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Arsenic and cancer
The chemical environment-Fd were carried out on a small number of blood samples taken rrom Japanese subjects. Both DNBP and DEHP were detectable in the blood of all but two of the 25 subjects sampled. The levels were some 30 timcb higher than those of polychlorinated biphenyls
THE Arsenic
and
CHEMICAL
cancer
Reymann. F., Moller. R. & Nielsen. A. (1978). Relationship between arsenic intake and internal malignant neoplasms. Arc/Is Drrfn. 114, 378. Skin cancer has developed after the chronic ingestion of potassium arsenite (Fowler’s solution) for the treatment of psoriasis or asthma (Cited irl F.C.T. 1972. IO. IO I ) and several cases of angiosarcoma of the liver have been reported after arsenic treatment of psoriasis or after exposure to arsenical pesticides (ihid 1976. 14. 507). The paper cited above analyses the treatment records of patients with various skin diseases in an attempt to assess the contribution of’ arsenic to subsequent malignant neoplasms. Records of I61 patients with lichen planus. 72 with verruca plana and 93 with psoriasis, all of whom had been treated internally with arsenic during the period lY30--1939, were examined. Included in the survey were small groups of arsenic-treated patients with multiple basal-cell carcinoma or Bowen’s disease, giving a total group of 389. Between 1943 and 1974, internal malignant neoplasms occurred in 41 of these patients. as against an expected 44.6 calculated from figures produced by the Danish Cancer Registry. The tumour incidence was apparently not affected by the total dose of arsenic or by the form in which it was administered (potassium arsenite. allylarsonic acid or unspecified arsenicals). A further 53 arsenic-treated patients were considered separately. as they had arsenical keratoses. On average. this group had received higher doses of arsenic than the group of 389 patients, although in about 43”,, of both groups, the total dose ingested could not be estimated. Other studies have also indicated that the development of arsenical keratoses is generally dose-dependent. The group with arsenical keratoses showed a markedly high incidence of internal malignancies. but the preselection of these patients prevented any assessment ol the statistical significance of this finding. There was no indication that the internal tumours developed more rapidly in the keratosis patients. In the main group, the only significant increase in the incidence of internal malignancies appeared in women who suffered from multiple basal-cell carcinoma. While these data fail to establish any clear pattern connecting past arsenical therapy with later internal malignancies. the authors conclude that evidence for the carcinogenicity of arsenic, even in the relatively low doses that have been used in dermatology in the past, is sufficiently strong to justify cessation of the use of arsenicals in human therapy.
Cosmu~. To.~ico/. Vol. 17. No. 3
309
and were found to be considerably higher in samples taken 2 hr after meals than in those taken before meals. In only a few cases, however. were the beforeand after-meal samples directly comparable in other respects.
ENVIRONMENT The
fate
of inhaled
chromate
Langird, S., Gundersen, N., Tsalev. D. L. & Gylseth, B. (1978). Whole blood chromium level and chromium excretion in the rat alter zinc chromate inhalation. Acttr phtrrmtrc. rox. 42, 142. Workers handling chrome pigments. particularly zinc chromate. have been reported to have an increased incidence of respiratory cancer (Cited irl F.C.T. 1979. 17, 97). The possible use of urinary or faecal excretion of chromium (Cr) as an index of exposure to chromate dusts has been considered as a step in the control of this hazard. In a pilot study. three pairs of rats were exposed in an inhalation chamber to 7.35 mg zinc chromate/m’ for 100, 250 or 350 min. and their blood, urine and faeces were assayed for Cr for the next 2 days. In the main exposure experiment, two groups of eight rats were exposed to zinc chromate for 6 hr on each of4 consecutive days or nights, and their urinary and faecal excretion of Cr was determined for 48 hr in the case of rats exposed in the daytime, and for 24 hr for those exposed at night. The zinc yellow pigment used. with 99% of the particles smaller than 5 pm. had a respirable rraction of 76%. The zinc chromate concentration in the chamber varied from 6.33-8.09 mg/m3 during the day and 9.98-10.5 during the night. The Cr concentration in whole blood rose rapidly with increased exposure time. After exposure to zinc chromate dust for lOOmin there was a five-fold increase in the whole-blood level of Cr, and a further similar increase was demonstrated over the next 150 min of exposure. Blood Cr appeared to be reaching a plateau level by day 4 of exposure. There were marked variations in individual urinary and faecal Cr concentrations. but the differences were smaller in the urine. Faecal Cr excretion appeared to reflect zinc chromate that was ingested rather than inhaled during exposure, and was probably useless as an index of inhalation exposure. Urinary Cr excretion increased rapidly from the start of each exposure and fell rapidly afterwards, but there was still a surplus of chromium in the urine 3 days after exposures had ended. The chromium level in the urine may thus give an indication of recent inhalation exposure levels. There was no significant difference in the.absorption and excretion of Cr between day and night exposures to zinc chromate. Chromate
carcinogenicity
in Japan
Ohsaki, Y.. Abe, S.. Kimura.
