Borak, Jonathan MD; Sirianni, Greg MS; Cohen, Howard PhD; Chemerynski, Susan BA; Jongeneelen, Frans PhD
Coal-derived creosote, a brownish-black oily liquid used as a wood preservative, is a distillation product of coal tars, which themselves are by-products of the high-temperature destructive distillation of bituminous coal to form coke. Creosote is a mixture of hundreds of distinct compounds, including polycyclic aromatic hydrocarbons (PAHs), phenols, heterocyclic oxygen, sulfur and nitrogen compounds, and simpler aromatic hydrocarbons. 1–3 A 1992 study found nearly 200 different PAH components in a sample of coal tar pitch. 4 There is also much component variation between creosote samples, although PAHs generally contribute at least 75% by weight. The components with the largest volume are naphthalene and its alkyl and hydroxyl congeners, which are also among the most volatile and therefore comprise even greater proportions of volatilized creosote.
The monitoring and control of occupational creosote exposures have been long-standing concerns among occupational physicians and industrial hygienists because of the recognized associations between creosote, coal tar, and cancer. 5,6 This has proved challenging for several reasons. There is no consensus about the best method for performing air monitoring: the Occupational Safety and Health Administration (OSHA) and the National Institutes for Occupational Safety and Health (NIOSH), for example, have recommended different methods yielding non-comparable results. 7–9 Also, because the compositions of various creosote samples differ and only a few of the components are carcinogenic, the most appropriate exposure metric has not been determined. Finally, most worksite programs monitor airborne exposure, but evidence indicates that dermal exposure to creosote is quantitatively more important than inhalation. 10,11
Historically, industrial hygiene monitoring of creosote workers has been conducted by measuring the quantity of solvent-extractable material found in airborne particulates collected on glass fiber filters in personal samplers. 12,13 Exposed filters are rinsed in benzene (or another appropriate solvent) to extract target material, samples are left to dry by allowing the solvent to evaporate, and the resulting residue is measured by gravimetric analysis. The results are referred to as benzene soluble fraction (BSF) or coal tar pitch volatiles (CTPV). Unfortunately, the tendency to regard BSF and CTPV as interchangeable terms is misleading, because BSF may contain a variety of compounds that are soluble in benzene but are not normally found in coal tar. 9 For example, petroleum oils and lubricants, hydrocarbon solvents, motor vehicle exhaust, and tobacco smoke can all contribute to BSF. The traditional BSF method does not identify the constituents of the measured fraction.
As a modification of this method, the solvent-extracted material is redissolved in an appropriate solvent for chromatographic analysis of its constituents, particularly the PAHs. This step allows discrimination between those BSF components that are actually derived from coal tar and those that are not, thereby identifying and eliminating positive interferences. The current OSHA analytical method for monitoring CTPV (Method #58) directs that “If the BSF exceeds the appropriate Permissible Exposure Limit, then the sample is analyzed by high performance liquid chromatography…to determine the presence of selected PAHs.”9
An alternative method for monitoring creosote workers uses sampling trains consisting of a Teflon filter followed by a resin-filled sorbent tube. The filters collect particulates and the sorbent collects vapors and gases. Filters and sorbent are bathed in solvent to extract BSF from filters and desorb organic volatiles from sorbent. Then, the sample components are identified and measured by high-performance liquid chromatography (HPLC). 7,8,13 Most often, 10 to 16 specific PAHs are individually measured and then summed to estimate total PAHs in the sample.
These monitoring refinements allow more specific and accurate measures of airborne exposures, but they do not address concerns about dermal exposure. Dermal uptake of creosote seems unrelated to air levels. In one study, creosote workers wore absorbent “whole-body dosimeters” under their work clothes and carried personal air samplers. 11 Dosimeter levels, analyzed for PAH content by chromatography, were unrelated to air levels of BSF and 11 individual PAHs. A second set of studies compared urine 1-hydroxypyrene (1-OHP) levels, a widely adopted biological marker of PAH exposure, 14,15 in creosote workers with differing skin exposures. 10,16 The use of protective coveralls and avoidance of contamination of skin and clothing were more important than air levels in determining the absorbed dose, and variations in 1-OHP levels seemed to be predicted by visible contamination on workers’ skin, gloves, and overalls. 10
This study was conducted to further characterize the relationship between inhalation and dermal exposures to creosote and urinary levels of 1-OHP in creosote-exposed wood treatment workers. The specific objectives were to compare simultaneous measurements of BSF and individual PAHs (as particulates and gases), to relate those measures of airborne exposure to total uptake as reflected by 1-OHP, and to evaluate the predictive value of job descriptions and visual inspection of work practices as predictors of creosote uptake.
