Documents body retention 11 results

"The review focused on the types of chemicals found in nail products, the potential adverse health effects associated with exposure to nail-product chemicals, evidence of chemical exposures in nail salon workers, and evidence supporting actions to reduce chemical exposures in nail salons. Many different types of products are used when providing nail specialty services. These products contain a large variety of chemical ingredients. Many nail-product ingredient s evaporate easily producing vapors and odors that may be inhaled or contact eyes and mucus membranes of nail salon workers and clients. Also, certain procedures during nail care generate dust which may be inhaled. Skin contact is also inherent in the use of nail-care products. Some types of chemicals commonly found in nail salon products are known to be associated with adverse health effects at relatively high exposure levels. Hence, concern has been raised about whether nail salon workers and clients could be at risk for such adverse health effects. The scope of this review is focused on summarizing existing information on the types of chemical ingredients found in nail salon products and in the nail salon indoor environment, the potential hazards of c hemicals in nail salon products , and the effectiveness of interventions to reduce potential hazards. ..."

"The purpose of this article is to provide an overview and practical guide to occupational health professionals concerning the derivation and use of dose estimates in risk assessment for development of occupational exposure limits (OELs) for inhaled substances. Dosimetry is the study and practice of measuring or estimating the internal dose of a substance in individuals or a population. Dosimetry thus provides an essential link to understanding the relationship between an external exposure and a biological response. Use of dosimetry principles and tools can improve the accuracy of risk assessment, and reduce the uncertainty, by providing reliable estimates of the internal dose at the target tissue. This is accomplished through specific measurement data or predictive models, when available, or the use of basic dosimetry principles for broad classes of materials. Accurate dose estimation is essential not only for dose-response assessment, but also for interspecies extrapolation and for risk characterization at given exposures. Inhalation dosimetry is the focus of this paper since it is a major route of exposure in the workplace. Practical examples of dose estimation and OEL derivation are provided for inhaled gases and particulates."

"Triphenyl phosphate (TPHP) is primarily used as either a flame retardant or plasticizer, and is listed as an ingredient in nail polishes. However, the concentration of TPHP in nail polish and the extent of human exposure following applications have not been previously studied. We measured TPHP in ten different nail polish samples purchased from department stores and pharmacies in 2013–2014. Concentrations up to 1.68% TPHP by weight were detected in eight samples, including two that did not list TPHP as an ingredient. Two cohorts (n = 26 participants) were recruited to assess fingernail painting as a pathway of TPHP exposure. Participants provided urine samples before and after applying one brand of polish containing 0.97% TPHP by weight. Diphenyl phosphate (DPHP), a TPHP metabolite, was then measured in urine samples (n = 411) and found to increase nearly seven-fold 10–14 h after fingernail painting (p < 0.001). To determine relative contributions of inhalation and dermal exposure, ten participants also painted their nails and painted synthetic nails adhered to gloves on two separate occasions, and collected urine for 24 h following applications. Urinary DPHP was significantly diminished when wearing gloves, suggesting that the primary exposure route is dermal. Our results indicate that nail polish may be a significant source of short-term TPHP exposure and a source of chronic exposure for frequent users or those occupationally exposed."

Background: The health effects of asbestos are intimately related to the fate of inhaled fibers in the lungs. The kinetics of asbestos fibers have been studied primarily in rodents. The objective of this study was to explore the application of these kinetic models to human autopsy data. Methods: We analyzed the asbestos fiber content of the lungs of 72 Quebec chrysotile miners and millers and 49 control subjects using analytical transmission electron microscopy. Statistical methods included standard multivariate linear regression and locally weighted regression methods. Results: The lung burdens of asbestos bodies and chrysotile and tremolite fibers were correlated, as were the concentrations of short, medium, and long fibers of each asbestos variety. There were significant associations between the duration of occupational exposure and the burdens of chrysotile and tremolite. The concentration of chrysotile decreased with the time since last exposure but the concentration of tremolite did not. The clearance rate varied inversely with the length of chrysotile fibers. For fibers greater than 10 in length the clearance half-time was estimated to be 8 years. Conclusions: The patterns in our data are compatible with both of the hypotheses suggested from rodent experiments; the existence of a long-term sequestration compartment and overload of clearance mechanisms in this compartment.