K.. Tsuneta. Y.. Mikami.
THE Arsenic
and
CHEMICAL
cancer
Reymann. F., Moller. R. & Nielsen. A. (1978). Relationship between arsenic intake and internal malignant neoplasms. Arc/Is Drrfn. 114, 378. Skin cancer has developed after the chronic ingestion of potassium arsenite (Fowler’s solution) for the treatment of psoriasis or asthma (Cited irl F.C.T. 1972. IO. IO I ) and several cases of angiosarcoma of the liver have been reported after arsenic treatment of psoriasis or after exposure to arsenical pesticides (ihid 1976. 14. 507). The paper cited above analyses the treatment records of patients with various skin diseases in an attempt to assess the contribution of’ arsenic to subsequent malignant neoplasms. Records of I61 patients with lichen planus. 72 with verruca plana and 93 with psoriasis, all of whom had been treated internally with arsenic during the period lY30--1939, were examined. Included in the survey were small groups of arsenic-treated patients with multiple basal-cell carcinoma or Bowen’s disease, giving a total group of 389. Between 1943 and 1974, internal malignant neoplasms occurred in 41 of these patients. as against an expected 44.6 calculated from figures produced by the Danish Cancer Registry. The tumour incidence was apparently not affected by the total dose of arsenic or by the form in which it was administered (potassium arsenite. allylarsonic acid or unspecified arsenicals). A further 53 arsenic-treated patients were considered separately. as they had arsenical keratoses. On average. this group had received higher doses of arsenic than the group of 389 patients, although in about 43”,, of both groups, the total dose ingested could not be estimated. Other studies have also indicated that the development of arsenical keratoses is generally dose-dependent. The group with arsenical keratoses showed a markedly high incidence of internal malignancies. but the preselection of these patients prevented any assessment ol the statistical significance of this finding. There was no indication that the internal tumours developed more rapidly in the keratosis patients. In the main group, the only significant increase in the incidence of internal malignancies appeared in women who suffered from multiple basal-cell carcinoma. While these data fail to establish any clear pattern connecting past arsenical therapy with later internal malignancies. the authors conclude that evidence for the carcinogenicity of arsenic, even in the relatively low doses that have been used in dermatology in the past, is sufficiently strong to justify cessation of the use of arsenicals in human therapy.
Cosmu~. To.~ico/. Vol. 17. No. 3
309
and were found to be considerably higher in samples taken 2 hr after meals than in those taken before meals. In only a few cases, however. were the beforeand after-meal samples directly comparable in other respects.
ENVIRONMENT The
fate
of inhaled
chromate
Langird, S., Gundersen, N., Tsalev. D. L. & Gylseth, B. (1978). Whole blood chromium level and chromium excretion in the rat alter zinc chromate inhalation. Acttr phtrrmtrc. rox. 42, 142. Workers handling chrome pigments. particularly zinc chromate. have been reported to have an increased incidence of respiratory cancer (Cited irl F.C.T. 1979. 17, 97). The possible use of urinary or faecal excretion of chromium (Cr) as an index of exposure to chromate dusts has been considered as a step in the control of this hazard. In a pilot study. three pairs of rats were exposed in an inhalation chamber to 7.35 mg zinc chromate/m’ for 100, 250 or 350 min. and their blood, urine and faeces were assayed for Cr for the next 2 days. In the main exposure experiment, two groups of eight rats were exposed to zinc chromate for 6 hr on each of4 consecutive days or nights, and their urinary and faecal excretion of Cr was determined for 48 hr in the case of rats exposed in the daytime, and for 24 hr for those exposed at night. The zinc yellow pigment used. with 99% of the particles smaller than 5 pm. had a respirable rraction of 76%. The zinc chromate concentration in the chamber varied from 6.33-8.09 mg/m3 during the day and 9.98-10.5 during the night. The Cr concentration in whole blood rose rapidly with increased exposure time. After exposure to zinc chromate dust for lOOmin there was a five-fold increase in the whole-blood level of Cr, and a further similar increase was demonstrated over the next 150 min of exposure. Blood Cr appeared to be reaching a plateau level by day 4 of exposure. There were marked variations in individual urinary and faecal Cr concentrations. but the differences were smaller in the urine. Faecal Cr excretion appeared to reflect zinc chromate that was ingested rather than inhaled during exposure, and was probably useless as an index of inhalation exposure. Urinary Cr excretion increased rapidly from the start of each exposure and fell rapidly afterwards, but there was still a surplus of chromium in the urine 3 days after exposures had ended. The chromium level in the urine may thus give an indication of recent inhalation exposure levels. There was no significant difference in the.absorption and excretion of Cr between day and night exposures to zinc chromate. Chromate
carcinogenicity
in Japan
Ohsaki, Y.. Abe, S.. Kimura.
K.. Tsuneta. Y.. Mikami.