TSCA's Impact on Society and Chemical Industry - ACS Publications

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Impact on P u b l i c H e a l t h

Downloaded by UNIV LAVAL on July 11, 2016 | http://pubs.acs.org Publication Date: May 1, 1983 | doi: 10.1021/bk-1983-0213.ch013

MICHAEL J. LIPSETT SRI International, MenloPark, CA 94025 Regulations promulgated under the Toxic Substances Control Act (TSCA) may have a beneficial impact on public health, though such an impact will be difficult to measure or to estimate. Such an evaluation of TSCA's effects is problematic because of: the difficulty in isolating impacts of TSCA regulations from other environmental or occupational health statutes; the insensitivity of epidemiologic studies in detecting chronic effects of low-level chemical exposure; and the preventive nature of the Act, which subjects new as well as existing chemicals to regulation. A more practical difficulty exists in that, five years after the enactment of TSCA, few chemical substances have been subject to regulation. This paper will discuss why an evaluation of the health impact of TSCA must of necessity remain somewhat speculative. I have been asked to discuss the human health impacts of TSCA. Any examination of such "impacts" of the Act should focus on effects that can be measured or estimated. However, in cases where the statutory goals are primarily preventive in nature, measurement or even estimation of health benefits may prove elusive. Although TSCA contains language that appears to require some consideration of the impact of regulation, it is unlikely that Congress intended that precise quantitative evaluation of the effects of TSCA be undertaken. As we shall see, such an evaluation is not feasible. Out of the universe of potential health effects that could be evaluated, I will focus on those specifically designated in the Act itself—cancer, birth defects and gene mutations. This is not to say that other potential health impacts of chemical exposure are unimportant. Rather, these three named effects represent a relatively circumscribed basis by which to evaluate the Act in terms of its explicit priorities. 0097-6156/83/0213-0169$06.00/0 © 1983 American Chemical Society Ingle; TSCA's Impact on Society and Chemical Industry ACS Symposium Series; American Chemical Society: Washington, DC, 1983.

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In the f i r s t s e c t i o n of my t a l k I hope to show why measurement of these e f f e c t s as a f u n c t i o n of regulatory actions under TSCA i s not p r a c t i c a l . I f such e f f e c t s are not measurable, then f o r regulatory purposes they must be estimated, u s u a l l y by e x t r a p o l a t i o n from animal experiments. I w i l l b r i e f l y i n d i c a t e that q u a n t i t a t i v e e x t r a p o l a t i o n i s an u n c e r t a i n business. In the second s e c t i o n , I w i l l summarize TSCA's probable impact on h e a l t h , methodological d i f f i c u l t i e s i n measurement notwithstanding. I w i l l conclude with some remarks about recent r e g u l a t o r y pronouncements which seem to i n d i c a t e that i f past p o l i c i e s have had l i t t l e d i s c e r n i b l e h e a l t h impact, future ones may have even l e s s .


P r a c t i c a l L i m i t a t i o n s on Measurement of Health

Impact

Assuming, f o r the sake of argument, that some f a r - r e a c h i n g r e g u l a t i o n s had been promulgated l i m i t i n g human exposure to one or more substances suspected of causing cancer, b i r t h defects, or gene mutations, i t would be d i f f i c u l t , i f not impossible, to measure any e f f e c t on the incidence of these conditions a t t r i b u t a b l e to such r e g u l a t i o n s . Some conceptual and p r a c t i c a l impediments to such measurement i n c l u d e : D i f f i c u l t y i s o l a t i n g the e f f e c t of TSCA from consumer p r o t e c t i o n and other environmental and occupational h e a l t h s t a t u t e s and r e g u l a t i o n s . R e l a t i v e i n s e n s i t i v i t y of epidemiologic studies i n d e t e c t i n g long-term e f f e c t s of low-level chemical exposures. I n a b i l i t y i n most instances to detect p o t e n t i a l b e n e f i c i a l h e a l t h e f f e c t s from reduced exposure to chemicals due to the chronic nature and m u l t i f a c t o r i a l e t i o l o g i e s of the c o n d i t i o n s i n question. The preventive nature of the Act, under which new as w e l l as e x i s t i n g chemicals may be subject to r e g u l a t i o n . I s o l a t i o n of TSCA's E f f e c t . There are at l e a s t 17 f e d e r a l statutes and numerous state laws purporting to regulate human exposure to hazardous substances. While many chemical substances that may pose chronic h e a l t h hazards are excluded from r e g u l a t i o n under TSCA (e.g., p e s t i c i d e s , drugs, cosmetics, a l c o h o l i c products, food a d d i t i v e s , tobacco), others are p o t e n t i a l l y subject to concurrent r e g u l a t i o n under several s t a t u t e s , i n c l u d i n g TSCA. For example, asbestos, a well-recognized human carcinogen, may be regulated by EPA under TSCA, and at the same time i s subject to r e g u l a t i o n by the same agency under the Clean A i r and Clean Water Acts. The Consumer

