ABSTRACT BACKGROUND: Exposure to air pollutants and illness by severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection can cause serious pulmonary impairment. OBJECTIVE: To identify a possible association between exposure to air pollutants and hospitalizations due to SARS-Cov-2. DESIGN AND SETTING: Ecological time-series study carried out in Taubaté, Tremembé, and Pindamonhangaba in 2020 and 2021. METHODS: Study with Sars-Cov-2 hospitalizations with information on hospitalization date, sex and age of the subjects, duration of hospitalization, type of discharge, and costs of these hospitalizations. Statistical analysis was performed through a negative binomial regression, with data on pollutant concentrations, temperature, air relative humidity, and hospitalization date. Coefficients obtained by the analysis were transformed into relative risk for hospitalization, which estimated hospitalizations excess according to an increase in pollutant concentrations. RESULTS: There were 1,300 hospitalizations and 368 deaths, with a predominance of men (61.7%). These data represent an incidence rate of 250.4 per 100,000 inhabitants and 28.4% hospital lethality. Significant exposure (P value < 0.05) occurred seven days before hospital admission (lag 7) for nitrogen dioxide (NO2) (relative risk, RR = 1.0124) and two days before hospital admission for PM2.5 (RR = 1.0216). A 10 μg/m3 in NO2 concentration would decrease by 320 hospitalizations and » US $ 240,000 in costs; a 5 μg/m3 in PM2.5 concentration would decrease by 278 hospitalizations and » US $ 190,000 in costs. CONCLUSION: An association between exposure to air pollutants and hospital admission due to Sars-Cov-2 was observed with excess hospitalization and costs for the Brazilian public health system.

ABSTRACT BACKGROUND: Exposure to air pollutants and illness by severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection can cause serious pulmonary impairment. OBJECTIVE: To identify a possible association between exposure to air pollutants and hospitalizations due to SARS-Cov-2. DESIGN AND SETTING: Ecological time-series study carried out in Taubaté, Tremembé, and Pindamonhangaba in 2020 and 2021. METHODS: Study with Sars-Cov-2 hospitalizations with information on hospitalization date, sex and age of the subjects, duration of hospitalization, type of discharge, and costs of these hospitalizations. Statistical analysis was performed through a negative binomial regression, with data on pollutant concentrations, temperature, air relative humidity, and hospitalization date. Coefficients obtained by the analysis were transformed into relative risk for hospitalization, which estimated hospitalizations excess according to an increase in pollutant concentrations. RESULTS: There were 1,300 hospitalizations and 368 deaths, with a predominance of men (61.7%). These data represent an incidence rate of 250.4 per 100,000 inhabitants and 28.4% hospital lethality. Significant exposure (P value < 0.05) occurred seven days before hospital admission (lag 7) for nitrogen dioxide (NO2) (relative risk, RR = 1.0124) and two days before hospital admission for PM2.5 (RR = 1.0216). A 10 μg/m3 in NO2 concentration would decrease by 320 hospitalizations and » US $ 240,000 in costs; a 5 μg/m3 in PM2.5 concentration would decrease by 278 hospitalizations and » US $ 190,000 in costs. CONCLUSION: An association between exposure to air pollutants and hospital admission due to Sars-Cov-2 was observed with excess hospitalization and costs for the Brazilian public health system.

ABSTRACT BACKGROUND: Exposure to particulate matter (PM) is associated with hospitalizations due to respiratory diseases among children. DESIGN AND SETTING: An ecological time series study was carried out to identify the role of coarse fractions of particulate matter (PM10-2.5) in hospitalizations among children up to 10 years of age, in Piracicaba (SP) in the year 2015. METHODS: A generalized additive model of Poisson regression was used to estimate the risk of hospitalization due to acute laryngitis and tracheitis, pneumonia, bronchitis, bronchiolitis and asthma. Lags of 0 to 7 days were considered, and the model was adjusted for the temperature and relative humidity of the air and controlled for short and long-term exposure. Proportional attributable ratios, population-attributable fractions and hospital costs were calculated with increasing concentrations of these pollutants. RESULTS: 638 hospitalizations were evaluated during this period, with a mean of 1.75 cases per day (standard deviation, SD = 1.86). The daily averages were 22.45 µg/m3 (SD = 13.25) for the coarse fraction (PM10-2.5) and 13.32 µg/m3 (SD = 6.38) for the fine fraction. Significant risks of PM10-2.5 exposure were only observed at lag 0, with relative risk (RR) = 1.012, and at lag 6, with RR = 1.011. An increase of 5 µg/m3 in the coarse fraction concentration implied an increase in the relative risk of hospitalizations of up to 4.8%, with an excess of 72 hospitalizations and excess expenditure of US$ 17,000 per year. CONCLUSIONS: This study showed the impact of coarse-fraction exposure on hospital admissions among children due to respiratory diseases.

