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Environmental influences on reproductive health: from conception to
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This presentation contains content that your browser may not be able to =
show
properly. This presentation was optimized for more recent versions of Micro=
soft
Internet Explorer.
If you would like to proceed anyway, click here.=
p>
"Everything that surrounds anything" web.mala.bc.ca
All the physical, chemical, biological and socialfactors that may affect the origin,
growth, development
and survival of an organism in a given setting.
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Environment and reproductive health
Causes =
span>and estimated number of deaths/ye=
ar in
children0 to 4 y<=
span
style=3D'mso-hansi-font-family:Arial'>rs
Acute respiratory infections:1000000
Diarrhoeal diseases: 1600000
Malaria <=
span
style=3D'mso-hansi-font-family:Arial'>and other vector-borne: 1 000000
Injuries (non-intentional) 300000=
Poisonings 16000=
span>
=
www.who.int/evidenc=
e 2002
data
The environment and health for children=
and
their mothers, Fact sheet WHO/284, 2005
Diseases strongly linked to
environmental threats are present in places
where children grow, live, learn and... work
WHO ACTIVITIES ON CHILDREN'S HEALTH & THE ENVIRONMEN=
T
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Over 5000000 children under 14 yrs die every year from diseases that relate to
environmental conditions, mainly in the developing <=
span
lang=3DEN-GB style=3D'font-size:111%;color:#0000CC'>world.www.who.int/world-health-day/2003=
=
div>
=
div>
=
div>
=
div>
MAIN GLOBAL ENVIRONMENTAL HEALTH RISKS
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Environment and reproductive health
=
RISKS
Physical=
div>
Chemical
Biological
Social
MEDIA
W=
ater,
Air, Food
<=
span
style=3D'mso-spacerun:yes'> Soil, Objects
SETTINGS
Rural/urban
Home, Park,
Field, Street,
Work
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Environment and reproductive health
=
RISKS
Physical=
div>
Chemical
Biological
Social
MEDIA
W=
ater,
Air, Food
<=
span
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SETTINGS
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ting,
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Environment and reproductive health
=
RISKS
Physical=
div>
Chemical
Biological
Social
MEDIA
W=
ater,
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<=
span
style=3D'mso-spacerun:yes'> Soil, Objects
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ACTIV=
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Habits, ….
SU=
SCEPTIBILITY
Cr=
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windows
Nu=
trition
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hnic
minorities
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Environment and reproductive health
=
RISKS
Physical=
div>
Chemical
Biological
Social
MEDIA
W=
ater,
Air, Food
<=
span
style=3D'mso-spacerun:yes'> Soil, Objects
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SU=
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EF=
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ON
Or=
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Fu=
nctions:
Reproduction=
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We=
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De=
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Su=
rvival
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Environment and reproductive health
=
RISKS
Physical=
div>
Chemical
Biological
Social
MEDIA
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ater,
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span
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/div>
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Environmental influences on reproductive health: from conception to
birth…and beyond - Jenny Pronczuk
Environment and reproductive health
v=
The
biological process of reproduction involves:
v
§=
Production of healthy germ cells
§=
Conception
§=
Viable conceptus (embryo)
§<=
/span>Growth & development of fetus in favourable maternal environment
§=
Successful delivery of baby
§Growth and development of baby =
into
healthy child and a healthy adult=
… and
parent!
§
v=
Any environmental factor that aff=
ects
one or more of these key stages can result in reproductive failure<=
/span>
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Environment and reproductive health
REPRODUCTIVE HEALTH
v
vFemales are born with all their ova
=
vExposure
to toxicants during the formation of fetal ovaries and ova will impact on fut=
ure
generations.
v
v
vMales produce sperm continuously
<=
/b>
§Past, rec=
ent, or
ongoing occupational/environmental exposures may alter spermatogenesis – with the =
possibility of "recovery"=
;
§
v
vE.g.: Lead and some pesticides have been detected in =
span>follicular fluid and semen<=
span
style=3D'font-size:86%;color:#0000CC;mso-special-format:lastCR;display:non=
e'>
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Environment and reproductive health
vEffects
on the female<=
/u> reproductive system:
v
§<=
/span>Sexual behaviour
§<=
/span>Onset of puberty and menstrual cycles
§<=
/span>Fertility (decreased)
§<=
/span>Gestation time
§<=
/span>Lactation (decreased)
§<=
/span>Menopause (cause premature menopause)
§<=
b>
§Eg:- =
Lead
exposure: menstrual disorders, infertility
§ =
span>- PCBs can bring irregularities in men=
strual
cycle.
v
REPRODUCTIVE TOXICANTS/FACTORS
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Environment and reproductive health
ENVIRONMENTAL THREATS TO FEMALE FERTILITY=
span>
vCauses of female infertility:
v
§Tu=
bal
factors36%
=
span>
§Ov=
ulatory
factors 33%
=
span>
§En=
dometriosis 6%
<=
/div>
§Un=
known 40% ??
§
v
v
v=
Eg. :
§Car exhaust fumes=
linked
to reduction in ovarian weight and n° offollicles
=
div>
§Coffee linked to =
higher
risk of not conceiving for 12 months
§Smoking and obesi=
ty
linked to ageing of genetic material
v=
span>
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Environment and reproductive health
REPRODUCTIVE HEALTH
vDES
(diethystilbestrol)
v<=
b>
vSynthetic hormone dev=
eloped
in 1930s to prevent mis=
carriage
v<=
b>
vMothers who took DES:=
v
vDaughters with vaginal adenocarcinoma=
13;
vBoys: reproductive organ abnormalitise&=
#13;
vHigher rates of breast cancer
<=
/span>
v
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Environment and reproductive health
=
=
v=
v
v
v=
Pre-conceptionPCBs
and Pb maternal body burdens are linked to abortion, stillbirth and learning disabilities
v=
Folate deficien=
cy
leads to neural tube defects
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Environment and reproductive health
REPRODUCTIVE TOXICANTS/FACTORS
vIn
the male=
b> reproductive system they can alte=
r:
v
§=
Sperm count and morphology
§=
Sexual behaviour
§=
Fertility (decreased)
§
§Eg:
§- Exposure to phtalates, PCBs and organochlorine
pesticides affect quality of sperm
§
§- Lead reduces male fertility
§
§- Carbon disulfide and some pesticides (chlordecone,
ethylene dibromide and dibromochloropropane)
§-=
Scrotal
hyperthermia
§
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Environmental influences on reproductive health: from conception to
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Environment and reproductive health
Environmental factors that influe=
nce
fertility:
DBCP
(dibromo-3-chloropropane)
Pesticide
used in banana & pineapple plantations
•<=
/span>Azoospermia and oligospermia in 64 to 9=
0% of
men exposed for 3 ys
•<=
/span>Failure of spermatogonial development(rats)
•<=
/span>DBCP-treated human sperm does not penet=
rate
the oocytes
Given the persistent nature of DBCP contami=
nation
in areas of past use, efforts should be made to remediate th=
ese
areas and to follow exposed populations for development of cert=
ain
human cancers, including breast, ovarian, stomach, respira=
tory,
oral and nasal cancers, among others.
