NEW JERSEY DEPARTMENT OF LABOR
DIVISION OF WORKERS’ COMPENSATION
MERCER COUNTY

 APPEARANCES:

WILENTZ, GOLDMAN & SPITZER, ESQS.,
By: ELIZABETH SISO BAIR
For Petitioner

HOWARD WILLIAM CRUSEY, JR., ESQ.,
By ANN DEBELLIS, ESQ.
For Respondent

WILLIAM L. BOYAN
Judge of Compensation

These Claim Petitioner hypothesize that George Owens contracted lung cancer from which he died as a result of employment with Respondent, H.M. Royal, Inc. They contend that asbestos caused the lung cancer.

It is not disputed that the cause of death was lung cancer, nor that the type of cancer is one that could be related to asbestos. It is disputed that petitioner was exposed to asbestos with sufficient intensity to bring on the cancer.

Respondent is neither a processor nor a manufacturer. It is a supplier of materials to other firms that do manufacturing. Respondent did not handle any asbestos in bulk, but solely material in packages. Petitioner contends that decedent came in contact with asbestos that escaped from the packaging.

It is not disputed that decedent was a very heavy smoker for many years, nor that he had stopped smoking some years ago. As to exactly when decedent stopped smoking, the widow’s testimony put it at a more remote time that the history in hospital records, presumably taken from decedent. I do not consider the difference decisive. There can be no question but that the intensity and duration of his smoking was sufficient to have been able to cause his cancer all by itself. Of course, under the liberal provisions of the workers’ compensation law, if asbestos significantly contributed to the cancer, whether by aggravation, exacerbation or acceleration, there is liability.

There is an interplay between cigarette smoking and asbestos in the causation of cancer. It is generally accepted that cigarette smoke contains a number of chemicals that have been shown to be carcinogens, i.e., capable without the presence of other chemicals to produce tumors in human tissue. Perhaps the most famous is benz-alpha-pyrene. When a drug manufacturer seeks approval to market a new drug as chemotherapy for cancer, it needs a lot of cancerous mice to test the drug on. Injecting the mice with benz-alpha-pyrene is an effective way to produce tumorous mice. Mice tissue is similar to human tissue in susceptibility to cancer. In addition, some cigarette smoke fractions are potent destroyers of a natural defense mechanism for lung tissue.

On the other hand, the biologic mechanism by which asbestos contributes to the causation of cancer is not well understood, even though epidemiological studies associate exposure to asbestos with lung cancers, and indicate a synergistic effect with cigarette smoke.

The unfortunate experience among shipyard workers during World War II turned out to be a perfect laboratory experiment. To meet the destruction of shipping by Nazi submarines, the United States undertook a vast shipbuilding program. The cargo vessels were almost all powered by reciprocating steam engines. Their efficiency could be increased if the steam was "superheated," i.e. heated much above the temperature (212 degrees Fahrenheit at sea level) that causes water to vaporize. This could only be accomplished by heavily insulating the pipes conducting the steam from the boilers to the cylinders. Asbestos was used in a manner that could be considered profligate. Many of the shipyard workers were employed for just one, two or three years during the war. Some were students who worked in the shipyards during summers. Many of the workers never came in contact with asbestos in an industrial setting for the rest of their lives. The data on the incidence of cancer among shipyard workers compared to the general population is the basis for much of the epidemiologic conclusions concerning asbestos’s potency for causing cancers, most notably mesothelioma, but including lung cancer generally.

The only known cause of mesothelioma is exposure to asbestos. Even so, only about seventy percent of the persons diagnosed with mesothelioma are known to have a history of exposure to asbestos. This shows one of the limitations of epidemiologic evidence. With respect to lung cancer generally, the most reasonable working hypothesis on the role asbestos plays in carcinogenicity seems to be that asbestos fibers in the lung tend to concentrate the carcinogenic chemicals in cigarette smoke.

