RESUMO
BACKGROUND: Rapid development and implementation of vaccines constituted a crucial step in containing the COVID-19 pandemic. A comprehensive understanding of physiological responses to these vaccines is important to build trust in medicine. OBJECTIVE: This study aims to investigate temporal dynamics before and after COVID-19 vaccination in 4 physiological parameters as well as the duration of menstrual cycle phases. METHODS: In a prospective trial, 17,825 adults in the Netherlands wore a medical device on their wrist for up to 9 months. The device recorded their physiological signals and synchronized with a complementary smartphone app. By means of multilevel quadratic regression, we examined changes in wearable-recorded breathing rate, wrist skin temperature, heart rate, heart rate variability, and objectively assessed the duration of menstrual cycle phases in menstruating participants to assess the effects of COVID-19 vaccination. RESULTS: The recorded physiological signals demonstrated short-term increases in breathing rate and heart rate after COVID-19 vaccination followed by a prompt rebound to baseline levels likely reflecting biological mechanisms accompanying the immune response to vaccination. No sex differences were evident in the measured physiological responses. In menstruating participants, we found a 0.8% decrease in the duration of the menstrual phase following vaccination. CONCLUSIONS: The observed short-term changes suggest that COVID-19 vaccines are not associated with long-term biophysical issues. Taken together, our work provides valuable insights into continuous fluctuations of physiological responses to vaccination and highlights the importance of digital solutions in health care. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): RR2-10.1186/s13063-021-05241-5.
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Vacinas contra COVID-19 , COVID-19 , Estudos Cross-Over , Frequência Cardíaca , Humanos , Feminino , Vacinas contra COVID-19/administração & dosagem , Masculino , Adulto , Estudos Prospectivos , COVID-19/prevenção & controle , Método Simples-Cego , Países Baixos , Taxa Respiratória , Ciclo Menstrual , SARS-CoV-2/imunologia , Temperatura Cutânea , Vacinação , Pessoa de Meia-Idade , Adulto JovemRESUMO
Household air pollution (HAP) from indoor combustion of solid fuel is a global health burden that has been linked to multiple diseases including lung cancer. In Xuanwei, China, lung cancer rate for non-smoking women is among the highest in the world and largely attributed to high levels of polycyclic aromatic hydrocarbons (PAHs) that are produced from combustion of smoky (bituminous) coal. Alu retroelements, repetitive mobile DNA sequences that can somatically multiply and promote genomic instability have been associated with risk of lung cancer and diesel engine exhaust exposure. We conducted analyses for 160 non-smoking women in an exposure assessment study in Xuanwei, China with a repeat sample from 49 subjects. Quantitative PCR was used to measure Alu repeat copy number relative to albumin gene copy number (Alu/ALB ratio). Associations between clusters derived from predicted levels of 43 HAP constituents, 5-methylchrysene (5-MC), a PAH previously associated with lung cancer in Xuanwei and was selected a priori for analysis, and Alu repeats were analyzed using generalized estimating equations. A cluster of 31 PAHs reflecting current exposure was associated with increased Alu copy number (ß:0.03 per standard deviation change; 95% confidence interval (CI):0.01,0.04; P-valueâ =â 2E-04). One compound within this cluster, 5-MC, was also associated with increased Alu copy number (P-valueâ =â 0.02). Our findings suggest that exposure to PAHs due to indoor smoky coal combustion may contribute to genomic instability. Additionally, our study provides further support for 5-MC as a prominent carcinogenic component of smoky coal emissions. Further studies are needed to replicate our findings.
