Methylene Chloride, Carboxyhemoglobin and Cardiac Risk

Abstract

We thank Dr Kales for his comments, but disagree with his conclusion that the permissible exposure limit (PEL) proposed by OSHA of 25 ppm (8-hour time-weighted average) for methylene chloride is appropriate and needed. We appreciate Dr Kales' concern about a potential for increased death secondary to ischemic heart disease at 50 ppm exposures to methylene chloride but, in fact, numerous human epidemiology studies do not support this concern. Exposures to methylene chloride in two different epidemiology studies averaged 500 ppm but were actually higher for most of the study years.1,2 Because HbCO levels are linearly related to methylene chloride exposure, one would expect significant levels of HbCO with exposures ten times greater than the current American Conference of Governmental Industrial Hygienists' standard of 50 ppm. If Dr Kales' suppositions are correct, a marked elevation in ischemic heart disease deaths should have been observed in both of these epidemiology studies. The facts are just the opposite. Neither study showed elevations in ischemic heart disease despite having a majority of employees that were older men. Another epidemiology study,3 in which employees were exposed to lower average concentrations of methylene chloride, also failed to show an increased risk of ischemic heart disease. The theory is nice but is not supported by numerous studies. We also determined whether there was an increase in employees' dying (while employed or within 30 days of being employed) from cardiac-related problems. This did not occur either. It should be noted that methylene chloride metabolism is rapid and that HbCO levels return to zero by the next day, so that any increased risk beyond 24 hours is not related to increased levels of HbCO as a result of methylene chloride exposure. Likewise, when the epidemiology studies were undertaken, the researchers questioned occupational medical professionals at both sites about any increase in non-fatal ischemic-related cardiac events in employees. No concerns were noted by the physicians or nurses questioned, and none were expressed by the employees at these sites. Although these impressions are anecdotal, any health-related concerns regarding exposure to methylene chloride would have become apparent. Initially, theory also held that methylene chloride would have an adverse impact on the liver. This too was disproved4 by studying employees exposed over 10 years to methylene chloride levels averaging 500 ppm. The end result of all of these studies is that there is no adverse impact on health, and the current PEL of 50 ppm for methylene chloride provides adequate protection for persons exposed at these levels. Finally, we must say that it is interesting that someone from NIOSH would raise this question again. We at Hoechst Celanese have also been very concerned about the issue of ischemic heart disease and, as a result, had urgently supplied our epidemiology data to researchers at NIOSH over 5 years ago. We also helped contribute to the protocol design for a study to answer this concern with an assurance that the work would be completed rapidly. We had assumed that our data had been adequately reviewed, no evidence of any problems with ischemic heart disease found, and this issue put to rest long ago. Kevin J. Soden, JD; Jonathan Amsel, ScD Hoechst Celanese Corporation; Charlotte, NC