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Santa Gertrudes (SG) and Rio Claro (RC), Sao Paulo, Brazil, are located in a ceramic industrial park zone, and their particulate matter with an aerodynamic diameter of less than 10 µm (PM10) concentration levels has been among the highest in recently monitored cities in Brazil. Local PM10 was mostly composed of silica. A cross-sectional study was designed to evaluate the lung functions of public high school students in SG, RC, and São Pedro (SP) (control location), Brazil, in 2018. The prevalence of asthma, mean PM10, FVC (forced vital capacity), and FEV1 (forced expiratory volume in the first second) were compared between the locations, and regression analyses were performed. A total of 450 students were included (SG: 158, RC: 153, and SP: 139). The mean FVC% (SG: 95.0% ± 11.8%, RC: 98.8% ± 12.9%, SP: 102.4% ± 13.8%, p < 0.05), the mean FEV1% (SG: 95.7% ± 10.4%, RC: 99.7% ± 12.0%, SP: 103.2% ± 12.0%, p < 0.05) and the mean PM10 (SG: 77.75 ± 38.08 µg/m3, RC: 42.59 ± 23.46 µg/m3, SP: 29.52 ± 9.87 µg/m3, p < 0.01) differed between locations. In regression models, each increase in PM10 by 10 µg/m3 was associated with a decrease in FVC% by 1.10% (95% CI 0.55%-1.65%) and a decrease in FEV1% by 1.27% (95% CI 0.75%-1.79%). Exposure to high levels of silica-rich environmental PM10 was found to be associated with lower FVC and FEV1.

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BACKGROUND: The identification of markers that can facilitate the early diagnosis of silicosis has remained challenging. We evaluated the association of inflammatory markers with the presence of silicosis and lung function impairment in individuals exposed to silica. METHODS: Individuals exposed and not exposed to silica were assessed by occupational history, clinical findings, lung function, chest imaging findings, and inflammatory markers. RESULTS: Among 297 men evaluated, 51 were unexposed controls (G1), 149 were exposed to silica without silicosis (G2), and 97 were exposed to silica with silicosis (G3). Inflammatory marker levels were higher in G3 than in G2 and G1. Platelet/lymphocyte ratio (PLR), lactate dehydrogenase (LDH), soluble tumor necrosis factor II (sTNFRII), and macrophage inflammatory protein-4 (MIP-4) were associated with silicosis, and LDH, neutrophil/lymphocyte ratio (NLR), sTNFRII, monocyte chemoattractant protein-1 (MCP-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and fibrinogen were negatively associated with lung function. CONCLUSION: Blood inflammatory markers are associated with silicosis and impaired lung function.

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This review aimed to provide an overview of pulmonary arteriovenous malformations, including the major clinical and radiological presentations, investigation, and treatment algorithm of the condition. The primary etiology of pulmonary arteriovenous malformations is hereditary hemorrhagic telangiectasia (HHT), also known as Rendu-Osler-Weber syndrome, with mutations in the ENG gene on chromosome 9 (HHT type 1) or in the ACVRL1/ALK1 complex (HHT type 2). Epistaxis should always be evaluated when repeated, when associated with anemia, and in some cases of hypoxemia. In the investigation, contrast echocardiography and chest CT are essential for evaluating this condition. Embolization is the best treatment choice, especially for correction in cases of hypoxemia or to avoid systemic infections. Finally, disease management was addressed in special conditions such as pregnancy. CT follow-up should be performed every 3-5 years, depending on the size of the afferent and efferent vessels, and antibiotic prophylactic care should always be oriented. Ultimately, knowledge of the disease by health professionals is a crucial point for the early diagnosis of these patients in clinical practice, which can potentially modify the natural course of the disease.

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BACKGROUND: Work-related asthma (WRA) is the most prevalent occupational respiratory disease, and it has negative effects on socioeconomic standing, asthma control, quality of life, and mental health status. Most of the studies on WRA consequences are from high-income countries; there is a lack of information on these effects in Latin America and in middle-income countries. METHODS: This study compared socioeconomic, asthma control, quality of life, and psychological outcomes among individuals diagnosed with WRA and non-work-related asthma (NWRA) in a middle-income country. Patients with asthma, related and not related to work, were interviewed using a structured questionnaire to assess their occupational history and socioeconomic conditions, and with questionnaires to assess asthma control (Asthma Control Test and Asthma Control Questionnaire-6), quality of life (Juniper's Asthma Quality of Life Questionnaire), and presence of anxiety and depression symptoms (Hospital Anxiety and Depression Scale). Each patient's medical record was reviewed for exams and use of medication, and comparisons were made between individuals with WRA and NWRA. RESULTS: The study included 132 patients with WRA and 130 with NWRA. Individuals with WRA had worse socioeconomic outcomes, worse asthma control, more quality-of-life impairment, and a higher prevalence of anxiety and depression than individuals with NWRA. Among individuals with WRA, those who had been removed from occupational exposure had a worse socioeconomic impact. CONCLUSIONS: Consequences on socioeconomic, asthma control, quality of life, and psychological status are worse for WRA individuals when compared with NWRA.

