Document NGYkbeGRqbg8Bnw81DbYezxNE
, halation of chlorob remove thane were narked visceral congestion, fltty degeneration of
the liver, kidney and occasionally heart, lipoid depletlon.of the adrenal cortex. In
terstitial pneiwonltls and, in animals that died, opacity of.the eyes. Such changes
were mlnlaul or absent even In nice given several consecutive dally exposures If they
were killed acre than 72 hours after the end of their first exposure. Necrosis and
cirrhosis of the liver of the type seen after carbon tetrachloride exposure was not
observed In mice, rats, rabbits and dogs even after *any Inhalation exposures.
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Katson and Dufour noted that a 2-hour exposure to 106 g/3 (tf by vol.) killed 2
ut of I gulme pigs (3).
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Constoet tnd Oierst (4) itported that rats <H#4 after # M-Hulmrta exposure to eon-
centratlons in the range 152-170 g/*3 (2.1-JJ5 If eol.) and Uft^M2J50 g/3 (2, 7-2.91
by val. )*; fstsl^feB^tte efter^ts^tmite expos urrrTwa its marcetle effects of
ehlorobrtawwethane In rats were studied In Petal 1 by these mwthorc ($). .
The present threshold limit value Is based larg. ely. m
ilv work of Torkel-
aoni, it *n1. (6f )` . These authors performed single and repeated vyor eKposwres, oral ad
ministration and topical application to skin and eyes In irlct, rats, guinea pigs, rabbits
nd dogs. In single Inhalation exposures with rats, no deaths were produced by 40,000 ''
for 0.1 hour, 20,000 ppm for 0.4 hour, 10,000 ppm for 1.5 hours or 5000 ppn for.7
Eits. la repeated Inhalation trials extending over 6 months, adverse effects were noted
fn a) 1 species at 1000 ppn. Only minor responses were observed In female rats at 500
ppu. Ha affects of consequence were seen at 370 ppm. They concluded that di1mbran>
ethrive c&mes a rather prolonged anesthesia at high concent rations and has only a
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slight capacity to produce a liver Injury
H revemfble,
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. On the basis of the above
WO ppn.
V data tew
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baen set at
btferences:
1
1. Svlrbely, J.L., Hlghwm. I., Alford, b.C., von Oettlngen, W.F.: I.'" Ind. Jta.
1t.
. X2 (1947).
High*an, 1., $v1rbely, J.l., eon Oettlngen, W.F., Alford, U.C., Pecora, L.J.:
Art*. Path. 45, 299 (114).
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1. Katson, A.F.TWfour, A.E.: Underwriters1 Laboratory, Inc., lull, of Res. Mo.
42, U.S.A. (1948).
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1 d. Cows took, C.C., Oberst, F.W.: Arch. Ind. Hyg. I 0co$. Ned. 117 (1953).
i, Comstock, C.C., Foglewan, R.W., Obent. F.b.: Arch. led. %f. IDceap. Ned. 7,
- 526 (1953).
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%t) I.
Tortelson, T.R., Oyen, F., tawe, TJL: Am. Ind. *'
^agt, 4, tL 175 (1960).
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CHLOTOoiPtecn - m ot-oam - 5ki
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Acne, systemic poisoning and avee death way rault from exposure to chlorinated
tlphenyls (1,2). A Is mt an Imiirtafcle warning rlgn of tipendlnf ,, mn severe, sys
temic toxicity. Neffs (3) hoc reported 7 cases of wild to moderate chloracne song 14
workers exposed to a few parts per million of the vapors of Arochlor (tfilorlaeted dip-
hepyl). Dm material has bttm sham to be absorbed thresh tte skin citslng fatty de
feneration of the liver (4). Treea, it al. (5) found Arochlor *1242* to be without de
tectable effect on laboratory arrivals after 150, 7-hour exposures it 1.9 f/*3 (0.18
ppm) and that 24, 7-4veur exposures at 8.6 wg/a3 were probably without effect. Trews
points out that the probtbllIty.ef Industrial occurrence of the latter vapor concen
i trations Is small, m they approach saturation; exposure to particulate matter ts con-
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gainst severe systemic toxicity but nay not guarantee complete freedom from chloracne
References:
! f '
1. Schwartz, l.: Am. J. Pub. Health 26, 586 (1936). ' ' '
2. Drinker, C.K., Warren, H.F., Bennett, G.A.: J. Ind. Hyg. I Tex. 19, 283 (1937).
3. Meigs, J.W., Alban, J.J., Kartln, B.L.: J. Am. Med. Assoc. 154, TTl7 (1954).
4. Parlbok, V.P.: Famakol. 1. Tokslkol. 17, 51 (1954).
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5. Tretsi-, JvT.,,^CTeveTand,
, Eappel. TTHttdHgy,
Am. hid. Hyg. Assoc.
Quart. 17 , 204 (1956). "
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. ' CHLORODIPHEKYL - 541 CHLORIWE - Skin * ^ -
0.5 mg/3
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From an extensive study of the penta-and hexachloro-naphthalenes, chlorinated
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diphenyls, and a mixture of these In animals by various routes of a4rin1 strati on. In
cluding chronic exposure via the respiratory tract, plus a study of Industrial expo
sures, Cecil Drinker, et al. (1,2) concluded that 0.5 mg/* 3 of chlorinated aromatic
compounds centaln1ng_more than 3 dilorlne atoms per molecule should represent the limit
ing concentration for htan exposure. '
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More recently Treon (3) studied the effects of two chlorinated diphenyl deriv-
atlves containing 421 and S4S chlorine respectively. In animals exposed 7 Pours daily
for 150 days during a period of 210 days. From the information derived from this care
fully done and extensive study, a level of 0.5 mg/m3 for chlorinated tflpheiyls containing
541 chlorine would appear reasonable for repeated dally exposures of industrial work
ers by analogy with chlerodlphenyl - 421 chlorine.
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References:
1. Drinker, C.K., Warren, M.F., Bennett, G.A.: J. Ind. Hjrg. S Tox. W, M3 (1937).
2. Drinker, C.K.: Ibid, 155 (1939),
3. Treon, J.F., Cleveland, F.P., Cappel, J., Atchley, R.W.: Am. Ind. Hyg- Assoc.
Quart. 17, 204 (1956). ^
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fS'* / X'w- C CHIOROPOM (Trlchloromethane)
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50 ppm (Approximately 250 ng/m)
Cook (1) noted that 100 ppm for chloroform Is generally accepted on the ^asls of
analogy with carbon tetrachloride whose action it resembles. He believed that this value may be high and suggested exposures be kept below 50 ppm until more data are avail able. Patty (2) suggests 300 to 400 ppm as a practical working level, but this Is ob
viously too high on the basis of subsequent experiences. Challen (3) and associates reported severe symptoms (lassitude, digestive disturbances, mental dullness) In wortars exposed to 80 to 240 ppm of chloroform and less severe symptoms In a group axposed to 20 to 70 ppm.
The limit of 50 ppm Is reccmnended as the basis of protecting against any serious short-term subjective effects and probably against long-term effects on the liver. Re
ported experience Is presently lacking on the latter, so that the TLV of 50 ppo should
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