Subjects and Study Design
The study was conducted in an impregnation plant where railroad ties were heat- and pressure-treated with creosote. A total of 34 plant employees, comprising all company personnel working at the plant on the days of the survey, were evaluated and monitored. A team of industrial hygienists conducted the monitoring campaign. Each worker completed a questionnaire and a short, scripted interview with a trained interviewer regarding job description work activities, diet, and smoking habits. The workers then each wore personal sampler trains (described subsequently) for the duration of their next full work shifts, the fourth day of a 5-day workweek. Because the mean half-time for urinary excretion of 1-OHP in exposed workers is about 12 to 18 hours, sampling near the end of the workweek is preferable. 15
For day-shift workers, spot urine samples were collected at the end of the monitored shift (post-shift urine) and at the beginning of the next shift (next-shift urine); about 12 to 16 hours elapsed between the urine collections. For night-shift workers, spot urine samples were collected at the start of the monitored shift (pre-shift urine) and at the end of the monitored shift (post-shift urine). In addition, two security guards assigned to, but not employed by, the plant completed questionnaires and interviews and then provided post-shift urine samples; they were not otherwise evaluated.
Based on information obtained by questionnaire and interview and by field observations in the workplace, three industrial hygienists each independently assigned workers to one of three exposure categories: low, moderate, and high. The low-exposure group included secretarial/clerical staff and others who did not work in the immediate area where creosote was used. The moderate-exposure group included those who worked in the area of creosote use but spent little or no time in the area where creosote impregnation was performed (the “retort” building). An example is a worker who transports cured ties to the shipment yard where creosote-covered ties were banded for shipment. The high-exposure group included workers who spent significant time in the retort building, who handled ties after application of creosote, or whose skin, gloves, or clothing were specifically noted to be contaminated. There was agreement on all of the category assignments. Depending on the tasks they performed on a given day, specific workers were required to wash and shower, using a skin cleanser formulated for removal of PAHs (KC Products, Portland, OR) at the end of that workshift. Such washing was required for 8 of the 36 workers included in this survey.
Analysis of Air Samples
Thirty-four workers were monitored for a full shift (approximately 8 hours). Prior to the shift, each worker was equipped with a personal air-sampling pump (PCXR-4 and AirChek 52, SKC, Eight Four, PA) calibrated at 2.0 L/min. Air was collected on closed-faced cassettes containing a 37-mm polytetrafluoroethylene 2-μm filter connected in a series with a ORBO 43 sorbent tube (Supelco, Bellefonte, PA). Samplers were placed in the breathing zone of each worker. Air sampling pumps were calibrated before and after monitoring and were inspected throughout the day to ensure proper operation. Only one pump needed to be exchanged during the shift (because of pump failure); a complete sample was received for this worker. Both the cassette and sorbent tube were wrapped in aluminum foil during sampling to eliminate sample degradation caused by ultraviolet light.
After sampling, the polytetrafluoroethylene filters and ORBO tubes were wrapped individually in aluminum foil, and sample pairs were placed into individual plastic sealed bags and stored in a refrigerator overnight. The following morning, the samples were placed in a light-opaque transport cooler, which contained iced freezer packs to keep the samples cold, and then shipped to an American Industrial Hygiene Association-accredited laboratory for analysis. On arrival, samples were stored in a freezer until analysis, which was conducted within 7 days.
The samples were analyzed according to methods published by OSHA 9 and NIOSH. 8 Particulate deposited on the polytetrafluoroethylene filters was extracted using benzene, which was then evaporated to dryness, and the resulting extract was weighed to determine the benzene soluble fraction (BSF). The extract was then redissolved in 5 mL of acetonitrile using an ultrasonic bath and was analyzed for 16 PAHs by reverse-phase HPLC with ultraviolet detection. Sorbent tubes were treated in a similar fashion, using benzene extraction followed by evaporation and dissolution of the resulting extract in acetonitrile for analysis of 16 component PAHs by HPLC.