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Poluição do Ar em Ambientes Fechados , Neoplasias Pulmonares , Hidrocarbonetos Policíclicos Aromáticos , Humanos , Feminino , Retroelementos/genética , Carvão Mineral/efeitos adversos , Carvão Mineral/análise , Variações do Número de Cópias de DNA/genética , China/epidemiologia , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Leucócitos , Poluição do Ar em Ambientes Fechados/análiseRESUMO
BACKGROUND: We previously found that occupational exposure to diesel engine exhaust (DEE) was associated with alterations to 19 biomarkers that potentially reflect the mechanisms of carcinogenesis. Whether DEE is associated with biological alterations at concentrations under existing or recommended occupational exposure limits (OELs) is unclear. METHODS: In a cross-sectional study of 54 factory workers exposed long-term to DEE and 55 unexposed controls, we reanalysed the 19 previously identified biomarkers. Multivariable linear regression was used to compare biomarker levels between DEE-exposed versus unexposed subjects and to assess elemental carbon (EC) exposure-response relationships, adjusted for age and smoking status. We analysed each biomarker at EC concentrations below the US Mine Safety and Health Administration (MSHA) OEL (<106 µg/m3), below the European Union (EU) OEL (<50 µg/m3) and below the American Conference of Governmental Industrial Hygienists (ACGIH) recommendation (<20 µg/m3). RESULTS: Below the MSHA OEL, 17 biomarkers were altered between DEE-exposed workers and unexposed controls. Below the EU OEL, DEE-exposed workers had elevated lymphocytes (p=9E-03, false discovery rate (FDR)=0.04), CD4+ count (p=0.02, FDR=0.05), CD8+ count (p=5E-03, FDR=0.03) and miR-92a-3p (p=0.02, FDR=0.05), and nasal turbinate gene expression (first principal component: p=1E-06, FDR=2E-05), as well as decreased C-reactive protein (p=0.02, FDR=0.05), macrophage inflammatory protein-1ß (p=0.04, FDR=0.09), miR-423-3p (p=0.04, FDR=0.09) and miR-122-5p (p=2E-03, FDR=0.02). Even at EC concentrations under the ACGIH recommendation, we found some evidence of exposure-response relationships for miR-423-3p (ptrend=0.01, FDR=0.19) and gene expression (ptrend=0.02, FDR=0.19). CONCLUSIONS: DEE exposure under existing or recommended OELs may be associated with biomarkers reflective of cancer-related processes, including inflammatory/immune response.
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Poluentes Ocupacionais do Ar , MicroRNAs , Exposição Ocupacional , Humanos , Emissões de Veículos/análise , Poluentes Ocupacionais do Ar/efeitos adversos , Poluentes Ocupacionais do Ar/análise , Estudos Transversais , União Europeia , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Biomarcadores/análiseRESUMO
OBJECTIVES: Diesel exhaust is an established human carcinogen, however the mechanisms by which it leads to cancer development are not fully understood. Mitochondrial dysfunction is an established contributor to carcinogenesis. Recent studies have improved our understanding of the role played by epigenetic modifications in the mitochondrial genome on tumorigenesis. In this study, we aim to evaluate the association between diesel engine exhaust (DEE) exposure with mitochondrial DNA (mtDNA) methylation levels in workers exposed to DEE. METHODS: The study population consisted of 53 male workers employed at a diesel engine manufacturing facility in Northern China who were routinely exposed to diesel exhaust in their occupational setting, as well as 55 unexposed male control workers from other unrelated factories in the same geographic area. Exposure to DEE, elemental carbon, organic carbon, and particulate matter (PM2.5) were assessed. mtDNA methylation for CpG sites (CpGs) from seven mitochondrial genes (D-Loop, MT-RNR1, MT-CO2, MT-CO3, MT-ATP6, MT-ATP8, MT-ND5) was measured in blood samples. Linear regression models were used to estimate the associations between DEE, elemental carbon, organic carbon and PM2.5 exposures with mtDNA methylation levels, adjusting for potential confounders. RESULTS: DEE exposure was associated with decreased MT-ATP6 (difference = -35.6%, P-value = 0.019) and MT-ATP8 methylation (difference = -30%, P-value = 0.029) compared to unexposed controls. Exposures to elemental carbon, organic carbon, and PM2.5 were also significantly and inversely associated with methylation in MT-ATP6 and MT-ATP8 genes (all P-values < 0.05). CONCLUSIONS: Our findings suggest that DEE exposure perturbs mtDNA methylation, which may be of importance for tumorigenesis.
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Exposição Ocupacional , Humanos , Masculino , Exposição Ocupacional/efeitos adversos , Emissões de Veículos/toxicidade , DNA Mitocondrial/genética , Metilação de DNA , Mitocôndrias/genética , Material Particulado/toxicidade , Carcinogênese/genética , Carbono/análiseRESUMO
It is unclear whether diet, and in particular certain foods or nutrients, are associated with lung cancer risk. We assessed associations of 92 dietary factors with lung cancer risk in 327 790 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC). Cox regression yielded adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) per SD higher intake/day of each food/nutrient. Correction for multiple comparisons was performed using the false discovery rate and identified associations were evaluated in the Netherlands Cohort Study (NLCS). In EPIC, 2420 incident lung cancer cases were identified during a median of 15 years of follow-up. Higher intakes of fibre (HR per 1 SD higher intake/day = 0.91, 95% CI 0.87-0.96), fruit (HR = 0.91, 95% CI 0.86-0.96) and vitamin C (HR = 0.91, 95% CI 0.86-0.96) were associated with a lower risk of lung cancer, whereas offal (HR = 1.08, 95% CI 1.03-1.14), retinol (HR = 1.06, 95% CI 1.03-1.10) and beer/cider (HR = 1.04, 95% CI 1.02-1.07) intakes were positively associated with lung cancer risk. Associations did not differ by sex and there was less evidence for associations among never smokers. None of the six associations with overall lung cancer risk identified in EPIC were replicated in the NLCS (2861 cases), however in analyses of histological subtypes, inverse associations of fruit and vitamin C with squamous cell carcinoma were replicated in the NLCS. Overall, there is little evidence that intakes of specific foods and nutrients play a major role in primary lung cancer risk, but fruit and vitamin C intakes seem to be inversely associated with squamous cell lung cancer.
