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Old Password. New Password. Password Changed Successfully Your password has been changed. Returning user. Request Username Can't sign in? No statistically significant excess incidence of tumors was observed in either sex of hamsters at any exposure level. This suggests that hamsters are less sensitive to the carcinogenic effects of MC than either mice or rats. Metabolism data gathered in hamsters indicate that hamsters have less capability to metabolize MC by the GST pathway than rats or hamsters or humans.

This correlation between lack of GST metabolism capacity and lack of tumor response supports the hypothesis that GST metabolism is important in MC carcinogenesis and also indicates that it would not be protective to use the hamster response to MC as the basis for a carcinogenic risk assessment. This study extended the finding of excess mammary tumors in rats to the ppm level.

However, because of the high background rates of mammary tumors in Sprague-Dawley rats, the NTP study showed a clearer dose-response relationship between MC exposure and incidence of mammary tumors. In a study conducted for the National Coffee Association [Ex. These factors most likely accounted for the lack of a positive tumor response. The NCA studies were used by Reitz et al.

Specifically, these studies helped to determine that the lack of tumor development was consistent with model predictions of the amount of GST metabolites in lung and liver of mice and that the MFO pathway was most likely not primarily responsible for the mouse tumor response. The Agency believes that the NTP studies show the clearest evidence of a carcinogenic effect of MC and has used these studies as the basis of its risk assessment for the following reasons: 1 The studies were well conducted and underwent extensive peer review.

OSHA believes that because of the clear tumor response, and quality of the studies, the NTP studies provide the best data for quantitative cancer risk assessment. OSHA concludes from these studies that MC causes cancer in two species of test animals by the inhalation route, and that a clear dose-response has been demonstrated. Epidemiological Studies Epidemiological studies of occupational exposure to MC have been conducted in the manufacturing of triacetate fibers, photographic film production, and the manufacturing of paint and varnish.

Those studies were reviewed by OSHA in the preamble to the proposed rule [56 FR ] and are summarized and updated in this document. In addition, an epidemiological study of MC exposure and astrocytic brain cancer is reviewed in this text. Studies of triacetate fiber production workers. Ott et al. In particular, Ott et al. In this study, Ott et al. In interpreting the results of this study, Ott noted that there may have been differences in hiring practices in the two plants which could have contributed to the observed differences in mortality.

In their conclusion, Ott et al. Mirer of UAW testified [Tr. Furthermore, when the MC epidemiological studies are looked at together, there is evidence, although limited, that MC exposure has an effect on cardiovascular mortality. On the other hand, Kodak [Ex. In an update to the Rock Hill study, Lanes et al. Lanes et al. Examination of the liver and biliary cancers indicated that the workers had ten or more years of employment and at least 20 years since first employment 4 observed v.

Approximate durations of employment for these three cases were 28 years, 20 years, and less than one year. No medical record for the third case could be obtained.

However, an autopsy report indicated adenocarcinoma of the liver for this case. To estimate the expected number of biliary cancer deaths, Lanes et al. The computed risk estimate, based on 0. The authors hypothesized that the biliary duct cancer cases may have been due to factors such as oral contraceptive use, gallstones, or ulcerative colitis. However, it appeared that medical records showed no indication of gallstones or ulcerative colitis in workers who died of biliary cancer. Moreover, although these factors were not specifically controlled for, there is no reason to believe the rates of these factors would be different in the exposed cohort compared to the general U.

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As before, York County, South Carolina was used as the comparison population. The overall SMR from all causes of death was 0. In this follow-up, the SMR for liver and biliary cancer dropped from 5. No additional deaths from biliary or liver cancer were observed. Using a Poisson distribution, Lanes et al. On the other hand, if MC had no effect on liver and biliary cancer mortality, Lanes et al. Because of the small number of cases involved and the instability of the numbers generated in this type of statistical analysis, OSHA believes that this study, overall, is suggestive but not definitive of an association between occupational exposure to MC and elevation of human cancer risk.

