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1.
Environ Int ; 158: 107003, 2022 01.
Artigo em Inglês | MEDLINE | ID: mdl-34991263

RESUMO

BACKGROUND: Accumulating evidence indicates early life exposure to air pollution, a suspected neurotoxicant, is negatively associated with children's neurodevelopment. OBJECTIVES: To explore the role of multiple exposure periods to ambient particulate matter with diameter <2.5 µm (PM2.5) and nitrogen dioxide (NO2) on emotion and behaviour, and early development in children <13 years. METHODS: We used data from Mothers and their Children's Health (MatCH) study, a 2016/17 sub-study from a prospective longitudinal study, the Australian Longitudinal Study on Women's Health. Annual PM2.5 and NO2 estimates since 1996 were obtained from a land-use regression model. Maternal residential proximity to roadways were used as a proxy measure of exposure to traffic-related air pollution. Child outcomes were maternal-rated emotional and behavioural problems (Strengths and Difficulties Questionnaire; SDQ, aged 2-12 years, n = 5471 children) and developmental delay in communication and gross motor skills (Ages and Stages Questionnaire; ASQ, aged 1-66 months, n = 1265 children). Defined exposure periods were early life exposure ('during pregnancy' and 'first year of life') and 'children's lifetime exposure'. Ambient air pollution was divided into tertiles and logistic regression was performed to estimate odds ratio (OR) for each child outcome, adjusting for potential confounders. RESULTS: Children exposed to moderate and high PM2.5 exposure, compared to low exposure, across all periods, had higher odds of emotional and behavioural problems, and gross motor delay. Children's lifetime exposure to moderate levels of PM2.5 (5.9-7.1 µg/m3) was associated with 1.27 (95% confidence interval 1.03, 1.57) fold higher odds of emotional/behavioural problems. Similar associations were found for moderate PM2.5 levels at 'first year of life' in a two-pollutant model only (OR: 1.30; 1.05, 1.60). However, there was insufficient evidence to suggest that NO2 exposure or living within 200 m of major roads was associated with emotional and behaviour problems or developmental delay across any exposure periods. CONCLUSION: We found isolated evidence that early life and childhood exposure to PM2.5 may be associated with emotional and behavioural problems and delays in gross motor skills, but most associations were null. Due to the limited number of longitudinal studies on low-exposure settings, further studies with more temporally refined exposure assessment are warranted.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Austrália/epidemiologia , Criança , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Feminino , Humanos , Estudos Longitudinais , Saúde Mental , Dióxido de Nitrogênio/análise , Material Particulado/análise , Material Particulado/toxicidade , Gravidez , Estudos Prospectivos
2.
Artigo em Inglês | MEDLINE | ID: mdl-35010792

RESUMO

COVID-19 has caused a global pandemic with considerable impact. Studies have examined the influence of socioeconomic status and air pollution on COVID-19 risk but in low detail. This study seeks to further elucidate the nuances of socioeconomic status, as defined by the Index of Multiple Deprivation (IMD), air pollution, and their relationship. We examined the effect of IMD and air pollution on the likelihood of testing positive for SARS-CoV-2 among 66,732 UKB participants tested for SARS-CoV-2 from 16 March 2020 through 16 March 2021. Logistic regression was performed controlling for age, sex, ancestry and IMD or air pollution in the respective models. IMD and its sub-scores were significantly associated with increased risk of testing positive for SARS-CoV-2. All particulate matter less than 2.5 µm (PM2.5), nitrogen oxide (NOx), and nitrogen dioxide (NO2) levels were associated with increased likelihood of testing positive for SARS-CoV-2. Measures of green space and natural environment around participants' homes were associated with reduced likelihood of SARS-CoV-2. Socioeconomic status and air pollution have independent effects on the risk of testing positive for SARS-CoV-2. Green space and natural environment space in the proximity of people's homes may mediate the effect of air pollution on the risk of testing positive for SARS-CoV-2.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , COVID-19 , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Bancos de Espécimes Biológicos , Humanos , Material Particulado/análise , Material Particulado/toxicidade , SARS-CoV-2 , Reino Unido/epidemiologia
3.
Artigo em Inglês | MEDLINE | ID: mdl-35010846

