How to reduce mosquito-born illnesses

[Guest guest]

Hi All,

 

> GBP wrote:

> > Perhaps we should reconsider DDT. Bart Paulding, LAc

 

Pete wrote:

> Hi Bart! Yes. I think some safeguards and a new protocol for safe

> handling. Perhaps only for mosquitoes, deer ticks and the like, not

> for farm crop pests. <http://www.junkscience.com/ddtfaq.htm>

 

I favour biological control of insects rather than chemical control. IMO,

DDT and its metabolite (DDE) are powerful toxins and should be

avoided if at all possible. See:

 

Sci Total Environ. 2005 May 12; [Epub ahead of print] DDT and

human health. Beard J; Australian Rural Health Research

Collaboration. University of Sydney and Southern Cross University, PO

Box 3074, Lismore NSW 2480, Australia. 1,1,1-Trichloro-2,2'bis(p-

chlorophenyl) ethane (DDT) was the first widely used synthetic pesticide

and is extremely persistent in both the environment and the human

body. The introduction of DDT revolutionised agricultural production and

has been credited with the elimination of malaria from the United States

and Europe. However, DDT is also known to have had major

environmental consequences and has been associated with dramatic

declines in many animal populations. Although DDT use has generally

been restricted since the early 1970s, exposure to the pesticide remains

widespread. In developed countries, slow elimination from the body

means a large proportion of the population still have detectable levels of

DDT, or its metabolite DDE, in their serum or adipose tissue. In

developing countries, the pesticide continues to be used for vector

control and a significant proportion of breast-fed babies has daily

intakes above recommended levels. This review considers the

epidemiological evidence for possible adverse effects of human

exposure to DDT. Much of this research is weakened by methodological

flaws. However, recent methods in breast cancer research using nested

studies in cohorts with stored biological samples have allowed a more

rigorous assessment of a putative role for DDT in disease aetiology.

While DDT does not appear to play a causative role in breast cancer

development, there is suggestive evidence for a role in the aetiology of

other conditions such as pancreatic cancer, neuropsychological

dysfunction, and reproductive outcomes. Research into these and other

conditions would benefit from the same rigorous approaches used in

breast cancer research. Until further high quality evidence is available, it

is still too early, even 60 years after the introduction of this once

ubiquitous chemical, to pass judgement on the role of DDT in a number

of common diseases. PMID: 15894351 [PubMed - as supplied by

publisher]

 

Environ Mol Mutagen. 2005 Jul;46(1):43-52. Induction of cell

proliferation, micronuclei and hyperdiploidy/polyploidy in the mammary

cells of DDT- and DMBA-treated pubertal rats. Uppala PT, Roy SK,

Tousson A, Barnes S, Uppala GR, Eastmond DA. Department of

Environmental & Occupational Health, School of Public Health, Loma

Linda University, Loma Linda, CA 92350, USA. puppala

The environmental estrogen, dichlorodiphenyltrichloroethane (DDT),

and its metabolites have been implicated in the development of breast

cancer through mechanisms that remain to be elucidated. It has been

hypothesized that exposure to DDT and its metabolites, during critical

periods of development, can contribute to an elevated risk for breast

cancer in adults. In the present study, we have investigated the effect of

o,p'-DDT on mammary gland cell proliferation and chromosomal

alterations, in a rat mammary cancer model (commonly used to study

human cancer), to gain insights into its potential role in the development

of breast cancer. Twenty-one-day-old female Sprague-Dawley (SD) rats

were administered o,p'-DDT, 7,12-dimethylbenz[a]anthracene (DMBA),

genistein, DDT+DMBA, or DDT+DMBA+genistein, over a 14-day period.

To determine changes in chromosome number and structure, we used

the micronucleus assay as well as multicolor fluorescence in situ

hybridization (FISH) region-specific DNA probes for rat chromosomes 4

and 19. Cell proliferation was evaluated using 5-bromo-2'-deoxyuridine

(BrdU). Significant increases in BrdU-incorporated cells were seen in

the rats treated with DDT+DMBA. Although micronucleus frequencies

were somewhat elevated in several of the treatment groups, significant

increases were not seen in any of them. Significant increases in

numerical chromosomal aberrations were detected in all of the DDT-

and DMBA-treated groups. Genistein significantly reduced BrdU

incorporation and polyploidy in the DDT+DMBA-treated rats. These

initial studies indicate that DDT and DMBA can induce cellular and

chromosomal alterations in the rat mammary gland, which is consistent

with the hypothesis that these agents can induce early events in

mammary carcinogenesis. © 2005 Wiley-Liss, Inc. PMID: 15880734

[PubMed - indexed for MEDLINE]

 

Endocrine. 2005 Jun;27(1):45-50. DDE-induced changes in aromatase

activity in endometrial stromal cells in culture. Holloway AC, Stys KA,

Foster WG. Reproductive Biology Division, Department of Obstetrics &

Gynecology, McMaster University, Hamilton, Ontario, Canada.

Environmental toxicants are thought to play a role in several estrogen-

dependent diseases including breast cancer and endometriosis.

