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PubMed1999

Lymphocyte subsets and sister-chromatid exchanges in the students exposed to formaldehyde vapor.

The present report evaluates the effects of formaldehyde (FA) exposure on peripheral lymphocytes by using both genetic and immunological parameters. Twenty-three non-smoking students in the study had inhalation exposure to 0.508 +/- 0.299 mg/m3 of FA for a period of 8 weeks (3h x 3 times each week) during anatomy classes. As for composition of lymphocyte subsets after FA exposure, significant increase was found in the percentage of CD19 (B cells), while significant decrease was observed in CD3 (total T cells), CD4 (T helper-inducer cells), and CD8 (T cytotoxic-suppressor cells) with a P < 0.01. Increase in the ratio of T-helper-inducer cells to T-cytotoxic-suppressor cells (T4/T8) was also observed with statistical significance after exposure (P < 0.001). In the meanwhile, no significant difference (P > 0.05) was reported between lymphocyte proliferation rate and sister-chromatid exchange (SCE) at the exposure level and duration. It is suggested that the lymphocyte subsets may be most susceptible to the effects of FA, though a single immunological endpoint is rarely related with pathophysiological interpretation.

Adult↗
PubMed2005

Aircraft disinsection: exposure assessment and evaluation of a new pre-embarkation method.

A new "pre-embarkation" method for aircraft disinsection was investigated using two different 2% d-phenothrin containing aerosols. Five experiments in aircrafts of the type Airbus 310 (4x) and Boeing 747-400 (1x) were performed. In the absence of passengers and crew the d-phenothrin aerosol was sprayed under the seat rows and in a second step at the height of approximately 1.60 m by moving from one end of the cabin to the other. Concentration levels of d-phenothrin were determined at different time periods after application of the aerosol spray. In a B 747-400 with the air conditioning system operating the concentrations ranged between 853 and 1753 microg/m3 during and till 5 min after the beginning of spraying at different locations in the cabin. Within 5-20min after the end of the spraying concentrations of 36-205 microg/m3 and 20-40 min thereafter only ca. 1 microg d-phenothrin/m3 were detectable (average values in relation to each period of measurement). On cabin interior surfaces the median values for mainly horizontal areas ranged from 100 to 1160 ng d-phenothrin/cm2. d-Phenothrin concentrations in the air were sufficient to kill flying insects like house flies and mosquitoes within 20 min. Horizontal surfaces were 100% effective against insects up to 24 h after spraying. Doses inhaled by sprayers determined by personal measurements were calculated to be 30-235 microg d-phenothrin per 100 g spray applied (30% in the respirable fraction for Arrow Aircraft Disinsectant; 10% for Aircraft Disinsectant Denka). If passengers will board, e.g., 20 min after the end of the disinsection operation, inhalation exposure is estimated to be practically negligible. Also possible dermal exposure from residues in seats and headrests is very low for passengers during the flight. Therefore any health effects for passengers and crew members are very unlikely.

Aedes↗
PubMed2005

Toxicity of hexamethylenediamine.

Hexamethylendiamine (HMDA; CAS No. 124-09-4; 6055-52-3 for the dihydrochloride salt) is moderately toxic following acute doses/exposures with oral lethal doses in rats ranging from 750 to 1500 mg/kg. HMDA is extremely irritating to the skin and eyes and is not a sensitizer in guinea pigs. Repeated exposure inhalation studies have defined the upper respiratory tract to be the first target of HMDA. The irritation seen is proportional to the exposure concentration. Systemic damage is limited. Genetic testing is not extensive, but there is no indication of activity. HMDA is neither a developmental nor a reproductive toxin, but in one developmental study, the fetal No-observed-adverse-effect-level (NOAEL) was lower than that of the maternal animal. No carcinogenicity studies have been conducted. Documented human experience is limited, but indications of HMDA's irritative properties are found in the literature. HMDA does not persist or bioaccumulate in the environment. The chemical is not particularly toxic to fish and aquatic invertebrates but is quite toxic to algae. HMDA is rapidly absorbed and metabolized by the rat with little tissue storage.

Animals↗
PubMed1990

Inhalation carcinogenesis of repeated exposures to high-fired 244CmO2 in rats.

