Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Inhalation Exposure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources
PubMed1992

Biochemical toxicology and disposition of Therminol 66 heat transfer fluid after inhalation or after dietary administration to male Sprague-Dawley rats.

The objectives of this study were to determine the disposition of Therminol 66 in rats and to determine the effects of this heat-transfer fluid on liver and kidney microsomal drug-metabolizing enzymes. Therminol 66 was administered to male Sprague-Dawley rats at various doses as either a single oral administration at 0, 100, or 300 mg/kg, or as a single 6-h inhalation exposure at 0 or 350 mg/m3. Animals were killed 48 h after gavage or after termination of inhalation exposure. Additional groups of animals were exposed to Therminol 66 via the diet at 0, 100, 500, or 5000 ppm for 14 d, or via repeated inhalation exposure at 0, 25, 250, or 1200 mg/m3 for 6 h/d for 14 d. These exposure scenarios represent approximately equivalent doses of Therminol 66 by the different routes of administration. No change in body weight was observed after acute oral or inhalation exposure, and little change in body weight was observed in animals administered Therminol 66 via the diet except at the highest dose. There was no change in kidney weight, and liver weights were increased only at the higher doses of Therminol 66. The body weight gain of animals exposed to Therminol 66 via inhalation decreased in a dose-dependent manner over the 2-wk exposure period. Results from the disposition study indicated that Therminol 66 did not appear to accumulate in the tissues examined and did not appear to be extensively absorbed after a single oral dose of 300 mg/kg. The whole-body elimination half-life was approximately 14 h and occurred primarily via the feces. There was no significant induction of hepatic aryl hydrocarbon hydroxylase (AHH) activity after single oral or inhalation exposures to Therminol 66. Ethoxycoumarin O-deethylase (ECOD) was significantly induced only in animals exposed to 350 mg/m3 via inhalation. Repeated dietary and inhalation exposures resulted in AHH and ECOD induction only at the highest doses, and the kidney appeared to be less sensitive than the liver. Animals exposed via inhalation demonstrated a greater hepatic inductive effect than did animals exposed via the diet, which may be due to absorption differences.(ABSTRACT TRUNCATED AT 400 WORDS)

7-Alkoxycoumarin O-Dealkylase↗
PubMed1997

Residential exposure to plasticizers and its possible role in the pathogenesis of asthma.

The plasticizer di(2-ethylhexyl) phthalate (DEHP) is widely used in building materials. DEHP is identified as the major plasticizer exposure in dwellings. We provide evidence that inhalation exposure to DEHP as aerosols adsorbed to particulate matter is as important, or more important, than vapor phase exposure. The particulate inhalation exposure to DEHP is considered to be significant due to its low clearance and extensive penetration into the pulmonary region. DEHP is capable of creating high local concentrations in the airways at the deposition site with subsequent local effects. The proposed mechanism of effect states that mono(2-ethylhexyl) phthalate (MEHP), the primary hydrolysis product of DEHP, mimics the inducing prostaglandins (PG) PGD(2), 9alpha,11betaPGF2, and PGF2alpha, and thromboxanes in the lungs, thereby increasing the risk of inducing inflammation in the airways, which is a characteristic of asthma.

Aerosols↗
PubMed1992

Toxicity of 2-methyl-5,6-cyclopentapyrimidine (MCPP).

2-Methyl-5,6-cyclopentapyrimidine (MCPP, CAS No. 36274-29-0) is a white dusty solid with a powerful lingering odor and is formed as a by-product in the polymer synthesis of an experimental polymer. The acute toxicity following both oral and inhalation exposures and the effects of repeated inhalation exposures in rats were determined. Mutagenic activity was assessed using Salmonella as the indicator organism. The chemical is moderately toxic, with the lethal dose following a single oral administration being 90 mg kg-1. Doses greater than or equal to 130 mg kg-1 produced strong convulsions. Excessive salivation, hyperactivity and twitching were seen at 90 mg kg-1 and only mild initial weight loss was seen in surviving rats (less than or equal to 60 mg kg). Liver injury was produced at doses as low as 17 (but not at 12) mg kg-1. The material was highly toxic by inhalation, with the approximate lethal concentration in rats following single 4-h exposures being 9 ppm. Convulsive-like movements were seen at greater than or equal to 9 ppm (not at 2 ppm). Histological findings suggest that MCPP causes dilation of blood vessels with hyperemia of various organs apparent in rats exposed to 1 ppm and sacrificed 1 or 2 days post-exposure. No evidence of liver or central nervous system damage was seen. Repeated (nine daily 4-h exposures) inhalation of 2 ppm MCPP failed to produce any signs of a toxic response. No mutagenic activity was seen. The material needs to be considered as a potent acute toxin.