RESUMO

In 2019, a novel coronavirus, SARS-CoV-2, was first reported in Wuhan, China. The virus causes the disease commonly known as COVID-19, and, since its emergence, it has infected over 252 million individuals globally and taken the lives of over 5 million in the same time span. Primary research on SARS-CoV-2 and COVID-19 focused on understanding the biomolecular composition of the virus. This research has led to the development of multiple vaccines with great efficacy and antiviral treatments for the disease. The development of biomedical interventions has been crucial to combating this pandemic; additionally, environmental confounding variables that could have exacerbated the pandemic need further assessment. In this research study, we conducted a spatial analysis of particulate matter (PM) concentration and its association with COVID-19 mortality in the United States. Results of this study demonstrate a significant positive correlation between PM concentration levels and COVID-19 mortality; however, this does not necessarily imply a causal relationship. These results are consistent with similar studies in Italy and China, where significant COVID-19 cases and corresponding deaths were exhibited. Furthermore, maps of the data demonstrate clustering of COVID-19 mortality which suggest further investigation into the social determinants of health impacting the pandemic.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , COVID-19 , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Humanos , Pandemias , Material Particulado/análise , Material Particulado/toxicidade , SARS-CoV-2 , Análise Espacial
4.
Environ Int ; 158: 106997, 2022 01.
Artigo em Inglês | MEDLINE | ID: mdl-34991257

RESUMO

BACKGROUND: Multiple health effects are associated with moisture damage in buildings. Studies explaining these associations and cell-level mechanisms behind the observed health effects are urgently called for. OBJECTIVES: We focused on characterizing gene expression in human airway epithelium after exposure to indoor air particulate matter (PM) sampled from houses with and without moisture damage, alongside determination of general toxicological markers. METHODS: We performed detailed technical building inspections in 25 residential houses and categorized them based on the detection of moisture damages and the probability of occupant exposure. PM sampling was complemented by microbiological and volatile organic compound assessment. We exposed human airway constructs to three dilutions (1:16, 1:8, 1:4) of collected PM from moisture-damaged (index) and non-moisture-damaged (reference) houses and imaged selected constructs with electron microscopy. We analyzed general toxicological markers and the RNA of exposed constructs was sequenced targeting genes associated with toxicological pathways. We did groupwise comparisons between index and reference houses and pairwise comparisons in matched index/reference houses. RESULTS: In groupwise comparison, gene Cytochrome P450 Family 1 Subfamily A Member 1 (CYP1A1) was statistically significantly over-expressed in index houses at all dilutions of collected PM and Nuclear Factor Kappa B Subunit 1 (NFKB1) at dilution 1:4 of collected PM. In pairwise index/reference house comparison, several genes related to multiple toxicological pathways were activated, largest expression differences seen for CYP1A1. However, none of the genes was consistently expressed in all the matched pairs, and general toxicological markers did not differentiate index and reference houses. DISCUSSION: The exposure to PM from index houses activated toxicology -related genes in airway constructs. Differential expression was not consistent among all the index/reference pairs, possibly due to compositional differences of bioactive particles. Our study highlights CYP1A1 and NFKB1 as potential targets in moisture damage -associated cellular responses.


Assuntos
Poluentes Atmosféricos , Poluição do Ar em Ambientes Fechados , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar em Ambientes Fechados/análise , Humanos , Material Particulado/análise , Material Particulado/toxicidade , Transcriptoma
5.
J Environ Sci (China) ; 115: 215-226, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-34969449

RESUMO

Particulate matter emissions (PM10) from the combustion, in a residential stove, of two commercial brands of certified (ENplus A1) pellets, a non-certified brand and laboratory made pellets of acacia were tested for their ability to induce ecotoxic, cytotoxic, and mutagenic responses in unicellular organisms and a human cell line. Ecotoxicity was evaluated through the Vibrio fischeri bioluminescence inhibition assay. Moreover, cytotoxicity was assessed at two time points (24- and 48-hr) through two complementary techniques in order to evaluate the cellular metabolic activity and membrane integrity of human lung epithelial cells A549. The Ames test using two Salmonella typhimurium strains (TA100 and TA98) was employed to assess the mutagenic potential of the polycyclic aromatic hydrocarbon fraction extracted from the PM10 samples. Results obtained with the bioluminescent bacteria indicated that only particles from the combustion of acacia pellets were toxic. All samples induced impairment on the A549 cells metabolic activity, while no significant release of lactate dehydrogenase was recorded. PM10 emissions from acacia pellets were the most cytotoxic, while samples from both certified pellets evoked significant cytotoxicity at lower doses. Cytotoxicity time-dependency was only observed for PM10 from the combustion of acacia pellets and one of the brands of certified pellets. Mutagenic activity was not detected in both S. typhimurium strains. This study emphasises the role of the raw material for pellet manufacturing on the toxicological profile of PM emissions. Alternative raw materials should be deeply investigated before their use in pelletisation and combustion in residential appliances.


