Criteria for the classification of carpal tunnel syndrome for use in epidemiologic studies were developed by means of a consensus process. Twelve medical researchers with experience in conducting epidemiologic studies of carpal tunnel syndrome participated in the process. The group reached agreement on several conceptual issues. First, there is no perfect gold standard for carpal tunnel syndrome. The combination of electrodiagnostic study findings and symptom characteristics will provide the most accurate information for classification of carpal tunnel syndrome. Second, use of only electrodiagnostic study findings is not recommended. Finally, in the absence of electrodiagnostic studies, specific combinations of symptom characteristics and physical examination findings may be useful in some settings but are likely to result in greater misclassification of disease status.
Increased weight and, more recently, body mass index (BMI), have been suggested as risk factors for carpal tunnel syndrome (CTS). In an effort to determine the relative risk (RR) of obesity in the development of CTS, 949 patients who had an evaluation of the right upper extremity that included motor and sensory conduction studies of the median and ulnar nerves were reviewed. Of these patients, 261 were diagnosed with a median mononeuropathy at the wrist. Those individuals who were classified as obese (BMI > 29) were 2.5 times more likely than slender individuals (BMI < 20) to be diagnosed with CTS. Forty-three percent of obese women and 32% of obese men had the diagnosis of CTS compared to 21% of slender women and 0% of slender men.
Human exposure to methylmercury (MeHg) and elemental mercury vapor (Hg 0 (g) ) are often estimated using total Hg concentrations in hair and urine, respectively. We investigated whether Hg stable isotopes could be used to better distinguish between exposure to Hg 0 (g) versus MeHg. We found that hair from North American dental professionals was characterized by high positive Δ 199 Hg values (mean = 1.86‰, 1 SD = 0.12‰, n = 11). This confirms that among people who regularly consume fish, total Hg concentrations in hair reflect exposure to MeHg. In contrast, we found that urine from the same individuals was characterized by a range of Δ 199 Hg values (0.29 to 1.77‰, 2 SD = 0.06‰, n = 12) that were significantly correlated to the number of dental amalgams in each individual's mouth. We hypothesize that fishderived MeHg is demethylated within the body, causing massdependent fractionation and the excretion of inorganic Hg in urine. Mercury in urine therefore represents a mixture of demethylated fish-derived MeHg and amalgam-derived inorganic Hg. We estimate that the majority (>70%) of Hg in urine from individuals with <10 dental amalgams is derived from ingestion of MeHg in fish. These data suggest that within populations that consume fish, urine total Hg concentrations may overestimate Hg exposure from personal dental amalgams.
Mercury is a potent toxicant of concern to both the general public and occupationally exposed workers (e.g., dentists). Recent studies suggest that several genes mediating the toxicokinetics of mercury are polymorphic in humans and may influence inter-individual variability in mercury accumulation. This work hypothesizes that polymorphisms in key glutathione synthesizing enzyme, glutathione s-transferase, and selenoprotein genes underlie inter-individual differences in mercury body burden as assessed by analytical mercury measurement in urine and hair, biomarkers of elemental mercury and methylmercury, respectively. Urine and hair samples were collected from a population of dental professionals (n=515), and total mercury content was measured. Average urine (1.06±1.24 ug/L) and hair mercury levels (0.49±0.63 ug/g) were similar to national U.S. population averages. Taqman assays were used to genotype DNA from buccal swab samples at 15 polymorphic sites in genes implicated in mercury metabolism. Linear regression modeling assessed the ability of polymorphisms to modify the relationship between mercury biomarker levels and exposure sources (e.g., amalgams, fish consumption). Five polymorphisms were significantly associated with urine mercury levels (GSTT1 deletion), hair mercury levels (GSTP1-105, GSTP1-114, GSS 5’), or both (SEPP1 3’UTR). Overall, this study suggests that polymorphisms in selenoproteins and glutathione-related genes may influence elimination of mercury in the urine and hair or mercury retention following exposures to elemental mercury (via dental amalgams) and methylmercury (via fish consumption).
To determine normative values for nerve conduction studies among workers, we selected a subset of 326 workers from 955 subjects who participated in medical surveys in the workplace. The reference cohort was composed exclusively of active workers, in contrast to the typical convenience samples. Nerve conduction measures included bilateral median and ulnar sensory amplitude and latency (onset and peak). Workers with upper extremity symptoms, medical conditions that could adversely affect peripheral nerve function, low hand temperature, or highly repetitive jobs were excluded from the “normal” cohort. Linear regression models explained between 21% and 51% of the variance in nerve function, with covariates of age, sex, hand temperature, and anthropometric factors. The most robust models were fitted for sensory amplitudes in the median and ulnar nerves for dominant and nondominant hands. The median–ulnar difference was least sensitive to adjustment, indicating it is the best measure to use if corrections are not made to account for relevant covariates. A key point was that the magnitude of variance increased with age and anthropometric factors. These findings provide strong evidence that to improve diagnostic accuracy, electrodiagnostic testing should control for relevant covariates, particularly age, sex, hand temperature, and anthropometric factors. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:999–1005, 1998.
Objective Arsenic in drinking water has been linked with the risk of urinary bladder cancer, but the dose–response relationships for arsenic exposures below 100 µg/L remain equivocal. We conducted a population-based case–control study in southeastern Michigan, USA, where approximately 230,000 people were exposed to arsenic concentrations between 10 and 100 µg/L. Methods This study included 411 bladder cancer cases diagnosed between 2000 and 2004, and 566 controls recruited during the same period. Individual lifetime exposure profiles were reconstructed, and residential water source histories, water consumption practices, and water arsenic measurements or modeled estimates were determined at all residences. Arsenic exposure was estimated for 99% of participants’ person-years. Results Overall, an increase in bladder cancer risk was not found for time-weighted average lifetime arsenic exposure >10 µg/L when compared with a reference group exposed to <1 µg/L (odds ratio (OR) = 1.10; 95% confidence interval (CI): 0.65, 1.86). Among ever-smokers, risks from arsenic exposure >10 µg/L were similarly not elevated when compared to the reference group (OR = 0.94; 95% CI: 0.50, 1.78). Conclusions We did not find persuasive evidence of an association between low-level arsenic exposure and bladder cancer. Selecting the appropriate exposure metric needs to be thoughtfully considered when investigating risk from low-level arsenic exposure.
This study followed workers over an extended period of time to identify factors which may influence the onset of Carpal Tunnel Syndrome (CTS). The purpose was to evaluate incidence of CTS and to create a predictive model of factors that play a role in the development of CTS. This prospective study followed 432 industrial and clerical workers over 5.4 years. Incident cases were defined as workers who had no prior history of CTS at baseline testing and were diagnosed with CTS during the follow-up period or at the follow-up screening. On the basis of logistic regression, significant predictors for CTS include baseline median-ulnar peak latency difference, a history of wrist/hand/finger tendonitis, a history of numbness, tingling, burning, and/or pain in the hand, and work above the action level of the peak force and hand activity level threshold limit value. This longitudinal study supports findings from previous cross-sectional studies identifying both work related ergonomic stressors and physical factors as independent risk factors for CTS.
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