Archive for category ‘Database‘

EPA Releases Guide to Help Scientists Understand Children’s Exposure to Pollutants

Pollutionmakes Children sick, Air pollution

WASHINGTON – The U.S. Environmental Protection Agency today released a user-friendly document to help risk assessors understand how children are exposed to pollution. The document, titled “Highlights of the Child-Specific Exposure Factors Handbook” serves as a quick-reference guide to the more comprehensive “Child-Specific Exposure Factors Handbook” published by EPA in 2008. It will serve as an additional resource for those who work on children’s health issues, which the agency has been highlighting during Children’s Health Month.

EPA developed the reference guide to provide important information necessary for answering questions about exposure through drinking water, breathing, and eating foods, such as:

  • How much exposure to environmental pollutants might children get if they live or play near contaminated sites?
  • How much dirt from a child’s hands might s/he inadvertently eat?
  • How much of a child’s exposure to various pollutants might come from skin contact?
  • Which age groups (childhood life stages) may inhale or ingest the most and thus may be at higher risks?

More information on the documents:

Reference: EPA Releases Guide to Help Scientists Understand Children’s Exposure to Pollutants, Release date: 10/27/2009

30. October 2009 | Air Pollution, Allergies, Chemical Exposure, Clinical Diagnostics, Database, Diagnosis Chemical Injury, Environmental Exposure, Environmental Illnesses, Indoor Air Pollution, Neurodevelopment, Neurotoxicity, Pesticides, Insecticides, Prevention, Sick Building Syndrome, Toxicology | Comments (0)

First approaches to the monetary impact of environmental health disturbances in Germany

Environmental related Diseases cost Billions

This article aims to describe essential conditions and starting-points for the monetary evaluation of environmentally attributable diseases. Furthermore, a cost calculation within a scenario analysis is conducted for Germany. 

To calculate the costs of environmental health effects we chose a disease-specific perspective. The national statistics of the Federal Statistical Office and the World Health Report burden of disease estimates were used to identify the most important disease categories for Germany. Based on an extensive literature research in computerized databases and the publications of national and international institutions, available costs of illness studies for Germany as well as environmental attributable fractions (EAFs) were identified. Based on these data environmental health costs were calculated with a top-down approach. 

Direct and indirect environmental costs of illness add up to 15-62 billion euro (2006) per year depending on the specific scenario. From our results a tentative scheme is deduced of how the monetary environmental burden of specific diseases is composed and how it can be assigned to major environmental exposures and economic sectors which can be used in setting intervention priorities and evaluating intervention efficiency. 

Within this article, we were able to calculate environmental health costs for Germany based on available, easy to access data and deduce implications for environmental policy decision-making. However, there are restrictions in data quality, as the aetiology of some diseases with respect to environmental impacts is not very well documented and data has not been collected particularly for Germany. 

Reference:   Haucke F, Brückner U., First approaches to the monetary impact of environmental health disturbances in Germany, Helmholtz Zentrum München – German Research Center for Environmental Health (GmbH), Institute of Health Economics and Health Care Management, Germany, Health Policy. 2009 Sep 8.

12. September 2009 | Air Pollution, Allergies, Chemical Exposure, Chemical Sensitivity, MCS, Chronic Fatigue Syndrome, Clinical Diagnostics, Database, Diagnosis Chemical Injury, Environmental Exposure, Environmental Illnesses, Hormone Disrupting Chemicals, Indoor Air Pollution, Neurodegenerative Diseases, Pesticides, Insecticides, Sick Building Syndrome | Comments (0)

Receptors play a role in regard to environmental toxins and in MCS

 

Information about some members (mainly TRPV1, TRPV3 and TRPA1) of the large group of receptors of the TRP ion channel family

 

I want to introduce you to some of the receptors of the TRP (transient receptor potential) ion channel family. Please keep in mind that I am not a scientist and that English is not my mother tongue. 

