Distractions and the risk of car crash injury: the effect of drivers' age

PROBLEM: Motor-vehicle accidents are one of the major causes of injury in most motorized countries. Driver distractions have been suggested as a contributor to traffic accidents. Moreover, age of the driver seems to have a role in the relationship between distractions and car crashes. But very few studies have investigated the effect of driver's age on this relationship. This exploratory study investigated the association between distractions, both inside and outside the vehicle, and the increased risk of car crash injury among drivers across different ages. METHOD: This study used a case series design to analyze data routinely collected by the NSW police in Australia. A special focus of this study was on how drivers' age affects the risk of car crash injury, which was determined by using a well-documented risk estimation methodology. RESULTS: The results obtained indicated that drivers of all ages, on the whole, are more susceptible to distractions inside the vehicle than distractions coming from outside. Age was shown to affect the relationship between in-vehicle distraction and the risk of car crash injury. A separate analysis was also conducted on hand-held phone usage while driving with results supplementing previous findings reported in the literature. IMPACT TO INDUSTRY: Safety strategies to countermeasure in-vehicle distractions have been suggested and discussed.     

Exposure Programme on Atmospheric Corrosion Effects of Acidifying Pollutants in Tropical and Subtropical Climates

Many national exposure programmes have been performed in tropical and subtropical climates during the last 50 years. However, ambitious programmes involving more than a few countries are scarce. In this paper a recently formed network of test sites is described involving 12 test sites in Asia (India, Vietnam, Thailand, Malaysia and China including Hong Kong) and four test sites in Africa (South Africa, Zambia and Zimbabwe). This effort is part of the 2001–2004 Swedish International Development Agency (SIDA) funded Programme on Regional Air Pollution in Developing Countries (RAPIDC). Corrosion attack after one (2002–2003) year of exposure (carbon steel, zinc, copper, limestone and paint coated steel) are presented together with environmental data (SO₂, NO₂, HNO₃, O₃, particles, amount and pH of precipitation, temperature and relative humidity) for all the test sites. The obtained corrosion values are substantially higher than expected for limestone, higher than expected for carbon steel and lower than expected for zinc compared to values calculated using the best available dose–response functions.     

CALCULATION OF CUMULATIVE PERCENTAGE AT SELECTED PARTICLE SIZES FROM BOTTOM WITHDRAWAL TUBE ANALYSIS

ABSTRACT: A new computation method is developed for the bottom withdrawal tube particle size analysis. A transformation on time scale is introduced so that the cumulative percentage of a selected particle size can be determined from a single continuous Oden cum.     

An integrative analysis of miRNA and mRNA expression in the brains of Alzheimer's disease transgenic mice after real-world PM2.5 exposure

Fine particulatematter (PM2.5) is associated with increased risks of Alzheimer’s disease (AD),yet the toxicologicalmechanisms of PM2.5 promoting AD remain unclear. In this study,wildtype and APP/PS1 transgenic mice (AD mice) were exposed to either filtered air (FA) or PM2.5 for eight weeks with a real-world exposure system in Taiyuan, China (mean PM2.5 concentration in the cage was 61 μg/m3). We found that PM2.5 exposure could remarkably aggravate AD mice’s ethological and brain ultrastructural damage, along with the elevation of the pro-inflammatory cytokines (IL-6 and TNF-α), Aβ-42 and AChE levels and the decline of ChAT levels in the brains. Based on high-throughput sequencing results, some differentially expressed (DE) mRNAs and DE miRNAs in the brains of AD mice after PM2.5 exposure were screened.Using RT-qPCR, seven DEmiRNAs (mmu-miR-193b-5p, 122b-5p, 466h-3p, 10b-5p, 1895, 384–5p, and 6412) and six genes (Pcdhgb8, Unc13b, Robo3, Prph, Pter, and Tbata) were evidenced the and verified. Two miRNA-target gene pairs (miR-125b-Pcdhgb8 pair and miR-466h-3p-IL-17Rα/TGF-βR2/Aβ-42/AChE pairs) were demonstrated that they were more related to PM2.5-induced brain injury. Results of Gene Ontology (GO) pathways and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways predicted that synaptic and postsynaptic regulation, axon guidance, Wnt, MAPK, and mTOR pathways might be the possible regulatory mechanisms associated with pathological response. These revealed that PM2.5- elevated pro-inflammatory cytokine levels and PM2.5-altered neurotransmitter levels in AD mice could be the important causes of brain damage and proposed the promising miRNA andmRNA biomarkers and potentialmiRNA-mRNA interaction networks of PM2.5-promoted AD.