Childhood cancers and atmospheric carcinogens

E G Knox

doi:10.1136/jech.2004.021675

Responses

Evidence based public health policy and practice

Childhood cancers and atmospheric carcinogens

Compose a Response to This Article

Compose Response

Title *

Author Information

Contributors
First Name and Middle Initial * First or given name, e.g. 'Peter'. Last Name * Your last, or family, name, e.g. 'MacMoody'. Email Address * Your email address, e.g. higgs-boson@gmail.com Occupation * Your role and/or occupation, e.g. 'Orthopedic Surgeon'. Affiliation * Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.

Statement of Competing Interests

Competing interests? *

Yes

Please describe the competing interests

PLEASE NOTE:

A rapid response is a moderated but not peer reviewed online response to a published article in a BMJ journal; it will not receive a DOI and will not be indexed unless it is also republished as a Letter, Correspondence or as other content. Find out more about rapid responses.
We intend to post all responses which are approved by the Editor, within 14 days (BMJ Journals) or 24 hours (The BMJ), however timeframes cannot be guaranteed. Responses must comply with our requirements and should contribute substantially to the topic, but it is at our absolute discretion whether we publish a response, and we reserve the right to edit or remove responses before and after publication and also republish some or all in other BMJ publications, including third party local editions in other countries and languages
Our requirements are stated in our rapid response terms and conditions and must be read. These include ensuring that: i) you do not include any illustrative content including tables and graphs, ii) you do not include any information that includes specifics about any patients,iii) you do not include any original data, unless it has already been published in a peer reviewed journal and you have included a reference, iv) your response is lawful, not defamatory, original and accurate, v) you declare any competing interests, vi) you understand that your name and other personal details set out in our rapid response terms and conditions will be published with any responses we publish and vii) you understand that once a response is published, we may continue to publish your response and/or edit or remove it in the future.
By submitting this rapid response you are agreeing to our terms and conditions for rapid responses and understand that your personal data will be processed in accordance with those terms and our privacy notice.

I agree to and have read the terms and conditions for rapid responses and BMJ Privacy Notice *

CAPTCHA

This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

Other responses

Jump to comment:

Re: Atmospheric carcinogens and childhood cancers -- Environmental Tobacco Smoke should be included
James M. Howard
Published on: 27 April 2016
This could be due to induced testosterone...
James M. Howard
Published on: 27 April 2016
Half of cases
Al Rio
Published on: 27 April 2016
Atmospheric carcinogens and childhood cancers -- Environmental Tobacco Smoke should be included
Norbert Hirschhorn
Published on: 27 April 2016

Published on: 27 April 2016
Re: Atmospheric carcinogens and childhood cancers -- Environmental Tobacco Smoke should be included
- James M. Howard, biologist
Dear Editor,
Environmental smoke may also induce testosterone production in women and their fetuses. This has been demonstrated in female rats and their fetuses.
Nicotine Tob Res. 2003 Jun;5(3):369-74.
Epidemiological studies have shown that smoking during pregnancy markedly increases the risk for future tobacco use by adolescent female offspring. It has been hypothesized that the increas...
Show More

Dear Editor,
Environmental smoke may also induce testosterone production in women and their fetuses. This has been demonstrated in female rats and their fetuses.
Nicotine Tob Res. 2003 Jun;5(3):369-74.
Epidemiological studies have shown that smoking during pregnancy markedly increases the risk for future tobacco use by adolescent female offspring. It has been hypothesized that the increased smoking risk in females is secondary to a nicotine-induced increase in fetal plasma testosterone levels that persist to adult life. To test this hypothesis, we randomized pregnant Sprague-Dawley rats to receive either saline or nicotine from Day 4 until the end of gestation. Blood samples for testosterone levels were obtained from 30- and 120-day-old offspring. In addition, blood samples for testosterone levels were obtained prior to and following a 2-day infusion of nicotine to chronically catheterized ovine fetuses. Maternal nicotine exposure resulted in increased plasma testosterone in 30-day-old female rat offspring, with no differences found in nicotine-exposed males. In addition, plasma testosterone levels increased in ovine fetuses in response to the nicotine infusion.
We conclude that prenatal nicotine exposure increases plasma testosterone levels chronically in adolescent female rat offspring and acutely in both male and female ovine fetuses. Although our findings lack correlative behavioral information on the female offspring, these data are consistent with human epidemiological data suggesting that prenatal environmental influences may have marked effects on the subsequent smoking behaviors of offspring.
Show Less

