Bisphenol A enter in aquatic environments through discharged off effluents,
principally from industrial plants, commercial areas and have great influence
on variety of aquatic biota, including fish. Evidence for changes of physiology
in fish as a result of exposure of BPA is global, with some of the most widely
reported effects on sexual development and function. In recent years, research
has shown that BPA has great influence on fresh water fishes which result in
behavioural changes of individual level and ultimately population level. This
review presents a critical assessment on reported effects of bisphenol A on
behavior in fish, mainly disturbance in reproduction behaviour. However, there
are many technical and interpretation challenges to predict the role of BPA in
endocrinal disruption and there is great criticism on how behaviors under
laboratory conditions

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Water is fundamental entity for all living
organisms to live. A satisfactory, safe, and good water supply should be
available for every individual and species. This is a duty of water suppliers
to provide good drinking quality of water to all living beings. However,
quality of drinking water is the affected by the presence of several
environmental pollutants, including endocrine disrupting chemicals (EDCs), pharmaceuticals
and personal care products (PPCPs), and other substances (Padhye et al., 2014).

A (BPA), one of the most studied EDCs, is an aromatic compound which used all
over the world as the precursor of plastics and chemical additives (Vandenberg et al., 2010). BPA is commonly used in
the production of polycarbonate plastics (very common for transparency, heat
resistance, and mechanical properties) and epoxy resins for coating of cans of
food and beverages.

In  aquatic 
environment,  BPA, Pharmaceuticals,  pesticides 
and  other  chemicals 
with  endocrine  disrupting chemicals enter through disposed
wastewater,  agricultural run-off,  and 
groundwater  discharge,  which may 
accumulate both  in  sediments and 
in biota  including  fish  (Hu  et  al., 2005). Fishes are most vulnerable
living organism when expose to pollutants like BPA because contaminated water
is directly in contact with fish organs like gills, skin can readily absorbed
BPA due to continuous exposure with BPA. BPA can also enter in fish body
through diet and drinking (gut). (Kwong et  al., 2008. In some  cases, BPA also found in developing eggs
which ultimately has influence on embryo and can retard the development of
embryo  (Daley  et 
al., 2009). Exposure of pollutants 
like BPA and other EDCs can also cause variations in behavior of fishes
in which includes  reduction the  capability 
for  avoidance from predators,  reducing/eliminating  the 
ability  to  detect 
chemical  alarm  substances released by conspecifics, affecting
schooling behavior, influencing feeding behavior, and may change social
hierarchies within a group (Scott and 
Sloman,  2004). Many studies have
been conducted to study the effect of BPA on fish physiology, normally on
features which relates to growth, development and reproduction (Hutchinson et al., 2006).

 In this paper, I present a review of the existing
literature in order to easily identify the current scope of information
available regarding effects of Bisphenol A in endocrine disruption for fresh
water fish species. This review critically analyses the information which
determine the possible effects of EDCs, on behavioral changes in fish, mainly
on behaviors related to sex and reproduction. The goal of this review is to
provide the state of the science related to role of BPA in endocrinal
disruption of fishes live in freshwater and estuarine fish, in which short-term
(i.e., physiology and behavior) and long-term effects (trans generational) are

Mechanisms of Action of BPA as an Endocrine Disrupting Chemical:

The general concept is that the estrogenic
activity of BPA is initiated when BPA is attach to estrogen receptors (ERs) in fisheries.
BPA has structural similarity to thyroid hormones (THs) bcause both have 2
benzoic rings. Due to structural similarity with thyroid hormone, BPA act as a
TH antagonist or agonist which result in disturbance of the thyroid system and
ultimately disturbance of whole body functions (Jung et al., 2007). For collection of data, models of fish metamorphosis
are mainly used. By using larval stages of fish, Iwamuro et al., (2006) found that in vivo, spontaneous and TH-induced
metamorphosis is blocked by BPA, as well as in vitro tail cell culture, tail
resorption is induced by throid hormones (THS). Corticotropin-releasing factor
(CRF) -inducible release of thyroid-stimulating hormone (TSH) and
thyrotropin-releasing hormone (TRH) -inducible release of both TSH and
prolactin from the pituitary gland are also inhibited by the compound. In fury,
the release of TSH and prolactin are not regulated by estradiol. This confirms
that ER binding is not related to the release of the pituitary hormones due to
BPA. In tail cell culture, the appearance of genes related to metamorphosis is
reduced by BPA, which reinforce the hypothesis that effects of BPA are induced
by directly binding to thyroid hormone receptors rather than estrogen receptors
(ERs)(Zoeller, 2005).

