al. (1982) has estimated that a downward shift in IQ of 4 points would double the proportion of children with IQ less than 80. Environmental exposures have been suggested for such diseases as parkinsonism, amyotrophic lateral sclerosis, Alzheimer's disease, and several peripheral neuropathies (Tanner et al., 1987; Ngim and Devathasan, 1989; Kalfakis et al., 1991; Bos et al., 1991; McLachlan et al., 1991). Improved means to evaluate more-subtle neurobehavioral and neurophysiologic effects (Valciukas and Lilis, 1980; Xintaras et al., 1979) have led to major advances in assessing neurotoxic effects. These methods are often specific for certain types of neurobehavioral effects, e.g., visual versus auditory memory. Hence, a careful selection of tests is required for field surveys. Consideration must also be given to possible confounders, such as age, alcohol intake, and education. Sometimes a battery of tests may be needed to screen workers for the effects of a neurotoxic substance. Such a battery should be specific enough to measure functions related to known effects of the substance and heterogeneous enough to cover a variety of neurobehavioral functions.
Neurologic and behavioral effects have been assessed for exposures to some indoor air pollutants. Otto et al. (1992) exposed 66 healthy young male subjects with no history of chemical sensitivity to air, to clean air, and to a complex mixture of volatile organic compounds (VOCs). Participants reported more fatigue and mental confusion after exposure to the organic compounds. However, performance on 13 neurobehavioral tests was not affected. In another part of the study, eye and throat irritation, headache, and drowsiness increased or showed no evidence of adaptation during exposure, even though the intensity of odors decreased by 30% (Hudnell et al., 1992). The investigators concluded that these results indicate that irritation intensity and other symptoms are not related in a simple way to odor intensity. The findings suggest that the symptoms may not be a psychosomatic response to the detection of an unpleasant odor and that environmental odor pollution may affect neurobehavior. Instead, subthreshold levels of VOCs may interact additively and stimulate trigeminal nerve receptors. Many nonspecific-symptom clusters have an odor component. Noxious environmental odors might trigger symptoms by a variety of physiologic mechanisms, including exacerbation of underlying medical conditions, innate odor aversions or aversive conditioning, stress-induced illness, and possible phenomenal reactions. Whereas relatively consistent patterns of subjective symptoms have been reported among individuals who live near environmental odor sources, documentation of objective correlates to such symptoms would require the development of new research tools.
An example of a common environmental neurotoxicant that produces a variety of chronic effects is lead. Lead has been known to cause serious