Analysis of Urine Samples
Following collection, urine specimens were labeled, placed in light-opaque containers, frozen, and shipped on dry ice to the laboratory (ABL Laboratories, Assen, Netherlands) for 1-OHP analyses according to the method of Jongeneelen. 17 Samples were stored in a freezer until analysis, which was conducted within 7 days. For purposes of quality assurance and control, ABL has participated since 1966 in the German DFG program of round-robin proficiency testing for urinary 1-OHP. Thawed samples were adjusted to pH 5.0 with 1 M hydrochloric acid, an equal volume of 0.1 M sodium acetate buffer (pH 5.0) was added, and the samples were incubated with beta-glucoronidase and aryl sulfatase in a water bath at 37°C for 16 hours to achieve enzymatic hydrolysis of the 1-OHP. After cooling, the hydrolysate was passed through a Bond-Elut C-18 cartridge, rinsed with 5 mL of water, and then eluted twice with 5 mL of methanol. The elutant was then evaporated until dry and the extract was combined with 1 mL of methanol.
The samples were analyzed for 1-OHP with a high-performance inverse-phase liquid chromatograph equipped with a C18 5-μm Nucleosil column, with dimensions of 150 × 4.6 mm. It was coupled with a fluorometric detector, with wavelengths set at 242 and 388 nm. Fifty μL of the methanol extract was injected into the column and eluted by a mobile phase of 60% acetonitrile and 40% demineralized water. The detection limit was 0.4 nmol/L.
Urinary creatinine levels were determined by means of Jaffés test. 18 The creatinine value was used to correct for variations in urine dilution and to convert the urinary 1-OHP measurements as μg 1-OHP per g creatinine.
Aliquots of pre-shift or next-day urine samples were transferred to clear plastic sample bottles, sealed and labeled, and shipped to National Medical Services (Willow Grove, PA) for determination of urinary cotinine, a key metabolite of nicotine and a biomarker of exposure to tobacco smoke. Phosphate-buffered samples were extracted by a solid phase technique, analytes were eluted in a solvent mixture containing methylene chloride, isopropanol, and ammonium hydroxide, and the extract was analyzed by capillary gas chromatography with nitrogen-selective detection.
The 34 plant employees included 6 women and 28 men who ranged in age from 29 to 58 years. On the basis of job descriptions and field observations, they were divided into high-, moderate-, and low-exposure categories. The low-exposure group consisted of 18 workers, the moderate-exposure group was comprised of 13 workers, and the high-exposure group included 3 workers. The two security guards were categorized as low-exposure.
The benzene soluble fraction (BSF) content of 34 personal airborne particulate samples was measured gravimetrically; 14 (41.2%) were below analytical limits of quantitation (<0.022 to 0.031 mg/m3). Three of the 34 samples (8.9%) had BSF values greater than 0.100 mg/m3, with one exceeding the OSHA permissible exposure limit of 0.200 mg/m3. However, levels of the 16 PAHs measured by HPLC in those three particulate samples were all below quantitation limits (limit of quantitation <0.1 to 0.041 μg/m3), thus indicating that the gravimetrically measured BSF levels reflected mainly interferences rather than coal tar-related material.
