Childhood cancer aetiology is poorly understood and is considered to originate in utero and early postnatal life. In this study, we investigated perinatal characteristics as potential risk factors by performing a population-based case-control study, including 1340 cancer cases diagnosed < 19y and born between 1989-2021 in southern Sweden, and 13400 controls matched by sex, year, and municipality of birth. Perinatal characteristics were obtained from seven national registries. Cox regression was used to examine the associations between perinatal characteristics and the risk of overall childhood cancer, leukaemia, CNS tumours, lymphoma, and other cancer types combined (OCT). Large for gestational age was associated with a higher risk of overall cancer (HR, 95%CI: 1.32, 1.02-1.69) and leukaemia (HR, 95%CI: 1.58, 1.01-2.5), while a 5-min Apgar score <7 indicated a higher risk of OCT (HR, 95%CI: 2.16, 1.12-4.15). Mechanical ventilation during neonatal care was associated with a higher risk of overall cancer (HR, 95%CI: 1.88, 1.39-2.53) and OCT (HR, 95%CI: 2.09, 1.19-3.39). The aforementioned characteristics were associated with up to a threefold increased risk among children diagnosed before six months of age compared to those diagnosed later. Additionally, maternal obesity was associated with a higher risk of CNS tumours (HR, 95%CI: 1.51, 1.04-2.21) and lymphoma (HR, 95%CI: 2.26, 1.31-3.88), and maternal underweight with a higher risk of leukaemia (HR, 95%CI: 2.43, 1.40-4.22). Planned caesarean delivery indicated an increased risk of OCT (HR, 95%CI: 1.52, 1.04-2.22). Our findings identify several perinatal characteristics associated with childhood cancer risk, highlighting the perinatal period as an important window for future etiological research.

[This corrects the article DOI: 10.1016/j.ekir.2024.08.035.].

Hexavalent chromium (Cr(VI)) can induce oxidative stress, genomic instability, and epigenetic modifications. In occupational settings, Cr(VI)-exposed workers may also be exposed to other toxicants, such as elements besides Cr, and per- and polyfluoroalkyl substances (PFAS). However, research on the extent of these co-exposures and their combined effects remains limited. The objective of this study was to characterize the exposure levels of ten elements and eight PFAS in Cr(VI)-exposed workers and to assess the combined effects of these exposure mixtures on biomarkers of oxidative stress and genomic instability. This study included 138 Cr(VI)-exposed workers and 96 controls from Swedish SafeChrom and Danish SAM-Krom studies. Concentrations of elements were measured by inductively coupled plasma mass spectrometry (ICP-MS), and PFAS were measured by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Effect biomarkers, including 8-hydroxy-2'-deoxyguanosine (8-OHdG), mitochondrial DNA copy number (mtDNA-cn), telomere length (TL) and O6-methylguanine-DNA methyltransferase promoter (MGMT) methylation, were analyzed in blood. Bayesian Kernel Machine Regression and quantile-based g-computation models were used to evaluate the mixture effects. Exposed workers had higher concentrations of Cr, manganese, copper, zinc, lead, and perfluoroheptanoic acid (PFHpA), lower mtDNA-cn and longer TL compared to controls. In the SAM-Krom study, perfluorooctane sulfonic acid (PFOS) levels were significantly elevated among exposed workers, with the P95 reaching 2044 ng/mL. The exposure mixtures were associated with increased 8-OHdG and MGMT hypermethylation. Together, these findings highlight the complexity of multiple occupational exposures in Cr(VI)-related work environments and suggest that combined exposure may contribute to early biological alterations related to oxidative stress and DNA methylation.