There will be two parts. In the first part today you will find general information about several receptors of the TRP family and the role these receptors play in regard to environmental irritants and MCS. In the second part you will find a list of substances which are able to activate these receptors.

 

Information about different receptors of the TRP family 

TRPV1

The most information can be found about the TRPV (vanilloid) subgroup and TRPA1.

The TRPV1 receptor is broadly expressed in all “port of entry” tissues (e.g., skin, gut, airways, conjunctiva) and the various cell types linings such tissues (i.e., keratinocytes, epithelia, endothelia, etc.). In addition TRPV1 receptors were found in various peripheral nonneuronal tissues (e.g., kidney, lung, testis, pancreas, spleen, liver, stomach, vascular smooth muscle, placenta, cornea, uterus, bladder). It exists in many areas of the CNS like hypothalamus, hippocampus, frontal cortex, motor neurons of the spinal cord and in CNS cells involved in inflammation (e.g. astrocytes, microglia). (Veronesi et al. (2006) 

TRPV1 is gated not only by vanilloids such as capsaicin, but also by noxious heat, acidosis and intracellular lipid mediators such as anandamide, lipoxygenase products and various pro-algesic pathways.  

If you read “vanilloid” it is likely that you are thinking of a piece of cake or vanilla ice cream. In addition to such a sweet food, vanillin can be found when paper becomes old (the smell of old books). But in contrast to your expectation vanilloids are substances, which are often hot and pungent like capsaicin in chillies. I am sure you know that burning sensation in your mouth if you have eaten something hot and spicy. This feeling of pain is caused by SP (substance P), which the TRPV1 releases together with neurokinin A [NKA], and calcitonin-gene-related-peptide [CGRP], which are leading to an inflammatory response.  

In addition various cell types, including mast cells, epithelial cells, and immune cells, have been shown to release pro-inflammatory cytokines (e.g., IL1beta, IL6, IL8, and TNF) in response to SP, CGRP, and NKA. (Veronesi 2006) 

After a while SP is used up and the result is that you will feel a reduction of pain (desensitization). Because of this mechanism capsaicin is sometimes used as a treatment in medicine. 

The problem with this is, that damage or even the death of cells, mentioned in several articles, can take place: 

“Cell death was characterized by cytoplasmic swelling, coalescence contents and eventual lysis” (Berkley Molecular Neurobiology Student Manuscripts- Term Paper Code 53)  

“After using capsaicin, the inflammatory reaction and lipid peroxidation may affect cellular functions and lead to cell death.” (Richeux et al. 2000) 

“Activation of the capsaicin receptor (VR1 or TRPV1) in bronchial epithelial cells by capsaicinoids and other vanilloids promotes pro-inflammatory cytokine production and cell death.” (Reilly 2005) 

“We show that activation of the intracellular subpopulation of TRPV1 causes endoplasmic reticulum (ER) stress and cell death in human bronchial epithelial and alveolar cells.” (Thomas et al. 2007) 

“In conclusion, the TRPV1 receptor is active in the brain microvasculature and has its permeability-increasing effect via substance P. It also plays a role in the immediate blood–brain barrierr disruption following ischaemia–reperfusion.” (Hu et al. 20005) 

“Activation of TRPV1 excites sensory neurons and induces the accumulation of intracellular Ca2+. This results in excessive mitochondrial Ca2+ loading and subsequent mitochondrial disruption, leading to neuronal cell death….”(Kim 2006) 

“…We recently reported that cytochrome c release from damaged mitochondria and caspase-3 activation are required for TRPV1-mediated neurodegeneration in mesencephalic cultures.” (Kim 2006)

TRPV3

The TRPV3 receptor is another member of the TRPV family. It behaves in a similar way as TRPV1. It can be activated by substances like camphor, carvacrol and thymol. 

In the article by Vogt-Eisele et al. 2007 terpenoids in essential oils, which are used cosmetically, were studied as agonists for TRPV3.

