717
1991 , 1997 ). Nevertheless, there are good data that long-term exposure to pollutants
has adversely affected the health of fi sh, especially in the North Sea and Great
Lakes. However, mortalities among fi sh populations do not necessarily imply disease. Furthermore, disease may develop long after the pollutant has been effectively
removed from the aquatic environment. Much of the work attempting to correlate
fi sh disease with aquatic pollution has resulted from surveys, many of which have
been carried out in the North Sea (e.g. Dethlefsen and Watermann 1980 ; Dethlefsen
et al . 1987 , 2000 ; McVicar et al . 1988 ; Vethaak and ap Rheinallt 1992 ). Briefl y, fi sh
are caught with nets, and the relative incidence of disease determined. One conclusion from these surveys is that larger numbers of diseased fi sh occur generally in the
polluted compared to clean/unpolluted locations (Dethlefsen et al. 2000 ). However,
the distinction between polluted and clean sites is imprecise. Therefore, there would
be some uncertainty as to what comprises a truly polluted or clean site. Moreover, it
is uncertain from surveys how long fi sh might have been in a polluted environment
prior to capture. Thus, the effects of fi sh migration on the incidence of disease needs
to be considered (Vethaak et al . 1992 ; Bucke et al . 1992 ; Jacquez et al . 1994 ).
Pollution has been associated with some bacterial diseases, namely fi n and tail
rot (Vethaak 1992 ; Vethaak et al . 1996 ), gill disease/hyperplasia (Kirk and Lewis
1993 ) and skin disease/ulceration (Vethaak 1992 ; Vethaak and Jol 1996 ). The trigger has been attributed to stressors including contaminated diets (Landsberg 1995 ),
heavy metals e.g. chromium (Rødsaether et al . 1977 ; Prabakaran et al . 2006 ), hydrocarbons (Khan 1987 ; Song et al . 2008 ), nitrogenous compounds, i.e. ammonia (Kirk
and Lewis 1993 ) and nitrites (Hanson and Grizzle 1985 ), pesticides (e.g. Voigt
1994 ), polychlorinated biphenyls (Eckman et al. 2004 ), sewage (e.g. Austin and
Stobie 1992 ), organic pollutants (Grawinski and Antychowicz 2001 ) and unspecifi ed pollutants (e.g. Vethaak and Jol 1996 ). In one example, organic pollution has
been attributed to the high occurrence of Ser. plymuthica infections in salmonid
farms in Poland since 1996 (Grawinski and Antychowicz 2001 ). Generally, the reasons for the association between pollution and disease need to be better researched.
However, proof of correlation between the occurrence of specifi c pollutants and
disease has seldom been documented. Surveys, which have pointed to a correlation
between pollution and disease, have generally not considered the nature or concentration of the pollutant(s).
An association has been made between fi sh diseases and unknown components
of sewage dumping (Siddall et al . 1994 ). For example in a survey of 16 sites in the
Dutch Wadden Sea, a higher incidence of skin ulcers and fi n rot was noted in fi sh
caught near fresh water drainage sluices than elsewhere (Vethaak 1992 ). Pollution
by domestic sewage, i.e. leakage from a septic tank, was attributed to a new skin
disease, which was characterised by the presence of extensive skin lesions and muscle necrosis, in rainbow trout (otherwise infected with ERM for which there might
also be a link with sewage sludge; Dudley et al . 1980 ) in Scotland during 1992
(Austin and Stobie 1992 ). Interestingly, the skin lesions – but not ERM – declined
substantially after the leaking septic tank was repaired.
There is accumulating evidence that contamination leads to a weakening of the
immune state, i.e. immunosuppression (Klesius and Shoemaker 2003 ). One example
The Effects of Environmental Stress Including Physical and Chemical Pollution
1991 , 1997 ). Nevertheless, there are good data that long-term exposure to pollutants
has adversely affected the health of fi sh, especially in the North Sea and Great
Lakes. However, mortalities among fi sh populations do not necessarily imply disease. Furthermore, disease may develop long after the pollutant has been effectively
removed from the aquatic environment. Much of the work attempting to correlate
fi sh disease with aquatic pollution has resulted from surveys, many of which have
been carried out in the North Sea (e.g. Dethlefsen and Watermann 1980 ; Dethlefsen
et al . 1987 , 2000 ; McVicar et al . 1988 ; Vethaak and ap Rheinallt 1992 ). Briefl y, fi sh
are caught with nets, and the relative incidence of disease determined. One conclusion from these surveys is that larger numbers of diseased fi sh occur generally in the
polluted compared to clean/unpolluted locations (Dethlefsen et al. 2000 ). However,
the distinction between polluted and clean sites is imprecise. Therefore, there would
be some uncertainty as to what comprises a truly polluted or clean site. Moreover, it
is uncertain from surveys how long fi sh might have been in a polluted environment
prior to capture. Thus, the effects of fi sh migration on the incidence of disease needs
to be considered (Vethaak et al . 1992 ; Bucke et al . 1992 ; Jacquez et al . 1994 ).
Pollution has been associated with some bacterial diseases, namely fi n and tail
rot (Vethaak 1992 ; Vethaak et al . 1996 ), gill disease/hyperplasia (Kirk and Lewis
1993 ) and skin disease/ulceration (Vethaak 1992 ; Vethaak and Jol 1996 ). The trigger has been attributed to stressors including contaminated diets (Landsberg 1995 ),
heavy metals e.g. chromium (Rødsaether et al . 1977 ; Prabakaran et al . 2006 ), hydrocarbons (Khan 1987 ; Song et al . 2008 ), nitrogenous compounds, i.e. ammonia (Kirk
and Lewis 1993 ) and nitrites (Hanson and Grizzle 1985 ), pesticides (e.g. Voigt
1994 ), polychlorinated biphenyls (Eckman et al. 2004 ), sewage (e.g. Austin and
Stobie 1992 ), organic pollutants (Grawinski and Antychowicz 2001 ) and unspecifi ed pollutants (e.g. Vethaak and Jol 1996 ). In one example, organic pollution has
been attributed to the high occurrence of Ser. plymuthica infections in salmonid
farms in Poland since 1996 (Grawinski and Antychowicz 2001 ). Generally, the reasons for the association between pollution and disease need to be better researched.
However, proof of correlation between the occurrence of specifi c pollutants and
disease has seldom been documented. Surveys, which have pointed to a correlation
between pollution and disease, have generally not considered the nature or concentration of the pollutant(s).
An association has been made between fi sh diseases and unknown components
of sewage dumping (Siddall et al . 1994 ). For example in a survey of 16 sites in the
Dutch Wadden Sea, a higher incidence of skin ulcers and fi n rot was noted in fi sh
caught near fresh water drainage sluices than elsewhere (Vethaak 1992 ). Pollution
by domestic sewage, i.e. leakage from a septic tank, was attributed to a new skin
disease, which was characterised by the presence of extensive skin lesions and muscle necrosis, in rainbow trout (otherwise infected with ERM for which there might
also be a link with sewage sludge; Dudley et al . 1980 ) in Scotland during 1992
(Austin and Stobie 1992 ). Interestingly, the skin lesions – but not ERM – declined
substantially after the leaking septic tank was repaired.
There is accumulating evidence that contamination leads to a weakening of the
immune state, i.e. immunosuppression (Klesius and Shoemaker 2003 ). One example
The Effects of Environmental Stress Including Physical and Chemical Pollution