Administration, Inhalation↗
PubMed2003

Inhalant nitrite exposure alters mouse hepatic angiogenic gene expression.

Inhalant nitrites are drugs of abuse that have been shown to enhance tumor growth rate in mice and are epidemiologically linked to an increased risk of Kaposi's sarcoma. Because nitrites produce nitric oxide, we hypothesized that their toxicological effects might be partly mediated via regulation of angiogenic factors such as vascular endothelial growth factor (VEGF). Preliminary studies showed that isobutyl nitrite (ISBN) incubation stimulated VEGF protein expression in J774 macrophage cells. C57BL/6 mice exposed to ISBN in air exhibited significant up-regulation of VEGF protein and mRNA in the liver, but not in the lung. Liver mRNA expression of VEGF receptor 2 (VEGFR-2), VEGFR-3, Smad5, and Smad7 was also significantly altered. These results demonstrate that in vivo exposure to an inhalant nitrite results in altered tissue expression of VEGF and its receptors, suggesting that some of its toxicological effects may be mediated partly through a mechanism involving angiogenesis.

Administration, Inhalation↗
PubMed1999

Emission testing and inhalational exposure-based risk assessment for candles having Pb metal wick cores.

Segments of seven candles with wicks having a Pb metal core have been tested in a purpose-built combustion chamber to assess air Pb emissions. Emissions were collected on glass fibre filters that have been digested in concentrated HNO3 and analysed by flame atomic absorption spectroscopy (FAAS). Despite an indication of a bimodal distribution in Pb emission rates, and a range from 450 to 1130 micrograms Pb/h, the mean rate from the seven candles was 770 micrograms Pb/h. The 38-cm long candles are, on average, capable of emitting 104,000 micrograms of Pb into the air over approximately 127 h. A mean value of 20% of the Pb metal in the wick consumed by the candle is emitted into the air, the remainder appears to accumulate at the base of a molten wax-pool adjacent to the wick. Individual Pb-bearing particles from the combustion of candles were observed in a field emission scanning electron microscope (FESEM) to have a diameter of 1 micron or less. The emission from the candles has been analysed by X-ray diffraction (XRD) and identified as Sodium Lead Carbonate Hydroxide [NaPb2(CO3)2OH]. This compound, being a Pb carbonate, is likely to be easily absorbed in the lungs and gastrointestinal tract. Risks associated with inhalational exposure have been assessed after determining indoor lead in air (PbA) concentrations. Given a lack of information on the duration of use of candles, a range of scenarios from worst possible case to daily and weekly burning regimes are evaluated. Detailed evaluations of PbA are based on the emission from a single candle at rates of 500 and 1000 micrograms Pb/h, room volumes of 25 and 50 m3, durations of emission of 1.5, 3 and 6 h and air infiltration rates of 0, 0.25, 0.5, 0.75 and 1.0 air volume changes per hour (ACH). A candle burnt for 3 h at 1000 micrograms/h in a 50 m3 room having poor ventilation at 0.25 ACH is estimated to yield a 24-h average lead in air concentration of 9.9 micrograms/m3 with a peak PbA value of 42.1 micrograms/m3. Daily exposure to such candle burning where children spend 80% of their time indoors is likely to elevate PbB in children by a minimum of 24 to 40 micrograms/dl, according to the PbB:PbA relationship of Brunekreef, 1984 (The relationship between air lead and blood lead in children: a critical review). Estimating child Pb uptake from first principles using a range of exposure factors, a child would obtain some 85 to 127% of the provisional tolerable weekly Pb intake (PTWI) from such daily exposure. Child blood lead levels could readily exceed levels of 10 micrograms/dl, largely due to exposure to emissions from burning Pb wick core candles for several hours once per week. The regular burning of multiple candles in small, poorly ventilated spaces could readily be associated with clinical Pb poisonings and death. High levels of exposure could occur with Pb metal core wick candles in less developed countries where candles are used on a daily basis for indoor lighting purposes in small dwellings. Prolonged burning of candles may occur in religious and in ceremonial circumstances or restaurants where they may be of particular concern. On the basis of the limited investigation carried out, candles having a wick with a Pb metal core have the potential to present highly unacceptable and avoidable risks to human health.

