), vascular and metabolic dysfunction (MESH:D002561), ischemic heart disease (MESH:D017202), IFG (MESH:D007003), CVD (MESH:D002318), MI (MESH:D009203), non-communicable diseases (MESH:D000073296), cerebrovascular accidents (MESH:D020521), obesity (MESH:D009765), dyslipidemia (MESH:D050171), cardiovascular and respiratory diseases (MESH:D012140), MetS (MESH:D024821), inflammation (MESH:D007249), pulmonary injury (MESH:D055370), CKD (MESH:D051436), prediabetes (MESH:D011236), cancers (MESH:D009369), diabetes (MESH:D003920), ischemic (MESH:D002545)
- **Chemicals:** Lipid (MESH:D008055), SO2 (MESH:D013458), Glucose (MESH:D005947), PM10 (-), O3 (MESH:D010126), Blood Glucose (MESH:D001786), Cholesterol (MESH:D002784), volatile organic compounds (MESH:D055549), oxygen (MESH:D010100), Diastolic Blood Pressure (MESH:D004145), carbon (MESH:D002244), TG (MESH:D014280), NO2 (MESH:D009585), CO (MESH:D002248)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12915351/full.md

## References

77 references — full list in the complete paper: https://tomesphere.com/paper/PMC12915351/full.md

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Source: https://tomesphere.com/paper/PMC12915351