Clark & Snedeker - Critical
evaluation of the cancer risk of bromochloropropane En=
viron Sci Health C Environ Carcinog
Ecotoxicol Rev.
2005;23(2):215-60.
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v=
Possible mechanism: impairment of a
paternal gene required for the normal growth and development of the fetus
=
;
v=
v=
v=
“The
special and unique vulnerability of children to environmental hazards”Bearer, Neurotoxicology, 2000,
21(6):925
FATHERS AND THEIR OFFSPRING=
b>
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Environment and reproductive health
REPRODUCTIVE TOXICANTS
v=
Eg: POPs (Persistent Organic Pollutants)
v=
Stockholm Convention
v
§CB-153 and DDE in semen of 149
Swedish fishermen fro=
m the
eastern Baltic coast had a high pro=
portion
of Y-chromosome bearing semen. Also high
levels of the POPs in blood.
§=
Higher prevalence of chryptorchidism in Lithuania
=
§
§Environmental factors may be changing the ra=
tio of
<=
i>sperm
carrying the X or Y (sex determining) chromosomes and may be contribu=
ting to
male reproductive
disorders
§
§Human Reproduction – 28 Apr=
il
2005
§www.eshre.com
<=
/span>
v
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Environmental influences on reproductive health: from conception to
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Environment and reproductive health
REPRODUCTIVE HEALTH
v=
Adverse occupational and environmental exposure=
s may result in adverse reproductive
outcomes:
v
§=
Reduced semen quality
§=
Ovarian dysfunction
§=
Infertility
§=
Fetal loss
§=
Growth retardation
§=
Altered parturition
§=
Still birth and birth defects
§
§Timing
of exposure is crucial!
v<=
/div>
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Environmental influences on reproductive health: from conception to
birth…and beyond - Jenny Pronczuk
Environment and reproductive health
FERTILIZATION
BIRTH
Placentation
Labor
Organ maturation
Implantation
Organ development
Environmental facto=
rs
influence:
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Environmental influences on reproductive health: from conception to
birth…and beyond - Jenny Pronczuk
Environment and reproductive health
FERTILIZATION
BIRTH
Placentation
Labor
Organ maturation
Implantation
Organ development
Environmental facto=
rs
influence:
Reproductive system
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Environmental influences on reproductive health: from conception to
birth…and beyond - Jenny Pronczuk
Environment and reproductive health
FERTILIZATION
BIRTH
Placentation
Labor
Organ maturation
Implantation
Organ development
Environmental facto=
rs
influence:
Reproductive system
CHILDHOOD
PERI-PUBERTY and PUBERTY
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Environmental influences on reproductive health: from conception to
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Environment and reproductive health
CRITICAL WINDOWS OF EXPOSURE IN REPRODUCTIVE HEAL=
TH
Fleming, T. P. et al. Biol Reprod =
2004;71:1046-1054
<=
/span>
Biology of Reproduction
Schematic representing the potenti=
al
interactions between the environment of the embryo, <=
span
lang=3DEN-GB style=3D'font-size:89%'>in vitro/ in vivo, the embryo's sh=
ort-term
responses & long-term consequences...
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Environmental influences on reproductive health: from conception to
birth…and beyond - Jenny Pronczuk
Environment and reproductive health
v=
vRecognize teratogens and learn about
them.
v=
vAsk=
for
policies and procedures dealing with reproductive health to be established in your
workplace
v=
vDo not rely only on material safety d=
ata
sheets and be careful
of misleading risk research.
v=
vDet=
ermine
if potential teratogenic agents can be replaced with safer materials.
v
vBe cautious … but not overly cautious=
.
v=
RECOMMENDATIONS
TO WORKING PARENTS
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Environmental influences on reproductive health: from conception to
birth…and beyond - Jenny Pronczuk
Environment and reproductive health
v"Improving
children and mothers' environmental health by addressing and
tackling issues affecting their health, presents an essential =
span>contribution
towards the achievement of the Millennium Development Goa=
ls
(MDGs)"
<<NOTE TO USER:Please add details of the date, time, =
place
and sponsorship of the meeting for which you are using this
presentation in the space indicated.>>
<<NOTE TO USER:Both emb=
ryonic
and fetal environmental health will be considered in this presentat=
ion.
The end of the eighth week of gestation marks the end of the
"embryonic period" and the beginning of the "fetal
period">>
Despite extraordinary advances in the=
twentieth century:
2000: 10.9 =
million
deaths in children under 5 years
1990: 12.7
millionBlack, Lancet,2003, 361: 2226
=
www.unicef.org/sowc02summary/table=
8.html
A number of public health accomplishment=
s, such
as improved sanitation, vaccinations, antibiotic=
s, improved
nutrition and medical surveil=
lance
programmes, have reduced morbidity and mortality among children, especially in the economi=
cally
developed countries.
In 2000 there were 10.9 million deaths <=
/span>among
children under the age of 5 years, whereas,
in 1990, there were 12.7 mill=
ion. Although
this reduction is remarkable,=
both
the deaths and the proportional reduction in mor=
tality
rates are distributed unevenly: over 98% of these deaths occurred in developing countries. &=
#13;
The five major childhood conditions whic=
h are
responsible for deaths in under-fives in low- and-middle income countries are:
diarrhoea, acute respiratory infections, malaria,
measles and perinatal conditions. Most of these
arethe consequence of poverty and
economic inequity, which have risen sharply in m=
any of
the least developed countries, reducing the reso=
urces
available for health care.
