Vapor Inhalation Research Articles

Spatial distribution, bioavailability, and health risk assessment of soil Hg in Wuhu urban area, China

Total mercury (Hg(T)) and bioavailability Hg (Hg(HCl)) concentrations in soil were determined in five districts in Wuhu urban area. Spatial pattern of soil Hg concentration was generated through kriging technology. Results showed that Hg concentration in soil ranged from 0.024 to 2.844 mg kg( -1) with an average of 0.207 mg kg( -1). Hg concentration in soil appeared to have a block distribution and decreased from downtown to surrounding district. And Hg concentrations appeared to have a medium scale spatial auto correlation, strongly affected by human activity. The maximal Hg average concentration (0.332 mg kg( -1)) in soil appeared in Jinghu district, where the high intensity of human activities is. Second highest Hg average concentration (0.263 mg kg( -1)) in soil appeared in development district, where the intensive industrial activities are. Bioavailability Hg concentration in soil ranged from 2.6 to 4.9 μg kg( -1) with an average of 3.8 μg kg( -1), which had a ratio of 0.28~6.44% to total Hg. The ratios of bioavailability Hg to total Hg in vegetable soil were bigger than those of park soil. Correlation analysis showed that total Hg, organic matter, total phosphorus, and bioavailability Hg concentrations in soil were significantly positively correlated. Hg concentration in vegetable ranged from 2.7 to 15.2 μg kg( -1) with an average of 6.5 μg kg( -1). Hg concentration in vegetable was positively correlated with Hg(HCl) concentration in soil. According to the calculation on hazard quotient (HQ) for children, inhalation of Hg vapor from soil is the main exposure pathway, in which HQ is 2.517 × 10( -2), accounting for 80.3% of the four exposure pathways. Hazard index (HI) of the four exposure pathways is lower than the "safe" level of HI = 1; therefore, exposure of soil Hg exhibited little potential health risk to children in Wuhu urban area.

A new methodology for estimating nerve agent (Sarin (GB)/VX) casualties as a function of time: Defining the Human Response Injury Profile nerve agent methodology

The Human Response Injury Profile (HRIP) methodology uses time-based progressions of underlying symptoms and their severity changes over time to determine user-defined casualty and fatality estimates from chemical, biological, radiological, and nuclear (CBRN) events. This paper provides an overview of the HRIP nerve agent methodology for use in estimating casualties resulting from Sarin (GB) and VX exposure. The injury severity terminology and injury profiles for the nerve agent vapor inhalation and VX liquid percutaneous exposure routes are provided to demonstrate the dosage and dose ranges and their associated progression of injury over time.

Dr. Campbell’s response to: Comment on “Minimal change nephrotic syndrome due to occupational mercury vapor inhalation” from M.J. Al Habbal

Dr. Campbell’s response to: Comment on “Minimal change nephrotic syndrome due to occupational mercury vapor inhalation” from M.J. Al Habbal

Effects of β-adrenoceptor antagonists on alcohol drinking by alcohol-dependent rats

Alcohol-dependent animals display enhanced stress responsivity, reward thresholds, and alcohol self-administration during alcohol withdrawal, and some of these aspects of alcohol dependence may be mediated by activation of brain norepinephrine (NE) systems. This study examined the effects of propranolol, a β-adrenoceptor antagonist, on operant alcohol-reinforced responding by alcohol-dependent and non-dependent rats. Adult male Wistar rats were trained to respond for alcohol in an operant conditioning paradigm on fixed-ratio-1 (FR-1) and progressive ratio (PR) reinforcement schedules. Rats were either made dependent on alcohol via chronic intermittent (14h ON/10h OFF) alcohol vapor inhalation or were not exposed to alcohol vapor. Rats were tested for the effects of propranolol (0-10mg/kg) or nadolol (0-20mg/kg) on operant alcohol-reinforced responding at the time point corresponding to 6-8h withdrawal in dependent animals. All doses of propranolol suppressed FR-1 operant alcohol-reinforced responding in alcohol-dependent rats, but only the highest dose suppressed FR-1 responding by controls. No dose of propranolol affected water responding. Nadolol did not affect operant behavior. Propranolol suppressed PR operant alcohol-reinforced responding across groups, an effect attributable to significant suppression of alcohol responding at the highest dose. Following development of alcohol dependence, rats exhibit hypersensitivity to the suppressive effects of propranolol on operant alcohol-reinforced responding. This effect is mediated by central actions of the drug, is not attributable to motor effects, and may reflect activation of brain NE systems that contributes to withdrawal-induced negative emotional states and drives alcohol drinking in the dependent organism.

