Document LJ8dDxbJ34e90LXVBEppY9g3q

CHEMICAL MANUFACTURERS ASSOCIATION March 13, 1989 To: VDC Panel Re: OSHA "Z-Table" Rule for VDC For your information, attached is a review of the final Z-Table regulation providing exposure limits for VDC for possible legal issues, as prepared by Mr. Bruce Dickson. Sincerely yours, Robert R. Romano, Ph.D. Associate Director, Special Programs Division & Manager, Vinylidene Chloride Program 2501 M Stroel, NW. Washington. DC 20037 202-887-1100 Telex 89617 (CMA WSH) SL 061771 COUNtCl LEG G, AUL ROBERT HASTINGS LECOHNARARLEDSSM,JAWNAOLK^SEKRT los anselcs office 555 south flower STREET lOS ANGELES, CALIFORNIA 90071 TELEPHONE (2131 03-0000 ORANGE COUNTY OFFICE 095 TOWN CENTER DRIVE COSTA mesa, California 92020 TELEPHONE (71A) Ai-HOO WEST LOS ANQELES OFFICE 1299 OCEAN AVENUE SANTA MONICA, CALIFORNIA 90*01 TELEPHONE (2(3) *51-1200 WRITER'S OlRECT DIAL NUMBER LAW OFFICES OF Paul, Hastings. Janofsky & Walker a batnrShib> including professional CORPORATIONS TWELFTH FLOOR IOSO CONNECTICUT AVENUE, N, W. WASHINGTON, D. C. 20036 TELEPHONE (202) 223-3000 TWx 710 -B22-3062 TELECOPIES' (202) *62-61+3 March 7, 1989 ATLANTA OFFICE Georgia-Pacific cents* 133 PEACHTREE STREET N E ATLANTA, GEORGIA 30303 TELEPHONE (40*1 58S-09OO CONNECTICUT OFFICE ONE CANTERBURY GREEN STAMFORD, CONNECTICUT OC9oi TELEPHONE (203) 357-0)00 NEW YORK OFFICE 9 WEST 57TM STREET NEW YORK, NEW YORK I0QI9 TELEPHONE 1212) 032-0100 TOKYO OFFICE TORANOMON OHTORl auiuOlNG *-3, TORANOMON l-CHOMC MINATO-KU, TOKYO iOS TELEPHONE (03) 507-0730 Our file no: MEMORANDUM TO CMA VINYLIDENE CHLORIDE PROGRAM PANEL Re: OSHA "2-Table11 Rule for VDC The Panel has asked that we review the final ZTable regulation providing exposure limits for vinylidene chloride for possible legal issues. We have reviewed it and discussed it with Dr. Romano. Specifically, we have looked into the question of whether the Panel has any reasonable objection to the final rule on the basis of an argument that the proposal gave insufficient notice that OSHA was considering a reduced exposure limit. Our conclusion is that the final rule probably was not sufficiently different from the proposed rule to warrant challenge on a theory of insufficient notice under the Administrative Procedure Act. This memorandum summarizes the law with respect to that issue and reaches the conclusion that litigation would probably not be fruitful. We have not addressed the question of whether OSHA's conclusions about the adequacy of the proposed 5 ppm TWA or the need to adopt a 1 ppm TWA are supported by the record. OSHA's rationale for adopting the final standard -- that studies show damage at 25 ppm and that VDC is a potential carcinogen -- does not seem to be so flawed as to justify an argument that the standard is not supported by the record. A. Proposed Rule In its proposed "Z-Table" rule, the Occupational Safety and Health Administration ("OSHA") or ("the Agency") suggested setting permissible exposure limits ("PELs") for SL 061772 Paul, Hastings, Janofsky & Walker March 7, 1989 Page 2 vinylidene chloride ("VDC") at an 8-hour time weighted average ("TWA") of 5 parts per million (''ppm") and a 15minute short-term exposure limit ("STEL") of 20 ppm. 53 Fed. Reg. 21106 (June 7, 1988). The Agency stated that it was concluding preliminarily that these limits would protect workers from the `'risk of liver and kidney damage and carcinogenity potentially associated with exposure to VDC at the levels permitted by the absence of any OSHA limit." Id. The Agency noted, however, that this standard might be an interim limit and that OSHA would promulgate a new limit "if it determined that such a new limit would substantially reduce significant risk." Id. OSHA indicated that the proposed rule adopted the same standard as the one advanced by the American Conference of Governmental Industrial Hygienists -- Threshold Limit Values ("ACGIH-TLV"). The proposal also noted that the National Institute on Occupational Health and Safety ("NIOSH") proposed that ''employee exposure to VDC be reduced to the lowest feasible level," and stated that NIOSH considered VDC to be a carcinogen. Although there does not appear to be a specific statement in the proposal defining what NIOSH meant by "the lowest feasible level," the final rule indicates that this NIOSH recommended exposure limit ("REL") was 1 ppm -- the same level as the one finally adopted by OSHA. 54 Fed. Reg. 2567 (January 19, 1989). The proposed OSHA rule also outlined various studies and the conclusions drawn therefrom on the toxicity and carcinogenicity of VDC. B. Final Rule After reviewing the studies cited and several comments (most notably, those submitted by CMA and the Worker's Institute for Safety and