# The Toxic Effects of Hydrated Cement, Autoclaved Aerated Concrete, and Demolition Dusts on the Respiratory System in Rats

## TL;DR

This study shows that exposure to dust from construction materials like cement and demolition waste causes lung damage and inflammation in rats.

## Contribution

The first experimental investigation of lung toxicity caused by hydrated cement, autoclaved aerated concrete, and demolition dust in rats.

## Key findings

- All dust types caused emphysema, with significant effects in hydrated cement and autoclaved aerated concrete groups.
- Demolition dust induced fibrosis, marked by increased CD68+ macrophages, TGF-β, and hydroxyproline.
- Exposure to all dusts activated the Akt/NF-κB pathway and increased apoptosis markers like caspase-9.

## Abstract

Background: Following the earthquakes that occurred in Türkiye in 2023, the resulting demolition dust (DD) negatively impacted air quality and led to an increase in respiratory diseases. Although the harmful effects of crystalline and amorphous silica are known, the effects of hydrated cement dust (HCD), autoclaved aerated concrete dust (AACD), and DD on the lungs have not been sufficiently investigated. This rat study presents the first experimental data on the toxicity of these dusts. Methods: In the study, the structural properties of dust particles smaller than 5 µm were characterized using XRD analysis. Subsequently, 48 female rats were divided into four groups: HCD, AACD, DD, and control. The relevant dust suspensions were administered to the experimental groups, and physiological saline was administered to the control group intranasally a total of five times over a 15-day period, once every 3 days. Subsequently, bronchoalveolar lavage fluid, blood, and lung tissues were analyzed. Results: An increase in emphysema was observed in all exposure groups, and this increase was significant in the AAC and HC groups. Inflammation and alveolar wall thickness increased in the HC and DD groups. Goblet cell hyperplasia was detected only in the HC group; increases in CD68+ macrophages and TGF-β, as well as elevated hydroxyproline, were detected only in the DD group and supported the fibrotic response (p < 0.05). Neutrophil increase was specific to the AAC group. In all exposure groups, Akt/NF-κB pathway proteins, caspase-9, and MPO levels increased, while Bcl-xl levels decreased (p < 0.05). The findings indicate that the examined dusts trigger inflammation and apoptosis. Conclusion: Exposure to HCD, AACD, and DD causes lung damage by modulating the Akt/NF-κB signaling cascade; it enhances the apoptotic process through Bcl-xl suppression and caspase-9 increase. DD also induces a marked fibrotic response.