Analysis by HPLC of the 34 particulate samples found that only six contained detectable levels of PAHs. Detectable levels of pyrene, fluoranthene, and phenanthrene were found in four samples, including those from the three high-exposure workers. Another two workers had detectable levels of phenanthrene but none of the other 15 PAHs. When quantifiable, such PAH levels were relatively low. The highest of the measured pyrene levels (0.33 μg/m3) was only 3.7% of the OSHA Method #58 Target Concentration of 9.0 μg/m3 for pyrene, whereas the highest phenanthrene level (0.60 μg/m3) was only 6.7% of its Target Concentration. 9 The Target Concentration is a technical benchmark set as the “preliminary estimate of airborne concentration of the contaminant of interest relative to the purpose of the testing”19
At least some PAHs were detectable in 32 of 34 sorbent tube samples, but the levels detected were generally very low. Most frequently detected were naphthalene, pyrene, fluorene, phenanthrene, and anthracene. By contrast, benzo(a)pyrene was not detectable in any sample. The highest naphthalene levels (210 to 330 μg/m3) were measured in samples from the high-exposure workers, but those levels were less than 1% of the OSHA permissible exposure limit (10 ppm, equivalent to 52,400 μg/m3 at 25°C). 20 Similarly, the highest sorbent tube levels of pyrene (1.5 to 2.5 μg/m3) were obtained from the same workers who had the highest naphthalene levels. Those pyrene levels were significantly below the corresponding OSHA Method #58 Target Concentration of 9.00 μg/m. 3,9 Even when pyrene levels from particulate and volatile fractions were summed, the highest resulting level for any worker (2.73 μg/m3) was only 30% of the OSHA Target Concentration.
No relationship was seen between particulate BSF levels and levels of sorbent tube PAHs from the same personal samplers. This is demonstrated in Fig. 1, which compares particulate BSF and sorbent pyrene levels from those samplers for which both were quantifiable. The negative slope and very poor correlation (r2 = 0.048) on regression analysis indicate the absence of a meaningful relationship between the two exposure measures.
There was also no apparent relationship between particulate BSF levels and predicted worker exposure categories. Figure 2 shows BSF levels aggregated by exposure group. Both visual inspection and statistical analysis by Aspin-Welch T-Test revealed no differences between the groups (P > 0.05).
On the other hand, statistically significant associations were found between exposure groups and sorbent tube PAH levels. That is shown in Fig. 3 for four PAHs. In each case, sorbent PAH levels increased significantly across groups, from low- to moderate- to high-exposure. For the low-exposure group, sorbent PAH levels were mostly below limits of quantitation (limit of quantitation <0.1 to 0.041 μg/m3).
Levels of 1-OHP and creatinine were measured in 68 urine samples from 36 workers. Post-shift and next-day urine samples were analyzed for each of 29 day-shift workers, whereas pre- and post-shift urine samples were analyzed for each of the three night-shift workers. In four cases, only a single urine specimen was analyzed: two workers provided post-shift urine samples but were unexpectedly absent the following day, and two security guards each provided only post-shift urine samples. There were also two post-shift samples for which 1-OHP levels were reported, but urinary creatinine concentrations could not be measured.
The distribution of 1-OHP levels is shown in Table 1. Values ranged from <0.1 to 63 μg/g creatinine. The two samples for which creatinine levels were unavailable contained 1-OHP levels of 249 and 458 nmol/L, among the four highest levels reported in this study. Although those two values cannot be specifically corrected for urinary creatinine, it is almost certain that they would have exceeded 20 μg/g creatinine. Accordingly, they were included in the group with 1-OHP levels >20 μg/g.
Among the workers for whom two urine samples were obtained, there was high correlation between their two 1-OHP measurements. For the 30 sets of urine results that could be compared in terms of μg/g creatinine, regression analysis revealed almost complete correlation (r2 = 0.99). Correlation was slightly lower when the 32 sets of urine results were compared without correction for creatinine (r2 = 0.87). Of interest was the differing relationship between post-shift and next-day urine values for workers who had showered after work as compared with those who had not. The slope of the regression line for the shower group workers was >1 (m = 1.03), whereas that for the no shower group was <1.0 (m = 0.92). This implies that during the post-shift period, absorbed doses decreased in those who showered but increased in the no shower group. Unfortunately, the small number of workers in the shower group limits the ability to test the statistical significance of this difference.
There was no apparent relationship between particulate BSF levels and post-shift urinary 1-OHP levels, as demonstrated in Fig. 4. The negative slope and very poor correlation (r2 = 0.051) on regression analysis indicate the absence of a meaningful relationship between those two exposure measures. Comparable results were obtained when uncorrected 1-OHP levels were regressed against BSF, a comparison that allowed the inclusion of the two workers with missing creatinine levels (data not shown).
