Air pollution accelerates the development of obesity and Alzheimer's disease: the role of leptin and inflammation - a mini-review.

Air pollution is an urgent concern linked to numerous health problems in low- and middle-income countries, where 92% of air pollution-related deaths occur. Particulate matter 2.5 (PM2.5) is the most harmful component of air pollutants, increasing inflammation and changing gut microbiota, favoring obesity, type 2 diabetes, and Alzheimer's Disease (AD). PM2.5 contains lipopolysaccharides (LPS), which can activate the Toll-like receptor 4 (TLR4) signaling pathway. This pathway can lead to the release of pro-inflammatory markers, including interleukins, and suppressor of cytokine signaling-3 (SOCS3), which inhibits leptin action, a hormone that keeps the energy homeostasis. Leptin plays a role in preventing amyloid plaque deposition and hyperphosphorylation of tau-protein (p-tau), mechanisms involved in the neurodegeneration in AD. Approximately 50 million people worldwide are affected by dementia, with a significant proportion living in low-and middle-income countries. This number is expected to triple by 2050. This mini-review focuses on the potential impact of PM2.5 exposure on the TLR4 signaling pathway, its contribution to leptin resistance, and dysbiosis that exacerbates the link between obesity and AD.

Air pollution aggravates renal ischaemia-reperfusion-induced acute kidney injury.

Chronic kidney disease (CKD) has emerged as a significant global public health concern. Recent epidemiological studies have highlighted the link between exposure to fine particulate matter (PM2.5) and a decline in renal function. PM2.5 exerts harmful effects on various organs through oxidative stress and inflammation. Acute kidney injury (AKI) resulting from ischaemia-reperfusion injury (IRI) involves biological processes similar to those involved in PM2.5 toxicity and is a known risk factor for CKD. The objective of this study was to investigate the impact of PM2.5 exposure on IRI-induced AKI. Through a unique environmentally controlled setup, mice were exposed to urban PM2.5 or filtered air for 12 weeks before IRI followed by euthanasia 48 h after surgery. Animals exposed to PM2.5 and IRI exhibited reduced glomerular filtration, impaired urine concentration ability, and significant tubular damage. Further, PM2.5 aggravated local innate immune responses and mitochondrial dysfunction, as well as enhancing cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway activation. This increased renal senescence and suppressed the anti-ageing protein klotho, leading to early fibrotic changes. In vitro studies using proximal tubular epithelial cells exposed to PM2.5 and hypoxia/reoxygenation revealed heightened activation of the STING pathway triggered by cytoplasmic mitochondrial DNA, resulting in increased tubular damage and a pro-inflammatory phenotype. In summary, our findings imply a role for PM2.5 in sensitising proximal tubular epithelial cells to IRI-induced damage, suggesting a plausible association between PM2.5 exposure and heightened susceptibility to CKD in individuals experiencing AKI. Strategies aimed at reducing PM2.5 concentrations and implementing preventive measures may improve outcomes for AKI patients and mitigate the progression from AKI to CKD. © 2024 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Exposure to urban ambient particles (PM2.5) before pregnancy affects the expression of endometrial receptive markers to embryo implantation in mice: Preliminary results.

Air pollution (AP) is one of the main recent concerns in reproductive healthy due to its potential to promote negative outcomes during pregnancy and male and female fertility. Several studies have demonstrated that AP exposure has been linked to increased embryonic implantation failures, alterations in embryonic, fetal and placental development. For a well-succeeded implantation, both competent blastocyst and receptive endometrium are required. Based on the lack of data about the effect of AP in endometrial receptivity, this study aimed to evaluate he particulate matter (PM) exposure impact on uterine receptive markers in mice and associate the alterations to increased implantation failures due to AP. For this study, ten dams per group were exposed for 39 days to either filter (F) or polluted air (CAP). At fourth gestational day (GD4), females were euthanized. Morphological, ultrastructural, immunohistochemical and molecular analysis of uterine and ovarian samples were performed. CAP-exposed females presented a reduced number of corpus luteum; glands and epithelial cells were increased with pinopodes formation impairment. Immunohistochemistry analysis revealed decreased LIF protein levels. These preliminary data suggests that PM exposure may exert negative effects on endometrial receptivity by affecting crucial parameters to embryonic implantation as uterine morphological differentiation, corpus luteum quantity and LIF expression during implantation window.