Rats were given single or multiple (10 exposures at about 21-d intervals) inhalation exposures to 244CmO2 starting at 70 d of age. Mean lung and bone doses (+/- standard deviation) were 1.4 +/- 1.3 and 0.74 +/- 1.1 Gy, respectively, in the single exposure group, and 1.8 +/- 2.9 and 0.53 +/- 0.74 Gy, respectively, in the multiple exposure group. After cessation of exposure in the multiple exposure group, mean cumulative lifetime radiation doses to lung and skeleton were not significantly different in the two groups. The percentages of rats with lung and bone tumors were 9.1 and 12%, respectively, in the single exposure group, and 20 and 24%, respectively, in the multiple exposure group. However, the multiple exposure regimen did not significantly alter survival times or tumor incidences in lung or bone from a single inhalation exposure to 244CmO2 when survival patterns were taken into account.

Administration, Inhalation↗
PubMed1998

K-ras mutations in 239PuO2 canine lung neoplasms.

Single-strand conformational polymorphism (SSCP) analysis and direct sequencing methods were used to examine lung tumors derived from a cohort of beagle dogs with inhalational exposures to 239PuO2. These exposures were done at Pacific Northwest Laboratories where 18-month-old beagle dogs were given 239PuO2 by single-dose inhalation and allowed to live out their life-spans. Formalin-fixed paraffin-embedded blocks of tissues from 25 dogs exposed to 239PuO2 by aerosol inhalation which later developed lung tumors were available for this study. Two of 25 tumors had mutations within exon 1 of K-ras detected by SSCP analysis. Both mutations were GGT to GAT transitions at codon 12 confirmed by direct sequencing experiments. One was an adenocarcinoma from the medium-high exposure group and the other was a broncheolo-alveolar carcinoma from the medium-low exposure group. The rate of K-ras mutations in plutonium-induced lung tumors described herein (8%) was greater than previously described in canine plutonium-induced lung tumors (0%), but was less than that which we have described in spontaneous canine lung cancer (16%), less than that reported for human spontaneous non-small cell lung cancer (13-36%) and less than that described in rats with spontaneous lung cancer (40%) or lung tumors following 239Pu inhalation exposure (46%).

Administration, Inhalation↗
PubMed1998

1,2- and 1,4-Cyclohexanediol: major urinary metabolites and biomarkers of exposure to cyclohexane, cyclohexanone, and cyclohexanol in humans.

The metabolism and toxicokinetics of cyclohexane (CH) and cyclohexanol (CH-ol), important solvents and chemical intermediates, were studied in volunteers after 8-h periods of inhalation exposure at concentrations of 1010 and 236 mg m(-3), respectively (occupational exposure limits: CH, 1050 mg m(-3); CH-ol, 200 mg m(-3)). Of the dose of absorbed parent compounds, the yields of urinary CH-ol and 1,2- and 1,4-cyclohexanediol (CH-diol) were 0.5%, 23.4%, and 11.3%, respectively, after exposure to CH and 1.1%, 19.1%, and 8.4%, respectively, after exposure to CH-ol as determined by a gas chromatography method involving hydrolysis of glucuronide conjugates. The metabolic patterns of CH and CH-ol were very similar to that of cyclohexanone (CH-one) studied in the laboratory previously. For all three compounds, peak excretion of CH-ol occurred at the end of the exposure period, after which it decayed rapidly. Excretion curves of 1,2- and 1,4-CH-diol reached maximal values within 0-6 h postexposure, with subsequent elimination half-lives being 14-18 h. The rate-limiting step in the elimination of CH compounds from the organism is renal clearance of CH-diols. Determination of CH-diols in end-of-shift urine samples is recommended as a useful new method of biomonitoring of CH, CH-ol, and CH-one at the workplace. However, due to accumulation of CH-diols in the body during repeated exposure, quantitative relationships between the exposure and the level of CH-diols have to be adjusted according to the day of sampling during the working week.

Adult↗
PubMedDate not supplied

A population-based exposure model for benzene.

