Measured removal rates of chrysotile asbestos fibers from air and comparison with theoretical estimates based on gravitational settling and dilution ventilation.

CONTEXT: Industrial hygiene assessments often focus on activity-based airborne asbestos concentration measurements, but few empirical data exist regarding the fiber removal rate from air after activities cease. OBJECTIVE: Grade 7T chrysotile indoor fiber settling (FS) rates were characterized using air sampling (NIOSH Method 7402). MATERIALS AND METHODS: Six replicate events were conducted in a 58 m(3) study chamber (ventilation 3.5 ACH), in which chrysotile-contaminated work clothing was manipulated for 15 min followed by 30 min of no activity. The fiber concentration decay constant and removal rate were characterized using an exponential decay model based on the measurements. RESULTS: Breathing zone airborne chrysotile concentrations decreased by 86% within 15-30 min after fiber disturbance, compared to concentrations during active disturbance (p < 0.05). Estimated mean time required for 99% of the phase contrast microscopy-equivalent (PCME) fibers to be removed from air was approximately 30 min (95% CI: 22-57 min). The observed effective FS velocity was 0.0034 m/s. This settling velocity was between 4.5-fold and 180-fold faster than predicted by two different particulate gravitational settling models. Additionally, PCME concentrations decreased approximately 2.5-fold faster than predicted due to air exchange alone (32 versus 79 min to 99% decrease in concentration). DISCUSSION: Other measurement studies have reported similar airborne fiber removal rates, supporting the finding that factors other than gravitational settling and dilution ventilation contribute measurably to PCM fiber removal from air (e.g. impaction, agglomeration). CONCLUSION: Overall, the scientific weight of evidence indicates that the time necessary for removal of 99% of fibers greater than 5 µm in length (with aspect ratios greater than 3:1) is approximately 20-80 min.

Evaluation of take-home exposure and risk associated with the handling of clothing contaminated with chrysotile asbestos.

The potential for para-occupational (or take-home) exposures from contaminated clothing has been recognized for the past 60 years. To better characterize the take-home asbestos exposure pathway, a study was performed to measure the relationship between airborne chrysotile concentrations in the workplace, the contamination of work clothing, and take-home exposures and risks. The study included air sampling during two activities: (1) contamination of work clothing by airborne chrysotile (i.e., loading the clothing), and (2) handling and shaking out of the clothes. The clothes were contaminated at three different target airborne chrysotile concentrations (0-0.1 fibers per cubic centimeter [f/cc], 1-2 f/cc, and 2-4 f/cc; two events each for 31-43 minutes; six events total). Arithmetic mean concentrations for the three target loading levels were 0.01 f/cc, 1.65 f/cc, and 2.84 f/cc (National Institute of Occupational Health and Safety [NIOSH] 7402). Following the loading events, six matched 30-minute clothes-handling and shake-out events were conducted, each including 15 minutes of active handling (15-minute means; 0.014-0.097 f/cc) and 15 additional minutes of no handling (30-minute means; 0.006-0.063 f/cc). Percentages of personal clothes-handling TWAs relative to clothes-loading TWAs were calculated for event pairs to characterize exposure potential during daily versus weekly clothes-handling activity. Airborne concentrations for the clothes handler were 0.2-1.4% (eight-hour TWA or daily ratio) and 0.03-0.27% (40-hour TWA or weekly ratio) of loading TWAs. Cumulative chrysotile doses for clothes handling at airborne concentrations tested were estimated to be consistent with lifetime cumulative chrysotile doses associated with ambient air exposure (range for take-home or ambient doses: 0.00044-0.105 f/cc year).

Airborne asbestos concentrations associated with heavy equipment brake removal.