Association of pulmonary black carbon accumulation with cardiac fibrosis in residents of Sao Paulo, Brazil.

Evidence suggests that myocardial interstitial fibrosis, resulting from cardiac remodeling, may possibly be influenced by mechanisms activated through the inhalation of airborne pollutants. However, limited studies have explored the relationship between lifetime exposure to carbon-based particles and cardiac fibrosis, specially using post-mortem samples. This study examined whether long-term exposure to air pollution (estimated by black carbon accumulated in the lungs) is associated with myocardial fibrosis in urban dwellers of megacity of Sao Paulo. Data collection included epidemiological and autopsy-based approaches. Information was obtained by interviewing the next of kin and through the pathologist's report. The individual index of exposure to carbon-based particles, which we designed as the fraction of black carbon (FBC), was estimated through quantification of particles on the macroscopic lung surface. Myocardium samples were collected for histopathological analysis to evaluate the fraction of cardiac fibrosis. The association between cardiac fibrosis and FBC, age, sex, smoking status and hypertension was assessed by means of multiple linear regression models. Our study demonstrated that the association of FBC with cardiac fibrosis is influenced by smoking status and hypertension. Among hypertensive individuals, the cardiac fibrosis fraction tended to increase with the increase of the FBC in both groups of smokers and non-smokers. In non-hypertensive individuals, the association between cardiac fibrosis fraction and FBC was observed primarily in smokers. Long-term exposure to tobacco smoke and environmental particles may contribute to the cardiac remodeling response in individuals with pre-existing hypertension. This highlights the importance of considering hypertension as an additional risk factor for the health effects of air pollution on the cardiovascular system. Moreover, the study endorses the role of autopsy to investigate the effects of urban environment and personal habits in determining human disease.

A custom, low-cost, continuous flow chamber built for experimental Sargassum seaweed decomposition and exposure of small rodents to generated gaseous products.

Since 2011, Sargassum events have increased in frequency along the Caribbean and Atlantic coasts. The accumulation and decomposition of large amounts of Sargassum seaweed on beaches pose socio-economic, ecological, and health risks due to the emission of hydrogen sulfide (H2S), methane, and ammonia. However, limited research exists on the emission processes and the health effects of subchronic and chronic exposure to low levels of H2S. Additionally, the absence of emission factor data for Sargassum decomposition on-site makes health risk assessments challenging. This study aimed to create a custom chamber to simulate real-world Sargassum decomposition, exposing experimental animals to the generated gases. Metal content was analyzed, and emission rates were estimated in a controlled environment. The decomposition-exposure system replicated reported environmental gas emissions from the Caribbean region, except for NH3. H2S bursts were observed during the decomposition process at intervals of 2-10 days, with higher frequency associated with larger masses of decomposing Sargassum. The decomposed gas was transferred to the exposure chamber, resulting in an 80-87% reduction in H2S concentration. The maximum H2S emission was 156 ppm, with a concentration ranging from 50.4 to 56.5 ppm. An estimated emission rate of 7-8 g/h for H2S was observed, and significant levels of lead, arsenic, and aluminum were found in beached Sargassum from the northeast coast of Brazil. This study's developed model provides an opportunity to investigate the effects and risks to human health associated with exposure to gases produced during the environmental decomposition of Sargassum seaweed.

Assessing socioeconomic bias of exposure to urban air pollution: an autopsy-based study in São Paulo, Brazil.