A model of daily-average inhalation exposures and total-absorbed doses of benzene to members of large populations was developed as part of a series of multimedia exposure and absorbed dose models. The benzene exposure and dose model is based upon probabilistic rather than sequential simulation of time-activity patterns, a simpler approach to modeling personal benzene exposures than other existing models. An important innovation of the benzene model is the incorporation of an anthropometric module for generating correlated exposure factors used to estimate absorbed doses occurring from inhalation, ingestion, and dermal absorption of benzene. A preliminary validation exercise indicates that the benzene model produces reasonable estimates of the distribution of benzene personal air concentrations expected for a large population. Uncertainty about specific percentiles of the predicted distributions of personal air concentrations was found to be dominated by uncertainty about microenvironmental benzene concentrations rather than time-activity patterns, and uncertainty about total absorbed doses was dominated by a lack of knowledge about the true absorption coefficient for benzene in the lung rather than knowledge gaps about microenvironmental concentrations or intake rates. The results of this modeling effort have implications for environmental control decisions, including evaluation of source control options, characterization of population and individual risk, and allocation of resources for future studies.

Air Pollution↗
PubMed2004

Effects of paving asphalt fume exposure on genotoxic and mutagenic activities in the rat lung.

Asphalt fumes are complex mixtures of aerosols and vapors containing various organic compounds, including polycyclic aromatic hydrocarbons (PAHs). Previously, we have demonstrated that inhalation exposure of rats to asphalt fumes resulted in dose-dependent induction of CYP1A1 with concomitant down-regulation of CYP2B1 and increased phase II enzyme quinone reductase activity in the rat lung. In the present study, the potential genotoxic effects of asphalt fume exposure due to altered lung microsomal enzymes were studied. Rats were exposed to air or asphalt fume generated under road paving conditions at various concentrations and sacrificed the next day. Alveolar macrophages (AM) were obtained by bronchoalveolar lavage and examined for DNA damage using the comet assay. To evaluate the systemic genotoxic effect of asphalt fume, micronuclei formation in bone marrow polychromatic erythrocytes (PCEs) was monitored. Lung S9 from various exposure groups was isolated from tissue homogenates and characterized for metabolic activity in activating 2-aminoanthracene (2-AA) and benzo[a]pyrene (BaP) mutagenicity using the Ames test with Salmonella typhimurium YG1024 and YG1029. This study showed that the paving asphalt fumes significantly induced DNA damage in AM, as revealed by DNA migration in the comet assay, in a dose-dependent manner, whereas the micronuclei formation in bone marrow PCEs was not detected even at a very high exposure level (1733 mg h/m3). The conversion of 2-AA to mutagens in the Ames test required lung S9-mediated metabolic activation in a dose-dependent manner. In comparison to the controls, lung S9 from rats exposed to asphalt fume at a total exposure level of 479+/-33 mg h/m3 did not significantly enhance 2-AA mutagenicity with either S. typhimurium YG1024 or YG1029. At a higher total asphalt fume exposure level (1150+/-63 mg h/m3), S9 significantly increased the mutagenicity of 2-AA as compared to the control. However, S9 from asphalt fume-exposed rats did not significantly activate the mutagenicity of BaP in the Ames test. These results show that asphalt fume exposure, which significantly altered both phases I and II metabolic enzymes in lung microsomes, is genotoxic to AM and enhances the metabolic activation of certain mutagens through altered S9 content.

Animals↗
PubMed1999

Long-lasting effects of chronic ozone exposure on rat nasal epithelium.

