Workplace inhalational hazards remain common worldwide, even though they are ameliorable. Previous American Thoracic Society documents have assessed the contribution of workplace exposures to asthma and chronic obstructive pulmonary disease on a population level, but not to other chronic respiratory diseases. The goal of this document is to report an in-depth literature review and data synthesis of the occupational contribution to the burden of the major nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity pneumonitis; other noninfectious granulomatous lung diseases, including sarcoidosis; and selected respiratory infections. Methods: Relevant literature was identified for each respiratory condition. The occupational population attributable fraction (PAF) was estimated for those conditions for which there were sufficient population-based studies to allow pooled estimates. For the other conditions, the occupational burden of disease was estimated on the basis of attribution in case series, incidence rate ratios, or attributable fraction within an exposed group. Results: Workplace exposures contribute substantially to the burden of multiple chronic respiratory diseases, including asthma (PAF, 16%); chronic obstructive pulmonary disease (PAF, 14%); chronic bronchitis (PAF, 13%); idiopathic pulmonary fibrosis (PAF, 26%); hypersensitivity pneumonitis (occupational burden, 19%); other granulomatous diseases, including sarcoidosis (occupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (occupational burden, 2.3% in silica-exposed workers and 1% in healthcare workers); and community-acquired pneumonia in working-age adults (PAF, 10%). Conclusions: Workplace exposures contribute to the burden of disease across a range of nonmalignant lung conditions in adults (in addition to the 100% burden for the classic occupational pneumoconioses). This burden has important clinical, research, and policy implications. There is a pressing need to improve clinical recognition and public health awareness of the contribution of occupational factors across a range of nonmalignant respiratory diseases.

Long-term opioid prescribing is increasing despite poor efficacy for non-cancer pain, potential harm, and incompatibility with best practice. Questions of equality of care arise from higher prescription rates in the north of England and in areas of greater social deprivation. A national registry of patients with high opioid use would improve patient safety for this high-risk demographic, as well as provide more focused epidemiological data regarding patterns of prescribing.

Recognition of the improvements in patient safety, quality of patient care, and efficiency that health care information systems have the potential to bring has led to significant investment. Globally the sale of health care information systems now represents a multibillion dollar industry. As policy makers, health care professionals, and patients, we have a responsibility to maximize the return on this investment. To this end we analyze alternative licensing and software development models, as well as the role of standards. We describe how licensing affects development. We argue for the superiority of open source licensing to promote safer, more effective health care information systems. We claim that open source licensing in health care information systems is essential to rational procurement strategy.

A 34-year-old Filipino lady presented to the emergency department with breathlessness and muscle cramping following a Bikram yoga workout. The patient reported sweating excessively while performing 90 min of strenuous exertion in a humidified room heated to an ambient temperature of 40.6°C. After the workout she drank 3.5 litres of water before experiencing breathlessness, severe muscle cramps, nausea and general malaise. Initial investigations revealed severe hyponatraemia (120 mmol/l). Despite early sodium replacement the patient dropped her Glasgow coma scale to 9/15 and developed tonic clonic seizures, requiring intubation and admission to the intensive care unit. The hyponatraemia was slowly corrected on the intensive care unit and the patient made a full recovery over the course of 5 days. This case highlights the dangers of overzealous fluid replacement following severe exertion in a hot environment.

BackgroundGastro-esophageal reflux disease (GERD) is associated with idiopathic pulmonary fibrosis (IPF) in observational studies. It is not known if this association arises because GERD causes IPF, or IPF causes GERD, or because of confounding by factors, such as smoking, associated with both GERD and IPF. We used bidirectional Mendelian randomisation (MR), where genetic variants are used as instrumental variables to address issues of confounding and reverse causation, to examine how, if at all, GERD and IPF are causally related.Methods and resultsA bidirectional two-sample MR was performed to estimate the causal effect of GERD on IPF risk, and of IPF on GERD risk, using genetic data from the largest GERD (78 707 cases and 288 734 controls) and IPF (4125 cases and 20 464 controls) genome-wide association meta-analyses currently available. GERD increased the risk of IPF, with an odds ratio (OR) of 1.6 (95% Confidence Interval, CI: 1.04–2.49; p=0.032). There was no evidence of a causal effect of IPF on the risk of GERD, with an OR of 0.999 (95%CI: 0.997–1.000; p=0.245).ConclusionWe found that GERD increases the risk of IPF, but found no evidence that IPF increases the risk of GERD. GERD should be considered in future studies of IPF risk, and interest in it as a potential therapeutic target should be renewed. The mechanisms underlying the effect of GERD on IPF should also be investigated.