Inflammatory Status in Trained and Untrained Mice at Different Pollution Levels.

Atmospheric pollution can be defined as a set of changes that occur in the composition of the air, making it unsuitable and/or harmful and thereby generating adverse effects on human health. The regular practice of physical exercise (PE) is associated with the preservation and/or improvement of health; however, it can be influenced by neuroimmunoendocrine mechanisms and external factors such as air pollution, highlighting the need for studies involving the practice of PE in polluted environments. Herein, 24 male C57BL/6 mice were evaluated, distributed into four groups (exposed to a high concentration of pollutants/sedentary, exposed to a high concentration of pollutants/exercised, exposed to ambient air/sedentary, and exposed to ambient air/exercised). The exposure to pollutants occurred in the environmental particle concentrator (CPA) and the physical training was performed on a treadmill specially designed for use within the CPA. Pro- and anti-inflammatory markers in blood and bronchoalveolar lavage (BALF), BALF cellularity, and lung tissue were evaluated. Although the active group exposed to a high concentration of pollution showed a greater inflammatory response, both the correlation analysis and the ratio between pro- and anti-inflammatory cytokines demonstrated that the exercised group presented greater anti-inflammatory activity, suggesting a protective/adaptative effect of exercise when carried out in a polluted environment.

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.

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.

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.

Sistema de avaliação de testes psicológicos: histórias contadas e não contadas / Psychological test evaluation system: stories told and untold / Sistema de evaluación de tests psicológicos: historias contadas y no contadas

O Sistema de Avaliação de Testes Psicológicos (SATEPSI) recebeu notoriedade entre brasileiros e estrangeiros por oferecer um complexo sistema de qualificação dos testes psicológicos, pouco visto em âmbito mundial. Sua elaboração dependeu de uma autarquia, que o financiou, normatizou e o mantém, mas também de pesquisadores docentes de avaliação psicológica, que trouxeram a expertise da área para que houvesse o pleno estabelecimento de seus parâmetros. Passadas duas décadas de seu lançamento, o SATEPSI foi tema de artigos, capítulos, lives e diálogos digitais, nos quais foram destaque, de modo geral, as Resoluções do Conselho Federal de Psicologia, que o normatiza, e seus impactos para a área de avaliação psicológica - como, por exemplo, o aumento do número de pesquisas e de testes brasileiros qualificados. O que se pretende neste artigo é mencionar sua construção, à luz dos autores que vivenciaram o SATEPSI em funções e tempos distintos. Atenção especial será dada aos Métodos Projetivos, cuja história ainda é pouco revelada.(AU)

The system to evaluate psychological tests (Satepsi) received notoriety among Brazilians and foreigners for offering a complex system of qualification of psychological tests, which is rarely seen worldwide. Its development depended on an autarchy (which financed, standardized, and maintains it) and on researchers teaching psychological assessment, who brought their expertise to the area so its parameters could be fully established. After two decades of its launch, Satepsi was the subject of articles, chapters, lives, and digital dialogues, which usually highlighted the Resolutions of the Federal Council of Psychology that normatize psychological evaluation and their impacts, such as the increase in the number of qualified Brazilian tests. This study aims to mention its construction in the light of the authors who experienced Satepsi in different functions and times, giving special attention to Projective Methods, whose history remains to be shown.(AU)

El Sistema de Evaluación de Tests Psicológicos (SATEPSI) ganó notoriedad entre los brasileños y los extranjeros por ofrecer un complejo sistema de calificación de los tests psicológicos, poco frecuente a nivel mundial. Su elaboración dependió de una autarquía, que lo financió, lo estandarizó y lo mantiene, pero también de investigadores docentes de evaluación psicológica, que trajeron la experiencia del área para que hubiera el pleno establecimiento de sus parámetros. Tras dos décadas de su lanzamiento, SATEPSI fue tema de artículos, capítulos, en directo y diálogos digitales, en los cuales destacaron, de modo general, las Resoluciones del Consejo Federal de Psicología que lo normatiza y sus impactos para el área de evaluación psicológica, como el aumento del número de investigaciones y de pruebas brasileñas calificadas. Lo que se pretende en este artículo es mencionar su construcción, a la luz de los autores que vivieron el SATEPSI en funciones y tiempos distintos. Se prestará especial atención a los métodos proyectivos cuya historia aún no se ha revelado.(AU)

Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice.