Background: The characterisation of individual exposure to air pollution in urban scenarios is a challenge in environmental epidemiological studies. We investigated if the city's pollution monitoring stations over or underestimate the exposure of individuals depending on their socioeconomic conditions and daily commuting times. Methods: The amount of black carbon accumulated in the lungs of 604 deceased who underwent autopsy in São Paulo was considered as a proxy for PM10. The concentrations of PM10 in the residence of the deceased were estimated by interpolating an ordinary kriging model. These two-exposure metrics allowed us to construct an environmental exposure misclassification index ranging from -1 to 1. The association between the index and daily commuting, socioeconomic context index (GeoSES), and street density as predictors was assessed by means of a multilevel linear regression model. Findings: With a decrease of 0.1 units in GeoSES, the index increases, on average, by 0.028 units and with an increase of 1 h in daily commuting, the index increases, on average, by 0.022 units indicating that individual exposure to air pollution is underestimated in the lower GeoSES and in people with many hours spent in daily commuting. Interpretation: Reduction of health consequences of air pollution demands not only alternative fuel and more efficient mobility strategies, but also should include profound rethink of cities. Funding: São Paulo Research Foundation (FAPESP-13/21728-2) and National Council for Scientific and Technological Development (CNPq-304126/2015-2, 401825/2020-5).

Maternal exposure to air pollution alters energy balance transiently according to gender and changes gut microbiota.

Introduction: The timing of maternal exposure to air pollution is crucial to define metabolic changes in the offspring. Here we aimed to determine the most critical period of maternal exposure to particulate matter (PM2.5) that impairs offspring's energy metabolism and gut microbiota composition. Methods: Unexposed female and male C57BL/6J mice were mated. PM2.5 or filtered air (FA) exposure occurred only in gestation (PM2.5/FA) or lactation (FA/PM2.5). We studied the offspring of both genders. Results: PM2.5 exposure during gestation increased body weight (BW) at birth and from weaning to young in male adulthood. Leptin levels, food intake, Agrp, and Npy levels in the hypothalamus were also increased in young male offspring. Ikbke, Tnf increased in male PM2.5/FA. Males from FA/PM2.5 group were protected from these phenotypes showing higher O2 consumption and Ucp1 in the brown adipose tissue. In female offspring, we did not see changes in BW at weaning. However, adult females from PM2.5/FA displayed higher BW and leptin levels, despite increased energy expenditure and thermogenesis. This group showed a slight increase in food intake. In female offspring from FA/PM2.5, BW, and leptin levels were elevated. This group displayed higher energy expenditure and a mild increase in food intake. To determine if maternal exposure to PM2.5 could affect the offspring's gut microbiota, we analyzed alpha diversity by Shannon and Simpson indexes and beta diversity by the Linear Discriminant Analysis (LDA) in offspring at 30 weeks. Unlike males, exposure during gestation led to higher adiposity and leptin maintenance in female offspring at this age. Gestation exposure was associated with decreased alpha diversity in the gut microbiota in both genders. Discussion: Our data support that exposure to air pollution during gestation is more harmful to metabolism than exposure during lactation. Male offspring had an unfavorable metabolic phenotype at a young age. However, at an older age, only females kept more adiposity. Ultimately, our data highlight the importance of controlling air pollution, especially during gestation.

Comparative stereological evaluation of the term allantochorion membrane in the mare pregnant with mule foals and equine foals.