Health ("WISH")), the Agency concluded that "these studies clearly demonstrate that VDC can cause adverse liver and kidney damage at airborne concentrations as low as 25 to 50 ppm and suggest that VDC is a potential occupational carcinogen." Id. Thus, on January 19, 1989, OSHA adopted a final rule setting the allowable limit for exposure to 1 ppm as an 8 hour TWA. SL 061773 'aul, Hastings, Janofsky & Walker March 7, 1989 Page 3 C. Notice of Rulemaking The Administrative Procedure Act, 5 U.S.C. 551 et sea., requires agencies to give public notice of a proposed rule and to give interested parties the "opportunity to participate in rule making through submission of written data, views, or arguments, with or without opportunity for oral presentation." Xd. at 553(b). This provision does not require a proposal to specify every aspect of the rule which may ultimately be adopted in final form. It does, nonetheless, require a sufficient description of the subjects and issues involved' so as to allow interested parties a meaningful opportunity to comment. Trans-Pacific Conference of Japan/Korea v. Federal Maritime Comm'n, 650 F.2d 1235 (D.C. Cir. 1980), cert, denied. 101 S. Ct. 2315 (1980). If notice of the proposed rule is too broad or the final agency rule deviates too sharply from the proposal, the affected parties will be deemed to have been deprived of notice and of an opportunity to comment. Small Refiner Lead Phase-down Task Force v. EPA. 705 F.2d 506, 547 (D.C. Cir. 1983); Chocolate Manufacturers Ass*n of the U.S. v. Block. 755 F.2d 1098 (4th Cir. 1985. This does not mean, however, that when an agency adopts a final rule which contains substantial changes from the proposed rule the new rule is automatically invalid and the agency needs to open a new comment period. International Harvester Co. v. Ruckleshaus. 478 F.2d 615, 632 n.51 (D.C. Cir. 1973). Nevertheless, to be valid, the change must represent a "logical outgrowth" of the prior notice and comments. South Terminal. 504 F.2d at 659. In determining whether a final regulation is a "logical outgrowth" of a proposed rule, the court must "proceed to compare carefully the specific language of the proposal with that of the final rule in light of the evidence adduced at the hearings." United Steelworkers v. Marshall. 647 F.2d 1180, 1221 (D.C. Cir. 1980). This standard essentially means that "given a new opportunity to comment, commenters would not have their first occasion to offer new and different criticisms which the agency might find convincing." BASF Wvandote Cort>. v. Costle. 598 F.2d SL 061774 Paul Hastings, Janofsky & Walker March 7, 1989 Page 4 637, 642 (1st cir. 1979), cert, denied. 444 U.S. 1096, 100 S. Ct. 1063 (1980). D. Case Law In the following cases, the court found that adequate notice had been given: 1. American Iron and Steel Institute v. EPA. 568 F.2d 284 (3rd Cir. 1977). EPA proposed regulations establishing maximum permissible levels of pollutants which could be discharged by certain manufacturing operations within the iron and steel industry. The proposed regulations surveyed the available pollution control techniques -- the best practable control technology currently available ("BPCTCA") -- that could be used in meeting these limitations. The court held that interested parties were sufficiently apprised that there was an issue as to whether recycling of partially clarified effluent was the BPCTCA and, therefore, that the Agency might adopt more stringent treatment technologies than those embodied in the proposed rule. Thus, the final rule was a "logical outgrowth" of the proposal. 2. South Terminal Com, v. EPA. 504 F.2d 646 (1st Cir. 1974). In order to reduce carbon monoxide emissions in the Boston area, EPA proposed (1) a ban on street parking in downtown; (2) prohibiting travel on certain routes one day a week through a $5 sticker system; and (3) limiting the supply of gasoline. The Agency also warned the public that other alternatives being considered, including a plan for fewer available parking spaces downtown. After extensive public comment, the sticker and gas supply options were dropped. The final rule adopted a plan which had not been previously recommended and that required a freeze on present and a review of future parking spaces. The court upheld the final rule stating that "[ajlthough the changes were substantial, they were in character with the original scheme and were additionally foreshadowed in proposals and comments advanced during the rulemaking. Parties had been SL 061775 Paul, Hastings, Janofsky & Walker March 7, 1989 Page 5 warned that strategies might be modified in light of their suggestions." Id. at 658. 