Neuropsychological correlates of manganese exposure: a meta-analysis.

The hypothesized effect of recurrent low-dose manganese (Mn) exposure on neuropsychological function is controversial because of inconsistent findings across three decades of research. We conducted a meta-analysis on 41 variables from nineteen neuropsychological studies of Mn-exposed workers. The results showed: Large effect size (ES) for biological markers of Mn and lead levels; thirteen of 26 neurocognitive measures showing a small average ES; only one of 26 tasks showed a moderate ES; and small to medium ES for confounding/competing variables such as education and aptitude. Tasks with the highest ES included clerical substitution tasks, digit span, tapping endurance, and Swedish Performance Evaluation System "Additions" reaction time, but none exceeded the ES for education or aptitude. The mean ES of dose-response relationships was zero. The data did not support a theory of preclinical ("early") neuromotor or cognitive dysfunction. Overall, the pooled data are more consistent with covariate effect than toxic effect, insofar as the pooled exposure group showed demographics less favorable to neuropsychological performance than the pooled referent groups. Future consideration of demographic and biological covariates is necessary before inferring subtle toxin-induced brain damage because neuropsychological tests are nonspecific.

Risk of false positives when identifying malingered profiles using the trauma symptom inventory.

The Trauma Symptom Inventory (TSI; Briere, 1995) is a 100-item self-report measure of posttraumatic symptomatology that includes an Atypical Response (ATR) validity scale designed to differentiate honest from malingered profiles. In this study, using an analogue design to experimentally manipulate honest and malingered responses on the TSI, we found that proposed ATR cut scores produce a significant risk of false positives. Furthermore, the functioning of proposed cut scores worsened when we used posttraumatic stress disorder relevant samples and low estimates of malingering base rates. In light of these findings, the TSI should be used with caution when assessing claims of posttraumatic stress in forensic or disability settings.

A meta-analysis of the neuropsychological effects of occupational exposure to manganese.

This article reports a meta-analysis of 25 samples in 20 peer-reviewed published neuropsychological studies of the cognitive, psychological, motor, and sensory/perceptual effects of exposure to manganese. These studies included 1,410 exposed participants and 1,322 controls, for a total N = 2,732. Studies were excluded from this analysis if they were unpublished, had uncodeable data, were based on fewer than four participants, failed to have a comparison group, or reported on manganese effects other than cognitive or sensory/motor (e.g., liver functioning). Because the independent variables defining manganese exposure varied across studies, effect sizes were calculated for exposed versus non-exposed workers. Dose-response relations were considered for measures of manganese levels in air/dust (84% of studies reported), blood (MnB; 76% reported), urine (MnU; 52% reported), and hair samples (4% reported). Level of exposure was also estimated by reported years of exposure (M = 13.1 years). Cohen's d statistic yielded a statistically significant weighted mean effect size of - .17, p < .0001 for manganese exposure. However, an effect this small is typically undetectable when evaluating individuals because it is smaller (about 1/6 SD) than the confidence intervals of most neuropsychological measures. Because the effect is so slight and the overlap so great between exposed and unexposed participants (87%), the error rate would exceed the hit rate if causal conclusions were rendered for occupational exposure to manganese as the source of an individual's cognitive, sensory, or motor impairments based on neuropsychological testing or symptom reports.

Commentary on cognitive impairment with toxigenic fungal exposure.

Recently, Gordon et al. (2004) published an article entitled "Cognitive Impairment Associated with Toxigenic Fungal Exposure: A Replication and Extension of Previous Findings." That article claims that neurocognitive deficits are pervasive in persons self-diagnosed with "toxic" mold exposure relative to historical norms. Further, Gordon et al. argue exposure to household molds causes brain damage similar to closed head injury. Examination of their methodology reveals unfounded and unreliable conclusions due to deviations from sound epidemiological principles, bias in participant selection, misleading data analysis, and implausible causal reasoning. The purpose of this critique is to outline the specific design and reasoning flaws that, if not addressed, would lead to unwarranted conclusions regarding the effects of mold exposure.

Methodological problems in the neuropsychological assessment of effects of exposure to welding fumes and manganese.

Recently, Kaiser (2003) raised concerns over the increase in brain damage claims reportedly due to exposure to welding fumes. In the present article, we discuss methodological problems in conducting neuropsychological research on the effects of welding exposure, using a recent paper by Bowler et al. (2003) as an example to illustrate problems common in the neurotoxicity literature. Our analysis highlights difficulties in conducting such quasi-experimental investigations, including subject selection bias, litigation effects on symptom report and neuropsychological test performance, response bias, and scientifically inadequate casual reasoning.

Toxic mold and mycotoxins in neurotoxicity cases: Stachybotrys, Fusarium, Trichoderma, Aspergillus, Penicillium, Cladosporium, Alternaria, Trichothecenes.

Presented is the argument that psychologists and neuropsychologists have no scientific basis for rendering opinions about causation given the current state of the literature. The critical question is whether in a residence or office inhalation of mold spores or mold metabolites, including mycotoxins, causes neuropsychological impairment or mental and emotional disorders. There has not been sufficient research to support such conclusions. Nonetheless, in the context of litigation, speculative opinions are rendered in lieu of scientifically well-founded conclusions. Resources for recognizing and coping with pseudoscientific arguments are suggested.

A statistical analysis of board certification in clinical neuropsychology.

In this paper, we use tools from decision theory to evaluate the effectiveness of the current psychology board certification process used by the American Board of Clinical Neuropsychology (ABCN). These analyses indicate that ABCN's current process is likely to be failing to certify too many competently trained candidates, and identifying relatively few truly competent neuropsychologists. In fact, we estimate that ABCN is only certifying between 16 and 52% of competent clinical neuropsychologists. This is in contrast to the processes of the American Board of Medical Specialties (ABMS), after which ABCN has indicated that it models its examination. ABMS estimates that 89% of all practicing physicians are board-certified by one of their member boards. Based on our analyses, specific recommendations for change are offered for credentialing the profession of neuropsychology.