Mules are derived from crossing horse mares with a donkey, in which the interest is due to gentleness and ability to work and equestrian sports. As the placenta is responsible for fetal development and maturation, knowing its typical microstructure allows us to understand how fetomaternal interactions occur in this interspecific pregnancy. Thus, the study performed a comparative stereological evaluation of volumetric composition and fetomaternal contact surface in the uterine body (UB), gravid uterine horn (GUH), and nongravid uterine horn (NGUH) of Mangalarga Paulista mare's term allantochorion membrane in mule and equine pregnancies. In equine gestation, the UB microcotyledon surface density was negatively correlated with the NGUH absolute area and the total volume of microvilli. In mule gestation, the base width and the number of microcotyledon were negatively correlated with the height and number of microcotyledons in the NGUH. Mule also showed a negative correlation between (1) the UB microcotyledon surface density and the GUH microcotyledons number per unit of membrane length, (2) the GUH total volume and the NGUH microcotyledon number. Such differences demonstrate a compensatory mechanism in conversion capacity among macrocompartments. A trend toward a greater total volume of allantoid vessels and total volume of allantoid mesoderm in UB microvilli was found in the equine and mule groups, respectively. There was a significant increase in the base width of microcotyledons in the NGUH of mules versus horses. These finds possibly influence the exchange capacity of each placental microregion and suggest a difference between mule versus horse term allantochorion membrane.

Effect of chronic exposure to fine particulate matter on cardiac tissue of NZBWF1 mice.

Epidemiological and toxicological studies have shown that inhalation of particulate matter (PM) is associated with development of cardiovascular diseases. Long-term exposure to PM may increase the risk of cardiovascular events and reduce life expectancy. Systemic lupus erythematosus (SLE) is a chronic inflammatory disease, autoimmune in nature, that is characterized by the production of autoantibodies that affects several organs, including the heart. Air pollution - which can be caused by several different factors - may be one of the most important points both at the onset and the natural history of SLE. Therefore this study aims to investigate whether exposure to air pollution promotes increased inflammation and cardiac remodelling in animals predisposed to SLE. Female NZBWF1 mice were exposed to an environmental particle concentrator. Aspects related to cardiac remodelling, inflammation and apoptosis were analysed in the myocardium. Body weight gain, cardiac trophism by heart/body weight ratio, relative area of cardiomyocytes and the fibrotic area of cardiac tissue were evaluated during the exposure period. Animals exposed to PM2.5 showed increased area of cardiomyocytes, and area of fibrosis; in addition, we observed an increase in IL-1 and C3 in the cardiac tissue, demonstrating increased inflammation. We suggest that air pollution is capable of promoting cardiac remodelling and increased inflammation in animals predisposed to SLE.

Prenatal exposure to Cannabis smoke induces early and lasting damage to the brain.

Cannabis is the most widely used illegal drug during pregnancy, however, the effects of gestational exposure to Cannabis smoke (CS) on the central nervous system development remain uncharacterised. This study investigates the effects of maternal CS inhalation on brain function in the offspring. Pregnant mice were exposed daily to 5 min of CS during gestational days (GD) 5.5-17.5. On GD 18.5 half of the dams were euthanized for foetus removal. The offspring from the remaining dams were euthanized on postnatal days (PND) 20 and 60 for evaluation. Brain volume, cortex cell number, SOX2, histone-H3, parvalbumin, NeuN, and BDNF immunoreactivity were assessed in all groups. In addition, levels of NeuN, CB1 receptor, and BDNF expression were assessed and cortical primary neurons from rats were treated with Cannabis smoke extract (CSE) for assessment of cell viability. We found that male foetuses from the CS exposed group had decreased brain volume, whereas mice at PND 60 from the exposed group presented with increased brain volume. Olfactory bulb and diencephalon volume were found lower in foetuses exposed to CS. Mice at PND 60 from the exposed group had a smaller volume in the thalamus and hypothalamus while the cerebellum presented with a greater volume. Also, there was an increase in cortical BDNF immunoreactivity in CS exposed mice at PND 60. Protein expression analysis showed an increase in pro-BDNF in foetus brains exposed to CS. Mice at PND 60 presented an increase in mature BDNF in the prefrontal cortex (PFC) in the exposed group and a higher CB1 receptor expression in the PFC. Moreover, hippocampal NeuN expression was higher in adult animals from the exposed group. Lastly, treatment of cortical primary neurons with doses of CSE resulted in decreased cell viability. These findings highlight the potential negative neurodevelopmental outcomes induced by gestational CS exposure.

