OSHA comments from the January 19, 1989 Final Rule on Air Contaminants Project extracted from 54FR2332 et. seq. This rule was remanded by the U.S. Circuit Court of Appeals and the limits are not currently in force.
CAS: 299-86-5; Chemical Formula: C12H19ClNO3P
OSHA had no former limit for crufomate. The ACGIH has a TWA-TLV of 5 mg/m3 and a STEL of 20 mg/m3 for this substance. The proposed PELs were 5 mg/m3 as an 8-hour TWA and 20 mg/m3 as a 15-minute STEL, and NIOSH (Ex. 8-47, Table N1) concurs. The final rule establishes this 8-hour TWA limit but does not establish a STEL for crufomate. Pure crufomate exists as crystals, and commercial crufomate is a yellow oil.
Crufomate actively inhibits both plasma and erythrocyte cholinesterase. A study in humans showed that ingestion of 200 mg of crufomate daily for seven days caused no apparent cholinesterase inhibition in the subjects of this controlled study; however, rats and dogs receiving higher doses (5 mg/kg/day) for two years did show this effect (McCollister, Olson, Rowe et al. 1968/Ex. 1-350).
The American Industrial Hygiene Association (AIHA) testified at the hearing that, in the AIHA’s opinion, OSHA should delete any STELs that the ACGIH has either deleted or indicated that it intends to delete (Ex. 8-16, Tr. p. 3-307). OSHA agrees that such limits should be reevaluated on the basis of current health information (see the discussion in Section VI.C.17); after reviewing the evidence of crufomate’s toxicity in short-term exposures, OSHA has determined that it is not appropriate to include a STEL for this substance in the final rule.
Because cholinesterase inhibition is a very sensitive indicator of exposure, OSHA concludes that the final rule’s 8-hour TWA limit of 5 mg/m3 is needed to provide an appropriate margin of safety below the ingestion NOEL of 200 mg/day for humans, which corresponds approximately to an 8-hour inhalation exposure of 20 mg/m3. The Agency finds that this PEL will protect workers from the significant risk of material health impairment in the form of cholinesterase inhibition, which was possible at the previously uncontrolled levels.