Air Pollution, Indoor↗
PubMed1990

The head dome: a simplified method for human exposures to inhaled air pollutants.

Acute controlled exposures of human subjects to air pollutants are customarily carried out with whole-body chambers, masks, or mouthpieces. The use of these methods may be limited by cost or technical considerations. To permit a study involving a highly unstable pollutant, artificial acid fog, administered to subjects during natural breathing, a head-only exposure chamber, called a head dome, was developed. It consists of a transparent cylinder with a neck seal which fits over the subject's head and rests lightly on his shoulders. The head dome does not constrain the upper airways or impede exercise on a bicycle ergometer. Ventilation can be monitored accurately and unobtrusively with a pneumotachograph at the exhaust port of the dome. A thermocouple may be used to monitor the onset and persistence of oronasal breathing. For short-term exposures to unstable or reactive pollutants lasting up to several hours, the head dome is an effective alternative to a whole-body chamber and probably superior to a face mask or mouthpiece.

Air Pollutants↗
PubMed2002

IgG and IgE antibody responses following exposure of Brown Norway rats to trimellitic anhydride: comparison of inhalation and topical exposure.

A variety of chemicals can cause sensitisation of the respiratory tract and occupational asthma, including certain acid anhydrides, diisocyanates and reactive dyes. As yet, no well-validated methods are available for the toxicological evaluation of the respiratory sensitising potential of chemicals. One approach which has been explored recently is the evaluation of induced IgE responses or cytokine expression patterns in rats or mice following topical exposure to chemical. Thus, it has been demonstrated that topical exposure of rodents to respiratory sensitising chemicals, but not to contact allergens, causes a dose-dependent and time-related increase in the concentration of total IgE. Using the reference respiratory allergen trimellitic anhydride (TMA), we have considered here the influence of route of exposure on the nature of induced immune responses. Specific IgG and IgE antibody responses and changes in total serum concentration of IgE have been measured following exposure of Brown Norway (BN) starin rats to TMA by topical administration or by inhalation. Exposure to TMA by both routes resulted in the stimulation of specific IgG and IgE antibody, although responses were considerably more vigorous after dermal exposure. Topical treatment also provoked marked and sustained increases in total serum IgE levels, whereas exposure via the respiratory tract stimulated a more transient elevation of this immunoglobulin in a minority of animals which reached statistical significance only at the highest dose group. The lesser vigour of the immune response following inhalation exposure is likely to be related to the considerably lower total antigenic dose which is delivered by this route. Nevertheless, these results show that the nature of immune response with respect to antibody isotype profile provoked by topical administration of TMA is qualitatively comparable with that stimulated by inhalation exposure to the same chemical. For the purposes of hazard assessment and identification of potential chemical respiratory allergens as a function of induced changes in serum IgE concentration, however, the evidence is that topical administration of test material is the preferred route of exposure.

Administration, Inhalation↗
PubMedDate not supplied

Identification of agricultural tasks important to cumulative exposures to inhalable and respirable dust in California.

Little data exists on the determinants of agricultural dust exposure, particularly in dry climates. Annual exposure indices to inhalable and respirable dust were constructed by exposure estimates for specific tasks, task duration, and task frequency. The estimates of exposure levels were based on actual field measurements and subjective dust exposure ranking. The task duration and frequency data were obtained by questionnaire from 546 farm operators in California. Annual exposure indices were analyzed to determine which tasks were major contributors to chronic dust exposure. The important tasks were identified by comparisons of the cumulative distribution of exposures for all tasks and the cumulative distribution of exposures with one task deleted. Thirteen and 11 tasks were identified to be important to both inhalable and respirable dust exposures, respectively. Tasks identified to be important to agricultural exposure may be ascribed to exposure duration more than to exposure intensity. Information on task-specific exposure is important for developing control strategies in the agricultural workplace.

Adult↗
PubMed2000

Dermal absorption of N,N-dimethylacetamide in human volunteers.