Assuntos
Poluentes Atmosféricos , Hidrocarbonetos Policíclicos Aromáticos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Humanos , Testes de Mutagenicidade , Mutagênicos , Material Particulado/análise , Material Particulado/toxicidade , Hidrocarbonetos Policíclicos Aromáticos/análise , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Emissões de Veículos , Madeira/química
6.
Environ Pollut ; 295: 118677, 2022 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-34906594

RESUMO

Air pollution exposure positively correlates with increased cardiovascular morbidity and mortality rates, mainly due to myocardial infarction (MI). Herein, we aimed to study the metabolic mechanisms underlying this association, focusing on the evaluation of cardiac mitochondrial function and dynamics, together with its impact over MI progression. An initial time course study was performed in BALB/c mice breathing filtered air (FA) or urban air (UA) in whole-body exposure chambers located in Buenos Aires City downtown for up to 16 weeks (n = 8 per group and time point). After 12 weeks, lung inflammatory cell recruitment was evident in UA-exposed mice. Interestingly, impaired redox metabolism, characterized by decreased lung SOD activity and increased GSSG levels and NOX activity, precede local inflammation in this group. At this selected time point, additional mice were exposed to FA or UA (n = 12 per group) and alveolar macrophage PM uptake and nitric oxide (NO) production was observed in UA-exposed mice, together with increased pro-inflammatory cytokine levels (TNF-α and IL-6) in BAL and plasma. Consequently, impaired heart tissue oxygen metabolism and altered mitochondrial ultrastructure and function were observed in UA-exposed mice after 12 weeks, characterized by decreased active state respiration and ATP production rates, and enhanced mitochondrial H2O2 production. Moreover, disturbed cardiac mitochondrial dynamics was detected in this group. This scenario led to a significant increase in the area of infarcted tissue following myocardial ischemia reperfusion injury in vivo, from 43 ± 3% of the area at risk in mice breathing FA to 66 ± 4% in UA-exposed mice (n = 6 per group, p < 0.01), together with a sustained increase in LVEDP during myocardial reperfusion. Taken together, our data unravel cardiac mitochondrial mechanisms that contribute to the understanding of the adverse health effects of urban air pollution exposure, and ultimately highlight the importance of considering environmental factors in the development of cardiovascular diseases.


Assuntos
Poluição do Ar , Infarto do Miocárdio , Poluição do Ar/análise , Animais , Peróxido de Hidrogênio , Camundongos , Mitocôndrias , Infarto do Miocárdio/induzido quimicamente , Material Particulado/toxicidade
7.
Ecotoxicol Environ Saf ; 229: 113087, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34922167

RESUMO

Levels and constituents of ambient air pollution have substantially changed in China over the last decade. Such changes may lead to the variations in health effects of air pollution. Very limited studies, however, have investigated the temporal variations in health effects of air pollution on a long-term scale, especially in China. We evaluated the temporal variations in short-term associations between PM10 and NO2 concentrations and emergency department (ED) visits during a 12-year period from 2008 to 2019 in Shanghai, China. A quasi-Poisson generalized linear regression was performed to assess the associations between PM10 and NO2 concentrations and ED visits during entire study period and three specific periods. We evaluated the temporal variations of period-specific associations with an interaction variable between pollutant concentrations and period indicators. We further investigated the concentration-response relationships for specific periods. The effects on specific subpopulations (males and females; 18-65 years old and >65 years old) were also examined. A 10 µg/m3 increase of PM10 and NO2 corresponded to 0.48% (95% CI: 0.36%, 0.59%) and 1.51% (95% CI: 1.25%, 1.78%) increase in ED visits at lag0-7 day for entire study period, respectively. The short-term associations between ED visits and NO2 remained unchanged over time (P-value > 0.05), while the effects from PM10 were significantly inconsistent (P-value < 0.05), with the highest effect observed during the intermediate period of 2012-2015 and the lowest effect observed during the initial period of 2008-2011. Similar temporal trends were found in subgroups, except for elderly group. Despite substantial reduction in ambient PM10 and NO2 concentrations, the short-term effects on ED visits for NO2 remained stable and even increased for PM10. More efforts were needed to reduce harmful components in air pollution mixture to reduce the health hazards of air pollution.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Adolescente , Adulto , Idoso , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , China , Serviço Hospitalar de Emergência , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Dióxido de Nitrogênio/análise , Material Particulado/análise , Material Particulado/toxicidade , Adulto Jovem
8.
Ecotoxicol Environ Saf ; 229: 113103, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34929501