Aerobic exercise training combined or not with okra consumption as a strategy to prevent kidney changes caused by metabolic syndrome in Zucker rats.

The complications of Metabolic Syndrome (MetS) include kidney disease, and most dialysis patients are diagnosed with MetS. The benefit of exercise training (ET) for MetS treatment is already well defined in the literature, but the antidiabetic and antihyperlipidemic benefits of okra (O) have been discovered only recently. The aim of this study was to evaluate the effects of O and/or ET supplementation on renal function and histology; serum urea and creatinine value; inflammation (IL-6, IL-10, TNF-α) and oxidative stress in renal tissue. For this, 32 Zucker rats (fa/fa) were randomly separated into four groups of 8 animals each: Metabolic Syndrome (MetS), MetS + Okra (MetS + O), MetS + Exercise Training (MetS + ET), and MetS + Exercise Training and Okra (MetS + ET + O), and 8 Zucker lean (fa/+) rats comprised the Control group (CTL). Okra was administered by orogastric gavage 2x/day (morning and night, 100 mg/kg) and ET performed on the treadmill, at moderate intensity, 1h/day, 5x/week for 6 weeks. Although the renal function was not altered, the animals with MetS showed greater fibrotic deposition accompanied by a worse stage of renal injury, in addition to increased kidney weight. Although all interventions were beneficial in reducing fibrosis, only ET combined with O was able to improve the degree of renal tissue impairment. ET improved the anti-inflammatory status and reduced nitrite levels, but the combination of ET and O was more beneficial as regards catalase activity. Okra consumption alone did not promote changes in inflammatory cytokines and oxidative stress in the kidney. In conclusion, ET combined or not with O seems to be beneficial in preventing the progression of renal disease when renal function is not yet altered.

Scientific Evidence about the Risks of Micro and Nanoplastics (MNPLs) to Human Health and Their Exposure Routes through the Environment.

Nowadays, a large amount and variety of plastic is being produced and consumed by human beings on an enormous scale. Microplastics and nanoplastics (MNPLs) have become ubiquitous since they can be found in many ecosystem components. Plastic particles can be found in soil, water, and air. The routes of human exposure are numerous, mainly involving ingestion and inhalation. Once ingested, these particles interact with the gastrointestinal tract and digestive fluids. They can adsorb substances such as additives, heavy metals, proteins, or even microorganisms on their surface, which can cause toxicity. During inhalation, they can be inhaled according to their respective sizes. Studies have reported that exposure to MNPLs can cause damage to the respiratory tract, creating problems such as bronchitis, asthma, fibrosis, and pneumothorax. The reports of boards and committees indicate that there is little data published and available on the toxicity of MNPLs as well as the exposure levels in humans. Despite the well-established concept of MNPLs, their characteristics, and presence in the environment, little is known about their real effects on human health and the environment.

Accumulation of trace element content in the lungs of Sao Paulo city residents and its correlation to lifetime exposure to air pollution.

Heavy metals are natural and essential elements of the environment and living beings, produced from natural (e.g. volcanic activity and cosmic ray-induced spallation) and anthropogenic processes (e.g. industrial and fossil fuel combustion). High-concentrations of heavy metals and radionuclides are also originated from anthropogenic activities in urban and industrial areas. In this preliminary study, we analyzed the levels of heavy metals and Polonium-210 (210Po) in lung tissues in autopsies from residents of the city of Sao Paulo, SP, Brazil. In order to identify the link among sources of the heavy metals in lungs, factor analysis was performed. Of the first four factors, which explain 66% of the total variability, three were associated with vehicular sources. The fitting of a regression model with 210Po as the response variable and with the four factors as explanatory variables, controlling for age, sex and tobacco, showed a significant association between the concentration of polonium and the first factor that is generated by catalysts and brakes (coefficient = 0.90, standard error = 0.33, p = 0.016). Our findings suggest an association between traffic-related trace metals and 210Po in lung autopsies.

