IRON OXIDE (DUST)
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: 1309-37-1; CHEMICAL FORMULA: Fe2O3
OSHA formerly had an 8-hour TWA limit of 10 mg/m3 for iron oxide fume. The ACGIH has established a limit of 5 mg/m3, measured as iron, total particulate. The proposed PEL was 5 mg/m3, and NIOSH (Ex. 8-47, Table N1) supported the proposed limit. However, the final rule retains OSHA’s former limit of 10 mg/m3 for this substance. The fume of iron oxide is red-brown in color.
Animals exposed to iron oxide or to iron oxide mixed with less than 5 percent silica by inhalation or by intratracheal injection did not develop pulmonary fibrosis (Naeslund 1940/Ex. 1-650; Harding, Grout, Durkan et al. 1950, as cited in ACGIH 1986/Ex. 1-3, p. 325). Inhalation of iron oxide dust also did not produce lung cancer in mice (Muller and Erhardt 1956/Ex. 1-648).
The evidence of iron oxide’s toxicity in humans is conflicting. Drinker, Warren, and Page (1935/Ex. 1-315) concluded that exposures to iron oxide fume should be maintained below 10 mg/m3, and a U.S. Department of Labor study (1941, as cited in ACGIH 1986/Ex. 1-3, p. 325) found that exposures below 30 mg/m3 were without adverse effect. There are several studies, on the other hand, that report chest X-ray abnormalities in miners, welders, silver polishers, electrolytic iron oxide workers, foundry workers, and boiler scalers (Doig and McLaughlin 1936/Ex. 1-626; Stewart and Faulds 1934/Ex. 1-764; Doig and McLaughlin 1948/Ex. 1-627; McLaughlin, Grout, Barrie, and Harding 1945/Ex. 1-642; Davidson 1951, as cited in McLaughlin 1951/Ex. 1-727; Pendergrass and Leopold 1945/Ex. 1-653; Dunner and Hermon 1944/Ex. 1-731) exposed to iron oxide dust or fume. Some of these workers developed disabling pneumoconiosis; however, the exposures of many of these workers were mixed and in some cases included exposure to varying amounts of silica.
McLaughlin (1951/Ex. 1-727), whose opinion on the subject is widely accepted, believes that the presence of iron oxide dust or fume in the lung causes a pigmentation (termed siderosis) that is responsible for the changes seen in exposed individuals’ chest X-rays. Siderosis is believed not to progress to fibrosis, and 6 to 10 years of exposure to about 15 mg/m3 iron oxide dust is required before this condition develops (Fawcett 1943/Ex. 1-736; Fleischer, Nelson, and Drinker 1945/Ex. 1-1051; Hamlin and Weber 1950/Ex. 1-698). However, no studies are available that correlate exposure levels with X-ray changes. Dr. Stuart M. Brooks (NIOSH 1986b, p. 425) notes that “[m]ore sophisticated physiologic testing, including measurement of the lung’s mechanical properties, is required to better document lung function changes that may occur following inhalation of iron-containing dusts. In vitro studies or animal experimentation might be helpful in determining dose-response relationships, understanding lung clearance mechanisms for iron, and elucidating any fibrogenic properties of various ferrous compounds.”
Some studies have shown that workers with exposures to iron oxide and such other substances as silica, radon gas, diesel exhaust, corn oils, and the thermal decomposition products of synthetic resins (Faulds 1957/Ex. 1-635; Dreyfus 1936/ Ex. 1-897; Bidstrup 1959/Ex. 1-1030; Boyd, Doll, Faulds, and Leiper 1970/Ex. 1-716; Braun, Guillerm, Pierson, and Sadoul 1960/Ex. 1-1141; Monlibert and Roubille 1960/Ex. 1-647; Jorgensen 1973/Ex. 1-1023; Muller and Erhardt 1956/Ex. 1-648; Koskela, Hernberg, Karava et al. 1976/Ex. 1-744; Gibson, Martin, and Lockington 1977/Ex. 1-1053) have a greater risk of developing lung cancer. However, OSHA agrees with the ACGIH that, “at this time, it is not generally accepted that exposure to iron oxide dust or fume causes cancer in man” (ACGIH 1986/ Ex. 1-3, p. 325). Stokinger (1984/Ex. 1-672) concluded that exposure to iron oxide dust and fume per se was not carcinogenic.
Several industry commenters (Exs. 8-22, 3-349, 3-829, 129, and 188; Tr. XI, pp. 137-138) objected to the proposed reduction in the PEL for iron oxide on the grounds that exposure to this substance does not cause fibrosis or pulmonary impairment, but rather siderosis, which is a benign pneumoconiosis. The American Iron and Steel Institute (Ex. 129, pp. 12-13) described siderosis as “simply a description of a condition that appears on radiographs.” OSHA disagrees with Mr. Hernandez’ assessment of the health effects potentially associated with exposure to iron oxide because the Agency believes that any occupational exposure that causes foreign substance to lodge in body tissues is undesirable. However, the Agency concurs with NIOSH’s Dr. Brooks (NIOSH 1986b, p. 425) that additional research is necessary to determine why the lung is unable to clear iron-containing dusts after inhalation.
Accordingly, OSHA finds it appropriate to retain the Agency’s former PEL for iron oxide dust and fume of 10 mg/m3, measured as total particulate. The Agency concludes, based on the evidence currently available, that this limit will protect workers from developing of siderosis, a benign pneumoconiosis that occurs after many years of exposure to levels of iron oxide dust or fume in excess of 15 mg/m3, and accumulation of iron dust in the lungs associated with ferric oxide exposure.