Current as of April 2008

The Science Behind Chromated Copper Arsenate (CCA)-Treated Wood

The chemistry behind CCA and its use in wood preservation is designed to keep the preservative in the wood so the product can perform as intended.  Over time, however, very small amounts of the preservative chemicals can be removed by contact with the surface of the wood.  The chemical of concern in relation to CCA is arsenic.  It is important to keep in mind that arsenic is a naturally occurring element; we are exposed to it every day in the food we eat, the water we drink, the air we breathe, and the soil around us.

There is an extensive amount of scientific literature related to arsenic in relation to CCA-treated wood, its toxicology, epidemiological studies, and exposure assessments.  These are discussed briefly below, and a partial list of pertinent references is provided.

CCA-Treated Wood and Arsenic

Very minute amounts of arsenic can be dislodged from the surface of treated wood through contact.  Arsenic in those minute amounts is in a complexed form and not readily available in terms of human exposure.  In fact, all studies evaluating potential exposure to arsenic from contact with CCA-treated wood confirm that the levels are far below and not distinguishable from background levels from normal diet and drinking water.

From the standpoint of dermal absorption, recent research published in the scientific literature confirmed that the arsenic in wood residues is poorly absorbed and does not result in detectable levels.

(Wester, R.C., X .Hui, S. Barbadillo, H.I. Maibach, Y.W. Lowney, R.A. Schoof, S.E. Holm, and M.V. Ruby.  2004.  In vivo percutaneous absorption of arsenic from water and CCA-treated wood residue.  Toxicological Sciences 79: 287-295)

In 2004, researchers at the University of Alberta, Canada, evaluated potential exposures to children playing on playsets made from CCA-treated wood.  They concluded that the levels of dislodgeable residues of arsenic found were far below those which normally occur in diet and drinking water. 

(Kwon, E., Zhang, H., Wang, Z., Ghangri, G.S., Lu, X., Fok, N.,Gabos, S., Li, X., and Le, X.C..  2004.  Arsenic on the hands of children after playing in playgrounds.  Environ Health Perspectives 112(14): 1375-1380)

In 2006, researchers in Florida reported that there were no detectable differences in exposure between children who played on playsets made from CCA-treated wood and those who played on playsets made from other materials.

(Shalat, S.L., H.M. Solo-Gabriele, L.E. Fleming, B.T. Buckley, K. Black, M. Jimenez, T. Shibata, M. Durbin, J. Graygo, W. Stephan, and G. Van De Bogart.  2006.  A pilot study of children's exposure to CCA-treated wood from playground equipment.  Science Total Environ 367(1):80-88)

To put this into perspective, several recent publications confirm that the very small potenial exposure from contact with CCA-treated wood is far below and indistinguishable from the background levels from diet and drinking water in US populations.

(Tsuji, J., L.J. Yost, L.M. Barraj, C.G. Scrafford, and P.J. Mink. 2007. Use of background inorganic arsenic exposures to provide perspective on risk assessment results. Reg Toxicol Pharmacol 48(1):59-69)

(Georgopoulos, P.G., S-W Wang, Y-C Yang, J Xue, VG Zartarian, T. McCurdy, and H. Ozkaynak. 2007. Biologically based modeling of multimedia, multipathway, multiroute population exposures to arsenic. J Expos Sci Environ Epidemiol (in press), advance online publication, 12 December 2007, doi:10/1038/sj.jes.7500637)

Comparison of Lifetime Exposure Estimates to Inorganic Arsenic from Natural Sources (Diet and Drinking Water) to Estimates for Children Contacting CCA-Treated Playsets and Decks.

After Tsuji, J., L.J. Yost, L.M. Barraj, C.G. Scrafford, and P.J. Mink.  2007.  Use of background inorganic arsenic exposures to provide perspective on risk assessment results.  Reg Toxicol Pharmacol 48(1):59-69.

Arsenic Toxicology and Epidemiology

At very high levels, arsenic can result in death when ingested over a short period of time.  However, the primary area of concern with arsenic is its potential to cause cancer.  Epidemiologic studies conducted in Taiwan, where levels of naturally-occurring arsenic in the drinking water are orders of magnitude higher than those in the US, have been used to evaluate the potential carcinogenic risk from oral exposure to inorganic arsenic.

In the past several years, there has been extensive reconsideration of the potential risks associated with low dose oral exposures to inorganic arsenic, largely related to intake via drinking water.  A large body of data has been published recently in peer-reviewed scientific journals, and the scientific and regulatory communities are reconsidering how these data should be used in regulatory models to assess risks in the U.S.

In 2007, after two years of evaluating the extensive new information and the many issues associated with interpretation of those data, the U.S. EPA Scientific Advisory Board (SAB) provided recommendations to U.S. EPA as it reconsidered the potential risks and how those risks should be modeled as part of regulatory assessment.  The SAB carefully considered the extensive amount of new research conducted on inorganic arsenic, including a large number of new epidemiologic studies, and recognized that there are many questions still to be answered.  It did not attempt to answer the questions but to provide advice on areas it deemed important for the Agency to take into account in its continued consideration.  The SAB clearly identified that data from low dose exposures supports the existence of a threshold response and recommended that EPA carefully evaluate those data separately from high dose data.  EPA’s evaluation of the data and how it should be used in regulatory decision-making processes currently is in progress.

The Agency for Toxic Substances and Disease Registry (ATSDR), an agency in the US Department of Health and Human Services, also completed an extensive review of inorganic arsenic in 2007.  ATSDR identified that there are no studies of US populations which identify any increased cancer risk from low dose oral exposures.  ATSDR also recognized the extensive recent information and ongoing evaluations and reconsiderations.

There is extensive data to support the conclusion that low dose oral exposures, such as those in the diet and drinking water of US populations, do not result in any increased cancer risk.  US populations differ substantially from those in other parts of the world where oral exposure to inorganic arsenic is orders of magnitude higher than in the US, and where dietary, cultural, and other factors can result in increased risk compared to the US.

As of the present time, the evaluation of the new data and consideration of how to assess risks in a regulatory decision-making framework continue.  It is important to note that there is extensive scientific research still in progress that will allow future improvements in regulatory decision-making processes.  The WPSC strongly supports the development of scientifically-based and transparent regulatory decisions and assessments.

There are numerous scientific publications from recent years, some of which are listed in References.