• Arsenic poisoning: acute or chronic?
  • Trace elements and chronic liver diseases.
  • Homicidal arsenic poisoning.

Portal cirrhosis associated with chronic inorganic arsenical poisoning.

Idiopathic portal hypertension and chronic arsenic poisoning.

[Noncirrhotic liver fibrosis after chronic arsenic poisoning].

[Chronic arsenic poisoning of Moselle vineyard-workers, with special reference to arsenic cancer].
Soil (section 5.2.4) may be a significant source of arsenic intake, particularly for children. However, the bioavailability may vary considerably.

Human health effects from chronic arsenic poisoning--a review.

The consequences of chronic arsenic poisoning among Moselle wine growers.
The accuracy and sensitivity of the methods employed for the analysis of arsenic in the studies described above is not clear. (This is true of most drinking-water studies throughout the world at that time.) The analytical series in Taiwan in the 1960s (Kuo, 1968; Tseng et al., 1968) were performed using the Natelson method, which has later been estimated to yield an imprecision (standard deviation) of 10% at concentrations of approximately 40 µg/litre or higher (Greshonig & Irgolic, 1997). In the first, limited series (Chen et al., 1962), and in the more extensive surveys done in the 1970s (Lo, 1975; Lo et al., 1977) the standard mercuric bromide staining method was used, which was later estimated to have an imprecision of 200 µg/litre, and to be quite unreliable for concentrations 100 µg/litre (Greshonig & Irgolic, 1997).


Arsenic is a chemical element with symbol As and atomic number 33

Extensive information concerning health effects of ingestion of inorganic arsenic in drinking-water comes from a series of studies performed in Taiwan. In the late 1960s, exposure to arsenic from drinking-water was suggested to be the cause of BFD (Ch'i & Blackwell, 1968). Since the 1910s artesian wells which contain high concentrations of arsenic have been used as a source of drinking-water in the area. In 1956 reservoir water was introduced to replace artesian wells as the source of drinking-water. A contemporary account (Tseng et al., 1968) reported that by early 1966 most of the villages had drinking-water with a low arsenic concentration. Another assessment (Chen & Wang, 1990), however, based on official health statistics, presents a view that the public water supply system served only 50% of the total Taiwanese population in 1974–1976, and because the water supply system primarily served metropolitan precincts, its coverage in urban and rural townships was as low as 30% in 1975. According to data from the Taiwan Water Supply Corporation (Tsai et al., 1998), the coverage of tap-water supply was 44% in Peimen, 41% in Hsuechia, 17% in Putai and 0% in Ichu in 1957. These figures increased respectively to 85%, 79%, 55% and 25% in 1967; to 97%, 88%, 60% and 61% in 1977, and to 95%, 94%, 71% and 85% in 1981.

A further Taiwanese study attempted to investigate the association between long-term arsenic exposure and PVD morbidity, rather than mortality, using Doppler ultrasound to measure the ankle–brachial index (blood pressure ratio between ankle and brachium, ABI) (Tseng et al., 1996). A cross-sectional study was undertaken, recruiting participants in a previous cohort study. Of the 941 subjects in the original cohort, 582 (62%) took part in the cross-sectional study, so a possible selection bias may have been operating. The study had several advantages over previous Taiwanese studies of BFD, including the use of an objective and more sensitive measure of PVD (i.e. ABI) rather than the physical examination used in previous studies, individual measures of arsenic exposure and the ability to adjust for potential confounders. The study found that the risk of PVD increased with increasing cumulative exposure to arsenic, with a statistically significant increase for the high subgroup ( 20 (mg/litre) year). This association persisted when different cut-off points for ABI were used to diagnose PVD.

arsenic poisoning in Bangladesh/India

Case reports of arsenic poisoning in pregnant women resulting in death of the fetus accompanied by toxic levels of arsenic in fetal organs and tissues demonstrate that arsenite (As2O3) readily passes through the placenta (Lugo et al., 1969; Bollinger et al., 1992). In a more recent study, Concha et al. (1998b) reported that arsenic concentrations were similar in cord blood and maternal blood (~9 µg/litre) of maternal–infant pairs exposed to drinking-water containing high levels of arsenic (~200 µg/litre). Another study of an "unexposed" population in the southern USA found that concentrations of arsenic in cord blood and maternal blood (about 2 µg/litre) were also similar, and suggests that arsenic readily crosses the placenta (Kagey et al., 1977).

chemical properties, health and environmental effects of arsenic

Studies in rabbits, rats, mice, hamsters and monkeys demonstrate that arsenic, administered orally or parenterally, in either the trivalent or pentavalent form, is rapidly distributed throughout the body (Lindgren et al., 1982; Marafante et al., 1982; Vahter et al., 1982; Vahter & Marafante, 1985; Yamauchi & Yamamura, 1985). Many of these studies have used radiolabelled arsenic, and it is noteworthy that arsenic-derived radioactivity is generally present in all tissues examined (Lindgren et al., 1982; Marafante et al., 1982; Vahter et al., 1982; Vahter & Marafante, 1985).

Arsenic In Your Food Investigated - Consumer Reports

Arsenic can cross the blood–brain barrier; it is found in brain tissue after oral or parenteral administration of trivalent or pentavalent inorganic arsenic in all species studied (e.g. see Table 16). However, the levels are uniformly low both across time and relative to other tissues, which indicates that arsenic (when administered in the form of sodium salts) does not readily cross the blood–brain barrier or accumulate in brain tissue after acute dosing (Lindgren et al., 1982; Marafante et al., 1982; Vahter et al., 1982; Vahter & Marafante, 1985; Yamauchi & Yamamura, 1985; Itoh et al., 1990).