Chemical pollution in drinking water is of great concern. Organotin compounds (OTCs) are a class of persistent toxic substances with the effect of disrupting endocrine function, but potential human health risk due to organotin pollution in drinking water is still less understood. Understanding the occurrence and sources of OTCs in drinking water is crucial. Seventy drinking water samples collected from tap water, water boiling machines and water vending machines in Shanghai were analyzed for seven target OTCs. It is shown that the summed concentrations of target OTCs (∑OTCs) were up to 129 ng Sn L−1, with the dominant species being dimethyltin (DMT), dibutyltin (DBT), monobutyltin (MBT) and monomethyltin (MMT). Furthermore, OTC pollution levels varied significantly among drinking water types and water source supply zones, with higher ∑OTC concentrations observed in tap water and zone A (supplied by an onshore reservoir next to the estuary). To quantify the sources of OTCs in drinking water, we employed two receptor models for comprehensive comparison: principal component analysis-multiple linear regression (PCA-MLR) and positive matrix factorization (PMF). Both models demonstrated excellent fit to the ∑OTC concentrations, with predicted ∑OTC values from each model showing a significant correlation (r = 0.9822, p < 0.05). Two main sources of OTCs were identified by using both models: materials used in pipes and drinking fountains and emissions from maritime, agricultural and industrial activities, and the PMF model further distinguished sources associated with degradation. The PMF model emerged as the most appropriate model for organotin source apportionment in drinking water due to its detailed and accurate results. In brief, this study revealed that levels of organotin vary across different water sources and supply zones and identified the main sources of pollution from water sources and water supply processes. This research not only addresses critical knowledge gaps but also provides essential information for informing policy and urban planning, particularly regarding the maintenance of community water purification facilities to ensure drinking water quality in rapidly urbanizing regions.

Background: Polychlorinated alkanes (PCAs) constitute a large group of individual congeners originating from commercial chlorinated paraffin (CP) products with carbon chain lengths of PCAs-C_10-13, PCAs-C_14-17, and PCAs-C_18-32, occasionally containing PCAs-C_6-9 impurities. The extensive use of CPs has led to global environmental pollution of PCAs. This study aimed to quantify PCAs in paired serum and breast milk of lactating Swedish mothers, exploring their concentration relationship.

Methods: Twenty-five paired samples of mothers’ blood serum and breast milk were analysed and concentrations were determined for PCAs C_6-32 and compared to 4,4′-DDE, the PCB congener 2,2′,4,4′,5,5′-hexachlorobiphenyl (CB-153), and hexachlorobenzene (HCB).

Results: The median concentrations of PCAs-C_6-9, PCAs-C_10-13, PCAs-C_14-17, PCAs-C_18-32 and ΣPCAs in serum were 14, 790, 520, 16 and 1350 ng/g lipid weight (lw), respectively, and in breast milk 0.84, 36, 63, 6.0 and 107 ng/g lw. Levels of 4,4′-DDE, CB-153 and HCB were comparable in the two matrices, serum and breast milk at 17, 12 and 4.9 ng/g lw. The results show significant differences of PCAs-C_10-13 and PCAs-C_14-17 in breast milk with 22– and 6.2-times lower lw-based concentrations than those measured in serum. On wet weight the differences serum/breast milk ratios of PCAs-C_6-9, PCAs-C_10-13, PCAs-C_14-17, PCAs-C_18-32 and ΣPCAs were 1.7, 3.2, 1.0, 0.4 and 1.6, respectively, while the ratio for 4,4′-DDE, CB-153 and HCB were each close to 0.1.

Conclusion: Swedish lactating mothers had high serum concentrations of PCAs-C_10-13 and PCAs-C_14-17, with the ΣPCAs median serum concentration of 1350 ng/g lw. The breast milk concentration, although considerably lower at 107 ng/g lw, still surpassed those of 4,4′-DDE, CB-153 and HCB, suggesting an exposure risk of infants to PCAs. The variation in blood and breast milk accumulation between PCAs and studied legacy POPs, is rarely discussed but warrants further studies on partitioning properties as well as associated toxicological implications.

Background: The European Food Safety Authority (EFSA) recommended lowering their estimated tolerable daily intake (TDI) for bisphenol A (BPA) 20,000-fold to 0.2 ng/kg body weight (BW)/day. BPA is an extensively studied high production volume endocrine disrupting chemical (EDC) associated with a vast array of diseases. Prior risk assessments of BPA by EFSA as well as the US Food and Drug Administration (FDA) have relied on industry-funded studies conducted under good laboratory practice protocols (GLP) requiring guideline end points and detailed record keeping, while also claiming to examine (but rejecting) thousands of published findings by academic scientists. Guideline protocols initially formalized in the mid-twentieth century are still used by many regulatory agencies. EFSA used a 21st century approach in its reassessment of BPA and conducted a transparent, but time-limited, systematic review that included both guideline and academic research. The German Federal Institute for Risk Assessment (BfR) opposed EFSA’s revision of the TDI for BPA.