Inflammatory effects of inhaled sulfur mustard in rat lung

Inhalation of sulfur mustard (SM), a bifunctional alkylating agent that causes severe lung damage, is a significant threat to both military and civilian populations. The mechanisms mediating its cytotoxic effects are unknown and were investigated in the present studies. Male rats Crl:CD(SD) were anesthetized, and then intratracheally intubated and exposed to 0.7–1.4 mg/kg SM by vapor inhalation. Animals were euthanized 6, 24, 48 h or 7 days post-exposure and bronchoalveolar lavage fluid (BAL) and lung tissue collected. Exposure of rats to SM resulted in rapid pulmonary toxicity, including focal ulceration and detachment of the trachea and bronchial epithelia from underlying mucosa, thickening of alveolar septal walls and increased numbers of inflammatory cells in the tissue. There was also evidence of autophagy and apoptosis in the tissue. This was correlated with increased BAL protein content, a marker of injury to the alveolar epithelial lining. SM exposure also resulted in increased expression of markers of inflammation including cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNFα), inducible nitric oxide synthase (iNOS), and matrix metalloproteinase-9 (MMP-9), each of which has been implicated in pulmonary toxicity. Whereas COX-2, TNFα and iNOS were mainly localized in alveolar regions, MMP-9 was prominent in bronchial epithelium. In contrast, expression of the anti-oxidant hemeoxygenase, and the anti-inflammatory collectin, surfactant protein-D, decreased in the lung after SM exposure. These data demonstrate that SM-induced oxidative stress and injury are associated with the generation of cytotoxic inflammatory proteins which may contribute to the pathogenic response to this vesicant.

Aromasticks in cancer care: An innovation not to be Sniffed at

To evaluate the effects of a new aromatherapy intervention introduced within an acute cancer care setting in the UK. Aromatherapy is a popular complementary therapy within oncology settings and is known to help relieve patients' anxiety. A new method of delivering aromatherapy to patients was adopted by a complementary therapy service at a UK hospital; aromasticks are similar in design to the Vicks® Vapour Inhaler®, with the intention of helping patients manage anxiety, nausea and sleep disturbance. A retrospective service evaluation. Patients referred to the complementary therapy service were, if appropriate, offered an aromastick. If the offer was accepted patients' details were captured on an evaluation form. One week later the patients were followed up by a different therapist. Frequency of using the aromastick and perceived benefits were documented. A total of 160 patients were included in this evaluation. 77% (n = 123) of all patients reported deriving at least one benefit from the aromastick. In anxious patients, 65% reported feeling more relaxed and 51% felt less stress. 47% of nauseous patients said that the aromastick had settled their nausea and 55% of those experiencing sleep disturbances felt that aromastick helped them sleep. The results also suggest that the effects of the aromastick may be directly proportional to the frequency of their use. Evidence demonstrating physiological changes associated with aroma inhalation plus the data presented in this paper highlight the potential for aromasticks within the clinical setting. Although the results of this evaluation of patient perspectives are not controlled, the data does underline the worth of further investigation. Future research is needed to show that aromasticks represent a tool patients can use to self-manage their own symptoms and help them retain an internal locus of control.

