Abstract
BackgroundIn animal experiments persistent organic pollutants (POPs) cause hepatosteatosis. In epidemiological studies POPs have positive associations with serum markers of nonalcoholic fatty liver disease (NAFLD) and together with obesity synergistic association with insulin resistance. Because insulin resistance and obesity are critical in NAFLD pathogenesis, we investigated the association of serum pollutant levels with liver histology and alanine aminotransferase (ALT) in morbidly obese.MethodsLiver biopsies were from 161 participants of the Kuopio Obesity Surgery Study (KOBS) who underwent bariatric surgery 2005–2011. Liver histology was categorized as normal, steatosis and non-alcoholic steatohepatitis (NASH). Liver phenotype at baseline and ALT at baseline and 12 months post-surgery were correlated to serum POP concentrations at respective time points. As lipophilic POPs concentrate to smaller fat volume during weight loss, serum levels before and 12 months after bariatric surgery were compared.ResultsBaseline serum concentration of PCB-118, β-HCH and several PFAAs had an inverse association with lobular inflammation possibly due to changes in bile acid metabolism. ALT had negative associations with many POPs at baseline that turned positive at 12 months after major clinical improvements. There was an interaction between some POPs and sex at 12 months, and in stratified data positive associations were observed mainly in females but not in males.ConclusionsWe found a negative association between serum concentrations of PCB-118, β-HCH and several PFAAs with lobular inflammation at baseline. Positive POPs-ATL associations at 12 months among women suggest that increased POP concentrations may decrease the degree of liver recovery.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-015-0066-z) contains supplementary material, which is available to authorized users.
Highlights
In animal experiments persistent organic pollutants (POPs) cause hepatosteatosis
POPs, perfluorinated alkyl acids (PFAAs) and liver histology at baseline Associations between liver histology at baseline and logtransformed concentrations of β -hexachlorocyclohexane (β-HCH) and PCB118 are shown in Table 3. β-HCH had significant negative association with lobular inflammation (2–4 foci per 200x field, p = 0.022)
For dioxin-like polychlorinated biphenyls (PCBs)-118 there was a negative association with non-alcoholic steatohepatitis (NASH) (p = 0.038), lobular inflammation (
Summary
In animal experiments persistent organic pollutants (POPs) cause hepatosteatosis. In epidemiological studies POPs have positive associations with serum markers of nonalcoholic fatty liver disease (NAFLD) and together with obesity synergistic association with insulin resistance. Decreasing time trends of exposure have been observed in the Nordic Countries e.g. for polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs) since 1960’s and 1970’s [13], for polybrominated diphenylethers (PBDEs) since 1990’s [14] and for perfluorinated alkyl acids (PFAAs) since 2000’s [15]. Due to their lipophilicity POP are stored in humans primarily in adipose tissue and in the liver [16], but animal and some human data indicate that dioxinlike compounds are selectively sequestrated to liver [16, 17]. Contrary to other POPs, PFAAs are not lipophilic and they have been shown to bind to proteins in blood and especially in the liver of animals [18] and to various protein rich tissues in humans [19]
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