A small but statistically significant association (r2 = 0.35) was found between urinary 1-OHP and sorbent tube pyrene levels for the 28 workers with quantifiable sorbent pyrene levels and both post-shift 1-OHP and creatinine levels. That association was largely determined by two outliers: the worker with the highest urinary 1-OHP and the worker with the highest sorbent pyrene level. When those two workers were excluded, the correlation nearly disappeared (r2 = 0.013).
In contrast to the low correlations between post-shift 1-OHP and air exposure measures, significant associations were found between exposure groups and post-shift 1-OHP levels. As shown in Fig. 5, urinary 1-OHP increased across exposure groups from low to moderate to high. That increase across groups demonstrated a significant linear trend (Pearson product moment coefficient of correlation [r]= 0.65, Cronbach’s alpha = 0.79), and the high-exposure group was significantly greater than the two other groups (Aspin-Welch T-Test, P < 0.05 and P < 0.01, respectively).
Diet and Smoking
The diet and smoking habits of workers were assessed by means of a questionnaire and urinary cotinine determination. At the time of each sample collection, workers were asked the number of servings of grilled or smoked meat or fish that they had eaten during the prior 24 and 72 hours. Seventeen of 36 workers denied consumption of grilled or smoked foods, whereas 19 had eaten between one and five servings in the 72 hours before sampling. Thirty-four of the 36 workers provided urine samples for cotinine analysis. Fourteen admitted smoking, whereas the other 20 denied both smoking and oral tobacco use. All of the smokers had positive urine cotinine levels (630 to >2000 ng/mL) consistent with their histories. Only one of those who denied smoking had a positive urine cotinine level, ie, >2000 ng/mL, which was almost certainly evidence of active smoking, and for analytical purposes he was classified as a smoker.
Levels of 1-OHP did not differ significantly between those who did and did not eat grilled foods, and the number of grilled servings was unrelated to urinary 1-OHP (P > 0.05, data not shown). Likewise, 1-OHP levels did not differ significantly between smokers and non-smokers or between groups of workers categorized by urine cotinine (non-detectable, 630 to 2000 ng/mL, and >2000 ng/mL) (P > 0.05, data not shown).
This study was conducted to characterize the relationship between inhalation and dermal exposures in creosote-exposed wood treatment workers. Full-shift breathing zone air samples were collected and analyzed for benzene soluble fraction (BSF) and 16 individual PAHs in both the particulate fraction and gaseous fraction of sampled air. Those exposure measures were compared with urinary 1-OHP levels in post-shift urine samples and, for most workers, in next-day urine samples. Urine 1-OHP has been shown to be a useful and widely used biological indicator of exposure to PAHs. 10,15,21–25
This study indicates the very limited value of air sampling to monitor and control occupational exposure in creosote workers. Gravimetrically measured BSF, the traditional approach for industrial hygiene monitoring of coal tar-exposed workers and the analytical basis for the current OSHA permissible exposure limit, was the least useful. Although 3 of 34 particulate samples had BSF levels >50% of the current permissible exposure limit (200 μg/m3), none of those three had HPLC-detectable levels of the 16 PAHs. In total, only 6 of 34 particulate samples contained quantifiable, albeit very low, levels of PAHs. Thus, the BSF measure mainly reflects positive interferences rather than coal tar. Accordingly, BSF does not seem appropriate for monitoring creosote exposure. That impression is supported by observations that BSF was unrelated to post-shift urinary 1-OHP, sorbent tube PAH levels, and worker exposure categories.
Determination of volatilized PAHs in the breathing zone was more useful for assessing exposure. Statistically significant associations were found between exposure groups and sorbent tube PAH levels, and a small but significant correlation was found between sorbent pyrene levels and post-shift 1-OHP. However, the levels of gaseous PAHs were very low, in most cases below quantitation limits (<0.022 to 0.031 mg/m3). For example, levels of benzo(a)pyrene, a carcinogenic PAH that is the basis of the German TRK for coal tar and coke oven exposures, 26 were below levels of quantitation (<0.18 to 0.22 μg/m3) in all samples. From these data, it is hard to conclude that the workers were exposed to biologically meaningful levels of coal tar pitch volatiles.