Sensory Detection and Responses to Toxic Gases: Mechanisms, Health Effects, and Countermeasures

The inhalation of reactive gases and vapors can lead to severe damage of the airways and lung, compromising the function of the respiratory system. Exposures to oxidizing, electrophilic, acidic, or basic gases frequently occur in occupational and ambient environments. Corrosive gases and vapors such as chlorine, phosgene, and chloropicrin were used as warfare agents and in terrorist acts. Chemical airway exposures are detected by the olfactory, gustatory, and nociceptive sensory systems that initiate protective physiological and behavioral responses. This review focuses on the role of airway nociceptive sensory neurons in chemical sensing and discusses the recent discovery of neuronal receptors for reactive chemicals. Using physiological, imaging, and genetic approaches, Transient Receptor Potential (TRP) ion channels in sensory neurons were shown to respond to a wide range of noxious chemical stimuli, initiating pain, respiratory depression, cough, glandular secretions, and other protective responses. TRPA1, a TRP ion channel expressed in chemosensory C-fibers, is activated by almost all oxidizing and electrophilic chemicals, including chlorine, acrolein, tear gas agents, and methyl isocyanate, the highly noxious chemical released in the Bhopal disaster. Chemicals likely activate TRPA1 through covalent protein modification. Animal studies using TRPA1 antagonists or TRPA1-deficient mice confirmed the role of TRPA1 in chemically induced respiratory reflexes, pain, and inflammation in vivo. New research shows that sensory neurons are not merely passive sensors of chemical exposures. Sensory channels such as TRPA1 are essential for maintenance of airway inflammation in asthma and may contribute to the progression of airway injury following high-level chemical exposures.

Behavioral effects of subchronic inhalation of toluene in adult rats

Whereas the acute neurobehavioral effects of toluene are robust and well characterized, evidence for persistent effects of repeated exposure to this industrial solvent is less compelling. The present experiment sought to determine whether subchronic inhalation of toluene caused persistent behavioral changes in rats. Adult male Long–Evans rats inhaled toluene vapor (0, 10, 100, or 1000 ppm) for 6 h/day, 5 days/week for 13 weeks and were evaluated on a series of behavioral tests beginning 3 days after the end of exposure. Toluene delayed appetitively-motivated acquisition of a lever-press response, but did not affect motor activity, anxiety-related behavior in the elevated plus maze, trace fear conditioning, acquisition of an appetitively-motivated visual discrimination, or performance of a visual signal detection task. Challenges with acute inhalation of toluene vapor (1200–2400 ppm for 1 h) and injections of quinpirole (0.01–0.03 mg/kg) and raclopride (0.03–0.10 mg/kg) revealed no toluene-induced latent impairments in visual signal detection. These results are consistent with a pattern of subtle and inconsistent long-term effects of daily exposure to toluene vapor, in contrast to robust and reliable effects of acute inhalation of the solvent.

Quantitative Risk Assessment of Trichloroethylene for a Former Chemical Works in Shanghai, China

ABSTRACT Assessment of the potential risks posed by chlorinated solvents in groundwater is the key to establish the extent of the contamination and derive achievable remedial targets should remediation deems necessary. This article first presents the application of the American Society for Testing and Materials (ASTM) Risk Based Corrective Actions (RBCA) Guidance to quantitatively evaluate human health and environmental risk for a former chemical works in Shanghai, China. The observed maximum trichloroethylene (TCE) concentration in groundwater at the site reached 1220 mg/l that exceeded its solubility of 1070 mg/l at 10°C (Soil annual average temperature is 10°C in Shanghai). The maximum concentration for cis-1, 2-DCE (DCE) was also found to be elevated at 264 mg/l. A critical exposure pathway was considered to be indoor vapor intrusion of TCE into the buildings with excess lifetime cancer risk for children being 1.7 × 10−3. This cancer risk exceeded regulatory limits of 1 × 10−4 to 1 × 10−6 for The Netherlands, the United Kingdom, and the United States. The calculated groundwater remedial targets for TCE and DCE are 7 mg/l and 904 mg/l, respectively, in order to protect child residents from inhalation of indoor vapors within the close proximity of the source area.

