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CHEMECOLOGY
SCIENCE NEWS SERVICE
Contacts:
James P. Turner (202) 887-1206
Beverly Lehrer (202) 887-1204
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CANCER INCIDENCE DECLINING
SPECIAL REPORT INDICATES
R ECeiVED ,\j
WASHINGTON-- Contrary to widespread impressions, there is no "cancer epidemic" taking place in America today -- indeed, many scientific authorities believe that cancer incidence is dropping, according to a special report in ChemEcology, a publication of the Chemical Manufacturers Association.
Analysis of mortality trends over the past decade show that, apart from increases in lung cancer deaths linked to cigarette smoking, there has been little overall change in cancer death patterns. For people under 65, recorded mortality is dropping. For those under 45, the picture is even brighter.
Lifestyle abuses -- including what we eat and how much we drink and smoke -- are the single biggest factor in cancer causation. Many scientists believe these behavior factors may account for more than two-thirds of cancer incidence, ChemEcology
explains. Factors such as occupational exposure to cancer-causing
substances and environmental pollution account for a small portion of the cancer burden. One recent analysis of cancer deaths attributes four percent to occupational exposure and two percent to pollution.
The report cites the American Medical Association's Council on Scientific Affairs, which stated: "There is no
(more)
definitive epidemiologic evidence that the United States has experienced an overall increase in the incidence of cancer related to high levels of pollutants or contaminants in the environment."
This view is shared by the American Cancer Society. Its report on a 20-year study of more than one million Americans finds that air pollution was not a major factor in causing lung cancer. "Smoking is the key," the Society concludes.
Prevention is likely to be an increasing direction for cancer research, according to one cancer authority cited in the report. Dr. John Cairns, a Harvard professor and chairman of the Scientific Advisory Board for the International Agency for Research on Cancer, thinks epidemiology will provide the key that unlocks cancer's mysteries.
"The practical experience is to try to work out what factors in our lifestyles, our customs and our habits are the cause of common cancers," Dr. Cairns explains.
In seeking cures, chemotherapy is effective with rapid spreading and generalized forms of the disease. It is also used to supplement treatment by surgery or radiation therapy of clinically localized cancers.
Today, about 50 chemical compounds out of thousands tested have been found effective against some forms of cancer, and more are being investigated.
The American Cancer Society lists 14 cancers that a few decades ago had poor prognoses. Today, ACS states they are being cured in many cases, largely because of advances in chemotherapy.
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Dr. Philip Handler
No Cancer Epidemic, NAS President Says
These comments on risk assessment by Dr. Philip Handler, president of the National Academy of- Sciences, are ex cerpted from "The National Research Council in 19 79."
Dr. Handler, a biochemist, has been president of the academy since 1969.
Concern for the possibility of en vironmentally induced cancer has become the predominant theme ot much risk assessment.
The assertion that virtually all cancer derives from environmental factors was made in consequence of the disparate geographic distribution of diverse forms of cancer combined with the absence ot any evidence that predisposition to a locally frequent form of cancer is associated with a specific ethnic group.
The environmental postulate has been confused with the possibility of car cinogenesis due to the thousands of man made chemicals recently introduced into the economy and hence into the environ ment. It is, perhaps, conceivable that a "cancer time bomb" has been implanted into human affairs. But if so, it has not yet erupted.
On the evidence, the environmental postulate must refer to the natural, not to the man-made, world. Only a very tiny fraction of all current deaths due to cancer, in the United States or elsewhere, could be due to man-made chemicals.
Moreover, only one or two percent of cancers can be traced to occupational ex
posure in such workplaces as coal mines, asbestos mines, and factories; "pollu tants" of all sorts may contribute to -- rather than cause -- perhaps five percent of all cancers. Radiation exposure, prin cipally medical use of X-ray, occasions no more than one percent of all cancers.
Indeed, the United States is not suffer ing an "epidemic of cancer," it is ex periencing an "epidemic of life" -- in that an ever greater fraction of the population survives to the advanced ages at which cancer has always been prevalent. JC The age-corrected incidences of only
two forms of cancer have changed significantly in the last half-century: The incidence of cancer of the lung has increased markedly due to cigarette smoking, which has less dramatically con tributed to cancer of other organs. Mean while, the incidence of cancer of the stomach, formerly as prevalent in the United States as today in Japan, has declined dramatically for reasons that are quite unknown. (We've been doing something right and don't know what it is!) The overall, age-corrected incidence of cancer has not been increasing; it has been declining slowly for some years.
Those who first directed attention to the role of "environmental factors" in influenc ing the geographic distribution of the various forms of cancer -- notably John Higginson of the International Agency for Research on Cancer in Lyons, France -- are well aware of these circumstances.
f
However, they associate that varied
distribution with neither man-made chemicals, radiation, industrial pollutants, nor natural "initiators" but, rather, with dif ferences in regional "lifestyles" -- for ex ample, the relative consumption of such items as tobacco, coffee, alcohol, dietary fat, and fiber, or voluntary exposure to the sun. Indeed, neither any specific cancer nor total cancer incidence is correlated with the degree of industrialization or energy consumption per capita of dif ferent world regions.
Nevertheless, regulatory policy in the United States has heavily emphasized measures to minimize exposure to man made chemicals which laboratory- tests have proved carcinogenic in rodents. Quite apart from the social and economic costs of such measures, they are ad dressed to a relatively minor fraction of the current mortality rate from cancer of all sorts.
To quote Higginson, "There is no justification for ignoring minor hazard because a greater evil exists, but, con versely, there is no justification for overemphasizing a minor risk to the detri ment of control of a major hazard."
It should be clear that man-made chemicals and radiation are, in this sense, a relatively minor hazard that must not distract the scientific community from the task of understanding fundamental cancer biology and addressing the difficult, com plex problem of the influence of ''life style" factors on the incidence and tissue site distribution of cancer.
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The urban environment, not air pollution or occupational exposure to chemicals, is a major factor in causing cancer, Or. Harry Demopoulos, Associate Professor of Pathology at the New York University Medical Center believes.
Data from the National Cancer Institute's Third National Cancer Survey support his hypothesis, he told a meeting of the Synthetic Organic Chemical Manufacturers Association.
That survey examined seven cities with combined populations of 16 million. Four cities -- San Francisco. Dallas, Min neapolis, and Atlanta -- are "clean" cities without heavy, polluting industry. Three cities -- Detroit, Pittsburgh and Birm-
An environmental health laboratory for research and testing of existing and new chemical products has been opened by Mobay Chemical Corporation.
The 60,000 square-foot-facility will help meet the need for increased tox icology data required by government agencies about many chemical industry products.
'OBT Ths-ortes
ingham -- are "dirty," heavily industrial ized cities.
Overall cancer rates in white and black males were eight percent lower in '`dirty" than in "clean" cities, the survey found.
"If the hypothesis was correct that in dustrial air pollution or urban air pollution were a major factor in cancer causation, we would have expected to have seen that four "clean1' cities had lower cancer rates than the three "dirty" cities," Dr. Demopoulos said.
In addition, the incidence of certain sitespecific cancers such as lung, larynx, bladder and stomach, which have been linked with industrial worker exposure, were no higher in the industrialized cities
"The rapid escalation of requirements for toxicology data has placed a strain on private and public facilities (hat conduct toxicology research. This made it obvious that, from a practical and scientific stand point, the corporation's requirement in this area, could be met only with a new facility," Dr, K. M. Weis, Mobay's presi dent and chief executive officer, said.
than the nonindustrialized ones, the survey showed.
The existence of thresholds for cancercausing substances explains why the cancer incidences in the "dirty" cities were no higher than those for the "clean" cities, Dr. Demopoulos claimed.
"Now, clearly the exposures, although seemingly horrendous in the three "dirty'' cities, were well below threshold levels because there was no effect. Recall, the Third National Cancer Survey showed eight percent less cancer in the "dirty" cities," he noted.
University medical researchers are disturbed by the federal government posi tion concerning cancer causes. Dr. Demopoulos said. If society follows the federal government approach that blames industry and pollution of air and water for cancer incidence, it will be led away from answers that already are being defined through laboratory and epidemiological research.
"Whoever attempts to lead the nation toward less cancer had better be correct, because the selection of the wrong path is the equivalent of leading millions of Americans to certain death," Dr. Demopoulos warned.
Some predominant causes of cancer were analyzed and ranked at a series of symposia sponsored by the New York Academy of Sciences and the American Health Federation, with cooperation of the American Cancer Society. Looking at these causes, we do know how to avoid certain potentially cancer-causing situa tions, Dr. Demopoulos said.
Approximately 35 percent of cancer deaths are attributable to smoking high-far cigarettes and excessive consumption of distilled liquor; 45 to diet; five percent to occupational exposure, with the re mainder related to factors such as exposure to background radiation, pre existing medical conditions and certain drugs, he said.
There is evidence that the occupational exposure deaths may have peaked and are on the way down since controls have been imposed on previously unregulated chemicals. Certain types of cancer, such as those related to asbestos and vinyl chloride exposure, have reached a plateau, Dr. Demopoulos noted.
CURRENT REPORT
The OCAW brief attacked three provisions contained in the present lead standard. The provision giving certain in dustries five years to achieve the airborne exposure limit for lead was attacked as contravening the language of the Oc cupational Safety and Health Act and undermining the Act's fundamental purpose. According to the OCAW brief, the Oc cupational Safety and Health Administration, by statute, is required to provide workers with the maximum protection that is economically viable, but the Secretary of Labor in stead attempted to "minimize the costs to industry by seriously sacrificing worker health and safety."
The present medical removal provision is claimed to be deficient by OCAW, because it allows workers suffering adverse effects from previous lead exposure to continue to be subjected to high lead concentrations for long periods of time. OCAW blames this deficiency on the secretary's im permissible policy of minimizing the employer's economic costs rather than simply ensuring the feasibility of adequate protections.
The Secretary of Labor violated his "statutory obligation to constantly upgrade and improve occupational health stan dards" by exempting the construction industry from com pliance with the lead standard, the OCAW brief asserted. The union requested that three provisions of the lead stan dard -- the five year compliance delay, the medical removal provision, and the exemption of the construction industry -- be set aside.
The Act imposes on the secretary the affirmative duty to make regulations that most adequately assure that no worker will be affected by lead exposure, the union's brief reasoned. The five-year delay in compliance and the medical removal provision both violate the Act by allowing continued exposure to harmful amounts of lead, according to OCAW.
Finally, OCAW contended that the secretary's decision to deny construction workers the protection of the lead stan dard was arbitrary, irrational and inconsistent with the Secretary's statutory obligations. OCAW claimed that there is no evidence that lead poses no hazard to construction workers or that the lead standard would be peculiarly dif ficult to implement in the construction industry. In the absence of such evidence, the secretary's decision to exempt the construction industry W3S arbitrary and irrational,
OCAW concluded.
capital Ugai Foundation
An arnicas brief in the lead standard case was submitted
by the Capital Legal Foundation, a nonprofit public interest
organization Organized in 1977 to engage in nonpartisan legal
research. The foundation's brief contended that the secretary does
not have the requisite statutory authority to require medical removal protection. This argument was based on the fact'
that a provision authorizing the Occupational Safety and Health Administration to adopt standards similar to the medical removal protection provision was dropped from the Occupational Safety and Health Act during congressional debate. The amicus brief also attacked the medical removal protection provision as being an attempt to supersede or supplant state workers' compensation laws.