Background Exposure to hexavalent chromium (Cr(VI)) can occur during occupational activities and leading lung cancer. MicroRNA (miRNA) plays an important part in carcinogenesis. Whether Cr(VI) exposure causes cancer-related miRNA changes is yet uncharacterized. Methods This study included 89 Cr(VI) exposed workers and 47 controls. MiRNAs were extracted from plasma followed by library preparations, miRNA sequencing, and differentially expressed miRNAs (DEMs) analysis. To understand the underlying biological functions, we used bioinformatics approaches, and qPCR was performed to validate the expression of potential target genes. Results A total of 2100 miRNAs were detected. In the exposed workers, 59 DEMs were identified: 21 up-regulated and 38 down-regulated. Target genes for both up- and down-regulated DEMs were significantly enriched in: miRNAs in cancer, small cell lung cancer and non-small cell lung cancer. Protein-protein interactions showed a high number of interactions, in which CCNE2, CDK4 and E2F1 were predicted as hub genes, and the messenger RNA expression of those genes was significantly higher in the exposed workers compared with controls. Conclusions Our study suggests that low-to-moderate Cr(VI) exposure results in differential expression of lung-cancer-related miRNAs and associated target genes. Further studies are needed to validate our findings and clarify whether these changes predict cancer risk.

BACKGROUND:Hexavalent chromium (Cr(VI)) is a lung cancer carcinogen. However, the genotoxic and mutagenic effects of Cr(VI) in humans at low-to-moderate occupational exposure levels are unknown. This study aims to investigate the relationship between occupational exposure to Cr(VI) and the presence of oxidative damage, genetic and epigenetic alterations. METHODS:We included 113 Cr(VI) exposed workers in 14 companies and 72 controls recruited within the SafeChrom project. Cr(VI) was measured in inhalable dust and total chromium in urine (U-Cr) and red blood cells (RBC-Cr). Analysed effect biomarkers included urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), micronuclei in peripheral blood reticulocytes (MNRET), blood relative mitochondrial DNA copy number (mtDNA-cn), relative telomere length (TL), and blood DNA methylation of four lung cancer-related genes (F2RL3, LINE-1, MGMT promoter and SEMA4B). RESULTS:The median inhalable Cr(VI) concentration among the exposed workers was 0.11 μg/m3 (5th-95th percentile: 0.02-8.44). Exposed workers showed higher 8-OHdG, TL, and MGMT promoter methylation levels and lower mtDNA-cn and MNRET compared with controls. Company-based differences in biomarkers were observed. Univariate analysis showed that TL was positively correlated with U-Cr, and 8-OHdG and MGMT promoter methylation were positively correlated with RBC-Cr. Multivariate analyses with adjustment for possible confounders showed higher 8-OHdG, TL, and MGMT promoter methylation in exposed workers compared with controls. CONCLUSIONS:Low-to-moderate Cr(VI) exposure was associated with higher oxidative stress, longer telomeres and epigenetic alterations, changes that previously have been linked to lung cancer risk. This study highlights the molecular impacts of Cr(VI) exposure, underscoring the importance of reducing the exposure to Cr(VI).

Background Lead is an established causal risk factor for coronary heart disease. Atherosclerosis may be the key mediator for this association, but evidence from studies in humans is limited. Our objective was to test the hypothesis that environmental lead exposure is associated with coronary atherosclerosis. Methods We used cross‐sectional data from the SCAPIS (Swedish Cardiopulmonary Bioimage Study), including 5627 men and women aged 50 to 64 years. Coronary artery calcium score (CACS), measured using computed tomography, was used as a marker of atherosclerosis, and blood lead was used as a biomarker of lead exposure. The prevalence ratio (PR) of positive (>0) and high (≥100) CACSs in relation to blood lead (continuous variable) was modeled using Poisson regression with robust SEs, adjusted for age, sex, smoking, low‐density lipoprotein/high‐density lipoprotein ratio, waist circumference, heredity for cardiovascular diseases, statin use, diabetes, blood cadmium, low physical activity, and educational level. Results Median blood lead was 14.2 μg/L. Positive CACS (prevalence, 41%) was not significantly associated with blood lead (PR per Δ10 μg/L, 1.02 [95% CI, 0.99–1.04]), whereas the association was stronger for high CACS (prevalence, 13%; and PR per Δ10 μg/L, 1.05 [95% CI, 1.00–1.11]). The estimate for high CACS was stronger in men (PR per Δ10 μg/L, 1.07 [95% CI, 1.01–1.13]) than among women (PR per Δ10 μg/L, 1.01 [95% CI, 0.85–1.20]). Conclusions Our study, which found that lead is associated with coronary artery calcification in men, provides further evidence that lead is a risk factor for atherosclerosis and coronary heart disease.

