Childhood Cancer, Possible Increase in Childhood Cancer, Engine Emissions, the Secular Trend and Testosterone

Copyright 2005, James Michael Howard, Fayetteville, Arkansas, U.S.A.

(Re: Journal of Epidemiology and Community Health 2005; 59: 101-105

Main results: Significant birth proximity relative risks were found within 1.0 km of hotspots for carbon monoxide, PM10 particles, VOCs, nitrogen oxides, benzene, dioxins, 1,3-butadiene, and benz(a)pyrene. Calculated attributable risks showed that most child cancers and leukaemias are probably initiated by such exposures.

Conclusions: Reported associations of cancer birth places with sites of industrial combustion, VOCs uses, and associated engine exhausts, are confirmed. Newly identified specific hazards include the known carcinogens 1,3-butadiene, dioxins, and benz(a)pyrene. The mother probably inhales these or related materials and passes them to the fetus across the placenta. )

This report may be explained by increased maternal testosterone as a result of exposure to these chemicals, especially nitrogen dioxide.

In 2004, I wrote "Negative Effects of Nitrogen Dioxide May be due to Testosterone" (http://www.anthropogeny.com/NO2%20and%20testosterone.htm )

"Nitrogen dioxide is a “pollutant” that is created by burning fuels. The main sources are power plants and motor vehicles. It is known to cause problems for people including increased susceptibility to respiratory infections, snoring, lung problems, etc. I suggest nitrogen dioxide may cause its problems because nitrogen dioxide may increase testosterone in humans as it does in rats (below). Increased testosterone may be involved in a number of diseases and mortality.

This areas has not been studied very much; in rats, nitrogen dioxide increases testosterone (Environ Health Perspect 2001; 109: 111-9 and ibid 1999; 107: 539-44)."

Baik, et al., recently reported "These findings indicate that levels of growth factors and hormones [testosterone] are strongly associated with stem cell potential in human umbilical cord blood and point to a potential mechanism that may mediate the relationship between in utero exposure to hormones and cancer risk in the offspring." (Cancer Res. 2005 Jan 1;65(1):358-63).

I suggest the basis of this report may be directly connected to induction of increased maternal testosterone levels which may induce future malignant transformations.

In 1994 I first suggested that testosterone may be involved in causing cancer (International Journal of Cancer 2005; 115: 497 and Annals of Internal Medicine 2005; 142: 471-472). Since there may be some indication that increased maternal testosterone may be involved in childhood cancers (the foregoing part of this treatise), I concluded that childhood cancer should be increasing because of the “secular trend.” It is my hypothesis that the "secular trend," the increase in size and earlier puberty in our children is actually caused by an increase in percentage of individuals of higher testosterone within our population over time. This is driven by women of higher testosterone. I did find information from the “National Cancer Institute” that childhood cancer may be increasing (2005). Therefore, I suggest this possible increase in childhood, and adult, cancers may be due, alone, to the secular trend and this may be exacerbated by exposure to chemicals, especially engine exhausts.