ToxiCity:

A. INTRODUCTION

1. Excessive Toxin Levels -- This is a summary and discussion of the 22- page Environmental Protection Agency (EPA) report entitled "A Toxic Inventory of the Bay View Hunters Point Community," Judy Quan, 9-15-95. It refers to ZIP code 94124 and comprises 13 percent of the city and county of San Francisco.

From a medical point of view, the report is somewhat disconnected since it is primarily focusing on the contents of various databases rather than tracing the story of a poisoned city.

However, it leaves no doubt that numerous toxins and carcinogens exist in great excess of their safe limits. These substances include heavy metals, anthracenes, petrochemicals, PCBs (polychlorinated biphenyls), DDT, DDE, and many others. (Table 1).

2. Damage to Health -- Since excessive rates of breast cancer, leukemias, childhood cancers, together with respiratory and other diseases were revealed by the 1995 DPH (Dept. of Public Health) study, Bernal Heights, Twin Peaks, Bayview Hunters Point, and other neighborhoods, are greatly disturbed by the presence of a massive Hazardous Superfund site in the midst of our City -- and by the absence of clean up efforts. Many advocate a moratorium on new polluting industries, such as the proposed third power plant, in an effort to slow excessive diseases until cleanup is completed.

B. CONTAMINATION

1. Levels of Contamination --

a. There are more than nine heavy metals present which exceed their toxic levels by an average of 20 times (ranging from 2 to 100 times their toxic levels) and half of these are carcinogenic They include thallium, nickel, antimony, sil-ver, chromium, beryllium, butyl tin, mercury, and copper (Table 1, column 2).

b. Nearby Islais Creek is another one of the "hot spots" of contamination in San Francisco with more than 10 hazardous toxins including cadmium, chromium, lead, mercury, nickel, DDT, DDE, anthracene, manganese, and silver (Table 1).

c. Over 730,000 tons of toxic metal-laden Naval Shipyard wastes were dumped along the shoreline between 1945 and 1986. One business on Shipyard property continues to generate hazardous wastes although the Shipyard is essentially closed. However, 95 percent of the Superfund site (aka CERCLIS) remains toxic.

d. PGE discharges over 450,000 pounds per year of heavy metals, petrochemicals, and other pollutants. In addition, 800 million gallons of waste water each day are treated by chlorine shock, dechlorination, and filtration before discharge; the majority is contributed by PGE. Petrochemical wastes are placed in storage tanks since their new permit now limits the amount of toxic effluents. However, neither the toxic levels in the waste water nor the seepage from storage tanks is mentioned. Only copper and oils are monitored monthly.

e. PGE also discharges well over 100 tons per year into the air including PM10 particles, carbon monoxide, sulfur dioxide, nitrogen dioxide, lead, ozone, and volatile organic compounds. These are monitored only quarterly to yearly.

f. The "Large Quantity" polluters generate more than 1,000 kilograms per month of hazardous wastes and include PGE Plants, the Shipyard, and 27 other facilities. There are 9 of these polluters whose leaking storage tanks are merely being "tracked" by the San Francisco Department of Public Health and CALSITES.

g. There are 51 facilities which have reported leaks or spills, but these are either in "studying" mode, or are "in the process" of clean up and are only being "tracked." The cases of another 20 facilities have been "closed."

C. SUMMARY

There presently exists in southeast San Francisco a number of serious problems:

1. Double the expected number of people are contracting cancer and several other diseases in Bayview Hunters Point ‹ this rate is the highest in the world!

2. Over 53 hazardous toxins are in greatly excessive levels above their safe level, and over 50% of these are carcinogens.

3. The PGE Hunters Point and Potrero Plants annually discharge over 425,000 pounds of toxins, over 200 tons of air emissions, and 240 billion gallons of waste water.

4. PGE plus 27 other "Large Quantity" polluters generate more than 1,000 kilograms of hazardous waste each month.

5. Less than 5% of this massive Superfund hazardous waste site has been cleaned up.

6. Most polluters are "studying" or "in the process of" cleaning up their spills and leaks, while there is still no cleaned up in sight.

For decades, America has paid for the "latest and the best" styles in most products in acceptance of the planned obsolescence principle. Now appears to be an appropriate time to begin utilizing some of these funds to properly dispose of hazardous wastes and in support of planned chemical safety.

The excessive contamination together with the massive disease rates speak for themselves. No more polluting industries can be allowed until the present situation has been cleaned up. Research has shown that the above chemicals can induce immunotoxicity as indicated by altered immune parameters including CD4, CD8, NK thymocytes, bone marrow cellularity, spleen weight, and splenic antibody-forming cells (14, 15), immune regulation and cytokinins (16), cerebral functions (17), derangement of cellular metabolism (20,24), and immunotoxicity (18), In addition, these compounds have been shown to expedite the conversion of an ARC patient into highly symptomatic AIDS (19).