BACKGROUND:Hexavalent chromium (Cr(VI)) is a carcinogen. Exposure to Cr(VI) may occur in different industrial processes such as chrome plating and stainless steel welding. The aim of this study was to assess occupational exposure to Cr(VI) in Denmark. METHODS:This cross-sectional study included 28 workers and 8 apprentices with potential Cr(VI) exposure and 24 within company controls, all recruited from six companies and one vocational school. Use of occupational safety and health (OSH) risk prevention measures were assessed through triangulation of interviews, a questionnaire and systematic observations. Inhalable Cr(VI) and Cr-total were assessed by personal air exposure measurements on Cr(VI) exposed participants and stationary measurements. Cr concentrations were measured in urine and in red blood cells (RBC) (the latter reflecting Cr(VI)). Genotoxicity was assessed by measurement of micronuclei in peripheral blood reticulocytes (MNRET). RESULTS:At announced visits, a consistent high degree of compliance to OSH risk prevention measures were seen in 'chromium bath plating' for both technical devices (e.g. ventilation, plastic balls, sheet coverings) and in the use of personal protective equipment (e.g. gloves, respirators), yet a lesser degree of compliance was observed in 'stainless steel welding'. The geometric mean of the air concentration of Cr(VI) was 0.26 μg/m3 (95% confidence interval (CI): 0.12-0.57) for the Cr(VI)-exposed workers and 3.69 μg/m3 (95% CI: 1.47-9.25) for the Cr(VI)-exposed apprentices. Subdivided by company type, the exposure levels were 0.13 μg/m3 (95% CI: 0.04-0.41) for companies manufacturing and processing metal products, and 0.81 μg/m3 (95% CI: 0.46-1.40) for bath plating companies. Workers with occupational exposure to Cr(VI) had significantly higher median levels of urinary Cr (2.42 μg/L, 5th-95th percentile 0.28-58.39), Cr in RBC (0.89 μg/L, 0.54-4.92) and MNRET (1.59 ‰, 0.78-10.92) compared to the within company controls (urinary: 0.40 μg/L, 0.16-21.3, RBC: 0.60 μg/L, 0.50-0.93,MNRET: 1.06 ‰, 0.71-2.06). When sub-dividing by company type, urinary Cr (4.61 μg/L, 1.72-69.5), Cr in RBC (1.33 μg/L, 0.95-4.98) and MNRET (1.89 μg/L, 0.78-12.92) levels were increased for workers with potential Cr(VI) exposure in bath-plating companies, and when subdividing by work task, workers engaged in process operation had increased levels of urinary Cr (8.51 μg/L, 1.71-69.5), Cr in RBC (1.33 μg/L, 0.95-4.98) and MNRET (1.89 μg/L, 0.82-12.92) levels. CONCLUSION:This biomonitoring study shows that bath platers were highly exposed to Cr(VI), as suggested by relatively high levels of urinary Cr, Cr in RBC and increased levels of micronuclei. The urinary Cr concentrations were high when compared to the French biological limit value of 2.5 μg Cr/L, corresponding to the Danish occupational exposure limit of 1 μg/m3. This, in turn, indirectly suggests that additional exposure routes than via air may contribute to the exposure. For welders, no statistically significant increases compared to within company controls were observed, however, the observed urinary Cr levels were similar to the levels observed in a European study (HBM4EU), and were higher than the levels observed for welders in Sweden (SafeChrom). In spite of a high degree of self-reported and observed compliance to OSH risk prevention measures during announced visits, the biomarkers of exposure reflecting recent exposure (urinary Cr) or exposure during the last four months (Cr in RBC) may point to variation in compliance to OSH risk prevention measures in general. Reduced occupational exposure to Cr(VI) may be achieved by applying the hierarchy of controls in eliminating or substituting Cr(VI), and the use of more effective technical solutions (e.g. automation).