RESUMO

BACKGROUND: Cooking oil fume (COF) is an important source of indoor air pollution which severely affects human health, and sufficient vitamin D3 (VitD3) is necessary for maternal and child health. However, the effects of cooking oil fume-derived PM2.5 (COF-PM2.5) on birth outcomes and whether VitD3 could protect from adverse effects caused by COFs-PM2.5 are still unclear. METHODS: Twenty-four pregnant rats were divided into 4 groups and treated with various treatments: normal feeding, COFs-PM2.5 intratracheal instillation, VitD3 intragastric administration, and COFs-PM2.5 and VitD3 co-treatment, respectively. The fetal rats were obtained in pregnant 21 days and the development of them was recorded. Morphological changes in umbilical cord were measured with HE staining, and the oxidative stress and inflammatory levels were also investigated. Western blotting and RT-PCR was used to detect the expression of angiogenesis related factors. RESULTS: We successfully established an intrauterine growth restriction model in rats induced by COFs-PM2.5 where fetus weight significantly decreased after COFs-PM2.5 exposure. As for the umbilical cord vasculature, the wall thickened and the lumen narrowed down, and the contractility of the umbilical cord vasculature enhanced after COFs-PM2.5 exposure. COFs-PM2.5 exposure also increased the oxidative stress and inflammation level and activated the HIF-1α/eNOS/NO and VEGF/VEGFR2/eNOS signaling pathway. Interestingly, VitD3 intervention significantly increased the fetus weight and attenuated the injury of umbilical cord vascular, and partly or completely reversed the changes in the ROS/eNOS/ET-1 axis caused by COF-PM2.5. CONCLUSIONS: The findings of this study suggested that COF-PM2.5 exposure could contribute to intrauterine growth restriction through disturbing the ROS/eNOS/ET-1 axis, while VitD3 supplementation could be an effective prophylactic measurement.


Assuntos
Poluição do Ar em Ambientes Fechados , Material Particulado , Animais , Colecalciferol , Culinária , Feminino , Retardo do Crescimento Fetal/induzido quimicamente , Retardo do Crescimento Fetal/prevenção & controle , Material Particulado/toxicidade , Gravidez , Ratos
9.
Environ Pollut ; 295: 118720, 2022 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-34953947

RESUMO

Particulate matter with aerodynamic diameter not larger than 2.5 µm (PM2.5) escalated the risk of respiratory diseases. Mitochondrial dysfunction may play a pivotal role in PM2.5-induced airway injury. However, the potential effect of PM2.5 on mitochondrial permeability transition pore (mPTP)-related airway injury is still unknown. This study aimed to investigate the role of mPTP in PM2.5-induced mitochondrial dysfunction in airway epithelial cells in vitro. PM2.5 significantly reduced cell viability and caused apoptosis in BEAS-2B cells. We also found PM2.5 caused cellular and mitochondrial morphological alterations, evidenced by the disappearance of mitochondrial cristae, mitochondrial swelling, and the rupture of the outer mitochondrial membrane. PM2.5 induced mPTP opening via upregulation of voltage-dependent anion-selective channel (VDAC), leading to deprivation of mitochondrial membrane potential, increased mitochondrial reactive oxygen species (ROS) generation and intracellular calcium level. PM2.5 suppressed mitochondrial respiratory function by reducing basal and maximal respiration, and ATP production. The mPTP targeting compounds cyclosporin A [CsA; a potent inhibitor of cyclophilin D (CypD)] and VBIT-12 (a selective VDAC1 inhibitor) significantly inhibited PM2.5-induced mPTP opening and apoptosis, and preserved mitochondrial function by restoring mitochondrial membrane potential, reducing mitochondrial ROS generation and intracellular calcium content, and maintaining mitochondrial respiration function. Our data further demonstrated that PM2.5 caused reduction in nuclear expressions of PPARγ and PGC-1α, which were reversed in the presence of CsA. These findings suggest that mPTP might be a potential therapeutic target in the treatment of PM2.5-induced airway injury.


Assuntos
Proteínas de Transporte da Membrana Mitocondrial , Poro de Transição de Permeabilidade Mitocondrial , Células Epiteliais/metabolismo , Potencial da Membrana Mitocondrial , Mitocôndrias/metabolismo , Proteínas de Transporte da Membrana Mitocondrial/metabolismo , Material Particulado/metabolismo , Material Particulado/toxicidade
10.
Chemosphere ; 286(Pt 1): 131566, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34293557