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Neoplasias Pulmonares , Vitamina A , Ácido Ascórbico , Estudos de Coortes , Dieta/efeitos adversos , Europa (Continente)/epidemiologia , Humanos , Neoplasias Pulmonares/epidemiologia , Neoplasias Pulmonares/etiologia , Países Baixos/epidemiologia , Nutrientes , Estudos Prospectivos , Fatores de RiscoRESUMO
BACKGROUND: Millions of workers worldwide are exposed to diesel engine exhaust (DEE), a known genotoxic carcinogen. Alu retroelements are repetitive DNA sequences that can multiply and compromise genomic stability. There is some evidence linking altered Alu repeats to cancer and elevated mortality risks. However, whether Alu repeats are influenced by environmental pollutants is unexplored. In an occupational setting with high DEE exposure levels, we investigated associations with Alu repeat copy number. METHODS: A cross-sectional study of 54 male DEE-exposed workers from an engine testing facility and a comparison group of 55 male unexposed controls was conducted in China. Personal air samples were assessed for elemental carbon, a DEE surrogate, using NIOSH Method 5040. Quantitative PCR (qPCR) was used to measure Alu repeat copy number relative to albumin (Alb) single-gene copy number in leucocyte DNA. The unitless Alu/Alb ratio reflects the average quantity of Alu repeats per cell. Linear regression models adjusted for age and smoking status were used to estimate relations between DEE-exposed workers versus unexposed controls, DEE tertiles (6.1-39.0, 39.1-54.5 and 54.6-107.7 µg/m3) and Alu/Alb ratio. RESULTS: DEE-exposed workers had a higher average Alu/Alb ratio than the unexposed controls (p=0.03). Further, we found a positive exposure-response relationship (p=0.02). The Alu/Alb ratio was highest among workers exposed to the top tertile of DEE versus the unexposed controls (1.12±0.08 SD vs 1.06±0.07 SD, p=0.01). CONCLUSION: Our findings suggest that DEE exposure may contribute to genomic instability. Further investigations of environmental pollutants, Alu copy number and carcinogenesis are warranted.
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Poluentes Ocupacionais do Ar/análise , Elementos Alu , Exposição Ocupacional/efeitos adversos , Emissões de Veículos/análise , Adulto , Carbono/análise , Estudos Transversais , Humanos , Masculino , Pessoa de Meia-Idade , Exposição Ocupacional/análise , Retroelementos , FumarRESUMO
BACKGROUND: Accruing epidemiological evidence suggests that prenatal exposure to emissions from cooking fuel is associated with increased risks of adverse maternal and perinatal outcomes including hypertensive disorders of pregnancy, low birth weight, stillbirth and infant mortality. We aimed to investigate the relationship between cooking fuel use and various pregnancy related outcomes in a cohort of urban women from the Accra region of Ghana. METHODS: Self-reported cooking fuel use was divided into "polluting" (wood, charcoal, crop residue and kerosene) and "clean" fuels (liquid petroleum gas and electricity) to examine 12 obstetric outcomes in a prospective cohort of pregnant women (N = 1010) recruited at < 17 weeks of gestation from Accra, Ghana. Logistic and multivariate linear regression analyses adjusted for BMI, maternal age, maternal education and socio-economic status asset index was conducted. RESULTS: 34% (n = 279) of 819 women with outcome data available for analysis used polluting fuel as their main cooking fuel. Using polluting cooking fuels was associated with perinatal mortality (aOR: 7.6, 95%CI: 1.67-36.0) and an adverse Apgar score (< 7) at 5 min (aOR:3.83, 95%CI: (1.44-10.11). The other outcomes (miscarriage, post-partum hemorrhage, pre-term birth, low birthweight, caesarian section, hypertensive disorders of pregnancy, small for gestational age, and Apgar score at 1 min) had non-statistically significant findings. CONCLUSIONS: We report an increased likelihood of perinatal mortality, and adverse 5-min Apgar scores in association with polluting fuel use. Further research including details on extent of household fuel use exposure is recommended to better quantify the consequences of household fuel use. STUDY REGISTRATION: Ghana Service Ethical Review Committee (GHS-ERC #: 07-9-11).