Ingle; TSCA's Impact on Society and Chemical Industry ACS Symposium Series; American Chemical Society: Washington, DC, 1983.

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Product Safety Commission regulates the presence of asbestos i n various consumer products. Workplace ambient standards f o r asbestos have been e s t a b l i s h e d under the Occupational Safety and Health Act, though the b a s i s f o r such r e g u l a t i o n i s not c a r c i n o g e n i c i t y . Many other chemical substances are subject to overlapping r e g u l a t i o n with respect to d i f f e r e n t aspects of human a c t i v i t y . Thus, with the exception of chemical exposures uniquely subject to r e g u l a t i o n under TSCA, the p o t e n t i a l i n f l u e n c e of t h i s s t a t u t e on o v e r a l l human exposure to hazardous chemicals w i l l be d i l u t e d by the e f f e c t s of r e g u l a t i o n s promulgated under other environmental, o c c u p a t i o n a l , and consumer p r o t e c t i o n s t a t u t e s . I n s e n s i t i v i t y of Epidemiologic Studies. There are obvious e t h i c a l and l e g a l l i m i t a t i o n s on administering p o t e n t i a l carcinogens, mutagens and teratogens to humans i n an experimental s e t t i n g . Therefore, to evaluate whether p a r t i c u l a r chemical agents increase the r i s k of chronic h e a l t h e f f e c t s , one must r e l y on epidemiologic studies of populations exposed to such agents. Since epidemiologic i n v e s t i g a t i o n s are not c o n t r o l l e d experiments, and since they are u s u a l l y undertaken r e t r o s p e c t i v e l y , they are subject to l i m i t a t i o n s that a f f e c t t h e i r s e n s i t i v i t y t o detect chronic e f f e c t s . One of the most important l i m i t a t i o n s i s the lack of good exposure data. With the exception of i n d u s t r i a l hygiene data f o r s e l e c t e d i n d u s t r i e s and ambient a i r q u a l i t y monitoring f o r Clean A i r Act " c r i t e r i a " p o l l u t a n t s , there i s l i t t l e more than sporadic sampling of environmental media and human environments f o r chemicals that could be subject to TSCA r e g u l a t i o n . In attempting to study whether human exposure to a p a r t i c u l a r chemical i s a s s o c i a t e d with a given chronic disease outcome, one must t r y to a s c e r t a i n past exposure to that chemical. However, i n s e t t i n g s other than the workplace, measurements of t h i s kind are v i r t u a l l y nonexistent. In a d d i t i o n , people who work with chemicals are t y p i c a l l y exposed to m u l t i p l e substances, and such overlapping exposures may be d i f f i c u l t to c o n t r o l f o r e i t h e r i n the design or the a n a l y s i s of epidemiologic s t u d i e s . In non-occupational contexts, u n c o n t r o l l e d and unmonitored low-level exposures to m u l t i p l e substances i n food, a i r , and water are a t y p i c a l feature of everyday l i f e that may make epidemiologic i d e n t i f i c a t i o n of independent r i s k f a c t o r s even more d i f f i c u l t . For most chemicals p o t e n t i a l l y subject to TSCA r e g u l a t i o n , epidemiologic studies w i l l not be able to r e s o l v e questions of a s s o c i a t i o n s of chemical exposures with p a r t i c u l a r disease outcomes. Chronic Nature of Diseases i n Question. Cancer i s a disease c h a r a c t e r i z e d i n most cases by a latency period of 15 to 40 years. That i s , there i s a l a g of 15 years or more between i n i t i a l exposure to a carcinogen and the m a n i f e s t a t i o n of the



