Patterns of domestic exposure to carbon monoxide and particulate matter in households using biomass fuel in Janakpur, Nepal

Household Air Pollution (HAP) from biomass cooking fuels is a major cause of morbidity and mortality in low-income settings worldwide. In Nepal the use of open stoves with solid biomass fuels is the primary method of domestic cooking. To assess patterns of domestic air pollution we performed continuous measurement of carbon monoxide (CO) and particulate Matter (PM2.5) in 12 biomass fuel households in Janakpur, Nepal. We measured kitchen PM2.5 and CO concentrations at one-minute intervals for an approximately 48-h period using the TSI DustTrak II 8530/SidePak AM510 (TSI Inc, St. Paul MN, USA) or EL-USB-CO data logger (Lascar Electronics, Erie PA, USA) respectively. We also obtained information regarding fuel, stove and kitchen characteristics and cooking activity patterns. Household cooking was performed in two daily sessions (median total duration 4 h) with diurnal variability in pollutant concentrations reflecting morning and evening cooking sessions and peak concentrations associated with fire-lighting. We observed a strong linear relationship between PM2.5 measurements obtained by co-located photometric and gravimetric monitoring devices, providing local calibration factors of 4.9 (DustTrak) and 2.7 (SidePak). Overall 48-h average CO and PM2.5 concentrations were 5.4 (SD 4.3) ppm (12 households) and 417.6 (SD 686.4) μg/m3 (8 households), respectively, with higher average concentrations associated with cooking and heating activities. Overall average PM2.5 concentrations and peak 1-h CO concentrations exceeded WHO Indoor Air Quality Guidelines. Average hourly PM2.5 and CO concentrations were moderately correlated (r = 0.52), suggesting that CO has limited utility as a proxy measure for PM2.5 exposure assessment in this setting. Domestic indoor air quality levels associated with biomass fuel combustion in this region exceed WHO Indoor Air Quality standards and are in the hazardous range for human health

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

The genetic architecture of the human cerebral cortex

INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function

On fine particulate matter and COVID-19 spread and severity: An in vitro toxicological plausible mechanism

COVID-19 pandemic had a significant impact on global public health. The spread of the disease was related to the high transmissibility of SARS-CoV-2 virus but incidence and mortality rate suggested a possible relationship with environmental factors. Air pollution has been hypothesized to play a role in the transmission of the virus and the resulting severity of the disease. Here we report a plausible in vitro toxicological mode of action by which fine particulate matter (PM2.5) could promote a higher infection rate of SARS-CoV-2 and severity of COVID-19 disease. PM2.5 promotes a 1.5 fold over-expression of the angiotensin 2 converting enzyme (ACE2) which is exploited by viral particles to enter human lung alveolar cells (1.5 fold increase in RAB5 protein) and increases their inflammatory state (IL-8 and NF-kB protein expression). Our results provide a basis for further exploring the possible synergy between biological threats and air pollutants and ask for a deeper understanding of how air quality could influence new pandemics in the future

Genome-wide gene-air pollution interaction analysis of lung function in 300,000 individuals

Background: Impaired lung function is predictive of mortality and is a key component of chronic obstructive pulmonary disease. Lung function has a strong genetic component but is also affected by environmental factors such as increased exposure to air pollution, but the effect of their interactions is not well understood. Objectives: To identify interactions between genetic variants and air pollution measures which affect COPD risk and lung function. Additionally, to determine whether previously identified lung function genetic association signals showed evidence of interaction with air pollution, considering both individual effects and combined effects using a genetic risk score (GRS). Methods: We conducted a genome-wide gene-air pollution interaction analysis of spirometry measures with three measures of air pollution at home address: particulate matter (PM2.5 & PM10) and nitrogen dioxide (NO2), in approximately 300,000 unrelated European individuals from UK Biobank. We explored air pollution interactions with previously identified lung function signals and determined their combined interaction effect using a GRS. Results: We identified seven new genome-wide interaction signals (P<5×10-8), and a further ten suggestive interaction signals (P<5×10-7). Additionally, we found statistical evidence of interaction for FEV1/FVC between PM2.5 and previously identified lung function signal, rs10841302, near AEBP2, suggesting increased susceptibility as copies of the G allele increased (but size of the impact was small - interaction beta: -0.363 percentage points, 95% CI: -0.523, -0.203 per 5 µg/m3). There was no observed interaction between air pollutants and the weighted GRS. Discussion: We carried out the largest genome-wide gene-air pollution interaction study of lung function and identified potential effects of clinically relevant size and significance. We observed up to 440 ml lower lung function for certain genotypes when exposed to mean levels of outdoor air pollution, which is approximately equivalent to nine years of average normal loss of lung function in adults

Is aircraft noise exposure associated with cardiovascular disease and hypertension? Results from a cohort study in Athens, Greece

Background We followed up, in 2013, the subjects who lived near the Athens International Airport and had participated in the cross-sectional multicountry HYENA study in 2004-2006. Objective To evaluate the association of exposure to aircraft and road traffic noise with the incidence of hypertension and other cardiovascular outcomes. Methods From the 780 individuals who participated in the cross-sectional study, 537 were still living in the same area and 420 accepted to participate in the follow-up. Aircraft and road traffic noise exposure was based on the estimations conducted in 2004-2006, linking geocoded residential addresses of the participants to noise levels. We applied multiple logistic regression and Cox proportional hazards models, adjusting for potential confounders. Results The incidence of hypertension was significantly associated with higher aircraft noise exposure during the night. Specifically, the OR for hypertension per 10 dB increase in Lnight aircraft noise exposure was 2.63 (95% CI 1.21 to 5.71). Doctor-diagnosed cardiac arrhythmia was significantly associated with Lnight aircraft noise exposure, when prevalent and incident cases were considered with an OR of 2.09 (95% CI 1.07 to 4.08). Stroke risk was also increased with increasing noise exposure but the association was not significant. Twenty-four-hour road traffic noise associations with the outcomes considered were weaker and less consistent. Conclusions In conclusion, our cohort study suggests that long-term exposure to aircraft noise, particularly during the night, is associated with incident hypertension and possibly, also, cardiovascular effects. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted

Noise annoyance - A modifier of the association between noise level and cardiovascular health?