Furthermore, the Agency has determined that the study results are not inconsistent with the results of the NTP cancer bioassay. Hoechst-Celanese [Ex. They argued that the reported excess in biliary tract cancer did not support the conclusion that MC exposure is associated with an increased risk of cancer. Specifically, they noted that, 1 Biliary cancers have not been reported in any of the animal cancer studies of MC; 2 no statistically significant increase in biliary cancers was seen in the Cumberland study described below ; 3 no statistically significant excess in biliary cancers was reported in the Kodak studies described below ; 4 It was unlikely that MC could have been responsible for the biliary tract cancer observed in one employee who had been exposed to MC for less than one year; and 5 the Rock Hill study did not control for other chemical exposures.

Shy, on behalf of Kodak, asserted [Tr. Shy acknowledged that animal bioassays have demonstrated liver tumors from MC exposure, but he noted that there is no evidence in humans that liver and biliary tract cancers have the same etiology. Furthermore, Dr. Shy argued that, 1 the results from the Lanes study is not supported by in vitro or pharmacokinetic studies. Moreover, the 20 year time interval between first exposure and death from biliary tract cancer provided evidence that "exposure preceded cancer with an appropriate interval for induction of the tumor [Ex.

The Agency believes that the risks of biliary cancer observed in these studies is consistent with risks derived from its pharmacokinetic analysis see the Quantitative Risk Assessment, Section VI. Regarding the biological plausibility, the Agency notes that human biliary cells appear to contain high concentrations of the mRNA for GST the enzyme many investigators believe to be responsible for MC-induced carcinogenesis [Exs. Although this requires more investigation to determine if there is a direct relationship, OSHA believes there is a plausible mechanistic argument for MC causality in human biliary tract cancers.

The Agency agrees with Dr. Shy, however, that the lack of dose-response data and the small number of cases in this cohort limit the strength of conclusions that can be drawn from this study. After weighing these considerations, the Agency has determined that there is suggestive evidence of a causal role for MC in these cases of biliary cancer. Gibbs et al. This plant, which ceased to operate in , had operations similar to the plant in Rock Hill, and it was assumed to have had similar MC exposure levels as well.

However, exposure measurements were not submitted for the Cumberland plant and it is unknown whether the Cumberland employees experienced the same exposures as their Rock Hill counterparts. The Gibbs study investigated the mortality of 3, workers who were employed at this plant on or after January There were 2, men and 1, women in the cohort. Most of the workers in the cohort were hired prior to 2, total. The study population was divided into three subcohorts based on their estimated exposure to MC: 1 men and women in the "high exposure" group estimated to be ppm , 2 men and women in the "low but never high exposure" group estimated to be ppm , and 3 men and 46 women in the "no exposure" group.

This cohort was followed through December The observed mortality was compared to expected death rates for Allegany County, Maryland where the plant was located and where most of the cohort deaths occurred , the State of Maryland, and the United States. The author of this study believed that the county rates were the most appropriate to use because the city of Cumberland is located in a rural area of Maryland and the state rates may have been influenced by rates in large urban areas such as Baltimore. In addition, local rates tend to adjust for social, economic, ethnic, and cultural factors which may be related to disease risk, access to medical care, etc.

However, if the fiber plant was the major employer in this rural area, then county rates may reflect the cohort's mortality rather than the background risk, in which case, state rates or U. The overall mortality rate for the high MC-exposed group was below the expected rates for Allegany County, Maryland, and the U. As in the Rock Hill study, mortality from biliary tract cancer was observed in the Cumberland study, although no statistically significant elevated incidence of biliary cancer was found two cases of biliary tract cancer were observed. In the high exposure group, there was one death 1.

For the high MC-exposed subcohort, Gibbs et al. This cohort should be followed for a longer period of time to help clarify the suggested association between MC exposure and biliary cancer observed in the Rock Hill cohort. Statistically significant excess mortality was also observed from prostate, uterine, and cervical cancers, although these also represented small numbers of cases: 13, 2, and 1, respectively. The excess of prostate cancer in the Gibbs et al. According to Gibbs et al. In support of this hypothesis, no other epidemiological or animal studies of MC exposure have suggested a relationship between prostate cancer and MC.

Thus, these men may have had longer exposure to other chemicals; 3 the study did not control for other personal risk factors; 4 Gibbs reported an increased incidence of prostate cancer elsewhere in the textile industry; and 5 the large number of statistical tests may have increased the probability of finding the death rate of a specific cause to be elevated or depressed.