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Poluição do Ar/efeitos adversos , Complicações do Trabalho de Parto/epidemiologia , Resultado da Gravidez/epidemiologia , Fumaça/efeitos adversos , Índice de Apgar , Culinária , Feminino , Gana/epidemiologia , Humanos , Complicações do Trabalho de Parto/etiologia , Mortalidade Perinatal , GravidezRESUMO
Coal types vary around the world because of geochemical differences in their source deposits; however, the influence of coal emissions from different deposits on human health remains unexplored. To address this issue, we conducted the first study of the relationship between coal use from various deposits and lung cancer risk in Xuanwei and Fuyuan, counties in China where lung cancer rates are among the highest in the world among female never-smokers due to use of bituminous ("smoky") coal for heating and cooking. We conducted a population-based case-control study of 1031 lung cancer cases and 493 controls among never-smoking women in Xuanwei and Fuyuan. Logistic regression models were used to estimate associations between coal use from various deposits across the lifecourse and lung cancer risk. There was substantial heterogeneity in risks by coal deposit (p = 7.8E-05). Compared to non-smoky coal users, risks by smoky coal deposit ranged from OR = 7.49 (95% CI: 3.43-16.38) to OR = 33.40 (95% CI: 13.07-85.34). Further, women born into homes that used smoky coal and subsequently changed to non-smoky coal had a higher risk (OR = 10.83 (95% CI: 4.61-25.46)) than women born into homes that used non-smoky coal and changed to smoky coal (OR = 4.74 (95% CI: 2.03-11.04, pdifference = 0.04)). Our study demonstrates that various sources of coal have considerably different impact on lung cancer in this population and suggests that early-life exposure to carcinogenic emissions may exert substantial influence on health risks later in life. These factors should be considered when evaluating the health risks posed by exposure to coal combustion emissions.
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Carvão Mineral/classificação , Neoplasias Pulmonares/epidemiologia , Poluição do Ar em Ambientes Fechados , Estudos de Casos e Controles , China/epidemiologia , Carvão Mineral/análise , Carvão Mineral/estatística & dados numéricos , Culinária , Exposição Ambiental , Feminino , Humanos , Modelos Logísticos , Neoplasias Pulmonares/etiologia , Pessoa de Meia-Idade , Fumaça/análiseRESUMO
BACKGROUND: Multiple lines of evidence have associated exposure to ambient air pollution with an increased risk of respiratory malignancies. However, there is a dearth of evidence from low-middle income countries, including those within South America, where the social inequalities are more marked. OBJECTIVES: To quantify the association between exposures to traffic related air pollution and respiratory cancer incidence and mortality within São Paulo, Brazil. Further, we aim to investigate the role of socioeconomic status (SES) upon these outcomes. METHODS: Cancer incidence between 2002 and 2011 was derived from the population-based cancer registry. Mortality data (between 2002 and 2013) was derived from the Municipal Health Department. A traffic density database and an annual nitrogen dioxide (NO2) land use regression model were used as markers of exposure. Age-adjusted Binomial Negative Regression models were developed, stratifying by SES and gender. RESULTS: We observed an increased rate of respiratory cancer incidence and mortality in association with increased traffic density and NO2 concentrations, which was higher among those regions with the lowest SES. For cancer mortality and traffic exposure, those in the most deprived region, had an incidence rate ratio (IRR) of 2.19 (95% CI: 1.70, 2.82) when comparing the highest exposure centile (top 90%) to the lowest (lowest 25%). By contrast, in the least deprived area, the IRR for the same exposure contrast was.1.07 (95% CI: 0.95, 1.20). For NO2 in the most deprived regions, the IRR for cancer mortality in the highest exposed group was 1.44 (95% CI: 1.10, 1.88) while in the least deprived area, the IRR for the highest exposed group was 1.11 (95% CI: 1.01, 1.23). CONCLUSIONS: Traffic density and NO2 were associated with an increased rate of respiratory cancer incidence and mortality in São Paulo. Residents from poor regions may suffer more from the impact of traffic air pollution.
