Chloroform is rapidly absorbed. Inhalation is the main route of exposure owing to the high vapour pressure and high blood/air partition coefficient (Davidson et al., 1982).

In a study of the uptake of chloroform in 16 patients under general anaesthesia (eight ventilated patients, eight breathing spontaneously), uptake was rapid with a plateau being achieved after 45-50 minutes. In spontaneously breathing patients the arterial concentration reached 25% of the inspired concentration after 1 hour, and in ventilated patients the concentration reached 20% of the inspired concentration in 10 minutes and 40% after 1 hour (Poobalasingham and Payne, 1978).

About 80% of chloroform was absorbed after a single inhalation exposure of approximately 5 mg (38Cl-labelled) chloroform in a volunteer (Morgan et al., 1970).

Chiou (1975) reanalysed the data of Fry et al. (1972) and calculated an apparent volume of distribution of 160 l for chloroform. The hepatic first-pass metabolism was estimated to be 32% and the pulmonary firstpass effect to be about 16%. So, after a single oral dose of 0.5g of chloroform, approximately 52% is available for absorption (IPCS, 1994).

Ingestion of 500 mg of chloroform in volunteers produced a maximum blood concentration exceeding 1 mg/l at about 1 hour (Fry et al., 1972). Inhalation of chloroform from an open container for 7 seconds (until the volunteer felt faint) produced a peak blood concentration of 4 mg/l at 20 minutes (Allan et al., 1988).

In a survey of 40 individuals with no known occupational exposure, all had non-detectable blood concentrations (<0.10 |g/l) of chloroform. However, 127 subjects using indoor swimming pools had an average blood chloroform concentration of 0.94 |g/l with a range of 0.10-3.1 |g/l (Aggazzotti et al., 1990). In another study, competitive swimmers using indoor pools had an average blood chloroform concentration of 0.89 |g/l, whereas none of the controls or those using outdoor pools had chloroform concentrations above the detection limit of 0.5 |g/l (Aiking et al., 1994). Chloroform is one of the trihalomethanes produced as a by-product of water chlorination.

In the industrial situation, chloroform absorption through the skin is only likely to be a problem following contact with the liquid rather than the vapour. Dick et al. (1995) examined dermal absorption of chloroform in volunteers. Chloroform in water or ethanol was applied to the ventral forearm and left on for eight hours. Absorption of chloroform was 7.8% when water was used and 1.6% when ethanol was used as the vehicle.

Toxicology of Solvents Distribution

There is limited information on the distribution of chloroform in humans. In an individual who died after inhalation of chloroform, the postmortem concentrations of chloroform were 47 mg/l in blood, 188 mg/l in liver, 144 mg/l in kidney, 74 mg/l in brain and 2 mg/l in urine (Meichsner et al., 1998). In a similar case the chloroform concentrations were: brain 113 |g/g, lung 72 |g/g, liver 178 |g/g, kidney 58 |g/g, urine 5 |g/g and stomach contents 63 |g/g (Nadjem and Logemann, 1998). In a murder victim where chloroform was used to facilitate robbery, the chloroform concentrations were heart blood (left) 280 mg/l, heart blood (right) 200 mg/l, urine 1.4 mg/l, stomach contents 21 mg/l, liver 800 |g/g, kidney 250 |g/g, lung 190 |g/g and brain 770 |g/g (Vendura et al., 1996).

Chloroform distribution was studied in mice using 14C-labelled chloroform. Following inhalation of 14C-chloroform the highest concentration of radioactivity was found in the body fat, particularly brown fat. Radioactivity was also high in the liver with lesser amounts in the blood, brain, lung, kidney and muscle. After 15 minutes there was a further increase in radioactivity in the fat. By 120 minutes, total radioactivity in the animals decreased and was essentially confined to the liver, duodenum and fat (Cohen and Hood, 1969).

This study also measured the concentration of volatile and non-volatile radioactivity in the liver. In animals killed immediately after anaesthesia the proportion of non-volatile radioactivity in the liver was 13.5%. At 15 minutes it was 43.7% and by 120 minutes the proportion was 85.6%. A similar increase in non-volatile radioactivity was also found in the duodenum (Cohen and Hood, 1969).

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