OBJECTIVEThe prevalence of type 2 diabetes is increasing alarmingly in both developed and developing countries. Recently, exposure to persistent organic pollutants (POPs) has been associated with the prevalence of type 2 diabetes. The purpose of this cross-sectional study is to examine the association between type 2 diabetes and POP exposure in the Helsinki Birth Cohort Study.RESEARCH DESIGN AND METHODSThe cohort consists of 8,760 people born in Helsinki during 1934–1944, before the global POP emission peak. In 2003, a clinical examination was performed, including blood sampling for laboratory analyses of serum lipids and POPs. Complete data from the examination were available for 1,988 participants. The concentrations of each POP were categorized into four groups on the basis of percentile intervals, and logistic regression was performed to examine diabetes prevalence across the POP categories, adjusting for sex, age, waist circumference, and mean arterial pressure and using the lowest category as the reference group.RESULTSAmong the participants with the highest exposure to oxychlordane, trans-nonachlor, 1,1-dichloro-2,2-bis-(p-chlorophenyl)-ethylene (p,p’-DDE, and polychlorinated biphenyl 153, the risk of type 2 diabetes was 1.64–2.24 times higher than that among individuals with the lowest exposure (Plin = 0.003–0.050, where Plin is the P value for linear trend across POP categories). In the stratified analysis, the associations between type 2 diabetes and oxychlordane and trans-nonachlor remained significant and were strongest among the overweight participants. Exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE 47) and 2,2′,4,4′,5,5′-hexabromodiphenyl ether (BDE 153) was not associated with type 2 diabetes.CONCLUSIONSThis study confirms the association between type 2 diabetes and adult-only exposure to organochlorine pesticides in a general urban population.

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.

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BackgroundHumans are exposed to tributyltin (TBT), previously used as an antifouling paint in ships, mainly through fish consumption. As TBT is a known obesogen, we studied the association of placenta TBT and other organotin compounds (OTCs) with ponderal index (PI) and growth during the first 18 months of life in boys.MethodsIn a prospective Finnish study, 110 placenta samples were collected from mothers of boys born in 1997–1999 with (n = 55) and without (n = 55) cryptorchidism. To account for the original study design, linear regression, weighted for sampling fractions of boys with (121/55) and without (5677/55) cryptorchidism from the total cohort, was used to study the association between placenta OTCs and children’s weight, length, growth rates and PI up to 18 months of age.ResultsPlacenta TBT concentrations were above the limit of quantification (LOQ) in 99% of the samples. However, monobutyltin (MBT), dibutyltin (DBT) and triphenyltin (TPhT) concentrations were below LOQ in 90%, 35% and 57% of samples, respectively. Placenta TBT was positively associated (p = 0.024) with weight gain during the first three months of life, but no other significant associations were observed for weight or length gain. Also, no significant associations between placenta OTC concentrations and child length, weight or PI at any time point were found.ConclusionsWe observed a trend towards higher weight gain from birth to 3 months of age with increasing placenta TBT concentration. These results should be interpreted with caution because obesogenic effects in animal experiments were seen after in-utero TBT exposures to doses that were orders of magnitude higher. Also the number of study subjects included in this study was limited.

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This is the first study to measure the concentrations of OTCs from human placenta samples, and to associate these concentrations to cryptorchidism. As opposite results were obtained with regard to OTC concentration in placenta and cryptorchidism status in Finland and Denmark, and no mechanism is known at the moment by which OTCs could affect testicular descent, these results cannot be generalized to other populations. However, some animal tests described in the literature show opposite effects of OTCs on fat deposition at different ranges of exposure. It is also clearly shown in the literature that TBT has an impact on sexual development of gastropods through RXR. As TBT is known to activate human RXR, further laboratory studies should be designed to explore the potential impact of TBT on male sexual development.

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We recently reported that differential gene expression and DNA methylation profiles in blood leukocytes of apparently healthy smokers predicts with remarkable efficiency diseases and conditions known to be causally associated with smoking, suggesting that blood-based omic profiling of human populations may be useful for linking environmental exposures to potential health effects. Here we report on the sex-specific effects of tobacco smoking on transcriptomic and epigenetic features derived from genome-wide profiling in white blood cells, identifying 26 expression probes and 92 CpG sites, almost all of which are affected only in female smokers. Strikingly, these features relate to numerous genes with a key role in the pathogenesis of cardiovascular disease, especially thrombin signaling, including the thrombin receptors on platelets F2R (coagulation factor II (thrombin) receptor; PAR1) and GP5 (glycoprotein 5), as well as HMOX1 (haem oxygenase 1) and BCL2L1 (BCL2-like 1) which are involved in protection against oxidative stress and apoptosis, respectively. These results are in concordance with epidemiological evidence of higher female susceptibility to tobacco-induced cardiovascular disease and underline the potential of blood-based omic profiling in hazard and risk assessment.