The "big killers" are diseases=
that
have a strong environmental c=
omponent:
indoor air pollution from biomass fuels (causes =
acute respiratory infections (ARI)), unsa=
fe water
and food (cause diarrhoea)and the proliferation of vectors i=
n the
environment (cause various other diseases such as malaria).
<<NOTE
TO USER: Insert regional figures.>>
Refs:
•World Health Report 2002 =
span>(www.who.int/whr/en/).=
div>
•www.who.int/evidence (2002 data, available in 2004).
•Black. Where
and why are 10 million children dying every year? Lancet,2003,
361:2226.
•UNICEF.<=
i> The
state of the world' s children 2002: leadership: the rate of progress (www.unicef.org/sow=
c02summary/table8.html).
•WHO. =
The
environment and health for children and their mothers, Fact sheet WHO/284, 2005.
According to WHO, there aresix main GLOBAL environmental risk factors for children.=
13;
=
<<NOTE T=
O USER:
The six risk fac=
tors will be described i=
n more detail in the following slides.>>
=
•<=
/span>Household water inse=
curity.This is =
one of the main causes =
of diarrhoea. Safe
drinking-water, as defined by the WHO Guidelines, does not represent any
significant risk to health over a lifetime of consumption, including diffe=
rent
sensitivities that may occur at diffe=
rent
life stages. • =
span>Poor hygiene and san=
itation. This leads to
inadequate washing and cleaning practices, and therefore
to disease=
.•Air pollution,
both indoor
and outdoor. This=
span> triggers or aggravates=
span>respiratory diseases.•Disease vectors. These cause o=
ne
million deaths a year in children, due to malaria, dengue fever, leishmaniasis, Japanese encephalitis =
and others.
•Chemical hazards.
•<=
/span>Injuries and accidents. I=
njuries
including road accidents, drowning, burns and poisoning cause
400=
000 deaths per y=
ear.
•=
EMERGING ISSUES! These includeglobal change (climate and others), ozone depletion, electromagnetic radiation, contamination by persistent organic
pollutants...
•
Refs: =
3;
•<=
/span>Healthy <=
span
style=3D'mso-hansi-font-family:Arial'>environments for children and a healthier planet.
Booklet. Geneva, WHO, 2002.=
13;•=
WHO Guidelines for drinking-water
quality,3rded. Geneva, World He=
alth
Organization, 2004 <=
/i>(www.who.int/water_sanitation_health/dwq/gdwq3/en/).
The biological process of reproduction involves key stages:
Production of healthy germ cells
Conception
Viable conceptus
Growth and development of fetus in favourable maternal environment=
3;
Successful delivery of baby
Growth and development of baby into healthy child and healthy adult &=
#13;
=
Any environmental (chemical, physical, biological, social<=
span
lang=3DEN-GB style=3D'mso-hansi-font-family:Arial;font-size:83%'>) factor =
that
affects one or more of these key stages can result in reproductive
failure.
Ref:
Xu, Reproductive health and pesticide ex=
posure.
From "Silent invaders, Pesticides, liveliho=
ods an
women's health". Ed: Jacobs, Pesticide Acti=
on
Network, UK, 2003.
=
span>
Reproductive disorders can be a result of exposures of their parents,
and/or in utero, and/or childhood and adulthood.
Females are born with all their ova they will release during their
reproductive life.
Exposure to toxic substances for a female carrying a female fetus can
affect her grandchildren if toxic effects occur during the formation of fetal
ovaries and ova.
Sperm (produced continuously during adult reproductive years) may be
influenced by past, recent, or ongoing occupational/environmental
exposures
Lead and pesticides have been detected in follicular fluid and semen =
Ref:
CPCHE, Child health and the environment: a primer, CPCHE, 2005.
Reasons for female infertility
Tubal factors36%=
Ovulatory factors 33%
Endometriosis 6%
unknown cause 40%
Car exhaust linked to reduction in ovarian weight and in number ofovarian follicles
Coffee linked to higher risk of not conceiving for 12 months
Smoking and obesity are linked to ageing genetic material
=
Jobs:
Women working in rubber, plastics or synthetics industry: 50% increas=
e in
preterm delivery.
Rylander, Reproductive outcomes among
hairdressers, Scand J Work Environ Health (2005)=
31
(3): 212.
Exposure before concep=
tion
can result in chromosomal abnormalities or mutation in DNA of ov=
a or
sperm that will have developmental effects in offspring.
If alterations are
permanent, result can have multigenerational effect
Example: DES
(diethystilbestrol): synthetic hormone developed in 1930s to prevent
miscarriage, among other indications. Off the market in the 1970s.
Mothers who took DES=
13;
Higher rates of breast
cancer
Sons and daughters had
higher rates of reproductive organ abnormalities, reduced fertility, adverse pregnancy
outcomes, rare reproductive cancers (specially vaginal adenocarcinoma) and
immune system disorders
Ref:
CPCHE, Child health an=
d the
environment: a primer, CPCHE, 2005.
Mother=
s’ exposures both prior to conception and during pregnancy are =
associated with a variety of outcomes including spontaneous
abortion, stillbirth or neonatal death, poor
intrauterine growth, major birth defects and
functional deficits.
<<READ SLIDE.>>
<<NOTE TO USER:you may want to stress exposures/o=
ccupations
that are regionally specific if there are data to
support prenatal or preconception effects.>>
Ref:
CPCHE, Child health and the environment: a primer,
CPCHE, 2005.<=
/div>
Display Show
All: 1&=
nbsp;
Review: 0
1: Int =
J Occup
Environ Health. 1999 Apr-Jun;5(2):116-22.=
Related A=
rticles,Links =
13;
Azoospermia and oligospermia among a large c=
ohort
of DBCP applicators in 12 countries.<=
/span> Slutsky M=
, Levin JL<=
/a>, Levy BS=
a>. The University of Texas Health Center at Tyler,=
11937
U.S. Highway 271, P.O. Box 2003, Tyler, Texas
75708-3154, USA. Azoospermia and oligospermia have been well
demonstrated among workers exposed to
1,2-dibromo-3-chloropropane (DBCP) in manufactur=
ing
and formulation of this pesticide. After DBCP was banned
in the United States in the late 1970s, two American companies continued to export it to many less developed countries. In t=
he
early to mid-1990s, attorneys assembled a cohort=
of
approximately 26,400 male plaintiffs who, as wor=
kers
on banana and pineapple plantations in 12 of the=
se
countries, had been exposed to DBCP, primarily during its application. These attorneys, for the purpose of a lawsuit ag=
ainst
the two American companies, developMedian exposu=
re ed
from interrogatories a database on these men that
included information about stated periods of
occupational DBCP exposure. Seminal fluid analys=
is
results were also entered into the database. Analyzing information in this database, the authors found that, after a
median exposure to DBCP of three years, 64.3% of=
these
men overall, and 90.1% of men studied from the
Philippines, had azoospermia or oligospermia. Th=
e mean
number of children reported by the men was 2.5
overall. The percentage of men with no children was 28.5% overall. =
This report represents the largest cohort of DBCP-exposed wor=
kers
in which adverse reproductive health effects hav=
e been
described, and the first report of the adverse e=
ffects
on the reproductive health of workers exposed to=
DBCP
primarily through its application in a cohort of this size.
