Consumer products in the United States have not had significant levels of benzene for decades, yet Plaintiffs’ counsel have filed thousands of cases, often called trace benzene suits, asserting that various consumer products such as degreasers, carburetor cleaners, mineral spirits, and paints have caused their clients to contract Leukemia, aplastic anemia or other blood related diseases. Since benzene has not been a known and intended ingredient of these products for many years, the claimants assert that other solvents that have been substituted for benzene, such as Toluene, Xylene, Hexane, Stoddards Solvent and VM&P Naphtha contain benzene and cause users to be exposed to benzene.
These suits are premised on exaggerated claims that these products contain much higher levels of benzene than they actually do, pointing to published references that are decades old or which rely on old references. (1), (2), (3), (4). Plaintiffs then add exaggerated usage claims to puff up exposure levels, and rely on a well known group of experts who promote a no threshold, any level of exposure is enough theory of causation. In doing so, Plaintiffs thrive on vague lay testimony of co-workers, the lack of recent published peer reviewed literature on benzene content of these solvents, and the lack of actual air or content test results during the Plaintiff’s exposure period to weave together a superficially plausible, but flawed, claim hoping to get past a Daubert challenge and get to a sympathetic jury.
An aggressive three pronged attack can expose Plaintiff’s claims as lacking substance.
First, establishing the benzene content of the product is in most jurisdictions the Plaintiff’s burden of proof, and is by and large a fact issue, not a matter for expert opinion. Expert opinions must be based on reliable data. Decades old references do not establish benzene content of current or recently used products or solvents not tested in a comparable time period as the references. Unless Plaintiff can establish by direct test results, MSDS’ or other documentation on Defendant’s products during the alleged exposure period, Plaintiff may not be able to prove with admissible evidence that the products at issue contained any detectible levels of benzene or any specific amount of benzene, that could then be used to estimate the Plaintiff’s exposure or dosage.
In response to Plaintiff’s expert, Melvyn Kopstein’s old references in his published article (1), a number of arguments can be made. First, the Consumer Product Safety Commission commissioned two studies resulting in reports in 1978 and 1980 and found nearly all consumer products already had less than .1% benzene content and 3 of 5 carburetor cleaners had no detectible levels of benzene. (5) (6). These reports lead the Consumer Product Safety Commission to withdraw their proposed ban on consumer products with over 0.1% benzene, as there was no need for the ban (7). Kopstein’s references were also attacked by the chemical industry which provided proof of the low current levels of benzene in their solvents. (2, 4). Kopstein has testified in litigation that benzene levels trended downward after his older references were issued. (22, 23).
The second prong of the attack should be against asserted high exposures based on unrealistic usage assumptions, and vague or selective statements of co-workers. High estimated exposures are often based on continuous use of multiple cans of spray or product per job.
Another expert frequently used by Plaintiffs recently published an article which indirectly contradicts many of Plaintiff’s usage claims and benzene exposure claims finding total VOC exposures from use of these products to be less than OSHA limits (8). Amazingly, this study did not address benzene exposures, directly. However, indirectly, it helps establish low benzene exposures by establishing low total volatile organic compound (VOC) levels. Detailed discovery of purchase and job records can also be used to show that the Plaintiff’s actual usage is far less than estimated by Plaintiff’s experts. In addition, actual simulated testing done by one of Plaintiff’s experts recently showed only intermittent use. (8) Also, many repair jobs performed by the claimant mechanic may not use these products at all.
The fourth prong is to attack the low dose, no threshold claims of Plaintiff’s experts.
Most reliable epidemiology studies have concluded that cumulative exposures of at least 50 ppm-years and most likely 200-400 ppm-years is required to cause AML, the only form of Leukemia that has clearly been linked to benzene exposures. (9-14). Other studies, such as the Glass, et al studies of the Australian Petroleum Industry Cohort and studies of the Chinese Cohort have been found to be flawed and not a reliable basis for establishing causation. (15-19).
Finally, some experts have put forth an unproven hypothesis that certain types of chromosome damages are markers of benzene induced Leukemia. However, even those Plaintiff experts putting forth such hypothesis have not been able to prove any particular pattern of chromosome damage as a basis to claim benzene as the cause. (20) In fact, one recent study surprised these scientists by disproving their hypothesis that topoisomerase inhibitors act like benzene in causing chromosome damage and Leukemia. (21).
So called Trace Benzene cases can be successfully defended with an aggressive multi-pronged attack on exposure related and causation issues.
