Recent empirical work on the distribution, determinants, and consequences of children and adolescents' witnessing of community violence are reviewed. Major findings across studies indicate that males, ethnic minorities, and urban residents are at increased risk for witnessing violence, and that higher rates of PTSD, depression, distress, aggression, and externalizing behavior disturbances are reported among those who witness violence. Degree of family conflict, domestic violence, and family support were demonstrated to modify the impact of exposure to violence. Research and policy recommendations are offered.

Background The etiology of autism is unknown, although prenatal exposures have been the focus of epidemiologic research for over 40 years. Aims To provide the first quantitative review and meta-analysis of the association between maternal pregnancy complications and pregnancy-related factors and risk of autism. Methods PubMed, Embase, and PsycInfo databases were searched for epidemiologic studies that examined the association between pregnancy-related factors and autism. Forty studies were eligible for inclusion in the meta-analysis. Summary effect estimates were calculated for factors examined in multiple studies. Results Over 50 prenatal factors have been examined. The factors associated with autism risk in the meta-analysis were advanced parental age at birth, maternal prenatal medication use, bleeding, gestational diabetes, being first born vs. third or later, and having a mother born abroad. The factors with the strongest evidence against a role in autism risk included previous fetal loss and maternal hypertension, proteinuria, preeclampsia, and swelling. Conclusions There is insufficient evidence to implicate any one prenatal factor in autism aetiology, although there is some evidence to suggest that exposure to pregnancy complications may increase the risk.

WHAT'S KNOWN ON THIS SUBJECT: Autism etiology is unknown, although perinatal and neonatal exposures have been the focus of epidemiologic research for more than 40 years. Although studies show that obstetrical and neonatal complications may increase autism risk, the specific complications and magnitude of effect have been inconsistent. WHAT THIS STUDY ADDS: Our study provides the first review and meta-analysis of all 64 studies of perinatal and neonatal risk factors for autism published through March 2007. abstract BACKGROUND: The etiology of autism is unknown, although perinatal and neonatal exposures have been the focus of epidemiologic research for over 40 years. OBJECTIVE: To provide the first review and meta-analysis of the association between perinatal and neonatal factors and autism risk. METHODS: PubMed, Embase, and PsycInfo databases were searched for studies that examined the association between perinatal and neo-natal factors and autism through March 2007. Forty studies were eligible for the meta-analysis. For each exposure, a summary effect estimate was calculated using a random-effects model. Heterogeneity in effect estimates across studies was examined, and, if found, a meta-regression was conducted to identify measured methodological factors that could explain between-study variability. RESULTS: Over 60 perinatal and neonatal factors were examined. Factors associated with autism risk in the meta-analysis were abnormal presentation, umbilical-cord complications, fetal distress, birth injury or trauma, multiple birth, maternal hemorrhage, summer birth, low birth weight, small for gestational age, congenital malformation, low 5-minute Apgar score, feeding difficulties, meconium aspiration, neonatal anemia, ABO or Rh incompatibility, and hyperbilirubinemia. Factors not associated with autism risk included anesthesia, assisted vaginal delivery, postterm birth, high birth weight, and head circumference. CONCLUSIONS: There is insufficient evidence to implicate any 1 perinatal or neonatal factor in autism etiology, although there is some evidence to suggest that exposure to a broad class of conditions reflecting general compromises to perinatal and neonatal health may increase the risk. Methodological variations were likely sources of heterogeneity of risk factor effects across studies. Pediatrics 2011;128: 344-355

The heterogeneity of associations is mostly accounted for by study design features that have largely been neglected in this literature. Enhanced attention to size of region and measurement strategies provide a clearer picture of how suicide rates vary by region. Resources for suicide prevention should be targeted to high poverty/deprivation and high unemployment areas.

Fast-food restaurants are concentrated within a short walking distance from schools, exposing children to poor-quality food environments in their school neighborhoods.