This serious and extensive occurrence of adverse reproductive health effects due to the export of a hazardous pesticide bef=
ore
and after its ban in the United States illustrat=
es a
number of needs for monitoring, research, educat=
ion,
and policy development.
Dibromochloropropane (DBCP): a 17-year
reassessment of testicular function and
reproductive performance. Potashnik=
G, Porath A<=
/a>. Department of Obstetrics and Gynecology, Soroka
Medical Center of Kupat Holim, Beer-Sheva,
Israel. The current study summarizes a 17-year reevalua=
tion
of testicular function and reproductive performa=
nce of
15 production workers with dibromochloropropane
(DBCP)-induced testicular dysfunction. Sperm cou=
nt
recovery was evident within 36 to 45 months in t=
hree
of the nine azoospermic and in three of the six =
oligozoospermic
men with no improvement thereafter. A significant
increase in plasma follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) and a nonsignificant decrease in testosterone level were detected in the severely affected individuals. There was no increase in the rate of spontaneous=
abortions and congenital malformations among pregnancies conceived during or after exposure. A low prevalence of male =
infants conceived during paternal exposure was found as compared with the preexposure period (16.6% versus 52.9%; P<.025). Restoration of fertility was followed by a gradua=
l increase of this value to 41.4%.
=
3;
These factors=
have a
more negative impact if men already have a higher level of damaged sperm.
Ref:
www.chem-tox.vom/infertility/default.htm=
3;
Tiido, Exposure to persistent organochlorine pollutants
associates with human sperm X:Y ratio, Human
Reproduction (2005) 20 (7): 1903
Preconception paternal exposures are now increasingly recognized as
important to the health =
and
development of the fetus.
Such exposures may increase the chance of certain diseases or adverse
pregnancy outcomes as seen in
the offspring. This is supported by research in animals and may well have a genetic or epigenetic
mechanism.
<<READ SLIDE.>>
<<NOTE TO USER: =
=
you
may want to stress exposures/occupations that are regionally specific if there are data to support
prenatal or preconception effects.>>
Refs:
•<=
/span>Bearer. The special and unique vulnerability=
of
children to environmental hazards.Neurotoxicology,
2000, 21:925.
A case–=
i>control study was conducted to exa=
mine the
relationship between Wilms' tumour
and paternal occupational exposures. The case group consisted of 200 <=
/span>children diagnosed as having Wilms=
' tumour
who were registered at selected National Wilms' Tumour Study institutions during the per=
iod 1
June, 1984, to 31 May, 1986. Disease-free controls were matched to each case using a random dig=
it
dialling procedur=
e. The
parents of cases and controls completed a self-administered questionnaire. There was no consis=
tent
pattern of increased risk for paternal occupational exposure to hydrocarbons or lead f=
ound
in this study. However, certain paternal occupations were found to have an elevated odds ratio (OR=
) of
Wilms' tumour, in=
cluding
vehicle mechanics, auto body repairmen, and welders. Offspring of fathers who were auto mechanics ha=
d a 4-
to 7-fold increased risk of Wilms' tumour for all three time periods. The largest increas=
ed odds
ratio for auto mechanics was in the preconception period [OR =3D 7.58; 95% confiden=
ce
interval (CI) =3D 0.90–63.9]. Welders had a 4- to 8-fold increased odds =
ratio,
with the strongest association during pregnancy (OR =3D 8.22; CI =3D 0.95<=
span
lang=3DEN-GB style=3D'font-size:83%'>–71.3). Although chance cannot be excluded as a =
possible explanation, association =
of
Wilms' tumour with these occupations has been reported in previous studies. Further study is =
needed
to provide data on the specific occupational exposures involved.
•=
span>Savitz. Effect of parents' occupational expo=
sures on
risk of stillbirth, preterm delivery, and small-for-gestational-age infants. Am J
Epidemiol,1989,<=
span
lang=3DEN-GB style=3D'font-size:83%'> 129:1201.
Ref:
Human Reprod=
uction –
28 April 2005
www.eshre.co=
m
Ref:
Xu, Reproductive health and pesticide exposure. From
"Silent invaders, Pesticides, livelihoods an
women's health". Ed: Jacobs, Pesticide Acti=
on
Network, UK, 2003.
=
span>
Health-damaging exposure to environmental risks can begin
before birth. Lead in air, mercury in food and other chemicals can result in long-term,
often irreversible effects, such as infertility, miscarriage, and birth
defects. Women's exposure to pesticides, solvents and persistent organic pollutants may
potentially affect the health of the fetus. Additionally, while the overal=
l benefits of breastfeed=
ing
are recognized, the health of the newborn may be affected by high <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>levels of contaminants=
in
breast milk. Small children, whose bodies are rapidly developing, are particularly susceptib=
le -
and in some instances the health impacts may only emerge later in <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>life.
Furthermore, children =
as
young as five years old sometimes work in hazardous settings. Pregnant women living =
and
working in hazardous environments and poor mothers and their children are at a high=
er
risk, as they are exposed to the most degraded environments, are often unaware of the h=
ealth
implications, and lack access to information on potential solutions.
<=
/span>
Health-damaging exposure to environmental risks can begin
before birth. Lead in air, mercury in food and other chemicals can result in long-term,
often irreversible effects, such as infertility, miscarriage, and birth
defects. Women's exposure to pesticides, solvents and persistent organic pollutants may
potentially affect the health of the fetus. Additionally, while the overal=
l benefits of breastfeed=
ing
are recognized, the health of the newborn may be affected by high <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>levels of contaminants=
in
breast milk. Small children, whose bodies are rapidly developing, are particularly susceptib=
le -
and in some instances the health impacts may only emerge later in <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>life.