Abstract Introduction Hexavalent chromium Cr(VI) is a human carcinogen, but the current exposure to Cr(VI) at Swedish workplaces is unknown. Methods Recruitment of 113 workers with potential Cr(VI) exposure and 72 controls was combined with measurements of inhalable Cr(VI) (only exposed workers) and total Cr in urine and red blood cells (RBC), Bayesian analysis of occupational exposure limit (OEL) compliance was used, as well as the Swedish job-exposure-matrix. Results Exposed workers performed processing of metal products, steel production, welding, and plating. The geometric mean concentration of inhalable Cr(VI) in exposed workers was 0.15 μg/m3. Eight workers (7%) exceeded the Swedish OEL (5 μg/m3), and the share of OEL exceedances was estimated to be up to 19.6% for stainless steel welders. Urine- and RBC-Cr were significantly higher in exposed workers compared with controls. Workers with inferred non-acceptable local exhaustion ventilation showed significantly higher inhalable Cr(VI), urine- and RBC-Cr than those with acceptable ventilation. Workers with inferred correct use of respiratory protection had higher inhalable Cr(VI), and, paradoxically, higher urine- and RBC-Cr concentrations than workers with incorrect use. We estimate that ~17 900 Swedish workers are occupationally exposed to Cr(VI) today. Discussion Our study showed that although most air measurements were relatively low, 7% exceeded the OEL, and particularly stainless steel workers are at risk for exceeding the OEL. The existing protective measures implemented at workplaces are still inadequate and insufficient. Conclusion Some workers in Sweden are exposed to high levels of the non-threshold carcinogen Cr(VI). National strategies aligned with European strategies are needed to eliminate occupational cancer.

Abstract Introduction Hexavalent chromium, Cr(VI), is classified as a Group 1 human carcinogen and causes lung cancer. This study was to investigate associations between occupational exposure to Cr(VI) and lung cancer-related non-coding RNAs. Methods The study included 111 Cr(VI) exposed workers and 72 controls in Sweden, 91.4% non-smokers. Cr concentration in red blood cells (RBC-Cr) was measured. MicroRNA (miRNA) and long non-coding RNA (lncRNA) were extracted from plasma followed by DNAse treatment, cDNA synthesis, and qPCR using target-specific assays for four miRNAs (miR-142-3p, miR-15b-5p, miR-3940-5p, miR-451a), and three lncRNAs (H19, MALAT1, NORAD). Results Median RBC-Cr concentrations were significantly higher in the exposed group (0.73 µg/L, 5-95% 0.51-2.33) compared with controls (0.53 µg/L, 0.42-0.72). Plasma relative expression levels of all miRNAs, MALAT1 and NORAD were significantly lower in the exposed workers compared with controls. In the exposed group, significant negative correlations (rS=-0.19 - -0.27) were found between RBC-Cr and miR-142-3p, miR-15b-5p, miR-451a and NORAD. NORAD correlated with miR-142-3p (rS=0.34) and miR-15b-5p (rS=0.28). In multivariate regression models adjusting for confounders, expression of the miRNAs, MALAT1 and NORAD was still significantly lower in the exposed group compared with controls, and the expression decreased with increasing RBC-Cr. Discussion Cr(VI) exposure was associated in a dose-response manner with differential expression of circulating non-coding RNAs in exposed workers, which suggests non-coding RNAs as potential toxicological biomarkers for Cr(VI). Relations between miRNAs and lncRNAs suggest that they participate in the same lncRNA-miRNA-mRNA regulatory axes, which may play important roles in Cr(VI) carcinogenesis. Conclusion Occupational Cr(VI) exposure may impact circulating lung-cancer-related non-coding RNAs expression.

