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Background As Colorado ranked among the top nationally in non-medical use of opioids, a pilot medication for opioid use disorder (MOUD) program was developed to increase the number of NPs and PAs providing MOUD in order to bring this evidence- based treatment to 2 counties showing disproportionally high opioid overdose deaths. Over the first 18 months, the MOUD Pilot Program led to 15 new health care providers receiving MOUD waiver training and 1005 patients receiving MOUD from the 3 participating organizations. Here we evaluate patient centered clinical and functional outcomes of the pilot MOUD program implemented in 2 rural counties severely affected by the opioid crisis. Methods Under state-funded law (Colorado Senate Bill 17–074), three rural agencies submitted de-identified patient-level data at baseline (N = 1005) and after 6 months of treatment (N = 190, 25%) between December 2017 and January 2020. The Addiction Severity Index, PhQ9 and GAD-7 with McNemar-Bowker, and Wilcoxon Signed Rank tests analysis were used to measure patient outcomes across after participation in the program. . Results Patients in treatment reported using less heroin (52.1% vs 20.4%), opioids (22.3% vs 11.0%), and alcohol (28.6% vs 13.1%, all P < 0.01). Patients reported improved health (53.4% vs. 68.2%, P = 0.04), less frequency of disability (8.69 vs. 6.51, P = 0.02), symptoms (29.8% vs 21.3%), pain (67.5% to 53.6), worry (45.3% vs 62.3%), anxiety (49.7% vs 23.2%), depression (54.1% vs 23.3%, all P < 0.02) after treatment. Conclusions This study shows decreased substance use, improved physical and mental health, and reduced symptoms after 6 months of MOUD. Although more research on retention and long-term effects is needed, data shows improved health outcomes after 6 months of MOUD. Lessons learned from implementing this pilot program informed program expansion into other rural areas in need to address some of Colorado’ major public health crises.

Background: Glyphosate is the most commonly used herbicide in the world and is purported to have a variety of health effects, including endocrine disruption and an elevated risk of several types of cancer. Blood DNA methylation has been shown to be associated with many other environmental exposures, but to our knowledge, no studies to date have examined the association between blood DNA methylation and glyphosate exposure. Objective: We conducted an epigenome-wide association study to identify DNA methylation loci associated with urinary glyphosate and its metabolite aminomethylphosphonic acid (AMPA) levels. Secondary goals were to determine the association of epigenetic age acceleration with glyphosate and AMPA and develop blood DNA methylation indices to predict urinary glyphosate and AMPA levels. Methods: For 392 postmenopausal women, white blood cell DNA methylation was measured using the Illumina Infinium MethylationEPIC BeadChip array. Glyphosate and AMPA were measured in two urine samples per participant using liquid chromatography–tandem mass spectrometry. Methylation differences at the probe and regional level associated with glyphosate and AMPA levels were assessed using a resampling-based approach. Probes and regions that had an false discovery rate in of 1,000 subsamples of the study population were considered differentially methylated. Differentially methylated sites from the probe-specific analysis were combined into a methylation index. Epigenetic age acceleration from three epigenetic clocks and an epigenetic measure of pace of aging were examined for associations with glyphosate and AMPA. Results: We identified 24 CpG sites whose methylation level was associated with urinary glyphosate concentration and two associated with AMPA. Four regions, within the promoters of the MSH4 , KCNA6 , ABAT , and NDUFAF2 / ERCC8 genes, were associated with glyphosate levels, along with an association between ESR1 promoter hypomethylation and AMPA. The methylation index accurately predicted glyphosate levels in an internal validation cohort. AMPA, but not glyphosate, was associated with greater epigenetic age acceleration. Discussion: Glyphosate and AMPA exposure were associated with DNA methylation differences that could promote the development of cancer and other diseases. Further studies are warranted to replicate our results, determine the functional impact of glyphosate- and AMPA-associated differential DNA methylation, and further explore whether DNA methylation could serve as a biomarker of glyphosate exposure. https://doi.org/10.1289/EHP10174

