Synthesis of Harvard Environmental Protection Agency (EPA) Center studies on traffic-related particulate pollution and cardiovascular outcomes in the Greater Boston Area

The association between particulate pollution and cardiovascular morbidity and mortality is well established. While the cardiovascular effects of nationally regulated criteria pollutants (e.g., fine particulate matter [PM_2.5] and nitrogen dioxide) have been well documented, there are fewer studies on particulate pollutants that are more specific for traffic, such as black carbon (BC) and particle number (PN). In this paper, we synthesized studies conducted in the Greater Boston Area on cardiovascular health effects of traffic exposure, specifically defined by BC or PN exposure or proximity to major roadways. Large cohort studies demonstrate that exposure to traffic-related particles adversely affect cardiac autonomic function, increase systemic cytokine-mediated inflammation and pro-thrombotic activity, and elevate the risk of hypertension and ischemic stroke. Key patterns emerged when directly comparing studies with overlapping exposure metrics and population cohorts. Most notably, cardiovascular risk estimates of PN and BC exposures were larger in magnitude or more often statistically significant compared to those of PM_2.5 exposures. Across multiple exposure metrics (e.g., short-term vs. long-term; observed vs. modeled) and different population cohorts (e.g., elderly, individuals with co-morbidities, young healthy individuals), there is compelling evidence that BC and PN represent traffic-related particles that are especially harmful to cardiovascular health. Further research is needed to validate these findings in other geographic locations, characterize exposure errors associated with using monitored and modeled traffic pollutant levels, and elucidate pathophysiological mechanisms underlying the cardiovascular effects of traffic-related particulate pollutants.

Implications: Traffic emissions are an important source of particles harmful to cardiovascular health. Traffic-related particles, specifically BC and PN, adversely affect cardiac autonomic function, increase systemic inflammation and thrombotic activity, elevate BP, and increase the risk of ischemic stroke. There is evidence that BC and PN are associated with greater cardiovascular risk compared to PM_2.5. Further research is needed to elucidate other health effects of traffic-related particles and assess the feasibility of regulating BC and PN or their regional and local sources.     

Seasonal nitrogen fluxes of the Lena River Delta

The Arctic is nutrient limited, particularly by nitrogen, and is impacted by anthropogenic global warming which occurs approximately twice as fast compared to the global average. Arctic warming intensifies thawing of permafrost-affected soils releasing their large organic nitrogen reservoir. This organic nitrogen reaches hydrological systems, is remineralized to reactive inorganic nitrogen, and is transported to the Arctic Ocean via large rivers. We estimate the load of nitrogen supplied from terrestrial sources into the Arctic Ocean by sampling in the Lena River and its Delta. We took water samples along one of the major deltaic channels in winter and summer in 2019 and sampling station in the central delta over a one-year cycle. Additionally, we investigate the potential release of reactive nitrogen, including nitrous oxide from soils in the Delta. We found that the Lena transported nitrogen as dissolved organic nitrogen to the coastal Arctic Ocean and that eroded soils are sources of reactive inorganic nitrogen such as ammonium and nitrate. The Lena and the Deltaic region apparently are considerable sources of nitrogen to nearshore coastal zone. The potential higher availability of inorganic nitrogen might be a source to enhance nitrous oxide emissions from terrestrial and aquatic sources to the atmosphere.Supplementary InformationThe online version contains supplementary material available at 10.1007/s13280-021-01665-0.     

Microcontroller PIC 16F877A standard based on solar cooker using PV—evacuated tubes with an extension of heat integrated energy system

Environmental Science and Pollution Research - The unavailability of sunlight during nighttime and cloudy weather condition has limited the usage of solar cookers throughout the day. This study...     

Degrading permafrost river catchments and their impact on Arctic Ocean nearshore processes

Arctic warming is causing ancient perennially frozen ground (permafrost) to thaw, resulting in ground collapse, and reshaping of landscapes. This threatens Arctic peoples'' infrastructure, cultural sites, and land-based natural resources. Terrestrial permafrost thaw and ongoing intensification of hydrological cycles also enhance the amount and alter the type of organic carbon (OC) delivered from land to Arctic nearshore environments. These changes may affect coastal processes, food web dynamics and marine resources on which many traditional ways of life rely. Here, we examine how future projected increases in runoff and permafrost thaw from two permafrost-dominated Siberian watersheds—the Kolyma and Lena, may alter carbon turnover rates and OC distributions through river networks. We demonstrate that the unique composition of terrestrial permafrost-derived OC can cause significant increases to aquatic carbon degradation rates (20 to 60% faster rates with 1% permafrost OC). We compile results on aquatic OC degradation and examine how strengthening Arctic hydrological cycles may increase the connectivity between terrestrial landscapes and receiving nearshore ecosystems, with potential ramifications for coastal carbon budgets and ecosystem structure. To address the future challenges Arctic coastal communities will face, we argue that it will become essential to consider how nearshore ecosystems will respond to changing coastal inputs and identify how these may affect the resiliency and availability of essential food resources.Supplementary InformationThe online version contains supplementary material available at 10.1007/s13280-021-01666-z.