BPA as Endocrine disrupting chemicals and their biological effects:

an organism, BPA acts via mimicking or blocking natural hormone functions. An array
of hormonal systems including estrogen, androgen, progestagen, corticosteroid
and  thyroid  signaling 
systems are affected by BPA. Sex steroid action and sexual development and reproduction
are seriously affected by BPA. Almost all aspects of reproduction, including
mediating sexual differentiation, gonadal growth, and reproductive behaviors
are controlled by sex steroid hormone (Goodhead and  Tyler, 

efforts show that at comparatively high concentrations (up to 21 µg l?1)
of BPA in streams and rivers cause serious biological effects in fisheries.
Results of experiments show that BPA is responsible to cause feminizing effects
in vivo and to induce zona radiata proteins (ZRPs) synthesis in a diverse range
of fish species. There are few examples of fisheries which are affected at
different concentration of BPA i.e. carp 100 µg l?1; fathead minnow
160 µg l?1,cod 50 µg l?1,medaka 1000 µg l?1;
rainbow trout 500 µg l?1 Lindholst et al. 2001).. In vivo studies
have shown that many other biological processes are influenced by BPA. Androgen
and estrogen synthesis and metabolism disorders are seriously affected by
exposure of BPA. Studies have been conducted  in carp and results showed that exposure of
low concentrations of BPA (1–10 µg l?1)  results in decrease the ratio of estrogen to
androgen in the plasma, while exposure to high concentrations (1000 µg l?1)
increases estrogen to androgen ratio (Mandich et al., 2007).

which are induces in the ratio between estrogens and androgens have biological
consequences which are diverse in nature which may comprise masculinization or feminization
of organisms, and/or alterations in other processes controlled by these hormones
(including growth, bone morphogenesis, insulin signaling, neural development,
cell division and apoptosis). Different studies provide evidence that different
species are sensitive at different concentration of BPA. For example, when
Atlantic cod (Gadus morhua) and
turbot (Scophthalmus maximus) both are exposed to 59 µg BPA l?1
via the water, then cod was more vulnerable than turbot because ZRP was more quickly
induced in the cod than in turbot which can interfere with fertility (Larsen et al., 2006). Rate of metabolic
transformation of BPA is possible reason for variation in sensitivity of
different species when exposed to BPA. Supporting this argument, removal and
metabolism of BPA occur more rapidly in zebra fish (D. rerio) than in the rainbow trout (Oncorhynchus mykiss)
(Lindholst et al., 2001).

Evidence for endocrine
disruption in wild fish

fish evidence for endocrine disruption in both undomesticated and wild
populations is broad. Cases  of  feminized 
responses  in  fish, 
include  production  of 
female proteins  in  males 
– vitellogenin  (VTG), and  amendments in 
germ cell  development –
production of  oocytes in  the testis 
(Lange  et al.,  2011) in 
fish exposed to BPA.

In  the 
USA  reported  androgenic 
reactions  include  masculinized 
secondary  sex characters  in 
female  mosquitofish (Gambusia 
holbrooki) exposed  to BPA
(Parks et 
al., 2001),  and  androgenic 
enhancement of  secondary  sex characters in male fathead minnows (Pimephales promelas) exposed to BPA(Ankley
et al., 2003). Effects of BPA on wild
fish populations have not yet been approached, although numerous modeling analyses
have tried to report this issue

Effects of BPA (estrogens)
in fish:

properties of BPA were first reported in 1936. Wide  range of 
(anti-)estrogenic effects and influences have  been 
investigated  in  a  wide-ranging  series 
of  laboratory 


Zebrafish  (Danio  rerio), medaka (Oryzias 
latipes),  fathead  minnow,  
and  three-spined  stickleback 
(Gasterosteus aculeatus) are
mostly used model species fisheries which are used to investigate the impacts of
BPA (Ankley and Johnson, 2004). Reproductive organs are mostly affected by
estrogens. Estrogens can skew the sex ratio towards females, reduce or prevent
spermatogenesis and delay   maturation of
the ovaries at higher concentration of BPA(Weber et al.,  2003).

