Attorney Joseph W. Belluck of Belluck & Fox, LLP says research provides new evidence of the deadly risks associated with asbestos exposure. 

A new study by prominent researchers shows that sheet metal workers are at higher risk of contracting and dying from asbestos-related diseases, a well-known New York attorney says. 

“Like other important studies, this research is strong evidence of the deadly risks associated with asbestos exposure,” said Joseph W. Belluck, a New York attorney who concentrates in litigation involving asbestos-related disease. “This study hammers home what too many sheet metal workers and their families already know: Asbestos exposure can make for a deadly profession.”

The study was published in the August issue of the American Journal of Industrial Medicine and was conducted by researchers at Duke University and the Center for Construction Research and Training in Silver, Spring Maryland. The researchers found higher mortality among sheet metal workers for mesothelioma, asbestosis and cancers of the pleura or lining of the chest and abdomen. Mesothelioma is a rare cancer nearly always related to asbestos exposure. 

Led by John Dement of Duke’s Division of Occupational and Environmental Medicine, researchers analyzed the overall mortality patterns of 17,345 workers with 20 years or more in the sheet metal trade and found significantly higher risk of asbestos-related diseases including mesothelioma, lung cancer and asbestosis. 

The researchers said the study offered additional evidence that workers who experienced periodic exposure to asbestos are at increased risk of asbestos-related diseases. Many workers do not begin showing symptoms until decades after exposure. Asbestos exposure continues to threaten workers who work in older structures or who work in the field of asbestos removal. 

Other professions already linked to asbestos-related diseases and death include construction workers, miners, shipyard workers, drywallers, asbestos removal workers, demolition workers and auto mechanics and textile workers who produced asbestos products. 

The U.S. Environmental Protection Agency and the World Health Organization Asbestos classify asbestos as a human carcinogen. But until the 1970s, asbestos was widely used in manufacturing, particularly for building materials, because of its properties of heat resistance and durability.  

Reference:    Belluck & Fox Law, Belluck & Fox Law Firm Notes New Asbestos Research Showing Higher Death Risk for Sheet Metal Workers, New York, NY (PRWEB) August 25, 2009.

Role of detoxification genes in response to xenobiotics 

The effect of exposure of Aedes aegypti larvae for 72h to sub-lethal concentrations of the herbicide glyphosate and the polycyclic aromatic hydrocarbon benzo[a]pyrene on their subsequent tolerance to the chemical insecticides imidacloprid, permethrin and propoxur, detoxification enzyme activities and transcription of detoxification genes was investigated. Bioassays revealed a significant increase in larval tolerance to imidacloprid and permethrin following exposure to benzo[a]pyrene and glyphosate. Larval tolerance to propoxur increased moderately after exposure to benzo[a]pyrene while a minor increased tolerance was observed after exposure to glyphosate.  

Cytochrome P450 monooxygenases activities were strongly induced in larvae exposed to benzo[a]pyrene and moderately induced in larvae exposed to imidacloprid and glyphosate. Larval glutathione S-transferases activities were strongly induced after exposure to propoxur and moderately induced after exposure to benzo[a]pyrene and glyphosate. Larval esterase activities were considerably induced after exposure to propoxur but only slightly induced by other xenobiotics. Microarray screening of 290 detoxification genes following exposure to each xenobiotic with the DNA microarray Aedes Detox Chip identified multiple detoxification and red/ox genes induced by xenobiotics and insecticides.  

Further transcription studies using real-time quantitative RT-PCR confirmed the induction of multiple P450 genes, 1 carboxy/cholinelesterase gene and 2 red/ox genes by insecticides and xenobiotics.  

Overall, this study reveals the potential of benzo[a]pyrene and glyphosate to affect the tolerance of mosquito larvae to chemical insecticides, possibly through the cross-induction of particular genes encoding detoxification enzymes. 

Reference:  Riaz MA, Poupardin R, Reynaud S, Strode C, Ranson H, David JP. Impact of glyphosate and benzo[a]pyrene on the tolerance of mosquito larvae to chemical insecticides. Role of detoxification genes in response to xenobiotics, Aquat Toxicol. 2009 Jun 4;93(1):61-9. Epub 2009 Mar 31

Diesel exhaust exposure may cause acute irritant-induced asthma and potentiate allergen-induced asthma. There are no previous reports of occupational asthma due to diesel exhaust. Aim of the study was to describe occupational asthma with latency in workers exposed to diesel exhaust in bus garages.  

The Shield database of occupational asthma notifications in the West Midlands, UK, was searched between 1990 and 2006 for workers where diesel exhaust exposure was thought to be the cause of the occupational asthma. Those without other confounding exposures whose occupational asthma was validated by serial peak expiratory flow (PEF) analysis using Oasys software were included.  

Fifteen workers were identified with occupational asthma attributed to diesel exhaust. Three had validated new-onset asthma with latency. All worked in bus garages where diesel exhaust exposure was the only likely cause of their occupational asthma. Occupational asthma was confirmed by measures of non-specific reactivity and serial measurements of PEF with Oasys scores of 2.9, 3.73 and 4 (positive score > 2.5).  

