Objective To determine if an evidence-based, behavioral lifestyle intervention program delivered at a worksite setting is effective in improving type 2 diabetes and CVD risk factors. Methods A randomized six-month delayed control design was utilized, with two-thirds of the participants assigned to begin intervention immediately and one-third beginning six months later. The year-long program (weekly for 3 months transitioning to monthly) focused on weight loss and increasing physical activity. Results The immediate intervention group had greater mean weight loss (−10.4 lbs., 5.1%, vs. −2.3 lbs., 1%, p=0.0001) than the delayed control group at 6 months and relatively greater improvements in activity, HbA1c and other risk factors. The delayed group experienced similar improvements after completing the intervention program. Conclusions A worksite behavioral lifestyle intervention is feasible and effective in significantly improving risk factors for diabetes and CVD.
Context Diisocyanates have been associated with respiratory and dermal sensitization. Limited number of case reports, and a few case studies, media, and other references suggest potential neurotoxic effects from exposures to toluene diisocyanate (TDI), 1,6 hexamethylene diisocyanate (HDI), and methylene diisocyanate (MDI). However, a systematic review of the literature evaluating the causal association on humans does not exist to support this alleged association.ObjectiveTo perform systematic review examining the body of epidemiologic evidence and provide assessment of causal association based on principles of the Sir Austin Bradford Hill criteria or considerations for causal analysis.MethodsA comprehensive search of public databases for published abstracts, case reports, cross-sectional surveys, and cohort studies using key search terms was conducted. Additional searches included regulatory reviews, EU IUCLID and EU Risk Assessment databases, and unpublished reports in the International Isocyanate Institute database. An expert panel consisting of physicians, toxicologists, and an epidemiologist critically reviewed accepted papers, providing examination of epidemiologic evidence of each report. Finally, the Hill criteria for causation were applied to the summative analysis of identified reports to estimate probability of causal association.ResultsTwelve papers reporting exposed populations with a variety of neurological symptoms or findings suitable for analysis were identified, including eleven case or case series reports, and one cross-sectional study. Three papers reported on the same population. Each of the papers was limited by paucity of diisocyanate exposure estimates, the presence of confounding exposures to known or suspected neurotoxicants, a lack of objective biological measures of exposure or neurotoxic effects, and lack of relative strength of association measures. Additionally, reported health symptoms and syndromes lacked consistency or specificity. No plausible mechanism of toxicity was found. Application of a predictive mathematical model for determining probability of causal association for neurotoxicity was calculated to be 21%.ConclusionThere is insufficient evidence for a causal association of neurotoxic effects and diisocyanate exposure based on lack of evidence in all categories of the Hill criteria for causality except for temporal association of reported symptoms and alleged exposure. Future reports should attempt to address more rigorous exposure assessment and control for confounding exposures.
This study provides support for the current American Conference of Governmental Industrial Hygienists threshold limit value time-weighted average of 5 ppb.
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