3. Small Refiner Lead-Phase Down Task Force v. EPA, 705 F.2d 506 (D.C. Cir. 1983). EPA proposed setting lead content limits for small refineries ("SRs") at 2.5 grams per leaded gallon ("gplg") which was more lenient than the level proposed for large refineries ("LRs"). The final rule set a much stricter level of l.l gplg, which was based on past production levels, for both SRs and LRs. This final rule reflected an attempt to close certain loopholes created by the disparate treatment of SRs and LRs. The notice has raised this concern but had not specifically listed which loopholes EPA might attempt to close. Nevertheless, the court found that SRs were on adequate notice of the past production requirements because they were generally aware that EPA was seeking to seal unidentified loopholes that might affect them and they were in fact aware that the LRs had proposed considering past production requirements. Thus, the final rule flowed logically from the earlier proposal. In addition, the court noted that the SRs' attorney had attended the public hearings and was closely monitoring the docket and that the SRs had responded to other information to which they objected. In the following cases the Court found that there had not been adequate notice: 1. AFL-CIO v. Donovan, 757 F.2d 330 (D.C. Cir.; 1985). Prior to the final regulation amending the Service Contract Act, the definition under that Act of "in the United States" covered situations where any part of the contract was performed in the U.S. The two proposals amending the Act highlighted the sections to be amended. Neither notice indicated that the definition of "in the United States" was to be changed to cover only those actions actually performed in the U.S. The court held that because the change appeared only in the final rule itself without indication of the pending change, the modification was not a "logical outgrowth" of the proposed rule. SL 061776 Paul, Hastings, Janofsky & Walker March 7, 1989 Page 6 2. Chocolate Manufacturers Ass'n ("CMA") v. Block, 755 F.2d 1098 (4th Cir. 1985). Where the Food and Nutrition Services of the USDA proposed a rule that would limit the sugar content allowed in supplemental foods -- without indicating that chocolate flavored milk would be affected by the final regulation -- the court held that the agency had not given CMA adequate notice. The court noted that although the final rule was an outgrowth of the proposed regulation, it wasn't a logical one, as chocolate milk had always been a permissible supplemental food in the program and there had never been any hint that it would be removed therefrom. Thus, CMA could not have anticipated such a provision in the final rule and therefore had not been adequately alerted of the need for comment. Conclusion Insufficient notice does not appear to be a valid basis for objecting to OSHA's final rule on VDC exposure limits. In its proposal, OSHA implied that several alternatives were being considered, including NIOSH's REL. CMA knew that OSHA and NIOSH had jointly recommended a 1 ppm VDC exposure level in 1978 and that NIOSH proposed that VDC be designated an occupational carcinogen. In its comments, CMA responded directly to that allegation and attempted to establish the NIOSH's proposal was unsupported by scientific evidence. CMA also recommended that ACGIH-TLVs be adopted (5/20 ppm) rather than NIOSH RELs (l ppm). Because NIOSH's low TLV recommendation was mentioned in the proposed rule, even if in passing, and CMA referred to it in its comments, the proposed rule would probably be held to give adequate notice, and the final rule would be held to be a "logical outgrowth" of the proposed standard. In addition, if a comment period were to be re opened, CMA would not be getting its first opportunity to offer new criticisms or suggestions that the agency might find convincing. CMA has already advocated that VDC is not a likely carcinogen and that ACGIH-TLVs be used as the basis for updating the Z-Table limits. OSHA addressed these claims but concluded that a lower exposure limit was warranted. Paul, Hastings, Janofsky & Walker March 7, 1989 Page 7 Further, OSHA specifically stated in the proposal that it might promulgate a new limit in the final rule if doing so would substantially reduce a significant risk. This statement, coupled with OSHA's direct evaluation of CMA's comment and other studies in the final rule and its notice in the proposal that it was considering the 1 ppm limit, makes it difficult to argue that the final rule deviated too sharply from the proposed one, thereby depriving CMA of notice. On the basis of the above discussion, it would be difficult to argue that the VDC Panel did not have sufficient notice of OSHA's consideration given to reducing the exposure levels for VDC to a level below the proposal. Consequently, it is unlikely that CMA could argue that there was insufficient notice of the proposed change in exposure limits to VDC. RBD/mbl R. Bruce Dickson Leslie A. Gonzalez SL 061778 2566 Federal Register / Vol. 54, No. 12 / Thursday, January 19. 