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Poluentes Atmosféricos , Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Neoplasias do Sistema Respiratório/epidemiologia , Emissões de Veículos , Brasil/epidemiologia , Incidência , Dióxido de NitrogênioRESUMO
The study aim was to investigate whether household bituminous ("smoky") coal use and personal exposure to combustion emissions were associated with immunologic/inflammatory marker levels. A cross-sectional study of healthy never-smoking women from rural Xuanwei and Fuyuan, China was conducted, which included 80 smoky coal and 14 anthracite ("smokeless") coal users. Personal exposure to fine particulate matter (PM2.5) and benzo[a]pyrene (BaP) was assessed using portable devices, while 67 circulating plasma immunologic/inflammatory markers were measured using multiplex bead-based assays. Multivariable linear regression models were employed to estimate associations between smoky coal versus smokeless coal use, indoor air pollutants, and immunologic/inflammatory markers. Six markers were altered among smoky coal users compared to smokeless coal, including significantly decreased interferon-inducible T-cell alpha chemoattractant (CXCL11/I-TAC), and increased serum amyloid P component (SAP). CXCL11/I-TAC was previously found to be reduced in workers exposed to high levels of diesel engine exhaust, which exhibits similar constituents as coal combustion emissions. Further, there was evidence that elevated PM2.5 and BaP exposure was associated with significantly diminished levels of the serum amyloid A (SAA); however, the false discovery rates (FDRs) were >0.2 after accounting for multiple comparisons. Inflammatory processes may thus mediate the carcinogenic effects attributed to smoky coal emissions.
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Poluição do Ar em Ambientes Fechados/efeitos adversos , Benzo(a)pireno/efeitos adversos , Biomarcadores/sangue , Carvão Mineral/efeitos adversos , Material Particulado/efeitos adversos , Adulto , Idoso , China , Culinária , Estudos Transversais , Feminino , Humanos , Pessoa de Meia-Idade , População Rural/estatística & dados numéricos , Adulto JovemRESUMO
Households in Xuanwei and Fuyuan, China, possess hazardous levels of fine particulate matter with an aerodynamic diameter <2.5 microns (PM2.5) and polycyclic aromatic hydrocarbons (PAHs) from coal combustion. Previous studies found that increased exposure to PM2.5 and benzo[a]pyrene (BaP; a PAH) were associated with decreased mitochondrial DNA copy number (mtDNAcn), a marker of oxidative stress. We further evaluated these associations in a cross-sectional study of 148 healthy non-smoking women from Xuanwei and Fuyuan. Personal exposure to PM2.5 and BaP was measured using portable devices. MtDNAcn was measured using qPCR amplification of leukocyte DNA that was collected after air measurements. Linear regression models were used to estimate the associations between personal exposure to PM2.5 and BaP, and mtDNAcn adjusted for age, body mass index (BMI) and fuel type. We found inverse associations between exposure to PM2.5 and BaP, and mtDNAcn. Each incremental log-µg/m3 increase in PM2.5 was associated with a significant decrease in mtDNAcn of -10.3 copies per cell [95% confidence interval (95% CI): -18.6, -2.0; P = 0.02]. Additionally, each log-ng/m3 increase in BaP was associated with a significant decrease in mtDNAcn of -5.4 copies per cell (95% CI: -9.9, -0.8, P = 0.02). Age, BMI, fuel type and coal mine type were not significantly associated with mtDNAcn. Exposure to PM2.5 and BaP may alter mitochondrial dynamics in non-smoking Chinese women. MtDNAcn may be a potential mediator of indoor air pollution on chronic disease development.
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Poluição do Ar em Ambientes Fechados/efeitos adversos , Benzo(a)pireno/efeitos adversos , Variações do Número de Cópias de DNA , DNA Mitocondrial/genética , Exposição Ambiental , Mitocôndrias/metabolismo , Material Particulado/efeitos adversos , Adulto , Idoso , Biomarcadores , China/epidemiologia , Estudos Transversais , DNA Mitocondrial/sangue , Demografia , Doença Ambiental/etiologia , Feminino , Humanos , Leucócitos/metabolismo , Pessoa de Meia-Idade , Estresse OxidativoRESUMO
In China's rural counties of Xuanwei and Fuyuan, lung cancer rates are among the highest in the world. While the elevated disease risk in this population has been linked to the usage of smoky (bituminous) coal as compared to smokeless (anthracite) coal, the underlying molecular changes associated with this exposure remains unclear. To understand the physiologic effects of smoky coal exposure, we analyzed the genome-wide gene-expression profiles in buccal epithelial cells collected from healthy, non-smoking female residents of Xuanwei and Fuyuan who burn smoky (n = 26) and smokeless (n = 9) coal. Gene-expression was profiled via microarrays, and changes associated with coal type were correlated to household levels of fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs). Expression levels of 282 genes were altered with smoky versus smokeless coal exposure (P < 0.005), including the 2-fold increase of proinflammatory IL8 and decrease of proapoptotic CASP3. This signature was more correlated with carcinogenic PAHs (e.g. Benzo[a]pyrene; r = 0.41) than with non-carcinogenic PAHs (e.g. Fluorene; r = 0.08) or PM2.5 (r = 0.05). Genes altered with smoky coal exposure were concordantly enriched with tobacco exposure in previously profiled buccal biopsies of smokers and non-smokers (GSEA, q < 0.05). This is the first study to identify a signature of buccal epithelial gene-expression that is associated with smoky coal exposure, which in part is similar to the molecular response to tobacco smoke, thereby lending biologic plausibility to prior epidemiological studies that have linked this exposure to lung cancer risk.