Furthermore, children =
as
young as five years old sometimes work in hazardous settings. Pregnant women living =
and
working in hazardous environments and poor mothers and their children are at a high=
er
risk, as they are exposed to the most degraded environments, are often unaware of the h=
ealth
implications, and lack access to information on potential solutions.
<=
/span>
Health-damaging exposure to environmental risks can begin
before birth. Lead in air, mercury in food and other chemicals can result in long-term,
often irreversible effects, such as infertility, miscarriage, and birth
defects. Women's exposure to pesticides, solvents and persistent organic pollutants may
potentially affect the health of the fetus. Additionally, while the overal=
l benefits of breastfeed=
ing
are recognized, the health of the newborn may be affected by high <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>levels of contaminants=
in
breast milk. Small children, whose bodies are rapidly developing, are particularly susceptib=
le -
and in some instances the health impacts may only emerge later in <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>life.
Furthermore, children =
as
young as five years old sometimes work in hazardous settings. Pregnant women living =
and
working in hazardous environments and poor mothers and their children are at a high=
er
risk, as they are exposed to the most degraded environments, are often unaware of the h=
ealth
implications, and lack access to information on potential solutions.
<=
/span>
1: Int =
J Occup
Environ Health. 1999 Apr-Jun;5(2):116-22.=
Related A=
rticles,Links =
13;
Azoospermia and oligospermia among a large c=
ohort
of DBCP applicators in 12 countries.<=
/span> Slutsky M=
, Levin JL<=
/a>, Levy BS=
a>. The University of Texas Health Center at Tyler,=
11937
U.S. Highway 271, P.O. Box 2003, Tyler, Texas
75708-3154, USA. Azoospermia and oligospermia have been well
demonstrated among workers exposed to
1,2-dibromo-3-chloropropane (DBCP) in manufactur=
ing
and formulation of this pesticide. After DBCP was banned
in the United States in the late 1970s, two American companies continued to export it to many less developed countries. In t=
he
early to mid-1990s, attorneys assembled a cohort=
of
approximately 26,400 male plaintiffs who, as wor=
kers
on banana and pineapple plantations in 12 of the=
se
countries, had been exposed to DBCP, primarily during its application. These attorneys, for the purpose of a lawsuit ag=
ainst
the two American companies, developMedian exposu=
re ed
from interrogatories a database on these men that
included information about stated periods of
occupational DBCP exposure. Seminal fluid analys=
is
results were also entered into the database. Analyzing information in this database, the authors found that, after a
median exposure to DBCP of three years, 64.3% of=
these
men overall, and 90.1% of men studied from the
Philippines, had azoospermia or oligospermia. Th=
e mean
number of children reported by the men was 2.5
overall. The percentage of men with no children was 28.5% overall. =
This report represents the largest cohort of DBCP-exposed wor=
kers
in which adverse reproductive health effects hav=
e been
described, and the first report of the adverse e=
ffects
on the reproductive health of workers exposed to=
DBCP
primarily through its application in a cohort of this size.
This serious and extensive occurrence of adverse reproductive health effects due to the export of a hazardous pesticide bef=
ore
and after its ban in the United States illustrat=
es a
number of needs for monitoring, research, educat=
ion,
and policy development.
Dibromochloropropane (DBCP): a 17-year
reassessment of testicular function and
reproductive performance. Potashnik=
G, Porath A<=
/a>. Department of Obstetrics and Gynecology, Soroka
Medical Center of Kupat Holim, Beer-Sheva,
Israel. The current study summarizes a 17-year reevalua=
tion
of testicular function and reproductive performa=
nce of
15 production workers with dibromochloropropane
(DBCP)-induced testicular dysfunction. Sperm cou=
nt
recovery was evident within 36 to 45 months in t=
hree
of the nine azoospermic and in three of the six =
oligozoospermic
men with no improvement thereafter. A significant
increase in plasma follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) and a nonsignificant decrease in testosterone level were detected in the severely affected individuals. There was no increase in the rate of spontaneous=
abortions and congenital malformations among pregnancies conceived during or after exposure. A low prevalence of male =
infants conceived during paternal exposure was found as compared with the preexposure period (16.6% versus 52.9%; P<.025). Restoration of fertility was followed by a gradua=
l increase of this value to 41.4%.
=
3;
Display Show
All: 1&=
nbsp;
Review: 0
1: Int =
J Occup
Environ Health. 1999 Apr-Jun;5(2):116-22.=
Related A=
rticles,Links =
13;
Azoospermia and oligospermia among a large c=
ohort
of DBCP applicators in 12 countries.<=
/span> Slutsky M=
, Levin JL<=
/a>, Levy BS=
a>. The University of Texas Health Center at Tyler,=
11937
U.S. Highway 271, P.O. Box 2003, Tyler, Texas
75708-3154, USA. Azoospermia and oligospermia have been well
demonstrated among workers exposed to
1,2-dibromo-3-chloropropane (DBCP) in manufactur=
ing
and formulation of this pesticide. After DBCP was banned
in the United States in the late 1970s, two American companies continued to export it to many less developed countries. In t=
he
early to mid-1990s, attorneys assembled a cohort=
of
approximately 26,400 male plaintiffs who, as wor=
kers
on banana and pineapple plantations in 12 of the=
se
countries, had been exposed to DBCP, primarily during its application. These attorneys, for the purpose of a lawsuit ag=
ainst
the two American companies, developMedian exposu=
re ed
from interrogatories a database on these men that
included information about stated periods of
occupational DBCP exposure. Seminal fluid analys=
is
results were also entered into the database. Analyzing information in this database, the authors found that, after a
median exposure to DBCP of three years, 64.3% of=
these
men overall, and 90.1% of men studied from the
Philippines, had azoospermia or oligospermia. Th=
e mean
number of children reported by the men was 2.5
overall. The percentage of men with no children was 28.5% overall. =
This report represents the largest cohort of DBCP-exposed wor=
kers
in which adverse reproductive health effects hav=
e been
described, and the first report of the adverse e=
ffects
on the reproductive health of workers exposed to=
DBCP
primarily through its application in a cohort of this size.
