Day 038 - 19 Oct 94 - Page 31


     
     1        indicating different sensitivity of different species, my
     2        evidence indicates that the official regulatory bodies are
     3        not always doing what nominally they say they are going to
     4        do; they do not always rely on no effect levels from the
     5        most sensitive species when setting the ADI.
     6
     7   Q.   Is it your opinion that is the most relevant result from
     8        the most sensitive species?
     9        A.  Most certainly, yes.  That is how I understand the
    10        rationale underlying the use of the concept of the ADI.
    11
    12   Q.   You did touch on the carcinogenicity.  If a test shows up
    13        or finds a non-genotoxic carcinogenicity, or whatever, what
    14        is your conclusion for safety implications?
    15        A.  My most common response to that is to want to know
    16        quite a lot more before I make an evaluation, but it seems
    17        to me that, without further information, it would be unwise
    18        and imprudent to assume that there is a threshold for
    19        non-genotoxic carcinogenesis.
    20
    21        The concept of the ADI, the acceptable daily intake, is
    22        quantitative in figure, chisled into the regulations.  The
    23        assumption underlying that is that there is a threshold and
    24        it can be identified.  Before I would be happy to endorse
    25        an ADI for a known animal carcinogen, I would want to be
    26        sure that we understood the mechanism whereby the compound
    27        caused cancer in laboratory animals, and we would want to
    28        know not just that, say, the metabolism of that compound
    29        was different in humans from the laboratory animal, we
    30        would need to know how it was metabolised by humans as well
    31        as by the laboratory animal and that the roots were
    32        significantly different; that that significant difference
    33        enabled us to be confident that it would not cause cancer
    34        in humans, either at the same site as it did in the
    35        animals, or at other sites, and that we knew enough about
    36        the metabolic root in humans to know that it was subject to
    37        a threshold.  Under those circumstances, I might be
    38        prepared to countenance or endorse setting an ADI for a
    39        non-genotoxic carcinogen; but otherwise not.
    40
    41   Q.   Is it true that if carcinogenicity is shown in results
    42        whether it is benign or toxic ----?
    43        A.  Malignant.
    44
    45   Q.  -- malignant, as far as you are concerned, that is evidence
    46        that that compound is not safe?
    47        A.  I would not quite characterise it like that.  I would
    48        characterise it as prima facie evidence that it may not be
    49        safe and sufficient evidence not to authorise it for
    50        general use in the food supply without a considerable 
    51        amount of further information of the kind I indicated in my 
    52        previous answer. 
    53
    54   MR. JUSTICE BELL:  Unless there is something which is so related
    55        that you want to deal with it before one o'clock,
    56        I understand that Mr. Cannon may not be required to come
    57        back.
    58
    59   MR. RAMPTON:  Not by me.
    60

Prev Next Index