Ozone, the principal oxidant pollutant in photochemical smog, causes airway epithelial injury in the upper and lower respiratory tract of laboratory animals. We have recently reported that long-term inhalation exposure to ozone causes mucous-cell metaplasia (MCM) in the surface epithelium lining the nasal airways of F344 rats. The principal objective of the present study was to determine the persistence of ozone-induced MCM in the nasal epithelium after the end of a chronic exposure. Male F344/N rats were exposed to 0, 0.25, or 0.5 ppm ozone, for 8 h/d, 7 d/wk for 13 wk. Animals were killed 8 h, 4 wk, or 13 wk after the end of the chronic exposure. Ozone-related alterations in the nasal epithelium were qualitatively and quantitatively characterized through histochemistry, image analysis, and morphometric techniques. Some rats were exposed for an additional 8 h to 0.5 ppm ozone at 13 wk after the end of the chronic exposure to determine whether previous ozone exposure results in persistent changes in the sensitivity of nasal epithelium to acute injury. At the end of the chronic exposure, hyperplasia was present in the nasal epithelium of rats exposed to 0.25 and 0.5 ppm ozone. By 13 wk postexposure, this proliferative alteration was still evident only in the rats exposed to 0.5 ppm ozone. Ozone-induced MCM with associated intraepithelial mucosubstances was evident only in the nasal tissues of rats exposed to 0.5 ppm ozone. Though attenuated, these alterations in the nasal mucous apparatus were still detectable at 13 wk after the end of the exposure. At this same time after the chronic exposure, an acute (8 h) exposure to 0.5 ppm ozone induced an additional increase of mucosubstances in the nasal epithelium of rats previously exposed to 0.5 ppm ozone, but not in rats chronically exposed to 0 or 2.5 ppm ozone. The persistent nature of the ozone-induced MCM in rats documented in this report suggests that ozone exposure may have the potential to induce similar long-lasting alterations in the airways of humans.

Animals↗
PubMed1989

Establishing aerosol exposure concentrations for inhalation toxicity studies.

Criteria for the selection of aerosol concentrations to be used in inhalation studies assessing the toxicity and carcinogenicity of chemical substances were discussed by the authors in a meeting sponsored by the National Toxicology Program. Concepts in the design of aerosol inhalation studies emerged from that meeting and are being communicated through this publication. Inhalation studies assessing the toxicity and carcinogenicity of aerosols have often used maximum exposure levels on the basis of technological feasibility. Evidence has now accumulated that the amount of pulmonary burden of deposited particles impacts on particle clearance above some as yet not well-defined exposure concentration. The sequelae are such that lung clearance decreases with increased particulate burden to the point of approaching complete cessation. This paper focuses on the major determinants in establishing maximal aerosol concentrations for use in inhalation toxicity studies with special emphasis on experimental design features to assess lung retention. The subject matter of this paper is a rapidly developing area in terms of knowledge. Accordingly, the contents of this article are intended as guidelines and not as absolute rules for the conduct and interpretation of inhalation exposure studies.

Administration, Inhalation↗
PubMed1994

The effects of high-dose toluene on embryonic development in the rat.

Developmental disability, intrauterine growth retardation, renal anomalies, and dysmorphic features have been described in offspring of women who abuse toluene during pregnancy. A Sprague-Dawley rat model was developed to study this clinical syndrome. During d 6-19 of gestation, 11 treated dams received daily gavage doses of toluene, 520 mg/kg body weight, diluted in corn oil, and 11 control dams received corn oil. This dose of toluene simulates the blood toluene levels obtained after an inhalation exposure to 3290 ppm toluene, an inhalation level in the lower end of the range experienced by toluene abusers. Maternal weight gain was 24% less in the toluene-exposed group (p < 0.002); however, there were no maternal deaths. The fetuses were delivered on d 19 of gestation, and 287 fetuses (148 toluene exposed, 139 control) were examined. Toluene treatment did not affect the number of implantations or stillbirths. There were no toluene-induced major congenital malformations or neuropathologic changes noted. In the toluene-treated group, the weights of the fetuses were reduced by 9.4% (p < 0.004) and placental weights were reduced by 10.3% (p < 0.01). Toluene exposure also reduced fetal organ weights as follows: brain 4.6%, heart 5.9%, liver 13.2% (p < 0.02), and kidney 13% (p < 0.05). Organ weight/body weight ratios did not differ significantly, suggesting that prenatal toluene exposure produced a generalized growth retardation.

Animals↗
PubMedDate not supplied

Risk from inhaled mycotoxins in indoor office and residential environments.

