Histological changes in lung tissues related with sub-chronic exposure to ambient urban levels of PM2.5 in Córdoba, Argentina

Polycyclic Aromatic Hydrocarbon Levels in Wistar Rats Exposed to Ambient Air of Port Harcourt, Nigeria: An Indicator for Tissue Toxicity

“…Most of the PAHs found in the study were mostly of the carcinogenic class. There is strong evidence that injuries to the lung tissues and DNA damage could result from sub-chronic exposure to low amounts of particles, even below the WHO's 24-h-threshold [33].…”

“…Dose-dependent absorption kinetics have also been demonstrated in the lungs of perfused rats at low exposure concentrations, and the absorption of PAHs in the mucosa follows the first-order kinetics with substantial local metabolism. However, at high-exposure doses, the capacity of epithelium to dissolve and metabolize PAHs becomes saturated, and the absorption rate turns zero-order kinetics [17,[30][31][32][33]. In the indoor environment, human exposure is likely to follow the low-dose, while first-order kinetics are likely to be observed in ambient air inhalation where concentrations are higher [30][31][32].…”

“…The lipophilic and hydrophobic toxicokinetic and metabolism in animal tissues [10,17,29] and plant metabolism [53] differ widely. Additionally, humans are not physiologically designed for controlled and episodic fumes inhalation, which is likely to destroy human cells within the inhalation time through carboxyhemoglobin pathogenesis, resulting from carbon monoxide poisoning [55,56] as against normal ambient air [33]. Consequently, simulated findings from such study methods most probably do not correlate relatively to animal health or an indicator for toxicity in human tissues, compared to studies that expose experimental animals (from hydrocarbon and petrochemical pollution-free environment) to the normal atmospheric ambient air accustomed to human respiration [33,54].…”

“…Additionally, humans are not physiologically designed for controlled and episodic fumes inhalation, which is likely to destroy human cells within the inhalation time through carboxyhemoglobin pathogenesis, resulting from carbon monoxide poisoning [55,56] as against normal ambient air [33]. Consequently, simulated findings from such study methods most probably do not correlate relatively to animal health or an indicator for toxicity in human tissues, compared to studies that expose experimental animals (from hydrocarbon and petrochemical pollution-free environment) to the normal atmospheric ambient air accustomed to human respiration [33,54]. To this end, this study, using an animal model [57], compared the PAH level concentrations in the blood tissue of Wistar rats exposed to the indoor and outdoor ambient air of a polluted environment in Port Harcourt and how they deviate from the established baseline obtained from the nonpolluted environment.…”

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

“…PM 2.5 , which are atmospheric PM with a diameter <2.5 µm, are composed of biological components, particles, PAHs, organic carbon, elemental carbon, inorganic water-soluble ions and heavy metals ( 15 ). In recent years, due to its adverse effects on the climate, environment and health, PM 2.5 has attracted attention and extensive research examining its effects have been performed ( 16 ). Research has indicated that the PM 2.5 is harmful to the respiratory system, since it accumulates in lung tissue and stimulates alveoli ( 17 ).…”