RESUMO

It is well documented that fine particles matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) are associated with a range of adverse health outcomes. However, most epidemiologic studies have focused on understanding their additive effects, despite that individuals are exposed to multiple air pollutants simultaneously that are likely correlated with each other. Therefore, we applied a novel method - Bayesian Kernel machine regression (BKMR) and conducted a population-based cohort study to assess the individual and joint effect of air pollutant mixtures (PM2.5, O3, and NO2) on all-cause mortality among the Medicare population in 15 cities with 656 different ZIP codes in the southeastern US. The results suggest a strong association between pollutant mixture and all-cause mortality, mainly driven by PM2.5. The positive association of PM2.5 with mortality appears stronger at lower percentiles of other pollutants. An interquartile range change in PM2.5 concentration was associated with a significant increase in mortality of 1.7 (95% CI: 0.5, 2.9), 1.6 (95% CI: 0.4, 2.7) and 1.4 (95% CI: 0.1, 2.6) standard deviations (SD) when O3 and NO2 were set at the 25th, 50th, and 75th percentiles, respectively. BKMR analysis did not identify statistically significant interactions among PM2.5, O3, and NO2. However, since the small sub-population might weaken the study power, additional studies (in larger sample size and other regions in the US) are in need to reinforce the current finding.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Idoso , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Teorema de Bayes , Estudos de Coortes , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Humanos , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Ozônio/análise , Ozônio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade
11.
Chemosphere ; 286(Pt 1): 131615, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34303049

RESUMO

BACKGROUND: Systematic evaluations of the cumulative effects and mortality displacement of ambient particulate matter (PM) pollution on deaths are lacking. We aimed to discern the cumulative effect profile of PM exposure, and investigate the presence of mortality displacement in a large-scale population. METHODS: We conducted a time-series analysis with different exposure-lag models on 13 cities in Jiangsu, China, to estimate the effects of PM pollution on non-accidental, cardiovascular, and respiratory mortality (2015-2019). Over-dispersed Poisson generalized additive models were integrated with distributed lag models to estimate cumulative exposure effects, and assess mortality displacement. RESULTS: Pooled cumulative effect estimates with lags of 0-7 and 0-14 days were substantially larger than those with single-day and 2-day moving average lags. For each 10 µg/m3 increment in PM2.5 concentration with a cumulative lag of 0-7 days, we estimated an increase of 0.50 % (95 % CI: 0.29, 0.72), 0.63 % (95 % CI: 0.38, 0.88), and 0.50 % (95 % CI: 0.01, 1.01) in pooled estimates of non-accidental, cardiovascular, and respiratory mortality, respectively. Both PM10 and PM2.5 were associated with significant increases in non-accidental and cardiovascular mortality with a cumulative lag of 0-14 days. We observed mortality displacement within 30 days for non-accidental, cardiovascular, and respiratory deaths. CONCLUSIONS: Our findings suggest that risk assessment based on single-day or 2-day moving average lag structures may underestimate the adverse effects of PM pollution. The cumulative effects of PM exposure on non-accidental and cardiovascular mortality can last up to 14 days. Evidence of mortality displacement for non-accidental, cardiovascular, and respiratory deaths was found.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doenças Cardiovasculares , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Doenças Cardiovasculares/epidemiologia , China/epidemiologia , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Humanos , Mortalidade , Material Particulado/análise , Material Particulado/toxicidade
12.
Chemosphere ; 286(Pt 1): 131614, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34325257

RESUMO

Particulate matter (PM)-induced airway inflammation contributes to the development and exacerbation of chronic airway diseases. Circular RNA (circRNA) is a new class of non-coding RNA that participates in gene regulation in various respiratory diseases, but the regulatory role of circRNA in PM-induced airway inflammation has not been fully elucidated. In this study, we performed the human circRNA microarray to reveal differentially expressed circRNAs in PM-induced human bronchial epithelial cells (HBECs). A total of 176 upregulated and 15 downregulated circRNAs were identified. Of these, a new circRNA termed circTXNRD1 was upregulated by PM exposure in a dose- and time-dependent manner. Knockdown of circTXNRD1 significantly attenuated PM-induced expression of proinflammatory cytokine interleukin 6 (IL-6). CircRNA pull-down, dual-luciferase reporter assay and fluorescence in situ hybridization showed that circTXNRD1 acted as an endogenous sponge to decrease miR-892a levels in HBECs. Downregulation of miR-892a could increase cyclooxygenase-2 (COX-2) expression and eventually promote IL-6 secretion in PM-induced HBECs. Taken together, our findings reveal circTXNRD1 as a novel inflammatory mediator in PM-induced inflammation in HBECs via regulating miR-892a/COX-2 axis. These results provide new insight into the biological mechanism underlying PM-induced inflammation in chronic airway diseases.


