Gas chromatography with pulsed flame photometric detection multiresidue method for organophosphate pesticide and metabolite residues at the parts-per-billion level in representatives commodities of fruits and vegetable crop groups.

A gas chromatographic method with a pulsed flame photometric detector (P-FPD) is presented for the analysis of 28 parent organophosphate (OP) pesticides and their OP metabolites. A total of 57 organophosphates were analyzed in 10 representative fruit and vegetable crop groups. The method is based on a judicious selection of known procedures from FDA sources such as the Pesticide Analytical Manual and Laboratory Information Bulletins, combined in a manner to recover the OPs and their metabolite(s) at the part-per-billion (ppb) level. The method uses an acetone extraction with either miniaturized Hydromatrix column partitioning or alternately a miniaturized methylene dichloride liquid-liquid partitioning, followed by solid-phase extraction (SPE) cleanup with graphitized carbon black (GCB) and PSA cartridges. Determination of residues is by programmed temperature capillary column gas chromatography fitted with a P-FPD set in the phosphorus mode. The method is designed so that a set of samples can be prepared in 1 working day for overnight instrumental analysis. The recovery data indicates that a daily column-cutting procedure used in combination with the SPE extract cleanup effectively reduces matrix enhancement at the ppb level for many organophosphates. The OPs most susceptible to elevated recoveries around or greater than 150%, based on peak area calculations, were trichlorfon, phosmet, and the metabolites of dimethoate, fenamiphos, fenthion, and phorate.

Acute toxicity, genotoxicity, and dermal carcinogenicity assessment of isooctyl acrylate.

Isooctyl acrylate (IOA) monomer is a complex mixture comprised predominantly of isomeric, eight-carbon alkyl esters of acrylic acid. Limited evidence from animal studies suggests that certain acrylate esters may be carcinogenic by the dermal route of exposure. The following studies were performed with IOA monomer: acute oral toxicity limit test in rats, primary dermal and ocular irritancy in rabbits, Ames Salmonella microsome assay, Saccharomyces cerevisiae D3 recombinogenicity assay, L5178Y TK +/- mouse lymphoma cell assay, and C3H/10T1/2 mouse embryo cell transformation assay. Finally, a limited dermal carcinogenicity bioassay was performed in which aliquots (25 microliters) of IOA monomer (5% v/v in acetone), IOA polymer (19% w/v in 70:30 acetone/heptane), or acetone (vehicle control) were applied to the shaved backs of male C3H/HeJ mice three times per week for the animals' lifetimes. IOA monomer had an acute oral LD50 in rats greater than 5000 mg/kg, was slightly irritating to the eyes and skin of rabbits on single exposures, and exhibited no genotoxic or cell-transforming potential. In the dermal carcinogenicity bioassay, no significant difference in mean survival times was observed between either treatment group and the control group. Animals treated with IOA monomer exhibited moderate dermatitis, surface crusting, hyperkeratosis, epidermal hyperplasia, diffuse melanosis, and one benign melanoma at the treatment size. Animals treated with IOA polymer exhibited varying degrees of dermatitis, surface crusting, and hyperkeratosis. Neither IOA monomer nor IOA polymer was carcinogenic under the conditions of the study.

Pulmonary response and transmigration of inorganic fibers by inhalation exposure.

Rats, hamsters, and guinea pigs were exposed by inhalation to different concentrations of potassium octatitanate fibers. Following 3 months of exposure, the animals were sacrificed between the 15th and 24th month. The exposed animals showed dose-related dust deposition and pulmonary fibrosis mainly in the respiratory bronchiolar region. Most short fibers (less than 5 micrograms) were phagocytized by alveolar macrophages, but long fibers (greater than 10 micrograms) were phagocytized by foreign body giant cells. Dust-laden macrophages (dust cells) entered into the lumen of bronchial lymphatic or pulmonary blood vessels. Numerous dust cells were transported from the lung to the tracheobronchial and mediastinal lymph nodes where some dust cells penetrated into the blood or lymphatic circulation. Massive direct cell migration of the mediastinal adipose tissue from the lymph nodes occurred occasionally. Dust-laden giant cells were found only occasionally in the liver, and there was widespread migration of the fibers into other vital organs and tissues without any significant responses.

Animal toxicity studies with ammonium perfluorooctanoate.

These studies were conducted to evaluate the potential toxicity of ammonium perfluorooctanoate, a commercial surfactant. They include acute and subchronic feeding studies with rabbits, mice, rats and monkeys as well as in vitro mutagenicity assays with Salmonella typhimurium and Saccharomyces cerevisiae. The compound was non-irritating to the skin and moderately irritating to the eyes of rabbits. The rat oral LD50 was 540 mg/kg; no deaths resulted from a one hour rat inhalation exposure at a nominal concentration of 18.6 mg/L. All in vitro assays were negative. The liver was the target organ in rodents in both the 28 day and 90 day feeding studies with males showing a greater response than females. Serum and liver concentrations of organic fluorine were greater in male than in female rats. In a 90 day oral study in rhesus monkeys the gastrointestinal tract and the reticuloendothelial system were the sites of toxic effects. The gastrointestinal effects were attributed to the potent surface activity of the compound. Histopathological effects wer noted in the spleen, lymph nodes and bone marrow. Unlike the rats, sex related differences were not evident in the monkeys. Toxicological evaluations of ammonium perfluorooctanoate are continuing.