OBJECTIVES: We investigated the potential for the dermal absorption of N,N-dimethylacetamide (DMAC: CAS No. 127-19-5) vapor, the biological half-life of N-methylacetamide (NMAC) in urine as the biological exposure item of DMAC, and the adjustment method for urinary concentrations. METHODS: Twelve healthy male volunteers (mean age 25.2 years, range 21-43 years) were exposed to DMAC for 4 h on two occasions at intervals of 96 h or above. Each volunteer sat inside a whole-body-type exposure chamber for the dermal exposure experiment or outside the chamber for the inhalation exposure experiment. The temperature and relative humidity in the chamber were controlled at approximately 26 degrees C and 40% in order to keep the skin (90% naked) of the volunteers dry. DMAC concentrations were 6.1 +/- 1.3 ppm for dermal exposure and 6.1 +/- 1.3 ppm for inhalation exposure. Urine samples were collected from 0 h through 36 h and at 48 h and 72 h after the exposure. Extrapolations from exposure concentrations for 4 h to 10 ppm for 8 h were performed. RESULTS: Mean dermal absorption was estimated to be 40.4% of the total DMAC uptake. The biological half-lives of urinary NMAC were 9.0 +/- 1.4 h and 5.6 +/- 1.3 h via skin and lung, respectively. Mean NMAC in urine just after 5 consecutive workdays (8 h/day) at 10 ppm DMAC exposure was assumed to be 33.7 mg/g x Cr (18.6-70.0 mg/g x Cr). Creatinine-adjusted NMAC concentration in urine for each volunteer within 12 h after the exposure was more closely correlated with the total excretion amount of NMAC up to 36 h than with urinary-volume-adjusted or specific-gravity-adjusted NMAC concentration in both the dermal and inhalation exposure experiments. CONCLUSIONS: DMAC vapor was significantly absorbed through the skin. Estimated NMAC values indicate that 20 mg/g x Cr NMAC seems to be appropriate as the biological exposure index.

Acetamides↗
PubMed1999

Measurement of HPRT mutations in splenic lymphocytes and haemoglobin adducts in erythrocytes of Lewis rats exposed to ethylene oxide.

Young adult male Lewis rats were exposed to ethylene oxide (EO) via single intraperitoneal (i.p.) injections (10-80 mg kg-1) or drinking water (4 weeks at concentrations of 2, 5, and 10 mM) or inhalation (50, 100 or 200 ppm for 4 weeks, 5 days week-1, 6 h day-1) to measure induction of HPRT mutations in lymphocytes from spleen by means of a cloning assay. N-ethyl-N-nitrosourea (ENU) and N-(2-hydroxyethyl)-N-nitrosourea (HOENU) were used as positive controls. Levels of N-(2-hydroxyethyl)valine (HOEtVal) adducts in haemoglobin (expressed in nmol g-1 globin) were measured to determine blood doses of EO (mmol kg-1 h, mM h). Blood doses were used as a common denominator for comparison of mutagenic effects of EO administered via the three routes. The mean HPRT mutant frequency (MF) of the historical control was 4.3 x 10(-6). Maximal mean MFs for ENU (100 mg kg-1) and HOENU (75 mg kg-1) were 243 x 10(-6) and 93 x 10(-6), respectively. In two independent experiments, EO injections led to a statistically significant dose-dependent induction of mutations, with a maximal increase in MF by 2.3-fold over the background. Administration of EO via drinking water gave statistically significant increases of MFs in two independent experiments. Effects were, at most, 2.5-fold above the concurrent control. Finally, inhalation exposure also caused a statistically significant maximal increase in MF by 1.4-fold over the background. Plotting of mutagenicity data (i.e., selected data pertaining to expression times where maximal mutagenic effects were found) for the three exposure routes against blood dose as common denominator indicated that, at equal blood doses, acute i.p. exposure led to higher observed MFs than drinking water treatment, which was more mutagenic than exposure via inhalation. In the injection experiments, there was evidence for a saturation of detoxification processes at the highest doses. This was not seen after subchronic administration of EO. The resulting HPRT mutagenicity data suggest that EO is a relatively weak mutagen in T-lymphocytes of rats following exposure(s) by i.p. injection, in drinking water or by inhalation.

Administration, Inhalation↗
PubMed2001

High-level, but not low-level, occupational exposure to inhaled anesthetics is associated with genotoxicity in the micronucleus assay.

