As with any potential toxic exposure, the dose and duration of exposure of asbestos matter. And these factors matter varyingly in connection to specific outcomes of interest. By 1930, virtually everyone understood that all the asbestos minerals caused asbestosis. While no one thought that just any exposure could cause asbestosis, everyone agreed that some asbestos exposures, of sufficient intensity and duration, and with some minimal latency from first exposure to manifestation, caused asbestosis.
The first serious attempt to quantify the nature and extent of asbestos exposure that caused asbestosis came in 1938, with a report from the United States government. Directed by the United States Surgeon General, the report was the first to quantify asbestos exposure in relation to the diagnosis of asbestosis. Its authors studied a cohort of over 500 North Carolina asbestos textile workers, and reported “the only cases of asbestosis, three in number, found below 5 million particles per cubic foot were diagnosed as doubtful; well-established cases occurred at higher concentrations. It appears from these data that if asbestos dust concentrations in the air breathed are kept below this limit new cases of asbestosis would not appear.”[1] From their analysis of the data, the federal government authors concluded provisionally that “5 million particles per cubic foot [5 mppcf] may be regarded tentatively as the threshold value for asbestos-dust exposure….”[2]
Eight years after this Public Health Service publication, the American Conference of Governmental Industrial Hygienists (ACGIH), in 1946, set its threshold limit value (TLV) at 5 mppcf.[3] In the period between the 1938 Public Health Service report and the 1946 ACGIH adoption of a TLV of 5 mppcf, the United States was engaged as both an employer and a contractor for products made with asbestos. The government cited and relied upon the 5 mppcf standard as protective of workers throughout the wartime manufacturing effort, as well as afterwards, into the 1960s. Whether the 5 mppcf standard protected workers from asbestosis proved to be an academic question because the government itself often failed to control asbestos exposures to that level among its own employees, most notably in government owned and contracted shipyards.[4]
By the early 1960s, the increasing prevalence of asbestosis among insulators and other end-users of asbestos-containing products became clear evidence that either the 5 mppcf TLV was being exceeded or that it was inadequately protective or both. In 1968, the ACGIH urged a change in the metric for measuring occupational exposure and the acceptable TLV to 12 fibers per cubic centimeter (f/cc). Two years later, the ACGIH further refined its TLV to a recommended TLV of 5 f/cc, counting fibers longer than 5 micrometers (µm), with a recommended excursion ceiling of 10 f/cc not to exceed 15 minutes.
Some states had adopted the ACGIH TLV as a regulatory standard, although some of the states failed to enforce the standard, and other states had no standard at all. The regulatory landscape shifted seismically for private, non-governmental employers when President Nixon signed the Williams-Steiger Act (The Occupational Safety and Health Act of 1970) into law on December 29, 1970. The following year, the newly created Occupational Health & Safety Administration (OSHA) established a permissible exposure level (PEL) for asbestos of 12 f/cc, time-weighted average over 8 hours.
The TLV and the initial OSHA PEL were set for “asbestos,” although there is no one mineral fiber that is asbestos. When the principal outcome of interest was asbestosis, the unitary standard made some sense. By the time that OSHA came upon the regulatory scene, the scientific evidence was rapidly converging upon a conclusion that not all asbestos minerals had the same carcinogenic potency or properties. The principal outcome of concern was shifting to a very specific cancer, mesothelioma, which the pathologist Christopher Wagner identified, in 1960, as almost uniquely associated with crocidolite (“blue asbestos”), one of the six asbestos minerals.[5] Indeed, by 1983, Dr. Harriet Hardy would reflect on the evolution of knowledge of the causes of mesothelioma to note that:
“A fatal malignancy [mesothelioma] associated with inhalation of a single form (crocidolite) of asbestos invaded the chest wall (pleura) and/or the abdominal wall.”[6]
By 2000, the differential mesothelioma potency of the six different asbestos minerals (amphiboles: crocidolite, amosite, tremolite, anthophyllite, and actinolite, and serpentine: chrysotile) was clear beyond cavil. Crocidolite was orders of magnitude more pathogenic than chrysotile with respect to mesothelioma, with a ratio of upwards of 500:1, with the 1 itself in doubt, and amosite somewhere in between.[7]
In more enlightened countries, such as the United Kingdom, manufacturing industry voluntarily abandoned importing crocidolite in 1970, while continuing to use chrysotile asbestos. In the United States, however, the regulatory agencies, OSHA and EPA, engaged in fiber-type egalitarianism. The federal agencies persisted, in the face of very strong contradictory evidence, in promulgating standards and rules that applied equally to all asbestos fiber types. Over the years, OSHA reduced the asbestos PEL to 0.2 f/cc, in 1983, and then to 0.1 f/cc, in 1994, where it remains today. The standard grossly overprotects against chrysotile, and grossly underprotects against crocidolite.
The rationales for the fiber-type egalitarianism was always thin to non-existent. On one theory, federal regulations do not distinguish among the six different mineral fibers because they are all capable of causing asbestosis and mesothelioma. This rationale simply confuses hazard with risk, and it ignores the shifting basis for lowering the PEL based upon perceived cancer risk, not for asbestosis risk.
Early in OSHA’s existence, the technical equipment to distinguish among mineralogical fiber types was relatively expensive and not widely distributed. One potential argument for a single standard for all fiber types was the supposed difficult of distinguishing among fiber types in the field. This rationale evaporated with the advance of technology and the spread of the necessary equipment into many work-a-day industrial hygiene laboratories.