Safety Hazards
nUSTRY APPROVES PROPOSED STANDARD V Qf MULTI-PIECE RIM WHEELS AT HEARING
* <ustry groups voiced their approval of the Occupational
i, and Health Administration's proposed standard for Vvicing of multi-piece rim wheels at a June 19 hearing.
The proposed standard would regulate the tire servicing employees, would establish a i procedure for servicing multi-piece rim wheeh quire mandatory use of restraining devices. . develop criteria for interchangeability of rim co . clients (Current Report, April 26. p. 1689: text, p. 1702).
The American Trucking Association stated that the proposal is `'acceptable." but that the wording should be clarified to reflect more accurately the nature of the hazard as it relates to the proposed requirement. The association suggested that the proposal's definition of a restraining device is "unduly restrictive" and does not allow the use of alternative protective measures.
The Firestone Tire and Rubber Company testified that the proposed standard is "superior" and reflects "a conscien tious and in-depth consideration of the problems of truck and bus rim and wheel maintenance." In addition, Firestone noted that the economic cost is "modest."
Firestone suggested that the proposal should be modified to include 15 inch rims and wheels rather than only rims 16 inches and larger as currently proposed. The company also asserted that the standard should prohibit welding of a rim unless the tire is deflated and removed from the rim beforehand.
The National Wheel and Rim Association stated that it "enthusiastically supports" the proposal as did the Rubber Manufacturers Association.
The Rubber Manufacturers Association, which originally petitioned OSHA in 1976 for adoption of the standard, urged OSHA to act promptly in deciding on a final rule.
Private citizens, stated their approval of the proposal, but added that OSHA should require comprehensive training in vocational schools for the servicing of multi-piece rim wheels.
The comment deadline is July 6 and issuance of the final standard is expected by October 1, according to osha pro ject officer John Klocko.
Carcinogens
cAwcrffoGENESIS THRESHOLD found AT LOW DOSAGE levels in nctr study
The theory that there IS HO "threshold dose level" below Which a carcinogenic substance would be safe was supported by a recently completed carcinogenesis study using more than 24.000 mice.
The Study, conducted by the Food and Drug Ad ministration's National Center for Toxicological Research (NCTR) "has provided a massive and overwhelming ex perimental profile and data base which lends support to regulatory policies," according to Thomas Cairns, NCTR acing director.
One such regulatory policy is the Occupational Safety and Health Administration's proposal for regulating carcinogens in the workplace, which States "there is presently no means to determine a safe exposure level to a carcinogen.
"Explanation of the dose-response relationship at low doses is fundamental to the regulatory agencies posture that there is no threshold level below which a carcinogen cannot exert its carcinogenic effect." Cairns said at June 15 sym posium in Washington, D.C., announcing the preliminary
results of the study. The study, using the carcinogen 2-acetylaminofluorine
(2-AAF), was designed to determine with precision the effects of a known carcinogen at low dose levels, according
to NCTR.
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Among significant findings of the study were the follow ing:
No threshold response effect was found at the lowest dose level used in the study.
The mice in the study developed a significant number of liver tumors which did not appear until after 18 months, at which point many current bioassay tests are ended.
The incidence of bladder tumors in the dosed mice dropped substantially when feeding of 2-AAF was stopped after the first nine months of the study. However, liver tumors continued to develop after 18 months, even when dosage was ended at nine months.
800 Cans of Diet Soda
The concept of a threshold dose level has been debated by regulatory agencies and industry groups concerned with cancer risk assessment.
The controversy arises from the standard practice of testing suspected carcinogens by administering massive doses of a substance to a relatively small number of test animals. The results of such experiments are extrapolated to predict the effect of very low exposure levels on human pop ulations.
Such tests. Cairns said, "have been challenged on scien tific grounds and are confused, even distrusted, by laymen who see only the differences between the experimental process and ordinary life situations."
"The `800 cans of diet soda' perception of toxicological research and its validity is undoubtedly a serious impedi ment to the credibility of our research and the regulatory decisions that may.be based on it," Cairns said.
NCTR scientists are still examining the data generated by the study. Detailed results will be reported in scientific jour nals.
For further information, contact Jeffrey Staffa. Associate Director for Research Operations and Planning, NCTRFDA. Room 9-39, 5600 Fishers Lane, Rockville, Md., 20857, telephone t301) 443-3155.
Coke Ovens
EMPLOYER MUST FURNISH CLOTHING FOR COKE OVEN PROTECTION, OSHA SAYS
The Occupational Safety and Health Administration June 19 reaffirmed its requirements that employers must provide protective clothing for workers exposed to coke oven emissions.
In response to a complaint by workers at the Jones and Laughlin Steel Corporation, Aliquippa, Pa., OSHA stated that the coke oven emissions standard at 29 CFR 1910.1029(h) (2>(i) (Reference File, 31:8461) requires employers to provide clean and dry protective clothing at least weekly.
The Jones and Laughlin workers petitioned OSHA for a waiver from the requirements to allow them to purchase and launder their own clothing because they feared the standard did not provide for enough changes of clothing to protect them adequately.
OSHA noted that the standard requires "appropriate" clothing and equipment and special changing rooms. The standards also prohibits workers from taking protective clothing home with them. It also stated that weekly changes of clothing are the minimum requirement. Nothing in the regulation prohibits more frequent changes, the agency added.
OCCUPATIONAL SAFETY & HEALTH REPORTER
Oregon
STATE ROLLOVER PROTECTION RULE FACES TENTATIVE REJECTION BY OSHA
Oregon's job safety and health standards requiring rollover protection for agricultural tractors are not as effec tive as federal regulations and probably will be rejected by the Occupational Safety and Health Administration. OSHA announced June 22.
In its notice of tentative intention to reject the state rules (44 FR 36506), OSHA indicated that Oregon's exemption of track-type tractors was deficient. Although hearings es tablished that there never had been a rollover of these types of tractors in the state. OSHA said evidence indicated that such rollovers had occurred elsewhere and had resulted in deaths and serious injuries.
OSHA noted that it will consider exceptions filed in quadruplicate by persons who participated in public hearings on the subject within 30 days. An additional 15 days will be allowed for objections to exceptions, also to be submitted in quadruplicate. Submissions should be made to the Assistant Secretary of Labor. OSHA, U.S. Department of Labor. Third St. and Constitution Ave,, Washington, D.C. 20210.
The OSHA notice of tentative intent to reject the Oregon standard appears in the Full Text section of this Current Report.
Program Directives
OSHA DETAILS REVISED PROCEDURES FOR TEMPORARY LABOR CAMP INSPECTIONS
Revised procedures for the handling of temporary labor camp and migrant housing facility inspections were detailed by the Occupational Safety and Health Administration in a June 15 instruction.
OSHA instruction CPL 2.37, from the Office of Field Coor dination, clarified the procedures for temporary labor camp inspections in light of the Employment and Training Ad ministration's migrant housing standard at 20 CFR 620 and OSHA's own regulations at 29 CFR 1910.142.
Before inspections are undertaken, employers are to be asked which standards, or variances therefrom, they prefer as applied to the temporary facilities. OSHA noted that, where the ETA standards govern, hazards which violate the ETA standards but comply with OSHA standards at 1910.142 are not to be cited. A possible exception would be serious violations of Section 5(a)(1) of the Occupational Safety and Health Act, the instruction noted. The ETA standards may not be cited by OSHA inspectors, the agency added, but where OSHA standards are selected or for facilities con structed after January 1, 1979, 1910.142 applies.
The OSHA instruction also recommended that compliance safety and health officers should focus on facilities and con ditions which relate closely to employee safety and health during migrant housing facility inspections. Specific items of concern to the inspector include site location, adequate shelter, approved water supplies, adequate toilet facilities, first aid provisions, and facilities for laundry, handwashing, and bathing. Inspectors are required to document the age of the dwelling units; the number of units and number of oc cupants per unit; the size of the housing area; the distances between dwelling units and water supply, toilets, livestock, and service buildings; the identity of the employer; and the extent to which the provision of housing is related to employ ment, the instruction stated. If the operation of the camp is related directly to the employment of the occupants, OSHA
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Occupational Health & Safety Letter, May 8, 1982
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health, and the occupational health nurse must be able to relate the workers' environment to the commun ity at large. The nurse must take a pro-active role rather than a reactive one by educating and encouraging / employees to develop healthy lifestyles."
DR. BUNDY RETIRES FROM U.S. STEEL, JOINS NAVY MEDICAL CENTER:
Dr. Merle Bundy has retired as Director of Industrial Medicine for United States Steel Corp. and will become Medical Officer at the Naval Regional Medical Center, San Diego. Dr. Joseph J. Schwerha is pro moted to succeed Dr. Bundy.
Dr. James A. Macka;, , former medical director of bankrupt White Motor Co., has joined the medical department of United States Steel's Duquesne (Pa.) Works.
Joel Broida and Jack Shad, both toxicologists at NIOSH headquarters in Rockville, Md., have joined the National Cancer Institute.
Hank Wilson has been appointed liaison with labor for NIOSH, headquartering in Washington (not Rockville).
E. Ross Buckley, from the Justice Department, has been appointed general counsel of the Occupa tional Safety & Health Review Commission.
SCHWEIKER DISAVOWS CALIFANO'S OCCUPATIONAL CANCER ESTIMATES:
HHS Secretary Richard Schweiker has disavowed the report of his predecessor, Joseph Califano, on the estimates of cancer related to occupational factors. In a letter to the Asbestos Information Associa tion, Schweiker called the estimates too high.
The Califano "Estimates Paper," prepared by a group of HHS scientists and published in 1978, calcu lated that more than 25 percent of all cancer deaths in the U.S. could be attributed to occupational factors and that 17 percent of current cancer deaths were associated with previous exposure to asbestos. The estii mates, presented by Califano to an AFL-CIO Conference on Occupational Health and Safety, were widely publicized and caused counter-reaction by much of industry and a number of scientists.
B.J. Pigg, Executive Director of the Asbestos Information Association, had written to Schweiker to urge that the Estimates paper be formally withdrawn by the Department from the record in OSHA's cur rent review of the genetic cancer policy. It had been previously used by OSHA in development of the can cer policy, although it has never been a formal HHS position.
In his reply of April 29, Schweiker said that "more recent estimates imply that the original estimates of cancer associated with asbestos exposure were too high. Current estimates for over-all workplaceassociated cancer mortality vary within a range of five to fifteen percent. Recent estimates for the contri bution of asbestos to cancer mortality range from one to three percent."
"In sum," he continued, "the current state of knowledge does not allow us to give a precise estimate; responsible scientists simply do not agree on a single estimate of cancers caused or contributed to by envi ronmental factors, or on the contribution of asbestos in particular.
"Our mutual concern for public health dictates that we all take appropriate action to prevent expos ures to hazardous substances. Whatever the exact contribution of occupational factors to cancer, these factors remain a source of concern to this Department. Thus, the central issue is that all of us must do what we can to make the workplace less hazardous, particularly for those who continue to work with mate rials like asbestos for which society has not yet found a substitute.
"As you know, OSHA has announced its intention to reevaluate and revise the Generic Cancer Stand ard. This will provide an opportunity to consider the most recent estimates and scientific judgment about occupationally-related cancer."
In his letter, Pigg said that the claims made by the original "Estimates Paper" have been repeatedly discredited by the scientific community. "Indeed," he said, "all but two of its nine co-contributors have expressed doubt as to the Paper's correctness. It nonetheless continues to receive prominent attention and ; is often referred to as the official government position on occupation and cancer.
