Abstract  In a 1997 public health assessment (PHA), ATSDR concluded that people were exposed to contaminants of concern in MCB Camp Lejeune drinking water. Although ATSDR declared those past exposures a public health hazard, it did so on the information that was available at the time, which was limited. Since publication of the 1997 PHA, additional scientific analyses and studies have expanded the knowledge base regarding contaminants of concern in MCB Camp Lejeune drinking water. This assessment evaluates exposures based on these new analyses and studies, particularly the findings from ATSDR’s historical reconstruction modeling efforts. For this public health assessment, ATSDR developed estimates of exposure doses for the following groups who lived or worked at—or lived and worked at—MCB Camp Lejeune: • Children who lived onbase with their families • Adults who lived onbase (inclusive of pregnant women) • Workers employed at the base, but who lived off-base • Marine personnel who trained and lived onbase This PHA also investigates how MCB Camp Lejeune is preventing lead exposure. The lead exposure assessment is conducted separately from the historical reconstruction contaminants of concern because the time frames of exposure do not overlap and are separated by approximately 20 years. If lead is present in the drinking water, the contamination occurs after the water leaves the treatment plant. Groundwater is not the source of lead in the drinking water. The discussion of the lead evaluation begins in the section titled Lead in Drinking Water and is separate from this PHA’s discussions on the other contaminants of concern.

Abstract  The purpose of this Toxicological Review is to provide scientific support and rationale for the hazard and dose-response assessment in IRIS pertaining to chronic exposure to tetrachloroethylene. It is not intended to be a comprehensive treatise on the chemical or toxicological nature of tetrachloroethylene.

Abstract  The neurotoxic effects of organic solvents are reviewed. Organic solvents have been used in extraction, dissolution or suspension of fats, waxes and resins. Studies have shown that acute neurotoxicity is similar for human and laboratory animal exposures and is characterized by narcosis, anesthesia, central nervous system depression, respiratory arrest, loss of consciousness and death. Chronic effects have been studied to a limited extent in animals and have been documented epidemiologically for workers and solvent abusers. Reported effects included peripheral neuropathy and mild toxic encephalopathy. Three severity levels were defined for chronic human exposures: minimal, organic affective syndrome; moderate, mild, chronic toxic encephalopathy; and pronounced, severe, chronic toxic encephalopathy. Neurophysiological effects (electromyogram or electroencephalogram abnormalities, decreased nerve conduction velocities) have also been reported in exposed workers. Neurobehavioral effects such as reversible subjective symptoms, prolonged personality or mood changes and intellectual impairment have been studied epidemiologically and in volunteers. Severe exposure has produced irreversible impairment of intellect and memory (dementia) and structural central nervous system damage. Metabolic aspects of organic solvent exposure were discussed. Guidelines for minimizing worker exposure are discussed in relation to exposure monitoring; control of exposure through contaminant control, worker isolation, use of personal protective equipment and worker education; and medical surveillance. A table containing a summary of NIOSH recommended exposure limits for organic solvents is presented. Examples of solvents neurotoxic to humans discussed include carbon-disulfide (75150), n-hexane (110543), methyl-n-butyl-ketone (591786), trichloroethylene (79016), perchloroethylene (127184) and toluene (108883)