UNLABELLED: To minimize the possible health risks posed by waste anesthetic gases, the National Institute of Occupational Safety and Health (NIOSH) recommends exposure limits. We investigated the genotoxicity of a previously established occupational exposure exceeding these limits (high-level exposure) and of one within these limits (low-level exposure). Genotoxicity was assessed by the formation of micronucleated lymphocytes in 25 anesthetists and anesthetic nurses of an Eastern European (High-Level Exposure Group) and a German (Low-Level Exposure Group) university hospital. Each exposed group was compared with a group of nonexposed personnel of the same hospital. Compared with its Control Group, there was an increased fraction of micronucleated lymphocytes per 1000 binucleated cells in the High-Level Exposure Group (median 14.0, range 9.0-26.7 vs median 11.3, range 3.2-19.4; P < 0.05) but not in the Low-Level Exposure Group (median 9.8, range 4.2-20.0 vs median 10.5, range 5.0-20.5). We conclude that a high-level exposure to inhaled anesthetics is associated with an increase in chromosome damage, and measures are recommended to decrease exposure levels. As evidenced by the formation of micronucleated lymphocytes, the threshold values recommended by NIOSH appear to be safe. IMPLICATIONS: A high level of occupational exposure to inhaled anesthetics is associated with genotoxicity (as defined by formation of micronucleated lymphocytes), whereas a low-level exposure (within National Institute of Occupational Safety and Health limits) is not.

Adult↗
PubMed1994

Evaluation of the humoral immune response of CD rats following a 2-week exposure to the pesticide carbaryl by the oral, dermal, or inhalation routes.

The objective of this study was to examine the immunotoxicological effects of the methyl-carbamate pesticide carbaryl via the oral, dermal, or inhalation routes. Male CD rats were exposed to carbaryl 5 d/wk for a 2-wk period. During nose-only inhalation exposures, rats received either 36, 137, or 335 mg/m3 carbaryl in acetone for 6 h. Air only and acetone/air controls were run concurrently. Orally exposed animals received either 1 ml corn oil or 10, 25, or 50 mg/kg carbaryl, while dermally exposed animals received either 2 ml acetone or 100, 500, or 1000 mg/kg carbaryl on their dorsal flank for 6 h. Four days prior to sacrifice, animals from all exposure groups were injected iv with 2 x 10(8) sheep red blood cells (SRBC). The primary immunoglobulin M (IgM) humoral immune response to SRBC was then assessed by measuring SRBC-specific antibody-forming cells (AFC) and levels of serum anti-SRBC IgM antibody, respectively, using the hemolytic plaque assay and an enzyme-linked immunosorbent assay. Individual body weights, spleen, thymus, and liver weights, spleen cell number, and red and white blood cell (RBC, WBC) counts were obtained for each animal. Following nose-only inhalation exposures, dose-dependent decreases in thymus weights, spleen cell number, AFC/spleen, AFC/10(6) splenocytes, and serum levels of SRBC-specific IgM antibody were observed. Significant decreases of 33, 57, and 22% in spleen cell number, AFC/spleen, and thymus weight, respectively, were found at the 335 mg/m3 exposure level. Animals exposed orally to 25 mg/kg carbaryl had a 34% decrease in WBC counts. A 34% decrease in WBC and a 13% increase in RBC counts were observed at the 50 mg/kg oral dose. Significant decreases in liver weights ranging from 11 to 13% were found at all oral exposure levels. Dermal exposure to carbaryl revealed no significant toxicological effects. Results indicate that humoral immune suppression was observed following inhalation, but not following oral or dermal exposures to carbaryl. Immunotoxicological studies evaluating pesticides need to consider relevant exposure routes and dosages for appropriate risk assessment procedures and exposure limits to be established.

Administration, Cutaneous↗
PubMed1994

An overview of animal models for assessing synthetic vitreous fibers (SVFs) safety.