The chemical structure of asbestos is quite simple and is well known. First of all, it is to be noted that it is not an organic chemical. Many, perhaps most, of the well recognized carcinogens are organic compounds, including benzene and its derivatives, such as benz-alpha-pyrene, referred to above, polyvinyl chloride (PVC), some aromatic hydrocarbons and beta-napthalamine, just to name a few that are quite well known.

The asbestos in this case was hydrous magnesium silicate. The chemical formula is 3MgO2SiO2, 2H2O. That these three chemical formulas are written with commas between them means that they are physically associated together, but not combined chemically. MgO is magnesium oxide. It is the insulator used in just about every electric oven in use in the United States today. If you look at either end of the heating element in an electric oven you will probably be able to see about 1&1/2 inch of tubular white material. That is magnesium oxide.

SiO2 is silicon dioxide. If you washed all the dirt out of beach sand, you would be left with silicon dioxide alone. When finely divided grains of silicon dioxide are inhaled, they are capable of causing the lung disease known as silicosis. However, silicon dioxide has not been associated with lung cancer. In contrast, asbestos is not granular. It is fibrous.

H2O, as "every schoolboy knows," is pure water. These three materials are physically combined without any of them being chemically changed in the formation of asbestos. It is surprising that scientists are largely baffled in trying to determine the mechanism by which three such simple, familiar chemicals play a role in the development of such a complex phenomenon as cancer.

Respondent handled asbestos from 1963 to 1986. The entire supply came from one source in Canada. Respondent had a relatively small number of customers for the product, probably less than ten. Most of the product was shipped from the source in Canada directly to the customers. Respondent got a percent of the sales price for its efforts in arranging the sales. The supplier in Canada apparently found this arrangement commercially more feasible than setting up its own sales organization.

Although respondent’s role was primarily that of a salesman, it kept some asbestos on hand in its Trenton warehouse. Several asbestos customers were in the Trenton area (one put asbestos in clutch plates for automobiles; another put it in floor tiles). Generally speaking, respondent sold asbestos to manufacturers of rubber, plastic and coatings.

The customers tried to anticipate and arrange for their needs, by arranging for timely shipments through respondent directly from the source in Canada. From time to time, they either misjudged their requirements or something went wrong with the shipping arrangement. Then they needed product right away to continue their operations. This was accommodated by respondent shipping from stock in its Trenton warehouse.

Although respondent handled asbestos until 1986, it was not present in its warehouse after 1983. From 1983 to 1986, it still made arrangements for direct shipments from the source in Canada to the customers’ place of business.

The asbestos was packaged in bags at the source in Canada. None was shipped in bulk. None was handled by respondent in bulk at any location.

In the beginning, the bags were made of a multi-ply type of paper. Later, the asbestos was placed in plastic-enclosed bags. This latter type of packaging allowed the contents to be put in under pressure, resulting in a firm package of uniform dimensions. It seems that before the introduction of the plastic-enclosed packages, there was a certain amount of slack in the packages. This made them subject to damage if handled roughly in contact with hard objects, resulting in spills.

From 1952 to 1958 decedent was employed as a laborer in respondent’s warehouse in Trenton. It was only in 1963 that respondent began handling asbestos. So decedent could not have been called upon, in his role as a common laborer, to clean up any spilled asbestos. As of 1963, decedent was appointed supervisor of the warehouse. He performed that job to the satisfaction of his employer. Ultimately, he received an annual salary of over $100,000.

Decedent’s health forced him to stop working for the company in 1993. Thus, during his management of the warehouse, asbestos was handled from 1963 to 1983. However, the sales tailed off greatly in the mid-1970's. I take judicial notice of the fact that the federal government greatly restricted the use of asbestos at that time.

Respondent kept records of the shipment of goods through the warehouse only for ten years, destroying a year’s worth of records ten years old at the end of each successive year. No evidence suggests this was done for any reason other than normal records retention considerations. However, because of this, there was only a scattering of records obtained from other sources giving any numerical values for the amount of product going through the warehouse.

