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This study investigated time trends in occupational exposure to various chemicals in Sweden and the distribution across demographic and labor market sectors. Exposure to six chemicals was investigated from 1980 to 2013 by application of a job exposure matrix to national population registers. Respirable crystalline silica (RCS), diesel engine exhaust, welding fumes, wood dust, chlorinated hydrocarbon solvents, and lead were selected to represent different groups of chemicals. Trends in exposure prevalence were investigated by linear regression and compared to the occupationally active population. Confidence intervals for the rate of change over time were obtained by bootstrapping. The proportion of workers born outside the Nordic countries increased over time in those exposed to RCS, diesel exhaust and wood dust. There was a shift of exposed jobs to small companies (<50 employees), especially for RCS, welding fumes, wood dust, and chlorinated hydrocarbon solvents. For RCS and welding fumes, there was a marked drop in exposure levels from 1980 to 1990 but small changes thereafter. Exposure to lead diminished, both in terms of prevalence and intensity. Over time, several exposures tended to shift to small companies, the construction sector, and migrant workers, all factors being indicative of less well-controlled working conditions. Occupational exposure to chlorinated organic solvents and lead diminished, while exposure levels to RCS and welding fumes have changed little since 1990. In view of the serious and well-established negative health effects, increased efforts to reduce exposure to RCS and welding fumes are needed.

There is emerging evidence that background exposure to persistent organic pollutants (POPs) are important in the development of conditions predisposing to diabetes as well as of type 2 diabetes itself. We recently reported that low dose POPs predicted incident type 2 diabetes in a nested case-control study. The current study examined if low dose POPs predicted future adiposity, dyslipidemia, and insulin resistance among controls without diabetes in that study. The 90 controls were diabetes-free during 20 years follow-up. They were a stratified random sample, enriched with overweight and obese persons. POPs measured in 1987-88 (year 2) sera included 8 organochlorine (OC) pesticides, 22 polychlorinated biphenyls (PCBs), and 1 polybrominated biphenyl (PBB). Body mass index (BMI), triglycerides, HDL-cholesterol, LDL-cholesterol, and homeostasis model assessment value for insulin resistance (HOMA-IR) were study outcomes at 2005-06 (year 20). The evolution of study outcomes during 18 years by categories of serum concentrations of POPs at year 2 was evaluated by adjusting for the baseline values of outcomes plus potential confounders. Parallel to prediction of type 2 diabetes, many statistically significant associations of POPs with dysmetabolic conditions appeared at low dose, forming inverted U-shaped dose-response relations. Among OC pesticides, p,p'-DDE most consistently predicted higher BMI, triglycerides, and HOMA-IR and lower HDL-cholesterol at year 20 after adjusting for baseline values. Oxychlordane, trans-nonachlor, and hexachlorobenzene also significantly predicted higher triglycerides. Persistent PCBs with [greater than or equal to]7 chlorides predicted higher BMI, triglycerides, and HOMA-IR and lower HDL-cholesterol at year 20 with similar dose-response curves. Simultaneous exposure to various POPs in the general population may contribute to development of obesity, dyslipidemia, and insulin resistance, common precursors of type 2 diabetes and cardiovascular diseases. Although obesity is a primary cause of these metabolic abnormalities, POPs exposure may contribute to excess adiposity and other features of dysmetabolism.

Background Early disruption of the microbial community may influence life-long health. Environmental toxicants can contaminate breast milk and the developing infant gut microbiome is directly exposed. We investigated whether environmental toxicants in breastmilk affect the composition and function of the infant gut microbiome at 1 month. We measured environmental toxicants in breastmilk, fecal short-chain fatty acids (SCFAs), and gut microbial composition from 16S rRNA gene amplicon sequencing using samples from 267 mother-child pairs in the Norwegian Microbiota Cohort (NoMIC). We tested 28 chemical exposures: polychlorinated biphenyls (PCBs), polybrominated flame retardants (PBDEs), per- and polyfluoroalkyl substances (PFASs), and organochlorine pesticides. We assessed chemical exposure and alpha diversity/SCFAs using elastic net regression modeling and generalized linear models, adjusting for confounders, and variation in beta diversity (UniFrac), taxa abundance (ANCOM), and predicted metagenomes (PiCRUSt) in low, medium, and high exposed groups. Results PBDE-28 and the surfactant perfluorooctanesulfonic acid (PFOS) were associated with less microbiome diversity. Some sub-OTUs of Lactobacillus , an important genus in early life, were lower in abundance in samples from infants with relative “high” (> 80th percentile) vs. “low” (< 20th percentile) toxicant exposure in this cohort. Moreover, breast milk toxicants were associated with microbiome functionality, explaining up to 34% of variance in acetic and propionic SCFAs, essential signaling molecules. Per one standard deviation of exposure, PBDE-28 was associated with less propionic acid (− 24% [95% CI − 35% to − 14%] relative to the mean), and PCB-209 with less acetic acid (− 15% [95% CI − 29% to − 0.4%]). Conversely, PFOA and dioxin-like PCB-167 were associated with 61% (95% CI 35% to 87%) and 22% (95% CI 8% to 35%) more propionic and acetic acid, respectively. Conclusions Environmental toxicant exposure may influence infant gut microbial function during a critical developmental window. Future studies are needed to replicate these novel findings and investigate whether this has any impact on child health.