Cecilioni VA - “Lung Cancer in a Steel City- A Personal Historical Perspective” Fluoride 23(3):101-103 (1990)

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Lung Cancer in a Steel City- A Personal Historical Perspective

by Dr. V.A. Cecilioni
Hamilton, Ontario, Canada

Almost twenty years have passed  since my first study on "Lung Cancer in a Steel City - Its Possible Relation to Fluoride Emissions" (1). This was followed two years later by "Further Observations on Cancer in a Steel  City" (2). Both studies presented evidence of a connection  between industrial air pollution in Hamilton and the high mortality  rates for cancer of the lung, as well as cancer of the gastro-intestinal  tract and genito-urinary system. The zonal distribution of deaths revealed a definite geographic pattern - a "cancer belt"  - quite similar to the isopleth lines of equal concentrations for  many atmospheric pollutants (including fluorides) previously reported by the Ontario Ministry of the Environment and by Environment Canada.  The highest mortality rate for lung cancer was in the northeast  area of the city, close to the large steel mills. The victims were  mostly men who had worked therein or had resided nearby for many years, although some had moved away after retiring.

The major source of the excessive amounts of fluorides in the Hamilton atmosphere is the huge amounts of fluorspar (Spar) used in steelmaking.  Thousands of tons of this calcium fluoride are used daily by the two huge and one medium-sized steel mills in Hamilton; all three  mills are located in the northeast section of the city. An analysis  of dust from one Hamilton steel mill gave the following result (a "control" dust sample is shown in brakets):

Arsenic 4.3 ppm [1.81]
Cadmium 1.6 ppm [0.21]
Fluoride 3.46% [0.063]
Lead 160 ppm [13]
Mercury 0.26 ppm [0.08]
Zinc 1100 ppm [70]

The most striking aspect of the dust composition is its high fluoride content of 3.46% or 34,600 ppm, 55 times higher than in "control"  dust. Fluoride can be emitted from open hearth steel furnaces both as gaseous and particulate matter, i.e. HF and SiF (3); also the  fluoride content of SiF is 73%. Therefore, it doesn't take much  SiF4 contamination to yield a dustborne fluoride content that is  3.46%. Also relevant is the observation that fluoride fallout values near a fluoride-emitting factory can be 90 times higher than in a more distant zone (4).

In my 1972-74 studies, the male death rate from lung cancer in the  most heavily polluted residential zone was 65/100,000, which was  2.83 times higher than the national average of 23/100,000 (2), compared with a 2.42 times higher rate reported in a 1988 study of the same zone involving a correction for age which reduced the ratio to 1.99, along with an additional correction for smoking which further decreased  the ratio to 1.40 (5). In terms of my own experience, I suspect that the correction(s) for smoking might be excessive, because the  lung cancer victims which I studied had not smoked as many cigarettes  as did their "white collar" colleagues. Nevertheless,  the main point to remember is that even a suspected over-correction  of the raw data revealed a significant difference in lung cancer  deaths between the heavily polluted zone and other areas, even when based on "guestimates" calculated 14 years later.

Another point to consider is that, of the 300-or-so histological examinations of lung cancer tissue I had reported, 48% were of the  small undifferentiated "oat cell" type of cancer. This kind of cancer usually constitutes 20%-or-less of lung cancers in male smokers (1,2). The same type of "oat cell" cancer also predominated in Newfoundland fluorspar miners (6). In this connection, the conclusions of Little et al. are extremely relevant, i.e.,

The high incidence of bronchial cancer in Newfoundland fluorspar miners is of interest . . . . If we assume that the age distribution and smoking histories are comparable, the incidence of bronchial cancer appears to be at least five times higher among the Newfoundland fluorspar miners than among the Colorado uranium miners for similar  radiation exposures . . . . (and) suggests that an additional factor or co-carcinogen is present, and the possibility that fluorspar itself is the co-carcinogen (7).

The authors of the 1988 Hamilton study mention co-carcinogens,  but did not discuss fluoride(s) (5).

Finally, the fact that fluoride has recently been implicated as a likely carcinogen responsible for osteosarcomas (8) should warn  epidemiologists not to ignore the carcinogenic potential of atmospheric fluoride(s).

References

1. Cecilioni, V.A.: Lung Cancer in a Steel City - Its Possible Relation to Fluoride Emissions. Fluoride, 5:172-181, 1972.

2. Cecilioni, V.A.: Further Observations of Cancer in a Steel City.  Fluoride, 7:153-165, 1974.

3. Schueneman, J.J., High, M.D. and Bye, W.E.: Air Pollution Aspects  of the Iron and Steel Industry. U.S. Dept. of Health, Education and Welfare, Public Health Service, Division of Air Pollution, Cincinnati,  Ohio, June 1963 (see p. 49).

4. Macuch, P., Hluchan, E., Mayer, J. and Able, E.: Air Pollution  by Fluoride Compounds near an Aluminum Factory. Fluoride, 2:28-32,  1969.

5. Shannon, H.S., Hertzman, C., Julian, J.A., Hayes, M.V. and Henry, N.: Lung Cancer and Air Pollution in an Industrial City - A Geographical Analysis. Canad. J. Public Health, 79:255-259, 1988.

6. Saccomanno, G.: In: Royal Commission Report Respecting Radiation,  Compensation, and SW-ety at the Fluorspar Mines, St. Lawrence, Newfoundland, 1969.

7. Little, J.B., Radford, E.P., McCombs, H.L. and Hunt, V.R.: Distribution of Polonium-210 in Pulmonary Tissues of Cigarette Smokers. N. Eng).  J. Med., 273:1343-1351, 1965.

8. National Toxicology Program Study: Sodium Fluoride in Drinking Water, NTP TR 393, NIH Publication No. 90-2848, March 26, 1990.

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