(I am) half the man I used to be
Workers in chemical factories, petrol pumps, plastic units, dyeing industries, mining and
smelting are greatest risk of mutating their sperms from risks at work. Infections and
other behaviour and individual risks also cause temporary or permanent harm. But
increasingly new chemicals once considered safe are proving to be affecting human
hormones. Recently some papers have shown that increased air pollution, specially
particulate and volatile organic compounds can reduce successful fusion of the egg and the
sperm — an arduous event made even more improbable, considering air pollution is the
bane of most cities.4 In some cases, some recovery of sperm
activity and function is possible, if the exposure source is removed. 5 This
is possible is some cases of users of anabolic steroids (like testosterone and
dihydroepiandrosterone sulfate), systemic fever illness (spinal abscess, chicken pox),
neurological drugs and sedatives (like carbamazepine and GABA-B). This also means that
discrete exposure to drugs and other environmental gonadotoxins can have real and profound
effects on sperm production. This study recommended that emphasis must be made during
physical examination and needs to have a good medical history in the evaluation of male
infertility. Possibly the biggest perpetrator are a class of compounds called dioxins.
They are commonly produced during the process of plastic production and more importantly
in unsafe food packaging and burning of plastic wastes.6 Dioxins inhibit enzymatic action and reduces transcription in
sperm, which predisposes some men to greater risk of abnormalities of the sperm as a
result of exposure to hydrocarbons and dioxins. Artificial food additives and packaging
contaminants can also be extremely toxic to the sperm. A study compared the oestrogenic
potency of the synthetic oestrogen Zeranol, (used as a growth promoter in meat production)
and five related compounds, 17ß-oestradiol, diethylstilboestrol (DES), genistein, and
Bisphenol-A (a plastic additive). Zeranol, 17ß-oestradiol and DES were about equally
potent, genistein was four to six orders of magnitude less potent than 17ß-oestradiol but
an order of magnitude more potent than Bisphenol-A. Most of these chemicals act as genetic
modulators. The very high potency of Zeranol compared with other potential endocrine
disruptors suggests that Zeranol intake from beef products could have greater impact on
consumers than the amounts of the known or suspected endocrine disruptors that have been
found in food.7 Metals like lead and cadmium also affect genetic transcription and
translation — a step important in the reproduction of genetic information within
rapidly produced sperms in the gonads. Lead for example degenerates transcription
processes in immature sperms in human testis that leads to infertility.8
Aluminium concentrations in the spermatozoa and seminal plasma can lead to permanent or
irreversible sterility. In a study of 27 employees of two industrial companies, a refinery
and a polyolefin factory found that high concentration of aluminium in spermatozoa was
correlated with decreased sperm motility.9
Sperm
speak |
Endocrine toxicity is defined as adverse effects on the
structure and /or functioning of the endocrine system that result from exposure to
chemical substances. The endocrine system is composed of many organs and glands that
secrete hormones directly into the bloodstream, including the pituitary, hypothalamus,
thyroid, adrenals, pancreas, thymus, ovaries, and testes. Once synthesised, hormones are
conveyed to a target tissue, where they function as chemical messengers that transmit
information between cells. Hormone levels and interactions control normal physiological
processes, maintaining the body’s homeostasis.
Chemical
cocktail |
| Chemical group |
Per cent |
*Organic Compounds
of which insecticides and pesticides |
78
31 |
*Cleaning agents 12
of which volatile compounds |
54 |
*Metals and metallic compounds
of which inorganic metallic compounds 12 |
7 |
| *Others |
3 |
| Source: Based on data from US- Environmental
Protection Agency, (EPA), World Wide Fund for Nature (WWF) and Environment Defense Fund
(EDF), available at http://www.scorecard.org/ranking, as viewed on November 10, 2002. |
Because the endocrine system is complex, a toxicant may
interfere at any of a number of points along a hormone’s pathway of production,
regulation, and action. Some chemicals may injure the glands that synthesise and secrete
hormones, while others disrupt hormonal actions at the target organ. Compounds that are
toxic to the endocrine system may cause diseases such as hypothyroidism, diabetes
mellitus, hypoglycemia, reproductive disorders, and cancer. A wide variety of toxic
substances can disrupt the function of the endocrine system. For example, chemicals that
resemble the hormone oestrogen can bind to oestrogen receptors located throughout the body
and either mimic the natural hormone or inhibit its actions. Exposure to
endocrine-disrupting chemicals such as PCBs and DDT have caused a host of toxic effects in
wildlife, including impaired reproduction and development. Other endocrine toxicants, such
as persistent organochlorine pesticides (POPs) and dioxins, are being studied for their
possible role in promoting hormone — induced cancers (such as breast cancer) and in
lowering sperm counts and male fertility. |
Effect of pesticides and other biocides on sperm and
chromosomes has not been extensively researched. Almost all studies indicate that
occupational exposure to pesticides induces genetic changes in human sperm. One Finnish
study found that some pesticides individually change the genetic constitutions
irreversibly.10,11 Almost half of 700 Danish army recruits have been found to have
sperm counts low enough to make it hard for them to father children. French military
personnel found that heat and nuclear exposure have been responsible in decrease in sperm
counts. Pesticides can also adversely affect male reproductive function.12
Damage caused by environmental toxins during critical periods of growth have been found to
be irreversible.