Background: Hexavalent chromium (Cr(VI)) is classified as a group 1 human carcinogen and increases the risk of lung cancer. Non-coding RNAs (ncRNAs) have key regulatory roles in lung cancer, but less is known about their relation to Cr(VI) exposure. Objectives: We aimed to 1) measure the expression of lung cancer-related circulating ncRNAs in exposed workers and controls; 2) assess associations between ncRNAs expression and Cr concentrations in red blood cells (RBC) and urine; and 3) evaluate correlations between the ncRNAs. Methods: The study included 111 Cr(VI) exposed workers and 72 controls recruited from the SafeChrom project. Cr concentrations were measured in RBC (biomarker of long-term exposure) and urine (biomarker of short-term exposure) samples. Long ncRNA (lncRNA) and microRNA (miRNA) were extracted from plasma followed by deoxyribonuclease treatment, complementary DNA synthesis, and quantitative real-time polymerase chain reaction using target-specific assays for three lncRNAs (H19, MALAT1, NORAD), and four miRNAs (miR-142-3p, miR-15b-5p, miR-3940-5p, miR-451a). Results: Expression levels of lncRNAs MALAT1 and NORAD, and all four miRNAs, were significantly lower in Cr (VI) exposed workers compared with controls, and correlated significantly with RBC-Cr concentrations (rS = -0.16 to -0.38). H19 was non-significantly increased in exposed workers but significantly correlated with miR142-3p (rS = -0.33) and miR-15b-5p (rS = -0.30), and NORAD was significantly positively correlated with all four miRNAs (rS = 0.17 to 0.46). In multivariate regression models adjusting for confounders, expressions of lncRNAs MALAT1 and NORAD and all miRNAs were still significantly lower in the exposed group compared with controls, and the expression decreased with increasing RBC-Cr concentrations. Conclusions: Cr(VI) exposure was inversely and in a dose-response manner associated with the expression of circulating non-coding RNA, which suggests ncRNAs as potential biomarkers for Cr(VI)-induced toxicity.

Relatively little is known about the relationship between socio-demographic factors and the chemical exposome in adolescent populations. This knowledge gap hampers global efforts to meet certain UN sustainability goals. The present work addresses this problem in Swedish adolescents by discerning patterns within the chemical exposome and identify demographic groups susceptible to heightened exposures. Enlisting the Riksmaten Adolescents 2016-17 (RMA) study population (N = 1082) in human-biomonitoring, and using proportional odds ordinal logistic regression models, we examined the associations between concentrations of a diverse array of substances (N = 63) with the determinants: gender, age, participant/maternal birth country income per capita level, parental education levels, and geographic place of living (longitude/latitude). Participant/maternal birth country exhibited a significant association with the concentrations of 46 substances, followed by gender (N = 41), and longitude (N = 37). Notably, individuals born in high-income countries by high-income country mothers demonstrated substantially higher estimated adjusted means (EAM) concentrations of polychlorinated biphenyls (PCBs), brominated flame retardants (BFRs) and per- and polyfluoroalkyl substances (PFASs) compared to those born in low-income countries by low-income country mothers. A reverse trend was observed for cobalt (Co), cadmium (Cd), lead (Pb), aluminium (Al), chlorinated pesticides, and phthalate metabolites. Males exhibited higher EAM concentrations of chromium (Cr), mercury (Hg), Pb, PCBs, chlorinated pesticides, BFRs and PFASs than females. In contrast, females displayed higher EAM concentrations of Mn, Co, Cd and metabolites of phthalates and phosphorous flame retardants, and phenolic substances. Geographical disparities, indicative of north-to-south or west-to-east substance concentrations gradients, were identified in Sweden. Only a limited number of lifestyle, physiological and dietary factors were identified as possible drivers of demographic inequalities for specific substances. This research underscores birth country, gender, and geographical disparities as contributors to exposure differences among Swedish adolescents. Identifying underlying drivers is crucial to addressing societal inequalities associated with chemical exposure and aligning with UN sustainability goals.

