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Effects of natural stressors such as copper (Cu 2+ ), temperature, hypoxia, chloroform and adrenaline on physiological and biochemical responses were investigated in the Mediterranean green crab Carcinus aestuarii from tidal shallow waters of Narta Lagoon, Albania. For this purpose, hemolymph glucose levels, total and differential hemocyte count, in normal and eye-stalked individuals, exposed to above mentioned stressors like, were assessed. In addition, lysosomal membrane stability was evaluated as biomarker of hemocyte toxicity, with possible implications on crab immune response. Hemolymph glucose levels were significantly increased in all treatment groups with 1.25-to 3.5-fold above baseline levels of 37.8 ± 2.7 mgdL -1 . Response times were being manifested within 30-120 min following exposure and recovery happened within 2 h of restoration of pretreatment conditions. Total hemocyte count (THC) and differential hemocyte count (DCH) showed a significant decrease for all stressors, except for copper, were an increase of semi-granular hemocyte fraction were recorded. Meanwhile, significant reduction of neutral red retention time (NRRT), in both eyestalk-ablated and exposed animals, were recorded, indicated the loss of hemocyte lysosomal membrane integrity. The responsiveness of hemolymph blood levels to all stressors, the decrease in total hemocyte count, as well as the loss of lysosomal membrane integrity demonstrated that exposure to environmentally realistic stressors placed a heavy metabolic load on C. aestuarii, modulating their immune competence and overall physiological wellness. Overall, results suggest that monitoring cellular and biochemical parameters like hemolymph glucose titres, TCH, DHC and NRRT, may be useful and sensitive means of evaluating the crustacean's ability to cope with the wide variety of environmental stressors through modulation of the immune parameters., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier Inc.)

Exposure to disinfection by-products (DBP) such as trihalomethanes (THM) in swimming pools has been linked to adverse health effects in humans, but their biological mechanisms are unclear. We evaluated short-term changes in blood gene expression of adult recreational swimmers after swimming in a chlorinated pool. Volunteers swam 40min in an indoor chlorinated pool. Blood samples were drawn and four THM (chloroform, bromodichloromethane, dibromochloromethane and bromoform) were measured in exhaled breath before and after swimming. Intensity of physical activity was measured as metabolic equivalents (METs). Gene expression in whole blood mRNA was evaluated using IlluminaHumanHT-12v3 Expression-BeadChip. Linear mixed models were used to evaluate the relationship between gene expression changes and THM exposure. Thirty-seven before-after pairs were analyzed. The median increase from baseline to after swimming were: 0.7 to 2.3 for MET, and 1.4 to 7.1μg/m 3 for exhaled total THM (sum of the four THM). Exhaled THM increased on average 0.94μg/m 3 per 1 MET. While 1643 probes were differentially expressed post-exposure. Of them, 189 were also associated with exhaled levels of individual/total THM or MET after False Discovery Rate. The observed associations with the exhaled THM were low to moderate (Log-fold change range: -0.17 to 0.15). In conclusion, we identified short-term gene expression changes associated with swimming in a pool that were minor in magnitude and their biological meaning was unspecific. The high collinearity between exhaled THM levels and intensity of physical activity precluded mutually adjusted models with both covariates. These exploratory results should be validated in future studies., (Copyright © 2017. Published by Elsevier B.V.)

Adsorption of non-polar compounds by suspended fullerene nanoaggregates (nC 60 ) may enhance their toxicity and affect the fate, transformation, and transport of non-polar compounds in the environment. The potential of stable fullerene nanoaggregates as contaminant carriers in aqueous systems and the influence of chloromethanes (trichloromethane and dichloromethane) were studied on the midgut epithelial cells of Daphnia magna by light and electron microscopy. The size and shape of fullerene nanoaggregates were observed and measured using dynamic light scattering, transmission electron microscopy, and low vacuum scanning electron microscopy. The nC 60 in suspension appeared as a bulk of aggregates of irregular shape with a surface consisting of small clumps 20-30 nm in diameter. The presence of nC 60 aggregates was confirmed in midgut lumen and epithelial cells of D. magna. After in vivo acute exposure to chloromethane, light and electron microscopy revealed an extensive cytoplasmic vacuolization with disruption and loss of specific structures of D. magna midgut epithelium (mitochondria, endoplasmic reticulum, microvilli, peritrophic membrane) and increased appearance of necrotic cells. The degree of observed changes depended on the type of treatment: trichloromethane (TCM) induced the most notable changes, whereas fullerene nanoaggregates alone had no negative effects. Transmission electron microscopy also indicated increased lysosomal degradation and severe peroxidative damages of enterocyte mitochondria following combined exposure to chloromethane and fullerene nanoaggregates. In conclusion, the adsorption of chloromethane by fullerene nanoaggregates enhances their toxicity and induces peroxidative mitochondrial damage in midgut enterocytes.

