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PubMed2003

Pleural dosimetry and pathobiological responses in rats and hamsters exposed subchronically to MMVF 10a fiberglass.

Interspecies differences in pulmonary and pleural responses to the inhalation of natural mineral and synthetic vitreous fibers have been observed in chronic and subchronic studies. However, the reasons for these differences are not clearly understood. There are also fiber-specific differences in the outcome of chronic inhalation exposure to natural mineral and synthetic vitreous fibers. Whether these differences are dependent upon the ability of these fibers to translocate to the pleural space is unknown. The present study was conducted to compare retained fiber burdens and selected pathological responses in the pleural compartments of rats and hamsters following subchronic inhalation of MMVF 10a fiberglass, a fiber negative for tumorigenesis or fibrosis in chronic studies. Fischer 344 rats and Syrian golden hamsters were exposed for 4 or 12 weeks by nose-only inhalation at nominal aerosol mass concentrations of 45 mg/m3 (610 WHO fibers/cc). Pulmonary fiber burdens and pulmonary inflammatory responses were greater in rats than in hamsters. The total number of fibers in the lung was approximately three orders of magnitude greater than in the pleural compartment. Pleural burdens in the hamster (160 fibers/cm2 surface area) were significantly greater than burdens in similarly exposed rats (60 fibers/cm2 surface area) following 12 weeks of exposure. With time postexposure, pleural burdens decreased in hamsters but were essentially unchanged in rats. Pleural inflammatory responses in both species were minimal. In rats, pleural inflammation was characterized by increased numbers of macrophages and increases in mesothelial cell replication during the period of fiber exposure. In contrast, hamsters had increased numbers of macrophages and lymphocytes, and mesothelial-cell replication indices were elevated on the parietal pleura of the costal wall and diaphragm, with some of these responses persisting through 12 weeks of postexposure recovery. Taken together, the results suggest that differences among rodent species in pleural responses to inhaled fibers are due to a delivered dose of fibers and to the biological responses to the presence of the fibers.

Administration, Inhalation↗
PubMed2005

Inhalation of concentrated particulate matter produces pulmonary inflammation and systemic biological effects in compromised rats.

Although significant progress has been made over the past few years, there is still debate on the causal fractions that are responsible for particulate matter (PM)-associated adverse health effects. A series of 1-d inhalation exposures to concentrated ambient particles (CAPs) were performed in compromised rats, focusing on pulmonary inflammation and changes in blood factors as biological outcomes. Studies were carried out in The Netherlands at an urban background location in Bilthoven, an industrialized location in the city of Utrecht, as well as at a location that is heavily dominated by freeway emissions. It was hypothesized that exposure to CAPs resulted in oxidative stress in the lung, producing a release of inflammatory mediators, which in turn can result in cardiovascular effects. Both spontaneously hypertensive rats and rats preexposed to ozone were studied. The effects were studied at 2d postexposure, focusing on pathology and cell proliferation, bronchoalveolar lavage fluid (BALF) analysis (including cytokines, biochemistry, cell differentials, cell viability and proliferation, and Clara-cell 16 protein), and blood analyses (fibrinogen, Clara-cell 16 protein, Von Willebrand factor, and cell differentials). Using CAPs exposures as a binary term, mild inflammation (increased numbers of neutrophils) and increased lung permeability (protein and albumin leakage in BALF) were evident. In addition, CAPs also produced increased fibrinogen concentrations in blood of spontaneously hypertensive rats. In conclusion, inhalation up to 3700 microg/m3 CAPs in the size range of 0.15-2.5 microm did induce statistically significant effects in the lung and blood, but the effects observed may not potentially be very biologically relevant. PM mass concentrations and lung permeability were weakly associated. This suggests that other PM metrics might be more appropriate.

Air Pollutants↗
PubMedDate not supplied

Chronic effects of the novel glucocorticosteroid RPR 106541 administered to beagle dogs by inhalation.