This serious and extensive occurrence of adverse reproductive health effects due to the export of a hazardous pesticide bef=
ore
and after its ban in the United States illustrat=
es a
number of needs for monitoring, research, educat=
ion,
and policy development.
Dibromochloropropane (DBCP): a 17-year
reassessment of testicular function and
reproductive performance. Potashnik=
G, Porath A<=
/a>. Department of Obstetrics and Gynecology, Soroka
Medical Center of Kupat Holim, Beer-Sheva,
Israel. The current study summarizes a 17-year reevalua=
tion
of testicular function and reproductive performa=
nce of
15 production workers with dibromochloropropane
(DBCP)-induced testicular dysfunction. Sperm cou=
nt
recovery was evident within 36 to 45 months in t=
hree
of the nine azoospermic and in three of the six =
oligozoospermic
men with no improvement thereafter. A significant
increase in plasma follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) and a nonsignificant decrease in testosterone level were detected in the severely affected individuals. There was no increase in the rate of spontaneous=
abortions and congenital malformations among pregnancies conceived during or after exposure. A low prevalence of male =
infants conceived during paternal exposure was found as compared with the preexposure period (16.6% versus 52.9%; P<.025). Restoration of fertility was followed by a gradua=
l increase of this value to 41.4%.
=
3;
Schematic representing the poten=
tial
interactions between the environment of the embryo, either in vitro or in
vivo, the embryo's short-term responses, and their long-term consequences.
Different stages and lineages of embryo development are shown in different
colors representing undifferentiated cells (pink), trophectoderm (yellow),=
ICM
(pale blue), and primitive endoderm (deep blue).
Ref: Fleming, The emb=
ryo and
its future, Biology of Reproduction (2004) 71: 1046. www.biolre=
prod.org/cgi/content/full/71/4/1046
Picture: Copyright pending.
Physiological
differences manifest in more ways than immature metabolic pathways. Becaus=
e important systems are still differentiating and gr=
owing,
the fetus and then the child, has unique susceptibilities
compared to adults — and critical time windows in those susceptibilities.&=
#13;
•<=
/span>Preconception
•<=
/span>Gestation
–
thalidomide, DES
–
ionizing radiation
–
methylmercury, Pb
–
second-hand tobacco smoke
–
lead.
There
has been an explosion of knowledge about development in past decade or so,=
and
it is hard to remember that it was on=
ly
about 50 years ago that the discovery was made that the fetus is vulnerable to exposures. The phocomelia
epidemic resulting from use of thalidomide in pregnancy was an early and dramatic example of the ability of chemica=
ls
to cross the placenta and damage the
fetus.Additionally, thalidomide
administered during a small, 4-day window between
gestational days 20 and 24, may increase the risk of autism (Stromland, 1994).More than one system can be susceptible and different
pathology may occur depending upon the dose
and timing of exposure.
Now
we know that other exposures during gestation can harm systems, and some a=
re
listed here. We also know that
preconception exposure of both parents can cause harm to children, =
as well as postnatal exposures.
<<NOTES
TO USER:It is important to point=
out
the different responses to insults shown on the bottom bar of the figure.Significant insult during the embryonic phase will result in pregnancy loss (first 2 weeks) or major organ
malformation. During the fetal stage, damage
is more subtle and related to system dysfunction.>>
<=
/div>
Ref:
•<=
/span>Stromland,
Autism in thalidomide embryopathy: a population study, Developmental Medic=
ine
& Child Neurology (1994)
36(4):351. Of a population of 100 Swedish
thalidomide embryopathy cases, at least four met full criteria for DSM-III-R autistic disorder and ICD-10 childhood
autism. Thalidomide embryopathy of the kind encountered in these cases affects fetal development early in
pregnancy, probably on days 20 to 24
after conception. It is argued that the possible association of thalidomide
embryopathy with autism may sh=
ed
some light on the issue of which neural circuitries may be involved in autism pathogenesis.
Figure:
Reprinted from The developing human, Moore, Elsevier Inc., 1973. Used with
copyright permission (2004) fr=
om
Elsevier.
Display Show
All: 1&=
nbsp;
Review: 0
1: Int =
J Occup
Environ Health. 1999 Apr-Jun;5(2):116-22.=
Related A=
rticles,Links =
13;
Azoospermia and oligospermia among a large c=
ohort
of DBCP applicators in 12 countries.<=
/span> Slutsky M=
, Levin JL<=
/a>, Levy BS=
a>. The University of Texas Health Center at Tyler,=
11937
U.S. Highway 271, P.O. Box 2003, Tyler, Texas
75708-3154, USA. Azoospermia and oligospermia have been well
demonstrated among workers exposed to
1,2-dibromo-3-chloropropane (DBCP) in manufactur=
ing
and formulation of this pesticide. After DBCP was banned
in the United States in the late 1970s, two American companies continued to export it to many less developed countries. In t=
he
early to mid-1990s, attorneys assembled a cohort=
of
approximately 26,400 male plaintiffs who, as wor=
kers
on banana and pineapple plantations in 12 of the=
se
countries, had been exposed to DBCP, primarily during its application. These attorneys, for the purpose of a lawsuit ag=
ainst
the two American companies, developMedian exposu=
re ed
from interrogatories a database on these men that
included information about stated periods of
occupational DBCP exposure. Seminal fluid analys=
is
results were also entered into the database. Analyzing information in this database, the authors found that, after a
median exposure to DBCP of three years, 64.3% of=
these
men overall, and 90.1% of men studied from the
Philippines, had azoospermia or oligospermia. Th=
e mean
number of children reported by the men was 2.5
overall. The percentage of men with no children was 28.5% overall. =
This report represents the largest cohort of DBCP-exposed wor=
kers
in which adverse reproductive health effects hav=
e been
described, and the first report of the adverse e=
ffects
on the reproductive health of workers exposed to=
DBCP
primarily through its application in a cohort of this size.
This serious and extensive occurrence of adverse reproductive health effects due to the export of a hazardous pesticide bef=
ore
and after its ban in the United States illustrat=
es a
number of needs for monitoring, research, educat=
ion,
and policy development.