Precocious puberty
So what is the probability of reversing toxic-induced male
sterility? Considering the diversity of chemicals and the different ways in which they
work it is difficult to make an assessment. Many forms of sterility and fertility problems
are irreversible. It depends on the time and duration of exposure, intensity (dosage) of
exposure and extent of damage. Men alone are not affected. Girls too have been
experiencing changes in reaching puberty.
A retrospective study of 145 girl patients in Belgium during a 9-year period for
treatment of precocious puberty, 28 per cent appeared to be foreign children (39 girls,
one boy) who immigrated 4 to 5 years earlier from 22 developing countries, without any
link to a particular ethnic or country background. These children were either adopted or
newly settled in Belgium. This led to the hypothesis that the mechanism of precocious
puberty might involve previous exposure to oestrogenic endocrine disruptors-DDT.
Dichlorodiphenylethylene (DDE), a derivative of DDT was 1.20 and 1.04 nanogramme/ml in
foreign adopted and non-adopted girls with precocious puberty, while the Belgian native
girls did not show any detectable concentrations. A possible relationship between
transient exposure to endocrine disruptors and sexual precocity is suggested. 13 An
unpublished research paper by H N Saiyed, director of National Institute of Occupational
Health (NIOH), Ahmedabad, shows that schoolgirls whose school is situated close to a lead
smelter in Kolkata matured sexually quicker than other girls in the city.14 Lead
is mostly accumulated in the bones but also targets soft organs causing particular damage
to the brain and nervous system, kidneys, liver, reproductive system and the
cardiovascular system.
Key issues
In Japan, in the last few years there has been a public
frenzy after exaggerated reporting by the media on the effects of endocrine disruptors. In
response the government initiated a large research programme accompanied by a large
research budget, building new laboratories and providing funds for national research.
Concern amongst the US public and pressure from environmental groups has prompted the
government to undertake a similarly significant research stance. The research budget for
endocrine disruptors in 1999 was in excess of $26 million in the US. 15
The primary focus of research in Europe is on occupational risk factors as opposed to the
US and Japanese focus on environmental risk factors. Hard data shows that in the last 25
years the incidence of testicular cancer has increased three fold as well as major
increases in hypospadias, cryptochidism and male infertility. This has caused a
significant reaction amongst the European community to investigate and to work together on
the endocrine disruptor problem; the main aim being to justify policy reviews and hence
improve health standards. Few studies in developing countries have been done. Most of the
studies are observations and anecdotal evidences focussing on sperm quality or sperm
quantity.16, 17 In India, no authoritative studies have been done comparing trends in sperm
count or quality.
Aniruddha Malpani of the Malpani Infertility Clinic,
Mumbai says, "We really don’t have population based data on semen analyses,
sperm counts and motility in India, so it’s not possible to provide statistics. These
are based on experience with semen analyses at large laboratories which perform lots of
semen analyses daily, but these patients are not representative of the population at
large." He attributes the decline in sperm count to effect of stress, effect of
smoking and effect of phytoestrogens and dioxins, a group of strong endocrine disruptors.
Malpani also laments that, "There is very little hard evidence in this field in
India, and population-based studies are very difficult and expensive to carry out. Since
infertility has never been a priority for the government, no one has really looked at this
field. With no regulations existing for the setting up of infertility clinics, there is
really no way of even determining whether the doctors who head these clinics are qualified
or not. Getting the true picture will hence be a difficult task. "
Manju Jilla, gynaecologist at the Jilla Hospital, Aurangabad opines, "Around 30
per cent of the cases that come to my hospital have the problem of male infertility.
History of the patients states that patients who have those problems are either working in
the industrial areas, pesticide industries, or doing drilling work."
The seriousness of the endocrine disruptor issue necessitates further research.
There is a need to:
- develop rapid and reliable assay systems to identify the oestrogenic effects of
chemicals currently used and chemicals that will be developed
- determine the related health effects of endocrine disruptor chemicals
- determine concentrations and periods of exposure that cause adverse effects
- develop universal analytical techniques for chemical identification and health related
epidemiological studies so that fair comparisons can be made
- understand all the confounding factors of how these chemicals effect humans and other
species - this may help identify who is most at risk
- understand the geographical factors involved
- determine how synergistic combinations of endocrine disruptors and other chemicals act
This research will help governments to decide what can be done and form policies to
restrict the use of certain chemicals in industry, agriculture the home and other areas.