The preclinical safety of RPR 106541, a novel 17-thiosteroid, was evaluated in young adult and mature dogs by inhalation exposure for 26 weeks and 52 weeks, respectively. A dry powder formulation of RPR 106541 in lactose was administered to young adult dogs (approximately 6 months of age at initiation) at doses of 0 (air and placebo controls), 10, 100, or 1,000 microg/kg/d for 26 weeks. A solution-based aerosol formulation was administered to mature dogs (approximately 10 months at initiation) from a pressurized metered dose inhaler at 0 (air and placebo controls), 10, 50, and 150 microg/kg/d for 52 weeks. Clinical evidence of glucocorticosteroid-induced immunosuppression was observed by weeks 20-26 following relatively high dose exposures (100 microg/kg/d and 1,000 microg/kg/d) in young dogs receiving the dry powder formulation for 26 weeks. Classic glucocorticosteroid effects were observed, including adrenocortical atrophy, reduced bone mass with retention of epiphyseal growth plates in long bones, prominence of stromal adipose tissue in bone marrow, and atrophy of lymphoid tissues. Inhalation administration of RPR 106541 to sexually mature dogs facilitated more definitive characterization of endocrine affects of RPR 106541 as compared with administration in younger, sexually immature animals. Significant effects in female reproductive organs included absence of corpora lutea in association with atresia of vesicular follicles within the ovaries, endometrial hyperplasia, and lobular development of mammary tissue. Discordant development of mammary tissue, accumulation of secretory material within hyperplastic endometrial glands, and hypertrophy of uterine lining epithelium in absence of ovulation were consistent with a secondary progestin effect by a potent glucocorticosteroid.

Administration, Inhalation↗
PubMed1992

Cytogenetic analysis of pulmonary lavage and bone marrow cells of rats after repeated formaldehyde inhalation.

Cytogenetic analyses were conducted on bone marrow and pulmonary lavage cells from rats that received repeated inhalation exposures to formaldehyde. Male Sprague-Dawley rats were exposed to 0, 0.5, 3, or 15 ppm formaldehyde for 6 h per day, 5 days per week, for 1 and 8 weeks. There was no significant increase in chromosomal abnormalities in the bone marrow cells of formaldehyde-exposed rats relative to controls. There was a statistically significant increase in chromosomal aberrations in the pulmonary lavage cells from rats that inhaled 15 ppm. There were 7.6 and 9.2% of the scored pulmonary lavage cells that had aberrations following 1 and 8 weeks, respectively, of 15 ppm formaldehyde exposure (with control levels of 3.5 and 4.8%, respectively). The predominant damage seen was chromatid breaks. These findings indicate that marginal but statistically significant genotoxic effects could be detected locally in lung alveolar macrophages, but not distally in bone marrow, following repeated formaldehyde exposures only at a high concentration that is carcinogenic to rats. The biological significance of this effect is uncertain since formaldehyde is not considered to be a lung carcinogen in rats.

Administration, Inhalation↗
PubMed1999

Effect of low-level short-term o-xylene inhalation of benzo[a]pyrene (BaP) metabolism and BaP-DNA adduct formation in rat liver and lung microsomes.

o-Xylene is a commonly used solvent that alters mixed-function oxidase (MFO) activity in an organ- and isozyme-specific pattern following intraperitoneal (ip) administration. Similar MFO alterations have been observed after ip or inhalation exposure to other methyl benzenes. These MFO alterations shifted the metabolism of the carcinogen benzo[a]pyrene (BaP) toward formation of toxication metabolites in lung. The purpose of this study was to determine whether o-xylene inhalation caused similar MFO changes and whether these alterations were reflected in altered BaP metabolism and BaP-DNA adduct formation. o-Xylene (300 ppm, 6 h) decreased the activity of arylhydrocarbon hydroxylase (AHH) in lung. CYP2B1 activity (benzyloxyresorufin O-dealkylase; BROD), which is responsible for metabolism of BaP to relatively nontoxic metabolites, was decreased in lung, as was, to a lesser extent, CYP1A1 (ethoxyresorufin O-dealkylase; EROD), which is responsible for metabolism of BaP to reactive/toxic metabolites. The BROD/EROD ratio, an indirect indicator of the pattern of BaP toxication/detoxication, was decreased in lung, suggesting that BaP metabolism is shifted toward toxication. No MFO alterations were observed in liver. In lung microsomes, o-xylene increased formation of 7,8-BaP-diol, while 9,10-BaP-diol, 3-OH BaP, and 9-OH BaP were decreased. In liver, o-xylene increased 9-OH BaP formation, while 4,5- and 9,10-diols as well as total diols were decreased. The toxication/detoxication ratios for BaP individual and total metabolite groups were increased in lung microsomes and unaltered in liver. The major BaP-DNA adduct, BaP diol epoxide-N2-deoxyguanosine, was increased in lung but decreased in liver microsomes from o-xylene-exposed rats. Four minor BaP-DNA adducts were formed in lung and three in liver, only one of which (liver adduct 3) was decreased. The o-xylene-induced increase in BaP adduct formation in lung and decrease in liver indicate that coexposure to organic solvents such as the methyl benzenes may alter the carcinogenesis of BaP, or other PAHs, in an organ-specific fashion.

