1979 Preamble to the 40 CFR 257 Solid Waste Regulation

In 1979, EPA assumes Cadmium is the only hazardous toxic pollutant in sewage sludge disposed of as a
fertilizer. EPA assumes cigarette smoke is the major source of Cadmium in the body. Twenty-six years later,
we know leafy vegetables will take up toxic pollutants as well as tobacco. Today,
we also know Cadmium is
one of many toxic cancer causing pollutants in sewage sludge. Yet,
laws are passed to ban cigarette
smoking and at the same time promote the dumping of these unlabelled toxic cancer causing pollutants on
food crops, parks, gardens and lawns.

1981 - Cornell studies found that organic extracts from "non- toxic" sludge killed mice quicker than that from "toxic
sludge. Also noted
that mutagenic components of sludge could be transported through crops to animals.

1981 - EPA, FDA, and USDA issued beneficial sewage sludge statement SW905. Yet, the methodology was not
available to test for dioxins or pathogens and EPA "assumed" only Cadmium and PCB's in sludge could effect human
health. (PF
#100, #109)

1981 - Municipalities began pilot projects to use liquid and semi-dried pathogen contaminated sludge as a fertilizer on
food crop production land.
(PF #113)

Page 53450    Federal Register / Vol. 44. No. 179 / Thursday, September 13, 1979 / Rules and Regulations
(a) Health effects; (b) trace amounts of cadmium; [c] maximum cumulative loadings; (d) annual rates of application; and
[e] closely controlled facilities.

(a) Health Effects of Cadmium.—The comments that were received exhibited widely divergent views on the health
implications of cadmium contained in solid waste. As a result, the Agency reexamined the available scientific data and
reached the following conclusions.

A variety of adverse health effects have been documented in humans and experimental animals under conditions of
acute as well as chronic exposure to cadmium.
While acute health effects in humans are generally caused by
high-level occupational exposure through inhalation, chronic health effects may result through the diet and
cigarette smoking, which are the major routes of cadmium intake for most people.
The kidney is considered
the main target organ for chronic exposure to cadmium, although chronic respiratory effects have been observed in
long-term occupational settings. Upon ingestion or inhalation, the metal gradually accumulates in the kidney cortex.
According to both clinical-epidemiological and model-calculation data, the critical concentration of cadmium in the kidney
cortex is approximately 200 micrograms per gram (ug/g), wet weight, in the average human. At that level renal tubular
dysfunction, characterized by proteinuria, is expected to occur. This condition is manifested by the excretion of B2-
microglobulin, which is the earliest discernible laboratory evidence of organ damage. Although mild or moderate
increases in excretion of B2-microglobulin, per se, are not life-threatening, the condition is often irreversible, and
continued excessive exposure to cadmium can lead to other renal function abnormalities (such as glycosuria, amino-
acid uria, and phosphaturia).

Several autopsy studies have been performed to determine the "cadmium content of various types of body tissue,
such as  the kidney and the liver. These studies confirm that the kidney is the organ which contains the Highest       
concentration of cadmium and that the concentration of the metal increases with age; Further; the autopsy data       
indicate that for the general United States population (smokers included)  the mean cadmium levels reached in the
kidney cortex are in the range""of 20-35 micrograms per gram wet weight.        

Smoking would tend to raise the mean cadmium concentration since the data  also show that smokers have                 
approximately double the concentration"