Mycotoxins are known to produce veterinary and human diseases when consumed with contaminated foods. Mycotoxins have also been proposed to cause adverse human health effects after inhalation exposure to mold in indoor residential, school, and office environments. Epidemiologic evidence has been inadequate to establish a causal relationship between indoor mold and nonallergic, toxigenic health effects. In this article, the authors model a maximum possible dose of mycotoxins that could be inhaled in 24 h of continuous exposure to a high concentration of mold spores containing the maximum reported concentration of aflatoxins B1 and B2, satratoxins G and H, fumitremorgens B and C, verruculogen, and trichoverrols A and B. These calculated doses are compared to effects data for the same mycotoxins. None of the maximum doses modeled were sufficiently high to cause any adverse effect. The model illustrates the inefficiency of delivery of mycotoxins via inhalation of mold spores, and suggests that the lack of association between mold exposure and mycotoxicoses in indoor environments is due to a requirement for extremely high airborne spore levels and extended periods of exposure to elicit a response. This model is further evidence that human mycotoxicoses are implausible following inhalation exposure to mycotoxins in mold-contaminated home, school, or office environments.

Adult↗
PubMed1992

Alveolar macrophages and lung lesions after combined exposure to nickel, cobalt, and trivalent chromium.

In earlier inhalation exposures of rabbits, nickel increased the production of surfactant by type II cells, with secondary effects on morphology and function of alveolar macrophages. Cobalt induced mainly a nodular growth pattern of the type II cells. Trivalent chromium seemed to impair the capacity of macrophages to catabolize surfactant but did not affect the type II cells. We exposed rabbits by inhalation to combinations of nickel (0.6 mg/m3 as NiCl2) and trivalent chromium [1.2 mg/m3 as Cr(NO3)3] (Ni-Cr), cobalt (0.5 mg/m3 as CoCl2) and nickel (0.5 mg/m3) (Co-Ni), or cobalt (0.5 mg/m3) and chromium (1.2 mg/m3) (Co-Cr) for 4 months, 5 days/week, 6 hr/day. Alveolar macrophages, alveolar type II cells, and lung content of phospholipids were determined. All combined exposures induced more pronounced lung lesions than exposures for each of the metals. Phospholipid concentrations were significantly higher. There were significantly higher percentages of macrophages filled with surfactant-like inclusions and a smooth surface. Accumulations of macrophages in alveoli were more widespread. Chromium potentiated the effects of nickel and cobalt on the type II cells, which led to secondary effects on the macrophages. Nickel potentiated the specific effects of cobalt, i.e., type II cell nodule formation. The result indicates that noxious effects could also be induced in man by combined exposure to nickel, cobalt, and trivalent chromium in concentrations similar to those occurring in some occupational settings.

Animals↗
PubMed1986

Toxicity of formaldehyde vapor in B6C3F1 mice exposed for 13 weeks.

Groups of 10 male and 10 female B6C3F1 mice were exposed to 0, 2, 4, 10, 20, or 40 ppm of formaldehyde vapor 6 h/day, 5 days/week for 13 weeks. Clinical abnormalities (dyspnea, listlessness, and hunched posture), significant mortality, and body weight loss were observed in the 40 ppm groups. Pathologic changes were observed in the nose, larynx, trachea, and bronchi of treated males and females and in the uterus and ovaries of treated females. Squamous metaplasia and inflammation were present in the nasal tissues of male and female mice in the 10, 20, and 40 ppm groups and in the larynx of males and females in the 20 and 40 ppm groups. The trachea had squamous metaplasia and hyperplasia of the epithelium in addition to submucosal fibrosis and inflammation in the 20 and 40 ppm groups. In some mice, epithelial-lined, irregular connective tissue bands spanned the tracheal lumen. Metaplasia of the bronchial epithelium was confined to the 40 ppm exposure groups. These effects on the respiratory system were more prevalent in male than in female mice. Hypoplasia of the uterus and ovaries, probably secondary to body weight loss, was confined to the 40 ppm exposure group. In conclusion, 13-week inhalation exposures of B6C3F1 mice to 10, 20, and 40 ppm of formaldehyde vapor induced histologic lesions in the upper respiratory system and concentrations of 40 ppm were lethal to those mice.

Animals↗
PubMed1997

Effects of combined exposure to noise and toxic substances--critical review of the literature.