Administration, Inhalation↗
PubMed2004

Poisoning due to chlorophenoxy herbicides.

Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1986

Ranking the carcinogenic hazards of occupational exposures: Exposure-Potency Index (EPI) values for nine volatile industrial chemicals.

Employers, employees, and occupational health professionals need a a simple index to rank carcinogens according to their potential danger at exposure levels which are commonly encountered in workplaces. We describe such an index, the Exposure-Potency Index (EPI). This simple proportion, dose level (mg/kg body weight/day) to which workers are permitted to be exposed/cancer-causing dose (mg/kg body weight/day) in test animals, permits comparisons among carcinogens. We have calculated this index for inhalation exposures to 1,3-butadiene, 1,2-dibromo-3-chloropropane (DBCP), 1,2-dibromoethane (EDB), ethylene oxide, formaldehyde, methylene chloride, propylene oxide, tetrachloroethylene (perchloroethylene), and trichloroethylene (TCE). The permitted worker exposure levels have frequently been close to the levels which induce tumors in laboratory animals. More recently, Permissible Exposure Limits (PEL's) for for some chemicals have been markedly reduced, and this is reflected in lowered EPI values. Combining EPI values with information on the numbers of exposed workers provides a simple means of identifying and ranking dangers to populations of workers.

Animals↗
PubMedDate not supplied

A quantitative definition of exposure and related concepts.

This paper develops a unified theoretical framework for understanding exposure to environmental pollutants and other agents. It reviews the scientific literature to describe the many diverse and often confusing ways in which the term "exposure" is being used. Using six criteria proposed for a useful framework, a set of quantitative definitions, which encompass and expand upon existing definitions, is developed. After "agent" (e.g., a pollutant) and "target" (e.g., a person's hand) are defined, "exposure" is defined as the contact between an agent and a target. An "instantaneous point exposure" is defined as the joint occurrence of two events: 1) point i of a target is located at (xi, yi, zi) at time t, and 2) an agent of concentration Ci is present at location (xi, yi, zi) at time t. It is shown that the definition of instantaneous point exposure is fundamental in that all other functions of exposure with respect to space or time-such as the average exposure and the integrated exposure-can be derived from it. Because exposure and dose are closely related and often confused, our framework also includes a general definition of dose that is consistent with common usage. Finally, the definitions in this unified theoretical framework are shown to apply to inhalation exposure, dermal exposure, and ingestion exposure. In addition to the literature review and the quantitative definitions of exposure, this paper includes a glossary of terms that are proposed to help establish a common language for the exposure sciences.

Carbon Monoxide↗
PubMed2001

A coupled airflow and source/sink model for simulating indoor VOC exposures.

In this paper, a numerical model is presented to study the indoor air quality (IAQ) in a room with different emission sources, sinks, and ventilation methods. A computer program, ACCESS-IAQ, is developed to simulate the airflow pattern, the time history of the contaminant concentrations in the occupied zone, and the inhalation exposures. The program developed may be useful for IAQ professional to design healthy and comfortable indoor environments. A numerical study has been carried out to predict the effectiveness of a displacement ventilation and a mixing ventilation on volatile organic compound (VOC) removal in a model office. Results from the numerical predictions show that when a "wet" emission source (a freshly painted wood stain) is distributed uniformly across the floor area with sinks (gypsum board) from the four vertical walls, displacement ventilation has consistently lower exposure at the breathing level of the occupant in the room. Such an effect is mainly due to the higher ventilation efficiency of displacement ventilation compared to the mixing ventilation. The simulation results also show that the walls adsorb significant amounts of VOCs during the first hour and act as secondary sources thereafter.

Absorption↗
PubMed1997

Significance of the biodurability of man-made vitreous fibers to risk assessment.

