Limits...
How much should we involve genetic and environmental factors in the risk assessment of mycotoxins in humans?

Creppy EE, Moukha S, Bacha H, Carratu MR - Int J Environ Res Public Health (2005)

Bottom Line: Within the same range of toxins concentrations in the blood some people develop a disease while others do not.Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy.Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria.

View Article: PubMed Central - PubMed

Affiliation: Dept of Toxicology, University of Bordeaux 2, 146, rue Lóo-Saignat, 33076 Bordeaux, France. edmond.creppy@tox.u-bordeaux2.fr

ABSTRACT
Despite consented efforts in prevention, mycotoxins remain a problem of human health concern in several parts of the world including developed countries. Within the same range of toxins concentrations in the blood some people develop a disease while others do not. Could this inequality in front of mycotoxins effects be explained by environment factors and/or genetic predisposition? Among recent advances in environmental health research Correlation between chronic diseases and mycotoxins in humans deserves attention through several questions: Are genetic factors involved in disease causation of mycotoxins? How much are these factors currently taken into account for mycotoxins risk assessment and how much should we involve them? Answers are still to come. Genetic and environment factors deserve therefore more attention when dealing with regulatory limits, since among the general population, those who are at risk and will develop specific diseases are likely those bearing genetic predispositions. We have addressed these questions for the specific case of ochratoxin A in humans by investigating in Tunisia, county of Jelma, in four rural families forming a household of 21 persons all exposed to ochratoxin A in diet. Our results confirm that ochratoxin A induces chronic tubular nephropathy in humans and mainly point at those having the HLA haplotype A3, B27/35, DR7 to be more sensitive to the disease for quantitatively similar or lower exposure. Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy. Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria. Several mechanisms are discussed that could be put ahead to explain how the HLA haplotype could lead to tubular cells lyses and renal failure. In the mean time it is urgent to search for mass screening biomarkers for mycotoxins in humans and related genetic factors to set-up more appropriate regulation.

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Related in: MedlinePlus

Genealogical tree of people included in the study.
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f2-ijerph-02-00186: Genealogical tree of people included in the study.

Mentions: The prospected community is made up of 21 members (11 women and 10 men, aged from 32 to 65 years) of four families (see genealogical tree, Fig. 2). For each subject, blood and urine samples were collected for OTA assays and for the evaluation of the renal function. For this nephropathy, several etiological agents have been incriminated seriously considered and disqualified. The cases that remained without any possible aetiology are categorised as CIN of unknown aetiology presumably related to OTA since only this causal agent remained correlated to the disease [5, 7].


How much should we involve genetic and environmental factors in the risk assessment of mycotoxins in humans?

Creppy EE, Moukha S, Bacha H, Carratu MR - Int J Environ Res Public Health (2005)

Genealogical tree of people included in the study.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3814714&req=5

f2-ijerph-02-00186: Genealogical tree of people included in the study.
Mentions: The prospected community is made up of 21 members (11 women and 10 men, aged from 32 to 65 years) of four families (see genealogical tree, Fig. 2). For each subject, blood and urine samples were collected for OTA assays and for the evaluation of the renal function. For this nephropathy, several etiological agents have been incriminated seriously considered and disqualified. The cases that remained without any possible aetiology are categorised as CIN of unknown aetiology presumably related to OTA since only this causal agent remained correlated to the disease [5, 7].

Bottom Line: Within the same range of toxins concentrations in the blood some people develop a disease while others do not.Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy.Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria.

View Article: PubMed Central - PubMed

Affiliation: Dept of Toxicology, University of Bordeaux 2, 146, rue Lóo-Saignat, 33076 Bordeaux, France. edmond.creppy@tox.u-bordeaux2.fr

ABSTRACT
Despite consented efforts in prevention, mycotoxins remain a problem of human health concern in several parts of the world including developed countries. Within the same range of toxins concentrations in the blood some people develop a disease while others do not. Could this inequality in front of mycotoxins effects be explained by environment factors and/or genetic predisposition? Among recent advances in environmental health research Correlation between chronic diseases and mycotoxins in humans deserves attention through several questions: Are genetic factors involved in disease causation of mycotoxins? How much are these factors currently taken into account for mycotoxins risk assessment and how much should we involve them? Answers are still to come. Genetic and environment factors deserve therefore more attention when dealing with regulatory limits, since among the general population, those who are at risk and will develop specific diseases are likely those bearing genetic predispositions. We have addressed these questions for the specific case of ochratoxin A in humans by investigating in Tunisia, county of Jelma, in four rural families forming a household of 21 persons all exposed to ochratoxin A in diet. Our results confirm that ochratoxin A induces chronic tubular nephropathy in humans and mainly point at those having the HLA haplotype A3, B27/35, DR7 to be more sensitive to the disease for quantitatively similar or lower exposure. Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy. Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria. Several mechanisms are discussed that could be put ahead to explain how the HLA haplotype could lead to tubular cells lyses and renal failure. In the mean time it is urgent to search for mass screening biomarkers for mycotoxins in humans and related genetic factors to set-up more appropriate regulation.

Show MeSH
Related in: MedlinePlus