"We write to you now because the `Estimates Paper' has once again been comprehensively criticized in the June issue of the Journal of the National Cancer Institute. An extensive review of the causes of
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4 Occupational Health & Safety Letter, May S. 1982
incer commissioned by the U.S, Congress' Office of Technology Assessment, and written by the eminent British scientists Sir Richard Doll and Richard Peto. concludes the Paper 'should not be regarded as a seri ous contribution to scientific thought and should not be used or cited as if it were"."
EVERYONE WANTS TO CUT HEALTH CARE COSTS-BUT NOW?:
The name of the game today in occupational medicine is cutting health care costs--so it was appropri ate that the American Occupational Medical Association meeting in Toronto have a pane! on the subject for what turned out to be a commendable exchange of views--views not always known to occupational health practitioners.
For example. Steven Sieverts, vice president for institutional affairs and health care cost containment of Blue Cross and Blue Shield of Greater New York, described ways his organization--frequently criticized for providing open-ended hospital cost protection without questions--said that's all undergoing a chance.
He declared that inpatient hospital utilization is going down, fewer people are admitted to hospitals and they are having shorter stays. In addition, many of the marginal short-stay cases are being treated out side the hospital.
"We are also doing a substantial number of things with a positive thrust. For example, we are in the midst of a substantial effort to promote ambulatory surgery as an alternative to inpatient hospital care." he said. "Other less costly and more appropriate alternatives to hospital care also are being encouraged b\ our plan, such as home health which Blue Cross and Blue Shield of Greater New York pioneered during the 1950s and 1960s. pre-admission diagnostic testing, and the like."
Dr. Thomas J. Doyle, assistant vice president and chief medical officer of Consolidated Edison of New York, said that business groups are being established in several communities and coalitions are being formed to investigate the causes of continuing cost increases and to exert, collectively, an influence on cost con tainment.
He cited the experience of the New York Business Group on Health, formed with the early assistance of the New York State Chamber of Commerce and Industry follow ing successful programs of groups w ork ing together in Philadelphia.
Dr. Doyle, who is chairman of the New York Business Group on Health's Data Analysis Committee, reviewed extensive 1980 Blue Cross data and an annual comparison is planned to monitor trends and con firm progress. Each company member of the NYBGH will have access to a manual being written by the committee to assist them in evaluation of the data from their own company. The manual will also provide information for data comparison guidance with other groups.
"Benefit plan design can be modified as more cost effective alternatives are identified." he said. "The participation of physicians, health benefit administrators and others involved in health care planning through the NYBGH has been an exciting new activity. We believe the companies involved will have a more health) workforce through more cost-cfficient over-all health care as a result of this participation."
Dr. C. Craig Wright. Director of Health Services for Xerox, made the point that multiple health pro motion programs in a company can contribute significantly to reduction of health care costs. Worksite and leisure time physical fitness activities, lifestyle and behavior modification programs are all part of a larger wellness concept which reduces illness and therefore health care costs, he said.
7 hey also have a positive effect on employee self-image and sense of securit}. job satisfaction, com pany loyalty and identification, morale and productivity. Dr. Wright said.
Note: A seminar-workshop on private philanthrophy in health, to explore the private sector's support for health-relaied projects and services, will be held June 23 at the New York Telephone Co., under spon sorship of the New York Business Group in Health. Details available from the Group. 200 Madison A\e.. 3rd Floor. New York. N.Y. 1 001 6: (21 2) 561-2059.
NIOSH SAYS COAL DUST AIR SAMPLING TECHNIQUES MAY BE FAULTY:
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The possibility that coal miners may be exposed to more coal dust than the Mine Safety and Health Administration standard is suggested by a letter from NJOSH questioning MHSA's method of air sampling. The letter resulted from a request by MSHA to conduct a statistical srudy of a larger investigation of the
A full pound of cure is still a long way off
Cancer is'a genera! name attached to a variety of dis eases that afflict man and animals, and in which affected tissues enter a stage oi a neoni rolled gross th that can lead to premature death. C-ncer. in ail its forms, accounts for approximate's l of death* in the United Stales (.Table 1). Data derived from epidemic-logs. from migrant stud ies. and from occupational health suggest that SO to 90b of human cancers are due to environmental factors. most of which are made bv man and, thus, can be presented bv man.
We often note a fair!;, direct connect:-.-:; between expo sure to ccrt.'.in environmental factors <c.g.. radiation or chemicai) and cancer. 1 lossevcr. the lime clement fre
quent!}. causes coniroverss about this relationship. Forexample. a workman exposed to carcinogenic JsostuiT inter mediates for 5 sears m.is show bladder cancer 25-35 scar- later. A heavs cigarette smoker mas base overt lung cancer unis utter 30-40 sear*, of -.mokin>:. It is thus that cancer, with its long latent period between exposure and the actual occurrence of the disease, is quite different from more acute's to.xie events.
Occupational exposure is responsible for a relatisels small proportion of the annual death rate from cancer (Table 2). 1 lowever, such cases have, over a period of time, received a lot of public notice, floncfulls. increased axsarencss, new er means of detecting carcinogens, and the introduction of preventive methods will eliminate both -- occupational cancer risks and those caused b> our life styles.
Chemical e mcinogens
In recent sears sve have learned a great deal about chemical carcinogens. We have data on harmiul vs. innoc uous dosages, dusc-rcspon.se curves, threshold levels, or threshold limit values, relationship to mutagenesis, and the like.
Many different types of chemical structures can induce a neoplastic change, but this nruperts mas dtifer in ani mal models and in man. Chemicai carcinogens can be ali phatic or aromatic compounds, straight or branched chain, saturated or unsaiurated. homo- or hetcrocsclic. and also inorganic chemicals. The- can be noses, licuids.
734 CHEMTECH DECEMBER 1977
A! 0 0 0 0 44/' 0 V
!
Table 1. Estimated cancer deaths by sex for all sites--
1975*
SHe AD SUM Buccal cavity & pharynx (Oral)
Both MXM 355 000 8200
Mel* Female 199 OOO IBS 000
5900 2300
Up 225 200 25
Tongue
1950
1400
550
Salivary gland
650 400 250
Floor of mouth
525 400 125
Other and unspecified mouth
1250
800 450
Pharynx
3600
2700
900
Digestive Organs Esophagus Stomach Small intestine Large intestine (colon) Rectum Liver and biliary passages Pancreas Other and unspecified digestive
101 700 6500
14 400 700
38 600 10 600
9800 19 500
1600
53 800 4700 8500 350
17 900 5900 4800
10 900 750
47 900 1800 5900 350
20 700 4700 5000 6600 850
Respiratory System Larynx Lung, bronchus, trachea Other and unspecified respiratory
85 700 3250
61 100 1350
67 150 2800
63 500 850
18 550 450
17 600 500
Bone, Tissue, Skin Bone Connective tissue Skin
8600 1900 1700 5000
4900 1100
900 2900
3700 800 800
2100
Breast
32 900
300 32 600
Genital Organs
Cervix, invasive )
Corpus uteri j Werus
Ovary Other female genital
Prostate Other male genital
42 700 7800 3300
10 800 1000
18 700 1100
19 800 -- -- --
--
18 700 1100
22 900 7800 3300
10 800 1000
--
--
Urinary Organs Bladder Kidney and other urinary
16 500 9400 7100
11 000 6500 4500
5500 2900 2600
Eye 400 200 200
Brain and central nervous system
8500
4800 3700
Endocrine Glands Thyroid Other endocrine
1650 1150 500
650 1000 350 800 300 200
Leukemia
15 200
8500 6700
Lymphomas Lymphosarcoma and reticulosarcoma Hodgkin's disease Multiple myeloma Other lymphomas
18 600 7800
3500 5100 2200
10 000 4200
2100 2700 1000
8600 3600
1400 2400 1200
All other and unspecified sites
24 350 12 QQ0 12 350
Incidence estimates are based on rates from National Cancer Institute Third National Cancer Survey.
J After Silverberg, .. and Holleb. A., Major trends in cancer 25 year survey, ca., Cancer Journal for Clinicians, 25, 2.21 (1975).
John H. Weisburger is Vice Presi dent for Research of the American Health Founda tion, Naylor Dana Institute for Dis ease Prevention and Research Pro fessor of Patholo gy. New York Medical College. He served as Head of the Carcinogen Screening Section and Director of the Bioassay Seg ment of the Carcinogenesis Programs at the National Cancer In stitute. Author of over 225 publications. Dr. Weisburger has di rected his research toward cancer prevention, with emphasis on the gastrointestinal and respiratory tract, and endocrine-controlled organs.
or solids. But within each of these classes the capability to cause cancer is highly structure-specific. Such chemicals may also have other diverse pathologic or toxic effects, which may or may not be related to the carcinogenic ef fect.
With one exception, that of inorganic arsenical com pounds, chemicals that cause cancer in man also cause cancer in animal models. It is highly probable that chemi cals which reliably cause cancer in animals also constitute a carcinogenic hazard to man. In recent years, bioassay in animals to detect carcinogenicity is being complemented by in vitro tests through cell and organ culture, and also by examining mutagenicity in microbiologic systems. Considerably more research is required to validate the ap plication of in vitro systems to detect carcinogens reliably, even if such tests are used only as selective prescreens.
Types of carcinogens
There are several types of chemical carcinogens:
Direct-acting or ultimate-chemical carcinogens have a chemical structure such that they can cause cancer with out host-mediated enzymic activation. A number of syn thetic chemicals, industrial products, and drugs fall into this class. * Procarcinogens, which constitute the majority of chemi cal carcinogens, require host-mediated biochemical acti vation to be effective. Whether or not they will cause can cer depends on such factors as species, strain, sex. age. diet, intestinal microflora. and the presence of other agents that modify the enzymic capability. As a rule, the younger the individual, the more sensitive he is. Man is heterogeneous, and different individuals present distinct response patterns.
CocaTcinogens do not cause cancer by themselves but potentiate the effect of a carcinogen, sometimes quite dra matically. Examples are tobacco smoke, coal and petrole um tars and oils, and some natural products, such as cer tain bile acids. In contrast to carcinogens, cocarcinogens
CHEMTECH DECEMBER 1977 735
do not act irreversibly. They need to be present in sizeable amounts over long periods of time. Thus their total or even partial removal from the environment would assist in delaying or preventing the development of cancer. This is a fruitful area for additional research and development.
Current concepts hold that the ultimate carcinogen, like the mutagen, is a reactive molecule that modifies DMA. The thesis that properly activated carcinogens can be de tected because they are also mutagenic in microbiological systems is now under active investigation,
This raises the further question as to whether chemicals that are carcinogens also represent a long-term mutagenic hazard to man. Theoretically, this may well be so. How ever, the activated carcinogen would have to reach the germ cells, rather than the somatic cells, or the germ cells would have to be able to activate a procarcinogen reaching it through the circulation. There is at present no good evi dence for this; much more research is required. Chemical carcinogens are often quite toxic, especially to dividing cells, and thus at higher dose levels may induce sterility.
Threshold levels
Because active chemical carcinogens interact with DNA and yield a long-lived adduct, we consider that their effect is largely irreversible. This is in contrast to other
toxic agents and drugs, the effects of which are not herita
ble and are reversible, There is some new evidence that an.altered DNA can
be repaired through a complex, multi-enzyme system (other point metabolic activation). This may explain why under some conditions with certain chemical carcinogens a single dose does not induce cancer. However, there are other chemical carcinogens that are active after a single
dose. In any case, once a cell containing abnormal DNA has undergone DNA synthesis and mitosis, the repair sys tem fails to recognize the abnormal DNA and thus is inef fective in restoring normal DNA structure and function.
