Understanding the impact on human health during peak episodes in air pollution is invaluable for policymakers. Particles less than PM2.5 can penetrate the respiratory system, causing cardiopulmonary ...and other systemic diseases. Statistical regression models are usually used to assess air pollution impacts on human health. However, when there are databases missing, linear statistical regression may not process well and alternative data processing should be considered. Nonlinear Artificial Neural Networks (ANN) are not employed to research environmental health pollution even though another advantage in using ANN is that the output data can be expressed as the number of hospital admissions. This research applied ANN to assess the impact of air pollution on human health. Three well-known ANN were tested: Multilayer Perceptron (MLP), Extreme Learning Machines (ELM) and Echo State Networks (ESN), to assess the influence of PM2.5, temperature, and relative humidity on hospital admissions due to respiratory diseases. Daily PM2.5 levels were monitored, and hospital admissions for respiratory illness were obtained, from the Brazilian hospital information system for all ages during two sampling campaigns (2008–2011 and 2014–2015) in Curitiba, Brazil. During these periods, the daily number of hospital admissions ranged from 2 to 55, PM2.5 concentrations varied from 0.98 to 54.2 μg m−3, temperature ranged from 8 to 26 °C, and relative humidity ranged from 45 to 100%. Of the ANN used in this study, MLP gave the best results showing a significant influence of PM2.5, temperature and humidity on hospital attendance after one day of exposure. The Anova Friedman's test showed statistical difference between the appliance of each ANN model (p < .001) for 1 lag day between PM2.5 exposure and hospital admission. ANN could be a more sensitive method than statistical regression models for assessing the effects of air pollution on respiratory health, and especially useful when there is limited data available.
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•Artificial Neural Networks (ANN) was applied to predict PM2.5 impact on human health.•Multilayer perceptron (MLP) showed best results.•Study of annual behavior of PM2.5 revealed high pollution events on winter.•PM2.5 elemental composition is mainly from anthropogenic activities.•Main contributions to PM2.5 emissions were from traffic sources.
ANN models predict respiratory hospital admissions from meteorological conditions and PM2.5 concentrations.
Aims
Brazil ranks high in the number of coronavirus disease 19 (COVID‐19) cases and the COVID‐19 mortality rate. In this context, autopsies are important to confirm the disease, determine associated ...conditions, and study the pathophysiology of this novel disease. The aim of this study was to assess the systemic involvement of COVID‐19. In order to follow biosafety recommendations, we used ultrasound‐guided minimally invasive autopsy (MIA‐US), and we present the results of 10 initial autopsies.
Methods and results
We used MIA‐US for tissue sampling of the lungs, liver, heart, kidneys, spleen, brain, skin, skeletal muscle and testis for histology, and reverse transcription polymerase chain reaction to detect severe acute respiratory syndrome coronavirus 2 RNA. All patients showed exudative/proliferative diffuse alveolar damage. There were intense pleomorphic cytopathic effects on the respiratory epithelium, including airway and alveolar cells. Fibrinous thrombi in alveolar arterioles were present in eight patients, and all patients showed a high density of alveolar megakaryocytes. Small thrombi were less frequently observed in the glomeruli, spleen, heart, dermis, testis, and liver sinusoids. The main systemic findings were associated with comorbidities, age, and sepsis, in addition to possible tissue damage due to the viral infection, such as myositis, dermatitis, myocarditis, and orchitis.
Conclusions
MIA‐US is safe and effective for the study of severe COVID‐19. Our findings show that COVID‐19 is a systemic disease causing major events in the lungs and with involvement of various organs and tissues. Pulmonary changes result from severe epithelial injury and microthrombotic vascular phenomena. These findings indicate that both epithelial and vascular injury should be addressed in therapeutic approaches.
•We hypothesized that O3 and NO2 may influence fetal and birth weight and umbilical Doppler velocimetry.•We measured O3 and NO2 in each pregnancy trimester using passive personal samplers.•O3 and NO2 ...did not influence fetal and birth weight.•Exposure to O3 influenced placental resistance.
We determined the influence of maternal air pollution exposure during each trimester of pregnancy on fetal and birth weight and fetoplacental hemodynamics. In total, 366 women with singleton pregnancies were prospectively followed in the city of São Paulo, Brazil. Nitrogen dioxide (NO2) and ozone (O3) were measured during each trimester using passive personal samplers. We evaluated fetal weight and Doppler velocimetry data from the umbilical, middle cerebral, and uterine arteries in the 3rd trimester, and birth weight. Multivariate analysis was performed, controlling for known determinants of fetal weight. Exposure to higher levels of O3 during the 2nd trimester was associated with higher umbilical artery pulsatility indices (PIs) p=0.013; beta=0.017: standard error (SE)=0.007. Exposure to higher levels of O3 during the 3rd trimester was associated with lower umbilical artery PIs (p=0.011; beta=−0.021; SE=0.008). Our results suggest that in the environment of São Paulo, O3 may affects placental vascular resistance.