It is generally agreed that the biodurability of man-made vitreous fibers is a major factor for the characterization of potential health effects. As there is currently no standardization of experimental protocols to determine biodurabilty, the results of the clearance assays have not been used up to now for regulatory purposes. Methods used to analyze biodurability in animal models are short-term inhalational exposure and intratracheal instillation of rat respirable fibers. Both test methods have strengths and limitations for regulatory purposes. We outline recommended procedures for standardized biodurability assays that can be used to compare different fiber types. In animal experiments, biodurability is difficult to separate from biopersistence, as mucociliary and macrophage-mediated clearance occur simultaneously with dissolution and disintegration. For intratracheal instillation, a sized rat respirable sample must be used. Precautions should be taken to prevent aggregation of fibers in the lungs. Although from a scientific point of view questions remain about quantifying the influence of fiber length, diameter, dose, and exposure route, consistent data on the biodurability of vitreous glass fibers are available which may be used for regulatory purposes.

Administration, Inhalation↗
PubMed1985

Human exposures to volatile halogenated organic chemicals in indoor and outdoor air.

Volatile halogenated organic chemicals are found in indoor and outdoor air, often at concentrations substantially above those in remote, unpopulated areas. The outdoor ambient concentrations vary considerably among sampling stations throughout the United States, as well as diurnally and daily. The vapor pressures and air-water equilibrium (Henry's Law) constants of these chemicals influence considerably the likely relative human exposures for the air and water routes. Volatilization of chemicals from indoor uses of water can be a substantial source of exposure, as shown for radon-222. Measurements of air concentrations of trichloroethylene (TCE) in showers using TCE contaminated groundwater show increases with time to as high as one-third of occupational threshold limit values. Using a scaled down experimental shower, such volatilization and subsequent decay in air was also demonstrated. Using a simplified indoor air model and assuming complete volatilization from a full range of typical water uses within the home, calculations indicate that the expected air inhalation exposures can be substantially higher than those from ingestion of these chemicals in drinking water. Although the regulation of toxic chemicals in potable water supplies has focused traditionally on direct ingestion, the volatilization and inhalation from other much greater volume indoor uses of water should be considered as well.

Air Pollutants, Occupational↗
PubMed1987

A linear systems approach to analyzing the pharmacokinetics of carbon tetrachloride in the rat following repeated exposures of 8 and 11.5 h/day.

Ten- and 12-h workdays are relatively common in the chemical and other non-labor intensive industries both in the United States and Europe. Based on pharmacokinetic principles, persons who work 10-12 h shifts and are exposed to chemicals with a terminal half-life between 5 and 200 h will absorb a larger quantity of the toxicant or have higher peak blood levels than persons who work 8-h shifts. To evaluate the effects of exposure duration and repeated exposure on the elimination of carbon tetrachloride (CCl4), rats were repeatedly exposed to 100 ppm 14CCl4 for either 8 or 11.5h/day. Pharmacokinetic equations which describe the plasma concentration and pulmonary elimination during and following single and repeated inhalation exposures were developed. These equations are based on a diffusional type of input function and a linear systems analysis approach. They can be used to make predictions of the cumulation of toxicant following repeated exposure, the relative change in the plasma level following multiple exposures, and the steady-state plasma level based only on the elimination of the chemical in the breath. The pharmacokinetic analysis indicated that rats repeatedly exposed to 100 ppm CCl4 for 11.5 h/day for 4 days per week, or 8 h/day for 5 days per week, will not have increasing plasma levels. The analysis also predicted no significant difference in the peak plasma concentration of CCl4 between the 8 and 11.5h/day schedules following either 1 or 2 weeks of exposure. Due to rapid pulmonary elimination by the rat, the steady state plasma level of CCl4 was reached after only three consecutive exposures for both schedules. The alpha and beta half-lives (X +/- SE) of pulmonary elimination for the 8 h/day group were 84 +/- 9 min and 400 +/- 32 min, respectively. The half-lives for the 11.5 h group were 91 +/- 6 min and 496 +/- 32 min, indicating that the beta phase half-life was significantly longer than that of the 8-h group. This observation, coupled with the tissue distribution data (Paustenbach et al. 1986), suggests that during the longer exposure period a greater fraction of CCl4 is placed in the poorly perfused tissues like fat, thus altering the time-course of elimination in the breath. A general formula for adjusting TLVs for unusually long work schedules is also developed and presented.