OSHA believes that the increased risk of prostate cancer should be noted as a possible positive effect of MC exposure on cancer risk, particularly considering the exposure-response relationship. However, because of potential confounding factors and lack of corroborating findings in other studies, OSHA believes this is suggestive rather than conclusive evidence of a human carcinogenic effect. Studies of film production workers. In their original study of film production workers, Friedlander et al.

The cohort in these studies consisted of workers who worked in any department in film production that used MC as its primary solvent for approximately thirty years. The cohort was followed through Proportionate mortality analysis for those workers ever employed in the study area versus a comparison group of workers in other Kodak Park departments produced a proportionate mortality ratio PMR of For ischemic heart disease, Friedlander et al.

No statistically significant differences were observed at p less than or equal to 0. For the cohort mortality study, Friedlander et al. Forty-five deaths from circulatory diseases were observed in the MC-exposed cohort versus Also, 6 deaths from respiratory diseases were reported in the MC-exposed group versus 3. No liver deaths were observed in this cohort. Thirty-three deaths from ischemic heart disease were observed in this cohort compared with None of these observed differences in mortality reached statistical significance.

Hearne et al. In the first update, the study cohort was followed through Two referent groups were utilized in this study: the general population of upstate New York men, excluding New York City, and Kodak Park employees. No statistically significant findings were observed for any cause of death. However, Hearne et al. This observation did not achieve statistical significance and a dose-response relationship was not observed when Hearne et al. In the update, nonsignificant deficits in observed-expected ratios for lung and liver cancer were found. Also, overall mortality from to was significantly less than in both referent groups.

Since , the number of pancreatic cancer deaths remained the same. As before, dose-response analysis showed no statistically significant pattern when latency or dose were considered. The update showed that deaths due to liver cancer, lung cancer, and ischemic heart disease were below the expected numbers in both referent groups. Also, no additional pancreatic cancer deaths were observed in this second update. Since the start of the follow-up, Hearne et al. The 1, men in the cohort were followed through An occupational control group could not be formed because death rates for Kodak employees before were unavailable.

Instead, male residents of upstate New York living outside of the five New York City counties were used. The mean career individual exposure was approximately 40 ppm for 17 years and the average interval between first exposure and end of follow-up was about 32 years. Circulatory diseases and ischemic heart disease mortality were also statistically significantly below expectation. For lung cancer there were 22 deaths Also, since the number of observed pancreatic cancer deaths in this cohort was similar to the expected number, Hearne et al.

Kodak [Tr. Using person-years of active employment only in their analysis, Hearne observed 27 deaths 36 were expected in the internal Kodak reference group from ischemic heart disease in the Kodak cohort; in the cohort, Kodak recorded 33 deaths compared with 43 expected in the New York State comparison population. The HWE is likely to be less of a factor when occupational comparison groups are used. However, there are two potential problems with using occupational comparison groups in this instance: 1 Cancer rates are more stable in larger populations, so comparison with state and national rates may be more appropriate.

Study of workers in paint and varnish manufacturing. The NPCA submitted to the record an epidemiological study of employees who worked for at least one year in the manufacture of paint or varnish [Ex. Although no statistically significant excess of mortality was reported, OSHA noted that there were 4 pancreatic cancers 1. Astrocytic brain cancer among workers in electronic equipment production and repair. Heineman et al.

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Cases were defined as white males who died from brain or other central nervous system tumors in southern Louisiana, northern New Jersey, and Philadelphia, Pennsylvania. Controls were randomly selected from death certificates and included white males who died of causes other than brain tumors, cerebrovascular diseases, epilepsy, suicide, and homicide. Controls were frequency-matched to cases by age, year of death, and geographic area. These codes linked work histories to job-exposure matrices which "characterized likely exposure to the six CAHs and to organic solvents" [Ex.

Gomez et al. As noted by Gomez et al. Odds ratios were calculated for exposure intensity categories to refrain from using weights. These categories did not include duration in jobs with lower intensity for subjects with high or medium intensity jobs. In their statistical analyses, Heineman et al. Astrocytic brain cancer was not found to be associated with "ever" being exposed to organic solvents as a group or to any of the six CAHs examined in this study.

However, as probability of exposure to organic solvents as a group, and MC in particular, increased, the risk of brain cancer increased chi-squared statistics for trend for organic solvents and MC were 1. For MC there was a 2. Similar results were seen for organic solvents and methyl chloroform for all probabilities combined chi-squared statistics for trend were 2. Lagging exposure by 10 years produced findings analogous to those noted above.