Background
Long-term exposure to fine particles ≤2.5 μm in diameter (PM
2.5
) has been linked to cancer mortality. However, the effect of wildfire-related PM
2.5
exposure on cancer mortality risk is ...unknown. This study evaluates the association between wildfire-related PM
2.5
and site-specific cancer mortality in Brazil, from 2010 to 2016.
Methods and findings
Nationwide cancer death records were collected during 2010–2016 from the Brazilian Mortality Information System. Death records were linked with municipal-level wildfire- and non-wildfire-related PM
2.5
concentrations, at a resolution of 2.0° latitude by 2.5° longitude. We applied a variant difference-in-differences approach with quasi-Poisson regression, adjusting for seasonal temperature and gross domestic product (GDP) per capita. Relative risks (RRs) and 95% confidence intervals (CIs) for the exposure for specific cancer sites were estimated. Attributable fractions and cancer deaths were also calculated. In total, 1,332,526 adult cancer deaths (age ≥ 20 years), from 5,565 Brazilian municipalities, covering 136 million adults were included. The mean annual wildfire-related PM
2.5
concentration was 2.38 μg/m
3
, and the annual non-wildfire-related PM
2.5
concentration was 8.20 μg/m
3
. The RR for mortality from all cancers was 1.02 (95% CI 1.01–1.03,
p
< 0.001) per 1-μg/m
3
increase of wildfire-related PM
2.5
concentration, which was higher than the RR per 1-μg/m
3
increase of non-wildfire-related PM
2.5
(1.01 95% CI 1.00–1.01,
p =
0.007, with
p
for difference = 0.003). Wildfire-related PM
2.5
was associated with mortality from cancers of the nasopharynx (1.10 95% CI 1.04–1.16,
p =
0.002), esophagus (1.05 95% CI 1.01–1.08,
p =
0.012), stomach (1.03 95% CI 1.01–1.06,
p =
0.017), colon/rectum (1.08 95% CI 1.05–1.11,
p <
0.001), larynx (1.06 95% CI 1.02–1.11,
p =
0.003), skin (1.06 95% CI 1.00–1.12,
p =
0.003), breast (1.04 95% CI 1.01–1.06,
p =
0.007), prostate (1.03 95% CI 1.01–1.06,
p =
0.019), and testis (1.10 95% CI 1.03–1.17,
p =
0.002). For all cancers combined, the attributable deaths were 37 per 100,000 population and ranged from 18/100,000 in the Northeast Region of Brazil to 71/100,000 in the Central-West Region. Study limitations included a potential lack of assessment of the joint effects of gaseous pollutants, an inability to capture the migration of residents, and an inability to adjust for some potential confounders.
Conclusions
Exposure to wildfire-related PM
2.5
can increase the risks of cancer mortality for many cancer sites, and the effect for wildfire-related PM
2.5
was higher than for PM
2.5
from non-wildfire sources.
There are no reports of the systemic human pathology of the novel swine H1N1 influenza (S-OIV) infection.
The autopsy findings of 21 Brazilian patients with confirmed S-OIV infection are presented. ...These patients died in the winter of the southern hemisphere 2009 pandemic, with acute respiratory failure.
Lung tissue was submitted to virologic and bacteriologic analysis with real-time reverse transcriptase polymerase chain reaction and electron microscopy. Expression of toll-like receptor (TLR)-3, IFN-gamma, tumor necrosis factor-alpha, CD8(+) T cells and granzyme B(+) cells in the lungs was investigated by immunohistochemistry.
Patients were aged from 1 to 68 years (72% between 30 and 59 yr) and 12 were male. Sixteen patients had preexisting medical conditions. Diffuse alveolar damage was present in 20 individuals. In six patients, diffuse alveolar damage was associated with necrotizing bronchiolitis and in five with extensive hemorrhage. There was also a cytopathic effect in the bronchial and alveolar epithelial cells, as well as necrosis, epithelial hyperplasia, and squamous metaplasia of the large airways. There was marked expression of TLR-3 and IFN-gamma and a large number of CD8(+) T cells and granzyme B(+) cells within the lung tissue. Changes in other organs were mainly secondary to multiple organ failure.
Autopsies have shown that the main pathological changes associated with S-OIV infection are localized to the lungs, where three distinct histological patterns can be identified. We also show evidence of ongoing pulmonary aberrant immune response. Our results reinforce the usefulness of autopsy in increasing the understanding of the novel human influenza A (H1N1) infection.
