We analyzed international patterns and socioeconomic and rural-urban disparities in all-cause mortality and mortality from homicide, suicide, unintentional injuries, and HIV/AIDS among US youth aged 15-24 years. A county-level socioeconomic deprivation index and rural-urban continuum measure were linked to the 1999-2007 US mortality data. Mortality rates were calculated for each socioeconomic and rural-urban group. Poisson regression was used to derive adjusted relative risks of youth mortality by deprivation level and rural-urban residence. The USA has the highest youth homicide rate and 6th highest overall youth mortality rate in the industrialized world. Substantial socioeconomic and rural-urban gradients in youth mortality were observed within the USA. Compared to their most affluent counterparts, youth in the most deprived group had 1.9 times higher all-cause mortality, 8.0 times higher homicide mortality, 1.5 times higher unintentional-injury mortality, and 8.8 times higher HIV/AIDS mortality. Youth in rural areas had significantly higher mortality rates than their urban counterparts regardless of deprivation levels, with suicide and unintentional-injury mortality risks being 1.8 and 2.3 times larger in rural than in urban areas. However, youth in the most urbanized areas had at least 5.6 times higher risks of homicide and HIV/AIDS mortality than their rural counterparts. Disparities in mortality differed by race and sex. Socioeconomic deprivation and rural-urban continuum were independently related to disparities in youth mortality among all sex and racial/ethnic groups, although the impact of deprivation was considerably greater. The USA ranks poorly in all-cause mortality, youth homicide, and unintentional-injury mortality rates when compared with other industrialized countries.

Prior studies have raised concern about maternal acetaminophen use during pregnancy and increased risk of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) in their children; however, most studies have relied on maternal self-report.OBJECTIVE To examine the prospective associations between cord plasma acetaminophen metabolites and physician-diagnosed ADHD, ASD, both ADHD and ASD, and developmental disabilities (DDs) in childhood. DESIGN, SETTING, AND PARTICIPANTSThis prospective cohort study analyzed 996 mother-infant dyads, a subset of the Boston Birth Cohort, who were enrolled at birth and followed up prospectively at the Boston Medical Center from October 1, 1998, to June 30, 2018.EXPOSURES Three cord acetaminophen metabolites (unchanged acetaminophen, acetaminophen glucuronide, and 3-[N-acetyl-L-cystein-S-yl]-acetaminophen) were measured in archived cord plasma samples collected at birth. MAIN OUTCOMES AND MEASURESPhysician-diagnosed ADHD, ASD, and other DDs as documented in the child's medical records. RESULTSOf 996 participants (mean [SD] age, 9.8 [3.9] years; 548 [55.0%] male), the final sample included 257 children (25.8%) with ADHD only, 66 (6.6%) with ASD only, 42 (4.2%) with both ADHD and ASD, 304 (30.5%) with other DDs, and 327 (32.8%) who were neurotypical. Unchanged acetaminophen levels were detectable in all cord plasma samples. Compared with being in the first tertile, being in the second and third tertiles of cord acetaminophen burden was associated with higher odds of ADHD diagnosis (odds ratio [OR] for second tertile, 2.26; 95% CI, 1.40-3.69; OR for third tertile, 2.86; 95% CI, 1.77-4.67) and ASD diagnosis (OR for second tertile, 2.14; 95% CI, 0.93-5.13; OR for third tertile, 3.62; 95% CI, 1.62-8.60). Sensitivity analyses and subgroup analyses found consistent associations between acetaminophen buden and ADHD and acetaminophen burden and ASD across strata of potential confounders, including maternal indication, substance use, preterm birth, and child age and sex, for which point estimates for the ORs vary from 2.3 to 3.5 for ADHD and 1.6 to 4.1 for ASD. CONCLUSIONS AND RELEVANCECord biomarkers of fetal exposure to acetaminophen were associated with significantly increased risk of childhood ADHD and ASD in a dose-response fashion. Our findings support previous studies regarding the association between prenatal and perinatal acetaminophen exposure and childhood neurodevelopmental risk and warrant additional investigations.

Key Points Question What are the prenatal risk factors and perinatal and postnatal outcomes associated with maternal opioid use during pregnancy? Findings In this cohort study based on data from 8509 mother-child pairs in the Boston Birth Cohort, in utero opioid exposure was significantly associated with higher risks of fetal growth restriction, preterm birth, lack of expected physiological development, childhood conduct disorder or emotional disturbance in preschool-aged children, and attention-deficit/hyperactivity disorder in school-aged children. Meaning Prenatal opioid exposure was associated with higher risks of adverse perinatal and postnatal physical health and neurodevelopmental outcomes, suggesting that efforts to mitigate the health consequences of the opioid epidemic require more intergenerational research.

ObjectivesThis study examined global inequalities in cervical cancer incidence and mortality rates as a function of cross-national variations in the Human Development Index (HDI), socioeconomic factors, Gender Inequality Index (GII), and healthcare expenditure.MethodsAge-adjusted incidence and mortality rates were calculated for women in 184 countries using the 2008 GLOBOCAN database, and incidence and mortality trends were analyzed using the WHO cancer mortality database. Log-linear regression was used to model annual trends, while OLS and Poisson regression models were used to estimate the impact of socioeconomic and human development factors on incidence and mortality rates.ResultsCervical cancer incidence and mortality rates varied widely, with many African countries such as Guinea, Zambia, Comoros, Tanzania, and Malawi having at least 10-to-20-fold higher rates than several West Asian, Middle East, and European countries, including Iran, Saudi Arabia, Syria, Egypt, and Switzerland. HDI, GII, poverty rate, health expenditure per capita, urbanization, and literacy rate were all significantly related to cervical cancer incidence and mortality, with HDI and poverty rate each explaining >52% of the global variance in mortality. Both incidence and mortality rates increased in relation to lower human development and higher gender inequality levels. A 0.2 unit increase in HDI was associated with a 20% decrease in cervical cancer risk and a 33% decrease in cervical cancer mortality risk. The risk of a cervical cancer diagnosis increased by 24% and of cervical cancer death by 42% for a 0.2 unit increase in GII. Higher health expenditure levels were independently associated with decreased incidence and mortality risks.Conclusions and Public Health ImplicationsGlobal inequalities in cervical cancer are clearly linked to disparities in human development, social inequality, and living standards. Reductions in cervical cancer rates are achievable by reducing inequalities in socioeconomic conditions, availability of preventive health services, and women’s social status.