Elemental mercury poisoning caused by subcutaneous and intravenous injection: An unusual self-injury

Elemental mercury poisoning most commonly occurs through vapor inhalation as mercury is well absorbed through the lungs. Administering subcutaneous and intravenous elemental mercury is very uncommon but with only a few isolated case reports in the literature. We present an unusual case of elemental mercury poisoning in a 20-year-old young male who presented with chest pain, fever, and hemoptysis. He had injected himself subcutaneously with elemental mercury obtained from a sphygmomanometer. The typical radiographic findings in the chest, forearm, and abdomen are discussed, with a review of the literature.

Toxic Leukoencephalopathy after Heroin Abuse without Heroin Vapor Inhalation

Toxic leukoencephalopathy has been associated with illicit heroin vapor inhalation. Despite the nonspecific and variable clinical presentation of these patients, they show typical radiologic findings. Previous studies evaluated typical radiologic findings with symmetric infratentorial hyperintense signal changes and similar alteration in the posterior limb of the internal capsule, the splenium of corpus callosum, the medial lemniscus and the lateral brainstem. In context with the reviewed literature, a series of another three cases with toxic leukoencephalopathy after heroin abuse other than vapor inhalation is presented. All three patients underwent magnet resonance imaging (MRI) including additional diffusion- weighted imaging and apparent diffusion coefficient maps. Clinical and laboratory findings were recorded. MRI of all three patients revealed similar symmetric supratentorial hyperintense signal changes involving the frontal, parietal, occipital and temporal lobes. The cortex was spared and the subcortical U fibers were partially involved. Further, the brainstem and the cerebellar white matter were not affected. Toxic leukoencephalopathy without involvement of the cerebellum and brainstem is a rare complication of heroin abuse. The pattern of heroin-induced toxic leukoencephalopathy on MRI might not only be related to an unknown adulterant, but also to the mode of drug administration.

Running Phthalates to Ground: Pinpointing Exposure Sources in a Virtual Home

Vol. 118, No. 2 NewsOpen AccessRunning Phthalates to Ground: Pinpointing Exposure Sources in a Virtual Home Naomi Lubick Naomi Lubick Search for more papers by this author Published:1 February 2010https://doi.org/10.1289/ehp.118-a80aAboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Methods to measure concentrations of chemicals in adults and children, a science known as biomonitoring, can be costly and burdensome. And, although biomonitoring data provide useful aggregate information on exposure to all sources, it is almost impossible to tell how much comes from a specific source. A new mechanistic model may offer a way to identify the strongest sources of exposure to semivolatile organic compounds by showing how chemicals move from a single product through a home and which model parameters have the greatest influence on exposure [EHP118:253–258; Xu et al.].Researchers created a model of a hypothetical three-room house equipped with adjustable airflow systems to illustrate how human exposure to phthalates released by a specific source—in this case, vinyl flooring—might be predicted. Phthalates are plasticizers that are used in products as diverse as nail polish, plastic wiring, and children’s toys. Data from the Centers for Disease Control and Prevention suggest that more than three-quarters of the U.S. population may be exposed to these suspected endocrine disruptors.The research team built on an earlier model that described how diethylhexyl phthalate (DEHP)—one of the most prevalent phthalates—is released from vinyl flooring into air and sorbs strongly to interior surfaces (walls, ceilings, floors, furniture, etc.) and suspended particles. Here the researchers used the model to explore the relative importance of inhalation of vapor, inhalation of particles, dermal sorption of DEHP, and oral ingestion of household dust on total exposure levels. To test which parameters might change the amount of total DEHP exposure through different routes, the researchers varied model parameters such as the amount of ventilation and velocity of air moving through their model house.For example, they calculated that a fan pushing air through the house would cause more skin contact with phthalates by increasing the release rate from the vinyl surfaces to the air. The fan also thinned the layer of air cushioning the skin, increasing the transfer of DEHP from air to skin. Stagnant air without the fan caused less transfer of DEHP from air to skin, thus protecting against dermal uptake of DEHP.The new model suggests that levels of phthalates measured in adults and children may result in part from contact with surfaces that may absorb high concentrations of DEHP, such as clothing. Changing the variables in the model house—from airflow to the amount of DEHP in the vinyl flooring to square footage in a room—made a difference in estimated exposure levels. Varying the parameters in this simple model demonstrated the potential for DEHP exposures arising from a single product to differ by as much as 40 times from one situation to another. That variability underscores the wide range of possible exposures across the population—and the difficulty of relying on biomonitoring alone to identify the most harmful sources.Exposure to gas-phase phthalates from vinyl flooring can occur through ingestion, inhalation, or dermal absorption.FiguresReferencesRelatedDetails Vol. 118, No. 2 February 2010Metrics About Article Metrics Publication History Originally published1 February 2010Published in print1 February 2010 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Pulmonary delivery of nicotine pyruvate: Sensory and pharmacokinetic characteristics.