Animals↗
PubMed2004

Exposure to beta-carbolines norharman and harman.

The aromatic beta-carbolines norharman and harman have been implicated in a number of human diseases including Parkinson's disease, tremor, addiction and cancer. It has been shown that these compounds are normal body constituents formed endogenously but external sources have been identified. Here, we summarise literature data on levels of norharman and harman in fried meat and fish, meat extracts, alcoholic drinks, and coffee brews. Other sources include edible and medicinal plants but tobacco smoke has been identified as a major source. Exposure levels from these different dietary sources are estimated to a maximum of 4 microg norharman per kg body weight (bw) per day and 1 microg harman per kg bw per day. Exposure via tobacco smoke depends on smoking habits and type of cigarettes but can be estimated to 1.1 microg/kg bw for norharman and 0.6 microg/kg bw for harman per package of cigarettes smoked. Studies on toxicokinetics indicate that inhalative exposure leads to a rapid increase in plasma levels and high bioavailability of norharman and harman. Oral bioavailability is lower but there are indications that sublingual absorption may increase dietary uptake of beta-carbolines. Endogenous formation can be estimated to be 50-100 ng/kg bw per day for norharman and about 20 ng/kg bw per day for harman but these rates may increase with high intake of precursors. Biomarker studies on plasma levels of beta-carbolines reported on elevated levels of norharman, harman or both in diseased patients, alcoholics and following tobacco smoking or consumption of beta-carboline-containing food. Cigarette smoking has been identified as major influence but dietary exposure may contribute to exposure.

Biological Availability↗
PubMed2000

Asthma and rhinitis induced by exposure to raw green beans and chards.

BACKGROUND: Although the vast majority of IgE-mediated allergic reactions to foods occurs through ingestion, a few cases of unexpected allergic reactions to foods may occur through the exposure to airborne food allergen particles. METHODS: Case reports. Skin prick tests and serum-specific IgE (CAP-FEIA) were used to identify specific IgE antibodies. Bronchial provocation tests were performed to determine the clinical relevance of inhaled exposure to raw and cooked green beans and raw chards. After demonstrating specific reactivity to them, SDS-PAGE and immunoblotting of raw and cooked green beans were carried out to identify relevant antigens. RESULTS: Three women developed bronchial asthma and rhinitis after exposure to raw green beans, and one of them also when exposed to raw chards. All women tolerated ingestion of green beans. Patients reported multiple episodes while handling these vegetables for cooking activities. Allergy to green beans and chards was demonstrated by skin testing and serum-specific IgE. Bronchial challenge test with these allergens showed positive responses to raw, but not cooked, green beans and chards. Oral food challenges with green beans (raw and cooked) and chards were negative in all patients. In order to further characterize the allergenic components of these extracts, SDS-PAGE and electroblotting studies were also performed. Immunoblots of raw and cooked green beans extract showed two IgE-binding bands with apparent molecular weights of 41.1 and 70.6 kD. Interestingly, a 47-kD IgE-binding protein was detected only in raw green bean extracts. CONCLUSIONS: We report three patients who developed asthma and rhinitis caused by exposure to raw, but not to cooked, green beans and chards in a non-occupational environment. Only minor differences of IgE reactivity between nitrocellulose-blotted raw and boiled green bean extract were found.

Adult↗
PubMed1995

HFA-134a (1,1,1,2-tetrafluoroethane); lack of oncogenicity in rodents after inhalation.

1. Groups of 60 male and 60 female B6C3F1 mice or HanIbm Wistar rats were exposed to HFA-134a using snout-only inhalation exposure techniques for periods of one hour daily for at least 104 weeks. HFA-134a was delivered directly from cylinders at vapour concentrations of 2500, 15,000 and 75,000ppm for mice and from metered-dose inhalers at vapour concentrations of 2500, 10,000 and 50,000ppm for rats. 2. Intended dosages were achieved. 3. Evidence of absorption was found at each dose level and was dose related. 4. Neither species suffered treatment related effects on survival, clinical signs, body weights, haematology nor on the type, incidence, site or severity of gross lesions. 5. There was no effect of treatment on the type, incidence, site or severity of neoplasms in mice or rats. 6. There were no non-neoplastic findings related to treatment in mice. 7. HFA-134a was considered not to be oncogenic and to provide a safe alternative to chlorofluorocarbons for use in pharmaceutical metered-dose inhalers.