One of the owners of the company testified that the plastic covered bag that replaced the paper bags was a "beautiful package." Its uniform, firm shape made it much easier to handle and store. It also made the packages less subject to damage. But to what extent can we infer a level of breakage of the prior multi-layer paper packages based on the reference to the plastic as a beautiful package?" The breakage of the paper bags was described as rare.

When a package of any material in respondents warehouse tore and a spill resulted, the packaging was repaired and reclosed and sold to the customer. There was no evidence that there was any discount for spillage. That there was none impresses me that the amount lost by spillage was not commercially significant to the customer. The customer would see that some of the packages had been resealed, so they knew some of the product could have been lost. If a significant fraction had been lost due to spillage, I would expect the customers to have been looking for a rebate or else seek a different supplier. Neither of these things have been shown to have happened.

On the other hand, asbestos fiber is a very light material and could become airborne if spilled.

The handling of asbestos during the peak years amounted to 6 or 7% of respondent’s total business. I assume that is in terms of dollar value. But the total dollar figures for the business were not in evidence, and only a small proportion of the asbestos sold by respondent passed through the Trenton warehouse. The warehouse is the only site that was posited as being the locale of decedent’s exposure to asbestos. So we have no measure of the quantity of asbestos that decedent was actually exposed to, nor even what he was potentially exposed to.

Sometimes in the case of death in which asbestos is thought to have played a role, an autopsy may produce physical evidence of the presence of asbestos in lung tissue. Asbestos fibers are very tiny, and, in the purest state, can only be seen with very special microscopes not generally available even in hospitals. Rather, "asbestos bodies," asbestos fibers to which other minerals have become attached, can be found in the ashes resulting from the combustion by the medical examiner f lung tissue exposed to asbestos during lifetime. Where the minerals adhering to the asbestos fibers include iron, the material in question is referred to as "ferruginous bodies." Such autopsy evidence would give direct evidence that asbestos fibers had found their way into the lungs. This would support an inference that a cancer of the lungs was contributed to by the exposure to asbestos. In the present case, however, no autopsy was done. This, of course, is a matter not under the control of respondent. No adverse inference to respondent can be drawn from the non-production of autopsy evidence.

Some probabilities with respect to the relative contribution of cigarette smoking and asbestos to the development of a lung cancer may sometimes be drawn from the primary site of the cancer. The "windpipe" i.e. the trachea, together with the chief airways leading into the lungs, the bronchi, forms an upside down capital letter "Y", the trachea being the stem. The point where the two arms of the "Y" branch out is known as the bifurcation. When cancer originates at the bifurcation, it is reasonable to assume that an inhaled carcinogen played a role. An aerosol is a solid floating in air or another gas. Cigarette smoke contains aerosols which are carcinogens. The solid particles in inhaled aerosols have an inertia that, according to one of Newton’s laws, makes them tend to continue their movement in the same direction unless and until something interferes. Inhaled aerosols are, thus, likely to impact on the tissue of the bifurcation.

On the other hand, inhaled light, straight fibers, such as crocidolite asbestos, are much more likely to be carried in the air stream and follow along past the bifurcation through the bronchi to much more distal portions of the lungs.

Reference was made in the case to the fact that asbestos that respondent marketed was "chrysotile." Chrysotile itself is a curly fiber. Other types, such as crocidolite, are straight fibers. It is generally accepted that the long, straight fibers are much more likely to stay in the air stream of inhaled breath as it passes through the nasal passages, the throat, the trachea, the bronchi and into the lung tissue itself, going all the way to the farthest reaches. Chrysotile fiber is less likely to reach pulmonary tissues that the long and straight fibers, and is less likely to cause cancer of the lung. It may be filtered out by nasal hairs.