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disease. (The p r i n c i p a l exceptions to t h i s observation are cancers of the hematopoetic t i s s u e s , which have a minimum latency period of around 5 years.) Thus, to measure the e f f e c t s of some h y p o t h e t i c a l r e g u l a t i o n s , one would have to look at cancer incidence 15 or more years a f t e r t h e i r adoption among a defined group o f people who would otherwise be exposed to the chemical or chemicals i n question. For e x i s t i n g chemicals that are recognized human carcinogens, i t might be p o s s i b l e to estimate the number of cancers avoided by reducing exposure over a l i f e t i m e . In theory t h i s could be c a l c u l a t e d using dose-response information to estimate the b e n e f i t s o f a percentage r e d u c t i o n of exposure to p a r t i c u l a r chemical substances. Unfortunately, such human dose-response data are u n a v a i l a b l e f o r a l l but a few carcinogens, and even f o r these, the e f f e c t s of low doses can only be guessed. With respect to b i r t h d e f e c t s , the time l a g between exposure and outcome i s not so much of a problem as i s the case with cancer. However, a t t r i b u t i n g human b i r t h defects to chemical exposures (other than pharmaceutical products, smoking, a l c o h o l , and a few occupational exposures), i s d i f f i c u l t . Even i f a p a r t i c u l a r substance i s capable o f causing b i r t h defects i n humans, the occurrence of such an outcome depends on the dose, on the route of maternal exposure, and on the timing of the exposure. Nevertheless, epidemiologic i n v e s t i g a t i o n s ( p r i n c i p a l l y c a s e - c o n t r o l s t u d i e s ) have a s c e r t a i n e d causal r e l a t i o n s h i p s between chemical exposures and adverse reproductive outcomes, such as c o n g e n i t a l anomalies. Most f e t a l defects are incompatible with f e t a l s u r v i v a l and r e s u l t i n spontaneous a b o r t i o n . This p o t e n t i a l l y s e n s i t i v e parameter of b i r t h d e f e c t s — i . e . , spontaneous a b o r t i o n — i s not r o u t i n e l y monitored, and therefore provides no b a s e l i n e from which to measure the p o t e n t i a l e f f e c t of reducing a given chemical exposure. Defects among l i v e b i r t h s are, however, r o u t i n e l y but not s y s t e m a t i c a l l y monitored nationwide by the Centers f o r Disease Control (CDC). This monitoring system probably does not convey an accurate p i c t u r e of the prevalence of b i r t h d e f e c t s , though, since i t i s based on h o s p i t a l discharge a b s t r a c t s , which o f t e n do not c o n t a i n information about any but the most severe and obvious c o n g e n i t a l anomalies. These a b s t r a c t s c o n t a i n l i t t l e or no information on maternal f a c t o r s , such as occupational exposures. Thus t h i s system would probably not be s e n s i t i v e enough to detect the e f f e c t s of e l i m i n a t i n g or s i g n i f i c a n t l y reducing chemical exposures, i f such exposures do i n f a c t have a major i n f l u e n c e on the incidence o f b i r t h d e f e c t s . Recent estimates of the percentage of b i r t h defects a t t r i b u t a b l e to environmental exposures o f a l l kinds, i n c l u d i n g smoking, drugs, i n f e c t i o n s , r a d i a t i o n , and general environmental chemicals, i n d i c a t e that t h i s category probably represents about 10% of b i r t h defects.(I) Most c o n g e n i t a l anomalies (about 2/3) are of