In humans, adverse pregnancy outcomes (low birth weight, prematurity, and intrauterine growth retardation) are associated with exposure to urban air pollution. Experimental data have also shown that ...such exposure elicits adverse reproductive outcomes. We hypothesized that the effects of urban air pollution on pregnancy outcomes could be related to changes in functional morphology of the placenta. To test this, future dams were exposed during pregestational and gestational periods to filtered or nonfiltered air in exposure chambers. Placentas were collected from near-term pregnancies and prepared for microscopical examination. Fields of view on vertical uniform random tissue slices were analyzed using stereological methods. Volumes of placental compartments were estimated, and the labyrinth was analyzed further in terms of its maternal vascular spaces, fetal capillaries, trophoblast, and exchange surface areas. From these primary data, secondary quantities were derived: vessel calibers (expressed as diameters), trophoblast thickness (arithmetic mean), and total and mass-specific morphometric diffusive conductances for oxygen of the intervascular barrier. Two-way analysis of variance showed that both periods of exposure led to significantly smaller fetal weights. Pregestational exposure to nonfiltered air led to significant increases in fetal capillary surface area and in total and mass-specific conductances. However, the calibers of maternal blood spaces were reduced. Gestational exposure to nonfiltered air was associated with reduced volumes, calibers, and surface areas of maternal blood spaces and with greater fetal capillary surfaces and diffusive conductances. The findings indicate that urban air pollution affects placental functional morphology. Fetal weights are compromised despite attempts to improve diffusive transport across the placenta.
•It was unknown whether there was an association with cancer hospitalizations.•Long-term exposure to ambient PM2.5 was positively associated with hospitalization for many cancer types in ...Brazil.•Inpatient days and cost would be saved if the annual PM2.5 exposure was reduced.
Long-term exposure to PM2.5 has been linked to cancer incidence and mortality. However, it was unknown whether there was an association with cancer hospitalizations.
Data on cancer hospitalizations and annual PM2.5 concentrations were collected from 1,814 Brazilian cities during 2002–2015. A difference-in-difference approach with quasi-Poisson regression was applied to examine State-specific associations. The State-specific associations were pooled at a national level using random-effect meta-analyses. PM2.5 attributable burden were estimated for cancer hospitalization admissions, inpatient days and costs.
We included 5,102,358 cancer hospitalizations (53.8% female). The mean annual concentration of PM2.5 was 7.0 μg/m3 (standard deviation: 4.0 μg/m3). With each 1 μg/m3 increase in two-year-average (current year and previous one year) concentrations of PM2.5, the relative risks (RR) of hospitalization were 1.04 (95% confidence interval CI: 1.02 to 1.07) for all-site cancers from 2002 to 2015 without sex and age differences. We estimated that 33.82% (95%CI: 14.97% to 47.84%) of total cancer hospitalizations could be attributed to PM2.5 exposure in Brazil during the study time. For every 100,000 population, 1,190 (95%CI: 527 to 1,836) cancer hospitalizations, 8,191 (95%CI: 3,627 to 11,587) inpatient days and US$788,775 (95%CI: $349,272 to $1,115,825) cost were attributable to PM2.5 exposure.
Long-term exposure to ambient PM2.5 was positively associated with hospitalization for many cancer types in Brazil. Inpatient days and cost would be saved if the annual PM2.5 exposure was reduced.
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•PM2.5 was associated with reduced life expectancy from all-causes, cancer, cardiovascular and respiratory diseases.•Regional inequalities and different trends were observed in PM2.5 ...attributable loss of life expectancy in Brazil.•Life expectancy would be improved by setting new WHO air quality guideline PM2.5 level as the acceptable threshold.
Long-term exposure to PM2.5 is proved to be linked with mortality. However, limited studies have estimated the PM2.5 related loss of life expectancy (LLE) and its changing trends. How much life expectancy would be improved if PM2.5 pollution is reduced to the new WHO air quality guideline (AQG) level is unclear.
Data on deaths from all-causes, cancer, cardiovascular and respiratory diseases were collected from 5,565 Brazilian municipalities during 2010–2018. A difference-in-differences approach with quasi-Poisson regression was applied to examine the PM2.5-years of life lost (YLL) associations and PM2.5 associated LLE.