Metals are significant contributors to water pollution, posing serious threats to human health. This study aims to assess the carcinogenic and non-carcinogenic health risks associated with metals in Isfahan drinking water. Eighty water samples were randomly collected from the city's distribution network between January and March 2020–2021. Inductively coupled plasma Optical Emission Spectrometry was used to measure toxic metals, namely Pb, Cr, Cd, Ni, and As concentrations. Results revealed that the mean concentration of Ni (70.03 µg/L) exceeded the WHO reference value (70 µg/L), while the other metals were below the standard values. The average chronic daily intake order of toxic metals was Ni > Cr > Pb > As > Cd. Non-carcinogenic risk assessment through hazard quotient (HQ) and hazard index (HI) demonstrated that both THI for adults (HQingestion + HQdermal = 4.02E−03) and THI for children (HIingestion + HIdermal = 3.83E−03) were below the acceptable limit (less than 1). This indicated no non-carcinogenic risk to residents through water ingestion or dermal exposure. However, findings indicated that the ingestion route was the primary exposure pathway, with HQ values for ingestion exceeding HQ values for dermal adsorption. Carcinogenic risk assessment showed that the risk associated with As metal exceeded the acceptable limit (1 × 10−6). Therefore, implementing treatment improvement programs and appropriate control measures is essential to safeguard the health of Isfahan City residents.

To prevent diseases arising from exposure to toxic metals, more knowledge about their temporal changes is needed, especially in children, the most vulnerable group.This study follows temporal changes in blood lead (BPb), mercury (BHg) and cadmium (BCd) levels in schoolchildren (8-11 years old) from two cities in southern Sweden. One blood sample per 773 children was used for time trend analyses between 2007-2022. One further blood sample re-sampled after 2 years, were used to assess intra-individual time trends of BPb (n=377), BCd (n=102) and BHg (n=53) between 1979-2019.Geometric mean (range) of BPb, BCd and BHg concentrations during 2007-2022 was 9.9 (2.3-59), 0.09 (0.03-0.34) and 0.73 (0.02-8.2) µg/L, respectively. Living close to a Pb smelter resulted in higher levels of all three metals compared with living in the city or rural area. Annually, the concentrations clearly decreased for BPb (-4.9%, p<0.001) and weakly for BCd (-0.6%, p=0.013), while BHg slightly increased (+1.4%, p=0.029). When stratified by residential area, the decrease of BCd and increase of BHg were significant only in the urban area (-1.8% and +2.8%, respectively; p<0.01). The BPb decrease rate was the highest in the urban area followed by the rural and Pb smelter areas (-5.8%>-4.5%>-3.9%; p<0.001). For children re-analysed during 1979-2019, a significant decrease was observed only for BPb (-6.8%; p<0.001), with a 2% higher decrease rate in the period before than after the Pb-gasoline ban in 1994.The preventive measures against Pb pollution are reflected in the constant decrease of BPb levels over time. However, the area close to a Pb smelter, as indicated by a slower Pb decrease rate, might need further and stricter preventive measures. Exposure to Hg and Cd was low, however, the slight increase in BHg and only a minor decrease in BCd, indicate the need for continuous biomonitoring of children.