With the increasing concerns about the harmful effects of disinfection products, the process of chlorination is becoming questionable. Bromoform and chloroform are among the most frequently occurring disinfection by-products. Haematological parameters are an important indicator of human well-being which is why the prime objective of the current study was to conduct a dose-response assessment to investigate the effects of trihalomethanes on human haematological count. Blood samples of healthy subjects were exposed to different concentrations (10, 30 and 50 μg/mL) of chloroform and bromoform in vitro to analyse how these compounds affected the haematological count with increasing dose concentrations. Headspace gas chromatography analysis was also conducted on samples to assess the difference between measured and spiked values of doses. The results indicated that the damage caused by bromoform was statistically more significant as compared to chloroform. Haemoglobin (HGB) and mean corpuscular haemoglobin concentration levels lowered as they were significantly affected (p < 0.05) by bromoform at all administered doses. It also significantly damaged platelet level at doses of 30 (p < 0.05) and 50 μg/mL (p < 0.01). Conversely, the damage caused by chloroform was statistically less significant (p > 0.05).

The study covered genetically determined lipid metabolism disorders due to oral intake of technogenic hyperchlorination drinkable water products. Findings are that overweight and obese children in a main group appeared to have serum chloroform level 2.3 times higher than that in a reference group. In oral intake of hyperchlorination drinkable water products, the study revealed main genes having polymorphism associated with endocrine disorders: overweight and obesity--APOE, PPARG, HTR2A, characterizing antioxidant system state--SOD2 and detoxication--SULTA. Polymorphism of candidate genes HTR2A and SOD2 was characterized by increased occurrence of mutant homo-- and heterozygous genotype, relative risk of pathologic allele presence in population exceeded the refrence group values. Probability of increased serum serotonin and lower Cu/Zn in children with mutant homozygous genotype HTR2A and SOD2 is 1.2-1.3 times higher than in those with heterozygous and normal homozygous genotypes.

Drinking water quality standard (DWQS) criteria for chemicals for which there is a threshold for toxicity are derived by allocating a fraction of tolerable daily intake (TDI) to exposure from drinking water. We conducted physiologically based pharmacokinetic model simulations for chloroform and have proposed an equation for total oral-equivalent potential intake via three routes (oral ingestion, inhalation, and dermal exposures), the biologically effective doses of which were converted to oral-equivalent potential intakes. The probability distributions of total oral-equivalent potential intake in Japanese people were estimated by Monte Carlo simulations. Even when the chloroform concentration in drinking water equaled the current DWQS criterion, there was sufficient margin between the intake and the TDI: the probability that the intake exceeded TDI was below 0.1%. If a criterion that the 95th percentile estimate equals the TDI is regarded as both providing protection to highly exposed persons and leaving a reasonable margin of exposure relative to the TDI, then the chloroform drinking water criterion could be a concentration of 0.11mg/L. This implies a daily intake equal to 34% of the TDI allocated to the oral intake (2L/d) of drinking water for typical adults. For the highly exposed persons, inhalation exposure via evaporation from water contributed 53% of the total intake, whereas dermal absorption contributed only 3%., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Disinfection byproducts were measured in the finished drinking water from ten water treatment plants in three Chinese cities - Guangzhou, Foshan and Zhuhai. A total of 155 water samples were collected in 2011 and 2012. The median (range) of trihalomethane (THM) and haloacetic acid (HAA) levels were 17.7 (0.7-62.7) μg/L and 8.6 (0.3-81.3) μg/L, respectively. Chloroform, dichloroacetic acid and trichloroacetic acid were the dominant species observed in Guangzhou and Foshan water, while brominated THMs predominated in water from Zhuhai. Haloacetonitriles, haloketones, chloral hydrate and trichloronitromethane were usually detected at levels ranging from unquantifiable (<0.2μg/L) to 12.2μg/L (choral hydrate). THMs and HAAs showed clear seasonal variations with the total concentrations higher in winter than in summer. Correlations among DBP levels varied, with the strongest linear correlation observed between chloroform and chloral hydrate levels (R(2)=0.77). The risk of cancer from ingestion, inhalation and dermal contact exposure to THMs was estimated. CHCl2Br contributed the highest percentage of the cancer risk from ingestion pathway and CHCl3 contributed the highest of cancer risk from inhalation pathway., (Copyright © 2013 Elsevier B.V. All rights reserved.)