The aim of this study was to evaluate pharmacokinetic and subjective responses to a prototype nicotine pyruvate (NP) aerosol generation system. In nine healthy adult daily cigarette smokers, plasma nicotine levels and subjective responses were assessed after double-blind administration of 10 inhalations of: NP (10 μg/puff, 20 μg/puff, and 30 μg/puff); Nicotrol/Nicorette nicotine vapor inhaler (NV) cartridge; and placebo (room air). Plasma nicotine concentrations increased to a significantly greater extent after inhalations of 20 μg/puff or 30 μg/puff NP (by 5.0 ± 3.4 ng/ml and 8.3 ± 3.1 ng/ml) than after placebo and NV conditions. Satisfaction ratings were higher for all NP conditions than for placebo, and harshness/irritation was lower for the NP 20 condition than for the NV control condition. Pulmonary function showed no adverse changes. These results demonstrate that NP inhalations produce rapid increases in plasma nicotine concentrations, provide satisfaction and are well tolerated. At the 20 μg/puff dose, peak nicotine concentrations were higher than with the Nicotrol/Nicorette nicotine vapor inhaler cartridge. Further trials of this promising nicotine inhalation technology are warranted to assess its safety and efficacy in smoking cessation treatment or harm reduction approaches.

Silver acetate interactions with nicotine and non-nicotine smoke components.

Oral topical silver-containing formulations were marketed in the 1970s and 1980s as smoking deterrents, based on the finding that when using such formulations, an unpleasant taste occurs upon smoking. This approach has not been widely adopted, however, in part because of a lack of efficacy data. The advent of new pharmacologic treatments for smoking cessation renews the possibility that such a taste aversion approach may be a useful adjunct to smoking cessation treatment. This study explored the basic mechanistic question of whether topical oral silver acetate solution interacts with nicotine as opposed to non-nicotine smoke constituents. We recruited 20 smoking volunteers to rate nicotine-containing or denicotinized cigarettes, as well as the Nicotrol nicotine vapor inhaler and sham (air) puffs. In two sessions, subjects rated the sensory and hedonic qualities of puffs after rinsing their mouths with either silver acetate solution or deionized water (placebo). Silver acetate relative to placebo solution substantially reduced liking and satisfaction ratings for the usual brand and denicotinized cigarettes; in contrast, for the nicotine inhaler these ratings were unaffected by the silver-based treatment. These results support the conclusion that silver acetate not only renders the taste of cigarette smoke less appealing, but also that the compound appears to interact selectively with non-nicotine smoke constituents. Moreover, these data suggest silver acetate would be compatible with buccal nicotine delivery systems (e.g., nicotine lozenge or gum). Combined use of taste aversion with nicotine replacement therapy could provide the smoker with additional assistance to resist relapse. Further exploration is warranted of the use of silver-based preparations as a short-term adjunct to smoking cessation treatment.

Inhalation exposure systems for the development of rodent models of sulfur mustard-induced pulmonary injury

Sulfur mustard (SM) is a chemical threat agent for which its effects have no current treatment. Due to the ease of synthesis and dispersal of this material, the need to develop therapeutics is evident. The present manuscript details the techniques used to develop SM laboratory exposure systems for the development of animal models of pulmonary injury. These models are critical for evaluating SM injury and developing therapeutics against that injury. Iterative trials were conducted to optimize a lung injury model. The resulting pathology was used as a guide, with a goal of effecting homogeneous and diffuse lung injury comparable to that of human injury. Inhalation exposures were conducted by either nose-only inhalation or intubated inhalation. The exposures were conducted to either directly vaporized SM or SM that was nebulized from an ethanol solution. Inhalation of SM by nose-only inhalation resulted in severe nasal epithelial degeneration and minimal lung injury. The reactivity of SM did not permit it to transit past the upper airways to promote lower airway injury. Intratracheal inhalation of SM vapors at a concentration of 5400 mg · min/m3 resulted in homogeneous lung injury with no nasal degeneration.