Pulmonary response to glass fiber by inhalation exposure.

Rats, hamsters, and guinea pigs were exposed to airborne glass fiber at a gravimetric concentration of 0.42 mg. per liter for 6 hours per day, 5 days per week for 90 days. The number of dust particles greater than 5 micron. in length was 0.73 x 10(6) per liter with an average diameter of approximately 1.2 micron. Most particles were less than 2 micron. in size and only 15% of the dust particles had a fibrous shape. Few fibers were longer than 10 micron. The pulmonary response was characterized by macrophage reaction with alveolar proteinosis at 90 days of inhalation. The light and ultrastructural alterations were similar to the other experimental or human alveolar proteinosis. The alveolar proteinosis disappeared at 1-year postexposure, but focal dust cell accumulation with proliferating granular pneumocytes persisted throughout the 2-year recovery period. No significant fibrosis or stromal changes were found in the dust-deposited areas. In hamsters and guinea pigs, most ferruginous bodies were developed from fibrous fibers but not from tiny dust particles. The tracheobronchial lymph nodes were markedly swollen and laden with dust cells.

Toxicological evaluations of some brominated biphenyls.

Extensive toxicological studies were carried out to define the probable hazard of octabromobiphenyl (OBB) to workers, users, and the environment. OBB had low acute toxicity in mammals and birds by various routes of administration. It was essentially non-irritating to rabbit eyes, non-irritating to human skin and caused only mild skin irritation and no sensitization in the guinea pig. OBB caused equivocal effects in the rat fetus. OBB was stored in the body fat of rats and caused liver enlargement at high single doses or low repeated doses. The studies indicate probable low safety factors in application and use and probable bioaccumulation. Hexabromobiphenyl (HBB) was more acutely toxic than OBB by skin absorption in the rabbit and caused liver enlargement at lower single doses.

Pathologic analysis of mink mortality in New England mink.

The underlying cause of death of a group of New England mink, which died in 1969 to 1970 was explored. PCB and chlorinated hydrocarbon pesticide levels were measured. Aroclor 1254 levels in these mink were elevated 73 fold over levels in healthy mink in 1974. DDT levels were elevated 5 times and DDE 3 times over those control animals. Gross pathology revealed desions of the lungs, liver and kidneys. There lesions were confirmed microscopically. The lungs of the New England mink showed inflammation and congestion. Areas of inflammation were also present in the liver. Massive areas of necrosis were seen in the kidneys, both in the medullary and cortical areas. Kidney involvement was greater than any other organ. P.A.S. positive material was seen in each of these organs with the kidneys showing largest amounts of this material. Since the New England mink did not show lesions of the G.I. tract, did not exhibit fatty degeneration of the liver, which PCB toxicity is known to induce in mink and because they showed areas of congestion, inflammation and positive P.A.S. material, PCB's were not considered the toxic agent. However, fungus or bacterial infection might be the causative agent.

Experiments on the effect of carbon monoxide on aminolevulinic acid dehydrase (ALAD).

The inverse relationship between blood lead concentration and aminolevulinic acid dehydrase (ALAD) is well known. Recently, it has been suggested that a similar relationship exists between carboxyhemoglobin (COHb) and ALAD activity. This study was undertaken to examine more closely the possible effect of carbon monoxide on ALAD. Blood from 19 human volunteers was analyzed for both carboxyhemoglobin and ALAD activity. Smokers had significantly lower concentrations of ALAD than nonsmokers and a rise in carboxyhemoglobin concentration was assocaited with a fall in ALAD activity. The in vitro bubbling of carbon monoxide into human blood did not significantly effect ALAD activity. Four groups of rats (10 per group) wre exposed to carbon monoxide or dietary lead acetate according to the following design: (I) Control--no Pb or CO; (II) 500 ppm Pb acetate in diet; (III) 250 ppm CO four hours/day X 5 days/week X 4 weeks; (IV) Both Pb and CO. Analysis of the rat data showed a significant depression of ALAD by lead. The activity of ALAD in the rats exposed to CO was significantly increased suggesting the possibility of an adaptive phenomenon.

Blood organochlorine pesticide levels in Virginia residents.

This study attempts to establish 1972 baseline levels for 31 organochlorine pesticides and industrial chemicals in postmortem human whole blood in Virginia. These pesticides and industrial chemicals have been detected previously in other parts of the food chain and environment. In the present study DDT and its metabolites, DDE and TDE, were detected most frequently and at highest levels. DDT and DDE tended to appear more frequently as people grew older although TDE levels remained constant. Dieldrin and lindane showed peak levels in the middle age group. Analyzing distribution of pesticides in blood by sex showed that females had higher levels of lindane and dieldrin and males had higher levels of DDT, DDE, and TDE. Analyzing racial distribution showed blacks with higher levels of DDT, TDE, and DDE and indicated little difference from whites for lindane and dieldrin. Higher levels were found in Richmond and Norfolk than in the Fairfax and Roanoke regions.