Between January, 1986 and September, 1988, the Taiwan National Poison Center recorded 97 telephone consultations (49 male, 48 female) on cases of ingestion of glyphosate-surfactant herbicide concentrate containing the isopropylamine salt of glyphosate (N-phosphonomethyl glycine, CAS 1071-83-6) and a non-ionic tallow amine surfactant. Eleven of the cases resulted in fatalities, all among those attempting suicide. The average amount ingested by survivors was 120 +/- 112 mL and by nonsurvivors was 263 +/- 100 mL (p less than or equal to 0.0001). The average age of survivors was 35 +/- 15 years compared to 54 +/- 11 years for fatalities (p less than or equal to 0.0002). Irritation of the oral mucous membrane and gastrointestinal tract was the most frequently reported effect. Other effects recorded were pulmonary dysfunction, oliguria, metabolic acidosis, hypotension, leukocytosis and fever. Fourteen patients received either atropine or pralidoxime plus atropine despite the fact that glyphosate does not inhibit acetylcholinesterase. Thirteen percent of patients received a urine test for paraquat or treatment customarily used for paraquat ingestion, possibly reflecting similar initial presentations following ingestion of these two herbicides. Laboratory differentiation is essential if any doubt exists about which herbicide was ingested. Patients ingesting large volumes of concentrated glyphosate-surfactant herbicide formulations require close observation and supportive treatment.
Monoclonal antibodies recognizing the stable imidazole ring-opened form of the major N7-guanine aflatoxin B1-DNA adduct have been used in competitive enzyme-linked immunosorbent assays (ELISA) and indirect immunofluorescence assays to quantitate adduct levels in liver tissue. Methods were developed in AFB1-treated animals, then applied to paired tumor and nontumor liver tissues of hepatocellular carcinoma patients from Taiwan. An avidin-biotin complex staining method was also used for of the detection of hepatitis B surface (HBsAg) and X (HBxAg) antigens in liver sections. A total of 8 (30%) hepatocellular carcinoma (HCC) samples and 7 (26%) adjacent nontumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent nontumorous liver samples were positive, and 9 (33%) HCC samples and 11 (41%) adjacent nontumor liver samples were HBxAg positive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These methods should be useful in determining the role of exposure in the induction of HCC in Taiwan.
Using a urinary immunoassay to measure aflatoxin metabolites, we examined the associations between exposure to aflatoxin, chronic infection with the hepatitis-B virus (HBV) and background rates of hepatocellular carcinoma (HCC) mortality in a cross-sectional survey of 250 residents from 8 areas of Taiwan with a 4-fold variation in age-adjusted HCC mortality. Specimens of fasting blood and overnight urines were used to determine HBV carrier status and excretion of aflatoxin in the subjects surveyed. While the prevalence of hepatitis-B virus carriers showed moderate variability, there was a 500-fold range in urinary aflatoxin levels. Mean log-transformed levels of aflatoxin metabolites were similar in males and females and in HBV carriers and non-carriers. In the 8 townships, HCC mortality correlated positively with both area HBV carrier prevalence and mean aflatoxin levels. The primary analyses, however, were conducted at the individual level. Each subject's aflatoxin level was treated as the response variable in a multiple regression model, and the corresponding sex-specific area HCC rate was included as a predictor along with the individual's carrier status, age and sex; alcohol consumption and cigarette smoking were also considered. In these analyses, a significant association was again observed between the marker of aflatoxin exposure and the background rate of HCC mortality. In females, the slope of the regression line was somewhat steeper in HBV carriers, but this pattern was not seen in males and formal testing yielded no statistically significant evidence of an interaction. Our findings are consistent with the hypothesis that aflatoxin plays an independent role in hepatocellular carcinoma in Taiwan.
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