The carcinogenicity of chromium (7440473) was investigated among chromate factory workers. The autopsy results of three workers who died of lung cancer and were hired between 1931 and 1932 were examined. The first case described a man who worked as a welder for 15 years. Cumulative exposures to chromium were 2.85mg/m3 years for insoluble chromium, 0.60mg/m3 years for soluble chromium, and 3.45mg/m3 years for total chromium. Chromium concentrations in the left lung ranged from 330+/-10 to 456+/-10 micrograms per 10 grams of tissue (microg/10g). The second case described a man who worked for the factory for 10.2 years. Cumulative exposures to chromium were 3.26mg/m3 years for insoluble chromium, 1.33mg/m3 years for soluble chromium, and 4.59mg/m3 years for total chromium. Although 18 years had passed since the last exposure, chromium concentrations in the lungs ranged from 30.4+/-1.8 in the left lung to 126+/-1.8microg/10g in the right lung. Within a tumor in the left lung, chromium concentration was as high as 178+/-9.0microg/10g. Chromium was detected in the heart and aorta 18 years after exposure and in the blood 17 years after exposure. The third case involved a man who worked for 31.8 years in ore mill, ore preparation, and boiler operations. Cumulative chromium exposures were 10.74mg/m3 years for insoluble chromium, 0.63mg/m3 years for soluble chromium, and 11.38mg/m3 years for total chromium. Chromium lung concentrations ranged from 1,150microg/10g in the left lung to 1,920microg/10g in the right lower lobe. Nine months before his death, a chromium level of 2,060microg/10g was detected in the right middle lobe. A chromium concentration of 4,280microg/10g was found in the left hilar node. Chromium was also observed in the testicle, heart, aorta, and blood. The author concludes that the above findings demonstrate the carcinogenic effects of chromium exposure.

"Ultrafine particles (UFP, particles <100 nm) are ubiquitous in ambient urban and indoor air from multiple sources and may contribute to adverse respiratory and cardiovascular effects of particulate matter (PM). Depending on their particle size, inhaled UFP are efficiently deposited in nasal, tracheobronchial, and alveolar regions due to diffusion. Our previous rat studies have shown that UFP can translocate to interstitial sites in the respiratory tract as well as to extrapulmonary organs such as liver within 4 to 24 h postexposure. There were also indications that the olfactory bulb of the brain was targeted. Our objective in this follow-up study, therefore, was to determine whether translocation of inhaled ultrafine solid particles to regions of the brain takes place, hypothesizing that UFP depositing on the olfactory mucosa of the nasal region will translocate along the olfactory nerve into the olfactory bulb. This should result in significant increases in that region on the days following the exposure as opposed to other areas of the central nervous system (CNS). We generated ultrafine elemental (13)C particles (CMD = 36 nm; GSD = 1.66) from [(13)C] graphite rods by electric spark discharge in an argon atmosphere at a concentration of 160 microg/m(3). Rats were exposed for 6 h, and lungs, cerebrum, cerebellum and olfactory bulbs were removed 1, 3, 5, and 7 days after exposure. (13)C concentrations were determined by isotope ratio mass spectroscopy and compared to background (13)C levels of sham-exposed controls (day 0). The background corrected pulmonary (13)C added as ultrafine (13)C particles on day 1 postexposure was 1.34 microg/lung. Lung (13)C concentration decreased from 1.39 microg/g (day 1) to 0.59 microg/g by 7 days postexposure. There was a significant and persistent increase in added (13)C in the olfactory bulb of 0.35 microg/g on day 1, which increased to 0.43 microg/g by day 7. Day 1 (13)C concentrations of cerebrum and cerebellum were also significantly increased but the increase was inconsistent, significant only on one additional day of the postexposure period, possibly reflecting translocation across the blood-brain barrier in certain brain regions. The increases in olfactory bulbs are consistent with earlier studies in nonhuman primates and rodents that demonstrated that intranasally instilled solid UFP translocate along axons of the olfactory nerve into the CNS. We conclude from our study that the CNS can be targeted by airborne solid ultrafine particles and that the most likely mechanism is from deposits on the olfactory mucosa of the nasopharyngeal region of the respiratory tract and subsequent translocation via the olfactory nerve. Depending on particle size, >50% of inhaled UFP can be depositing in the nasopharyngeal region during nasal breathing. Preliminary estimates from the present results show that approximately 20% of the UFP deposited on the olfactory mucosa of the rat can be translocated to the olfactory bulb. Such neuronal translocation constitutes an additional not generally recognized clearance pathway for inhaled solid UFP, whose significance for humans, however, still needs to be established. It could provide a portal of entry into the CNS for solid UFP, circumventing the tight blood-brain barrier. Whether this translocation of inhaled UFP can cause CNS effects needs to be determined in future studies."