Assuntos
MicroRNAs , RNA Circular , Ciclo-Oxigenase 2/genética , Células Epiteliais , Humanos , Hibridização in Situ Fluorescente , Inflamação/induzido quimicamente , Inflamação/genética , MicroRNAs/genética , Material Particulado/toxicidade , RNA/genética
13.
J Hazard Mater ; 421: 126710, 2022 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-34332479

RESUMO

The particulate matter (PM) in livestock houses, one of the primary sources of atmospheric PM, is not only detrimental to the respiratory health of animals and farmworkers but also poses a threat to the public environment and public health and warrants increased attention. In this study, we investigated the variation in the pulmonary microbiome and metabolome in broiler chickens exposed to PM collected from a broiler house. We examined the pulmonary microbiome and metabolome in broilers, observing that PM induced a visible change in α and ß diversity. A total of 66 differential genera, including unclassified_f_Ruminococcaceae and Campylobacter, were associated with pulmonary inflammation. Untargeted metabolomics was utilised to identify 63 differential metabolites induced by PM and correlated with differential bacteria. We observed that PM resulted in injury of the broiler lung and disruption of the microbial community, as well as causing changes in the observed metabolites. These results imply that perturbations to the microbiome and metabolome may play pivotal roles in the mechanism underlying PM-induced broiler lung damage.


Assuntos
Metaboloma , Microbiota , Animais , Galinhas , Inflamação/induzido quimicamente , Pulmão , Material Particulado/toxicidade
14.
J Hazard Mater ; 422: 126771, 2022 01 15.
Artigo em Inglês | MEDLINE | ID: mdl-34391975

RESUMO

The present study investigates potential nanomaterial releases and occupational health risks across the lifecycle of nano-enabled building materials (NEBMs), namely, insulations and coatings. We utilized real-world degradation scenarios of a) sanding (mechanical), b) incineration (thermal), and c) accelerated UV-aging (environmental) followed by incineration. Extensive physicochemical characterization of the released lifecycle particulate matter (LCPM) was performed. The LCPM2.5 aerosol size fraction was used to assess the acute biological, cytotoxic and inflammatory effects on Calu-3 human lung epithelial cells. RNA-Seq analysis of exposed cells was performed to assess potential for systemic disease. Findings indicated that release dynamics and characteristics of LCPM depended on both the NEBM composition and the degradation scenario(s). Incineration emitted a much higher nanoparticle number concentration than sanding (nearly 4 orders of magnitude), which did not change with prior UV-aging. Released nanofillers during sanding were largely part of the matrix fragments, whereas those during incineration were likely physicochemically transformed. The LCPM from incineration showed higher bioactivity and inflammogenicity compared to sanding or sequential UV-aging and incineration, and more so when metallic nanofillers were present (such as Fe2O3). Overall, the study highlights the need for considering real-world exposure and toxicological data across the NEBM lifecycle to perform adequate risk assessments and to ensure workplace health and safety.


Assuntos
Saúde do Trabalhador , Material Particulado , Aerossóis/análise , Materiais de Construção , Humanos , Incineração , Material Particulado/toxicidade
15.
J Hazard Mater ; 421: 126760, 2022 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-34396970

RESUMO

Large amounts of epidemiological evidence have confirmed the atmospheric particulate matter (PM2.5) exposure was positively correlated with the morbidity and mortality of respiratory diseases. Nevertheless, its pathogenesis remains incompletely understood, probably resulting from the activation of oxidative stress, inflammation, altered genetic and epigenetic modifications in the lung upon PM2.5 exposure. Currently, biomarker investigations have been widely used in epidemiological and toxicological studies, which may help in understanding the biologic mechanisms underlying PM2.5-elicited adverse health outcomes. Here, the emerging biomarkers to indicate PM2.5-respiratory system interactions were summarized, primarily related to oxidative stress (ROS, MDA, GSH, etc.), inflammation (Interleukins, FENO, CC16, etc.), DNA damage (8-OHdG, γH2AX, OGG1) and also epigenetic modulation (DNA methylation, histone modification, microRNAs). The identified biomarkers shed light on PM2.5-elicited inflammation, fibrogenesis and carcinogenesis, thus may favor more precise interventions in public health. It is worth noting that some inconsistent findings may possibly relate to the inter-study differentials in the airborne PM2.5 sample, exposure mode and targeted subjects, as well as methodological issues. Further research, particularly by -omics technique to identify novel, specific biomarkers, is warranted to illuminate the causal relationship between PM2.5 pollution and deleterious lung outcomes.


