Search

In human exposure studies involving Polychlorinated Biphenyls (PCBs), it is useful to establish when an individual was potentially exposed. Age dating PCB exposure is complex but assessments can be made because different PCB congeners have different residence times in the human body. The less chlorinated congeners generally tend to have shorter residence times because they are biotransformed and eliminated faster than more chlorinated congeners. Therefore, the presence of high proportions of less chlorinated congeners is often indicative of recent exposure. The 2003-04 National Health and Nutrition Examination Survey (NHANES) dataset contains results for the concentration of 37 PCBs in a sub-sample of the US population. Multivariate statistical analysis of the NHANES data showed that less chlorinated congeners are not always biotransformed faster than higher chlorinated compounds. For example, PCB 28 (a tri-chlorobiphenyl) appears to be more resistant to biotransformation than PCB 101 and 110 (penta-chlorobiphenyls). Using statistical analysis of the NHANES data in conjunction with previously published studies on PCB persistence in humans, it was possible to identify the structural relationships that determine if a PCB is likely to be from a recent exposure (termed 'episodic') or from steady state exposure. Congeners with chlorine atoms in the 2,5- and 2,3,6-positions appear to be more susceptible to biotransformation whereas congeners with chlorine bonds in the 2,3,4- 2,4,5- 3,4,5- and 2,3,4,5-positions appear to be more persistent. This work shows that future investigations to date PCB exposure would benefit from the analysis of a wide range of congeners, including the selection of key congeners based not only on the degree of chlorination but also on the positions of the chlorine atoms on the biphenyl., (Copyright © 2013 Elsevier B.V. All rights reserved.)

A major concern raised about photostability studies of sunscreen products is that the photodegradation of sunscreens does not readily translate into changes in product performance. This study examines the correlation between photochemical degradation of sunscreen agents and changes in protection provided by sunscreen films. Films of a commercial sunscreen product containing avobenzone, oxybenzone and octinoxate were irradiated using a fluorescent UV-A phototherapy lamp with additional UV-B blocking filter. Periodically, during irradiation the transmittances of the films were measured and samples collected for chemical analysis of the sunscreen agents using high-performance liquid chromatography techniques. The results show that UV-induced changes in UV transmittance of sunscreen films correlate with changes in concentration of sunscreen agents. In a parallel experiment, we also irradiated a thin film of the same product in the cavity of an electron spin resonance (ESR) spectrometer. We report the concomitant photolysis of avobenzone and octinoxate that predominates over expected E/Z photoisomerization and that irradiation of a film of this product produced free radicals detected by ESR spectroscopy that persisted even after exposure had ended.

Drinking water is supplied by individual roof-catchment systems for homes and businesses near a dissolving sulfite pulp mill (now closed) located just north of Ketchikan in southeast Alaska. This study was conducted to determine if polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDDs/Fs) found in the sediments of the roof-catchment cisterns resulted from historical deposition of stack emissions from the pulp mill's multi-fuel power boilers. Fly ash from the power boilers had maximum total PCDD/F concentrations of 3.08 x 10(5)-3.10 x 10(6) ng/kg, which resulted from combustion of bleach plant wastewater sludge and saltwater-soaked wood waste. Cistern sediments had maximum total PCDD/F concentrations of 7.71 x 10(4) ng/kg. Potential sources of PCDDs/Fs in the cistern sediments were considered to be automobile exhaust, heating oil combustion, and private trash burning as well as pulp mill boiler emissions. Discriminant analysis was used to analyze differences between profiles of tetra through octa homologue classes of PCDDs/ Fs (defined as proportional contributions to total concentration) from different source terms. Homologue profiles of potential sources from Ketchikan included in this analysis were fly ash collected from the mill's power boilers and soils collected from background areas (areas with similar PCDD/F sources as the residences [e.g., auto exhaust and burn barrels] near the mill but beyond the zone of aerial deposition of emissions from the mill). Profiles for emissions from automobile exhaust, fertilizers, oil heating, residential trash burning, and residential wood heating were also included in the source "training" data set (for the discriminant analysis) using data from published literature. The classification rules developed from the discriminant analysis were applied to the following test media sampled at Ketchikan: roof-catchment cistern sediments and soils collected from areas in the vicinity of the mill's power boilers (i.e., nearby residential or commercial [developed] areas, on the mill property, and nearby forestlands). The homologue profiles of cistern sediment and nearby developed area soil samples were similar to background soils, whereas the profiles for the forestland soil samples (influenced by emissions from the mill but not other anthropogenic sources) closely matched the fly ash pattern. The homologue profiles of the emission sources from published data were more similar to one another than either background soils or fly ash. Soil samples from the mill property were classified as members of all source groups. On the basis of these analyses, the composition of PCDDs/Fs detected in the cistern sediments is typical of Ketchikan background conditions and not reflective of mill emissions.