Pleural plaquing, scarring of the outermost reaches of the cavity containing the lungs, is per se taken to indicate insult by asbestos. See Rybski v. Johns-Manville Corp., 185 N.J. Super. 433 (App. Div. 1982). This is probably due to the effect of long, straight fibers such as crocidolite, for example.

Although chrysotile is the type of fiber marketed by respondent, what is commercially sold as chrysotile is probably not really 100% of any one type of fiber, and probably contains some admixture with other types of asbestos fiber. Does the location of decedent’s tumor in this case help assess the probabilities that it was caused either by cigarette smoke or by asbestos? The primary site was neither at the bifurcation nor at a remote area of the lungs, but in a mid-point. The location gives little basis to inculpate the primarily chrysotile asbestos in this case.

What about inter vivos x-ray evidence? Day after day in the Workers’ Compensation court, we hear evidence of interstitial markings on x-rays indicating fibrosis by inhalation of asbestos or other fibers. There is an unresolved controversy among experts in industrial hygiene whether the occurrence of asbestosis is a necessary part of the disease process of any lung cancer that can be said to have been due to exposure to asbestos. The argument for this proposition is based on epidemiology. Since epidemiology is the only presently scientifically demonstrated basis for believing asbestos contributes to lung cancer, proponents of the hypothesis that asbestosis is a necessary part of the disease process of cancer contend they are just as much entitled to rely on epidemiology showing strong co-relation between the occurrence of an asbestos related lung cancer and asbestosis.

There are a number of objections to the hypothesis that I have had occasion to discuss in another case in the past. Whether or not asbestosis is a necessary part of the disease process leading to lung cancer due to asbestos, the presence of x-ray findings of asbestosis would at least offer convincing proof that the person had been exposed to a significant quantity of asbestos. But in the present case, there was no x-ray finding of asbestosis, nor any other asbestos caused condition, before the diagnosis of cancer. Petitioner’s expert did not discuss this subject. Respondent’s expert did. He pointed out the lack of such findings in x-rays before the diagnosis was made of the cancer. He testified that the changes on the x-rays after the cancer was diagnosed were to the cancerous process. Since the cancer spread quite a bit, this seems plausible. In addition, it was not controverted. There was no rebuttal.

Histology is the branch of biology that deal with the minute structure of tissues, including cells. Different cancers have different cell structures. Looking at the present evidence from the histologic standpoint, the type of cancer cell that affected decedent could have been caused by cigarette smoke in a person never exposed to asbestos. No histologic evidence was offered that would justify an inference that asbestos is more likely to have contributed to the causation of decedent’s cancer than cigarette smoking alone.

We are left with evidence that is very lacking in proof that there was any substantial asbestos exposure. The widow, who obviously has a financial interest in the outcome of the case, testified that when decedent came home from his work, his clothes sometimes had a white appearance, although sometimes they looked like carbon black. She did not do decedent’s laundry herself, so she was only able to tell us what she saw being in the same room with decedent. There was no testimony that she hugged decedent when he came home and she got white material on her clothes which she observed more closely when she undressed.

She described the material she saw on decedent’s clothes as "looking like talc." If it was talc, it obviously was not asbestos. The widow did not tell us how she knew what talc looked like.

Some of the evidence put in by petitioner stated that the asbestos fibers shipped from respondent’s source in Canada were white with a greenish tinge. The supplier was very proud of it’s quality control. It had apparently made a large investment in the elaborate mill in Canada that processed the asbestos to reduce it to clean fibers of specified lengths. Each category of product was uniform. The greenish tinge was probably there. But no witness described any material on decedent’s clothes nor that was seen to have spilled in respondent’s warehouse as having a greenish tinge.

I know from experience in many other cases that during the hey-day of industry in Trenton, talc was extensively used to prevent latex surfaces from sticking together. That is true in the manufacture of latex gloves and condoms. Talc may well have been in a product in respondent’s warehouse. No one inculpates talc as a carcinogen.