A number of studies have been conducted in recent years investigating the potential effects on various health endpoints of the combination of noise and a variety of different industrial substances. This review indicates that the information available in both animals and humans on this subject is limited particularly with respect to assessing occupational risk. Most studies have focused on auditory effects in animals, although investigations have been performed for other toxicological endpoints. For some substances, notably toluene, the information from animals studies does suggest an interaction but these were performed only at exposure levels to both noise and chemicals which were each individually ototoxic. Single simultaneous exposure to noise and styrene did not result in any enhancement of auditory impairment above that produced by noise or styrene alone. Single simultaneous exposure to noise and carbon monoxide (CO), however, showed some evidence of enhancement of ototoxicity beyond that produced by noise or carbon monoxide alone, although only at high atmospheric concentrations of CO. When 1,3-dinitrobenzene was administered parentally at neurotoxic dose levels with continuous noise exposure, there was an increased severity of effects in the brain stem. Combined exposure to noise and lead and/or cadmium resulted in histopathological heart lesions of undefined severity, a finding which was not observed for either of those agents in isolation. Dermal exposure to dimethylformamide and noise or inhalation exposure to xylene and noise resulted in some biochemical changes in cardiac muscle which were of doubtful toxicological significance. In developing mice, there was evidence that combined exposure to cadmium sulphate and noise caused an increased incidence of external and skeletal malformations but only at dose levels of cadmium which would have induced developmental effects. Overall, for each of these chemicals and endpoints observed there is a suggestion of some interaction with noise exposure. From the data that are currently available, however, inferences cannot be drawn on whether or not interactions would have occurred at lower, more occupationally relevant, levels of exposure. A number of studies have investigated human populations exposed to both noise and industrial chemicals. Due to confounding factors, however, it was concluded that these data were inadequate for assessing the combined effects of noise and chemical exposure on hearing.

Animals↗
PubMed2000

[Poisonings with the herbicides glyphosate and glyphosate-trimesium].

Generally the herbicide glyphosate is considered harmless to humans. Glyphosate-trimesium is labelled harmful (Xn), whereas glyphosate-isopropylamine carries no warning sign. As cases of serious poisoning have emerged contacts to the Poison Information Centre have been reviewed. The persons exposed were mainly smaller children and adults 20 to 59 years of age. Oral exposure was recorded in 47 persons, inhalation exposure in 24 and topical contact in 42. About one fourth of the exposed persons were asymptomatic. Most of the symptomatic poisonings demonstrated complaints from the mouth, the gastrointestinal tract and the airways. Eleven patients were admitted to hospital. Two died, one of them having ingested the isopropylamine salt, the other the trimesium salt. Death ensued quickly in the latter patient. A similar fate was observed in a child--not included in the present material--who had also ingested the trimesium compound.

Adult↗
PubMed2001

The application of physiologically based pharmacokinetic modelling in the analysis of occupational exposure to perchloroethylene.

A physiologically based pharmacokinetic model for perchloroethylene was parameterized, calibrated and validated using anatomic, physiologic, biochemical and physicochemical data obtained from the literature. The model was used to analyse human exposure data obtained under controlled conditions and from dry cleaning establishments in the Padua area of northern Italy. Whilst the model satisfactorily simulated the urinary excretion of trichloroacetic acid, following experimental inhalation exposure to 10, 20 and 40 ppm perchloroethylene under controlled conditions the opposite was true for the occupational exposure data. However, further model refinement to incorporate inter-individual variability of anatomical, physiological and biochemical parameters which have an impact on model output, would further improve the predictive capabilities of the model. The possibility of perchloroethylene and trichloroethylene co-exposure in the occupational setting was indicated by the model.

Calibration↗
PubMed2004

Biochemical effects of low level exposure to soman vapour.

The aim of this study was to demonstrate changes in acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities, tyrosine aminotransferase activity (TAT) and plasma corticosterone level, neuroexcitability and behavior following 24 hours and 4 weeks of soman sublethal inhalation exposure at low level. AChE activity in erythrocytes and BuChE activity in plasma was decreased (dependent on the concentration of soman) 24 h and 4 weeks after the exposure. Similar decrease in AChE activity in different brain parts was observed. One of stressogenic parameters (TAT) was changed after 24 h exposure only. 4 weeks after the exposure, these parameters (corticosterone and TAT) were in the range of normal values. Behaviour of experimental animals was changed 24 h after the exposure persisting 4 weeks after the exposure as well as neuroexcitability.

Acetylcholinesterase↗