Asbestos-containing brake linings were used in heavy-duty construction equipment such as tractors, backhoes, and bulldozers prior to the 1980s. While several published studies have evaluated exposures to mechanics during brake repair work, most have focused on automobiles and light trucks, not on heavy agricultural or construction vehicles. The purpose of this study is to characterize the airborne concentration of asbestos to workers and bystanders from brake wear debris during brake removal from 12 loader/backhoes and tractors manufactured between 1960 and 1980. Asbestos content in brake lining (average 20% chrysotile by polarized light microscopy) and brake wear debris [average 0.49% chrysotile by transmission electron microscopy (TEM)] was also quantified. Breathing zone samples on the lapel of mechanics (n = 44) and area samples at bystander (n = 34), remote (n = 22), and ambient (n = 12) locations were collected during 12 brake changes and analyzed using phase contrast microscopy (PCM) [National Institute for Occupational Safety and Health (NIOSH) 7400] and TEM (NIOSH 7402). In addition, the fiber distribution by size and morphology was evaluated according to the International Organization for Standardization method for asbestos. Applying the ratio of asbestos fibers:total fibers (including non-asbestos) as determined by TEM to the PCM results, the average airborne chrysotile concentrations (PCM equivalent) were 0.024 f/cc for the mechanic and 0.009 f/cc for persons standing 1.2-3.1 m from the activity during the period of exposure ( approximately 0.5 to 1 h). Considering the time involved in the activity, and assuming three brake jobs per shift, these results would convert to an average 8-h time-weighted average of 0.009 f/cc for a mechanic and 0.006 f/cc for a bystander. The results indicate that (i) the airborne concentrations for worker and bystander samples were significantly less than the current occupational exposure limit of 0.1 f/cc; (ii) approximately 2% of respirable fibers were >20 microm in length; and (iii) approximately 95% of chrysotile in the brake linings degraded in the friction process. The industrial hygiene data presented here should be useful for conducting retrospective and current exposure assessments of individuals, as well as hazard assessments of work activities that involve repairing and replacing asbestos-containing brakes in heavy construction equipment.

Beryllium and lung cancer: a weight of evidence evaluation of the toxicological and epidemiological literature.

The potential carcinogenicity of beryllium has been a topic of study since the mid-1940s. Since then, numerous scientific and regulatory bodies have assigned beryllium to various categories with respect to its carcinogenicity. Past epidemiologic and animal studies, however, have been marked with notable methodological shortcomings. Because it has been about 16 yr since IARC evaluated beryllium and approximately 50 relevant papers on the topic have been published since that time, we conducted a weight-of-evidence analysis of the historical as well as recent animal and human literature. We also assessed whether recently published studies improved upon methodological shortcomings or shed light upon uncertainties in prior studies. Thirty-three animal studies, principally designed to evaluate the cancer hazard or related mechanisms, and seventeen epidemiologic studies were considered in this assessment. Based on this analysis, the evidence for carcinogenicity of beryllium is not as clear as suggested by previous evaluations, because of the inadequacy of the available smoking history information, the lack of well-characterized historical occupational exposures and shortcomings in the animal studies. We concluded that the increase in potential risk of lung cancer was observed among those exposed to very high levels of beryllium and that beryllium's carcinogenic potential in humans at exposure levels that exist in modern industrial settings should be considered either inadequate or marginally suggestive.

Exposure to chrysotile asbestos associated with unpacking and repacking boxes of automobile brake pads and shoes.

Industrial hygiene surveys and epidemiologic studies of auto mechanics have shown that these workers are not at an increased risk of asbestos-related disease; however, concerns continue to be raised regarding asbestos exposure from asbestos-containing brakes. Handling new asbestos-containing brake components has recently been suggested as a potential source of asbestos exposure. A simulation study involving the unpacking and repacking of 105 boxes of brakes (for vehicles ca. 1946-80), including 62 boxes of brake pads and 43 boxes of brake shoes, was conducted to examine how this activity might contribute to both short-term and 8-h time-weighted average exposures to asbestos. Breathing zone samples on the lapel of a volunteer worker (n = 80) and area samples at bystander (e.g., 1.5 m from worker) (n = 56), remote area (n = 26) and ambient (n = 10) locations collected during the unpacking and repacking of boxes of asbestos-containing brakes were analyzed by phase contrast microscopy and transmission electron microscopy. Exposure to airborne asbestos was characterized for a variety of parameters including the number of boxes handled, brake type (i.e. pads versus shoes) and the distance from the activity (i.e. worker, bystander and remote area). This study also evaluated the fiber size and morphology distribution according to the International Organization for Standardization analytical method for asbestos. It was observed that (i) airborne asbestos concentrations increased with the number of boxes unpacked and repacked, (ii) handling boxes of brake pads resulted in higher worker asbestos exposures compared to handling boxes of brake shoes, (iii) cleanup and clothes-handling tasks produced less airborne asbestos than handling boxes of brakes and (iv) fiber size and morphology analysis showed that while the majority of fibers were free (e.g. not associated with a cluster or matrix), <30% were respirable and even fewer were of the size range (>20 microm length) considered to pose the greatest risk of asbestos-related disease. It was found that average airborne chrysotile concentrations (30 min) ranged from 0.086 to 0.368 and 0.021 to 0.126 f cc(-1) for a worker unpacking and repacking 4-20 boxes of brake pads and 4-20 boxes of brake shoes, respectively. Additionally, average airborne asbestos exposures (30 min) at bystander locations ranged from 0.004 to 0.035 and 0.002 to 0.011 f cc(-1) when 4-20 boxes of brake pads and 4-20 boxes of brake shoes were handled, respectively. These data show that a worker handling a relatively large number of boxes of brakes over short periods of time will not be exposed to airborne asbestos in excess of its historical or current short-term occupational exposure limits.