Objectives: We identify the flaws in the assumptions that the German BfR, as well as the FDA, have used to justify maintaining the TDI for BPA at levels above what a vast amount of academic research shows to cause harm. We argue that regulatory agencies need to incorporate 21st century science into chemical hazard identifications using the CLARITY-BPA (Consortium Linking Academic and Regulatory Insights on BPA Toxicity) nonguideline academic studies in a collaborative government–academic program model.

Discussion: We strongly endorse EFSA’s revised TDI for BPA and support the European Commission’s (EC) apparent acceptance of this updated BPA risk assessment. We discuss challenges to current chemical risk assessment assumptions about EDCs that need to be addressed by regulatory agencies to, in our opinion, become truly protective of public health. Addressing these challenges will hopefully result in BPA, and eventually other structurally similar bisphenols (called regrettable substitutions) for which there are known adverse effects, being eliminated from all food-related and many other uses in the EU and elsewhere.

Black-crowned night heron (Nycticorax nycticorax) eggs have been identified as useful indicators for biomonitoring the environmental pollution in China. In this study, we investigated thirty eggs of black-crowned night heron collected from the upper Yangtze River (Changjiang) Basin, Southwest China, for the occurrence of legacy persistent organic pollutants (POPs), including polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs), and polybrominated diphenyl ethers (PBDEs). Our results showed a general presence of POPs in night heron eggs with OCPs being the dominant contaminants, having a geometric mean concentration of 22.2 ng g(-1) wet weight (ww), followed by PCBs (1.36 ng g(-1) ww), PBDEs (0.215 ng g(-1) ww), and PCDD/Fs (23.0 pg g(-1) ww). The concentration levels were found to be significantly higher in night heron eggs than in poultry eggs by one or two magnitude orders. Among OCP congeners, p,p & PRIME;-DDE was found to be predominant in night heron eggs, with a geometric mean concentration of 15.1 ng g(-1) ww. Furthermore, species-specific congener patterns in eggs suggested similar or different sources for different POPs, possibly associated with contaminated soil and parental dietary sources. Additionally, estimated daily intakes (EDIs) were used to evaluate non-carcinogenic and carcinogenic risk associated with consumption of bird eggs. Our results revealed non-negligible non-cancer and cancer risk for humans who consume wild bird eggs as a regular diet instead of poultry eggs.

Despite several decades of study, ambiguities persist in terms used to express environmental and biotic occurrences of polychlorinated alkanes (PCAs), the main ingredient of chlorinated paraffins (CPs). This can lead to misinterpretation of data between analytical chemists, toxicologists, risk assessors/managers and regulators. The terms recommended here to harmonise reporting and reduce ambiguity use the conventional definition of PCAs - linear chlorinated alkanes (typically, C_≥10) with one chlorine per carbon, although some evidence of multiple chlorination exists. Other recommendations include.

● reporting the “Sum of measured PCAs” because “Total PCAs” is currently unquantifiable.

●reporting individual chain lengths, e.g., ΣPCAs-C₁₁, ΣPCAs-C₁₃, allows easier comparability and allows toxicology and risk assessment to consider different PCA combinations.

● maintain studies on individual PCAs in order to better characterise chemical, environmental and health risk behaviour.

The terms could be extended in future to assimilate new findings on individual PCAs, multiple chlorination and chirality.

Indoor environments may impact human health due to chemical pollutants in the indoor air and house dust. This study aimed at comparing the bioavailability and distribution of PFOA following both an inhalation and an oral exposure to PFOA coated house dust in rats. In addition, extractable organofluorine (EOF) was measured in different tissue samples to assess any potential influence of other organofluorine compounds in the experimental house dust. Blood samples were collected at sequential time points after exposure and at the time of termination; the lungs, liver, and kidney were collected for quantification of PFOA and EOF. The concentration of PFOA in plasma increased rapidly in both exposure groups attaining a C_max at 3 h post exposure. The C_max following inhalation was four times higher compared to oral exposures. At 48 h post exposure, the levels of PFOA in the plasma, liver, and kidney were twice as high from inhalation exposures. This shows that PFOA is readily bioavailable and has a rapid systemic distribution following an inhalation or oral exposure to house dust coated with PFOA. The proportion of PFOA to EOF corresponded to 65–71% and 74–87% in plasma and tissues, respectively. The mass balance between EOF and target PFOA indicates that there might be other unknown PFAS precursor and/or fluorinated compounds that co-existed in the house dust sample that can have accumulated in rats.

