Pulmonary Inflammation and Cell Death in Mice After Acute Exposure to Air Particulate Matter From an Industrial Region of Buenos Aires

Epidemiological studies have shown that air particulate matter (PM) can increase respiratory morbidity and mortality being the lungs the main target organ to PM body entrance. Even more, several in vivo and in vitro studies have shown that air PM has a wide toxicity spectra depending among other parameters, on its size, morphology, and chemical composition. The Reconquista River is the second most polluted river from Buenos Aires, and people living around its basin are constantly exposed to its contaminated water, soil and air. However, the air PM from the Reconquista River (RR-PMa) has not been characterized, and its biological impact on lung has yet not been assessed. Therefore, the present investigation was undertaken to study (1) RR-PMa morphochemical characteristic and (2) RR-PMa lung acute effects after intranasal instillation exposure through the analysis of three end points: oxidative stress, inflammation, and apoptosis. A single acute exposure of RR-PMa (1 mg/kg body weight) after 24 h caused significant (p < 0.05) enrichment in bronchoalveolar total cell number and polymorphonuclear (PNM) fraction, superoxide anion generation, production of pro-inflammatory cytokines TNF-α and IL-6, and induction of apoptosis. It was also observed that in lung homogenates, none of the antioxidant enzymes assayed showed differences between exposed RR-PMa and control mice. These data demonstrate that air PM from the Reconquista River induce lung oxidative stress, inflammation, and cell death therefore represents a potential hazard to human health.     

Images of the respiratory system in ancient Egypt: Trachea,bronchi and pulmonary lobes

Examination of ancient Egyptians’ depictions of the respiratory tract, dating back to the 30th century BC, reveals their awareness of the pulmonary anatomy: reinforced with cartilaginous rings, the trachea is split into two main bronchi, which then enter the lungs (lungs being divided into pulmonary lobes).     

Occupational Rhinosinusitis and Upper Airway Disease: The World Trade Center Experience

The World Trade Center disaster and its recovery work involved a range of hazardous occupational exposures that have not been fully characterized but that can be reasonably assumed to have the potential to cause mucosal inflammation, preferentially (but not exclusively) in the upper airway. A high prevalence of rhinosinusitis and upper airway disease (UAD) symptoms was reported by several early surveys. Clinical studies demonstrated objective, clinically significant, and persistent chronic perennial rhinosinusitis and UAD—with or without seasonal exacerbation—in a large proportion of patients. Demonstration of an association between UAD and available exposure indicators has been limited. Atopy seemed to be associated with increased UAD symptom severity and to be a risk factor for upper, but not lower, airway disease. World Trade Center-related UAD is considered an irritant-induced disease but not, in many cases, of acute onset. No data thus far suggest an increased upper airway cancer incidence.     

Activation of muscarinic acetylcholine receptors via their allosteric binding sites.

Ligands that bind to the allosteric-binding sites on muscarinic acetylcholine receptors alter the conformation of the classical-binding sites of these receptors and either diminish or increase their affinity for muscarinic agonists and classical antagonists. It is not known whether the resulting conformational change also affects the interaction between the receptors and the G proteins. We have now found that the muscarinic receptor allosteric modulators alcuronium, gallamine, and strychnine (acting in the absence of an agonist) alter the synthesis of cAMP in Chinese hamster ovary (CHO) cells expressing the M2 or the M4 subtype of muscarinic receptors in the same direction as the agonist carbachol. In addition, most of their effects on the production of inositol phosphates in CHO cells expressing the M1 or the M3 muscarinic receptor subtypes are also similar to (although much weaker than) those of carbachol. The agonist-like effects of the allosteric modulators are not observed in CHO cells that have not been transfected with the gene for any of the subtypes of muscarinic receptors. The effects of alcuronium on the formation of cAMP and inositol phosphates are not prevented by the classical muscarinic antagonist quinuclidinyl benzilate. These observations demonstrate for the first time that the G protein-mediated functional responses of muscarinic receptors can be evoked not only from their classical, but also from their allosteric, binding sites. This represents a new mechanism of receptor activation.     

Dynamics of the heart rate variability and oxygen saturation response to acute normobaric hypoxia within the first 10 min of exposure

Although the heart rate variability (HRV) response to hypoxia has been studied, little is known about the dynamics of HRV after hypoxia exposure. The purpose of this study was to assess the HRV and oxygen saturation (SpO₂) responses to normobaric hypoxia (FiO₂ = 9·6%) comparing 1 min segments to baseline (normoxia). Electrocardiogram and SpO₂ were recorded during a 10‐min hypoxia exposure in 29 healthy male subjects aged 26·0 ± 4·9 years. Baseline HRV values were obtained from a 5‐min recording period prior to hypoxia. The hypoxia period was split into 10 non‐overlapping 1‐min segments and time domain HRV indexes (RMSSD and SDNN) were calculated for each segment. Differences (Δ) from baseline values were calculated and transformed using natural logarithm (Ln). This study revealed that the decrease in ΔSpO₂ became significant (P<0·001) in the first minute of hypoxia, the decrease in ΔLn RMSSD became significant (P = 0·002) in the second minute, and the decrease in ΔLn SDNN became significant (P = 0·001) in the third minute. Between the second and fifth minute of hypoxia, ΔSpO₂ correlated with ΔLn RMSSD (r = 0·57, P<0·001) and ΔLn SDNN (r = 0·44, P<0·001). Five min after the onset of hypoxia, ΔSpO₂ was significantly (P = 0·002) decreased but changes in ΔLn RMSSD (P = 0·344) and ΔLn SDNN (P = 0·558) were not significant. In conclusion, the decrease in HRV was proportional to desaturation but only during the first 5 min of hypoxia.