The transformation of two benzophenone UV filters (Oxybenzone and Dioxybenzone) was examined over the pH range 6-11 in the presence of excess aqueous chlorine. Under these conditions, both UV filters were rapidly transformed by aqueous chlorine just above circumneutral pH while transformation rates were significantly lower near the extremes of the pH range investigated. Observed first-order rate coefficients (k(obs)) were obtained at each pH for aqueous chlorine concentrations ranging from 10 to 75 μM. The k(obs) were used to determine the apparent second-order rate coefficient (k(app)) at each pH investigated as well as determine the reaction order of aqueous chlorine with each UV filter. The reaction of aqueous chlorine with either UV filter was found to be an overall second-order reaction, first-order with respect to each reactant. Assuming elemental stoichiometry described the reaction between aqueous chlorine and each UV filter, models were developed to determine intrinsic rate coefficients (k(int)) from the k(app) as a function of pH for both UV filters. The rate coefficients for the reaction of HOCl with 3-methoxyphenol moieties of oxybenzone (OXY) and dioxybenzone (DiOXY) were k(1,OxY) = 306 ± 81 M⁻¹s⁻¹ and k(1,DiOxY) = 154 ± 76 M⁻¹s⁻¹, respectively. The k(int) for the reaction of aqueous chlorine with the 3-methoxyphenolate forms were orders of magnitude greater than the un-ionized species, k(2,OxY) = 1.03(±0.52) × 10⁶ M⁻¹s⁻¹ and k(2&#95;1,DiOxY) = 4.14(±0.68) × 10⁵ M⁻¹s⁻¹. Also, k(int) for the reaction of aqueous chlorine with the DiOXY ortho-substituted phenolate moiety was k(2&#95;2,DiOxY) = 2.17(±0.30) × 10³ M⁻¹s⁻¹. Finally, chloroform formation potential for OXY and DiOXY was assessed over the pH range 6-10. While chloroform formation decreased as pH increased for OXY, chloroform formation increased as pH increased from 6 to 10 for DiOXY. Ultimate molar yields of chloroform per mole of UV filter were pH dependent; however, chloroform to UV filter molar yields at pH 8 were 0.221 CHCl₃/OXY and 0.212 CHCl₃/DiOXY., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Characterization of water quality from indoor swimming pools, using chorine-based disinfection techniques, was performed during a 6-mo period to study the occurrence, distribution, and concentration factors of trihalomethanes (THM). Several parameters such as levels of water THM, water and air chloroform, water bromodichloromethane (BDCM), water dibromochloromethane (DBCM), water bromoform (BF), free residual chlorine (FrCl), pH, water and air temperature, and permanganate water oxidizability (PWO) were determined in each pool during that period. Chloroform (CF(W)) was the THM detected at higher concentrations in all pools, followed by BDCM, DBCM, and BF detected at 99, 34, and 6% of the samples, respectively. Water THM concentrations ranged from 10.1 to 155 μg/L, with 6.5% of the samples presenting values above 100 μg/L (parametric value established in Portuguese law DL 306/2007). In this study, air chloroform (CF(Air)) concentrations ranged from 45 to 373 μg/m³ with 24% of the samples presenting values above 136 μg/m³ (considered high exposure value). Several significant correlations were observed between total THM and other parameters, namely, CF(W), CF(Air), FrCl, water temperature (T(W)), and PWO. These correlations indicate that FrCl, T(W) and PWO are parameters that influence THM formation. The exposure criterion established for water THM enabled the inclusion of 67% of Lisbon pools in the high exposure group, which reinforces the need for an improvement in pool water quality.

