Residues chlordane

McCaskey TA, Liska BJ. 1967. Effect of milk processing methods on endosulfan, endosulfan sulfate, and chlordane residues in milk. J Dairy Sci 50 1991-1993. 

There is much confusion among food manufacturers concerning municipal and state restrictions on the use of DDT and chlordan residual sprays in their plants. 

Chlordane is readily absorbed by warm-blooded animals through skin, diet, and inhalation. It is quickly distributed in the body and tends to concentrate in liver and fat (WHO 1984). Up to 75% of a single oral dose of chlordane administered to rats and mice was absorbed in the gut, and up to 76% of an aerosol dose was absorbed in the respiratory tract (Nomeir and Hajjar 1987). Rabbits absorbed 33% in the gut following oral administration (USEPA 1988). Chlordane residues in mammals were usually not measurable 4 to 8 weeks after cessation of exposure (Ingle 1965). Chlordane persistence in human serum and whole body was estimated at 88 days and 21 days, respectively this compares to a Tb 1/2 of about 23 days in rats fed chlordane for 56 days (USEPA 1980). 

Maximum concentrations of chlordanes in American oysters (Crassostrea virginica) taken in the Gulf of Mexico in 1976 were near 0.1 pg/kg dry weight (Table 13.2). Chlordane concentrations were substantially lower than concentrations of other organochlorines measured in oysters, such as DDT (28 pg/kg) and polychlorinated biphenyls (90 pg/kg), suggesting a need for additional studies on interaction effects of chlordane residues with those of other environmental chemicals (Rosales et al. 1979). 

Chlordane residue data for amphibians and reptiles are extremely limited. Maximum concentrations of chlordane isomers did not exceed 70 pg/kg FW of oxychlordane in eggs of the American crocodile, Crocodylus acutus, or 250 pg/kg FW in carcass of the common garter snake, Thamnophis sirtalis (Table 13.2). However, California newts, Tarichia torosa, taken near a lake treated with 10 pg/L technical chlordane had greatly elevated chlordane residues in liver and comparatively low concentrations in carcass, stomach, and stomach contents. After 14 days, livers contained about 34 mg/kg total chlordanes lipid weight — about 19% chlordanes, 9% nonachlors, and 6% chlor-denes (Albright et al. 1980). After 2.8 years, 98% of the total chlordanes was lost. 7ra .v-nonachlor was the most persistent component in newt liver, accounting for up to 55% of the total chlordanes in specimens collected 2.8 years after application (Table 13.2) (Albright et al. 1980). 

Gooch, J.W., F. Matsumura, and M.J. Zabik. 1990. Chlordane residues in Great Lakes trout acute toxicity and interaction at the GABA receptor of rat and lake trout brain. Chemosphere 21 393-406. 

Tojo, Y., M. Wariishi, Y. Suzuki, and K. Nishiyama. 1986. Quantitation of chlordane residues in mothers milk. Arch. Environ. Contam. Toxicol. 15 327-332. 

Miyazaki, T., et al. Chlordane residues in human milk, Bull. Environ. Contam. Toxicol., 25,518, 1980. 

Extremely sensitive analytical methods have been developed for the detection of heptachlor and heptachlor epoxide in various environmental and biological samples (detection limits as low as 10 ng/L). Although most methods were developed for detecting heptachlor and heptachlor epoxide in environmental media, the technology is readily adaptable to biological materials including breast milk, adipose tissue, and serum. These methods can be used to determine whether exposure has occurred. The presence of heptachlor may reflect an exposure to heptachlor or chlordane because it is a metabolite of chlordane. The presence of heptachlor epoxide may reflect an exposure to heptachlor or to chlordane since it is a metabolite of both these pesticides. However, in the absence of stable chlordane residues (e.g., nonachlor and oxychlordane), the heptachlor epoxide would most likely have been derived from heptachlor. 

MacMonegle CW Jr, Steffey KL, Bruce WN. 1984. Dieldrin, heptachlor, and chlordane residues in soybeans in Illinois 1974, 1980. J Environ Sci Health B19 39-48. 

Trany-nonachlor, a major component of technical chlordane, was frequently found as the major chlordane residue in humans, whereas oxychlordane was the major component in rats fed technical chlordane (Nomeir and Hajjar 1987). Trany-nonachlor is converted efficiently by rat liver microsomes to trany-chlordane, but this ability is lacking in humans, resulting in the accumulation of ran -nonachlor in humans (Nomeir and Hajjar 1987). 

A Michigan daily farmer, who had a history of health complaints after 1976, developed malignant cancer of the esophageal and stomach wall in 1986 the man subsequently died in 1988 (Sherman 1991). Samples of adipose tissue, collected in 1976 and 1987, revealed PBB concentrations of 0.83 and 0.85 ppm, respectively. Also detected in the fat tissue collected in 1987 were polychlorinated biphenyl (PCB) at 3.57 ppm and chlordane residues at concentrations ranging from 0.018 to 0.039 ppm. 

