Height-related changes in body mass index: a reappraisal

OBJECTIVES: To study the relationship between body mass index (BMI) and height in 20-22 year-old patients. METHODS: A research questionnaire filled by a representative sample of military personnel upon discharge from service was analyzed. At the same time, weight and height were measured, and BMI was calculated (BMI = weight (Kg)/height(2)(m(2))). RESULTS: There were 35,951 participants in the study, including 16204 females and 19747 males. There was a positive correlation between BMI and height in men (regression slope = 0.00717, r = 0.015, p = 0.03), while the correlation was negative in women (regression slope = -0.02811, r = -0.05, p < 0.0001). In multiple regression analysis, when BMI was used as the dependent variable and height, gender, ethnic origin, smoking, oral contraceptive use, and level of recreational exercise as the independent variables, only height, gender, and ethnic origin remained significant in the final analysis (R-square 0.0205, p < 0.0001). CONCLUSION: In young adults, BMI is affected in a subtle, but opposite manner in males and females. In males, BMI increases with increasing height, while in females, BMI decreases with increasing height.     

Epidemiologic studies of glyphosate and cancer: A review

The United States Environmental Protection Agency and other regulatory agencies around the world have registered glyphosate as a broad-spectrum herbicide for use on multiple food and non-food use crops. Glyphosate is widely considered by regulatory authorities and scientific bodies to have no carcinogenic potential, based primarily on results of carcinogenicity studies of rats and mice. To examine potential cancer risks in humans, we reviewed the epidemiologic literature to evaluate whether exposure to glyphosate is associated causally with cancer risk in humans. We also reviewed relevant methodological and biomonitoring studies of glyphosate. Seven cohort studies and fourteen case-control studies examined the association between glyphosate and one or more cancer outcomes. Our review found no consistent pattern of positive associations indicating a causal relationship between total cancer (in adults or children) or any site-specific cancer and exposure to glyphosate. Data from biomonitoring studies underscore the importance of exposure assessment in epidemiologic studies, and indicate that studies should incorporate not only duration and frequency of pesticide use, but also type of pesticide formulation. Because generic exposure assessments likely lead to exposure misclassification, it is recommended that exposure algorithms be validated with biomonitoring data.     

Switching from long-term benzodiazepine therapy to pregabalin in patients with generalized anxiety disorder: a double-blind, placebo-controlled trial

To evaluate the efficacy of pregabalin in facilitating taper off chronic benzodiazepines, outpatients (N = 106) with a lifetime diagnosis of generalized anxiety disorder (current diagnosis could be subthreshold) who had been treated with a benzodiazepine for 8-52 weeks were stabilized for 2-4 weeks on alprazolam in the range of 1-4 mg/day. Patients were then randomized to 12 weeks of double-blind treatment with either pregabalin 300-600 mg/day or placebo while undergoing a gradual benzodiazepine taper at a rate of 25% per week, followed by a 6-week benzodiazepine-free phase during which they continued double-blind study treatment. Outcome measures included ability to remain benzodiazepine-free (primary) as well as changes in Hamilton Anxiety Rating Scale (HAM)-A and Physician Withdrawal Checklist (PWC). At endpoint, a non-significant higher proportion of patients remained benzodiazepine-free receiving pregabalin compared with placebo (51.4% vs 37.0%). Treatment with pregabalin was associated with significantly greater endpoint reduction in the HAM-A total score versus placebo (-2.5 vs +1.3; p < 0.001), and lower endpoint mean PWC scores (6.5 vs 10.3; p = 0.012). Thirty patients (53%) in the pregabalin group and 19 patients (37%) in the placebo group completed the study, reducing the power to detect a significant difference on the primary outcome. The results on the anxiety and withdrawal severity measures suggest that switching to pregabalin may be a safe and effective method for discontinuing long-term benzodiazepine therapy.     

A critical review of the epidemiology of Agent Orange/TCDD and prostate cancer

To inform risk assessment and regulatory decision-making, the relationship between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and prostate cancer requires clarification. This article systematically and critically reviews the epidemiologic evidence on the association between exposure to TCDD or Agent Orange, a TCDD-contaminated herbicide used during the Vietnam War, and prostate cancer risk. Articles evaluated include 11 studies of three cohorts, four case–control or cross-sectional studies, and three case-only studies of military veterans with information on estimated Agent Orange or TCDD exposure; 13 studies of seven cohorts, one case–control study, and eight proportionate morbidity or mortality studies of Vietnam veterans without information on Agent Orange exposure; 11 cohort studies of workers with occupational exposure to TCDD; and two studies of one community cohort with environmental exposure to TCDD. The most informative studies, including those of Vietnam veterans involved in Agent Orange spraying or other handling, herbicide manufacturing or spraying workers with occupational TCDD exposure, and community members exposed to TCDD through an industrial accident, consistently reported no significant increase in prostate cancer incidence or mortality. Only some potentially confounded studies of Vietnam veterans compared with the general population, studies with unreliable estimates of Agent Orange exposure, and analyses of selected subgroups of Vietnam veterans reported positive associations. Overall, epidemiologic research offers no consistent or convincing evidence of a causal relationship between exposure to Agent Orange or TCDD and prostate cancer. More accurate exposure assessment is needed in large epidemiologic studies to rule out a causal association more conclusively.     

