The Environmental “Riskscape” and Social Inequality: Implications for Explaining Maternal and Child Health Disparities

BACKGROUND: Research indicates that the double jeopardy of exposure to environmental hazards combined with place-based stressors is associated with maternal and child health (MCH) disparities. OBJECTIVE AND DISCUSSION: Our aim is to present evidence that individual-level and place-based psychosocial stressors may compromise host resistance such that environmental pollutants would have adverse health effects at relatively lower doses, thus partially explaining MCH disparities, particularly poor birth outcomes. Allostatic load may be a physiologic mechanism behind the moderation of the toxic effect of environmental pollutants by social stressors. We propose a conceptual framework for holistic approaches to future MCH research that elucidates the interplay of psychosocial stressors and environmental hazards in order to better explain drivers of MCH disparities. CONCLUSION: Given the complexity of the link between environmental factors and MCH disparities, a holistic approach to future MCH research that seeks to untangle the double jeopardy of chronic stressors and environmental hazard exposures could help elucidate how the interplay of these factors shapes persistent racial and economic disparities in MCH

HIV vaccine trial safety and retention among 18-20 year olds in the HVTN 503/Phambili study support the inclusion of adolescents in future trials

Worldwide, many adolescents, especially women, acquire HIV before age 18. Yet to date, no HIV vaccine trials have enrolled adolescents. Reasons for excluding adolescents from these trials include regulations protecting vulnerable subjects and concerns regarding informed consent, social harms, adverse events, and loss to follow-up

The Impact of HAART on the Respiratory Complications of HIV Infection: Longitudinal Trends in the MACS and WIHS Cohorts

Objective: To review the incidence of respiratory conditions and their effect on mortality in HIV-infected and uninfected individuals prior to and during the era of highly active antiretroviral therapy (HAART). Design: Two large observational cohorts of HIV-infected and HIV-uninfected men (Multicenter AIDS Cohort Study [MACS]) and women (Women's Interagency HIV Study [WIHS]), followed since 1984 and 1994, respectively. Methods: Adjusted odds or hazards ratios for incident respiratory infections or non-infectious respiratory diagnoses, respectively, in HIV-infected compared to HIV-uninfected individuals in both the pre-HAART (MACS only) and HAART eras; and adjusted Cox proportional hazard ratios for mortality in HIV-infected persons with lung disease during the HAART era. Results: Compared to HIV-uninfected participants, HIV-infected individuals had more incident respiratory infections both pre-HAART (MACS, odds ratio [adjusted-OR], 2.4; 95% confidence interval [CI], 2.2-2.7; p<0.001) and after HAART availability (MACS, adjusted-OR, 1.5; 95%CI 1.3-1.7; p<0.001; WIHS adjusted-OR, 2.2; 95%CI 1.8-2.7; p<0.001). Chronic obstructive pulmonary disease was more common in MACS HIV-infected vs. HIV-uninfected participants pre-HAART (hazard ratio [adjusted-HR] 2.9; 95%CI, 1.02-8.4; p = 0.046). After HAART availability, non-infectious lung diseases were not significantly more common in HIV-infected participants in either MACS or WIHS participants. HIV-infected participants in the HAART era with respiratory infections had an increased risk of death compared to those without infections (MACS adjusted-HR, 1.5; 95%CI, 1.3-1.7; p<0.001; WIHS adjusted-HR, 1.9; 95%CI, 1.5-2.4; p<0.001). Conclusion: HIV infection remained a significant risk for infectious respiratory diseases after the introduction of HAART, and infectious respiratory diseases were associated with an increased risk of mortality. © 2013 Gingo et al

Predictors for neonatal death in the rural areas of Shaanxi Province of Northwestern China: a cross-sectional study

Background Almost all (99%) neonatal deaths arise in low-income and middle-income countries. Approximately 450 new-born children die every hour, which is mainly from preventable causes. There has been increased recognition of the need for these countries to implement public health interventions that specifically target neonatal deaths. The purpose of this paper is to identify the predictors of neonatal death in Type 4 rural (poorest) counties in Shaanxi Province of northwestern China. Methods A cross-sectional study was conducted in Shaanxi Province, China. A single-stage survey design was identified to estimate standard errors. Because of concern about the complex sample design, the data were analysed using multivariate logistic regression analysis. Socioeconomic and maternal health service utilization factors were added into the model. Results During the study period, a total of 4750 women who delivered in the past three years were randomly selected for interview in the five counties. There were 4880 live births and 54 neonatal deaths identified. In the multiple logistic regression, the odds of neonatal death was significantly higher for multiparous women (OR = 2.77; 95% CI: 1.34, 5.70) and women who did not receive antennal health care in the first trimester of pregnancy (OR = 2.49; 95% CI: 1.41, 4.40). Women who gave birth in a county-level hospital (OR = 0.18; 95% CI: 0.04, 0.86) and had junior high school or higher education level (OR = 0.20; 95% CI: 0.05, 0.84) were significantly protected from neonatal death. Conclusions Public health interventions directed at reducing neonatal death should address the socioeconomic factors and maternal health service utilization, which significantly influence neonatal mortality in rural China. Multipara, low educational level of the women, availability of prenatal visits in the first trimester of pregnancy and hospital delivery should be considered when planning the interventions to reduce the neonatal mortality in rural areas

Smoking Cessation Among Women with and at Risk for HIV: Are They Quitting?

