Background: It is increasingly accepted that patients want information about their proposed treatment, and that provision of such information may alleviate fear and may improve the process of obtaining informed consent. It is not yet clear what form such information should take. Objective: Based on differences shown previously between patients receiving standard treatment and those in clinical trials, a system of routine appointments with a chemotherapy nurse at least one day before the patient offered consent to treatment was established for all patients receiving chemotherapy in Leicestershire, at which time patients were given standardised written information regarding outpatient chemotherapy and specific drugs. Method: In order to complete the audit cycle, the previous questionnaire study was repeated. Results: From 160 questionnaires distributed, 131 complete replies were received. Compared with the previous audit, a significantly higher proportion of patients receiving standard chemotherapy remembered being given written information about chemotherapy from a nurse before starting their treatment and remembered signing a consent form. The significant difference in feelings of involvement in the decision to have chemotherapy between patients receiving standard chemotherapy and those in clinical trials detected in the previous audit was no longer detectable, suggesting the clinical effectiveness of the intervention performed. Conclusion: Implementation of nurse-led appointments with provision of standardised information before formal consent being taken should be studied further for its potential to improve patients' involvement in medical decision making.

Diesel exhaust (DE) is a major contributor to ambient air pollution around the world. It is a known human carcinogen that targets the respiratory system and increases risk for many diseases, but there is limited research on the effects of DE exposure on the epigenome of human bronchial epithelial cells. Understanding the epigenetic impact of this environmental pollutant can elucidate biological mechanisms involved in the pathogenesis of harmful DE-related health effects. To estimate the causal effect of short-term DE exposure on the bronchial epithelial epigenome, we conducted a controlled single-blinded randomized crossover human experiment of exposure to DE and used bronchoscopy and Illumina 450K arrays for data collection and analysis, respectively. Of the 13 participants, 11 (85%) were male and 2 (15%) were female, and 12 (92%) were White and one (8%) was Hispanic; the mean age was 26 years (SD = 3.8 years). Eighty CpGs were differentially methylated, achieving the minimum possible exact P-value of P = 2.44 × 10−4 (i.e. 2/213). In regional analyses, we found two differentially methylated regions (DMRs) annotated to the chromosome 5 open reading frame 63 genes (C5orf63; 7-CpGs) and unc-45 myosin chaperone A gene (UNC45A; 5-CpGs). Both DMRs showed increased DNA methylation after DE exposure. The average causal effects for the DMRs ranged from 1.5% to 6.0% increases in DNA methylation at individual CpGs. In conclusion, we found that short-term DE alters DNA methylation of genes in target bronchial epithelial cells, demonstrating epigenetic level effects of exposure that could be implicated in pulmonary pathologies.

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