Resumo Objetivo: Estimar a associação entre exposição ao material particulado fino com diâmetro aerodinâmico inferior a 2,5 micra (PM2.5) e as internações por pneumonia e asma em crianças. Métodos: Estudo ecológico de séries temporais com indicadores diários de internação por pneumonia e asma, em crianças com até 10 anos, residentes em Taubaté (SP), e concentrações estimadas de PM2.5, entre agosto de 2011 e julho de 2012. Modelo aditivo generalizado de regressão de Poisson foi usado para estimar o risco relativo, com defasagem de zero até cinco dias após a exposição; o modelo unipoluente foi ajustado pela temperatura aparente, medida definida a partir da temperatura e umidade relativa do ar, sazonalidade e dia da semana. Resultados: Os valores dos riscos relativos para internações por pneumonia e asma foram significativos para lag 0 (RR=1,051; IC95% 1,016-1,088); lag 2 (RR=1,066; IC95% 1,023-1,113); lag 3 (RR=1,053; IC95% 1,015-1,092); lag 4 (RR=1,043; IC95% 1,004-1,088) e no lag 5 (RR=1,061; IC95% 1,018-1,106). O incremento de 5mcg/m3 de PM2.5 contribui para aumento no risco relativo para internações entre 20,3 a 38,4 pontos percentuais; no entanto, a diminuição de 5µg/m3 na concentração do PM2.5 resulta em menos 38 internações. Conclusões: A exposição ao PM2.5 esteve associada às internações por pneumonia e asma em crianças menores de 10 anos, mostrou o papel do material particulado fino na saúde da criança e forneceu subsídios para implantação de medidas preventivas para diminuírem esses desfechos.

Abstract Objective: To estimate the association between exposure to fine particulate matter with an aerodynamic diameter <2.5 microns (PM2.5) and hospitalizations for pneumonia and asthma in children. Methods: An ecological study of time series was performed, with daily indicators of hospitalization for pneumonia and asthma in children up to 10 years of age, living in Taubaté (SP) and estimated concentrations of PM2.5, between August 2011 and July 2012. A generalized additive model of Poisson regression was used to estimate the relative risk, with lag zero up to five days after exposure; the single pollutant model was adjusted by the apparent temperature, as defined from the temperature and relative air humidity, seasonality and weekday. Results: The values of the relative risks for hospitalization for pneumonia and asthma were significant for lag 0 (RR=1.051, 95%CI; 1.016 to 1.088); lag 2 (RR=1.066, 95%CI: 1.023 to 1.113); lag 3 (RR=1.053, 95%CI: 1.015 to 1.092); lag 4 (RR=1.043, 95%CI: 1.004 to 1.088) and lag 5 (RR=1.061, 95%CI: 1.018 to 1.106). The increase of 5mcg/m3 in PM2.5 contributes to increase the relative risk for hospitalization from 20.3 to 38.4 percentage points; however, the reduction of 5µg/m3 in PM2.5 concentration results in 38 fewer hospital admissions. Conclusions: Exposure to PM2.5 was associated with hospitalizations for pneumonia and asthma in children younger than 10 years of age, showing the role of fine particulate matter in child health and providing subsidies for the implementation of preventive measures to decrease these outcomes.

A colonização do Helicobacter pylori está associada com gastrite crônica, úlcera péptica, metaplasia intestinal, adenocarcinoma e linfoma gástrico. O objetivo desse estudo foi comparar os resultados do diagnóstico histológico usado de rotina na detecção do H. pylori com o diagnóstico molecular. Foram utilizadas amostras de 80 lesões gástricas (gastrite crônica, gastrite atrófica, úlcera gástrica e metaplasia intestinal), 18 amostras de adenocarcinoma gástrico e 10 amostras de mucosa gástrica normal H. pylori negativas (controle). Todas as amostras foram avaliadas histologicamente (coloração com hematoxilina-eosina e Giemsa) e pela PCR com a amplificação dos genes antígeno espécie-específico (H3H4) e urease A (H5H6) do H. pylori e pelo gene humano CYP1A1, como controle da qualidade do DNA. Nas amostras de lesão benigna e adenocarcinoma gástrico, a infecção foi detectada em 43% (42/98) e 71% (70/98), respectivamente, para os diagnósticos histológico e molecular (p = 0,0001). O teste de PCR detectou o H. pylori em 27,5% (22/80) das lesões gástricas benignas e em 50% (9/18) dos adenocarcinomas gástricos, com diagnóstico histológico negativo para essa bactéria. Cerca de 2,5% das amostras, exclusivamente de lesões benignas, com diagnóstico histológico positivo apresentaram resultado molecular negativo, para ambos os primers. Diferenças estatisticamente significantes foram encontradas entre os métodos histológico e molecular, em metaplasia intestinal (p = 0,0461) e adenocarcinoma gástrico (p = 0,0011), devido à subdetecção do H. pylori pelo método histológico, e provavelmente pela baixa densidade da bactéria conseqüente à atrofia severa da mucosa gástrica, nesses dois tipos de lesões. Nossos achados demonstram que o método de PCR é mais eficaz para diagnosticar a infecção por H. pylori, principalmente, em metaplasia intestinal e adenocarcinoma gástrico.

