The Agency for Toxic Substances and Disease Registry (ATSDR) once again ignores their own data on mercury vapor to exclude it from their “Interaction profile for:Chlorpyrifos, Lead, Mercury, and Methylmercury”, of which the primary effect of concern for this mixture is neurological, and the sub-population of concern is children. ATSDR has thus chose to not acknowledge or address the primary exposure of mercury in the population, that of dental mercury amalgam fillings.
INTERACTION PROFILE FOR: CHLORPYRIFOS, LEAD, MERCURY, AND METHYLMERCURY
U.S. Department of Health and Human ServicesPublic Health ServiceAgency for Toxic Substances and Disease Registry.
…Metallic and inorganic mercury can be transformed by microorganisms into methylmercury, which bioaccumulates in the food chain. For the general population, and particularly for subsistence fishers and hunters, the most important pathway of exposure to mercury is ingestion of methylmercury in foods. Fish (including tuna, a food commonly eaten by children), other seafood, and marine mammals contain the highest concentrations….
…The primary effect of concern for this mixture is neurological, and the sub-population of concern is children. Neurological effects are the critical effects for chlorpyrifos, lead, and methylmercury, and children are known (for lead and methylmercury) or predicted on the basis of animal studies (for chlorpyrifos) to be more sensitive than adults. Although metallic mercury causes neurological effects when inhaled, this route is of concern primarily for occupational exposure.
According to the CDC’s NHANES data, children as young as 3 have amalgams installed.
This is actually incorrect as the majority of the population has mercury fillings (over 120 million people), and they have the highest exposure to mercury from their mercury fillings as noted by…
WHO (1991) concluded that “estimated average daily intake and retention” from dental amalgam was 3.8-21 (3-17) μg/day (values in brackets representingretained (absorbed) dose (WHO, 1991, Table 2).
PHS(1993) acknowledged that estimates of mercury exposure from amalgam span 1 μg/day to 29μgs/day (see PHS, 1993, Appendix III), with higher estimates appropriately acknowledged for the sizable population of persons who have more than ten amalgam fillings.
In the Executive Summary of this document (WHO 2003), WHO clearly states “Dental amalgam constitutes a potentially significant source of exposure to elemental mercury, with estimates of daily intake from amalgam restorations ranging from 1 to 27 μg/day.”
Children may be exposed to metallic mercury if they play with it after finding it in abandoned warehouses or taking it from school laboratories. Broken thermometers and some electrical switches are other sources of metallic mercury. Some absorption of metallic mercury occurs from dental amalgam fillings, probably following volatilization from the fillings.
Clear evidence of adverse effects from this pathway of exposure is lacking, as are joint action studies with the other components of this mixture, so this form of mercury is not considered further in the interaction profile. The critical effect of inorganic mercury is on the kidney,which is not a sensitive target organ for the other components of the mixture….
Mark Richardson P.h.D. explains part 2 of the amalgam risk assessment he presented to the FDA
The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) mandatesthat the Agency for Toxic Substances and Disease Registry (ATSDR) shall assess whether adequateinformation on health effects is available for the priority hazardous substances. Where such informationis not available or under development, ATSDR shall, in cooperation with the National ToxicologyProgram (NTP), initiate a program of research to determine these health effects. The Act further directsthat where feasible, ATSDR shall develop methods to determine the health effects of substances incombination with other substances with which they are commonly found.
To carry out these legislative mandates, ATSDR’s Division of Toxicology and EnvironmentalMedicine(DTEM) has developed and coordinated a mixtures program that includes trend analysis toidentify the mixtures most often found in environmental media, in vivo and in vitro toxicological testingof mixtures, quantitative modeling of joint action, and methodological development for assessment ofjoint toxicity.
The purpose of an Interaction Profile is to evaluate data on the toxicology of the “whole” priority mixture(if available) and on the joint toxic action of the chemicals in the mixture in order to recommendapproaches for the exposure-based assessment of the potential hazard to public health. Joint toxic actionincludes additivity and interactions. A weight-of-evidence approach is commonly used in thesedocuments to evaluate the influence of interactions in the overall toxicity of the mixture. The weight-ofevidenceevaluations are qualitative in nature, although ATSDR recognizes that observations oftoxicological interactions depend greatly on exposure doses and that some interactions appear to havethresholds. Thus, the interactions are evaluated in a qualitative manner to provide a sense of whatinfluence the interactions may have when they do occur.
ATSDR will use the following process for the development of interaction profiles:
• ATSDR will select substances/chemicals for development of interaction profiles throughinter/intra agency communications and literature reviews.
