The Center for Regulatory Effectiveness invokes the data quality act to reject published studies on atrazine toxicity.

Should chemical toxicity data from the peer-reviewed, published scientific literature be considered reliable enough for government risk assessors to use? The Center for Regulatory Effectiveness (CRE) says no, arguing that studies subject to rigorous peer review and published in prominent scientific journals may not be sufficiently "reliable" to be used by the government. The CRE, self-described as a regulatory watchdog group supported by business and trade associations, relies on the so-called Data Quality Act (2001), an obscure provision of a spending bill, which requires governmental agencies to develop guidelines for "ensuring and maximizing the quality, objectivity, utility, and integrity of information" they disseminate.

The issue of whether the Data Quality Act will promote greater scientific rigor or whether it will stand in the way of regulatory decision making is coming to a head as the U.S. Environmental Protection Agency (EPA) assesses atrazine, one of most widely used herbicides in the United States. Atrazine has been banned or restricted in numerous countries, and significant published literature suggests that atrazine is an endocrine disruptor (Hayes et al. 2002a, 2002b, 2003; Laws et al. 2000; Stoker et al. 1999; 2000; Tavera-Mendoza et al. 2002; Sass 2003). Nevertheless, the CRE recently objected that since

   there are no validated test methods for assessing any
   such effects, these pages of the Environmental Risk
   Assessment should be corrected to state that there is
   no reliable evidence that atrazine causes endocrine
   effects in the environment. (Frankenberry et al.
   2003)

On the surface, the CRE's call for validated tests sounds innocuous, even responsible. On closer inspection, the CRE seems to be arguing that a federal agency may not base any regulatory action on scientific research unless it has been performed in accordance with a preexisting, government-approved test protocol. However, the government lacks standard protocols to assess many health effect end points and many types of studies. For example, there is no accepted government benchmark for data from epidemiologic research, for the use of pharmacokinetic models, or for most molecular methodologies. Accidental poisoning data are likewise useful to a risk assessor looking at a given chemical, but they are obviously not the result of experiments carried out under government-approved test conditions. If accepted, the CRE's arguments could jeopardize the government's ability to consider most published scientific research.

Atrazine provides an unnerving example of how the CRE approach could undermine sound policy decisions. In recent articles published in Nature, Environmental Health Perspectives, and the Proceedings of the National Academy of Sciences, Berkeley researcher Tyrone Hayes described a series of adverse affects on amphibian sexual development associated with atrazine exposure (Hayes et al. 2002a, 2002b, 2003). The endocrine effects reported in flogs are consistent with published studies of endocrine effects in atrazine-exposed rats, including delayed puberty in male (Stoker et al. 2000) and female (Laws et al. 2000) Wistar rat pups, prostatitis in the male pups suckling from atrazine-treated dams (Stoker et al. 1999), and reduced testosterone levels in atrazine-treated Sprague-Dawley rat pups (Friedmann 2002). All of these studies inform the U.S. EPA in its assessment of atrazine as a potential endocrine disruptor. Such studies are consistent with the Data Quality Act's goal of promoting reliable information in agency decision making, given that they were published in respected peer-reviewed journals. However, the CRE argued that these data were unreliable and should not be considered by the U.S. EPA in its atrazine assessment.

Government scientists are capable of assessing the reliability of data in order to generate scientifically defensible assessments. For example, the U.S. EPA determined that a number of studies sponsored by the atrazine manufacturer and designed to assess atrazine effects on amphibians were uninformative because of flawed study designs, insufficient statistical power, or high variability (U.S. EPA 2003).

The U.S. EPA has thus far defended its authority to consider all available data, notwithstanding these Data Quality Act objections (Frankenberry et al. 2003). The agency clearly recognizes that it needs all available data to generate a full and informed assessment of any risks. In assessing the data, the greatest consideration should be given to those data from robust and well-designed studies, particularly from studies published in the peer-reviewed scientific literature and therefore available for public scrutiny and scientific debate.

The authors are employed by an environmental nonprofit group concerned with strengthening regulation of toxic chemicals.

REFERENCES

Data Quality Act. 2001. Public Law 106-554, H.R. 5658, Sec. 515(a).

Frankenberry M, Lin J, Bargar T, Urban D, Steeger T. 2003. January 28 EPA Response to Comments from Syngenta and Its Contractors, the Triazine Network, the Center for Regulatory Effectiveness, the American Water Works Association, the State of New York Office of Attorney General, the US Department of Interior Fish and Wildlife Service, The California Regional Water Control Board, the American Farm Bureau Federation, and the Louisiana Farm Bureau Federation, about the EPA Reregistration Eligibility Science Chapter for Atrazine, Environmental Fate and Effects Chapter, dated April 22, 2002. Washington, DC:U.S. Environmental Protection Agency. Available: http://cascade.epa.gov/RightSite/getcontent /Tempfile.pdf?DMW_OBJECTID=O90007d480135e24&DMW_FORMAT=pdf [accessed 21 November 2003].

Friedmann AS. 2002. Atrazine inhibition of testosterone production in rat males following peripubertal exposure. Reprod Toxicol 16:275-279.

Hayes TB, Collins A, Lee M, Mendoza M, Noriega N, Stuart AA, et al. 2002a. Hermaphroditic, demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Proc Natl Acad Sci USA 99:5476-5480.

Hayes T, Haston K, Tsui M, Hoang A, Haeffele C, Vonk A. 2002b. Herbicides: feminization of male frogs in the wild. Nature 419:895-896.

Hayes T, Haston K, Tsui M, Hoang A, Haeffele C, Vonk A. 2003. Atrazine-induced hermaphroditism at 0.1 ppb in American leopard frogs (Rana pipiens): laboratory and field evidence. Environ Health Perspect 111:558-575

Laws SC, Ferrell JM, Stoker TE, Schmid J, Cooper RL. 2000. The effects of atrazine on female Wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Toxicol Sci 58:366-376.

Sass J. 2003. MacLennan et al report on an elevated incidence of prostate cancer among workers in a triazine manufacturing plant [Letter]. J Occup Environ Med 45:343-344.

Stoker TE, Laws SC, Guidici DL, Cooper RL. 2000. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Toxicol Sci 58:50-59.

Stoker TE, Robinette CL, Cooper RL. 1999, Maternal exposure to atrazine during lactation suppresses suckling-induced prolactin release and results in prostatitis in the adult off-spring. Toxicol Sci 52:68-79.

Tavera-Mendoza L, Ruby S, Brousseau P, Fournier M, Cyr D, Marcogliese D. 2002. Response of the amphibian tadpole (Xenopus laevis) to atrazine during sexual differentiation of the testis. Environ Toxicol Chem 21:527-531.

U.S. EPA. 2003. White Paper on Potential Developmental Effects of Atrazine on Amphibians: In Support of an Interim Reregistration Eligibility Decision on Atrazine. Washington, DC:U.S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances.

Jennifer B. Sass

Jon P. Devine, Jr.

Health and Environment Program

Natural Resources Defense Council

Washington, DC

E-mail: [e-mail]