The known non-specific irritant effects of diesel exhaust suggest that this is an example of low-dose irritant-induced asthma and that exposures to diesel exhaust in at least some bus garages are at a sufficient level to cause this. 

Reference:   Adewole F, Moore VC, Robertson AS, Burge PS., Diesel exhaust causing low-dose irritant asthma with latency? Occup Med (Lond). 2009 Sep;59(6):424-7.

Chronic fatigue syndrome (CFS) is characterized by debilitating fatigue, often accompanied by widespread muscle pain that meets criteria for fibromyalgia syndrome (FMS). Symptoms become markedly worse after exercise. Previous studies implicated dysregulation of the sympathetic nervous system (SNS), and immune system (IS) in CFS and FMS.  

We recently demonstrated that acid sensing ion channel (probably ASIC3), purinergic type 2X receptors (probably P2X4 and P2X5) and the transient receptor potential vanilloid type 1 (TRPV1) are molecular receptors in mouse sensory neurons detecting metabolites that cause acute muscle pain and possibly muscle fatigue. These molecular receptors are found on human leukocytes along with SNS and IS genes.  

Real-time, quantitative PCR showed that 19 CFS patients had lower expression of beta-2 adrenergic receptors but otherwise did not differ from 16 control subjects before exercise. After a sustained moderate exercise test, CFS patients showed greater increases than control subjects in gene expression for metabolite detecting receptors ASIC3, P2X4, and P2X5, for SNS receptors alpha-2A, beta-1, beta-2, and COMT and IS genes for IL10 and TLR4 lasting from 0.5 to 48 hours (P < .05). These increases were also seen in the CFS subgroup with comorbid FMS and were highly correlated with symptoms of physical fatigue, mental fatigue, and pain. These new findings suggest dysregulation of metabolite detecting receptors as well as SNS and IS in CFS and CFS-FMS.  

Muscle fatigue and pain are major symptoms of CFS. After moderate exercise, CFS and CFS-FMS patients show enhanced gene expression for receptors detecting muscle metabolites and for SNS and IS, which correlate with these symptoms. These findings suggest possible new causes, points for intervention, and objective biomarkers for these disorders. 

Reference:  Light AR, White AT, Hughen RW, Light KC., Moderate Exercise Increases Expression for Sensory, Adrenergic, and Immune Genes in Chronic Fatigue Syndrome Patients But Not in Normal Subjects, Department of Anesthesiology, Department of Neurobiology and Anatomy, Utah, University of Utah Salt Lake City, Utah, J Pain. Jul 30, 2009.

Non-profit hospitals more likely to have smoke-free campuses than for-profit entities 

While hospital buildings are often smoke-free, a new study finds that by February 2008, 45 percent of US hospitals had adopted “smoke-free campus” policies, meaning that all the property owned or leased by the hospital, both indoors and outdoors, was smoke-free and there were no designated smoking areas on those properties.  

The study, “The Adoption of Smoke-Free Hospital Campuses in the United States,” is the first of its kind to examine the national prevalence of smoke-free hospital campus policies. It was conducted by The Joint Commission, the world’s largest healthcare standards setting and accrediting body, and researchers from the Henry Ford Health System’s Center for Health Promotion and Disease Prevention. The study was funded by the Substance Abuse Policy Research Program of the Robert Wood Johnson Foundation and appears in the online version of the peer-reviewed journal Tobacco Control.  

“Besides the 45 percent that already had smoke-free campuses, another 15 percent indicated that they would be implementing similar policies in the near future. Hence, it is safe to assume on the basis of these results that the majority of US hospitals will have smoke-free campuses by the end of 2009,” according to Scott C. Williams, PsyD, of The Joint Commission.  

The 2008 data shows that not-for-profit hospitals were more likely to have smoke-free campuses than for-profit hospitals. The 2008 data also shows that hospitals in Arkansas, Iowa, Massachusetts, Minnesota, Oklahoma and Wisconsin had among the highest proportion of smoke-free campuses. Hospitals in several tobacco states also had significant proportion of smoke-free campuses.  

“In 1992, The Joint Commission implemented a standard which required hospitals to adopt a non-smoking policy throughout all buildings, limiting smoking to separate, ventilated areas. At that time, fewer than 3 percent of hospitals extended this indoor smoking ban to include the entire hospital campus, both indoors and outdoors. Our study shows that around 2004-2005 this began to change dramatically. Now a majority of the nation’s hospitals do not allow smoking anywhere on their property,” Williams said.  

The study examined the current smoking policies and future plans of 1,916 Joint Commission-accredited hospitals to determine the prevalence of smoke-free hospital campus policies and whether such policies had an impact on smoking cessation counseling offered in those hospitals. The study found that not-for-profit hospitals were slightly more likely to offer smoking cessation counseling than for-profit hospitals.  

The study also found that federally owned hospitals were less likely to have smoke-free campuses. This, according to the study, was likely due to the influence of federal legislation requiring all Veterans Administration (VA) hospitals to have a suitable and accessible patient indoor smoking area for patients and residents. “Such legislation makes it virtually impossible for VA hospitals to adopt a completely smoke-free campus,” Williams said.  

Reference:  Substance Abuse Policy Research Program, Majority of US hospitals will have smoke-free campuses by end of year, WASHINGTON DC, Aug. 20, 2009