1989 / Rules and Regulations tungsten (1977h, as cited in ACGIH exposed continuously to VDC significant increase in tumors (Viola and ` 1986/Ex. 1-3, p. 614), NIOSH states that concentrations of 5,15, 25. or 47 ppm for Caputo 1977/Ex. 1-937). Other information on the effects of exposure to 90 days; only the animals exposed to 5 investigators exposed rats to 25 or 75 soluble tungsten compounds in the ppm showed no increases in mortality . ppm by inhalation for six hours/day, working population is not available. The (Prendergast, Jones. Jenkins, and Siegel five days/week for 18 months, or to 60, ^WtCGIH (1988/Ex. 1-3, p. 614) 1967/Ex. 1-928). 100, or 200 ppm VDC in their drinking ^^recommends a lower TLV for the Nasal irritation, liver cell water for two years, and found no soluble, as compared to the insoluble, degeneration, and retarded weight gain increase in tumor incidence in these compounds of tungsten because of the were reported in rats following 20 six- animals (Rampy, Quast, Humiston et al. former's greater systemic toxicity. No - hour exposures to 500 ppm VDC (Gage 1977, as cited in ACGIH 1986/Ex 1-3, p. comments other titan those of NIOSH -' 1970/Ex. 1-318); at 200 ppm. only nasal 628). In mice, VDC was not active eithe'- (Ex. 8-47) were received on this irritation occurred. Studies by Torkelson as a whole mouse skin carcinogen or by substance. and Rowe (1981b, as cited in ACGIH subcutaneous injection. In the final rule, OSHA is establishing 1986/Ex. 1-3, p. 628) in which rats, an 8-hour TWA of 1 mg/m' and a STEL ; rabbits, guinea pigs, and dogs were In other studies, VDC proved : mutagenic in both B. coli and S. of 3 mg/m* for tungsten and its soluble - exposed to 25,50, or 100 ppm VDC for compounds, measured as tungsten. The > eight hours per day, five days per week typhimurium strains (Greim, Bonse, Radwan et aL 1975/Ex 1-904; Bartsch. Agency concludes that these limits will ; for six months revealed injury of the Malaveille. Montesano, and Tomatis protect workers against the significant kidneys and liver in all animals at all 1975/Ex 1-889). VDC has been risks of systemic toxicity, anorexia, . levels of exposure. Maltoni (1977/Ex. 1- implicated as a tumor initiator in a colic, incoordination, trembling, and 985) andMaltoni, Cotti, Morisi, and carcinogenesis bioassay by Van Duuren, dyspnea, all of which constitute material Chieco (1977/Ex. 1-1090) conducted an Goldschmidt, Loewengart et al. (1979/ health impairments that are associated evaluation of VCD's carcinogenicity in Ex. 1-938). Studies by Reitz, Watanabe, with exposure to these compounds at which mice, rats and hamsters were McKenna et al (1980/Ex-1-927) suggest levels above the new PELs. exposed to levels from 10 to 150 ppm for that VCD's tumorigenicity is a result of VTNYIJDENE CHLORIDE fl.l- four hours per day, five days per week its ability to initiate cell injury, rather PICHLOROETHYLENE) for 52 weeks, with results reported than of its ability to alter the genetic CAS: 75-35-4: Chemical Formula: CHa= CD, HS.No.1428 - Previously, OSHA's Z tables did not include a limit for vinylidene chloride , (VDC), The ACGIH has established 5 ,* ppm as an 8-hour TWA and 20 ppm as a 15-minute STEL NIOSH and OSHA, in 1978, jointly recommended that employee exposure to VDC be reduced ^tathe lowest feasible level on the basis . ^H/DCs carcinogenicity (NIOSH/ ^KHA 1978/Ex. 1-1119). OSHA proposed a PEL of 5 ppm (8-hour TWA) and a STEL of 20 ppm. However, in through, week 98 of the study. In those mice exposed to 25 ppm VCD, 21 percent of the males and 1.5 percent of the females developed kidney adenocarcinomas; these tumors were . not seen in rats exposed to amounts of i VDC up to 150 ppm.Exposures of 100 or 150 ppm in rats did produce a significant increase In mammary adenocarcinomas, and this response was dose-related (Maltoni 1977/Ex. 1-985; Maltoni. Cotti. Morisi. and Chieco 1977/Ex. 1-1090), ' * Overt toxicity and mortality occurred early in the studies after four-hour . exposures at levels of 50 ppm in mice . material of an injured cell. However, VDC has been shown to alkylate DNA in situ and increase the rate of DNA repair to a small extent in mice (Norris and Reitz 1984/Ex. 134B). The actual cell injury is caused by VDC metabolites, which are highly Teactive and cytotoxic (Maltoni 1977/Ex, 1-985; Hathway 1977/ Ex. 1-906; Hensehler and Bonse 1977/Ex. 1-908). A cohort study of 138 VCD-exposed workers did not identify any VCD- related health effects in these workers (Ott, Fishbeck. Townsend, and . response to record comments, the final and 200 ppm in rats; hamsters exposed Schneider 1978/Ex. 1-924). The cohort rule promulgates a 1-ppm limit as an 8- to 20 ppm VDC'showed no increase in was too small to provide any evidence hour TWA. Vinylidene chloride is a `' tumor incidence (Maltoni 1977/Ex. 1- . that VDC is not likely to be, .,. colorless liquid that polymerizes readily;' 985; Maltoni, Cotti, Morisi, and Chieco -- carcinogenic. 