Characteristics of Single Vehicle Crashes with a Teen Driver in South Carolina, 2005-2008.

OBJECTIVE: Teens' crash risk is highest in the first years of independent driving. Circumstances surrounding fatal crashes have been widely documented, but less is known about factors related to nonfatal teen driver crashes. This study describes single vehicle nonfatal crashes involving the youngest teen drivers (15-17 years), compares these crashes to single vehicle nonfatal crashes among adult drivers (35-44 years) and examines factors related to nonfatal injury producing crashes for teen drivers. METHODS: Police crash data linked to hospital inpatient and emergency department data for 2005-2008 from the South Carolina Crash Outcomes Data Evaluation System (CODES) were analyzed. Nonfatal, single vehicle crashes involving passenger vehicles occurring on public roadways for teen (15-17 years) drivers were compared with those for adult (35-44 years) drivers on temporal patterns and crash risk factors per licensed driver and per vehicle miles traveled. Vehicle miles traveled by age group was estimated using data from the 2009 National Household Travel Survey. Multivariable log-linear regression analysis was conducted for teen driver crashes to determine which characteristics were related to crashes resulting in a minor/moderate injury or serious injury to at least one vehicle occupant. RESULTS: Compared with adult drivers, teen drivers in South Carolina had 2.5 times the single vehicle nonfatal crash rate per licensed driver and 11 times the rate per vehicle mile traveled. Teen drivers were nearly twice as likely to be speeding at the time of the crash compared with adult drivers. Teen driver crashes per licensed driver were highest during the afternoon hours of 3:00-5:59 pm and crashes per mile driven were highest during the nighttime hours of 9:00-11:59 pm. In 66% of the teen driver crashes, the driver was the only occupant. Crashes were twice as likely to result in serious injury when teen passengers were present than when the teen driver was alone. When teen drivers crashed while transporting teen passengers, the passengers were >5 times more likely to all be restrained if the teen driver was restrained. Crashes in which the teen driver was unrestrained were 80% more likely to result in minor/moderate injury and 6 times more likely to result in serious injury compared with crashes in which the teen driver was restrained. CONCLUSIONS: Despite the reductions in teen driver crashes associated with Graduated Driver Licensing (GDL), South Carolina's teen driver crash rates remain substantially higher than those for adult drivers. Established risk factors for fatal teen driver crashes, including restraint nonuse, transporting teen passengers, and speeding also increase the risk of nonfatal injury in single vehicle crashes. As South Carolina examines strategies to further reduce teen driver crashes and associated injuries, the state could consider updating its GDL passenger restriction to either none or one passenger <21years and dropping the passenger restriction exemption for trips to and from school. Surveillance systems such as CODES that link crash data with health outcome data provide needed information to more fully understand the circumstances and consequences of teen driver nonfatal crashes and evaluate the effectiveness of strategies to improve teen driver safety.

Motorcycle helmet effectiveness in reducing head, face and brain injuries by state and helmet law.

BACKGROUND: Despite evidence that motorcycle helmets reduce morbidity and mortality, helmet laws and rates of helmet use vary by state in the U.S. METHODS: We pooled data from eleven states: five with universal laws requiring all motorcyclists to wear a helmet, and six with partial laws requiring only a subset of motorcyclists to wear a helmet. Data were combined in the Crash Outcome Data Evaluation System's General Use Model and included motorcycle crash records probabilistically linked to emergency department and inpatient discharges for years 2005-2008. Medical outcomes were compared between partial and universal helmet law settings. We estimated adjusted relative risks (RR) and 95 % confidence intervals (CIs) for head, facial, traumatic brain, and moderate to severe head/facial injuries associated with helmet use within each helmet law setting using generalized log-binomial regression. RESULTS: Reported helmet use was higher in universal law states (88 % vs. 42 %). Median charges, adjusted for inflation and differences in state-incomes, were higher in partial law states (emergency department $1987 vs. $1443; inpatient $31,506 vs. $25,949). Injuries to the head and face, including traumatic brain injuries, were more common in partial law states. Effectiveness estimates of helmet use were higher in partial law states (adjusted-RR (CI) of head injury: 2.1 (1.9-2.2) partial law single vehicle; 1.4 (1.2, 1.6) universal law single vehicle; 1.8 (1.6-2.0) partial law multi-vehicle; 1.2 (1.1-1.4) universal law multi-vehicle). CONCLUSIONS: Medical charges and rates of head, facial, and brain injuries among motorcyclists were lower in universal law states. Helmets were effective in reducing injury in both helmet law settings; lower effectiveness estimates were observed in universal law states.

