Capacity of Ugandan public sector health facilities to prevent and control non-communicable diseases: an assessment based upon WHO-PEN standards

Abstract Background Non-communicable diseases (NCDs) are increasing in prevalence in low-income countries including Uganda. The Uganda Ministry of Health has prioritized NCD prevention, early diagnosis, and management. However, research on the capacity of public sector health facilities to address NCDs is limited. Methods We developed a survey guided by the literature and the standards of the World Health Organization Pacakage of Essential Noncommunicable Disease Interventions for Primary Health Care in Low-Resource Settings. We used this tool to conduct a needs assessment in 53 higher-level public sector facilities throughout Uganda, including all Regional Referral Hospitals (RRH) and a purposive sample of General Hospitals (GH) and Health Centre IVs (HCIV), to: (1) assess their capacity to detect and manage NCDs; (2) describe provider knowledge and practices regarding the management of NCDs; and (3) identify areas in need of focused improvement. We collected data on human resources, equipment, NCD screening and management, medicines, and laboratory tests. Descriptive statistics were used to summarize our findings. Results We identified significant resource gaps at all sampled facilities. All facilities reported deficiencies in NCD screening and management services. Less than half of all RRH and GH had an automated blood pressure machine. The only laboratory test uniformly available at all surveyed facilities was random blood glucose. Sub-specialty NCD clinics were available in some facilities with the most common type being a diabetes clinic present at eleven (85%) RRHs. These facilities offered enhanced services to patients with diabetes. Surveyed facilities had limited use of NCD patient registries and NCD management guidelines. Most facilities (46% RRH, 23% GH, 7% HCIV) did not track patients with NCDs by using registries and only 4 (31%) RRHs, 4 (15%) GHs, and 1 (7%) HCIVs had access to diabetes management guidelines. Conclusions Despite inter-facility variability, none of the facilities in our study met the WHO-PEN standards for essential tools and medicines to implement effective NCD interventions. In Uganda, improvements in the allocation of human resources and essential medicines and technologies, coupled with uptake in the use of quality assurance modalities are desperately needed in order to adequately address the rapidly growing NCD burden.https://deepblue.lib.umich.edu/bitstream/2027.42/145194/1/12913_2018_Article_3426.pd

Urinary Polycyclic Aromatic Hydrocarbon Metabolites and Attention/Deficit Hyperactivity Disorder, Learning Disability, and Special Education in U.S. Children Aged 6 to 15

Exposure to polycyclic aromatic hydrocarbons (PAHs) adversely affects child neurodevelopment, but little is known about the relationship between PAHs and clinically significant developmental disorders. We examined the relationship between childhood measures of PAH exposure and prevalence of attention deficit/hyperactivity disorder (ADHD), learning disability (LD), and special education (SE) in a nationally representative sample of 1,257 U.S. children 6–15 years of age. Data were obtained from the National Health and Nutrition Examination Survey (NHANES) 2001–2004. PAH exposure was measured by urinary metabolite concentrations. Outcomes were defined by parental report of (1) ever doctor-diagnosed ADHD, (2) ever doctor- or school representative-identified LD, and (3) receipt of SE or early intervention services. Multivariate logistic regression accounting for survey sampling was used to determine the associations between PAH metabolites and ADHD, LD, and SE. Children exposed to higher levels of fluorine metabolites had a 2-fold increased odds (95% C.I. 1.1, 3.8) of SE, and this association was more apparent in males (OR 2.3; 95% C.I. 1.2, 4.1) than in females (OR 1.8; 95% C.I. 0.6, 5.4). No other consistent pattern of developmental disorders was associated with urinary PAH metabolites. However, concurrent exposure to PAH fluorine metabolites may increase use of special education services among U.S. children

Maternal arsenic exposure and impaired glucose tolerance during pregnancy

Background: Accumulating evidence has shown an increased risk of type 2 diabetes in general populations exposed to arsenic, but little is known about exposures during pregnancy and the association with gestational diabetes (GD). Objectives: We studied 532 women living proximate to the Tar Creek Superfund Site to investigate whether arsenic exposure is associated with impaired glucose tolerance during pregnancy. Methods: Blood glucose was measured between 24 and 28 weeks gestation after a 1-hr oral glucose tolerance test (GTT) as part of routine prenatal care. Blood and hair were collected at delivery and analyzed for arsenic using inductively coupled plasma mass spectrometry with dynamic reaction cell. Results: Arsenic concentrations ranged from 0.2 to 24.1 μg/L (ppb) (mean ± SD, 1.7 ±1.5) and 1.1 to 724.4 ng/g (ppb) (mean ± SD, 27.4 ± 61.6) in blood and hair, respectively. One-hour glucose levels ranged from 40 to 284 mg/dL (mean ± SD, 108.7 ± 29.5); impaired glucose tolerance was observed in 11.9% of women when using standard screening criterion (> 140 mg/dL). Adjusting for age, Native-American race, prepregnancy body mass index, Medicaid use, and marital status, women in the highest quartile of blood arsenic exposure had 2.8 higher odds of impaired GTT than women in the lowest quartile of exposure (95% confidence interval, 1.1–6.9) (p-trend = 0.008). Conclusions: Among this population of pregnant women, arsenic exposure was associated with increased risk of impaired GTT at 24–28 weeks gestation and therefore may be associated with increased risk of GD

Maternal iron metabolism gene variants modify umbilical cord blood lead levels by gene-environment interaction: a birth cohort study