In contrast, urinary 1-OHP measurements gave strong evidence that some of these workers had been exposed to coal tar material and that systemic absorption had occurred. As summarized in Table 1, seven urine samples from four of the workers had 1-OHP levels >10 μg/g creatinine. Although there is no specific benchmark level for assessing exposure in creosote workers, these levels exceed the benchmark levels recommended for workers occupationally exposed in the coke oven and primary aluminum industries. 14 In the present study, 1-OHP levels could not be explained by dietary or smoking differences; therefore, they were likely due to workplace exposures.
Such evidence from urine analyses of exposure and systemic absorption, coupled with the apparent lack of evidence for significant inhalation exposure, suggests that workers were mainly exposed by the dermal route. These findings are consistent with those of other creosote studies that demonstrated peak 1-OHP excretion hours after the shift, with next-morning samples often higher than post-shift samples: “a phenomenon more or less explained by the apparent dermal absorption continuing even after working hours.”10
The importance of dermal exposure can also be shown by estimating the magnitude of absorbed doses attributable to dermal versus inhalation exposure. The following simplified toxicokinetic model relates the quantity of 1-OHP excreted in urine to the quantity of pyrene absorbed from the lungs. 10,27,28 The model deliberately overestimates uptake from the lungs, thus ensuring that estimates of dermal uptake are conservative.
* Assume that 100% of inhaled pyrene is absorbed from the lungs, that 50% is metabolized to 1-OHP, 29 and that 10% of the resulting 1-OHP is excreted in the urine. 30,31
* Assume that the average creosote worker breathes 10 m3 of air per 8-hour shift and excretes 2 L of urine and 2 g of creatinine per 24 hours.
* Then, the quantity of urinary 1-OHP attributable to inhalation (QI) can be estimated from the inhaled pyrene concentration (PI) according to the following equation: MATH
In this study, the four highest inhaled pyrene concentrations ranged from 1.72 to 2.73 μg/m3 (calculated as the sum of particulate plus sorbent pyrene levels). When those inhaled pyrene values are substituted for PI in the equation, the equation predicts that urinary 1-OHP levels will range from 0.48 to 0.6825 μg/g. Those predicted values are less than 1% of the highest 1-OHP level actually measured and less than 5% to 10% of the nine highest levels. Most of the workers had inhaled pyrene levels that were much lower and would have predicted essentially undetectable urine levels of 1-OHP. Thus, it is likely that more than 90% to 99% of measured 1-OHP excretion derived from dermal uptake rather than inhalation. This conclusion is consistent with findings in earlier studies of workers exposed to creosote 10,16 and other forms of coal tar. 27,28
These results have several important implications. First, traditional approaches to the industrial hygiene monitoring of creosote workers seem inappropriate and inadequate. As described by the American Conference of Governmental Industrial Hygienists, adoption of a threshold limit value based on the BSF of coal tar pitch was a “practical compromise” made “in the absence of more definitive information.”12 In this study, BSF was unrelated to measures of both internal exposure (ie, urinary 1-OHP) and external exposure (ie, volatile PAHs). Moreover, gravimetrically determined BSF mainly reflected positive interferences rather than coal tar pitch. Accordingly, the concepts of BSF and coal tar pitch volatiles must be clearly differentiated, and more effective methods must be found to monitor creosote workers.
An example of such a more effective method may be the measurement of specific volatilized PAHs in workplace air. This study found a weak association between urinary 1-OHP and sorbent tube pyrene levels. Likewise, a significant association was found between sorbent tube PAH levels and exposure groups. Such findings indicate that gaseous coal tar components, rather than particulates, are better indicators of workers’ exposure to creosote. However, there are limitations to this method. As inhalation accounts for only a small proportion of the absorbed dose, inhalation exposure measures can predict only a small proportion of the internal dose. There are also few benchmarks by which to evaluate such measures. For example, the OSHA Method #58 Target Concentrations 9 are based on analytical constraints rather than health-based endpoints. Likewise, documentation for NIOSH Method #5800 (“Total Polycyclic Aromatic Compounds”) contains no comparative reference levels, 7 and that for NIOSH Method #5506 (“Polynuclear Aromatic Hydrocarbons by HPLC”) refers to OSHA permissible exposure limits for coal tar pitch volatiles and naphthalene. 7 Without exposure limits or benchmarks, such as the German TRK for benzo(a)pyrene, 26 this approach has limited utility.