Retrospective estimation of Plutonium-239 doses from transfer to the fetus for Mayak PA workers.

PURPOSE: The estimation of plutonium fetal transfer and the calculation of individual in utero and postnatal doses for the Mayak Production Association (PA) offspring cohort. MATERIALS AND METHODS: The model developed by the International Commission on Radiological Protection (ICRP) for the transfer of plutonium to the fetus following maternal intakes before and during pregnancy has been adjusted for application to analysis of the fetal transfer of (239)Pu for Mayak workers. Improved estimates of fetal to maternal concentration ratios (CF:CM) have been obtained based on a correlation observed between adult offsprings' measured daily urine (239)Pu activity and estimates of their mothers' systemic activity at conception. Data on (239)Pu activity in daily urine samples were collected from 13 selected adults whose mothers worked at the Mayak PA facility during the period from 1948-1953, before and/or during pregnancy. RESULTS: A comparison of measured and modeled excretion data enabled a mean value of 0.18 ± 0.02 (n = 21) to be inferred for the Pu CF:CM ratio, with a coefficient of variation of 60%. CONCLUSIONS: Point estimates of the individual in utero and postnatal absorbed doses for the red bone marrow and liver were in the range 2…13 mGy in 95% of the cases for the cohort of 1936 offspring.

Underreporting of driver alcohol involvement in United States police and hospital records: capture-recapture estimates.

This paper analyzes what portion of US nonfatal crashes are alcohol-involved and how well police and hospitals detect involvement. A capture recapture model estimated alcohol involvement from levels detected by police and hospitals and the extent of detection overlap. We analyzed 550,933 Crash Outcome Data Evaluation System driver records from 2006-2008 police crash report censuses probabilistically linked to hospital inpatient and emergency department (ED) discharge censuses for CT, KY (admissions only), MD, NE, NY, SC, and UT. We computed national estimates from NHTSA's General Estimates System.Nationally an estimated 7.5% of drivers in nonfatal crashes and 12.9% of nonfatal crashes were alcohol-involved. (Crashes often involve multiple drivers but rarely are two alcohol-involved.) Police correctly identified an estimated 32% of alcohol-involved drivers in non-fatal crashes including 48% in injury crashes. Excluding KY, police in the six states reported 47% of alcohol involvement for cases treated in EDs and released and 39% for admitted cases. In contrast, hospitals reported 28% of involvement for ED cases and 51% for admitted cases. Underreporting varied widely between states. Police reported alcohol involvement for 44% of those who hospitals reported were alcohol-involved, while hospitals reported alcohol involvement for 33% of those who police reported were alcohol-involved. Police alcohol reporting completeness rose with police-reported driver injury severity. At least one system reported 62% of alcohol involvement. Police and hospitals need to communicate better about alcohol involvement. Despite the proven effectiveness of brief alcohol intervention, EDs rarely detect, much less intervene with crash-involved drinking drivers. Both police and EDs particularly need to assess alcohol involvement in minor injury better.

RNase L activity does not contribute to host RNA degradation induced by herpes simplex virus infection.

In early herpes simplex virus (HSV) infection, the virion host shutoff (vhs) protein mediates the degradation of mRNA and subsequent shutoff of host protein synthesis. It is unclear whether vhs acts alone or in concert with virus-induced cellular factors for this activity. This paper examines whether RNase L, a virally induced endoribonuclease, contributes to HSV-induced mRNA decay. Results showed that RNA degradation was comparable in wild-type and RNase L(-/-) cells, demonstrating that HSV-mediated RNA degradation is independent of RNase L activity. Furthermore, the data show that HSV-1 does not significantly induce RNase L activity in murine embryo fibroblasts.

Pathogenesis of herpes simplex virus type 2 virion host shutoff (vhs) mutants.