Adolescence is a period of significant physiological changes, and likely a sensitive window to chemical exposure. Few nation-wide population-based studies of chemical body burdens in adolescents have been published. In the national dietary survey Riksmaten Adolescents (RMA) 2016-17, over 13 chemical substance groups, including elements, chlorinated/brominated/fluorinated persistent organic pollutants (POPs) were analysed in blood, and in urine metabolites of phthalates/phthalate alternatives, phosphorous flame retardants, polycyclic aromatic hydrocarbons (PAHs), and pesticides, along with bisphenols and biocide/preservative/antioxidant/UV filter substances (N = 1082, ages 11-21). The aim was to characterize the body burdens in a representative population of adolescents in Sweden, and to compare results with human biomonitoring guidance values (HBM-GVs). Cluster analyses and Spearman's rank order correlations suggested that concentrations of substances with known common exposure sources and similar toxicokinetics formed obvious clusters and showed moderate to very strong correlations (r & GE; 0.4). No clusters were formed between substances from different matrices. Geometric mean (GM) concentrations of the substances were generally less than 3-fold different from those observed among adolescents in NHANES (USA 2015-16) and GerES V (Germany 2014-17). Notable exceptions were brominated diphenyl ethers (PBDEs) with >20-fold lower GM concentrations, and the biocide triclosan and ultraviolet (UV) filter benzophenone-3 with >15-fold lower mean concentrations in RMA compared to NHANES. Exceedance of the most conservative HBM-GVs were observed for aluminium (Al, 26% of subjects), perfluorooctanesulfonic acid (PFOS, 19%), perfluorooctanoic acid (PFOA, 12%), lead (Pb, 12%), MBP (dibutyl phthalate metabolite, 4.8%), hexachlorobenzene (HCB, 3.1%) and 3-phenoxybenzoic acid (PBA, pyrethroid metabolite, 2.2%). Males showed a higher proportion of exceedances than females for Pb, HCB and PFOS; otherwise no gender-related differences in exceedances were observed. A higher proportion of males than females had a Hazard Index (HI) of substances with liver and kidney toxicity and neurotoxicity >1. Industrialized countries with similarly high standards of living, with some exceptions, show comparable average body burdens of a variety of toxic chemicals among adolescents from the general population. The exceedances of HBM-GVs and HIs strongly suggests that further efforts to limit chemical exposure are warranted.

BACKGROUND:Lead exposure is associated with cardiovascular disease. Atherosclerosis has been hypothesized to be one of the underlying mechanisms behind this association. AIM:To investigate whether lead exposure is associated with an increased risk of atherosclerosis in the carotid arteries in a large Swedish population-based cohort. METHODS:We performed a cross-sectional study using data from the population-based Swedish CardioPulmonary bioImage Study (SCAPIS), including 5622 middle-aged men and women, enrolled 2013-2018. Blood lead (B-Pb), measured by inductively coupled plasma mass spectrometry, was used as exposure biomarker. The presence of atherosclerotic plaque in the carotid arteries (yes/no), total plaque area (mm2) and the presence of large plaques (>25 mm2) were determined by ultrasonography. Associations between B-Pb and the different outcomes were analysed using Poisson and linear regression models, adjusted for potential confounders. RESULTS:Atherosclerotic plaque was present in 57% of the individuals, for whom the median total plaque area was 16 mm2 (range: 0.2-222). The median B-Pb concentration was 14 μg/L (range: 0.75-203). After adjusting for potential confounders, individuals in the fourth quartile of B-Pb (Q4) had a prevalence ratio (PR) for plaque of 1.08 (95% CI: 1.01, 1.16) when compared with the first quartile (Q1). A 10 μg/L increase in B-Pb concentrations was associated with an increase of 0.92 mm2 (95% CI: 0.14, 1.71) in total plaque area. The PR for large plaque was 1.09 (95% CI: 0.84, 1.42 for Q4 vs Q1). CONCLUSIONS:This study shows an association between B-Pb and atherosclerosis in the carotid arteries providing some support for the hypothesis that atherosclerosis is one of the mechanisms underlying the association between lead exposure and cardiovascular disease.