By contrast, the use of urinary 1-OHP as a biological exposure marker is practical and appropriate, and previous studies have shown its value in creosote workers. 10,16,21 Although pyrene levels may vary among creosote samples, pyrene is always present in PAH mixtures and therefore serves as an indirect indicator of all PAHs. Extensive research has led to the recognition of a range for normative “background” levels of 1-OHP against which workers’ levels can be compared. 14,15 It is also useful without regard to the route of exposure.
Biological monitoring does, however, face potential obstacles. Background levels vary from country to country, probably because of different ambient levels, lifestyles, diet, and smoking. 15 Thus it is may be necessary to determine background levels before workplace monitoring is conducted. Fortunately, such concerns may be of little relevance to the monitoring of creosote workers. This study and others 10 found that smoking and diet did not confound exposure assessments based on urinary 1-OHP. Another potential obstacle is the lack of a single 1-OHP benchmark for PAH-exposed workers and the absence of authorized biological exposure limits. Different biological exposure limits have been proposed for two specific groups of industrial workers: 4.4 μg/g for coke oven workers and 9.3 μg/g for workers in the primary aluminum industry. 14,32–34 Although these two benchmarks serve as guidelines for assessing exposure in creosote workers, it is likely that neither is specifically correct. A possible solution stems from a recent proposal that 1-OHP limits be adapted to specific work environments by means of correction factors linked to worksite-specific ratios of airborne benzo(a)pyrene and pyrene. 25 Ultimately, more reliable limits for workers exposed to creosote and other PAHs workers will require long-term epidemiological studies of exposed worker cohorts.
The present study findings also seem relevant to neighbors of industrial creosote facilities, some of whom may have concerns about airborne contamination. Atmospheric releases of creosote from wood-preserving facilities have generally not been well defined, but it is widely accepted that the more volatile components of creosote are generally the less toxic. 2 This suggests that airborne risks to neighbors would be significantly less than corresponding risks to facility workers. The current findings support that view. Among facility workers, evidence of exposure was almost entirely restricted to workers with direct dermal contact to creosote and creosote-treated products. In addition, measured breathing zone PAH exposures were very low. As shown in Fig. 3, volatilized PAH levels declined rapidly as workers moved from high- to low-exposure groups. Considering that most low-exposure workers had airborne exposures at or below analytical levels of quantitation, it seems unlikely that more distant, off-site neighbors could experience higher exposure levels.
A recent Quebec study provides further evidence that people residing near creosote facilities do not experience substantial PAH exposure. 35 Urinary 1-OHP levels in “exposed” non-smoking adults who lived <360 m downwind from a facility were compared with levels in non-smoking adult “controls” living 1.9 to 2.7 km upwind. Measured 1-OHP levels were nearly identical in both groups. Geometric mean levels were ≤0.11 μg/g (0.05 to 0.06 μmol/mol creatinine), comparable with baseline levels reported previously for non-smoking, non-occupationally exposed Quebec residents. 36,37 These levels were nearly tenfold lower than those determined in samples from the 18 low-exposure workers in the present study (geometric mean, 1.05 μg/g; 95% confidence interval, 0.8 to 1.3), a difference which strongly suggests that facility neighbors experience lower levels of exposure than do low-exposure workers at creosote facilities.
In summary, this study documented very low airborne exposure to creosote-related materials in workers employed at a creosote wood-treatment facility. Among workers with evidence of exposure, almost the entire internal dose could be attributed to dermal rather than inhalation uptake. Traditional approaches to industrial hygiene monitoring at creosote facilities, as currently mandated by OSHA, seem inappropriate and inadequate. By contrast, biological monitoring of creosote workers by means of urinary 1-OHP is currently the most practical and appropriate means to ensure that exposures are not excessive.
We gratefully acknowledge the professional assistance of Robert Wheeler, CIH, and Bobby J. Gunter, PhD, CIH. John Gibbs, MD, provided advice and encouragement. This study was supported by the Kerr-McGee Corporation.
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