disruptor chemicals (BPA) can cause increasing masculinizing effect on  males, increasing  testis 
size  and speed up  spermatogenesis. Ovulation and manufacture of
VTG or yolk in females, skew sex ratio towards males and lessening ovary size
are adverse effects of BPA in females (Seki et  al., 2005). Some of the effects of BPA could
lessen the production of offspring which are documented through controlled
laboratory studies and therefore have a population significance. Effects on reproductive
development and fertility has been revealed due to exposure of environmental

endocrine-disrupting chemicals such as BPA are introduce in fisheries habitat,
the possible adverse effects of these pollutants are not only passed on to
their offspring, but also onto their offspring’s offspring, and their offspring
too. Ramji et al., (2015) selected Medaka fish for this study due to their
shorter generations, which made it the perfect candidate for the research study
at hand. Results showed a 30% decrease in the fertilization rate of fish, two generations
after exposure and  20% reduction after
three generations. If those trends sustained, the potential for declines in
overall population numbers might be expected in generations.

the work of Nash et al. (2004) it was shown that exposure to BPA (5 and 0.5
ng/L) had no chief effects on reproductive production, growth, or fertilization
in the F0 generation of fishes. However, when the interaction was continued
into the F1, their breeding was intensely affected and the population failed
completely due to reduced sperm quality /infertility in the  males. 
Interestingly the sterile males still showed typical male spawning
behavior. These  consequences were
confirmed  on a  larger scale when  a lake in 
Canada dosed  with  4-6  ng/L  over 
a  period  of 
3  years  caused 
in the  failure of  the fathead 
minnow  population,  which 
then  consequently  recovered 
two  years  after cessation of dosing (Kidd et al., 2007). When  addressing 
population  level  effects 
of BPA,  however,
extrapolating  between  laboratory 
conclusions and  effects  in 
the  wild  is generally 
more difficult. Additionally, wild populations are normally exposed to BPA
with  diverse  means    

action,  rather  than 
a  single chemical exposure,
as  occurs in most laboratory  studies.

Reproductive and
developmental toxicity of BPA:

reproductive effects

is abundant qualitative evidence on reproductive and developmental toxicity of
BPA to aquatic organisms.  Crain et al.
(2007) reviewed the environmental toxicology of Bisphenol A (BPA), concluding
that BPA can disrupt the endocrine system of a diversity of species at
environmentally relevant concentrations of 21 µg/L or less.  Reported male reproductive effects
include:  apotosis of testicular cells in
swordtail freshwater fish (Kwak et al., 2001), inhibition of gonadal growth and
spermatogenesis in fathead minnows (Sohoni et al., 2001), decreased sperm
density & motility in brown trout (Lahnsteiner et al., 2005), reduction of
testosterone and 11-ketotestosterone in turbot (Labadie and Budzinski, 2006),
and introduction of an intersex condition known as ?testis–ova? in medaka
(Metcalfe et al., 2001). Additionally, when male medaka were interact to 10
µmol/L BPA and placed with fertile females, reduced number of eggs and
hatchlings were observed; no significant decreases were observed at BPA
concentrations of 0.3, 1 and 3 µmol/L (Shioda and Wakabayashi, 2000).. 

reproductive effects:

 Reported female reproductive effects
include:  inhibition of gonadal growth
and egg production in fathead minnows (Sohoni et al., 2001), reduced
hatchability of in flathead minnow larvae (Sohoni et al., 2001), delay in, or
complete stopage of ovulation in brown trout (Lahnsteiner et al., 2005), less
number of eggs and hatchlings in medaka (Shioda and Wakabayashi, 2000), introduction
of Atlantic salmon eggshell zona radiata protein (Arukwe et al., 2000), and
increased choriogenin mRNA expression in medaka (Tyl et al., 2002). BPA
exposure at 59 µg/L for 3 weeks led to an promotion of estrone level in turbot
(Labadie and Budzinski, 2006).  High
concentrations of BPA may have both morphological and histological effects on
salmon yolk-sac fry; at three concentrations (10, 100 and 1000 µg/L) variations
in behaviour, morphology and histological structure were observed containing
fluid accumulation (oedema) in the yolk sac and haemorrhages in the front part
of the yolk sac and in the head around the gill arches at 1000 µg/L (Honkanen
et al., 2004). Embryo lesions and deformities have been observed in medeka at
200 µg/L (Pastva et al., 2001).  Effects
on the offspring include embryo lesions and deformities at 200 µg/L, and
yolk-sac hemorrhages and edema at 1000 µg/L (Honkanen et al., 2004 ; Kishida et
al., 2001; Pastva et al., 2001 ).  