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unknown e t i o l o g y . Chemicals that have been l i n k e d to b i r t h defects or other reproductive e f f e c t s have been detected as e t i o l o g i c agents because pregnant women have had r e l a t i v e l y l a r g e , well-documented exposures i n the form of i n g e s t i o n of drugs or a l c o h o l , a c c i d e n t a l poisoning, or occupational exposure. Epidemiologic studies are, i n general, too i n s e n s i t i v e to detect e f f e c t s at lower exposure l e v e l s , unless the substance of i n t e r e s t i s extremely potent. With respect to the t h i r d chronic h e a l t h e f f e c t mentioned s p e c i f i c a l l y i n TSCA—gene m u t a t i o n s — a g a i n the nature of the e f f e c t i n question i s such that h i s t o r i c a l measurement i s not f e a s i b l e . Mutagenic p r o p e r t i e s are studied i n m i c r o b i a l , c e l l c u l t u r e , and animal systems. Human body f l u i d s can be monitored for the presence of mutagenic substances, but t h i s does not a c t u a l l y measure genetic e f f e c t s . While several methods f o r monitoring mutational events i n humans are being developed, none i s ready yet f o r general use.(2_) There are, however, cytogenetic techniques to examine p o t e n t i a l genetic e f f e c t s of chemical exposure on humans. These look at a higher l e v e l of genetic organization—chromosomal and chromatid a b e r r a t i o n s . Some studies of persons exposed to chemicals demonstrate an increase of such a b e r r a t i o n s c o r r e l a t i n g with the time of exposure. In other i n v e s t i g a t i o n s , i n d i v i d u a l v a r i a b i l i t y has overshadowed any d i f f e r e n c e s that might be a t t r i b u t a b l e to chemical exposure. Such i n v e s t i g a t i o n s are complicated by a lack of knowledge about the frequency and p e r s i s t e n c e of spontaneous chromosomal a b e r r a t i o n s . Furthermore, there i s l i t t l e evidence l i n k i n g such changes to s p e c i f i c diseases, though i n t u i t i v e l y one would expect such an a s s o c i a t i o n . (Several types of human cancers have been reported to be associated with s p e c i f i c chromosomal rearrangements.) In general, mutational events are considered d e t r i m e n t a l . T e l e o l o g i c a l l y speaking, t h i s i s why l i v i n g systems have evolved m u l t i p l e DNA r e p a i r mechanisms. Some i n v e s t i g a t o r s have estimated that about 90% of known carcinogens a c t through mutational mechanisms. (_3) Furthermore, many human diseases, i n c l u d i n g s i c k l e c e l l anemia, thalassemia, mucopolysaccharidoses and others, are known to have a genetic b a s i s . However, my point i s that while the s t a t e - o f - t h e - a r t of genetic t o x i c o l o g y i s r a p i d l y e v o l v i n g , i t i s not yet capable of measuring mutagenic events i n complex human systems. Cytogenetic techniques can detect chromosomal e f f e c t s , though experience with these techniques i s l i m i t e d . Regulation of New As Well As E x i s t i n g Chemicals. An e v a l u a t i o n of TSCA s impact would d i f f e r from that of most environmental s t a t u t e s i n that the former purports to regulate new as w e l l as e x i s t i n g chemicals. The o b j e c t i v e of the premanufacturing n o t i f i c a t i o n (PMN) system under s e c t i o n 5 i s to permit EPA to make a reasoned e v a l u a t i o n of new chemicals' 1


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t o x i c i t i e s p r i o r to t h e i r production and d i s t r i b u t i o n i n commerce. EPA has a u t h o r i t y to impose a broad spectrum of c o n t r o l s to prevent or minimize human and environmental exposure to chemicals that could r e s u l t i n d i s e a s e . This a u t h o r i t y has been used mainly to require more extensive t e s t i n g of s e v e r a l suspect chemicals. In the cases where EPA has formally required such t e s t i n g , the manufacturers have withdrawn t h e i r a p p l i c a t i o n s and suspended plans to produce the chemicals. While the d e c i s i o n not to produce a p o t e n t i a l l y t o x i c substance may serve the goal of TSCA to i d e n t i f y and prevent hazards before people are exposed, how can one q u a n t i t a t e the h e a l t h impact of the manufacturers d e c i s i o n s ? I pose t h i s question r h e t o r i c a l l y , since EPA's requests f o r a d d i t i o n a l t e s t i n g stemmed from a data base inadequate to assess r i s k . In other words, since there was not enough information i n the f i r s t place to know whether there might even be a s u b s t a n t i a l h e a l t h r i s k , i t would be impossible to estimate the h e a l t h impact of d e c i d i n g not to produce such chemicals. By now I hope i t i s c l e a r that measurement of the human h e a l t h impact of TSCA, at l e a s t with respect to cancer, b i r t h defects, and genetic mutations, i s not c u r r e n t l y f e a s i b l e , f o r both p r a c t i c a l and t h e o r e t i c a l reasons. Thus, any e v a l u a t i o n of r e g u l a t i o n s under TSCA i n terms of p o t e n t i a l h e a l t h b e n e f i t s must be based on p r e d i c t i o n s from epidemiologic or c l i n i c a l data, and from animal and m i c r o b i a l models. Risk assessment without human t o x i c i t y data i s unavoidable under s e c t i o n 5 regulatory d e c i s i o n s concerning new chemicals, though f o r r e g u l a t i o n s of e x i s t i n g chemicals, c l i n i c a l and epidemiologic evidence may be a v a i l a b l e . However, i n most cases where exposure to chemical substances (other than drugs or c i g a r e t t e s ) has been shown to be associated with cancer or b i r t h d e f e c t s i n humans, accurate exposure data are not a v a i l a b l e , and therefore dose-response curves can be only crudely approximated. In animal experiments exposures can be c a r e f u l l y c o n t r o l l e d , and dose-response curves can be formally estimated. E x t r a p o l a t i n g such information to the human s i t u a t i o n i s o f t e n done f o r regulatory purposes. There are several models f o r estimating a l i f e t i m e cancer r i s k i n humans based on e x t r a p o l a t i o n from animal data. These models, however, are premised on e m p i r i c a l l y u n v e r i f i e d assumptions that l i m i t t h e i r usefulness f o r q u a n t i t a t i v e purposes. While q u a n t i t a t i v e cancer r i s k assessment i s widely used-, i t i s by no means u n i v e r s a l l y accepted. Using d i f f e r e n t models, one can a r r i v e at estimates of p o t e n t i a l cancer incidence i n humans that vary by several orders of magnitude f o r a given l e v e l of exposure. Such v a r i a t i o n s make i t rather d i f f i c u l t to place confidence i n t e r v a l s around b e n e f i t s estimations f o r regulatory purposes. Furthermore, low dose r i s k e s t i m a t i o n methods have not been developed f o r chronic h e a l t h e f f e c t s other than cancer. The 1