However, risk did not increase monotonically with cumulative exposure. Few individuals had high cumulative scores when exposure was lagged 20 years for the individual CAHs. Compared with jobs with medium or low intensity exposures to organic solvents and all six CAHs, risk of brain cancer was higher for subjects who worked in jobs with high intensity exposures.

Since many subjects were determined to have been exposed to more than one of the CAHs, sometimes even in the same job, Heineman et al. Risks associated with MC increased when adjustments for exposure to the other agents were made. Among the six CAHs examined in this study Heineman et al. According to Heineman et al. Next-of-kin data, poor specificity of some work histories for specific solvents, and the interchangeability of solvents may have resulted in misclassification of individuals with respect to any of the exposure measurements used in this study.

However, Heineman et al. Another limitation of this study, pointed out by Heineman et al. Heineman further remarked that differential misclassification was probably not a problem in this study because occupational histories came from next-of-kin of both cases and controls. In light of the limitations of this study, however, Heineman et al. Moreover, Heineman et al. Several commenters [Exs.

Information provided by next-of-kin concerning jobs held, job descriptions, dates of employment, and hours worked per week may be flawed with recall bias. Next-of-kin may not be able to accurately recall job-related information, especially for jobs held early in life. If next-of-kin for cases or controls had better recall than the other group, differential misclassification could occur. HSIA [Ex. However, NIOSH noted that misclassification "is a typical problem in population based case-control studies of this type [Ex.

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ORC stated that exposure values were assigned to all SIC and SOC codes, and not developed based on job history information, which would have given the study more validity. Kodak also expressed some concern regarding this study due to lack of accurate records of past exposures, reliance on expert judgement to a large degree, use of next-of-kin to determine potential exposure, and undocumented qualifications of those making judgements concerning the different occupations and industries involved.

In addition, Kodak felt that the exposure data were "at best, unsubstantiated semi-qualitative judgements of likelihood and intensity of exposure [Ex. Vulcan Chemicals [Ex. However, lack of exposure verification does not nullify the results of the study. The Agency believes that the associations observed are suggestive of a human carcinogenic effect of MC. Another issue that Kodak [Ex. Vulcan [Ex. Although they offered no explanation of how this selection bias would operate, Vulcan did suggest that this issue should be investigated further.

Vulcan was also concerned that the matching of controls and cases with respect to occupations and socioeconomic status may be inadequate. In particular, Vulcan criticized the Heineman study for not presenting the occupations of the control group and for not matching the socioeconomic status of the two groups. Similarly, Kodak [Ex. Kodak [Ex.

OSHA believes that there is no evidence that this is the case in this study. HSIA argued that Gomez et al. Furthermore, there was a remarkably high correlation between exposure to MC and brain tumors. OSHA concludes that the results from this study strongly suggest a possible association between MC and brain cancer. However, in the absence of quantified exposure data for these workers, it remains relatively speculative to attempt to estimate a quantitative dose-response relationship.

Therefore, OSHA concludes that the risk estimate based on the animal data is the best available and accordingly it retains that estimate for its significant risk analysis. Summary of epidemiological studies. Considered as a whole, the available epidemiologic evidence did not demonstrate a strong, statistically significant cancer risk associated with occupational exposures to MC. In addition, the non-positive epidemiological studies summarized here are not of sufficient power to rule out the positive results from the animal studies.

This issue is addressed further in the Quantitative Risk Assessment section of this document. In summary, the epidemiological results are suggestive of an association between occupational exposure to MC and elevated cancer risk which offers supporting evidence to the positive animal bioassay results. Conclusion OSHA concludes from the mutagenicity, animal bioassay and human epidemiology data that MC causes cancer in test animals and that it is a potential occupational carcinogen.

The Agency has determined that, because of the quality of the studies, the clear dose-response relationship and the appropriateness of the route of administration, the NTP rodent bioassay data are the best available for quantitative cancer risk assessment. OSHA also concludes that the epidemiology data, in some cases, suggest a positive association between human MC exposure and cancer incidence, but the dose-response relationships are not clear.