The objective of this study was to assess the impact of the exposure route on the human kinetic adjustment factor (HKAF), for which a default value of 3.16 is used in non-cancer risk assessment. A multi-route PBPK model was modified from the literature and used for computing the internal dose metrics in adults, neonates, children, elderly and pregnant women following three route-specific scenarios to chloroform, bromoform, tri- or per-chloroethylene (TCE or PERC). These include 24-h inhalation exposure, body-weight adjusted oral exposure and 30 min dermal exposure to contaminated drinking water. Distributions for body weight (BW), height (BH) and hepatic cytochrome P450 2E1 (CYP2E1) content were obtained from the literature, whereas model parameters (flows, volumes) were calculated from BW and BH. Monte Carlo simulations were performed and the HKAF was calculated as the ratio of the 95th percentile value of internal dose metrics in subpopulation to the 50th percentile value in adults. On the basis of the area under the parent compound's arterial blood concentration vs time curve (AUC(pc)), highest HKAFs were obtained in neonates for every scenario considered, and were the highest for bromoform (range: 3.6-7.4). Exceedance of the default value based on AUC(PC) was also observed for an oral exposure to chloroform in neonates (4.9). In all other cases, HKAFs remained below the default value. Overall, this study has pointed out the dependency of the HKAF on the exposure route, dose metrics and subpopulation considered, as well as characteristics of the chemicals investigated., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Background, Aim, and Scope: Quantitative risk comparison of toxic substances is necessary to decide which substances should be prioritized to achieve effective risk management. This study compared the ecological risk among nine major toxic substances (ammonia, bisphenol-A, chloroform, copper, hexavalent chromium, lead, manganese, nickel, and zinc) in Tokyo surface waters by adopting an integrated risk analysis procedure using Bayesian statistics., Methods: Species sensitivity distributions of these substances were derived by using four Bayesian models. Environmental concentration distributions were derived by a hierarchical Bayesian model that explicitly considered the differences between within-site and between-site variations in environmental concentrations. Medians and confidence intervals of the expected potentially affected fraction (EPAF) of species were then computed by the Monte Carlo method., Results: The estimated EPAF values suggested that risk from nickel was highest and risk from zinc and ammonia were also high relative to other substances. The risk from copper was highest if bioavailability was not considered, although toxicity correction by a biotic ligand model greatly reduced the estimated risk. The risk from manganese was highest if a conservative risk index estimate (90% upper EPAF confidence limit) was selected., Conclusion: It is suggested that zinc is not a predominant risk factor in Tokyo surface waters and strategic efforts are required to reduce the total ecological risk from multiple substances. The presented risk analysis procedure using EPAF and Bayesian statistics is expected to advance methodologies and practices in quantitative ecological risk comparison.

The paper presents the results of studying the carcinogenic effect of chloroform and its combination with carbon tetrachloride, 1,2-dichloroethane, trichloroethylene during chronic oral administration to F1(CBAxC57Bl6) mice. There is a relationship between the manifestation of carcinogenesis to the dose of chloroform and a combination of chemicals, as well as its enhancement upon exposure to the combination as compared with acute administration of chloroform. Exposure to a combination of substances at the level of their maximum permissible concentrations does not affect carcinogenesis. The possible mechanisms of the specific features of carcinogenesis in this experiment are discussed.

Chloroform can be formed as a disinfection by-product during water chlorination, one of the primary modalities for purifying municipal water supplies for human consumption. The aim of this study was to characterize the immunotoxic effects of chloroform in female B6C3F1 mice when exposure occurred via the drinking water. Consistent with human exposure, female B6C3F1 mice were exposed to chloroform-containing drinking water at 2.5, 10, 25, 100, and 250 ppm for 28 days. The examined endpoints included the effects of chloroform on body and organ weights, water consumption, hematology, innate immunity, humoral immunity, and cell-mediated immunity. The functions of natural killer, B-, and T-cells were not altered by chloroform in drinking water at the concentrations tested, except that an increase in splenocyte basal proliferation was observed at chloroform levels of 100 and 250 ppm. Following chloroform administration, there was a decreased number of circulating neutrophils in the blood in all treatment groups, but neutrophil function in lung homogenates, as evaluated using an assay for myeloperoxidase activity following lipopolysaccharide and N-Formyl-Met-Leu-Phe stimulation, was not compromised. Further, the results of host resistance to Listeria monocytogenes infection also suggested that neutrophil function was normal. At the highest treatment level of chloroform (250 ppm), erythrocyte number and hemoglobin levels were significantly decreased. Some significant changes were also observed for body weights, water consumption, and organ weights; however, most of these effects were only observed at the highest treatment level of chloroform (250 ppm). Taken together, the results demonstrate that while chloroform administered via the drinking water affects body weight and selected hematological parameters at high dose levels, overall immune responses, as measured in several tests for immune function, are not compromised.

