Document peMYgnYzQ4pzzE6eq2aMjNEww

FILE NAME: Oil Industry and American Petroleum Institute (API) DATE: 1950 Apr 28 DOC#: API067 DOCUMENT DESCRIPTION: Internal Report, Shell Oil Co. - Problems of Environmental Cancer in the Petroleum Industry S H E LL D E V E LO P l^ f& ir^ ^ ^ A N Y TO FROM $|pril 28, 1950 I C. H. EINE, M.D., CONSULTING TOXICOLOGIST s u b j e c t CERTAIN PR0BI2MS OP ENVIRONMENTAL CANCER IN THE PETROLEUM INDOSTRT As you are undoubtedly aware there has arisen in many aourcee an in creased concern about the incidence of cancer in the productive working age group. Since it is my understanding that certain Departments of the Company will have occasion in the future to have an increased contact with high boiling ani non volatile petroleum mixtures, I have prepared the following memorandum for your Information. I can see no cause for immediate concern, however, it is rightly the province of your group to have acceso to information about the problem of occupational cancer. Any chemical agent which on proper exposure, directly or indirectly, causes cancerous growth in one, several, or all types of human tissues represents an environmental carcinogen. There is considerable evidence substantiating the increase in cancer due to environmental causea. While such factors as improvement in diagnosis and treatment doubtlessly increase the number of cases recognized, there is little doubt that there ia a quantitative widening of the spectrum of environmental carcinogens. For example there has been a marked increase in the number of lung cancers recorded during the past AO years from many parts of the world. The extrinsic origin of this phenomenon is suggested by the fact that the increase has been more pronounced in males than in females. At present there is a lack of proof that a single extrinsic agent is wholly responsible for this development. It is well established that several agenta with highly different physical and chemical properties may cause pulmonary malignancies of occupational origin. In only relatively few instances can the origin of environmental cancer be traced to contact with well defined chemical agenta possessing established carcinogenic qualities. Among such compounds are arsenic, benzol, and aromatic amines, in addition to radio--active elements. . A large group of environmental tumors are caused by exposure to ill defined mixtures of organic chemicals, the carcinogenic components of which are in completely known. The members of this group include tar, pitch, asphalt, soot, crude mineral oils, paraffin oil, abale oil, anthracene oil, lubricating and fuel oil, creosote and bitumens. The highly diverse chemical and physical properties of these compounds make it improbable that they exert their specific pathogenic action on a common mechanism. Certain theories have been proposed concerning the possible Bv-tfhanl in producing cancer. The first of these theories is baaed on the known action of the aromatie aminea and carciaegans contained in tar, and 003343 -2~ ...resulting in the formations of allergens. -A second theory relates that carcino gens do not poesess.direct carcinogenic properties, hut that they* act through' ' changing sons normal chemical constituent of the cell or. tissue fluid so that it becomes endowed with carcinogenic properties. A third theory concerns agents which may cause quantitative or qualitative changes in acne intricate endocrine gland or the liver, which responds with generation within the body of abnormal endogenous carcinogenic products. Cancers of this type may be produced by hepatotoxic agents such as azo dyes or chlorinated hydrocarbons. Human contacts with soot, carbon black, pitch, asphalt, crude petroleum, shale oil, paraffin oil, lubricating and fuel oil, anthracene oil and other dis tillations and fractionation products of coal and petroleum apparently cause tha majority of environmental cancers in man. The specific carcinogenic agent or agents in these products is not known. However, it is probable that 3,.-benzpyrene account for at least a portion of this activity. . Despite the observation that tar products, petroleum, and oil shale pro ducts account for the majority of environmental cancer in man, Gafafer, on analyz ing the incidence rate of cancer among the employees of an oil refinery, did not find any significant difference from that of the general population. Hueper, an authority in Occupational Cancer Problems states that he feels that tha validity of this report is highly questionable, due to difficulty in obtaining factual data. The A.P.I. is in the process of undertaking a survey among certain members of the Institute who have kept adequate medical records; their report should be forthcoming in about a year. Information of a highly confidential type has reached me that Esso has conducted such a survey and has obtained information which is causing con siderable concern. The role which the inhalation of tar dust and fumes plays in the production of cancer in man is still unsettled. Animal experimental evidence shows that soot containing gasoline motor exhaust products cause cancer of the lungs after inhalation, or sarcoma of the subcutaneous tissue after injection in mice and rats. However, the lung cancer rate among males in Pittsburgh was found to be lower