Aggregate Exposure and Cumulative Risk Assessment--Integrating Occupational and Non-occupational Risk Factors.

Occupational exposure limits have traditionally focused on preventing morbidity and mortality arising from inhalation exposures to individual chemical stressors in the workplace. While central to occupational risk assessment, occupational exposure limits have limited application as a refined disease prevention tool because they do not account for all of the complexities of the work and non-occupational environments and are based on varying health endpoints. To be of greater utility, occupational exposure limits and other risk management tools could integrate broader consideration of risks from multiple exposure pathways and routes (aggregate risk) as well as the combined risk from exposure to both chemical and non-chemical stressors, within and beyond the workplace, including the possibility that such exposures may cause interactions or modify the toxic effects observed (cumulative risk). Although still at a rudimentary stage in many cases, a variety of methods and tools have been developed or are being used in allied risk assessment fields to incorporate such considerations in the risk assessment process. These approaches, which are collectively referred to as cumulative risk assessment, have potential to be adapted or modified for occupational scenarios and provide a tangible path forward for occupational risk assessment. Accounting for complex exposures in the workplace and the broader risks faced by the individual also requires a more complete consideration of the composite effects of occupational and non-occupational risk factors to fully assess and manage worker health problems. Barriers to integrating these different factors remain, but new and ongoing community-based and worker health-related initiatives may provide mechanisms for identifying and integrating risk from aggregate exposures and cumulative risks from all relevant sources, be they occupational or non-occupational.

AND YOU THOUGHT HORMONES WERE THE PROBLEM IN PREGNANCY.

A 20-year-old woman, G2P1, presented to the labor and delivery triage with right flank pain and emesis of sudden onset without any precipitating factors. The patient denied history of trauma, anticoagulant therapy, or hypertension. At the time of admission, the patient was in severe pain, was afebrile, had a blood pressure of 139/79, and heart rate of 96. Abdominal exam revealed no tenderness to palpation without guarding or rebound. Musculoskeletal tenderness was elicited from infra-scapular region to the sacroiliac joint on the right side. Mild right costovertebral tenderness was noted. Her cervix was dilated 3cm, effaced 50 percent, with fetal station at -3, unchanged from previous visit. Fetal monitor tracing was reassuring and obstetric ultrasonogram at 22 weeks showed normal fetal anatomy. Magnetic resonance imaging (MRI) revealed T2 hyperintense signal involving and surrounding the right adrenal gland suggesting infarct.

Effect of periodontal therapy on lactoferrin levels in gingival crevicular fluid.

BACKGROUND: The aim of this study was to evaluate lactoferrin quantification as a sensitive and objective method of detecting the degree of periodontal inflammation, oxidative stress and to monitor the effects of periodontal therapy. METHODS: Fifty subjects were divided into two groups based on gingival index, probing pocket depth, clinical attachment loss and alveolar bone loss: healthy group and periodontitis group with generalized chronic periodontitis. Non-surgical periodontal therapy was rendered and crevicular fluid samples collected at baseline and four weeks after therapy for lactoferrin quantification using enzyme linked immunosorbent assay. The correlation between clinical parameters and lactoferrin levels was drawn and analysed for both groups. RESULTS: The mean level of crevicular lactoferrin in the periodontitis group was 1857.21 ng/ml. The mean level decreased to 1415.03 ng/ml after treatment. The lowest lactoferrin concentration was seen in the healthy group (75.34 ng/ml). All clinical parameters correlated positively with lactoferrin levels. CONCLUSIONS: The lactoferrin level was higher in the periodontitis group compared to the healthy group, and reduced with periodontal therapy. Higher levels were associated with higher values of clinical parameters, both before and after therapy. The data indicates that Lactoferrin plays an important role in periodontal disease and crevicular lactoferrin quantification can be a marker for detecting periodontal inflammation, oxidative stress and monitoring periodontal therapy.

Comparison of periodontal open flap debridement versus closed debridement with Er,Cr:YSGG laser.

BACKGROUND: Traditional periodontal open flap debridement (OFD) results in reduced pocket depth (PD), clinical attachment loss (CAL), gingival recession (GR) and postoperative pain and discomfort. The quest to overcome these shortcomings has led to research into Er,Cr:YSGG laser assisted pocket therapy (ELAPT). This study was designed to compare the clinical outcomes of ELAPT versus OFD. METHODS: Fifteen patients with a PD of ≥5 mm and ≤8 mm at two sites were selected. Test sites (Group 1) were treated by ELAPT and the control (Group 2) by OFD. Clinical parameters were recorded at baseline, 3 and 6 months and included Plaque Index (PI), Gingival Index (GI), modified Sulcular Bleeding Index (mSBI), PD, CAL and GR. RESULTS: Both treatments produced a reduction in PI, GI, mSBI and PD, an increase in GR, and a gain in CAL at 3 and 6 months. The mean gain of CAL in Group 1 at 3 and 6 months (1.60 ± 0.78 and 1.80 ± 0.63) was similar (p > 0.05) to the value of Group 2 (1.93 ± 0.88 and 2.00 ± 0.54). GR increased significantly (p < 0.05) only in Group 2 at 3 and 6 months (1.80 ± 0.56 and 1.87 ± 0.64) compared to Group 1 (0.50 ± 0.68 and 0.60 ± 0.74). CONCLUSIONS: ELAPT compared with OFD results in similar CAL gains with less GR and significant reductions in PD, GI and mSBI, and may be considered as an alternative to surgical therapy.

Cancer mortality patterns among hairdressers and barbers in 24 US states, 1984 to 1995.

We evaluated cancer mortality patterns among hairdressers and barbers, according to occupation, coded on 7.2 million death certificates in 24 states from 1984 to 1995. Of the 38,721 deaths among white and black hairdressers and barbers of both sexes, 9495 were from all malignant neoplasms. Mortality odds ratios were significantly elevated for all malignant neoplasms, lung cancer, and all lymphatic and hemopoietic cancers among black and white female hairdressers. White female hairdressers had significant excess mortality from cancers of the stomach, colon, pancreas, breast, and bladder and from non-Hodgkin's lymphoma and lymphoid leukemia; mortality from these cancers was also elevated among black female hairdressers. White male hairdressers had significantly elevated mortality from non-melanoma skin cancer and non-Hodgkin's lymphoma. Mortality from all malignant neoplasms, although significantly elevated among both white and black female hairdressers, was significantly below the null for white male hairdressers. Black and white male barbers had significantly elevated mortality from stomach and pharyngeal cancer, respectively. A significant deficit in mortality from all neoplasms and cancers of the pancreas, lung, and prostate was noted for white male barbers. This large study of cancer mortality among hairdressers and barbers showed some differences in mortality patterns by gender and race. Further studies are required to determine if specific occupational exposures may explain some of the elevated cancer rates.