Operant behavior and alcohol levels in blood and brain of alcohol-dependent rats.

The purpose of the present investigation was to more clearly define blood-alcohol parameters associated with alcohol dependence produced by alcohol vapor inhalation and alcohol-containing liquid diet. Alcohol levels in blood and brain were compared during and after 4 hours of acute alcohol vapor exposure; also, brain-alcohol levels were assessed in alcohol-exposed (14-day alcohol vapor) and alcohol-naïve rats during and after 4 hours of acute alcohol vapor exposure. A separate group of rats were implanted with i.v. catheters, made dependent on alcohol via vapor inhalation, and tested for operant alcohol responding; blood-alcohol levels (BALs) were measured throughout operant alcohol drinking sessions during alcohol withdrawal. A final group of rats consumed an alcohol-liquid diet until they were dependent, and those rats were then tested for operant behavior at various withdrawal time points; BALs were measured at different withdrawal time points and after operant sessions. Blood- and brain-alcohol levels responded similarly to vapor, but brain-alcohol levels peaked at a higher point and more slowly returned to zero in alcohol-naïve rats relative to alcohol-exposed rats. Alcohol vapor exposure also produced an upward shift in subsequent operant alcohol responding and resultant BALs. Rats consumed large quantities of alcohol-liquid diet, most of it during the dark cycle, sufficient to produce high blood-alcohol levels and elevated operant alcohol responding when tested during withdrawal from liquid diet. These results emphasize that the key determinants of excessive alcohol drinking behavior are the BAL range and pattern of chronic high-dose alcohol exposure.

Health risk assessment of heavy metal exposure to street dust in the zinc smelting district, Northeast of China

Heavy metal contamination in the street dust due to metal smelting in the industrial district of Huludao city was investigated. Spatial distribution of Hg, Pb, Cd, Zn and Cu in the street dust was elucidated. Meanwhile, noncancer effect and cancer effect of children and adults due to exposure to the street dust were estimated. The maximum Hg, Pb, Cd, Zn and Cu contents in the street dust are 5.212, 3903, 726.2, 79,869, and 1532 mg kg − 1 , and respectively 141, 181, 6724, 1257 and 77.4 times as high as the background values in soil. The trends for Hg, Pb, Cd, Zn and Cu are similar with higher concentrations trending Huludao zinc plant (HZP). The exponential equation fits quite well for the variations of Pb, Cd, Zn and Cu contents with distance from the pollution sources, but not for Hg. The biggest contribution to street dust is atmospheric deposition due to metal smelting, but traffic density makes slight contribution to heavy metal contamination. According to the calculation on Hazard Index (HI), in the case of noncancer effect, the ingestion of dust particles of children and adults in Huludao city appears to be the route of exposure to street dust that results in a higher risk for heavy metals, followed by dermal contact. The inhalation of resuspended particles through the mouth and nose is almost negligible. The inhalation of Hg vapour as the fourth exposure pathway to street dust is accounting for the main exposure. Children are experiencing the potential health risk due to HI for Pb larger than safe level (1) and Cd close to 1. Besides, cancer risk of Cd due to inhalation exposure is low.

Intensity and duration of chronic ethanol exposure is critical for subsequent escalation of voluntary ethanol drinking in mice.