The Agency has determined that the remaining epidemiology data the non-positive studies are not of sufficient power to rule out the results obtained in the animal bioassay data and that the animal data provide the best available data for quantitative risk assessment. Other Toxic Responses 1. This depression in CNS activity was manifested as increased tiredness, decreased alertness and decreased vigilance.

These effects could compromise worker safety by leading to an increased likelihood of accidents following MC exposure. Animal studies. Savolainen et al. On the fifth day, after 3 and 4 hours of exposure to MC, levels of acid proteinase in rat brains were significantly increased, but no change in brain RNA levels was reported. The authors suggested that the increase in acid proteinase may have been the result of increased levels of CO from metabolism of MC.

OSHA believes that this study shows that MC can cause specific changes in the neurological system at a biochemical level. The Agency intends to monitor the scientific literature for additional developments on these effects, but has not used this information in setting the MC exposure limits because it is presently unclear how changes in acid proteinase are related to the observed CNS depressive effects of MC in humans.

Rosengren et al. Because of high mortality in the 2 higher doses, no data were collected at ppm and exposure was terminated after 10 weeks at ppm. Exposure to ppm was continued for three months. Exposure to MC was followed by four months of no exposure before animals were examined for irreversible CNS effects.

The authors found increased levels of glial cell marker proteins in the frontal cerebral cortex and sensory motor cortex after exposure to ppm MC. These findings are consistent with glial cell hypertrophy or glial cell proliferation. Levels of DNA were decreased in the hippocampus of gerbils exposed to both and ppm and in the cerebellar hemispheres after ppm MC. Decreased DNA concentrations indicate decreased cell density resulting from cell death or inhibition of DNA synthesis.

The neurotoxic mechanism of action of MC in gerbil brains is not understood. However, since the metabolism of MC to CO was determined to be saturated at both and ppm COHb levels were equivalent at both exposure concentrations , the changes in glial cell proteins and DNA concentrations was attributed to either a direct effect of MC or an effect of a metabolite of the GST pathway.

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Although this study describes biochemical changes in the CNS subsequent to MC exposure, the high mortality of the experimental animals and the lack of MC toxicity data in the gerbil make it difficult to determine the significance of this study for extrapolation to other species. It is also unclear how these effects would relate to CNS depression observed in humans after MC exposure. In addition, continuous exposure to MC has been shown in other experimental situations [Exs. Exposure on a 6 or 8-hour per day schedule is also more like occupational exposure scenarios and therefore those experiments are generally easier to interpret when assessing risk to workers.

In summary, OSHA believes that the rat and gerbil data described above shows that MC can cause specific changes in the neurological system at a biochemical level. The Agency intends to monitor the scientific literature for additional developments on these effects to determine if these types of effects have implications for human CNS risks. Human studies. MC causes CNS depression which is characterized by tiredness, difficulty in maintaining concentration, decreased task vigilance, dizziness, headaches, and, at high concentrations, loss of consciousness and death.

Accidental human overexposures to MC [Exs. CNS depression has been described after humans were exposed to experimental MC concentrations as low as ppm [Ex. Experimental studies. CNS depression was detected in human subjects exposed to MC at concentrations as low as ppm for 4 hours or ppm for 1. In these experiments, which measured subtle CNS depression such as dual task performance and visual evoked response , it was not possible to determine a no observed effect level NOEL , because the lowest experimental concentration used ppm elicited CNS effects.

The HSIA questioned whether bias was introduced into the results of these studies by inadequate procedures to establish a "double blind. However, since Putz et al. OSHA believes that these studies were well conducted and is relying on the quality of the studies overall as evidence of the validity of the results. Absent evidence demonstrating the inadequacy of the blinding procedures, OSHA has determined that these studies show that MC can cause mild CNS depression in humans exposed at concentrations as low as ppm.

Although there are insufficient data to draw firm conclusions, extrapolation from existing studies suggests that the proposed STEL of ppm may not fully protect physically active workers from CNS impairment. Therefore, a lower STEL should be considered, if feasible. This analysis [Ex. Putz et al. The model also predicted that minute exposures to ppm while the subject was exercising at 50 watts would produce brain MC concentrations substantially less than that predicted for the 4 hour exposure to ppm MC. Workers engaged in strenuous activity while exposed to MC should take special precautions, such as frequent breaks in fresh air, especially if dizziness or lightheadedness occurs.