Background: Given the relationship between iron metabolism and lead toxicokinetics, we hypothesized that polymorphisms in iron metabolism genes might modify maternal-fetal lead transfer. The objective of this study was to determine whether maternal and/or infant transferrin (TF) and hemochromatosis (HFE) gene missense variants modify the association between maternal blood lead (MBL) and umbilical cord blood lead (UCBL). Methods: We studied 476 mother-infant pairs whose archived blood specimens were genotyped for TF P570S, HFE H63D and HFE C282Y. MBL and UCBL were collected within 12 hours of delivery. Linear regression models were used to examine the association between log-transformed MBL and UCBL, examine for confounding and collinearity, and explore gene-environment interactions. Results: The geometric mean MBL was 0.61 μg/dL (range 0.03, 3.2) and UCBL 0.42 (<0.02, 3.9). Gene variants were common with carrier frequencies ranging from 12-31%; all were in Hardy-Weinberg equilibrium. In an adjusted linear regression model, log MBL was associated with log UCBL (β = 0.92, 95% CI: 0.82, 1.03; p < 0.01) such that a 1% increase in MBL was associated with a 0.92% increase in UCBL among infants born to wild-type mothers. In infants born to C282Y variants, however, a 1% increase in MBL is predicted to increase UCBL 0.65% (βMain Effect = −0.002, 95% CI: −0.09, −0.09; p = 0.97; βInteraction = −0.27, 95% CI: −0.52, −0.01; p = 0.04), representing a 35% lower placental lead transfer among women with MBL 5 μg/dL. Conclusions: Maternal HFE C282Y gene variant status is associated with greater reductions in placental transfer of lead as MBL increases. The inclusion of gene-environment interaction in risk assessment models may improve efforts to safeguard vulnerable populations. Electronic supplementary material The online version of this article (doi:10.1186/1476-069X-13-77) contains supplementary material, which is available to authorized users

Levels of Lead in Breast Milk and Their Relation to Maternal Blood and Bone Lead Levels at One Month Postpartum.

Despite the many well-recognized benefits of breast-feeding for both mothers and infants, detectable levels of lead in breast milk have been documented in population studies of women with no current environmental or occupational exposures. Mobilization of maternal bone lead stores has been suggested as a potential endogenous source of lead in breast milk. We measured lead in breast milk to quantify the relation between maternal blood and bone lead levels and breast-feeding status (exclusive vs. partial) among 310 lactating women in Mexico City, Mexico, at 1 month postpartum. Umbilical cord and maternal blood samples were collected at delivery. Maternal breast milk, blood, and bone lead levels were obtained at 1 month postpartum. Levels of lead in breast milk ranged from 0.21 to 8.02 microg/L (ppb), with a geometric mean (GM) of 1.1 microg/L; blood lead ranged from 1.8 to 29.9 microg/dL (GM = 8.4 microg/dL); bone lead ranged from less than 1 to 67.2 microg/g bone mineral (patella) and from less than 1 to 76.6 microg/g bone mineral (tibia) at 1 month postpartum. Breast milk lead was significantly correlated with umbilical cord lead [Spearman correlation coefficient (r$_S$) = 0.36, p less than 0.0001] and maternal blood lead (r$_S$= 0.38, p less than 0.0001) at delivery and with maternal blood lead (r$_S$ = 0.42, p less than 0.0001) and patella lead (r$_S$= 0.15, p less than 0.01) at 1 month postpartum. Mother's age, years living in Mexico City, and use of lead-glazed ceramics, all predictive of cumulative lead exposure, were not significant predictors of breast milk lead levels. Adjusting for parity, daily dietary calcium intake (milligrams), infant weight change (grams), and breast-feeding status (exclusive or partial lactation), the estimated effect of an interquartile range (IQR) increase in blood lead (5.0 microg/dL) was associated with a 33% increase in breast milk lead [95% confidence interval (CI), 24 to 43%], whereas an IQR increase in patella lead (20 microg/g) was associated with a 14% increase in breast milk lead (95% CI, 5 to 25%). An IQR increase in tibia lead (12.0 microg/g) was associated with a 5% increase in breast milk lead (95% CI, -3% to 14%). Our results indicate that even among a population of women with relatively high lifetime exposure to lead, levels of lead in breast milk are low, influenced both by current lead exposure and by redistribution of bone lead accumulated from past environmental exposures

Assessment of cleaning to control lead dust in homes of children with moderate lead poisoning: treatment of lead-exposed children trial

In this article we describe the assessment and control of lead dust exposure in the Treatment of Lead-exposed Children (TLC) Trial, a clinical trial of the effects of oral chelation on developmental end points in urban children with moderately elevated blood lead levels. To reduce potential lead exposure from settled dust or deteriorated paint during the drug treatment phase of the trial, the homes of 765 (98%) of the randomized children (both active and placebo drug treatment groups) were professionally cleaned. Lead dust measurements were made in a sample of 213 homes before and after cleaning. Geometric mean dust lead loadings before cleaning were 43, 29, 308, and 707 micro g/ft2 in the kitchen floor, playroom floor, playroom windowsill, and playroom window well samples respectively. Following cleaning, floor dust lead loadings were reduced on average 32% for paired floor samples (p < 0.0001), 66% for windowsills (p < 0.0001), and 93% for window wells (p < 0.0001). Cleaning was most effective for 146 homes with precleaning dust lead levels above the recommended clearance levels, with average reductions of 44%, 74%, and 93% for floors (p < 0.0001), windowsills (p < 0.0001), and window wells (p < 0.0001), respectively. Despite these substantial reductions in dust lead loadings, a single professional cleaning did not reduce the lead loadings of all dust samples to levels below current federal standards for lead in residential dust. Attainment of dust levels below current standards will require more intensive cleaning and lead hazard reduction strategies