Assuntos
Poluentes Atmosféricos , MicroRNAs , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Biomarcadores , Humanos , Pulmão , Estresse Oxidativo , Material Particulado/análise , Material Particulado/toxicidade
16.
Environ Res ; 203: 111930, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34425111

RESUMO

In June 2020, we published a review focused on assessing the influence of various air pollutants on the transmission of SARS-CoV-2, and the severity of COVID-19 in patients infected by the coronavirus. The results of most of those reviewed studies suggested that chronic exposure to certain air pollutants might lead to more severe and lethal forms of COVID-19, as well as delays/complications in the recovery of the patients. Since then, a notable number of studies on this topic have been published, including also various reviews. Given the importance of this issue, we have updated the information published since our previous review. Taking together the previous results and those of most investigations now reviewed, we have concluded that there is a significant association between chronic exposure to various outdoor air pollutants: PM2.5, PM10, O3, NO2, SO2 and CO, and the incidence/risk of COVID-19 cases, as well as the severity/mortality of the disease. Unfortunately, studies on the potential influence of other important air pollutants such as VOCs, dioxins and furans, or metals, are not available in the scientific literature. In relation to the influence of outdoor air pollutants on the transmission of SARS-CoV-2, although the scientific evidence is much more limited, some studies point to PM2.5 and PM10 as potential airborne transmitters of the virus. Anyhow, it is clear that environmental air pollution plays an important negative role in COVID-19, increasing its incidence and mortality.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , COVID-19 , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Humanos , Incidência , Material Particulado/análise , Material Particulado/toxicidade , SARS-CoV-2
17.
Chemosphere ; 286(Pt 2): 131833, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34426128

RESUMO

Due to the poor living and healthcare conditions, preterm birth (PTB) in rural population is a pressing health issue. However, PTB studies in rural population are rare. To explore the effects of air pollutants on PTB in rural population, we collected 697,316 medical records during 2014-2016 based on the National Free Preconception Health Examination Project. Logistic regression models were used to estimate the association between air pollutants and PTB and the modifying effects of demographic characteristics. Relative contribution and principal component analysis-generalized linear model (PCA-GLM) analysis were used to explore the most significant air pollutant and gestational period. Our results demonstrated that PTB risk is positively associated with exposure to air pollutants including PM10, PM2.5, SO2, NO2, and CO, while negatively associated with O3 exposure (P < 0.05). In addition, we found that NO2 was the largest contributor to the risk of PTB caused by air pollutants (26.5%). The third trimester of pregnancy was the most sensitive exposure window. PCA-GLM analysis showed that the first component (a combination of PM, SO2, NO2, and CO) increased the risk of PTB. Moreover, we found that rural women who are younger, had higher educated, multi-parity, or smoke appeared to be more sensitive to the association between air pollutants exposure and PTB (P-interaction<0.05). Our findings suggested that increased air pollutants except O3 were associated with elevated PTB risk, especially among vulnerable mothers. Therefore, the effects of air pollutants exposure on PTB should be mitigated by restricting emission sources of NO2 and SO2 in rural population, especially during the third trimester.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Nascimento Prematuro , Efeitos Tardios da Exposição Pré-Natal , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , China/epidemiologia , Feminino , Humanos , Recém-Nascido , Exposição Materna/estatística & dados numéricos , Material Particulado/análise , Material Particulado/toxicidade , Gravidez , Nascimento Prematuro/induzido quimicamente , Nascimento Prematuro/epidemiologia , População Rural
18.
Chemosphere ; 286(Pt 3): 131963, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34426263

RESUMO

BACKGROUND: Exposure to air pollution has been linked with altered immune function in adults, but little is known about its effects on early life. This study aimed to investigate the effects of exposure to air pollution during prenatal and postnatal windows on cell-mediated immune function in preschoolers. METHODS: Pre-school aged children (2.9 ± 0.5 y old, n = 391) were recruited from a mother-child cohort study in Wuhan, China. We used a spatial-temporal land use regression (LUR) model to estimate exposures of particulate matter with aerodynamic diameters ≤2.5 µm (PM2.5) and ≤10 µm (PM10), and nitrogen dioxide (NO2) during the specific trimesters of pregnancy and the first two postnatal years. We measured peripheral blood T lymphocyte subsets and plasma cytokines as indicators of cellular immune function. We used multiple informant models to examine the associations of prenatal and postnatal exposures to air pollution with cell-mediated immune function. RESULTS: Prenatal exposures to PM2.5, PM10, and NO2 during early pregnancy were negatively associated with %CD3+ and %CD3+CD8+ cells, and during late pregnancy were positively associated with %CD3+ cells. Postnatal exposures to these air pollutants during 1-y or 2-y childhood were positively associated with IL-4, IL-5, IL-6, and TNF-α. We also observed that the associations of prenatal or postnatal air pollution exposures with cellular immune responses varied by child's sex. CONCLUSIONS: Our results suggest that exposure to air pollution during different critical windows of early life may differentially alter cellular immune responses, and these effects appear to be sex-specific.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Criança , Pré-Escolar , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Feminino , Humanos , Imunidade Celular , Masculino , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Material Particulado/análise , Material Particulado/toxicidade , Gravidez
19.
Am J Rhinol Allergy ; 36(1): 81-90, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34236242