The perinatal period and early infancy are considered critical periods for lung development. During this period, adversities such as environmental exposures, allergic sensitization, and asthma are believed to impact lung health in adulthood. Therefore, we hypothesized that concomitant exposure to allergic sensitization and urban-derived fine particulate matter (PM2.5) in the early postnatal period of mice would cause more profound alterations in lung alveolarization and growth and differently modulate lung inflammation and gene expression than either insult alone in adult life. BALB/c mice were sensitized with ovalbumin (OVA) and exposed to PM2.5 from the fifth day of life. Then, we assessed lung responsiveness, inflammation in BALF, lung tissue, and alveolarization by stereology. In addition, we performed a transcriptomic analysis of lung tissue on the 40th day of life. Our results showed that young adult mice submitted to allergic sensitization and exposure to ambient PM2.5 since early life presented decreased lung growth with impaired alveolarization, a mixed neutrophilic-eosinophilic pattern of lung inflammation, increased airway responsiveness, and increased expression of genes linked to neutrophil recruitment when compared to animals that were OVA-sensitized or PM2.5 exposed only. Both, early life allergic sensitization and PM2.5 exposure, induced inflammation and impaired lung growth, but concomitant exposure was associated with worsened inflammation parameters and caused alveolar enlargement. Our experimental data provide pathological support for the hypothesis that allergic or environmental insults in early life have permanent adverse consequences for lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice. Together with our data, current evidence points to the urgent need for healthier environments with fewer childhood disadvantage factors during the critical windows of lung development and growth.

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.

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.

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.

LPS Response Is Impaired by Urban Fine Particulate Matter.

Fine particulate matter (PM2.5) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM2.5 on LPS-induced lung injury onset. BALB/c male mice were exposed to either filtered air or ambient fine PM2.5 in an ambient particle concentrator for 5 weeks. Then, an acute lung injury was induced with nebulized LPS. The animals were euthanized 24 h after the nebulization to either LPS or saline. Inflammatory cells and cytokines (IL-1ß, IL-4, IL-5, IL-6, IL-10, IL-17, TNF) were assessed in the blood, bronchoalveolar lavage fluid (BALF), and lung tissue. In addition, lung morphology was assessed by stereological methods. Our results showed that the PM+LPS group showed histological evidence of injury, leukocytosis with increased neutrophils and macrophages, and a mixed inflammatory response profile, with increased KC, IL-6, IL-1ß, IL-4, and IL-17. Our analysis shows that there is an interaction between the LPS nebulization and PM2.5 exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM2.5 exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM2.5 exposure.

Heterogeneous impacts of mobility restrictions on air quality in the State of Sao Paulo during the COVID-19 pandemic.

Air quality in the State of Sao Paulo was evaluated during the first general State plan of mobility restrictions due to the COVID-19 pandemic (24th March to May 31, 2020). Nitrogen dioxide (NO2), ozone (O3), particulate matter PM10 and PM2.5 and sulphur dioxide (SO2) concentrations were assessed in cities of the Sao Paulo State with a monitoring station and compared to historical data. Linear regression models were built to investigate the relationship between the isolation of the population - determined using mobile phone monitoring data - and the concentration of each pollutant during the studied period. Although the reduction of pollutants such as NO2, SO2 and PM2.5 is very clear, the economic and climatic characteristics of each region were decisive in the general behaviour of O3 and PM10. It was not possible to establish a correlation between the pollutants and the isolation index, partly due to the lack of data, partly due to the compliance of the population to those measurements, which was variable over time. Another important limitation factor was the absence of data related to the pollutants of interest in many of the stations. However, the isolation measures carried out in the State opened the opportunity to individually assess the air quality measurements in each of the stations, enabling an understanding that will allow in the future the design of air quality policies together with local sanitary policies.

Safe in the womb? Effects of air pollution to the unborn child and neonates.

OBJECTIVE: In this brief review, the authors focus on the effects of gestational exposures to urban air pollution on fetal development and neonatal outcomes. SOURCE OF DATA: In this review the authors used PubMed, Web of Science and SciELO research platforms, analyzing papers from the last 30 years. SUMMARY OF THE FINDINGS: Epidemiological and experimental evidence agree that gestational exposure to air pollution in urban increases the risks for low birth weight, preterm birth, congenital malformation, intrauterine growth restriction, and neonatal mortality. Furthermore, exposures are associated with increased risks for preeclampsia, hypertension, gestational diabetes. CONCLUSIONS: Therefore, it is time for greater involvement and engagement of the health sector in the discussion of public policies that may affect the quality of the environment, and that directly or indirectly impact the health of those who were not yet born.

Safe in the womb? Effects of air pollution to the unborn child and neonates

Abstract Objective: In this brief review, the authors focus on the effects of gestational exposures to urban air pollution on fetal development and neonatal outcomes. Source of data: In this review the authors used PubMed, Web of Science and SciELO research platforms, analyzing papers from the last 30 years. Summary of the findings: Epidemiological and experimental evidence agree that gestational exposure to air pollution in urban increases the risks for low birth weight, preterm birth, congenital malformation, intrauterine growth restriction, and neonatal mortality. Furthermore, exposures are associated with increased risks for preeclampsia, hypertension, gestational diabetes. Conclusions: Therefore, it is time for greater involvement and engagement of the health sector in the discussion of public policies that may affect the quality of the environment, and that directly or indirectly impact the health of those who were not yet born.

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.