Organochlorine contaminants (OCs) – organochlorine pesticides (OCPs) and industrial products and byproducts – are included in different monitoring programmes and surveys, involving various animal species. Fish-eating birds are suitable indicator species for OCs. Adult birds may be difficult to capture, but chicks can be sampled more easily. Blood of birds is a potentially suitable non-destructive matrix for analysis, as OC levels in blood reflect their concentrations in the body. The study was aimed at investigating how age of fast-growing Grey heron (Ardea cinerea) chicks affects contaminant levels in their blood and thus how important is sampling at exact age for biomonitoring purposes. In 1999 on Lake Engure in Latvia whole blood samples of heron chicks were collected at three different time points, with seven and nine days in between the first and second and second and third sampling points, respectively. Twenty-two chicks were sampled at all three times. In total, 102 samples were analysed for 19 polychlorinated biphenyl (PCB) congeners, DDT metabolites – DDE and DDD, hexachlorobenzene (HCB), α-, β-, γ-hexachlorocyclohexane (HCH), and trans-nonachlor. Total PCB concentrations averaged around 2000 ng/g dry extracted matter (EM). DDE was the dominant individual contaminant (ca. 800 ng/g EM), followed by CB-153, -138, and −118. Most of the other analysed OCs were below 100 ng/g EM. No significant (p > 0.05) differences in OC concentrations were found between the three sampling occasions, except for trans-nonachlor. This means that blood can safely be sampled for biomonitoring purposes during the 17 days’ time window. The analysed legacy contaminants may serve as model substances for other persistent organic pollutants.

Even though the chlorinated paraffins (CPs) have been on the environmental pollution agenda throughout the last 50 years it is a class of chemicals that only now is discussed in terms of an emerging issue with extensive annual publication rates. Major reviews on CPs have been produced, but a deeper understanding of the chemical fate of CPs, including formation of metabolites in animals and humans, is still missing. Thus, the present review aims to critically compile our present knowledge on the disposition, i.e. Adsorption, Disposition, Metabolism, and Excretion (ADME) of CPs in biota and to identify research needs.

We conclude that CPs could be effectively absorbed from the gastro-intestinal tract (GI) tract, and probably also from the lungs, and transported to various organs. A biphasic elimination is suggested, with a rapid initial phase followed by a terminal phase, the latter (e.g., fat tissues) covering half-lives of weeks and months. CPs are metabolized in the liver and excreted mainly via the bile and faeces, and the metabolic rate and type of metabolites are dependent on chlorine content and chain length. Results that strengthen CP metabolism are in vivo findings of phase II metabolites in bile, and CP degradation to carbon fragments in experimental animals. Still the metabolic transformations of CPs are poorly studied, and no metabolic scheme has yet been presented. Further, toxicokinetic mass balance calculations suggest that a large part of a given dose (not found as parent compound) is transformation products of CPs, and in vitro metabolism studies present numerous CP metabolites (e.g., chloroalkenes, chlorinated ketones, aldehydes, and carboxylic acids).

The toxicity of PCB-156 (2,3,3′,4,4′,5-hexachlorobiphenyl) was investigated in rats following subchronic dietary exposure. Groups of 10 male and female Sprague-Dawley rats were administered PCB-156 in the diet at 0, 0.01, 0.1, 1 or 10 ppm for 90 days. Dose-dependent increases were detected for the liver, lung and kidney weights, as well as for the liver EROD, PROD and UDPGT enzyme activities and liver uroporphyrin concentration. Dose-dependent decreases were observed in final body weight, body weight gain, and thymus weight. Apolar retinoid concentrations were decreased in the liver and lungs and increased in the kidneys. Histopathological examination of the liver, thyroid, and thymus showed mild to moderate dose-related changes.

A LOAEL of 0.01 ppm was established, based on reduced apolar liver retinoid concentration. Benchmark dose-modelling corroborated the sensitivity of liver retinoid endpoints. The lower confidence limits (BMDL) for a 5% decrease in apolar liver retinoid concentrations were 0.0009 and 0.0007 ppm, respectively, in males and females, corresponding to a daily dose of 0.06 μg PCB-156 per kg body weight. Organizing dose-response data for the individual hepatic endpoints along the PCB-156 dosing scale revealed a sequence of events compatible with a causal link between depletion of apolar retinoids and the other liver biochemistry and pathology findings. Taken together, data suggest that the retinoid endpoints should be further evaluated for a causal relationship to PCB-induced liver toxicity and that retinoid system endpoints are identified and characterized to support health risk assessment in the emerging research fields of endocrine disruption and mixture toxicology.