Another rationale sometimes asserted by extreme advocacy groups such as the Collegium Ramazzini is the precautionary principle. This principle is not, however, a rational basis; it simply assumes what is to be proven in the face of contradictory evidence. The net result is that precautionary reasoning kept the much more dangerous fiber, crocidolite, in use for an intolerably long period, while subjecting chrysotile to unreasonable regulation.
Another early rationale was that many occupational epidemiologic studies involved exposures to mixtures of asbestos fiber types. This rationale was evaporated by the publication of many studies of workplaces that used a single type of asbestos fiber, which allowed reasonable, evidence-based estimates of relative pathogenicity of fiber types.
Perhaps the real reason for the embrace of fiber type egalitarianism by advocacy scientists and the lawsuit industry was that the companies that mined and sold commercial amphibole fibers (amosite and crocidolite) were mostly in South Africa, a country that refused to honor and domesticate the judgments of American courts. Advocates for the lawsuit industry needed to ensure that the chrysotile mining and milling companies could not escape liability in cases involving “mixed” fiber type exposures, by raising the differential pathogenicity. Some manufacturing companies that used commercial amphiboles such as crocidolite and amosite joined in the attack because they were concerned that companies that used only chrysotile would escape liability, leaving them to pay the entirety of verdicts. The lawsuit industry and segments of manufacturing industry worked in cahoots to subvert the evidentiary base for distinguishing among fiber types.
Fiber type egalitarianism led the Environmental Protection Agency to attempt a ban on asbestos, regardless of fiber type, in 1989. The EPA rulemaking was unceremoniously vacated in 1991, by the United States Court of Appeals, for lacking substantial evidentiary support.[8]
Advocates at the EPA, with support from NGO zealots, including the Collegium Ramazzini, have been urging a complete ban, irrespective of mineral fiber type, ever since. Asbestos found its way to the EPA’s short list of priority substances for review under amendments to the Toxic Substances Control Act. In 2019, a friendlier Circuit for the advocates declared that the Act required the EPA to address legacy uses as well.[9]
After 2019, the EPA rulemaking proceeded with a predictable disregard for the vast differences in mineral fiber types and their respective pathogenicities. In the first part of the ongoing rulemaking, the EPA invaded the jurisdictional turf of OSHA to ban the very few remaining industrial uses of chrysotile. Predictably, the EPA’s rulemaking cited epidemiology of mixed fiber type usage. This part of EPA’s rulemaking has been challenged in court. The case was argued, on June 1, 2026, on an appeal before the Fifth Circuit, in Texas Chemistry Council v. EPA (No. 24-60193).
The EPA is currently considering accepting comments on part two of its rulemaking to evaluate risks involved with legacy uses of asbestos minerals. Professor Robert Nolan and I (more the former than the latter) have filed comments in the form of a report on the “Necessary Considerations for a Science-Based Risk Evaluation of Asbestos Fiber Types in the EPA’s Planned Rulemaking.” On behalf of the International Environmental Research Foundation, we urged the agency to abandon its willful disregard of mineralogical and pathogenic differences between and among the different asbestos minerals, in order to promulgate a sane, scientific, legally defensible risk evaluation of legacy asbestos use, by fiber type.[10] The comment period has been extended to September 23, 2026.
[1] Waldemar C. Dreeseen, J. M. Dallavalle, Thomas I. Edwards, J.W. Miller & R.R. Sayers, A Study of Asbestosis in the Asbestos Textile Industry, Public Health Bulletin No. 241, at ix (1938).
[2] Id. at 91.
[3] American Conference of Governmental Industrial Hygienists, Documentation of threshold limit values – asbestos (1946).
[4] Kara Franke & Dennis Paustenbach, Government and Navy knowledge regarding health hazards of asbestos: A state of the science evaluation (1900 to 1970), 23(S3) INHALATION TOXICOL. 1, 4 (2011).
[5] Christopher Wagner, C.A. Sleggs & Paul Marchand, Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province, 17 BR. J. INDUS. MED. 260 (1960); J. Christopher Wagner, The discovery of the association between blue asbestos and mesotheliomas and the aftermath, 48 BR. J. INDUS. MED. 399 (1991).
[6] Harriet Hardy, CHALLENGING MAN-MADE DISEASE: THE MEMOIRS OF HARRIET L. HARDY, M.D. 95 (1983).
[7] John T. Hodgson & Andrew A. Darnton, The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure, 14 ANN. OCCUP. HYGIENE 565 (2000); David H. Garabrant & Susan T. Pastula, A comparison of asbestos fiber potency and elongate mineral particle (EMP) potency for mesothelioma in humans,” 361 TOXICOL. & APPLIED PHARMACOL. 127 (2018) (“relative potency of chrysotile:amosite:crocidolite was 1:83:376”). See also D. Wayne Berman & Kenny S. Crump, Update of Potency Factors for Asbestos-Related Lung Cancer and Mesothelioma, 38(S1) CRIT. REV. TOXICOL. 1 (2008).
[8] Corrosion Proof Fittings v. EPA, 947 F.2d 1201 (5th Cir. 1991).
[9] Safer Chemicals, Healthy Families v. EPA, 943 F.3d 397 (9th Cir. 2019).
[10] Robert P. Nolan & Nathan A. Schachtman, on behalf of the International Environmental Research Foundation, Necessary Considerations for a Science-Based Risk Evaluation of Asbestos Fiber Types in the EPA’s Planned Rulemaking; Submission in response to the EPA’s Request for Additional Information to Protect Americans from Legacy Uses and Associated Disposal of Asbestos (Aug. 22, 2026).