Recent prominence and public awareness of the environment has prompted governments to
initiate and accelerate research into these chemicals.
Tinkering randomly with the chemicals, that can disrupt human growth and survival of
future progeny, is dangerous and unwise. Meantime, while various chemical companies and
others are making a good living tinkering and arguing among themselves, 46,000 American,
32,000 European, 11,000 Indian, 16,000 Chinese, 72 Inuit, and many many more women the
world over will die of breast cancer this year and another 400,000 will undergo surgery,
radiation treatment or chemotherapy for the disease. The 250 plus confirmed
hormone-mimicking chemicals are still being pumped and dumped into the environment in
tonnes each year. We allow this to happen because we (as a society) assume chemicals are
innocent until proven guilty. Isn’t it time we turned that assumption on its head,
requiring corporate polluters to demonstrate the absence of harm from their products
before they are released? Why do we tolerate these chemical trespasses into our most
intimate property, our bodies? The present regulatory system where greater harm is caused
before we can even begin to restrict the output of dangerous chemicals, seems — to
put it bluntly — so unworthy of great nations as to be called uncivilised.
| References |
1.
J Pajarinen et al 1997, Incidence of disorders of spermatogenesis in middle aged
Finnish men 1981-91: two necropsy studies, in The British Medical Journal, The BMJ
Publishing House, London, Vol 314, No 13.
2. J Auger et al 1995,
Decline in semen quality among fertile men in Paris during the past 20 years, in the
New England Journal of Medicine, Massachusetts Medical Society, Boston, Vol 332, No 5,
pp 281-285.
3. A Giwercman et al 1993, The human testisan organ at
risk?, in International Journal of Andrology, American Society of Andrology,
Schaumburg, Vol 15, pp 373-375.
4. K C Worrilow et al 2001, A retrospective analysis:
the examination of a potential relationship between particulate (P) and volatile organic
compound (VOC) levels in a class 100 IVF laboratory cleanroom (CR) and specific parameters
of embryogenesis and rates of Implantation (IR), in Fertility & Sterility,
American Society for Reproductive Medicine, USA.
5. S Cayan et al 2001, Spermatogenic recovery after
discrete periods of unusual gonadotoxin exposure, in Fertility and Sterility,
American Society for Reproductive Medicine, USA, Vol 76, No 3, p 154.
6. O A Khorram et al 2001, Expression of aryl
hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT)
messenger ribonucleic acid in human spermatozoa, in Fertility and Sterility,
American Society for Reproductive Medicine, USA, Vol 76, No 3, Supp 1, pp 259-260.7. Henrik Leffers et al 2001, Oestrogenic potencies of
zeranol, oestradiol, diethylstilboestrol, bisphenol-A and genistein: implications for
exposure assessment of potential endocrine disrupters, in Human Reproduction,
Oxford University Press, Oxford, Vol 16, No 5, pp 1037-1045.
8. S H Benoff et al 2001, Environmental Lead (Pb2)
exposures modulate testicular RNA expression, in Fertility and Sterility, American
Society for Reproductive Medicine, USA, Vol 76, No 3, Supp 1, September, p 260.
9. O Hovatta et al, Aluminium, lead and cadmium
concentrations in seminal plasma and spermatozoa, and semen quality in Finnish men, in Human
Reproduction, Oxford University Press, Oxford, Vol 13, pp 115-119.
10. K Härkonen et al 1999, Aneuploidy in sperm and
exposure to fungicides and lifestyle factors, ASCLEPIOS, A European Concerted Action on
Occupational Hazards to Male Reproductive Capability, in Environmental Molecular
Mutagen, Vol 34, pp 39-46.
11. J Lähdetie et al 1997, Incidence of aneuploid spermatozoa
among infertile men studied by multicolor fluorescence in situ hybridization. American
Journal of Medical Genetics, John Wiley and Sons, Utah, Vol 71, pp 115-121.
12. E Tielemans et al 1999, Pesticide exposure and decreased
fertilisation rates in vitro, in The Lancet, The Lancet Publishing House, New York, Vol
354, August 7.
13. M Krstevska-Konstantinova 2001, Sexual precocity after
immigration from developing countries to Belgiium: evidence of previous exposure to
organochlorine pesticides, in Human Reproduction, Oxford University Press, Oxford, Vol
16, No 5, May 16, pp 1020-1026.
14. H N Saiyed 2002, Effects of lead exposure on sexual
maturity rate (SMR) in girls, presentation at MoEF-CII conference on Environmental Health,
November 20-21, New Delhi.
15. USEPA, Annual Budget and Expenditure 2001, Vol 1, Research
and Outreach programs, Washington DC.
16. E Chou 1999, Workplace and declining sperm count, in Occupational
Health and Industrial Medicine, January, Vol 12, No 1, p 73.
17.
H Fisch et al 1996, Worldwide variations in sperm count, in Urology, Vol 48, No 6,
December, pp 909-911. |
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