Toxicant-induced increased aromatase activity, an enzyme complex that

catalyzes the final rate-limiting step in the conversion of androgens to

estrogens, has been reported in assays using placental microsomes

and cancer cells in vitro. These data suggest that environmental

toxicants can increase aromatase activity and thus increase local tissue

estrogen levels, which could have implications for estrogen- dependent

functions in target tissues. The objective of this study was therefore to

quantify the effect of the stable breakdown product of DDT, 2,2-bis(p-

chlorophenyl)ethylene (p,p'-DDE), a toxicant broadly detected in human

adipose tissue, serum and follicular fluid, on aromatase activity in the

endometrium, an estrogen-sensitive target tissue. Specifically, the effect

of increasing log concentrations of p,p'-DDE on aromatase activity was

determined in cultures of endometrial stromal cells (ESC). Relative to

controls p,p'-DDE treatment significantly increased aromatase activity in

ESC (135%). Moreover, ESC cells treated with p,p'-DDE were

immunopositive for aromatase, whereas no aromatase staining could be

demonstrated in control cultures. Our data demonstrate that p,p'-DDE

treatment can increase aromatase activity in ESC in culture. PMID:

16077170 [PubMed - in process]

 

Brain Res Bull. 2005 Apr 15;65(3):241-7. Epub 2004 Dec 18.

Activation of brain estrogen receptors in mice lactating from mothers

exposed to DDT. Mussi P, Ciana P, Raviscioni M, Villa R, Regondi S,

Agradi E, Maggi A, Di Lorenzo D. Department of Pharmacological

Sciences, Center of Excellence on Neurodegenerative Diseases,

University of Milan, Via Balzaretti 9, 20133 Milan, Italy. The insecticide

dichlorodiphenyltrichloroethane (DDT) interferes with physiological

endocrine processes modulating estrogens receptor activity. Most of the

data describing the DDT mechanism of action have been collected in

vitro or in reproductive tissues in vivo. Here we use a new transgenic

mouse model to investigate the DDT effects on estrogens receptor

activation in vivo in non-reproductive tissues. In particular, we

demonstrate that DDT is able to activate estrogen receptors in the brain

and the liver of adult mice after acute administration, and it is active in

lactating mice when accumulated in the mother's milk. Furthermore, we

demonstrate that the acute administration of DDT activates estrogen

receptors with a different kinetics with respect to 17beta-estradiol.

Experiments with a breast cancer cell line engineered to express

luciferase under the transcriptional control of activated estrogen

receptors reveal that the microsomal metabolization of DDT is required

for its full activity on estrogen receptors. Taken together these data lead

to hypothesize that the delayed DDT time course on estrogen receptor

activation in vivo might be due to a necessary step of metabolism of the

compound. PMID: 15811587 [PubMed - indexed for MEDLINE]

 

Epidemiology. 2005 Mar;16(2):182-90. Exposure to organochlorine

compounds and effects on ovarian function. Windham GC, Lee D,

Mitchell P, Anderson M, Petreas M, Lasley B. Environmental Health

Investigations Branch, Department of Health Services, Oakland,

California 94612, USA. gwindham BACKGROUND: Some

chemicals appear to have hormonally active properties in animals, but

data in humans are sparse. Therefore, we examined ovarian function in

relation to organochlorine compound levels. METHODS: During 1997-

1999, 50 Southeast Asian immigrant women of reproductive age

collected urine samples daily. These samples were assayed for

metabolites of estrogen and progesterone, and the women's menstrual

cycle parameters were assessed. Organochlorine compounds (including

DDT, its metabolite DDE, and 10 polychlorinated biphenyl [PCB]

congeners) were measured in serum. RESULTS: All samples had

detectable DDT and DDE, with mean levels higher than typical U.S.

populations. Mean cycle length was approximately 4 days shorter at the

highest quartile concentration of DDT or DDE compared with the lowest.

After adjustment for lipid levels, age, parity, and tubal ligation, and

exclusion of a particularly long cycle, the decrements were attenuated to

less than 1 day, with wide confidence intervals (CIs). The adjusted

mean luteal phase length was shorter by approximately 1.5 days at the

highest quartile of DDT (95% CI = -2.6 to -0.30) or DDE (-2.6 to -0.20).

With each doubling of the DDE level, cycle length decreased 1.1 day (-

2.4 to 0.23) and luteal phase length decreased 0.6 days (-1.1 to -0.2).

Progesterone metabolite levels during the luteal phase were consistently

decreased with higher DDE concentration. PCB levels were not

generally associated with cycle length or hormone parameters after

adjustment, and they did not alter the DDE associations when included

in the same models. CONCLUSIONS: This study indicates a potential

effect of DDE on ovarian function, which may influence other end points

such as fertility, pregnancy, and reproductive cancers. PMID: 15703532

[PubMed - indexed for MEDLINE]

 

 

Best regards,

 

 

Tel: (H): +353-(0) or (M): +353-(0)

 

 

 

 

Ireland.

Tel: (W): +353-(0) or (M): +353-(0)

 

 

 

" Man who says it can't be done should not interrupt man doing it " -

Chinese Proverb

 

 

 

[Guest guest]

wrote:

 

>>> Perhaps we should reconsider DDT. Bart Paulding, LAc

 

> Pete wrote:

>

>> Hi Bart! Yes. I think some safeguards and a new protocol for safe

>> handling. Perhaps only for mosquitoes, deer ticks and the like, not

>> for farm crop pests. <http://www.junkscience.com/ddtfaq.htm>

>

> I favour biological control of insects rather than chemical control.

> IMO, DDT and its metabolite (DDE) are powerful toxins and should be

> avoided if at all possible. See:

 

Hi Dr. Phil!

 

Do biological controls reliably kill mosquitoes in sufficient numbers to

stop the mosquito borne illnesses? If so, then by all means.

 

Regards,

 

Pete