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Fluoride - Cause of Asthma?

Numerous recent studies in workers exposed to fluorides, as well as
children living near fluoride polluting industries have shown a direct
correlation between fluoride levels in plasma/urine and asthma
(Romundstad et al, 2000a, b; Soyseth et al,1994;1995).

Already in 1986, investigating 253 North American Indian children 11 to
17 years of age living on the Akwasasne reserve, Ernst et al found a
significant linear relationship between respiratory abnormalities and
fluoride urine samples.

In 1995 Soyseth et al. reported that exposure to low fluoride
concentrations during early childhood was associated with an increased
prevalence of bronchial hyper-responsiveness in schoolchildren.

Earlier Soyseth et al (1994) had reported that "a positive association
was found between bronchial responsiveness and plasma fluoride levels,
such that an increase in the plasma fluoride level of 10 ng/ml was
associated with an increase in the dose-response slope by a factor of
1.11 (95% confidence interval 1.05 to 1.17).

To put this figure in perspective:

In 8-16-year old Swiss students exposed to either drinking water
fluoridation or salt fluoridation, the average fluoride concentration
in plasma was 12.7 ng/ml (+/- 3.8)(Ziegler et al, 1991).

In 2000 Romundstad et al conducted a mortality analysis in aluminum
workers exposed to fluorides and reported an association between
exposure to fluorides and mortality from chronic bronchitis, emphysema
and asthma. Mortality from these diseases was associated with
cumulative exposure to fluorides.

In 2001, Negoita et al. reported of increases in asthma and
hypothyroidism among the Akwasasne natives.
What is the association of asthma with hypothyroidism

As mentioned above, Soyseth et al showed that bronchial responsiveness
was related to plasma fluoride levels. Bronchial responsiveness is
regulated by thyroid hormones (T3). Higher plasma fluoride levels mean
lower iodine (Free T3) levels. In the 1930s May and Litzka showed in
great detail how fluoride reduced iodine levels in blood. The more
iodine in the blood, the more fluoride had to be used. Armed with this
knowledge, they treated thousands of patients effectively from
hyperthyroidism caused by excess iodine intake (Basedow's Disease).

Giving this amount of fluoride to a normal person, this would bring
about iodine deficiency, or reduced Free T3 levels.

Numerous studies have now shown that the "continuing deficiency of
thyroid hormones influences the development of the inflammatory
component of asthma" (Manzolli et al, 1999).

It comes therefore also as no surprise that T3 supplementation has
shown great benefits in the treament of asthma (abdel Khalek et al,
1991).

References

Abdel Khalek K, el Kholy M, Rafik M, Fathalla M, Heikal E - "Effect of
triiodothyronine on cyclic AMP and pulmonary function tests in
bronchial asthma" Asthma 28(6):425-31 (1991) pub med link

   * "... This study was undertaken to evaluate the effect of
triiodothyronine, determined by pulmonary function tests and c-AMP
plasma and sputum levels, in asthmatic children. Twenty-three children
clinically euthyroid and complaining of chronic bronchial asthma were
given a triiodothyronine (T3) supply for a period of 30 days. Pulmonary
function tests, plasma and sputum cyclic AMP and plasma T3 levels were
performed prior to and after T3 therapy. Patients were requested to
continue on their usual antiasthma medicines and to try reduction of
the doses of the drugs they needed as possible. All patients tolerated
well the T3 regimen without any adverse effect. They all reported at
the end of the 30 days an obvious subjective improvement of their
asthmatic conditions with a decrease in the number of exacerbations.
Seven patients stopped their usual antiasthmatic medicines, being
maintained on T3 only and 3 have decreased the amount of
bronchodilators needed. A significant improvement of pulmonary function
tests was noted in all patients. Also, significantly increased levels
of plasma and sputum c-AMP were observed after T3 administration in
comparison to the control and pretest values. No statistical
differences were found in plasma T3 between the control and the
patients either before or after T3 therapy. The study revealed that T3
administration to clinically euthyroid chronic asthmatic children
induced a beneficial effect. This might be through improvement of c-AMP
synthesis. T3 in the doses used is devoid of side effects, proves to be
a useful adjuvant to classic antiasthma therapy, and may reduce the
amount of bronchodilators needed."

Refsnes M, Becher R, Lag M, Skuland T, Schwarze PE - "Fluoride-induced
interleukin-6 and interleukin-8 synthesis in human epithelial lung
cells" Hum Exp Toxicol 18(11):645-52 (1999) pub med link

   * Exposure to fluorides has been associated with asthmatic symptoms
among workers in the aluminium industry. In a recent experimental study
hydrogen fluoride (HF) was found to induce a weak inflammatory response
in humans. In the present study the potential of sodium fluoride (NaF)
and HF to induce cytokine response was examined and how these responses
are modulated by Al3+ in a human epithelial lung cell line (A549).
Dose-response experiments showed a maximal release of IL-6 and IL-8 at
a concentration of 5 mM NaF 24 h after addition. The responses to HF
were of a similar magnitude as for NaF. Time-course experiments showed
a NaF-induced IL-6 response at 5 h, whereas an IL-8 response was
observed after 10 h. Cycloheximide treatment completely abolished the
NaF-induced cytokine responses. A marked increase in the mRNA level for
IL-6 was observed already 2 h after exposure to 5 mM NaF, and
presumably is a prerequisite for the subsequent increase of IL-6. The
fluoride-induced effects on IL-6 and IL-8 release were strongly reduced
by pretreatment with deferoxamine (an Al3+-chelator), and enhanced by
addition of Al3+. This indicates that an AlF4-- complex, a known
activator of GTP-binding proteins, is involved in fluoride-induced IL-6
and IL-8 responses in A549 cells."

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