Dominance of Female

Dutch database on freshwater bream populations comprises of comprehensive
information on some 25,000 fish from approximately 25 different populations.
Assuming that the normal sex ratio should be equivalent, these populations were
examined and found that 11 of them had considerably more females than males. In
most cases, between 60 and 65% of the fish were female, but in one case, more
than 70% of the fish were female. No case showed a significant majority of
males. There are many factors that can affect sex ratio data on fish
populations and of the risks around the assumption of sexual equality, but introduction
to environmental BPA could be one interpretation of these data. Obviously, this
type of investigation can never display cause and effect, but it does at least increase
the possibility of the influences of endocrine disruption at the population
level but the question of toxic impacts of estrogenic emissions on fish
populations is one of the most important that still needs to be answered (Oehlmann et al, 2000).

Overview on the effect
of BPA on reproductive behaviors in fish        

 In fish many laboratory studies have shown
effects of BPA on reproductive behavior in individuals, with a  principal focus  on estrogen 
in  males. Examples include
disruption of nest building in adult male, delayed onset of nest building or
reduced care for the nest have all been reported. In sand gobies exposure of
adult fish to 4 ng /L  was  shown 
to  reduce  the 
ability of  males  to 
gain  and keep  a 
nest  and reduced their display of
sexual behaviors (Saaristo et al.,
2009). Similarly, adult male fathead minnows exposed to 20 ng/L showed reduced
care for the spawning site (Salierno and Kane, 2009). Similarly, females
exposed to BPA (at 9.86 ng/L) showed diminished courting response towards males
and had lower reproductive success than unexposed females.


from available data in fresh water fisheries, there is agreement on the fact
that BPA is a chemical of potential concern for the ecosystem. In many cases,
the concentrations of BPA necessary to cause such effects exceeded the average
concentrations in the environment or were in the upper range. The laboratory
studies cannot account for the life-long animal exposure to BPA, since it is
continuously released in large amounts. Thus, an underestimation of the effects
is conceivable, also considering that wildlife species may be exposed to higher
BPA concentrations in specific matrices (leachates, plants effluents, river,
and marine sediments). Differences in behavior, including boldness, shoaling,
startling response, or anxiety, do occur between different strains of laboratory
zebrafish and zebrafish of different origins and between different wild

of behavioral changes are not always easily measured, nor can then be
attributed to specific BPA or even modes of action. BPA also not only  affect 
sexual  behaviors  but 
non-sexual  behaviors  too, 
and  a  response 
in  behavior specific to an BPA has not been identified. Whilst
begin to understand the effects of single concentration of BPA on behavior in
fish, in the wild fish experience multiple chemical exposure events which will
increase the complexity for interpreting behavior responses.

One  of 
the  greatest  challenges 
for  studies  on  the  effects 
of  BPA  on 
fish behavior  is  translating 
them to  the  population 
level.  Much of this depends on
the significance of the behavior trait to successful reproduction. Clearly, if
an BPA alters a  behavior  to 
prevent  male female  interactions 
in  the  spawning 
process  and  this occurs 
for  the  whole population,  then the 
population  becomes  extinct, even 
if  the individuals are capable of
producing viable gametes.

of the information on the effects of EDCs on sexual behavior in fish has come
from laboratory studies, on a very limited number of fish species. Furthermore,
most  of 
these studies  have  been 
conducted  on  laboratory 
strains  derived  from  a
population maintained in captivity for many generations and thus with limited
genetic influx and exchange, which in turn may not be representative of wild
populations. In general  both individuals  and 
populations  with  lower 
genetic  diversity  show 
lower tolerance and phenotypic variability.

current understanding of the role of behavior in reproduction and population
maintenance is still very limited and very little  work 
has  been conducted  investigating 
the link  between genetic  diversity and responses  in  behavior  to  BPA  exposure 
in  either  laboratory 
or  wild  populations. So. arguably a lot of
fundamental research work is required to obtain a more detailed understanding
of fish sexual behaviors and implications for alterations in these behaviors
before they can be applied into a risk assessment framework, or into predictive
population modeling.

















conclusion, the collective findings in this review indicate that BPA can affect
sexual behaviors with reproductive consequences for fish and potentially fish populations.
The  information  available, 
however, derive  from  a 
very  limited  number 
of  species  of 
fish  and  many 
of  the  behavioral phenotypes are  not necessarily  specific to 
BPA. Future efforts should focus on developing an understanding of role
of BPA as endocrinal disruptor which threaten fresh water fish population as
well as species.


Ø  Develop
a full toxicological assessment on BPA to determine an acceptable freshwater
exposure level.

Ø  Identify
which fresh water species are most at risk to environmental BPA levels.

Perform more studies
in the natural