One mechanism for reduced physical activity among youth may be the influence of unsafe neighborhoods. Neighborhood interventions to increase safety and reduce disorder may be efficacious in increasing physical activity, thereby reducing risk of overweight and cardiovascular disease.

ObjectiveTo generate a national multiple sclerosis (MS) prevalence estimate for the United States by applying a validated algorithm to multiple administrative health claims (AHC) datasets.MethodsA validated algorithm was applied to private, military, and public AHC datasets to identify adult cases of MS between 2008 and 2010. In each dataset, we determined the 3-year cumulative prevalence overall and stratified by age, sex, and census region. We applied insurance-specific and stratum-specific estimates to the 2010 US Census data and pooled the findings to calculate the 2010 prevalence of MS in the United States cumulated over 3 years. We also estimated the 2010 prevalence cumulated over 10 years using 2 models and extrapolated our estimate to 2017.ResultsThe estimated 2010 prevalence of MS in the US adult population cumulated over 10 years was 309.2 per 100,000 (95% confidence interval [CI] 308.1–310.1), representing 727,344 cases. During the same time period, the MS prevalence was 450.1 per 100,000 (95% CI 448.1–451.6) for women and 159.7 (95% CI 158.7–160.6) for men (female:male ratio 2.8). The estimated 2010 prevalence of MS was highest in the 55- to 64-year age group. A US north-south decreasing prevalence gradient was identified. The estimated MS prevalence is also presented for 2017.ConclusionThe estimated US national MS prevalence for 2010 is the highest reported to date and provides evidence that the north-south gradient persists. Our rigorous algorithm-based approach to estimating prevalence is efficient and has the potential to be used for other chronic neurologic conditions.

Objective-Adolescence is an important period of risk for the development of lifelong smoking behaviors. Compelling, although inconsistent, evidence suggests a relation between parental smoking and the risk of smoking initiation during adolescence. This study investigates unresolved issues concerning the strength and nature of the association between parent smoking and offspring smoking initiation.Methods-We enrolled 564 adolescents aged 12-17, along with one of their parents, into the New England Family Study between [2001][2002][2003][2004]. Lifetime smoking histories were obtained from parents and their adolescent offspring. Discrete-time survival analysis was used to investigate the influence of parental smoking histories on the risk of adolescent smoking initiation.Results-Parental smoking was associated with a significantly higher risk of smoking initiation in adolescent offspring (odds ratio=2.81, 95% CI=1.78, 4.41). In addition, the likelihood of offspring smoking initiation increased with the number of smoking parents and the duration of exposure to parental smoking, suggesting a dose-response relation between parental smoking and offspring smoking. Offspring of parents who had quit smoking were no more likely to smoke than offspring of parents who had never smoked. The effects of parental smoking on offspring initiation differed by sex (with a stronger effect of father's smoking on boys than girls), developmental period (with a stronger effect of parental smoking before the adolescent was age 13 than afterwards), and residence of parents (with effects of father's smoking being dependent on living in the same household as the adolescent). Parental smoking was also associated with stronger negative reactions to adolescents' first cigarette, a potential marker of the risk of progression to higher levels of use.Conclusions-Parental smoking is an important source of vulnerability to smoking initiation among adolescents, and parental smoking cessation might attenuate this vulnerability. KeywordsSmoking; adolescents; parent-offspring transmissionMost adult smokers began smoking during adolescence; 1-3 preventing adolescent smoking initiation is therefore important for reducing the public health burden of smoking-related illnesses over the life course. There is accumulating evidence that parental smoking increases the risk for adolescent smoking initiation; 4-19 however, unresolved issues persist concerning the strength and nature of the association between parent smoking and initiation of smoking in offspring. 20 For example, while parental smoking and parental nicotine dependence have each been linked with an increased risk of offspring smoking, 21,22 few studies of intergenerational transmission have addressed their comparative effects. Evidence from one such study suggests that the effect of maternal smoking on offspring smoking is largely irrespective of maternal nicotine dependence. 18Prior evidence of a dose-response relationship between parental smoking and offspring initiation is also mixed. In...