We report the first case known to us of an apparent bilateral association of essential iris atrophy (EIA) and keratoconus (KC), with coincident features of posterior polymorphous dystrophy (PPD). Based on this case and the published natural history and findings of both the irido corneal endothelial (ICE) syndrome and PPD, we propose a new hypothesis for the pathogenesis of the ICE syndrome with associated KC and/or PPD. We suggest that, similar to the genetics of retinoblastoma, the predisposition for either the ICE syndrome or for PPD is inherited as an inactive allele, the so-called "first hit." Inactivation of the second allele, or "second hit," which could occur at any time, might be the product of the background mutation rate or of an environmental trigger. Dedifferentiation or an abnormality in normal development could occur after the first or second hit, resulting in varying clinical patterns. We also concur with other investigators that PPD could be part of the spectrum of the ICE syndrome, owing to similarities in their clinical presentations, histopathology, specular and electron microscopy, and natural history.

We examined 57 patients with symptoms of chronic blepharitis using meibomian gland expression, meibography, tear osmolarity, and the Schirmer's test. We also performed meibography on 20 normal patients free of chronic blepharitis. We found that 42 blepharitis patients (74%) had evidence of meibomian gland loss, whereas only four of 20 normal patients (20%) had any gland dropout. We performed cluster analysis on the data from the patients with blepharitis and found that these patients tended to fall into distinct groups with clinically relevant characteristics. We also found that tear osmolarity correlated positively with gland dropout (+0.413) and negatively with excreta volume (-0.499). This study demonstrates that an objective analysis of meibomian gland function may be used to assess chronic blepharitis and define subsets of blepharitis with measurable differences. It also supports the significance of meibomian gland dysfunction on tear osmolarity and the evaporative state of the eye.

We evaluated the meibomian gland function of 11 patients before and during treatment with isotretinoin (Accutane) by assessing tear osmolarity, meibomian gland morphology, tear production, rose bengal staining, and meibomian gland excreta. We found, during Accutane use, that meibomian glands appeared significantly less dense and atrophic by meibography. Excreta thickness increased from 1.7 +/- 0.9 to 3.1 +/- 1.2 (p less than 0.005), and expressible excreta volume decreased from 1.52 +/- 0.68 to 1.10 +/- 0.3 (p less than 0.05) (scale 1-4). We also found a significant increase in tear osmolarity from 304.9 +/- 11 to 316.3 +/- 10 mosmol/L (p less than 0.005). There was no significant change in the Schirmer test during treatment. We suggest that the clinical symptoms of blepharitis during Accutane therapy are related to decreased meibomian gland function and consequent increased tear evaporation and tear osmolarity.

We report nine cases of corneal infiltrates and/or ulceration in patients using disposable extended wear contact lenses. None of the nine patients had worn the lenses more than the recommended 7 days. Cultures were performed on six of the patients; all cultures were negative. One of the six cultured patients had been treated with topical antibiotics prior to culture. All responded promptly to cessation of lens wear and topical antibiotic therapy. Although all of the infiltrates/ulcers were paracentral, none of the patients sustained any permanent visual loss.

Ciguatera is a type of food poisoning that results from eating certain tropical fish which have become toxic. It is common in Australia: 175 outbreaks, which involved 527 people, were reported in Queensland between 1965 and 1984. It seems restricted to certain areas around the Australian coastline. Most reports have involved the narrow-barred Spanish mackerel, Scomberomorus commersoni, most of which were caught in southern Queensland waters. Up to 2100 cases may have occurred in north Queensland between 1965 and 1984, which were not recorded by the writers. The symptoms of ciguatera in Australia are similar to those reported elsewhere in the South Pacific. Ciguatoxin acts by increasing the permeability of excitable membranes to sodium ions. This type of membrane is found throughout the body in nerve tissue as well as in heart and skeletal muscle. The treatment of ciguatera remains symptomatic and supportive only. Major advances in treatment for ciguatera and detection of ciguatoxin await the means of producing additional ciguatoxin.