Environmental exposures are ubiquitous and play a significant, and sometimes understated, role in public health as they can lead to the development of various chronic and infectious diseases. In an ideal world, there would be sufficient experimental data to determine the health effects of exposure to priority environmental contaminants. However, this is not the case, as emerging chemicals are continuously added to this list, furthering the data gaps. Recently, simulation science has evolved and can provide appropriate solutions using a multitude of computational methods and tools. In its quest to protect communities across the country from environmental health threats, ATSDR employs a variety of simulation science tools such as Physiologically Based Pharmacokinetic (PBPK) modeling, Quantitative Structure-Activity Relationship (QSAR) modeling, and benchmark dose (BMD) modeling, among others. ATSDR's use of such tools has enabled the agency to evaluate exposures in a timely, efficient, and effective manner. ATSDR's work in simulation science has also had a notable impact beyond the agency, as evidenced by external researchers' widespread appraisal and adaptation of the agency's methodology. ATSDR continues to advance simulation science tools and their applications by collaborating with researchers within and outside the agency, including other federal/state agencies, NGOs, the private sector, and academia.

In a recent article, TP Clement (2010, hereafter referred to as TPC) discusses the complexities and limitations of "hindcasting" models and criticizes the use of complex models when undertaking investigations of subsurface reactive transport processes. TPC implies that complex numerical models that stimulate reactive transport processes in groundwater are likely if not always an inappropriate tool to apply to "hindcasting" investiagtions and that scientists and engineers who implement these investiagtions using such models are somehow not aware of teh technical and scientific complexities and limitations of such methods and approaches. To illustrate his point of view, TPC uses a case study of an ongoing health study of exposure to volatile organic compounds (VOCs) in drinking water at US Marine Corps Base Camp Lejeune, North Carolina (hereafter referred to as the case-control health study at Camp Lejeune). The article presents some thought-provoking points-of-view. However, we believe there is a lack of detail on several key issues that require specificity and clarification, particularly with respect to modleing approaches and methods, the physics of containment occurrence and reactive transport in teh subsurface, and agency policies for the review and dissemination of data and reports.

Two of three water-distribution systems that have historically supplied drinking water to family housing at U.S. Marine Corps Base Camp Lejeune, North Carolina, were contaminated with volatile organic compounds (VOCs). Scientific data relating to the harmful effects of VOCs on a child or fetus are limited. Therefore, the U.S. Agency for Toxic Substances and Disease Registry (ATSDR) is conducting an epidemiological study to evaluate potential associations between in utero and infant (up to 1 year of age) exposures to VOCs in contaminated drinking water at Camp Lejeune and specific birth defects and childhood cancers. The study includes births that occurred during the period 1968-1985 to women who were pregnant while they resided in family housing at Camp Lejeune. To support the epidemiological study, water-modeling techniques are being used to reconstruct historical conditions of groundwater flow, contaminant fate and transport, and the distribution of drinking water contaminated with VOCs. Results for this phase of the study indicate that PCE concentrations in drinking water, delivered to the Tarawa Terrace housing area, exceeded the current maximum contaminant level for PCE of 5 micrograms per liter (µg/L) for 346 months-November 1957-February 1987; the maximum simulated PCE concentration in Tarawa Terrace drinking water was 183 µg/L during March 1984 compared to a measured concentration of 215 µg/L during February 1985.