In addition, it has been shown that immuno-toxicity is highly correlated with the carcinogenic properties of a large number of chemical substances (1, 2, 3, 4). Those compounds which exert the most potent immunotoxic effects have been shown to be the most carcinogenic, to produce tumors at the greatest number of sites, and at the highest frequency when compared to non-immunotoxic compounds (5).

Lending credence to the immunological surveillance of neoplasms are observations of an inordinately high frequency of malignant neoplasms in immunosuppressed transplant recipients, children with inherited immunodeficiency, and individual with AIDS (6).

The most common neoplasms that occur in immunodeficient patients are of the heterogenous lymphoid and reticuloendothelial types (5). Most immunosuppressants are antiproliferative which exert their effects by altering DNA (7).

Please do not hesitate to call if further information or a copy of the entire report is desired.

[Note: References (#) appear following the tables.]

Column headings for Table 1:
Level: Safe Level as Time Weighted Average in ppm
*: Exceptions: m â mg/m3; s â skin exposure
Carcinogenic: Rated by either IARC, NTP, ACGIH, or NIOSH
HP Levels: Excessive BVHP levels above the toxic limit

(not in sequential order)

1) Internat Agency for Research on Cancer 1987, Monographs on the carcinogenic risks to humans Overall Evaluations of Carcinogenicity An Updating of IARC Monographs, Vols 1-42 (Suppl 7) Lyon, France.

2) Gold, LW, Ames, BN, et al (1987) Carcinogenic potency database: Standardized results of animal bioassays, by the National Toxicology Program through May 1986 Environmental Health Perspectives 74, 237-329.

3) Haseman JK Huff JE Zeiger E McConnell EE (1987) Comparative results of 327 chemical car-cinogenicity, Environ Health Persp 74, 229-235

4) Huff J et al (1991a) Chemicals associated with site-specific neoplasia in 1372 long-term carcinogenesis experiments in laboratory rodents Environ Health Persp 93, 247-270.

5) Luster, MI, et al (1988) Assessment of chemical-induced immunotoxicity: National Toxicology Program1Ú4s guidelines for immunotoxicity evaluation in mice Fundam Appl Toxicol 10 2-19.

6) Purtilo, D.T., & Linder, J (1983) Oncological consequences of impaired immune surveillance against ubiquitous viruses J Clin Immunol 3, 197-206; D Kim, B.S., Haggerty, H.G., & Holsapple, M.P (1989) Production of DNA single-stranded breaks in unstimulated splenocytes by dimethylnitrosamines Mutat Res 213, 185-193.

7) Wilmer, J.L., Erexson, G.L., & Kligerman, A.D (1990) Effect of acrolein on phosphoramide mustard-induced sister chromatid exchanges in cultured human lymphocytes Cancer Res 50, (15), 4635-4638.

8) Alavanja MCR, Blair A, Merkle S, et al : Mortality among agricultural extension agents Am J Ind Med 14:167-176, 1988.

9) Alavanja MCR, Blair A, Merkle S, et al : Mortality among forest and soil conservationists Arch Environ Health 44:94-101, 1981.

10) Blair A, Zahm SH Mehtodologic issues in exposure assessment for case- control studies of cancer & herbicides Am J Ind Med 18:285-293, 1990.

14) Pruett, SB et al; Fundamental Applied Toxicology 18,40 1Ú492.

15) Worthing, C.R.(1987) Pesticide Manual, pp 541-542 Lavenham Press, Lavenham.

16) Edwards, BS, et al, (1984) Effects of diethyldithiocarbamate, an inhibitor of interferon antiviral activation, upon human natural killer cells J Immunol 132, 2868-2875.

17) Renoux, G, et al; (1984) Involvement of brain neocortex and liver in the regulation of T cells: The mode of action of sodium diethyldithiocarbamate Immunopharmacology 7, 89-100.

18) Street, J.C.(1981) Immunotoxicity of Pesticides In Immunological Considerations in Toxicology (R.P Sharma, Ed.), Vol 1, pp 59-60 CRC Press, Boca Raton.

19) Merieux Institute of France, 1991.

20) Barrett PB; Harwood JL The inhibition of fatty acid elongation by a thiocarbamate herbicide and its sulphoxide Biochemical Society Transactions, 1993 May, 21(2):184S.

24) Peffer RC; Campbell DD; Ritter JC Metabolism of the thiocarbamate herbicide SUTAN in rats Xenobiotica, 1991 Sep, 21(9):1139-52.