Dibromochloropropane (DBCP): a 17-year
reassessment of testicular function and
reproductive performance. Potashnik=
G, Porath A<=
/a>. Department of Obstetrics and Gynecology, Soroka
Medical Center of Kupat Holim, Beer-Sheva,
Israel. The current study summarizes a 17-year reevalua=
tion
of testicular function and reproductive performa=
nce of
15 production workers with dibromochloropropane
(DBCP)-induced testicular dysfunction. Sperm cou=
nt
recovery was evident within 36 to 45 months in t=
hree
of the nine azoospermic and in three of the six =
oligozoospermic
men with no improvement thereafter. A significant
increase in plasma follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) and a nonsignificant decrease in testosterone level were detected in the severely affected individuals. There was no increase in the rate of spontaneous=
abortions and congenital malformations among pregnancies conceived during or after exposure. A low prevalence of male =
infants conceived during paternal exposure was found as compared with the preexposure period (16.6% versus 52.9%; P<.025). Restoration of fertility was followed by a gradua=
l increase of this value to 41.4%.
=
3;
Display Show
All: 1&=
nbsp;
Review: 0
1: Int =
J Occup
Environ Health. 1999 Apr-Jun;5(2):116-22.=
Related A=
rticles,Links =
13;
Azoospermia and oligospermia among a large c=
ohort
of DBCP applicators in 12 countries.<=
/span> Slutsky M=
, Levin JL<=
/a>, Levy BS=
a>. The University of Texas Health Center at Tyler,=
11937
U.S. Highway 271, P.O. Box 2003, Tyler, Texas
75708-3154, USA. Azoospermia and oligospermia have been well
demonstrated among workers exposed to
1,2-dibromo-3-chloropropane (DBCP) in manufactur=
ing
and formulation of this pesticide. After DBCP was banned
in the United States in the late 1970s, two American companies continued to export it to many less developed countries. In t=
he
early to mid-1990s, attorneys assembled a cohort=
of
approximately 26,400 male plaintiffs who, as wor=
kers
on banana and pineapple plantations in 12 of the=
se
countries, had been exposed to DBCP, primarily during its application. These attorneys, for the purpose of a lawsuit ag=
ainst
the two American companies, developMedian exposu=
re ed
from interrogatories a database on these men that
included information about stated periods of
occupational DBCP exposure. Seminal fluid analys=
is
results were also entered into the database. Analyzing information in this database, the authors found that, after a
median exposure to DBCP of three years, 64.3% of=
these
men overall, and 90.1% of men studied from the
Philippines, had azoospermia or oligospermia. Th=
e mean
number of children reported by the men was 2.5
overall. The percentage of men with no children was 28.5% overall. =
This report represents the largest cohort of DBCP-exposed wor=
kers
in which adverse reproductive health effects hav=
e been
described, and the first report of the adverse e=
ffects
on the reproductive health of workers exposed to=
DBCP
primarily through its application in a cohort of this size.
This serious and extensive occurrence of adverse reproductive health effects due to the export of a hazardous pesticide bef=
ore
and after its ban in the United States illustrat=
es a
number of needs for monitoring, research, educat=
ion,
and policy development.
Dibromochloropropane (DBCP): a 17-year
reassessment of testicular function and
reproductive performance. Potashnik=
G, Porath A<=
/a>. Department of Obstetrics and Gynecology, Soroka
Medical Center of Kupat Holim, Beer-Sheva,
Israel. The current study summarizes a 17-year reevalua=
tion
of testicular function and reproductive performa=
nce of
15 production workers with dibromochloropropane
(DBCP)-induced testicular dysfunction. Sperm cou=
nt
recovery was evident within 36 to 45 months in t=
hree
of the nine azoospermic and in three of the six =
oligozoospermic
men with no improvement thereafter. A significant
increase in plasma follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) and a nonsignificant decrease in testosterone level were detected in the severely affected individuals. There was no increase in the rate of spontaneous=
abortions and congenital malformations among pregnancies conceived during or after exposure. A low prevalence of male =
infants conceived during paternal exposure was found as compared with the preexposure period (16.6% versus 52.9%; P<.025). Restoration of fertility was followed by a gradua=
l increase of this value to 41.4%.
=
3;
Display Show
All: 1&=
nbsp;
Review: 0
1: Int =
J Occup
Environ Health. 1999 Apr-Jun;5(2):116-22.=
Related A=
rticles,Links =
13;
Azoospermia and oligospermia among a large c=
ohort
of DBCP applicators in 12 countries.<=
/span> Slutsky M=
, Levin JL<=
/a>, Levy BS=
a>. The University of Texas Health Center at Tyler,=
11937
U.S. Highway 271, P.O. Box 2003, Tyler, Texas
75708-3154, USA. Azoospermia and oligospermia have been well
demonstrated among workers exposed to
1,2-dibromo-3-chloropropane (DBCP) in manufactur=
ing
and formulation of this pesticide. After DBCP was banned
in the United States in the late 1970s, two American companies continued to export it to many less developed countries. In t=
he
early to mid-1990s, attorneys assembled a cohort=
of
approximately 26,400 male plaintiffs who, as wor=
kers
on banana and pineapple plantations in 12 of the=
se
countries, had been exposed to DBCP, primarily during its application. These attorneys, for the purpose of a lawsuit ag=
ainst
the two American companies, developMedian exposu=
re ed
from interrogatories a database on these men that
included information about stated periods of
occupational DBCP exposure. Seminal fluid analys=
is
results were also entered into the database. Analyzing information in this database, the authors found that, after a
median exposure to DBCP of three years, 64.3% of=
these
men overall, and 90.1% of men studied from the
Philippines, had azoospermia or oligospermia. Th=
e mean
number of children reported by the men was 2.5
overall. The percentage of men with no children was 28.5% overall. =
This report represents the largest cohort of DBCP-exposed wor=
kers
in which adverse reproductive health effects hav=
e been
described, and the first report of the adverse e=
ffects
on the reproductive health of workers exposed to=
DBCP
primarily through its application in a cohort of this size.
This serious and extensive occurrence of adverse reproductive health effects due to the export of a hazardous pesticide bef=
ore
and after its ban in the United States illustrat=
es a
number of needs for monitoring, research, educat=
ion,
and policy development.
