Coke Plant Emissions from March 3 Accident

This is from Dennis Stratton:

After the air emission accident at Erie Coke on Wed 3/10 people have been asking what they were exposed to. PAHs are known to be part of the particulate matter that was the dark cloud, or coke breeze. Do you know that in most cases when you catch a fish that has a tumor, it was caused by PAHs.

In the last email that I sent out, EPA Compliance Report for Erie Coke, and Tonawanda Coke, there were 6 chemicals listed under TRI.

TRI Total Releases and Transfers by Chemical and Year Chemical releases and transfers are in pounds except where otherwise noted.

First on the list is POLYCYCLIC AROMATIC COMPOUNDS,

Most people haven't ever heard of PAH's. Below is a multi-year study done in Western New York that was released in 2005. There is a map showing Lake Erie, with the concentrations along it.

http://cebp.aacrjournals.org/content/14/1/53.full
Breast Cancer Risk and Exposure in Early Life to Polycyclic Aromatic Hydrocarbons

The Western New York Exposures and Breast Cancer Study (WEB Study) is a population-based, case-control study conducted with women living in Erie and Niagara Counties in Western New York State during 1996-2001. All participants were aged 35-79 years. Cases included 1,166 women with histologically confirmed, primary, incident breast cancer. In addition, cases under the age of 65 years were restricted to women with a driver's license. Controls (n = 2,105) were frequency matched by age, race, and county of residence to cases. Controls under the age of 65 years were randomly selected from the New York State Department of Motor Vehicles driver's license list and controls 65 years of age and over were randomly selected from the Centers for Medicare and Medicaid Services rolls. For these analyses, cases and controls were restricted to participants who were residents of Erie and Niagara Counties during each of the three pertinent time periods: birth, menarche, and first birth. A total of 1,638 cases and 3,396 controls met our inclusion criteria of between 35 and 79 years of age, current resident of Erie or Niagara County, no previous cancer diagnosis other than nonmelanoma skin cancer and an ability to speak English. The response rates were 71% (1,166 of 1,638) and 62% (2,105 of 3,396) for cases and controls, respectively. All participants provided informed consent; the protocol was approved by the Institutional Review Boards of the University at Buffalo School of Medicine and Biomedical Sciences and of participating hospitals.

Polycyclic aromatic hydrocarbons (PAH) are ubiquitous in the environment and commonly present in particulate air pollution (1, 2). PAHs are a broad category of chemical compounds composed of carbon and hydrogen and are formed as a byproduct during combustion of organic material. Important sources of PAHs include cigarette smoke, steel mills, foundries, automobiles, coal combustion for electricity production and many other industrial and nonindustrial processes.

Most of these sources not only contribute to the release of PAHs into the environment, but also contribute to particulate air pollution. Ninety to 95% of particulate phase PAHs are physically associated with particulate matter <3.3 μm (2, 4). These small particles are thought to have particular biological relevance because they can be inhaled and deposited in the lower respiratory tract (5). PAHs are lipophilic (6, 7), have been shown to be mammary carcinogens in animal models (1, 8, 9), and there is evidence that they may also be human mammary carcinogens (10, 11). In addition, PAHs may also have estrogenic and antiestrogenic properties that could potentially affect breast cancer risk

To our knowledge, no studies have examined exposure to total suspended particulates (TSP) and breast cancer risk and only a few epidemiologic investigations of breast cancer have examined PAHs. Petralia et al. (13) examined premenopausal breast cancer and occupational exposure to benzene and PAHs using job exposure matrices in a population-based, case-control study. High probability of occupational exposure to benzene and PAHs was associated with premenopausal breast cancer. However, because women were exposed to a mixture of compounds, the independent effect of PAHs was difficult to estimate.

Rundle et al. (11) examined PAH-DNA adducts in breast tumor tissue. They found a 2-fold increase in PAH-DNA adducts in malignant tumors compared with tissue from controls with benign breast disease with atypia. Gammon et al. (10) examined PAH-DNA adducts in mononuclear cells in relation to the risk of breast cancer in a case-control study of Long Island residents. They found a nearly 50% increase in the risk of breast cancer for subjects in the highest quintile of PAH-DNA adducts in mononuclear cells; there was no dose-response relationship.

More on the same study.

Polycyclic aromatic hydrocarbons (PAH) are ubiquitous in the environment. We hypothesized that early life exposure to PAHs may have particular importance in the etiology of breast cancer. We conducted a population-based, case-control study of ambient exposure to PAHs in early life in relation to the risk of breast cancer.

This is the link to the study. http://cebp.aacrjournals.org/cgi/content/full/14/1/53

Cancer Epidemiology Biomarkers & Prevention Vol. 14, 53-60, January 2005
© 2005 American Association for Cancer Research
Breast Cancer Risk and Exposure in Early Life to Polycyclic Aromatic Hydrocarbons Using Total Suspended Particulates as a Proxy Measure

Matthew R. Bonner1, Daikwon Han1, Jing Nie1, Peter Rogerson2, John E. Vena4, Paola Muti1, Maurizio Trevisan1, Stephen B. Edge3 and Jo L. Freudenheim3
1 Department of Social and Preventive Medicine, School of Public Health and Health Professions; 2 Department of Geography, University at Buffalo;3 Department of Breast and Soft Tissue Surgery, Roswell Park Cancer Institute, Buffalo, New York; and 4 Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina



Several previous studies have examined exposure to PAHs in adult life in relation to cancer (10, 11). There is evidence that PAH-DNA adducts in tumor tissue and peripheral blood tends to be higher in breast cancer cases that in controls. Tumor PAH-DNA adducts levels are markers of recent exposure and PAH-DNA adducts in mononuclear cells are at best indicative of exposure several years before collection. Our findings are based on historical estimates of early life exposure. They support the hypothesis that exposure to PAHs may be associated with breast cancer risk and indicate that early life exposure to these compounds may have particular relevance to the etiology of breast cancer.

Other exposures, particularly ionizing radiation, have been observed to increase risk of breast cancer with early age at exposure. Similarly, exposure to PAHs in early life may also confer increased risk of breast cancer compared with adult exposure to PAHs. In addition, there is some evidence that early life exposure to PAHs could affect the developing fetus. In a study of early life exposure to high PAHs concentrations in air, Perera et al. found exposure to PAHs was associated with reduced birth weight, birth length, and head circumference (28). Several studies investigating the relationship between birth weight and the risk of breast cancer have observed a j-shaped curve with birth weight; those <2,500 g at birth had increased risk of breast cancer compared with women with birth weights of 2,500 to 2,999 g (29, 30).