Cigarette smoking is an important risk factor for adverse health events in HIV-infected populations. While recent US population-wide surveys report annual sustained smoking cessation rates of 3.4–8.5%, prospective data are lacking on cessation rates for HIV-infected smokers. To determine the sustained tobacco cessation rate and predictors of cessation among women with or at risk for HIV infection. Prospective cohort study. A total of 747 women (537 HIV-infected and 210 HIV-uninfected) who reported smoking at enrollment (1994–1995) in the Women’s Interagency HIV Study (WIHS) and remained in follow-up after 10 years. The participants were mostly minority (61% non-Hispanic Blacks and 22% Hispanics) and low income (68% with reported annual incomes of less than or equal to $12,000). The primary outcome was defined as greater than 12 months continuous cessation at year 10. Multivariate logistic regression was used to identify independent baseline predictors of subsequent tobacco cessation. A total of 121 (16%) women reported tobacco cessation at year 10 (annual sustained cessation rate of 1.8%, 95% CI 1.6–2.1%). Annual sustained cessation rates were 1.8% among both HIV-positive and HIV-negative women (p = 0.82). In multivariate analysis, the odds of tobacco cessation were significantly higher in women with more years of education (p trend = 0.02) and of Hispanic origin (OR = 1.87, 95% CI = 1.4–2.9) compared to Black women. Cessation was significantly lower in current or former illicit drug users (OR = 0.42 95% CI = 0.24–0.74 and OR = 0.65, 95% CI = 0.49–0.86, respectively, p trend = 0.03) and women reporting a higher number of cigarettes per day at baseline (p trend &lt; 0.001). HIV-infected and at-risk women in this cohort have lower smoking cessation rates than the general population. Given the high prevalence of smoking, the high risk of adverse health events from smoking, and low rates of cessation, it is imperative that we increase efforts and overcome barriers to help these women quit smoking

Ambient air pollution exposure and full-term birth weight in California

<p>Abstract</p> <p>Background</p> <p>Studies have identified relationships between air pollution and birth weight, but have been inconsistent in identifying individual pollutants inversely associated with birth weight or elucidating susceptibility of the fetus by trimester of exposure. We examined effects of prenatal ambient pollution exposure on average birth weight and risk of low birth weight in full-term births.</p> <p>Methods</p> <p>We estimated average ambient air pollutant concentrations throughout pregnancy in the neighborhoods of women who delivered term singleton live births between 1996 and 2006 in California. We adjusted effect estimates of air pollutants on birth weight for infant characteristics, maternal characteristics, neighborhood socioeconomic factors, and year and season of birth.</p> <p>Results</p> <p>3,545,177 singleton births had monitoring for at least one air pollutant within a 10 km radius of the tract or ZIP Code of the mother's residence. In multivariate models, pollutants were associated with decreased birth weight; -5.4 grams (95% confidence interval -6.8 g, -4.1 g) per ppm carbon monoxide, -9.0 g (-9.6 g, -8.4 g) per pphm nitrogen dioxide, -5.7 g (-6.6 g, -4.9 g) per pphm ozone, -7.7 g (-7.9 g, -6.6 g) per 10 <it>μ</it>g/m³particulate matter under 10 μm, -12.8 g (-14.3 g, -11.3 g) per 10 <it>μ</it>g/m³particulate matter under 2.5 μm, and -9.3 g (-10.7 g, -7.9 g) per 10 <it>μ</it>g/m³of coarse particulate matter. With the exception of carbon monoxide, estimates were largely unchanged after controlling for co-pollutants. Effect estimates for the third trimester largely reflect the results seen from full pregnancy exposure estimates; greater variation in results is seen in effect estimates specific to the first and second trimesters.</p> <p>Conclusions</p> <p>This study indicates that maternal exposure to ambient air pollution results in modestly lower infant birth weight. A small decline in birth weight is unlikely to have clinical relevance for individual infants, and there is debate about whether a small shift in the population distribution of birth weight has broader health implications. However, the ubiquity of air pollution exposures, the responsiveness of pollutant levels to regulation, and the fact that the highest pollution levels in California are lower than those regularly experienced in other countries suggest that precautionary efforts to reduce pollutants may be beneficial for infant health from a population perspective.</p

Risk of breast, ovary, and uterine corpus cancers among 85 268 women with AIDS

By linking HIV/AIDS and cancer surveillance data in 12 US regions, breast and reproductive cancer risks with AIDS were compared to those in the general population. Trends in standardized incidence ratios (SIRs) were assessed by CD4 count, AIDS-relative time, and calendar time. Standardized incidence ratios were indirectly adjusted for cancer risk factors using data from AIDS cohort participants and the general population. With AIDS, 313 women developed breast cancer (SIR 0.69, 95% confidence interval (CI) 0.62–0.77), 42 developed ovary cancer (SIR 1.05, 95% CI, 0.75–1.42), and 31 developed uterine corpus cancer (SIR 0.57, 95% CI, 0.39–0.81). Uterine cancer risk was reduced significantly after age 50 (SIR 0.33). Breast cancer risk was reduced significantly both before (SIR 0.71) and after (SIR 0.66) age 50, and was lower for local or regional (SIR 0.54) than distant (SIR 0.89) disease. Breast cancer risk varied little by CD4 count (Ptrend=0.47) or AIDS-relative time (Ptrend=0.14) or after adjustment for established cancer risk factors. However, it increased significantly between 1980 and 2002 (Ptrend=0.003), approaching the risk of the general population. We conclude that the cancer deficit reflected direct or indirect effects of HIV/AIDS and that anti-HIV therapy reduced these effects