The annual PM2.5 concentration in each municipality from 2010 to 2018 was 7.7 µg/m3 in Brazil. Nationally, with each 10 μg/m3 increase in five-year-average (current and previous four years) concentrations of PM2.5, the relative risks (RRs) were 1.18 (95% CI: 1.15–1.21) for YLL from all-causes, 1.22 (1.16–1.28) from cancer, 1.12 (1.08–1.17) from cardiovascular and 1.17 (1.10–1.25) from respiratory diseases. Life expectancy could be improved by 1.09 (95% CI: 0.92–1.25) years by limiting PM2.5 concentration to the national lowest level (2.9 µg/m3), specifically, 0.20 (0.15–0.24) years for cancer, 0.16 (0.11–0.22) years for cardiovascular and 0.09 (0.05–0.13) years for respiratory diseases, with significant disparities across regions and municipalities. Life expectancy would be improved by 0.78 (0.66–0.90) years by setting the new WHO AQG PM2.5 concentration level of 5 μg/m3 as an acceptable threshold.
Using nationwide death records in Brazil, we found that long-term exposure to PM2.5 was associated with reduced life expectancy from all-causes, cancer, cardiovascular and respiratory diseases with regional inequalities and different trends. PM2.5 pollution abatement to below the WHO AQG level would improve this loss of life expectancy in Brazil.
Long-term exposure to PM2.5 has been linked to lung cancer incidence and mortality, but limited evidence existed for other cancers. This study aimed to assess the association between PM2.5 on cancer ...specific mortality. An ecological study based on the cancer mortality data collected from 5,565 Brazilian cities during 2010–2018 using a difference-in-differences approach with quasi-Poisson regression, was applied to examine PM2.5-cancer mortality associations. Globally gridded annual average surface PM2.5 concentration was extracted and linked with the residential municipality of participants in this study. Sex, age stratified and exposure-response estimations were also conducted. Totalling 1,768,668 adult cancer deaths records of about 208 million population living across 5,565 municipalities were included in this study. The average PM2.5 concentration was 7.63 μg/m3 (standard deviation 3.32) with range from 2.95 μg/m3 to 28.5 μg/m3. With each 10 μg/m3 increase in three-year-average (current year and previous two years) concentrations of PM2.5, the relative risks (RR) of cancer mortality were 1.16 (95% confidence interval CI: 1.11–1.20) for all-site cancers. The PM2.5 exposure was significantly associated with several cancer-specific mortalities including oral, nasopharynx, oesophagus, and stomach, colon rectum, liver, gallbladder, larynx, lung, bone, skin, female breast, cervix, prostate, brain and leukaemia. No safe level of PM2.5 exposure was observed in the exposure-response curve for all types of cancer. In conclusion, with nationwide cancer death records in Brazil, we found that long-term exposure to ambient PM2.5 increased risks of mortality for many cancer types. Even low level PM2.5 concentrations had significant impacts on cancer mortality.
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•Long-term exposure to ambient PM2.5 increased risks of mortality for many cancer types.•There is no threshold for the effects of PM2.5 on mortality from all cancer sites.•Even low level PM2.5 concentrations had significant impacts on cancer mortality.
Air pollution is one of the most environmental health concerns in the world and has serious impact on human health, particularly in the mucous membranes of the respiratory tract and eyes. However, ...ocular hazardous effects to air pollutants are scarcely found in the literature.
Panel study to evaluate the effect of different levels of ambient air pollution on lacrimal film cytokine levels of outdoor workers from a large metropolitan area.
Thirty healthy male workers, among them nineteen professionals who work on streets (taxi drivers and traffic controllers, high pollutants exposure, Group 1) and eleven workers of a Forest Institute (Group 2, lower pollutants exposure compared to group 1) were evaluated twice, 15 days apart. Exposure to ambient PM2.5 (particulate matter equal or smaller than 2.5 μm) was 24 hour individually collected and the collection of tears was performed to measure interleukins (IL) 2, 4, 5 and 10 and interferon gamma (IFN-γ) levels. Data from both groups were compared using Student's t test or Mann- Whitney test for cytokines. Individual PM2.5 levels were categorized in tertiles (lower, middle and upper) and compared using one-way ANOVA. Relationship between PM2.5 and cytokine levels was evaluated using generalized estimating equations (GEE).
PM2.5 levels in the three categories differed significantly (lower: ≤22 μg/m3; middle: 23-37.5 μg/m3; upper: >37.5 μg/m3; p<0.001). The subjects from the two groups were distributed unevenly in the lower category (Group 1 = 8%; Group 2 = 92%), the middle category (Group 1 = 89%; Group 2 = 11%) and the upper category (Group 1 = 100%). A significant relationship was found between IL-5 and IL-10 and PM2.5 levels of the group 1, with an average decrease of 1.65 pg/mL of IL-5 level and of 0.78 pg/mL of IL-10 level in tear samples for each increment of 50 μg/m3 of PM2.5 (p = 0.01 and p = 0.003, respectively).
High levels of PM2.5 exposure is associated with decrease of IL-5 and IL-10 levels suggesting a possible modulatory action of ambient air pollution on ocular surface immune response.
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