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i m p l i c a t i o n of the l i m i t a t i o n s of r i s k assessment methodology and h e a l t h impact measurement i s that, with narrowly defined exceptions, h e a l t h b e n e f i t s of TSCA r e g u l a t i o n s cannot be r e a l i s t i c a l l y estimated.


Few

E f f e c t s of TSCA Regulatory

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I f the h e a l t h impact o f TSCA r e g u l a t i o n s i s not p o s s i b l e to measure, and i f estimates of health b e n e f i t s of r e g u l a t i o n s are d i f f i c u l t to q u a n t i f y , l i t t l e has been achieved under TSCA that could be measured or estimated. In the next s e c t i o n of t h i s paper, I w i l l be d i s c u s s i n g r e g u l a t i o n under s e c t i o n 5, which deals with new chemicals and s i g n i f i c a n t new uses of e x i s t i n g chemicals, and under s e c t i o n 6, which involves chemical substances and mixtures known to be hazardous. I w i l l not discuss actions under s e c t i o n 8, concerning p o t e n t i a l health hazard r e p o r t i n g , nor w i l l I cover the e f f e c t s of actions undertaken by the i n d i v i d u a l states with s e c t i o n 28 grants. Impacts d i r e c t l y a t t r i b u t a b l e to TSCA r e g u l a t i o n s include s e v e r a l proposed and f i n a l r e g u l a t i o n s d i r e c t e d at s p e c i f i c chemical substances under s e c t i o n 6 — p o l y c h l o r i n a t e d biphenyls (PCBs), d i o x i n , chlorofluorocarbons (CFCs), and a s b e s t o s — a n d orders issued under s e c t i o n 5(e). PCBs. Congress s i n g l e d out PCBs from a l l other environmental contaminants f o r regulatory a t t e n t i o n under s e c t i o n 6(e) o f TSCA. EPA was d i r e c t e d to develop r e g u l a t i o n s for l a b e l l i n g , use and d i s p o s a l , as w e l l as to promulgate r u l e s f o r implementing a s t a t u t o r y ban on manufacturing, processing and d i s t r i b u t i o n of PCBs other than i n a " t o t a l l y enclosed manner" o r i n a way that the EPA Administrator considered safe. In a l e g a l challenge to these r e g u l a t i o n s e a r l y l a s t year, the D.C. Court o f Appeals found EPA s d e f i n i t i o n of " t o t a l l y enclosed uses" to be unsupported by the procedural record, and d i r e c t e d EPA to rewrite some parts of these r e g u l a t i o n s . Subsequently the judge's order was stayed f o r 18 months to allow EPA to gather a d d i t i o n a l evidence. Thus, the reformulation o f these r u l e s w i l l not be completed u n t i l l a t e r t h i s year or e a r l y 1983. Those PCB r e g u l a t i o n s s t i l l on the books may have helped to diminish human exposure to PCBs, though f o r the reasons discussed e a r l i e r , the h e a l t h impact of such diminished exposure i s not measurable. 1

Dioxin. Two years ago, EPA promulgated a r u l e p r o h i b i t i n g Vertac Chemical Corporation from d i s p o s i n g of waste contaminated by d i o x i n . Other p a r t i e s intending to dispose of s i m i l a r l y contaminated wastes were required to n o t i f y EPA 60 days i n advance of t h e i r i n t e n t i o n s . This order may have prevented some exposure to t h i s h i g h l y t o x i c substance, though the human h e a l t h impact of t h i s s i n g l e p r o h i b i t i o n cannot be c a l c u l a t e d .