Basically for this reason individual dosages of chemical carcinogens, although given at intervals, appear to have an additive carcinogenic effect. Therefore we must combine individual doses with a time element to answer the ques tion as to whether a threshold can or does exist, a key dif ference and distinction from non-carcinogenic toxicants. Instances are known where intake of low levels of carcino gens gave no cancer, which may be evidence for no-effect levels. However, more research is required to delineate this important problem and also to evaluate synergistic ef fects. We should consider dosage and time together when selecting individuals where exposure to carcinogens might occur. In older persons, low total doses would be possible over the remaining years of employment since the total
Table 2. Proportion (%) ol cancers at selected sites for which there are sound etlologic hypotheses0
Site
Mouth (140, 141, 143, 144) Salivary Gland (142) Esophagus(150) Stomach (151) Colon and rectum (153, 154) Liver (155.0)
(155.0) Africa Lung (162) Breast (170) Cervix uteri (171) Corpus uteri (172) Ovary (175.0) Other female genitals (176) Prostate and testis (177, 178) Penis (179.0) Bladder (181.0) W. industrial
(181.0) Africa Skin (190, 191) Brain tumors (193) Leukemia and lymphoma (200, 205)
Children Adults
Cultural (.)<
90 -- 80 4 -- 70 -- 80 --
-- -- -- -- -- -- 50 -- -- --
Exogenou* lectors________________
Occup*tftonol
Iatrogenic
(to)45 (e)*
1-- ----
---- _--
----
---- ----
1-2 _
----
----
----
----
-- <1
----
<1 --
10-20 --
<1 --
2--
--2
<7 -- -- <1
Miec. <d)>
5 --
4
1 1 1 -- 8 -- --
-- --
-- --
95 __ 50 . 80 --
Congenital/Familial
Of Acquired
()* -- --
<1 -- <1 -- -- --
--
-- -- -- --
-- -- __ -- 10
<1
Unknown (Db <5 100 15 95 99 30 100 <10 100 100
100 100
99 100 <5 30-40
50 <8 98
1 __ __
92 99
After Higginson, J,, and Muir, C, S.. Epidemiology. In Cancer Medicine. J. F. Holland and E. Frei, Eds., Lea and Febiger, Philadelphia, 1973. J Unless slated, these estimates refer predominantly to a Western-type industrial population.
6 See letters in footnote For remarks. Mouth, (a) In India almost 100% caused by betel chewing. Alcohol and tobacco are main factors elsewhere. Esophagus, (a) Alcohol and tobacco major factors in France, U.S.A.; not in S. Africa, Kazakhstan, Iran, (d) Precise role of iron deficiency still to be clarified, (e) Tylosis. Stomach, (a) Role of tobacco at cardia. Colon and rectum, (d) Mineral oil possible factor. Liver (Western industrial), (a) Alcohol predominant factor. Liver (Asia), (d) Parasitic infection. Liver (Africa), (f) Role of aftatoxin and hepatitis still not known. Lung, (a) Doll estimates up to 50% of cigarette caused cancer may also be dependent on synergistic effect of atmospheric pollution. Breast. (0 Evidence concerning influence of maternal age at birth of first child, ethnic differences, familial tendency, and
possible viral transmission make ft difficult to assign etiology to the previous columns. Cervix uteri, (f) Role of age at first intercourse, herpes virus, circumcision,
and Jewishness not sufficiently clear. Corpus uteri, (f) Role of height, obesity, multiparity, and other factors not sufficiently clear. Other female genitals, (c) Maternal
stllbestrol causing vaginal adenocarcinoma in offspring. Penis, (d) Inadequate circumcision and cleanliness. Bladder, (a) Possible role ol cigarettes; (W. industrial). (b) Chemical exposure; (Africa), (d) Schistosomiasis. Skin, (d) Includes outdoor workers and others exposed to sun. <e) Pigmented spots and malignant melanoma; albinism and xeroderma pigmentosum in other skin cancers. Brain tumors, (c) Maternal and other radiation. Leukemia and lymphoma (children & adults), (c) Ionizing radiation In embryonic and adult life.
736 CHEMTECH DECEMBER 1977
3 i'-ii... 0 () 0 0 A A / J.
i
1
life span available for cancer development would be limit ed.
Background on occupational cancer
Chemical carcinogenesis actually was first observed in the last century in people who were exposed to cancercausing environments: the chimney sweeps of Percival Pott, the chemical factory workers of Rehn, and the indi viduals with radiation-induced cancer.
Because the cause of occupational cancers, once estab lished, is usually quite definitive, it is, as a rule, possible to recommend and institute successful preventive measures. In some instances, this involves total elimination of the carcinogenic factor by omitting production. Where the material appears essential for various reasons, systems can be designed to avoid exposure to staff. This includes not only a consideration of contact by production workers but also contact by maintenance workers, repair persons, and the like.
The types of cancer seen depend on a number of factors, including structure of the chemical, age and sex of the pa tient, interactions with other chemicals, length and peri odicity of exposure. At this time, we have demonstrated only about 20 chemicals or mixtures that cause cancer in man (Table 3). Exposure to these chemicals may be due to occupational and environmental settings as well as person al habits. We must be concerned both with the interaction between chemicals and possible synergistic effects. For ex ample, exposure to asbestos or certain minerals and ores in the course of mining operations has led to lung cancer. Analysis of this situation, however, revealed that lung can cer was most frequent in cigarette smokers while the risk in non-smokers was greatly reduced. The latter developed mainly mesotheliomas, not bronchogenic carcinomas. Oc cupational exposure to asbestos enhanced several-fold the risk of developing lung cancer in smokers. The risk can be lowered quite appreciably, not only by minimizing expo sure at the work place, but also by actively discouraging personnel from smoking.
There is need to examine, in detail, other such interac tions. For example, in animal models, which often mirror the human situation, we have observed interactions be tween exposure to chlorinated solvents such as carbon tet rachloride, and other carcinogens.
Radiation-induced cancer
Various types of radiation are carcinogenic to man. For instance, excessive exposure to sunlight causes cancer of the skin, which actually has a high incidence but a low mortality. Early detection of the lesions results in success ful treatment.
Skin cancer can arise occupationally in individuals who work outside, like farmers or construction workers, or vol untarily through sunbathing.
In the past, cancer incidence was also higher in staff using x-ray equipment. In modern times, much be ,er con trol of emitted dosages has been effected through various modalities, including shielding. More sensitive emulsions permit shorter exposure times, and, thus, the risk is mini mized appreciably.
Populations exposed to the atomic bomb explosions in Hiroshima and Nagasaki exhibit a slightly higher inci dence of cancer, particularly of lymphomas and leukemia. Considering the latent period for cancer development, it is possible that the sequelae of radiation exposure in 1945 have not fully manifested themselves at this time.
Table 3. Carcinogens In man*
Polynuclear aromatic hydrocarbons: soots, pitch, coal tar and products, creosote, shale, mineral, petroleum and cutting oils; cigarette, cigar, and pipe smoke
Aromatic amines: 2-naphthytamine, benzidine and derivatives, 4biphenylamine. 4-nitrobiphenyl. auramine and magenta
Alkylating agents: Chlornaphazine [bis(2-chloroethyl)2naphthylamine], mustard gas [bis(2-chloroethy!)sulfide], melphalan 4-(bis(2-chloroethylaminoy-L-pheriylalanine)], busullan (1,4-bvrtanediol dimetharvesullonate), bis(chlorometriyl)ether, dimethyl sulfate
Nickel carbonyl, vinyl chloride, acrylonitrile Isopropyl oil manufacture (process discontinued) Betel nut, nass, tobacco chewing Chromates, inorganic arsenicals, asbestos Radiation ionizing, ultraviolet (solar), x-rays, nuclear fission
products, uranium, radon, radium, thorotrast Mixtures of agents
Benzene? Mycotoxins, Senecio alkaloids, plant carcinogens? Hormonal imbalance?
Viruses?
After Wefsburger, j. H., Chemical carcinogenesis. In Cancer Medicine. J. F. Holland and E. Frei, Eds., Lea and Febiger, Philadelphia, 1973.
Major causes of cancer
The incidence and mortality from various types of can cer stem mainly from factors other than occupational ex posure. Broadly, they are the result of:
use of tobacco products, especially cigarette smoking, and
personal dietary habits,
There are interactions which, in some cases, potentiate
the effect of these two major causes. For example, lung
cancer is higher in cigarette smokers living in an indus
trial, urban environment with consequent air pollution,
compared to a similar smoker in a rural, non-polluted en
vironment. Certain cancers are the result of interaction
between two distinct types of personal habits. Cancer of
the esophagus is seen upon chronic intake of some alcohol
ic beverages and cigarette smoking. It is much less fre
quent in people who only smoke, and not seen usually in
people who only drink.
a ( ,, ,,
Smoking and cancer
All types of tobacco smoke have carcinogenic proper ties. Cigarette smoking, however, leads mainly to lung cancer because addicted cigarette smokers inhale while pipe and cigar smokers who don't inhale usually develop cancer in the oral cavity and the lip. Some smoking prac tices, like inverse smoking, lead to cancer in the oral cavi ty, both as a reaction to the smoke and the heat of the burning tobacco. The relationship between smoking of cigarettes and lung cancer has been well documented. There is a proportionality between the amount smoked, the length of time smoked, and the development of lung cancer. The age at which smoking is begun is important and inversely related to risk.
In addition to lung cancer, cigarette smoking is also a major cause, perhaps acting together with diet, of cardio vascular disease. (Diet alone in some individuals suffices to elicit coronary heart disease,) Smokers also present an increased risk to the so-called minor cancers, namely can cer in the urinary bladder, pancreas, esophagus, larynx.
CHEMTECH DECEMBER 1977 737
and other portions of the upper respiratory tract. Emphy sema is often an accompanying disease.
Prevention of tobacco-related diseases
These important diseases are quite often fatal at rela tively young ages. We must therefore develop information programs to persuade the public to give up smoking alto gether. Such programs must be directed to sensitive and susceptible age groups, probably best late in elementary or early on in high school. This is important, because the younger the individual is at the beginning of his or her smoking career, the more likely he or she will develop lung cancer and other adverse sequelae.
For the already addicted smokers, two courses of pre vention are open. One is individual and relates to enticing the smoker to participate in smoking withdrawal clinics or programs, as discussed in part by Dr. Paul White. Pro grams by the American Cancer Society and by the Feder al Government, particularly the Cancer Control Division of the National Cancer Institute, are beginning to have an impact, mainly in males in the upper socioeconomic groups. Privately operated clinics that teach smokers to stop for a fee have varying success rates. It is important to motivate the smoking public to participate and to increase the success rate of permanent withdrawal.
Exposure to tobacco smoke does not seem to lead to ir reversible damage, except after long excessive use. This is because this product consists of a mixture of small amounts of primary carcinogens with large amounts of co carcinogens, the effect of the latter being reversible. There are now data to document that stopping habitual smoking often leads to a reversal of the risk so that ex-smokers, after about 10 years, have the same risk as if they had never smoked.