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Poluição do Ar em Ambientes Fechados , Carvão Mineral , Exposição por Inalação , Mucosa Bucal/metabolismo , Fumaça , Transcriptoma , Adulto , Idoso , Feminino , Perfilação da Expressão Gênica , Humanos , Pessoa de Meia-Idade , Família MultigênicaRESUMO
Exposure to polycyclic aromatic hydrocarbons (PAHs) from burning "smoky" (bituminous) coal has been implicated as a cause of the high lung cancer incidence in the counties of Xuanwei and Fuyuan, China. Little is known about variations in PAH exposure from throughout the region nor how fuel source and stove design affects exposure. Indoor and personal PAH exposure resulting from solid fuel combustion in Xuanwei and Fuyuan was investigated using repeated 24 h particle bound and gas-phase PAH measurements, which were collected from 163 female residents of Xuanwei and Fuyuan. 549 particle bound (283 indoor and 266 personal) and 193 gas phase (all personal) PAH measurements were collected. Mixed effect models indicated that PAH exposure was up to 6 times higher when burning smoky coal than smokeless coal and varied by up to a factor of 3 between different smoky coal geographic sources. PAH measurements from unventilated firepits were up to 5 times that of ventilated stoves. Exposure also varied between different room sizes and season of measurement. These findings indicate that PAH exposure is modulated by a variety of factors, including fuel type, coal source, and stove design. These findings may provide valuable insight into potential causes of lung cancer in the area.
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Poluição do Ar em Ambientes Fechados/análise , Carvão Mineral , Hidrocarbonetos Policíclicos Aromáticos/análise , Adulto , Idoso , Idoso de 80 Anos ou mais , Poluição do Ar em Ambientes Fechados/efeitos adversos , China/epidemiologia , Culinária/instrumentação , Estudos Transversais , Análise Fatorial , Características da Família , Feminino , Humanos , Neoplasias Pulmonares/epidemiologia , Pessoa de Meia-Idade , Modelos Teóricos , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Fatores de RiscoRESUMO
The combustion of biomass and coal is the dominant source of household air pollution (HAP) in China, and contributes significantly to the total burden of disease in the Chinese population. To characterize HAP exposure related to solid fuel use and ventilation patterns, an exposure assessment study of 163 nonsmoking female heads of households enrolled from 30 villages was conducted in Xuanwei and Fuyuan, two neighboring rural counties with high incidence of lung cancer due to the burning of smoky coal (a bituminous coal, which in health evaluations is usually compared to smokeless coal--an anthracite coal available in some parts of the area). Personal and indoor 24-h PM2.5 samples were collected over two consecutive days in each household, with approximately one-third of measurements retaken in a second season. The overall geometric means (GM) of personal PM2.5 concentrations in Xuanwei and Fuyuan were 166 [Geometric Standard Deviation (GSD):2.0] and 146 (GSD:1.9) µg/m(3), respectively, which were similar to the indoor PM2.5 air concentrations [GM(GSD):162 (2.1) and 136 (2.0) µg/m(3), respectively]. Personal PM2.5 was moderately highly correlated with indoor PM2.5 (Spearman r = 0.70, p < 0.0001). Burning wood or plant materials (tobacco stems, corncobs etc.) resulted in the highest personal PM2.5 concentrations (GM:289 and 225 µg/m(3), respectively), followed by smoky coal, and smokeless coal (GM:148 and 115 µg/m(3), respectively). PM2.5 levels of vented stoves were 34-80% lower than unvented stoves and firepits across fuel types. Mixed effect models indicated that fuel type, ventilation, number of windows, season, and burning time per stove were the main factors related to personal PM2.5 exposure. Lower PM2.5 among vented stoves compared with unvented stoves and firepits is of interest as it parallels the observation of reduced risks of malignant and nonmalignant lung diseases in the region.