Air Pollution: A Neglected Risk Factor for Dementia in Latin America and the Caribbean.

The risk of dementia and Alzheimer's disease in Latin America and the Caribbean (LAC) rises with increasing age and polluted air. Currently, at least 172 million people breathe unhealthy levels of air pollution in LAC countries. Several cohort studies have indicated that air pollution increases the risk of developing dementia and neurodegenerative diseases, but the mechanisms underlying the association are still not clear. Air pollution causes and aggravates five established risk factors for dementia (obesity, hypertension, stroke, diabetes mellitus, and heart diseases) and is linked to three other risk factors (physical inactivity, cognitive inactivity, and depression). Some of these risk factors could be mediating the association between air pollution and dementia. Reducing the risks for dementia is crucial and urgently needed in LAC countries. There is room for improving air quality in many urban areas in the LAC region and other low- and middle-income countries (LMICs), a routealready explored by many urban areas in developing regions. Moreover, reducing air pollution has proved to improve health outcomes before. In this article, we propose that despite the ongoing and valid scientific discussion, if air pollution can or cannot directly affect the brain and cause or aggravate dementia, we are ready to consider air pollution as a potentially modifiable risk factor for dementia in LAC and possibly in other LMICs. We suggest that controlling and reducing current air pollution levels in LAC and other LMIC regions now could strongly contribute.

Lasting effects of prenatal exposure to Cannabis in the retina of the offspring: an experimental study in mice.

BACKGROUND: Prenatal exposure to Cannabis is a worldwide growing problem. Although retina is part of the central nervous system, the impact of maternal Cannabis use on the retinal development and its postnatal consequences remains unknown. As the prenatal period is potentially sensitive in the normal development of the retina, we hypothesized that recreational use of Cannabis during pregnancy may alter retina structure in the offspring. To test this, we developed a murine model that mimics human exposure in terms of dose and use. METHODS: Pregnant BalbC mice were exposed daily for 5 min to Cannabis smoke (0.2 g of Cannabis) or filtered air, from gestational day 5 to 18 (N = 10/group). After weaning period, pups were separated and examined weekly. On days 60, 120, 200, and 360 after birth, 10 pups from each group were randomly selected for Spectral Domain Optical Coherence Tomography (SD-OCT) analysis of the retina. All retina layers were measured and inner, outer, and total retina thickness were calculated. Other 37 mice from both groups were sacrificed on days 20, 60, and 360 for retinal stereology (total volume of the retina and volume fraction of each retinal layer) and light microscopy. Means and standard deviations were calculated and MANOVA was performed. RESULTS: The retina of animals which mother was exposed to Cannabis during gestation was 17% thinner on day 120 (young adult) than controls (P = 0.003) due to 21% thinning of the outer retina (P = 0.001). The offspring of mice from the exposed group presented thickening of the IS/OS in comparison to controls on day 200 (P < 0.001). In the volumetric analyzes by retinal stereology, the exposed mice presented transitory increase of the IS/OS total volume and volume fraction on day 60 (young adult) compared to controls (P = 0.008 and P = 0.035, respectively). On light microscopy, exposed mice presented thickening of the IS/OS on day 360 (adult) compared to controls (P = 0.03). CONCLUSION: Gestational exposure to Cannabis smoke may cause structural changes in the retina of the offspring that return to normal on mice adulthood. These experimental evidences suggest that children and young adults whose mothers smoked Cannabis during pregnancy may require earlier and more frequent clinical care than the non-exposed population.

The impact of chronic exposure to air pollution over oxidative stress parameters and brain histology.

