Ocular effects of exposure to triethylamine in the sand core cold box of a foundry.

OBJECTIVES--To assess the acute and chronic ophthalmological effects of triethylamine exposure among foundry workers. METHODS--Ocular effects on people currently, previously, and never exposed to triethylamine in a foundry cold box were studied at two points in time. The initial phase included an ocular examination with a slit lamp to assess corneal health, a visual acuity test, and a questionnaire to assess vision symptoms. The follow up included measurements of corneal thickness with an ultrasonic pachymeter and the vision symptoms questionnaire before and after the shift and at the beginning and end of the week. Personal air measurements for triethylamine were also obtained during the follow up. RESULTS--The vision symptoms of blurriness, halos around lights, and blue hazy vision occurred more often in currently exposed workers than those previously or never exposed to triethylamine. Air concentrations of triethylamine ranged from < 0.33 mg/m3 to 20.3 mg/m3. Among currently exposed workers, symptoms were more common among those with exposure to > 10 mg/m3 of triethylamine (odds ratio (OR) = 3.0, 95% confidence interval (95% CI) 0.35-25.6). No differences in corneal thickness were found in currently or previously exposed workers and those never exposed. No increase in corneal thickness was found after v before the shift. CONCLUSION--Despite low concentrations of triethylamine and no corneal oedema, workers exposed to triethylamine reported vision symptoms. Possible explanations for these symptoms without corneal oedema are that triethylamine affects ciliary muscle function or that the corneal oedema was transient and not present when corneal thickness measurements were taken. No chronic effects were found in previously exposed workers. Further research is needed to elucidate the mechanism for the reported vision symptoms, which occurred below the current United States eight hour time weighted standard of 100 mg/m3 and the American Conference of Governmental Industrial Hygienists (ACGIH) recommended value at the time of our study of 40 mg/m3. We recommend that air concentrations be maintained to meet the current recommended ACGIH threshold of 4.1 mg/m3.     

Acculturation and Nutritional Health of Immigrants in Canada: A Scoping Review

Although recent immigrants to Canada are healthier than Canadian born (i.e., the Healthy Immigrant Effect), they experience a deterioration in their health status which is partly due to transitions in dietary habits. Since pathways to these transitions are under-documented, this scoping review aims to identify knowledge gaps and research priorities related to immigrant nutritional health. A total of 49 articles were retrieved and reviewed using electronic databases and a stakeholder consultation was undertaken to consolidate findings. Overall, research tends to confirm the Healthy Immigrant Effect and suggests that significant knowledge gaps in nutritional health persist, thereby creating a barrier to the advancement of health promotion and the achievement of maximum health equity. Five research priorities were identified including (1) risks and benefits associated with traditional/ethnic foods; (2) access and outreach to immigrants; (3) mechanisms and coping strategies for food security; (4) mechanisms of food choice in immigrant families; and (5) health promotion strategies that work for immigrant populations.     

Levofloxacin-induced toxic epidermal necrolysis in an elderly patient

Stevens-Johnson syndrome and toxic epidermal necrolysis (TEN) are mild-to-life-threatening adverse reactions that have been described after exposure to fluoroquinolones. No published reports, however, exist of exfoliative disease after treatment with levofloxacin. A 78-year-old woman with many medical problems, including chronic obstructive pulmonary disease, was treated with parenteral levofloxacin for community-acquired pneumonia. She was discharged with oral levofloxacin to complete an additional 3 days of treatment as an outpatient. Two days after completing this regimen, the patient developed a rash with blistering. The rash progressed to TEN in 7 days, and she was transferred to a burn treatment center. She was treated with fluid resuscitation, wound dressing, and antibiotics. Her condition improved, and she was discharged after 22 days. To our knowledge, this case is the first published report of levofloxacin-induced TEN.     

Evaluating the Michigan SENSOR Surveillance Program for work-related asthma

BACKGROUND: Most Occupational Safety and Health Administration (OSHA) inspections are based on employee complaints or targeting of industry groupings. Limited use has been made of illness data to target inspections and evaluation of such targeting is even more limited. METHODS: This study compared 545 Michigan OSHA (MIOSHA) inspections performed as follow up to reports of work-related asthma (WRA) with 12,268 non-disease initiated OSHA inspections performed during the same time period (1989-2002). RESULTS: SENSOR asthma inspections were more likely to be conducted in larger, unionized employers. Although the likelihood of citations ( approximately 50%), type of citation, and monetary penalties ( approximately 30%) were not different between disease and non-disease initiated inspections, the number of citations and amount of monetary penalties were less in disease initiated inspections. Citations and penalties were more likely for small as compared to large employers, and were less likely at unionized worksites. CONCLUSIONS: Even without the availability of specific standards for agents that cause WRA, inspections triggered by a WRA index case are very much like other inspected worksites in terms of the prevalence of violations observed at the worksite. The advisability of making referrals to OSHA and additional ways to evaluate the effectiveness of this type of intervention model are discussed.     

Comparisons of risk prediction methods using nested case‐control data

Using both simulated and real datasets, we compared two approaches for estimating absolute risk from nested case‐control (NCC) data and demonstrated the feasibility of using the NCC design for estimating absolute risk. In contrast to previously published results, we successfully demonstrated not only that data from a matched NCC study can be used to unbiasedly estimate absolute risk but also that matched studies give better statistical efficiency and classify subjects into more appropriate risk categories. Our result has implications for studies that aim to develop or validate risk prediction models. In addition to the traditional full cohort study and case‐cohort study, researchers designing these studies now have the option of performing a NCC study with huge potential savings in cost and resources. Detailed explanations on how to obtain the absolute risk estimates under the proposed approach are given. Copyright © 2016 John Wiley & Sons, Ltd.     