EFFECTS OF CONCURRENT OZONE EXPOSURE ON THE PATHOGENESIS OF CIGARETTE SMOKE-INDUCED EMPHYSEMA IN B6C3F 1 MICE

Episodic elevation of air pollutants may exacerbate respiratory distress associated with chronic obstructive pulmonary disease (COPD), yet few experiments have been performed to determine how continuously polluted atmospheres may contribute to the etiology of COPD, in general and pulmonary emphysema in particular. This study describes the effects of concurrent exposure to ozone (O 3) in the pathogenesis of cigarette smoke (CS)-induced emphysema in the mouse. Female B6C3F 1 mice were whole-body exposed either to filtered air (FA) or to mainstream CS at a concentration of 250 mg total particulate material/m 3 for 6 h/day, 5 days/wk for 15 or 32 wk. Concurrently, mice were exposed either to FA or to O 3 at 0.3 ppm for 8 h/night, 5 nights/wk for the same time periods. At necropsy, mouse lungs were lavaged, and bronchoalveolar lavage fluid (BALF) was analyzed for inflammatory cell numbers, total protein, lactate dehydrogenase (LDH) and alkaline phosphatase (AP) activities, superoxide production by isolated alveolar macrophages, glutathione content, inflammatory cytokines, and proteolytic activity. Other lungs were inflated at constant pressure for 6 h with formalin for fixation, routine histopathology, and stereology. After 32 wk of exposure, CS with or without concurrent O 3 exposure produced stereologic evidence of emphysema as previously described. Concurrent O 3 exposure did not worsen any of these parameters, nor did O 3 by itself cause stereologic changes that were consistent with emphysema. The O 3 exposure caused only slight elevations of BALF macrophages, while CS exposure caused marked increases in the numbers of both BALF macrophages and neutrophils. Neutrophils in the BALF in response to CS exposure were also more numerous at 32 wk than at 15 wk. Exposure to CS caused an increase in BALF total protein, LDH, AP, and interleukin (IL)-1β. After 32 wk, CS exposure was associated with decreased superoxide production from isolated alveolar macrophages. The CS exposure elevated BALF total glutathione primarily at 15 wk. Overall, O 3 had little effect on endpoints that were significantly affected by CS exposure. We conclude that concurrent O 3 exposure has no effect on the induction of emphysema by CS in this animal model.     

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

The respective contribution of occupational and behavioural factors to social disparities in all-cause mortality has been studied very seldom. The objective of this study was to evaluate the role of occupational and behavioural factors in explaining social inequalities in premature and total mortality in the French working population. The study population consisted of a sample of 2,189 and 1,929 French working men and women, who responded to a self-administered questionnaire in mid-1996, and were followed up until the end of 2008. Mortality was derived from register-based information and linked to the baseline data. Socioeconomic status was measured using occupation. Occupational factors included biomechanical and physical exposures, temporary contract, psychological demands, and social support, and behavioural factors, smoking, alcohol abuse, and body mass index. Significant social differences were observed for premature and total mortality. Occupational factors reduced the hazard ratios of mortality for manual workers compared to managers/professionals by 72 and 41%, from 1.88 (95% CI: 1.17–3.01) to 1.25 (95% CI: 0.74–2.12) for premature mortality, and from 1.71 (95% CI: 1.18–2.47) to 1.42 (95% CI: 0.95–2.13) for total mortality. The biggest contributions were found for biomechanical and physical exposures, and job insecurity. The role of behavioural factors was very low. Occupational factors played a substantial role in explaining social disparities in mortality, especially for premature mortality and men. Improving working conditions amongst the lowest social groups may help to reduce social inequalities in mortality.     

A mechanism of S-(1,2,3,4,4-pentachloro-1,3-butadienyl)-L-cysteine toxicity to rabbit renal proximal tubules

S-(1,2,3,4,4-Pentachloro-1,3-butadienyl)-L-cysteine (PCBC) has been identified as the penultimate compound responsible for hexachlorobutadiene-induced nephrotoxicity. The primary goal of these studies was to determine the mechanism of PCBC-induced toxicity in rabbit renal proximal tubules by examining the early changes in tubular physiology. PCBC (20-500 microM) induced a specific sequence of toxic events. Following 15 min of exposure, 200 microM PCBC increased basal (25%) and ouabain-insensitive (78%) respiration. This was followed by a decrease in basal (46%), nystatin-stimulated (54%), and ouabain-insensitive (21%) respiration and a decrease in glutathione content (79%). Finally, there was a decrease in cell viability as measured by a decrease in LDH retention at 60 min. Direct probing of mitochondrial function revealed that the initial increase in respiration resulted from the uncoupling of oxidative phosphorylation, while the late changes in respiration appeared to result from gross mitochondrial damage characterized by inhibited state 3 respiration, inhibited cytochrome c-cytochrome oxidase, and inhibited electron transport. Studies utilizing tubules with decreased glutathione content revealed that glutathione plays little if any role in the early events of PCBC-induced toxicity. These results suggest that PCBC-induced mitochondrial dysfunction may initiate the renal proximal tubule injury.     

Selection of elderly controls using random digit dialing.

The experience of identifying and soliciting elderly male controls, using a nonclustered random digit dialing procedure in a case-control study, is presented. For elderly controls (ages 65-84) 3.5 times more residential telephone numbers were required than for controls encompassing a much broader age range (ages 40-84). This is a function of the proportion of elderly in the population and their lower response to telephone identification. Elderly controls, age 70 and older, also had lower participation rates.