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Poluentes Atmosféricos/análise , Poluição do Ar em Ambientes Fechados/análise , Culinária , Material Particulado/análise , Adulto , Idoso , China/epidemiologia , Carvão Mineral , Monitoramento Ambiental , Feminino , Utensílios Domésticos , Humanos , Incidência , Neoplasias Pulmonares/epidemiologia , Pessoa de Meia-Idade , População Rural , Ventilação , MadeiraRESUMO
Over half of the world's population is exposed to household air pollution from the burning of solid fuels at home. Household air pollution from solid fuel use is a leading risk factor for global disease and remains a major public health problem, especially in low- and mid-income countries. This is a particularly serious problem in China, where many people in rural areas still use coal for household heating and cooking. This review focuses on several decades of research carried out in Xuanwei County, Yunnan Province, where household coal use is a major source of household air pollution and where studies have linked household air pollution exposure to high rates of lung cancer. We conducted a series of case-control and cohort studies in Xuanwei to characterize the lung cancer risk in this population and the factors associated with it. We found lung cancer risk to vary substantially between different coal types, with a higher risk associated with smoky (i.e., bituminous) coal use compared to smokeless (i.e., anthracite) coal use. The installation of a chimney in homes resulted in a substantial reduction in lung cancer incidence and mortality. Overall, our research underscores the need among existing coal users to improve ventilation, use the least toxic fuel, and eventually move toward the use of cleaner fuels, such as gas and electricity.
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Poluição do Ar em Ambientes Fechados/efeitos adversos , Carvão Mineral/efeitos adversos , Neoplasias Pulmonares/etiologia , Neoplasias Pulmonares/mortalidade , Fumaça/efeitos adversos , China , Carvão Mineral/classificação , Estudos de Coortes , Culinária , Combustíveis Fósseis , Calefação , Humanos , Incidência , Fatores de Risco , FumarRESUMO
INTRODUCTION: Environmental exposures, such as ambient air pollution and household fuel use affect health and under-5 mortality (U5M) but there is a paucity of data in the Global South. This study examined early-life exposure to ambient particulate matter with a diameter of 2.5 µm or less (PM2.5), alongside household characteristics (including self-reported household fuel use), and their relationship with U5M in the Navrongo Health and Demographic Surveillance Site (HDSS) in northern Ghana. METHODS: We employed Satellite-based spatiotemporal models to estimate the annual average PM2.5 concentrations with the Navrongo HDSS area (1998 to 2016). Early-life exposure levels were determined by pollution estimates at birth year. Socio-demographic and household data, including cooking fuel, were gathered during routine surveillance. Cox proportional hazards models were applied to assess the link between early-life PM2.5 exposure and U5M, accounting for child, maternal, and household factors. FINDINGS: We retrospectively studied 48,352 children born between 2007 and 2017, with 1872 recorded deaths, primarily due to malaria, sepsis, and acute respiratory infection. Mean early-life PM2.5 was 39.3 µg/m3, and no significant association with U5M was observed. However, Children from households using "unclean" cooking fuels (wood, charcoal, dung, and agricultural waste) faced a 73 % higher risk of death compared to those using clean fuels (adjusted HR = 1.73; 95 % CI: 1.29, 2.33). Being born female or to mothers aged 20-34 years were linked to increased survival probabilities. INTERPRETATION: The use of "unclean" cooking fuel in the Navrongo HDSS was associated with under-5 mortality, highlighting the need to improve indoor air quality by introducing cleaner fuels.
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Poluição do Ar em Ambientes Fechados , Culinária , Material Particulado , Gana , Humanos , Pré-Escolar , Lactente , Feminino , Material Particulado/análise , Masculino , Poluição do Ar em Ambientes Fechados/estatística & dados numéricos , Poluição do Ar em Ambientes Fechados/análise , Poluição do Ar em Ambientes Fechados/efeitos adversos , Exposição Ambiental/estatística & dados numéricos , Mortalidade da Criança , Poluentes Atmosféricos/análise , Características da Família , Estudos Retrospectivos , Recém-Nascido , Poluição do Ar/estatística & dados numéricosRESUMO
BACKGROUND: The incidence of severe asthma exacerbations (SAE) requiring a pediatric intensive care unit (PICU) admission during the coronavirus disease 2019 (COVID-19) pandemic (and its association with public restrictions) is largely unknown. We examined the trend of SAE requiring PICU admission before, during, and after COVID-19 restrictions in Amsterdam, the Netherlands, and its relationship with features such as environmental triggers and changes in COVID-19 restriction measures. METHODS: In this single-center, retrospective cohort study, all PICU admissions of children aged ≥2 years for severe asthma at the Amsterdam UMC between 2018 and 2022 were included. The concentrations of ambient fine particulate matter (PM2.5 ) and pollen were obtained from official monitoring stations. RESULTS: Between January 2018 and December 2022, 228 children were admitted to the PICU of the Amsterdam UMC for SAE. While we observed a decrease in admissions during periods of more stringent restriction, there was an increase in the PICU admission rate for SAE in some periods following the lifting of restrictions. In particular, following the COVID-19 restrictions in 2021, we observed a peak incidence of admissions from August to November, which was higher than any other peak during the indicated years. No association with air pollution or pollen was observed. CONCLUSION: We hypothesize that an increase in clinically diagnosed viral infections after lockdown periods was the reason for the altered incidence of SAE at the PICU in late 2021, rather than air pollution and pollen concentrations.