Synthetic vitreous fibers (SVFs) are materials with many important commercial applications. The fibrous nature of the SVFs raises concerns about their potential human health hazards. However, sufficient epidemiological data do not exist to establish the hazardous nature of all SVFs. In addition, the cellular and molecular mechanisms underlying the induction of pulmonary lesions are only partially understood. Without sufficient evidence to associate fiber exposure and lung disease, animal bioassays have been used to identify specific hazardous fibers. These bioassays include inhalation exposures, intratracheal instillation, and intracavitary injection (intrapleural and intraperitoneal). Inhalation exposures of animals most closely represent the human experience, but these exposures are costly and time-consuming to conduct. Intratracheal and intracavitary administrations of fiber are alternatives to inhalation exposures; however, they do not represent human exposures and can give false positive results. The limitations of the noninhalation approaches must be considered when addressing the potential for a respirable fiber to induce human lung disease. In addition, when the results from inhalation exposures do not agree with the alternative animal assays, most weight should be given to the animal inhalation assays because of the limitations of the alternative approaches. To determine the safety of SVFs, both the inhalation and noninhalation approaches are suggested.

Air Pollutants, Occupational↗
PubMedDate not supplied

The impact of a change to inhalable occupational exposure limits: strontium chromate exposure in the U.S. Air Force.

The American Conference of Governmental Industrial Hygienists has announced its intention to replace all total particulate threshold limit values (TLVs) with size-selective TLVs. Because the U.S. Air Force has adopted the TLVs as its occupational exposure limits, the impact of this change is of interest, specifically for hexavalent chromium. This article reviews historical strontium chromate sampling data in the Air Force and the impact of its reinterpretation in comparison to an inhalable TLV. Based on the measured conversion factor between the 37-mm cassette and the IOM inhalable sampler, inhalable strontium chromate exposures will continue to exceed the TLV during all aircraft priming and most sanding procedures. In addition, inhalable exposures are expected to exceed 1000 times the TLV, greater than the highest currently assigned protection factor for airline respirators, during 25% of priming procedures. Without a change in the value of the current TLV time-weighted average of 0.5 microg/m(3), the Air Force will need to reduce strontium chromate levels, either by incorporating work practices that decrease worker productivity or considering a change to nonchromated primers.

Air Pollutants, Occupational↗
PubMed1996

Worker exposures to inhalable and total aerosol during nickel alloy production.

This paper describes a study that was carried out at a North American nickel alloy production facility to compare the levels of personal exposures to inhalable and total nickel-containing aerosols. It is part of a large body of work aimed at assessing the impact of introducing new personal sampling instrumentation with performance consistent with the latest criteria proposed by the International Standards Organization (ISO), the Comité Européen Normalisation (CEN) and the American Conference of Governmental Industrial Hygienists (ACGIH). Side-by-side sampling using the 37-mm filter holder (for total aerosol) and the so-called IOM inhalable aerosol sampler was conducted for the personal exposures of workers in a range of workplaces throughout the facility. The results showed that inhalable aerosol exposure levels-for both overall aerosol and for total nickel-were consistently and significantly higher than the corresponding total aerosol levels. Weighted least-squares linear regression yielded factors ranging from about 1.3 to 2.4 for overall dust and from about 1.5 to 3.5 for nickel. Inspection of the statistical distribution of the exposures for the whole plant suggested that it was log-normal.

Aerosols↗
PubMed1999

Correlation of urinary nickel excretion with observed 'total' and inhalable aerosol exposures of nickel refinery workers.

An investigation of the relationship between observed nickel aerosol exposures and urinary nickel excretion was undertaken at a Scandinavian nickel refinery. The goal of the study was to assess the impact of nickel aerosol speciation, the use of particle size-selective sampling instrumentation and adjustment of urinary levels for creatinine excretion on the usefulness of urinary nickel excretion as a marker for exposure. Urinary nickel measurements and paired 'total' and inhalable aerosol exposure measurements were collected each day for one week from refinery workers in four process areas. The mean observed urinary nickel concentration was 12 micrograms L-1 (11 micrograms of Ni per g of creatinine). The strongest relationships between urinary excretion and aerosol exposure were found when urinary nickel levels were adjusted for creatinine excretion and when exposure to only soluble forms of nickel aerosol was considered. No significant difference was observed between measures of 'total' and inhalable aerosol in the ability to predict urinary excretion patterns. In the light of these results, it is recommended that consideration be given to the chemical species distribution of nickel aerosol in the use of urinary nickel measurements as a screening tool for cancer risk in occupationally-exposed populations.

Adult↗
PubMed2006

Occupational exposure to inhalable wood dust in the member states of the European Union.