The integration of risk assessment into clinical breast screening holds promise in increasing health care efficiency and decreasing morbidity and mortality associated with breast cancer diagnosis. While the National Cancer Comprehensive Network recommends risk counseling and increased screening for women with a 5-year risk of ≥1.7% based on the Gail model or other risk model (1,2), the US Preventive Services Task Force recommends that women who are at increased risk for breast cancer and at low risk for adverse medication effects be offered risk-reducing medications, such as tamoxifen or raloxifene, by their clinicians (3). However, neither recommendation clearly specifies which risk model to use; rather, they mention a number of different risk models. Thus, clinicians seeking to integrate breast cancer risk assessment into their practice are faced with uncertainty on how to assess risk in their patients.Concerns have been expressed regarding the limited clinical applicability of the Gail model (4,5). In addition, the Gail model does not consider some established risk factors, including breast density, obesity, and hormone use. We sought to determine the potential impact of adding two other models, the Breast Cancer Surveillance Consortium (BCSC) and the Tyrer-Cuzick models, on assessing screening mammography patients' breast cancer risk in the University of California, Irvine (UCI) Athena Breast Health Network Risk Assessment Program (6).After obtaining approval by the UCI Institutional Review Board, 3,426 research participants were recruited from the risk assessment program between March 2011 and January 2014. For this pilot study, a sample of 325 research participants were consecutively selected starting with the most recent enrollment date, based on age and race/ethnicity, resulting in~25% between 40-49, 50-59, 60-69, and 70-79 in each of the three most populous race/ethnicity categories in our patient population: non-Hispanic White, Hispanic, and Asian. Patients who met exclusionary criteria for the Gail, BCSC, or Tyrer-Cuzick models were excluded, resulting in 307 participants in our analytic pilot study cohort. All data except breast density data were obtained from the Athena Breast Health Questionnaire, which also served as an electronic intake form for the patients. Breast density data, categorized as BIRADS 1-4, were extracted from radiologist-dictated mammogram reports accessed through patients' electronic medical records. The data were used to calculate each patient's breast cancer risk scores using three risk assessment tools: (a) the Breast Cancer Risk Assessment Tool (www.cancer.gov/bcrisktool), based on the modified Gail model (7); (b) the BCSC Risk Calculator (tools.bcsc-scc.org/BC5yearRisk) (8); and (c) the IBIS Breast Cancer Risk Evaluation Calculator (www.ems-trials.org/riskevaluator), which calculates Tyrer-Cuzick scores (9). The distinct and overlapping risk factors considered in each of these models are depicted in Figure 1.As expected, the average risk scores for White women (1.66-1.86%) w...

Environmental factors have been linked to many diseases and health conditions, but reliable assessment of environmental exposures is challenging. Developing biomarkers of environmental exposures, rather than relying on self-report, will improve our ability to assess the association of such exposures with disease. Epigenetic markers, most notably DNA methylation, have been identified for some environmental exposures, but identification of markers for additional exposures is still needed. The rationale behind the Markers for Environmental Exposures (MEE) Study was to (1) identify biomarkers, especially epigenetic markers, of environmental exposures, such as pesticides, air/food/water contaminants, and industrial chemicals that are commonly encountered in the general population; and (2) support the study of potential relationships between environmental exposures and health and health-related factors. The MEE Study is a cross-sectional study with potential for record linkage and follow-up. The well-characterized cohort of 400 postmenopausal women has generated a repository of biospecimens, including blood, urine, and saliva samples. Paired data include an environmental exposures questionnaire, a breast health questionnaire, dietary recalls, and a food frequency questionnaire. This work describes the rationale, study design, and cohort characteristics of the MEE Study. In addition to our primary research goals, we hope that the data and biorepository generated by this study will serve as a resource for future studies and collaboration.