1v1 '.' `.1, . The acute oral LD for male rats is .. 1977/Ex. 1-1090).`.v:~ V ' , `1 . The Chemical Manufacturers 2500 mg/kg (Jenkins, Trabulus, and ,'\ A study by.Murray. Nitschke. Rampy, ! Association submitted the results of an ' Murphy 1972/Ex. 1^960). The LC#for `0,/` and Schwetz (1979/Ex. 1-920) ' - NTP gavage study of VDC in mice and rats exposed to a single four-hour investigated the embryotoxic, fetotoxic, " 1 rats (NTP 1982/Ex. 134B). The only exposure oFVDC vapor was reported as " and teratogenic effects of inhaled and , observed significant increase in tumor 8350 ppm in onestudy (Siegel Jones, ingested VDC (in rats) and Inhaled VDC. .. incidence occurredln low-daseiemale Coon, and Lyon 1971/Ex. 1-371) andr/n' (in rabbits). In the inhalation studies, mice; this increase was hot considered 32.000 ppm in an earlier study ' ; rats wen exposed to Z0.80, or 160 ppnC ! to be related to"VDC administration. (Carpenter, Smyth, and Pozzani 1949/Ex' VDC for seven hours per day. VDC was .. because similar effects were not . 1-722). liquid VDC causes transients toxic to both the adults and their J observed in high-dose female mice, male irritation-to the eyes of rats but has little J embryos at levels of 80 and 160 ppm mice, or rats-He NTP(1982/Ex 134B) effect on exposed skin if the VDC is " among the rats, and at 160 ppm in ,, concluded that VDC was not allowed to evaporate (Torkelson and ' rabbits. At exposure levels of 20 ppm in carcinogenic in mice or rats exposed by Rowe 1981b, as cited in ACGIH 1988/Ex.' rats and 80 ppm in rabbits, neither. gavage, but cautioned that a maximum 1-3, p.628). .' - maternal toxicity nor effects on tolerated, dose had not been Prendergast and co-workers (1967/Ex. embryonic or fetal development were \7. demonstrated and that previously .. . 1-92Q) exposed rats, rabbits, guinea pigs, noted. In the ingestion study with rats, ' - reported studies had ahownrthat. <. and monkeys eight houra/day, five ' ^ r;' drinking water containing 200 ppm VDC carcinogenicity is associated with.VDC days/week for six weeks to 395 mg/m?. ; caused no toxic effects In either the rats inhalationhy animals.-.-,,.> ..... . (100 ppm); these authors saw no visible .or their offspring. Based on the carcinogenicity evidence signs of toxicity while the exposure was";^ -Two strains of rata exposed to 75 or, described above. NIOSH (Ex 8-47,,, in process, butTabbits and monkeys lostV lOOppnr VDC for five days/week, six' Table N6B) indicated that VDC is a . weight These same species were "' -v hours/day for 12 months did not show a suitable candidate for an individual 6(b) [Snaki. of th demo >nse jjience ies-s _ isu ..to bt jSobje iSHa ijh'gei IAII lider iuse jylchl itemer icity < latthi :hew jaltb T oposet %VDC jotectk [ej.Tht 'enderj 'ppm t [crease (eTork rACGI mhdli' lese ct ,cgit tvide ibhtan lould c Spinas isk ass' Lt" (E> [OSH/ idenc ISH.; _jpose [bt affc Imsy ,j'estio: &967/E Baerve yiels v, istopa: scposet elated i.expc -.lpuPa (day, fb- liver tc iter e: 125 ppm (month: _ OSH (dearly Eadvers tairborr ISO pptr Tpotent Fand ki. const:'. /wifi- SL 061779 iJL Federal Register / VoL 54, No. 12 / Thursday. January 19. 1989 / Rules and Regulations Z567 (Vio! atl(j r ^R60, irinkino d no these ston et al. Etc. 1-3, p, dve either 8ti or by 1 mse, tertsch, niatis tn a l Duuren, (1979/ afanabe, ) suggest result of rather netic ever, J DMA >NA Norris :tual cell lites, totoxic 1yl977/ ifIMEk. 0rkers ihort lence o/an and y unor male ered in male J4BJ 5d by was VDC ience Jeanaking. However, the CMA (Ex. 1651 within the meaning of the Act. freshly formed metal fume, results in the 5 of the opposite opinion, stating that Therefore, OSHA concludes that the appearance of delayed, flu-like ^demonstrated lack of tumor proposed limits of 5 ppm as an 8-hour symptoms, including dyspnea, coughing, bonse in most studies, coupled with TWA and 20 ppm as a STEL will not pains in muscles and joints, fever, and gdence that VDC metabolism is sufficiently protect workers from the chills. Recovery usually requires one or aes-specific, "demonstrates that significant risk of organ damage, and two days of time away from work. In ' is unlikely to pose an oncogenic that a further reduction in the PEL is