Dibromochloropropane (DBCP): a 17-year
reassessment of testicular function and
reproductive performance. Potashnik=
G, Porath A<=
/a>. Department of Obstetrics and Gynecology, Soroka
Medical Center of Kupat Holim, Beer-Sheva,
Israel. The current study summarizes a 17-year reevalua=
tion
of testicular function and reproductive performa=
nce of
15 production workers with dibromochloropropane
(DBCP)-induced testicular dysfunction. Sperm cou=
nt
recovery was evident within 36 to 45 months in t=
hree
of the nine azoospermic and in three of the six =
oligozoospermic
men with no improvement thereafter. A significant
increase in plasma follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) and a nonsignificant decrease in testosterone level were detected in the severely affected individuals. There was no increase in the rate of spontaneous=
abortions and congenital malformations among pregnancies conceived during or after exposure. A low prevalence of male =
infants conceived during paternal exposure was found as compared with the preexposure period (16.6% versus 52.9%; P<.025). Restoration of fertility was followed by a gradua=
l increase of this value to 41.4%.
=
3;
Display Show
All: 1&=
nbsp;
Review: 0
1: Int =
J Occup
Environ Health. 1999 Apr-Jun;5(2):116-22.=
Related A=
rticles,Links =
13;
Azoospermia and oligospermia among a large c=
ohort
of DBCP applicators in 12 countries.<=
/span> Slutsky M=
, Levin JL<=
/a>, Levy BS=
a>. The University of Texas Health Center at Tyler,=
11937
U.S. Highway 271, P.O. Box 2003, Tyler, Texas
75708-3154, USA. Azoospermia and oligospermia have been well
demonstrated among workers exposed to
1,2-dibromo-3-chloropropane (DBCP) in manufactur=
ing
and formulation of this pesticide. After DBCP was banned
in the United States in the late 1970s, two American companies continued to export it to many less developed countries. In t=
he
early to mid-1990s, attorneys assembled a cohort=
of
approximately 26,400 male plaintiffs who, as wor=
kers
on banana and pineapple plantations in 12 of the=
se
countries, had been exposed to DBCP, primarily during its application. These attorneys, for the purpose of a lawsuit ag=
ainst
the two American companies, developMedian exposu=
re ed
from interrogatories a database on these men that
included information about stated periods of
occupational DBCP exposure. Seminal fluid analys=
is
results were also entered into the database. Analyzing information in this database, the authors found that, after a
median exposure to DBCP of three years, 64.3% of=
these
men overall, and 90.1% of men studied from the
Philippines, had azoospermia or oligospermia. Th=
e mean
number of children reported by the men was 2.5
overall. The percentage of men with no children was 28.5% overall. =
This report represents the largest cohort of DBCP-exposed wor=
kers
in which adverse reproductive health effects hav=
e been
described, and the first report of the adverse e=
ffects
on the reproductive health of workers exposed to=
DBCP
primarily through its application in a cohort of this size.
This serious and extensive occurrence of adverse reproductive health effects due to the export of a hazardous pesticide bef=
ore
and after its ban in the United States illustrat=
es a
number of needs for monitoring, research, educat=
ion,
and policy development.
Dibromochloropropane (DBCP): a 17-year
reassessment of testicular function and
reproductive performance. Potashnik=
G, Porath A<=
/a>. Department of Obstetrics and Gynecology, Soroka
Medical Center of Kupat Holim, Beer-Sheva,
Israel. The current study summarizes a 17-year reevalua=
tion
of testicular function and reproductive performa=
nce of
15 production workers with dibromochloropropane
(DBCP)-induced testicular dysfunction. Sperm cou=
nt
recovery was evident within 36 to 45 months in t=
hree
of the nine azoospermic and in three of the six =
oligozoospermic
men with no improvement thereafter. A significant
increase in plasma follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) and a nonsignificant decrease in testosterone level were detected in the severely affected individuals. There was no increase in the rate of spontaneous=
abortions and congenital malformations among pregnancies conceived during or after exposure. A low prevalence of male =
infants conceived during paternal exposure was found as compared with the preexposure period (16.6% versus 52.9%; P<.025). Restoration of fertility was followed by a gradua=
l increase of this value to 41.4%.
=
3;
Health-damaging exposure to environmental risks can begin
before birth. Lead in air, mercury in food and other chemicals can result in long-term,
often irreversible effects, such as infertility, miscarriage, and birth
defects. Women's exposure to pesticides, solvents and persistent organic pollutants may
potentially affect the health of the fetus. Additionally, while the overal=
l benefits of breastfeed=
ing
are recognized, the health of the newborn may be affected by high <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>levels of contaminants=
in
breast milk. Small children, whose bodies are rapidly developing, are particularly susceptib=
le -
and in some instances the health impacts may only emerge later in <=
span
style=3D'mso-hansi-font-family:Arial;font-size:83%'>life.
Furthermore, children =
as
young as five years old sometimes work in hazardous settings. Pregnant women living =
and
working in hazardous environments and poor mothers and their children are at a high=
er
risk, as they are exposed to the most degraded environments, are often unaware of the h=
ealth
implications, and lack access to information on potential solutions.
<=
/span>
Houlihan, Body
Burden, The pollution in newborns, EWG, 2005
Ref:
Houlihan, Body
Burden, The pollution in newborns, EWG, 2005
ehp.niehs.nih.gov/docs/2001/109-5/ss.html
<=
/i>
Ref:
The March of Dimes Global Report on Birth Defects, The Hidden Toll of <=
/i>Dying
and Disabled Children. http://www.marchofdimes.com/professionals/871_18587.asp
Fleming, The embryo and its future, Biology of Reproduction
(2004) 71: 1046.
1) Recognize teratogens an=
d learn
about them.<=
/div>
Ask for policies and procedures=
dealing
with reproductive health to be established in your workplace
Do not rely only on material sa=
fety
data sheets and be careful of misleading risk research.
Determine if potential ter=
atogenic
agents can be replaced with safer materials.
Be cautious … but not over=
ly
cautious.
It is impossible to face "no exposure". This =
is not
an acceptable recommendation. Otherwise the whole
world would be off-limits to pregnant patients.&=
#13;
CB-153 and DDE in semen of 149 Swedish fishermen from the eastern
Baltic coast had a high proportion of Y-chromosome bearing semen. A=
lso
high levels of the POPs in blood.
Higher prevalence of chryptorchidism in Lithuania
Environmental factors may be changing the ratio of sperm carrying t=
he X
or Y (sex determining) chromosomes and may be contributing to male
reproductive disorders
"Improving children =
and
mothers' environmental health by addressing and tackling issues
affecting their health, presents an essential contribution towards t=
he
achievement of the Millennium Development Goals (MDGs)"