Air pollution (AP) triggers neuroinflammation and lipoperoxidation involved in physiopathology of several neurodegenerative diseases. Our study aims to investigate the effect of chronic exposure to ambient AP in oxidative stress (OS) parameters and number of neurons and microglial cells of the cortex and striatum. Seventy-two male Wistar rats were distributed in four groups of exposure: control group (FA), exposed throughout life to filtered air; group PA-FA, pre-natal exposed to polluted air until weaning and then to filtered air; group FA-PA, pre-natal exposed to filtered air until weaning and then to polluted air; and group PA, exposed throughout life to polluted air. After 150 days of exposure, the rats were euthanized for biochemical and histological determinations. The malondialdehyde concentration in the cortex and striatum was significantly higher in the PA group. The activity of superoxide dismutase was significantly decreased in the cortex of all groups exposed to AP while activity of catalase was not modified in the cortex or striatum. The total glutathione concentration was lower in the cortex and higher in the striatum of the FA-PA group. The number of neurons or microglia in the striatum did not differ between FA and PA. On the other hand, neurons and microglia cell numbers were significantly higher in the cortex of the FA-PA group. Our findings suggest that the striatum and cortex have dissimilar thresholds to react to AP exposure and different adaptable responses to chronically AP-induced OS. At least for the cortex, changing to a non-polluted ambient early in life was able to avoid and/or reverse the OS, although some alterations in enzymatic antioxidant system may be permanent. As a result, it is important to clarify the effects of AP in the cortical organization and function because of limited capacity of brain tissue to deal with threatening environments.

Chronic exposure to PM2.5 aggravates SLE manifestations in lupus-prone mice.

BACKGROUND: Air pollution causes negative impacts on health. Systemic lupus erythematosus (SLE) is an autoimmune disease with diverse clinical manifestations and multifactorial etiology. Recent studies suggest that air pollution can trigger SLE and induce disease activity. However, this association has not been deeply investigated. Thus, the aim of this study was to evaluate whether exposure to fine particulate matter (PM2.5) exacerbates SLE manifestations, focusing on renal complications, in a lupus-prone animal model. Female NZBWF1 mice were exposed daily to 600 µg/m3 of inhaled concentrated ambient particles (CAP) or filtered air (FA). Survival rate, body weight, weight of organs (kidney, spleen, thymus, liver and heart), blood cell count, proteinuria, kidney stereology, renal histopathology, gene expression and oxidative stress were analyzed. RESULTS: Female NZBW mice exposed to CAP showed decreased survival, increased circulating neutrophils, early onset of proteinuria and increased kidney weight with renal cortex enlargement when compared to NZBW mice exposed to FA. CONCLUSIONS: This work shows that air pollution aggravates some SLE manifestations in lupus-prone mice. These results reinforce the need of reducing air pollutant levels in order to promote a better quality of life for individuals diagnosed with SLE.

Air pollution impairs recovery and tissue remodeling in a murine model of acute lung injury.

Evidence regarding the impact of air pollution on acute respiratory distress syndrome (ARDS) is limited, and most studies focus on ARDS onset. Our study aimed to evaluate whether exposure to fine particulate matter interferes with lung recovery and remodeling in a murine model of acute lung injury. Forty-eight mice received nebulized LPS or the vehicle (controls). Blood, BALF, lungs and spleen were collected after 5 weeks of exposure to either PM2.5 (PM and LPS + PM group) or filtered air (control and LPS5w groups). Inflammatory cells and cytokines were assessed in the blood, BALF, lungs and spleen. Stereological analyses and remodeling assessments were performed by histology. The LPS + PM group showed increased BALF leukocytes, characterized by increased macrophages, increased IL-1ß and IL-6 levels, anemia and thrombocytopenia. Moreover, we also observed septal thickening, decreased alveolar air space total volume and, septa surface density. Finally, regarding tissue remodeling, we observed elastosis of the lung parenchyma, and unlike in the LPS5w group, we did not observe fibrosis in the LPS + PM group. In conclusion, the delayed inflammation resolution due to subchronic exposure to PM2.5 could be influenced by low systemic and local lymphocyte counts, which lead to impaired lung injury recovery and tissue remodeling.