To the extent that these effects occur, the STEL would not be protective. Mild and reversible CNS depression was detected at ppm for 4 hours and ppm for 1. Impairment of the CNS would also increase the risk from accidents. Measured data show risks at ppm for four hours of exposure. A lower level at shorter duration is needed to avoid that risk. NIOSH's calculations show that for active workers a level lower than ppm may be needed.

However, because of feasibility concerns, which would be greater at lower levels and the suggestion that short duration of exposure i.

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Occupational exposure studies. Weiss [Ex. After 3 years of exposure, the worker developed neurological symptoms, characterized by restlessness, palpitations, forgetfulness, poor concentration, sleep disorders, and finally, acoustical delusions and optical hallucinations. No hepatic damage or cardiac toxicity was found. At the first appearance of symptoms, cessation of exposure produced an immediate cessation of symptoms. Later, longer and longer periods were required after termination of exposure in order to alleviate the symptoms. The increasing persistence of symptoms is consistent with a diagnosis of toxic encephalosis.

Hanke et al. Clinical examination of 14 of the workers who had neurological symptoms headache, vertigo, sleep disturbance, digestive complaints and lapses in concentration and memory revealed changes in the EEG patterns of the exposed workers which persisted over a weekend pause in exposure. These EEG changes were characteristic of a toxic encephalosis produced by chronic intoxication with a halogenated solvent MC. Although these studies represent a small number of cases with very high chronic exposures, the evidence is suggestive of a relationship between chronic MC exposure and toxic encephalosis.

In a case study report, Barrowcliff et al. Axelson [Ex. In the NPRM, OSHA expressed the opinion that these studies, taken together, "provide suggestive evidence of a permanent toxicity [different from the observed reversible CNS depression] which may be the result of chronic exposure to MC. The first study was provided as an English translation of a Czechoslovakian paper by Kuzelova et al. These investigators examined workers in a film production plant who were exposed to MC concentrations from 29 to ppm.

Toxicity associated with chronic MC exposure was observed in workers exposed to MC for up to two years, but the authors recommended continuing studies of the long-term health effects. The Agency agrees with the authors that this study was not sufficient to adequately characterize the long-term CNS health effects that may be induced by MC exposure. Cherry et al. In a study, the authors found a marginal increase in self-reported neurological symptoms among exposed workers. This increase disappeared when an appropriate reference group was used for comparison.

However, in a investigation, Cherry [Ex. Ambient MC exposures for this population ranged from 28 to ppm for the full shift. This study demonstrated CNS effects due to occupational MC exposures below ppm the lowest dose which was administered in the experimental studies.

To the contrary, OSHA believes that the occupational studies discussed above demonstrate that MC has an effect on the CNS at occupational exposure levels as low as ppm. Although the study, which relied on self-report of neurological symptoms, did not demonstrate a CNS effect, the study examined more objective measures of CNS depression and correlated the observed effects with a direct measure of MC exposure. OSHA believes that this study demonstrates that, although the CNS depression may be mild, it is demonstrable in occupational settings and at concentrations in the range of the STEL although the exposures in this study were over an 8-hour work day.

As described above, OSHA is sufficiently concerned about the potential for health effects at concentrations below the STEL of ppm that it will continue to gather information and revisit this issue, if warranted. Cardiovascular stress has been observed after exposure to CO, so it is reasonable to suspect that similar health effects would be observed after exposure to MC and metabolism to CO [Ex. Carbon monoxide successfully competes with oxygen and blocks the oxygen binding site on hemoglobin, producing carboxyhemoglobin COHb and reducing delivery of oxygen to the tissues.

This reduces the oxygen supply to the heart itself, which can result in myocardial infarction heart attack [Ex. The cardiac health effects anticipated from exposure to MC itself or CO as the result of metabolism of MC are described below. There is no evidence from animal studies in the MC rulemaking record that MC has a direct toxic effect on cardiac tissue. Chlorinated solvents have been shown to sensitize the cardiac tissue to epinephrine-induced fatal cardiac arrhythmias [Ex. However, MC is less effective in sensitizing cardiac tissue than other chlorinated analogues.

MC caused sensitization of cardiac tissues only at doses well above doses which produce a narcotic effect. This finding indicates that compliance with an 8-hour TWA of 25 ppm MC would likely be sufficient to protect against such sensitization.