Dear Editor:Published by MAC on 2003-01-10
It is not the normal role of university scientists to debate with industry CEOs in the press; however, a response from us regarding John Mayberrys (Dofasco Inc.) attack on our Air pollution induces heritable DNA mutations study is warranted. For the moment we are willing to ignore the fact that we were labeled speculative and irresponsible by Mayberry, and stick to a discussion of the science.
The response to our publication would have been more appropriate had Mr. Mayberry actually read and referred to the published article rather than to the media reports. Below we present the comments made by Mr. Mayberry, followed by our response.
There appeared to be no effort whatsoever to scientifically establish the actual cause of the gene damage among the test mice.
We state in the introduction of our paper that the mouse exposures were performed with the objective of testing inhalation of industrial air pollution as a route of chemical mutagen exposure. This encompasses all air pollution sources in the industrial area of Hamilton Harbour, including the steel mills, which were found to be important in previous research on mutations in herring gulls. Contrary to the remark above, we did establish the cause of the mutations in general terms breathing the air in Hamilton Harbour. This was the objective of the study, and ultimately the conclusion that we drew.
The researchers test site was near the Hamilton Beach Strip, downwind from the entire city of Hamilton, including the industrial core, and adjacent to the Queen Elizabeth Highway, one of the busiest stretches of highway in North America. There would have been at least 100,000 vehicles passing within a stone's throw of the mice each day over the course of the study.
We saw no evidence of the researchers distinguishing steel mills from other sources upwind of the test site. We saw no evidence of them distinguishing steel mill emissions from vehicle exhaust. We do not believe there were adequate research controls in the study in regards to identifying or distinguishing the potential sources of emissions or their effects."
We do not deny that there are other sources of air pollution in our study area. In fact, we clearly identify the same sources as Mayberry in the Discussion section of our paper. We state that Integrated steel mills in Hamilton are not the only local source of PAHs and other toxic airborne emissions. A nearby major commuter highway, diesel powered industrial vehicles, and the surrounding population of > 640 000 humans also contribute. Previous research of ours, published similarly in scientific peer-reviewed journals, has shown elevated mutation rates in gulls nesting near steel mills. Steel mill colonies showed the highest rates of mutations, while urban sites, including a site near Toronto, revealed mutation rates that were intermediate between the Steel mill colonies and rural colonies. The classification into the categories steel, urban and rural explained the data in a statistically significant way. Importantly, while the steel mill colonies had mutation rates that were significantly elevated above rural colonies, the colony located in Toronto, a much larger city than Hamilton with both industry and traffic (the gull colony is on the Leslie St. Spit, down-wind from Lakeshore Blvd., the Gardiner Expressway, and the Don Valley Parkway) but lacking steel mills, did not. Furthermore, the distance of a colony from the nearest steel mill was significantly correlated with the rate of germ- line mutations (the closer to the steel mills, the higher the mutation rate). This analysis included data from colonies near 4 totally different steel mill sites both in Canada and the USA. This is strong evidence that steel mills contribute significantly to mutation induction.
Further, the study concluded polycyclic aromatic hydrocarbons (PAHs) were the cause of the genetic mutations in test mice. The researchers isolated this element from other elements found in the ambient air and declared it the cause of the gene damage in mice, but they do not provide compelling evidence or explanation for this linkage.
We have clearly not concluded that PAHs are responsible for the mutations. With respect to the chemicals responsible, we state that At the present time, however, we can only state that some portion of the air in Hamilton Harbour caused elevated heritable mutation frequency. Later in the same paragraph We suggest that PAHs from incomplete coal combustion are a likely candidate group for causing elevated germline mutation rates in the steel mice exposed in our study. Clearly the uncertainty over the chemical mutagens responsible is expressed here. We know the air caused elevated mutation frequency, and PAHs are the hypothesized cause. Many species of PAHs with high molecular weights (large molecules) are known to be mutagenic to bacterial and mammalian cells, as well as transgenic mice, and some have been shown to cause cancer. PAHs are known to be emitted by steel mills, which are the largest point sources in the Hamilton Harbour area upwind of the study site. More research will have to be done to confirm that PAHs are responsible.
A consultant from GlobalTox, an international consulting firm, commented on the issue earlier today. "It looks like from the study that we have no idea what these animals were exposed to, Coreen A. Robbins is quoted as saying. She went on to characterize the causal relationships of the research findings as a big stretch.
In making this criticism, it is clear that Robbins did not understand the nature of the study. Clearly, we were after one simple question: could air pollution in Hamilton Harbour induce mutations. We did not make any attempt to measure chemical exposure, nor did we claim to. Robbins statement is therefore meaningless as a criticism. It is also important that the general public and Mayberry be aware that our manuscript underwent rigorous scientific review by four independent experts prior to being published in the Proceedings of the National Academy of Science, USA.
Dofasco encourages academic research that benefits the community. We are committed to the well-being of our environment and our community, which is reflected in our performance and through third party validation of our industry leadership. We would welcome and encourage more accurate and thorough research to definitively identify the cause of the gene damage."
In recent history, both Dofasco and Stelco have made significant efforts to reduce their environmental impact, and we commend them for these efforts. Our data, however, show that at least up to the fall 1999, these efforts may not have been sufficient. This research, in showing a biological impact resulting from pollution exposure, may not be in the best economic interest of the steel industry, however, most would consider our work beneficial to the local community of living organisms, including people. As for performing further studies on genetic damage, we couldnt agree more. We dont have all of the answers; in fact, we dont have most of the answers because this is the first time anybody has asked questions about air pollution and heritable mutations directly. We are currently performing follow-up studies that continue to examine air pollution in Hamilton Harbour, and to provide some directions for remediation efforts. Rather than trying to undermine our research, we invite the steel companies to cooperate in our efforts to understand these elevated mutation rates. With ongoing studies we may be in a position to document improvements in the air quality in Hamilton Harbour. This was a stated goal when this research first began in the early 1990s. In the end, it is to the ultimate benefit of the community to sort this out.
James S. Quinn and Christopher M. Somers
Department of Biology
1280 Main St. West,