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Asma , COVID-19 , Criança , Humanos , COVID-19/epidemiologia , Pandemias , Estudos Retrospectivos , Controle de Doenças Transmissíveis , Asma/epidemiologia , Asma/diagnóstico , Unidades de Terapia Intensiva PediátricaRESUMO
Background: While some long-term effects of COVID-19 are respiratory in nature, a non-respiratory effect gaining attention has been a decline in hemoglobin, potentially mediated by inflammatory processes. In this study, we examined the correlations between hemoglobin levels and inflammatory biomarkers and evaluated the association between hemoglobin and fatigue in a cohort of Long-COVID patients. Methods: This prospective cohort study in the Netherlands evaluated 95 (mostly hospitalized) patients, aged 40-65 years, 3-6 months post SARS-CoV-2 infection, examining their venous hemoglobin concentration, anemia (hemoglobin < 7.5 mmol/L in women and <8.5 mmol/L in men), inflammatory blood biomarkers, average FSS (Fatigue Severity Score), demographics, and clinical features. Follow-up hemoglobin was compared against hemoglobin during acute infection. Spearman correlation was used for assessing the relationship between hemoglobin concentrations and inflammatory biomarkers, and the association between hemoglobin and fatigue was examined using logistic regression. Results: In total, 11 (16.4%) participants were suffering from anemia 3-6 months after SARS-CoV-2 infection. The mean hemoglobin value increased by 0.3 mmol/L 3-6 months after infection compared to the hemoglobin during the acute phase (p-value = 0.003). Whilst logistic regression showed that a 1 mmol/L greater increase in hemoglobin is related to a decrease in experiencing fatigue in Long-COVID patients (adjusted OR 0.38 [95%CI 0.13-1.09]), we observed no correlations between hemoglobin and any of the inflammatory biomarkers examined. Conclusion: Our results indicate that hemoglobin impairment might play a role in developing Long-COVID fatigue. Further investigation is necessary to identify the precise mechanism causing hemoglobin alteration in these patients.
RESUMO
Considering sex as a biological variable in modern digital health solutions, we investigated sex-specific differences in the trajectory of four physiological parameters across a COVID-19 infection. A wearable medical device measured breathing rate, heart rate, heart rate variability, and wrist skin temperature in 1163 participants (mean age = 44.1 years, standard deviation [SD] = 5.6; 667 [57%] females). Participants reported daily symptoms and confounders in a complementary app. A machine learning algorithm retrospectively ingested daily biophysical parameters to detect COVID-19 infections. COVID-19 serology samples were collected from all participants at baseline and follow-up. We analysed potential sex-specific differences in physiology and antibody titres using multilevel modelling and t-tests. Over 1.5 million hours of physiological data were recorded. During the symptomatic period of infection, men demonstrated larger increases in skin temperature, breathing rate, and heart rate as well as larger decreases in heart rate variability than women. The COVID-19 infection detection algorithm performed similarly well for men and women. Our study belongs to the first research to provide evidence for differential physiological responses to COVID-19 between females and males, highlighting the potential of wearable technology to inform future precision medicine approaches.
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COVID-19 , Masculino , Humanos , Feminino , Adulto , COVID-19/diagnóstico , Estudos Retrospectivos , SARS-CoV-2 , Algoritmos , BiofísicaRESUMO
Environmental risks are a substantial factor in the current burden of disease, and their role is likely to increase in the future. Model-based scenario analysis is used extensively in environmental sciences to explore the potential effects of human activities on the environment. In this Review, we examine the literature on scenarios modelling environmental effects on health to identify the most relevant findings, common methods used, and important research gaps. Health outcomes and measures related to climate change (n=106) and air pollution (n=30) were most frequently studied. Studies examining future disease burden due to changes or policies related to dietary risks were much less common (n=10). Only a few studies assessed more than two environmental risks (n=3), even though risks can accumulate and interact with each other. Studies predominantly covered high-income countries and Asia. Sociodemographic, vulnerability, and health-system changes were rarely accounted for; thus, assessing the full effect of future environmental changes in an integrative way is not yet possible. We recommend that future models incorporate a broader set of determinants of health to more adequately capture their effect, as well as the effect of mitigation and adaptation efforts.