addition to fume fever, exposure to Jjlto humans" (Etc 165, p. 42). CMA (p objected to die statement by warranted. Accordingly, OSHA is establishing a 1-ppm 8-hour TWA limit welding fume may damage the small airways, causing interstitial pneumonia 3SH and OSHA in the joint Current for vinylidene chloride in jhe final rule. (Abraham 1983). tjligence Bulletin on VDC (NIOSH/ . WELDING FUMES Several commenters, the American SA 1978/Ex. 1-1119} that VDC be CAS: None; Chemical Formula: Not available Iron and Steel Institute (Exs. 129,188), jSidered a potential carcinogen H.S. No. 1430 the Abbott Laboratories (Tr. 9-155 to 9- Eause of its structural similarity to, yl chloride: the CMA considered this Btement inappropriate, given the - "ticity data available.' ' ifatthew Gillen and Scott Schneider Rhe Workers Institute for Safety and gaitH (WISH) commented that the ; , OSHA formerly had no limit for exposure to welding fumes, which are defined as fumes that are generated by '. the manual metal arc or oxy-acetylene welding of iron, mild steel, or aluminum. The ACGIH has set an 8-hour TWA of 5 mg/m*for these welding fumes. , 156), and the American Welding Society (Ex. 3-860), were of the opinion that OSHA's discussion of welding fumes in the NPRM was not clear with regard to whether the limit applied to exposure samples taken inside or outside of the welding helmet OSHA wishes to clarify "posed 5*ppm PEL and 20-ppm STEL measured as total particulate in the , that welding fume is to be measured in SrVDC would not provide sufficient - welder'3 breathing zone. OSHA the breathing zone of the welder the "btection from systemic effects (Ex. proposed an 8-hour TWA of 5 mg/m' for specific details of the appropriate Jg). They pointed out that the study by these fumes; this limit is established in positioning of the sampler should be fendergast et al. (1967/Ex. 1-926) found the final rule. This limit applies to the determined on the basis of guidance in 5 ppin to be the lowest effect level for total fume concentration generated the Field Operations Manual (OSHA ncreased mortality in animals, and that during the welding of iron, mild steel, or 1984). This is consistent with a past Ke Torkelson and Rowe (1981b, as cited aluminum; the fumes generated by the OSH Review Commission decision (8 [jnXCGiH 1986/Ex. 1-3, p. 828) study welding of stainless steel, cadmium, or . OSHRC1049). ; - ouhd liver and kidney injury in animals, lead-coated steel, or other metals such NIOSH (Ex. 8-47) stated at the : bese commenters stated that the as copper, nickel, or chrome are r ,, , hearing that welding fumes 'should be - kCGIH TLV cannot be considered to - considerably more toxic and should be " designated as a carcinogen. This view - rovide adequate protection for this - kept at or below the levels required by was also endorsed by Dr.- James Melium. ubitance. Given this fact OSHA their respective PELs. Welding fumes. . . i of the New York State Department of : hould consider the NIOSH REL of 1 'f' consist of metallic oxides generated by . Health (Tr. p. 11-104). frr response to. _ pin as an interim value until further ' ' the heating of metal being welded, the. . these commenters, OSHA notes that.. sk assessment studies can be carried " welding rod. or its coatings. - -- there are few data- sufficient to -r 1 . out" (Ex. 118). Although these types of welding establish a-dose-response for the fumes. J^OSHA has re-examined the health generally produce fumes consisting of Accordingly, OSHA believes it would be Evidence in light of the comment by aluminum, iron, or zinc oxides, other premature to identify these fumes as . 1SH, and has determined that the toxic gases may also be produced in potential occupational carcinogens.. proposed 5-ppm TWA PEL for VDC does large amounts (Ferry and Ginther 1952/ OSHA concludes that a PEL for not afford workers sufficient protection Ex. 1-900; Ferry 19S4/Ex. 1-782; welding fumes is needed to protect r (from systemic effects. Although it is Silverman 1956/Ex. 1-1169; Homer and workers involved in the welding of' questionable, in the Prendergast et al. / Mohr 1957/Ex. 1-787). The welding of aluminum, iron.,or mild steel from the [(1967/Ex. 1-928/ study, that file - - iron metals may give off fumes of significant risk of metal fume fever and (observed deaths at lower exposure manganese, silicate, and various organic ' respiratory irritation associated with the Revels were compound-related, - -- : binders. Aluminum welding may - . generation of welding fumes. In the final Jstopathologic examination of animals generate fumes consisting of fluorine,. Tl rule, OSHA is establishing.a TWA of 5 Exposed to 47 ppm showed treatment-1 t ! arsenic, copper, silicon, and beryllium . ^ mg/m* for these particular types of ,c Delated liver and Iddney damage. Using: :! (NIOSH 1975h and American Welding, .