Excessive alcohol drinking continues to be an important health problem. Recent studies from our laboratory and others have demonstrated that animal models of ethanol dependence and relapse can contribute to understanding factors that contribute to excessive drinking. In this study, we tested the hypothesis that the amount and duration of ethanol exposure is critical for promoting the escalation in drinking by mice given access to ethanol in a limited access paradigm. We used several methods of chronic intermittent ethanol exposure in male C57BL/6J mice that would vary in the amount and duration of exposure to ethanol as indicated by blood ethanol concentrations (BEC). After establishing baseline drinking in the mice using a 2 hours, 2 bottle choice drinking paradigm, each study involved alternating between periods of ethanol exposure and periods of limited access to ethanol (1 cycle) for a total of 3 cycles. In Study 1, mice were allowed extended access (16 hours) to ethanol for oral consumption or remained in the home cage. In Study 2, the ethanol exposure consisted of intragastric gavage of increasing doses of ethanol or isocaloric sucrose as the control. Study 3 compared intragastric gavage combined with pyrazole, an alcohol dehydrogenase inhibitor, with vapor inhalation of ethanol using procedures known to lead to increased drinking in mice. Finally, Study 4 was a retrospective review of several studies conducted in our laboratory using inhalation procedures. The retrospective review encompassed a range of postvapor chamber BEC values and ethanol intakes that would allow a relationship between increased drinking and BEC to be examined. Allowing mice to drink for longer periods of time did not cause increased drinking in subsequent limited access sessions. Likewise, gastric intubation of ethanol which produced high BEC (>300 mg/dl) with or without pyrazole did not increase drinking. Only the vapor inhalation procedure, which was associated with sustained BEC above 175 mg/dl for the entire exposure period resulted in increased drinking. The retrospective study provided further evidence that sustained BEC levels above 175 mg/dl was critical to the escalation in drinking. We found that the intensity (amount) and duration of ethanol exposure, indexed by BEC, is critical to produce increased drinking in mice. Specifically, BEC must regularly exceed 175 mg/dl for the escalation in drinking to occur. Future studies will examine neurobiological adaptations that may underlie the increased drinking behavior caused by chronic intermittent ethanol exposure.

Minimal-change nephrotic syndrome due to occupational mercury vapor inhalation

A 25-year-old man developed nephrotic syndrome and severe hypertension following occupational exposure to mercury vapor whilst working at a fluorescent light factory. A renal biopsy confirmed minimal-change disease on light microscopy, immunofluorescence and electron microscopy. He was also noted to be polycythemic which was initially treated with venesection. His blood and urinary mercury levels were elevated and so he was given chelation therapy with 2,3-dimercaptopropane-1-sulfonate (DMPS), along with steroids for his minimal-change disease, resulting in full resolution of his nephrotic syndrome within 6 weeks. He remains well with normal renal function, blood pressure and normal blood and urine mercury concentrations.

Effect Of Ginger Extract On Gasoline Associated Immunitoxicities In Wistar Rats

Effect of ginger extracts on gasoline associated immunotoxicities in wistar rats was studied. Fifteen wistar rats were randomly assigned into three study groups. Group 1 was the control, while groups 2 and 3 received daily treatment by inhalation of gasoline vapour. The animals in group3 were also treated with 100mg ginger/kg body weight. The experiment lasted for 60 days. One day after the final exposure, the animals were euthanized by overdose of chloroform. Blood was collected by cardiac puncture into EDTA sterilized sample bottles and used for the analysis of hemoglobin(Hb),packed cell volume(PCV),red blood cells(RBC),white blood cells and erythrocyte indices-mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH),mean corpuscular hemoglobin concentration(MCHC). The results showed that gasoline alone decreased the levels of Hb, RBC, WBC, PCV, MCV and MCHC, but it had no significant effect on the MCH of the rats. However, treatments with ginger extracts nearcompletely abrogated /mitigated any effects that have been induced by inhalation of gasoline alone. It appears that ginger extracts inhibited the chain reaction, caused by free radicals, and acted to remove the catabolic wastes from the lymphocytes and reticulocytes, thereby accelerating metabolism and lymph drainage. It also appears that ginger extracts promoted the sloughing-off of wasted tissues and corrected the imbalance of elevated inflammatory prostaglandins, leading to increased erythrocytes synthesis and improved immune system.