Association between diesel engine exhaust exposure and lung function in Australian gold miners.

Previous studies have reported that miners (and other workers) exposed to high levels of diesel engine exhaust (DEE) have an increased risk of lung function decline. The main objective of this study was to evaluate associations between exposure to different components associated with DEE in relation to lung function across a 12-h working shift. Eighty underground gold miners and twenty surface miners completed spirometry and questionnaires at the beginning and end of their 12 h work shift. Personal exposure to elemental carbon (EC), volatile organic compounds (VOCs), nitrogen dioxide (NO2), particle size and particle number were monitored during their shift. Multiple regression models were used to examine the associations between DEE and lung function, adjusting for a range of covariates. Underground miners were exposed to higher levels of EC, VOCs, NO2, and particle number and larger mean particle size than surface miners. Cross-shift reduction in Z-score value of FEV1/FVC in underground miners was statistically significantly greater than those of surface miners. The cross-shift change in Z-score value of FEV1/FVC was associated with exposure to higher concentration of EC and particle number, but not with VOCs, NO2 and particle size. Occupational exposure to diesel engine exhaust in current Australian gold mines is substantial. Exposures were higher in underground miners and had a negative association with their lung function over a single 12-h shift.

Measurement of urinary 1-aminopyrene and 1-hydroxypyrene as biomarkers of exposure to diesel particulate matter in gold miners.

Metabolites of polycyclic aromatic hydrocarbons measured in human samples are often used as biomarkers of exposure to diesel engine exhaust (DEE). The aim of this study was to assess the changes in urinary levels of 1-aminopyrene (1-AP) and 1-hydroxypyrene (1-OHP) and their relationship with Elemental Carbon (EC), as a component of diesel engine exhaust exposure, among a hard-rock gold-mining population. Urine samples were collected at the beginning and end of a 12-hour work shift from 100 underground and above ground gold miners. Miners were fitted with personal exposure monitoring equipment to quantify exposure to DEE, measured as Elemental Carbon (EC), across their 12-hour work shift. General linear regression assessed associations of the post-shift urinary 1-AP and 1-OHP concentrations with EC, controlling for age, gender, the pre-shift biomarker level, Body Mass Index (BMI), days on current shift, time in mining, smoking status and second-hand smoke exposure. The concentrations of 1-AP and 1-OHP increased significantly across a 12-hour mining work shift. Moreover, consistent with the sensitivity analysis, the concentration of 1-AP was significantly associated with EC after adjustments. Urinary 1-OHP, but not 1-AP was significantly associated with current smoking. Urinary 1-AP may be a more robust and specific biomarker of DEE than 1-OHP.

Effect of the velopharynx on intraluminal pressures in reconstructed pharynges derived from individuals with and without sleep apnea.

The most collapsible part of the upper airway in the majority of individuals is the velopharynx which is the segment positioned behind the soft palate. As such it is an important morphological region for consideration in elucidating the pathogenesis of obstructive sleep apnea (OSA). This study compared steady flow properties during inspiration in the pharynges of nine male subjects with OSA and nine body-mass index (BMI)- and age-matched control male subjects without OSA. The k-ωSST turbulence model was used to simulate the flow field in subject-specific pharyngeal geometric models reconstructed from anatomical optical coherence tomography (aOCT) data. While analysis of the geometry of reconstructed pharynges revealed narrowing at velopharyngeal level in subjects with OSA, it was not possible to clearly distinguish them from subjects without OSA on the basis of pharyngeal size and shape alone. By contrast, flow simulations demonstrated that pressure fields within the narrowed airway segments were sensitive to small differences in geometry and could lead to significantly different intraluminal pressure characteristics between subjects. The ratio between velopharyngeal and total pharyngeal pressure drops emerged as a relevant flow-based criterion by which subjects with OSA could be differentiated from those without.

Second thoughts on psychedelic drugs.

Psychedelic drugs are making a comeback. Proponents of psychedelics point to the widespread medical experimentation with mescaline and lysergic acid diethylamide-125 (LSD) in the 1950s as proof of their safety and efficacy. However, a review of the private and published writings of Sidney Cohen, MD, who conducted the first study of the safety of psychedelics, reveals that serious medical concerns about psychedelics arose before the public backlash against the drugs in the 1960s. The story of psychedelic research is a reminder of the inevitable complications involved in testing drugs on human subjects.

LSD before Leary. Sidney Cohen's critique of 1950s psychedelic drug research.

In 1962 Sidney Cohen presented the medical community with its first warning about the dangers of the drug LSD. LSD had arrived in the United States in 1949 and was originally perceived as a psychotomimetic capable of producing a model psychosis. But in the mid 1950s intellectuals in Southern California redefined LSD as a psychedelic capable of producing mystical enlightenment. Though LSD was an investigational drug, authorized only for experimental use, by the late 1950s psychiatrists and psychologists were administering it to cure neuroses and alcoholism and to enhance creativity. Cohen's 1960 study of LSD effects concluded that the drug was safe if given in a supervised medical setting, but by 1962 his concern about popularization, nonmedical use, black market LSD, and patients harmed by the drug led him to warn that the spread of LSD was dangerous. The subsequent government crackdown and regulation of LSD preceded the 1960s drug movement and was prompted by medical, not social, concerns.