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Asbestos. EPA issued a proposed r u l e concerning i d e n t i f i c a t i o n and c o r r e c t i o n of f r i a b l e asbestos-containing m a t e r i a l s i n schools. Based on data v o l u n t a r i l y submitted, EPA estimated that at l e a s t 8,600 p u b l i c schools attended by over 3 m i l l i o n c h i l d r e n contain such m a t e r i a l s . However, EPA r e p o r t e d l y has no information on another 44,000 schools. Classroom concentrations of asbestos f i b e r s i n some schools have been found to approximate concentrations i n homes of asbestos workers who do not have shower or laundry f a c i l i t i e s at work. Since c h i l d r e n exposed to asbestos w i l l l i v e long enough to allow the cancer latency period to elapse, the presence of f r i a b l e asbestos m a t e r i a l s i n schools represents a p o t e n t i a l l y enormous p u b l i c h e a l t h problem. The f i n a l asbestos r u l e w i l l r e p o r t e d l y be promulgated i n the near f u t u r e . (The r u l e was published May 27, 1982.) No other r e g u l a t i o n s regarding asbestos have been issued. CFCs. A l l " n o n e s s e n t i a l " uses of CFCs i n a e r o s o l p r o p e l l e n t s were banned i n 1978—the f i r s t and only major c o n t r o l a c t i o n under TSCA not s p e c i f i c a l l y mandated by the s t a t u t e . This a c t i o n may have helped to reduce the future incidence of s k i n cancer by diminishing CFCs d e s t r u c t i v e e f f e c t s on s t r a t o s p h e r i c ozone. Making appropriate assumptions about rates of ozone d e p l e t i o n and e x t r a p o l a t i n g from current disease r a t e s , one could estimate a range of cancers avoided because of t h i s p r o h i b i t i o n . However, any h e a l t h b e n e f i t due to the ban on a e r o s o l CFC uses may be masked by the continued increase i n non-aerosol uses. 1

A l l i n a l l , regulatory actions under s e c t i o n 6 are not l i k e l y to have achieved a major e f f e c t on human h e a l t h . One reason f o r t h i s i s that under TSCA s e c t i o n 9, regulatory deference i s accorded to other statutes and, where appropriate, to other regulatory agencies. Another i s that TSCA i s conceptually more d i f f i c u l t to administer than other environmental statutes that set target goals and dates f o r p o l l u t i o n r e d u c t i o n . TSCA focuses instead on the prevention of "unreasonable r i s k s , " i n which the d e f i n i t i o n of what i s unreasonable depends i n part on p o t e n t i a l h e a l t h b e n e f i t s that are d i f f i c u l t to q u a n t i f y . While there have been other impediments to the r e g u l a t i o n of known hazards, one c r i t i c a l f a c t o r has been EPA's de-emphasis of such regulatory actions i n favor of gathering data and s e t t i n g up a system to screen and monitor new chemicals. PMNs f o r New Chemicals. How w e l l has the PMN system worked from the perspective of p r o t e c t i n g human health? As was noted e a r l i e r , there i s no way to d i r e c t l y measure the b e n e f i t s . Nine chemicals have been withdrawn from production as a r e s u l t of orders r e q u i r i n g more extensive t e s t i n g . Informal negotiations


