Chlorinated Naphthalenes Research Articles

A cytotoxicity and mechanistic investigation of mono- and di-chloro naphthalenes

Polychlorinated naphthalenes (PCNs) were characterized as persistent organic pollutants (POPs) that were widely distributed in the environment. Although the striking in vivo toxicity of these pollutants towards both animals and humans was well documented, their cytotoxicity and mechanism of action have not been extensively investigated. In this study, the in vitro antiproliferative activity of mono- and di-chloronaphthalenes as representative PCNs were evaluated and the results indicated strong growth inhibitory effects against mammalian cells, especially the human breast MCF-10A cell and human hepatic HL-7702 cells. 2-Chloronaphthalene with the most potent antiproliferative effects within the tested PCNs, which showed IC50 values ranging from 0.3 mM to 1.5 mM against selected human cell lines, was investigated for its working mechanisms. It promoted cellular apoptosis of MCF-10A cells upon the concentration of 200 μM. It also induced the autophagy of MCF-10A cells in a dose-dependent manner, resulting in cell death via the interaction of autophagy and apoptosis. Thus, these findings supported the theoretical foundation for interventional treatment of PCNs toxicity and also provided implications for the use of chemopreventive agents against the toxic chlorinated naphthalenes in the environments.

Materials Contamination and Indoor Air Pollution Caused by Tar Products and Fungicidal Impregnations: Intervention Research in 2014-2019.

Construction materials containing tar products are a source of indoor air pollution in buildings. This particularly concerns old buildings, in which wooden structures were impregnated with tar compositions (creosote oil and Xylamite oil containing tar products) and buildings in which bituminous seal containing hydrocarbon solvents was used. During the 1970s and 1980s, an impregnant known as Xylamite was commonly used in Polish buildings. This material still emits organic vapors into the building’s environment, significantly worsening indoor air quality (IAQ). Xylamites and other impregnating materials are a source of indoor air pollution through toxic organic compounds, such as phenol, cresols, naphthalenes, chlorophenols (CPs), and chloronaphthalenes (CNs), which emit specific odors. TD-GC/MS enables detailed identification of the reasons behind chemical indoor air pollution. The results of laboratory tests on the chemical emissions of bitumen-impregnated materials were presented in 32 case studies. In turn, the results of indoor air pollution by volatile bitumen components were presented on 11 reference rooms and 14 case studies, including residential buildings, office buildings, and others. Laboratory tests of samples of construction products confirmed the main emission sources into indoor air. The research results for the period 2014–2019 are tabulated and described in detail in this manuscript.

Differences in the action of lower and higher chlorinated polychlorinated naphthalene (PCN) congeners on estrogen dependent breast cancer cell line viability and apoptosis, and its correlation with Ahr and CYP1A1 expression.

There are data showing that exposition to PCNs mixture increased incidence of gastrointestinal and respiratory neoplasms, but data regarding incidence of hormone-dependent cancer so far not shown. The objective was to determine if exposure to single lower and higher chlorinated PCN congeners is associated with altered proliferation and apoptosis of estrogen dependent breast cancer cells, and whether such effects are related to induction of AhR and CYP1A1 protein expression. MCF-7 cells were exposed to PCN 34, 39, 42, 46, 48, 52, 53, 54, 66, 67, 70, 71, 73 and 74 at concentrations of 100-10,000pg/ml. We evaluated the action of these PCN congeners on cell proliferation, DNA fragmentation and caspase-8,-9 activity. AhR and CYP1A1 protein expression and CYP1A1 activity was evaluated at a concentration of 1000pg/ml. An opposite action of tri- to tetraCNs than of penta-to heptaCNs on cell proliferation and apoptosis was evident. Tetra PCNs increased cell proliferation, but had no effect on DNA fragmentation nor caspase activity. Fast induction of CYP1A1 protein expression under the influence of lower chlorinated PCNs suggests faster metabolism and a possible stimulatory action of locally formed metabolites on cell proliferation. None of the higher chlorinated PCNs affected cell proliferation but all higher chlorinated PCNs increased caspase-8 activity, and hexa PCNs also increased caspase-9 activity. The rapid activation of the Ah receptor and CYP1A1 protein expression by higher chlorinated PCNs point to their toxicity; however, it is not sufficient for potential carcinogenicity. Action of lower chlorinated naphthalenes metabolites should be explored.

Thermal degradation of octachloronaphthalene over as-prepared Fe(3)O(4) micro/nanomaterial and its hypothesized mechanism.

Decomposition of octachloronaphthalene (CN-75) featuring fully substituted chlorines was investigated over as-prepared Fe3O4 micro/nanomaterial at 300 °C. It conforms to pseudo-first-order kinetics with kobs = 0.10 min(-1) as comparable to that of hexachlorobenzene and decachlorobiphenyl. Analysis of the products indicates that the degradation of CN-75 proceeds via two competitive hydrodechlorination and oxidation pathways. The onset of hydrodechlorination producing lower chlorinated naphthalenes (CNs) is more favored on α-position than β-position. Higher amounts of CN-73, CN-66/67, CN-52/60, and CN-8/11 isomers were found, while small content difference was detected within the tetrachloronaphthalene and trichloronaphthalene homologues, which might be attributed to lower energy principle and steric effects. The important hydrodechlorination steps, leading to CN-73 ≫ CN-74 in two heptachloronaphthalene isomers contrary to that in technical PCN-mixtures, were specified by calculating the charge of natural bond orbitals in CN-75 and the energy of two heptachloronaphthalene radicals. On the basis of the molecular electrostatic potential of CN-75, the nucleophilic O(2-), and eletrophilic O2(-) and O(-), present on the Fe3O4 surface, might attack the carbon atom and π electron cloud of naphthalene ring, producing naphthol species with Mars-van Krevelen mechanism, and formic and acetic acids.

From Hyperkeratosis to Apoptosis: Lessons Learned from 65 Years of Research

In 1950, shortly after completing my Ph.D. degree requirements and joining the faculty of the Animal Science Department at Cornell University, I heard about X-disease, or, more accurately, bovine hyperkeratosis, from Dr. Kenneth McEntee, a pathologist in the Veterinary College at Cornell. Affected animals developed thick skins, resembling armor plate. This was a consequence of their inability to convert carotene to vitamin A [1]; they lacrimated profusely so that their faces were constantly wet and they lost weight and eventually died. The disease, at first thought to be caused by a virus, was increasing rapidly in the United States and Europe, especially in Germany, prompting the U.S. Department of Agriculture to establish a special research program for the disease. Dr. McEntee and I, along with Dr. Peter Olafson, chairman of the Pathology Department, set out to find the cause of this disease. Luckily, we found some bread crumbs collected from beneath the slicer in a bakery in Burlington, VT, that had been fed to calves that later developed the disease. We extracted the active compound with ether and subjected the extract to column chromatography, testing each fraction for potency by monitoring plasma levels of vitamin A in test calves. Finally, we were able to crystallize the active compound(s) and identify them by spectrophotometry as highly chlorinated naphthalenes [2]. These compounds had been added to heat-resistant lubricants and fire-retardant paints and were also found in a wood preservative made in Germany. When these discoveries were published, and the napthalenes were removed, the disease rapidly disappeared, and few scientists today have ever heard of it. In retrospect, this early research achievement was a great morale booster, at a critical time in my career. My major research project—the measurement of steroids and gonadotropins in blood and tissues of cattle—was floundering. Plasma levels of steroids, particularly estrogens, proved to be lower than found in other species, and the methods we were using (differential extractions followed by column chromatography and measurement by spectrophotometry) were not adequate. The first comprehensive data correlating plasma luteinizing hormone (LH), estrogen, and progesterone levels during the bovine estrous cycle were not published until 1972 [3]. The Lesson Learned

Dioxin-like compound load in bulk of Chlorofen–A technical chlorobiphenyl formulation from Poland

The results from inventory aiming to quantify production of individual chlorobiphenyl (CB) constituents and by-product impurities such as chlorodibenzo-p-dioxins (CDDs), chlorodibenzofurans (CDFs) and chloronaphthalenes (CNs) contained in the bulk of manufactured Chlorofen presented. 2,2′,3,4,4′,5,5′-Heptachlorobiphenyl (#180) is the most abundant constituent of Chlorofen and its historical production is estimated as 210 tones, and followed in decreasing order other major constituents are 2,2′,3,3′,4,4′,5′,6-/2,2′,3,4,4′,5,5′,6-OcCB (#196/203), 2,2′,3,3′,4,4′,5,5′-OcCB (#194), 2,2′,3,3′,4,5,6,6′-OcCB (#200) 2,2′,3,3′,4,5′,6-HpCB (#175), 2,2′,3,3′,4,5,5′,6-OcCB (#198) 2,2′,3,3′,4,5,5,′6′-OcCB (#199), 2,2′,3,3′,4,5′,6-HpCB (#175), 2,2′,3,4,5,5′,6-HpCB (#185) and 2,2′,4,4′,5,5′-HxCB (#153), which contributed from 150 to 53 tones, respectively. Production of non-ortho CBs was 30.277 kg with 23 kg input from 3,3′4,4′,5-PeCB (#126), while of mono-ortho CBs was 390 kg with 200 kg input from 2,3′,4,4′,5-PeCB (#118). 3,3′4,4′,5-PeCB (#126) and 3,3′,4,4′,5,5′-HxCB (#169) with 2300 and 99 g of dioxin TEQ were major dioxin-like contributors among planar CBs in this formulation. CDDs and CDFs content of the bulk of Chlorofen was estimated as 0.11 and 319 kg, respectively, and the most toxic members are 0.355 and 99.6 g TEQ. 1,2,3,4,5,6,7-HpCN (#73) with 5.3 kg (53 g TEQ) 1,2,3,4,5,6,8-HpCN (#74) with 2.9 kg (29 g TEQ) and OCN with 370 kg (37000 g TEQ) dominated among CNs in bulk of Chlorofen. An especially large contribution form OCN is due to its relatively high extrapolated REP value and absolute concentration value reported.

Quantitative structure—activity relationships for the prediction of relative in vitro potencies (REPs) for chloronaphthalenes

Chloronaphthalenes (CNs), due to their structural similarities to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the other “dioxin-like” compounds, can bind to the aryl hydrocarbon receptor (AhR) and induce a wide range of pleotrophic effects. Relative potency of individual dioxin analogues can be measured relative to that of TCDD. Relative effects potencies (REP) can be based on many responses, including in vivo and in vitro responses. Both in vivo and in vitro tests, based on either indigenous responses such as the induction of ethoxyresorufin O-deethylase (EROD) or exogenous reporter genes under the control of the AhR such as luciferase can be used to determine REP values. Here we used measured REP values determined for CNs in two assays. Both assays are based on H4IIE rat hepatoma cells. The H4IIE assay is based on expression of the endogenous reporter gene (CYP-1 A) that codes for the expression of EROD and the H4IIE-luc assay which is based on the exogenous reporter gene (luciferase) transfected into the H4IIE cell line. Experimentally determined REP were available for only 17 and 18 of the 75 possible choronaphthalene congeners, for the H4IIE and H4IIE-luc assays, respectively. For this reason computational models were developed to allow prediction of the relative potencies of the other CN congeners. Predictive relationships were based on quantum chemical descriptors obtained from Density Functional Theory (DFT) calculations (B3LYP/6–311++G**). The final models were found by means of a hybrid method combining a genetic algorithm and artificial neural networks. REP values estimated for individual CNs based on the H4IIE assay ranged from 4.3 × 10− 9 to 3.2 × 10− 2 while those based on the H4IIE-luc assay ranged from 4.0 × 10− 8 to 1.8 × 10− 3. CN congeners nos. 66, 67, 70 and 73 were exhibited the greatest REP values in both assays. The 1,2,3,5,6,8-hexaCN congener (no. 68) had a REP value that was 10-fold less. The remaining congeners had REP values that were less or did not cause sufficient up-regulation of the monitored genes to allow for the calculation of a REP. Interactions of CNs with the AhR could be affected by three possible factors: molecular size, steric interactions and electrostatic interactions. These findings are discussed relative to the use of consensus TCDD equivalency factors' (TEFs) for use in risk assessments of CNs for regulatory purposes.

QSPR Modeling of Partition Coefficients and Henry’s Law Constants for 75 Chloronaphthalene Congeners by Means of Six Chemometric Approaches—A Comparative Study

n -octanol/water and n-octanol/air partition coefficients were calculated for 75 chloronaphthalenes (CNs) by means of quantitative structure-property relationship (QSPR) strategy to fill significant lacks in the empirical data. The QSPR models based on quantum-chemical descriptors computed on the level of density functional theory using B3LYP functional and 6-311++G** basis set. For each property, six models were identified using chemometric approaches such as: multiple regression method, principal component regression, partial least square regression, partial least square regression with initial elimination of the uninformative variables, partial least square regression with variable selection by a genetic algorithm (GA-PLS), and neural networks with variable selection by a genetic algorithm (GA-NN). They were calibrated and validated using the experimentally measured values of logKOW available for 16 congeners and the values of logKOA existing for 43 congeners. The models were compared regarding to their complexity and prediction ability. For best predictive model logKOW values of 75 CNs varied from 3.93 to 6.68, while that of logKOA, from 5.93 to 11.64. Root mean square errors of prediction for the best (GA-NN) models were 0.065 and 0.091, respectively. Further, values of logKAW and KH of CNs were calculated based on predicted logKOW and logKOA data. Depending on the CN congener logKAW varied from −1.68 to −5.21 and that of KH from 0.02 to 51.24. The errors of partitioning data computed in this study were of the same order of magnitude as reported for experimentally derived partitioning data, which confirmed applicability of the proposed modeling scheme for successful determination of logKOW and KOA. Accordingly, a new procedure of the computational partitioning data generation based on partial least square regression with variable selection by a genetic algorithm (GA-PLS) and neural networks with variable selection by a genetic algorithm (GA-NN) was optimized and proposed for future use.

Polychlorinated naphthalenes and other chlorinated tricyclic aromatic hydrocarbons emitted from combustion of polyvinylchloride

Chloronaphthalenes (CNs) and phenanthrenes or/and anthracenes (CP/CAs) were detected in the emissions of polyvinylchloride (PVC) combustion at 900 °C. The presence of metallic iron, copper, or aluminum increased the formation of highly chlorinated CNs (tri- to octachloro-homologues) in the PVC combustion process. Total levels of CNs and CP/CAs were 40–48 and 76–116 mg/kg PVC, respectively, in the emissions from combustion of PVC with metals. Monochloronaphthalenes, dichloronaphtahlenes, monochlorophenanthrenes, and monochloroanthracenes were the predominant homologues. The other CN homologues were minor combustion byproducts. Detection of CNs in the PVC combustion emissions suggests that CN formation from solid waste incineration is a source of CNs in the environment.

Congener-specific composition of polychlorinated naphthalenes, coplanar PCBs, dibenzo-p-dioxins, and dibenzofurans in the Halowax series.

Concentrations and congener compositions of polychlorinated naphthalenes (PCNs), coplanar polychlorinated biphenyls (Co-PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), and dibenzofurans (PCDFs) were determined in seven Halowax (HW) preparations. In HW 1000 and 1031, low-chlorinated naphthalenes (CNs) and in HW 1051, highly chlorinated naphthalenes were dominant, whereas tri- through penta-CNs were major homologues in other Halowaxes. Concentrations of Co-PCBs were in the range of 2.0-2600 ng/g. CB 105 and 118 were dominant in all Halowaxes. Concentrations of PCDDs/DFs were in the range of 92-5900 ng/g. The 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TEQs) in Halowaxes calculated from the amounts of PCNs, Co-PCBs, and PCDDs/DFs were in the range of 2800-220,000 ng-TEQ/g. PCNs accounted for most of the total TEQs in Halowaxes, and the contribution of PCDDs/DFs and Co-PCBs to total TEQs was less than 1/1000 that of PCNs. Congeners that most significantly contributed to TEQs were CN 69, 73, 70, and 63. Total TEQs roughly estimated from the Japanese production of technical PCNs, 210 kg-TEQ, was about half from technical PCBs, 440 kg-TEQ on average.

Biochemical Responses of Fish Sac Fry and a Primary Cell Culture of Fish Hepatocytes Exposed to Polychlorinated Naphthalenes

Chlorinated naphthalenes are planar halogenated aromatic compounds, which are widespread in the environment. Knowledge of their biochemical and toxicological actions in aquatic biota is, however, limited. The objective of this study was to assess the toxicity of highly chlorinated naphthalene congeners found in the aquatic environment on fish sac fry and to study their effects on xenobiotic metabolizing enzymes (CYP) using a short-term primary culture of fish hepatocytes and liver microsomes. A few days after hatching, rainbow trout sac fry were administered either Hallovax 1014, a mixture of 1,2,3,4,6,7-hexachloronaphthalene and 1,2,3,5,6, 7-hexachloronaphthalene (HxCN-mix), or 1,2,3,4,5,6, 7-heptachloronaphthalene (HpCN) (0.08, 0.8, and 4 microg/sac fry injected into the yolk sac). The exposure was terminated 2 weeks later. The naphthalene preparations did not cause any clinical signs of toxicity or difference in mortality rates between the control and treated groups. Immunohistochemical analysis of CYP1A expression in the treated sac fry revealed that staining was most pronounced in the hepatocytes and thereafter in kidney tubular epithelial cells. Moderate CYP1A staining was also seen in the mucosal epithelium of pyloric caecae and mild staining in the epithelium of olfactory organ. Staining in control sac fry was weak or absent. Exposure of the primary cell culture of trout hepatocytes to a low doses (</=10 ng/ml) of the chlorinated naphthalenes increased significantly CYP1A-associated EROD activity and CYP1A mRNA content, HxCN-mix being the most potent and thereafter HpCN and Hallovax 1014. The higher doses (50-100 ng/ml) of each naphthalene also inhibited EROD activity. However, the content of CYP1A mRNA or the intensity of the CYP1A protein band (58 kDa) recognized by anti-trout CYP1A peptide antibodies were not decreased with increasing polychlorinated naphthalene (PCN) concentration, indicating that the inhibition was not due to reduced protein synthesis. Furthermore, in vitro analyses of the inhibitory potential of PCNs on CYP1A activity with trout liver microsomes suggested that these naphthalene preparations may be CYP1A substrates and act as competitive inhibitors of CYP1A catalyst. Our results demonstrate that highly chlorinated naphthalenes are potent modulators of fish CYP1A enzyme and suggest that hepatocytes and tubular epithelial cells are the cell types that may be vulnerable to their metabolic products for cell injury in fish sac fry.

POLYCHLORINATED NAPHTHALENES AND OTHER ORGANOCHLORINE CONTAMINANTS IN HUMAN ADIPOSE AND LIVER TISSUE

Chlorinated naphthalenes (CNs) and chlorinated biphenyls (CBs), hexachlorobenzene (HCB), and p,p '-DDE were determined in human adipose and liver tissues collected at autopsy of 5 men and 2 women (Swedish), 47-80 yr of age. In paired adipose tissue and liver samples, the differences of the distribution of CNs, CBs, HCB, and p,p '-DDE were small, but the concentrations of the compounds (lipid weight basis) varied between the subjects. Generally, the profiles of the contaminants were similar in the subjects. However, in one of the male subjects (80 yr of age) the concentrations of 1,2,3,5,7/1,2,4,6,7-pentaCN and 1,2,3,4,6,7/1,2,3,5,6,7-hexaCN were much higher in the liver: 6 and 20 times higher than in adipose tissue, respectively. The concentration of the toxic coplanar 3,3',4,4',5-pentaCB (CB-126) was also high in the liver from this individual, three times higher concentration than in adipose tissue. It is suggested that the multiplicity of contaminants found in humans should be taken into consideration in risk assessment and that further studies are needed on the distribution of contaminants in different tissues.

Congener-specific analysis of chloronaphthalenes in white-tailed sea eagles Haliaeetus albicilla breeding in Poland

Forty-four congeners of higher chlorinated naphthalenes were identified and quantified in the breast muscles, liver and adipose fat of a few specimens of white-tailed sea eagle collected from the Baltic coastal and inland breeding areas in Poland in 1991–1992. Many of the identified chloronaphthalenes (CNs) were well resolved as single peaks on the Rtx-5 HRGC-MS/EI-SIR chromatograms; but still some of them coeluted in pairs (four tetra-, two penta- and six hexa-CNs) or triplicate (six tetra-CNs) on the chromatograms. All tetra-, penta-, hexa- and hepta-CNs present in Halowax 1014, a technical mixture of CNs, were found in the tissues of white-tailed sea eagles indicating a high persistency of these ubiquitous environmental contaminants. The profile and pattern of chloronaphthalenes found in sea eagles differed largely from that of Halowax 1014, suggesting a selective and structure-related metabolism of many CN congeners. Among the most persistent and highly bioaccumulating CNs in tissues of the sea eagles were congeners such as 1,3,5,7-T4CN (CA' no. 42), 1,2,4.6-/1,2,4,7-/1,2,5,7-T4CN (CN nos. 33/34/37) and 1,4,6,7-T4CN (CN no. 47); 1,2,3,5,7-/1.2,4,6,7-P5CN (CNnos. 52/60) and 1,2,4,6,8-P5CN (CN no. 61), and 1,2,3,4,6,7-/1,2,3,5.6,7-H6CN. Differences in the metabolic potency of some of the most persistent tetra- and penta-CNs were observed between juvenile and adult white-tailed sea eagles. The CN congener no. 54 (1,2,3,6,7-P5CN) also is present in tissues of white-tailed sea eagles. It is formed during combustion processes and has not been found in the technical mixtures of PCNs of the Halowax series.

Comparative toxicity of PCBs and related compounds in various species of animals.

There are several basic principles that apply to the clinicopathologic syndrome produced by polychlorinated biphenyls (PCBs). They are as follows: The degree of halogenation and position of the halogen atoms determine the potency of PCB, PBB, CDD, CDF and CN; in a given species of animals, the clinicopathologic syndrome induced by PCB is comparable to that induced by polybrominated biphenyls (PBB), chlorinated dibenzo-p-dioxins (CDD), chlorinated dibenzofurans (CDF), and chlorinated naphthalenes (CN) when an equitoxic dose is achieved; The clinicopathologic syndrome is different in each species of animals; Different species of animals vary in their susceptibility to intoxication; intoxication is more readily effected in young animals that in adults; at lethal doses the time between exposure and death is prolonged (greater than 2 weeks).