Objectives: The effect modifying impact of annoyance due to aircraft noise and road traffic noise on the relationships between the aircraft noise level and road traffic noise level on the prevalence of hypertension was investigated in 4861 subjects of the HYENA study (HYpertension and Exposure to Noise near Airports). Methods: Different models were investigated either including the noise level and noise annoyance variables separately, or simultaneously, or together with an interaction term referring to the same noise source for the noise level and the noise annoyance. Results: Significant effect modification was found with respect to the association between aircraft noise and hypertension. The association was stronger in more annoyed subjects. No clear interaction was found with respect to road traffic noise. The comparison of the magnitude of the main effects (per standard deviation or inter-quartile range) of noise level and noise annoyance variables revealed stronger associations with hypertension for the noise levels. Conclusion: There is some indication that the noise level has a stronger predictive meaning for the relationship between noise exposure and hypertension than the reported noise annoyance (main effects). The results from the Hyena study support the hypothesis that noise annoyance acts as an effect modifier of the relationship between the noise level and hypertension. © 2013 Elsevier B.V

Exposure to aircraft and road traffic noise and associations with heart disease and stroke in six European countries: A cross-sectional study

Background: Although a number of studies have found an association between aircraft noise and hypertension, there is a lack of evidence on associations with other cardiovascular disease. For road traffic noise, more studies are available but the extent of possible confounding by air pollution has not been established. Methods. This study used data from the Hypertension and Environmental Noise near Airports (HYENA) study. Cross-sectional associations between self-reported &apos;heart disease and stroke&apos; and aircraft noise and road traffic noise were examined using data collected between 2004 and 2006 on 4712 participants (276 cases), who lived near airports in six European countries (UK, Germany, Netherlands, Sweden, Greece, Italy). Data were available to assess potential confounding by NO§ssub§2§esub§ air pollution in a subsample of three countries (UK, Netherlands, Sweden). Results: An association between night-time average aircraft noise and &apos;heart disease and stroke&apos; was found after adjustment for socio-demographic confounders for participants who had lived in the same place for ≥ 20 years (odds ratio (OR): 1.25 (95% confidence interval (CI) 1.03, 1.51) per 10 dB (A)); this association was robust to adjustment for exposure to air pollution in the subsample. 24 hour average road traffic noise exposure was associated with &apos;heart disease and stroke&apos; (OR: 1.19 (95% CI 1.00, 1.41), but adjustment for air pollution in the subsample suggested this may have been due to confounding by air pollution. Statistical assessment (correlations and variance inflation factor) suggested only modest collinearity between noise and NO§ssub§2§esub§ exposures. Conclusions: Exposure to aircraft noise over many years may increase risks of heart disease and stroke, although more studies are needed to establish how much the risks associated with road traffic noise may be explained by air pollution. © 2013 Floud et al.; licensee BioMed Central Ltd

The role of aircraft noise annoyance and noise sensitivity in the association between aircraft noise levels and medication use: results of a pooled-analysis from seven European countries

Background: Few studies have considered aircraft noise annoyance and noise sensitivity in analyses of the health effects of aircraft noise, especially in relation to medication use. This study aims to investigate the moderating and mediating role of these two factors in the relationship between aircraft noise levels and medication use among 5860 residents of ten European airports included in the HYENA and DEBATS studies. Methods: Information on aircraft noise annoyance, noise sensitivity, medication use, and demographic, socio-economic and lifestyle factors was collected during a face-to-face interview at home. Medication was coded according to the Anatomical Therapeutic Chemical (ATC) classification. Outdoor aircraft noise exposure was estimated by linking the participant’s home address to noise contours using Geographical Information Systems (GIS) methods. Logistic regressions with adjustment for potential confounding factors were used. In addition, Baron and Kenny’s recommendations were followed to investigate the moderating and mediating effects of aircraft noise annoyance and noise sensitivity. Results: A significant association was found between aircraft noise levels at night and antihypertensive medication only in the UK (OR = 1.43, 95%CI 1.19–1.73 for a 10 dB(A)-increase in Lnight). No association was found with other medications. Aircraft noise annoyance was significantly associated with the use of antihypertensive medication (OR = 1.33, 95%CI 1.14–1.56), anxiolytics (OR = 1.48, 95%CI 1.08–2.05), hypnotics and sedatives (OR = 1.60, 95%CI 1.07–2.39), and antasthmatics (OR = 1.44, 95%CI 1.07–1.96), with no difference between countries. Noise sensitivity was significantly associated with almost all medications, with the exception of the use of antasthmatics, showing an increase in ORs with the level of noise sensitivity, with differences in ORs among countries only for the use of antihypertensive medication. The results also suggested a mediating role of aircraft noise annoyance and a modifying role of both aircraft noise annoyance and noise sensitivity in the association between aircraft noise levels and medication use. Conclusions: The present study is consistent with the results of the small number of studies available to date suggesting that both aircraft noise annoyance and noise sensitivity should be taken into account in analyses of the health effects of exposure to aircraft noise. © 2021, The Author(s)