The aim of this study was to estimate occupational exposure to inhalable wood dust by country, industry, the level of exposure and type of wood dust in 25 member states of the European Union (EU-25) for the purposes of hazard control, exposure surveillance and assessment of health risks. National labour force statistics, a country questionnaire (in 15 member states, EU-15), a company survey (in Finland, France, Germany and Spain), exposure measurements (from Denmark, Finland, France, Germany, The Netherlands and the United Kingdom) and expert judgements were used to generate preliminary estimates of exposure to different types of wood dust. The estimates were generated according to industrial class (six wood industries, four other sectors) and level of exposure (five classes). These estimates were reviewed and finalized by national experts from 15 member states. Crude estimates were generated also for 10 new member states (EU-10). The basic data and final estimates were included in the WOODEX database. In 2000-2003, about 3.6 million workers (2.0% of the employed EU-25 population) were occupationally exposed to inhalable wood dust. Of those, construction employed 1.2 million exposed workers (33%), mostly construction carpenters. The numbers of exposed workers were 700,000 (20%) in the furniture industry, 300,000 (9%) in the manufacture of builders' carpentry, 200,000 (5%) in sawmilling, 150,000 (4%) in forestry and <100,000 in other wood industries. In addition, there were 700,000 exposed workers (20%) in miscellaneous industries employing carpenters, joiners and other woodworkers. The numbers of exposed workers varied by country ranging from <3,000 in Luxembourg and Malta to 700,000 in Germany. The highest exposure levels were estimated to occur in the construction sector and furniture industry. Due to limited exposure data there was considerable uncertainty in the estimates concerning construction woodworkers. About 560,000 workers (16% of the exposed) may be exposed to a level exceeding 5 mg m(-3). Mixed exposure to more than one species of wood and dust from wooden boards was very common, but reliable data on exposure to different species of wood could not be retrieved. This kind of assessment procedure integrating measurement data, company data, country-specific data and expert judgement could also serve as one model for the assessment of other occupational exposures.

Air Pollutants, Occupational↗
PubMed1989

Effects of adsorption of benzo[a]pyrene onto carbon black particles on levels of DNA adducts in lungs of rats exposed by inhalation.

Exposure of rodents to benzo[a]pyrene (BaP) associated with particles has previously been shown to result in increased retention of BaP and metabolites in lungs. To determine if DNA damage might be enhanced, DNA adducts were measured in lungs of F344 rats following inhalation of pure BaP aerosols or BaP absorbed on carbon black particles. Groups of rats were exposed nose only to filtered air, [14C]BaP (2 mg/m3), or [14C]BaP (2 mg/m3) adsorbed on carbon black (97 mg/m3) (BaP/CB) for 4 hr/day, 1 day/week, for 12 weeks. Groups of rats were terminated at 4, 8, 12, 16, 20, and 24 weeks after the beginning of the 12-week exposure period. Retention of total 14C in lungs was used as an indicator of total reactive metabolites. DNA isolated from lungs was analyzed for adducts using a 32P-postlabeling assay. Inhalation of BaP/CB resulted in 100-fold higher levels of 14C in lungs at the end of the 12-week exposure than did inhalation of pure BaP. The halftime for the decline in 14C levels was 34 +/- 3 weeks (mean +/- SE) for rats exposed to BaP/CB and 6 +/- 2 weeks for rats exposed to pure BaP. At the end of 12 weeks of exposure, DNA adducts in lungs of rats exposed to pure BaP ranged from 2-15 adducts per 10(9) bases (mean = 7, n = 4) and in rats exposed to pure BaP absorbed on carbon black ranged from 10-12 adducts per 10(9) bases (mean = 11, n = 4); DNA adducts in lungs of sham-exposed rats ranged from 0-2 adducts per 10(9) bases (mean = 1, n = 4). The halftimes for the decline in DNA adducts in lungs were 3 +/- 1 weeks (mean +/- SE) for the rats exposed to BaP/CB and 5 +/- 2 weeks for the rats exposed to BaP. One of the DNA adducts found following exposure to both BaP and BaP/CB was tentatively identified as the BaP diol epoxide deoxyguanosine (BPDE) adduct. Levels of both total and BPDE DNA adducts were significantly increased (p less than 0.05) in lungs of rats exposed to both BaP and BaP/CB compared to levels in lungs of sham-exposed rats. There were no significant differences in levels of DNA adducts in lungs of rats exposed to BaP or BaP/CB, although the pattern of adducts was different between the two exposure modes.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