RESUMO

BACKGROUND: Exposure to urban particulate matter (UPM) is linked to the aggravation of various health problems. Although the nasal cavity is the first barrier to encounter UPM, there is a lack of studies on the impact of UPM on the olfactory area. The purpose of this study was to investigate the cytotoxic effects of UPM on mouse olfactory epithelium, the underlying pathophysiology involved, and changes in cytokine levels. METHODS: Mice were divided into 4 groups: control, 400UPM (administered 400 µg UPM daily; standard reference material 1649b; average particle diameter 10.5 µm) 1week, 400UPM 2weeks, and recovery 1week after 400UPM 2weeks (n = 10, 6, 6, and 6, respectively). Olfactory function was evaluated by conducting a food-finding test once a week. The olfactory neuroepithelium was harvested for histologic examination, gene ontology, quantitative real-time polymerase chain reaction, and western blotting. RESULTS: Compared to those in the control group, olfactory marker protein, olfactory receptor 1507, adenylyl cyclase 3, and GNAL mRNA levels were lower and S-100, 2',3'-cyclic nucleotide 30-phosphodiesterase, nerve growth factor receptor-associated protein, brain-derived neurotrophic factor, and tachykinin receptor mRNA levels were higher in the 400UPM group olfactory neuroepithelium. There were no significant differences in neuroepithelial inflammatory marker levels between the 400UPM and saline group. CONCLUSIONS: UPM decreased olfactory function and might have cytotoxic effects on the olfactory epithelium. Olfactory ensheathing cells and trigeminal nerve might be related to the regeneration of the olfactory epithelium after olfactory destruction associated with UPM.


Assuntos
Citocinas , Material Particulado , Animais , Modelos Animais de Doenças , Camundongos , Mucosa Olfatória , Material Particulado/toxicidade , RNA Mensageiro , Olfato
20.
Environ Res ; 203: 111859, 2022 01.
Artigo em Inglês | MEDLINE | ID: mdl-34389348

RESUMO

BACKGROUND: Evidence for the metabolic impact of long-term exposure to air pollution on diabetes is lacking. We investigated the association of particulate matter <10 µm (PM10) and <2.5 µm (PM2.5) with yearly averages of HbA1c, daily insulin dose (IU/kg) and rates of severe hypoglycaemia in type 1 diabetes (T1D). METHODS: We studied data of 44,383 individuals with T1D < 21 years which were documented in 377 German centres within the diabetes prospective follow-up registry (DPV) between 2009 and 2018. Outcomes were aggregated by year and by patient. PM10-and PM2.5-yearly averages prior to the respective treatment year were linked to individuals via the five-digit postcode areas of residency. Repeated measures linear and negative binomial regression were used to study the association between PM-quartiles (Q1 lowest, Q4 highest concentration) and yearly averages of HbA1c, daily insulin dose and rates of severe hypoglycaemia (confounders: sex, time-dependent age, age at diabetes onset, time-dependent type of treatment, migratory background, degree of urbanisation and socioeconomic index of deprivation). RESULTS: Adjusted mean HbA1c increased with PM10 (Q1: 7.96% [95%-CI: 7.95-7.98], Q4: 8.03% [8.02-8.05], p-value<0.001) and with PM2.5 (Q1: 7.97% [7.95-7.99], Q4: 8.02% [8.01-8.04], p < 0.001). Changes in daily insulin dose were inversely related to PM (PM10 and PM2.5: Q1 0.85 IU/kg [0.84-0.85], Q4: 0.83 IU/kg [0.82-0.83], p < 0.001). Adjusted rates of severe hypoglycaemia increased with PM-quartile groups (PM10 Q1:11.2 events/100 PY [10.9-11.5], PM10 Q4: 15.3 [14.9-15.7], p < 0.001; PM2.5 Q1: 9.9 events/100 PY [9.6-10.2], PM2.5 Q4: 14.2 [13.9-14.6], p < 0.001). DISCUSSION: Air pollution was associated with higher HbA1c levels and increased risk of severe hypoglycaemia in people with T1D, consequently indicating a higher risk of diabetes complications. Further studies are needed to explore causal pathways of the observed associations.


Assuntos
Poluentes Atmosféricos , Diabetes Mellitus Tipo 1 , Hipoglicemia , Adolescente , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Criança , Diabetes Mellitus Tipo 1/induzido quimicamente , Diabetes Mellitus Tipo 1/epidemiologia , Humanos , Hipoglicemia/induzido quimicamente , Hipoglicemia/epidemiologia , Material Particulado/análise , Material Particulado/toxicidade , Estudos Prospectivos
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