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It is feasible to recruit diverse families at risk for hereditary cancer from a population-based cancer registry. This recruitment approach can be used as a paradigm for harmonizing processes and increasing internal and external validity of large-scale public health genomic initiatives in the era of precision medicine.

BackgroundCarriers of breast cancer gene (BRCA) mutations are asked to communicate genetic test results to their biological relatives to increase awareness of cancer risk and promote use of genetic services. This process is highly variable from family to family. Interventions that support communication of genetic test results, coping, and offer decision support in families harboring a pathogenic variant may contribute to effective management of hereditary cancer.ObjectiveThe aim of this paper was to describe the development of the Family Gene Toolkit, a Web-based intervention targeting BRCA carriers and untested blood relatives, designed to enhance coping, family communication, and decision making.MethodsWe present findings from focus groups regarding intervention acceptability and participant satisfaction and from a pre-post pilot study with random allocation to a wait-listed control group regarding intervention feasibility and usability.ResultsThe Family Gene Toolkit was developed by a multidisciplinary team as a psycho-educational and skills-building intervention. It includes two live webinar sessions and a follow-up phone call guided by a certified genetic counselor and a master’s prepared oncology nurse. Each live webinar includes two modules (total four modules) presenting information about BRCA mutations, a decision aid for genetic testing, and two skill-building modules for effective coping and family communication. Participants in focus groups (n=11) were highly satisfied with the intervention, reporting it to be useful and describing clearly the important issues. From the 12 dyads recruited in the pre-post pilot study (response rate 12/52, 23%), completion rate was 71% (10/14) for intervention and 40% (4/10) for wait-listed control groups.ConclusionsAcceptability and satisfaction with the Family Gene Toolkit is high. On the basis of the findings from usability and feasibility testing, modifications on timing, delivery mode, and recruitment methods have been implemented.Trial RegistrationClinicalTrials.gov NCT02154633; https://clinicaltrials.gov/ct2/show/NCT02154633 (Archived by WebCite at http://www.webcitation.org/6yYNvLPjv)

BackgroundToxicological research suggests that coarse particles (PM10–2.5) are inflammatory, but responses are complex and may be best summarized by multiple inflammatory markers. Few human studies have investigated associations with PM10–2.5 and, of those, none have explored long-term exposures. Here we examine long-term associations with inflammation and coagulation in the Multi-Ethnic Study of Atherosclerosis.MethodsParticipants included 3,295 adults (45–84 years of age) from three metropolitan areas. Site-specific spatial models were used to estimate 5-year concentrations of PM10–2.5 mass and copper, zinc, phosphorus, silicon, and endotoxin found in PM10–2.5. Outcomes included interleukin-6, C-reactive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin–antiplasmin complex, and inflammation and coagulation scores. We used multivariable regression with multiply imputed data to estimate associations while controlling for potential confounders, including co-pollutants such as fine particulate matter.ResultsSome limited evidence was found of relationships between inflammation and coagulation and PM10–2.5. Endotoxin was the PM10–2.5 component most strongly associated with inflammation, with an interquartile range (IQR) increase (0.08 EU/m3) associated with 0.15 (95% CI: 0.01, 0.28; p = 0.03) and 0.08 (95% CI: –0.07, 0.23; p = 0.28) higher inflammation scores before and after control for city, respectively. Copper was the component with the strongest association with coagulation, with a 4-ng/m3 increase associated with 0.19 (95% CI: 0.08, 0.30; p = 0.0008) and 0.12 (95% CI: –0.05, 0.30; p = 0.16) unit higher coagulation scores before and after city adjustment, respectively.ConclusionsOur cross-sectional analysis provided some evidence that long-term PM10–2.5 exposure was associated with inflammation and coagulation, but associations were modest and depended on particle composition.CitationAdar SD, D’Souza J, Mendelsohn-Victor K, Jacobs DR Jr, Cushman M, Sheppard L, Thorne PS, Burke GL, Daviglus ML, Szpiro AA, Diez Roux AV, Kaufman JD, Larson TV. 2015. Markers of inflammation and coagulation after long-term exposure to coarse particulate matter: a cross-sectional analysis from the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 123:541–548; http://dx.doi.org/10.1289/ehp.1308069