 

TRPA1

TRPA1 can be activated by allyl isothiocyanate, which you can find in mustard oil (cabbage, cress …) or by the thiosulfinate allicin (garlic and onions).  

TRPA1, also plays an important role in modulating nociceptor excitability and neurogenic inflammation in the setting of tissue injury. Bradykinin is produced in response to tissue injury, inflammation and ischemia and it binds to the PLC-coupled receptors on sensory neurons. It causes acute pain through immediate excitation of nociceptors like TRPA1, followed by a longer sensitization of thermal and mechanical stimuli. This hypersensitization is produced through PLC-mediated potentiation of TRPV1. TRPA1 is often coexpressed with TRPV1. (Bautista et al. 2006)

 

TRPM2

Peroxynitrite and other reactive species induce oxidative DNA damage and activate poly(ADP-ribose) polymerase 1 (PARP-1). 

Overactivation of PARP-1 depletes its substrate NAD(+), slowing the rate of glycolysis, electron transport, and ATP formation, eventually leading to functional impairment or death of cells, as well as up-regulation of various proinflammatory pathways (Pacher, Szabo 2008) 

TRPM2 is gated by (PARP-1). (Pacher, Szabo 2008)

 

TRPM8

This receptor is responsible for sensing cool temperatures. If you eat menthol, it gives you a cool feeling, which is created by the activation of this receptor.

 

These receptors play a role in regard to environmental toxins and in MCS

I want to share now a few quotes in regard to sensitization of the receptors with you.

“In general, sensitization may be governed by a change in conformation status of the receptor or ion channel itself, rendering an enhanced activation state. Sensitization may further be governed by increased expression of functional receptors on the cell surface.” (Veronesi and Oortgiesen 2006) 

“In particular, upregulation of TRPV1 is often produced after exposure to proinflammatory agents, thus suggesting the general hypothesis that under inflammatory circumstances, a ’sensitized’ TRPV1 can be activated by agonist concentrations much lower than those tested under conventional experimental conditions.” (Geppetti 2004) 

“Furthermore, activation by one ligand can potentiate the response to a second activator.” (Kauer 2008)

In several articles researchers of different teams looked at environmental irritants and their role in activation/sensitization of these receptors: 

Toxicologists have reported an initiating role for TRPV1 in mediating airway inflammation (e.g., hyperresponsiveness, asthma) caused by chemical irritants and air pollutants (e.g., particulate matter, ozone, pesticides (Veronesi et al., 2001 )). Identifying this receptor as a common responder to multiple chemical toxicants could explain how diverse pollutants and inhaled substances produce the respiratory dysfunction associated with environmental contaminants. (Veronesi and Oortgiesen 2006) 

In the article by Andre et al. (2008) is mentioned that unsaturated aldehydes (mainly acrolein and crotonaldehyde) in cigarette smoke stimulated TRPA1 and caused airway neurogenic inflammation.  

Acrolein is present in tear gas, vehicle exhaust, and smoke from burning vegetation, including tobacco products. Acrolein can induce apnea, shortness of breath, cough, airway obstruction, and mucous secretion. It is also a toxic metabolite of cyclophosphamide and ifosfamide, chemotherapeutic agents widely used in the treatment of cancer, severe arthritis, multiple sclerosis, and lupus. (Bautista et al. 2006) 

Shiba et al. (2009) found out that phthalate esters are able to activate TRPV1 and TRPA1 receptors. 

Macpherson showed in 2007 that formaldehyde activates the ion channel TRPA1. In addition it was discovered that the endogenous aldehyde hydroxynonenal is able to activate TRPA1, too. 