than that of any other large city surveyed with the exception of Denver. Hueper has pointed out that the great majority of cancers which can be traced to occupational origin in modern times have resulted from carcinogens which entered industrial processing during the last 50 years. In the following table are presented all* the known or commonly suspected chemical agents causing cancer that are present in the oil industry. As a general rule occupational cancers arise at the site where the particular carcinogen has the most prolonged and intense contact with the tissue. Consequently, we would expect the majority of cancers in the petroleum industry to occur on the skin, mucous membrane and surface organs. , CHH/mu cc: N. V. Jacobsen R. R. Ward 003344 _____ _ C. H. HISS, M.D., Consulting Tmlcologlst CARTER lAflLg T CERTAIN RECOGNIZED AND SOSASCTED CARCINOGENIC AGENTS BCCOONTERED IN THE OTT. IKKJSTRT ^ .... .... SHOWING THE ORGANS OR SYSTEMS CHIEFLY AFFECTED .... ~ T ~ 3~~" . .Substance ' " " ' ' ` ' Organ or System . ' M U n a and derivatives `. . . .. Bladder, ureter, kidney Anthracene, crude . Aromatic organic chamicala - ' Skin Liver Asphalt Skin Eye Benzidine and derivatives Bladder, ureter, kidney Benzol Blood forming organs Benzol derivatives Blood forming organs Chlorinated aliphatic hydrocarbons (?) liver Creosote Skin lip Eye Mineral oil, crude Skin Lip Respiratory system I5re Naphthylamlne, beta Bladder, ureter, kidney Oil shale Skin Paraffin oil, crude Skin Pitch Skin lip Bladder Eye Soot Spindle oil Tar i I Skin Bladder sttn 00334 Lip Skin Respiratory syatem Bladder Blood forming organs Eye CARTER 3539 TABIZ 1 - Page 2* . 4 A number of agents encountered in the petroleum industry elicit pre-cancerous reactions which are characteristic to a certain extent of causative agents and which represent various transitional stages between the original normal tissue wi the final cancer. In Table 2 are enumerated certain of the more common of these agents together with the portion of the body affected and a description of the lesion. 003346 CARTEK ric: a ^ -.ix,wo-TiuAuuj lAA.nrA'H AL LESIOtCS . - . *' * . . * ' * ` '* Precancerous Lesions" . ' ' ' - . Etiologie Agent ' iKIN: - Atrophy: ' 1i ' Eczema: | : Keratosis: !i1 k i S 1 . _ \ j Hyperkeratosis: l 4 j Skiir-groasly thinned and glistening . in patches, associated with . ' keratotic areas ' * Fitch, tar, asphalt, radio active substances, radia tion (including ultraviole rays). ' Dry seborrheic patches on skin Arsenic, asphalt, pitch, soot, tar. Flat, discrete, scaly area on skin with raised pearly borders. Usually on parts of skin exposed to carcinogen, but may occur in unexposed parts, par ticularly about sweat glands, with arsenic. Rough, fissured keratotic plaques with small, hard, wart-like horns, usually on hands and soles. May became nodular and ulcerate. Anthracene, arsenic, asphalt creosote, crude mineral oil paraffin, pitch, sodium nitrate, soot, tar, radio active substances, radiatio (including ultraviolet rays Verrucae: Form of hyperkeratosis. * Ulceration:_________ Breakdown of keratotic lesiona. i Leukoderma: Absent pigmentation alone. 1 Leuko-melanoderma: ijl ft| Patchy increased and absent pigmenta tion of skin. Most common in areas of highest pigmentation, and may involve oral mucosa. I Anthracene, arsenic, asphalt creosote, crude mineral oil paraffin, pitch, tar, radio active substances, radiatio (including ultraviolet rays T Melanoderma: y Scleroderma: i" Increased pigmentation alone. Dry, scaly, parchment-like akin, with ' enlarged pores, associated with leukomelanoderma Crude mineral oil, paraffin oil, radioactive substances radiation. BLADDER: Hemorrhage: 1 submucosal: * fa Papillomas: P" -- * 1ES: J Papillomas: |H ' Varying size with telangiectasia. Located mainly in trigone and about Aniline, benzidine, beta- ureteral orifices. naphthylamine and deriva Polypous or villous, pedunculated or sessile, often multiple about trigone tives. 003347 nd ureteral orifices. " Pedunculated, develop mainly on lids, occasionally on eyeball. Arsenic, asphalt, creosote, crude mineral oil, pitch, tar, radiation (including ultre^nT^t ravai. rAPTtrp i V* ,, . f- TABI2 2 - Page 2. - . . . . . Precanceroua Lesions .-. ... . . _ . Etiologie Agent BONES AND BONE MARROW: Blood dyscrasiaa: iI . I * Hyperplastic, hypoplastic, aplastic, or hemolytic anemia. .Thrombocytopenic purpura with spleen not markedly en larged. Transitory leukopenia, mono cytosis. Benzol and derivatives, radioactive subatancee, radiation. - LUNGS: ' Pneumoconioses: Chronic pneumonia : Bituminosis, asbestosis, "lipoid" pneumonia, chronic chemical pneu monia, arsenical dermatosis, chromate ulcer of hands, perforated nasal septum (chromate, arsenic). Asbestos, arsenic, tar, s oil, mist, chrome salts, -''chrome pigments, nickel carbonyl. -------------- ----------T 15 Many of these pre-cancerous manifestations regress spontaneously .from exposure ' to the causative agent ceases, however, some of them are followed by or transformed into malignant growths It is advised, therefore, to examine certain workers pjriodically for such reactions when they are known to be exposed to these carcinogenic agents, and when sue ii warning signals appear the worker should be removed from his environment. Q a D 003348 J CARTER 0 3542