Identifying an apppropriate occupational exposure limit (OEL) for beryllium: data gaps and current research initiatives.

The occupational exposure limit of 2.0 microg/m3 for beryllium has been used in the workplace since the late 1940s. In particular, the adequacy of the American Conference of Governmental Industrial Hygienists (ACGIH) Threshold Limit Value (TLV) for beryllium has recently come into question. The symposium "Beryllium: Effect on Worker Health" was convened in September 1999, to bring together leading scientists to present and discuss current research activities on beryllium exposure and chronic beryllium disease (CBD). One of the key questions to be resolved at the symposium was, "Is there a sufficient understanding of exposure and the cause of CBD that would allow us to develop a TLV that we believe would prevent disease?" Seven scientists presented information regarding the current understanding of the disease, possible causes, and ongoing research. The topics were (1) biomonitoring approaches and their relationship with clinical effects, (2) historical and current exposure assessments, (3) sampling methods and aerosol characterization, and (4) epidemiology. Six basic hypotheses regarding the relationship between exposure to beryllium and CBD were generated from the information presented at the symposium. The six hypotheses that are related to issues such as beryllium form, particle size, industrial hygiene practices, extrapulmonary routes of exposure, and genetic susceptibility also appear to be the focus of ongoing and likely future research initiatives. This article summarizes both the presentations made at the meeting and the hypotheses generated. It is expected that an understanding of these issues should explain the inconsistent dose-response relationship observed between exposure and CBD. The ongoing and planned research is anticipated to provide sufficient data within two to three years to develop one or more scientifically sound TLVs for the different chemical forms of beryllium.

Is total mass or mass of alveolar-deposited airborne particles of beryllium a better predictor of the prevalence of disease? A preliminary study of a beryllium processing facility.

Cases of chronic beryllium disease (CBD) and beryllium (Be) sensitization continue to be identified among Be industry workers. The currently accepted method for measuring exposure, which involves measuring the total mass of airborne Be per cubic meter, shows an inconsistent dose-response relationship with the prevalence of CBD. This study was conducted to evaluate which Be aerosol characteristics other than total mass may be more informative in understanding the dose-response relationship between exposure to Be and disease. Personal (n = 53) and general (n = 55) area airborne Be samples were collected in five furnace areas at a Be manufacturing facility where prevalence rates of CBD and Be sensitization had been previously studied among 535 employees with significant Be exposure. In the five furnace areas, particle-size specific personal samples and area samples were collected using an Andersen impactor and a microorifice uniform deposit impactor (MOUDI), respectively. The calculated concentrations were expressed in terms of total mass per cubic meter, and in forms of mass, number, and surface area of particles less than 10 microm or less than 3.5 microm mass median aerodynamic diameter per cubic meter that are predicted to deposit in the alveolar region of the lung. Tests for linear trend of the relationships of the various exposure metrics to prevalence of CBD and sensitization demonstrated highly significant associations between mass concentration (MOUDI) of particles less than 10 microm, and less than 3.5 microm, predicted to deposit in the alveolar region of the lung and CBD (p = 0.0004 and 0.000003, respectively) and sensitization (p = 0.025 and 0.003, respectively). However, no statistically significant association was found between these two exposure metrics and personal (Andersen) samples. The number and surface area concentration (MOUDI) of alveolar-deposited particles (less than 10 microm) also showed significant relationships with CBD (p = 0.03 and 0.03, respectively). No other exposure parameters showed significant relationships with CBD or Be sensitization. These results suggest that the concentration of alveolar-deposited particles less than 10 microm or, more particularly, the concentration of alveolar-deposited particles less than 3.5 microm may be a more relevant exposure metric for predicting the incidence of CBD or sensitization than the total mass concentration of airborne Be.

A comparison and critique of historical and current exposure assessment methods for beryllium: implications for evaluating risk of chronic beryllium disease.