Background: One problem of interpreting population-based biomonitoring data is the reconstruction of corresponding external exposure in cases where no such data are available., Objectives: We demonstrate the use of a computational framework that integrates physiologically based pharmacokinetic (PBPK) modeling, Bayesian inference, and Markov chain Monte Carlo simulation to obtain a population estimate of environmental chloroform source concentrations consistent with human biomonitoring data. The biomonitoring data consist of chloroform blood concentrations measured as part of the Third National Health and Nutrition Examination Survey (NHANES III), and for which no corresponding exposure data were collected., Methods: We used a combined PBPK and shower exposure model to consider several routes and sources of exposure: ingestion of tap water, inhalation of ambient household air, and inhalation and dermal absorption while showering. We determined posterior distributions for chloroform concentration in tap water and ambient household air using U.S. Environmental Protection Agency Total Exposure Assessment Methodology (TEAM) data as prior distributions for the Bayesian analysis., Results: Posterior distributions for exposure indicate that 95% of the population represented by the NHANES III data had likely chloroform exposures < or = 67 microg/L [corrected] in tap water and < or = 0.02 microg/L in ambient household air., Conclusions: Our results demonstrate the application of computer simulation to aid in the interpretation of human biomonitoring data in the context of the exposure-health evaluation-risk assessment continuum. These results should be considered as a demonstration of the method and can be improved with the addition of more detailed data.

We investigated the concentration of trihalomethanes (THMs) in tap water and swimming pool water in the area of the Nakhon Pathom Municipality during the period April 2005-March 2006. The concentrations of total THMs, chloroform, bromodichloromethane, dibromochloromethane and bromoform in tap water were 12.70-41.74, 6.72-29.19, 1.12-11.75, 0.63-3.55 and 0.08-3.40 microg/L, respectively, whereas those in swimming pool water were 26.15-65.09, 9.50-36.97, 8.90-18.01, 5.19-22.78 and ND-6.56 microg/L, respectively. It implied that the concentration of THMs in swimming pool water was higher than those in tap water, particularly, brominated-THMs. Both tap water and swimming pool water contained concentrations of total THMs below the standards of the World Health Organization (WHO), European Union (EU) and the United States Environmental Protection Agency (USEPA) phase I, but 1 out of 60 tap water samples and 60 out of 72 swimming pool water samples contained those over the Standard of the USEPA phase II. From the two cases of cancer risk assessment including Case I Non-Swimmer and Case II Swimmer, assessment of cancer risk of non-swimmers from exposure to THMs at the highest and the average concentrations was 4.43 x 10(-5) and 2.19 x 10(-5), respectively, which can be classified as acceptable risk according to the Standard of USEPA. Assessment of cancer risk of swimmers from exposure to THMs at the highest and the average concentrations was 1.47 x 10(-3) and 7.99 x 10(-4), respectively, which can be classified as unacceptable risk and needs to be improved. Risk of THMs exposure from swimming was 93.9%-94.2% of the total risk. Cancer risk of THMs concluded from various routes in descending order was: skin exposure while swimming, gastro-intestinal exposure from tap water intake, and skin exposure to tap water and gastro-intestinal exposure while swimming. Cancer risk from skin exposure while swimming was 94.18% of the total cancer risk.

Water chlorination results in the formation of trihalomethanes (THMs) including chloroform. In human stud-ies, fetal growth restriction has been associated with exposure to THMs during pregnancy and impaired fetal growth has been associated with an increased risk of type 2 diabetes. Therefore, the objective of this study was to determine the effect of in utero and lactational exposure to chloroform on birthweight and postnatal indicators of type 2 diabetes. Female Wistar rats were given chloroform (0 microg/L, 75 microg/L) in their drinking water for 2 wk prior to mating until parturition (in utero exposure only) or until weaning (in utero+lactational exposure). At postnatal d 1 (PND1) pups of dams exposed to chloroform had significantly higher serum glucose levels and lower insulin levels, but this effect was not due to b-cell depletion in the neonatal pancreas. Glucose homeostasis in response to a glucose challenge was not changed by chloroform treatment. Chloroform exposure did not affect birthweight; however, offspring of dams exposed to chloroform had significantly impaired postnatal growth. Although fetal and neonatal exposure to chloroform did not elicit physiological changes associated with the onset of type 2 diabetes, there were physiological changes resulting in impaired postnatal growth.