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r e p o r t e d l y r e s u l t e d i n l a b e l l i n g and use r e s t r i c t i o n s or f u r t h e r t e s t i n g on about 60 others.(4^ There i s no way to assess the impact of these a c t i o n s on h e a l t h , since the content of these informal n e g o t i a t i o n s i s not p u b l i c knowledge. Although TSCA s e c t i o n 2 assigns the r e s p o n s i b i l i t y f o r developing adequate t o x i c i t y data to manufacturers and processors o f chemicals, i t has been s t a f f members of EPA who have been doing most of the t o x i c o l o g i c work under s e c t i o n 5. As of the end of 1980, two-thirds of PMNs submitted contained no t o x i c i t y information whatsoever. P r e l i m i n a r y s t a t i s t i c s from 1981 i n d i c a t e that a greater percentage of PMNs during the past year contained more t o x i c i t y t e s t i n g information. S t i l l , there were few chronic t o x i c i t y data. The l a c k of such information has meant that EPA s evaluations have had to be conducted on the basis of s t r u c t u r e - a c t i v i t y r e l a t i o n s h i p s . Such analyses involve comparing the PMN chemicals t o e x i s t i n g ones with s i m i l a r s t r u c t u r e s whose t o x i c i t i e s are known. S t r u c t u r e - a c t i v i t y studies are probably adequate f o r some substances. An example would be i n e r t polymers whose monomeric components have been w e l l - c h a r a c t e r i z e d t o x i c o l o g i c a l l y . For other chemicals, analyses based on a review of s t r u c t u r a l analogues may prove inadequate f o r a t l e a s t three reasons. F i r s t , minor molecular m o d i f i c a t i o n s may have a dramatic e f f e c t on t o x i c o l o g i c p r o p e r t i e s . For instance, 2,6-heptanedione i s r e l a t i v e l y harmless, while 2,5-heptanedione i s a neurotoxin.(_5) Second, there may not be any corresponding chemicals f o r which adequate chronic t o x i c i t y data e x i s t , since most e x i s t i n g chemicals have not been subject to such t e s t i n g . T h i r d , the molecular bases f o r chronic t o x i c e f f e c t s have been thoroughly worked out only f o r c e r t a i n c l a s s e s of mutagens, carcinogens, and a n t i m e t a b o l i t e s . Within these c l a s s e s , s t r u c t u r e - a c t i v i t y analyses can be u s e f u l i n i d e n t i f y i n g p o t e n t i a l "bad a c t o r s , " and, indeed, have led to informal requests f o r more extensive t o x i c i t y data or to s e c t i o n 5(e) orders. However, other mechanisms of c a r c i n o g e n i c i t y and mutagenicity, as w e l l as molecular explanations f o r t e r a t o g e n i c i t y , other adverse reproductive e f f e c t s , n e u r o t o x i c i t y and other chronic t o x i c e f f e c t s , have not been w e l l - c h a r a c t e r i z e d and cannot be incorporated i n t o s t r u c t u r e - a c t i v i t y reviews. Thus, i n the absence of t e s t i n g o f new chemicals f o r chronic t o x i c e f f e c t s , the PMN review process probably cannot provide an adequate screening at the present time. A former A s s i s t a n t Administrator f o r Toxic Substances observed that such analyses are "based upon a fundamental lack of information and data. This i n turn means that our information w i l l be h i g h l y u n c e r t a i n . " ^ ) On the other hand, p r i o r to the establishment of the PMN system, those chemicals for which EPA requested b e t t e r data might otherwise have been produced or d i s t r i b u t e d i n commerce with l i t t l e or no t e s t i n g whatever. 1