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ABSTRACT This review aimed to provide an overview of pulmonary arteriovenous malformations, including the major clinical and radiological presentations, investigation, and treatment algorithm of the condition. The primary etiology of pulmonary arteriovenous malformations is hereditary hemorrhagic telangiectasia (HHT), also known as Rendu-Osler-Weber syndrome, with mutations in the ENG gene on chromosome 9 (HHT type 1) or in the ACVRL1/ALK1 complex (HHT type 2). Epistaxis should always be evaluated when repeated, when associated with anemia, and in some cases of hypoxemia. In the investigation, contrast echocardiography and chest CT are essential for evaluating this condition. Embolization is the best treatment choice, especially for correction in cases of hypoxemia or to avoid systemic infections. Finally, disease management was addressed in special conditions such as pregnancy. CT follow-up should be performed every 3-5 years, depending on the size of the afferent and efferent vessels, and antibiotic prophylactic care should always be oriented. Ultimately, knowledge of the disease by health professionals is a crucial point for the early diagnosis of these patients in clinical practice, which can potentially modify the natural course of the disease.

RESUMO Esta revisão teve como objetivo fornecer uma visão geral das malformações arteriovenosas pulmonares, incluindo as principais apresentações clínicas e radiológicas, investigação e algoritmo de tratamento da condição. A principal etiologia das malformações arteriovenosas pulmonares é a telangiectasia hemorrágica hereditária (THH), também conhecida como síndrome de Rendu-Osler-Weber, com mutações no gene ENG no cromossomo 9 (THH tipo 1) ou no complexo ACVRL1/ALK1 (THH tipo 2). A epistaxe sempre deve ser avaliada quando repetida, quando associada à anemia e em alguns casos de hipoxemia. Na investigação, a ecocardiografia e TC de tórax com contraste são essenciais para avaliar essa condição. A embolização é a melhor escolha terapêutica, especialmente para correção em casos de hipoxemia ou para evitar infecções sistêmicas. Por fim, o manejo da doença foi abordado em condições especiais, como a gravidez. O acompanhamento por TC deve ser feito a cada 3-5 anos, dependendo do tamanho dos vasos aferentes e eferentes, e a antibioticoprofilaxia deve sempre ser orientada. Em última análise, o conhecimento da doença pelos profissionais de saúde é um ponto crucial para o diagnóstico precoce desses pacientes na prática clínica, o que pode potencialmente modificar o curso natural da doença.

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Chronic thromboembolic pulmonary hypertension (CTEPH) is a serious and debilitating disease caused by occlusion of the pulmonary arterial bed by hematic emboli and by the resulting fibrous material. Such occlusion increases vascular resistance and, consequently, the pressure in the region of the pulmonary artery, which is the definition of pulmonary hypertension. The increased load imposed on the right ventricle leads to its progressive dysfunction and, finally, to death. However, CTEPH has a highly significant feature that distinguishes it from other forms of pulmonary hypertension: the fact that it can be cured through treatment with pulmonary thromboendarterectomy. Therefore, the primary objective of the management of CTEPH should be the assessment of patient fitness for surgery at a referral center, given that not all patients are good candidates. For the patients who are not good candidates for pulmonary thromboendarterectomy, the viable therapeutic alternatives include pulmonary artery angioplasty and pharmacological treatment. In these recommendations, the pathophysiological bases for the onset of CTEPH, such as acute pulmonary embolism and the clinical condition of the patient, will be discussed, as will the diagnostic algorithm to be followed and the therapeutic alternatives currently available.

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Malignant pleural mesothelioma (MPM) is an aggressive neoplasm that originates from hyperplasia and metaplasia of the mesothelial cells that cover the pleural cavity. Previous exposure to asbestos is the main risk factor. Since MPM is often diagnosed at an advanced stage with rapid evolution and resistance to treatment, it is associated with an unfavorable outcome. Mesothelioma in situ (MIS) has been postulated as a preinvasive phase of MPM; however, its diagnostic criteria have been defined only recently. Diagnosis of MIS may represent an opportunity for early therapies with better results, but the optimal approach has not been defined thus far. Here, we report on a case of a 74-year-old man with right-sided pleural effusion and a previous history of occupational exposure to asbestos for 9 years who was diagnosed with MIS after a latency of 36 years. During follow-up, spontaneous disease regression was observed 5 months after the initial diagnosis; however, it recurred in the form of invasive epithelioid MPM. There is a paucity of literature on MIS and its evolution; however, our case provides relevant knowledge of this unusual behavior, which is important to define follow-up and therapeutic strategies for future cases.

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Resumo Muitos avanços ocorreram nas últimas décadas na terapêutica da hipertensão arterial pulmonar (HAP), uma doença grave, progressiva, incurável e potencialmente fatal. Para seu tratamento adequado, são fundamentais o diagnóstico hemodinâmico e a classificação de sua etiologia, em que várias delas (colagenoses, hipertensão portal, cardiopatia congênitas, esquistossomose) requerem medidas específicas, além do tratamento farmacológico característico para HAP. O tratamento com fármacos-alvo para HAP baseia-se em produtos farmacêuticos que interferem em três vias fisiopatológicas moleculares: da prostaciclina, da endotelina e do óxido nítrico. Tais fármacos apresentam múltiplas apresentações (oral, endovenosa, subcutânea e inalatória) e mudaram a história da HAP. Essas medicações e suas estratégias de uso, assim como particularidades das diferentes formas de HAP, são o foco desta revisão.

Abstract In the last decades, important advances have been made in the treatment of pulmonary arterial hypertension (PAH), a severe, progressive, incurable, and potentially fatal disease. For an adequate therapy, correct hemodynamic diagnosis and etiology classification are fundamental. Many etiologies - rheumatic disease, portal hypertension, congenital heart diseases, schistosomiasis - require specific measures, in addition to drug therapy for PAH. The specific therapy for PAH is based on medications that act on three pathophysiological pathways - prostacyclin, endothelin, and nitric oxide pathways. These drugs have multiple presentations (oral, intravenous, subcutaneous, and inhaled) and have changed the history of PAH. This review presents an overview of drug therapy strategies and different forms and peculiarities of PAH.

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