Absorption↗
PubMed1997

A recommended occupational exposure limit for formaldehyde based on irritation.

In recent years, several regulatory agencies and professional societies have recommended an occupational exposure limit (OEL) for formaldehyde. This article presents the findings of a panel of experts, the Industrial Health Foundation panel, who were charged to identify an OEL that would prevent irritation. To accomplish this task, they critiqued approximately 150 scientific articles. Unlike many other chemicals, a large amount of data is available upon which to base a concentration-response relationship for human irritation. A mathematical model developed by Kane et al. (1979) for predicting safe levels of exposure to irritants based on animal data was also evaluated. The panel concluded that for most persons, eye irritation clearly due to formaldehyde does not occur until at least 1.0 ppm. Information from controlled studies involving volunteers indicated that moderate to severe eye, nose, and throat irritation does not occur for most persons until airborne concentrations exceed 2.0-3.0 ppm. The data indicated that below 1.0 ppm, if irritation occurs in some persons, the effects rapidly subside due to "accommodation." Based on the weight of evidence from published studies, the panel found that persons exposed to 0.3 ppm for 4-6 h in chamber studies generally reported eye irritation at a rate no different than that observed when persons were exposed to clean air. It was noted that at a concentration of 0.5 ppm (8-h TWA) eye irritation was not observed in the majority of workers (about 80%). Consequently, the panel recommended an OEL of 0.3 ppm as an 8-h time-weighted average (TWA) with a ceiling value (CV) of 1.0 ppm (a concentration not to be exceeded) to avoid irritation. The panel believes that the ACGIH TLV of 0.3 ppm as a ceiling value was unnecessarily restrictive and that this value may have been based on the TLV Committee's interpretation of the significance of studies involving self-reported responses at concentrations less than 0.5 ppm. The panel concluded that any occupational or environmental guideline for formaldehyde should be based primarily on controlled studies in humans, since nearly all other studies are compromised by the presence of other contaminants. The panel also concluded that if concentrations of formaldehyde are kept below 0.1 ppm in the indoor environment (where exposures might occur 24 h/d) this should prevent irritation in virtually all persons. The panel could not identify a group of persons who were hypersensitive, nor was there evidence that anyone could be sensitized (develop an allergy) following inhalation exposure to formaldehyde. The panel concluded that there was sufficient evidence to show that persons with asthma respond no differently than healthy individuals following exposure to concentrations up to 3.0 ppm. Although cancer risk was not a topic that received exhaustive evaluation, the panel agreed with other scientific groups who have concluded that the cancer risk of formaldehyde is negligible at airborne concentrations that do not produce chronic irritation.

Animals↗
PubMed1997

Benzene-induced hematotoxicity and bone marrow compensation in B6C3F1 mice.

Long-term inhalation exposure of benzene has been shown to cause hematotoxicity and an increased incidence of acute myelogenous leukemia in humans. The progression of benzene-induced hematotoxicity and the features of the toxicity that may play a major role in the leukemogenesis are not known. We report the hematological consequences of benzene inhalation in B6C3F1 mice exposed to 1, 5, 10, 100, and 200 ppm benzene for 6 hr/day, 5 days/week for 1, 2, 4, or 8 weeks and a recovery group. There were no significant effects on hematopoietic parameters from exposure to 10 ppm benzene or less. Exposure of mice to 100 and 200 ppm benzene reduced the number of total bone marrow cells, progenitor cells, differentiating hematopoietic cells, and most blood parameters. Replication of primitive progenitor cells in the bone marrow was increased during the exposure period as a compensation for the cytotoxicity induced by 100 and 200 ppm benzene. In mice exposed to 200 ppm benzene, the primitive progenitor cells maintained an increased percentage of cells in S-phase through 25 days of recovery compared with controls. The increased replication of primitive progenitor cells in concert with the reported genotoxicity induced by benzene provides the components necessary for producing an increased incidence of lymphoma in mice. Furthermore, we propose this mode of action as a biologically plausible mechanism for benzene-induced leukemia in humans exposed to high concentrations of benzene.

Animals↗