Unique gene expression and hepatocellular injury in the lipopolysaccharide-ranitidine drug idiosyncrasy rat model: comparison with famotidine.

Rats cotreated with lipopolysaccharide (LPS) and ranitidine (RAN) but not LPS and famotidine (FAM) develop hepatocellular injury in an animal model of idiosyncratic drug reactions. Evaluation of liver gene expression in rats given LPS and/or RAN led to confirmation that the hemostatic system, hypoxia, and neutrophils (PMNs) are critical mediators in LPS/RAN-induced liver injury. We tested the hypothesis that unique gene expression changes distinguish LPS/RAN-treated rats from rats given LPS or RAN alone and from those cotreated with LPS/FAM. Rats were treated with a nonhepatotoxic dose of LPS (44.4 x 10(6) endotoxin units/kg, iv) or its vehicle. Two hours thereafter they were given RAN (30 mg/kg, iv), FAM (either 6 mg/kg, a pharmacologically equi-efficacious dose, or 28.8 mg/kg, an equimolar dose, iv), or vehicle. They were killed 2 or 6 h after drug treatment for evaluation of hepatotoxicity (2 and 6 h) and liver gene expression (2 h only). At a time before the onset of hepatocellular injury, hierarchical clustering distinguished rats treated with LPS/RAN from those given LPS alone. 205 probesets were expressed differentially to a greater or lesser degree only in LPS/RAN-treated rats compared to LPS/FAM or LPS alone, which did not develop liver injury. These included VEGF, EGLN3, MAPKAPK-2, BNIP3, MIP-2, COX-2, EGR-1, PAI-1, IFN-gamma, and IL-6. Expression of these genes was confirmed by real-time PCR. Serum concentrations of MIP-2, PAI-1, IFN-gamma, and IL-6 correlated with their respective gene expression patterns. Overall, the expression of several gene products capable of controlling requisite mediators of injury (i.e., hemostasis, hypoxia, PMNs) in this model were enhanced in livers of LPS/RAN-treated rats. Furthermore, enhanced expression of MAPKAPK-2 in RAN-treated rats and its target genes in LPS/RAN-treated rats suggests that p38/MAPKAPK-2 signaling is a regulation point for enhancement of LPS-induced gene expression by RAN.     

Effect of choice of outcome measure on studies of the etiology of obesity in children

PurposeEpidemiologic studies of the etiology of childhood obesity often use proxies for adiposity as outcomes. This study aimed to compare the ability of a range of proxy measures to detect associations with sedentary behavior.MethodsLongitudinal study of children in the Gateshead Millennium Study who were 7 years at baseline and 9 years at follow-up. Associations between 2-year changes in objectively measured sedentary behavior and changes in proxies for adiposity (waist circumference, waist Z score, body mass index, body mass index Z score) and measurement of body composition (fat mass index from bioelectric impedance) were examined. Associations were tested with linear regression.ResultsAssociations between 2-year increases in sedentary behavior and increases in adiposity were detectable by using the fat mass index as the outcome, but not the simple proxy measures of adiposity, as outcomes.ConclusionsProxy measures are inferior to measures of body composition as outcomes in epidemiologic studies.     

Proceedings of the Symposium ‘Angiotensin AT1 Receptors: From Molecular Physiology to Therapeutics’: REGULATION OF RENAL TUBULAR SODIUM TRANSPORT BY ANGIOTENSIN II AND ATRIAL NATRIURETIC FACTOR

• 1 The effects of angiotensin II (AngII) on water and electrolyte transport are biphasic and dose-dependent, such that low concentrations (10^?12 to 10^?9 mol/L) stimulate reabsorption and high concentrations (10^?7 to 10^?6 mol/L) inhibit reabsorption. Similar dose-response relationships have been obtained for luminal and peritubular addition of AngII.
• 2 The cellular responses to AngII are mediated via AT₁ receptors coupled via G-regulatory proteins to several possible signal transduction pathways. These include the inhibition of adenylyl cyclase, activation of phospholipases A₂, C or D and Ca²⁺ release in response to inositol-1,4,5,-triphosphate or following Ca²⁺ channel opening induced by the arachidonic acid metabolite 5,6,-epoxy-eicosatrienoic acid. In the brush border membrane, transduction of the AngII signal involves phospholipase A₂, but does not require second messengers.
• 3 Angiotensin II affects transepithelial sodium transport by modulation of Na⁺/H⁺ exchange at the luminal membrane and Na⁺/HCO₃ cotransport, Na⁺/K⁺-ATPase activity and K⁺ conductance at the basolateral membrane.
• 4 Atrial natriuretic factor (ANF) does not appear to affect proximal tubular sodium transport directly, but acts via specific receptors on the basolateral and brush border membranes to raise intracellular cGMP levels and inhibit AngII-stimulated transport.
• 5 It is concluded that there is a receptor-mediated action of ANF on proximal tubule reabsorption acting via elevation of cGMP to inhibit AngII-stimulated sodium transport. This effect is exerted by peptides delivered at both luminal and peritubular sides of the epithelium and provides a basis for the modulation by ANF of proximal glomerulotubular balance. The evidence reviewed supports the concept that in the proximal tubule, AngII and ANF act antagonistically in their roles as regulators of extracellular fluid volume.