It is produced when reactive oxygen species peroxidate membrane phospholipids in response to tissue injury, inflammation, and oxidative stress and it promotes acute pain, neuropeptide release, and neurogenic inflammation. (Trevisani 2007) 

Cyclohexanone is known to activate TRPV1 and it is used as an intermediate in the production of nylon, fungicices, herbicides, paint thinners and lubricant oils. (Silver et al. 2006) 

But the most important work was done by Pall and Anderson (2004). They investigated the role of many substances especially solvents and VOCs in regard to the TRP ion channels and they mention in their article 12 points, which provide the support that TRPVs plays a role in MCS. Here are a few examples: 

  • Chemicals, which stimulate the TRP receptors are similar to the diversity to chemicals in MCS.
  •  TRPVs increase NO and stimulate NMDA receptors.
  •  Substance P is increased on vanilloid stimulation and it is elevated in MCS
  •  Neurogenic inflammation is caused by the activation of TRPVs and it plays a role in MCS

Professor Pall describes the connection between the receptors of the TRP family, NO and the NMDA receptor as follows: 

“The vanilloid receptor (TRPV1 or VR1), widely distributed in the central and peripheral nervous system, is activated by a broad range of chemicals similar to those implicated in Multiple Chemical Sensitivity (MCS) Syndrome. The vanilloid receptor is reportedly hyperresponsive in MCS and can increase nitric oxide levels and stimulate N-methyl-D-aspartate (NMDA) receptor activity, both of which are important features in the previously proposed central role of nitric oxide and NMDA receptors in MCS. Vanilloid receptor activity is markedly altered by multiple mechanisms, possibly providing an explanation for the increased activity in MCS …”(Pall and Anderson 2004)

While I worked on this subject I had the feeling I looked through a keyhole. I was able to see some parts of the room in front of me, but other parts I was not able to see. I am convinced that during the next years more parts of the “room” will be discovered and we will get a bigger view in which in additional areas, these receptors play a role and maybe even more substances will be discovered by which these receptors are activated.   

Author: Namid   

References:

First I want to give you a few additional links to articles, which I found helpful: 

Geppetti, P., et al. (2006). The transient receptor potential vanilloid 1: role in airway inflammation and disease. Eur J Pharmacol. 2006 Mar 8;533(1-3):207-14.  

Geppetti et al (2004).: Activation and sensitisation of the vanilloid receptor: role in gastrointestinal inflammation and function. British Journal of Pharmacology (2004) 141, 1313–1320  

If you want to read more about the role of these receptors in diseases I would recommend that you read Nilius et al.:Transient Receptor Potential Cation Channels in Disease. Physiol. Rev. 87: 165-217, 2007

It contains several good figures like: fig. 7 – TRPV1, fig.8 – TRPA1, fig. 11 – respiratory tract. 

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10. August 2009 | Chemical Exposure, Chemical Sensitivity, MCS, Clinical Diagnostics, Database, Diagnosis Chemical Injury, Environmental Exposure, Environmental Illnesses, Neurotoxicity, Toxicology | Comments (0)

German Federal Institute for Occupational Safety and Occupational Medicine mentioned MCS – Multiple Chemical Sensitivity at Thesaurus “Safety and Health at Work”

The Federal Institute for Occupational Safety and Occupational Medicine has published an alphabetical and systematic Thesaurus “Safety and Health at Work”. The Thesaurus has been created in a long-standing cooperation between documentalists, librarians and scientists from the Federal Institute of Occupational Safety and Occupational Medicine.    

The disease MCS – Multiple Chemical Sensitivity (ICD-10 T78.4) is mentioned at the Thesaurus “Safety and Health at Work”, alphabetical Part, Status May 2009, as: 

MCS - Multiple Chemical Sensitivity at Thesaurus

Multiple Chemical Sensitivity (B02.19.00)     

At the systematic Part MCS – Multiple Chemical Sensitivity is found at the category B02:  

“Work related Disease and Occupational Disease/Disease”  

integrated in Part:  

  • B02.19 Other Disease 
  • B02.19.00 Multiple Chemical Sensitivity  

Chronic Fatigue Syndrome (CFS) is integrated analogue.  