One of the owners of respondent’s family-owned business testified that he never saw decedent wear clothes in the condition described by his widow. This individual in his younger years worked side by side with decedent. He wore the same type of uniform as decedent. He took his uniform off at the end of one day and put the same uniform back on the next day. It could hardly have been full of dust of any kind. I consider this witness’s testimony more credible that the widow’s on this point. He had a much smaller financial interest in the outcome of the case than she did. His firm is covered by insurance. The potential effect of this case on rates for the future seems negligible. Rates are set by a state agency on an industry-wide basis for particular classes of job titles. They are not individualized for each employer. The respondent’s owner-witness referred to in this paragraph seemed very knowledgeable about the business and the product. He seemed quite candid.

Petitioner’s expert, Dr. Goodman, did not really come to grips with the issue of whether the quantity of asbestos with which decedent may have come in contact in the course of his employment was sufficient to cause his lung cancer. His attitude was that any asbestos exposure would have been enough. To illustrate this point, he brought up the experience with the Johns-Manville plant in Manville, New Jersey. Some family members of the workers in the Johns-Manville plant developed asbestos related diseases without ever having been in the plant. Of course, there is a great difference between the Johns-Manville plant and respondent’s warehouse. Johns-Manville mixed ingredients, including asbestos fibers, to be made into shingles. There was dumping and stirring of the asbestos-containing materials, as part of the regular, daily operation of the plant for many years.

That is not analogous to respondent’s warehouse operation where nothing was handled in bulk, and the only possible exposure to asbestos was on the occasional, rare breakage of packages containing asbestos that decedent was not personally handling.

Dr. Goodman indirectly admitted there is a dose-relation between asbestos exposure and disease, even though he refused to accept that terminology. He acknowledged that a person just driving through the town of Manville would not be expected to come down with an asbestos related cancer. That being so, it follows that there is a level of exposure that would have to be shown before there can be a sound connection of the causal relation of the disease to the exposure. Petitioner has not shown that this is the case by a preponderance of the evidence.

As is the case with all disabilities manifested after January 1980, petitioner must establish a claim for permanent disability benefits by a preponderance of the demonstrable, objective, medical evidence. This histology does not preponderate in favor of asbestos contributing to the causation of the cancer. Neither does the site of the origin of the cancer. The inter vivos x-ray findings do not show any marks asbestos exposure. There are not post mortem findings. If one or more of these factors did inculpate asbestos, I might then excuse the lack of direct evidence that decedent was exposed to asbestos at all.

I sympathize with the widow on the difficulty in obtaining evidence of commercial transactions many years ago when nobody at the time had commercial or any other reasons for preserving the records more than ten years. The widow was able to testify she had been in the plant with her husband on Sundays. But she was unable to testify that decedent himself cleaned up any spills of asbestos. He was the supervisor of the entire warehouse during the entire time that the company handled asbestos in the warehouse. There was testimony that occasionally packages broke in the years when the product was shipped in paper. During the time decedent was supervisor, after 1963, there was a lot of testimony that decedent made sure that the warehouse was spotless. Any spills must have been promptly cleaned up. But there was no substantial evidence that decedent, with his $100,000 salary, himself engaged in cleaning up spills of asbestos.

There was very clear evidence decedent, for a very significant period, was a very heavy cigarette smoker. One pack per day is generally considered quite dangerous for a lot of reasons. Decedent smoked a lot more than that for many years.

Since I do not find the evidence persuasive that decedent’s disease or death was caused by exposure during employment with respondent, there is no entitlement to any benefits.

There will be a stenographic reporting fee of 4500.00 payable by respondent to Trainor Reporting Service.

The respondent, as a prevailing party, should submit a form of Judgment consistent with this opinion either consented to as to form under the ten day rule. When signed, the Judgment constitutes the final action of the Division of Workers’ Compensation.

______________________

William L. Boyan
Judge of Compensation

Dated: May 2, 2000