The second broad means of controlling the risk is through managerial preventive medicine. Basic research efforts have led to the periodic release of data on tar and nicotine contents of cigarettes. The public thus has a choice of selecting a smoke on the basis of such informa tion. Cooperative research efforts of the Federal Govern ment, the American Cancer Society, the American Heart Association, and the relevant industries, have led to pro gressively lower tar content of existing smoking products and to new materials with even lower content of potential. ly harmful products. It is important to continue this trend and to foster the development of even less harmful smok ing materials. It would be useful to recommend also that some of the higher tar- and nicotine-containing products now on the market be progressively deleted and to encour age the greater use, if at all, of the lower risk materials. This approach has already started to yield results, for the dramatic documented increase in lung cancer rales in men in the United States for the last 40 years is beginning to plateau and, indeed, possibly to decline.
In women who started smoking more recently the in creased cancer rale has not approached t'.at of men and is not expected to reach the same high levels. .
Nutrition and cancer
Epidemiology and studies of migrant populations lead to the conclusion that a number of cancers with high inci dence and mortality result from dietary habits. In most in stances, this means that the macronutrients, and balances therein, are involved, rather than micronutrients, addi tives, or minor constituents. Again, we need more research on the contribution of micronutrients.
In the United States, cancers of the large bowel, endo crine-responsive organs (e.g., breast and prostate), ovary, pancreas, and kidneys are the result of Western-style di etary habits. These types of cancer are much less frequent in population groups with different eating habits, such as the Japanese. On the other hand, Japanese descendents living in the United States have rates comparable to those of other people living in the U.S. The key change in such migrants and their descendents is diet. Both Japan and the United States are industrialized countries with similar pollution problems, but their main cancer patterns, as re gards types of cancer and incidence of each form, are dif ferent. This fact reinforces the concept that diet rather than industrial activity per se is responsible for the main human cancers.
We don't yet know by what mechanisms Western-style diets lead to the types of cancer mentioned above or to the development of cardiovascular disease. Thus a study of the key etiologic factors related to such diets and their al teration would have impressive consequences and signifi cance for disease prevention.
The key difference between Western-style and Japanese diet is the amount of fat, particularly of animal origin, and the neutral unsaponifiable fraction, i.e., cholesterol. In the United States, 40 to 45% of calories are derived from fat, whereas in the Orient it is 15 to 20%. A number of White Papers on diet and chronic disease, including that of the American Health Foundation, the American Heart Association, and the Committee on Nutrition of the National Academy of Sciences, have recommended that Norman Jolliffe's "prudent diet" be adopted. This diet lowers the fat component to 30-35% of total calories, and recommends a daily intake of 300 mg cholesterol, or less. These adjustments in diets rely on persuading individuals or groups of individuals to alter their habits through vol untary action.
In addition, as with cigarettes, managerial prevention can be applied for nutrition-connected cancers. In this case, the success rate may be even better and possibly be achieved more readily. The U.S. food industries are an important component of industrial life and they have con siderable impact on the public through their merchandiz ing procedures, It is possible to enlist the industry's re search departments to assist in managerial prevention. Recently, in connection with a research program in the prevention of cardiovascular disease, the food and agricul tural industries have begun to produce pilot quantities of beef with a lower level of saturated fat. Also, indirectly, the high cost of grain has resulted in having cattle coming to market with leaner meat. This trend should be encour aged for health rather than immediate economic reasons. In the long run, the maintenance of improved health has, aside from its moral and ethical aspect, an important eco nomic impact.
In other areas'of the world, such as Japan or Africa, the overall incidence of cancer is also high, but the distribu tion of cancer is quite different. Gastric cancer, the main type in Japan, has declined in the U.S. over the last 40 years. This decline may stem from more wholesome food practices, especially refrigeration and the lower consump tion of meats (especially pork and ham) and fish treated with high levels of nitrate or nitrite-containing preserva tives. At the same time, improved supplies of micronu trients, vitamins from fresh fruits, vegetables, and salads may counteract nitrite and provide belter tissue integrity. Similar such trends are also evident in Eastern Europe,
738 CHEMTECH DECEMBER 1977
and even in Japan. Other types of cancer (liver, esopha gus) are likewise due to environmental and dietary prac tices prevalent in Africa or'southern Asia, and would re spond to a modification of habits or agricultural practices.
Micro-elements and contaminants in water consumed by man play, as yet. an undetermined role in the develop ment of cancer. Workers in the asbestos industry not only have a higher risk of pulmonary disease, but may also have a higher risk of cancer in the large bowel, presum ably because of ingestion of asbestos. These data need confirmation, and in fact more research is required to de fine the role of small amounts of contaminants such as as bestos, petroleum derivatives, hydrocarbons and halogenated derivatives thereof, phenolic components, and inor ganic chemicals in public waters. Nonetheless, it would seem that assuring the purity of water, to which everyone is exposed from birth, would prevent possible synergistic interactions between environmental factors and such water impurities.
It thus appears that individual and managerial alter ation of diet, of smoking habits, and products, and to a lesser but more feasible way, of occupational situations, would go a long way toward a necessary decrease in a se ries of neoplastic and other chronic diseases, which lead to untimely death.
Personal hygiene and cancer
Cancer of the cervix and, to some extent, cancer of the penis, is seen in population groups with poor sexual hy giene. Recent implication of herpes-type viruses with these types of cancer may open the road to prevention. An im mediately feasible preventive action is through the teach ing of individual sexual hygiene and the managerial devel opment of housing that permits proper hygiene practice. Also, early detection of neoplastic lesions by regular phys ical examinations, including "pap" smears, especially in high-risk groups, contributes to secondary prevention by reducing mortality caused by advanced disease.
Mutagenesis
The relationship of carcinogenesis and mutagenesis is being used to develop a test for chemical carcinogens through mutagen screening in microbiologic systems, a much faster process than carcinogen bioassay in animals. Procarcinogens properly activated to ultimate carcinogens are usually mutagenic. However, not all mutagens in mi crobiologic systems are carcinogenic.
It is difficult to assess the potential mutagenic hazard from exposure to chemical and environmental carcino gens. There is a given incidence of births with genetic ab normalities. Some of these relate to a recessive trait that is expressed by combination of alleles. This problem is being studied extensively. Early detection in high-risk groups through genetic counseling and also aminocentesis pro vides the means of jucicious decision-making.
Exposure of father or mother to mutagenic environmen tal agents may result in offspring with genetic abnormali ties. This area requires further research. In fact, more data are needed just to define the limits of the problem.
Teratogenesis
Teratogenic events are due to abnormal transcriptional features during differentiation of the fertilized ovum and as such are quite distinct from mutagenic or carcinogenic events.
Physically or mentally abnormal newborns constitute a portion of live births. As in the case of genetic abnormali ties, a fair proportion of abnormal-offspring are due to un known causes, There is evidence that exposure of the fetus to radiation and to specific chemicals (e.g., thalidomide) results in malformed individuals.
It is true that some carcinogens can also act as terato gens. In the majority of instances, however, this is not so. Thus bioassay systems to detect carcinogens cannot be used as a rule to develop information on the possible tera togenic effect of a chemical or a mixture. The effect of teratogens is revealed usually in multi-generation studies, utilizing several species since not all chemical teratogens act alike in diverse species. Clearly, we need more re search in this area.
Recommendations
t. Life-style related cancers
A. Tobacco. Both human and animal evidence support the view that several types of cancer, especially lung, mouth, and larynx cancer, and non-neoplastic diseases such as emphysema and cardiovascular diseases are caus ally related to smoking
Exert major efforts to develop smoking withdrawal clinics. Advise the public of the consequences of smoking, and the hazards of starting to smoke at an early age.
Accelerate research on the development and appre ciation of less harmful smoking products.
Develop more information on the interaction between smoking and other environmental or occupational situa tions leading to synergistic augmentation of the hazard.
Develop more information on conditions other than cancer that stem from smoking, such as emphysema and cardiovascular disease.
B. Nutrition. In various parts of the world, the main
human cancers are associated with one of several dietary conditions. Efforts need to be made to perform more re search to validate current concepts and to secure changes in the mode of living and dietary environment for the de finitive prevention of several types of cancer.
Breast, ovary, endometrium, and prostate cancer ap pear associated with high diet intake of fat. We must have more research to secure knowledge about the underlying mechanism. Inform the public of the need to lower the fat intake and adopt the "prudent diet" in which fat is at the most 35% of calories, and cholesterol is less than 300 mg per day. Inform the agricultural and food industries of the need to distribute and market products with lower fat and cholesterol content.
Colorectal cancer. This disease is also associated with high fat intake and adoption of the "prudent diet" by the public is indicated. More research is needed to gather an understanding of the mechanisms involved in its devel opment. We should encourage managerial prevention through work with the food and agricultural industries in lowering the fat content of foods, especially of meats and dairy products.
Gastric cancer. Gastric cancer appears associated with the consumption of foods containing a high carbohydrate/fat ratio, low micronutrients, and sizable amounts of nitrite or nitrate. Detailed investigations are needed to document the underlying mechanisms. We must advise the public of the need to store food at low' temperatures to
CHEMTECH DECEMBER 1977 739
prevent the formation of nitrite from nitrate through mi crobiological reduction. Also, improved diets with respect to micronutrients, especially vitamin C, a nitrite antago nist, should be recommended. Managerial prevention in cludes control of the addition of nitrite and nitrate to foods. This area is currently under discussion by USDA and industry Advisory Groups.
H. Occupational cancer
Exposure in an occupational setting to certain chemi cals or mixtures has resulted in cancer in man, sometimes after a long, latent period. With few exceptions, the prod ucts responsible have also caused cancer in animal models. We must
minimize exposure of workers, maintenance people, and allied personnel to known chemical carcinogens;
avoid the release of chemical carcinogens into the en vironment through air, water, or solid effluents, including sewage, where the public at large might be affected;
take advantage of the data generated by the National Cancer Institute, the National Institute of Environmental Health Sciences and other programs, on improved and more rapid methods of bioassay, including mutagen test ing, to acquire information on, as yet, untested chemicals
to which individuals may be exposed. Perform bioassays of chemicals revealed by such prescreens, and for which ex posure parameters of specific groups or the population at large denotes the existence of potential risk;
in view of a number of lines of evidence mentioned in this document on the lesser sensitivity of older individuals to chemical carcinogens, and considering the latent period required for overt cancer appearance, select older individ uals, typically above age 45, for employment in situations where contact with carcinogens might occur. Of course, as noted above, systems should be designed to ensure mini mal exposure to actual or potential carcinogens.
III. Prevention of cancer
(1) Develop additional research efforts on the causes of all types of cancer and the mechanisms of carcinogenesis in order to provide a sound and reliable data base for the elaboration of rational preventive measures.
(2) Establish health-action groups to give wide publici ty to currently available methods of cancer prevention.
(3) Through informational, managerial, and legislative efforts, lower the cancer risk of the work environment, and the risk from personal habits, such as smoking and poor dietary practices.
Current reading references
Arcos, I.C.. Argus, M.F., Chemical Induction of Cancer, Academic Press, New York, 1974.
Becker, F.F., Ed., Cancer. Plenum Publishing Company. New York. 1975. Casarett. L.J.. Doull, J.. Eds., Toxicology, The Basic Science ofPoisons. Mac
millan Publishing Co., Inc., New York, 1975. Doll, R., Vodopija, L, Davis, W,, Eds., Host Enoironment Interactions in the
Etiology of Cancer in Man. JARC Scientific Publications, No. 8, International Agency for Research on Cancer, Lyon, France, 1973. Hathway, D.E., Foreign Compound Metabolism in Mammals, Vol. 2, The Chemical Society, London, England, 1972. Hollaender, A.. Ed.. Chemical Mutagens. Principles and Methods for Their Detection. Vols. 1 & 2, Plenum Press, New York, 1971. Holland, J. F,, Frei, E., Eds., Cancer Medicine. Lea and Febiger, Philadelphia, 1973. Hamburger, F., Ed., Phystopathology ofCancer. S. Karger, Basel, Switzerland, 1974. Huepcr, W.C., Conway, W.D., Chemical Carcinogenesis and Cancers. Charles C Thomas, Springfield, III., 1964. Schotienfeld, D,, Cancer Epidemiology and Prevention. Current Concepts, Charles C Thomas, Springfield, III., 1975. Ts'o, P.O.P., DiPaolo, J.A., Eds., Chemical Carcinogenesis. Parts A&B. Marcel Dekker Inc., New York, 1974. Wynder, E.L., Hoffmann, D., Tobacco and Tobacco Smoke: Studies in Ex perimental Carcinogenesis. Academic Press. New York, 1967. Busch, H., Ed.. Methods in Cancer Research: serial publication currently vol. 10, Academic Press, Inc., New York, 1973.
Homburger, F., Ed,, Progress in Experimental Tumor Research: serial publi cation, currently vol. 19, S. Karger, Basel and New York, 1975.
Klein. G., Weinhouse, S.. Haddow. A.. Eds., Advances in Cancer Research: serial publications, currently vol. 21, Academic Press, Inc., New York. 1975.
Wynder, E.L., Ed., Preventive Medicine; serial publication, currently vol. 6, Academic Press, Inc., New York, 1977.
McCann. J.. CHEMTECH, Nov. 1976, p 682. Williams. G.M., Cancer Res.. 37, 1845-1851 (1977).
Author's address: Naylor Dana Institute for Disease Prevention, American Health Foundation. Valhalla, N. Y. 10595.
Research in the laboratory of Dr. Weisburger is supported in part by Public Health Service Grants CA-12376, CA-I4298, CA-15400 (National Large Bowel Cancer Project). CA-17613, Contracts CP-33208, CP-55705, CP65818, CP-75978 from the National Cancer Institute, ES-6-2130 from N1EHS, and grant OH-00611 from NIOSH.
This review is based on a document developed for Task Force II, Theory, Practice and Application of Prevention in Environmental Health, part of the National Conference on Preventive Medicine, sponsored by the Fogarty International Center of the National Institutes of Health, Belhesda, Maryland, and the American College of Preventive Medicine.
Adapted from Journal of Occupational Medicine. Vol. 18, No. 4, April 1976.
OPERATION HALLEY'S COMET
From the Colonel "Tomorrow evening at approximately 2000 hours
Halley's Comet will be visible in this area, an event which occurs only once every 75 years. Have the men fall out in the battalion area in fatigues, and 1 will e> plain this rare phenomenon to them. In case of rain, we will not be able to see anything, so assemble the men in the theater and I will show them films of it."
Executive Office to Company Commanders "By order of the Colonel, tomorrow at 2000 hours,
Halley's Comet will appear above the battalion area. If it rains, fall the men out in fatigues, then march to the theater where the rare phenomenon will take place; something which occurs only once every 75 years."
740 CHEMTECH DECEMBER 1977
Company Commanders to Lieutenants "By order of the Colonel in fatigues at 2000 hours
tomorrow evening, the phenomenal Halley's Comet will appear in the theater. In case of rain, the Colonel will give another order, which occurs once every 75 years."
Lieutenants to Sergeants "Tomorrow at 2000 hours, the Colonel will appear
in the theater with Halley's Comet. If it rains, the Colonel will order the Comet into the battalion area in fatigues."
Sergeants to Squads "When it rains tomorrow at 2000 boars, the phe
nomenal 75-year old General Halley, accompanied by the Colonel, wilt drive his Comet through the bat talion area theater in fatigues."
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/ Mm Mi hrsdUn# prmblemm he |Ml *br wmlM *r m. 7 vwt
MM peflwrtMnm. jtome ^ the draw are n>tnl IrHhuC and
Instances, of nonregular heavy exposure during accidental leaks and/or spills at worksites. In these case* the average exposure may be
Tor the worker that has developed Iaocyanate sensitivity, there la usually such a decrease In the FEV.
over the woriodvlft.
MM are Mitri aMMur.* r MMl l an by nwlelM
under the 8-hour time-weighted tandsrd.
EAST TEST Art there any blood or akin testa
MM<lr mM mU / men Mn/M
How doe* the doctor make the
which can 100 percent confirm the
NtaMI asthma, bat be vMfdat
diagnosis of Isocyanate sensitivity
diagnosis of Isocyanate sensitivity?
Ma /br an satfl be MM mm MM MM FOT awl a CAST teat (b<rt |WMI me awe about thzss
equal Isocyanate Induced asthma? Most Important to a work history of exposure to Isocyanate* (don't
The answer atthe present time Is no. Obviously, it would be useful to haw a simple Mood test in order to screen
MWf IV doeer mmiImmI Che Mi mt
*r----. `MM,* `toJtarvfc'
expect your family doctor to know anything about them) and a medical history of recurrent shortness of
ter sensitised workers. However, the
varioes blood teats that have been developed to measure 'antibodies'or
mmd
rtberflaa, fM le Me
breath, cough and possibly wheezing
proteins made by the body to stick
e|0bM batman all tbeaef I*
that occurs after exposure. In the
onto foreign substance* such as
IVi I a bare for Job re/afed
antkmmf
case of liocyaaate asthma In partlcetar. or occupational asthma
toocyanate molecules, haw thus hr proved unreliable. The RACT test is
Dear ICWU Member
in general, shortness of breath, chest
one such test that unfortunately Is
. Aa yon already know from jour van experience, exposure to poly urethane* from either their produc tion or urn can cauee or women breathing problem*. Polyurethane*
lAWTAMIAprodnet*--foam, lacquers,coatlr^
of aO aorta -- are need widely In tha American economy. Polyurethane to
I a polymer, bi other word*, a chain of
tengleafethawe Malta. Myuvertoatkm of vretbanaa Involve* the urn of toocyanatea. taoeyanatea are a poop of chemical compound* that are tut of the moat `sensitising' subatancee known to exlat In the Indaatrial environment
ht do are mean by aetvsZUdng?
X-BAV9Senatttxatkm to a auhatance mean*
that the body haa developed the tendency to react In an exrasahw way when axpoeed to the offending substance. Btpoeure aaually occun either through Inhalation ar akin contact Airway* hypers*nshMty or aathma occur* after expoidre throw |h breathing; contact
i tightness and cough are more frequently found than wheezing. Wheezing Is usually found in classic allergic asthma. Symptoms of occu pational aathma won't occur Immediately after expomir* to the offending agent; they may not occur uadi 48 Hours after' exposure. In other words, after the worker to already at home. That to why you have to help the doctor make the dtagnoato. He or 4** I* unlikely to think ofR withoutyourtalktoigap the reintionshtp to work. An extremely Important question la, do the symptom* go away on weekends and vacations?
<3iest x-ray* are almost always normal with asthma of any kind so they wont be of much use In diag nosing occupational asthma. Breathing tests are of much more uk, but only during and perhaps Immediately after an attack of asthma.
not always poaith* when a worker has Isocyanate asthma and Is not always negatha when an exposed worker la weft. Skin tests have proved equally unreliable.
You Uao asked about 1rrttant'sub stance*in your shop. Manychemteats Including some dusts, vapors and fume* are directly Irritating to the lining of the respiratory tract. It to quite common for occupational doctors to see workers with chronic bronchitis or inflammation of breathing tube* due to long term exposure to Irritating subatancea such as ammon|s, sulfur dloxkle, nitrogen dloxkle, chlorine, ozone, manganese, chromium, silks, arid mists and FTuortdes-
It luma out that In high concen trations, laocyanatea are quite Irritating and will cause respiratory symptoms in moat workers, not just those who are toocyanate sensitized. One clue that a substance to directly
denaatttto and/or hbaa occur* after
UJWG FUNcnoH nm
irritating rather th*h sensitizing, Is
exposure throa^i *Mn contact
When an attack of asthma occurs
the finding that most people on the
To pat hawk . to laocyanatea,
the bronchi or breathing tube*
job seem to complain ofbumlng eyes,
approxtooaitatyB partttot of woricar*
become narrow so that It to hard to
nose and throat when exposed to the
;1.9
expoaad to AM Ah U^#)ob can be
exhale after taking In a breath; there
airborne chemicals.
x> expacaad ta devaldp' aenMtivUy tc
to an obstruction In exhalation. This
Workers with chronic bronchitis .
r them, aaaaflytn the form of aathma.
obstruction usually reverses Itself In
win usually Improve with reduction
Expo*ore to iaocyanate occur*
time but the process can be speeded'
of exposure. Exposure ran be
before the polyurethane roam or
o lacquer totallypolymerised. Once the o polyurethane la complately
up with the use of certain medication. In other words, asthma Is- a reversible obstructive lung
reduced through Improved ventilation, enclosure of the work process, or adequate respiratory
potymu tod or set," there ahould be
disease. If breathing tests are done In
protection. Worker* with occupa
IKtie or no free Isocyanate present
between asthma attacks, they win
tional asthma, on the other hand,
Once sensitivity to an toocyanmte ha*
usually be normal.
often have to change jobs to get
developed, the sensitized worker la
rev.
completely away from the substance
often not able to work where there
The most Important breathing test
to whkh their airways are sensitized.
are even minimal concentration*
for occupational asthma to the FEV,
Even If they are taking anil-
peasant Reaction can occur at
(forced expiratory volume In one
anlhmalk drugs, the sensitized
exposure level* below the QftHA right
second) which I* the measure ofhow
worker may have to change jobs lo
hour time-weighted average thresh-
much air a worker can blow out In
avoid further Illness.
hold limit value (TLV). The current
one second with the maximum effort.
Dr. Mark Callen
HEALTM ft SAFETY NEWS
Cancer . . . Is A Six-Letter Word!
Cancer is a word that to frightening to moat people. And a look at some statistics for this disease provide*ample reason for such a reaction.
One nut of every four Americana can expect lo get cancer.and two out of every three families will haw a member who develops some form of cancer. Although rarly diagnosis and improved treatment techniques Increase th* Chance* of survival, the rate of cancer deaths (and reported cases) to rising. In 1873.361,000 American* died ofcancer, but by 1976 the numbers had increased lo 384.000.
One reason more case* are seen had to do wKh our Increased Ufe expectancy. There I* a long delay between exposure to a cancer causing substance and appearance of the disease. Since life expectancy to greater today, more people live long enough For cancers to appear. But the Increased rate ofcancer cannot be explained antriy by longer life span. We must took beyond life ex pectancy and examine the evidence which points to potential occupational and environment*! cause*.
This article will explore what cancer Is. potential and known causes, testing of cancer suspects, regulation of car cinogens. resources, and prevention of ranret. Because evidence strongly points to occupational and environ mental exposures as mftor causes of cancer, the article focuses on thta aspect.
CANCE* -- WHAT IS ITT
The term 'cancer*describes a number of different diseases with a variety of causes. But basically, in all forms of cancer the body's cell division system becomes damaged, which leads to a rapid, out-uf-conlrol growth of ahnormsl cell*. Generally cancer starts iff as a disease localized In one area (often on the surface of an organ such * the akin or liver). As growth continue*, the rancer can spread deeper into the organ and evcnftially spread to other pHrla of Mir h>dy (metastasize) by way Ilf the IiIihkI nr. lymph systems.
WHAT CAUSE* CANCEST IVre are many substances in our environment that are linked to develop ment of rancer. In fact, environments] poUutanta tot air, water, soft, and the workplace are now estimated to cause bttwti.li 76 and 86 percent of eB human cancers. The Increase in manufacture and uk of petrochemical* to directly connected to the proliferation of tancer-causing aubatancea In the environment.
I 't A *1 `o
*\ <
Although we often hear that 'everything causes cancer,* this is not the rase. From human sturile*. about 3ft substance* or agenls have been Identified as rarclnogens. and about 641
others ahow evidence ofcarcinogenicity faMtfcy lo cause cancer) based oa epidemiological evidence. Knows cancer-causers (carcinogen*) Include chemicals such as benzidine and other organic amine*, mbestos. nickel and chromium, benzene, and arsenic, a* well as Ionizing radiation and ultraviolet radiation.
Some cancers seem to have multiple cause*, and exposure to mom than am carcinogen may Increase risk of rancer development. Tor example, both cigarette smoking and asbestos are linked to Increased tuiW cancer rtoh. Aabestoa Workers who donlamofce have att right limes greater risk ofdeveloping lung cancer than an anexpoaad popula tion, while asbestos workers who do tavtoke hare a 98-thnes greater chance when compared to an unexpoasd population. On the whole, however, the potential for producing cancer when two chemicals Interact la largely unstudied.
Although all occupational and environmental carcinogen* have not been Identified, there are numerous substances which are considered human carcinogen* based on results of rpldemlologlral studies m well as animal studies.
'TRACKING DOWN CAECINOOENB
Unfortunately, the malorlty of known rmrrlndgens have not been discovered by any systematic method of testing rriemlcato before Introducing them kilo the workplace or general environment. Instead, workers have been exposed to subatancea for many years, and after Increased cancer rate* are aeeh, confirming testa In animals may he con Hurled Because moat chemical carcino gens haw a long latency period (time between initial exposure and the appearance of cancer), by the time a chemical la confirmed as a cardnogen large numbers of workers may have already been exposed.
Epidemiological studies are one of the msijnr methods for determining that a
(ronllnoed on next page)
i
chemical It carcinogen. In such t study, aeieatlscx follow a grou p of people who haw been exposed to a certain subUK*. They compare the number of cancer cun and deaths with a similar group (control group) who were not exposed to the lubatancr. Epidemiologjeel studies are the beat evidence that a substance la a human carcinogen. Their obrjcu drawback la that people continue to be exposed white waiting for tha results. So we have a altuatlon where, aa BUI Lloyd of OSHA ha* aald, "Akwoat everything we know now about occupational cancer comet from count ing dead bodlea."
Ofrviouaiy other method* tnuit be uaed to determine If a chemical la capable of causing cancer. The moat widely uaed testa are long-term animal Studies, although ahnrt-term teat* tn bacteria Insect*, or plant* are being uaed mote frequently.
ANIMAL TESTS
The basic aim of an animal test la to measure the effect* of exposing * particular group of animal* to a*peclflc substance. Two groups of animals are used: experimental (exposed to the sub stance) and control (unexposed). These groups are further divided into *ubVoups, e.g, 60 animal* of one sex and specisa Generally, testing Is performed hi two strain* of animals. Because of
their short Weapon (shout lour year*) rata, mice, and hamsters are the common teat animal*.
The anLmais are normally expoaed In the way that moat closely resemble* human exposure (for example. Inhala tion of asbestos fibers) OenemUy, at least two doses should be used: the maximum tolerated dose, which b the largest dode that wW not shorten the atanalb Ufeapan by causing adme other toxic effect; and either one-half or onequarter of that doe*. At the end of the teat period the animal* are killed and their organ* examined for evidence of cancer. If the number of cancer* In the expoaed group la significantly greater than la the Control group, the subetence I* considered a carcinogen.
Animal testa are considered ap
propriate tn determining the cancer-
causing potential of a substance
because evidence of carcbtogenicky In
animal testa agrees with known human
experience. OneacSenUat who reviewed
animal teat dtofcda ffl substance* for
which then
nfM.tptdemtologic*!
evidence of Mmtiui ``carcinogenicity
found that only one of the chemical*,
araeote, did not cause cancer In lest animals.
Although meat scimtlau agree that ehemlceli which cause canrer in
Common Chemicals and Cancer Risks >
Agent
Arwnk (S) Atoe*u>s (B)
prnwne Chromium PCME (bi* chleromethjl ether) genzldine (R) Alpha-nBpthrfamlM (R) Beu-napthytamlne |R) t-aminodlphenyt (R) 4-nKrodlpheayl (R) Wood dual
Coke oven byproducts | R), shale, and mineral oU* Vinyl chloride (ft) AneWhetlc* leiraviojei radlstloa Uranium (radon daughlrn)
Caster Site
Rtin, lunge Brer Lange ptcoral and prekseteal meaoUwRamfcB rectum Bone marrow (leukemia) Nasal cavity, Mrynx, lung Lung Bfedder Bladder Bladder Bladder Bladder Nasal cavity and skmae* Nasal caWly. larynx, lung, skin, scrotum
Uv*r. brain ffeM marrow (leukemia) SUn Lung
humans wil also cause cancer In new chemicals introduced Into the
animals, the reverse ke not true. One workplace each year, but also to test
major reason that people realm using those already in use. So there Is a great
animal teat data u> predict effect* In deal of interest In short-term lest* such
human* relate* to dose. The dose* given as the one developed by Bruce Amei at
to test animal* are high, and this leads the University of Cattfomia, Berkeley.
to the misconception that anything will The teat Identifies substance* which are
cause cancer If the dose la high enough. mutagen* (capable of changing genetic
Vet, numerous chemical* have been material). Ames and other scientists
tested in animals at the normal high believe that most muutgeni are also
doses and have not been found to be carcinogen* In fact, nearly 90 percent
carcinogenic.
of those chemicals which are known
High doses an* used *o that the poimible effects win be easier to detect,
since the group of test animal* I* rela tively small when compared with the number of potentially expoaed humane For example, what If a low dose of a substancecaused cancer In one ofevery 10.000 persons (or 10,000 tumors bi 100 million American*)! If you used the same corresponding dose In a group of 60 rats (a* opposed to 10,000 rats) clearly the chance ofcancer showing up
carcinogens test positive aa mutagen* In the Ames teat. Numerous other short term testa are in use or being studied.
Despite problems with short-term and animal tests, some such testing program must continue. Fast experi ence with sibesto*. BCME, vinyl chloride, and numerous other carcino gens has clearly shown thst we cannot wait for absolute proof of carcinogeni city in humans before regulating exposure to potential carcinogens
would be minimal. Reliable conclusions can't be drawn from such a small test
PREVENTION
Kple In addition, the costs of using a r number of test animal* would be
Because the vast majority of cancers are caused by agent* In the
prohibitive. When dose* are high, theenvironment, h follows that they are
cancer* are more likely to be men In a potentially preventable -- remove the
mU group of test animals because the substance, remove the risk. Experience
cancer rate would be Increased propor has shown, however, thst It Is not that
tionately. And negative result* at high simple. In fact, this country has failed
doae* Increase the likelihood that the abysmally In controlling exposure to
substance le not a carcinogen.
carcinogens. When other countriel have
banned substances (for example, Italy
OTHEt TESTS
and England banning benzidine and other organic amines) the II.S. has
Because animal teat* are expensive continued its quest for 'safe" exposure
(up to $400,000 per teat) and involve at least U.6 to 4 year* per test, it would be sn impossible task not only to lest all the
levels. So despite knowledge of rsrclno genicity, workers continue l<> Ite exposed to benzene, coke oven emit
alona, asbestos, and other carcinogens. should receive a copy of the carcinogen
And In many cases they continue use report form.
working without befog told that sub stances to which they are exposed cause, or are suspected of causing cancer.
Efforts must be made to find and contact workers formerly exposed to cmctnqgraa, *o that they can ba channeled Into aereeobvg programs
The reasons for this country* foist* aimed alearty detection ofcancer, and
to regulate carcinogens and adequately receive medical smaikm Ifniciwny.
protect worker* and the genscol public
Bmsarch M nttabfo sbort-tarm
include:
Mta to kfowUfr rsiitouffnaffionhl ba
Pressure from industry related to : pcrfcrmod.
economic coma tM control This Is evident In industry** support of cornbenefit analysis for new health
New chemieals' fotredured Into todmuy awl tha environment bmmc ba tested for carcinogenicity. Chemicals
standards. But, as Samuel Epttofo points out in hit book. The ftWlto tf Conor, the benefits of using a carcino
alreadyla use dwsld Jaaboatreomd.A method tor prioritfotag chemicals to bo tested should bo dreufopad. (Ths Tbxle
gen gs to one group of people (corpora tion* and stockholders) wtile the real
coota la tenaa of Hfoesa, death, loot
Babotancas Control Art aalwced bythe
Environmental HmmUm Agency aa * as OfiHAh new eaoesr patty fens
wages, medical expenses, and so on, paid by workers and society are dh>wrisaed or ignored.
on this aapareofr min nguu ngtilatlnn)
Efforts Aould atao bo made to Identify effects of interacting labwancea.
Lack of a coordinated approach.
Tumor registries, where el cancer
The many government agendas which cases would ba reported, Mtould be
have authority in lernu of jraearch, . drrelogod throughout thecountry. Cur
control, prevention of esnear, or rently very few such registries exist enforcement of eardmgtn regulations
have different approaches to these areas. Some efforts have been made to arrive ml a uniform approach, but thus far such at* approach has not boon developed.
The long latency period. Because at cancer's long latent period M's often difficult to identify cause wtth effect. And regulations are directed toward short-term, acute health effect*.
A SOCIAL DISEASE
The abovfe are Sperifle avenues tor dealing with the epidemic of cancer related to occupational and environ mental exposure*. But Imp!*menting such proffama Is not enough. Cancer Is not just a biologicai phfianmrir~Ti It Mo disease with social,' political, and
economic aspects. Carcinogenic chemicals are produced and uaed
PROGRAM NEEDED
despite their effect on humans because Industry consider* them necessary, and
An effective program to prevent efforts to control such thtnilcato are
cancer la necessary. Such a program must ala6 be aimed at those workers
met with the argument that bi many case* It I* not economically fooidble to do
who have already been exposed. What so. Caotrola or substitutions would be
are some of the aspects of such a costly, and increased product price
program?
would then be passer! on to the
Workers currently exposed to known carcinogens must be Informed of their exposures and the hazards involved. In addition, controls must be Instituted in those situations where car cinogens are used (for example, protec
consumer. These .angiiminta caused,
delays In standards firsubstances such a* coke own fisjaakgia and arsenic, and will continue to' do so aa long as economic Impact statement* remain a crucial Issue In standard retting.
tive clothing, air-supplied respirator*,
Cancer Is afro a social disease. It rob*
closed systems handling carcinogen*). the victims, their famUea, and society.
Education and training programs And It heaps ever-increasing Insurance
should be developed for such work and medical roots on society a* a whole.
place*. Labeling requirement* should Yet we demand certain good* that are
also be developed and enforced.
manufactured using carcinogen* --
All carcinogen use should be reported to government agencies for enforcement and compliance purposes. As part of the reporting fystem, workers
pesticides, hair dyes, dyes for other materials, plastic*, and so on. So we must determine how Important such things are In light at their terrible coal Cenrar lepotentially preventable, but all
sector* of society mwR be committed to
meoriMKT
, z w iw imhumw*
IVmbIW'*h#*vt"fou*Rfodhffph*
Ike M'foll IM pan kfito fh-rpfow*J
**
fraftb AMfonrelku M.an. EltmMrtftArf toNM
Ei i iniaftf> ivtfoi the vtom. of lb* t'n TVfipniP^wl >4
Ijfoe K4ii<teI Affhe fo ififtg v Htihfi id Allw.
prevention Ifwearies see an end to the
cancer epldehtic.'
(Niliail to taker Ocrepatlaasl Hsslrh Frsgreai Meatier. Eepriated with penelaslea five tuber Occepetieual Realfo Program Meeker Vel. t Ik. t Mserb-April ISM.)
H&S Reports
Available To
Local Unions
There are immornw reports, beaks, pumphhu and other mainriM for focal ualau Health and MriyCMamltieoa, afl of wbJdt baW a weak* of pardaent daut
From time to time.wevrifl preview tow* of theoe and IM oddrmma wtwre ICWU Health awl Safety Coot* milw*o May writ# directly tor them. Unlew otherwise noted, these pubUcattoni are free of coot., V
AT"rTaalkaba^gMBeuacnksO! auwr NAesa*lrShatfety
and HialUi for BUeh sad Urt* WortosU"
The combig yeoro do aot hold ffeat promise .for Black and Latino worker*. As the economy worsen*, the race of unemployment for there mothers wfl be Meggering many wig be displaced from their comma*kk* as employment opportunities evapo rate.
Yet mom adult*from the Black aud Latino communities will remain active workers. And a* such, theywM
be confronted with dlscrimlnstlou and uahealthful working conditions on a growing seals, since the current admlntatration hm made ft a policy to dilute the already Inadequate number of(Undents and regulation* promulgated by the Occupational Safety and Health Administration (OSHA), and to reduce OfiKA'. enforcement actlvky to near nonexbtcnt levels.
Job placemeat dtarrimlnstion has inevfufdy guaranteed the dirtiest and most dangerous Jobs for mom Black and Latino worker* wKh Iktlr prospect of advancement or transfer to leas hatardout locations. As a result, Black and Latino workers are probably over-represented in the current occupational disease and Injury epidemic that a/TUrt* all American worker* (available statistic* indicate that each year aa many aa lOO/MQ worker* die front Job-retated illness while another 22 million suffer disabling Injuries; that 2d-40 percent of aU cancer* are Job related).
Copies of report are available from
Tbs Urban Bavirenmcat Cow freeace Inc.
M IIU Street. NW, Bah IMl Washington, DC SB0OI
~-<*ij*f<e*jj-S- * . ?y.:
Cancer and Lifestyle: An Expert View
Does air pollution cause cancer? What is meant by the statement that lifestyle is responsible? What's the best way to tackle prevention and cure of this disease?
Questions like these are being asked by scientists, doctors, policy makers and pri vate citizens. They must be answered to properly direct re search and the regulatory pro cess.
Dr. John Higginson is a senior scientist for a consortium of universities called Universi ties Associated for Research and Education in Pathology. He was founding director for the International Agency for Re search in Cancer, an agency of the World Health Organization, and has been working in the
cancer field for more than 30 years.
In this interview he com ments on some issues that are Or. John Higginson part of the cancer controversy.
CE: You have stated most
causes of cancer are environ Dr. Higginson: We have cig
mental. What is covered by arette smoking, alcoholic bever
that statement? What per^.-.- ages, sunbathing. In terms of
centage of cancer does that-fJ. the work environment, we have
include?
exposures In the workplace to
Dr. Higginson: If one uses^j- Chemicals, we have the envi
the term environment In a wideJI' ronment that's related to medi
sense, the cultural environment, cine or radiation. Certain drugs
the work environment, the which are used in fact to treat
chemical environment, be cancer are also highly carcino
havioral environment, diet and genic in themselves.
so on, it covers a wide amount CE: What does this Imply
of the cancer problem.
then for cancer prevention or
There's a lot of indirect for cancer protection?
evidence to indicate that these Dr. Higginson: There are
various factors influence about three major implications. One,
80 to 90 percent of human where the carcinogenic agent is
cancers.
easily definable. It is control
CE: When you talk about lable. The possibilities for pre
environmental causes, you vention are almost 100 percent.
name diet as one. Can you In terms of cigarette smoking,
define a few of the others? cigarette-related cancer are
almost theoretically completely preventable.
Secondly, in the work envi ronment, removal of the highly carcinogenic substances or substitution by a less harmful substance may have a highly effective action.
Third, I don't think it has a major implication for detection, except in situations where you know people are at exceptional ly high risk. Then you may wish to build into the system methods of trying to identify and diagnose those cancers earlier so that you are going to be able to treat hopefully at a curable level.
tf your prevention is good, early detection in that particular cancer ceases to be very impor tant.
CE: In your opinion, what direction should cancer re search be taking? Where should research money and scientific effort be focused?
only major hope is to be able to cure it.
Fourthly, these all add up to a common packet where each particular problem is in vestigated, and the most satis factory approach developed. It's a mixture of applied and basic research. These are not contra dictory, they're complementary. CE: Has industrialization affected overall cancer rates?
Dr. Higginson: The^.evidence at present that wq/have is that industrialization G| the
sense that we understand it of mass exposure to chemicals in the general environment has had very little impact.,
Of course, where industri alization has led to exposure to compounds at a very high level, such as certain dyes that cause bladder cancer or asbestos that causes cancer of the lung and
Dr. Higginson: That is a
question that everybody
answers, and there is no univer sal agreement. Speaking per
" .. industrialization
sonally, I believe it has to be in the sense that we
tackled at four levels. One, the application of known knowledge such as the role of cigarettes, the role of occupational haz
understand it of mass exposure to chemicals in the
ards, things like that.
general environment
Secondly, when we're has had very little
dealing with those agents that are less clearly defined, we
impact
have to do the basic research to
see if by understanding mecha
nisms we could possibly identify
what for example is the role of
late full-term pregnancy in caus
ing cancer of the breast in
females.
of the covering of the lung, it
Thirdly, because we don't has had an impact.
know the cause, obviously we
But I think the question
have to do a lot more research you're posing is the total com
and better treatment, because if munity. There it doesn't seem to
you can't prevent a cancer, the /fcave had much of an impact.
SAL. 000044783 CHEMECOLOGY
CE: Why do some environ mental groups keep trying to link cancer with industrial pollutants?
Dr. Higginson: I think one must go back historically to'the period when industrial cancer was ignored and many com panies showed a high degree of insensitivity lo the problems of the workplace. It wasn't only cancer but general working con ditions, accidents in the work place, and so on.
Now, this then was fol lowed by a period in which many people believed cancer was due to viruses. But if it was due to a virus, there wasn't very much you could do about it. Then when one started moving back again to the chemical field, nearly all the chemical agents that have been defined as caus ing cancer in humans were first identified in the workplace. There was a kind of associa tion--that environment meant chemical environment, and that the chemicals would be auto matically man-made.
The reason it was discov ered in the workplace was that these were high-risk popula tions of relatively modest num bers of individuals who showed very high frequencies. Because in those days the exposures in the workplace were often ex traordinarily high and therefore you were really getting a very, very high frequency which is almost impossible to miss.
CE: The environmental groups are concerned as much about air pollution out side the plant as they are with workplace exposure. ~
There is still an attempt to link overall cancer ratesjo environmental pollution. Would you comment on that?
Dr. Higginson: It started back in the early '50s, at a time when I entered the cancer research field.
A1 that time, many people said it wasn't cigarettes that were the major cause of lung cancer; it was air pollution due to industrialization. And this view was expressed by a con siderable number of distin guished scientists.
Now Doll and Peto and myself and Winder all came up with these low figures for occupation. We were not able to identify significantly a large group of cancers due to general pollution. The most we could say was that possibly general pollution had an effect on lung cancer in cigarette smokers.
On the other hand, I can understand that not only envi ronmentalists but many other people really don't believe that breathing dirty air full of soot is good for you. And certainly it had significant effect in terms of bronchitis and emphysema and other respiratory diseases in the United Kingdom.
There's a gut feeling that it must be carcinogenic. And cer tainly, dust contains cancercausing agents. So people are very unwilling to believe some thing they can do something about in terms of air cleanness may have much less impact on the problem than they would wish.
CE: What role does work place exposure to chemicals play in overall cancer Inci dence?
Dr. Higginson: I feel that up to five percent is probably in reason. One tends to push the figure up rather than down because one doesn't want to miss something that you can do something about.
CE: What's the best way to lower even further the num bers of work-related can cers?
Dr. Higginson: I think we would make considerable prog ress if we can get rid of cigarette smoking, because whatever you look at, whether it is lung, larynx, mouth, pancreas, blad der, many of which are workrelated cancers, it's awfully diffi cult to unravel what proportion might be attributable to the workplace because of the over whelming impact of the ciga rette habit. This makes it almost impossible to identify other possible agents.
Certainly, for example, Dr. Selikoff has shown that in terms of asbestos workers and ciga
rette smoking, cigarettes so potentiate the effect of asbestos as to be enormous. And asbes tos is a much less important problem from the public health point of view if you don't smoke cigarettes, because they do potentiate each other.
CE: Dr. Higginson, Is there now or can we expect an epidemic of cancer In the United States that would be caused by Industrial chemi cals In the air?
Dr. Higginson: In the 30-odd years I have been working in the cancer field, I have seen a number of situations called epi demics of cancer. The vast majority of them have laded out, and have obviousfy been a chance observation.
There has been a major epidemic in cigarette-produced lung cancer in the United States and elsewhere. A much smaller epidemic, but still very impor tant for those concerned, has been asbestos.
The third possible epidem ic, if one wants to use that term,
chronic bronchitis and diseases of that type.
But it has had a surprisingly low or no effect on lung cancer. This has been looked at in great depth, especially in the '50s. When people started blaming cigarettes, many people stated that it wasn't the cigarettes, it was air pollution factor, due to industrialization.
Now, no one can ever deny that something couldn't happen in the future, But I think with what we know today it's most unlikely that any chemical could escape to the general environ ment in such quantities, except perhaps atomic war where radiation would occur, that would in fact lead to a major epidemic in the general popula tion,
In fact, air injjtany coun tries such as the Suited King dom, is better todaflhan it was In 1950. . Thij& Is well documented. In.,tn# U.S. It's been somewhat, slower. But I don't think we will'see another epidemic due to air pollution, provided we maintain reason able controls. I'm talking about a reasonable, balanced public health approach.
"We have not been able to define any group or individual group of cancers due to pollution of the general air. "
CE: You said we probably should not expect another epidemic from air pollution. Was there one before this?
Dr. Higginson: There was a personal epidemic due to per sonal pollution of your own environment by the cigarette. Now it Is possible that this is going to cause problems and that passive smoking may turn out to be much more dangerous than people believe.
is melanoma of the skin due to
sunlight, due to the marked
change of (sunbathing) habits among the community. That is
the situation up to today. We have not been able to
define any group or individual
group of cancers due to pollu tion of the general air. There
seems to be some effect of air pollution on smokers. Also, air
pollution does have an effect on
cardio-respiratory disease^
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There are two studies which suggest tliat people ex posed to other people smoking, one in Greece, one in Japan, does lead to an increase in lung cancer. If that is the case, we might be able to say that some of the increase in lung cancer or some of the cases of lung cancer in ordinary individuals are produced due to passive smoking.
To be Continued Next Month
MAY 1982
5
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