-T: ; welding fumes, measured as total fan exposure regimen similar to - - Society 1974, both as cited in ACGIH . particulate inside the welder's breathing ^occupational exposure (i.e., eight hours/-, 1986/Ex. 1-3, p. 634). Eighteen different . zone. The Agency finds that this limit . raay, five days/week), Torkelson and r substances, including fluoride, t 4 will substantially reduce the significant [Rowe (1981b,' as cited in ACGIH1986/ - manganese, silicon, titanium, and " V risk of material health impairment to FEx. 1-3, p. 628) demonstrated kidney and sodium and potassium silicates, have - which manual metal arc or oxy- . ; liver toxicity in four species of animals been measured in the fumes resulting acetylene welders of iron, mild steel, or after exposure to VDC levels as low as from the welding of mild steel (ACGIH . aluminum were previously exposed in 25 ppm were administered for only six : 1986/Ex. 1-3, p. 634). -. - the absence of any OSHA limit months. -1 , .*. fc; OSHA believes that these studies clearly demonstrate that VDC can cause adverse liver and iddney damage at Excessive exposure to welding fume can cause a variety of disorders, most notably metal fume fever. It has been estimated that 30 to 40 percent of all ZINC OXIDE (FUME) CAS: 1314-13-2; Chemical Formula: ZnO HA No. 1437 - :' v airborne concentrations as low as 25 to welders have experienced metal fume , OSHA's former exposure limit for zir 50 ppm and suggest that VDC is a fever at some time (Abraham 1983, in oxide fume was 5 mg/m* as an 8-hour potential occupational carcinogen. Liver Environmental and Occupational ,. TWA The ACGIH recommends a 5-mg and kidney damage and cancer clearly. - Medicine, W.N. Rom, e<L,p. 146). This aHTWA and also has a STEL of 10 mg. constitute material health impairments disorder, which results from exposure to m*. NIOSH recommends a 5-mg/m* 10- SL 061780 dssis lor proposing a new limit for adenocarcinomas: these tumors were (Ott, Fishbeck. Townsend, and tungsten a'nd compounds (soluble). At not seen in rats exposed to amounts of Schneider 1976). the time of the final rule. OSHA will VCD up to 150 ppm. Exposures of 100 or OSHA U proposing an 8-hour TWA of promulgate a new limit if the Agency 150 ppm in rats did produce a significant 5 ppm and a 15-minute STEL of 20 ppm determines that this limit will increase in mammary adenocarcinomas, for vinylidene chloride. The Agency substantially reduce significant risk. and this response was dose-related preliminarily concludes that these limits VINYLIDENE CHLORIDE fl.l---- dichluruethyUnei (Maltoni 1977; Maltoni, Cotti, Morisi. and Chieco 1977). Overt toxicity and will protect workers from the risk of kidney and liver damage and CAS: 75--35--A; Chemical Formula: C1L =CClj mortality occurred early in the studies carcinogenicity potentially associated H.S. No. 1428 after 4-hour exposures at levels of 50 with exposure to VCD at the levels Currently, OSHA's Z tables do not ppm in mice and 200 ppm in rats; permitted by the absence of any OSHA have a limit for vinylidene chloride hamsters exposed to 20 ppm VCD limit. This limit may be an interim limit; (VCD). The ACGIH has established 5 showed no increase in tumor incidence as future priorities permit, the Agency ppm as an 8-hour TWA and 20 ppm as a (Maltoni 1977; Maltoni, Cotti. Morisi. may perform a quantitative risk 15-minute STEL. NIOSH recommends and Chieco 1977). assessment for VCD and consider that employee exposure to VCD be A study by Murray, Nitschke, Rampy, further rulemaking. This health evidence reduced to the lowest feasible level, and and Schwetz (1979) investigated the forms a reasonable basis forproposing a considers VCD a carcinogen. Vinylidene embryotoxfc. fetotoxic, and teratogenic r hew limit for vinylidene chloride (1,1- chloride is a colorless liquid that effects of inhaled and ingested VCD (in ' dichloroethylene). At the time of the polymerizes readily. rats) and inhaled VCD (in rabbits). In - final rule. OSHA will promulgate a new The acute oral LD for male rats i3 ~~ the inhalation studies, rats were- * . limit if the Agency determines that this 2500 mg/kg (Jenkins,'Trabulus, and exposed to 20, 80, or 160 ppm VCD for . limit will substantially reduce - Murphy 1372). The LC*o for rats exposed hours per day. VCD was toxic to both - significant risk. to a single 4-hour exposure of VCD the adults and their embryos at levels of - FUMES ~" vapor was reported as 6350 ppm in one study (Siegel, Jones, Coon, and Lyon 1971) and 32,000 ppm in an earlier study (Carpenter, Smyth, and Pozzani 1949). Liquid VCD causes transient irritation to the eyes of