• After the selection, a letter will be sent to individuals and agencies on ATSDR’s mailing listproviding notice of ATSDR’s intent to create an interaction profile.
• A notice will also be posted in the Federal Register to inform the public of ATSDR’s intent todevelop a particular interaction profile.
• The draft interaction profile will undergo both internal and external peer review processes.
• A Federal Register notice will announce the release of the official draft for public comment.
• ATSDR will post a link to the draft interaction profile on its Website, giving the public anopportunity to provide comments.
• ATSDR will review all public comments and revise the draft, as appropriate, before issuing thefinal version.
A component-based approach is recommended for the exposure-based screening assessment of potentialhazards to public health from exposure to this mixture. The recommendations include the estimation of ahazard index for the neurological effects of the chlorpyrifos, lead, and methylmercury components of thismixture. The subpopulation of greatest concern for neurological effects of this mixture includes infants,young children, and fetuses.
Appendix C: Background Information for Mercury and Methylmercury
For the general population, the most important pathway of exposure to mercury is ingestion of methylmercury in foods, with fish, otherseafood, and marine mammals containing the highest concentrations (ATSDR 1999). Another source of exposure for the general population is intake of metallic mercury from dental amalgams. Infants can be exposed to inorganic mercury and methylmercury from breast milk, and the developing fetus can be exposed through transplacental transfer of metallic mercury and methylmercury (ATSDR 1999).
Hana Pohl, M.D., Ph.D.ATSDR, Division of Toxicology and Environmental Medicine, Atlanta, GA
Joan Colman, Ph.D.Syracuse Research Corporation, Syracuse, NY
A peer review panel was assembled for this profile. The panel consisted of the following members:1. Christopher J. Borgert, Ph.D., Applied Pharmacology and Toxicology, Inc., Consulting &Research Services, Gainesville, FL2. Kannan Krishnan, Ph.D., Human Toxicology Research Group, University of Montreal,Montreal, PQ, Canada3. Harihara Mehendale, Ph.
Despite ATSDR’s assertion that
“The critical effect of inorganic mercury is on the kidney,which is not a sensitive target organ for the other components of the mixture”
ATSDR’s own literature (Toxicological Profile on Mercury) states several times that “The major target organs of metallic mercury-induced toxicity are the kidneys and the central nervous system.”
ATSDR TOXICOLOGICAL PROFILE OF MERCURY 1999
2.2.1 Inhalation Exposure pg33
Most of the studies on inhalation exposure concern exposure to metallic mercury vapor. For this reason, the term “metallic mercury” will be used in this section instead of “inorganic mercury.” Other forms of inorganic mercury do not pose a risk by the inhalation pathway. Inhalation of sufficient levels of metallic mercury vapor has been associated with systemic toxicity in both humans and animals. The major target organs of metallic mercury-induced toxicity are the kidneys and the central nervous system. At high exposure levels, respiratory, cardiovascular, and gastrointestinal effects also occur.
126.96.36.199 Neurological Effects Metallic Mercury. pg58
The central nervous system is probably the most sensitive target organ for metallic mercury vapor exposure.
2.5 RELEVANCE TO PUBLIC HEALTH (pg 220) OVERVIEW
Once in the central nervous system, however, metallic mercury vapor is oxidized to themercuric ion (Hg++), which is then trapped in the central nervous system due to the limited ability of themercuric ion to cross the blood-brain barrier.
The absorption of metallic mercury vapors from lungs is high (about 80%) (Hursh et al. 1976), and the most sensitive target following inhalation exposure to metallic mercury is the central nervous system. Absorbed metallic mercury crosses the placenta, and the fetal blood may concentrate mercury to levels 10 or more times the levels found in the maternal blood. Therefore, the developing fetal nervous system may be quite sensitive to maternal exposures to mercury vapors.
Even small amounts of nonpolar mercury(<2 g) in the body may eventually lead to central nervous system damage (Neirenberg et al. 1998). The low capacity for central nervous system tissues to regenerate and the fact that even subtle damage to small areas of the brain can have profound overall effects, makes this tissue very susceptible to the highly toxic mercuricion. These factors, and a slow but inevitable trapping of mercuric ions may lead to the mercury-induceddelayed central nervous system toxicity observed months to years after exposure ceases (Neirenberg et al.1998, Rice 1996a). Even potent chelators have not been effective in interfering with progressive central nervous system damage once a nonpolar mercury compound gains access to the circulatory system and begins to concentrate in tissues (Neirenberg et al. 1998, Taueg et al. 1992).
UPDATE 2/14/2011 From Mark Richardson: