Abstract  BIOSIS COPYRIGHT: BIOL ABS. RRM REVIEW PESTICIDE WASTEWATER EPA GAS CHROMATOGRAPHY HIGH PERFORMANCE LIQUID CHROMATOGRAPHY ANALYTICAL METHOD USA

Abstract  BIOSIS COPYRIGHT: BIOL ABS. RRM EPA ENVIRONMENTAL LAW ENVIRONMENTAL SURVEILLANCE

Abstract  Risk assessment of metal-contaminated soil depends on how precisely one can predict the solubility of metals in soils. Responses of plants and soil organisms to metal toxicity are explained by the variation in free metal ion activity in soil pore water. This study was undertaken to predict the free ion activity of Zn, Cu, Ni, Cd, and Pb in metal-contaminated soil as a function of pH, soil organic carbon, and extractable metal content. For this purpose, 21 surface soil samples (0-15 cm) were collected from agricultural lands of various locations receiving sewage sludge and industrial effluents for a long period. One soil sample was also collected from agricultural land which has been under intensive cropping and receiving irrigation through tube well water. Soil samples were varied widely in respect of physicochemical properties including metal content. Total Zn, Cu, Ni, Cd, and Pb in experimental soils were 2,015 ± 3,373, 236 ± 286, 103 ± 192, 29.8 ± 6.04, and 141 ± 270 mg kg(-1), respectively. Free metal ion activity, viz., pZn(2+), pCu(2+), pNi(2+), pCd(2+), and pPb(2+), as estimated by the Baker soil test was 9.37 ± 1.89, 13.1 ± 1.96, 12.8 ± 1.89, 11.9 ± 2.00, and 11.6 ± 1.52, respectively. Free metal ion activity was predicted by pH-dependent Freundlich equation (solubility model) as a function of pH, organic carbon, and extractable metal. Results indicate that solubility model as a function of pH, Walkley-Black carbon (WBC), and ethylenediaminetetraacetic acid (EDTA)-extractable metals could explain the variation in pZn(2+), pCu(2+), pNi(2+), pCd(2+), and pPb(2+) to the extent of 59, 56, 46, 52, and 51 %, respectively. Predictability of the solubility model based on pH, KMnO4-oxidizable carbon, and diethylenetriaminepentaacetic acid-extractable or CaCl2-extractable metal was inferior compared to that based on EDTA-extractable metals and WBC.

Abstract  BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN EPIDEMIOLOGY OCCUPATIONAL FACTORS METAL HOT ENVIRONMENTS MICROWAVES NOISE

Abstract  The use and toxicity of fumigants was examined. Methods included space fumigation, soil fumigation, and structural fumigation. Worker exposures have been reported in all three types of fumigation, with structural fumigation posing the greatest risk to workers as well as to the public health. The use of the fumigant 1,2-dibromo-3-chloropropane (96128) (DBCP) has caused reproductive problems in exposed workers and has been considered to be a potent mutagen. Ethylene-dibromide (106934) (EB) has been shown to be more toxic than DBCP and acute dermal exposure has resulted in local inflammation, swelling, and blistering. EB has been shown to be a carcinogen as well as a mutagen in experimental studies. Exposure to the fumigants 1,2-dichloropropene (563542) and 1,3-dichloropropene (542756) have resulted in kidney and liver damage in experimental studies and both have been implicated as being carcinogens. Methyl-bromide (74839) poisonings have been reported in a number of cases and acute exposures to high concentrations have resulted in narcosis and death from respiratory failure. Its principle toxic effect has been on the nervous system and visual and hearing disorders, peripheral neuropathy, and central nervous system symptoms have been seen following chronic exposures. Methyl-bromide has also been demonstrated to be a mutagen in experimental studies. The effects of exposure to fumigants including sulfuryl-fluoride (2699798), chloropicrin (76062), boron-trifluoride (7637072), aluminum-phosphate (7784307), zinc-phosphate (7779900), 1,2-dichloropropane (78875), 1,1-dichloro-1-nitroethane (594729), hydrogen-cyanide (74908), carbon-disulfide (75150), aluminum-phosphide (20859738), and carbon-tetrachloride (56235) were discussed.

Abstract  In recent years, evidence from disparate observations has indicated adverse changes in the reproductive health and fecundity of animals and humans. In humans, there is strong evidence for such trends in the incidences of testicular and female breast cancer, and concern has also been expressed regarding semen quality, cryptorchidism, hypospadias and polycystic ovaries. Laboratory studies have indicated that some chemicals in the environment, both natural and synthetic, have the potential to disrupt the endocrine system and that these could, at least theoretically, be partly responsible for the observed changes. Chemicals thus identified include the naturally occurring steroid hormones, phyto- and myco-estrogens, and anthropogenic chemicals such as synthetic hormones, organotins, organochlorine pesticides, polychlorinated biphenyls, dioxins, alkylphenol polyethoxylates, phthalates and bisphenol-A. While there is no direct evidence from human studies to confirm a causal link between exposure and effect, concern exists and is strengthened by reports of adverse reproductive and developmental effects in wildlife, possibly mediated via endocrine disruptive pathways. The development of imposex in neogastropod molluscs exposed to tributyltin has been attributed to such a mechanism and in wild populations of fish, alligators and birds, instances of masculinisation or feminisation in polluted areas have been noted. Among mammals, disturbed fertility of Florida panthers and some marine species has also been reported. A concentrated research and monitoring programme is required to clarify the nature and extent of effects on reproductive health in humans and wildlife, and to assess human and wildlife exposure to relevant naturally occurring or anthropogenic endocrine disrupting substances. This will enable a more robust evaluation of the contribution that environmental chemical exposure may have on adverse trends in the reproductive health of humans and wildlife.

Abstract  A classification scheme is proposed for degrees of experimental evidence for the carcinogenicity of chemicals for animals. The classification stems from the suggestions of an IARC Working Group that the evaluation of bioassays include consideration of whether an increase in malignant tumours occurred and whether it occurred to an unusual degree or in multiple experiments. We extended the evaluative process to chemical experiments with no evidence of carcinogenicity and gave increased emphasis to results from more than one animal species. Although the proposed classification was developed for a group of NCI bioassays which were similar in design and conduct, it may provide a general framework for the evaluation of carcinogenesis bioassays and stimulate development and application of evaluative methods.

Abstract  BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN POLLUTION CONTROL GOVERNMENT REGULATION TOXICITY PREVENTION PROTECTIONISM FEDERAL COMMUNICABLE DISEASE CONTROL ACT PUBLIC HEALTH RISK MANAGEMENT GROUNDWATER RESTORATION EUROPEAN COMMISSION ECC STANDARD GERMANY

Abstract  BIOSIS COPYRIGHT: BIOL ABS. RRM ANIMAL WEIGHT-OF-EVIDENCE ANALYSIS CARCINOGENS

Abstract  In 1976, Crump, Heel, Langley, and Peto described how almost any dose-response relationship for carcinogens becomes linear at low doses when background cancers are taken into account. This has been used, by the U.S. Environmental Protection Agency, USEPA, as partial justification for a regulatory posture that assumes low-dose linearity, as is illustrated by a discussion of regulation of benzene as a carcinogen. The argument depends critically on the assumption that the pollutant and the background proceed by the same biological mechanism. In this paper we show that the same argument applies to noncancer end points also. We discuss the application to a number of situations: reduction in lung function and consequent increase in death rate due to (particulate) air pollution; reduction in IQ and hence (in extreme cases) mental deficiency due to radiation in utero; reduction of sperm count and hence increase in male infertility due to DBCP exposure. We conclude that, although the biological basis for the health effect response is different, in each case low-dose linearity might arise from the same mathematical effect discussed by Crump et al. (1976). We then examine other situations and toxic end points where low-dose linearity might apply by the same argument. We urge that biologists and chemists should concentrate efforts on comparing the biological and pharmacokinetic processes that apply to the pollutant and the background. Finally, we discuss some public policy implications of the possibility that low dose linearity may be the rule rather than the exception for environmental exposures.

Abstract  HEEP COPYRIGHT: BIOL ABS. Further findings of a survey of manufacturers, processors and importers of chemicals determined by the International Agency for Research on Cancer (IARC) to be animal carcinogens, but whose carcinogenicity in humans was considered uncertain because of inadequate epidemiologic data, are reported. Epidemiologic studies were obtained from companies marketing or using any of the 75 IARC animal carcinogens in commerce in the USA. Eighteen of the 75 IARC animal carcinogens had volumes listed of \ 106 lb/yr, with 8 of the 13 chemicals for which studies had been completed or are in progress in this high volume category. The use category with the largest number of chemicals was drugs-19 of the 75 IARC animal carcinogens were in this category. None of the 13 chemicals included in epidemiologic studies was a drug. Seven of the 13 chemicals included in studies were used primarily as pesticides. Little information was obtained on dyes and dye intermediates, experimental carcinogens and drugs, all of which are produced in relatively low volumes; these categories represent 42 of the 75 IARC animal carcinogens. Low volumes and declining usage/production appear to be barriers to performance of epidemiologic studies. Information received suggests that sometimes the problem of low production volume may be avoided by studying users rather than production workers. Overall, few additional epidemiologic studies of the 75 IARC animal carcinogens are expected.

Abstract  It is generally recognized that reductive processes are more important than oxidative ones in transforming, degrading and mineralizing many environmental contaminants. One process of particular importance is reductive dehalogenation, i.e., the replacement of a halogen atom (most commonly a chlorine atom) by a hydrogen atom. A number of different mechanisms are involved in these reactions. Photochemical reactions probably play a role in some instances. Aliphatic compounds such as chloroethanes, partly aliphatic compounds such as DDT, and alicyclic compounds such as hexachlorocyclohexane are readily dechlorinated in the laboratory by reaction with reduced iron porphyrins such as hematin. Many of these are also dechlorinated by cultures of certain microorganisms, probably by the same mechanism. Such compounds, with a few exceptions, have been found to undergo reductive dechlorination in the environment. Aromatic compounds such as halobenzenes, halophenols and halobenzoic acids appear not to react with reduced iron porphyrins. Some of these however undergo reductive dechlorination both in the environment and in the laboratory. The reaction is generally associated with methanogenic bacteria. There is evidence for the existence of a number of different dechlorinating enzymes specific for different isomers. Recently it has been found that many components of polychlorinated biphenyls (PCBs), long considered to be virtually totally resistant to environmental degradation, may be reductively dechlorinated both in the laboratory and in nature. These findings suggest that many environmental contaminants may prove to be less persistent than was previously feared.

Abstract  The development of occupational epidemiology has been steadily accelerating, both with regard to methodology and the number of studies being conducted. This chapter reviews the general applications of occupational epidemiology and illustrates some of the various studies reported in the literature in order to assist in the practical application of the epidemiologic approach.