 

MCS is not classified as a mental disease

To clear up occurring doubts, it is to point out that MCS – Multiple Chemical Sensitivity is not integrated into chapter B02.15: Mental diseases, Depression, Neurosis, Post traumatic Stress Disorder or psychosomatic diseases. 

Thesaurus “Safety and Health at Work”

The Thesaurus offers a quick overview on the broad group of themes “Safety and Health at Work”. It contains about 3 500 main keywords and is the joining of the keywords from the two previous Thesauri “Safety at Work” and “Occupational Medicine”. The Thesaurus is based on the practical work of the Library group, documentation at the content development and their research of technical literature. It is a tool for documentation.   

The Thesaurus is intended for all who search for literature about “Safety and Health at Work”. It is supportive for prearrangement of research inquiries at the data pool LITDOK and can be helpful for searching in topic related databases.  

Author: Silvia K. Müller, CSN – Chemical Sensitivity Network, July 23, 2009  

Reference:  Thesaurus „Sicherheit und Gesundheit bei der Arbeit“ Alphabetischer Teil, Systemischer Teil, Dortmund/Berlin/Dresden 2009. 

23. July 2009 | Chemical Sensitivity, MCS, Chronic Fatigue Syndrome, Database, Diagnosis Chemical Injury, Environmental Illnesses, Toxicology | Comments (0)

First Step in Protecting Children from Toxic Chemicals

State Identifies Dangerous Chemicals 

Waiting for the BabyThe Maine Department of Environmental Protection (DEP) and the Maine Center for Disease Control and Prevention (CDC) announce the publication of Maine’s List of Chemicals of High Concern. Publishing the list of about 1700 chemicals is the first step toward implementing Maine’s new Toxic Chemicals in Children’s Products law.  

The law aims to make children’s products safer and less toxic. Maine DEP and CDC have taken the first step, which is to identify and list chemicals known to governments as causing cancer and other health concerns.  

“Increasing public awareness of toxic chemicals and their presence in children’s products will promote the use of safer chemicals in Maine and move us toward our long term goal of protecting the public and the environment,” said DEP Commissioner David Littell. “We also hope this list will prove helpful to businesses, including manufacturers, as they work to improve the chemical safety of their products.”

The CHC list was compiled from existing government lists which identified chemicals that are known to pose specific health threats including those that cause cancer. Some of the commonly recognized chemicals on the list include: lead, mercury, formaldehyde, and bisphenol A. 

“Far too often we are forced to confront the risks and benefits of chemicals in products only after we discover they are present in children’s bodies at levels of possible concern,” said Dr. Dora Anne Mills, State Health Officer and Director of the Maine Center for Disease Control and Prevention. “We need to be assured that children’s products are safe from toxic chemicals when they are put on the market. The Maine CHC list is an important first step toward that critical goal.”

In the past, Maine and other states have targeted specific chemicals or products. The CHC listing takes a more holistic approach – it sets up a process to, prioritize, access chemical information, and replace some of the harmful chemicals in children’s products. The law gives the state the authority to phase out the use of dangerous chemicals in children’s products when safer alternatives are effective and available at a comparable cost. 

Next year, the DEP and CDC will begin to look more closely at these chemicals, the extent of their use, the level of exposure to children, and documented presence in the human body or environment. The law required the DEP to move at least two “priority chemicals” forward for further scrutiny and possible regulatory action.  

Maine is one of several states to implement news laws to reduce toxic chemicals in consumer products. Maine is the first state to publish a List of Chemicals of High Concern. 

Reference:Department of Environmental Protection Maine, State Takes First Step in Protecting Children from Toxic Chemicals, Identifies Dangerous Chemicals, July 17, 2009

18. July 2009 | Air Pollution, Chemical Exposure, Database, Diagnosis Chemical Injury, Environmental Exposure, Hormone Disrupting Chemicals, Indoor Air Pollution, Neurodegenerative Diseases, Neurodevelopment, Neurotoxicity, Pesticides, Insecticides, Prevention, Sick Building Syndrome, Toxicology | Comments (0)

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