During lytic infection, the virion host shutoff (vhs) protein mediates the rapid degradation of mRNA and the shutoff of host protein synthesis. In vivo, herpes simplex virus type 1 (HSV-1) mutants lacking vhs activity are profoundly attenuated. Homologs of vhs exist in all of the neurotropic herpesviruses, and the goal of this study was to determine the virulence of HSV-2 mutants lacking vhs. Two HSV-2 recombinants were used in this study: 333-vhsB, which has a lacZ cassette inserted into the N terminus of vhs, and 333d41, which has a 939-bp deletion in vhs. As expected, both 333-vhsB and 333d41 failed to induce the cellular RNA degradation characteristic of HSV. Corneal, vaginal, and intracerebral routes of infection were used to study pathogenesis. Both viruses grew to significantly lower titers in the corneas, trigeminal ganglia, vaginas, dorsal root ganglia, spinal cords, and brains of mice than wild-type and rescue viruses, with a correspondingly reduced induction of disease. Both viruses, however, reactivated efficiently from explanted trigeminal ganglia, showing that vhs is dispensable for reactivation. The lethality of 333d41 following peripheral infection of mice, however, was significantly higher than that of 333-vhsB, suggesting that some of the attenuation of 333-vhsB may be due to the presence of a lacZ cassette in the vhs locus. Taken together, these data show that vhs represents an important determinant of HSV-2 pathogenesis and have implications for the design of HSV-2 recombinants and vaccines.

Herpes simplex virus type 2 virion host shutoff protein regulates alpha/beta interferon but not adaptive immune responses during primary infection in vivo.

The herpes simplex virus (HSV) virion host shutoff (vhs) protein, the product of the UL41 (vhs) gene, is an important determinant of HSV virulence. vhs has been implicated in HSV interference with host antiviral immune responses, down-regulating expression of major histocompatibility complex molecules to help HSV evade host adaptive immunity. The severe attenuation of vhs-deficient viruses in vivo could reflect their inability to escape immune detection. To test this hypothesis, BALB/c or congenic SCID mice were infected intravaginally (i.vag.) with the HSV type 2 (HSV-2) vhs null mutant 333d41 or the vhs rescue virus 333d41(R). vhs-deficient virus remained severely attenuated in SCID mice compared with rescue virus, indicating that vhs regulation of adaptive immune responses does not influence HSV pathogenesis during acute infection. Innate antiviral effectors remain intact in SCID mice; prominent among these is alpha/beta interferon (IFN-alpha/beta). The attenuation of HSV-2 vhs mutants could reflect their failure to suppress IFN-alpha/beta-mediated antiviral activity. To test this hypothesis, 129 and congenic IFN-alpha/beta receptor-deficient (IFN-alpha/betaR(-/-)) mice were infected i.vag. with wild-type virus, vhs null mutants 333-vhsB or 333d41, or the vhs rescue virus 333d41(R). Whereas vhs-deficient viruses showed greatly reduced replication in the genital mucosa of 129 mice compared with wild-type or vhs rescue viruses, they were restored to nearly wild-type levels of replication in IFN-alpha/betaR(-/-) mice over the first 2 days postinfection. Only wild-type and vhs rescue viruses caused severe genital disease and hind limb paralysis in 129 mice, but infection of IFN-alpha/betaR(-/-) mice restored the virulence of vhs-deficient viruses. vhs-deficient viruses replicated as vigorously as wild-type and rescue viruses in the nervous systems of IFN-alpha/betaR(-/-) mice. Restoration was specific for the vhs mutation, because thymidine kinase-deficient HSV-2 did not regain virulence or the capacity to replicate in the nervous systems of IFN-alpha/betaR(-/-) mice. Furthermore, the defect in the IFN-alpha/beta response was required for restoration of vhs-deficient virus replication and virulence, but the IFN-alpha/beta-stimulated protein kinase R pathway was not involved. Finally, vhs of HSV-2 has a unique capacity to interfere with the IFN-alpha/beta response in vivo, because an HSV-1 vhs null mutant did not recover replication and virulence after i.vag. inoculation into IFN-alpha/betaR(-/-) mice. These results indicate that vhs plays an important role early in HSV-2 pathogenesis in vivo by interfering with the IFN-alpha/beta-mediated antiviral response.