Background:The Global Burden of Disease (GBD) study, coordinated by the Institute for Health Metrics and Evaluation (IHME), produces influential, data-driven estimates of the burden of disease and premature death due to major risk factors. Expanded quantification of disease due to environmental health (EH) risk factors, including climate change, will enhance accuracy of GBD estimates, which will contribute to developing cost-effective policies that promote prevention and achieving Sustainable Development Goals.Objectives:We review key aspects of the GBD for the EH community and introduce the Global Burden of Disease–Pollution and Health Initiative (GBD-PHI), which aims to work with IHME and the GBD study to improve estimates of disease burden attributable to EH risk factors and to develop an innovative approach to estimating climate-related disease burden—both current and projected.Methods:We discuss strategies for improving GBD quantification of specific EH risk factors, including air pollution, lead, and climate change. We highlight key methodological challenges, including new EH risk factors, notably evidence rating and global exposure assessment.Discussion:A number of issues present challenges to the scope and accuracy of current GBD estimates for EH risk factors. For air pollution, minimal data exist on the exposure–risk relationships associated with high levels of pollution; epidemiological studies in high pollution regions should be a research priority. For lead, the GBD’s current methods do not fully account for lead’s impact on neurodevelopment; innovative methods to account for subclinical effects are needed. Decisions on inclusion of additional EH risk–outcome pairs need to be guided by findings of systematic reviews, the size of exposed populations, feasibility of global exposure estimates, and predicted trends in exposures and diseases. Neurotoxicants, endocrine-disrupting chemicals, and climate-related factors should be high priorities for incorporation into upcoming iterations of the GBD study. Enhancing the scope and methods will improve the GBD’s estimates and better guide prevention policy. https://doi.org/10.1289/EHP5496
Air pollution exposure and HIV infection can each cause neurocognitive insult in children. The purpose of this study was to test whether children with combined high air pollution exposure and perinatal HIV infection have even greater risk of neurocognitive impairment. This was a cross-sectional study of HIV-uninfected unexposed (HUU) and HIV-infected children and their caregivers in Nairobi, Kenya. We used a detailed neuropsychological battery to evaluate neurocognitive functioning in several domains. We measured caregiver 24-h personal CO exposure as a proxy for child CO exposure and child urinary 1-hydroxypyrene (1-OHP), a biomarker for exposure to polycyclic aromatic hydrocarbons (PAHs). Median 24-h caregiver CO exposure was 6.1 and 3.7 ppm for 45 HIV-infected (mean age 6.6 years) and 49 HUU (mean age 6.7 years), respectively; 48.5% of HIV-infected and 38.6% of HUU had caregiver 24-h CO levels exceeding the WHO recommended level. Median 1-OHP exposure was 0.6 and 0.7 µmol/mol creatinine among HIV-infected and HUU children, respectively. HIV-infected children with high urinary 1-OHP (exceeding 0.68 µmol/mol creatinine) had significantly lower global cognition (p = 0.04), delayed memory (p = 0.01), and attention scores (p = 0.003). Among HUU children, urinary 1-OHP and caregiver 24-h caregiver CO were not significantly associated with neurocognitive function. Our findings suggest that combined chronic exposure to air pollutants and perinatal HIV infection may be associated with poorer neurocognitive outcomes. High prevalence of air pollution exposure highlights the need to reduce these exposures.
Background: With climate change, adverse human health effects caused by heat exposure are of increasing public health concern. Forests provide beneficial ecosystem services for human health, including local cooling. Few studies have assessed the relationship between deforestation and heat-related health effects in tropical, rural populations. We sought to determine whether deforested compared to forested landscapes are associated with increased physiological heat strain in a rural, tropical environment. Methods: We analyzed data from 363 healthy adult participants from ten villages who participated in a two-by-two factorial, randomized study in East Kalimantan, Indonesia from 10/1/17 to 11/6/17. Using simple randomization, field staff allocated participants equally to different conditions to conduct a 90-minute outdoor activity, representative of typical work. Core body temperature was estimated at each minute during the activity using a validated algorithm from baseline oral temperatures and sequential heart rate data, measured using chest band monitors. We used linear regression models, clustered by village and with a sandwich variance estimator, to assess the association between deforested versus forested conditions and the number of minutes each participant spent above an estimated core body temperature threshold of 38.5°C. Results: Compared to those in the forested condition (n=172), participants in the deforested condition (n=159) spent an average of 3.08 (95% CI 0.57, 5.60) additional minutes with an estimated core body temperature exceeding 38.5°C, after adjustment for age, sex, body mass index, and experiment start time, with a larger difference among those who began the experiment after 12 noon (5.17 [95% CI 2.20, 8.15]). Conclusions: In this experimental study in a tropical, rural setting, activity in a deforested versus a forested setting was associated with increased objectively measured heat strain. Longer durations of hyperthermia can increase the risk of serious health outcomes. Land use decisions should consider the implications of deforestation on local heat exposure and health as well as on forest services, including carbon storage functions that impact climate change mitigation.
Background: Cadmium is a ubiquitous, toxic heavy metal associated with several adverse health outcomes, including high blood pressure, in adults. The impact of maternal cadmium burden on offspring birth weight and have not been thoroughly explored. We investigated associations of prenatal cadmium burden with birth weight and offspring blood pressure in childhood and adolescence. Methods: We analyzed data from 202 mother-child pairs who were recruited for the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) study in Mexico City (1997-2000). Prenatal cadmium burden was characterized using maternal urine collected in the third trimester of pregnancy - continuous and quartile specific-gravity adjusted cadmium (log-UCd, μg/L). Outcomes were offspring birth weight and blood pressure (measured at age 7-15 years). Blood pressure status (normal, elevated, stage 1 hypertension) was defined based on the 2017 American Academy of Pediatrics Guidelines. Those with elevated or stage 1 hypertension were categorized as having high blood pressure. Linear and logistic regression models were used to examine associations, adjusted for potential confounders. Potential effect modification by offspring sex was assessed using interaction terms and sex-stratified models. Results: Study participants included 93 males and 109 females, with a mean age of 10.0 (SD=1.5) years. Median third trimester urinary cadmium concentration was 0.17 μg/L (IQR=0.12, 0.26). The prevalence of high blood pressure was 19.3% (39/202). Prenatal cadmium was not associated with birthweight (β=-58.94 grams, 95%CI: -138.07, 20.19), offspring systolic blood pressure (β=-0.90 mmHg, 95%CI: -2.87, 1.06), diastolic blood pressure (β=-1.21 mmHg, 95%CI: -2.68, 0.26), or high blood pressure (OR=0.64, 95%CI: 0.34, 1.21). We found similar results when prenatal cadmium was modeled with quartiles. There was no evidence of effect modification by sex for any of the outcomes. Conclusions: In the current study, maternal third trimester was not associated with offspring blood pressure or birth weight, however future studies are needed to confirm these findings.
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