OBJECTIVES:Hexavalent chromium (Cr(VI)) is classified as a human carcinogen. Occupational Cr(VI) exposure can occur during different work processes, but the current exposure to Cr(VI) at Swedish workplaces is unknown. METHODS:This cross-sectional study (SafeChrom) recruited non-smoking men and women from 14 companies with potential Cr(VI) exposure (n = 113) and controls from 6 companies without Cr(VI) exposure (n = 72). Inhalable Cr(VI) was measured by personal air sampling (outside of respiratory protection) in exposed workers. Total Cr was measured in urine (pre- and post-shift, density-adjusted) and red blood cells (RBC) (reflecting Cr(VI)) in exposed workers and controls. The Bayesian tool Expostats was used to assess risk and evaluate occupational exposure limit (OEL) compliance. RESULTS:The exposed workers performed processing of metal products, steel production, welding, plating, and various chemical processes. The geometric mean concentration of inhalable Cr(VI) in exposed workers was 0.15 μg/m3 (95% confidence interval: 0.11-0.21). Eight of the 113 exposed workers (7%) exceeded the Swedish OEL of 5 μg/m3, and the Bayesian analysis estimated the share of OEL exceedances up to 19.6% for stainless steel welders. Median post-shift urinary (0.60 μg/L, 5th-95th percentile 0.10-3.20) and RBC concentrations (0.73 μg/L, 0.51-2.33) of Cr were significantly higher in the exposed group compared with the controls (urinary 0.10 μg/L, 0.06-0.56 and RBC 0.53 μg/L, 0.42-0.72). Inhalable Cr(VI) correlated with urinary Cr (rS = 0.64) and RBC-Cr (rS = 0.53). Workers within steel production showed the highest concentrations of inhalable, urinary and RBC Cr. Workers with inferred non-acceptable local exhaustion ventilation showed significantly higher inhalable Cr(VI), urinary and RBC Cr concentrations compared with those with inferred acceptable ventilation. Furthermore, workers with inferred correct use of respiratory protection were exposed to significantly higher concentrations of Cr(VI) in air and had higher levels of Cr in urine and RBC than those assessed with incorrect or no use. Based on the Swedish job-exposure-matrix, approximately 17 900 workers were estimated to be occupationally exposed to Cr(VI) today. CONCLUSIONS:Our study demonstrates that some workers in Sweden are exposed to high levels of the non-threshold carcinogen Cr(VI). Employers and workers seem aware of Cr(VI) exposure, but more efficient exposure control strategies are required. National strategies aligned with the European strategies are needed in order to eliminate this cause of occupational cancer.

To prevent diseases arising from exposure to toxic metals, more knowledge about their temporal changes is needed, especially in children, the most vulnerable group.

BACKGROUND:Lead (Pb), cadmium (Cd) and mercury (Hg) are all nephrotoxic metals, and a large part of the body burden of Cd and Hg is found in the kidneys. There are, however, few studies on associations between exposure to these toxic metals and renal biopsy findings, and none at low-level exposure. AIM:To examine the hypothesis that low-level concentration of Pb, Cd or Hg in the kidneys is associated with histopathological changes in the kidneys. METHODS:We determined concentrations of Pb, Cd and Hg in kidney, blood and urine in 109 healthy kidney donors, aged 24-70 years. The renal biopsies were scored according to the Banff classification regarding tubular atrophy, interstitial fibrosis, glomerulosclerosis, arteriosclerosis, and arteriolohyalinosis. Kidney function was assessed based on glomerular filtration rate (GFR) as well as urinary excretion of albumin, low molecular weight proteins, kidney injury molecule 1 and N-acetylglucose aminidase. Associations between metal concentrations and histopathological changes, were assessed in models also including age, sex and smoking. RESULTS:The median kidney concentrations of Pb, Cd and Hg were 0.08, 13 and 0.21 μg/g, respectively. There were signs of tubular atrophy in 63%, interstitial fibrosis in 21%, glomerulosclerosis in 71%, arteriosclerosis in 47%, and arteriolohyalinosis in 36% of the donors, but, as could be expected, the histopathological findings were limited, mostly Banff grade 1. In models adjusted for age, sex and smoking, kidney Cd was positively associated with tubular atrophy (p = 0.03) and possibly with arteriolohyalinosis (p = 0.06). Kidney Hg was associated with arteriosclerosis (p = 0.004). DISCUSSION AND CONCLUSIONS:The results suggest that even low levels of Cd in the kidney can induce a mild degree of tubular atrophy. This is in line with previous findings at high-level Cd exposure. The association between kidney Hg and renal arteriosclerosis was unexpected, and may be a chance finding.