Attorney Jim Love of the IAOMT
B. The Fawer Study, Relied on by Both EPA and ATSDR, isa Study of Chloralkali Workers and not Appropriate for RfC or MRL Derivation.
Most of the occupational studies underlying our knowledge of mercury vapor toxicity and, therefore, underlying all current RELs for Hg°, were conducted on chloralkali workers.Although air–Hg° concentrations are generally elevated among such workers, concomitantexposure to chlorine gas (Cl2) occurs. Data on airborne Cl2 levels in chloralkali plants wererecently summarized by the European Union (EU, 2007). Cl2 levels in the air of chloralkali plantsaverages about 1 ppm (0.3 mg/m3) and ranges between 0 ppm and 6.5 ppm (0–19.5 mg/m3) depending on the specific work environment where sampling was conducted.
The concomitant exposure to Cl2 and Hg° effectively reduces worker exposure by decreasing the amount of airborne Hg° available for inhalation and absorption. Mercury converts to HgCl2 in the presence of Cl2 at room temperature (Menke and Wallis, 1980; Viola andCassano, 1968). The inhalation absorption of HgCl2 is only half or less of that of Hg° (ATSDR,1999; Viola and Cassano, 1968). Hg° deposition to the brain is also altered. Hg2+ (associatedwith HgCl2) does not cross the blood–brain barrier as does Hg° (Lorscheider et al., 1995;Viola and Cassano, 1968). Following Hg° exposure, the red blood cell (RBC) to plasma Hg°concentration ratio typically ranges between 1:1 and 2:1 (WHO, 1991). However, much less Hg°is associated with RBCs in the blood of chloralkali workers (with Cl2 present).
Suzuki, et al. (1976), investigating Hg°-exposed chloralkali workers versus workers from two other industrial sectors (who were all exposed to Hg° at similar airborne concentrations(0.01–0.03 mg/m3)), observed that the RBC to plasma Hg° concentration ratio in the chloralkaliworkers was only 0.02:1 whereas workers of the two other industries (with no concomitantexposure to Cl2), had RBC to plasma Hg concentration ratios between 1.5:1 and 2:1. A studyby Viola and Cassano (1968) of rodents (rats, mice) exposed to Hg° alone or in the presence ofCl2, demonstrated reduced Hg° absorption in the presence of Cl2 and the deposition of Hg° to thebrain of rodents exposed concomitantly to Hg0 and Cl2 was only 1/5th of that when exposure wasto Hg° alone.
There is other evidence of the interaction of Cl2 with Hg°. Cl2 injection is employed as a direct Hg° emissions control technology to reduce Hg° levels in industrial stack emissions(Pavlish et al., 2003). Increasing chlorine quantity/concentration in the process improves the efficiency of Hg° emission control (Richards, 2005). In the presence of chlorine, Hg° is convertedto Hg2+, which precipitates with stack particulate matter that is subsequently removed (‘scrubbed’) from stack emissions.
It is evident, therefore, that all studies of uptake and toxicity of Hg° exposure in chloralkali workers will be confounded by concomitant Cl2 exposure and, as a result, studies ofchloralkali workers should not form the primary basis for a REL for Hg°; the application andextrapolation of those results to other occupational groups and the general public, whose Hg°exposure occurs in the absence of Cl2, is invalid.
James M. Love
TITUS HILLIS REYNOLDS LOVE DICKMAN & McCALMON, P.C.
3700 First Place Tower 15 East Fifth Street
Tulsa, Oklahoma 74103-4334