Abstract  HEEP COPYRIGHT: BIOL ABS. HUMAN FETAL TOXICITY METAL TOXICITY PESTICIDE

Abstract  A series of halogenated propanes were studied for renal and testicular necrogenic effects in the rat and correlated to their ability to induce in vivo renal and testicular DNA damage and in vitro testicular DNA damage. l,2-Dibromo-3-chloropropane (DBCP) and 1,2,3-tribromo-propane were most potent in causing organ damage in both kidney and testes. Extensive necrosis was evident at 85 /μmol/kg in kidney and at 170 μmol/kg in testis. The dibromomonochlorinated analogue l,3-dibromo-2-chloropropane was less organ toxic than DBCP and 1,2,3-tribromo-propane, but induced more organ damage than the dichloromonobrominated analogues 1-bromo-2,3-dichloropropane and l,3-dichloro-2-bromopropane. Dihalogenated propanes were even less necrogenic. These observed differences in toxic potency between the halogenated propanes could not be explained by relative differences in tissue concentrations. The ability of the halogenated propanes to induce DNA damage in vivo correlated well with their ability to induce organ damage. However, DNA damage occurred at lower doses and at a shorter period of exposure than organ necrosis. This indicates that DNA damage might be an initial event in the development of organ necrosis by halogenated propanes in general. Further, testicular DNA damage induced by the halogenated propanes in vivo correlated well with the DNA damage observed in isolated testicular cells in vitro, showing that toxicity was due to in situ activation. The numbers, positions, and the types of halogen substituents appear to be important determinants in causing DNA damage and necrogenic effects. The toxic potential of the halogenated propanes was in the following order: 1,2,3-tribromopropane > l,2-dibromo-3-chloropropane >l,3-dibromo-2-chloropropane > l,3-dichloro-2-bromopropane a; l-bromo-2,3-dichloropropane> 1,2,3-trichloropropane =* 1,2-dibromopropane > 1,3-dibromopropane > l-bromo-3-chloro-propane. The most toxic analogues contain three halogens with at least two vicinal bromines.

Abstract  BIOSIS COPYRIGHT: BIOL ABS. The transformation of 1,2-dichloropropane (1,2-D) was observed in anaerobic microcosms and enrichment cultures derived from Red Cedar Creek sediment. 1-Chloropropane (1-CP) and 2-CP were detected after an incubation period of 4 weeks. After 4 months the initial amount of 1,2-D was stoichiometrically converted to propene, which was not further transformed. Dechlorination of 1,2-D was not inhibited by 2-bromoethanesulfonate. Sequential 5% (vol/vol) transfers from active microcosms yielded a sediment-free, nonmethanogenic culture, which completely dechlorinated 1,2-D to propene at a rate of 5 nmol min-1 mg of protein-1. No intermediate formation of 1-CP or 2-CP was detected in the sediment-free enrichment culture. A variety of electron donors, including hydrogen, supported reductive dechlorination of 1,2-D. The highest dechlorination rates were observed between 20? and 25?C. In the presence of 1,2-D, the hydrogen threshold concentration was below 1 ppm by volume (ppmv). In

Abstract  Case histories which illustrated the adverse health consequences associated with exposure to environmental pollutants were presented. Exposure of male factory workers to dibromochloropropane (35691657) or kepone (143500) resulted in sterility. Epidemics of poisoning from heavy metals were discovered among children who lived in the vicinity of smelters. Consumption of fish from a river in Japan contaminated with factory waste containing methylmercury resulted in an epidemic of neurologic disorders and the births of 40 children with cerebral palsy. In South Africa, a cluster of cases of mesothelioma were found to be associated with living near open pit asbestos (1332214) mines as children. Accidental contamination of cooking oil with polychlorinated-biphenyl (1336363) resulted in an epidemic of chloracne in Kyushu, Japan. Cattle feed contaminated with polybrominated biphenyls caused devastating debilitation and death among livestock in Michigan. Inappropriate disposal of chemical byproducts of hexachlorophene (70304) onto floors of horse arenas caused deaths of 63 horses and illnesses among children who played on the floor. Nearly all known teratogens and carcinogens were first recognized through clinical observations by patients or their physicians and were subsequently tested epidemiologically and experimentally. Proposed steps for the epidemiologic study of areawide contamination were outlined. A list of available resources which may aid in the study of environmental contamination was provided. The special susceptibilities of the child and fetus, and of the reproductive system to chemical pollutants were emphasized. The author concludes that priorities need to be set and plans formulated for the evaluation of health hazards of environmental contamination.

Abstract  Biosis copyright: biol abs. rrm book