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While there has been l i t t l e regulatory a c t i o n under sections 5 and 6, TSCA may have had some i n d i r e c t health e f f e c t s . For example, chemical companies are more aware now than they were f i v e and a h a l f years ago, when TSCA was enacted, about chronic h e a l t h hazards i n the workplace. In general, t h e r e f o r e , workplace exposures to chronic t o x i c hazards are l i k e l y to be lower than i n the past. To some indeterminate extent, the compiling of the TSCA inventory and the TSCA r e p o r t i n g requirements may have played a r o l e i n c r e a t i n g a new awareness of chemical hazards. Other s o c i a l and l e g a l developments, however, have probably been more important i n the c r e a t i o n of such an awareness. Among such other i n f l u e n c e s would have to be included product l i a b i l i t y l i t i g a t i o n , OSHA r e g u l a t i o n s , union pressures, and a more general i n c r e a s i n g consciousness of p o t e n t i a l adverse e f f e c t s of chemical production and use, due to greater media coverage of these and r e l a t e d issues. Conclusion In t h i s paper I have t r i e d to show that measurement of h e a l t h b e n e f i t s a t t r i b u t a b l e to TSCA i s not f e a s i b l e . I hope that i n doing so I have not belabored the obvious. For new chemicals and f o r most e x i s t i n g chemicals, prospective e v a l u a t i o n of h e a l t h b e n e f i t s to be achieved by v a r i o u s exposure c o n t r o l s w i l l have to be based on e x t r a p o l a t i o n from m i c r o b i a l and animal data. However, while such e x t r a p o l a t i o n may be u s e f u l i n a q u a l i t a t i v e sense, q u a n t i t a t i v e r i s k assessment techniques involve considerable u n c e r t a i n t y , and i n any case have not been developed f o r chronic e f f e c t s other than cancer. Measurement or e s t i m a t i o n of h e a l t h impacts under TSCA would be premature, since r e l a t i v e l y l i t t l e has been done to regulate new or e x i s t i n g chemicals that could r e s u l t i n h e a l t h b e n e f i t s . The p r i n c i p a l exception to t h i s g e n e r a l i z a t i o n i s the ban on a e r o s o l uses of CFCs, whose chronic e f f e c t s on human h e a l t h derive from t h e i r environmental impact rather than d i r e c t biological toxicity. Compared with other environmental laws, such as the Clean A i r Act, the regulatory accomplishments of TSCA are somewhat i n s u b s t a n t i a l . A large part of the d i f f i c u l t y i n developing r e g u l a t o r y i n i t i a t i v e s under TSCA may be the lack of s p e c i f i c s t a t u t o r y direction. Preventing unreasonable r i s k s i s harder to implement as a p o l i c y than achieving percentage reductions i n a i r emissions of p a r t i c u l a r p o l l u t a n t s . The implementation of t h i s Act has therefore tended to focus on information-gathering o b j e c t i v e s rather than c o n t r o l a c t i v i t i e s . Deciding what are reasonable or unreasonable r i s k s depends on the quantity and q u a l i t y of i n f o r m a t i o n about c o s t s , r i s k s and b e n e f i t s of d i f f e r e n t l e v e l s of production and exposure c o n t r o l s with respect to a p a r t i c u l a r chemical or c l a s s of



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chemicals. To the extent that human epidemiological data are available, regulatory decisions should take them into account. However, to postpone such decisions (as has recently been done in the case of formaldehyde) on the grounds that ongoing or future epidemiologic studies will resolve critical health issues is, in my opinion, misguided. Such studies (particularly cohort mortality studies) typically take several years to complete, and may not yield definitive answers. Because of the inherent limitations of such investigations, the usual standard of proof of causation in epidemiology is consistent results from multiple studies conducted under different conditions. Such studies cannot disprove the carcinogenicity of a chemical—at best, they can indicate only an upper limit of risk. The expense and relative insensitivity of epidemiologic investigations insure that they will be of limited importance in identifying chronic health effects attributable to specific chemical exposures. Finally, a policy of delay pending the results of epidemiologic studies implies that an apparently higher threshold of certainty regarding health risks must be reached before initiating regulatory action. This would make sections 5 and 6 even more difficult to implement, and would portend that the health impact of TSCA will continue to be of marginal significance. Literature Cited 1.

2. 3.

4. 5.

Wilson, J. G. "Environment and Birth Defects;" Academic Press: New York, 1973, cited in Klingberg, Μ. Α.; Papier, C. M. "Environmental Teratogens;" in "Contributions to Epidemiology and Biostatistics;" Klingberg, Μ. Α., Weatherall, J.A.C., Eds., Karger: Basel, 1979. Bloom, A. D., Ed. "Guidelines for Studies of Human Populations Exposed to Reproductive Hazards;" March of Dimes Birth Defects Foundation: New York, 1981, passim. McCann, J.; Ames, B. "The Salmonella/Microsome Mutagenicity Test: Predictive Value for Animal Carcinogenicity;" in "Origins of Human Cancer;" Hiatt, Η. Η., Watson, J. D., Winsten, J. Α., Eds., Cold Springs Harbor Laboratory: Cold Springs Harbor, New York, 1977, pp. 1431-50. U.S. Environmental Protection Agency, Office of Toxic Substances. "Priorities for OTS Operation;" Washington, D.C., January 1982. Schaumburg, H. H.; Arezzo, J. C.; Markowitz, L.; Spencer, P. S. "Neurotoxicity Assessment at Chemical Disposal Sites;" in "Assessment of Health Effects at Chemical Disposal Sites;" Proceedings of a Symposium held in New York City on June 1-2, 1981, Lowrance, W. W., Ed., The Rockefeller University.


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Jellinek, S. D. Paper presented at Fuji Techno Systems Seminar on the Impact of Regulatory Requirements on Chemical Substances, Tokyo, Japan, Oct. 30, 1980, cited in U.S. Office of Technology Assessment, "Assessment of Technologies for Determining Cancer Risks from the Environment;" 1981, p. 148. November 22, 1982


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