Comparative Toxicity of PCBs and Related Compounds in Various Species of Animals

There are several basic principles that apply to the clinicopathologic syndrome produced by polychlorinated biphenyls (PCBs). They are as follows: The degree of halogenation and position of the halogen atoms determine the potency of PCB, PBB, CDD, CDF and CN; in a given species of animals, the clinicopathologic syndrome induced by PCB is comparable to that induced by polybrominated biphenyls (PBB), chlorinated dibenzo-p-dioxins (CDD), chlorinated dibenzofurans (CDF), and chlorinated naphthalenes (CN) when an equitoxic dose is achieved; The clinicopathologic syndrome is different in each species of animals; Different species of animals vary in their susceptibility to intoxication; intoxication is more readily effected in young animals that in adults; at lethal doses the time between exposure and death is prolonged (greater than 2 weeks).

Hepta-, hexa-, tetra- and dichloronaphthalene congeners as inducers of hepatic microsomal drug-metabolizing enzymes

Pretreatment of immature male Wistar rats with 1,2,3,4,5,6,7-hepta-, 1,2,3,4,5,6,8-hepta- and 1,2,3,4,5,6-hexachloronaphthalene resulted in the induction of several hepatic microsomal drug-metabolizing enzymes. The enzymic activities, reduced cytochrome P-450: CO and ethylisocyanide binding difference spectra and electrophoretic mobilities of the induced microsomal proteins were comparable to those observed after administration of the classical inducer of microsomal aryl hydrocarbon hydroxylase, 3-methylcholanthrene. The 1,2,3,4,5,6,7-heptachloronaphthalene congener, which is fully substituted in the lateral 2,3,6 and 7 positions, was more potent than the 1,2,3,4,5,6,8-hepta- and the 1,2,3,4,5,6-hexachloronaphthalene congeners which contain only 3 lateral chloro substituents. 1,2,3,4-Tetra- and several lower chlorinated naphthalenes were inactive as inducers of microsomal aryl hydrocarbon hydroxylase. The effects of structure on the induction activities of the polychlorinated naphthalenes were similar to those observed for other halogenated aryl hydrocarbons.

ChemInform Abstract: SUBSTITUENT EFFECTS AND ADDITIVITY IN THE CARBON‐13 NUCLEAR MAGNETIC RESONANCE SPECTRA OF CHLORINATED NAPHTHALENES AND THEIR CHLORINATED NAPHTHOL METABOLITES

Chemischer InformationsdienstVolume 9, Issue 37 Physical Organic Chemistry ChemInform Abstract: SUBSTITUENT EFFECTS AND ADDITIVITY IN THE CARBON-13 NUCLEAR MAGNETIC RESONANCE SPECTRA OF CHLORINATED NAPHTHALENES AND THEIR CHLORINATED NAPHTHOL METABOLITES N. K. WILSON, N. K. WILSONSearch for more papers by this authorR. D. ZEHR, R. D. ZEHRSearch for more papers by this author N. K. WILSON, N. K. WILSONSearch for more papers by this authorR. D. ZEHR, R. D. ZEHRSearch for more papers by this author First published: September 12, 1978 https://doi.org/10.1002/chin.197837072AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume9, Issue37September 12, 1978 RelatedInformation

Metabolism of chlorinated naphthalenes.

Metabolism of chlorinated naphthalenes.

A simple differentiation of polychlorobiphenyls from chlorinated naphthalenes.

A simple differentiation of polychlorobiphenyls from chlorinated naphthalenes.

Behavior of Chlorinated Naphthalenes in Analytical Methods for Organochlorine Pesticides and Polychlorinated Biphenyls

Abstract Chlorinated naphthalenes are industrial chemicals with properties similar to those of polychlorinated biphenyls (PCB); they are recovered from foods by analytical methods for multiple residues of organochlorine pesticides. The chlorinated naphthalenes may interfere with the gas chromatographic determination of several organochlorine pesticides. A silicic acid column chromatographic method previously developed to separate PCB from organochlorine pesticide residues, particulary DDT and its analogs, also separates chlorinated naphthalenes from the pesticides and permits GLC determination without interference.