rats but has little effect on , exposed skin if the VCD is allowed to-. . evaporate (Torkelson and Rowe 1981). Prendergast and co-workers exposed rats, rabbits, guinea pigs, and monkeys 8 hours/day, 5 days/week for 6 weeks to 395 mg/m5 (100 ppm); these authors saw no visible signs of toxicity while the ~' exposure was in process, but rabbits " and monkeys lost weight' These same 80 and 160 ppm among the rats, and 160 ppm in rabbits. At exposure levels of 20 ppm in rats and 80 ppm in rabbits, neither maternal toxicity nor effects on embryonic or fetal development were noted. In the ingestionstudy with rats, :. drinking water containing 200 ppm VCD caused no toxic effects in either the rats or their offspring; -- - - Two strains of rats exposed to 75 or 100 ppm VCD for 5 days/week, 6 hours/ day forl2 months didriot show a ' '*" significant increase in tumors (Viola and Caputo 1977). Other investigators " exposed rats to 25 or 75 ppm by CAS: None; Chemical Formula.-Not available H.S. No. 1430 - OSHA currently has no limits for exposure to welding fumes, which it defines as fumes that are generated by the manual metal areor oxy-acetylene welding of iron, mild steel, or aluminum. The ACGIH has set an 8-honr TWA of 5 mg/m5 for welding fumes, measured as total particulate inside the welding helmet ; -- Although welding of these types generally produces fumes made up of aluminum, iron, or zinc oxides, other species were exposed continuously to VCD concentrations of 5,15,25. or 47 ppm for 90 days; only the animals inhalation for 6 hours/day, 5 days/week toxic gases may be produced in large for 18 months or to 60,100. or 200 ppm . amounts (Ferry and Ginther 1952; Ferry VCD in their drinking water for 2 years ' 1954; Silverman 1956; Homer et al. 1957). exposed to 5 ppm showed no increases and found no increase in tumor in mortality (Prendergast, Jones, Jenkins, :- incidence in these animals (Rampy, and Siegel 1967), v.. . ; ; Quast, Humiston et al. 1977). In mice,.. Iron metals may give off fumes of manganese, silicate, and various organic binders. Aluminum welding may result Nasal irritation, liver cell VCD was not active either as a whole in fumes consisting of fluorine, arsenic, degeneration, and retarded weight gain mouse skill carcinogen or by copper, silicon, and beryllium (NIOSH werereported in rats following twenty. ., subcutaneous injection. ` * . . r - n.d.; American Welding Society 1973). 6-hour exposures to 500 ppm VCD_(Gage In other'studiesi VCD proved ' ' Eighteen different substances, including 1970); at ZOO ppm, only nasal irritation mutagenic in both fi. coli and S. : T. . fluoride, manganese, silicon, titanium, occurred. Studies byTorkelson and , typhimuriumstrains (Greim. Bouse, and sodium anff potassium silicates, Rowe (1981) in whlqh rats, rabbits, ., `,.,1 Radwari et aL 1975; Bartsch.Malavellle^*: have^been measured in'the fumes'' guinea pigs, and dogs were exposed to . Moritesano, and Toniatis 1975). VCD has; resulting from the welding of mild steel 25.50, or 100 ppm VCD for 8 hours per 1 j . been implicated as a tumor initiator in a' - (ACGIH 1986, p. 634).' The process of day, 5 days per weekibr 6 months . 7 l '': , carcinogenesis bioassay by Van Duuren- ^shielded arc welding is known to. revealed injury of the kidneys and liver (1979). Studies by Reitz; Watanabe, ' -T produce ozone, and when carbon in all animals at all levelsof exposure. 1 ^McKenna et al. (1980) suggest that T _ dioxfde is' used aeVshield gas, carbon Maltoni (1977) and Maitoni, .Cotti, 4 } VCD's tumorigenicity ls a result of its _ monoxide Is given'jff (NIOSH ri.d.; Morisi, and Chieco (1977) conducted an J ability to initiate cell injury and nof of":~`- American'Welding Society 1973). evaluation of VCD's carcinogenicity in ; V its ability to alter the genetic material of The adversaries!theffects associated which mice, rats and hamsters were i (fan injured cell. The actual cell injury is ' with over exposure to welding fumes are exposed to levels from 10 ppm to 150 caused by VCD metabolites which are ' those of metal.fume fever--chills and ppm for 4 hours per day, 5 days per highly reactive and cytotoxic (Maltoni . fever, profuse sweating, and week for 52 weeks; with results reported' 1977; Hathaway 1977; Henschler and, ~ --weaknesv-and respiratory irritation. through week 98 of the study. In those Bonsel977). 'OSHA preliminarily concludes that a mice exposed to 25 ppm VCD, 21 percent A cohort study of 138 VCD-exposed PEL'for welding fumes is needed to of the males and 1.5 percent of the . workers did not identify any VDC- protect workers involved in the welding females developed kidney ; related health effects in these workers . of aluminum. Iron, or ntild steel from the SL 061781