The primary beryllium industry has generated a large amount of data on airborne beryllium concentrations that has been used to characterize exposure by task-specific activities, job category, individual worker, and processing area using a variety of methods. These methods have included high-volume breathing zone sampling, high-volume process sampling, high- and low-volume respirable and area sampling, real-time monitoring, and personal sampling. Many of the beryllium studies have used these air sampling methods to assess inhalation exposure and chronic beryllium disease (CBD) risk to beryllium; however, available data do not show a consistent dose-response relationship between airborne concentrations of beryllium and the incidence of CBD. In this article, we describe the air sampling and exposure assessment methods that have been used, review the studies that have estimated worker exposures, discuss the uncertainties associated with the level of beryllium for which these studies have reported an increased risk of CBD, and identify future investigative exposure assessment strategies. Our evaluation indicated that studies of beryllium workers are often not directly comparable because they (1) used a variety of exposure assessment methods that are not necessarily representative of individual worker exposures, (2) rarely considered respirator use, and (3) have not evaluated changes in work practices. It appears that the current exposure metric for beryllium, total beryllium mass, may not be an appropriate measurement to predict the risk of CBD. Other exposure metrics such as mass of respirable particles, chemical form, and particle surface chemistry may be more related to the prevalence of CBD than total mass of airborne beryllium mass. In addition, assessing beryllium exposure by all routes of exposure (e.g., inhalation, dermal uptake, and ingestion) rather than only inhalation exposure in future studies may prove useful.

Alteration in lung particle translocation, macrophage function, and microfilament arrangement in monocrotaline-treated rats.

Individuals with preexisting cardiopulmonary disease are thought to be more susceptible to acute episodes of particulate pollution resulting in increased morbidity and mortality. Our study was designed to evaluate particle fate and macrophage function in an animal model of monocrotaline (MCT)-induced pulmonary hypertension. Two weeks following a single MCT injection, Sprague-Dawley rats were exposed sequentially to two different colored fluorescent microspheres 1.0 micron in diameter by aerosolization. Morphometric evaluation of lung sections was performed 0 and 24 h following the final particle exposure to determine the intrapulmonary location of inhaled microspheres. A decrease in the number of particles phagocytized by alveolar macrophages and an increase of free particles overlying the epithelium were found in MCT-treated animals compared with control. Pulmonary macrophages recovered by bronchoalveolar lavage were evaluated for chemotactic and phagocytic ability. Macrophage chemotaxis was significantly impaired following MCT treatment compared with controls, whereas phagocytic activity of macrophages lavaged from MCT and control treatment groups was similar. Macrophages were stained for filamentous (F) and globular (G) actin using Texas-Red-labeled phalloidin and Oregon-green-labeled DNase I, respectively. The area of microfilament staining for F and G actin increased, but the ratio of F/G actin was significantly decreased in animals with MCT treatment compared with control. While the responses observed with MCT treatment, such as pulmonary edema, polymorphonuclear leukocytes influx, and unique macrophage morphology may contribute to impaired macrophage function, the change in microfilament arrangement suggests that MCT may inhibit macrophage chemotaxis and impair particle clearance from the lungs.

Lung parenchyma and type II cell morphometrics: effect of surfactant treatment on preterm ventilated lamb lungs.

The effect of exogenous surfactant treatment on lung and type II cell structure of ventilated lambs of 137-138 days gestational age was studied. Thirty-four lambs were delivered and randomized to control or 100 mg/kg of natural sheep surfactant treatment groups. Lungs from one group of lambs not treated with surfactant were fixed before ventilation, and the other animals were ventilated to maintain normal blood gas values for 3, 24, or 48 h. Morphometric assessment of the inflation-fixed lung parenchyma of ventilated lungs was compared with the architectural appearance of alveoli and alveolar ducts in the unventilated lungs. Mechanical ventilation resulted in distension of alveolar ducts accompanied by the shallowing and loss of well-defined alveoli and areas of atelectasis at 3 h. These abnormalities increased in severity after 24 and 48 h of ventilation. Surfactant treatment before ventilation significantly reduced the extent and degree of dilatation and concomitant atelectasis. The fraction of normal parenchyma was 38 +/- 7% in untreated lambs vs. 64 +/- 6% in treated lambs after 24 h of ventilation. After 48 h of ventilation, significant differences between control (39 +/- 6%) and surfactant-treated (55 +/- 6%) lambs were still evident. Alveolar type II cells contained approximately 15% lamellar bodies by volume. Neither surfactant treatment nor time of ventilation altered the volume density of lamellar bodies or other organelles, except for a decrease in glycogen from 8% in nonventilated lungs to 2.5% in lungs ventilated for 24 h. These findings indicate that a surfactant treatment at birth results in the maintenance of more normal parenchyma with less atelectasis during prolonged ventilation of the immature lung.(ABSTRACT TRUNCATED AT 250 WORDS)