(1)Kopstein M. 2006, Potential uses of petrochemical products can result in significant benzene exposures: MSDS must list benzene as an ingredient. J. Occup. Environment. Hyg. 3(1): 1-8;
(2)Jacques A.M. 2006 Benzene Levels in Hydrocarbon Solvents. J. Occup. Environment. Hyg. 3:D85-D87. [Benzene levels in modern solvents generally do not exceed .01% or 100 ppmv];
(3)Fedoruk, M.J., et al 2003, Benzene Exposure Assessment for Use of a Mineral Spirits – Based Degreaser. App. Occupational & Environment Hyg. 18:764-771. [spiked mineral spirits used. Natural benzene content of mineral spirits was 3 to10 ppm; nonrepresentative aggressive and vigorous simulated cleaning procedures used to obtain worst case scenario];
(4)McKee, R.H., 2007, Benzene Levels in Hydrocarbon Solvents – Response to Author’s Reply J. Occup. Environment. Hyg. 4:060-D62. [Benzene levels in modern solvents have been below .1% for 20 years and below 100 ppm for solvents produced by the members of the Hydrocarbon Solvents Panel];
(5)Battelle Columbus Laboratories, “Technical & Economic Feasibility of a Ban on Consumer Products Containing More Than 0.1% or More Benzene” 1978 Report to United States Consumer Product Safety Commission (CPSC -C-78-0091) dated December 22, 1978;
(6)Hodgkins, Doris, 1980, “Benzene Analysis of Consumer Products” Report to United States Consumer Product Safety Commission, dated March 13, 1980;
(7)Proposed to Withdraw Proposed Ban, 46 FR 3034-01; 1981 WL 108534(F.R.), January 13, 1981;
(8)Wilson, M.P., Hammond S.K., Nicas, M, and Hubbard, A.E., 2007 “Worker Exposure to Volatile Organic Compounds in the Vehicle Repair Industry” J. Occup. Envir. Hyg. 4:301-310;
(9)Wong O (1995), Risk of Acute Myeloid Leukemia and Multiple Myeloma In Workers Exposed to Benzene. Occup. Envir. Med. 52:380-384;
(10)Wong O, Raabe, G.K. (1998), Acute Myeloid & Monocytic Leukemia and Benzene Exposure in Petroleum Distribution Workers in the United Kingdom. Occup. Envir. Med. 55: 360-362;
(11)Wong O (1998), Re: Benzene and Dose Related Incidence of Hematologic Neoplasms in China. J. National Cancer Institute 90: 469-670;
(12)Rinsky, R.A., et al (2002) Benzene Exposure and Hematopoietic Mortality; Long Term Epidemiologic Risk Assessment. Am J. Ind. Med. 42: 474-480;
13.Crump K. (1996) Risk of Benzene – Induced Leukemia Predicted From Pliofilm Cohort Envir. Health Perspect. 104: 1437-1441;
14.Paustenbach D.J., et al (1992) Reevaluation of Benzene Exposure for the Pliofilm (rubber workers) Cohort (1936-1976) Toxicol Envir. Health 36(3):177-231;
15.Wu, W. (1988) Occupational Cancer Epidemiology in the Peoples Republic of China J. Occp. Med. 30:968-974;
16.U.S. Environmental Protection Agency Integrated Risk Information System, Benzene (CASRN 71-43-2), 2003;
17.Travis L.B., et al (1994) Hematopoietic Malignancies and related disorders among benzene – exposed workers in China. Leukemia and Lymphoma 14:91-102;
18.Wong O. (1999) A Critique of the Exposure Assessment in the Epidemiologic Study of Benzene – exposed workers in China conducted by the Chinese Academy of Preventive Medicine and U.S. National Cancer Institute. Reg. Tax and Pharm. 30:259-267;
19.Natelson, E.A. (2007) Benzene Induced Acute Myeloid Leukemia – A Clinician’s Perspective, Am. J. Hematol. 00:000-000, 2007 Accepted 2/13/07;
20.Zhang L, Eastmond, D.A., Smith M.T., The Nature of Chromosomal Aberrations Detected in Humans Exposed to Benzene Crit. Rev. Tox. 32(1):1 – 42 (2002);
21.Escobar, P.A., Smith, M.T., Visishta A, Hubbard A. E., Zhang, L. (2007) Leukemia Specific Chromosome Damage Detected by COMET with fluorescence in situ hybridization (COMET-FISH). Mutagenesis 2007 June 16 [E-publication available only];
22.Deposition of Melvyn J. Kopstein, 1/5/99 in Jill Edwards, et al v. Safety-Kleen Corporation, U.S. Dist. Ct., S.D. Fla. Case,. #97-7180-CV at pp 86-89;
23.Deposition of Melvyn J. Kopstein, 10/20/06, Parker v. The Goodyear Tire & Rubber Company, et al, 14th Judicial District Court, Texas, Cause #05-0390-B at pp 69-72, 126.