Objective: The objective of this article was the construction of injury risk functions (IRFs) for front row occupants in oblique frontal crashes and a comparison to IRF of nonoblique frontal crashes from the same data set.
Method: Crashes of modern vehicles from GIDAS (German In-Depth Accident Study) were used as the basis for the construction of a logistic injury risk model. Static deformation, measured via displaced voxels on the postcrash vehicles, was used to calculate the energy dissipated in the crash. This measure of accident severity was termed objective equivalent speed (oEES) because it does not depend on the accident reconstruction and thus eliminates reconstruction biases like impact direction and vehicle model year. Imputation from property damage cases was used to describe underrepresented low-severity crashes―a known shortcoming of GIDAS. Binary logistic regression was used to relate the stimuli (oEES) to the binary outcome variable (injured or not injured).
Results: IRFs for the oblique frontal impact and nonoblique frontal impact were computed for the Maximum Abbreviated Injury Scale (MAIS) 2+ and 3+ levels for adults (18–64 years). For a given stimulus, the probability of injury for a belted driver was higher in oblique crashes than in nonoblique frontal crashes. For the 25% injury risk at MAIS 2+ level, the corresponding stimulus for oblique crashes was 40 km/h but it was 64 km/h for nonoblique frontal crashes.
Conclusions: The risk of obtaining MAIS 2+ injuries is significantly higher in oblique crashes than in nonoblique crashes. In the real world, most MAIS 2+ injuries occur in an oEES range from 30 to 60 km/h. 相似文献
Objective: Evaluating the biofidelity of pedestrian finite element models (PFEM) using postmortem human subjects (PMHS) is a challenge because differences in anthropometry between PMHS and PFEM could limit a model's capability to accurately capture cadaveric responses. Geometrical personalization via morphing can modify the PFEM geometry to match the specific PMHS anthropometry, which could alleviate this issue. In this study, the Total Human Model for Safety (THUMS) PFEM (Ver 4.01) was compared to the cadaveric response in vehicle–pedestrian impacts using geometrically personalized models.
Methods: The AM50 THUMS PFEM was used as the baseline model, and 2 morphed PFEM were created to the anthropometric specifications of 2 obese PMHS used in a previous pedestrian impact study with a mid-size sedan. The same measurements as those obtained during the PMHS tests were calculated from the simulations (kinematics, accelerations, strains), and biofidelity metrics based on signals correlation (correlation and analysis, CORA) were established to compare the response of the models to the experiments. Injury outcomes were predicted deterministically (through strain-based threshold) and probabilistically (with injury risk functions) and compared with the injuries reported in the necropsy.
Results: The baseline model could not accurately capture all aspects of the PMHS kinematics, strain, and injury risks, whereas the morphed models reproduced biofidelic response in terms of trajectory (CORA score = 0.927 ± 0.092), velocities (0.975 ± 0.027), accelerations (0.862 ± 0.072), and strains (0.707 ± 0.143). The personalized THUMS models also generally predicted injuries consistent with those identified during posttest autopsy.
Conclusions: The study highlights the need to control for pedestrian anthropometry when validating pedestrian human body models against PMHS data. The information provided in the current study could be useful for improving model biofidelity for vehicle–pedestrian impact scenarios. 相似文献
The aim of this study was to determine the level of 26 polycyclic aromatic hydrocarbons (PAHs) at parking garages and to provide the necessary annual information based on occupational inhalation exposure and non-occupational inhalation exposure, which carry risks for the environment. For this purpose, 22 samples were collected continuously from both gas and particulates phase PAHs from two parking garages at Konya City Center, Turkey. The exposure-based risk of these samples was evaluated using concentrations of the carcinogenic PAH compounds. None of the 26 PAHs measured had values exceeding the recommended exposure limits (RELs) standard values for inhalation rate recommended by the World Health Organization (WHO). Exposure levels of gas and particulate PAHs for the occupational group and the public (children and adults who spend time in shopping centers) were found to be 0.07–28.24 μgm?3 and 0.05–5.753 μgm?3, respectively, representing levels two to four times higher than those at the control site. Maximum daily inhalation of B[a]Py was estimated at 1.33 ngd?1 for exposure of the public and as 274 ngd?1 for the occupational group. It is believed that traffic makes a substantial contribution to the PAH profile, which had relatively high concentrations of naphthalene (Napth) and coronene (Coro). Highly carcinogenic dibenzo(a,l)pyrene (B[al]Pyre) was found in the ambient air at two parking garages. Napth and phenanthrene (Phen) were the main compounds found in nearly all the tested samples. In this study, benzo[e]pyrene (B[e]Py) was used as a reference for PAHs because its concentration is stable and does not change seasonally. Considering the importance of these compounds in relation to human health, the aim of this work was to characterize and quantify the more toxic PAHs in parking garages. Conducting PAH sampling and their chemical analysis is very costly and labor intensive. This study produced data that can be a powerful tool for environmental forensics. 相似文献
In this study, a cohort of farmers from the Mateur region in the North of Tunisia, were interviewed and examined for the biochemical effects of pesticides. We studied their haematological profile, lipid parameters, serum markers of nephrotoxicity and hepatotoxicity. We also evaluated the activities of Butyrylcholinesterase (BChE), Acetylcholinesterase (AChE) and thiolactonase-paroxonase (PON). Moreover, lipid peroxidation and activities of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were determined. The duration of pesticide use and the farmers’ age were considered in the analysis. Our results revealed significant differences in some haematological parameters, in liver and kidney functions, in the lipidic status of the pesticide-exposed group. We also reported an increase in the index of incidence of cardiovascular risk in farmer populations. A significant decrease in AChE, BChE and PON levels was found among farmers. Lipid peroxidation, however, increased. The activities of SOD and CAT were remarkably elevated in farmer populations. There was a significant relation between changes in biological markers, the duration of pesticide use and the farmers’ age. This study indicates that a long-term exposure to pesticides may play an important role in the development of vascular diseases via metabolic disorders of lipoproteins, lipid peroxidation and oxidative stress, inhibition of BChE and decrease in thiolactonase-PON levels. 相似文献
SO2 remains a common air pollutant, almost half of the world’s population uses coal and biomass fuels for domestic energy. Limited evidence suggests that exposure to SO2 may be associated with neurotoxicity and increased risk of hospitalization and mortality of many brain disorders. However, our understanding of the mechanisms by which SO2 causes harmful insults on neurons remains elusive. To explore the molecular mechanism of SO2-induced neurotoxic effects in hippocampal neurons, we evaluated the synaptic plasticity in rat hippocampus after exposure to SO2 at various concentrations (3.5 and 7 mg m−3, 6 h d−1, for 90 d) in vivo, and in primary cultured hippocampal neurons (DIV7 and DIV14) after the treatment of SO2 derivatives in vitro. The results showed that SYP, PSD-95, NR-2B, p-ERK1/2 and p-CREB were consistently inhibited by SO2/SO2 derivatives in more mature hippocampal neurons in vivo and in vitro, while the effects were opposite in young hippocampal neurons. Our results indicated that in young neurons, SO2 exposure produced neuronal insult is similar to ischemic injury; while in more mature neurons, SO2 exposure induced synaptic dysfunctions might participate in cognitive impairment. The results implied that SO2 inhalation could cause different neuronal injury during brain development, and suggested that the molecular mechanisms might be involved in the changes of synaptic plasticity. 相似文献