Helicobacter pylori colonization is associated with chronic gastritis, peptic ulcers, intestinal metaplasia, adenocarcinoma and lymphoma of the stomach. The objective of this study was to compare the results of the routinely used histology with molecular diagnosis for the detection of H. pylori. Eighty samples from gastric lesions (chronic gastritis, atrophic gastritis, gastric ulcer, and intestinal metaplasia), 18 gastric adenocarcinoma and 10 normal mucosa H. pylori-negative (control) samples were obtained. All samples were examined histologically (hematoxylin-eosin and Giemsa staining), and PCR amplifications of the species-specific antigen gene (H3H4) and urease A gene segment (H5H6) of H. pylori were made, using the human gene CYP1A1 for DNA quality control. In the benign lesion and adenocarcinoma the infection was detected in 43% (42/98) and 71% (70/98) by histological and molecular diagnosis (p = 0.0001), respectively. The PCR test detected H. pylori in 27.5% (22/80) of the benign gastric lesions and in 50% (9/18) of the gastric adenocarcinoma cases, the histological diagnosis being negative for this bacterium. About 2.5% of the samples, exclusively from benign lesions and with a positive histological diagnosis, showed negative molecular results for both primers. Statistically significant differences were found between the histological and the molecular method in intestinal metaplasia (p = 0.0461) and gastric adenocarcinoma (p = 0.0011), due to underdetection of H. pylori by the histological method, which is probably due to the low density of the bacterium as a consequence of the severe atrophy of the gastric mucosa. Our findings suggest that PCR is the more efficient method for the assessment of H. pylori infection, especially in metaplasia and gastric adenocarcinoma.

RACIONAL: O câncer de estômago é o segundo tipo mais comum de neoplasia no mundo. A carcinogênese de estômago é processo de múltiplos passos, podendo manifestar-se em várias etapas como gastrite superficial, gastrite atrófica crônica, metaplasia intestinal, displasia e, finalmente, como um carcinoma. Essas condições costumam ser seqüenciais e ocorrer num período de muitos anos como resultado da exposição a uma variedade de fatores endógenos e exógenos, que causam alterações genéticas. Os recentes avanços da genética molecular têm mostrado que o acúmulo dessas várias anormalidades, incluindo a ativação de oncogenes e a inativação de genes supressores de tumores, resultam no desenvolvimento do câncer. Alterações genéticas descritas em carcinomas gástricos incluem amplificações e mutações dos genes c-ERBB2, K-RAS, c-MET e TP53. O ganho de cromossomos também foi encontrado em várias combinações com perda de outros cromossomos e pode estar associado com a expressão elevada de oncogenes, que contribuem com a progressão tumoral. CONCLUSÃO: Essas mudanças genéticas em carcinomas evidenciam o processo de múltiplas etapas da carcinogênese gástrica, por meio do acúmulo de uma série de alterações.

BACKGROUND: Gastric cancer is considered to be the second most common cancer worldwide. Carcinogenesis of the stomach is a multi-stage process. The progression from normal epithelial to tumor cells may involve at least five stages: superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia and carcinoma. These sequential changes in the gastric mucosa may occur over a period of many years as a result of exposure to a variety of exogenous and/or endogenous factors which cause genetic alterations. Recent developments in molecular genetics have shown that the accumulation of these multiple genetic alterations, including activation of oncogenes and inactivation of tumor-suppressor genes, results in cancer development. Genetic alterations previously reported in gastric carcinomas include amplifications or mutations of the c-ERBB2, K-RAS, c-MET and TP53. Chromosomal gains were also found in various combinations with chromosomal losses and may be associated with the overexpression of dominant oncogenes contributing to tumor progression. CONCLUSIONS: These accumulated genetic changes in carcinomas provide evidences for the stepwise mode of gastric carcinogenesis through the accumulation of a series of genetic alterations.