Conflict of Interest:
None declared.
- Back to top
Published on: 27 April 2016
This could be due to induced testosterone...
- James M. Howard, biologist
Dear Editor,
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:/...
Show More

Dear Editor,
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.
Show Less

Conflict of Interest:
None declared.
- Back to top
Published on: 27 April 2016
Half of cases
- Al Rio, Analyst
Dear Editor,
We are greatly disappointed to see the strange wording of the article by Prof E G Knox "Childhood cancers and atmospheric carcinogens", J. Epidemiol. Community Health [1], which says that "[t]he case material was extracted from a file of all 22 458 deaths from leukaemia or other cancer occurring before the 16th birthday in Great Britain between 1953 and 1980. They were classified into 11 main groups...
Show More

Dear Editor,
We are greatly disappointed to see the strange wording of the article by Prof E G Knox "Childhood cancers and atmospheric carcinogens", J. Epidemiol. Community Health [1], which says that "[t]he case material was extracted from a file of all 22 458 deaths from leukaemia or other cancer occurring before the 16th birthday in Great Britain between 1953 and 1980. They were classified into 11 main groups [...]". In the introduction, the author says that he worked with "fatal child cancers in Great Britain between 1966 and 1980, were linked with high local atmospheric emissions of different chemical species." We think that this wording, in which the classification was done before the date split, implies that more cases were analyzed than really were.
And it is not a problem with us and an over-susceptibility to this wording. BMJ's press release "Childhood cancers strongly linked to air pollution in early life" [2], incorrectly states that "[t]he postal addresses of 22,500 children who had died of cancer in Britain between 1955 and 1980 were linked to emissions hotspots for specific chemicals," when in fact about half of those twenty-two thousand cases were analyzed.
Respectfully,
Al Rio
Atlantic-Pacific Alliance
References
[1] E G Knox: Childhood cancers and atmospheric carcinogens , J. Epidemiol. Community Health 2005;59;101-105, doi:10.1136/jech.2004.021675,
http://jech.bmjjournals.com/cgi/content/full/59/2/101
[2] Emma Dickinson, BMJ Specialty Journals: Childhood cancers strongly linked to air pollution in early life,
http://www.eurekalert.org/pub_releases/2005-08/bsj-ccs080905.php
Show Less

Conflict of Interest:
None declared.
- Back to top
Published on: 27 April 2016
Atmospheric carcinogens and childhood cancers -- Environmental Tobacco Smoke should be included
- Norbert Hirschhorn, Physician, public health
Dear Editor,
Professor Knox has provided a valuable analysis on atmospheric carcinogens and their association with childhood cancers. Omitted, however, was a major source of air pollution, environmental tobacco smoke (ETS), which contains many of the same carcinogens mentioned such as benzene, benz(a)pyrene, [1,3] butadiene, cadmium and arsenic. ETS exposure, particularly in utero, due to smoking by either pare...
Show More

Dear Editor,
Professor Knox has provided a valuable analysis on atmospheric carcinogens and their association with childhood cancers. Omitted, however, was a major source of air pollution, environmental tobacco smoke (ETS), which contains many of the same carcinogens mentioned such as benzene, benz(a)pyrene, [1,3] butadiene, cadmium and arsenic. ETS exposure, particularly in utero, due to smoking by either parent has been identified as a potential risk factor for childhood brain tumors and lymphoma- leukemia [1,2,3].
Norbert Hirschhorn MD
References
(1) Sasko AJ, Vainio H. From in utero and childhood exposure to parental smoking to childhood cancer: a possible link and the need for action. Hum Exp Toxicol. 1999;18:192-201.
(2) Filippini G, Farinotti M, Ferrarini M. Active and passive smoking during pregnancy and risk of central nervous system tumours in children. Paediatr Perinat Epidemiol.2000;14:78-84.
(3) Boffeta P, Tredaniel J, Greco A. Risk of childhood cancer and adult lung cancer after childhood exposure to passive smoke: A meta- analysis. Environ Health Perspect. 2000;108:73-82.
Show Less

Conflict of Interest:
None declared.
- Back to top

Main menu

Plain text

PLEASE NOTE:

Vertical Tabs

Other responses

Jump to comment:

Log in using your username and password

Main menu

Log in using your username and password

You are here

Plain text

PLEASE NOTE:

Vertical Tabs

Other responses

Jump to comment:

Read the full text or download the PDF:

Log in using your username and password