Kawano, M., Inoue, T., Hidaka, H., Tatsukawa, R. (1986) Chlordane residues in krill, fish and Weddell seal from the Antarctic. Toxicol. Environ. Chem. 11, 137. 

Eitzer, B.D. Mattina, M.I. lannucci-Berger, W., Compositional and chiral profiles of weathered chlordane residues in soil Environ. Toxicol Chem. 2001, 20, 2198-2204. 

Generally, levels of total chlordane residues in blood and milk fat increase as duration of exposure increases (Ogata and Izushi 1991 Saito et al. 1986 Taguchi and Yakushiji 1988 Takamiya 1987). Human milk fat contained total mean chlordane residues of <188 ppm, and blood levels were 0.015 ppm in exposed individuals (Ogato and Izushi 1991 Taguchi and Yakushiji 1988). Levels in fat and liver exceeded levels in the blood (Mussalo-Rauhamaa 1991). 

Data regarding tissue levels of chlordane residues in humans after purely inhalation exposure were not located. 

Lactation is probably the route of excretion of most interest, because of concern that nursing mothers may pass chlordane residues to their infants in this manner. Documentation of toxicity in infants induced in this manner, however, was not located in the available literature. While cis- and frans-chlordane have not been identified in human milk, chlordane metabolites and related chemicals present in commercial products (e.g., oxychlordane, frans-nonachlor and heptachlor epoxide) have been identified in human milk. Oxychlordane residues were detected in 46% of 57 human milk samples in Arkansas/Mississippi (Strassman and Kutz 1977), in 68% of 6 samples in low pesticide usage areas of Mississippi (Barnett et al. 1979), and in 100% of 50 samples in Hawaii (Jensen 1983). On a whole milk basis, mean concentrations of oxychlordane ranged from 0.002 to 0.005 mg/L (Barnett et al. 1979 Strassman and Kutz 1977). All three routes of exposure (inhalation, oral, dermal) may have been involved in the accumulation of chlordane residues in the mothers. 

Chlordane residues stored in fat in the human body are probably innocuous. It is possible that toxicity may occur when stores of body fat are mobilized in response to stress or dieting, or in the case of nursing mothers, who mobilize substantial amounts of body fat to maintain lactation, although examples were not located in the available literature. 

It is possible to measure chlordane and/or a number of its metabolites in a variety of human tissues and fluids (i.e., blood, adipose tissue, brain, liver, kidney, milk, sebum (or skin lipids), urine, and feces). Generally, total chlordane residue levels are higher in fat and liver than in the blood (Mussalo-Rauhamaa 1991). There is no information in the literature, however, correlating the levels found in these tissues and fluids with the environmental chlordane concentrations to which the individual was exposed. Furthermore, the data do not reveal how long after exposure residues may be detected in the various body tissues and fluids. 

Several components of chlordane trans- and c/s-chlordane, trans- and c/s-nonachlor, heptachlor, gamma-chlordene) were detected in the skin lipids of humans (Sasaki et al. 1991b). The samples were taken by swabbing the face with cotton soaked with 70% ethanol 3-4 hours after the face was washed with soap. Because all samples from inhabitants of an area known to be contaminated with chlordane contained chlordane residues, and because the profile of chlordane components in skin lipids closely resembled those in technical chlordane, the authors suggested that skin lipid analysis is a satisfactory indicator of dermal exposure to airborne chlordane, such as occurs in homes treated for termites. Oxychlordane in the skin lipids was positively correlated (correlation coefficient = 0.68, p<0.01) with concentrations in internal adipose tissue. The authors concluded that the concentration of oxychlordane in skin lipids was a satisfactory indicator of body accumulation of chlordane. 

A later study in monkeys confirmed that chlordane residues in skin lipids correlate closely with residues in blood (Sasaki et al. 1992). In this study, monkeys were given 5 consecutive, weekly, subcutaneous doses of 1 or 10 mg trans-chlordane/kg, and blood, adipose tissue and skin lipids were sampled up to 28 weeks after the last treatment for analysis for trans- chlordane and oxychlordane. Trans-chlordane concentrations in adipose tissue declined rapidly after the last dose oxychlordane concentrations increased for about 5 weeks and leveled off. The correlation coefficients for trans-chlordane in the adipose tissue and blood, and in the adipose tissue and skin lipids were 0.93 and 0.72, respectively. The correlation coefficients for oxychlordane in the adipose tissue and blood, and in the adipose tissue and skin lipids were 0.94 and 0.83, respectively. These data suggest that /rans-chlordane concentrations in skin lipids are a satisfactory biomarker of recent exposure, and that oxychlordane concentrations in skin lipids are a satisfactory marker of previous exposure and of the body burden (in adipose tissue) of oxychlordane. 

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